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Biomedical subjects

Y Shin

Publications and source records attributed to Y Shin.

At least 91 records · Page 5Linked to original sources
PubMed1995

Maitotoxin-elicited calcium influx in cultured cells. Effect of calcium-channel blockers.

Maitotoxin elicited a marked influx of 45Ca2+ into NIH 3T3 fibroblast cells. The influx was blocked by imidazoles (econazole, miconazole, SKF 96365, clotrimazole, calmidazolium) with IC50 values from 0.56 to 3 microM. Phenylalkylamines (verapamil, methoxyverapamil) and nitrendipine were less potent, and diltiazem was very weak. Among other calcium blockers, the diphenylbutylpiperidines fluspirilene and penfluridol, the diphenylpropylpiperidine loperamide, and the local anesthetic proadifen were quite active with IC50 values of 2-4 microM. The pattern of inhibition of maitotoxin-elicited calcium influx did not correspond to the ability of the agents to block elevation of calcium that ensues through calcium-release activated calcium (CRAC) channels after activation of phosphoinositide breakdown by ATP in HL-60 cells. The imidazoles did block CRAC channels, but fluspirilene, penfluridol, loperamide and proadifen were ineffective. Loperamide actually appeared to enhance influx of calcium via the activated CRAC channels. The imidazoles, in particular calmidazolium, caused an apparent influx of calcium and caused a stimulation of phosphoinositide breakdown in HL-60 cells.

3T3 Cells↗
PubMed1995

Enhancement of Escherichia coli H(+)-ATPase caused by binding of monoclonal antibodies is attributed to structural changes of Leu-456 and Ser-440 in the alpha subunit.

Five monoclonal antibodies against the alpha subunit of F1-ATPase from Escherichia coli alpha 104, alpha 105, alpha 107, alpha 109, and alpha 110 were prepared. The monoclonal antibodies alpha 104 and alpha 110 enhanced the F1-ATPase activity maximally to 1.6- and 1.7-fold that of the wild-type, respectively, while alpha 105 did not. Both antibodies bound to a peptide corresponding to the region between residues 354 and 513. Mutations in this region which caused reduced binding of the alpha subunit to the antibodies were identified at residues Ser-440, Leu-456, Leu-471, Leu-482, Met-483, and Ser-506 for alpha 104 and residues Ser-440, Leu-456, Leu-471, Asp-476, Leu-482, Met-483, and Ser-506 for alpha 110. These residues are possibly involved in the epitopes for the antibodies and are located close together on the surface of the alpha subunit. Among the mutations, Leu-456 to Pro and Ser-440 to Pro mutations caused increase of the F1-ATPase activity up to 1.9 and 1.2 times that of the wild-type, respectively, while Leu-471 to Pro mutation caused a defect in assembly of the F1-ATPase on the membrane. The other mutations caused no significant change in ATPase activity. These results suggested that Ser-440 and Leu-456 have an important role in regulating catalysis by the F1-ATPase, but that the neighboring residue Leu-471 has an important role in assembly of the F1-ATPase complex. It was also suggested that binding of the monoclonal antibodies alpha 104 and alpha 110 to residues Ser-440 and Leu-456 caused local conformational changes, leading to enhancing effects on F1-ATPase activity similar to the Ser-440 to Pro and Leu-456 to Pro mutations.

Animals↗
PubMed1995

A new variant of type IV glycogenosis with primary cardiac manifestation and complete branching enzyme deficiency. In vivo detection by heart muscle biopsy.

Type IV glycogenosis (polyglucosan body disease) is a rare congenital autosomal recessive inherited disorder, caused by lack of the branching enzyme (amylo-1,4-1,6 transglucosidase). This deficiency leads to storage of abnormal glycogen (polyglucosan bodies) in the liver and other tissues. The clinical onset of the disease is insidious with non-specific gastrointestinal symptoms followed by progressive hepatic failure. Usually patients die due to hepatic cirrhosis within 4 years. Sometimes myopathy of the heart and skeletal muscle is also present. In these cases, the clinical onset is often later than in typical cases. We report on two brothers with primarily cardiac manifestation and late onset of the disease. The older one started to suffer from progressive dilated cardiomyopathy at the age of 18 years, presenting with severe heart failure, hepatosplenomegaly, ascites and peripheral oedema. He also demonstrated myopathy and muscular atrophy especially of the shoulder and lower limbs. Initially he improved on medical therapy, but one year later severe heart failure recurred followed shortly afterwards by sudden cardiac death. Right heart and skeletal muscle biopsies were performed while he was alive. These, as well as the autopsy, revealed massive accumulation of polyglucosan bodies. In both heart and skeletal muscle, complete branching enzyme deficiency could be proven. His 14-year-old brother showed similar clinical findings of mild dilated cardiomyopathy. His muscle biopsy also revealed polyglucosan body myopathy. Thus, in young patients presenting with congestive cardiomyopathy, type IV glycogenosis has to be considered in the differential diagnosis.

1,4-alpha-Glucan Branching Enzyme↗
PubMed1995

A new inherited muscular disorder in Japanese quails (Coturnix coturnix japonica).

Thirteen adult mutant (LWC strain) Japanese quails (Coturnix coturnix japonica), between the ages of 8 and 60 weeks were examined for a progressive muscular disorder. The disorder, inherited as an autosomal dominant trait, was clinically apparent as early as 28 days of age; it was characterized by generalized myotonia, muscle stiffness, and muscle weakness. Affected birds were identified by their inability to lift their wings vertically upward and by their inability to right themselves when placed on their dorsum. Electromyographic studies in two mutant quails showed high-frequency repetitive discharges comparable to those of myotonic runs. These discharges persisted after nerve resection. The distinctive histopathologic changes in the various muscles examined were ring fibers, sarcoplasmic masses, and internal migration of sarcolemmal nuclei. A slight decrease in the size of type IIB muscle fibers and a slight increase in the size of type IIA fibers were observed in the M. pectoralis thoracicus of affected quails. In older affected birds, inter- and intrafascicular fatty infiltration with replacement of type IIB fibers by fat cells was seen in the pectoral muscles. Single fiber necrosis, nonspecific lymphorrages, and variations in the muscle fiber size and shape were also noted. The typical muscle lesions and multisystem involvement, which was manifested by testicular degeneration and atrophy in the male LWC specimens and bilateral lenticular cataracts in 6 of 13 affected mutant quails, suggest resemblance of this new inherited muscular disorder to myotonic dystrophy in man.

Animals↗
PubMed1995

Detection of canine distemper virus nucleocapsid protein gene in canine peripheral blood mononuclear cells by RT-PCR.

For a rapid diagnosis of canine distemper virus (CDV) infection, the reverse transcription-PCR (RT-PCR) was carried out to detect CDV nucleoprotein (NP) gene from canine peripheral blood mononuclear cells (PBMCs). Two sets of primers were targeted to two regions of NP gene of CDV Onderstepoort strain. The NP gene fragments were well amplified by the RT-PCR in each of the RNA extracts from Vero cells infected with 6 laboratory strains of CDV including Onderstepoort strain, and from PBMCs of a dog experimentally infected with CDV. The amplified NP gene was detected in 17 of 32 samples from dogs which were clinically suspected for CDV infection at veterinary hospitals. No RT-PCR product was found in 52 samples from healthy dogs including 40 specific pathogen free beagles vaccinated with an attenuated live virus-vaccine for CDV and 12 stray dogs. The RT-PCR provides a fast, sensitive, and supplementary method for the diagnosis of CDV infection in dogs.

Animals↗
PubMed1995

Prevalence of diabetes and IGT in Yonchon County, South Korea.

OBJECTIVE: To determine the prevalence of diabetes and impaired glucose tolerance (IGT) in Yonchon County of South Korea and to investigate their associated factors. RESEARCH DESIGN AND METHODS: We performed a population-based cross-sectional study with random cluster sampling of residents > or = 30 years of age. Among the 3,804 residents sampled, a total of 2,520 participants had a standard 75-g oral glucose tolerance test and answered a detailed questionnaire. We also collected standard anthropometric data. RESULTS: If the data for participants in the age range of 30-64 years were adjusted to the standard world population, the prevalence of diabetes was 7.2% and the prevalence of IGT was 8.9%. It was observed that the significant factors associated with diabetes were waist-to-hip circumference ratio, serum triglyceride levels, age, systolic blood pressure, family history of diabetes, and locality. CONCLUSIONS: The prevalence of diabetes in Yonchon County was substantially higher than was previously suggested. The risk of diabetes increased with the increased central obesity and metabolic disturbances associated with insulin resistance.

Adult↗
PubMed1995

The health insurance system in Korea and its implications.

The national health insurance system was introduced in Korea in 1977 and achieved universal coverage in July 1989. This article briefly describes the general features of the insurance scheme: coverage, management, benefit package, financing provision of medical services and method of reimbursement. Generally speaking, the system mirrors that of the German and Japanese experiences. Although the Korean health insurance system achieved universal coverage during a remarkably short time-span, there is much room for improvement. In this regard, the article also highlights the problems related to Korea's health insurance system and the attempts to improve equity and efficiency in both financing and provision of services.

Cost-Benefit Analysis↗
PubMed1995

Cigarette smoking among Korean adolescents: prevalence and correlates.

The purpose of this study was to examine the prevalence of cigarette smoking and to explore its relationship with individual, family, school, and psychological factors among Korean adolescents. As part of the Korean Institute for Health and Social Affairs' Adolescent Health Survey, 5,209 eighth graders and 4,677 eleventh graders from 70 junior and senior high schools completed a self-administered questionnaire during school hours in 1989. Current prevalence of cigarette smoking was 8.45% (15.43% of boys and 1.28% of girls). Smoking prevalence increased with age among boys. Based on logistic regression analyses, perceived peer use was most strongly associated with smoking status (OR = 9.97 for boys; and 68.27 for girls). Academic stress, grade, and type of school were also associated with smoking status for both boys and girls. In addition, mother's smoking, birth order, and urbanity were associated with smoking status for boys. Implications of the results for prevention efforts to inhibit the onset of cigarette smoking among Korean adolescents are discussed.

Achievement↗
PubMed1994

Effects of ATP and UTP in pheochromocytoma PC12 cells: evidence for the presence of three P2 receptors, only one of which subserves stimulation of norepinephrine release.

1. In pheochromocytoma PC12 cells ATP and, to a lesser extent, 2-methylthioATP stimulate phosphoinositide breakdown, release of intracellular calcium, and influx of external calcium, leading to stimulation of norepinephrine release. In contrast, although UTP also stimulates phosphoinositide breakdown, release of intracellular calcium, and influx of external calcium, there is no stimulation of norepinephrine release. 2. 2-MethylthioATP, presumably acting at P2y receptors, and UTP, presumably acting at P2u receptors, in combination elicit a phosphoinositide breakdown greater than that elicited by either alone. Intracellular levels of calcium measured with Fura-2 increase to greater levels with ATP than with UTP and are sustained, while the UTP intracellular levels of calcium rapidly return to basal values. Both ATP and UTP cause a similar influx of 45 Ca2+ presumably by stimulation of a P2 receptor directly linked to a cation channel. 3. It is proposed that PC12 cells contain two distinct G protein-coupled P2 receptors that activate phospholipase C and a P2 receptor linked to a cation channel. The P2y receptor sensitive to ATP (and to 2-methylthioATP) causes the depletion of a pool of intracellular calcium, sufficient to activate so-called "receptor-operated calcium entry". The sustained elevation of intracellular calcium after ATP treatment is proposed to result in stimulation of norepinephrine release and activation of calcium-dependent potassium channels and sodium-calcium exchange pathways. 4. The P2u receptor sensitive to UTP (and to ATP) causes only a transient elevation in levels of intracellular calcium, perhaps from a different pool, insufficient to activate so-called receptor-operated calcium entry. Further sequelae do not ensue, and the functional role of the UTP-sensitive P2u receptor is unknown.

Adenosine Triphosphate↗
PubMed1994

Effects of the amphiphilic peptides mastoparan and adenoregulin on receptor binding, G proteins, phosphoinositide breakdown, cyclic AMP generation, and calcium influx.

1. The amphiphilic peptide mastoparan is known to affect phosphoinositide breakdown, calcium influx, and exocytosis of hormones and neurotransmitters and to stimulate the GTPase activity of guanine nucleotide-binding regulatory proteins. Another amphiphilic peptide, adenoregulin was recently identified based on stimulation of agonist binding to A1-adenosine receptors. 2. A comparison of the effects of mastoparan and adenoregulin reveals that these peptides share many properties. Both stimulate binding of agonists to receptors and binding of GTP gamma S to G proteins in brain membranes. The enhanced guanyl nucleotide exchange may be responsible for the complete conversion of receptors to a high-affinity state, complexed with guanyl nucleotide-free G proteins. 3. Both peptides increase phosphoinositide breakdown in NIH 3T3 fibroblasts. Pertussis toxin partially inhibits the phosphoinositide breakdown elicited by mastoparan but has no effect on the response to adenoregulin. N-Ethylmaleimide inhibits the response to both peptides. 4. In permeabilized 3T3 cells, both adenoregulin and mastoparan inhibit GTP gamma S-stimulated phosphoinositide breakdown. Mastoparan slightly increases basal cyclic AMP levels in cultured cells, followed at higher concentrations by an inhibition, while adenoregulin has minimal effects. 5. Both peptides increase calcium influx in cultured cells and release of norepinephrine in pheochromocytoma PC12 cells. The calcium influx elicited by the peptides in 3T3 cells is not markedly altered by N-ethylmaleimide. 6. Multiple sites of action appear likely to underlie the effects of mastoparan/adenoregulin on receptors, G proteins, phospholipase C, and calcium.

3T3 Cells↗
PubMed1994

Angiotensin and ANP secretion during chronically controlled increments in atrial pressure.

The primary objective of this study was to determine whether angiotensin II (ANG II) has direct effects on the atrium to chronically stimulate the secretion of atrial natriuretic peptide (ANP) by actions that are independent of its vasoconstrictor and fluid-retaining effects that increase ANP secretion indirectly by raising atrial pressure. In five dogs, right atrial pressure (RAP) was controlled at approximately 5.5 mmHg above control levels for 8 days by employing an externally adjustable occluder around the pulmonary artery and a servo-control system, and plasma levels of ANG II were fixed at either normal (days 1-3 and 7-8) or high (days 4-6) physiological concentrations by chronic infusion of captopril+ANG II. When plasma ANG II was maintained at normal levels during servo-control of RAP, plasma ANP concentration increased five- to sixfold and sodium balance was achieved at a reduced arterial pressure (-14 mmHg). In contrast, despite increased plasma levels of ANP, the high rate of ANG II infusion produced marked sodium retention during the initial 24 h; however, the antinatriuresis was not sustained because the servo-control system partially deflated the pulmonary artery occluder to prevent fluid-induced increments in RAP. Moreover, in the absence of a change in RAP, high plasma levels of ANG II did not influence plasma ANP concentration. These findings indicate that the plasma levels of ANP achieved in heart failure increase renal excretory capability and allow fluid balance to be achieved at a substantial fall in mean arterial pressure as long as there is minimal involvement of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1993

Halogen-substituted trimetoquinol analogs as thromboxane A2 receptor antagonists in platelets and aorta.

Trimetoquinol (TMQ) is a non-prostanoid compound that blocks prostaglandin H2/thromboxane A2 (TXA2) receptor-mediated responses initiated by a prostaglandin (PG) H2 analog, U46619, in human platelets and rat aorta. Ring fluorine-substituted TMQ analogs selectively antagonized PG-dependent human platelet activation induced by U46619, arachidonic acid, collagen, ADP or epinephrine; and were about 300-fold less potent as inhibitors of PG-independent responses mediated by thrombin or bacterial phospholipase C. For each inducer of the PG-dependent pathway, the rank order of inhibitory potency was identical (TMQ > 8-fluoro-TMQ > 5-fluoro- TMQ). Iodine substitution yielded a similar rank order of antagonism against U46619-induced platelet activation (TMQ > 8-iodo-TMQ > 5-iodo-TMQ), and all TMQ analogs inhibited platelet aggregation in whole blood as well as in platelet-rich plasma. Inhibition of specific [3H]SQ 29,548 binding by TMQ analogs was highly correlated with inhibition of functional responses to U46619. Radioligand binding experiments using TMQ analogs with rat platelets showed no interspecies difference in comparison with human platelets. The rank order of inhibitory potencies for the fluorinated (but not iodinated) TMQ analogs changed in rat thoracic aorta with 8-fluoro-TMQ > TMQ > or = 5-fluoro-TMQ as antagonists of U46619-induced vascular contraction. These findings demonstrate that the primary mechanism of antiplatelet action of TMQ analogs is related to a blockade of TXA2 receptor sites, and ring-halogenated TMQ analogs distinguish between TXA2-mediated functional responses in vascular smooth muscle and platelets.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗