prep4md

What Is Cryptorchidism? (undescended testis)

2012-01-29T18:27:00.001+02:00

Cryptorchidism is the absence of one or both testes from the scrotum. It is the most common birth defect regarding male genitalia. In unique cases, cryptorchidism can develop later in life, often as late as young adulthood. About 3% of full-term and 30% of premature infant boys are born with at least one undescended testis. However, about 80% of cryptorchid testes descend by the first year of life (the majority within three months), making the true incidence of cryptorchidism around 1% overall. Cryptorchidism is distinct from monorchism the condition of having only one testicle.

A testis absent from the normal scrotal position can be:

-found anywhere along the "path of descent" from high in the posterior (retroperitoneal) abdomen, just below the kidney, to the inguinal ring;
-found in the inguinal canal;
-ectopic, that is, found to have "wandered" from that path, usually outside the inguinal canal and sometimes even under the skin of the thigh, the perineum, the opposite scrotum, or the femoral canal;
-found to be undeveloped (hypoplastic) or severely abnormal (dysgenetic);
-found to have vanished (also see anorchia).

About two thirds of cases without other abnormalities are unilateral; one third involve both testes. In 90% of cases an undescended testis can be palpated in the inguinal canal; in a minority the testis or testes are in the abdomen or nonexistent (truly "hidden").

Undescended testes are associated with reduced fertility, increased risk of testicular germ cell tumors and psychological problems when the boy is grown. Undescended testes are also more susceptible to testicular torsion and infarction and inguinal hernias. To reduce these risks, undescended testes are usually brought into the scrotum in infancy by a surgical procedure called an orchiopexy.

Although cryptorchidism nearly always refers to congenital absence or maldescent, a testis observed in the scrotum in early infancy can occasionally "reascend" (move back up) into the inguinal canal. A testis which can readily move or be moved between the scrotum and canal is referred to as retractile.

Cryptorchidism is derived from the Greek words "crypto" (meaning "hidden") and "orchid" (meaning "testicle"). During the last century, cryptorchidism was sometimes restricted to the subset of undescended testes that were not palpable above the scrotum or in the inguinal canal – those that were truly hidden in the abdomen or completely absent. In recent decades the distinction is no longer made in most contexts, and the two terms are used interchangeably. Cryptorchism is an older variant of the same term.

Normal fetal testicular development and descent:

The testes begin as an immigration of primordial germ cells into testicular cords along the genital ridge in the abdomen of the early embryo. The interaction of several male genes organizes this developing gonad into a testis rather than an ovary by the second month of gestation. During the 3rd to 5th months, the cells in the testes differentiate into testosterone-producing Leydig cells, and anti-müllerian hormone-producing Sertoli cells. The germ cells in this environment become fetal spermatogonia. Male external genitalia develop during the 3rd and 4th months of gestation and the fetus continues to grow, develop, and differentiate.

The testes remain high in the abdomen until the 7th month of gestation, when they move from the abdomen through the inguinal canals into the two sides of the scrotum. It has been proposed that movement occurs in two phases, under control of somewhat different factors. The first phase, movement across the abdomen to the entrance of the inguinal canal appears controlled (or at least greatly influenced) by anti-müllerian hormone (AMH). The second phase, in which the testes move through the inguinal canal into the scrotum, is dependent on androgens (most importantly testosterone).Maldevelopment of the gubernaculum, or deficiency or insensitivity to either AMH or androgen therefore can prevent the testes from descending into the scrotum. Some evidence suggests there may even be an additional paracrine hormone, referred to as descendin, secreted by the testes.

In many infants with inguinal testes, further descent of the testes into the scrotum occurs in the first 6 months of life. This is attributed to the postnatal surge of gonadotropins and testosterone that normally occurs between the first and fourth months of life.

Spermatogenesis continues after birth. In the 3rd to 5th months of life, some of the fetal spermatogonia residing along the basement membrane become type A spermatogonia. More gradually, other fetal spermatogonia become type B spermatogonia and primary spermatocytes by the 5th year after birth. Spermatogenesis arrests at this stage until puberty.

Most normal-appearing undescended testis are also normal by microscopic examination, but reduced spermatogonia can be found. The tissue in undescended testes becomes more markedly abnormal ("degenerates") in microscopic appearance between 2 and 4 years after birth. There is some evidence that early orchiopexy reduces this degeneration.

Causes and risk factors

In most full-term infant boys with cryptorchidism but no other genital abnormalities, a cause cannot be found, making this a common, sporadic, unexplained (idiopathic) birth defect.

Severely premature infants can be born before descent of testes.

There is a strong association of cryptorchidism with low birthweight due to either prematurity or intrauterine growth retardation. In these infants there is usually no evidence of hormonal malfunction. Inguinal hernias associated with low birthweight are common.

A contributing role of environmental chemicals – endocrine disruptors – that interfere with normal fetal hormone balance has been proposed and is rarely possible to implicate a specific chemical exposure for an individual child.

Environmental risk factors may include exposure to regular alcohol consumption during pregnancy (5 or more drinks per week, associated with a 3x increase in cryptorchidism, when compared to non-drinking mothers).

A small percentage of cases of isolated cryptorchidism are familial.

Cryptorchidism occurs at a much higher rate in a large number of congenital malformation syndromes. Among the more common are Prader-Willi syndrome, Noonan syndrome, and cloacal exstrophy.

Diagnosis

The most common diagnostic dilemma in otherwise normal boys is distinguishing a retractile testis from a testis that will not/cannot descend spontaneously into the scrotum. Retractile testes are more common than truly undescended testes and do not need to be operated on. In normal males, as the cremaster muscle relaxes or contracts, the testis moves lower or higher ("retracts") in the scrotum. This cremasteric reflex is much more active in infant boys than older men. A retractile testis high in the scrotum can be difficult to distinguish from a position in the lower inguinal canal. Though there are various maneuvers used to do so, such as using a crosslegged position, soaping the examiner's fingers, or examining in a warm bath, the benefit of surgery in these cases can be a matter of clinical judgement.

In the minority of cases with bilaterally non-palpable testes, further testing to locate the testes, assess their function, and exclude additional problems is often useful. Pelvic ultrasound or magnetic resonance imaging performed and interpreted by a radiologist can often, but not invariably, locate the testes while confirming absence of a uterus. A karyotype can confirm or exclude forms of dysgenetic primary hypogonadism, such as Klinefelter syndrome or mixed gonadal dysgenesis. Hormone levels (especially gonadotropins and AMH) can help confirm that there are hormonally functional testes worth attempting to rescue, as can stimulation with a few injections of human chorionic gonadotropin to elicit a rise of the testosterone level. Occasionally these tests reveal an unsuspected and more complicated intersex condition.

In the even smaller minority of cryptorchid infants who have other obvious birth defects of the genitalia, further testing is crucial and has a high likelihood of detecting an intersex condition or other anatomic anomalies. Ambiguity can indicate either impaired androgen synthesis or reduced sensitivity. The presence of a uterus by pelvic ultrasound suggests either persistent müllerian duct syndrome (AMH deficiency or insensitivity) or a severely virilized genetic female with congenital adrenal hyperplasia. An unambiguous micropenis, especially accompanied by hypoglycemia or jaundice, suggests congenital hypopituitarism.

Treatment

The primary management of cryptorchidism is surgery, called orchiopexy. It is usually performed in infancy, if inguinal testes have not descended after 4–6 months, often by a pediatric urologist or pediatric surgeon, but in many communities still by a general urologist or surgeon.

When the undescended testis is in the inguinal canal, hormonal therapy is sometimes attempted and occasionally successful. The most commonly used hormone therapy is human chorionic gonadotropin. A series of hCG injections (10 injections over 5 weeks is common) is given and the status of the testis/testes is reassessed at the end. Although many trials have been published, the reported success rates range widely, from roughly 5 to 50%, probably reflecting the varying criteria for distinguishing retractile testes from low inguinal testes.

Hormone treatment does have the occasional incidental benefits of allowing confirmation of Leydig cell responsiveness (proven by a rise of the testosterone by the end of the injections) or inducing additional growth of a small penis (via the testosterone rise). Some surgeons have reported facilitation of surgery, perhaps by enhancing the size, vascularity, or healing of the tissue. A newer hormonal intervention used in Europe is use of GnRH analogs such as nafarelin or buserelin; the success rates and putative mechanism of action are similar to hCG, but some surgeons have combined the two treatments and reported higher descent rates. Limited evidence suggests that germ cell count is slightly better after hormone treatment; whether this translates into better sperm counts and fertility rates at maturity has not been established. The cost of either type of hormone treatment is less than that of surgery and the chance of complications at appropriate doses is minimal. Nevertheless, despite the potential advantages of a trial of hormonal therapy, many surgeons do not consider the success rates high enough to be worth the trouble since the surgery itself is usually simple and uncomplicated.

In cases where the testes are identified preoperatively in the inguinal canal, orchiopexy is often performed as an outpatient and has a very low complication rate. An incision is made over the inguinal canal. The testis with accompanying cord structure and blood supply is exposed, partially separated from the surrounding tissues ("mobilized"), and brought into the scrotum. It is sutured to the scrotal tissue or enclosed in a "subdartos pouch." The associated passage back into the inguinal canal, an inguinal hernia, is closed to prevent re-ascent.

When the testis is in the abdomen, the first stage of surgery is exploration to locate it, assess its viability, and determine the safest way to maintain or establish the blood supply. Multi-stage surgeries, or auto-transplantation and anastomosis, are more often necessary in these situations. Just as often, intra-abdominal exploration discovers that the testis is non-existent ("vanished"), or dysplastic and not salvageable.

The principal major complication of all types of orchiopexy is loss of the blood supply to the testis, resulting in loss of the testis due to ischemic atrophy or fibrosis.

Pathophysiology

At least one contributing mechanism for reduced spermatogenesis in cryptorchid testes is temperature. The temperature of testes in the scrotum is at least a couple of degrees cooler than in the abdomen. Animal experiments in the middle of the 20th century suggested that raising the temperature could damage fertility. Some circumstantial evidence suggests tight underwear and other practices that raise testicular temperature for prolonged periods can be associated with lower sperm counts. Nevertheless, research in recent decades suggests that the issue of fertility is more complex than a simple matter of temperature. It seems likely that subtle or transient hormone deficiencies or other factors that lead to lack of descent also impair the development of spermatogenic tissue.

The inhibition of spermatogenesis by ordinary intra-abdominal temperature is so potent that continual suspension of normal testes tightly against the inguinal ring at the top of the scrotum by means of special "suspensory briefs" has been researched as a method of male contraception, and was referred to as "artificial cryptorchidism" by one report.

An additional factor contributing to infertility is the high rate of anomalies of the epididymis in boys with cryptorchidism (over 90% in some studies). Even after orchiopexy, these may also affect sperm maturation and motility at an older age.

The most common type of testicular cancer occurring in undescended testes is seminoma. It is usually treatable if caught early, so urologists often recommend that boys who had orchiopexy as infants be taught testicular self-examination, to recognize testicular masses and seek early medical care for them. Cancer developing in an intra-abdominal testis would be unlikely to be recognized before considerable growth and spread, and one of the advantages of orchiopexy is that a mass developing in a scrotal testis is far easier to recognize than an intra-abdominal mass.

The risk of malignancy in the undescended testis is 4 to 10 times higher than that in the general population and is approximately 1 in 80 with a unilateral undescended testis and 1 in 40 to 1 in 50 for bilateral undescended testes. The peak age for this tumor is 15–45 yr. The most common tumor developing in an undescended testis is a seminoma (65%); in contrast, after orchiopexy, seminomas represent only 30% of testis tumors.

What Is Intussusception?

2012-01-29T00:46:00.001+02:00

An intussusception is a medical condition in which a part of the intestine has invaginated into another section of intestine, similar to the way in which the parts of a collapsible telescope slide into one another. This can often result in an obstruction. The part that prolapses into the other is called the intussusceptum, and the part that receives it is called the intussuscipiens.

Early symptoms can include nausea, vomiting (sometimes bile stained (green color), pulling legs to the chest area, and intermittent moderate to severe cramping abdominal pain. Pain is intermittent not because the intussusception temporarily resolves, but because the intussuscepted bowel segment transiently stops contracting. Later signs include rectal bleeding, often with "red currant jelly" stool (stool mixed with blood and mucus), and lethargy. Physical examination may reveal a "sausage-shaped" mass felt upon palpation of the abdomen.

In children or those too young to communicate their symptoms verbally, they may cry, draw their knees up to their chest or experience dyspnea (difficult or painful breathing) with paroxysms of pain.

Fever is not a symptom of intussusception. However, intussusception can cause a loop of bowel to become necrotic, secondary to ischemia due to compression to arterial blood supply. This leads to perforation and sepsis, which causes fever.

Diagnosis

Intussusception is often suspected based on history and physical exam, including observation of Dance's sign. Per rectal examination is particularly helpful in children as part of the intussusceptum may be felt by the finger. A definite diagnosis often requires confirmation by diagnostic imaging modalities. Ultrasound is today considered the imaging modality of choice for diagnosis and exclusion of intussusception due to its high accuracy and lack of radiation. A target-like mass, usually around 3 cm in diameter, confirms the diagnosis. An x-ray of the abdomen may be indicated for evaluation of intestinal obstruction or the presence of free intraperitoneal gas; the latter finding would imply that bowel perforation has already occurred. In some institutions, air enema is used for diagnosis as the same procedure can be used for treatment.

Differential diagnosis

Intussusception has three main differential diagnoses. These are acute gastroenteritis, Henoch–Schönlein purpura, and rectal prolapse. Abdominal pain, vomiting, and stool with mucus and blood are present in acute gastroenteritis, but diarrhea is the leading symptom. Rectal prolapse can be differentiated by projecting mucosa that can be felt in continuity with the perianal skin, whereas in intussusception the finger may pass indefinitely into the depth of sulcus. Henoch–Schönlein purpura presents the characteristic rash.

Treatment

The condition is not usually immediately life-threatening. The intussusception can be treated with either a barium or water-soluble contrast enema or an air-contrast enema, which both confirms the diagnosis of intussusception, and in most cases successfully reduces it. The success rate is over 80%. However, approximately 5–10% of these recur within 24 hours.

If it cannot be reduced by an enema or if the intestine is damaged, then a surgical reduction is necessary. In a surgical reduction, the abdomen is opened and the part that has telescoped in is squeezed out (rather than pulled out) manually by the surgeon or if the surgeon is unable to successfully reduce it or the bowel is damaged, the affected section will be resected. More often, the intussusception can be reduced by laparoscopy, whereby the segments of intestine are pulled apart by forceps.

Prognosis

The outlook for intussusception is excellent when treated quickly, but when untreated it can lead to death within 2–5 days. Fast treatment is a necessity, because the longer the intestine segment is prolapsed the longer it goes without bloodflow, and the less effective a non-surgical reduction will be. Prolonged intussusception also increases the likelihood of bowel ischemia and necrosis, requiring surgical resection.

Kathryn Schulz: On being wrong

2012-01-26T01:05:00.000+02:00

Are Electronic Cigarettes Bad For You?

2012-01-20T13:01:00.000+02:00

What Is Burkitt's Lymphoma?

2011-12-28T22:34:00.001+02:00

Burkitt's lymphoma (or "Burkitt's tumor", Burkitt lymphoma or "malignant lymphoma, Burkitt's type") is a cancer of the lymphatic system (in particular, B lymphocytes).

Burkitt's lymphoma can be divided into three main clinical variants: the endemic, the sporadic and the immunodeficiency-associated variants. Burkitt's lymphoma is usually associated with over 90% of AIDS cases.

The endemic variant occurs in equatorial Africa. It is the most common malignancy of children in this area. Children affected with the disease often also had chronic malaria, which is believed to have reduced resistance to Epstein-Barr virus (EBV), allowing it to take hold. The disease characteristically involves the jaw or other facial bone, distal ileum, cecum, ovaries, kidney or the breast.

The sporadic type of Burkitt lymphoma (also known as "non-African") is another form of non-Hodgkin lymphoma found outside of Africa. The tumor cells have a similar appearance to the cancer cells of classical African or endemic Burkitt lymphoma. Again it is believed that impaired immunity provides an opening for development of the Epstein-Barr virus. Non-Hodgkin lymphoma, which includes Burkitt's, accounts for 30-50% of childhood lymphoma. The jaw is less commonly involved, compared to the endemic variant. The ileo-cecal region is the common site of involvement.

Immunodeficiency-associated Burkitt lymphoma is usually associated with HIV infection or occurs in the setting of post-transplant patients who are taking immunosuppressive drugs. Burkitt lymphoma can be one of the diseases associated with the initial manifestation of AIDS.

By morphology (i.e. microscopic appearance) or immunophenotype, it is almost impossible to differentiate these three clinical variants. Immunodeficiency-associated Burkitt lymphoma may demonstrate more plasmacytic appearance or more pleomorphism, but these features are not specific.

The tumor consists of sheets of a monotonous (i.e. similar in size and morphology) population of medium size lymphoid cells with high proliferative activity and apoptotic activity. The "starry sky" appearance seen under low power is due to scattered tingible body-laden macrophages (macrophages containing dead body of apoptotic tumor cells). The old descriptive term of "small non-cleaved cell" is misleading. The tumor cells are mostly medium in size (i.e. tumor nuclei size similar to that of histiocytes or endothelial cells). "Small non-cleaved cells" are compared to "large non-cleaved cells" of normal germinal center lymphocytes. Tumor cells possess small amount of basophilic cytoplasm. The cellular outline usually appears squared off.

Almost by definition, Burkitt's lymphoma is associated with a chromosomal translocation of the c-myc gene. This gene is found at 8q24.

Treatment includes dose-adjusted EPOCH with Rituxan (rituximab).

Effect of the chemotherapy, as with all cancers, depends on the time of diagnosis. With faster growing cancers, such as Burkitt's, the cancer actually responds faster than with slower growing cancers. This rapid response to chemotherapy can be hazardous to patient, as a phenomenon called "tumor lysis syndrome" could occur. Close monitoring of patient and adequate hydration is essential during the process.

Chemotherapy:
cyclophosphamide
doxorubicin
vincristine
methotrexate
cytarabine
ifosfamide
etoposide
rituximab

Other treatments are immunotherapy, bone marrow transplants, surgery to remove the tumor, and radiotherapy.

http://en.wikipedia.org/wiki/Burkitt's_lymphoma

AIDS Defining Clinical Condition

2011-12-26T23:40:00.005+02:00

AIDS Defining Clinical Condition

Candidiasis of bronchi, trachea, or lungs
Candidiasis esophageal
Coccidioidomycosis, disseminated or extrapulmonary
Cryptococcosis, extrapulmonary
Cryptosporidiosis, chronic intestinal for longer than 1 month
Cytomegalovirus disease (other than liver, spleen or lymph nodes)
Cytomegalovirus retinitis (with loss of vision)
Encephalopathy (HIV-related)
Herpes simplex: chronic ulcer(s) (for more than 1 month); or bronchitis, pneumonitis, or esophagitis
Histoplasmosis, disseminated or extrapulmonary
Isosporiasis, chronic intestinal (for more than 1 month)
Kaposi's sarcoma
Lymphoma, Burkitt's
Lymphoma, immunoblastic (or equivalent term)
Lymphoma, primary, of brain
Mycobacterium avium complex or Mycobacterium kansasii, disseminated or extrapulmonary
Mycobacterium, other species, disseminated or extrapulmonary
Mycobacterium tuberculosis, any site (extrapulmonary)
Pneumocystis jiroveci pneumonia (formerly Pneumocystis carinii)
Progressive multifocal leukoencephalopathy
Salmonella septicemia (recurrent)
Toxoplasmosis of the brain
Tuberculosis, disseminated
Wasting syndrome due to HIV
Cervical cancer (invasive)
Mycobacterium tuberculosis, any site (pulmonary)
Pneumonia (recurrent)

And in Children < 13 years:

Bacterial infections, multiple or recurrent
Lymphoid interstitial pneumonia or pulmonary lymphoid hyperplasia complex

What Is Kaposi's Sarcoma?

2011-12-26T19:10:00.000+02:00

Kaposi's sarcoma (KS) is a tumor caused by Human herpesvirus 8 (HHV8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV). It became more widely known as one of the AIDS defining illnesses in the 1980s. The viral cause for this cancer was discovered in 1994. Although KS is now well-established to be caused by a virus infection, there is widespread lack of awareness of this even among persons at risk for KSHV/HHV-8 infection.

Restated, Kaposi’s sarcoma (KS) is a systemic disease which can present with cutaneous lesions with or without internal involvement. Four subtypes have been described: Classic KS, affecting middle aged men of Mediterranean and Jewish descent, African endemic KS, KS in iatrogenically immunosuppressed patients, and AIDS-related KS. The erythematous to violaceous cutaneous lesions seen in KS have several morphologies: macular, patch, plaque, nodular, and exophytic. The cutaneous lesions can be solitary, localized or disseminated. KS can involve the oral cavity, lymph nodes, and viscera. Classic KS tends to be indolent, presenting with erythematous or violaceous patches on the lower extremities. African endemic KS and AIDS-related KS tend to be more aggressive. The AIDS-related KS lesions often rapidly progress to plaques and nodules affecting the upper trunk, face, and oral mucosa. The diagnosis can be made with a tissue biopsy and, if clinically indicated, internal imaging should be done.

Once the diagnosis of KS has been made, treatment is based on the subtype and the presence of localized versus systemic disease. Localized cutaneous disease can be treated with cryotherapy, intralesional injections of vinblastine, alitretinoin gel, radiotherapy, topical immunotherapy (imiquimod), or surgical excision. Extensive cutaneous disease and/or internal disease may require IV chemotherapy and immunotherapy. Discontinuation or reduction of immunosuppressive therapy is recommended when KS arises in the setting of iatrogenic immunosuppression. However, with AIDS-related KS, HAART has been shown to prevent or induce regression of KS. Some AIDS patients have complete resolution of the lesions and prolonged remission while continuing the therapy. Therefore, HAART should be considered first-line treatment for these patients, though they may require other concomitant treatments.

Types

Since Moritz Kaposi first described this malignant neoplasm, the disease has been reported in five separate clinical settings, with different presentations, epidemiology, and prognoses

Classic Kaposi sarcoma
African cutaneous Kaposi sarcoma
African lymphadenopathic Kaposi sarcoma
AIDS-associated Kaposi sarcoma
Immunosuppression-associated Kaposi sarcoma

Signs and symptoms

KS lesions are nodules or blotches that may be red, purple, brown, or black, and are usually papular (i.e. palpable or raised).
They are typically found on the skin, but spread elsewhere is common, especially the mouth, gastrointestinal tract andrespiratory tract. Growth can range from very slow to explosively fast, and is associated with significant mortality andmorbidity.

Skin

Commonly affected areas include the lower limbs, back, face, mouth and genitalia. The lesions are usually as described above, but may occasionally be plaque-like (often on the soles of the feet) or even involved in skin breakdown with resulting fungating lesions. Associated swelling may be from either local inflammation or lymphoedema (obstruction of local lymphatic vessels by the lesion). Skin lesions may be quite disfiguring for the sufferer, and a cause of much psychosocial pathology.

Mouth

Is involved in about 30%, and is the initial site in 15% of AIDS related KS. In the mouth, the hard palate is most frequently affected, followed by the gums. Lesions in the mouth may be easily damaged by chewing and bleed or suffer secondary infection, and even interfere with eating or speaking.

Gastrointestinal tract

Involvement can be common in those with transplant related or AIDS related KS, and it may occur in the absence of skin involvement. The gastrointestinal lesions may be silent or cause weight loss, pain, nausea/vomiting, diarrhea, bleeding (either vomiting blood or passing it with bowel motions), malabsorption, or intestinal obstruction.

Respiratory tract

Involvement of the airway can present with shortness of breath, fever, cough, hemoptysis (coughing up blood), or chest pain, or as an incidental finding on chest x-ray. The diagnosis is usually confirmed by bronchoscopy when the lesions are directly seen, and often biopsied.

Pathophysiology

Despite its name, it is generally not considered a true sarcoma, which is a tumor arising from mesenchymal tissue. KS actually arises as a cancer of lymphatic endothelium and forms vascular channels that fill with blood cells, giving the tumor its characteristic bruise-like appearance. KSHV proteins are uniformly detected in KS cancer cells.

KS lesions contain tumor cells with a characteristic abnormal elongated shape, called spindle cells. The tumor is highly vascular, containing abnormally dense and irregular blood vessels, which leak red blood cells into the surrounding tissue and give the tumor its dark color. Inflammation around the tumor may produce swelling and pain.

Although KS may be suspected from the appearance of lesions and the patient's risk factors, definite diagnosis can only be made by biopsy and microscopic examination, which will show the presence of spindle cells. Detection of the KSHV protein LANA in tumor cells confirms the diagnosis.

Treatment

Blood tests to detect antibodies against KSHV have been developed and can be used to determine if a patient is at risk for transmitting infection to their sexual partner, or if an organ is infected prior to transplantation. Unfortunately, these tests are not available except as research tools and thus there is little screening for persons at risk for becoming infected with KSHV, such as transplant patients.

Kaposi's sarcoma is not curable (in the usual sense of the word) but it can often be effectively palliated for many years and this is the aim of treatment. In KS associated with immunodeficiency or immunosuppression, treating the cause of the immune system dysfunction can slow or stop the progression of KS. In 40% or more of patients with AIDS-associated Kaposi's sarcoma, the Kaposi lesions will shrink upon first starting highly active antiretroviral therapy (HAART). However, in a certain percentage of such patients, Kaposi's sarcoma may again grow after a number of years on HAART, especially if HIV is not completely suppressed. Patients with a few local lesions can often be treated with local measures such as radiation therapy or cryosurgery. Surgery is generally not recommended as Kaposi's sarcoma can appear in wound edges. More widespread disease, or disease affecting internal organs, is generally treated with systemic therapy with interferon alpha, liposomal anthracyclines (such as Doxil) or paclitaxel.

With the decrease in the death rate among AIDS patients receiving new treatments in the 1990s, the incidence and severity of epidemic KS also decreased. However, the number of patients living with AIDS is increasing substantially in the United States, and it is possible that the number of patients with AIDS-associated Kaposi's sarcoma will again rise as these patients live longer with HIV infection.

What Is Fragile X Syndrome?

2011-12-24T12:31:00.003+02:00

Fragile X syndrome (FXS), Martin–Bell syndrome, or Escalante's syndrome, is a genetic syndrome that is the most commonly known single-gene cause of autism and the most common inherited cause of intellectual disability. It results in a spectrum of characteristic physical and intellectual limitations and emotional and behavioral features which range from severe to mild in manifestation.

The syndrome is associated with the expansion of a single trinucleotide gene sequence (CGG) on the X-chromosome, and results in a failure to express the protein coded by the FMR1 gene, which is required for normal neural development. There are four generally accepted states of the chromosome region involved in Fragile X syndrome which relate to the length of the repeated CGG sequence; Normal (6-50 CGG repeats)(not affected by the syndrome) , Premutation (59-200 CGG repeats)(occasionally affected in later years with the development of Fragile X associated tremor/ataxia syndrome), and Full Mutation (more than 200 CGG repeats)(affected).

Aside from intellectual disability, prominent characteristics of the syndrome include an elongated face, large or protruding ears, flat feet, larger testes (macroorchidism), and low muscle tone. Speech may include cluttered speechor nervous speech. Behavioral characteristics may include stereotypic movements (e.g., hand-flapping) and atypical social development, particularly shyness, limited eye contact, memory problems, and difficulty with face encoding.

Some individuals with the fragile X syndrome also meet the diagnostic criteria for autism. Most females who have the syndrome experience symptoms to a lesser degree because of their second X-chromosome; however, they can develop symptoms just as severe as their male counterparts. While full mutation males tend to present with severe intellectual disability, the symptoms of full mutation females run the gamut of minimally affected to severe intellectual disability, which may explain why females are underdiagnosed relative to males.

Physical phenotype:

Prominent ears (one or both)
Long face (vertical maxillary excess)
High-arched palate (related to the above)
Hyperextensible finger joints
Double-jointed thumbs
Flat feet
Larger testes in men after puberty (postpubescent macroorchidism)
Low muscle tone

Social interaction

FXS is characterized by social anxiety, including gaze aversion, prolonged time to commence social interaction, and challenges forming peer relationships. Social anxiety in individuals with FXS is related to challenges with face encoding. Face encoding is the ability to recognize a face that one has seen before.

Individuals with FXS show decreased activation in the prefrontal regions of the brain. These regions are associated with social cognition. A child with FXS is likely to have hyperactivity, anxiety, and social deficits. Individuals with fragile X-associated tremor/ataxia syndrome (FXTAS) are likely to experience dementia, mood and/or anxiety disorders. Males with the FMR1 premutation and clinical evidence of FXTAS were found to have increased occurrence of somatization,obsessive–compulsive disorder, interpersonal sensitivity, depression, phobic anxiety and psychoticism.

Fragile X syndrome was originally diagnosed by culturing cells in a folate deficient medium and then assessing the cultures for X-chromosome "breakage" by cytogenetic analysis of the long arm of the X-chromosome (the appearance of a broken chromosome being caused by discontinuity of staining in the region of the trinucleotide repeat). This technique proved unreliable for both diagnosis and carrier testing.

The fragile X abnormality is now directly determined by analysis of the number of CGG repeats and their methylation status using restriction endonuclease digestion and Southern blot analysis.

Not everyone with fragile X syndrome has the same signs and symptoms. Even affected people in the same family don’t show the same symptoms. The signs and symptoms fall into six categories:

Intelligence and learning
Physical
Social and emotional
Speech and language
Sensory
Disorders commonly associated or sharing features with Fragile X

Fragile X syndrome is an X-linked dominant condition with variable expressivity and possibly reduced penetrance.

Alberto Cairo: There are no scraps of men

2011-12-24T00:05:00.000+02:00

What Is Antiphospholipid Syndrome?

2011-12-23T16:06:00.004+02:00

Antiphospholipid syndrome or antiphospholipid antibody syndrome (APS or APLS or), often also Hughes syndrome, is an autoimmune, hypercoagulable state caused by antibodies against cell-membranephospholipids that provokes blood clots (thrombosis) in both arteries andveins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, or severe preeclampsia. The syndrome occurs due to the autoimmune production of antibodies against phospholipid (aPL), a cell membrane substance. In particular, the disease is characterised by antibodies against cardiolipin (anti-cardiolipin antibodies) and β2 glycoprotein I. The term "primary antiphospholipid syndrome" is used when APS occurs in the absence of any other related disease. APS however also occurs in the context of other autoimmune diseases, such as systemic lupus erythematosus (SLE), in which case the term "secondary antiphospholipid syndrome" is used.

Antiphospholipid syndrome can cause (arterial/venous) blood clots (in any organ system) or pregnancy-related complications. In APS patients, the most common venous event is deep vein thrombosis of the lower extremities (blood clot of the deep veins of the legs) and the most common arterial event is stroke. In pregnant women affected by APS, miscarriage can occur prior to 20 week of gestation, while pre-eclampsia is reported to occur after that time. Placental infarctions, early deliveries and stillbirth are also reported in women with APS. In some cases, APS seems to be the leading cause of mental and/or development retardation in the newborn, due to an aPL-induced inhibition of trophoblastdifferentiation. The antiphospholipid syndrome responsible for most of the miscarriages in later trimesters seen in concomitant systemic lupus erythematosus and pregnancy.

Other common findings, although not part of the APS classification criteria, are thrombocytopenia (low platelet count), heart valve disease, and livedo reticularis (a skin condition). Some patients report headaches, migraines, and oscillopsia (Oscillopsia is a visual disturbance in which objects in the visual field appear to oscillate). Very few patients with primary APS go on to develop SLE.

Antiphospholipid syndrome is tested for in the laboratory using both liquid phase coagulation assays (lupus anticoagulant) and solid phase ELISA assays (anti-cardiolipin antibodies).

Genetic thrombophilia is part of the differential diagnosis of APS and can coexist in some APS patients. Presence of genetic thrombophilia may determine the need for anticoagulation therapy. Thus genetic thrombophilia screening can consist of: Further studies for Factor V Leiden variant and the prothrombin mutation, Factor VIII levels, MTHFR mutation. Levels of protein C, free and total protein S, Factor VIII, antithrombin, plasminogen, tissue plasminogen activator (TPA) and plasminogen activator inhibitor-1 (PAI-1)

The testing of antibodies to the possible individual targets of aPL such as β2 glycoprotein 1 and antiphosphatidyl serine is currently under debate as testing for anticardiolipin appears to be currently sensitive and specific for diagnosis of APS even though cardiolipin is not considered an in vivo target for antiphospholipid antibodies. Lupus anticoagulant: This is tested for by using a minimum of two coagulation tests that are phospholipid sensitive, due to the heterogeneous nature of the lupus anticoagulant antibodies. The patient on initial screening will typically have been found to have a prolonged APTT. These tests must be carried out on a minimum of two occasions at least 6 weeks apart and be positive on each occasion demonstrating persistent positivity to allow a diagnosis of antiphospholipid syndrome. This is to prevent patients with transient positive tests (due to infection etc.) being diagnosed as positive.

Distinguishing a lupus antibody from a specific coagulation factor inhibitor (e.g.: Factor VIII). This is normally achieved by differentiating the effects of a lupus anticoagulant on factor assays from the effects of a specific coagulation factor antibody. The lupus anticoagulant will inhibit all the contact activation pathway factors (Factor VIII, Factor IX, Factor XI and Factor XII). Lupus anticoagulant will also rarely cause a factor assay to give a result lower than 35 iu/dl (35%) where as a specific factor antibody will rarely give a result higher than 10 iu/dl (10%). Monitoring IV anticoagulant therapy by the APTT ratio is compromised due to the effects of the lupus anticoagulant and in these situations is generally best performed using a chromogenic assay based on the inhibition of Factor Xa by antithrombin in the presence of heparin.

Classification with APS requires evidence of both one or more specific, documented clinical events (either a vascular thrombosis and/or adverse obstetric event) and the confirmed presence of a repeated aPL. The Sapporo APS classification criteria (1998, published in 1999) were replaced by the Sydney criteria in 2006.

Based on the most recent criteria, classification with APS requires one clinical and one laboratory manifestation:

Clinical:

A documented episode of arterial, venous, or small vessel thrombosis—other than superficial venous thrombosis in any tissue or organ by objective validated criteria with no significant evidence of inflammation in the vessel wall and/or
1 or more unexplained deaths of a morphologically normal fetus (documented by ultrasound or direct examination of the fetus) at or beyond the 10th week of gestation and/or 3 or more unexplained consecutive spontaneous abortions before the 10th week of gestation, with maternal anatomic or hormonal abnormalities and paternal and maternal chromosomal causes excluded or at least 1 premature birth of a morphologically normal neonate before the 34th week of gestation due to eclampsia or severe pre-eclampsia according to standard definitions, or recognized features of placental insufficiency plus

Laboratory:

Anti-cardiolipin IgG and/or IgM measured by standardized, non-cofactor dependent ELISA on 2 or more occasions, not less than 12 weeks apart; medium or high titre (i.e., > 40 GPL or MPL, or > the 99th percentile) and/or
Anti-β2 glycoprotein I IgG and/or IgM measured by standardized ELISA on 2 or more occasions, not less than 12 weeks apart; medium or high titre (> the 99th percentile) and/or
Lupus anticoagulant detected on 2 occasions not less than 12 weeks apart according to the guidelines of the International Society of Thrombosis and Hemostasis.

Often, this disease is treated by giving aspirin to inhibit platelet activation, and/or warfarin as an anticoagulant. The goal of the prophylactic treatment is to maintain the patient's INR between 2.0 - 3.0. In refractory cases plasmapheresis may be used.

What Are The Most Common STDs in Men?

2011-12-23T01:43:00.000+02:00

HIV/AIDS
Gonorrhea
Chlamydia
Herpes Simplex Virus-2 (HSV-2)
Human Papillomavirus (HPV)
Syphilis

Remember your "ABCs." A is for “abstinence.” B is for “be faithful.” C is for “condom.”

What are G protein-coupled receptors (GPCRs)?

2011-12-21T10:40:00.004+02:00

G protein-coupled receptors (GPCRs), also known as seven-transmembrane domain receptors, 7TM receptors, heptahelical receptors, serpentine receptor, and G protein-linked receptors (GPLR), comprise a large protein family of transmembrane receptors that sensemolecules outside the cell and activate inside signal transduction pathways and, ultimately, cellular responses. G protein-coupled receptors are found only in eukaryotes, including yeast, choanoflagellates, and animals. The ligands that bind and activate these receptors include light-sensitive compounds, odors, pheromones, hormones, and neurotransmitters, and vary in size from small molecules to peptides to large proteins. G protein-coupled receptors are involved in many diseases, and are also the target of approximately 40% of all modern medicinal drugs.

There are two principal signal transduction pathways involving the G protein-coupled receptors: the cAMP signal pathway and the Phosphatidylinositol signal pathway. When a ligand binds to the GPCR it causes a conformational change in the GPCR, which allows it to act as a guanine nucleotide exchange factor (GEF). The GPCR can then activate an associated G-protein by exchanging its bound GDP for a GTP. The G-protein's α subunit, together with the bound GTP, can then dissociate from the β and γ subunits to further affect intracellular signaling proteins or target functional proteins directly depending on the α subunit type (Gαs, Gαi/o, Gαq/11, Gα12/13).

GPCRs are involved in a wide variety of physiological processes. Some examples of their physiological roles include:

The visual sense: the opsins use a photoisomerization reaction to translate electromagnetic radiation into cellular signals. Rhodopsin, for example, uses the conversion of 11-cis-retinal to all-trans-retinal for this purpose
The sense of smell: receptors of the olfactory epithelium bind odorants (olfactory receptors) and pheromones (vomeronasal receptors)
Behavioral and mood regulation: receptors in the mammalian brain bind several different neurotransmitters, includingserotonin, dopamine, GABA, and glutamate
Regulation of immune system activity and inflammation: chemokine receptors bind ligands that mediate intercellular communication between cells of the immune system; receptors such as histamine receptors bind inflammatory mediators and engage target cell types in the inflammatory response
Autonomic nervous system transmission: both the sympathetic and parasympathetic nervous systems are regulated by GPCR pathways, responsible for control of many automatic functions of the body such as blood pressure, heart rate, and digestive processes
Cell density sensing: A novel GPCR role in regulating cell density sensing.
Homeostasis modulation (e.g., water balance).

Structurally GPCRs are characterized by an extracellular N-terminus, followed by seventransmembrane (7-TM) α-helices (TM-1 to TM-7) connected by three intracellular (IL-1 to IL-3) and three extracellular loops (EL-1 to EL-3), and finally an intracellular C-terminus. The GPCR arranges itself into atertiary structure resembling a barrel, with the seven transmembrane helices forming a cavity within the plasma membrane that serves a ligand-binding domain that is often covered by EL-2. Ligands may also bind elsewhere, however, as is the case for bulkier ligands (e.g., proteins or large peptides), which instead interact with the extracellular loops, or, as illustrated by the class C metabotropic glutamate receptors (mGluRs), the N-terminal tail. The class C GPCRs are distinguished by their large N-terminal tail, which also contains a ligand-binding domain. Upon glutamate-binding to an mGluR, the N-terminal tail undergoes a conformational change that leads to its interaction with the residues of the extracellular loops and TM domains. The eventual effect of all three types of agonist-induced activation is a change in the relative orientations of the TM helices (likened to a twisting motion) leading to a wider intracellular surface and “revelation” of residues of the intracellular helices and TM domains crucial to signal transduction function (i.e., G-protein coupling). Inverse agonists andantagonists may also bind to a number of different sites, but the eventual effect must be prevention of this TM helix reorientation.

A final common structural theme among GPCRs is palmitoylation of one or more sites of the C-terminal tail or the intracellular loops. Palmitoylation is the covalent modification of cysteine (Cys) residues via addition of hydrophobic acyl groups, and has the effect of targeting the receptor to cholesterol- and sphingolipid-rich microdomains of the plasma membrane called lipid rafts. As many of the downstream transducer and effector molecules of GPCRs (including those involved in negative feedback pathways) are also targeted to lipid rafts, this has the effect of facilitating rapid receptor signaling.

GPCRs respond to extracellular signals mediated by a huge diversity of agonists, ranging from proteins to biogenic aminesto protons, but all transduce this signal via a mechanism of G-protein coupling. This is made possible by virtue of a guanine-nucleotide exchange factor (GEF) domain primarily formed by a combination of IL-2 and IL-3 along with adjacent residues of the associated TM helices.

The G protein-coupled receptor is activated by an external signal in the form of a ligand or other signal mediator. This creates a conformational change in the receptor, causing activation of a G protein. Further effect depends on the type of G protein.

GPCRs include receptors for sensory signal mediators (e.g., light and olfactory stimulatory molecules); adenosine, bombesin, bradykinin,endothelin, γ-aminobutyric acid (GABA), hepatocyte growth factor (HGF),melanocortins, neuropeptide Y, opioidpeptides, opsins, somatostatin, tachykinins, members of the vasoactive intestinal peptidefamily, and vasopressin; biogenic amines (e.g.,dopamine, epinephrine, norepinephrine,histamine, glutamate (metabotropic effect),glucagon, acetylcholine (muscarinic effect), and serotonin); chemokines; lipid mediators of inflammation (e.g., prostaglandins,prostanoids, platelet-activating factor, and leukotrienes); and peptide hormones (e.g.,calcitonin, C5a anaphylatoxin, follicle-stimulating hormone (FSH), gonadotropin-releasing hormone (GnRH), neurokinin, thyrotropin-releasing hormone (TRH), andoxytocin). GPCRs that act as receptors for stimuli that have not yet been identified are known as orphan receptors.

There are two principal signal transduction pathways involving the G protein-linked receptors: cAMP signal pathway and Phosphatidylinositol signal pathway.

cAMP signal pathway

The cAMP signal transduction contains 5 main characters: stimulative hormone receptor (Rs) or inhibitory hormone receptor (Ri)

Stimulative hormone receptor (Rs) is a receptor that can bind with stimulative signal molecules, while inhibitory hormone (Ri) is a receptor that can bind with inhibitory signal molecules.

Stimulative regulative G-protein is a G protein-linked to stimulative hormone receptor (Rs) and its α subunit upon activation could stimulate the activity of an enzyme or other intracellular metabolism. On the contrary, inhibitory regulative G-protein is linked to an inhibitory hormone receptor and its α subunit upon activation could inhibit the activity of an enzyme or other intracellular metabolism.

The Adenylyl cyclase is a 12-transmembrane glucoprotein that catalyzes ATP to form cAMP with the help of cofactor Mg2+ or Mn2+. The cAMP produced is a second messenger in cellular metabolism and is an allosteric activator to Protein kinase A.

Protein kinase A is an important enzyme in cell metabolism due to its ability to regulate cell metabolism by phosphorylating specific committed enzymes in the metabolic pathway. It can also regulate specific gene expression, cellular secretion, and membrane permeability. The protein enzyme contains two catalytic subunits and two regulatory subunits. When there is no cAMP the complex is inactive. When cAMP binds to the regulatory subunits, their conformation is altered, causing the dissociation of the regulatory subunits, which activates protein kinase A and allows further biological effects.

cAMP phosphodiesterase is an enzyme that can degrade cAMP to 5'-AMP, which will terminate the signal.

Phosphatidylinositol signal pathway

In the phosphatidylinositol signal pathway, the extracellular signal molecule binds with the G-protein receptor (Gq) on the cell surface and activates phospholipase C, which is located on the plasma membrane. The lipase hydrolyzes phosphatidylinositol 4,5-bisphosphate (PIP2) into two second messengers: Inositol 1,4,5-trisphosphate (IP3) and Diacylglycerol (DAG). IP3 binds with the receptor in the membrane of the smooth endoplasmic reticulum and mitochondria, help open the Ca2+ channel. DAG will help activate Protein Kinase C (PKC), which phosphorylates many other proteins, changing their catalytic activities, leading to cellular responses. The effects of Ca2+ is also remarkable: it cooperates with DAG in activating PKC and can activate CaM kinase pathway, in which calcium modulated protein calmodulin (CaM) binds Ca2+, undergoes a change in conformation, and activates CaM kinase II, which has unique ability to increase its binding affinity to CaM by autophosphorylation, making CaM unavailable for the activation of other enzymes. The kinase then phosphorylates target enzymes, regulating their activities. The two signal pathways are connected together by Ca2+-CaM, which is also a regulatory subunit of adenylyl cyclase and phosphodiesterase in cAMP signal pathway.

Hemoglobin/ Red Blood Cell Recycling Animation

2011-12-17T23:18:00.000+02:00

RNA interference: by Nature Video

2011-12-17T00:10:00.000+02:00

Nephron Function & Electrolytes

2011-12-15T18:01:00.001+02:00

Key topic for USMLE Step 1. Dont forget where different classes of diuretics work.

Sketch of a nephron:

http://static.newworldencyclopedia.org/7/72/Renal_Diuretics.gif

The nephron carries out nearly all of the kidney's functions. Most of these functions concern the reabsorption and secretion of various solutes such as ions (e.g., sodium), carbohydrates (e.g., glucose), and amino acids (e.g., glutamate). Properties of the cells that line the nephron change dramatically along its length; consequently, each segment of the nephron has highly specialized functions.

The proximal tubule as a part of the nephron can be divided into an initial convoluted portion and a following straight (descending) portion. Fluid in the filtrate entering the proximal convoluted tubule is reabsorbed into the peritubular capillaries, including approximately two-thirds of the filtered salt and water and all filtered organic solutes (primarily glucose and amino acids).

The loop of Henle, is a U-shaped tube that extends from the proximal tubule. It consists of a descending limb and ascending limb. It begins in the cortex, receiving filtrate from the proximal convoluted tubule, extends into the medulla as the descending limb, and then returns to the cortex as the ascending limb to empty into the distal convoluted tubule. The primary role of the loop of Henle is to concentrate the salt in the interstitium, the tissue surrounding the loop.

Considerable differences distinguish the descending and ascending limbs of the loop of Henle. The descending limb is permeable to water and noticeably less impermeable to salt, and thus only indirectly contributes to the concentration of the interstitium. As the filtrate descends deeper into the hypertonic interstitium of the renal medulla, water flows freely out of the descending limb by osmosis until the tonicity of the filtrate and interstitium equilibrate. Longer descending limbs allow more time for water to flow out of the filtrate, so longer limbs make the filtrate more hypertonic than shorter limbs.

Unlike the descending limb, the ascending limb of Henle's loop is impermeable to water, a critical feature of the countercurrent exchange mechanism employed by the loop. The ascending limb actively pumps sodium out of the filtrate, generating the hypertonic interstitium that drives countercurrent exchange. In passing through the ascending limb, the filtrate grows hypotonic since it has lost much of its sodium content. This hypotonic filtrate is passed to the distal convoluted tubule in the renal cortex.

The distal convoluted tubule has a different structure and function to that of the proximal convoluted tubule. Cells lining the tubule have numerous mitochondria to produce enough energy (ATP) for active transport to take place. Much of the ion transport taking place in the distal convoluted tubule is regulated by the endocrine system. In the presence of parathyroid hormone, the distal convoluted tubule reabsorbs more calcium and excretes more phosphate. When aldosterone is present, more sodium is reabsorbed and more potassium excreted. Atrial natriuretic peptide causes the distal convoluted tubule to excrete more sodium. In addition, the tubule also secretes hydrogen and ammonium to regulate pH.

After traveling the length of the distal convoluted tubule, only about 1% of water remains, and the remaining salt content is negligible.

Though the collecting duct is normally impermeable to water, it becomes permeable in the presence of antidiuretic hormone(ADH). ADH affects the function of aquaporins, resulting in the reabsorption of water molecules as it passes through the collecting duct. Aquaporins are membrane proteins that selectively conduct water molecules while preventing the passage of ions and other solutes. As much as three-quarters of the water from urine can be reabsorbed as it leaves the collecting duct by osmosis. Thus the levels of ADH determine whether urine will be concentrated or diluted. An increase in ADH is an indication of dehydration, while water sufficiency results in low ADH allowing for diluted urine.

Lower portions of the collecting organ are also permeable to urea, allowing some of it to enter the medulla of the kidney, thus maintaining its high concentration.

Urine leaves the medullary collecting ducts through the renal papillae, emptying into the renal calyces, the renal pelvis, and finally into the urinary bladder via the ureter.

The juxtaglomerular apparatus is a specialized region of the nephron responsible for production and secretion of the enzyme Renin, involved in the renin-angiotensin system. This apparatus occurs near the site of contact between the thick ascending limb and the afferent arteriole. It contains three components: the macula densa, juxtaglomerular cells, and extraglomerular mesangial cells.

Yoav Medan: Ultrasound surgery -- healing without cuts

2011-12-14T23:34:00.000+02:00

Ultra sound surgery.

Charity Tillemann-Dick: After a lung transplant, an aria

2011-12-14T00:31:00.000+02:00

Quyen Nguyen: Color-coded surgery

2011-12-14T00:28:00.000+02:00

Spell of the Albino - Africa

2011-12-12T01:55:00.000+02:00

Since 2008, at least 62 albinos have been killed in Tanzania, 16 have been violently assaulted and had their limbs amputated and the bodies of 12 albinos have been exhumed from graves and dismembered.

Spell of the Albino - Africa Investigates - Al Jazeera English

Twelve Health and Safety Tips for the Holidays

2011-12-07T21:15:00.003+02:00

Wash hands often.
Bundle up to stay dry and warm. Wear appropriate outdoor clothing: layers of light, warm clothing; mittens; hats; scarves; and waterproof boots.
Manage stress. Don't over-commit yourself and prevent holiday anxiety and pressure.
Get enough sleep.
Be smoke-free. Avoid smoking and second-hand smoke. There is NO safe amount of tobacco or secondhand smoke. Breathing even a little secondhand smoke can be dangerous.
Get your vaccinations, which help prevent diseases and save lives.
Prepare food safely. Remember these simple steps: wash hands and surfaces often, avoid cross-contamination, cook foods to proper temperatures, and refrigerate promptly.
Eat healthy, and get moving. Eat fruits and vegetables. Limit your portion sizes and foods high in fat and sugar.
Be active for at least 2½ hours a week and help kids and teens be active for at least 1 hour a day.
...

Read full list at: http://www.cdc.gov/Features/HealthyTips/

Conjoined Twins: Twin Girls, A Medical Wonder

2011-12-07T21:05:00.000+02:00

Video: Top Tips to Survive Medical School

2011-11-30T18:50:00.000+02:00

Why Is College So Expensive?

2011-11-29T02:49:00.000+02:00

Intravenous line insertion

2011-10-20T01:06:00.000+02:00

How Herd Immunity Works (and Why Anti-Vaccination Is Dangerous)

2011-01-01T16:55:00.000+02:00