Sunday, 2 September 2012

Peutz—Jeghers syndrome

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.



Thursday, 30 August 2012

Dew 2

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

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.


Tuesday, 21 August 2012

An Appeal!

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Monday, 13 August 2012

PATHOGENESIS in ALCOHOLIC LIVER DISEASE

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