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Biomedical subjects

M Kitamura

Publications and source records attributed to M Kitamura.

At least 109 records · Page 6Linked to original sources
PubMed1999

Severe aspiration pneumonia after surgery for reconstructed gastric tube cancer treated with extracorporeal life support.

A 68-year-old man who had received resection for thoracic esophageal cancer 8 years ago, was operated on for the cancer of the reconstructed gastric tube. On the day of the operation, he accidentally swallowed gastric juice due to an obstruction in the reconstructed gastric tube. He suffered from acute hypoxic respiratory failure which could not be controlled with conventional therapy on postoperative day 1. Therefore, extracorporeal life support was employed at 3.0 L/min. extracorporeal flow for 11 days. Before extracorporeal life support data: PO2/FiO2 = 45, A-aDO2 = 600. During extracorporeal life support, the ventilator setting was pressure control (16 cmH2O) ventilation with a positive end expiratory pressure of 8 cmH2O, respiratory rate of 5 breaths/min., and FiO2 of 0.4. The patient was successfully weaned from extracorporeal life support and extubated on postoperative day 12. After extracorporeal life support data: PO2/FiO2 = 225, A-aDO2 = 465. We report on a successful weaning case from extracorporeal life support and discuss the efficacy these of regarding this patient.

Aged↗
PubMed1999

Effect of hepatocyte growth factor on tacrolimus-induced nephrotoxicity in spontaneously hypertensive rats.

Renal toxicity is a serious side effect of therapy with tacrolimus (FK506), an immunosuppressive agent administered to renal transplant recipients. We investigated the effect of hepatocyte growth factor (HGF) on tacrolimus-induced nephrotoxicity in spontaneously hypertensive rats (SHR). After a right nephrectomy, rats received a continuous perfusion of either HGF in a dose of 5 microg/kg daily (tacrolimus + HGF group) or normal saline (tacrolimus group) into the left renal artery at a rate of 1 microl/h for 7 days after surgery. Tacrolimus was injected intramuscularly in a dose of 4 mg/kg daily for 10 days after surgery. HGF significantly inhibited the tacrolimus-induced increase in the serum creatinine (SCr) level (P < 0.05). HGF also prevented the tacrolimus-induced loss in body weight. The bromodeoxyuridine (BrdU) index was significantly higher in kidney specimens from the tacrolimus + HGF group. These findings suggest that HGF induces the regeneration of renal tubular cells and suppresses tacrolimus-induced renal toxicity in SHR.

Animals↗
PubMed1999

Current strategy of temporary circulatory support for severe cardiac failure after operation.

BACKGROUND: After open heart operations about 1% of patients still need temporary circulatory support for severe cardiac failure, and over half of those patients die during or after the support. This study assessed the efficacy of the current strategy of circulatory support. METHODS: We assessed clinical outcome of 64 consecutive patients (1.5% of pump cases) who had temporary circulatory support associated with perioperative variables. The results were analyzed by logistic regression analysis. RESULTS: The weaning and discharge rates were 50.0% and 26.7% with venoarterial bypass, 76.2% and 57.1% with biventricular bypass, 87.5% and 37.5% with isolated left ventricular bypass, and 60.0% and 40.0% with pulsatile left ventricular assistance, respectively. Logistic regression analysis identified presupport cardiogenic shock (odds ratio, 9.922) and support type (14.684) as factors significantly associated with nonweaning from the temporary support, and cardiogenic shock (28.268), support duration (2.948), and support type (14.184) as factors significantly associated with mortality during or after the circulatory support. CONCLUSIONS: The current strategy of temporary circulatory support improved clinical outcome of patients with severe cardiac failure. Early application of circulatory support before profound cardiogenic shock and proper selection of the support type might be key factors for successful circulatory support postoperatively after operation.

Adult↗
PubMed1999

Behavioural and neurochemical effects of cholinergic and dopaminergic agonists administered into the accumbal core and shell in rats.

The first goal of this study was to investigate whether turning behaviour elicited by unilateral injections of the cholinergic agonist carbachol into the shell of the nucleus accumbens differs from that elicited by similar injections into the core of this nucleus, and to compare the behavioural effects with the known effects of such injections of the mixture of the dopamine D1 and D2 receptor agonists SKF 38393 (5 microg) and quinpirole (10 microg). The second goal was to investigate whether these injections of carbachol produce neurochemical alterations in the ventrolateral striatum that differ from similar injections of the mixture of the dopamine D1 and D2 receptor agonists into these brain regions. Injections of carbachol into the shell produced predominantly (a) contralateral circling marked by normal stepping and running in wide circles during the initial 50 min and (b) postural asymmetry during the following 75 min; similar injections into the core produced (a) contralateral pivoting, namely pathological head-to-tail turning marked by abnormal hindlimb stepping during the initial 50 min and (b) postural asymmetry during the next 75 min. The postural asymmetry seen after the carbachol injections was closely associated with the drug-induced increase in the dopamine release measured by microdialysis in the ipsilateral striatum. Injections of the mixture of dopamine agonists into the shell, but not core, also produced pivoting. These shell injections increased the dopamine release in the ipsilateral striatum, and decreased it in the contralateral striatum. The relative increase in the ipsilateral striatum was closely associated with the drug-induced pivoting. The data show that stimulation of cholinergic and dopaminergic receptors in the shell and core elicit effects that vary according to the subregion of the nucleus accumbens. It is concluded that the accumbens-specific, cholinergic effects are mediated via substrates that differ from those involved in the shell-specific, dopaminergic effects.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1999

Prolonged nocturnal penile tumescence caused by epinastine.

PURPOSE: We report a case of prolonged nocturnal penile tumescence (NPT) caused by the antiallergic agent epinastine. METHODS/RESULTS: We measured NPT using Rigiscan-Plus (DacoMed, Minneapolis, MN, USA) with or without the patient having taken epinastine. CONCLUSIONS: Considering its pharmacological effects on cyclic nucleotides, epinastine may have an effect on erectile function.

Dibenzazepines↗
PubMed1999

The concept of glomerular self-defense.

The balance between local offense factors and defense machinery determines the fate of tissue injury: progression or resolution. In glomerular research, the most interest has been on the offensive side, for example, the roles of leukocytes, platelets, complement, cytokines, eicosanoids, and oxygen radical intermediates. There has been little focus on the defensive side, which is responsible for the attenuation and resolution of disease. The aim of this review is to address possible mechanisms of local defense that may be exerted during glomerular injury. Cytokine inhibitors, proteinase inhibitors, complement regulatory proteins, anti-inflammatory cytokines, anti-inflammatory eicosanoids, antithrombotic molecules, and extracellular matrix proteins can participate in the extracellular and/or cell surface defense. Heat shock proteins, antioxidants, protein phosphatases, and cyclin kinase inhibitors may contribute to the intracellular defense. This article outlines how the glomerulus, when faced with injurious cells or exposed to pathogenic mediators, defends itself via the intrinsic machinery that is brought into play in resident glomerular cells.

Glomerulonephritis↗
PubMed1999

Inhibition of glomerular cell apoptosis by heparin.

BACKGROUND: Heparin, the multifunctional glycosaminoglycan, has been considered a therapeutic agent for glomerular diseases. Although a number of biological properties are postulated to explain its therapeutic utility, it is unknown whether heparin affects cell survival in the glomerulus. In this report, we investigated the effect of heparin on apoptosis of glomerular cells. METHODS: Cultured rat mesangial cells were pretreated with heparin or heparan sulfate proteoglycan (HSPG) and were exposed to proapoptotic stimuli. To examine an effect of heparin on spontaneous apoptosis that occurs in explanted glomeruli, isolated rat glomeruli were incubated in the presence or absence of heparin. Apoptosis was evaluated by Hoechst 33258 staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, and agarose gel electrophoresis to detect DNA fragmentation. The effect of heparin on activator protein 1 (AP-1), a crucial mediator for oxidant-induced apoptosis, was examined by Northern blot analysis and a reporter assay. RESULTS: Heparin and HSPG inhibited apoptosis of mesangial cells triggered by hydrogen peroxide. It was associated with blunted expression of c-fos/c-jun mRNAs and suppression of AP-1 activation. The cytoprotective effect of heparin was also observed in other cell types and in apoptosis triggered by different stimuli. That is, (a) heparin inhibited mesangial cell apoptosis induced by staurosporine, pyrrolidine dithiocarbamate, and ultraviolet light, and (b) heparin suppressed oxidant-induced apoptosis of NRK49F fibroblasts and Madin-Darby canine kidney epithelial cells. Furthermore, heparin attenuated spontaneous apoptosis of podocytes in explanted glomeruli. CONCLUSIONS: These results indicate the novel potential of heparin as an inhibitor of apoptosis in several cell types, including glomerular cells.

Animals↗
PubMed1999

Oxidant-induced apoptosis of glomerular cells: intracellular signaling and its intervention by bioflavinoid.

Oxidant stress plays a crucial role in the generation of a wide range of glomerular disease. In the first part of this article, we describe intracellular signaling pathways involved in the oxidant-initiated apoptosis of mesangial cells, especially highlighting the tyrosine kinase-c-Jun/AP-1 pathway. In the second part, we address a novel potential of bioflavonoid quercetin as an inhibitor of apoptosis in glomerular cells. Possible mechanisms for the antiapoptotic action of quercetin and its therapeutic utility are discussed.

Animals↗
PubMed1999

Clinical experience of left ventricular assist systems at the Heart Institute of Japan.

The main indications for left ventricular assist system (LVAS) support are postcardiotomy ventricular failure as temporary circulatory support and end-stage cardiomyopathy as chronic circulatory support. To clarify the efficacy of LVAS support, we assessed the clinical outcome of a pneumatic LVAS and an electromagnetic LVAS for patients with severe ventricular failure. As of March 1998, 5 patients with postcardiotomy ventricular failure had received the pneumatic LVAS support, and 2 other patients with end-stage idiopathic cardiomyopathy had undergone implantation of the electromagnetic LVAS. The drive control of the LVAS was mainly counterpulsation in the diastole of the native heart. In the 5 postcardiotomy patients, the duration of pneumatic LVAS support ranged from 30 to 312 h (mean, 109.2). All 3 patients with more than 72 h support were successfully weaned, and 2 of them survived. The other 2 patients with cardiogenic shock and less than 36 h support could not be weaned from the LVAS. In the 2 cardiomyopathy patients, 1 patient was well maintained by the electromagnetic LVAS support and underwent successful heart transplantation 7 months later. The other patient has been chronically supported by the LVAS for 2 months and is doing well so far. These results suggest that selective application of the pneumatic LVAS as a temporary support and the electromagnetic LVAS as a chronic support might be appropriate for maximizing the effectiveness of LVAS treatment for profound cardiac failure.

Adult↗
PubMed1999

Ras family GTPases control growth of astrocyte processes.

Astrocytes in neuron-free cultures typically lack processes, although they are highly process-bearing in vivo. We show that basic fibroblast growth factor (bFGF) induces cultured astrocytes to grow processes and that Ras family GTPases mediate these morphological changes. Activated alleles of rac1 and rhoA blocked and reversed bFGF effects when introduced into astrocytes in dissociated culture and in brain slices using recombinant adenoviruses. By contrast, dominant negative (DN) alleles of both GTPases mimicked bFGF effects. A DN allele of Ha-ras blocked bFGF effects but not those of Rac1-DN or RhoA-DN. Our results show that bFGF acting through c-Ha-Ras inhibits endogenous Rac1 and RhoA GTPases thereby triggering astrocyte process growth, and they provide evidence for the regulation of this cascade in vivo by a yet undetermined neuron-derived factor.

Actins↗
PubMed1999

Two cases of metastatic bladder cancers showing diffuse thickening of the bladder wall.

Metastatic bladder cancer showing diffuse thickening of the bladder wall is very rare. We report two cases of metastatic bladder cancer arising from a stomach cancer and acute lymphocytic leukemia. Hydronephrosis and diffuse thickening of the bladder wall were revealed by ultrasonography and computed tomography. Transurethral biopsy and percutaneous whole wall needle biopsy of the bladder were useful for diagnosis. The possibility of metastasis or recurrence of prior and other malignancies should therefore be considered when the clinical features described here are encountered.

Adenocarcinoma↗
PubMed1999

Adoptive transfer of genetically modified macrophages elucidated TGF-beta-mediated 'self-defence' of the glomerulus against local action of macrophages.

TGF-beta has several anti-inflammatory properties which may be relevant to prevention of or recovery from acute glomerular inflammation. Using genetically modified mesangial cells and a technique for in vivo macrophage transfer, this article provides evidence for TGF-beta-mediated 'self-defence' of the glomerulus against macrophages. Rat mesangial cells stably transfected with TGF-beta1 showed a blunted response to the macrophage-derived, proinflammatory cytokine IL-1beta. In contrast, mesangial cells expressing the dominant-interfering TGF-beta receptor showed an enhanced response to IL-1. Similarly, externally added TGF-beta1 inhibited the cytokine response of normal glomeruli, and isolated nephritic glomeruli producing active TGF-beta1 showed a depressed response to IL-1beta, compared to normal glomeruli. Consistent with these in vitro results, in vivo transfer of activated macrophages revealed that the TGF-beta-producing glomeruli are insensitive to the effector action of macrophages. These results indicate that TGF-beta1 functions as an endogenous 'defender' that counteracts local action of activated macrophages in the glomerulus.

Adoptive Transfer↗
PubMed1999

Crystallization and preliminary crystallographic studies of FMN-binding protein from Desulfovibrio vulgaris miyazaki F.

The flavin mononucleotide binding protein from Desulfovibrio vulgaris (Miyazaki F) was crystallized using the vapour-diffusion method. The crystal belongs to the monoclinic space group P21 with unit-cell parameters a = 37.2, b = 84.6, c = 41.1 A, beta = 94.1 degrees, contains two molecules per asymmetric unit and diffracts beyond 1.2 A resolution with a synchrotron radiation X-ray source.

Bacterial Proteins↗
PubMed1999

Regeneration of periodontal tissues by basic fibroblast growth factor.

Several growth factors (or cytokines) have recently received attention because of their ability to actively regulate various cellular functions of periodontal ligament (PDL) cells and the effects of topical application of such factor(s) on periodontal tissue regeneration has been evaluated. In this study, we examined the role of basic fibroblast growth factor (bFGF) in the wound healing and regeneration of periodontal tissues. Alveolar bone defects (such as 2-wall, 3-wall and furcation class II bone defects) were created surgically in beagle dogs and primates. Recombinant bFGF was topically applied to the artificial bony defects. Six or 8 wk after application, the periodontal regeneration was morphologically and histomorphometrically analyzed. In all sites where bFGF was applied, significant periodontal ligament formation with new cementum deposits and new bone formation was observed in amounts greater than in the control sites. We found it noteworthy that no instances of epithelial down growth, ankylosis or root resorption were observed in the bFGF sites. In vitro studies demonstrated that bFGF enhances the proliferative responses of human PDL cells, which express FGF receptor-1 and -2, but inhibits the induction of alkaline phosphatase activity and mineralized nodule formation by PDL cells. Interestingly, we observed that the mRNA level of laminin in PDL cells, which plays an important role in angiogenesis, was specifically upregulated by bFGF stimulation, but that of type I collagen was downregulated. The present study demonstrates that bFGF can be applied as one of the therapeutic modalities which actively induce periodontal tissue regeneration. The results of in vitro studies suggest that by suppressing the cytodifferentiation of PDL cells into mineralized tissue forming cells, bFGF may play important roles in wound healing by promoting angiogenesis and inducing the growth of immature PDL cells, and may in turn accelerate periodontal regeneration.

Administration, Topical↗
PubMed1999

In vitro antibacterial activity of LJC 11,036, an active metabolite of L-084, a new oral carbapenem antibiotic with potent antipneumococcal activity.

LJC 11,036 is the active metabolite of L-084, a novel oral carbapenem that exhibits potent broad-spectrum activity. Antibacterial activities of LJC 11,036 against clinical isolates from respiratory infections, such as Streptococcus pneumoniae (n = 52), Streptococcus pyogenes (n = 19), Haemophilus influenzae (n = 50), Klebsiella pneumoniae (n = 53), and Moraxella catarrhalis (n = 53), and from urinary-tract infections, such as Escherichia coli (n = 53) (MICs at which 90% of the isolates were inhibited [MIC(90)s], 0.1, </=0.006, 0.39, 0.05, 0.05, and 0.05 microg/ml, respectively), were 2- to 64-fold higher than those of imipenem, cefdinir, and faropenem. Moreover, against these bacterial species, except for H. influenzae, the MIC(90)s of LJC 11,036 were 4- to 512-fold lower than those of levofloxacin. LJC 11,036 showed bactericidal activity equal or superior to that of imipenem. Bactericidal activity against penicillin-resistant S. pneumoniae (PRSP) did not vary with the phase of growth. LJC 11,036 had potent activity against various beta-lactamase-producing strains, excluding carbapenemase producers. Against renal dehydropeptidase-I, LJC 11,036 was more stable than imipenem. Furthermore, LJC 11,036 produced in vitro postantibiotic sub-MIC effects against PRSP HSC-3 (6.0 h at one-fourth the MIC) and H. influenzae LJ5 (9.2 h at one-half the MIC). LJC 11,036 showed high binding affinities for PBP1A, -1B, -2A/2X, -2B, and -3 of PRSP and for PBP1B, -2, -3A, and -3B of H. influenzae.

Anti-Bacterial Agents↗
PubMed1999

Bioflavonoid quercetin inhibits interleukin-1-induced transcriptional expression of monocyte chemoattractant protein-1 in glomerular cells via suppression of nuclear factor-kappaB.

Flavonoids are semiessential food components that possess anti-inflammatory properties. This report describes a novel potential of bioflavonoid quercetin as an inhibitor of monocyte chemoattractant protein-1 (MCP-1) in glomerular cells. Cultured mesangial cells as well as isolated glomeruli expressed MCP-1 mRNA in response to interleukin-1beta (IL-1beta). Quercetin dramatically inhibited the cytokine-triggered MCP-1 expression. To explore the mechanisms involved, effects of quercetin on the putative transcriptional activators of MCP-1, nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), were examined. Exposure of the cells to IL-1beta caused activation of NF-kappaB without significant upregulation of AP-1 activity. NF-kappaB inhibitor MG132 diminished the IL-1-induced expression of MCP-1 in mesangial cells and isolated glomeruli, whereas c-Jun/AP-1 inhibitor curcumin did not affect this process. Consistently, NF-kappaB-inactive mesangial cells expressing a super-repressor mutant of IkappaBalpha showed blunted expression of MCP-1 by IL-1beta. In contrast, AP-1-inactive mesangial cells expressing a dominant-negative mutant of c-Jun exhibited the same level of MCP-1 mRNA as that in control cells. These results suggest that: (1) quercetin has the ability to attenuate activation of NF-kappaB; and (2) it inhibits IL-1-triggered MCP-1 expression via suppression of NF-kappaB, but not AP-1, in glomerular cells.

Animals↗
PubMed1999

The antioxidant N-acetylcysteine induces mesangial cells to create three-dimensional cytoarchitecture that underlies cellular differentiation.

Prolonged culture of mesangial cells produces multifocal nodular structures, i.e., "hillocks," consisting of cells and extracellular matrix. Hillock formation is associated with induction of a differentiated phenotype of mesangial cells, with suppressed mitogenesis and downregulation of alpha-smooth muscle actin (alpha-SMA). Currently, little is understood regarding physiologically relevant factors that facilitate this cytodifferentiation. This study explores whether and how the cellular redox state modulates hillock formation. Exposure of confluent rat mesangial cells to the antioxidant N-acetylcysteine (NAC), an inducer of glutathione, dramatically facilitated hillock formation. This effect was mimicked by external addition of the reduced form of glutathione ethyl ester. In contrast, the oxidizing agents diamide and menadione inhibited the development of hillocks triggered by either NAC, glutathione, or prolonged culture. The induction of hillocks by NAC was correlated with downregulation of alpha-SMA as well as attenuated activity of the CArG box element (the cis-element relevant to the expression of the alpha-SMA gene and growth-associated genes). These results indicate that, by a redox-sensitive mechanism, NAC induces mesangial cells to create three-dimensional cytoarchitecture that underlies cellular differentiation.

Acetylcysteine↗