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Biomedical subjects

M Koide

Publications and source records attributed to M Koide.

At least 91 records · Page 5Linked to original sources
PubMed1996

Oral glucose ingestion stimulates cholecystokinin release in normal subjects and patients with non-insulin-dependent diabetes mellitus.

The role of glucose in the regulation of plasma cholecystokinin (CCK) level was investigated in healthy control subjects and patients with non-insulin-dependent diabetes mellitus (NIDDM). Plasma CCK concentration was determined by a specific and sensitive bioassay and by a highly sensitive and reliable double-antibody radioimmunoassay using OAL-656 as an antiserum. In control subjects, ingestion of Trelan G-75 (1,200 mOsm/L,225 mL), which is equivalent to 75 g glucose as metabolic products, caused a rapid and significant increase in plasma CCK bioactivity from 1.3 +/- 0.2 to a peak of 5.8 +/- 0.6 pmol/L and immunoreactive CCK concentration from 1.2 +/- 0.1 to 4.6 +/- 0.6 pmol/L. Ingestion of 75 g glucose in 225 mL water (33.3% solution) increased plasma CCK bioactivity to a similar degree to that observed following Trelan G-75 (peak response, 4.5 +/- 0.4 pmol/L). The same volume of 0.9% NaCl solution or water failed to increase plasma CCK concentration. A smaller dose of glucose (50 b/150 mL water) increased plasma CCK concentration, although the peak level (3.0 +/- 0.5 pmol/L) was less than that observed following 75 g glucose. In patients with NIDDM, Trelan G-75 ingestion increased CCK concentration, but the peak level was lower, albeit insignificantly, than that of normal subjects. When the maximal increment of plasma CCK above the basal value was compared between control and NIDDM subjects, the differences were statistically significant (NIDDM, 3.6 +/- 0.1 pmol/L; control, 5.0 +/- 0.4; P < .01). However, integrated CCK responses to Trelan G-75 in NIDDM (165.8 +/- 15.5 pmol/120 min) were not significantly different from those in control subjects (189.8 +/- 15.9 pmol/120 min). Peak CCK bioactivity occurred within 10 to 30 minutes of ingestion, preceding the increase in glucose and insulin. These results suggest a possible effect of CCK on insulin release in humans, and that the CCK secretory response to glucose in well-controlled diabetic patients is not significantly altered.

Administration, Oral↗
PubMed1996

Heparin-induced thrombocytopenia in hemodialysis patients.

This study was conducted to determine the incidence of heparin-induced thrombocytopenia (HIT), an important complication in heparin therapy, in 154 hemodialysis patients, with characterization of the subtypes using an enzyme-linked immunosorbent assay. The etiology of the immunologic type of HIT is suggested to involve the binding of a specific antibody for platelet factor 4-heparin complex to platelets and their consequent activation. The 154 consecutive patients were newly treated with hemodialysis due to chronic or acute renal failure between January 1993 and July 1995. Heparin-induced thrombocytopenia was suspected in six patients (3.9%), and its presence was confirmed by platelet aggregation testing. Five of the patients with HIT had anti-platelet factor 4-heparin complex antibody detected by the enzyme-linked immunosorbent assay and were diagnosed with immunologic HIT. The patient who did not have the antibody was thought to have another type of HIT.

Acute Kidney Injury↗
PubMed1996

Atrial natriuretic peptide accelerates proliferation of chick embryonic cardiomyocytes in vitro.

The developing embryonic heart has been reported to contain significant levels of atrial natriuretic peptide (ANP). In this study, the role of ANP in cardiac development was evaluated using cultured cardiomyocytes isolated from chick embryos. We analyzed the effect of ANP on cell number, DNA synthesis, total RNA level, the expression of cell-cycle-specific and sarcomeric proteins, and levels of lactate dehydrogenase and creatine phosphokinase. ANP increased overall DNA synthesis (measured by BrdU incorporation, P < 0.01) and enhanced cell proliferation. Morphologically, the development of the cardiomyocyte network was distinctly enhanced in the ANP-treated cells. Cellular RNA content was elevated; likewise, myosin and tropomyosin biosynthesis was significantly greater in ANP-treated cells. In addition, expression of G1/S-specific protein increased, whereas G2/M-specific protein remained unchanged by ANP treatment. An antibody against ANP and a specific ANP receptor antagonist, HS-142-1, antagonized and/or attenuated the action of ANP on both cell proliferation and protein biosynthesis. These results indicate that ANP accelerates myocardial cell proliferation by enhancing entry into S phase and by increasing DNA synthesis during S phase specifically through receptor mediated pathway. The in vitro effects of ANP on myocardial cell proliferation, together with the elevated levels of ANP seen in vivo during normal heart formation, suggest a possible autocrine function of ANP in embryonic cardiac development.

Animals↗
PubMed1996

Ethanol inhibits CCK-induced enzyme secretion by affecting calcium-pump activity in isolated rat pancreatic acini.

The aim of this study was to clarify the effect of ethanol on stimulus-secretion coupling in pancreatic exocrine secretion. We investigated the effects of 600 mM ethanol on cholecystokinin octapeptide (CCK-8)-stimulated amylase release, cytosolic free Ca2+ concentration ([Ca2+]i) and Ca2+ fluxes using in vitro isolated rat pancreatic acini. Ethanol, given alone, stimulated both the initial and the sustained phases of amylase release. On the other hand, ethanol inhibited only the sustained phase of amylase release stimulated by CCK-8. Ethanol also inhibited amylase release in response to fluoride, a direct activator of guanine nucleotide-binding protein, suggesting that ethanol affects intracellular signal transduction molecules. Ethanol had no influences on the initial rise but increased the sustained rise in [Ca2+]i stimulated by CCK-8 and inhibited CCK-8-stimulated Ca2+ outflux without affecting Ca2+ influx. 8-Bromoguanosine 3':5'-cyclic monophosphate, a membrane-permeable analogue of cGMP regulating membrane Ca(2+)-pump activity in various cells, completely reversed the ethanol-induced inhibition of amylase release and Ca2+ outflux in response to CCK-8 as well as fluoride. Given that Ca2+ plays a critical role in stimulus-secretion coupling in pancreatic exocrine secretion, our results indicate that 600 mM ethanol inhibits CCK-8-stimulated amylase release by inhibiting Ca(2+)-pump activity on the plasma membrane.

Amylases↗
PubMed1996

The effect of a collagenous implant on deep dermo-periosteal defects in the rabbit.

In plastic surgery, extensive wounds with exposed bone and loss of the periosteum (i.e., deep dermo-periosteal defects) are difficult to treat, even with split-thickness skin grafts, because such grafts rarely survive. Even when these grafts do survive, functional impairment often occurs subsequently. The application of a collagen sponge (Terudermis, Terumo, Tokyo) to such wounds has previously been reported to accelerate granulation tissue formation, resulting in would healing and graft survival. However, this previous report only presented data relating to gross morphological appearance. In this paper, we present histological evidence to demonstrate the beneficial effect of the collagen sponge on experimental dermo-periosteal scalp defects in rabbits. About two weeks after the application of collagen sponge to the experimental wounds, a well-vascularized granulation tissue was formed. Autologous split-thickness skin grafts applied to this new granulation tissue were found to be viable one week after grafting. The results confirm histologically that collagen sponge is effective for the treatment of deep dermo-periosteal defects which would not have regenerated skin cover with conventional therapies such as skin grafting or the temporary use of dermoprotective materials followed by skin grafting.

Animals↗
PubMed1996

[Diagnosis of legionellosis by microagglutination test--comparison to indirect immunofluorescent antibody method].

We studied the micro-agglutination method (MAT) for the diagnosis of legionellosis. Serum samples were collected from 44 clinically legionellosis suspected patients (17 positive with indirect immunofluorescent antibody technique [IFA] and 27 IFA negatives) and 20 healthy adults (25-30 years old). MAT showed negative results with sera collected from healthy adults and IFA negative patients, 8 out of 17 cass of IFA positive patients showed positive results in MAT. The remaining 9 cases out of 17 were negative in MAT judging from our criteria (1:256 in single serum or fourfold rise to 1:128 in pair sera). MAT had good proportion to IFA in samples collected within three weeks after onset of each disease. All sera that became positive in MAT were sampled within four weeks after onset of each illness. It was noted that MAT was mainly related to IgM-class antibodies. These relationships must be decided by investigating more cases of legionellosis. According to the result of this study, the MAT method was thought to be useful for rapid diagnosis of legionellosis.

Adult↗
PubMed1996

Effects of pressure- or volume-overload hypertrophy on passive stiffness in isolated adult cardiac muscle cells.

It has been hypothesized that the changes in myocardial stiffness induced by chronic hemodynamic overloading are dependent on changes in the passive stiffness of the cardiac muscle cell (cardiocyte). However, no previous studies have examined the passive constitutive properties of cardiocytes isolated from animals with myocardial hypertrophy. Accordingly, changes in relative passive stiffness of cardiocytes isolated from animals with chronic pressure- or volume-overload hypertrophy were determined by examining the effects of anisosmotic stress on cardiocyte size. Anisosmotic stress was produced by altering superfusate osmolarity. Hypertrophied cardiocytes were enzymatically isolated from 16 adult cats with right ventricular (RV) pressure-overload hypertrophy induced by pulmonary artery banding (PAB) and from 6 adult cats with RV volume-overload hypertrophy induced by creating an atrial septal defect (ASD). Left ventricular (LV) cardiocytes from each cat served as nonhypertrophied, normally loaded, same-animal controls. Superfusate osmolarity was decreased from 305 +/- 3 to 135 +/- 5 mosM and increased to 645 +/- 4 mosM. During anisosmotic stress, there were no significant differences between hypertrophied RV and normal LV cardiocytes in pressure overload PAB cats with respect to percent change in cardiocyte area (47 +/- 2% in RV vs. 48 +/- 2% in LV), diameter (46 +/- 3% in RV vs. 48 +/- 2% in LV), or length (2.4 +/- 0.2% in RV vs. 2.0 +/- 0.3% in LV), or sarcomere length (1.5 +/- 0.1% in RV vs. 1.3 +/- 0.3% in LV). Likewise, there were no significant differences in cardiocyte strain between hypertrophied RV and normal LV cardiocytes from ASD cats. In conclusion, chronic pressure-overload hypertrophy and chronic volume-overload hypertrophy did not alter the cardiocyte response to anisosmotic stress. Thus chronic overload hypertrophy did not alter relative passive cardiocyte stiffness.

Animals↗
PubMed1996

Major risk factors for atherosclerosis are manifested in experimental Ca-deficiency.

The eggshell is the major source of Ca required during growth of chick embryos. Therefore, chick embryos placed ex ovo for long-term (SL) are rendered severe systemic calcium deficiency. We report here that SL chick embryos express Ca-deficiency related atherogenic disorders, and that in vitro Ca-deficiency induces dedifferentiation, i.e. loss of cell-type specific features and accelerated proliferative activities, in the various types of cultured cells. Systemic blood pressure is significantly higher and an accelerated weight gain of the heart is noted in SL compared to normal embryos (NL) at the incubation Day-14. Plasma cholesterol was lower, while triglyceride and glucose were higher in SL. Varying Ca in the culture medium (FCa, 1.8 mM; HCa, 2.8 mM; Ca/2, 0.9 mM) clearly affected the phenotype of the cultured cardiomyocytes and vascular cells isolated from the chick embryos. The cell number and total DNA were significantly larger and the level of LDH and proliferating cell nuclear antigen (PCNA) was elevated in Ca/2 compared to FCa. On the contrary, the level of CPK and contractile proteins were lowered in Ca/2. Thus, it is indicated that Ca-deficiency induces atherogenic disorders in vivo, and accelerates cell proliferation and decelerates sarcomeric protein expression in vitro. Taken together, it is suggested that the atherogenic, developmental disorders in SL may be the integrated result of the phenotype alteration in the various cell types directly induced by Ca-deficiency.

Animals↗
PubMed1996

Cytoskeletal role in the contractile dysfunction of cardiocytes from hypertrophied and failing right ventricular myocardium.

We have shown on the levels of the sarcomere and the cardiocyte that increased microtubule density accounts, to a remarkable degree, for the contractile dysfunction characteristic of pressure-overload right ventricular hypertrophy. In this study, we have asked whether these linked phenotypic and contractile abnormalities persist during the transition to right heart failure in this model and whether, following this transition, microtubule depolymerization remains effective in restoring normal cellular contractile function when characterized in terms of sarcomere mechanics. 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. These measurements were made in control cats and in operated cats having right ventricular hypertrophy alone or hypertrophy with associated right heart failure; the left ventricle from each heart served as a normally loaded same-animal control. We show here both that alterations in microtubule density and sarcomere mechanics are a persistent and progressive feature of the hypertrophied and then failing cat right ventricle and that the ratio of polymerized to free tubulin is selectively increased in the failing right ventricle. The mechanical defect, though more severe in failing than in hypertrophied right ventricles, was normalized by microtubule depolymerization. Because we find persistent and progressive increases both in microtubules and in the functional consequence of aberrant sarcomere mechanics during the transition from hypertrophy to failure when right ventricular pressure overloading is severe, this cytoskeletal abnormality may well contribute to the contractile dysfunction characteristic of right heart failure in this model.

Animals↗
PubMed1995

Effective anticoagulation by argatroban during immunoadsorption therapy for malignant rheumatoid arthritis with a high polymorphonuclear leukocyte elastase level.

Polymorphonuclear leukocyte elastase (PMNE) is a glycoprotein with a molecular weight of about 30000 and exists in 3 isozymes (1). It has a biological role in host defense mechanisms, but it sometimes induces abnormal blood coagulation and injury of the vascular intima (1,2). We were not able to obtain a satisfactory anticoagulant effect when using heparin during immunoadsorption therapy in a patient with malignant rheumatoid arthritis and high PMNE level, but found that argatroban, a selective antithrombin agent, produced satisfactory anticoagulation. This finding is interesting as far as the various pathologic roles of PMNE are attracting increasing clinical attention (1,2,3).

Antithrombins↗
PubMed1995

Diagnosis of Legionella pneumophila infection by polymerase chain reaction.

We examined the application of the polymerase chain reaction (PCR) for the diagnosis of legionellosis. Eight intratracheal aspirates were collected from a patient with pneumonia caused by Legionella pneumophila serogroup 2, and serial 10-fold dilutions of the samples were obtained. Two samples were positive for L. pneumophila by the direct fluorescent antibody (DFA) method down to a 10(-2) concentration, and one was positive down to a 10(-4) concentration. PCR was positive for all eight samples, and the sensitivity was greater than that of the DFA method. Only one of the eight samples yielded organisms in culture: the L. pneumophila serogroup 2 strain was isolated on buffered charcoal yeast extract alpha agar as an atypical white, papillate colony.

Aged↗
PubMed1995

Thrombin inhibition in the acute phase of ischaemic stroke using argatroban.

We studied the effect of argatroban, a new selective thrombin inhibitor, on the haemostatic system in seven patients with acute ischaemic stroke (the argatroban group). Argatroban was infused continuously at 2.5 mg/h for the first 48 h, and then 10 mg of argatroban was infused over 3 h twice a day on days 3-7. The placebo group consisted of six acute ischaemic stroke patients. As a combination therapy, intravenous administration of glycerol was also performed at the same time in five of the seven patients in the argatroban group and in four of the six patients in the placebo group. D-dimer levels were measured by a latex photometric immunoassay that allowed immediate quantitative assessment. The D-dimer levels of our 13 patients with acute ischaemic stroke were raised at the time of admission (day 1) and 69% of the values were above the 97th percentile ( > 500 ng/ml) in healthy subjects. D-dimer levels were significantly reduced in the argatroban group on days 2 and 7 after admission when compared with the placebo group (day 2: P = 0.032; day 7: P = 0.046). Thus, haemostatic activation occurred in acute ischaemic stroke was effectively blocked by argatroban.

Aged↗