DREAM

Easy way to end BAD HABITS

noreply@blogger.com (NICE) — Tue, 10 Feb 2015 03:46:00 +0000

Cardionice greetings folks,

Wondered always how to terminate minor unfruitful wrong thoughts and ha bits.

Recently found a reasonable solution,

We NICE group friends,thought of Displaying here,

it goes like this. .....

There are number of distraction techniques helped children delay gratification more effectively. Such techniques included singing songs, thinking about something else, or covering the eyes.

Delaying gratification isn't always so cut-and-dry in the real world, however. While the children in Mischel's study had the promise of a secondary reward for waiting just a short period of time, everyday scenarios don't always come with this guarantee. If you give up that brownie, you still might not lose weight. If you skip a social event to study, you still might do poorly on the exam.

It is this uncertainty that makes giving up immediate rewards so difficult. That delicious treat in front of you now is a sure thing, but your goal of losing weight seems much further off and not so certain. uncertainty about future rewards is what makes delaying gratification such a challenge. " we don't know when these long-term rewards will arrive – or even if they will ever arrive. Give definitive time-frames: In situation where people are not sure when they will receive an expected reward, giving feedback on just how long they will have to wait can be beneficial. Train stations might post wait times, for example, while teachers might give students a definitive deadline for when students will receive a promised reward.

Set realistic deadlines: When trying to achieve a goal, such as losing weight, people are sometimes prone to either setting unrealistic deadlines. For example, a dieter might set himself up for failure if he makes a completely unrealistic goal of losing 10 pounds per week. When he fails to lose those first 10 pounds, he might then give up and give in to temptation. A more realistic goal of one pound per week would allow the dieter to see real results of his efforts.

So, friends answer is simple - deadline. .

<Let's do it, and may it be one step in making a better world around us />

noreply@blogger.com (NICE) — Thu, 29 Jan 2015 08:06:00 +0000

Imagine your home.
# you are going inside your room.
# there was a box.
# people are standing around it.
# you trespassing them to see what is in the box.
# you are hearing what people talking
# you were lying inside the box.
...
What you want to hear from your people at your condolence, is what you lived.
So live like what you want to live

noreply@blogger.com (NICE) — Thu, 29 Jan 2015 08:00:00 +0000

We all know this thing. If I do good, I get good. No one came up with the recipe to remain good. I am waiting for that

Mitotane and infertility

noreply@blogger.com (NICE) — Thu, 20 Nov 2014 12:13:00 +0000

Men with classic 21-hydroxylase deficiency are at risk for infertility.

The mechanisms are complex and involve three factors:

gonadotropin inhibition due to the excessive secretion of progestin by the adrenal glands,

obstruction of the rete testis, and

destruction of the testes by testicular adrenal rest tumors.

Antisecretory and antitumoral activities of mitotane, a drug that induces “chemical adrenalectomy restore the fertility of a man with both 21-hydroxylase deficiency and azoospermia.

The 21-hydroxylase deficiency was suspected at birth because of salt wasting and was confirmed by elevated serum levels of 17-hydroxyprogesterone and molecular analysis of CYP21A2.

Posted via Blogaway

noreply@blogger.com (NICE) — Thu, 19 Jun 2014 11:42:00 +0000

hashCode and equals

Lets understand with a small example where and why hashCode and equals are used.

Java.lang.Object has methods called hasCode() and equals(). These methods play a significant role in the real time application. However its use is not always common to all applications. In some case these methods are overridden to perform certain purpose. I will explain you some concept of these methods and why it becomes necessary to override these methods.

Lets say, you have a Map containing employees object as the key and String as value. Eg: Map<Employee,String> where Employee Object -> EmpId,EmpName,Age. Lets assume there are many entries in the map and you want to find if two employee objects are equal. So following will be the basic implementation of a java developer.

package com.test;

public class Employee {

String EmpName;

int EmpNo;

int age;

public Employee(String EmpName,int EmpNo,int age) {

this.EmpName = EmpName;

this.EmpNo = EmpNo;

this.age = age;

}

public static void main(String[] args) {

/* 3 Employee Objects Created and checking if e1 and e3 objects are equal */

Employee e1 = new Employee("Sri",02,27);

Employee e2 = new Employee("Priya",03,28);

Employee e3 = new Employee("Sri",02,27);

/* e1 and e3 objects will not be equal */

System.out.println("Are E1 and E3 equal:" +e1.equals(e3));

System.out.println("e1 hash code:" +e1.hashCode());

System.out.println("e2 hash code:" +e2.hashCode());

System.out.println("e3 hash code:" +e3.hashCode());

}

Output:

Are E1 and E3 equal:false

e1 hash code:28117098

e2 hash code:17008065

e3 hash code:4354460

Why did it return false. As per the above code,e1 and e3 objects seem to have the same values in the Employee Object and hence it should be equal right?

Whenever we create a object, JVM allocates a memory/address space on the heap for the object. Object generates a HashCode based on the memory address of the instance of the object. This hash code generation is done internally and need not worry about the generation. For us, hashCode is just a random number generated by the JVM.

So in this case, e1 will have one hashcode generated ad e2 will have another hashcode generated and e3 will have another hashcode generated. So, when we say e1.equals(e3), it checks if e1 hashcode is equal to e3 hashcode. It will be different and hence it returned false. It checks if two different objects are equal.

What can we do to overcome this situation? We can generate hashcode of our own with any logic of developer choice and check the equality which will result in a positive scenario.

package com.test;

public class Employee {

String EmpName;

int EmpNo;

int age;

public Employee(String EmpName,int EmpNo,int age) {

this.EmpName = EmpName;

this.EmpNo = EmpNo;

this.age = age;

}

public int hashCode(){

int hashCode = EmpNo*age;

return hashCode;

}

public static void main(String[] args) {

/* 3 Employee Objects Created and checking if e1 and e3 objects are equal */

Employee e1 = new Employee("Sri",02,27);

Employee e2 = new Employee("Priya",03,28);

Employee e3 = new Employee("Sri",02,27);

/* e1 and e3 objects will not be equal */

System.out.println("Are E1 and E3 equal:" +e1.equals(e3));

System.out.println("e1 hash code:" +e1.hashCode());

System.out.println("e2 hash code:" +e2.hashCode());

System.out.println("e3 hash code:" +e3.hashCode());

}

Output:

Are E1 and E3 equal:false

e1 hash code:54

e2 hash code:84

e3 hash code:54

Now, we have similar hashcodes generated with our logic but still e1 and e3 are unequal.Because, it uses java out of box equals method to check equality. There is a contract between the hashCode and equals that they have to go hand in hand else you may encounter issues. So, whenever we implement hashCode method, we will also implement equals method. Lets write a equals method now. Lets say, if empId is unique in e1 and e3, we will declare that they are equal and will return a boolean true/false.

package com.test;

public class Employee {

String EmpName;

int EmpNo;

int age;

public Employee(String EmpName,int EmpNo,int age) {

this.EmpName = EmpName;

this.EmpNo = EmpNo;

this.age = age;

}

public int hashCode(){

int hashCode = EmpNo*age;

return hashCode;

}

public boolean equals(Object obj) {

boolean flag=false;

if(this.EmpNo == ((Employee)obj).EmpNo)

flag=true;

return flag;

}

public static void main(String[] args) {

/* 3 Employee Objects Created and checking if e1 and e3 objects are equal */

Employee e1 = new Employee("Sri",02,27);

Employee e2 = new Employee("Priya",03,28);

Employee e3 = new Employee("Sri",02,27);

/* e1 and e3 objects will not be equal */

System.out.println("Are E1 and E3 equal:" +e1.equals(e3));

System.out.println("e1 hash code:" +e1.hashCode());

System.out.println("e2 hash code:" +e2.hashCode());

System.out.println("e3 hash code:" +e3.hashCode());

}

Output:

Are E1 and E3 equal:true

e1 hash code:54

e2 hash code:84

e3 hash code:54

We have got the two objects equal now. So, Whenever there is any Object equality check, we should implement hashCode and equals method to avoid problems with Object manipulations/retrievals.

Hope this post helps.

The Frey's.....

noreply@blogger.com (NICE) — Fri, 18 Apr 2014 05:31:00 +0000

Frey....
2 terminologies in medicine.

Frey s syndrome :
Gustatory sweating.

Etio: misdirected regeneration of auriculotemporal nerve following parotid injury or surgery.
First case reported by polish neurologist Lucja Frey.. 1923.

Frey's procedure:
In Chronic pancreatitis...
For:
Disease in head of pancreas
How:
Diseased head chopped off. Competed with Pancreaticojejunostomy ..
This is named for the American surgeon C. F. Frey...1987

The henle's...

noreply@blogger.com (NICE) — Thu, 17 Apr 2014 16:19:00 +0000

Loop of henle, between PCT and DCT -kidneys ,
The other Henle's anatomical & pathological findings are:

Crypts of Henle: Microscopic pockets located in the conjunctiva of the eye.

Hassall-Henle bodies: Transparent growths in the periphery of the Descemet membrane of the eye.

Henle's fissure: Fibrous tissue between the cardiac muscle fibers.

Henle's ampulla: Ampulla of the uterine tube.

Henle's layer: Outer layer of cells of root sheath of a hair follicle.

Henle's ligament: Tendon of the transversus abdominis muscle.

Henle's membrane: Bruch’s layer forming inner boundary of the choroid of the eye.

Henle's sheath: Connective tissue which supports outer layer of nerve fibres in a funiculus.

Henle's spine: The supra-meateal spine that serves as a landmark in the mastoid area.

Potter syndrome

noreply@blogger.com (NICE) — Thu, 17 Apr 2014 16:16:00 +0000

Features :
POTTER:

Pulmonary hypoplasia
Oligohydrominios
Twisted skin (wrinkly skin)
Twisted face (Potter facies)
Extremities defects
Renal agenesis (bilateral)

Potter syndrome refers to the typical physical appearance and associated pulmonary hypoplasia of a neonate as a direct result of oligohydramnios (lack of amniotic fluid and kidney failure )and compression while in utero.

Potter phenotype refers to a typical facial appearance that occurs in a newborn when there is no amniotic fluid. The lack of amniotic fluid is called oligohydramnios. Without amniotic fluid, the infant is not cushioned from the walls of the uterus. The pressure of the uterine wall leads to an unusual facial appearance, including widely separated eyes .

Potter phenotype may also lead to abnormal limbs, or limbs that are held in abnormal positions or contracturescontractures. Oligohydramnios also stops development of the lungs, so the lungs do not work properly at birth.

Success secrets

noreply@blogger.com (NICE) — Tue, 15 Apr 2014 05:44:00 +0000

"Our greatest weakness lies in giving up. The most certain way to succeed is always to try just one more time"

On the “powerful blend of instruction, encouragement, and constant practice

“The trick to creativity … is to identify your own peculiar talent and then to settle down to work with it for a good long time ”

Red chilli onion chutney

noreply@blogger.com (NICE) — Fri, 11 Apr 2014 16:50:00 +0000

Shallots 10
Garlic 10small

Tamarind -little
Tomato —3
Salt—as required

1) Grind raw onion garlic redchilli into a paste

2)Then grind raw tomato tamarind and salt into a fine paste

3)In a kadai, put one spoon of oil, mustard, channa dhal, ulunthu dal, curry leaves, pour the onion garlic redchilli paste and fry till raw smell leaves. Now pour the tomato puree and tamarind paste and mix it well, for five minutes.Fry till the Entire raw smell of tomato is gone.

Spicy chilli chutney is ready !

This goes well with paniyaram,dosa,idly.

Medical Sites

noreply@blogger.com (NICE) — Fri, 11 Apr 2014 15:25:00 +0000

These are all some of nice medical websites , share and contribute other useful medical websites.

free streaming videos
http://www.medimaps.co.uk

http://www.memorablemedicine.com
http://www.dpd.cdc.gov/dpdx/
http://www.osceskills.com/
http://www.popfossa.com/
http://www.medicalisland.net/
http://digital-medicine.blogspot.com/
http://meducationtechnology.blogspot.com/
http://medispot123.blogspot.com/
http://www.abcdfree.com/
http://www.elnosocomio.com/
http://www.eophtha.com/eophtha/

the next set of sites we should know

1 AIPGE/AIIMS,NewDelhi

www.aiims.edu

2 AMU. Aligarh

www.amu.ac.in

3 AFMC, Pune

www.armedforces.nic.in

4 Association-CET (Maharashtra)

www.amupmdc.org

5 Association-CET (Karnataka)

www.comedk.org

6 BHU, Varanasi

www.bhu.ac.in

7 CMC, Ludhiana

www.cmcludhiana.org

8 CMC, Vellore

www.home.cmcvellore.ac.in

9 Chandigarh (U.T.)

www.puchd.ac.in

10 DMER (MD/MS)

www.dmer.org

11 Karnataka (MD/MS)

www.rguhs.ac.in

12 Delhi State PG

www.du.ac.in

13 Diplomate of National Board (DNB)

www.natboard.nic.in

14 NIMHANS, Bangalore

www.nimhans.kar.nic.in

15 Dr TN MGR Tamilnadu Medical University

www.tnmmu.ac.in

16 Nizams Institute,Hyderabad

http://nims.ap.nic.in/

17 St.Johns, Bangalore

www.stjohns.in

18 KGMC, Lucknow

www.kgmcindia.edu

19 West Bengal University

www.thewbuhs.org

20 Dr.D Y Patil University

www.dypatiluniversity.org

21 PGI, Chandigarh

www.pgimer.nic.in

22 Rajasthan PG Entrance

www.ruhsraj.org

23 UPSC

www.upsc.gov.in

23 Dental council of India

www.dciindia.org

24 Medical Council of India

www.mciindia.org

25 Family and health welfare

www.mohfw.nic.in

Rare and interesting case

noreply@blogger.com (NICE) — Fri, 15 Feb 2013 08:09:00 +0000

We had a patient who is left alone in his life for about ten years. To be more clear he was bedridden for those years. The only thing he will do is eat,sometimes pee and poop, but he rarely walks.
People around him thought it was the attitude of elderly. But none of them know the disease he is Developing secretly in his private part. No body touched him or bothered to talk to him so we cannot know anything about fever or anyother ailments. All of their attention turned to him only when foul smell emanated that's about few days before hospitalisation. A pathetic astonishment awaited when they opened his dhoti.
A huge swelling with multiple foul-smelling pus discharging ulcers over his scrotum.
Disgusting!!!!
Immediately took him to hospital where we seen him very badly dehydrated and anemic.,obeys commands but very few verbal response. He was conscious. Except for Bilateral crepitations and wheeze, Systems were normal. His penis got buried into the swelling. The swelling was irreducible, warm and red,tender to touch. Amazingly he was a vegan without any addictions but with diabetes and hypertension . Such an old poor man.
Ultrasound abdomen- bilateral chronic ureteric obstruction with some duodenal wall thickening.
Ultrasound scrotum- bilateral inguinoscrotal hernia with scrotal skin inflammation features.
Planned for bilateral herniorrhaphy and scrotal exploration with debridement .
He was started with piperacillin tazobactam and iv fluids.
On Foley s catheterization, about one litre of urine was drained following that frank pus came out through that catheter about 200ml.
Blood picture showed leucocytosis,renal failure? Chronic,anemia. Chest X-ray showed pulmonary shadows.
Echocardiogram came up with age related cardiac changes.
Decided and posted him for surgery.
Under general anaesthesia, abdomen opened first through lower abdomen transverse incision in layers. On opening about 2/3rd of small bowel loops were herniated through the defect in the anterior abdominal wall on both sides. The herniated bowel loops were lifted up from scrotum on both sides. Fortunately there is no bowel obstruction. Defect was closed with vicryl. While trying to push bowel loops inside the abdominal cavity it was found that his mesentery got elongated due to chronic bowel drag such that abdominal cavity could not accommodate those herniated bowel loops. Decision of resection and anastomosis was made and executed. With drain tube and on attaining hemostats abdomen closed.
Following that scrotum was opened, yaks very foul smelling.
Necrotic areas were removed. Hernial sacs were identified and closed. Scrotal skin was closed and approximated following debridement. Care was taken not to injure urethra.
He was shifted to intensive care with ventilator support.
Surgery was completed without major blood loss.
Vitals got stable. Abdomen became soft and extubated on second post operative day.
But his renal parameters were On its rise, rales and rhonchi never decreased. He was desaturated on post op day three but came up with diuretics and nebulisers. Nephrologist added the dose of diuretics.
He passed flatus with sluggish bowel sounds,and appeared well on fourth post operative day.
Unfortunately on fifth post op night he again desaturated, he was intubated and kept on ventilator. Few hours later, he desaturated again with bradycardia. With in minutes, there was a cardiac arrest.
CPR started ,every efforts were made as per ACLS protocol, but life could not be revived.
He is dead.
Ofcourse,loss at his age would not bring much tragedy to his family yet nature proved its superiority over medical science again.
Cause of death:
Cardiorespiratory arrest
Renal failure
Sepsis
Fournier s gangrene
Diabetes mellitus
Systemic hypertension
Bilateral inguinoscrotal hernia

Non antibiotic approach to UTI treatment

noreply@blogger.com (NICE) — Sun, 30 Sep 2012 15:13:00 +0000

Most important step in causing uti bu uropathogenic Escherichia coli, is the "adhesion" of bacteria to urothelial cells.

This attachment is mediated by "FimH", a mannose-binding adhesin, which is expressed on the bacterial surface.

To date, UTIs are mainly treated with antibiotics, leading to the ubiquitous problem of increasing resistance against most of the currently available antimicrobials. Therefore, new treatment strategies are urgently needed, avoiding selection pressure and thereby implying a reduced risk of resistance.

A new class of highly active antimicrobials, anti adhesive molecule targeting the virulence factor FimH - indolinylphenyl mannoside

When it was administered in a mouse model at the low dosage of 1 mg/kg (corresponding to approximately 25 μg/mouse), the minimal therapeutic concentration to prevent UTI was maintained for more than 8 h. In a treatment study, the colony-forming units in the bladder could be reduced by almost 4 orders of magnitude, comparable to the standard antibiotic treatment with ciprofloxacin (8 mg/kg, sc).

So with the help of this novel anti adhesive molecule UTIs can be managed very simply without antibiotics.

Q: What are the causative organisms of bacterial meningitis?

noreply@blogger.com (NICE) — Sun, 30 Sep 2012 14:40:00 +0000

Haemophilus influenzae, which used to be the most common cause of the disease in infants and young children before the HiB vaccine was introduced.

Listeria monocytogenes can infect people of any age, but pregnant women, very young children, and the elderly are at most risk. L. monocytogenes can be acquired through contaminated foods.

Neisseria meningitidis is highly contagious and causes meningococcal meningitis. This form is commonly found in children and young adults, including college students living in dorms.

Staphylococcus aureus may present itself after head trauma or brain surgery

Streptococcus pneumoniae, the most common cause of bacterial meningitis in children, may appear along with pneumonia, an ear infection, or a sinus infection

Q:Why patient needs to be in supine position after a spinal procedure?

noreply@blogger.com (NICE) — Fri, 21 Sep 2012 08:32:00 +0000

A: Because of spinal headache which is due to dural drag. Dura is the pain sensitive part of the whole nervous system. So after a spinal procedure due to the loss of CSF dura gets pulled down just like pulling down of cloth in umbrella while closing it, but it's very minimal drag that is limited to just headache

Dew 4:a single pill!

noreply@blogger.com (NICE) — Tue, 04 Sep 2012 17:42:00 +0000

A new pill to treat HIV infection that combines four medicines and only has to be taken once a day was approved by the U.S. Food and Drug Administration.

Stribild
which will be marketed by maker Gilead Sciences, contains the HIV drugs elvitegravir, cobicistat, emtricitabine and tenofovir disoproxil fumarate. It will be prescribed to people who have never been treated for HIV infection, the agency said in a statement. Two of the drugs, elvitegravir and cobicistat, are new, the FDA noted. Elvitegravir interferes with one of the enzymes that HIV needs to multiply, while cobicistat inhibits an enzyme that metabolizes certain HIV drugs and so prolongs the effect of elvitegravir.

The combination of emtricitabine and tenofovir disoproxil fumarate is already marketed as Truvada, and they work in concert to block another enzyme that HIV needs to replicate.

dew 5: h2o2 potential!

noreply@blogger.com (NICE) — Tue, 04 Sep 2012 17:31:00 +0000

Q:Is it safe to use hydrogen peroxidein cleaning dirty wounds?

A:Yes, but it is not advisable now a days because Peroxide is a solution made up of hydrogen and oxygen. It is a strong oxidizer and can be used as a cleaning agent and to prevent infections. When used topically, this antiseptic foams due to the enzyme catalase. As the catalase comes in contact with the skin it turns the hydrogen peroxide into water and oxygen gas.

According to health experts at the Swedish Medical Center in Colorado, hydrogen peroxide contains too much oxygen for the blood leading to potential issues. When your skin absorbs hydrogen peroxide, it can reduce the amount of fibroblasts, a particular cell that is imperative for cleaning and repairing damaged tissue

http://www.medicaldaily.com/articles/11831/20120830/the-dangers-of-peroxide.htm#zr2duG06mcuqzeiV.99

Peutz—Jeghers syndrome

noreply@blogger.com (NICE) — Sun, 02 Sep 2012 15:51:00 +0000

Dew3:

There is a congenital condition which presents with acute onset of abdominal pain, vomiting, and abdominal distention in adolescents.

Peutz–Jeghers syndrome, an autosomal dominant disorder characterized by the development of multiple hamartomatous gastrointestinal polyps, mucocutaneous pigmented lesions on the lips or buccal mucosa, and an increased risk of cancer within and outside the gastrointestinal tract.

Dew 2

noreply@blogger.com (NICE) — Thu, 30 Aug 2012 08:21:00 +0000

Single-dose drug cure for malaria

Scientists claim to have discovered a drug that could cure all strains of malaria with a single oral dose and also block transmission of the deadly parasite from person to person. The compound from the aminopyridine class (code named MMV390048) shows potent activity against multiple points in the malaria parasite’s lifecycle. The drug is the first compound researched on African soil to enter preclinical development in partnership with Medicines for malaria venture (MMV), a not-for-profit public-private partnership, in Switzerland. The synthetic molecule from the aminopyridine class, which has been described as novel and potent, not only has the potential to become a single-dose cure for malaria, but researchers are convinced that it could block transmission of the malaria parasite from person to person. The aminopyridine series was initially identified by Griffith University scientists in Australia as part of MMV’s extensive malaria screening campaign of around 6 million compounds. A team of scientists from the University of Cape Town’s (UCT) Drug Discovery and Development Centre (H3-D) in South Africa, led by Professor Kelly Chibale then scrutinised and explored the anti-malarial potential of the series further. With parasitological and pharmacological support from the Swiss Tropical and Public Health Institute and Monash University, respectively, Kelly’s team selected the most promising compounds from the series to be optimized and re-tested. In just 18 months the team had identified and developed a candidate suitable for preclinical development. “We are very excited that this promising compound, researched by African scientists, has been selected by MMV for further development,” Chibale, Founder and Director, UCT H3-D, said. “This is truly a proud day for African science and African scientists! Our team is hopeful that the compound will emerge from rigorous testing as an extremely effective medicine for malaria — a disease that accounts for 24 per cent of total child deaths in sub-Saharan Africa,” Chibale said.

Courtesy : the hindu.

Dew 1

noreply@blogger.com (NICE) — Thu, 30 Aug 2012 02:01:00 +0000

Q:What is the feature shown here?

A:black eyes or racoon's eyes or pandas sign. One of the features of basal skull fracture. Other signs include CSF rhinnorhea.

An Appeal!

noreply@blogger.com (NICE) — Tue, 21 Aug 2012 17:45:00 +0000

We Nice Ventures found that most lengthy not attract viewers or readers and most of our cardionice folks will be expecting to present our content precisely.After Considering many facts,we like to present our cardionice blog audience some DEWS,which are the precise medical contents presented neatly.We need our cardionice folks to continue their support for this new initiative as always.

Thanks

Cardionice,

NICE Ventures

PATHOGENESIS in ALCOHOLIC LIVER DISEASE

noreply@blogger.com (NICE) — Mon, 13 Aug 2012 06:09:00 +0000

Ethanol is mainly absorbed by the small intestine and, to a lesser degree, through the stomach. Gastric alcohol dehydrogenase (ADH) initiates alcohol metabolism. Three enzyme systems account for metabolism of alcohol in the liver. These include cytosolic ADH, the microsomal-oxidizing system (MEOS), and peroxisomal catalase. The majority of ethanol oxidation occurs via ADH to form acetaldehyde, which is a highly reactive molecule that may have multiple effects. Ultimately, acetaldehyde is metabolized to acetate by aldehyde dehydrogenase (ALDH). Intake of ethanol increases intracellular accumulation of triglycerides by increasing fatty acid uptake and by reducing fatty acid oxidation and lipoprotein secretion. Protein synthesis, glycosylation, and secretion are impaired. Oxidative damage to hepatocyte membranes occurs due to the formation of reactive oxygen species; acetaldehyde is a highly reactive molecule that combines with proteins to form protein-acetaldehyde adducts. These adducts may interfere with specific enzyme activities, including microtubular formation and hepatic protein trafficking. With acetaldehyde-mediated hepatocyte damage, certain reactive oxygen species can result in Kupffer cell activation. As a result, profibrogenic cytokines are produced that initiate and perpetuate stellate cell activation, with the resultant production of excess collagen and extracellular matrix. Connective tissue appears in both periportal and pericentral zones and eventually connects portal triads with central veins forming regenerative nodules. Hepatocyte loss occurs, and with increased collagen production and deposition, together with continuing hepatocyte destruction, the liver contracts and shrinks in size. This process generally takes from years to decades to occur and requires repeated insults

Ideal for tasting Death!!!

noreply@blogger.com (NICE) — Fri, 03 Aug 2012 18:34:00 +0000

When farmers were in search of a cheap, most efficacious and easy to use and freely available pesticide fumigant,they found Aluminium Phosphide(ALP) in 1940.

But the First idiot who tasted it for death was in 1981,since then, the number of cases is progressively increasing throughtout the North
India so much so that it is now the single most suicidal
method and the problem has acquired an epidemic
proportion

Physical Properties:
Chalky white or brown 3 gm. tablets containing 56% of ALP and 44% of ammonium carbonate.

The Way it is being used:
The tablets are taken out of sealed container and placed on stored grains and storage container is closed for few days to combat moles and vermines in granaries.

celphos were not used as routine pesticide,it is a fumigant.

Reactions:
ALP has relatively high
vapour pressure that allows it to penetrate porous material
effectively. On coming into contact with water or
moisture or OH radical of air or hydrochloric acid in
stomach,3 gm. tablet of ALP liberates 1gm. of phosphine
or phosphorus hydrogen and each 0.6 gm pellet
0.2 gm of phosphine gas, i.e.,
ALP + 3H20 ----->AL(OH)3 + PH3(in air)
ALP + 3HCL------>ALCL3 + PH3 (in air and stomach)

Few facts about Phosphine (PH3):
PH, is a colourless gas with fishy or garlic odour .
It is removed with half life of 5-24 hours.
The non-toxic residues i.e. phosphites and
hypophosphites of aluminum left in the grains, are less
than 0.1 mg/kg of PH3 for raw cereals, the WHO/FAO
recommended permissible levels regarded safe for human
consumption.

Pathogenesis of toxic effects:
Irrespective of routes of exposure, viz., the
inhalation, ingestion or ocular, the toxic effects of
PH3 are same except initially and are dose dependent.
Some of ALP is directly absorbed from stomach to reach
liver to liberate PH3 slowly to prolong the toxic effects of poisoning.

PH3 is rapidly absorbed from stomach or lungs by
simple diffusion, oxidized slowly.The systemic toxic effects appears in 1-60 minutes after ingestion.This is what the problem of celphos,it reaches and bites the heart soon,so patient will be dying by the time he reaches hospital.

It is excreted in urine as hypophosphite and also excreted unchanged through
lungs significantly.

Basic Act behind the effect:
PH3 inhibits the electron transport resulting from
preferrential inhibition of cytochrome oxidase leading
to respiratory chain inhibition which leads to cellular
hypoxia and small vessel injury which is further
potentiated by cardiotoxicity
due to anoxic myocardial
damage and shock

Direct toxic effect of ALP on myocardium or
hypomagnesemia brought on by focal myocardial
damage leads to arrhythmia s. Hypo tension and shock
ensue within 3-6 hours of ingestion of ALP. In survivors,
the cardiotoxicity and hypoxia disappear within 5-7 days
due to excretion of PH3 and restoration of normal cellular
metabolism.

ECG changes in Celphos poisoning:
The toxic chemical myocarditis leads to
varied fatal ECG changes, 6 to 24 hours after ingestion

in non-survivors, in the form of VE beats, conduction
disturbance, LBBB, ventricular fibrillation, aberrant
conduction and idioventricular rhythm terminally leading

to asystole. The non-fatal ECG changes appear
within 12 to 24 hours in survivors and disappear within
56 to 80 hours. Death in first 24 hours appears to be
cardiogenic as evidenced by shock and ECG abnormality.

The serum electrolytes are within normal limits and not
correlated with ECG changes. Since the survivors show
complete normal ECG recovery, it denotes that the effect
of poisoning is due to some reversible factor leading to
disturbance in the permeability of sodium (Na+),
potassium (K+), calcium (Ca2+) and magnesium (Mg2+)
ions leading to change in trans membrane action potential
due to focal myocardial involvement and subsequent
myocardial necrosis, resulting in release of reactive species and intermediates.

Chugh et al. has shown that ingestion
leads to high superoxide dismutase activity and low
catalase levels that result in increased formation of free
radicals and accelerated lipid peroxidation. Lipid
peroxidation in turn results in damage to cellular
membrane, disruption of ionic barrier, nucleic acid
damage and cell death

Hypomagenesemia seen in ALP poisoning may be due
to an oxidative stress which buffers the Mg2+ resulting
in increased susceptibility of oxygen free radicals injury
and accerlated lipid peroxidation . High level of SOD
(Superperoxide Dismutase) and MDA (Malonyl
dialdehyde) seen in non-survivors suggests their direct
relation to mortality, whereas the catalase has inverse
relationship. The return of SOD and MDA to normal suggests abolition of an oxidative stress due to elimination of phosphine.
Intractable shock may be due to arrhythmia,
conduction disturbance and myocardial damage. The
peripheral circulatory failure (PCF) due to wide spread
small vessel injury leads to peripheral vasodilatation
leading to shock. Excessive vomiting due to fluid loss
results into shock. Direct toxic effects of PH3 on adrenal
cortex accompanied by decreased cortisol levels, leads
to shock and high mortality .
Injury to alveolar capillary membrane by PH3 while
being inhaled, leads to ARDS (Adult Respiratory Distress
Syndrome) which may also occur rarely if patient has
consumed more than 2 to 3 tablets of ALP.
Wide spread capillary damage leads to bleeding
diathesis, disseminated intravascular coagulation (DIC)
and acute tubular necrosis (ATN).

Shock and DIC lead
to terminal renal failure.

Direct toxic effects of ALP or its adsorbed products
or metabolic acidosis on muscles leads to muscular
ischemia and degeneration of nonspecific nature leading
to myopathy.
In blood, the PH3 changes the circular dichroitic
spectra of hemoglobin and change in haem iron leading
to conformational changes of the prosthetic group.
The blood PH3 levels are positively co-related to the
clinical grades of ALP toxicity and to the dose of the
pesticide consumed . The occurrence of intravascular
hemolysis with ALP poisoning in a patient with normal
G6PD levels is of significance as jaundice in patients
with this poisoning is often attributed to the hepatic
damage alone.
In addition to the effect on the adrenal cortex, ALP
also affects glucose metabolism leading to hypoglycemia,
hyperglycemia or no change effects which can be attributed
to the wide variety of changes in Mg2+, Ca2+, phosphate,
citrate or cortisol levels which act as active stimulatory or
inhibitory modulators to enzymes and hormones that
catalyze and regulate glucose metabolism.

Fatal dose
The specified fatal dose is 0.15-0.5 gm. However, most
of the patients present with ingestion of three or more
tablets which invariably results in death.

Management of celphos poisoning:
As with any other poisoning,the primary aim is to decontaminate the stomach.But in this circumstance,to reduce the absorption of
phosphine, gastric lavage with potassium permanganate
(1:10,000) is done. Permanganate is used as it oxidizes
PH3 to form non-toxic phosphate.
This is followed by a slurry of activated charcoal (approximately 100 gm)
given through a naso gastric tube. A cathartic (liquid
paraffin) is given to accelerate the excretion of
aluminium phosphide and phosphine. Antacids and
proton pump blockers are added for symptomatic
relief
Treatment of Shock
• Intravenous fluids 4 to 6 liters within 3-6 hours
the 50% of which should be normal saline, with
concommitent central venous pressure (CVP)
monitoring to raise it to 10 cm. of H20.

Inj.hydrocortisone 400 mg every 4 to 6 hours is
highly effective to decrease capillary leakage in
lungs in ARDS and to potentiate the
responsiveness of the shock to the endo-or
exogenous catecholamines.

Low dose dopamine (4-6 μg/kg/min) is given to keep
systolic blood pressure >90 mm Hg

Send Out the criminal:
Phosphine excretion can be increased by maintaining
adequate hydration and renal perfusion with
intravenous fluids and low dose (4-6 μg/kg/min)
dopamine. Diuretics like frusemide can be given if
systolic blood pressure is >90 mm Hg to enhance
excretion as the main route of elimination of phosphine
is renal.

Treatment of Cardiac Arrhythmias
MgSo4 is effective in first 24 hours in dose of 1
gm. iv stat after dissolving in 100 ml of 5% dextrose or NS
and 1 gm. every hour for next 3 hours and then 1 gm.
every 6 hours for 5-7 days in continuous iv infusion in
5% dextrose. It corrects cardiac arrhythmias by
modulating sympathetic, parasympathetic and slow
channel kinetics. Mg2+ level should be
maintained at less than toxic levels of 10 meq/l. The
magnesium level achieved with said dosage schedule is
2.00 to 3.1 meq/I.
The conventional antiarrhythmic drugs, viz;
digoxin and xylocaine are not effective and cardioversion
is not attempted due to diffuse myocarditis

Metabolic Acidosis
Bicarbonate level less than 15 mEq/L requires sodabicarb in a dose of 50-100 mEq intravenously every 8 hour till the bicarbonate level rises to 18-20 mEq/L. Patients may
require up to 300-500 ml of sodium bicarbonate. The peritoneal or haemodialysis is useful in case, if metabolic acidosis persists in haemodynamically stable patients.

N-acetyl cysteine has also been tried in celphos poisoningto reduce oxidative stress.

The average time interval between intake of poison and death is three hours with a range of 1-48 hours, 95% of the patients
die within 24 hours and the commonest cause of death
in this group is arrhythmia. Death after 24 hours is
due to shock, acidosis, ARDS and arrhythmia

chlorthalidone for Females ????

noreply@blogger.com (NICE) — Fri, 27 Jul 2012 17:41:00 +0000

Cardionice feels happy to bring out a less know drug but with good efficacy and potency in the treatment of hypertension and edema.

Chlorthalidone-
An oral diuretic
prolonged action (48–72 hours) and low toxicity.
Excreted unchanged by the kidneys.
Onset of Diuretic effect - 2.6 hours and continues for up to 72 hours.
Mean half-life following a 50 to 200 mg dose is 40 hours. In the first order of absorption, the elimination half-life is 53 hours following a 50 mg dose, and 60 hours following a 100 mg dose. Approximately 75 percent of the drug is bound to plasma proteins, 58 percent of the drug being bound to albumin. This is caused by an increased affinity of the drug to erythrocyte carbonic anhydrase.

The drug produces copious diuresis with greatly increased excretion of sodium and chloride. At maximal therapeutic dosage, Chlorthalidone is approximately equal in its diuretic effect to comparable maximal therapeutic doses of benzothiadiazine diuretics. The site of action appears to be the cortical diluting segment of the ascending limb of Henle's loop of the nephron.

Hypertension

Initiation:
a single daily dose of 25 mg. If the response is insufficient , dosage may be increased to a single daily dose of 50 mg. If additional control is required, the dosage of Chlorthalidone may be increased to 100 mg once daily or a second antihypertensive drug (step 2 therapy) may be added. Dosage above 100 mg daily usually does not increase effectiveness. Increases in serum uric acid and decreases in serum potassium are dose-related over the 25 to 100 mg/day range.

Maintenance: Maintenance doses may be lower than initial doses and should be adjusted according to individual patient response. Effectiveness is well sustained during continued use.

Edema

Initiation: Adults, initially 50 to 100 mg daily, or 100 mg on alternate days. Some patients may require 150 to 200 mg at these intervals or up to 200 mg daily. Dosages above this level, however, do not usually produce a greater response.

Maintenance: Maintenance doses may often be lower than initial doses and should be adjusted according to individual patient response. Effectiveness is well sustained during continued use.

Think about a menopaused,hypertensive women who is prone for osteoporosis.what drug can kill birds with one arrow???------is the drug what we are discussing as above-chlorthalidone.

It reduces the calcium excretion in kidneys.hence it conserves calcium and helps in preventing osteoporosis.

Nice?????has to be!!!!!!!!!!!!!!!!

Difference between droplet and servlet

noreply@blogger.com (NICE) — Mon, 23 Jul 2012 14:00:00 +0000

Servlet	Droplet
Servlet is a java class which extends HttpServlet	Droplet is java class which extends DynamoServlet (customized in atg)
Servlet extends HttpServlet extends GenericServlet implements javax.servlet.Servlet	Droplet extends Dynamo Servlet extends HttpServletService extends ServletService implements javax.servlet.Servlet
Servlet can be invoked from a jsp giving the servlet path and name <jsp:forward page="/MyServlet"/> or <form method="POST" action="/ProfileSyncService">	Droplet can be embedded in jsp as <dsp:droplet name="sampleDroplet"> to fetch the information
Not applicable.	One or more droplets can be present in a jsp. Nested droplets are also applicable.
Servlet is used to submit data, it acts as a controller. It is not used to put data.	Droplet is used to render or put data in the db