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Biomedical subjects

J Lin

Publications and source records attributed to J Lin.

At least 37 records · Page 2Linked to original sources

Bovine brain microsomal CDP-diacylglycerol synthetase: solubilization and properties.

CDP-diacylglycerol(DAG) synthetase (EC 2.7.7.41) has been solubilized from bovine brain microsomes by the detergent CHAPS (3-[(3-cholamidopropyl) dimethylammonio] -1-propanesulfonate). Optimal solubilization with 1.5% CHAPS yielded 55-60% of the synthetase activity. The effect of CHAPS on the enzyme was biphasic inhibiting at 0.3% and giving maximal activity at 0.5% (the concentration used for all assays). The solubilized, but not the microsomal enzyme is activated by phosphatidylcholine (PC) and strongly inhibited by cardiolipin and lysoPC. Strong inhibition by N-ethylmaleimide, 5,5'-dithio-bis (2-nitrobenzoic acid) and p-chloromercuribenzoate supported a sulfhydryl requirement for the enzyme. Phosphatidic acid (PA) from egg lecithin and 1-stearoyl,2-arachidonoyl PA were preferred substrates for the microsomal synthetase. Solubilized synthetase showed selectivity for the latter PA which is consistent with this enzyme functioning to help form the preponderant 1-stearoyl,2-arachidonoyl species of phosphatidylinositol. Further attempts to purify the synthetase were unsuccessful. All findings suggested the enzyme exists as an unstable complex.

Animals

[A study on aetiological factors of primary hepato-carcinoma in Tianjin China].

In order to investigate the possible risk factors of primary hepato-carcinoma (PHC) in Tianjin, 122 clinical diagnosed PHC patients and matched hospital controls were interviewed and 99 pairs of their blood samples were examined for HBV. The findings confirmed the strong association between HBV infection and PHC. The individual's immune state during HBV infection might be an important factor for PHC development. Histories of hepatitis and cirrhosis and family history of PHC were risk factors of PHC. Cigarette smoking might have association with PHC. Smoking for more the years of, the higher the risk of PHC. The present study did not find association between PHC and drinking water, dietary habits, alcohol consumption, histories of blood transfusion and injection, exposure to pesticides and poison.

Adolescent

[Glycosaminoglycans associate with corneal transparency].

Keratoplasty specimens form 12 patients with macular corneal dystrophy, 1 patient with systemic glycosaminoglycan stored disease and 12 cases of normal cornea were studied by electron-histochemistry. The results showed that the normal cornea contains chondroitin sulfate in the basement membrane and bowman's membrane, Keratan sulfate and chondroitin sulfate between the collagen fibrils of strome, heparan sulfate on the cell membranes of various cells, and hyaluronic acid on the surface of endothelial cell. The chondroitin sulfate of the stroma of macular corneal dystrophy increases, but the keratan sulfate is absent. The keratocytes and endothelial cells of macular corneal dystrophy synthesize fibrillogranular material and abnormal glycosaminoglycan. The heparan sulfate is stored in the cytoplasm of corneal epithelial cell and keratocyte of systemic glycosaminoglycan stored disease and absent on the membrane of involved cells. The authors suggest that glycosaminoglycan play important role in maintaining corneal transparency and the changes of distribution, character and quantity of glycosaminoglycan in the cornea cause corneal opaqueness.

Cornea

Ribose facilitates thallium-201 redistribution in patients with coronary artery disease.

To investigate whether i.v. infusion of ribose, an adenine nucleotide precursor, postischemia facilitates thallium-201 (201Tl) redistribution and improves identification of ischemic myocardium in patients with coronary artery disease (CAD), 17 patients underwent two exercise 201Tl stress tests, performed 1-2 wk apart. After immediate postexercise planar imaging, patients received either i.v. ribose (3.3 mg/kg/min x 30 min) or saline as a control. Additional imaging was performed 1 and 4 hr postexercise. Reversible defects were identified by count-profile analysis. Significantly more (nearly twice as many) reversible 201Tl defects were identified on the post-ribose images compared to the post-saline (control) images at both 1 and 4 hr postexercise (p less than 0.001). Quantitative analyses of the coronary arteriogram was available in 13 patients and confirmed that the additional reversible defects were in myocardial regions supplied by stenosed arteries. We conclude that ribose appears to facilitate 201Tl redistribution in patients with CAD and enhances identification of ischemic myocardium.

Aged

Acanthamoeba keratitis successfully treated with prolonged propamidine isethionate and neomycin-polymyxin-gramicidin.

We report a case of Acanthamoeba castellanii keratitis that was successfully treated with intense propamidine isethionate and neomycin-polymyxin-gramicidin over 11 and nine days, respectively. The frequency with which the medications were applied, once every 30 minutes with each medication, has been surpassed only once before in reported cases. Additional medical treatment included topical miconazole 1% drops for five days and clotrimazole 1% drops for one day; the latter was discontinued due to corneal epithelial toxicity. Intense treatment of Acanthamoeba keratitis with these medications has not been reported before for as long as 11 days. Our aggressive approach was successful, and no clinically detectable significant side effects were observed. There has been no recurrence to date.

Acanthamoeba Keratitis

[Effects of endotoxin on the cochlear electrophysiology and Na(+)-K(+)-ATPase activity].

Hemophilus influenzae (type B) endotoxin 10 micrograms was put in the niche of the round window in guinea pigs. The CAP thresholds and N1 latencies were measured before and 12, 24 and 72 hours after experiments. The 10 kHz and 8 kHz CAP thresholds after experiments were significantly higher (P less than 0.01), the N1 latencies were prolonged (P less than 0.05). There were minute changes in 4kHz CAP thresholds and N1 latencies (P greater than 0.05). In all time groups, the Na(+)-K(+)-ATPase activity was outstandingly weakened. It suggested that: (1) endotoxin put in the niche of the round window is responsible for the cochlear function disturbances in high frequencies, and (2) the decrease of the Na(+)-K(+)-ATPase activity is an important factor for the electrophysiological disturbances in the inner ear.

Animals

In vitro influence of enkephalins on the proliferative response of mouse and rat splenic lymphocytes to phytohemagglutinin.

The opioid peptides leucine enkephalin (LENK) and methionine enkephalin (MENK) were investigated for their effect on the proliferative response of activated BALB/C mouse and Sprague-Dawley rat splenic lymphocytes in vitro. The results showed that LENK and MENK (1 x 10(-3) mg/ml to 1 x 10(-13) mg/ml) significantly suppressed the proliferative response of mouse lymphocytes to phytohemagglutinin (PHA) and enhanced the proliferation of rat lymphocytes at peptide concentrations similar to those effective in mice. It is proposed that endogenous ENKs play a neuroendocrine role between the central nervous system and the immune system.

Animals

[Effects of the enkephalins on natural killer cytotoxicity].

Spleen mononuclear cells of BALB/C mice and YAC-1 cells were used in this experiment. Leucine enkephalin or methionine enkephalin at time 0 was added to cell cultures and the amount of the enzyme lactate dehydrogenase released from lysed target cells was determined 22 hours after incubation. There were on average 41% (5% to 60.7%) and 63% (46.8% to 78%) enhancements of natural killer activity in the presence of leucine enkephalin (1 x 10(-11)-1 x 10(-3) mg/ml) and methionine enkephalin (1 x 10(-15)-1 x 10(-3) mg/ml) respectively. The results showed that opioid peptides can modify NK cell function.

Animals

[Studies on serum angiotensin-I-converting enzyme activity of experimental silicosis in rats].

The level of serum angiotensin-I-converting enzyme (SACE) activity on experimental silicosis in rats at different stages and under treatment with PVNO is reported. The results showed that levels of SACE in each dust groups begun to rise significantly higher than control groups as from the fifth day until 180th day (P less than 0.05). The levels of SACE of treatment groups with PVNO were significantly lower than the dust groups and similar to normal groups of the same age. It is suggested that SACE activity might be used as a reference index of silicosis.

Animals

Effect of human plasma apolipoproteins on the activity of purified lecithin: cholesterol acyltransferase.

An active preparation of lecithin: cholesterol acyltransferase (LCAT, EC 2.3.1.43) was isolated from human plasma by density ultracentrifugation, high-density lipoprotein affinity chromatography, DEAE-Sepharose and hydroxylapatite chromatography. This enzyme preparation gave a single band on polyacrylamide gel electrophoresis in 8 M urea and on sodium dodecyl sulfate gel electrophoresis. Upon analytical isoelectric focusing the enzyme separated into at least five isoforms with isoelectric points ranging from 5.1 to 5.5. The enzyme with an apparent molecular weight of 66,000 +/- 2,000 was characterized by a high content of glutamic acid, aspartic acid, leucine and glycine and contained approximately 31 moles of glucosamine/10(3) moles of protein and no galactosamine. The purified enzyme, stored at 20-40 microgram/ml at 4 degrees C, had a half-life of 26 +/- 4 days. The effect of purified human plasma apolipoproteins A-I, A-II, C-I, C-II, C-III and D on the activity of purified LCAT was studied, using egg-yolk lecithin (40 microM): cholesterol (10 microM) vesicles prepared in 1.25% ethanol in the absence or presence of 0.5% albumin. Addition of albumin to the incubation mixture nearly doubled the esterification rate of LCAT with A-I as activator (n=4), whereas it inhibited esterification by approximately 35% (n=3) if C-I was the activator. Maximum activation by C-I yielded only 13 +/- 6% (vesicles with albumin) or 42 +/- 5% (vesicles without albumin) of the LCAT activity obtained with A-I. Each of the apoproteins A-II, C-II, C-III and D inhibited the LCAT reaction in the presence of A-I or C-I at concentrations needed for maximal activation. Contrary to previous work, apolipoprotein D does not appear to be an activator of LCAT. LCAT activity is significantly affected by albumin and the apolipoproteins A-II, C-II, C-III, and D.

Amino Acids

Biochemical studies of a human low-activity galactose-1-phosphate uridyl transferase variant.

A low activity galactose-1-phosphate uridyl transferase (transferase) variant in a newborn infant has been demonstrated by biochemical studies in erythrocytes and cultured skin fibroblasts. The newborn infant was a galactosaemic suspect identified in a neonatal metabolic screening programme. On breast feeding, he did well without clinical symptoms of galactosaemia during the first 15 days of life. However, substantial amounts of erythrocyte galactose-1-phosphate and urinary galactitol corresponding to the levels in untreated galactosaemic patients, along with mild amino aciduria, were found. The transferase activity, as measured by a sensitive micro kinetic radioisotopic method, was about 7--10% of the normal. On starch gel electrophoresis, the enzyme from the haemolysate had similar mobility as the normal in Tris--glycine buffer, pH 8.8 and phosphate buffer, pH 7.0, but had a slower mobility than that of the normal in the histidine buffer, pH 7.8. The mobility difference was much clearer in a semipurified enzyme preparation. The transferase enzyme in the haemolysate appeared to be more heat labile.

Cells, Cultured

CT contrast enhancement in cerebral infarction.

Computed tomography was used to study 100 patients with ischemic cerebral infarcts. All cases were documented by autopsy, radionuclide imaging, cerebral angiography, or clinical course. Vascular distribution of infarcts was varied and included infarcts of cerebral hemispheres, basal ganglia, and cerebellum. Distinct patterns of enhancement are seen following administration of intravenous contrast material: predominantly peripheral, central, homogeneous, or heterogeneous. Enhancement of the infarcted area usually occurs 1-4 weeks after the onset of clinical symptoms, but was seen as early as the first day or as late as several months after the onset of symptoms. Infarcts showing contrast enhancement may or may not revert to a nonenhanced pattern on follow-up examination for several months. Lesions demonstrating contrast enhancement in cerebrovascular disease may at times be indistinguishable from tumor. Contrast enhancement was the only manifestation of infarction in some instances, and an infarcted area may be completely missed if a postcontrast examination is not performed.

Adolescent