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T Arai

Publications and source records attributed to T Arai.

At least 73 records · Page 4Linked to original sources
PubMed2002

Effects of propofol on lactate accumulation and oedema formation in focal cerebral ischaemia in hyperglycaemic rats.

BACKGROUND: In cerebral ischaemia, hyperglycaemia brings about severe lactate accumulation and neuronal damage when compared with normoglycaemia. Propofol has been known to suppress glucose metabolism in the brain and possess neuroprotective properties in cerebral ischaemia. Therefore, in this study we examined if propofol could attenuate lactate accumulation and neuronal damage in cerebral ischaemia under hyperglycaemic conditions. METHODS: Ten male wistar rats were divided into two experimental groups: low-dose (approximately 12 mg kg(-1) h(-1)) and high-dose (approximately 60 mg kg(-1) h(-1)) propofol groups (n=5 for each). Following injection of 2 g kg(-1) glucose intraperitoneally, the middle cerebral artery was occluded for 1 h, and then reperfused for the following 2 h. Lactate accumulation and oedema formation were estimated consecutively using nuclear magnetic resonance (NMR) techniques. RESULTS: Lactate accumulation and oedema formation increased continuously during ischaemia and reperfusion in the low-dose propofol group, which was attenuated in the high-dose propofol group. Lactate/NAA (N-acetylaspartate) ratio (as an index of lactate accumulation) 60 and 120 min after reperfusion were 2.67 and 3.26 in low-dose group and 0.30 and 0.10 in high-dose group. For NMR images the number of pixels with a low average diffusion coefficient (an index of the oedema formation), 60 and 120 min after reperfusion were 250.0 and 317.8 in low-dose group, and 16.0 and 12.4 in high-dose group. CONCLUSION: High-dose propofol attenuated lactate accumulation and oedema formation in cerebral ischaemia in hyperglycaemic rats.

Anesthetics, Intravenous↗
PubMed2002

Effects of hydrocortisone and beta-aminopropionitrile on stress-strain and stress-relaxation behaviors, and birefringent retardation of collagen fibers in the rat incisor periodontal ligament.

Three groups of male Wistar rats received daily subcutaneous injections of 10 mg/kg of hydrocortisone (HC group), 300 mg/kg of beta-aminopropionitrile (BAPN group), or saline (control group), for 10 days. The shear stress-strain and stress-relaxation properties of the incisor periodontal ligament were examined in transverse sections from dissected mandibles. Both the maximum shear stress and failure strain energy density increased significantly following the administration of hydrocortisone. The maximum shear stress decreased following the administration of BAPN. However, the stress-relaxations in the initial 10 min did not show significant differences among the three groups. Polarized light microscopic analysis revealed that the retardation value of the collagen fibers was highest in the HC group and lowest in the BAPN group for the bone-related area, but not for the tooth-related and middle areas of the ligament. It is suggested that the changes induced by hydrocortisone or BAPN occurred mainly in the elastic components and to a minor extent in the viscous components although the physical and biomechanical properties are determined by the interaction of all the various components. We also suggest that the main response to the drugs occurred in the collagen fibers in the bone-related area of the ligament.

Aminopropionitrile↗
PubMed2001

6-formylpterin intracellularly generates hydrogen peroxide and restores the impaired bactericidal activity of human neutrophils.

The effects of 6-formylpterin on the impaired bactericidal activity of human neutrophils were examined ex vivo. When neutrophils isolated from fresh blood were incubated with 6-formylpterin, the intracellular production of hydrogen peroxide (H(2)O(2)) occurred. The H(2)O(2) generation by 6-formylpterin in neutrophils occurred in the presence of diphenyleneiodonium (DPI), an inhibitor of NADPH-oxidase. When neutrophils were incubated with DPI, the killing rate of catalase-positive bacteria, Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus), significantly decreased. This impaired bactericidal activity of the DPI-treated neutrophils was a mimic for chronic granulomatous disease (CGD). However, the killing rate of the DPI-treated neutrophils against E. coli and S. aureus significantly increased when 6-formylpterin was administered. Since 6-formylpterin intracellularly generates H(2)O(2) independent from the NADPH-oxidase, it was considered to improve the impaired bactericidal activity of the DPI-treated neutrophils. The use of 6-formylpterin may serve as an option of therapy for CGD.

Adult↗
PubMed2001

Asynchronous development of the Benjamin-Feir unstable mode: solution of the Davey-Stewartson equation.

The long time evolution of the Benjamin-Feir unstable mode in two dimension is described by the growing-and-decaying mode solution to the Davey-Stewartson equation. The solution of the hyperbolic Davey-Stewartson (the so-called Davey-Stewartson I) equation is analyzed to show that the resonance between line soliton and growing-and-decaying mode exists. If the resonant condition is exactly satisfied, the growing-and-decaying mode exists only in the forward region of propagation of soliton and the soliton is accelerated (or decelerated). Under the quasiresonant condition, the growing-and-decaying mode grows at first in the forward region, and after the sequence of the evolution has done in the forward region the mode starts to grow in the backward region of the soliton.

Journal Article↗
PubMed2001

Age-related hypermethylation of the hMLH1 promoter in gastric cancers.

To determine whether methylation of the hMLH1 promoter is related to increasing age and gastric carcinogenesis, we examined hMLH1 methylation and expression in 100 gastric cancers. hMLH1 methylation and aberrant protein expression were observed in 9 and 13 cancers, respectively. Normal and intestinal metaplastic tissues adjacent to cancers with hypermethylation did not exhibit any hMLH1 methylation, indicating that it may be specific to gastric cancers. The frequency of hMLH1 methylation significantly increased with age. These results suggest that hMLH1 methylation plays an important role in gastric carcinogenesis in old people.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Autoreactive CD4(+) T-cell clones to beta2-glycoprotein I in patients with antiphospholipid syndrome: preferential recognition of the major phospholipid-binding site.

Autoreactive CD4(+) T cells to beta2-glycoprotein I (beta2GPI) that promote antiphospholipid antibody production were recently identified in patients with antiphospholipid syndrome (APS). To further examine antigen recognition profiles and T-cell helper activity in beta2GPI-reactive T cells, 14 CD4(+) T-cell clones specific to beta2GPI were generated from 3 patients with APS by repeated stimulation of peripheral blood T cells with recombinant beta2GPI. At least 4 distinct T-cell epitopes were identified, but the majority of the beta2GPI-specific T-cell clones responded to a peptide encompassing amino acid residues 276 to 290 of beta2GPI (KVSFFCKNKEKKCSY; single-letter amino acid codes) that contains the major phospholipid-binding site in the context of the DRB4*0103 allele. Ten of 12 beta2GPI-specific T-cell clones were able to stimulate autologous peripheral blood B cells to promote anti-beta2GPI antibody production in the presence of recombinant beta2GPI. T-cell helper activity was exclusively found in T-cell clones capable of producing interleukin 6 (IL-6). In vitro anti-beta2GPI antibody production induced by T-cell clones was inhibited by anti-IL-6 or anti-CD40 ligand monoclonal antibody. In addition, exogenous IL-6 augmented anti-beta2GPI antibody production in cultures of the T-cell clone lacking IL-6 expression. These results indicate that beta2GPI-specific CD4(+) T cells in patients with APS preferentially recognize the antigenic peptide containing the major phospholipid-binding site and have the capacity to stimulate B cells to produce anti-beta2GPI antibodies through IL-6 expression and CD40-CD40 ligand engagement. These findings are potentially useful for clarifying the pathogenesis of APS and for developing therapeutic strategies that suppress pathogenic antiphospholipid antibody production in these patients.

Adult↗
PubMed2001

Dexamethasone reduces energy utilization in ischemic gerbil brain.

Glucocorticoids have been reported to aggravate ischemic neuronal damage. Because energy failure is a crucial factor in the development of ischemic neuronal injury, the effects of dexamethasone on histologic outcome and energy metabolism were investigated in gerbil brain. Dexamethasone (3 microg, i.c.v.) was administered 1 h prior to ischemia, and its effect on delayed neuronal death caused by 2 min of bilateral common carotid artery occlusion was observed in hippocampal CA1 pyramidal neurons. The brain concentration of ATP after various durations of decapitation ischemia was determined, and the effect of dexamethasone (3 microg, i.c.v.) was examined. Na+,K+-activated adenosine triphosphatase (Na+,K+-ATPase) activity was evaluated after the administration of the agent. Forebrain ischemia for 2 min produced neuronal damage in animals pretreated with dexamethasone, although neuronal damage was not observed in vehicle-injected animals. Decapitation ischemia for 0.5 and 1 min reduced the brain ATP concentration to 44% and 15% of the basal level, respectively. Dexamethasone attenuated the ischemia-induced reduction in ATP, and the values were 58% and 25% of the basal level, respectively. Na+,K+-ATPase activity at pH 6.7 was suppressed to 47% by dexamethasone treatment (3 microg, i.c.v.), whereas the activity at pH 7.4 was not influenced by the agent. The results show that a contributing factor to the aggravation of ischemic neuronal damage may be a disturbance in Na+,K+-ATPase despite adequate levels of ATP.

Adenosine Diphosphate↗
PubMed2001

Identification of human ST2 protein in the sera of patients with autoimmune diseases.

Soluble human ST2 protein (IL1RL1-a) in the sera of patients with various autoimmune diseases was identified by a newly developed procedure using specific monoclonal antibodies. After immunoprecipitation and subsequent immunoblotting, a glycosylated protein of about 60 kDa was detected in the sera of SLE patients, but not in the sera of healthy controls. The experiments using gel filtration and SDS-PAGE under a nonreducing condition indicated the existence of the ST2 multimer in serum. The mobility of the natural protein was slower than that of the recombinant human ST2 protein produced by COS7 cells in SDS-PAGE, suggesting a difference of glycosylation between humans and monkeys. The identification of the natural human ST2 protein should be important both to fundamental researches and the further clarification of the clinical implications of the ST2 protein.

Animals↗
PubMed2001

Intracellular processing of aggregated tau differs between corticobasal degeneration and progressive supranuclear palsy.

Corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) are sporadic neurodegenerative diseases with intracytoplasmic aggregates of the microtubule-associated protein, tau, in neurons and glial cells. Immunoblot analysis of detergent-insoluble brain extracts of patients with CBD and PSP shows distinctive patterns of tau fragments. These results suggest differing intracellular processing of aggregated tau in these two diseases despite an identical composition of tau isoforms. Such biochemical differences may be related to the neuropathological features of these diseases.

Aged↗
PubMed2001

Adenovirus-mediated gene therapy specific for small cell lung cancer cells using a Myc-Max binding motif.

Recent clinical trials of gene therapy for patients with thoracic cancers have shown that these treatments were well tolerated with minimal side effects and that we need to further enhance specificity as well as efficiency of gene transfer to target cancer cells. We previously reported that myc-overexpressing SCLC cell lines became selectively sensitive to ganciclovir (GCV) by transducing the herpes simplex virus thymidine kinase (HSV-TK) gene under the control of the Myc-Max response elements (a core nucleotide sequence, CACGTG) and that this construct (MycTK) could be utilized to develop a novel treatment against chemo-radio-resistant SCLC. We report here in vivo antitumor effects and safety of a replication-deficient adenoviral vector containing the Myc-Max binding motif (AdMycTK) on SCLC cells. In vitro infection with AdMycTK selectively rendered myc-overexpressing SCLC cell lines 63- to 307-fold more sensitive to GCV. In vivo injections with AdMycTK followed by GCV administration markedly suppressed the growth of myc-overexpressing tumors established in the subcutis or in the peritoneal cavity of athymic mice. On the other hand, infection with AdMycTK did not significantly affect either in vitro GCV sensitivity of the cells expressing very low levels of the myc genes or the growth of their subcutaneous tumors. Moreover, we observed no apparent side effects of this treatment including body weight loss or biochemical abnormalities in contrast to the treatment with AdCATK that conferred strong but nonspecific expression of the HSV-TK gene. These results suggested that AdMycTK/GCV therapy is effective on SCLC patients whose tumors overexpress myc family oncogenes.

Adenoviridae↗
PubMed2001

6-formylpterin, a xanthine oxidase inhibitor, intracellularly generates reactive oxygen species involved in apoptosis and cell proliferation.

The chemical property of 6-formylpterin and its biological functions were examined. Polarographic studies revealed that 6-formylpterin reacted with NAD(P)H and consumed oxygen. In contrast, other conjugated pterins, such as biopterin and neopterin, showed no consumption of oxygen. The production analysis using high-performance liquid chromatography documented that 6-formylpterin catalyzes the conversion from NADH to NAD. Electroparamagnetic resonance spin trapping experiments demonstrated that this reaction is accompanied with the generation of reactive oxygen species (ROS), superoxide anion and hydrogen peroxide. When 6-formylpterin was administered to HL-60 cells, intracellular ROS generation was observed and apoptosis was induced. In contrast, other conjugated pterins induced neither intracellular ROS generation nor apoptosis in HL-60 cells. The intracellular ROS generation by 6-formylpterin was observed in other cells, such as PanC-1 cells and Jurkat cells. 6-formylpterin suppressed cell proliferation in PanC-1 cells and inhibited Fas-mediated apoptosis in Jurkat cells. These findings indicate that, among conjugated pterins, 6-formylpterin has the unique property to transfer electron from NAD(P)H to oxygen and that the property brings about intracellular ROS generation, which exerts various biological functions such as induction of apoptosis, suppression of cell proliferation, and inhibition of Fas-mediated apoptosis.

Apoptosis↗
PubMed2001

Nanosecond, high-intensity pulsed laser ablation of myocardium tissue at the ultraviolet, visible, and near-infrared wavelengths: in-vitro study.

BACKGROUND AND OBJECTIVE: A large number of clinical trials of transmyocardial laser revascularization (TMLR) have been conducted to treat severe ischemic heart diseases. A variety of laser sources have been used or tested for this treatment, however, no comprehensive study has been performed to reveal the mechanism and the optimum laser irradiation condition for the myocardium tissue ablation. There have been reported limited experimental data of the high-intensity pulsed laser ablation of myocardium tissues. STUDY DESIGN/MATERIALS AND METHODS: A 1064-nm Q-switched Nd:YAG laser and its 2nd (532 nm), 3rd (355 nm), and 4th (266 nm) harmonics were used for ablation experiments. At each wavelength, 25 laser pulses irradiated the porcine myocardium tissue samples at a constant laser intensity (peak laser power divided by laser spot area) of approximately 2 GW/cm(2) and the ablation depths were measured. During ablation, laser-induced optical and acoustic emissions were measured to investigate the ablation mechanism at each laser wavelength. For the ablated tissues, histological observation was made with a polarization optical microscope. RESULTS: It was shown that the ablation efficiency did not directly depend on the linear absorption coefficient of the tissue; the ablation depth was maximized at 355 and 1064 nm, and minimized at 532 nm. Strong laser-induced optical and acoustic emissions were observed for the 266- and 1064-nm laser irradiations. The histology showed that thermal denaturation of the tissue near the ablation walls decreased with decreasing wavelength for 266, 355, and 532 nm, but it was limited for 1064 nm. CONCLUSION: At the laser intensity of approximately 2 GW/cm(2), ablation characteristics were drastically changed for the different laser wavelengths. The results indicated that for 266, 355, and 532 nm, the tissue removal was achieved mainly through a photothermal process, but for 266 nm the intense laser-induced plasma formation would result in a reduced laser energy coupling to the tissue. For 1064 nm, a photodisruption was most probable as a dominant tissue removal process. Because of the high ablation rate and limited thermal denaturation, the 355- and 1064-nm lasers could be potential laser sources for TMLR, although further investigation is needed to discuss the clinical issues.

Angioplasty, Laser↗
PubMed2001

Use of a new ICG-dye-enhanced diode laser for percutaneous laser disc decompression.

BACKGROUND AND OBJECTIVE: The lasers used today for Percutaneous Laser Disc Decompression (PLDD) can not selectively ablate the nucleus pulposus (NP). We hypothesized that if indocyanine green dye were injected into the NP, 805 nm diode laser irradiation would result in selective and safe removal of NP tissue without damaging nearby tissues. STUDY DESIGN/MATERIALS AND METHODS: Twelve beagle dogs were used for three experiments, i.e., determination of attenuation coefficients of NP and AF, determination of weight of NP before and after laser irradiation, and histopathological study. RESULTS: The attenuation coefficient at 805 nm of NP which had been homogenized in the presence of ICG was 2521.3/cm. Upon application of the diode laser at a power of 1, 3, or 5 W (the intensity of laser irradiation: 0.353, 1.061, or 1.768 x 10(3) W/cm(2)) to NPs into which ICG had been injected, the weight of the NPs decreased by a mean 20, 45, and 65%, respectively. Macroscopic and microscopic examination of the discs after PLDD showed that only the NP where the tissues were stained by ICG were removed. CONCLUSIONS: These results indicated that the combined use of ICG and diode laser irradiation effectively and selectively ablates the NP with low laser power.

Animals↗
PubMed2001

Characterization of a novel gene, sperm-tail-associated protein (Stap), in mouse post-meiotic testicular germ cells.

During mammalian spermatogenesis, many specific molecules show the dynamics of expression and elimination, corresponding with the morphological differentiation of germ cells. We have isolated a novel cDNA designated F77 from mouse testis by cDNA subtractive hybridization between normal and sterile mice, using the C57BL/6 congenic strain for the hybrid sterilityhyphen;3 lpar;Hsthyphen;3rpar; allele from Mus spretus. The full-length F77 mRNA was 3.4 kb and showed significant nonmatching with entries in the databases. F77 was mapped at a proximal position between D8Mit212 and D8Mit138 on mouse chromosome 8, in which no corresponding genes related to its nucleotide sequence were found. F77 mRNA was not detected in any other organs except the testis of adult fertile mice. F77 protein was only seen in normal adult testis and epididymis. In contrast to normal C57BL/6 mice, F77 mRNA and protein were not seen in germ cell-deficient Kit(W)/Kit(Wv) mice. By in situ hybridization, F77 mRNA was detected mainly at round spermatids in the sexually mature testis, and immunohistochemical analysis revealed that F77 protein was located at the tail of elongated spermatids. We are proposing the name, sperm-tail-associated protein (Stap), for the gene encoding F77 cDNA. Mol. Reprod. Dev. 59: 350-358, 2001.

Amino Acid Sequence↗
PubMed2001

Toxic shock syndrome toxin-1 accelerated collagen-induced arthritis in mice.

The aim of this study was to explore the roles of toxic shock syndrome toxin-1 (TSST-1) in collagen-induced arthritis (CIA). DBA/1 mice were immunized with type II collagen (CII) and treated with TSST-1. Intraperitoneal and intravenous injections of TSST-1 aggravated CIA, enhancing its incidence and severity. CIA was accompanied by an increase in anti-CII IgG Ab levels. Intraperitoneal administration with TSST-1 enhanced IFN-gamma, TNF-alpha, and IL-4 production in DBA/1 mice. We discovered the mRNA expressions of IFN-gamma, IL-2, TNF-alpha, IL-1beta, and iNOS in spleen cells stimulated with TSST-1 in vitro. However, IL-12 and IL-4 mRNA expression were seen constitutively without stimulation. Only a little increase of IL-12 and IL-4 mRNA expression was seen at 2-3 h after treatment with TSST-1. Our experiments demonstrated that CIA was aggravated by the treatment with TSST-1, which may have induced various proinflammatory cytokines and the production of both Th1 and Th2 cytokines.

Animals↗
PubMed2001

Bilirubin impairs bactericidal activity of neutrophils through an antioxidant mechanism in vitro.

BACKGROUND: Liver failure accompanied by hyperbilirubinemia after major hepatic resection is profoundly associated with septic complications. Although the immune dysfunction in cholestasis has been intensively investigated, the contribution of increased serum bilirubin to the impaired resistance to bacterial infection remains to be elucidated. Because bilirubin possesses an antioxidant activity, we hypothesized that bilirubin may scavenge reactive oxygen species (ROS) produced by neutrophils and consequently impair neutrophil bacterial killing. To address this, we evaluated the effects of bilirubin on the bactericidal activity of ROS or of neutrophils in vitro. MATERIALS AND METHODS: The antioxidant activity of bilirubin was determined using an ROS-sensitive fluorophore, dichlorofluorescin diacetate (DCFH-DA). Bilirubin concentration in the buffer solution was monitored spectorophotometrically after incubation with ROS. The effect of bilirubin on killing of Escherichia coli by ROS or by isolated human neutrophils was determined by counting the viable E. coli after incubation on nutrient agar. RESULTS: The bilirubin concentration in the buffer solution was decreased by the addition of hydrogen peroxide, especially in the presence of peroxidase or ferrous iron. DCFH-DA oxidation by ROS or activated neutrophils was inhibited by bilirubin in a dose-dependent manner. The bactericidal activity of ROS or of isolated neutrophils was significantly attenuated by bilirubin. CONCLUSIONS: Bilirubin impairs bactericidal activity of neutrophils through scavenging ROS. Increased levels of serum bilirubin may well be responsible for the impaired bacterial clearance in patients with hyperbilirubinemia.

Antioxidants↗