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Biomedical subjects

T Murakami

Publications and source records attributed to T Murakami.

At least 451 records · Page 25Linked to original sources
PubMed1999

Cardiac surgery in patients with dialysis-dependent renal disease.

This study was designed to evaluate the operative outcome of dialysis patients undergoing cardiac surgery. A retrospective review was performed of 28 consecutive patients with end-stage renal disease dependent on maintenance hemodialysis (n = 26) or peritoneal dialysis (n = 2) who underwent cardiopulmonary bypass (CPB). The operations included isolated coronary artery bypass grafting (CABG) (n = 21), aortic valve replacement (n = 4) and CABG plus aortic valve replacement (n = 3). Seven operations were emergent or urgent. In 23 patients, a heparin-coated (HC) circuit with reduced systemic heparinization was used for CPB. The hospital mortality was 7.1%. Complications occurred in 13 patients (46%). Although thoracotomy for bleeding was required in 3 patients, only 1 had undergone CPB with an HC circuit. There were 7 late deaths. All survivors showed improvement in symptoms and overall functional status. The actuarial survival rates were 78% and 58% at 1 and 4 years, respectively. In the 10 patients with diabetes mellitus, the 4-year survival rate was 50%. In the patients who underwent non-elective surgery, the survival rate was 29%. Cardiac surgery can be performed with increased but acceptable mortality in dialysis patients. Good symptomatic relief can be expected. Surgery should be performed before the general condition deteriorates.

Actuarial Analysis↗
PubMed1999

[Molecular mechanism of insulin resistance in hyperlipidemia].

Several types of abnormal lipoprotein particles are observed in patients with insulin resistance: elevated VLDL-triglycerides, remnant lipoprotein, small dense LDL, reduced HDL-cholesterol. These patterns are caused by environmental and genetic factors that alter the lipoprotein metabolism. These lipoprotein abnormalities cause insulin resistance through several factors which decrease LPL and PPAR gamma, on the other hand increase ACS and MTP. It is considered that increased plasma level of FFA will closely associated with these factors and their regulations. Secretion of TNF-alpha from adipocytes increases in obesity and closely relates to the pathogenesis of insulin resistance. But the genetic mechanisms are not still clear. More studies about genetic factors which affect to lipoprotein metabolism will be needed and should be considered about the role on insulin resistance.

Humans↗
PubMed1999

Pilot study of schistosomiasis control in Poyang lake region.

AIM: To perform a longitudinal survey of the control of schistosomiasis in Fanhu Village hyperendemic for schistosomiasis, Poyang Lake region of Jiangxi Province from 1992 to 1996. METHODS: Annual mass chemotherapy and health education were implemented in all investigated individuals, in 1996, artesunate was used in high risk population in transmission season as a prophylactic measure. RESULTS: The prevalence of S. japonicum infection reduced from 26.0% in 1992 to 10.7% in 1994, the intensity of infection (geometric mean of EPG of feces) in residents decreased from 1.92 in 1992 to 0.55 in 1994, and the morbidity indicators such as hepatomegaly and splenomegaly in the cases also have been improved significantly after chemotherapy. In 1995, both the infection rate and intensity of infection of schistosomiasis were recurred from 10.7% and 0.55 in 1994 to 18.4% and 1.04 respectively due to the floods. In 1996, the infection rate reduced to 5.0% and the intensity of infection also decreased to 0.25 due to the additional measure. CONCLUSION: A mass chemotherapy in conjunction with health education and oral artesunate for preventing reinfection in transmission season is effective for the control of schistosomiasis in lake regions.

Adolescent↗
PubMed1998

Transforming growth factor-beta1 increases mRNA levels of osteoclastogenesis inhibitory factor in osteoblastic/stromal cells and inhibits the survival of murine osteoclast-like cells.

Osteoclastogenesis inhibitory factor (OCIF), also termed osteoprotegerin (OPG), is a secreted member of the tumor necrosis factor (TNF) receptor family. It inhibits bone resorption in vivo and osteoclast-like cell (OCL) formation in vitro. To better understand the biological role of OCIF, we first examined the effects of various osteotropic agents on OCIF mRNA levels in mouse calvarial osteoblasts. Northern blot analysis showed that stimulators of OCL formation such as 1,25-(OH)2D3, prostaglandin E2 (PGE2), parathyroid hormone (PTH), and interleukin 1 (IL-1) decreased OCIF mRNA levels. In contrast, transforming growth factor (TGF)-beta1 increased OCIF mRNA levels in primary osteoblasts as well as in osteoblastic/stromal cell lines. Since it was reported that both TGF-beta1 and OCIF not only inhibited OCL formation but also impaired the survival of OCL by inducing apoptosis in vitro, we next examined the possible involvement of OCIF in TGF-beta1-induced impairment of OCL survival. In a mouse bone marrow culture, we confirmed that addition of OCIF or TGF-beta1 decreased the number of surviving OCL. Anti-OCIF IgG, which completely neutralized the effect of OCIF, partially prevented the TGF-beta1-induced decrease in the number of OCL. Our results suggest that (i) downregulation of OCIF expression is one of the mechanisms for the stimulatory effects of 1,25(OH)2D3, PGE2, PTH, and IL-1 on osteoclastogenesis; and (ii) the TGF-beta1-induced apoptosis of OCL is mediated, at least in part, by upregulation of OCIF expression.

Animals↗
PubMed1998

Mouse placental cells secrete soluble leptin receptor (sOB-R): cAMP inhibits sOB-R production.

The aims of this study were to identify whether mouse placenta secretes soluble OB-R (sOB-R) and to find the regulating factor of OB-R expression. Total RNAs were extracted from placenta and decidua, and OB-R expression was assessed by Northern blot analysis. Decidua did not express OB-R mRNA. However, OB-R mRNA expression was detectable in the placenta on day 13 of pregnancy, and then it increased and reached a peak on day 17 of pregnancy. Mouse placental cells from day 12 of pregnancy were cultured and OB-R gene expression was assessed by Northern blot analysis. OB-R mRNA expression was detectable from the second day of culture and reached a peak on the third day of culture. To determine whether placental cells release sOB-R, supernatant of cultured placental cells was subjected to Western blot analysis. sOB-R was detected in the medium by the second day of culture and sOB-R release increased up to the fourth day of culture. Addition of leptin to the medium did not affect expression of OB-R mRNA. However, 8-bromo cAMP inhibited both steady-state levels of OB-R mRNA and the amount of sOB-R protein in the medium in a dose- and time-dependent manner. These results suggest that trophoblast cells differentiate, express, and release sOB-R both in vivo and in vitro and that cAMP is one of several potent regulators of sOB-R secretion by the mouse placenta.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

Skeletal muscle metabolism limits exercise capacity in patients with chronic heart failure.

BACKGROUND: Several studies have indicated that skeletal muscle is important in determining the exercise capacity of patients with chronic heart failure (CHF). However, this theory has been investigated only in experiments based on local exercise involving a small muscle mass. We investigated skeletal muscle metabolism during maximal systemic exercise to determine whether muscle metabolism limits exercise capacity in patients with CHF. We also studied the relationship between muscle metabolic abnormalities during local and systemic exercise. METHODS AND RESULTS: Skeletal muscle metabolism was measured during maximal systemic exercise on a bicycle ergometer by a combination of the metabolic freeze method and 31P magnetic resonance spectroscopy in 12 patients with CHF and 7 age- and size-matched normal subjects. We also evaluated skeletal muscle metabolism during local exercise while subjects performed unilateral plantar flexion. Muscle phosphocreatine (PCr) was nearly depleted during maximal systemic exercise in patients with CHF and normal subjects (12.5+/-0.04% and 12.3+/-0.07%, respectively, of initial level). PCr depletion occurred at a significantly lower peak oxygen uptake (peak VO2) in patients with CHF than in normal subjects (CHF, 20.2+/-3.0 versus normal, 31.8+/-3.7 mL . min-1 . kg-1, P<0. 0001). Muscle metabolic capacity, evaluated as the slope of PCr decrease in relation to increasing workload, was correlated with peak VO2 during maximal systemic exercise in patients with CHF (r=0.83, P<0.001). Muscle metabolic capacity during local exercise was impaired in patients with CHF and was correlated with capacity during systemic exercise (r=0.76, P<0.01) and with peak VO2 (r=0. 83, P<0.001). CONCLUSIONS: These results suggest that impaired muscle metabolism associated with early metabolic limitation determines exercise capacity during maximal systemic exercise in patients with CHF. There was a significant correlation between muscle metabolic capacity during systemic and local exercise in patients with CHF.

Adult↗
PubMed1998

Circulating leptin did not associate with the development of the hyperglycemia accompanied by insulin insensitivity in spontaneous noninsulin dependent diabetes mellitus model Otsuka-Long-Evans-Tokushima-Fatty rats.

Leptin, the product of the ob gene, has been reported to regulate feeding behavior and energy metabolism. Plasma leptin concentration was strongly correlated with body fat content in humans. It is well known that increased body fat content is accompanied by insulin insensitivity. In order to study the relationship between serum leptin level and metabolic variables, we performed caloric restriction on Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats, a model of noninsulin dependent diabetes mellitus. The male OLETF rats were allocated at random to three groups: 100% group, and 85% and 70% groups (which consumed 85% and 70% of the amount of food consumed by the 100% group, respectively). A significant correlation between serum leptin level and the body fat content, body weight, triglyceride, and fasting plasma glucose was observed. Using a partial correlation analysis to control for body fat content, however, the correlation between serum leptin and these variables disappeared. No significant changes in serum leptin levels were observed before and after a 1 h hyperinsulinemic euglycemic clamp test. In conclusion, serum leptin was significantly correlated with body fat content rather than fasting plasma glucose, serum insulin and insulin sensitivity. This suggests that circulating leptin per se may not result in hyperinsulinemia and insulin insensitivity in the OLETF rat.

Animals↗
PubMed1998

Interaction with P-glycoprotein and transport of erythromycin, midazolam and ketoconazole in Caco-2 cells.

The effect of cytochrome P-450 3A (CYP3A) substrates (erythromycin, midazolam) and an inhibitor (ketoconazole) on P-glycoprotein-mediated transport was studied in Caco-2, the human colon adenocarcinoma cell line expressing various functions of differentiated intestinal epithelial cells. The involvement of P-glycoprotein in the transport of these drugs was also examined. The basal-to-apical transport of rhodamine 123, a P-glycoprotein substrate, was inhibited by erythromycin, midazolam and ketoconazole, as well as by P-glycoprotein inhibitors such as verapamil. The apical-to-basal transport of rhodamine 123 was increased by these drugs. The transepithelial transport of erythromycin and midazolam, but not of ketoconazole, was much greater from the basal to apical side than from the apical to basal side. The inhibitory effect of verapamil was observed on the basal to apical transport of erythromycin, but not on midazolam and ketoconazole transport. In conclusion, erythromycin, midazolam and ketoconazole could interact with P-glycoprotein-mediated transport, and P-glycoprotein could be, at least in part, involved in the transport of erythromycin, but not of midazolam and ketoconazole, in the intestinal epithelia.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1998

Intracoronary aspiration thrombectomy for acute myocardial infarction.

To investigate the pathogenesis of acute myocardial infarction (AMI) and values of intracoronary aspiration thrombectomy (ICAT), we applied ICAT to reperfusion therapy using generally available intracoronary catheters to aspirate intracoronary occlusive tissues. We assigned ICAT or primary percutaneous transluminal coronary angioplasty (PTCA) to patients with evolving AMI (Thrombolysis In Myocardial Infarction (TIMI) trial grade 0), and investigated primary histopathologic, clinical, and angiographic outcomes in 43 patients treated with ICAT alone or followed by PTCA, and compared the outcomes with those in 48 patients treated with primary PTCA. No major complications (procedural death, emergent bypass graft surgery) occurred. Reconalization (TIMI grade 3 and 2) was achieved in 25 patients (58%) with ICAT alone and in 39 patients (91%) with ICAT alone or followed by PTCA. Aspirated thrombi were defined as recent thrombi in 21 cases (49%), atheroma in 6 (14%), no thrombi in 13 (30%), and organized thrombi in 1 case. In cases of recent thrombi, ICAT alone provided recanalization more frequently than in those of atheroma or no thrombi (18 of 21 [86%], 3 of 6 [50%], 4 of 13 [31%], respectively; p < 0.05; recent thrombi vs atheroma or no thrombi). There were no significant differences in primary recanalization rate (ICAT alone or followed by PTCA vs primary PTCA; 91% vs 92%) or incidence of complications between the 2 strategies. These results indicate that although the pathogenesis of AMI is heterogeneous in each individual case, intracoronary thrombus contributes little to the pathogenesis of average AMI, and therefore mechanical approaches may be feasible to maximize reperfusion therapies for AMI.

Angioplasty, Balloon, Coronary↗
PubMed1998

Osteoclastogenesis inhibitory factor suppresses osteoclast survival by interfering in the interaction of stromal cells with osteoclast.

Osteoclastogenesis inhibitory factor (OCIF) was originally identified as a factor inhibiting osteoclast (OC) formation. The number of OC in rats treated with OCIF decreased, suggesting that OCIF inhibits OC formation in vivo; however, it is also possible that OCIF affects the number of OC by promoting apoptosis of OC. To address this issue, the effects of OCIF on the survival of OC were examined using well established mouse culture systems. OCIF dose-dependently inhibited OC formation in mouse marrow cultures. Addition of OCIF during day 0-3 did not alter the peak levels of OC formation on day 7 and 8. However, the addition of OCIF during day 5 and thereafter resulted in the rapid decrease of the number of OC. OCIF inhibited the survival of OC formed in mouse marrow cultures in dose- and time-dependent manners. The involvement of stromal cells in OC survival was examined using crude and stromal cell-depleted OC populations. OCIF dramatically inhibited the survival of crude OC populations rich with stromal cells. However, in stromal cell-depleted OC populations, OC spontaneously decreased in the absence of OCIF and OCIF did not enhance the decrease further at least up to 48 h. Apoptotic OC were detected in detached cell populations treated with OCIF in mouse marrow cultures and a specific inhibitor for caspase-3 rescued the death of OC. OCIF mutant lacking the death domain homologous regions inhibited OC survival, though the potency was much less than native OCIF. Taken together, OCIF inhibited not only OC recruitment but also OC survival. OCIF inhibited OC survival by interfering the interaction of stromal cells with OC.

Animals↗
PubMed1998

Hepatoprotective and nitric oxide production inhibitory activities of coumarin and polyacetylene constituents from the roots of Angelica furcijuga.

The methanolic extract from the roots of Angelica furcijuga KITAGAWA was found to exhibit protective effects on liver injury induced by D-galactosamine (D-GalN) and lipopolysaccharide (LPS). From the methanolic extract, seventeen coumarins, two phenylpropanoids, and two polyacetylenes were isolated and examined their in vitro and in vivo hepatoprotective effects and inhibitory activity of NO production in macrophages. A acylated khellactone, isoepoxypteryxin, showed protective activity against D-GalN-induced cytotoxicity in primary cultured rat hepatocytes. On the other hand, six acylated khellactones (hyuganins A, B, C, and D, anomalin, isopteryxin) and two polyacetylenes [(-)-falcarinol and falcarindiol] strongly inhibited NO production induced by LPS in cultured mouse peritoneal macrophages, and also other acylated khellactones (isoepoxypteryxin, pteryxin, and suksdorfin) and a coumarin glycosides (praeroside II) were found to show the activity. By comparison of the inhibitory activities for acylated khellactones with those for other coumarins, acyl groups were found to be essential to exerting potent activity.

Acetylene↗
PubMed1998

Induction of nuclear respiratory factor-1 expression by an acute bout of exercise in rat muscle.

Nuclear respiratory factor 1 (NRF-1) is a regulatory factor of nuclear genes for respiratory subunits and for components of the mitochondrial transcription and replication machinery. This study investigated the effects of an acute bout of aerobic exercise on the postexercise expression of mRNA for NRF-1 and RNA moiety of endonuclease for mitochondrial RNA processing (MRP-RNA) in soleus muscle of 5 days-trained and untrained rats. In the trained group, rats were run on a motor-driven treadmill at a speed of 25 m/min for 90 min/day for 5 days. On the final day, rats were run by the same procedures and were sacrificed at various postexercise time points (0.5, 3, 6, and 24 h). The basal level of cytochrome oxidase activity was increased by the training, which was associated with the increase in the expression of mRNAs for subunit VIc and III of the enzyme. The NRF-1 mRNA expression was transiently increased by approximately 35% at the time point of 6 h after exercise, although the basal level of the expression was not altered by training. A similar transient increase (approximately 50%) in NRF-1 expression by the acute bout of exercise was also observed in untrained rats. In contrast to the NRF-1 expression, the basal level of MRP-RNA abundance was not altered by 5 days training and was not affected by the single exercise bout in either 5 days-trained or untrained rats. These results suggest that the postexercise increase in NRF-1 mRNA expression in rat skeletal muscle may be an early response to endurance exercise for an enhancement of the mitochondrial oxidative capacity.

Animals↗
PubMed1998

Leptin receptor signal transduction: OBRa and OBRb of fa type.

We report herein the characterization of activities of signal transduction for three types of leptin receptors (OBRs) from rats, the OBRa, OBRb, and OBRb with fa mutation (OBRb-fa), by measurement of the levels of tyrosine phosphorylation of STAT3 (signal transducers and activators of transcription 3) and MAPK (mitogen-activated protein kinase), which are induced by leptin stimulation of CHO cells stably expressing the OBR (CHO-OBRb, CHO-OBRa, or CHO-OBRb-fa cells). As the result of leptin stimulation, enhanced levels of tyrosine phosphorylation of STAT3 and MAPK were detected in CHO-OBRb cells. In CHO-OBRb-fa cells, enhancement levels for both were lower than those in CHO-OBRb cells. In CHO-OBRa cells, only the phosphorylation of MAPK was detected. These data suggest that these reduced signaling activities cause obesity in fa/fa rats and that OBRa, which has been generally thought to be inactive at signaling, actually transmits signals through the MAPK pathway.

Animals↗
PubMed1998

Autocrine inhibition of leptin production by tumor necrosis factor-alpha (TNF-alpha) through TNF-alpha type-I receptor in vitro.

The aim of this study was to find factors which regulate m-leptin secretion during pregnancy. Mouse parametrial adipocytes from day 13 of pregnancy were cultured with or without mouse placental lactogen (mPL)-I, mPL-II, or mouse tumor necrosis factor-alpha (mTNF-alpha) and mouse-leptin (m-leptin) concentration in the medium was assessed by RIA. Up to four days of mPL-I or mPL-II treatment did not affect m-leptin secretion. However, mTNF-alpha, which is produced by adipocytes, significantly inhibited m-leptin secretion in a dose- and time-dependent manner. Antibody to mTNF-alpha completely blocked the inhibitory effect of mTNF-alpha on m-leptin secretion. mTNF-alpha significantly inhibited the expression of m-leptin messenger RNA. Agonistic polyclonal antibody directed against the mTNF-type-I receptor (mTNF-RI) significantly inhibited m-leptin secretion, but the anti-mTNF-RII antibody did not change m-leptin secretion. Moreover, human TNF-alpha (h-TNF-alpha) also inhibited human-leptin (h-leptin) secretion by cultured human adipocytes collected from the subcutaneous fat of pregnant women. These results suggest that TNF-alpha, which is secreted by adipocytes, inhibits m-leptin secretion through mTNF-RI and suggest the presence of an autocrine or paracrine regulation of leptin secretion in human and mouse adipose tissue in vivo.

Adipocytes↗
PubMed1998

Expression of three calpain isoform genes in human skeletal muscles.

Calpain is thought to be involved in muscular degradation in progressive muscular dystrophy (PMD), especially Duchenne and Becker muscular dystrophies. To assess the expression of calpain genes in skeletal muscles of patients with myopathies, we examined mRNA levels of three calpain isoforms by the quantitative reverse transcriptase-polymerase chain reaction method in biopsied muscles from control, PMD and amyotrophic lateral sclerosis (ALS) patients. There was a statistically significant increase in calpain 1 and calpain 2 mRNA levels in PMD and ALS patients as compared to controls. In contrast, there was a decrease in expression of calpain 3 mRNA in PMD, but it was not statistically significant. Expression of calpain 1 and calpain 2 positively correlated with each other, but not with calpain 3. These results indicate that expression of calpain 1 and calpain 2, but not calpain 3, are upregulated in diseased human muscles, likely playing a regulatory role in the process of myofibrillar degradation at the transcriptional as well as posttranslational level.

Adolescent↗
PubMed1998

Nucleotide sequence homology to bovine viral diarrhea virus 2 (BVDV 2) in the 5' untranslated region of BVDVs from cattle with mucosal disease or persistent infection in Japan.

Cytopathogenic and non-cytopathogenic bovine viral diarrhea viruses (BVDVs) were isolated from cattle with mucosal disease or persistent infection in Japan. These isolates were compared for antigenic properties by cross-neutralization tests with Japanese reference strains of BVDV belonging to classical type 1. Significantly low cross-reactivity to reference strains was noted, indicating the viruses to possibly represent a new serotype in Japan. Thus, to determine the genotype of the isolates, nucleotide sequences of the 5' untranslated region were determined and compared with those of previously reported BVDV 1 and 2. The isolates were clearly shown to belong to BVDV 2, not to BVDV 1.

Animals↗
PubMed1998

A study of cell death in Werdnig Hoffmann disease brain.

We examined the occurrence of apoptotic cell death in the autopsied brains of four patients with Werdnig Hoffmann disease (WH), using TdT-mediated DIG-dUTP nick end labeling (TUNEL) and immunohistochemistry for apoptosis-related proteins. Three of the four patients, aged over 6 months, exhibited TUNEL-positive cells in the lateral nuclei of the thalamus, and one of the three patients also had TUNEL-positive cells in the cerebral cortex. The labeled nuclei did not show characteristic features such as nuclear fragmentation or apoptotic bodies, and synaptophysin-positive granules were observed around some of the TUNEL-positive cells, although none of the antibodies against glial markers could visualize TUNEL-positive cells. TUNEL-positive cells were not observed in other regions examined, including the spinal cord, medulla and cerebellum or in the brains of three age-matched controls. There were neither immunopositive structures for bcl-2 or p53 nor alteration of in situ expression of bcl-xs/l or bax in any subject, and the TUNEL-positive cells lacked immunopositivity against apoptosis-related proteins. The presence of these TUNEL-positive cells might suggest latent neurodegeneration in the thalamus before central chromatolysis of neurons or neuronal loss appears, although it is not clear whether apoptotic cell death is involved in this degenerative process.

Apoptosis↗