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Biomedical subjects

J Kang

Publications and source records attributed to J Kang.

At least 253 records · Page 14Linked to original sources
PubMed1992

[Intra-abdominal visceral fat in myotonic dystrophy].

We first clarified the relationship between abdominal visceral fat accumulation and impaired glucose and lipid metabolism in patients with myotonic dystrophy. Nineteen patients aged 44.2 +/- 11.4 years with a body mass index (BMI) of 20.5 +/- 2.8 kg/m2, and 18 controls aged 45.2 +/- 10.3 years, with a BMI 20.0 +/- 2.8 kg/m2 were examined. The distribution of abdominal visceral and subcutaneous fat was examined by CT scanning at the umbilical level. Visceral fat area was significantly greater in myotonic dystrophy than that in control (p < 0.05), and positively correlated with the levels of fasting plasma glucose (r = 0.65 p < 0.01), plasma glucose area under the curve of 75 g oral glucose tolerance test (r = 0.67 p < 0.01), fasting plasma insulin (r = 0.77 p < 0.001), serum total cholesterol (r = 0.71 p < 0.001) and serum triglyceride (r = 0.68 p < 0.01). From the present results, we speculate that excess visceral fat accumulation in myotonic dystrophy induces impaired glucose and lipid metabolism.

Abdomen↗
PubMed1992

[Effects of diprophylline on pulmonary hypertension in patients with chronic pulmonary disease].

The present study was undertaken to evaluate the short-term effects of diprophylline on hemodynamic and gases exchange in 10 patients in stable condition with chronic pulmonary disease. Diprophylline decreased the pulmonary vascular resistance by markedly reducing the mean pulmonary arterial pressure but didn't change cardiac output significantly. Diprophylline also caused a significant decrease in arterial carbon dioxide tension, but there was no significant difference between the level of PaO2, SaO2 and A-aDo2 before and after the administration of diprophylline.

Aged↗
PubMed1992

Membrane binding and autolytic activation of calpain-I in human platelets.

The binding of calpain-I (Ca2+ activated neutral protease with high Ca2+ sensitivity) to the membranes of human platelets and the subsequent autolytic activation of calpain-I were analyzed by an immunoblot technique. In A23187 stimulated platelets, cytosolic calpain-I translocated to the membranes with autolysis in a Ca2+ dependent manner and simultaneously underwent autolysis. Although calpeptin, a cell permeable calpain inhibitor, inhibited autolysis of calpain-I, it was unable to prevent the translocation of calpain-I. In a cell re-constituted system, the membrane binding of calpain-I was also Ca2+ dependent and was significantly inhibited by a substrate of calpain. It was suggested that the binding of calpain-I to the membranes required the substrate binding site of this enzyme.

Biological Transport↗
PubMed1991

Platelet activation by a synthetic hydrophobic polymer, polymethylmethacrylate.

Platelets adhere to artificial surfaces in the initial stage of thrombus formation, but the subsequent steps in signal transduction that lead to platelet activation by artificial surfaces are not understood. When 0.325-micron diameter beads composed of a hydrophobic polymer, polymethylmethacrylate (PMMA), were added to gel-filtered aequorin-loaded platelets suspended in media containing Ca2+, the platelets aggregated; addition of fibrinogen was not required. Platelet aggregation was preceded by an increase in cytoplasmic Ca2+ and was accompanied by phosphorylation of the 47-Kd substrate of protein kinase C (PKC), 5-hydroxytryptamine (5-HT) release, and accumulation of phosphatidic acid. All these effects were partially inhibited by apyrase and aspirin. Monoclonal antibodies (MoAbs) 7E3 and M148 and the synthetic peptides RGDS and fibrinogen gamma chain fragment 400-411, all of which bind to the platelet fibrinogen receptor glycoprotein IIb-IIIa (GPIIb-IIIa) and inhibit fibrinogen binding, prevented PMMA-induced aggregation but did not inhibit the Ca2+ increase. Chymotrypsin-treated platelets aggregated after addition of fibrinogen, but not PMMA. We conclude that platelets interact initially with PMMA at membrane sites other than those required for fibrinogen binding, leading to activation of membrane phospholipases and PKC, an increase in cytoplasmic Ca2+, release of 5-HT, ADP, and fibrinogen from storage granules, and to platelet aggregation.

Adenosine Diphosphate↗
PubMed1991

Digestive proteinases of larvae of the corn earworm, Heliothis zea: characterization, distribution, and dietary relationships.

Proteinases and peptidases from the intestinal tract of fifth-instar larvae of Heliothis (= Helicoverpa) zea (Boddie) (Lepidoptera:Noctuidae) were characterized based on their substrate specificity, tissue of origin, and pH optimum. Activity corresponding to trypsin, chymotrypsin, carboxypeptidases A and B, and leucine aminopeptidase was detected in regurgitated fluids, midgut contents, and midgut wall. High levels of proteinase activity were detected in whole midgut homogenates, with much lower levels being observed in foregut and salivary gland homogenates. In addition, enzyme levels were determined from midgut lumen contents, midgut wall homogenates, and regurgitated fluids. Proteinase activities were highest in the regurgitated fluids and midgut lumen contents, with the exception of leucine aminopeptidase activity, which was found primarily in the midgut wall. Larvae fed their natural diet of soybean leaves had digestive proteinase levels that were similar to those of larvae fed artificial diet. No major differences in midgut proteinase activity were detected between larvae reared under axenic or xenic conditions, indicating that the larvae are capable of digesting proteins in the absence of gut microorganisms. The effect of pH on the activity of each proteinase was studied. The pH optima for the major proteinases were determined to be pH 8.0-8.5 for trypsin, when tosyl-L-arginine methyl ester was used as the substrate; and pH 7.5-8.0 for chymotrypsin, when benzoyl-L-tyrosine ethyl ester was used as the substrate.

Animals↗
PubMed1991

Quasi-simultaneous measurement of ionized calcium and alpha-granule release in individual platelets.

The effect of alpha-thrombin and ADP on calcium mobilization and alpha-granule release in individual platelets was investigated by flow cytometry. alpha-Thrombin (4.5 nM) caused a uniform rise of free cytosolic calcium ([Ca2+]i) among indo-1-loaded human platelets. Despite the uniformity of this effect, approximately 20% of the cells failed to secrete alpha-granule content, as shown by binding of fluorescein isothiocyanate (FITC)-conjugated S12 monoclonal antibody. ADP (10 microM) caused a similar brisk and uniform rise of calcium but did not increase S12 binding to any platelets. On the other hand, with alpha-thrombin (0.5 nM), calcium mobilization was heterogeneous and paralleled granule release. [Ca2+]i increased rapidly in some platelets, while only slowly in others. When an electronic gate was set according to FITC-S12 fluorescence, cells with a greater secretory response proved to be those with a higher calcium level. With both alpha-thrombin and ADP, chelation of external calcium by EGTA (2 mM) reduced calcium response of individual cells. NiCl2 (1 mM) also inhibited calcium rise of individual platelets to the same extent as EGTA (2 mM) in spite of the presence of 1 mM CaCl2 in the extracellular media. The effects of EGTA and NiCl2 were not limited to a particular subpopulation of cells. These data suggest that the putative Ni2(+)-inhibitable divalent cation channel(s) may be responsible for the increased influx of calcium that occurs during platelet activation by alpha-thrombin and ADP. It appears that these calcium channels contribute to the elevation of [Ca2+]i among virtually all the platelets.

Adenosine Diphosphate↗
PubMed1990

Differential splicing of Alzheimer's disease amyloid A4 precursor RNA in rat tissues: PreA4(695) mRNA is predominantly produced in rat and human brain.

Alzheimer's disease is characterized by filamentous depositions of amyloid A4 protein in the brain. The first precursor of A4 protein that has been described consists of 695 amino acids (PreA4(695)). Until now, three types of amyloid precursor mRNAs (PreA4(770), PreA4(751) and PreA4(695)), produced by alternative splicing, have been detected. We analysed the differential expression of these mRNAs in various rat tissues by PCR and show that (1) there exists a fourth type of mRNA, PreA4(714); (2) in all tissues except the brain the PreA4(695) mRNA is less abundant than the other types of mRNAs; in the brain, however, the PreA4(695) mRNA predominates by far. The same observations hold true for human tissues. The possible function of this differential splicing is discussed.

Alzheimer Disease↗
PubMed1990

Clozapine for psychosis in Parkinson's disease.

The clinical efficacy of clozapine, an atypical antipsychotic, in treating levodopa-induced hallucinations was investigated in five patients with Parkinson's disease under open label conditions. Two patients could not tolerate clozapine, even in doses as low as 12.5-25 mg daily, because of extreme sedation. Three patients could tolerate clozapine and experienced improvement or elimination of their hallucinations at doses below 100 mg daily. Despite a significant risk of adverse effects, cautious use of clozapine in low doses may be beneficial for patients with levodopa-induced psychosis who do not respond to more conservative measures.

Aged↗
PubMed1990

The influence of intravesical volume upon contractile responses of the whole bladder preparation from streptozotocin-diabetic rats.

1. The in vivo whole bladder preparation was used to correlate bladder volume with the ability of urinary bladders from control, sucrose-drinking, and diabetic rats to develop pressure in response to bethanechol or nerve stimulation. 2. Both streptozotocin-induced diabetes mellitus and sucrose-diuresis caused an increase in rat urinary bladder capacity and mass. 3. There were significant decreases in the ability of bladders from control rats to develop pressure in response to bethanechol at 1.0 ml intravesical volume, but no change in responsiveness of bladders from sucrose-drinking or diabetic rats at different intravesical volumes. Bladders from sucrose-drinking and diabetic rats developed significantly less pressure in response to bethanechol stimulation at low intravesical volumes than did bladders from control rats. 4. Bladders from diabetic rats developed significantly less pressure in response to 32 Hz stimulation at 0.2 ml intravesical volume compared to larger volumes, however, there were no differences in the responses of bladders from sucrose-drinking or control rats at any intravesical volume. 5. Bladders from control and sucrose-drinking rats had a reduced ability to empty in response to bethanechol and field stimulation at large intravesical volumes. 6. Bladders from 8-week streptozotocin-diabetic rats are able to contract and empty efficiently in response to nerve stimulation and bethanechol over a wide range of intravesical volumes.

Animals↗
PubMed1990

Long-term expression of a T-cell receptor beta-chain gene in mice reconstituted with retrovirus-infected hematopoietic stem cells.

To determine the feasibility of retrovirus-mediated gene transfer into stem cells for studying T-cell development, we constructed a high-titer retrovirus vector containing the neomycin phosphotransferase (neo) gene and a murine T-cell receptor (TCR) beta-chain gene with the V beta 6 variable segment. The TCR gene was placed under the control of the human beta-actin promoter and enhancer. Bone marrow cells pretreated with 5-fluorouracil were infected by coculturing with psi-2 virus-producing cells in the presence of recombinant interleukins 1, 2, 4, and 6 as well as interleukin 3 from WEHI-3 conditioned medium. The infected cells were transplanted into irradiated mice, and expression of the exogenous V beta 6 gene was examined with a V beta 6-specific monoclonal antibody, RNase protection, and polymerase chain reaction amplification. Three of seven mice expressed the retroviral TCR gene on the surface of a significant proportion of mature T cells 5-6 months after transplantation. In mice analyzed less than 1 month after transplantation, up to 30% of mature T cells expressed V beta 6 TCRs, an increase of at least 20% above the level of endogenous V beta 6 expression. DNA analysis revealed that pluripotent hematopoietic stem cells were infected by the retroviral vector in a long-term reconstituted mouse that showed increased V beta 6 expression.

Actins↗