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W S Shin

Publications and source records attributed to W S Shin.

71 records · Page 4Linked to original sources
PubMed1994

Five cases of cytomegalovirus infection detected by in situ hybridization and antigenemia assay.

We report five cases of cytomegalovirus infection in immunocompromised patients which were detected by either cytomegalovirus antigenemia assay or in situ hybridization. Four cases had leukemia and the other had chronic renal failure. All the three BMT recipients suffered from GvHD. Interestingly, there was an unique case of CMV disease without a history of BMT, which reminded us that CMV could attack immunocompromised patients who had not undergone transplantation, too. Four out of five cases died. We think that cytomegalovirus infection or disease should not be regarded as a minor problem in post-transplantation infection in Korea.

Adolescent↗
PubMed1994

Acute herpetic esophagitis--a case report.

We report a case of acute herpetic esophagitis in a 33 year old man who was presumed to be immuno-compromised following prolonged steroid and cyclosporin treatment for acute rejection of a transplanted kidney. In Korea, all reported cases of herpetic esophagitis have been diagnosed in immuno-compromised and debilitated patients with a typical endoscopic appearance of ulcerating lesions. However, our patient showed multiple vesicular lesions without ulcer along the entire esophagus. The diagnosis was confirmed by colorimetric detection of herpes virus DNA using in situ hybridization. The endoscopic findings reported herein probably represent the typical early stage of acute herpetic esophagitis.

Acute Disease↗
PubMed1993

Determination of the degree of cure of dental resins using Raman and FT-Raman spectroscopy.

FT-IR spectroscopy has traditionally been used to determine the degree of conversion of dental resins. FT-Raman scattering provided an alternate method of obtaining degrees of conversion for these systems and was particularly useful for measuring spectra of materials without any sample preparation. Raman and FT-Raman spectroscopy gave identical results, but the latter technique was preferred for the highly fluorescent samples often encountered in commercial composites. Linear calibration curves were obtained for the aromatic mixtures Bis-GMA/TEGDMA and Bisphenol-A/TEGDMA using C = C/phi, and for the wholly aliphatic mixture EGDMA/EGDA using C = C/C = O, over a wide range of mole ratios. If both the mole and intensity ratios [C = C/phi or C = C/C = O] were known for an uncured dental resin, then the degrees of conversion could be obtained for the cured materials using Raman spectroscopy. However, if the mole ratios for the uncured resin were unknown, then the degree of conversion depended on the calibration curve, since the Raman scattering cross section of the vibrational modes depended on the molecules to which they were attached.

Benzhydryl Compounds↗
PubMed1992

Autocrine and paracrine effects of endothelium-derived relaxing factor on intracellular Ca2+ of endothelial cells and vascular smooth muscle cells. Identification by two-dimensional image analysis in coculture.

To elucidate the effects of endothelium-derived relaxing factor (EDRF) released from vascular endothelial cells (ECs) on handling of intracellular calcium ion (Ca2+i) in ECs themselves and vascular smooth muscle cells (VSMCs), we measured the Ca2+i by two-dimensional digital image analysis of fura-2-loaded ECs and VSMCs in tissue culture. In isoculture of one cell type, adenosine triphosphate (ATP, 1 microM) transiently increased the Ca2+i of both ECs and VSMCs. High-K+ depolarization or angiotensin II also elevated the Ca2+i of VSMCs, whereas neither stimulants changed the Ca2+i of ECs. In coculture of ECs with VSMCs, the same dose of ATP rapidly increased the Ca2+i of ECs and then transiently decreased the Ca2+i of VSMCs to below the resting level. The maximal Ca2+i-modulating effects of ATP on both cell types were reproducible after the second application of ATP. Three kinds of EDRF blockers (L-NG-monomethylarginine, methemoglobin, or methylene blue) potentiated the ATP-induced Ca2+i rise in ECs and attenuated the Ca2+i reduction in VSMCs, suggesting the autocrine and paracrine effects of EDRF on ECs and VSMCs, respectively. However, neither indomethacin, superoxide dismutase, nor neutralizing monoclonal antibody to endothelin-1 altered the second responses. Thus, two-dimensional Ca2+i image analysis of ECs and VSMCs in coculture enabled direct visualization of the EDRF actions in ECs and VSMCs and their modifications.

Adenosine Triphosphate↗
PubMed1991

Cell growth-dependent expression of endothelin-1 provocable Ca2+ channels in cloned vascular smooth muscle cells.

To analyze the action of endothelin-1 (ET-1) on intracellular Ca ion ([Ca2+]i) handling, we have measured the [Ca2+]i transients in a cultured vascular smooth muscle cell (VSMC) line, A7r5, using two-dimensional microfluorophotometry. In the presence of 1 mM extracellular Ca2+ ([Ca2+]e), ET-1 (100 nM) induced a transient increase in [Ca2+]i due to Ca2+ release from sarcoplasmic reticulum and a subsequent sustained [Ca2+]i increase, suggestive of the entry via the voltage-dependent Ca2+ channel. The transient phase was heterogenous in the VSMC population; only two-thirds of VSMCs showed the phase, whereas all cells showed the sustained phase. To elucidate the cause of heterogeneity, we measured the [Ca2+]i using VSMCs cultured under two extreme conditions. When the cell cycle was arrested at the quiescent phase in the defined serum-free medium, the transient phase was observed in most cells. In contrast, when cell growth was promoted by the above medium plus PDGF (50 ng/ml), the [Ca2+]i response was completely abolished, whereas both the voltage-dependent Ca2+ channel and vasopressin-operated Ca2+ mobilization mechanism were universally preserved, irrespective of the culture conditions. These results may imply that the ET-1-mediated Ca2+ release mechanism is closely influenced by cell growth and preferentially effective at the quiescent phase.

Calcium↗
PubMed1991

Increased plasma level of endothelin-1 and coronary spasm induction in patients with vasospastic angina pectoris.

To elucidate the pathogenic contribution of a potent vasoconstrictor, endothelin-1, to coronary artery spasm, we provoked spasm with intracoronary administration of acetylcholine or ergonovine and performed sensitive immunoassays of plasma levels of endothelin-1 and atrial natriuretic factor (ANF) in the peripheral vein and coronary sinus of patients with a tentative diagnosis of vasospastic angina (VSA, n = 19). The validity of coronary sinus blood sampling was verified by simultaneous measurement of the ANF level. The plasma endothelin-1 levels in venous and coronary sinus blood of the spasm-provoked patients (n = 12) were 1.71-fold and 2.16-fold higher, respectively, than those of nonprovoked cases (n = 5, p less than 0.01). During left coronary spasm, the endothelin-1 level in coronary sinus transiently decreased from 2.27 +/- 0.14 to 1.76 +/- 0.14 pg/ml (p less than 0.01) and returned to the control level (1.98 +/- 0.20 pg/ml) after the spasm resolved, whereas the change was equivocal during right coronary spasm. In contrast, the patients in whom spasm was not provoked showed no changes and maintained low endothelin-1 levels both before and after the maximal provocation (0.90 +/- 0.13 versus 0.90 +/- 0.13 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Subpopulations of rat vascular smooth muscle cells as discriminated by calcium release mechanisms from internal stores.

Transsarcolemmal influx and release from the sarcoplasmic reticulum (SR) through specific Ca2+ channels are the two main pathways to elevate cytosolic Ca2+ (Ca2+i) in vascular smooth muscle cells (VSMCs). To elucidate intercellular distribution and function of the Ca2+ channel in SR in cultured VSMCs, we observed Ca2+i transients by digital two-dimensional imaging with a fluorescent Ca2+ indicator, fura-2, and found an alternative response to either caffeine or angiotensin II under the condition that selectively enabled Ca2+ release from SR. Caffeine (20 mM) increased the Ca2+i by 292 +/- 36% (mean +/- SEM) over the basal level in one third of the VSMC population (n = 19), while the remaining cells in the same observation field showed no or very weak response (110 +/- 4%). In contrast, after the treatment with caffeine plus ryanodine (30 microM), which inactivates the caffeine-sensitive channel, and with 1 mM Ca2+ chelator (EGTA) instead of Ca2+ in the incubation medium to block the CA2+ entry from outside, angiotensin II (10 nM) induced the Ca2+i elevation (287 +/- 26%) in previously caffeine-nonresponsive cells, although caffeine-responsive cells retained quiescence (112 +/- 2%). These responses did not differ when the order of the reagent application was reversed. These heterogeneities of VSMCs in the Ca2+i response to vasoactive substances indicate that VSMCs are functionally divided into subgroups with different Ca2+ channel predominance on SR, necessitating reevaluation of the previous studies obtained from multiple VSMCs.

Angiotensin II↗
PubMed1991

Growth-dependent alterations of intracellular Ca(2+)-handling mechanisms of vascular smooth muscle cells. PDGF negatively regulates functional expression of voltage-dependent, IP3-mediated, and CA(2+)-induced Ca2+ release channels.

To examine the alterations of intracellular Ca2+ ([Ca2+]i)-handling mechanisms in cultured vascular smooth muscle cells (VSMCs) of rat aorta (Shin et al Circ Res 1991;69:551-556), we stimulated VSMCs by extracellular high K+, caffeine, and angiotensin II and evaluated Ca2+ influx through voltage-dependent Ca2+ channels, Ca(2+)-induced Ca2+ release, and inositol trisphosphate-dependent Ca2+ release from internal stores. Percentage of VSMCs responding to each stimulant (responder ratio) and degree of [Ca2+]i increase in the responding cells were analyzed by a two-dimensional fura-2 imaging system. The responder ratios to the three stimulants were high (70-90%) in the quiescent phase (days 1-2), although some cells selectively responded to one or two of the stimulants. Responder ratios prominently decreased to approximately 20% in the proliferating phase (days 2.5-3). In the subconfluent (days 3.5-4) and postconfluent (days 5-6) phases, the responder ratio to high K+ and angiotensin II recovered to the same level as during the quiescent phase, whereas that to caffeine remained low (approximately 10-20%). In responding cells, the degree of [Ca2+]i increase by caffeine and angiotensin II was stable (approximately 100%) during culturing, whereas that to high K+ was small (approximately 30-40%) in the quiescent and proliferating phases and rapidly increased threefold in the subconfluent and postconfluent phases. Furthermore, arrest of cell growth in serum-free medium prevented the reduction of responder ratios in the proliferating phase and restored the decreased ratio of the caffeine responder. Acceleration of VSMC proliferation by platelet-derived growth factor decreased the ratios in all phases. These results imply that 1) the functional expressions of [Ca2+]i-handling mechanisms in response to these vasoactive stimuli are influenced by cell growth and cytodifferentiation of VSMCs or platelet-derived growth factor and 2) they are regulated independently from each other.

Angiotensin II↗
PubMed1991

Effects of atrial natriuretic peptide on endothelin-induced vasoconstriction and intracellular calcium mobilization.

Mechanisms for the antagonistic action of atrial natriuretic peptide (ANP) toward endothelin were studied. We examined the effects of ANP on endothelin-induced vasoconstriction in isolated perfused kidney and the elevation of intracellular free calcium concentration using Fura-2 in cultured rat vascular smooth muscle cells (VSMC). Endothelin produced an increase in renal vascular resistance in isolated perfused kidney (2 x 10(-10) mol/l, +109%; P less than 0.01). ANP completely abolished renal vasoconstriction induced by endothelin. Endothelin produced a biphasic elevation in intracellular calcium concentration in the VSMC. Ethyleneglycol-bis-(beta-amino-ethylether)-N,N,N',N'-tetr aac etic acid (EGTA; 3 mmol/l) or nicardipine (10(-8) mol/l) decreased the sustained elevation of intracellular calcium concentration by 10(-8) mol/l endothelin to the basal level (endothelin, +15% versus EGTA + endothelin, -1%; P less than 0.05; endothelin, +18% versus nicardipine + endothelin, +5%; P less than 0.01). Pretreatment with 10(-6) mol/l ANP suppressed neither the peak phase of intracellular calcium concentration elevation (endothelin, 10(-8) mol/l, +35% versus endothelin + ANP, +31%; not significant) nor the sustained phase of intracellular calcium concentration elevation (endothelin, 10(-8) mol/l, +21% versus endothelin + ANP, +16%; not significant). ANP markedly increased the production of cyclic 3',5'-guanosine monophosphate (cGMP) in the VSMC (ANP, 10(-6) mol/l, +1100%; P less than 0.01). However, endothelin did not influence cGMP production in the presence or absence of ANP. ANP may antagonize the vasoconstrictive action of endothelin through an effect on the steps subsequent to the mobilization of intracellular calcium in the pathway of vascular smooth muscle contraction.

Animals↗
PubMed1989

Synergistic deleterious effect of micromolar Ca ions and free radicals on respiratory function of heart mitochondria at cytochrome C and its salvage trial.

Both Ca2+ and free radicals (FR) are accumulated in temporarily ischemic myocardium and might cause reperfusion injury. Respiratory function measured by polarography of isolated heart mitochondria before or after the in vitro treatment with Ca2+ (1.2 microM) and/or FR showed that Ca2+ or FR per se showed no or weak effect on state 3, but cotreatment of Ca2+ and FR prominently deteriorated state 3, state 4 and RCI. The injury was speculated to occur at cytochrome c itself or its reductase from enzyme assay in the respiratory chain. Furthermore, contrary to the published data, the synergistic action was not mitigated by phospholipase A2 inhibitors (dibucaine, mepacrine), membrane stabilizers (lidocaine, coenzyme Q10), Ca entry blocker (verapamil) or superoxide dismutase, suggesting refractory to therapy.

Animals↗
PubMed1989

Collagen-stimulated human platelet aggregation is mediated by endogenous calcium-activated neutral protease.

To clarify the physiological role of calcium-activated neutral protease (CANP) in human platelets, we loaded the platelets with a Ca2+ -sensitive fluorescent dye, fura-2, and measured the degree of aggregation, cytosolic calcium ion concentration [( Ca2+]i), and proteolysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). At physiological concentration of Ca2+ (1 mM) in the incubation medium, [Ca2+]i was below 0.5 microM and platelet aggregation was not shown. Ionomycin (0.15 microM) or collagen (50 micrograms/ml), but not ADP (10 microM), sharply enhanced the [Ca2+]i to near 1 microM and caused the aggregation. A calcium entry blocker, verapamil, completely abolished both the [Ca2+]i rise and the aggregation. NCO-700, a membrane permeable inhibitor against cysteine proteases (including CANP), dose-dependently blocked the aggregation but did not change the [Ca2+]i transient. SDS-PAGE revealed that filamin, talin, and 70 kDa protein were specifically degraded when platelets were aggregated by ionomycin or collagen and that the proteolysis was not observed when the aggregation was blocked by verapamil or NCO-700. These data provided evidence that Ca2+ entry exceeding 0.5 microM is essential, but not sufficient per se, and that activation of cysteine protease, most likely CANP, is involved in the platelet aggregation by collagen or calcium ionophore.

Blood Platelets↗
PubMed1989

Response of intracellular Ca2+ transients in cultured vascular smooth muscle cells to angiotensin II, vasopressin, acetylcholine and atrionatriuretic peptide.

Modulation of intracellular Ca2+ concentration [( Ca2+]i) is a signal for the contraction of vascular smooth muscle cells responding to vasoreactive substances. We prepared confluently cultured smooth muscle cells from rat aorta, loaded them with Ca2+ sensitive fluorescent dye, fura-2, and measured the [Ca2+]i transient by microscopic spectrofluorometry. The [Ca2+]i was distributed heterogeneously in cytosol. Angiotensin II (10 nM) transiently doubled the [Ca2+]i. It was also increased by arginine-vasopressin (10 nM), even after stimulation by angiotensin II was saturated. In contrast, acetylcholine (10 microM) or rat atrionatriuretic peptide (10 nM) did not change the [Ca2+]i in the same detecting field of the same cell, contradicting previous reports.

Acetylcholine↗