Biomedical subjects

M Koide

Publications and source records attributed to M Koide.

At least 73 records · Page 4Linked to original sources

PubMed1997

Hanshin-Awaji earthquake as a trigger for acute myocardial infarction.

On Jan. 17, 1995, the Hanshin-Awaji district was struck by the most destructive earthquake ever to occur in Japan. It is commonly believed that acute emotional stress such as that caused by an earthquake can trigger acute myocardial infarction (AMI). The objective of this study was to evaluate the effect of the quake stress on the onset of AMI in our district. The number of patients with AMI during the first 4 weeks after the quake increased by about 3.5-fold. The mean age of patients was 72.5 +/- 2.8 years, and the proportion of women (53%) was significantly greater than in the preceding years. The proportion of patients without prodromal angina pectoris was 53%. The mean post-traumatic stress disorder reaction index score (n = 14) was 40.1 +/- 4.1, which indicates a severe stress level. The mean score in the women (45.9 +/- 4.7; n = 7) was significantly higher than that in the men (34.3 +/- 6.4; n = 7). We concluded that after an earthquake, severe emotional stress can trigger AMI, more often than normal in women.

Aged↗

PubMed1997

Development of argatroban, a direct thrombin inhibitor, and its clinical application.

Argatroban, a direct thrombin inhibitor, is used clinically because of its safe and effective antithrombotic action. This drug of low molecular weight shows reversible inhibition of thrombin irrespective of whether thrombin is fibrin-bound or soluble. Optimal anticoagulant effects can easily be attained by monitoring with the activated partial thromboplastin time or whole-blood activated clotting time when a therapeutic range of argatroban equivalent to that of heparin is used. The antithrombotic action is simply detected with a chromogenic substrate assay. The clinical use of the drug in Japan was approved for the treatment of chronic peripheral arterial obstructive disease and acute ischemic stroke. For coronary artery disease in patients with deficiency of antithrombin activities attributable to either antithrombin III or heparin cofactor II deficiency, argatroban is effective as an anticoagulant. Acute coronary occlusion during and after percutaneous transluminal coronary angioplasty can be treated by argatroban as an alternative to heparin. The presence of platelets activated by a trace amount of thrombin is evidenced by modified methods of platelet aggregometry in acute ischemic stroke. Therefore, argatroban can render the platelets insensitive against the platelet hyperaggregation enhanced by thrombin.

Anticoagulants↗

PubMed1997

Pharmacokinetics of carboplatin and etoposide in a haemodialysis patient with Merkel-cell carcinoma.

We present a Merkel-cell carcinoma patient with chronic renal failure requiring haemodialysis and evaluate the pharmacokinetics of carboplatin and etoposide during haemodialysis. The area under the concentration-time curve of carboplatin was increased by prolonging the interval between administration and haemodialysis. However, that of etoposide was not changed. Carboplatin showed good membrane permeability in haemodialysis, while etoposide showed no permeability. In conclusion, the pharmacokinetics of carboplatin could be controlled by haemodialysis and the interval between chemotherapy and haemodialysis. However, the pharmacokinetics of etoposide were not affected.

Aged↗

PubMed1997

Early onset of immunological heparin-induced thrombocytopenia in acute myocardial infarction.

We studied five patients who developed a decrease in platelet count of more than 30000 x 10(6)/l within 24 h of heparin treatment and direct percutaneous transluminal coronary angioplasty and/or intracoronary thrombolytic therapy among 38 consecutive patients with acute myocardial infarction (AMI). Anti-platelet factor 4 (PF4)-heparin complex antibodies were detected in the sera of these five patients, although they had never previously been exposed to heparin. These patients might have had specific antibodies before heparin treatment. PF4 might be released from activated platelets and bind to endogenous heparin-like molecules, and antibodies with cross-reactivity to the PF4-heparin complex may have been generated by the endogenous complex before the first heparin treatment. We conclude that it is worthwhile to check the platelet count and screen for anti-PF4-heparin complex antibody in advance to prevent thrombotic complications due to heparin treatment in patients with AMI.

Acute Disease↗

PubMed1997

Evaluation of soluble cell adhesion molecules in atopic dermatitis.

Recent studies have indicated the importance of cell adhesion molecules (CAMs) between the vascular endothelium and activated leukocytes in various inflammatory skin diseases. Soluble forms of CAMs (sCAMs) have also been detected in sera from such diseases. In order to elucidate the role of the soluble forms in skin inflammation, we determined the serum levels of E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in patients with atopic dermatitis (AD). Using an enzyme-linked immunosorbent assay, we quantified sCAMs levels in 21 patients with atopic dermatitis and in 16 healthy controls. In severe AD patients, levels of these three types of sCAMs were markedly elevated. sE-selectin was significantly elevated in severe AD over the levels in mild AD. A positive correlation with individual clinical activity was found for changes in the sE-selectin and sVCAM-1 levels. sE-selectin levels were correlated with the serum IgE levels and the number of eosinophils. The sVCAM-1 level was also significantly correlated with the number of monocytes. Among these three molecules, sE-selectin appeared to be the most sensitive clinical parameter in monitoring the clinical course of AD patients.

Adolescent↗

PubMed1997

Application of argatroban, direct thrombin inhibitor, in heparin-intolerant patients requiring extracorporeal circulation.

This study describes the present knowledge regarding the clinical application of argatroban, a direct competitive thrombin inhibitor for heparin-intolerant patients, including those with congenital and acquired antithrombin III deficiencies, those with heparin-induced thrombocytopenia, and those with high levels of polymorphonuclear granulocyte elastase. These patients are often associated with intracircuit clot formation with heparin anticoagulation during extracorporeal circulation. Therefore, argatroban may be chosen as one of the alternate anticoagulants. Because the anticoagulant effect of argatroban is reflected in the prolongation of activated thromboplastin time, monitoring is easy, similar to that for heparin. Because argatroban has a fast acting anticoagulant effect without any cofactors such as antithrombin III, this drug is a favorable anticoagulant for heparin-intolerant patients with antithrombin III deficiencies requiring extracorporeal circulation. In adverse reactions to heparin, heparin acts as an antigen after complexing with platelet factor 4, which leads to life-threatening heparin-induced thrombocytopenia. As argatroban prevents heparin-induced platelet aggregation, it is effective for use as a therapeutic anticoagulant. In other clinical applications, heparin decreases antithrombin activity and causes intracircuit clot formation during extracorporeal circulation when the polymorphonuclear granulocyte elastase level is very high. The antithrombin activity shows less decrease when argatroban is substituted for heparin. These findings indicate that argatroban is a useful alternative anticoagulant in these heparin-intolerant patients.

Anticoagulants↗

PubMed1997

Gingival crevicular interleukin-1 and interleukin-1 receptor antagonist levels in periodontally healthy and diseased sites.

Interleukin-1 (IL-1) molecules, IL-1 alpha and IL-1 beta are cytokines involved in the acute-phase response against infection and in the pathogenesis of periodontal destruction. Administration of exogenous IL-1 receptor antagonist (IL-1ra) is effective in reducing the inflammatory reactions mediated by IL-1. However, the relationship between these three naturally occurring IL-1 molecules and periodontal diseases has been poorly characterized. We investigated the correlation of gingival crevicular IL-1 molecules and the clinical status of patients with different severities of periodontitis. IL-1 alpha, IL-1 beta, IL-1ra and the total IL-1/IL-1ra ratio (IL-1 activity index; IL-1AI) were measured in 75 gingival crevicular fluid (GCF) samples from non-inflamed gingiva sites in 2 healthy subjects and diseased sites in 7 patients with several types of periodontitis. IL-1 alpha, IL-1 beta and IL-1ra were measured by specific non-cross-reactive enzyme linked immunosorbent assay. The probing depth, gingival index and alveolar bone loss of each site was recorded at the time of GCF sampling. The total amount of IL-1 alpha, IL-1 beta and the IL-1AI, but not total IL-1ra, were found to be correlated with alveolar bone loss score. Three IL-1 molecules were also measured in the gingival tissue of patients with periodontitis. A similar progressive decrease of the IL-1AI was detected in gingival tissue with periodontitis. These results suggest that the amounts of both crevicular IL-1 and IL-1AI are closely associated with periodontal disease severity.

Acute-Phase Reaction↗

PubMed1997

Presence of Epstein-Barr virus genome in the bone marrow of patients with hematopoietic malignancies.

The Epstein-Barr virus (EBV) genome was detected by polymerase chain reaction (PCR) in mononuclear cells from bone marrows with diverse types of hematopoietic malignancies. Viral repeated sequences (BamHI-W region) were detected in 42 of 82 (51%) hematopoietic malignancies, including polycythemia vera, but not in nonneoplastic cases. EBV-positive cases were found to consist of various histological types. We did not detect any EBV PCR product in the peripheral blood. The EBV BamHI-Y, -H region, encoding EBV nuclear antigen 2 DNA, which is a single-copy gene in the viral genome, was detected in only 13 of 42 BamHI-W-positive cases, suggesting that the copy number of the EBV genome differed in each case. In all cases, the PCR band was verified by Southern blot hybridization using specific EBV probes. Whether the infected virus is an etiologic agent of the malignancy or merely a latent infection cannot be determined by the PCR assay performed under these conditions. These results, however, suggest that a novel form of EBV latent infection is present in the bone marrow of patients with hematopoietic malignancies.

Adult↗

PubMed1997

Specific inhibitors of vacuolar H(+)-ATPase trigger apoptotic cell death of osteoclasts.

Osteoclasts are multinucleated bone-resorbing cells that play a critical role in bone remodeling. Specific inhibitors of vacuolar H(+)-ATPase (V-ATPase), concanamycin A and bafilomycin A1, abolish bone resorption by osteoclasts. In this study, we examined whether these V-ATPase inhibitors trigger apoptotic cell death in osteoclasts, using murine osteoclast-like multinucleated cells (OCLs) formed in vitro. Acridine orange staining revealed that the treatment of OCLs with concanamycin A resulted in chromatin condensation and alterations in nuclear morphology within a few hours. The TdT-mediated dUTP-nick-end labeling (TUNEL) reaction confirmed the apoptotic features of OCLs treated with concanamycin A. The accelerated apoptotic cell death induced by concanamycin A occurred in OCLs treated with interleukin-1 alpha or macrophage colony-stimulating factor as well, which are known to elongate the survival time of osteoclasts. In contrast, these inhibitors did not induce cell death of osteoblastic cells isolated from mouse calvaria. These results suggest that functional impairment of V-ATPase triggers apoptotic cell death in osteoclasts.

Animals↗

PubMed1997

Dedifferentiation of atrial cardiomyocytes as a result of chronic atrial fibrillation.

Chronic atrial fibrillation was induced in goats by electrical pacing. After 9 to 23 weeks of sustained atrial fibrillation, the morphology of the atrial structures was examined. The majority of the cardiomyocytes exhibited marked changes in their cellular substructures, with the replacement of sarcomeres by glycogen as the main characteristic. Using immuno-histochemical staining procedures, we assessed the expression and organization of contractile and cytoskeletal proteins in these cases and compared them with the expression and organization of these proteins in normal atria. Part of the atrial cardiomyocytes acquired a dedifferentiated phenotype, as deduced from the re-expression of alpha-smooth muscle actin, the disappearance of cardiotin, and the staining patterns of titin, which resembled those of embryonic cardiomyocytes. From these results we conclude that chronic atrial fibrillation induces myocardial dedifferentiation. This model of chronic atrial fibrillation in goats offers the possibility to study the time course of changes in cardiac structure during sustained atrial fibrillation and after cardioversion.

Animals↗

PubMed1997

[A report of two cases of Carpentier-Edwards pericardial mitral valve malfunction due to neointimal overgrowth expanding to valve cusps].

Two cases of Carpentier-Edwards pericardial mitral valve malfunction due to neointimal overgrowth were reported. Case one was a 51-year-old female undergone redo mitral valve replacement at nine years after first operation. Removed valve showed remarkable overgrowth of neointima expanding to the valve cusps. Case two was a 67-year-old male. A valve removed at nine years after first operation and at 1.5 years after recovery of prosthetic valve endocarditis. Removed valve also showed neointimal overgrowth expanding to the valve cusps. Although we experienced only two cases of neointimal overgrowth, these findings were considered being important in durability of Carpentier-Edwards pericardial valve.

Aged↗

PubMed1997

[Surgical relief of airway obstruction from a double aortic arch associated with corrected transposition of the great arteries, pulmonary atresia and bilateral patent ductus arteriosus in a neonate].

A rare 20-day-old male with double aortic arch, corrected transposition of the great arteries (cTGA), pulmonary atresia and bilateral patent ductus arteriosus (PDA) was transported to our institute because of severe respiratory dysfunction and cyanosis. The patient had been already intubated and ventilated on respirator. A echocardiography and cine-angiography demonstrated that the both sides aortic arch had almost identical sizes, originating common carotid arteries and subclavian arteries and PDAs respectively, and the descending aorta located on the left side of the mid-line. At the first surgery, the distal of the right aortic arch was divided just proximal to the descending aorta after complete tissue dissection around the arch. The divided right sided aortic arch was mobilized from posterior to anterior aspect of the bronchus. Then the right subclavian artery was divided and an original Blalock-Taussig shunt was employed. The right sided PDA was ligated. After the first surgery, respiratory dysfunction lasted for weeks mainly because of the PGE1 dependent left sided PDA. At the second surgery, left sided modified Blalock-Taussig shunt was constructed and the left sided PDA was divided. These procedures resulted in stable respiratory status and oxygen saturation. The patient was extubated three days later and now in satisfactory clinical condition.

Abnormalities, Multiple↗

PubMed1997

Function of FK506 binding protein (FKBP) in chick embryonic cardiac development.

FK506 binding protein (BP) 12, an immunophilin of FK506-binding proteins, is involved in intra-cellular signal transduction through the calcineurin-nuclear factor pathway. FKBP12 is reported to be associated with the ryanodine-receptor and IP3 Ca2+ channels, and to regulate cell proliferation via binding transforming growth factor (TGF)-beta receptor and cyclin dependent kinase (CDK). To elucidate the function of FKBP12 in cardiac development, we analyzed the temporal profile and regulation of FKBP12 expression in chick heart and in cultured cardiomyocytes. FKBP12 is expressed in embryos as early as day 4 and is predominantly associated with cardiomyocytes and osteo-chondrocytes. Tissue FKBP level in the heart increases with development. Immunohistochemically, the distribution and levels of FKBP12 appear to be related to sarco-endoplasmic reticulum Ca-ATPase 2 (SERCA2) but not to sarcomeric proteins. In proliferating cells, FKBP12 expression correlates with cellular mitosis, but not with DNA synthesis. In earlier embryos (< day 8), suppressing the activity of FKBP by FK506 administration is lethal, and induces cardiomegaly at later stages. In cultured cardiomyocytes, FK506 reduces the level of contractile proteins and inhibits cell proliferation. These results show that FKBP12 is enriched in cell types involved in dynamic Ca handling, and is likely an important molecule for cardiac development. FKBP12 most likely functions by affecting cellular Ca handling, since its effects are modified by modulators of Ca handling by sarcoplasmic reticulum.

Animals↗

PubMed1997

[Improving surgical results for cardiovascular anomalies in neonates].

The surgical results for congenital cardiovascular anomalies in neonates between August 1987 and July 1997 were reviewed. Two hundred thirty-four neonates underwent the corrective surgery with the use of cardiopulmonary bypass (CPB) for the cardiac anomalies including transposition of the great arteries (d-TGA) (157 patients), total anomalous pulmonary venous connection (TAPVC) (44 patients), cardiac defects with the aortic arch anomalies (11 patients), and others (22 patients), with an early mortality rate of 12%. The survival rates through the arterial switch operation for d-TGA and correction for TAPVC in 30 days were satisfactory (92% and 89%, respectively). The early mortality rate of palliative surgery done without CPB in 115 neonates due to aortic arch anomalies, pulmonary outflow tract obstruction, or pulmonary hypertension was low (6%). In contrast with these results, the outcome of palliative surgery using CPB for hypoplastic left heart syndrome, the aortic arch anomalies with subaortic stenosis, or TAPVC in asplenia hearts was poor, with the surgical mortality of 80%.

Aortic Coarctation↗

PubMed1996

Basis for increased microtubules in pressure-hypertrophied cardiocytes.

BACKGROUND: We have shown the levels of the sarcomere and the cardiocyte that a persistent increase in microtubule density accounts to a remarkable degree for the contractile dysfunction seen in pressure-overload right ventricular hypertrophy. In the present study, we have asked whether these linked phenotypic and contractile abnormalities are an immediate and direct effect of load input into the cardiocyte or instead a concomitant of hypertrophic growth in response to pressure overloading. METHODS AND RESULTS: The feline right ventricle was pressure-overloaded by pulmonary artery banding. The quantity of microtubules was estimated from immunoblots and immunofluorescent micrographs, and their mechanical effects were assessed by measuring sarcomere motion during microtubule depolymerization. The biogenesis of microtubules was estimated from Northern and Western blot analyses of tubulin mRNAs and proteins. These measurements were made in control cats and in operated cats during and after the completion of right ventricular hypertrophy; the left ventricle from each heart served as a normally loaded same-animal control. We have shown that the alterations in microtubule density and sarcomere mechanics are not an immediate consequence of pressure overloading but instead appear in parallel with the load-induced increase in cardiac mass. Of potential mechanistic importance, both these changes and increases in tubulin poly A+ mRNA and protein coexist indefinitely after a new, higher steady state of right ventricular mass is reached. CONCLUSIONS: Because we find persistent increases both in microtubules and in their biosynthetic precursors in pressure-hypertrophied myocardium, the mechanisms for this cytoskeletal abnormality must be sought through studies of the control both of microtubule stability and of tubulin synthesis.

Animals↗

PubMed1996

Tryptophan modulates exocrine secretory function in rat pancreatic acini.

We investigated the effect of tryptophan (Trp) on exocrine secretory function, using isolated rat pancreatic acini. Trp inhibited cholecystokinin-octapeptide (CCK-8)-stimulated amylase secretion, causing a downward shift in the dose-response curve. The inhibitory effect of Trp was dose-dependent and was observed only on the sustained secretion, there being no effect on the initial phase of amylase secretion. Trp (10mM) also inhibited amylase secretion in response to carbachol and bombesin, as well as fluoride, a potent activator of guanine-nucleotide binding proteins. Since Ca2+ influx is necessary for sustained secretion, we examined the effect of Trp on Ca2+ influx and efflux. Trp increased the CCK-8-stimulated Ca2+ influx rate without affecting Ca2+ efflux, suggesting that Trp elevates intracellular Ca2+ levels. Increasing intracellular Ca2+ levels with A23187 resulted in the inhibition of CCK-8-stimulated amylase secretion. These results indicate that Trp inhibits CCK-stimulated sustained amylase secretion, in part by increasing Ca2+ influx into acinar cells.

Amylases↗

PubMed1996

Evaluation of an artificial dermis full-thickness skin defect model in the rat.

An artificial dermis product was applied to full-thickness skin defects in rats and cell infiltration into the collagen matrix was investigated. Host fibroblasts and capillaries infiltrated as far as the upper end of the collagen matrix by day 14 after application. Determination of glycosaminoglycan levels in the matrix showed that hyaluronic acid was generated in a similar amount to that seen in the intact skin by day 14. An autologous thin split-thickness skin graft was placed onto the artificial dermis simultaneously or several days after its application to the defect. The take rate was 100% when a split-thickness skin graft was performed on day 14 after application of the artificial dermis. At 6 weeks after the skin defect was created, the wound area was 80% of the original area and the dermis at the grafted site was as thick as that of normal skin. These results suggested that the artificial dermis provides a good matrix for thin split-thickness skin graft and is useful for the reconstruction of full-thickness skin defects. This method is considered to be an alternative to the conventional procedure using thick skin grafts or skin flaps.

Animals↗

PubMed1996

Histological evaluation of skin reconstruction using artificial dermis.

An artificial dermis, composed of a collagen matrix, was applied to a full-thickness skin defect prepared on the back of rats. Two weeks later, a thin split-thickness skin autograft was overlaid on the matrix at each recipient site. The dermal layer at the recipient sites was 1.02 mm thick with prior application of artificial dermis, as compared with the 0.46 mm thickness observed without such pretreatment. Histologically, the split-thickness skin graft normally lies with no gap on the artificial dermis, which looks like natural dermis. Six days after grafting, the epithelial basal cells in the grafts showed an active uptake of bromodeoxyuridine (a thymidine analogue), indicating high activity of cell proliferation. About 50 and 20% respectively of the artificial dermis remained at each recipient site at 12 and 20 weeks after its application (after the skin defect). This finding indicates that bovine collagen, which is a constituent of the artificial dermis, is gradually replaced by the host tissue.

Animals↗