Biomedical subjects
Publications and source records attributed to H Wong.
A group of black adolescents stratified by age and sexual maturity (Tanner stage) had electronic blood counts determined. Hemoglobin, hematocrit, and red cell count were lower than the means reported for white or Hispanic children of the same age. The difference could not be explained by iron deficiency, but the data were insufficient to exclude alpha thalassemia as a cause.
Immunoprecipitations of hepatic lipase from pulse-labeled rat liver have demonstrated that hepatic lipase is synthesized in two distinct molecular weight forms, HL-I (Mr = 51,000) and HL-II (Mr = 53,000). Both forms are immunologically related to purified hepatic lipase, but not to lipoprotein lipase. HL-I and HL-II are also kinetically related and represent different stages of intracellular processing. Glycosidase experiments suggest that HL-I is the high mannose microsomal form of the mature, sialylated HL-II enzyme. Hepatic lipase activity was detected in liver and adrenal gland but was absent in brain, heart, kidney, testes, small intestine, lung, and spleen. The adrenal and liver lipase activities were inhibited in a similar dose-dependent manner by hepatic lipase antiserum. Immunoblot analysis of partially purified adrenal lipase showed an immunoreactive band co-migrating with HL-II at 53,000 daltons which was absent in a control blot treated with preimmune serum. Adrenal lipase and authentic hepatic lipase yielded similar peptide maps, confirming the presence of the lipase in adrenal gland. However, incorporation of L-[35S]methionine into immunoprecipitable hepatic lipase was not detected in this tissue. In addition, Northern blot analysis showed the presence of hepatic lipase mRNA in liver but not adrenal gland. The presence of hepatic lipase in adrenal gland in the absence of detectable synthesis or messenger suggests that hepatic lipase originates in liver and is transported to this extrahepatic site.
The influence of chronic ethanol ingestion on hepatic acyl-CoA: cholesterol acyltransferase activity was investigated to determine the relationship between alcohol intake and cholesterol ester accumulation. Rats were given nutritionally complete liquid diets supplemented with 6.3% ethanol or an isocaloric equivalent of dextrin-maltose for 5 weeks. During this period, the hepatic acyl-CoA: cholesterol acyltransferase activity of ethanol-fed male rats remained constant, whereas the same activity in pair-fed controls as well as chow-fed rats exhibited a 30% decrease in activity. Unlike alcohol-fed male rats, the hepatic acyl-CoA: cholesterol acyltransferase activity of female rats decreased by approximately 30% by the fifth week of ethanol ingestion. Despite the fact that the gender of the animals led to disparate levels of acyl-CoA: cholesterol acyltransferase activity in response to ethanol ingestion, similar levels of cholesteryl ester accumulation were observed. The altered levels of acyl-CoA: cholesterol acyltransferase activity caused no significant change in the cholesterol concentration, cholesterol/phospholipid ratio, phospholipid fatty acid composition, or the membrane fluidity of the hepatic microsomes. We conclude that the altered hepatic acyl-CoA: cholesterol acyltransferase activity of ethanol-fed female rats cannot be directly responsible for ethanol-induced accumulation of cholesteryl esters.
Activated mouse N-ras gene transfected into PC12 rat pheochromocytoma cells suppressed proliferation and promoted neuronal differentiation. Normal mouse N-ras in a LTR-containing vector caused differentiation with a reduced efficiency, but normal N-ras in a vector lacking LTR sequences failed to alter the PC12 phenotype. Cultures of NGF-resistant PC12 variant subline U7 also showed outgrowth of neurites and cessation of cell division following transfection with the mutated ras gene. The present findings suggest that ras genes can, in certain cells, play a role in promoting differentiation and suppressing proliferation, in contrast to their established oncogenic neoplasia-promoting activity in other cells.
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Suspension of living hepatocytes were microencapsulated inside 300 micron mean diameter alginate artificial cells. The galactosamine fulminant hepatic failure rat model was used. 48 hours after the injection of galactosamine, grade II coma hepatic failure rats were divided into pairs. One of the pair was randomly chosen for the control group, and the other for the treated group. Each rat in the control group received one peritoneal injection of microcapsules containing no hepatocytes. Each rat in the treated group received one peritoneal injection of microcapsules containing hepatocytes. The survival of the treated group is significantly higher than the control group.
Amine-containing trichothecanes were prepared by reductive aminations of 3-ketoanguidin. In in vivo tests against P388 leukemia, most of them showed an improved activity compared to anguidin though their potency was decreased. 3-Ketoanguidin also produced some unexpected structures: oxazoline 5, dioxalane 7, and alpha-amino nitrile 13.
As analogues of pyrrolo[2,1-c][1,4]benzodiazepine antitumor antibiotics, such as anthramycin and tomaymycin, several benzo[1,4]diazepine imines and carbinolamine ethers were prepared and tested in vivo against P388 leukemia. Two different synthetic approaches, namely, a reduction of an aromatic nitro group with a concomitant cyclization and a reduction of a lactam, were employed to generate an imine or a carbinolamine moiety. Bicyclic analogues 6a', 6f, and 6g were found to be active, indicating that the pyrroline ring of anthramycin is not an absolute necessity for the antitumor activity. Compound 6g, 3,4-dihydro-9-hydroxy-4-propargyl-5H-1,4-benzodiazepin-5-one, was at least as active as neothramycin although it was 5 times less potent. Among the tricyclic analogues, compounds 5, 7a, and 8b were active against P388 leukemia, and they generally appear to be more potent than bicyclic analogues.
In children with congenital facial anomalies, body image and emotional indicators correlated with the timing and number of operations, rather than with the severity of the deformity. These data suggest that surgery should be performed at the earliest age possible and in the fewest number of stages.
We compared conventional bronchoscopic transbronchial biopsy (TBB) and bronchoalveolar lavage (BAL) with non-bronchoscopic bronchoalveolar lavage (NB-BAL) in nine patients with acquired immunodeficiency syndrome (AIDS) and bilateral lung infiltrates. NB-BAL was carried out with a control-tipped reusable catheter. In each patient, bronchoscopic procedures were performed in the right lung, followed immediately by NB-BAL in the left lung. The specimens obtained by NB-BAL confirmed the presence of P carinii pneumonia in seven of eight patients in whom the diagnosis was established by TBB or BAL. Viral cultures of NB-BAL specimens yielded cytomegalovirus (CMV) in four of five subjects with evidence of CMV via bronchoscopic technique, including two instances in which CMV was not detected by BAL. Complications were limited to right-sided pneumothorax attributable to TBB. Accuracy of NB-BAL appears to be comparable to that of conventional bronchoscopic approaches in the diagnosis of AIDS-related pulmonary infection with P carinii or CMV. NB-BAL may be a safer and more economical alternative to TBB and BAL in the diagnosis of pulmonary opportunistic infections.
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Sequential treatment of the chicken liver fatty acid synthetase by trypsin and subtilisin cleaved the Mr 267,000 subunit to 6-8 polypeptides, ranging in molecular weights from 15,000 to 94,000. Fractionation of the digest by ammonium sulfate and chromatography on a Procion Red HE3B affinity column permitted the isolation of a polypeptide (Mr = 94,000) containing the beta-ketoacyl reductase activity but no other partial activities normally associated with the synthetase. The specific activity of the beta-ketoacyl reductase increased 2 to 3 times in this fraction, an increase that is within the expected range based on relative molecular weight. The kinetic parameters of this fraction towards NADPH and N-acetyl-S-acetoacetyl cysteamine were essentially the same as the beta-ketoacyl reductase component of the intact synthetase. However, the purified fragment did not catalyze the reduction of acetoacetyl-S-CoA derivative, a substrate that is readily reduced by the intact synthetase. Fluorescence measurements with etheno-NADP+ indicate the binding of about 1 mol of NADP+/94,000 daltons, a value which is in agreement with the results obtained from fluorescence measurements with NADPH and the binding of a radiolabeled photoaffinity analog of NADP+. Phenylglyoxal inhibits the beta-ketoacyl reductase activity of either the intact synthetase or the isolated fragment, suggesting the involvement of an essential arginine at or near the active site. Another fragment (Mr 36,000) containing beta-ketoacyl reductase activity was isolated from the synthetase after kallikrein/subtilisin double digestion. Previous mapping studies had shown that this fragment lies adjacent to the COOH-terminal thioesterase domain and overlaps the tryptic Mr 94,000 peptide by approximately 21 daltons. This fragment, but not the Mr 94,000 fragment, was found to contain the phosphopantetheine prosthetic group, indicating that the acyl carrier protein moiety is located in the 15,000-dalton segment that separates the beta-ketoacyl reductase from the thioesterase domain.
The fatty acid synthetase of animal tissue consists of two subunits, each containing seven catalytic centers and an acyl carrier site. Proteolytic cleavage patterns indicate that the subunit is arranged into three major domains, I, II, and III. Domain I contains the NH2-terminal end of the polypeptide and the catalytic sites of beta-ketoacyl synthetase (condensing enzyme) and the acetyl-and malonyl-transacylases. This domain, therefore, functions as a site for acetyl and malonyl substrate entry into the process of fatty acid synthesis and acts in part as the site of carbon-carbon condensation, resulting in chain elongation. Domain II is the medial domain and contains the beta-ketoacyl and enoyl reductases, probably the dehydratase, and the 4'-phosphopantetheine prosthetic group of the acyl carrier protein site. Domain II, therefore, is designated as the reduction domain where the keto carbon is reduced to methylene carbon by sequential processes of reduction, dehydration, and reduction again. Throughout these processes, the acyl group is attached to the pantetheine-SH of the acyl carrier protein. The latter site is distal to the cysteine-SH of the beta-ketoacyl synthetase, constitutes the 15000-dalton polypeptide at the COOH-terminal end of Domain II, and connects to Domain III. When the growing chain reaches C16 carbon length, the fatty acyl group is released by the thioesterase activity, which is contained in Domain III. A functional model is proposed based on the aforementioned results and the recent evidence that the synthetase subunits are arranged in a head-to-tail fashion, such that the pantetheine-SH of the acyl carrier protein of one subunit and the cysteine-SH of the beta-ketoacyl synthetase of the second subunit are juxtaposed. In this model, a palmitate synthesizing site contains Domain I of one subunit and Domains II and III of the second subunit. Therefore, even though each subunit contains all of the partial activities of the reaction sequence, the actual palmitate synthesizing unit consists of one-half of a subunit interacting with the complementary half of the other subunit.
The behaviour of queues in ENT out-patients has been simulated by a computer program. This allowed various appointment systems to be studied and improved to allow a smooth flow of patients through the clinic, in such a way that the idle time of the clinic staff is reduced without increasing patient waiting times.
HLA-A, B and DR antigens were studied in Mainland Chinese diabetes mellitus patients and controls (31 Type I DM, 50 Type II DM, 105 controls). HLA-DR3 and HLA-A9 were increased in Type I diabetics only. An increase in HLA-DR4 was noted in Type I diabetics, but the increase was not statistically significant in this small series.
A specific radioimmunoassay for neurotensin in plasma has been developed with a sensitivity of 2 pmol/l of plasma. The antiserum was directed towards the amino terminal region of neurotensin and did not cross-react with other gastrointestinal peptides. Non-specific interference was eliminated and the sensitivity increased by extracting the plasma samples with ethanol prior to assay. Within- and between-assay coefficients of variation were 7.8% and .12% respectively. The mean plasma concentration of neurotensin in 30 fasting subjects was 29 +/- 4 pmol/l. A mixed meal increased plasma neurotensin from 16 +/- 2 to 53 +/- 6 pmol/l at 2 h.
Monitoring of 25 first cadaver transplant recipients was carried out weekly after transplantation. A total of 441 sera were tested from these patients against B and T lymphocytes at 4 degrees C and 37 degrees C for development of cytotoxic antibodies. Thirteen of the 25 patients (52%) developed B-cold antibodies as their first antibodies and all had functioning kidneys. Five of the patients developed B-warm antibodies initially, and all 5 rejected their transplants within 24 days. Of the seven patients who did not develop antibodies, 3 rejected their kidneys within 72 days. We conclude that it is important to distinguish between two types of antibodies to B lymphocytes--those reactive in the cold and those reactive in the warm--since they have opposite effects. Of the 17 successful grafts, 13 first developed B-cold cytotoxins.
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