Biomedical subjects
G Patel
Publications and source records attributed to G Patel.
Monoclonal antibodies against adenovirus type 5: preparation and preliminary characterization.
Eight different hybridoma cells lines producing monoclonal antibodies against the major antigens of human adenovirus type 5 have been obtained. They were selected by screening initial hybridomas by the fluorescent antibody technique followed by radioimmune precipitation and they reacted with hexon, penton, fibre and 100K polypeptides. Five apparently different epitopes against the hexon antigen were detected showing a spectrum of activity against the hexons of other serotypes, suggesting that the hexon contained a variety of subgroup specificities as well as the previously described group and type specificities.
Intraluminal pressure measurements during barium enema: full column vs. air contrast.
Intraluminal pressure measurements were made during enema examination of 10 patients undergoing full column studies and 10 patients receiving air-contrast studies. There was no significant difference between the pressure in the distal colon of the two groups. All pressures were less than those produced by Valsalva maneuver or straight leg raising, and were generally less than those previously found to be necessary to rupture the colon. The authors believe that the findings should dispel any fear that an air-contrast examination is more hazardous than a full column study. Perforations occurring during these procedures are more likely related to disease of the colon wall or local trauma.
Sensitive assays for trypsin, elastase, and chymotrypsin using new fluorogenic substrates.
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Comparison of pharmaceutical quality of laboratory made macroaggregated albumin with commercially available products.
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A new fluorogenic substrate for chymotrypsin.
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Mechanisms underlying potentiation of barbiturate action by sodium nitrite in the mouse: the role of methemoglobin-induced hypoxia.
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Studies of the nuclear residual proteins.
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Partial purification of DNA-polymerase from the non-histone chromatin proteins of rat liver.
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Amino acid incorporation system of the nuclear residual acidic proteins.
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Localization of DNA-polymerase in the cell nucleus of calf thymus.
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Insulin dependent diabetes in children.
We present our experience with twenty children with insulin dependent diabetes mellitus admitted during the past 2 1/2 years. Sixteen patients were admitted with acute onset of ketoacidosis while four were having gradual onset. Active and symptomatic treatment was started in all diabetic ketoacidotic patients. One patient died during the acute stage. Eleven patients were followed for 3-6 months or more. Glycosylated hemoglobin was considered as a criteria for control. Three had good control, two fair and six poor control; six developed diabetic ketoacidosis and three developed hypoglycemia.
Viral hepatitis in the 1990s, Part I: Current principles of management.
Recent years have brought major advances in the diagnosis and treatment of viral hepatitis. Treatment of acute uncomplicated hepatitis is supportive rather than curative. Treatment of fulminant hepatic necrosis is directed towards preventing and treating complications while preparing suitable patients for liver transplantation. Corticosteroids do not improve survival rates in patients with fulminant hepatic necrosis and should be avoided in nearly all patients with hepatitis A. Although liver histology in acute viral hepatitis is highly characteristic, biopsy is usually superfluous, except in transplant patients with acute hepatic dysfunction. Hepatitis A virus infection is frequently asymptomatic, and data on its incidence are poor. The virus is frequently transmitted before the patient becomes ill; therefore, curtailing hepatitis A spread depends in large measure on hygienic practices. Passive immunization is possible with immune globulin. Inactivated and attenuated vaccines may be licensed within the next 2 years.
Viral hepatitis in the 1990s, Part II: Hepatitis B and delta virus.
Parenterally shared blood and sexual transmission are the main routes of spread of hepatitis B in the United States. Most cases resolve spontaneously without specific treatment. Passive immunization provides temporary protection in certain postexposure settings. Active immunization achieves high protection rates. Duration of protection and the need for booster doses are not well defined. Many cases of fulminant B hepatitis, severe chronic active hepatitis, and end-stage cirrhosis secondary to hepatitis B are due to hepatitis delta virus infection. The delta virus requires the presence of hepatitis B for expression of disease. Hepatitis B prophylaxis should help eliminate delta hepatitis.
Viral hepatitis in the 1990s, Part III: Hepatitis C, hepatitis E, and other viruses.
Acute hepatitis can be caused by a number of viruses, especially A, B, C, E, delta, Epstein-Barr virus, and cytomegalovirus. Hepatitis A and B have been discussed previously in this series. The virus responsible for most cases of what commonly has been referred to as non-A non-B hepatitis has been tracked, and antibodies to certain proteins of this virus have been identified. This virus is now referred to as hepatitis C. The possible clinical outcomes after acute hepatitis C virus infection are similar to those for hepatitis B virus infection, except that hepatitis C is far more likely to become chronic. Clinical testing for hepatitis C virus infection is in its infancy and has certain limitations. Successful treatment of at least some cases of hepatitis C is possible. Hepatitis E has recently been described, primarily in third-world countries. It causes an acute hepatitis that may be particularly lethal for pregnant women. Herpesviruses may also cause hepatitis, particularly in the newborn or the immunocompromised. Exotic viruses causing acute hepatitis are enumerated.