WENDMANs VIEWS on NANOTECH

Rebuttal to NASA's Claim of No Effect of Earths' Magnetic Fields on Climate Change ( deleted by LinkedIn )

2021-10-04T13:39:00.005-07:00

NASA Climate Change Team is funny. This article of theirs is dead wrong missing all the salient details completely with whitewashing the real effects of actual salient changes in earth's magnetic field in south South Atlantic.

https://lnkd.in/de23bpzC

https://climate.nasa.gov/blog/3104/flip-flop-why-variations-in-earths-magnetic-field-arent-causing-todays-climate-change/ ( or why the earths magnetic field changes are in fact doing so and nothing from Carbon as a weakling greenhouse gas 100x smaller in GHG than CLOUDS despite NASA's blatant error )

The Nasa claims are out and out false by convenient omissions of facts throughout their blog post. Rife with irrelevant facts immaterial to actual causes of climate change.

My rebuttal follows ( deleted by LinkedIn and unclear if Google will permit either. )

Your ( the NASA ) article misses the main effects, huge drop in earth's magnetic field in south South Atlantic between South America and Southern most South Africa, and you totally ignore that a drop in earths regional local magnetic field only changes global warming by hugely affecting cloud formation and hence weather patterns across the world.

You skirt the issues with pablum of global averages and claiming that pole flips are the major effect which they are irrelevant presently. The sun's ions form clouds when hitting the earth's atmosphere and this is the major source of GHG warming and not carbon emissions in the slightest ( 1% effect of carbon bearing gases versus clouds and their formation and density )

It is convenient to ignore that the recent pandemic with reduction in carbon emissions had zero impact on climate change / chaos which is convenient to ignore but salient as a test of carbon based global warming ( none there in the slightest )

Your article skirts the salient actual mechanisms of magnetic field effects which is upon cloud formation and nothing else relevant. Your thesis is more like politics than science despite the source you are ( but are in fact not ).

I used to work in sustainability / climate change but found later it to be a farce as is your claim of no magnetic field effects ( surely dead wrong flat earth science bullshit ). Chew on this and fess up to the whitewashing of your non article, it is utter nonsense by avoidance of real science. Your article misses the main effects, huge drop in earth's magnetic field in south South Pacific between South America and South Africa, and you totally ignore that a drop in earths regional local magnetic field only changes global warming by hugely affecting cloud formation and hence weather patterns across the world.

You skirt the issues with pablum of global averages and claiming that pole flips are the major effect which they are irrelevant presently. The sun's ions form cloud when hitting the earth's atmosphere and this is the source of actual greenhouse gas warming and not carbon emissions in the slightest ( 1% effect of carbon bearing gases versus 100x GHG effects of clouds / water vapor, and the clouds formation and density )

It is convenient to ignore that the recent pandemic with reduction in carbon emissions had zero impact on climate change / chaos, which is convenient to ignore but salient as a test of carbon based global warming ( none there in the slightest )

Your article skirts the salient actual mechanisms of magnetic field effects which is upon cloud formation and nothing else relevant. The article's hypothesis is more like politics than science despite the source you are ( but seem not to be ).

I used to work in sustainability / climate change but found later it to be a farce as is your claim of no magnetic field effects ( surely dead wrong Carbon emissions is flat earth science bullshit ). Clouds are the main source of Green house Gas warming, not carbon bearing gases.

Chew on this and fess up to the whitewashing of your non article. It is utter nonsense by avoidance of the real science with smokescreen of irrelevant "facts". It is not about pole flips or magnetic field averages at issue, it is about the south South Atlantic's massive reduction in magnetic field's goings on.

Feel free to copy and repost this post as you deem useful and necessary.

I think what did it for me initially, was finding about about Penn State's Prof. Michael Mann's fraud ( and by association Al Gore's too ) validated in loss of a lawsuit by Prof. Dr. Tim Ball, an actual Climate Scientist trained in England and working in Winnipeg Canada. Dr. Mann ( no weather science training ) lost in BC Superior Court. Mann over 11 years, as Mann refused to hand over the input data used to Produce his falsehoods ( the infamous hockey-stick CO2 temperature graph ), and the BC Superior Court Judge deemed it false and unverifiable, unlike most all peer reviewed science is required to be vetted.

ECMO - an Effective ICU Aid in Treating Severe Swine Flu H1N1 Infection

2009-11-11T23:46:00.000-08:00

Recent news regarding treatment of severe H1N1 Swine Flu is interesting - promising but sobering.

In notable cases, H1N1 is a stubborn son of a bitch to shake off and get well from, and if not careful it can be overwhelming.

Many other pre-existing medical conditions can contribute to a stubborn case of H1N1.

But with a glimmer of hope, severe cases can be treated with somewhat better prognosis using a novel technique intensive care method called ECMO - ExtraCorporeal Membrane Oxygenation.

Essentially since H1N1 attacks the lungs, the virus is hitting the body's ability to deal with the infection itself by significantly impairing oxygen levels in the circulatory system, when stricken with a severe case of H1N1.

ECMO is an invasive means using a special catheter and external oxygenating membrane to assist in significantly reoxygenate the blood, deficient in oxygen from the reduced functioning of the lungs when infected with a stiff case of H1N1.

A procedure not for the faint of heart, expensive, and definitely a hospital beside procedure with its own risks. There is no huge hospital capacity for this treatment if a widespread pandemic might arrive, as the equipment is expensive and it is a somewhat risky procedure, due to the depth of insertion of a special catheter.

But the ECMO technique seems to be effective in treatment to help severe cases.

Here are some links to articles on ECMO for treatment of severe Swine Flu - H1N1 viral infections :

ECMO Is Better Than Conventional Ventilation For Treating Severe Respiratory Failure From Conditions Like Swine Flu

ECMO - Will We Have Sufficient Capacity for the Fall/Winter Flu Season?

ECMO respirators saving swine flu victims

Lung treatment for swine flu patients

Intensive care procedure saves lives: Swine flu study

Swine Flu: Everything You Need to Know

Swine Flu Pandemic Paradox Kills Few, Overwhelms ICUs

Swine flu - a new wall of silence

Swine flu - critical care bed shortage revealed

ECMO for Swine Flu - The Westmead Experience. Simon Zidar

Sturgeon: UK needs ECMO machines to treat swine flu cases Health minister makes plea for life-saving treatment

The ECMO Option

NOTABLE >>>>

Examining how swine flu killed a 'very healthy' teen
Complications from MRSA bacteria contribute to first local H1N1 fatality

Oxygen therapy in swine flu

News and Articles on ECMO - Surfwax

Mother positive after surviving virus

ECMO better for severe respiratory failure

Third Scot dies from swine flu in 24 hours

Sturgeon: UK needs ECMO machines to treat swine flu cases Health

Scots Researchers Pioneer Portable ECMO Treatment

Successful ECMO trial

Extracorporeal Membrane Oxygenation (ECMO) Can Be Invaluable During Influenza Season

High-tech treatment may save lives in swine flu outbreak

Swine flu deaths in Australia could have doubled without the use of a mechanical heart and lung treatment, says doctor.

Treatment for severe respiratory failure in swine flu is better with ECMO with conventional ventilation

Study provides clue to surviving Swine Flu

In any case, a simple means to help limit H1N1 severity, specifically by boosting the immune system, is to take large doses of VITAMIN D - of order of 1gm per day regularly, and if ill, taking 3 -> 4 gms per day, for short term of 3 -4 days duration.

Low vitamin D is apparently a simple risk factor for more severe prognoses of H1N1, and given that Vitamin D is cheap, USE IT.

Google VITAMIN D and H1N1 Swine Flu.

Hints that this Fall's / Winter's Swine Flu Might be Troubling

2009-06-09T05:46:00.000-07:00

from the Canadian Broadcasting Corporation's Manitoba Provincial News

Severe flu cases surge in Manitoba aboriginal community

Last Updated: Monday, June 8, 2009 | 4:05 PM CT

The Manitoba government is reporting a surge in the number of people requiring intensive care for influenza-like illnesses, particularly among a relatively young aboriginal population.

The vast majority of people reporting flu-like illnesses this spring are experiencing relatively mild cases and have not required hospitalization, Manitoba's chief medical officer of health, Dr. Joel Kettner, said at a press conference Monday afternoon.

'It's important to recognize that what we have observed is really more severe than what we would expect to see or what we have seen with typical seasonal influenza in the past.'—Dr. Joel Kettner, Manitoba's chief medical officer of health

However, there has been "an increased concentration of severe respiratory illness admitted to the intensive care units, which is higher in number than previous influenza outbreaks," officials with Manitoba Health and Healthy Living stated at the press conference.

As of Sunday night, 26 people were in the intensive care units on ventilators for flu-related reasons. It is expected many of them will be confirmed as cases of swine flu, or the H1N1 influenza A virus, officials said, noting more than half of the people are of aboriginal descent with an average age of 35, said Kettner.

The Winnipeg Regional Health Authority is taking steps to provide enough support to intensive-care units and prioritizing patients for personal-care home beds. The WRHA has also acquired 15 additional ventilators that will be put to use as needed, officials said.

Normally at this time of year, there are 30-35 patients using hospital ventilators for various reasons. The 26 people requiring the devices due to flu-like illnesses are in addition to those patients.

Typically, at this time of year, there are very few — if any — cases of severe flu.

"It's important to recognize that what we have observed is really more severe than what we would expect to see or what we have seen with typical seasonal influenza in the past," said Kettner.

Non-urgent surgeries may be postponed

The WRHA authority may also defer non-urgent surgical procedures that would normally require ICU care, said health officials.

As well, the Public Health Agency of Canada has provided three epidemiologists to Manitoba to assist in assessing cases of influenza-like illness.

There are 40 people in Manitoba with confirmed cases of swine flu. There were no new cases announced Monday.

Health authorities announced last week 27 new cases of the H1N1 virus in Manitoba, affecting people between the ages of one month and 56 years. Of the new cases, three patients required treatment in hospital.

Illnesses afflict communities of St. Theresa Point and Dauphin

As well, more than 200 people from St. Theresa Point First Nation, located about 500 kilometres from Winnipeg, reported being ill last week. Of those, 21 were transported to Winnipeg hospitals and two were confirmed to have swine flu. The majority of the ill are being treated in the community.

Also, a flu-like outbreak kept hundreds of students away from schools in Dauphin, Man., last week.

The provincial government is encouraging the public to maintain their immune systems by making healthy food choices, being physically active and getting enough sleep.

Other tips to prevent the spread of any germs include:

Covering a cough or sneeze, using a tissue or the inside of the elbow.
Washing hands often with soap and water, especially after a cough or sneeze.
Avoiding touching eyes, nose or mouth.

Those with flu-like symptoms, such as fever, cough, aches and fatigue, are most contagious for about one week. During that time, people are encouraged to stay home from school or work and limit contact with others to reduce the chance of spreading the virus.

Anyone seeking advice or care can call Health Links at 204-788-8200 or 1-888-315-9257.

Possible Light at the End of the MRSA tunnel ?

2008-04-07T23:27:00.000-07:00

here are some recent news releases about a strategy to possibly treat MRSA using extracts from Alligator blood. Now that would be neat ! Only hints of a strategy as yet but the old gators might have something to help out on the war on MRSA.

Alligator blood may beat MRSA

Alligator Blood May Put The Bite On Antibiotic-resistant Infections

Alligators To The Rescue

Alligator Blood May Lead to Powerful New Antibiotics

and here is the PI researcher

Mark Merchant at McNeese Univeristy

When is the Tipping Point on Gas Prices ?

2008-04-06T21:42:00.000-07:00

An interesting question to ask is - at what price level for US average Gasoline prices at the pump will serve to catalyze a change in automobile fueling? To biofuels or otherwise, that may render significant changes in the marketplace.

Will this take 5 dollar gasoline which is approaching with almost inevitability? Will industry - fueling and vehicle manufacturers actually react in a timely manner to make the most of the potential market opportunity? That biofuel manufacturers might have sufficient supplies of compatible fuels, or vehicles and fueling stations for alternative fuel vehicles might be available in sufficient quantity to have a material effect in providing a solution to power the economy?

Something to think about.

Visible speed of change in the market is presently slow, but will there be a solution in time to avoid an otherwise possible brake to the general economy? or a catalyst to a new vehicle and fueling infrastructure that takes up the slack?

not an idle question......

Adherex Receives Orphan Drug Designation for ADH-1 in Melanoma

2008-02-22T07:29:00.000-08:00

in plain english - after just a FDA Phase 1 B clinical testing, Adherex is granted the following status for ADH-1 in Melanoma combo with mephalan ( definition taken from FDA site )

""Orphan Product Designation

The Orphan Drug Act (ODA) provides for granting special status to a product to treat a rare disease or condition upon request of a sponsor. The combination of the product to treat the rare disease or condition must meet certain criteria. This status is referred to as orphan designation. Orphan designation qualifies the sponsor of the product for the tax credit and marketing incentives of the ODA. A marketing application for a prescription drug product that has been designated as a drug for a rare disease or condition is not subject to a prescription drug user fee unless the application includes an indication for other than a rare disease or condition.""

This milestone from the firm was a herculean task achieved by the brilliant team lead by Dr. Peters and Dr. Norris.

The news is so fresh firm this morning, that when I called their offices to congratulate the team, the receptionist was unaware that the FDA orphan drug status had been granted, nor did she understand the significance.

For a refresher of some things Adherex, google > "wendman adherex genesis" and read the post describing early days of the firm after renewal of management by the then fresh merger / takeover by the Oxiquant team.

This recent FDA orphan status approval is likely the mere beginning of realization of the promise of the firm's technology, a significant milestone in the quest by Prof. Orest Blaschuk of McGill and others to apply Cadherin technology to cancer treatments. It has been a long and arduous journey to this amazing first substantive FDA milestone by Adherex.

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

Press Release

Source: Adherex Technologies Inc.

Adherex Receives Orphan Drug Designation for ADH-1 in Melanoma
Friday February 22, 8:30 am ET

Additional centers to be added to ongoing Phase I/IIb trial

RESEARCH TRIANGLE PARK, NORTH CAROLINA--(MARKET WIRE)--Feb 22, 2008 -- Adherex Technologies Inc. (Toronto:AHX.TO - News)(AMEX:ADH - News), a biopharmaceutical company with a broad portfolio of oncology products under development, today announced that it has received orphan drug designation for ADH-1 from the U.S. Food and Drug Administration (FDA). The designation was granted for the use of ADH-1 in conjunction with melphalan for the treatment of Stage IIB/C, III, and IV malignant melanoma. Adherex is currently conducting a Phase IIb expansion trial in melanoma using systemic ADH-1 in combination with regional melphalan.

"FDA orphan drug designation for ADH-1 is an important asset in Adherex's development of this drug," said Dr. William P. Peters, CEO and Chairman of Adherex. "Orphan drug designation provides multiple incentives for Adherex to continue its accelerated development of ADH-1 for this significant clinical problem. Melanoma is a disease with an extremely poor prognosis and one in which the molecular target for ADH-1, N-cadherin, is frequently and often intensively expressed. N-cadherin is also intimately involved in the invasion and metastasis of melanoma. Our experience to date combining ADH-1 and melphalan for the treatment of in-transit melanoma has been very encouraging. To continue with the rapid development of this combination, two additional centers, Lehigh Valley and H. Lee Moffitt, have joined our Phase IIb trial which is ongoing at Duke and the MD Anderson. All four participating institutions are first-class medical centers with experienced investigators, and we are very pleased to have them involved in this development program."

The FDA orphan drug designation, administered by the Office of Orphan Products Development, provides potential incentives such as funding for clinical studies, study design assistance, waiver of FDA user fees, tax credits and, importantly, up to seven years of market exclusivity upon marketing approval.

Adherex is currently evaluating the synergy of systemic ADH-1 in combination with regionally-infused melphalan for the treatment of melanoma in a Phase I/IIb trial. The Lehigh Valley Hospital in Pennsylvania and the H. Lee Moffitt Cancer Center in Florida are being added as additional clinical trial sites to provide further multi-institutional experience. The Phase IIb portion of this trial is anticipated to complete patient accrual by approximately mid-2008, with data to be released at an appropriate scientific venue.

Another Phase I trial is also nearing completion at US Oncology in which systemic ADH-1 is being evaluated in combination with three different systemic chemotherapies: ADH-1 + docetaxel (Taxotere®), ADH-1 + carboplatin, and ADH-1 + capecitabine (Xeloda®). Subsequent Phase II and potential randomized, prospective trials of ADH-1 in combination with chemotherapy will be planned and based upon the results of the combination studies currently ongoing.

About Adherex Technologies

Adherex Technologies Inc. is a biopharmaceutical company dedicated to the discovery and development of novel cancer therapeutics. We aim to be a leader in developing innovative treatments that address important unmet medical needs in cancer. We currently have multiple products in the clinical stage of development, including eniluracil, ADH-1 and sodium thiosulfate (STS). Eniluracil, an oral dihydropyrimidine dehydrogenase (DPD) inhibitor, was previously under development by GlaxoSmithKline for oncology indications. ADH-1, our lead biotechnology compound, selectively targets N-cadherin, a protein present on certain tumor cells and established blood vessels that feed solid tumors. STS, a drug from our specialty pharmaceuticals pipeline, protects against the disabling hearing loss that can often result from treatment with platinum-based chemotherapy drugs. With a diversified portfolio of unique preclinical and clinical-stage cancer compounds and a management team with expertise in identifying, developing and commercializing novel cancer therapeutics, Adherex is emerging as a pioneering oncology company. For more information, please visit our website at www.adherex.com.

This press release contains forward-looking statements that involve significant risks and uncertainties. The actual results, performance or achievements of the Company might differ materially from the results, performance or achievements of the Company expressed or implied by such forward-looking statements. Such forward-looking statements include, without limitation, those regarding the development plans of the Company and the expected results of our development. We can provide no assurance that such development will proceed as currently anticipated or that the expected results of such development will be realized. We are subject to various risks, including the uncertainties of clinical trials, drug development and regulatory review, the early stage of our product candidates, our reliance on collaborative partners, our need for additional capital to fund our operations, our history of losses, and other risks inherent to the biopharmaceutical industry. For a more detailed discussion of related risk factors, please refer to our public filings available at www.sedar.com and www.sec.gov.

Contact:

     Contacts:
   Adherex Technologies Inc.
   D. Scott Murray
   Senior Vice President, Corporate Development
   919-484-8484
   info@adherex.com

Source: Adherex Technologies Inc.

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here are links to prior Adherex posts of mine

http://mark-nano.blogspot.com/2008/01/adherex-announces-phase-iib-expansion.html
http://mark-nano.blogspot.com/2007/06/adherex-trials-recruiting-and-closed.html
http://mark-nano.blogspot.com/2007/06/porf-orest-blaschuks-prolific-patents.html
http://mark-nano.blogspot.com/2007/01/adherex-phase-1-clinical-trial-for.html
http://mark-nano.blogspot.com/2005/12/cadherins-and-looming-revolution-in.html
http://mark-nano.blogspot.com/2006/03/adherex-receives-regulatory-approval.html

Recent 2008 winter cold snap helping Arctic sea ice

2008-02-18T06:41:00.000-08:00

Some folks in the north recently have been to put it mildly freezing their rears off. The past month of January 2008 has seen in the arctic temperatures well in the -30s C and -40s C range since late January, with the mercury dipping past -50 C in some areas. ref CBC article "Recent cold snap helping Arctic sea ice, scientists find" of Feb 15th 2008

Satellite telemetry image data is indicating that the cold snap is helping the Arctic ocean
ice increase in area by about 750,000 square miles, in comparison to average winter icepack area in the prior three years. For reference, the low in summer 2007 was 1.61 million square miles, so this recent cold snap icepack growth is not immaterial, but it is as yet unclear if this is any kind of trend. Not likely, more likely it is just a normal blip long overdue.

It is nice to get some real winter weather again, much like in the early 70's of my long lost youth. Makes for great skiing and other winter sports.

Adherex Announces Phase IIb Expansion of ADH-1 Combination Study in Melanoma

2008-01-30T17:22:00.000-08:00

Press Release

Source: Adherex Technologies Inc.

Adherex Announces Phase IIb Expansion of ADH-1 Combination Study in Melanoma
Thursday January 17, 4:40 pm ET

RESEARCH TRIANGLE PARK, NORTH CAROLINA--(MARKET WIRE)--Jan 17, 2008 -- Adherex Technologies Inc. (Toronto:AHX.TO - News)(AMEX:ADH - News), a biopharmaceutical company with a broad portfolio of oncology products under development, today announced that it has completed patient enrollment in the Phase I portion of the clinical trial of systemic ADH-1 in combination with isolated limb infusion melphalan and is proceeding with a multi-institutional Phase IIb expansion of the study.

"We have completed the Phase I portion of this study at Duke with a satisfactory safety profile at all three ADH-1 doses tested and initial tumor response data that have exceeded our expectations based upon the center's historical experience with mephalan alone," said William P. Peters, MD, PhD, Chairman and CEO of Adherex. "However, while positive, we consider the data to be early and limited both in terms of the number of patients and the length of follow-up. We have therefore decided to expand the trial to provide additional patients and more information for planning potential pivotal trials."

The Company plans to expand the clinical trial of systemic ADH-1 in combination with isolated limb infusion melphalan for the treatment of melanoma by up to 25 additional patients. Further, the M.D. Anderson Cancer Center in Houston, Texas has been added as an additional clinical trial site to gain multi-institutional experience. This Phase IIb expansion of the trial is anticipated to complete patient accrual by approximately mid-2008 and data will be released at an appropriate scientific venue.

About Adherex Technologies

This press release contains forward-looking statements that involve significant risks and uncertainties. The actual results, performance or achievements of the Company might differ materially from the results, performance or achievements of the Company expressed or implied by such forward-looking statements. Such forward-looking statements include, without limitation, those regarding the development plans of the Company and the expected timing or results of our development. We can provide no assurance that the development will proceed as currently anticipated or that the expected timing or results of the development will be realized. We are subject to various risks, including the uncertainties of clinical trials, drug development and regulatory review, the early stage of our product candidates, our reliance on collaborative partners, our need for additional capital to fund our operations, our history of losses, and other risks inherent to the biopharmaceutical industry. For a more detailed discussion of related risk factors, please refer to our public filings available at www.sedar.com and www.sec.gov.

Contact:

     Contacts:
   Adherex Technologies Inc.
   D. Scott Murray
   Senior Vice President, Corporate Development
   919-484-8484
   info@adherex.com

Source: Adherex Technologies Inc.

PhotoTechEDU Digital Photography Technology Short Course Videos - Google Tech Talks on YouTube

2008-01-22T17:16:00.000-08:00

Here is a series of video classes given at Google campus covering many subjects in Digital Photography and Imaging - the class series is called PhotoTechEDU - online at YouTube - in the Google Tech Talk topical section.

This series of engineering grade lectures covers in depth many aspects of digital imaging, image processing/ editing and photography.

The main entry to all of Google Tech Talks is linked above in the blog post title

The YouTube PhotoTechEDU videos are linked below .... you will need a broadband connection

PhotoTechEDU Day 1: Photo Technology Overview
PhotoTechEDU Day 2: Photo Technology Overview Continued
PhotoTechEDU Day 3: Ray Tracing, Lenses, and Mirrors
PhotoTechEDU Day 4: Contrast, MTF, Flare, and Noise
PhotoTechEDU Day 5: Silicon Image Sensors
PhotoTechEDU Day 6: Digital Camera Image Processing...
PhotoTechEDU Day 7: Lossy Image Compression
PhotoTechEDU Day 8: Diffraction and Interference in Imaging
PhotoTechEDU Day 9: Amateur Astrophotography
PhotoTechEDU Day 10: Image Compression Part 2
PhotoTechEDU Day 11: Document Image Analysis with Leptonica
PhotoTechEDU Day 12: High Dynamic Range Image Capture
PhotoTechEDU Day 14: Exposing Digital Forgeries from...
PhotoTechEDU Day 16: Multi-viewpoint Mosaics
PhotoTechEDU Day 18: Non-destructive, Selective, Editing...
PhotoTechEDU Day 19: Inkjet printing...
PhotoTechEDU Day 22: Measuring, Interpreting and...
PhotoTechEDU Day23: Raw Files and Formats
PhotoTechEDU Day 25: Open-source-based high-resolution...
PhotoTechEDU Day 26: Image quality testing and...
PhotoTechEDU Day27: Focus on Resolution
PhotoTechEDU Day 28: "Capturing more Light": Pragmatic...
PhotoTechEDU Day 29: Photographing VR Panoramas
PhotoTechEDU Day 30: Imaging optics for the next decade
PhotoTechEDU Day 31 - Color Balance: Babies, Rugs & Sunsets

CleanTech Google Tech Talks on YouTube

2008-01-21T11:35:00.000-08:00

Here is a partial list of videos of interesting presentations given at Google on various topics related to Clean Technologies. Makes for fascinating viewing from the numerous thought provoking speakers.

If one has access to a broadband connection be sure to have a look at these talks.

The page title link is to the entire topics of Google campus Tech Talks - with an emphasis on software, but covering many fascinating subject materials.

The talks liked below are those I have found so far that relate to clean technologies.

Biofuels: Think Outside The Barrel Vinod Khosla

Learn about Solar Energy and Solar Panel Installation...

Electricity use and efficiency of servers and data centers: A review of recen...

Geoengineering Earth's Climate

Should Google Go Nuclear? Clean, cheap, nuclear power...

Electricity from Orbit: The case for R & D

Windbelt Cheap Generator Alternative

My own solar system: Installing solar panels at my house

Climate Change and Health

Ocean Wave Energy

Tango EV Electric Sports Car

Fission is the new fire

Shames Mountain the Place Where POWDER Snow Falls Profusely

2008-01-02T18:36:00.000-08:00

So if you are a real powder hound snow skier and lust after the fluffy white stuff, unfettered by long lines or crowds, and are able to revel in amazing vistas and superb slopes, check out Shames Mountain in Terrace British Columbia, where snow falls even when further south it does not.

Here is an excellent blog showing hints of the astounding ski runs

Advances in Resuscitation Science ( revival after heart attacks etc. )

2007-07-14T23:54:00.000-07:00

Recent medical research is questioning fundamental ideas about how to best revive victims of heart attacks and oxygen deprivation. Dr. Lance Becker of Penn is on the forefront of research that indicates opportunities in patient revival exist where otherwise current practice of administering concentrated oxygen at normal body temperatures might actually be finalizing or contributing to unnecessary deaths.

A key technical observation seems to be that the rate/(concentration) at which oxygen is returned to the patient in present revival protocols, if too fast as presently quite common practice, seems to inadvertently kill the patient by permanently triggering a death sequence initiated by cell mitochondria.

Dr. Becker observes that cooling the patient and slowing the return of oxygen with revived heartbeat, might inhibit the catalysis of permanent death by a mitochondrial switch, and seems to offer increased chances of revival from death in numerous cases otherwise conventionally deemed hopeless.

Sounds like fantastic science and great experimental observations.

Here are some interesting links

Recent Newsweek article The Science of Death: Reviving the Dead
Dr. Becker's profile at Penn
and his research group
New York Times Chill Therapy Is Endorsed for Some Heart Attacks
Univ of Chicago Rapid Cooling Technique May Save Victims of Sudden Cardiac Death
Univ of Chicago Induced hypothermia is underused after resuscitation from cardiac
Wake County EMS Blog ICE - Induced Cooling by EMS
an Emergency Medical Service that is implementing these methods
University of Pittsburgh Health Sciences matching faculty found for hypothermia, induced
Laura’s Psychology Blog Rethinking death…
Maddy's ramblings straight to the heart of the matter
RN Web The big chill: Improving the odds after cardiac arrest
The Hypothermia Network
American Heart Association Therapeutic Hypothermia After Cardiac Arrest
Society of Cardiovascular Anesthesiologists Recommendation for Application of Therapeutic Hypothermia to Cardiac Arrest Victims
American College of Emergency Physicians Focus On: Therapeutic Hypothermia
Pulmonary Reviews THERAPEUTIC HYPOTHERMIA FOR TRAUMATIC BRAIN INJURY: GETTING IT RIGHT
EMS Responder COLD Care Wake County EMS develops protocols for induced hypothermia
Massachusetts General Hospital Hypothermia after Cardiac Arrest
Northern Hypothermia Network Protocols

8 commercial medical equipment suppliers for Critical Hypothermia induction needed to cool the body to prevent rapid permanent death from mitochondrial catalysis are linked below.

Of only about 225 hospitals, out of more than 5,700 hospitals in the United States have this critical equipment needed for saving lives from permanent death.

Ask if your local hospitals have this critical hypothermia(cooling) inducing equipment, if they don't, then bang the doors of complacency DOWN, crack open the inertia of the physicians, and get the hospital to both BUY the hypothermia induction equipment, and for staff in emergency medicine to read the later and earlier articles linked above, and many protocols to start saving heart attack victims NOW.

If your local hospital does not do this quickly, then plaster copies of these articles throughout hospital department staff mailboxes, and get your local newspapers to write articles about Dr. Becker's work ASAP.

If all it took was cooling your loved one soon after an otherwise fatal heart attack to bring them back to life, and your hospital did not do this just because of complacency with current commonly accepted but WRONG therapies, shame them into learning Dr. Becker's techniques NOW, even for ambulance treatments.

Cooling Device Manufacturers and Assigned Patents (note these may in some cases include patents unrelated to patient cooling)

Alsius Corporation (Irvine, CA; maker of endovascular cooling catheter system)
71 patents
Medivance, Inc. (Louisville, CO; maker of external cooling system)
27 patents
Radiant Medical (Redwood, CA; maker of endovascular cooling catheter system)
47 patents
Innercool Medical (San Diego, CA; maker of endovascular cooling catheter system)
78 patents
EMCOOLS (Austria; maker of external cooling blanket)
none in US under either EMCOOLS nor Emergency Medical Cooling Systems
note I have not searched at WIPO nor EU patent office, and firm is based in Austria
Adroit Medical(Loudon, TN; maker of internal and external cooling devices)
5 patents
MTRE Advanced Technologies - link from Adroit Medical
3 patents
Gaymar Industries
43 patents

A presentation by Penn "Hypothermia after cardiac arrest"

here is a list of hypothermia clinical protocols from different hospitals - links from Penn

Here is a list of research journal articles using the Medivance system for inducing hypothermia for medical treatment benefits.

Publications Referring to Medivance Arctic Sun^®

Calver P, Braungardt T, Kupchik N, Jensen A, Cutler C. The big chill: improving the odds after cardiac arrest. RN 2005; 68:58-62.
Carhuapoma JR, Gupta K, Coplin WM, Muddassir SM, Meratee MM. Treatment of refractory fever in the neurosciences critical care unit using a novel, water-circulating cooling device: a single-center pilot experience. J Neurosurg Anesthesiol 2003; 15:313-318.
Geocadin RG, Carhuapoma JR. Medivance Arctic Sun Temperature Management System. Neurocrit Care 2005; 3:63-67.
Holden M, Makic MB. Clinically induced hypothermia: why chill your patient? AACN Adv Crit Care 2006; 17:125-132.
Ly HQ, Denault A, Dupuis J, Vadeboncoeur A, Harel F, Arsenault A, Gibson CM, Bonan R. A pilot study: The Noninvasive Surface Cooling Thermoregulatory System for Mild Hypothermia Induction in Acute Myocardial Infarction (The NICAMI Study). Am Heart J 2005; 150:933.
Mahmood MA, Voorhees ME, Parnell M, Zweifler RM. Transcranial Doppler ultrasonographic evaluation of middle cerebral artery hemodynamics during mild hypothermia. J Neuroimaging 2005; 15:336-340.
Mayer SA, Kowalski RG, Presciutti M, Ostapkovich ND, McGann E, Fitzsimmons BF, Yavagal DR, Du YE, Naidech AM, Janjua NA, Claassen J, Kreiter KT, Parra A, Commichau C. Clinical trial of a novel surface cooling system for fever control in neurocritical care patients. Crit Care Med 2004; 32:2508-2515.
Scott BD, Hogue T, Fixley MS, Adamson PB. Induced Hypothermia Following Out-of-Hospital Cardiac Arrest; Initial Experience in a Community Hospital. Clin Cardiol. 29, 525-529 2006.
Zweifler RM, Voorhees ME, Mahmood MA, Alday DD. Induction and maintenance of mild hypothermia by surface cooling in non-intubated subjects. J Stroke Cere Dis 2003; 12:237-243.
Zweifler RM, Voorhees ME, Mahmood MA, Parnell M. Rectal Temperature Reflects Tympanic Temperature During Mild Induced Hypothermia in Nonintubated Subjects. J Neurosurg Anesthesiol 2004; 16:232-235.
Zweifler RM, Voorhees ME, Mahmood MA, Parnell M. Magnesium sulfate increases the rate of hypothermia via surface cooling and improves comfort. Stroke 2004; 35:2331-2334.

Here are more general research references

Two books

Therapeutic Hypothermia (Hardcover) by Stephan A. Mayer (Editor), Daniel I. Sessler (Editor)

Therapeutic Hypothermia (Molecular & Cellular Biology of Critical Care Medicine) (Hardcover) by Samuel A. Tisherman (Editor), Fritz Sterz (Editor)

There seem to be a few other research efforts in this area of controlled resuscitation by hypothermia.

This appears to be excellent innovative medical science, that might well soon transform patient prognoses for the better.

Here is an excerpt from the recent Newsweek article of July 2007
By Jerry Adler with Matthew Philips, Joan Raymond and Julie Scelfo

"How long has it been since you've read an article about heart attacks that didn't mention saturated fats? Our age is obsessed with "health," but when health fails, the last line of defense is in the emergency room, where doctors patrol the border between life and death—a boundary that they have come to see as increasingly uncertain, even porous. This is a story about what happens when your heart stops: about new research into how brain cells die and how something as simple as lowering body temperature may keep them alive—research that could ultimately save as many as 100,000 lives a year. And it's about the mind as well, the visions people report from their deathbeds and the age-old questions about what, if anything, outlives the body.

It begins with a challenge to something doctors have always been taught in medical school: that after about five minutes without a pulse, the brain starts dying, followed by heart muscle—the two most voracious consumers of oxygen in the body, victims of their own appetites. The emerging view is that oxygen deprivation is merely the start of a cascade of reactions within and outside the cells that can play out over the succeeding hours, or even days. Dying turns out to be almost as complicated a process as living, and somehow, among its labyrinthine pathways, Bondar found a way out.

Monica tried to recall what she had learned in a CPR class decades earlier. She bent over Bondar and began pushing down on his chest, then rushed back to the kitchen to dial 911. "My husband is dying!" she gasped to the operator.

Compressing Bondar's chest would have sent a trickle of blood to his brain, supplying a fraction of its normal oxygen consumption, not enough to bring him back to consciousness. But the West Deptford police station was only three blocks away, and within two minutes of Monica's call three officers arrived with a defibrillator. They placed the pads on Bondar's chest, delivered two jolts of electricity to his heart, and got a pulse back. Soon paramedics arrived with oxygen and rushed him to a nearby community hospital. The report Monica received there after an hour was equivocal: Bondar was "stable"—his heart rate and blood pressure back to near normal—but he was still in a coma. It was then that Monica made a decision that may have saved his life. She asked that her husband be moved the 15 miles to Penn, the region's leading university hospital.

Dr. Lance Becker, director of Penn's year-old Center for Resuscitation Science, frequently dreams about mitochondria: tubular structures within cells, encasing convoluted membranes where oxygen and glucose combine to produce the energy the body uses in moving everything from molecules across cell membranes to barbells. Recently mitochondria have been in the news because they have their own DNA, which is inherited exclusively down the female line of descent, making them a useful tool for geneticists and anthropologists.

But Becker is interested in mitochondria for another reason: he believes they are the key to his audacious goal of tripling the time during which a human being can go without a heartbeat and still be revived. That the five-minute rule is not absolute has been known for a long time, and the exceptions seem to involve low temperatures.

Children who fall through ice may survive unexpectedly long immersions in cold water. On Napoleon's Russian campaign, his surgeon general noticed that wounded infantrymen, left on the snowy ground to recover, had better survival rates than officers who stayed warm near the campfire. Becker is hoping to harness this effect to save lives today.

Becker is 53, slender and boyish in a way that belies his thinning hair; his typical greeting to colleagues is a jaunty "What's up, guys?" For his lab he has assembled a high-powered team from a wide range of specialties, including a brilliant young neuroscientist, Dr. Robert Neumar; an emergency-medicine specialist, Dr. Ben Abella; plus cardiologists, biochemists, bioengineers and a mouse-heart surgeon. His associate director, Dr. Vinay Nadkarni, comes from pediatrics.

Becker has in effect re-created at Penn, on a more ambitious scale, the laboratory he founded in 1995 at the University of Chicago, with a grant of $50,000 from the philanthropist Jay Pritzker. Ten years earlier Pritzker had walked into the emergency room at Chicago's Michael Reese Hospital complaining of chest pains, and crumpled to the floor. Becker resuscitated him, the beginning of both a rewarding friendship (Pritzker lived for 14 more years) and a new direction for Becker's career. "Every day since then," he says, "I would go home and wonder why Jay Pritzker got a second chance and so many other people didn't."

Becker's interest in mitochondria reflects a new understanding about how cells die from loss of circulation, or ischemia. Five minutes without oxygen is indeed fatal to brain cells, but the actual dying may take hours, or even days. Doctors have known for a long time that the consequences of ischemia play out over time. "Half the time in cardiac arrest, we get the heart going again, blood pressure is good, everything is going along," says Dr. Terry Vanden Hoek, director of the Emergency Resuscitation Center at the University of Chicago, "and within a few hours everything crashes and the patient is dead."

It took some time, though, for basic research to supply an explanation. Neumar, working with rats, simulates cardiac arrest and resuscitation, and then examines the neurons at intervals afterward. Up to 24 hours later they appear normal, but then in the next 24 hours, something kicks in and they begin to deteriorate. And Dr. James R. Brorson of the University of Chicago has seen something similar in neural cells grown in culture; deprive them of oxygen and watch for five minutes, or even much longer, and not much happens. "If your car runs out of gas, your engine isn't destroyed, it just needs fuel," he says.

Cell death isn't an event; it's a process. And in principle, a process can be interrupted. The process appears to begin in the mitochondria, which control the cell's self-destruct mechanism, known as apoptosis, and a related process, necrosis.

Apoptosis is a natural function, destroying cells that are no longer needed or have been damaged in some way. Cancer cells, which might otherwise be killed by apoptosis, survive by shutting down their mitochondria; cancer researchers are looking for ways to turn them back on. Becker is trying to do the opposite, preventing cells that have been injured by lack of oxygen from, in effect, committing suicide.

It's a daunting problem. "We're asking the questions," says one leading researcher, Dr. Norm Abramson of the University of Pittsburgh. "We just haven't found the answers." Until recently, the conventional wisdom was that apoptosis couldn't be stopped once it was underway. It proceeds by a complex sequence of reactions—including inflammation, oxidation and cell-membrane breakdown—none of which seems to respond to traditional therapies. Becker views cell death in cardiac arrest as a two-step process, beginning with oxygen deprivation, which sets up the cell for apoptosis; then the heart starts up again and the patient gets a lungful of oxygen, triggering what is called reperfusion injury. The very substance required to save the patient's life ends up injuring or killing him.

Researchers have ransacked their arsenal of drugs looking for ways to interrupt this sequence. Over the years they have tried various techniques on nearly 100,000 patients around the world. None has shown any benefits, according to Dr. A. Michael Lincoff, director of cardiovascular research at the Cleveland Clinic. But one thing does seem to work, something so obvious and low-tech that doctors have a hard time accepting it. It's hypothermia, the intentional lowering of body temperature, down to about 92 degrees Fahrenheit, or 33 Celsius.

Research by a European team in 2002 reported favorable results from a controlled study of several hundred cardiac-arrest patients; subjects who were cooled both had better survival rates and less brain damage than a control group. The first big international conference on cooling took place in Colorado this February. Despite favorable studies and the endorsement of the American Heart Association, "we were concerned that [hypothermia] still wasn't catching on," says the conference organizer, Dr. Daniel Herr of Washington Hospital Center in Washington, D.C.

The two leading manufacturers of cooling equipment—Medivance, Inc., and Gaymar Industries—say only about 225 hospitals, out of more than 5,700 in the United States, have installed machines for inducing hypothermia. Herr says the treatment requires a "paradigm shift" by doctors. "People have a hard time believing that something as simple as cooling can make such a big difference." Perhaps that's because no one quite understands how cooling works. It appears to work globally on apoptosis, rather than on any of the individual biochemical pathways involved in it. "The short answer is, we don't know," says Neumar.

Researchers have also been looking into the way patients get oxygen during resuscitation, and afterward. The treatment goal in cardiac arrest has been to rush oxygen to the heart and brain at maximum concentration; the mask the paramedic pops on your mouth supplies it at 100 percent. "The problem with that," says Dr. Ronald Harper of UCLA, "is it does some very nasty things to the brain." Harper believes a mixture containing 5 percent carbon dioxide would buffer those negative effects, but the idea is still controversial.

At the University of Maryland, Dr. Robert Rosenthal and Dr. Gary Fiskum have been looking into whether oxygen concentrations should be dialed down much more aggressively. In their lab, dogs with induced cardiac arrest recovered better when they were taken off full oxygen after just 12 minutes, compared with an hour in the control group. Rosenthal says in practice patients sometimes are left on pure oxygen for much longer than an hour—in one hospital he studied, for as much as 121 hours.

At Penn, Becker's Resuscitation Center coordinates with the Emergency Department on a protocol for cooling patients in cardiac arrest. "We look at their prior mental state," says Dr. Dave Gaieski. "If someone was in a coma in a nursing home, we're not going to cool them." The same goes for patients whose hearts stopped for longer than an hour. Since 2005 just 14 patients have met Penn's criteria for hypothermia. Eight survived, six of them with complete recovery. No one knows how many others were saved by cooling around the country.

Bondar arrived at Penn at about 1:30 a.m., still comatose, minutes ticking away while he was evaluated for cooling. Once the decision was made, the team sprang into action, injecting him with an infusion of chilled saline—two liters at about 40 degrees—then wrapping him in plastic tubes filled with chilled, circulating water. Becker believes, based on animal work, that cooling patients even sooner—ideally, on their way to the hospital—would be even more effective, and part of the work of his lab involves perfecting an injectable slurry of saline and ice that could be administered by a paramedic. Bondar was kept at about 92 degrees for about a day, then allowed to gradually return to normal temperature. He remained stable, but unresponsive, over the next three days, while Monica stayed at his bedside. She finally went home Sunday evening, and was awakened Monday by a call from the hospital that she was sure meant bad news.

"Guess what?" said the voice on the other end. "Bill's awake."

Bondar's first words were, "How did I get here?" He had lost track of a full week, from about two days before his heart attack until he woke up. That's not unusual; short-term memory is often the first casualty of cardiac arrest. Neumar says certain cells in the hippocampus, the part of the brain that forms new memories, are for unknown reasons especially sensitive to ischemia. Another Penn patient, Sean Quinn, was 20 and a student at Drexel University when he went into unexplained cardiac arrest in 2005. He was one of the earliest patients cooled at Penn, and there's reason to believe that it saved his life, but the continuing memory deficit has prevented him from returning to college."

........................

"We are, Becker believes, at the forefront of a revolution in emergency medicine destined to save millions of lives in the years ahead. This is doctoring at its most basic, wresting people back from death. "I have been fighting with death for 20 years," he says. "And I'll keep doing it, I think, until I meet him in person."

Bless you Dr. Becker .... we need more physicians using your excellent research work NOW.

Generous Gift from Virgil Elings & Betty Elings Wells to UCSB for California NanoSystems Institute

2007-06-27T16:35:00.000-07:00

UCSB Receives $12.5 Million Gift from Virgil Elings and Betty Elings Wells to Support Research and Innovation at the California NanoSystems Institute

June 4, 2007

	Click for downloadable imageBetty Elings Wells Credit: Randall Lamb Click for downloadable imageVirgil Elings Credit: Jeff Clark Click for downloadable imageThe California Nanosystems Institute at UC Santa Barbara will be named Elings Hall as depicted

(Santa Barbara, Calif.) – Virgil Elings and Betty Elings Wells have made a $12.5 million gift to UC Santa Barbara to support pioneering research at the California NanoSystems Institute (CNSI). In recognition of their recent gift, the new building that is home to the prestigious California Institute for Science and Innovation will be named in honor of Virgil Elings.

The CNSI is a multidisciplinary research partnership between UCLA and UC Santa Barbara established by the state in 2000 with the support of the state legislature and California industry. By exploring the power and potential of manipulating structures molecule-by-molecule, the CNSI is on its way to creating revolutionary new materials, devices, and systems that will enhance virtually every aspect of our lives – helping to drive California's economy through innovations in medical delivery and health care, powerful new information technologies, energy efficient devices, environmental improvements, and more.

The Elings and Wells gift is the largest contribution to The Campaign for UC Santa Barbara, which seeks to raise $500 million to ensure UCSB's excellence for future generations. With this recent gift, a total of $415 million has been contributed to the campaign by alumni and friends.

"UCSB is sincerely grateful to Virgil and Betty for their extraordinary generosity, we are pleased to have our building for the California NanoSystems Institute bear the Elings name," said UCSB Chancellor Henry T. Yang. "Virgil and Betty's vision for our campus began over 40 years ago, with their shared goals of scholarship and innovation in scientific and business pursuits. As a UCSB professor of physics, Virgil Elings had the foresight to bring the best science graduates and quality research and design together. This integration of science and industry proved to be a winning combination, as it is today at the California NanoSystems Institute."

Virgil Elings is a former UCSB professor of physics who made fundamental contributions leading to the scientific revolution at the nanoscale. In 1987, he co-founded Digital Instruments (DI), the first company to make the power of atomic scanning probe microscopy readily available to scientists and engineers, enabling them to view and explore nanoscale features and structures never seen before – a critical starting point in nanoscience and nanotechnology.

"Our company, Digital Instruments, was a part of the beginning of what people today call nanotechnology," said Virgil Elings. "We also made our money in Santa Barbara, and this is one of many gifts we are making to give back to the community in which we have prospered."

During their marriage, Betty Elings Wells was a real estate investor and business partner with her former husband, Virgil Elings. Together, they launched numerous entrepreneurial ventures, including Digital Instruments, where she was office manager and secretary of the corporation.

Wells said that she made the gift to UCSB to honor her former husband and mentor, the devoted employees at Digital Instruments – many of whom were UCSB graduates – , and to support the university she has been affiliated with since her arrival in Santa Barbara 40 years ago.

"Virgil has made a huge impact on the world by advancing nanoscience, and I think his name should be carried forward," said Wells. "He is a brilliant scientist, inventor, and educator who was able to accomplish what many men dream about and few make real. My desire to help fund education and research in Elings Hall is also an expression of gratitude to our employees at Digital Instruments, since the building will be dedicated to them as well. It is my hope that UCSB will continue the level of exciting research that transpired within the walls of Digital Instruments."

The CNSI building, now known as Elings Hall, stands near the eastern entrance to the campus and is the hub for nanoscience research at UCSB. The institute fosters collaborative research and builds on the substantial and collective strengths of the College of Engineering and the sciences. It also brings together innovators from California universities, industries, and national laboratories and trains the next generation of innovators and entrepreneurs.

The Elings and Wells gift will significantly advance nanoscience research at the institute as well as in engineering and the sciences. It will provide $9 million in unrestricted support to develop and implement innovative research and education initiatives and create new laboratory facilities. In addition, a $3.5 million endowment for the CNSI will generate ongoing resources to build and sustain state-of-the-art programs and to allow rapid response to new scientific and educational opportunities.

Evelyn Hu, UCSB professor of electrical and computer engineering and scientific director of the CNSI, noted that the factors leading to Digital Instruments' extraordinary success – innovation, ingenuity, hard work, dedication, and bringing together a core group of people who share a vision – "map so well onto what is underway today at CNSI."

"Virgil and Betty's gift and the confidence that it implies through its support of this new enterprise at UCSB is coming exactly at the right time, allowing us to bring nanoscience research to the next level," said Hu. "We are now well poised to launch a set of research and education programs that may define critical pathways in science and engineering for the next decade and beyond."

About the Donors

Virgil Elings and Betty Elings Wells are partners in their philanthropic support of the California NanoSystems Institute at UC Santa Barbara and several community projects, including Elings Park in Santa Barbara and the Elings Aquatic Center at Dos Pueblos High School.

Their $12.5 million gift to the campus is the largest contribution to The Campaign for UC Santa Barbara. With this recent gift, they join UCSB's Lancaster Society Leaders, which recognizes cumulative donors to the campus of $10 million and above.

In recognition of their generosity, the building housing the California NanoSystems Institute will be named Elings Hall.

Virgil Elings, who earned his Ph.D. in physics from the Massachusetts Institute of Technology, was a professor of physics at UCSB for more than 20 years before he co-founded Digital Instruments (DI) in 1987 with Gus Gurley, a UCSB alumnus.

Digital Instruments had a simple goal – to make the power of scanning probe microscopy readily available to scientists and engineers, enabling them to view and explore nanoscale features and structures never seen before. That year, they constructed the first commercially successful scanning tunneling microscope. It was a critical starting point for nanoscience and nanotechnology.

DI received several awards for business and engineering excellence, including three Photonics Circle of Excellence awards and local, state, and national new product awards from the Society of Professional Engineers. In 1992, DI was ranked No. 150 in the INC 500 list of the 500 fastest growing private companies in the U.S. In 1998, the corporation merged with Veeco Instruments, a leading supplier of instrumentation for the research, semiconductor, data storage, telecommunications, and other industries. By combining the technological strengths of each company, the newly formed company added the distinction of being the world leader in 3-D surface metrology.

Elings, who holds 42 patents, served as the company's president and chairman of the board until his retirement in 1999.

At UCSB, he has been a mentor for the Technology Management Program. He has also been a guest speaker in the program's entrepreneur lecture series and in the Economics Department.

Elings, who resides in Santa Ynez, is a rancher and lavender farmer. He displays his collection of vintage and rare motorcycles and European race bikes at his motorcycle museum in Solvang.

Betty Elings Wells is a successful real estate investor and property manager in the Santa Barbara area, Iowa, and Arizona.

She earned a B.A. in history with a minor in political science from the State College of Boston, while her former husband, Virgil Elings, was completing his Ph.D. in physics at the Massachusetts Institute of Technology.

After moving to Santa Barbara, Wells began her property management career in Isla Vista, building investment capital for the couple's business ventures in which she was actively involved. For Digital Instruments, the company co-founded by Virgil Elings, she was office manager and secretary of the corporation.

At UCSB, Wells served two terms as president of the Faculty Women's Club, and continues her involvement with the organization as a generous benefactor of student scholarships awarded by the club.

Betty Wells and Virgil Elings have two children, Michael and Jeffrey, who are both engineers. Michael graduated with a degree in electrical engineering from the University of Colorado, and Jeffrey was awarded a degree in mechanical engineering from UC San Diego.

Wells resides in Goleta.

###

ED - as typical, I tend to post on what I have known or had some connection to. I worked for Virgil directly as a grunt engineer, doing my nanotech process and device development in scanning microscope nano probes for some 6 years. The best scientist businessman I have ever met or had the pleasure of working for. BAR NONE. Pragmatic and down to earth to a fault ("don't ship till it works", "you don't know anything until it works completely"(ie don't exaggerate incremental partial successes and don't be prematurely content till it is DONE), competitive and thoughtful like few others.

Hated business BS puffery that did not contribute to profits, saw and understood and lived the imperative of healthy ongoing innovating, inventing and patenting, ( and taught many to understand this ). The old R&D Magazine editorial of his - Invent or Die for Technology Startups and Ventures, was tempered with the sage understanding of don't just patent willy nilly, but do so strategically ( he rarely wanted to patent / or bother with patenting until something worked - ie was worth putting the effort into protecting, rather than mere speculation of same ) and yet he licensed when strategic and worthwhile too. Oh and read the patent literature profusely, else how the heck can you invent? (file cabinet drawerS full of patents of competitors) This imperative for reading profusely is lost upon so many, as to defy common sense, but he made up for others weaknesses in spades !

Best of all is Virgil's priceless wit, sly mischievous smile, and sage guidance of many many folks over the years. There was an interesting anecdote about a dart board in his visitors chair in his office (next to a restored motorcycle), in days during the transition to the acquisition by the new acquiring firm, that was priceless and remains true to this very day. Darts eh? (or will that be a sales forecast you want Eduardo? ..... I'll give you darts instead.) Yet Virgil knew the imperative of a vigorous competitive sales staff and hired one of the best in the sales business ...

And to those who love motorcycles, Virgil always had bikes that he just completed restoration of in the company building and always one or 2 parked in his office. He raced competitively in a classic bike race circuit often with his son Jeff, and his collection of superbly restored historically significant mostly racing motorcycles, can be seen here at the Solvang Motorcycle Museum.

What a guy I tell you, brilliant beyond compare and despite at times a well known gruff outward demeanor, a heart of gold inside, and one of the most productive applied technologists I have ever seen. ( and success in applied technology innovation is the true litmus test of brilliance far beyond theory alone or half completed development, outside of commercial realm) Virgil is the real deal, a one in a million.

Under Virgil's sage leadership, the speed that Digital Instruments innovated at, could blind you if you bothered to look, and innovated successfully enough to both capture and retain 50% world wide SPM microscope market share. Moreover this invention machine achieved doing the unthinkable - a US firm owning the majority of SPM instrument market inside Japan due to the unparalleled reputation the instruments and company garnered in the worldwide scientific community.

Virgil is the real McCoy !

Adherex Trials - Recruiting and Closed listed at Clinicaltrials.gov on June23 2007

2007-06-23T17:57:00.000-07:00

Include trials that are no longer recruiting patients.

8 studies were found.

1.	No longer recruiting	A Study of the Safety and Effects of ADH-1 Given Intravenously as a Single Agent Condition: Neoplasms
2.	Terminated	A Study of the Safety and Effects of ADH-1 Given Daily to Subjects With Solid Tumors Condition: Neoplasms
3.	No longer recruiting	Study of ADH-1 Given Intravenously to Patients With Solid Tumors Condition: Neoplasms
4.	Recruiting	A Study of 5 Fluorouracil and the Anti-Tumor Activity of ADH300004 and 5 Fluorouracil in Subjects With Incurable Solid Tumors Condition: Neoplasms
5.	Completed	A Study of ADH300004 in Surgically Resected Primary or Metastatic Colorectal Cancer and Liver Biopsy, or Planned Hepatic Resection Condition: Neoplasms
6.	Recruiting	A Phase 1 Dose Escalation Study of ADH 1 in Combination With Carboplatin, or Docetaxel or Capecitabine Condition: Neoplasms
7.	Recruiting	A Phase 1 Dose Escalation Study of ADH-1 in Combination With Normothermic Isolated Limb Infusion of Melphalan Condition: Neoplasms
8.	Recruiting	A Study of the Safety, Pharmacokinetics, and Anti-Tumor Activity of ADH300004 and 5-Fluorouracil Administered Orally in a Weekly Schedule to Subjects With Locally Advanced, Recurrent, or Metastatic Hepatocellular Carcinoma Condition: Hepatocellular Carcinoma

Prof. Orest Blaschuk's Prolific Patents in Cadherin Cell Adhesion Science

2007-06-22T03:00:00.000-07:00

Prof Orest Blachuk of McGill University Dept. of Urology has racked up an impressive portfolio of patents and patent applications. He is cofounder of Adherex Technology and its scientific luminary. Adherex is on the path to some significant advances in cancer treatment prognoses.

1	US7138369	Compounds and methods for modulating apoptosis
2	US7122623	Compounds and methods for modulating cell adhesion
3	US20060183884	Compounds and methods for modulating cell adhesion
4	US7063842	Compounds and methods for inhibiting the interaction between .alpha.-catenin and .beta.-catenin
5	US6967238	Compounds and methods for modulating cell adhesion
6	US6962969	Compounds and methods for modulating nonclassical cadherin-mediated functions
7	US20050222037	Compounds and methods for modulating VE-cadherin-mediated function
8	US20050215482	Compounds and methods for modulating OB-cadherin-mediated function
9	US20050203025	Compounds and methods for modulating nonclassical cadherin-mediated functions
10	US-APP20050163786	Compounds and methods for modulating adhesion molecule function
11	US6914044	Compounds and methods for modulating cell adhesion
12	US20050129676	Compounds and methods for modulating functions of classical cadherins
13	US20050037973	Compounds and methods for cancer therapy
14	US20040254099	Compounds and methods for modulating beta-catenin mediated gene expression
15	US6830894	Compounds and methods for modulating claudin-mediated functions
16	US20040248219	Methods for diagnosing and evaluating cancer
17	US20040248220	Methods for diagnosing and evaluating cancer
18	US20040229811	Compounds and methods for modulating desmosomal cadherin-mediated functions
19	US6806255	Compounds and methods for modulating adhesion molecule function
20	US6797807	Compounds and methods for cancer therapy
21	US20040175361	Compounds and methods for modulating functions of nonclassical cadherins
22	US6780845	Compounds and methods for cancer therapy
23	US20040142854	Compounds and methods for stimulating beta-catenin mediated gene expression and differentiation
24	US20040132651	Compounds and methods for regulating cell adhesion
25	US6756356	Compounds and methods for modulating claudin-mediated functions
26	US20040106545	Compounds and methods for modulating cell adhesion
27	US6723700	Compounds and methods for modulating claudin-mediated functions
28	US20040058864	Peptidomimetic modulators of cell adhesion
29	US6706685	Compounds and methods for stimulating .beta.-catenin mediated gene expression and differentiation
30	US6682901	Methods for diagnosing and evaluating cancer
31	US6683048	Compounds and methods for stimulating gene expression and cellular differentiation
32	US6680175	Methods for diagnosing and evaluating cancer
33	US6677116	Methods for treating cancer by modulating .beta.-catenin mediated gene expression
34	US20040006011	Peptidomimetic modulators of cell adhesion
35	US20030236186	Compounds and methods for inhibiting the interaction between alpha-catenin and beta-catenin
36	US20030229199	Compounds and methods for modulating nonclassical cadherin-mediated functions
37	US20030224978	Compounds and methods for modulating apoptosis
38	US6638911	Compounds and methods for modulating desmosomal cadherin-mediated functions
39	US6610821	Compounds and methods for modulating endothelial cell adhesion
40	US6593297	Compounds and methods for inhibiting cancer metastasis
41	US20030109454	Compounds and methods for modulating adhesion molecule function
42	US6569996	Antibody that specifically binds to the cadherin-5 cell adhesion recognition sequence
43	US20030096746	Compounds and methods for inhibiting cancer metastasis
44	US6562786	Compounds and methods for modulating apoptosis
45	US20030087811	Compounds and methods for cancer therapy
46	US20030082166	Compounds and methods for modulating nonclassical cadherin-mediated functions
47	US6551994	Compounds and methods for inhibiting the interaction between .alpha.-catenin and .beta.-catenin
48	US20030065136	Compounds and methods for modulating cell adhesion
49	US20030027761	Compounds and methods for modulating junctional adhesion molecule-mediated functions
50	US20030013655	Compounds and methods for regulating cell adhesion

51	US20020193294	COMPOUNDS AND METHODS FOR MODULATING CLAUDIN-MEDIATED FUNCTIONS
52	US20020168761	Peptidomimetic modulators of cell adhesion
53	US20020169106	COMPOUNDS AND METHODS FOR INHIBITING CANCER METASTASIS
54	US6472368	Compounds and methods for modulating adhesion molecule function
55	US6472367	Compounds and methods for modulating OB-cadherin mediated cell adhesion
56	US20020151475	Compounds and methods for modulating cell adhesion
57	US6465427	Compounds and methods for modulating cell adhesion
58	US20020146687	METHODS FOR DIAGNOSING AND EVALUATING CANCER
59	US20020123044	METHODS FOR DIAGNOSING AND EVALUATING CANCER
60	US6433149	Compounds and methods for inhibiting cancer metastasis
61	US6417325	Compounds and methods for cancer therapy
62	US6391855	Compounds and methods for modulating junctional adhesion molecule-mediated functions
63	US6358920	Compounds and methods for modulating nonclassical cadherin-mediated functions
64	US6346512	Compounds and methods for modulating cell adhesion
65	US6333307	Compounds and method for modulating neurite outgrowth
66	US6326352	Compounds and methods for modulating cell adhesion
67	US6310177	Compounds and methods for modulating tissue permeability
68	US6303576	Compounds and methods for modulating .beta.-catenin mediated gene expression
69	US6277824	Compounds and methods for modulating adhesion molecule function
70	US6248864	Compounds and methods and modulating tissue permeability
71	US6207639	Compounds and methods for modulating neurite outgrowth
72	US6203788	Compounds and methods for regulating cell adhesion
73	US6169071	Compounds and methods for modulating cell adhesion
74	US6110747	Compounds and methods for modulating tissue permeability
75	US6031072	Compounds and methods for modulating cell adhesion

What a heck of a substantive patent portfolio.

Dr. Michael Kaplitt's Viral DNA Gene Therapy for Parkinsons

2007-06-21T21:44:00.000-07:00

Dr. Michael Kaplitt, a relatively young physician, leads a small new firm called Neurologix. The notable very preliminary result of the firm, is what seems to be very promising results from early stage testing of a means to attempt to inhibit the destructive effects of Parkinsons disease.

Here is a link to the article recently published in Lancet
An interview with a physician interpreting the preliminary results by Neurologix

Kaplitt's work is a novel effort to use a genetically modified virus as the vector to introduce modified DNA to afflicted brain tissues, in a manner that reverses a fundamental mechanism of Parkinsons disease, a deficit of GABA gamma-aminobutyric acid, the major inhibitory neurotransmitter in the brain. Note - Kaplitt is clearly the neurosurgical expert, and Matt During seems to be key to the use of a virus as a vector gene delivery system

When GABA is too weakly secreted, and hence in deficit, Parkinsons results, with its evident excessive uncontrolled neural activity of motor function. Proper levels of GABA appear to be useful if not critical to control the disease.
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About Parkinson’s disease (conventional description)

Parkinson’s disease is a debilitating neurological disorder; a person’s lifetime risk of getting it is 1 chance in 1,000. The risk of developing Parkinson’s disease increases as one gets older. The symptoms are a resting tremor, slowness of movement, muscular rigidity, and an unstable posture. Not all of these four symptoms need to be present for a diagnosis of Parkinson’s disease.

Medication can help relieve the symptoms of Parkinson’s disease, especially in the early stages. As the disease progresses, the symptoms are more difficult to control. Surgery is then an option for some Parkinson’s disease patients.

Parkinson’s disease is caused by the loss of brain cells that make dopamine. Dopamine is a neurotransmitter that is needed for normal movement. The majority of these cells need to be lost before Parkinson’s disease symptoms are seen.

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Neurologix's technique directly causes more GABA to be synthesized where it is needed, thus helping to calm the STN subthalmic nucleus over-activity - which is a core characteristic of Parkinsons, if not possibly an alternative interpretation of the actual disease itself.

The only technical point I sense I do not comprehend is how injecting a genetically modified virus into the brain tissue where GABA is synthesized, might not cause GABA synthesis in other tissues more widely than intended?

Can Kaplitt's methods result in overproduction of GABA, or alternately, can the genetically engineered viral infection only result in turning back on GABA production where it might otherwise only occur in a healthy patient, so the effect might prove to be self regulating in desirable manners? It appears at first glance to not be a concern.

It might be that Kaplitt has found a partial DNA fragment that can only result in GABA production where it originally occurred, and nowhere else in the body. If so, this might overcome plausible stumbling blocks of other genetically engineered attempts at treating Parkinson's.

The details of why the research team thinks there is a good case for this to work well over long term for the patient, might be interesting to learn about.

[ed - June 25 2007 - Mike Kaplitt's dad Dr. Martin Kaplitt who is COB of Neurologix just called me, to help clarify my questions re why this works, and does not cause an overproduction of GABA. Two main salient points - 1 - The blood brain barrier prevents the gene carrier of modified AAV Virus to not pass beyond the brain cavity, with the surgical procedure used to introduce the virus into the brain, and notably in proximity to the desired brain tissue desired to infect with the modified gene. 2 - GABA competes with some other factor (which Martin mentioned but I do not remember the specific name to) such that there is a constant regulation of free GABA versus the competing effect, with the result this works.

Martin also remarked that Dopamine based strategies for treating Parkinsons have their limits(described in the Neurologix patents) and this GABA restoration used by Neurologix is fundamentally a new strategy to treat Parkinson's not merely noted by the use of Gene Therapy, nor merely by the less common use of modified AAV vector as the means to infect the desired Gene per se, but notable in that the therapy targets an entirely new pathway to treat Parkinsons via the GABA route. ]

The experiment results were in a small phase 1 FDA test, where it is important to note that FDA Phase 1 clinical testing is mostly intended to address potential toxicity or dangers of a new pharma compound treatment, and not specifically intended to address a new treatment's efficacy.

Nevertheless, when something is novel and effective, there often are often hints in preliminary FDA Phase 1 tests that indicate the potential promise of a new method or pharma compound.

My impression is this is possibly stunning.

As yet far too early to claim a cure, but if ever a Phase 1 hinted that Parkinsons might have met its match, this hints of possible substantive success. This is discussed in an article at MSNBC and here in some greater depth in a recent Weill Cornell Neurosurgery news release dated June 21st 2007.

Kaplitt appears to have the insight, experimental expertise (Genetic engineering and Neurology) and deep technical understanding needed to tame the monster that Parkinsons is. I wish him and the Neurologix team all the best of luck in developing the real innovations undertaken.

Dr. Kaplitt seems to be a researcher who both observes closely, and tests his novel ideas well. Moreover the man has got game - patent game, and given he got his MD in 1995, he is likely going to be a very prolific innovator over his career.

Here are most of Kaplitt's patents and patent applications at present

1	US20070059290	Transcriptional regulation of target genes
2	US20060228776	PINK-1 promoter
3	US20060210538	Use of apotosis inhibiting compounds in degenerative neurological disorders
4	US20060129126	Infusion device and method for infusing material into the brain of a patient
5	US20060099179	Glutamic acid decarboxylase (GAD) based delivery system
6	US20050025746	Glutamic acid decarboxylase (GAD) based delivery systems
7	US6780409	Glutamic acid decarboxylase (GAD) based delivery system
8	US20030152914	Method for generating replication defective viral vectors that are helper free
9	US20030087264	Transcriptional regulation of target genes
10	US6503888	AAV-mediated delivery of DNA to cells of the nervous system
11	US20020091094	Glutamic acid decarboxylase (GAD) based delivery system
12	US6180613	AAV-mediated delivery of DNA to cells of the nervous system
13	US6162796	Method for transferring genes to the heart using AAV vectors
14	US6106824	Expression of growth associated protein B-50/GAP-43 in vitro and in vivo
15	US6040172	Defective DNA viral vector comprising a neural tissue-specific promoter for in vivo expression of a gene

I will also point out that the scientific advisory board (SAB) at Neurologix is substantive. Kaplitt has put together a SAB intellectual team that is notable for the breadth of the participants talents, most if not all experience directly relevant to the firm's efforts.

The Neuroligix SAB is comprised of people who include
1 - a surgeon for Parkinson's disease, who also is a member of the scientific advisory board for the Michael J. Fox Foundation,
2 - a molecular neuroscientist,
3 - a psychiatrist highly skilled in neuropsychopharmacology,
4- a neurologist specializing in molecular and cellular changes in neural networks, focused on Epilepsy,
5 - a pioneer of gene therapy of neurological diseases and human brain microdialysis,
6 - a Professor of Molecular and Cellular Neuroscience,
aside from Kaplitt's obvious brilliance.

Here are the company bios followed by academic research summaries of the SAB members, including that of the founder Dr. Michael Kaplitt

Andres M. Lozano, M.D. Ph.D.
Dr. Lozano is the acknowledged world leader in surgery for Parkinson's disease and other movement disorders, and is also an expert in surgery for epilepsy. Dr. Lozano has published over 100 papers and has recently edited a major book on this subject. He also directs a laboratory engaged in pioneering research attempting to identify potential causes of Parkinson's Disease. He is currently Professor of Neurosurgery and holds the Ronald Tasker Chair in Stereotactic and Functional Neurosurgery at The University of Toronto. Dr. Lozano received his MD from the University of Ottawa and Ph.D. from McGill University. He completed a residency in Neurosurgery at the Montreal Neurological Institute prior to joining the staff at The University of Toronto. He has held numerous official positions in Neurology and Neurosurgery societies, and is currently the Secretary of both the American Society for Stereotactic and Functional Neurosurgery and the World Society for Stereotactic and Functional Neurosurgery. He also serves on the editorial board of several major journals, and is a member of the scientific advisory board for the Michael J. Fox Foundation.

ACADEMIC RESEARCH SUMMARY -

Keywords: Parkinson's disease, neuroprotection, neurophysiology, dopamine, functional neurosurgery

Research Interests

Parkinson's Disease and Functional Neurosurgery
Our laboratory is interested in understanding the causes of Parkinson's disease and in developing novel treatments. Our experiments aim at uncovering the mechanisms through which dopamine neurons die and developing novel strategies to prevent their death using experiments on models of Parkinson's disease.

A second focus of our laboratory is functional neurosurgery. In these studies we aim to improve our understanding of how disruptions in neural activity in the brain of human patients lead to subthalamic nucleus and various areas of the cortex to obtain direct recordings to cellular activity in these nuclei. These approaches help understand the pathogenesis of these disorders and are leading the development of novel treatment strategies.

Pubmed Publications

Perform an automatic PubMed search of this researcher's publications.

Andrew Brooks, Ph.D.
Dr. Brooks is the Director of the Bionomics Research and Technology Center (BRTC) at the Environmental and Occupational Health Science Institute of the University of Medicine and Dentistry of New Jersey. He is also the Associate Director of Technology Development at Rutgers University's Cell and DNA Repository and an Associate Professor of Environmental Medicine and Genetics at UMDNJ. Dr. Brooks is a molecular neuroscientist whose research focuses on deciphering the molecular mechanisms that underlie memory and learning. These studies investigate gene-environment interactions in the context of aging, neurodegenerative disease and neurotoxicant exposure. His group is also involved in the development of novel informatics approaches to better understand complex genomics-based data sets for diagnostic development.

ACADEMIC RESEARCH SUMMARY - Dr. Brooks’ laboratory hasthree main areas of interest. First, his group works on decipheringthe molecular mechanisms that underlie memory and learning.They utilize a variety of technologies for genetic modificationas well as investigate gene–environment interactions inthe context of aging, neurodegenerative disease and neurotoxicantexposure. Their research utilizes many high-throughput genomicsbased technologies to study these areas. Second, his group isinvolved in the development of novel informatics approachesto better understand complex genomics-based data sets. The teamhas recently developed a novel method for interpreting complexgene expression data sets as a function of biological relevance.This approach is being utilized both in the basic science andclinical arenas. Lastly, Dr. Brooks’ team is engaged ina number of technology development programs. Currently, theyare developing new applications in the area of transcript profilingand protein profiling that can be applied to both standard andnovel technology platforms. More recently Dr. Brooks has beenappointed Director of the AMDeC Microarray Resource Center,which helps coordinate all micro array and genomics relatedactivities for New York State. Dr. Brooks has been activelyinvolved with ABRF for a number of years and currently chairsthe Microarray Research Group.

Eric J. Nestler, M.D., Ph.D.
Dr. Nestler is the Lou and Ellen McGinley Distinguished Chair in Psychiatric Research and Professor and Chairman of the Department of Psychiatry at the University of Texas Southwestern Medical Center. From 1992 to 2000, he was Director of the Abraham Ribicoff Research Facilities and of the Division of Molecular Psychiatry at Yale University. Dr. Nestler's research focuses on ways in which the brain responds to repeated perturbations under normal and pathological conditions, with a primary focus on drug addiction and depression. He has authored or edited seven books, and published more than 300 articles and reviews and 267 abstracts relating to the field of neuropsychopharmacology.

Dr. Nestler's awards and honors include the Pfizer Scholars Award (1987), Sloan Research Fellowship (1987), McKnight Scholar Award (1989), Efron Award of the American College of Neuropsychopharmacology (1994) and Pasarow Foundation Award for Neuropsychiatric Research (1998).

ACADEMIC RESEARCH SUMMARY - My laboratory is interested in understanding the molecular and cellular basis of neural and behavioral plasticity. One major focus of our group is on drug addiction: to characterize molecular and cellular adaptations induced in the brain after chronic administration of opiates, cocaine or other drugs of abuse. An important feature of this work is to relate specific molecular and cellular adaptations to drug-induced alterations in neuronal function and complex behavior that define an addicted state. A second major focus is on the long-term effects of stress and antidepressants on the brain in animal models of depression. We utilize methods of viral-mediated gene transfer and genetic mutations in mice (in particular, inducible, cell type-specific mutations) to establish causal relationships among molecular, cellular, and behavioral levels of analysis.

Daniel H. Lowenstein, M.D., Ph.D.
Dr. Lowenstein is Professor and Vice Chairman in the Department of Neurology at the University of California, San Francisco (UCSF), Founder and Director of the UCSF Epilepsy Center, and Director of Physician-Scientist Training Programs for the UCSF School of Medicine. He was previously at Harvard Medical School as the Dean for Medical Education and Carl W. Walter Professor of Neurology. During 2004, Dr. Lowenstein served as the President of the American Epilepsy Society.

His interests include the molecular and cellular changes in neural networks following seizure activity and injury and the contribution of neurogenesis to seizure-induced network reorganization in the adult central nervous system. He has received several national awards for excellence in teaching and numerous academic honors and awards, including the American Epilepsy Society's 2001 Basic Research Award. Most recently, Dr. Lowenstein's research has centered on approaches designed to advance understanding of the complex genetics that are thought to underlie a substantial portion of idiopathic epilepsies. In collaboration with other epilepsy researchers, he is working on the design of a venture entitled "The Epilepsy Phenome/Genome Project," with the intention of collecting detailed phenotypic and genotypic information on more than 5,000 patients in order to identify genetic mutations and post-translational mechanisms contributing to epilepsy.

Matthew J. During, M.D., DSc.

Dr. During is an internationally recognized leader in the fields of gene therapy of neurological diseases and human brain microdialysis, areas in which he is a world pioneer. He is currently Professor of Molecular Medicine and Pathology at University of Auckland in New Zealand and Director of the Molecular and Translational Neuroscience Laboratory, Department of Neurological Surgery, Weill Medical College of Cornell University. He also served as Director of the CNS Gene Therapy Center and Professor of Neurosurgery at Jefferson Medical College from 1998 through 2002.

At the University of Auckland, Dr. During directs major neuroscience and gene therapy programs. One of his most recent and important accomplishments in gene therapy field was completion of the first non-cancer CNS gene therapy trial, a subject of major articles in publications such as Science. In addition, Dr. During made a significant breakthrough in the development of a novel vaccine for stroke and epilepsy (again published in Science) as well as a novel oral gene delivery method for diseases like diabetes.

In addition to research and teaching, Dr. During has authored more than 100 groundbreaking papers in the fields of neuroscience, molecular biology, gene transfer and therapy, including many articles in such prestigious journals as Nature, Science, Nature Genetics and Nature Medicine.

Dr. During is a graduate of University of Auckland School of Medicine, and did further postgraduate training at M.I.T. (1985 - 1987), Harvard Medical School (1986 - 1989) and at Yale (1988 - 1989). He was on the Faculty at Yale University from 1989 through 1998, where he directed a program on the molecular basis of learning and memory, and headed Yale's first gene therapy protocol.

ACADEMIC RESEARCH SUMMARY - Research Areas - Our research interests are broad and range from the study of the molecular basis of learning and memory, to gene therapy of neurological disorders. The main common theme is the use of somatic cell gene transfer to study neuronal physiology and to treat human disease. Our research covers the full spectrum from molecular biology through to animal behaviour and human clinical trials. For our gene therapy program, in the first instance "proof of principle" experiments are conducted to test therapeutic concepts in an attempt to obtain phenotypic correction in models of neurological disease. Promising approaches are advanced to human clinical trials. Many of our research projects involve collaborations and our laboratory is of international standing and forms a key role in a major network of mammalian brain gene interventionists. Our gene therapy group is an international collaborative group of investigators at Auckland and Philadelphia.

Vectorology program
Our vectorology program is primarily orientated around adeno-associated virus (AAV) as a vector gene delivery system. Our efforts are focused on improvements in these systems including increased efficiency of gene transfer/transduction; stable and regulated transgene expression; gene silencing; vector targeting; and decreased toxicity/pathogenicity of the vector systems as well as development of animal models of neurological disease, including Parkinson's, Huntington's and Alzheimer's Disease.

Parkinson's Disease
We have an extensive Parkinson's Disease research program, ranging from generating novel genetic models of Parkinson's Disease, investigation of mechanisms underlying Parkinson's neuropathology, as well as the development of therapeutic strategies. Early work focused on dopamine replacement and growth factor strategies. More recently, we have developed a strategy to reset brain circuitry altered in Parkinson's. Following promising preclinical studies, we have obtained FDA approval for the world's first human Phase I clinical trial using a gene therapy approach for Parkinson's Disease.

Alzheimer's Disease/Huntington's Disease
New research directions for our lab include developing genetic models of Huntington's and Alzheimer's Diseases and the development of therapeutic strategies for these diseases.

Learning and Memory
We have a long-standing interest in the molecular mechanisms of learning and memory. Our current approach is focused on altering candidate molecular gene expression (signal transduction enzymes and transcription factors) in specific brain regions using viral vectors and defining alterations in brain neurochemistry and physiology which mediate phenotypic effects on learning and memory.

Epilepsy
Our laboratory has a long-standing interest in the use of microdialysis in the conscious human brain. Our major efforts have been to determine the mechanisms underlying epilepsy specifically focusing on the GABergic and glutamatergic transmitter systems. In addition we have looked at effects of novel antiepileptic drugs (AEDs) on brain chemistry to define mechanisms of action as well as the use of AEDs as probes to look at receptor and transporter changes in the human epileptic brain. We are currently developing approaches for gene therapy of the epilepsies.

Vaccines for neurological disease
We are characterising genetic and protein vaccine approaches as potential prophylactic approaches for stroke and epilepsy.

Effects of Environment on Brain Structure and Function
We have an interest in the effects of environment on brain structure and function. We and others have found that complex social and physical stimulation increases new cell birth within the hippocampus. This process called neurogenesis has implications for learning and memory as well as neurological disease.

Michael G. Kaplitt, M.D. Ph.D.
Dr. Michael Kaplitt is an expert and innovator in gene therapy who was among the first scientists to publish on the use of viruses for direct gene delivery in the living brain. Dr. Kaplitt published a breakthrough study on the use of defective herpes simplex virus vectors in the brain, and along with Dr. During, he was the lead author on the first publication reporting on the use of adeno-associated virus (AAV) vectors in the brain.

Dr. Kaplitt is currently Assistant Professor of Neurosurgery, Director of Stereotactic and Functional Neurosurgery and Director of the Laboratory of Molecular Neurosurgery at Weill Medical College of Cornell University. He is also Clinical Assistant Attending, Division of Neurosurgery, Dept. of Surgery at Memorial-Sloan Kettering Cancer Center, and Adjunct Faculty, Laboratory of Neurobiology and Behavior at The Rockefeller University. In addition to his neurosurgical practice and laboratory research, Dr. Kaplitt has received several awards for his work and has authored more than 40 papers and book chapters on gene therapy and stereotactic and functional neurosurgery, including articles which have appeared in scientific magazines such as Nature Genetics and Proceedings of the National Academy of Sciences.

Following his neurosurgical residency, Dr. Kaplitt completed a fellowship in Stereotactic and Functional Neurosurgery with Dr. Andres Lozano at the University of Toronto, where he received sub-specialty training in surgery for Parkinson's Disease, other movement disorders, pain and epilepsy. Dr. Kaplitt, together with Dr. Arthur Loewy, edited an internationally recognized book on the subject of gene therapy in the brain, titled "Viral Vectors" and published by Academic Press. Due to the success of the first volume, Dr. Kaplitt and Dr. During are currently working on a revised volume at the request of the publisher. Dr. Kaplitt graduated magna cum laude in molecular biology from Princeton University.

Dr. Kaplitt received his MD degree from Cornell University School of Medicine in 1995, where he completed his residency in Neurosurgery. Dr. Kaplitt also received a Ph.D. degree in molecular neurobiology from Rockefeller University, where he performed his groundbreaking work in viral gene transfer to the brain.

Paul Greengard, Ph.D. Chairman

Dr. Paul Greengard is the Vincent Astor Professor of Molecular and Cellular Neuroscience at The Rockefeller University. He began his exploration of nerve cells in 1948 when he joined the Johns Hopkins biophysics laboratory then headed by Detlev Bronk. After receiving his Ph.D. from Johns Hopkins in 1953, Greengard spent five years in England receiving advanced training in brain biochemistry at the University of London, at Cambridge University, and at the National Institute of Medical Research.

Upon his return to the United States, Greengard worked as Director of the Department of Biochemistry at Geigy Research Laboratories, in Ardsley, New York for eight years. He has remained intensely interested in the applications of basic scientific knowledge to the development of therapeutic agents for treatment of various neurological and psychiatric diseases. In 1967, he left the pharmaceutical industry to return to academia. He spent one year as Visiting Professor at Albert Einstein College of Medicine and Vanderbilt University School of Medicine. From 1968 to 1983 Greengard served as Professor of Pharmacology and Psychiatry at Yale University, at which time he moved to his current position at The Rockefeller University.

Over the years, Greengard’s achievements have earned him many distinguished awards including the Metropolitan Life Foundation Award for Medical Research, The Charles A. Dana Award for Pioneering Achievements in Health, the Ralph W. Gerard Prize in Neuroscience from the Society for Neuroscience, The National Academy of Sciences Award in the Neurosciences, the Bristol-Myers Award for Distinguished Achievement in Neuroscience Research, the 3M Life Sciences Award of the Federation of American Societies for Experimental Biology. In the year 2000, Greengard was awarded the Nobel Prize in Physiology or Medicine.

ACADEMIC RESEARCH SUMMARY -

The goals of our research group are to understand more fully the molecular basis of communication between neurons in the adult mammalian brain and to elucidate the molecular defects responsible for various neurological and psychiatric disorders.

Elucidation of the mechanism of action of neurotransmitters, therapeutic agents and drugs of abuse. Work over the past three decades has demonstrated that nerve cells communicate with each other through two mechanisms, referred to as fast and slow synaptic transmission. Fast-acting neurotransmitters, e.g., glutamate (excitatory) and GABA (inhibitory), achieve effects on their target cells within one millisecond, by virtue of opening ligand-operated ion channels. In contrast, all of the effects of the biogenic amine and peptide neurotransmitters, as well as many of the effects of glutamate and GABA, are achieved over hundreds of milliseconds to minutes, by slow synaptic transmission. This latter process is mediated through an enormously more complicated sequence of biochemical steps, involving second messengers, protein kinases, and protein phosphatases. Slow-acting neurotransmitters control the efficacy of fast synaptic transmission by regulating the state of phosphorylation of receptors for fast-acting neurotransmitters and thereby controlling the efficiency of the response of these postsynaptic receptors to the neurotransmitter. A major goal of our research at the present time is to elucidate the molecular mechanisms by which this regulation occurs. Our research uses techniques from the fields of molecular biology, cellular biology, biochemistry, electrophysiology and neuro-anatomy in a multidisciplinary approach to the problems of neuronal function and signal integration.

One major focus of our work is to elucidate the molecular and cellular basis of neuronal function and interactions in the basal ganglia. The basal ganglia play a critical role in the integration of sensorimotor, associative and limbic information to produce motor behaviors. In addition, abnormalities in dopaminergic, glutamatergic and serotonergic signaling in the basal ganglia have been implicated in many neurological and psychiatric disorders, including schizophrenia, Parkinson's disease, Huntington's disease, depression, anxiety, Attention Deficit Hyperactivity Disorder and drug abuse. The basal ganglia are composed of several subcortical nuclei, including the striatum, the globus pallidus, the subthalamic nucleus and the substantia nigra. The striatum is a central component of the basal ganglia as it integrates excitatory glutamatergic inputs, predominantly from the cortex and thalamus, with dopaminergic and serotonergic inputs from mesencephalon, and sends projections to the output structures of the basal ganglia.

Neurobiology of signaling in the brain. Our research group is elucidating the signal transduction pathways through which dopamine and other neurotransmitters elicit their physiological effects on their target neurons in the basal ganglia. We have found that about a dozen neurotransmitters which regulate the activity of these neurons do so in large measure by regulating the state of phosphorylation of a pivotal signaling switch referred to by the acronym DARPP-32 (dopamine and cyclic AMP-regulated phosphoprotein, Mr32kDA). They do so through a variety of mechanisms involving increased or decreased phosphorylation or increased or decreased dephosphorylation. We have found four specific residues in DARPP-32 that are phosphorylated by distinct protein kinases and dephosphorylated by distinct protein phosphatases. The DARPP-32 molecule itself can act either as an inhibitor of cyclic AMP-dependent protein kinase or as an inhibitor of protein phosphatase-1, depending upon the particular residue that is phosphorylated. This is the first known example of a molecule that can act either as a protein kinase or phosphatase inhibitor. The state of phosphorylation of DARPP-32, through control of protein kinase and phosphatase activities, regulates the state of phosphorylation and activity of virtually every known physiological effector, including a variety of ion pumps, ion channels, neurotransmitter receptors and transcription factors. Dopaminoceptive neurons integrate all information coming into the neostriatum and are the only efferent pathway out of the striatum. DARPP-32 provides a molecular mechanism by which all efferent information is integrated and converted into a meaningful physiological response. Animals with targeted deletion of the DARPP-32 gene show a total loss of effectiveness of dopamine, antipsychotic drugs and substances of abuse, including cocaine, amphetamine, LSD, PCP (angel dust), opiates, marijuana, alcohol, nicotine and caffeine. This research program has clarified a great deal of the signaling machinery involved in dopamine action and the action of other neurotransmitters that interact with the dopamine pathway, has elucidated new principles of signal transduction and is of clinical relevance, providing a variety of new targets for the development of drugs for the treatment of several major psychiatric and neurological disorders.

Finally, we have found recently that DARPP-32 plays a major role in signaling between nerve cells in many regions of the brain in addition to the dopamine-innervated regions. For example, the widely used antidepressant drug Prozac regulates DARPP-32 phosphorylation in the cortex and hippocampus. Moreover, the antidepressant effects of Prozac observed in wild-type mice are abolished in mice lacking the DARPP-32 gene. These data indicate that the essential role of DARPP-32 in cell signaling in the brain extends far beyond the dopamine cell-signaling system and appears to involve a large number of neurotransmitters in many brain regions.

Alzheimer Amyloid Precursor Protein (APP). We have demonstrated that the relative amounts of APP that are converted to the nontoxic soluble form of APP (APPs) and the toxic beta-amyloid are controlled by protein phosphorylation and dephosphorylation mechanisms. Thus, activators of various protein kinases, as well as inhibitors of various protein phosphatases, reduce the amount of beta-amyloid formed by nerve cells. We are now determining the components of the signal transduction cascade that are responsible for the regulation of APP breakdown, and the formation of beta-amyloid, with the aim of developing new targets for the treatment of Alzheimer's disease.

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Here is the firm's press release describing the early Phase 1 results.

Neurologix Announces Publication of Landmark Gene Therapy Study Demonstrating Safety and Statistically Significant Improvement in Patients With Advanced Parkinson's Disease

FORT LEE, N.J.--(BUSINESS WIRE)--June 21, 2007--Neurologix, Inc. (OTCBB:NRGX) today announced the publication in the June 23 issue of the journal The Lancet of positive results from the first ever gene therapy trial for Parkinson's disease and the first report of direct gene transfer into a patient's own brain cells for any adult neurodegenerative disease.

The open label Phase 1 study, conducted in 12 patients with advanced Parkinson's disease demonstrated both a lack of adverse events related to the gene therapy procedure and statistically significant improvements from baseline in both clinical symptoms and abnormal brain metabolism (as measured by positron emission tomography, or PET scanning). Although all patients had symptoms on both sides of the body, the procedure was performed on only one side of the brain, enabling the untreated side to serve as a study control. The reported improvements were observed primarily on the treated side of the body beginning three months after the gene therapy procedure and persisted through the 12 months formal study period.

Neurologix sponsored the study as part of its ongoing efforts to develop this and other gene therapy approaches to the treatment of neurodegenerative and metabolic diseases. Principal investigators Michael G. Kaplitt, MD, PhD, and Matthew J. During, MD, PhD, performed the procedures at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. Andrew Feigin, MD and David Eidelberg, MD of the Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System performed the clinical evaluations and the PET scans. Neurologix scientists were also co-investigators in the study.

"This ground-breaking study represents not only an encouraging first step in the development of a promising new approach to Parkinson's disease therapy, but also provides a platform to translate a variety of new gene therapy agents into human clinical trials for many devastating brain disorders," said Paul Greengard, PhD, chairman of the Neurologix Scientific Advisory Board and recipient of the 2000 Nobel Prize for Physiology or Medicine for his work related to how brain cells communicate. "The significant and sustained improvements in clinical symptoms following treatment of only one side of the brain are impressive. Moreover, the PET results offer an important window into the function of the living brain in these patients, which supports a normalization of brain activity specific to the treated hemisphere."

The study used an adeno-associated virus (AAV) vector to deliver an inhibitory gene (glutamic acid decarboxylase or "GAD") to the subthalmic nucleus (STN) of the brain. In Parkinson's disease, STN activity is abnormally increased, largely due to a deficit in GABA (gamma-aminobutyric acid), the major inhibitory neurotransmitter in the brain. Increasing GAD causes more GABA to be synthesized, thus helping to calm the STN over-activity. The value of this strategy has been demonstrated in previous human studies where reducing STN activity by either electrical stimulation or lesioning can help ameliorate the symptoms of advanced Parkinson's disease.

The Phase 1 study was not specifically designed to assess efficacy. Nonetheless, the researchers reported the clinical outcomes to be very encouraging, with treated patients showing significant improvement in both the "on" and "off" states of their illness (the time periods in which they achieve or do not realize benefit from drug therapy) beginning at three months following surgery and continuing through the end of the study. These improvements occurred predominantly on the side of the body corresponding to the side of the brain receiving treatment. Moreover, the absence of change at the earliest time point following treatment suggests that the improvement was not likely due to the surgical lesioning of the targeted brain region, as surgical approaches typically give rise to immediate, short-lasting benefit around the time of surgery, while prior studies of AAV-mediated gene therapy show that gene expression gradually increases to a maximal level over a period of weeks.

"We are very encouraged by the results of this trial and its publication in such a prestigious journal," said John Mordock, Neurologix President and Chief Executive Officer. "Since the inception of the company, we have been a leader in developing gene therapy for neurological disease, and we feel that rigorous peer-review and publication of the results from this first-ever trial is an important milestone for this entire field. These promising observations certainly warrant further, more definitive testing of Neurologix's technology, and we anticipate beginning a larger Phase 2 study in Parkinson's disease later this year. Moreover, the results also provide a solid foundation for the development of our other therapeutic programs, including epilepsy where we plan to initiate a Phase 1 gene therapy study this year."

Study Design

The study included 12 patients with advanced Parkinson's disease, with four patients in each of three dose-escalating cohorts. All procedures were performed under local anesthesia and all 12 patients were discharged from the hospital within 48 hours of the procedure. At one year, all 12 patients as a group demonstrated a clinical improvement of 25% in the Unified Parkinson's Disease Rating Scale (UPDRS) compared to baseline (p less than 0.005). Nine of the 12 patients showed an average of 37% and five of these patients had substantial improvement of between 40% and 65%. Clinical improvement also correlated well to metabolic changes in glucose utilization as measured by PET scan. The PET scan data revealed a significant improvement (p less than 0.001) in brain metabolism on the treated side of the brain compared to the untreated side. No adverse events related to the gene therapy procedure were reported throughout the duration of the 12-month study, or in the subsequent two years since the study formally ended.

About Neurologix

Neurologix, Inc. is a development-stage company engaged in the research and development of proprietary treatments for disorders of the brain and central nervous system utilizing gene therapies. The Company's initial development efforts are focused on gene therapy for treating Parkinson's disease, epilepsy and other neurodegenerative and metabolic disorders. Neurologix's core technology, "NLX," is currently in the clinical development stages, having recently been tested in a company-sponsored Phase I human clinical trial to treat Parkinson's disease.

Cautionary Statement Regarding Forward-looking Statements

This news release includes certain statements of the Company that may constitute "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, and which are made pursuant to the Private Securities Litigation Reform Act of 1995. These forward-looking statements and other information relating to the Company are based upon the beliefs of management and assumptions made by and information currently available to the Company. Forward-looking statements include statements concerning plans, objectives, goals, strategies, future events, or performance, as well as underlying assumptions and statements that are other than statements of historical fact. When used in this document, the words "expects," "promises," "anticipates," "estimates," "plans," "intends," "projects," "predicts," "believes," "may" or "should," and similar expressions, are intended to identify forward-looking statements. These statements reflect the current view of the Company's management with respect to future events. Many factors could cause the actual results, performance or achievements of the Company to be materially different from any future results, performance or achievements that may be expressed or implied by such forward-looking statements, including, but not limited to, the following:

The Company is still in the development stage and has not generated any revenues. From inception through March 31, 2007, it incurred net losses and negative cash flows from operating activities of approximately $22.7 million and $17.4 million, respectively. Management believes that the Company will continue to incur net losses and cash flow deficiencies from operating activities for the foreseeable future. Because it may take years to develop, test and obtain regulatory approval for a gene-based therapy product before it can be sold, the Company likely will continue to incur significant losses for the foreseeable future. Accordingly, it may never be profitable and, if it does become profitable, it may be unable to sustain profitability.

In order to obtain the regulatory approvals necessary to commercialize its current or future product candidates, from time to time the Company will need to raise funds through public or private equity offerings, debt financings or additional corporate collaboration and licensing arrangements. Availability of financing depends upon a number of factors beyond the Company's control, including market conditions and interest rates. The Company does not know whether additional financing will be available when needed, or if available, will be on acceptable or favorable terms to it or its stockholders. Management believes that the Company's current resources will enable it to continue as a going concern through at least March 31, 2008.

The Company will need to conduct future clinical trials for treatment of Parkinson's disease using the Company's NLX technology. If the trials prove unsuccessful, future operations and the potential for profitability will be materially adversely affected and the business may not succeed.

There is no assurance as to when, or if, the Company will be able to successfully receive permission from the FDA to begin a Phase I safety trial for treatment of epilepsy.

Other factors and assumptions not identified above could also cause the actual results to differ materially from those set forth in the forward-looking statements. Additional information regarding factors that could cause results to differ materially from management's expectations is found in the section entitled "Risk Factors" in the Company's 2006 Annual Report on Form 10-KSB. Although the Company believes these assumptions are reasonable, no assurance can be given that they will prove correct. Accordingly, you should not rely upon forward-looking statements as a prediction of actual results. Further, the Company undertakes no obligation to update forward-looking statements after the date they are made or to conform the statements to actual results or changes in the Company's expectations.

CONTACT:
Neurologix, Inc.
Marc Panoff, CFO, 201-592-6451 (Investors)
marcpanoff@neurologix.net
or
Kureczka/Martin Associates
Joan Kureczka, 415-821-2413 (Media)
Jkureczka@comcast.net

SOURCE: Neurologix, Inc.

.........................................

here are some more links to info about Dr. Michael Kaplitt

Crains New Yorkers Top 40 under 40
Weill Cornell Physicians listing
New York Best Doctors June 2004
Popular Science - Gambling on Gene Therapy ( ED - and winning is my guess)
Princeton Alumni Weekly October 22, 2003: A moment with...Michael Kaplitt ’87
Weill-CU/Auckland study shows efficacy of gene therapy for Parkinson's

........................................

Also I wish to highlight the apparent correlation of exposure to the metallic element / mineral Manganese, as a seemingly more than just a curious potential cause of Parkinsons, or at least Parkinsons like symptoms.

This is explored here in a web article from UC Davis and here at the University of Washington where there is apparently some parkinsons related data in dietary minerals of both manganese and iron .

This is a clear case where in the extreme taking too much of the wrong over the counter minerals (in for example vitamin supplements) one needs to exert caution, especially if already suffering from Parkinsons. Yet apparently some Manganese is required for healthy body functions? Are dietary supplements of Manganese ever properly indicated or justified? I do not know.

One osteopath physician describes some of these issues from a more experienced perspective than ever I could - Dr. Joseph Mercola

And here is an abstract of an academic research article substantiating the neurotoxic effects of manganese exposure to the nigrostriatal dopaminergic system, resulting in Parkinsons like effects. The main subject of the article seems actually to be effects of a particular protein kinase in the phenomena of damage to dopaminergic cells by manganese. I have not had time to look at the actual article, but hints are there in the abstract as to implied cautions re Manganese exposure.

Aside from obscure industrial sources of manganese exposure, one might be interested to know that stainless steel and aluminum foil both seem to have varying amounts of manganese in the practical alloys. The extent naturally will vary, but this might not be as well controlled in food cookware and aluminum foil as one might desire in the context of manganese risks in Parkinsons like issues.

A quick search indicates that typical aluminum foils might contain up to 1% manganese, typically fractional %. Most stainless steels have comparable low concentration, but there is one stainless variant that is called manganese substituted stainless steel that is curious in having 4% manganese... If this happened to be "accidentally" used in some stainless cookware and used to cook acidic foods regularly, my guess is this might be a curious area to investigate for a correlation to Parkinson's like symptoms in folks not exposed to industrial sources.

And excerpt from here http://www.argentumsolutions.com/tutorials/alloy_tutorialpg4.html
describes the stainless steel variant.
........................................................

Manganese Substituted Stainless Steels (2XX or S2XXXX)

The AISI 200 series of stainless steels (S2XXXX) was developed during the 1930’s. These alloys were used during the Korean War to preserve nickel. About 4 wt% of the nickel is replaced by manganese with small (<0.25>

A number of stainless steel alloys in this classification have the trade name "Nitronic". These alloys tend to have higher strength and good wear resistance. Some examples are Nitronic 50 (21.2 wt% chromium, 12.5 wt% nickel, 2.5 wt% molybdenum, and 5 wt% manganese) with corrosion resistance better than AISI 316 and Nitronic 60 (17.0 wt% chromium, 8.5 wt% nickel, 4 wt% silicon, and 8 wt% chromium) with excellent wear resistance.

...................................................

Just playing the amateur chemist for a nanosecond, would hint to me that some types of foods - likely more acidic in nature, would be more probable to leach some hypothetical small amounts of manganese, than foods closer to pH neutral? Which I do not know, but this as high alkalinity cooking with the wrong cookware that bore Manganese might be not so desirable ? It would be curious to test, as some stainless steels and aluminum foil might become an inadvertent health hazard in the wrong circumstances. Just speculation, but not entirely without rationale.

Far more notable is that welders can often be exposed to more directly hazardous Manganese fumes from some welding metallurgies, as will folks who do work in some basic metals / metallurgy processes where manganese fumes or vapors might be created at high temperatures. As usual, read your MSDS's and act accordingly.

Here is a link to a properly described MSDS for manganese oxide at the well respected chemical firm JT Baker, which correctly indicates the potential for central nervous system disorders and Parkinson's like symptoms. Some manganese element and inorganic manganese compound MSDS's are not so complete, nor as thorough. My compliments to JT Baker for doing it right. JT Baker makes well engineered products, I might add.

.....................................................
AUG 8th 2007.
I found an especially compelling web discussion about the correlation between the use of Manganese Dioxide ceramics glazes in RAKU Pottery firing and parkinsons symptoms here .

The discussion is almost shocking, as I used to do some pottery wheel work long long ago, although I did little glaze firing, I did paint glazes onto my works. This is indeed a warning regarding glazes other than those which are lead based. Given the possibility that manganese dioxide ceramics glazes might be prevalent in artwork and home made ceramics (cookware?) this is a warning light that is BRIGHT RED as in Beware. Given that some artlike glazes (yielding hues ranging from brown to pink and purple) might have very high concentrations of Manganese Dioxides, this is likely a stronger acting effect than the stainless steel curiousity I describe above.
.....................................................

A further but Very Important Note - Please visit the Michael J Fox Foundation for lots of good useful information about Parkinsons disease, research, and treatments existing and being developed. Superbly focused, practically oriented research efforts, bearing down like a laser to attempt to cure this terrible disease.

Michael deserves profuse compliments for the superb work he is doing through his foundation, as do the foundation team members. The team and its efforts are substantive and highly focused on practical innovations that can have large impacts on clinical results.

FOCUSED on important matters of where to best use all the intellectual horsepower - for the greater good ! Often implied in many research efforts, but often not done well .... but Mike's Got It Right Here !!!

My sincerest respect goes out to Michael, as well as best wishes to him for a speedy recovery from his illness.

God Bless You Mike !

You are a hell of a great role model to emulate !!
......................................
p.s. I wrote this article after reading an earlier news item at MSNBC and observing what was a very unusual advance in the quest to improve Parkinsons treatment prognoses. So MSNBC, as others had it first(it was released on news wires), but I might have written this fairly well, as Dr. Martin Kaplitt COB indicated as he complimented me on this article.

My compliments go back to the excellent team at Neurologix for superb thoughtful, applied medical research and development. All the respect goes out to this superb team !

NOTE - for some more interesting articles on another novel biotech firm - this one innovating in cancer pharmaceuticals, see the following prior posts of mine on Adherex Technology, a firm using Cadherin Cell Adhesion chemistry, to selectively and safely kill a good portion of tumor tissue, among other pharma strategies.

article-on-genesis-of-adherex

orest-blaschuks-prolific-patents

adherex-phase-1-clinical-trial-for

ottawas-missing-growth-gene

re-motley-fools-why-we-love-wild-penny

patents of Micheal Gertner President of Oraya Therapeutics

2007-06-18T17:45:00.000-07:00

These are patent publications of Dr. Michael Gertner, president and founder of Oraya Therapeutics, and includes IP from various sources, not restricted to license by nor assignment to Oraya (ie specifically it is not yet determined which IP is likely to be licensed or owned by Oraya) Some is assigned to Nanosys and some comes from UC, and some is indeterminate due to limited information published by applications for patents

1	US20070027358	Devices and methods to treat a patient
2	US7144381	Hemodialysis system and method
3	US20060271024	Nasal Cavity Treatment Apparatus
4	US20060264699	Extragastric minimally invasive methods and devices to treat obesity
5	US20060224100	HEMODIALYSIS ACCESS WITH ON-OFF FUNCTIONALITY
6	US20060212053	Extragastric minimally invasive methods and devices to treat obesity
7	US20060206173	Devices, Methods and Kits for Radiation Treatment via a Target Body Surface
8	US20060206171	Devices, methods and kits for radiation treatment via a target body surface
9	US20060195139	Extragastric devices and methods for gastroplasty
10	US20060195165	Optical therapy devices, systems, kits and methods for providing therapy to a body cavity
11	US20060189889	Management Systems For The Surgically Treated Obese Patient
12	US20060167531	Optical therapies and devices
13	US20060142790	Methods and devices to facilitate connections between body lumens
14	US20060121180	Metallic structures incorporating bioactive materials and methods for creating the same
15	US20060089571	Obesity treatment systems
16	US20060074473	Methods and devices for combined gastric restriction and electrical stimulation
17	US20060062820	Metallic structures incorporating bioactive materials and methods for creating the same
18	US20060013390	System and method for encrypting data in analog form
19	US20060015138	Emboli diverting devices created by microfabricated means
20	US20050267533	Methods and devices for the surgical creation of satiety and biofeedback pathways
21	US20050228415	Methods and devices for percutaneous, non-laparoscopic treatment of obesity
22	US20050221072	Medical device applications of nanostructured surfaces
23	US20050216042	Percutaneous gastroplasty
24	US20050216040	Devices and methods to treat a patient
25	US20050186250	Metallic structures incorporating bioactive materials and methods for creating the same
26	US20050106212	Metallic structures incorporating bioactive materials and methods for creating the same
27	US20050100779	Three dimensional polymeric fuel cell components
28	US20050038498	Medical device applications of nanostructured surfaces
29	US20030060873	Metallic structures incorporating bioactive materials and methods for creating the same
30	US20030014003	Hemodialysis system and method
31	US6090114	Tibial plateau resection guide
32	US5916219	Tibial plateau resection guide
33	US5911710	Medical insertion device with hemostatic valve

The Worlds Best Sandwich - Snowdon Delicatessen

2007-06-12T21:19:00.000-07:00

Binh while you are looking for a good place to eat, up you know where, check this out

Order
lean,
Hot, (meat kept kept in steamer till sliced just before serving )
double mustard (mustard on both side of bread )
smoked meat sandwich ( comes on rye bread, that is excellent and fresh )

order with (fresh cut ) french fries
( ask for vinegar for the fries else use conventional ketchup )
and coles slaw
and dill pickles on the side.

tres important !

Vinod Khosla's Biofuels Think Outside The Barrel

2007-06-02T19:22:00.000-07:00

re Motley Fool's "Why We Love Wild Penny Stocks" article misses the mark by not explaining Adherex's unusual story

2007-06-02T09:04:00.000-07:00

Dear Tim and Brian,

re your recent article on Motley Fool Why We Love Wild Penny Stocks

Your simple statements about Adherex do not do the firms efforts justice in the least, nor indicate the critical mass of promise Adherex holds likely to achieve in notable advances in cancer treatment prognoses.

Adherex's present modest valuation is a huge hangover from founding (business) management team's incompetence. The initial management now long since gone, since the merger/takeover by Oxiquant - bringing aboard Dr. Peters as CEO and refocusing the firms efforts far more productively. As such the present stock valuation in no way reflects the likely cancer pharma blockbuster successes the firm has moved forward well into FDA trials.

Granted most of Adherex's efforts are in FDA P1 / P2, but the scientific learning of substance has been significant, not merely promising, as there are numerous technical / scientific fundamentals that are hugely favorable with quite unusual characteristics for cancer pharmaceutical developments.

Some key technical points of note - there are 2 main cancer pharma programs pursued.

1st - ADH-1 - that of the the novel Cadherin technology which Adherex was founded on (Cadherin being a cell adhesion compound - the glue of the body's cells), developed initially by Prof. Orest Blaschuk of McGill University.

2nd - 5FU/ Eniluracil combo therapy - inlicensed from a failed Glaxo phase 3 trial ( described much further below )

back to ADH-1

The primary compound called ADH-1, is an N-Cadherin antagonist (early on was called Exherin, prior to merger with Oxiquant).

In laymans terms, a Cadherin antagonist will reduce the cell adhesion properties of the targeted Cadherin type by the chemical agent "antagonist". The practical significance to successful advances in cancer treatment will be described below, but in short there is selectivity in Cadherin targeting that means that destroying a particular soft tissue tumor Cadherin type, will not need to have any material effect on the rest of the body, both in primary targeting / tumor tissue destruction and in safety (almost total absence of side effects) for reasons that will elaborated below.

So keywords to note for ADH-1 here, are Safety, Absence of Side Effects, and Selective Targeting of ONLY Tumor Tissue.

There are various classes of Cadherin cell adhesion compounds in the body, and they perform different functions. In the case of tumors - tumor tissue can be classed as E-Cadherin marked or N-Cadherin marked. This is notable and fortuitous for a cadherin cancer pharma strategy.

These two cadherins (E&N) are important in tumor tissue evolution, as they reflect stages of how the tumor tissue grows. Generally speaking N-Cadherin tissue seems to be more immature and rapid growing cancer tissue, but there are greater subtleties. Plus as tumors grow there are pockets of regions of tumor tissue of each, such that both Cadherins E&N can coexist together in the tumor. The distribution and proportions of E&N Cadherins are not necessarily simple.

The two E & N Cadherins also present an unusual strategy to treat soft tissue tumors, that until the appearance of Adherex, were not addressed in the least as a possible means for cancer treatment.

In our case with ADH-1, N-Cadherin marked tumor tissue will offer up an opportunity to safely and quickly kill large amounts of N-Cadherin tumor tissue with unprecedented results using ADH-1's capability to cause N-Cadherin de-adhesion ( hence the firm's name Adherex ) ...

More specifically is that ADH-1 is effective in destroying N-Cadherin marked tumor soft tissue, and notably as yet largely unknown, is that most Chemos to date are effective mostly on E-Cadherin marked soft tumor tissue.

Very conveniently there is a complementary synergistic effect (N-Cadherin by ADH-1 & E-Cadherin by conventional Chemo ) with most present / prior chemos, and the potential for ADH-1 in combo to markedly improve cancer pharmaceutical efficacy.

This complementary characteristic only became apparent recently, from prior single agent ADH-1 FDA P1/P2 tests & subsequent preclinical Combo experiments, after Dr. Peters vigorous efforts to move single agent ADH-1 trials along. He learned brilliantly and the science is not merely superb in an academic sense, but amazing in the practical implications which seem to likely have promise across many soft tissue tumor types, using several existing conventional Chemos, in combination with ADH-1.

Salient characteristics of single agent ADH-1 -

Unusual natural compound normally produced in the body, and when tissue expression (production) of natural ADH-1 is lost, correlates to some small ~10-30% fraction of tumors. This is described in the open literature by some Cadherin research biologists?

One can infer from this, that natural ADH-1 is one of the human body's natural low level cancer scavengers.

But due to its natural presence in the body, ADH-1 has a near perfect metabolism (break down) in the liver (complete elimination in 4hrs by liver), so cumulative side effects are nil, so long as the dose RATE is kept below some critical threshold. In P1 single agent testing, Adherex found that if a rather unusually high dose RATE was exceeded, the common chemo side effect called Hands and Foot syndrome was observed, and if the ADH-1 dose RATE was reduced, no H&F ever appeared, and essentially no side effects were observed either.

But importantly there is NO limit to cumulative total DOSE in the least, also due to the unusual safe natural metabolic breakdown pathway in the liver, that ADH-1 possesses. This characteristic of ADH-1 as a cancer pharmaceutical agent having a safe natural metabolic (elimination) pathway is rare as hens teeth in chemotherapy agents, especially cancer chemo agents with as high activity as ADH-1 possesses..

Noting the 4 hrs to complete elimination by metabolic pathways, we can now also observe that the basic cancer action of ADH-1 - the chemical effect of destroying cell adhesion of N-cadherin marked tumor tissue, is noted by the rapid and selective onset of destruction N-Cadherin marked tumor blood vessels (vasculature) in 30 minutes.

N-cadherin tumor tissue blood vessels are well known to be very fragile, sort of immature thin spindly and almost leaky vasculature development structure. ADH-1 seems to safely and selectively target the N-Cadherin tumor vasculature with no significant effects on the rest of the body whose otherwise healthy vasculature is largely held together by E-Cadherin.

Furthermore onset of N-Cadherin tumor tissue vasculature destruction, by melting as it were, occurs in a rapid 30 minutes from ADH-1 infusion.... The result is that no blood can feed the N-Cadherin tissue, nor leave the tumor by the venous system, so the N-Cadherin tumor tissue will no longer be viable.

This fast rate of 30 minutes ADH-1 activity, is onset to beginning destruction of N-Cadherin marked tumors/ tumor tissue by melting the N-Cadherin blood vessels, is unprecedented.

Remember NO side effects below a critical level of dose RATE from ADH-1, and rapid N-cadherin tumor tissue blood vessel destruction !!!

The destruction of N-Cadherin marked tumor tissue blood vasculature by ADH-1, starts onset of N-Cadherin tumor tissue NECROSIS or tumor tissue death. IN 30 MINUTES. The actual tumor shrinkage from the necrosis onset is far slower (weeks to months), but necrosis onset by N-Cadherin vasculature destruction is relentless in shrinking the N-Cadherin marked tumor tissue.

[ June 5th 2007 - The second order effect is that residual N-cadherin tissue at the periphery of an N-cadherin region might survive ADH-1 treatment to some degree due to adjacent non-NCadherin blood supply. Notable but typically small effect ]

More subtly. tumor tissue seems to at times switch and evolve at some slow rate between N-Cadherin and E-Cadherin types. ADH-1 seems very effective against N-Cadherin tumor tissues in quite a number of soft tissue cancer tumors.

What is evident is that the COMBINATION of ADH-1 with its minimal to zero added side effects + the present normal conventional chemos of some good fraction of cancer treatments, will prove to be extraordinarily effective in cancer prognoses with few added side effects over existing chemo drugs used in combination therapies.

This unusual ADH-1 combo synergy/ efficacy arises due to the fact that most existing chemos are seemingly not effective against N-Cadherin marked tumor tissue (curiously, normal prior chemos seem to be mostly effective against E-Cadherin tumor tissue) and yet ADH-1 is devastatingly effective in quickly destroying N-Cadherin tumor tissue.

This is the salient technical advance for cancer treatment improvement that ADH-1 presents, derived from massive learnings of prior Cadherin cell adhesion science and recent single agent FDA p1/p2 tests of ADH-1.

At present ADH-1 has mostly completed single agent Phase 2 trials, and is now heading into P1 combo therapy trials.

Due to the fundamental confidence in the unusual properties of ADH-1, alone and in combination with conventional chemos, one of the first combo therapies being undertaken as a P1 combo for ADH-1 is MELANOMA.

The rational is unusual. Melanoma today is largely untreatable as is well known, if not caught very early. Apparently some early preclinical testing of ADH-1 with Mephalan for melanoma, has indicated unusual activity increases that arises in part from ADH-1's targeting of N-Cadherin tissue that conventional chemos do not attack well. One might infer that Melanoma might become the poster boy for Cadherin cancer treatment strategies, in that if the lethality of Melanoma is due largely to its possible unusual ratio of N-Cadherin melanoma tissue, this would all begin to make some unusual sense....

Adherex has indicated their likely intention to quickly move through Phase 1 Melanoma testing to an unusual Phase two randomized trial in an attempt to possibly gain an advanced approval by the FDA, possibly through a P2 phase alone without progressing to the typical P3. This strategy is unusual (done with Gleevec apparently) and is not without risks, but single agent ADH-1 properties and limits are well studied by now, and as such given the preclinical testing observations with ADH-1 combo with Mephalan for melanoma, there is some unprecedented promise here....

If Phase 2 combo ADH-1 / Mephalan for Melanoma was successful in a randomized P2 trial, the consequences for Adherex would be astounding as would be the improvement for Melanoma patient prognoses possibly be very unusually beneficial.

There is far more to the ADH-1 story at present, and there are intentions for numerous tumor types to be tested with Combo ADH-1 and various conventional chemos, and these will progress at a more normal pace for Adherex. But the Melanoma effort is very unusual, as one can gather Melanoma is a very tough nut to crack. This effort has some implications of risk and potentially huge upside for Adherex....

Clearly some soft tissue tumor types will likely respond better than others and this is what Adherex is presently exploring with a number of different tumors being brought into trial efforts. ADH-1 will not be a cure for cancer, but it seems to have unprecedented promise for a significant advance in cancer prognoses in the near to medium term, under the very capable even brilliant, Dr. Peters CEO and Dr. Norris President and COO.

some reading you might enjoy ...

a lead in blog post.
http://mark-nano.blogspot.com/2006/02/article-on-genesis-of-adherex.html

An article originally from Ottawa Citizen chronicling the early days till the aquisition / merger of the firm with Oxiquant - where Oxiquant's Dr. Peters takes over control of the firm, with Dr. Norris who had joined prior to the merger (and may have in fact suggested a merger, since the firm was nearly in bankruptcy prior to merger).

The key technical role of McGill University's Prof. Orest Blaschuk's development of Cadherin technchnology and his by now 40 issued patents held by Adherex is alluded to. [I had encouraged Bagnall to write this article for over 2 years till he succumbed to my pestering influence, and I contributed to guiding the subject matter contained. I was left off as 2nd co-author apparently since I own some small amount of Adherex stock]
http://www.investorshub.com/boards/read_msg.asp?message_id=9153690

http://mark-nano.blogspot.com/2006/03/adherex-receives-regulatory-approval.html

article originally from the Ottawa Citizen newspaper (less relevant to Adherex but interesting)
http://mark-nano.blogspot.com/2007/04/ottawas-missing-growth-gene-behind.html

BUT THERE IS STILL MORE ....

2nd - the second pharma compound being pursued, is a formerly failed Glaxo Smith Kline project, that failed Phase 3 after ~$80m invested by Glaxo, due to a technical error that Glaxo did in phase 3, improperly ratioing the mix of two compounds tried for the hoped for combo chemotherapy advance of 5FU & Eniluracil.

[Note this was approximately what Dr. Peters described in one of the webcast conference calls to Adherex investors in Q3/4 2006? possibly early 2007 about how the 5FU/Eniluracil matters transpired at GSK and later]

........................................................................
[ Note 6-4-2007 11:30pm pst - some readers are being referred here from a google finance discussion of issues of other matters of GSK(by someone else posting a link to the article of mine here). I dislike what is being said about GSK at the google GSK vioxx referral posts, and think it wrong to not present a balanced picture of events present and in historical context for any and every firm (life happens to be complicated - never as good in the best of times nor as bad in the worst of times FWIW).

GSK has had a long productive and prestigious tradition of playing significant POSITIVE role in the pharmaceutical products marketplace...so the tenor of some of the discussions about GSK at the referred link at the Google finance topic on Vioxx is troubling and likely unfair to the firm... MY 2 Cents .. I think it important to never exaggerate the bad especially leaving out the context of all the good done by any firm one discusses - just to be fair to all concerned - MW ]
..........................................................

The goal here is the intention of taking the common chemotherapy agent 5FU which is old and without patent protection, but a mainstay of intravenous (IV) cancer chemotherapy for many many years, and transform it into an orally administrable pill, of hopefully longer half-life duration of the 5FU compound in the bloodstream. Glaxo failed in their 5FU/Eniluracil P3, but in the course of some partnering discussions with Adherex re ADH-1, offered up the failed 5FU/Eniluracil program to Adherex for in-licensing by Adherex.

Dr. Peters the brilliant fellow he is, knew likely immediately what Glaxo did wrong in their P3 execution of this program, and within 3 months has mouse model experiment data supporting his excellent performing fix to Glaxos P3 errors, showing orally administered 5FU/Eniluracil has all the intended promise when the RATIOS of the 2 compounds were dosed in the appropriate manner ( that Glaxo erred in Glaxos Phase 3 efforts ).

Due to the fact that the new Adherex 5FU/Eniluracil effort (now after complete in-licensing of all Glaxo IP of same) is leveraging some extensive prior work of Glaxo's, and that 5FU is very well known from many many years of use in intravenous cancer treatments, Adherex has an unusual opportunity to make a more effective application of present IV intravenous 5FU that is currently unprotected by patents, to become a more effective, orally administrable PILL, with increase in 5FU efficacy....and PATENTABLE....

So that is the second major thrust of Adherex's cancer pharma development efforts. Adherex's 5FU/Eniluracil efforts are now heading back to a fast pace of P1s for the remix of 5FU/Eniluracil, obviously leveraging profuse prior efforts by Glaxo.

In the simplest sense of stock price valuation, Adherex is a penny stock. In the promise of the firm and even the substance of the technical advances to date, Adherex is no common penny stock in the least.

I was initially introduced to the firm's Cadherin technology by a McGill University professor on a trip back to my hometown many years ago, from my then work / home in Santa Barbara.

Initially I was skeptical of the technology, as the specific unnamed McGill professor had his quirks, but it became apparent to me 1-2 years later, what Prof. Orest Blaschuk, the developer and inventor, has discovered is indeed a novel and effective means to likely upend common poor cancer prognoses, with a new brilliant Cadherin based technical strategy of unusual effectiveness.

The quick addition of 5FU/Eniluracil to the firm's development efforts is an added bonus of unprecedented opportunity and a testament to Drs. Peters & Norris obvious brilliance, especially in the quick demo of the fix to Glaxo's technical missteps, in a mere 3 months.

Unmentioned here as yet, is that both these major programs ADH-1 and 5FU/Eniluracil will possibly result in pharmaceutical products with > $B markets.

So is Adherex just yet another penny stock?

I'll let you think that over.

[ed - more of my prior Adherex posts are linked just below]

adherex-phase-1-ADH-1_Combo-clinical-trial-announcement

adherex-receives-regulatory-approval-for-dosing-increase

article-on-genesis-of-adherex

cadherins-and-looming-revolution-in-cancer-treatment

wendman cancer cancer+treatment cancer+cure cancer+treatment+innovation cancer+innovation cancer+research cancer+pharmaceuticals pharmaceuticals biotech biotechnology pharma nano nanotech patents nanotechnology nano+cancer nanotech+cancer patents+cancer nanotechnology+cancer cadherin n-cadherin e-cadherin cancer+cadherin treatment+cadherin blaschuk+cadherin adherex

WISDOM of PAOLO GARGINI (process technology)

2007-05-15T14:29:00.000-07:00

I thought this series of quotes from Paolo, was very apt in guiding successful device technology development, or in fact any R&D effort which is complicated and substantive in technical challenge.

Oftentimes, people who ignore these words of wisdom, or sadder yet don't understand the nuggets within, find poor success in solving technology development challenges, and will often not comprehend the organizational root causes of project or team failure.

The best teams in development are often fluid and agile, taking this wise advice to heart.

5 (wise) LESSONS OF TECHNOLOGY DEVELOPMENT by PAOLO GARGINI

1] The Right Things may Happen for the Wrong Reasons

2] Predictors of Engineering Limits have Always been Proven Wrong by the Right Improvements

3] It Would be Wrong to Believe that the Right Fundamental Limits Don’t Exist

4] It is Wise to Look For The Right Solutions before Things Start to go Wrong

5] It Would be Wrong to Delay Taking Action and not Doing the Right Thing at the Right Time
............................

quote from PAOLO GARGINI (re: process technology)
Director of Intel Technology (process) Development Strategy
Intel Fellow, and Chairman of ITRS - Intl Tech Roadmap Semiconductors

Mine own edits to this are -> Try your best, hang in there and think about assumptions that might be able to be circumvented, where presently assumed to be impenetrable barriers. This is the essence of 2], and while one cannot bank on unusual solutions magically appearing that destroy assumptions of limits, one can look passively, actively, like a crouching tiger, or a ravenous reader, or experiment prolificly and efficiently, to find the fix to one's ills, that ails one's quest.

Unspoken here is that true breakthroughs, development thereof, and recognizing them when they might have been staring you in the face for some time, is a bit of a soft art. Overmanage and tightly control dissent, and you tightly often squeeze your endeavor into a rather tight corner...

An example of this was when an older researcher was almost grudgingly accepted to find a corner to do some work in a lab of a rather prestigious research scientist, and he proved key to the concepts to enable laser based microcantilever deflection sensing so critical to practical AFM - atomic force microscopes. All from attempts to test laser rangefinding to the moon on the lab ceiling, we now see molecules and atoms like never before.

Apparently complementary Heterostructure FETS (or something similar) were stumbled upon because of an error in the intended MBE EPI epitaxy layer growth sequence.

The major single yield improvement for the worlds first DRAM, The Intel 1101 256bit pMOS DRAM, occurred when a bright, humble, yet confident engineer, Tom Rowe, in the early 1970s, in the face of a plant wide edict by Gordon Moore to prohibit ANY and ALL process experiments on the 1101 Dram process (then running a miserable ~5-10% yield ), was ignored in secret by Tom Rowe.

Tom then found a means to >5x increase yield of the worlds first DRAM using, as Les Vadasz called it, a SOOPER DIP, which was Tom Rowe's secret wet etch chemical recipe to clear the metal contact openings without destroying the CVD deposited Field Oxide... And yes that was a Sooper Dip apparently and it both saved the day and led to the commercial success of Intel's efforts in fielding the first MOS Dram memories. Tom is a hell of a guy, fun to talk with and a kind people person. And a great raconteur...

Overconstrain technical innovation and problem solving, overcontrol and we all lose. Work your tail off and get a little loose, and we all win.

Work hard and think like the devil.

Paolo is not a personal friend, but I worked at Intel Livermore '84-86 when he headed Intel Logic TD......quoted from Paolo's 2004 Semicon West presentation

Originally posted 10/16/05
bumped up to refresh on May 15th 2007, as apt as ever.

wendman nanotechnology nanotech nano mems piezoresistive+Pressure+sensor Noyce Silicon+sensor
problem+solving R&D research+development yield+improvement semiconductor wafer+fab wafer+fabrication wafer+300mm brainstorming six+sigma pdf+solutions carnegie+mellon cmu intel hypothesis nano

Tim May's 1991 whitepaper on Parallel Nanoprobe Lithography

2007-05-06T01:03:00.000-07:00

In the early 90's, in the course of participating in the Palo Alto Nanotechnology Working Group, Tim May wrote an interesting whitepaper hypothesizing what scanned nanoprobes might offer in advanced potentially inexpensive high rate lithography. It was a very interesting series of ideas that predated much of the more formal IP generation in parallel nanoprobes, esp. from universities.

Tim is a brilliant scientist, and in the early days of DRAMS at Intel, had discovered the alpha particle effect causing RAM memory bit loss was from trace radioactive materials in some ceramic IC packages. He was an Intel R&D scientist and often had avant garde innovative ideas. There is some story of some lead bricks under a famous Intel executive's house that were used in Tim's experiment to verify that cosmic rays were not at root cause of the memory errors.

For some interesting perspective on the future foretold by Tim, as yet unrealized, I am posting his paper - scanned, to the web, with his full permission and credit to him.

I thought and continue to think that Tim May is far more creative than often given credit for. Brilliant, sometimes cuttingly sarcastic like some fraction of great scientists are(esp if in contact with similar Hungarians??!!), and a very witty guy.

I even remember his efforts in describing how AI techniques might be used to benefit wafer fab process diagnosis and control, by rule based analysis of electrical test data and in-process wafer fab metrology results, far predating others efforts much later...

After I received this hardcopy, I later joined Digital Instruments, and a few years into my stay at DI, when Minne began talking to Virgil Elings of the Quate group's later research into parallel nanoprobes, I gave a copy of this to Virgil, who in his usual effervescent manner, was slightly bemused.

Here are scanned images (with watermarks) of Tim May's brilliant whitepaper on Parallel Nanoprobe Lithography from around 1991 or earlier. (undoubtedly Tim will correct me later with a more accurate date and other details).

This posting is a series of 14 clickable high resolution images, reduced in size on the web page for faster page loading, but each will render in high resolution if you click on the smaller images. Or right click on each, to directly download in windows the high res images.

This does beg several unspoken questions re the IP filings on parallel nanprobes later by several other groups who may have read of, or listened to Tim's pathfinding ideas in the very early 90's, at the Palo Alto Nanotechnology Working Group, or same through the net.

Here are the page images of Tim May's brilliant whitepaper on Parallel Nanoprobe Lithography.

And yes, I used to kibutz with him over his name for the "pizza crawler" as he wittily called it....We had a few yuk yuks over it..

Nanoprobe Lithography Parallel Probe NanoLithographyMinne Manalis
Wilder wendman microscope+stm Tim+May Dan+Rugar
nanotechnology nano nanotech scanning+probe+microscope microscope+near+field microscope+atomic+force microscope+afm
microscope+tunneling afm+hansma quate elings
elings+digital+instruments elings+veeco
nanosensors sensors+budget nanoprobe

SmartTip 's NanoProbe Fountain Pen - a Dip Pen Nanolithography Tool

2007-05-03T05:50:00.000-07:00

SmartTip is an unusually innovative spinoff of the Netherlands' University of Twente's division of Transducer Science and Technology (formerly called MicMec), which has done prodigious amounts of R&D in micromachining of all kinds of microsensors and actuators, including the more conventional mems structures like pressure sensors and accelerometers and other more novel devices.

I enjoyed reading dissertations from Twente's institute, as invariably the research was fascinating, and often novel, and always well characterized. I learned of Twente's efforts when I was at IC Sensors, and Hal Jerman and Steve Terry had a couple of the interesting dissertations around the offices, which made for fascinating reading. Plus on staff there was an engineer Dedrick DeBruin, who came from Twente if I am not mistaken...

So recently it seems after SmartTip's few earlier efforts at mildly novel nanoprobe developments for SPM / AFM (notably the Canticlever for magnetics MFM and related devices), SmartTip is fielding an inking type scanned nanoprobe, derived from a standard atomic force microscope cantilever. The firm is calling the devices Fountain Pens and is going into a beta type customer sampling to learn of the application subtleties before attempting to field a product on a larger scale.

While there is little reference to Dip Pen Nanolithography at SmartTip's page, close examination of the mechanism used, seems like this is what it may very well be doing (ie using DPN(tm) 's described ink transfer methods), although not with dipping to preload the tip for wicked type inking from a solid tip nib. It is a curious connection...

The Smart Tip [aka DPN(tm)] Fountain Pen devices have taken a more common low stress silicon nitride AFM cantilever and incorporated an inking well in the body of the otherwise solid pyrex glass chip, drilled 1-2 holes in the pyrex and incorporated some recesses in the glass using the otherwise normal anodic bond side glass etch, and then added a fluid channel in the cantilever arm(s), plus an inlet coupling the cantilever fluidic channel to the pyrex glass region's ink well, and a tiny etched outlet from the far end of the fluidic channel just near the back of the pyramidal molded silicon nitride AFM tip.

[ed - postscript MAY 24th 2007 - this picture linked above, hints at the potential for IP in useful systems integration of continuous feed microfluidics, beyond the mere static reservoir shown in the hole drilled in the glass existing chip's design.

A systems level integration for near continuous feed, would embody an external larger reservoir, linked to the chip level reservoir which might include tubing, a demountable compression seal at the top of the drilled glass substrate chip and various combinations of external / internal valving, sensors for flow and level / volume remaining, and even integrated electrochemical sensors.

This basic device platform also might permit /enable microvalve fluidic chemistry switching either remotely with longer cycle time / dead volume or more closely coupled fluidic switching closer to the cantilever or a multi microvalve manifold microfabricated on or near the cantilever, even best near the tip to reduce the dead volume of chemistry switching from multiple microvalves - Mark Wendman]

Interesting structure, but possibly not novel enough? Granted this seems to be the 1st commercially fielded AFM cantilever that incorporates and integral microfluidic channel(s) in the cantilever arm, but it still seems to be a device using Dip Pen Nanolithography methods, as DPN(tm) if I am not mistaken, is described more generally as what transpires at a solid Tip apex to wick a meniscus of fluid to the scanned surface just as an ink nib does conventionally.

Also DPN(tm) is not restricted to applications that require dipping per se to provide the ink supply, but I might be mistaken, even if the name DPN(tm) implies dipping, the actual technology might not stipulate this with restrictions of DPN(tm) to dipped supply of "inks".

In short, DPN(tm) likely includes cases in which the fluidic supply to the tip is integrated into the cantilever, and specifically with cases of cantilever incorporates a microfluidic channel.

There seems to be a novel configuration enabled by the integrated inkwell and fluidics channel - where on this web page at Twente is described that the MFP probe enables AFM-based electrochemical conductor deposition by connecting the metal electrode on top of the probe chip (anode) and the sample substrate where conductor deposition is intended (cathode) to a bias power supply. The electrical circuit is formed using the electrolyte solution in the cantilever microchannels. The deposition is voltage regulated since well performing currents for this method are very tiny.

Regrettably they as yet have not acheived electrodeposit linewidths much smaller than 250nm, which I suspect might be due to the substrate spreading resistance, or the gap between the hole at the end of the microfluidics channel being further away from the tip apex. It could also be possible that the electrical biases and writing speeds need further optimization?

I like the structures, even if the ideas might not be as novel with respect to technology as Twente's MicMec / SmartTip might otherwise hope for.

In the Beta Field testing, I'd guess that 3 critical aspects of the device's features are implicitly being evaluated - 1] the fluid channel of the cantilever(lever stiffness and fluidics flow for various sample fluid viscosities), 2] the diameter of the fluid channel opening, in proximity to the tip (just behind the tip ) and 3] the desired sharpness of the tip...

Additionally one might ask if the reflected spot quality from the lever backside AFM laser reflection is in any way affected by the fluidics channel. This largely will be determined by how the fluidics channel fabrication was integrated into the cantilever process ( ie how flat the resulting reflecting surface is so that laser spot quality is not excessively degraded).

Fascinating stuff ...

note - DPN(tm) is a trademark of NanoInk inc.
Dip Pen NanoLithography is also a trademark of NanoInk, but has been used in academic contexts before trademarking

DPNDip Pen NanoLithographyMirkinChad MirkinNanoInk
BioForce Nanosciences wendman microscope+stm
nanotechnology nano nanotech scanning+probe+microscope microscope+near+field microscope+atomic+force microscope+afm
microscope+tunneling afm+hansma quate elings
elings+digital+instruments elings+veeco
nanosensors sensors+budget nanoprobe

Advanced Thin Silicon Solar Cells - Tom Rust's Photon Energy Systems of OAKLAND

2007-04-23T22:29:00.000-07:00

Photon Energy Systems has developed a process for making thin LT 50microns thickness and 3x->5X reduction in single crystal silicon wafers required - the major cost in modules is the silicon. Photon Energy Systems technology reduces the silicon cost by a factor of ~5X over conventional silicon wafers, and ~3x over unusual ultrathin fragile wafers, with fragility of the the ultrathin Photon Energy chip cells, not an issue at all due to the tiny chip size and simple methods of handling them.
2) 20X reduction in cell processing capital costs over conventional wafer cells. This allows smaller capital expenditures in processing equipment to have much greater throughput and reduces cell costs.
3) Cell output stability of single crystal silicon - near constant over life, versus commonly observed large power degradation of amorphous silicon thin film solar cells.

The manufacturing technique is comprised of 2 major manufacturing steps:

1) Thin Silicon Sub-Cells - this process uses conventional Cz or Fz single crystal silicon boules, cuts the boules into thick (typically 2mm) wafers, and then processes them into tens of thousands of thin cells. By processing the wafers from a small surface area to a very large surface area in each wafer, the wafer processing resources needed to make each module is reduced by a factor of more than 20X.

2) Sub-Module (pseudo wafer) - the cells are assembled using our unique parallel assembly tools into sub modules, similar in size to conventional solar cells. These sub modules are then formed into larger panels - assembled, laminated and framed into conventional solar panels.

Sub-module (pseudo wafer) of thin (50micron) single crystal silicon PhotoVoltaic cells (Top and bottom bars are solderable outputs)

Typical efficiency for Cz made cells - 15%

For More Info - contact
Tom Rust, President
Photon Energy Systems
tel - (510) 912-4662 fax - (510) 339-9636
info@photonenergysys.com

wendman solar+power solar+energy solar+panels solar+cells photovoltaic nanosys Sunpower konarka Cyrium Nanosolar Miasole powerfilm DFJ NEA Jurvetson Heeger Alivisatos quantum+dot quantum+dot+solar+cells nano nanotech nanotechnology global+warming renewable+energy clean+tech

Thoughtful Lecture by Sir Harold Kroto

2007-03-03T11:14:00.000-08:00

This is a lecture by Sir Harold Kroto - a nobel prize winner for chemistry with Richard Smalley and Robert Curl in 1996 - for discovery of C-60 the Buckyball form of carbon.

Kroto is a wonderful witty lecturer, with a sublime understanding of science, its meaning and purposes.

The lecture was given Nov 2006 in Alberta.