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Biomedical subjects

J Lin

Publications and source records attributed to J Lin.

At least 91 records · Page 5Linked to original sources
PubMed1984

Chemicomechanical transduction performed by enzymes activated by polymers.

Kinetic models for the mode of action of processive and non-processive DNA-helicases are detailed. Fluxes at the steady state are analyzed, and the random walk of the enzymes on the DNA is studied in connection with the rate constants of the chemical reactions involved in the transformation of substrate to products. Finally, the constants of the kinetic model for the processive helicase are related to the parameters of an analogous viscoelastic model.

Adenosine Triphosphatases↗
PubMed1984

Histopathologic studies on transscleral argon-krypton photocoagulation with an exolaser probe.

We performed argon and krypton laser photocoagulation of the retina and ciliary body on rabbit and monkey eyes using an exolaser probe. Clinically, transscleral retinal lesions produced a white circumscribed reaction. Histologically, we observed necrosis of the retina and choroid. Chronic lesions showed disorganization of the retina and formation of chorioretinal scars. Transciliary body laser coagulation damaged the ciliary body and its processes. The intraocular pressure was reduced in rabbits for one week and in monkeys for two weeks after 360 degrees transciliary laser coagulation. Scleral involvement was a common finding in transscleral laser coagulation.

Animals↗
PubMed1983

Febrile transfusion reaction following initial transfusion in a man with immunoblastic lymphadenopathy and granulocyte autoantibodies.

A 69-year-old man with immunoblastic lymphadenopathy and autoimmune hemolytic anemia who had no previous exposure to blood products developed a severe febrile nonhemolytic transfusion reaction following the initial infusion of packed red blood cells. The reaction recurred with transfusion of packed red blood cells, but not when freeze-thawed red blood cells were used. Immunofluorescence techniques demonstrated granulocyte antibodies in his serum and on the surface of his granulocytes. Circulating immune complex, HLA, and platelet antibodies were not present. The granulocyte antibodies fluctuated in titers with disease activities, and could be completely removed from the serum by autologous granulocyte absorption. We conclude that our patient had granulocyte autoantibodies which probably produced febrile transfusion reactions.

Aged↗
PubMed1983

Lectin- and ionophore-stimulated Ca2+ influx in murine lymphocytes: inhibition by disialoganglioside.

Gangliosides suppress lymphocyte mitogenesis when added exogenously to the cells. On the premise that the mechanism of ganglioside action may be an interference with primary induction events, mitogen-induced 45Ca2+ influx in murine lymphocytes was studied. Disialoganglioside (GD1a) at physiopathological concentrations inhibits concanavalin A-induced 45Ca2+ uptake as well as blast transformation. The suppressive action of GD1a is both concentration dependent (50% suppression at 13 microM) and very rapid (within 1 min). GD1a is not cytotoxic nor does it significantly alter the rate of Ca2+ efflux. The uptake studies were extended to A23187, a compound with mitogenic and specific divalent cation ionophore activities. Ca2+ uptake by lymphoid cells from AKR/J, Swiss, and CBA mice is stimulated by A23187; and GD1a, in a dose-dependent manner, inhibits the ionophore-induced 45Ca2+ influx. Pretreatment of thymocytes with GD1a renders the cells greatly insensitive to the subsequent ionophore activity of A23187. The results suggest that exogenous gangliosides may function as an inhibitor of some of the mitogen-triggered early events, including Ca2+ metabolism, and thus influence the immunological behavior of intact lymphoid cells.

Animals↗
PubMed1983

Prolymphocytic leukemia: postmortem findings after long-term survival.

A patient had prolymphocytic leukemia and survived for 44 months. A partial remission for more than 11 months and a short complete remission were induced by agents commonly used for the treatment of acute myelocytic leukemia. However, surface markers identified the disease as of B-cell origin.

Antineoplastic Agents↗
PubMed1981

The nucleotide sequence of the cloned rpoD gene for the RNA polymerase sigma subunit from E coli K12.

We have determined the nucleotide sequence of the rpoD gene which codes for the sigma subunit of RNA polymerase from E. coli K12. The gene, which we formerly cloned as a HindIII restriction fragment in the transducing phage, charon 25, was recloned into several plasmids. We have determined a 2600 base pair DNA sequence which includes the entire structural gene for sigma. The resulting amino acid sequence agrees with previous information obtained about sigma including the amino acid composition, partial sequence data for the N-terminus, the highly acidic nature of the polypeptide, and the cleavage pattern at cysteines. The molecular weight of 70,263 daltons calculated for the 613 amino acid polypeptides is significantly lower than had been determined previously by SDS polyacrylamide gel analysis.

Base Composition↗
PubMed1981

Influence of pancreatic duct ligation on gastric acid secretion.

The influence of pancreatic duct ligation (PDL) on gastric secretion was investigated in dogs with a Heidenhain pouch. A test meal was given to the dogs before PDL, and following PDL the dogs were administered with the test meal mixed with pancreatic enzymes and with the test meal alone in succession. The responses to the test meal were examined in the control period and every one week for a period of 1 to 6 weeks following PDL to identify the changes in gastric acid secretion, serum gastrin levels, immunoreactive glucagon (IRG) levels and immunoreactive insulin (IRI) levels. Gastric acid secretion in response to food stimulations markedly increased after PDL. However, the acid secretion was significantly inhibited by the administration of pancreatic enzymes. Serum gastrin levels began to increase from the second week and continued to increase until the sixth week after PDL, revealing no effect of pancreatic enzymes. IRG levels also increased following PDL, particularly in cases administered with pancreatic enzymes. IRI levels were higher at the first week of PDL than before PDL, but tended to decrease thereafter. It is assumed that gastric hypersecretion after PDL would have complicated relations with IRG, gastric inhibitory polypeptide (GIP) as well as with antral gastrin.

Animals↗
PubMed1979

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↗
PubMed1978

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↗
PubMed1978

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↗