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Biomedical subjects

G Patel

Publications and source records attributed to G Patel.

14 recordsLinked to original sources
PubMed1992

A new method for the isolation of recombinant baculovirus.

An improved method for the isolation of baculovirus recombinants is described. The method involves the replication and maintenance of the baculovirus genome in the yeast Saccharomyces cerevisiae which was accomplished by the isolation of a baculovirus recombinant containing yeast ARS and CEN sequences ensuring stable replication in yeast and a URA3 selectable marker. The viral DNA maintained its ability to replicate in insect cells. An efficient and rapid selection system was set up, to isolate viral recombinants in yeast; DNA from selected yeast colonies was transfected into insect cells to obtain recombinant virus. We demonstrate the utility of this system by isolating recombinant viruses that express two different members of the CREB/ATF family of transcription factors.

Animals↗
PubMed1992

Lithotripsy plus ursodiol is superior to ursodiol alone for cholesterol gallstones.

The safety and efficacy of gallbladder extracorporeal shock-wave lithotripsy combined with 600 mg/day ursodiol were examined in 85 patients with radiolucent gallstones, 15 with lightly calcified gallstones, and 12 with radiolucent stones pretreated for greater than or equal to 2 months with 600 mg/day ursodiol. Results were compared with those of a well-matched lithotripsy-eligible group of 32 subjects treated with ursodiol alone (no lithotripsy). Pretreatment with ursodiol significantly improved while gallstone calcification interfered with fragmentation. Small gallstone size and number also aided fragmentation. Biliary lithotripsy plus ursodiol increased efficacy twofold compared with ursodiol therapy alone (47% vs. 22% of subjects gallstone free; P less than 0.02). Gallstones did not disappear in any subject with calcified gallstones (P less than 0.001) vs. lithotripsy). Product-limit analysis showed that the efficacy for gallstone dissolution increases in the following order: ursodiol alone, lithotripsy-ursodiol, lithotripsy-ursodiol pretreated with ursodiol (P less than 0.02, pairwise). Similar mean gallstone-dissolution rate constants (stone size divided by time to disappear) of stone fragments and whole gallstones during ursodiol therapy suggest that most fragments disappear by dissolution not expulsion. This finding explains why fragmentation appears to be the key predictor of disappearance and even partial fragmentation accelerates gallstone clearance.

Alanine Transaminase↗
PubMed1992

Generation and possible significance of trypsinogen activation peptides in experimental acute pancreatitis in the rat.

Trypsinogen activation peptides (TAP) were quantified by radioimmunoassay in blood, urine, and peritoneal exudate of rats with experimental pancreatitis. Forty-four animals were studied, comprising a control group and four different induction techniques (cerulein, cerulein plus either 2- or 10-min intraductal glycodeoxycholic acid [GDOC] infusion, and cerulein plus intraductal GDOC with enterokinase [EK]). Significantly higher TAP concentrations were found at 6 h (or at death) in plasma and ascites of all pancreatitis groups compared with controls. TAP quantitation in hourly urine samples demonstrated significantly higher concentrations from the third hour onward in the most severe groups and from the fourth hour onward in the cerulein-treated rats. All nonsurviving rats had a plasma TAP of greater than 2.5 nM/L, whereas only 1 of 34 surviving animals had such a concentration (p less than 0.001). A significant stepwise increase in total TAP in ascites was found when comparing the cerulein group, the two GDOC groups, and the EK group (p less than 0.001). Chromatography of samples with a high TAP content demonstrated comigration with synthetic TAP. We conclude that free TAP are present in blood, urine, and peritoneal exudate of rats with experimental pancreatitis of different pathogenesis and that the amount of TAP may be indicative of the severity of the disease process.

Acute Disease↗
PubMed1992

Slow cumulative eye position to quantify optokinetic afternystagmus.

In 30 normal subjects we computed the slow cumulative eye position (SCEP) of optokinetic afternystagmus (OKAN) that followed 60 seconds of full-field optokinetic stimulation at 60 degrees/s. The mean SCEP was 112.8 degrees +/- 65.0 degrees. The lower and upper fifth percentile limits for directional preponderance of the SCEP were -38.8% and 44.3%, respectively. The time constant, which we calculated by dividing the SCEP by the initial velocity, was 12.0 +/- 7.4 seconds. This value is nearly identical to the time constant obtained from semilogarithmic regression of the decay of OKAN slow-phase velocity versus time. We conclude that the SCEP is a good measure of OKAN and that it reflects the substantial amount of variability and directional asymmetry observed in the optokinetic responses of normal subjects.

Algorithms↗
PubMed1992

Alternate mechanisms of ras activation are complementary and favor and formation of ras-GTP.

The mechanisms of ras activation by mutations in residue 61 and in the NKXD guanine nucleotide-binding consensus sequence (ras residues 116-119) have been evaluated. Weakly transforming mutations that either reduce intrinsic and GTPase-activating protein (GAP)-stimulated GTPase activities (61P) or enhance guanine nucleotide exchange rates (116H, 119E) were combined into the same H-ras proteins. The resulting double-mutant proteins exhibited significantly stronger transforming forming activities than are observed with each individual mutation, suggesting that the consequences of these two different mechanisms of activation favor maintenance of ras in the active form, which is GTP bound. In vivo nucleotide association analysis demonstrated a direct relationship between ras-GTP formation and transforming activity. Although both 61P and 61L mutations result in reduced intrinsic GTPase activity and loss of GAP stimulation in vitro, only H-ras(61L) exhibits strong transforming activity. While H-ras(61L) is found predominantly in the GTP-bound form, H-ras(61P) is predominantly complexed with GDP in vivo. Thus, in vitro GAP stimulation of GTPase activity does not directly correlate with transforming potential, suggesting that other ras-specific regulatory components may also be important in regulating the cycling of ras between CDP- and GTP-bound states.

3T3 Cells↗
PubMed1991

Development of enzyme-linked immunosorbent assay for free human pro-colipase activation peptide (APGPR).

Human pancreatic colipase is secreted as the inactive form procolipase. Activation involves tryptic cleavage of an N-terminal pentapeptide Ala-Pro-Gly-Pro-Arg (APGPR) which is known as procolipase activation peptide (CLAP). N-terminally haptenised synthetic APGPR was used to generate specific C-terminally directed anti-APGPR antibodies. The antiserum was used to develop a competitive enzyme linked immunosorbent assay (ELISA) specific for free CLAP with a detection limit of 12 nmol/l and an intra-assay coefficient of variation (CV) of 3.28% and an inter-assay CV of 5.82%. The release of immunoreactive CLAP from human pancreatic juice and chicken pancreas upon trypsinisation was demonstrated, as well as the absence of reactivity of the antisera with procolipase from which the CLAP is released. APGPR was found to be unstable in biological fluids. Immunoreactivity is rapidly lost with half life of 5 min and 4 h in human serum and urine respectively. This loss of reactivity can be significantly slowed by the addition of 20 mmol/l Zinc ions (Zn2+), while ethylenediaminetetra-acetic acid (EDTA) and other protease inhibitors were ineffective. In serum the moiety responsible for loss of immunoreactivity was found to have an estimated molecular mass of 200,000-300,000 Da. CLAP assay specifically reports procolipase activation and may help elucidate the mechanism of satiety as well as contribute to the recognition and understanding of the role of procolipase activation in diseases states such as pancreatitis.

Animals↗
PubMed1991

Percutaneous transluminal angioplasty of proximal subclavian artery stenosis after left internal mammary to left anterior descending artery bypass surgery.

A patient is described who underwent percutaneous transluminal angioplasty, through a brachial approach, of a high grade stenosis at the proximal portion of the left subclavian artery 1.5 years after coronary artery bypass grafting including left internal mammary to left anterior descending artery anastomosis. Symptoms of class IV angina, vertebrobasilar insufficiency and occupational arm claudication that developed after bypass surgery were promptly relieved after balloon dilation. Percutaneous transluminal angioplasty of the subclavian artery can be performed safely and provides an alternative to carotid-subclavian or axillary-axillary bypass surgery for treatment of internal mammary artery graft malfunction.

Angioplasty, Balloon↗
PubMedDate not supplied

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.

Adolescent↗
PubMedDate not supplied

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.

Acute Disease↗
PubMedDate not supplied

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.

Female↗
PubMedDate not supplied

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.

Cytomegalovirus↗