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Biomedical subjects

M Nishida

Publications and source records attributed to M Nishida.

At least 199 records · Page 11Linked to original sources
PubMed1998

[Ionic binding of 3H-gentamicin and short-term bactericidal activity of gentamicin against Pseudomonas aeruginosa isolates differing in lipopolysaccharide structure].

The clinical isolates of Pseudomonas aeruginosa can be roughly classified into long- and short-lipopolysaccharide (LPS) strains and LPS-deficient strains, based on the silver-stained patterns of their LPSs after SDS-PAGE. The ionic binding of 3H-gentamicin, a polycationic antibiotic, to the negatively charged sites on the surface structures of P. aeruginosa strains, often differing in LPS structure, was the highest in the long-LPS strains followed in descending order by the short-LPS strains and LPS-deficient strains. It was presumed that a clinical isolate of P. aeruginosa No. 45 is lacking in the O-polysaccharide chains and some structures of the core-regions consisting of its LPS-structure after SDS-PAGE. On the other hand, the binding of 3H-gentamicin to this strain was quite. high, i.e., similar to that to of the long-LPS strains. To clarify this finding, P. aeruginosa PAC1R and its LPS-deficient mutants were used as reference strains because the chemical structures of their LPSs containing the repeated units of O-polysaccharides and the neutral sugar contents in the core-regions were previously confirmed. The PAC605 strain of the LPS-mutants of the PAC series, was completely lacking in the repeated units of O-polysaccharide and also lacking in some neutral sugar residues of the core-oligosaccharide region. However, this strain was highly bound to 3H-gentamicin, suggesting that the negatively charged sites on the deep core-oligosaccharide region and/or on lipid A participated in the binding of 3H-gentamicin. This manner of binding may be also applied to P. aeruginosa No. 45. When P. aeruginosa PAC1R, PAC605 and No. 45 strains were each exposed to gentamicin (20 micrograms/ml) for 10 minutes, the viable cell counts of PAC1R decreased to about 70% of the initial count, whereas the viable cell counts of PAC605 and No. 45 strains decreased to 3.6 and 11.0% respectively, indicating the vulnerability of both types of the strains to be enhanced by the bactericidal action of gentamicin with short-term incubation.

Anti-Bacterial Agents↗
PubMed1998

Inducible nitric oxide synthase augments injury elicited by oxidative stress in rat cardiac myocytes.

The effects of nitric oxide (NO) produced by cardiac inducible NO synthase (iNOS) on myocardial injury after oxidative stress were examined: Interleukin-1 beta induced cultured rat neonatal cardiac myocytes to express iNOS. After induction of iNOS, L-arginine enhanced NO production in a concentration-dependent manner. Glutathione peroxidase (GPX) activity in myocytes was attenuated by elevated iNOS activity and by an NO donor, S-nitroso-N-acetyl-penicillamine (SNAP). Although NO production by iNOS did not induce myocardial injury, NO augmented release of lactate dehydrogenase from myocyte cultures after addition of H2O2 (0.1 mM, 1 h). Inhibition of iNOS with N omega-nitro-L-arginine methyl ester ameliorated the effects of NO-enhancing treatments on myocardial injury and GPX activity. SNAP augmented the myocardial injury induced by H2O2. Inhibition of GPX activity with antisense oligodeoxyribonucleotide for GPX mRNA increased myocardial injury by H2O2. Results suggest that the induction of cardiac iNOS promotes myocardial injury due to oxidative stress via inactivation of the intrinsic antioxidant enzyme, GPX.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Oxidized LDL increases and interferon-gamma decreases expression of CD36 in human monocyte-derived macrophages.

CD36 is a glycoprotein with an Mr of 88 kDa that is expressed on platelets, monocytes/macrophages, capillary endothelial cells, and adipocytes. We previously demonstrated that CD36 is involved in the uptake of oxidized low density lipoprotein (OxLDL) by using CD36-deficient macrophages (J Clin Invest. 1995;96:1859). However, the regulation of CD36 expression in human monocyte-derived macrophages has not been fully elucidated. The current study attempted to clarify the effect of OxLDL and cytokines, both of which are present in atherosclerotic lesions and may play an important role in atherogenesis, on the expression of CD36. A cell enzyme-linked immunosorbent assay and flow cytometry were used to detect CD36 protein. A ribonuclease protection assay was used to measure CD36 mRNA in human monocyte-derived macrophages. The expression of CD36 was increased during the differentiation of monocytes to macrophages. Incubation of macrophages with 25 microg/mL OxLDL for 24 hours increased the level of CD36 protein by 56% and that of CD36 mRNA by 58%. Lysophosphatidylcholine did not affect the expression of CD36. The effects of OxLDL were demonstrated in macrophages that had already differentiated to the point where CD36 expression was almost maximal. Interferon-gamma (IFN-gamma) reduced the expression of CD36 in a dose-dependent manner. A concentration of 1000 U/mL IFN-gamma significantly reduced the expression of CD36 protein by 57% and that of CD36 mRNA by 30%. In conclusion, CD36 may be important in the formation of foam cells by induction through its ligand (OxLDL). Moreover, some local factors, such as IFN-gamma, may suppress CD36 expression on macrophages in human atherosclerotic lesions.

CD36 Antigens↗
PubMed1998

Effectiveness of superficial temporal artery-middle cerebral artery anastomosis in adult moyamoya disease: cerebral hemodynamics and clinical course in ischemic and hemorrhagic varieties.

BACKGROUND AND PURPOSE: The efficacy of superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis in adult moyamoya disease was evaluated by clinicopathophysiological studies. METHODS: Fifteen patients with cerebral ischemic attacks (ischemia group) and 15 patients with intracranial hemorrhages (hemorrhage group) were investigated. Clinicoangiographic features and regional cerebral blood flow (rCBF) of the MCA territory were preoperatively and postoperatively investigated, and cortical arterial pressure (CAP) and anastomotic blood flow (AF) were intraoperatively measured. RESULTS: In the ischemia group, the preoperative rCBF of 38.4 mL/100 g per minute was significantly increased to 42.1 mL/100 g per minute with a diminution of angiographic moyamoya vessels in 67% of patients after surgery. The mean CAP and AF were 25.6 mm Hg and 34.7 mL/min, respectively. Proximal and distal cerebral vascular resistance (PCVR = [Mean Systemic Arterial Blood Pressure-Mean CAP]/rCBF and DCVR = [Mean CAP/rCBF]) were 1.78 and 0.68, respectively. One patient died perioperatively as a result of intracerebral hemorrhage. During follow-up (mean, 67 months), 12 of 14 patients recovered without neurological deficits, 1 was moderately disabled because of the initial insult, and another patient experienced an intracerebral hemorrhage but recovered fully. In the hemorrhage group, the preoperative rCBF of 38.0 mL/100 g per minute was significantly increased to 42.7 mL/100 g per minute with a diminution of moyamoya vessels in 60% after surgery. The mean CAP and AF were 29.1 mm Hg and 24.1 mL/min, respectively. PCVR and DCVR were 1.72 and 0.77, respectively. One patient became hemiparetic because of perioperative intracerebral hemorrhage. During follow-up (mean, 94 months), 3 patients had fatal intracranial hemorrhages, 10 had good recoveries, and 2 had moderate disabilities. CONCLUSIONS: This study revealed a high PCVR and a very low DCVR in both the ischemia and hemorrhage groups of patients. STA-MCA anastomosis partially normalized cerebral circulation and decreased moyamoya vessels but did not completely prevent rebleeding.

Adult↗
PubMed1998

Effect of side chains including the N-methyl-tetrazole-thiol group of beta-lactam antibiotics on transport in cultured kidney epithelial cells LLC-PK1.

In this study, the transcellular transport characteristics of four beta-lactam antibiotics (cefotaxime, cefmenoxime, cefmetazole, and cefotiam) were investigated in a kidney epithelial cell line LLC-PK1, especially focusing on the effect of the N-methyl-tetrazole-thiol (NMTT) group attached to 7-amino-cephalosporanic acid. There were no directional differences between the apical-to-basolateral and basolateral-to-apical transport of cefotaxime, cefmenoxime, and cefmetazole, suggesting that the NMTT group does not influence the transcellular transport behaviors of beta-lactam antibiotics. In contrast, cefotiam transport across LLC-PK1 cell monolayers was 1.3-fold greater in the basolateral-to-apical direction than in the apical-to-basolateral direction. It is considered that the ionization of nitrogen in the N-dimethylaminoethyl group attached to NMTT is a factor in the secretory-oriented movement of cefotiam. The transcellular transport of cefotiam in both directions was significantly depressed at a low temperature (4 degrees C) and by 2,4-dinitrophenol. The basolateral-to-apical transport of cefotiam was also shown to be concentration-dependent. These results suggest that a specialized transport process might participate in the transcellular transport of cefotiam. The lipophilicities of these beta-lactam antibiotics were not correlated to the degree of transcellular transport, directly.

Animals↗
PubMed1998

Magnetic resonance angiography visualization of four vessel (bilateral carotid and vertebral artery) occlusion--two case reports.

A 44-year-old female with transient vertigo and a 51-year-old female with headache and numbness of the hand presented with four vessel occlusion of the cerebral arteries (bilateral internal carotid arteries and bilateral vertebral arteries). This is an extremely rare entity, and the clinicoradiological features are not well documented. Magnetic resonance (MR) angiography visualized the cerebral arterial occlusion. Conventional angiography confirmed the diagnosis and demonstrated extensive collateral vessels. MR angiography is a useful method for screening patients with minimal or no symptoms for abnormalities in the cerebral circulation.

Adult↗
PubMed1998

Subarachnoid hemorrhage caused by Aspergillus aneurysm as a complication of transcranial biopsy of an orbital apex lesion--case report.

A 62-year-old male complaining of unilateral visual disturbance and pain in the involved eye had a small mass at the right orbital apex which was identified as an Aspergillus granuloma by transcranial biopsy. One month later, the patient became comatose because of fatal subarachnoid hemorrhage due to a newly developed aneurysm. Autopsy showed a ruptured aneurysm on the right internal carotid-posterior communicating artery. Histological examination demonstrated prominent Aspergillus invasion of the arterial wall. Aspergillus infection must be taken into consideration in patients with orbital apex syndrome, which may lead to serious cerebrovascular consequences. If sino-orbital lesions are detected by neuroimaging techniques, biopsy using an extradural approach should be performed to obtain a definitive diagnosis.

Aneurysm, Infected↗
PubMed1998

Induction of thymidine phosphorylase activity and enhancement of capecitabine efficacy by taxol/taxotere in human cancer xenografts.

Thymidine phosphorylase (dThdPase) is an essential enzyme for the activation of the cytostatics capecitabine (N(4)-pentyloxycarbonyl-5'-deoxy-5-fluorocytidine) and its intermediate metabolite [5'-deoxy-5-fluorouridine (5'-dFUrd)] to 5-fluorouracil in tumors. We have tried to identify the best partners of capecitabine in combination therapy, such as dThdPase up-regulators, which may enhance the efficacy of this compound. Among various cytostatics studied with the WiDr human colon cancer xenograft model, Taxol, Taxotere, and mitomycin C greatly increased levels of human dThdPase in tumors, and cyclophosphamide slightly increased the enzyme level. These cytostatics simultaneously increased the levels of human tumor necrosis factor alpha (TNFalpha), which is an up-regulator of dThdPase. In cultures of the WiDr cells, however, Taxol did not up-regulate TNFalpha to a detectable level and only slightly enhanced levels of dThdPase. These results suggest that Taxol might indirectly elevate TNFalpha in tumor cells, which in turn up-regulated dThdPase in the tumor cells in the WiDr cancer xenograft. In the combination therapy, the efficacy of Taxol and Taxotere with either capecitabine or 5'-dFUrd was more than just additive. In contrast, Taxol and either 5-fluorouracil or UFT (a mixture of tegafur and uracil) in combination showed only additive activity. Taxol and Taxotere might enhance the efficacy of capecitabine and 5'-dFUrd, probably by modulating dThdPase activity in tumor tissues.

Animals↗
PubMed1998

[Combined hepatic resection and removal of portal vein tumor thrombi].

Portal thrombectomy with extended hepatectomy for extensively progressive primary liver cancer (Vp 3), in which the tumor thrombus has spread beyond the first portal branches, will make other non-surgical treatments possible and improve patients quality of life. We have performed extensive resections in 15 cases of such Vp 3 liver cancer. One patient with huge HCC involving retrohepatic IVC underwent in situ extended left hepatectomy without reconstruction of IVC, resulting in postoperative renal failure because of thrombosis in the bilateral renal veins, but 14 other patients' postoperative courses were uneventful. Ten of 14 patients relapsed within one year, but these patients underwent non-surgical treatments, resulting in improvement in the quality of life. The 1-, and 3-year survival rates were 55.6% and 32.5%, respectively.

Adult↗
PubMed1998

[Effect of somatosensory disturbance to outcomes of motor function in thalamic hemorrhage: evaluation with short-latency somatosensory evoked potential (SSEP)].

We investigated the effect of the somatosensory functions to the outcomes of motor functions in 28 patients with thalamic hemorrhage. The disturbance of the pyramidal tracts was assessed by the destruction of the internal capsule found in computed tomography (CT). The disturbance of the somatosensory function was analyzed by the N20 component of short-latency somatosensory evoked potentials (SSEP). The outcomes of motor function was evaluated after 3 months of ictus. Correlations between the outcomes of motor function, disturbance of the pyramidal tract, and disturbance of the somatosensory function were discussed. The result indicated that functional outcomes statistically correlated with neither disturbance of the internal capsule alone nor disturbance of N20 alone. But, there was statistically significant between functional outcomes and the combination of disturbance of the internal capsule with disturbance of N20 (p < 0.05, Wilcoxon signed-rank). There was not statistical difference in hematoma volume or consciousness. The implications of these results suggest that somatosensory function may affect the recovery of motor functions.

Aged↗
PubMed1998

Lack of active lung anaphylaxis in congenitally mast cell-deficient Ws/Ws rats sensitized with the nematode Nippostrongylus brasiliensis.

Ws/Ws rats are deficient in both mucosal- and connective tissue-type mast cells. To study the role of mast cells in active anaphylaxis, changes in vascular permeability in the trachea upon intravenous antigen challenge with Evans blue dye were examined in Ws/Ws, heterogenic Ws/+, and normal +/ + rats sensitized with the nematode Nippostrongylus brasiliensis. Antigen challenge resulted in fatal anaphylactic shock in some +/+ and Ws/+ rats, but not in Ws/Ws rats. Marked dye leakage developed within 30 min in the trachea of +/+ and Ws/+ rats, while Ws/Ws rats showed no substantial increases in the levels of vascular permeability. Ex vivo stimulation of sensitized lung fragments from +/+ animals with specific antigen induced significant releases of histamine and leukotriene (LT) C4, while sensitized Ws/Ws rat-lung fragments did not. In Ws/Ws rats, levels of nematode-specific IgE, IgG1 and IgG2a antibodies as well as levels of lung eosinophilia were not significantly different from those in +/+ rats. These results show that mast cell-deficient Ws/Ws rats fail to develop active anaphylaxis, and this is mediated probably by the lack of mast cell-derived mediators required for initiation of the reaction.

Anaphylaxis↗
PubMed1998

[The role of nitric oxide in ischemia-reperfused heart].

We examined the role of nitric oxide (NO) in ischemia-reperfused hearts. In an occlusion-reperfusion model of hypercholesterolemic rabbits, the extent of myocardial infarction was increased because of the activation of neutrophils, possibly due to the impaired production of NO in atherosclerotic coronary circulation. It was reversed by the addition of exogenous NO releaser, SNAP. In a hypoxia-reoxygenation model of cultured cardiac myocytes, NO produced by endogenous cardiac iNOS augmented myocyte injury after exposure to hypoxia-reoxygenation. Inhibition of glutathione peroxidase activity was suggested to be the mechanism of sensitization to oxidative stress after exposure to NO. Therefore, NO is supposed to play two roles in ischemia-reperfused hearts, i.e., cardioprotective effect through coronary circulation and cardiotoxic effect through direct action on cardiac myocytes.

Animals↗
PubMed1998

[Relative valve area stenosis after replacement of a Starr-Edwards mitral valve (model 6520) for corrected TGA (S, L, L): report of a case].

The patient was a 38-year-old man who had undergone mitral valve replacement with a Starr-Edwards disc valve (model 6520, 3 M, phi 30 mm, functional valve area: 2.85 cm2) at the age of 15 years for TR combined with corrected TGA. He developed dyspnea on exertion and palpitations at the age of 30 years, and paroxysmal supraventricular tachycardia appeared at the age of 35 years. Cardiac catheterization revealed that the PCWP was 30 mmHg and the TVA was 1.1 cm2, and a diagnosis of stenosis of the prosthetic valve was made. Thus, replacement of the Starr-Edwards disc valve using a BICARBON double leaflet valve (phi 27 mm, functional valve area: 2.85 cm2) was performed. The operative findings of the Starr-Edwards disc valve revealed a normal appearance and no pannus growth. Postoperative echocardiography and cardiac catheterization found that the TVA was 3.7 cm2 and the PCWP was 13 mmHg. The actual valve area of the disc valve sewn on the ventrical, which was anatomically RV construction might have been smaller than the ideal area; however, the double leaflet valve proved efficient in our patient. This case report serves to demonstrate that because of the postoperative difference in measurement between the actual valve area and the prostheticin ball or disc valve, patients undergoing mitral valve replacement must be followed up carefully.

Adult↗
PubMed1998

[Macroscopic and pathohistological investigation of endarterial plaque after intraoperative balloon dilatation of the carotid artery during carotid endarterectomy].

Twelve patients associated with stenosis of the extracranial carotid artery underwent intraluminal balloon dilatation during carotid endarterectomy (CEA). There were 11 men and 1 woman, and age ranged from 56 to 73 years old. The rate of stenosis, shown by angiography, in each patient was from 60 to 85% in width. After securing carotid blood flow by a T-shaped shunt tube, a balloon catheter was inserted from the exposed common carotid artery into the internal carotid artery. The balloon was inflated three or four times with 2.5-3.5 atm. for 30-40 seconds. Immediately after balloon dilatation, endoscopic investigation was performed (Wolf; hard type endoscope, 2.7 mm diameter). Then CEA was performed using the usual procedure. The removed endarterial plaque was investigated pathohistologically. In macroscopic and endoscopic findings, there were 6 patients with mural thrombosis, 4 patients with laceration of the intima, and one patient with outflow of atheroma from the intima. Only 3 patients had increase in lumen after balloon dilatation. In pathohistological appearance, all patients had a moderate degree of fibrosis, calcification, and atheroma in the cross section of the plaque. Ten patients had intramural hemorrhage. Three typical patients were revealed by the use of angiographical, ultrasonographical, endoscopic, and pathohistological presentation. Case 10 showed laceration of the intima by balloon dilatation, and had moderate increase in lumen size macroscopically and endoscopically. There were moderate cases of fibrosis, calcification, atheroma, and intramural hemorrhage. Dilatation of the lumen seemed to be accomplished by a decrease in thickness of the atheroma and intramural hemorrhage. Case 8 demonstrated an increase in lumen size, but also laceration of the intima and outflow of atheroma from the arterial wall. There were much atheroma and large intramural hemorrhage in the intima, which might become a source of enbolism. Case 7 revealed no laceration of the intima and no increase in lumen size. Preoperative ultrasonography showed hyperechoic finding and postoperative pathohistological findings showed severe fibrosis and calcification, which were thought to have interrupted balloon dilatation. There have been small numbers of reports about pathohistological presentation after percutaneous transluminal angioplasty (PTA), because it is very difficult to take a specimen after PTA. In this report we were able to present the necessity of preoperative investigations by angiography, ultrasonography, and 3D-CT.

Aged↗
PubMed1997

Peg5/Neuronatin is an imprinted gene located on sub-distal chromosome 2 in the mouse.

We have established a systematic screen for imprinted genes using a subtraction-hybridization method with day 8.5 fertilized and parthenogenetic embryos. Two novel imprinted genes, Peg1/Mest and Peg3, were identified previously by this method, along with the two known imprinted genes, Igf2 and Snrpn. Recently three additional candidate imprinted genes, Peg5-7 , were detected and Peg5 is analyzed further in this study. The cDNA sequence of Peg5 is identical to Neuronatin, a gene recently reported to be expressed mainly in the brain. Two novel spliced forms were detected with some additional sequence in the middle of the known Neuronatin sequences. All alternatively spliced forms of Peg5 were expressed only from the paternal allele, confirmed using DNA polymorphism in a subinterspecific cross. Peg5/Neuronatin maps to sub-distal Chr 2, proximal to the previously established imprinted region where imprinted genes cause abnormal shape and behavior in neonates.

Alternative Splicing↗
PubMed1997

Heat shock-induced manganese superoxide dismutase enhances the tolerance of cardiac myocytes to hypoxia-reoxygenation injury.

We evaluated the mechanism of the heat shock-induced tolerance to ischemia-reperfusion using a model of hypoxia-reoxygenation tolerance in neonatal rat cardiac myocytes. Myocytes exposed to heat shock (42 degrees C, 1 h) exhibited a 1.8-fold increase in levels of manganese superoxide dismutase (Mn-SOD) mRNA after 40 min v control cells. The concentration of Mn-SOD increased from 0.49+/-0.04 microg/mg protein to 0.68+/-0.05 microg/mg protein after 24 h (P<0. 05). Levels of heat shock protein 72 (hsp72; inducible form) mRNA and protein also increased markedly after heat shock exposure. The release of creatine kinase (CK) from the myocytes and the depletion of ATP level in the myocytes exposed to hypoxia (pO2: 7 mmHg, 3 h) and reoxygenation (pO2: 143 mmHg) were significantly reduced following heat shock pretreatment (CK: 1.18+/-0.14 U/l v 0.62+/-0.13 U/l, ATP: 11.9+/-1.1 nmol/mg protein v 16.2+/-1.0 nmol/mg protein, P<0.05). Treatment with antisense oligodeoxyribonucleotides to Mn-SOD (1.5 micromol/l) completely inhibited the heat shock-associated induction of Mn-SOD (0.47+/-0.05 microg/mg protein), but not hsp72, and abolished the heat shock-induced decrease in CK release (1.04+/-0.15 U/l, P<0.05) and depletion of ATP level (11. 2+/-1.1 nmol/mg protein, P<0.05). Results indicate that Mn-SOD induction, not hsp72 induction, plays a pivotal role in the heat shock-induced acquisition of tolerance to hypoxia-reoxygenation in neonatal rat cardiac myocytes.

Animals↗
PubMed1997

Time course of tolerance to ischemia-reperfusion injury and induction of heat shock protein 72 by heat stress in the rat heart.

We compared the time course of tolerance to myocardial ischemia-reperfusion injury with the time course of heat shock protein 72 (hsp72; inducible form) induction after heat stress in a rat model. The size of the infarct resulting from ischemia-reperfusion was increased 12 h after whole-body hyperthermia (42 degrees C for 15 min), but was significantly decreased 48 and 72 h after hyperthermia, compared with the sham control. The infarct size was decreased as late as 96 h after hyperthermia, although the infarct-limiting effect was smaller at that time. The myocardial content of hsp72 was markedly increased for 3-72 h after hyperthermic treatment, and was decreased after 72 h in association with an increase in the infarct size. The hsp72 content remained elevated during the period of tolerance to ischemia-reperfusion injury, but the infarct size decreased after the hsp72 content peaked. Pretreatment with a protein kinase C (PKC) inhibitor, chelerythrine chloride, immediately before hyperthermia, significantly suppressed the delayed cardioprotective effect of hyperthermia and reduced hsp72 induction. These results suggest that newly synthesized hsp72 through PKC activation after heat stress may have to be post-translationally modified and compartmentalized prior to assuming to the development of the delayed tolerance to ischemia-reperfusion injury in rats.

Animals↗