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T Arai

Publications and source records attributed to T Arai.

At least 379 records · Page 21Linked to original sources
PubMed1997

Visceral fat accumulation as an important risk factor for obstructive sleep apnoea syndrome in obese subjects.

OBJECTIVES: It is well known that obstructive sleep apnoea-(OSA) is frequently associated with obesity. In the current study, we investigated the correlation between abdominal visceral fat accumulation and the presence of OSA in obese subjects. SUBJECTS: A consecutive series of 37 patients (17 men and 20 women) with primary obesity who were admitted to the Second Department of Internal Medicine. Osaka University Hospital, were investigated Patients with OSA were designated as those whose apnoea index (number of apnoea h-1 of sleep) was more than 5. MAIN OUTCOME MEASURES: The distribution of body fat was determined using computed tomographic sections. The upper airway dimensions were evaluated with indices obtained by cephalometry in both inspiratory and expiratory phases. RESULTS: Visceral adipose tissue (AT) area which was measured at the level of the umbilicus, and its ratio to total AT area were both significantly greater in OSA patients as compared with those in non-OSA patients. All subjects whose visceral AT area measured more than 220 cm2 manifested OSA. These two parameters also closely correlated with an increase in apnoea index. A multiple linear regression analysis revealed that the visceral AT area significantly correlated to apnoea index when age, AT mass and lean body mass were taken into account. The fluctuations of the upper airway were significantly greater in the large visceral fat group than in the small visceral fat group. CONCLUSIONS: These results suggest that visceral fat accumulation is an important risk indicator for OSA in obese subjects.

Adipose Tissue↗
PubMed1997

Relations between the extracellular concentrations of choline and acetylcholine in rat striatum.

Changes in extracellular levels of acetylcholine (ACh) and choline (Ch) in the striatum of rats were examined by in vivo microdialysis after intraperitoneal injections of drugs. A dopamine D2 antagonist, sulpiride (20 mg/kg), and a muscarinic antagonist, atropine (3.5 mg/ kg), increased ACh levels and decreased Ch levels. On the contrary, the D2 agonist (+/-)-2-(N-phenylethyl-N-propyl)amino-5-hydroxytetralin (N-434; 5 mg/kg) and an anesthetic, pentobarbital (50 mg/kg), decreased ACh levels and increased Ch levels. Perfusion of 10 microM hemicholinium-3 (HC-3), a Ch uptake inhibitor, through the striatum induced a complete inhibition of ACh release and increased Ch levels in all drug-treated groups. The degree of relative increase in the level of Ch induced by HC-3 differed among the drug-pretreated groups; compared with the control group, the relative increase was larger in the sulpiride- and atropine-treated groups and smaller in the N-434 and pentobarbital-treated groups. Thus, we demonstrated reciprocal relations between extracellular concentrations of Ch and ACh after treatments by drugs. The data suggest that in the striatum, which is rich in cholinergic innervation, the extracellular Ch concentration is to a large extent determined by activity of the cholinergic transmission reflected in high-affinity choline uptake.

Acetylcholine↗
PubMed1997

Raised plasma concentrations of parathyroid hormone related peptide in hypercalcemic multiple myeloma.

In order to clarify the pathogenesis of hypercalcemia in multiple myeloma, we measured plasma levels of parathyroid hormone related peptide (PTHrP), tumor necrosis factor alpha (TNF-alpha), tumor necrosis factor beta (TNF-beta), intact PTH and, serum 1,25-dihydroxyvitamin D in fifteen patients of multiple myeloma. We also measured serum levels of inorganic phosphorus (iP) and alkalinephosphatase activity (ALP). No significant differences in iP (3.2 +/- 0.4 vs. 4.0 +/- 2.2 mg/dl), ALP (150 +/- 28 vs. 335 +/- 305 IU/l) 1,25(OH)2 D (31.5 +/- 17.0 vs. 23.3 +/- 11.2 pg/ml) or TNF-alpha (7.8 +/- 2.1 vs. 8.0 +/- 2.0 pg/ml) were observed between normocalcemic and hypercalcemic patients. Plasma iPTH levels in hypercalcemic patients were significantly lower than those in normocalcemic patients (28.5 +/- 9.4 vs. 16.3 +/- 5.6 pg/ml, p = 0.01). Plasma levels of TNF-beta were less than 15.6 pg/ml in all subjects. On the other hand, the frequency of patients with abnormally high plasma levels of PTHrP was significantly greater (2/9 for normocalcemia vs 5/6 for hypercalcemia, chi 2 = 5.20, p = 0.02) in patients with hypercalcemia than in normocalcemic patients. Furthermore, a significant positive relationship between plasma PTHrP levels and corrected serum calcium levels (cCa) was observed using Spearman's correlation analysis by rank in fifteen myeloma cases (rs = 0.66, p = 0.013). These results suggest that PTHrP might be involved in the elevation of serum calcium levels in hypercalcemic myeloma patients. However, a few cases exhibit normocalcemia despite elevated plasma PTHrP levels or hypercalcemia without high plasma PTHrP levels. Therefore, further studies are necessary to elucidate the pathogenesis of hypercalcemia in multiple myeloma.

Aged↗
PubMed1997

Ultrastructural background of albuminuria in rats with passive Heymann nephritis.

BACKGROUND: Although it is widely known that proteinuria in rats with passive Heymann nephritis (PHN) is prevented by treatment with cobra venom factor (CVF), the precise mechanisms of complement-dependent proteinuria have not been fully elucidated. The aim of this study was to evaluate morphologically whether the size of subepithelial electron-dense deposits (EDDs) contributes to the onset of albuminuria. METHODS: The size of subepithelial EDDs and anionic sites in the lamina rarae externa (LRE) overlaid with subepithelial EDDs were evaluated by ruthenium red and compared between PHN and PHN treated with CVF in rats. RESULTS: Overt albuminuria was present on days 3 and 4 after injection of anti-Fx1A. CVF-treatment of rats with PHN prevented albuminuria (PHN + CVF: n = 6) (53.6 +/- 38.8 vs 1.02 +/- 0.55 mg/day, P < 0.01, on day 4). Rat C3 was detected along the glomerular capillary walls on day 4 post-injection in rats with PHN, but not in rats with PHN + CVF. Subepithelial EDDs were observed in both groups. Quantitative morphometric analysis revealed that CVF-treatment decreased the size of subepithelial EDDs as well as the extent of retraction of glomerular epithelial cells. In both groups the density of anionic sites in the LRE overlaid with EDDs was decreased compared with the LRE without subepithelial EDDs. However, no difference was noted between the two groups. CONCLUSIONS: Depletion of serum complement decreases subepithelial EDDs as well as the number of sites with decreased anionic charge underlying the EDDs. Thus, the size of subepithelial EDDs plays a pivotal role in the onset of albuminuria.

Albuminuria↗
PubMed1997

The expression of ST2 gene in helper T cells and the binding of ST2 protein to myeloma-derived RPMI8226 cells.

The ST2 gene, which is specifically induced by growth stimulation, encodes interleukin-1 receptor-related proteins. Using the RT-PCR method, we found that the ST2 gene was broadly expressed in hematopoietic cell lines. It was also expressed specifically in helper T cell lines among lymphocytic cell lines. We analyzed the expression of ST2 in mouse helper T cell subsets with Northern blotting analysis. Mouse Th1 cell lines so far studied did not express ST2 mRNAs. On the other hand, one of the Th2 cell lines, D10, expressed ST2L (transmembrane form) without stimulation, while co-stimulation by PMA and A23187 induced ST2 (soluble form) mRNA. These results suggest that the ST2 gene is involved in the regulation of the immune system. IL-1 alpha, IL-1 beta, and receptor antagonist did not bind to ST2L protein, which prompted us to search for the specific ligand of ST2. The recombinant human ST2 protein was purified and labeled with FITC. The labeled human ST2 protein bound with myeloma-derived RPMI8226 cells among the various B-cell lines, indicating possible involvement of ST2 in T-cell/B-cell interaction.

Animals↗
PubMed1997

Real time observation of binding of herpes simplex virus type 1 (HSV-1) to Vero cells and neutralization of HSV-1 by sulfonated human immunoglobulin.

A real time biomolecular interaction assay system involving an optical sensor was applied to the quantitative analysis of the binding of herpes simplex virus type 1 (HSV-1) to Vero cells, and the neutralization antibody titer against this virus with a commercially available sulfonated human immunoglobulin preparation. The virus titers in a viral solution and the neutralizing antibody titer in the human immunoglobulin preparation could be successfully estimated in a short time with this system without any difficult cytopathic effect analysis of cultured cells.

Animals↗
PubMed1997

The effect of xenon on spinal dorsal horn neurons: a comparison with nitrous oxide.

We compared the effects of xenon (Xe) on the spinal cord dorsal horn neurons with those of nitrous oxide (N2O) in cats anesthetized with chrolarose and urethane. We assessed the potency of both anesthetics by the inhibition of wide dynamic range neuron responses evoked by cutaneous noxious (pinch) stimulation to a hindpaw. During 70% Xe inhalation, the responses of 7 of 11 neurons to pinch stimulation were suppressed. N2O, 70%, suppressed it in 8 of 11 neurons. The potency of Xe and N2O was compared in six neurons that were suppressed by both anesthetics. After 20 min of Xe inhalation, the response to pinch was suppressed to 49.5% +/- 8.2% (mean +/- SE), while N2O, 70% in oxygen, suppressed it to 45.9% +/- 7.9%. The difference between N2O and Xe was not significant. We conclude that Xe and N2O suppress the spinal cord dorsal horn neurons to a similar degree.

Anesthetics, Inhalation↗
PubMed1997

Increase of glutamate uptake in astrocytes: a possible mechanism of action of volatile anesthetics.

BACKGROUND: Glutamate is the most ubiquitous excitatory neurotransmitter in the vertebrate central nervous system. Astrocytes play an important role in terminating glutamatergic neurotransmission by removing released glutamate from the synaptic cleft. The authors examined the effects of several anesthetics on the glutamate uptake activity of astrocytes. METHODS: Cultured astrocytes from hippocampi of rat embryos were incubated with solution containing [3H]glutamate, which was pre-equilibrated with 0-4% halothane at 37 degrees C. The uptake activity was evaluated as the amount of radioactivity per cell of protein. RESULTS: When the reaction solution was equilibrated with 4% halothane, glutamate uptake increased to about 165% of the control. The effect of halothane was dose-dependent, and a significant augmentation (30-50%) of glutamate uptake was observed at a range in clinical use concentrations (1-2%). On the other hand, the uptake of gamma-aminobutyric acid, an inhibitory transmitter, was hardly affected by 1-4% halothane. The effect of halothane on glutamate uptake was also examined in neuron-rich culture, and similar augmentation was observed, although the extent was less than that in astrocyte culture. Biochemical subcellular fractions (i.e., glial plasmalemmal vesicles and synaptosomes) were also examined, however, only slight (not significant) increase was detected in the glutamate uptake activity. Other volatile anesthetics, such as enflurane, isoflurane, and sevoflurane, also enhanced glutamate uptake, whereas the intravenous anesthetics ketamine and pentobarbital showed no effect on glutamate uptake. CONCLUSIONS: The increase of glutamate uptake by astrocytes in the presence of volatile anesthetics potentially attenuates excitatory synaptic transmission in the entire central nervous system, a finding that may explain in part the action of volatile anesthetics.

Adjuvants, Anesthesia↗
PubMed1997

Lidocaine suppresses the anoxic depolarization and reduces the increase in the intracellular Ca2+ concentration in gerbil hippocampal neurons.

BACKGROUND: The movement of ions, particularly Ca2+, across the plasma membrane of neurons is regarded as an initial element of the development of ischemic neuronal damage. Because the mechanism by which lidocaine protects neurons against ischemia is unclear, the effects of lidocaine on the ischemia-induced membrane depolarization, histologic outcome, and the change in the intracellular Ca2+ concentration in the gerbil hippocampus were studied. METHODS: The changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 4 min were compared in animals given lidocaine (0.8 micromol administered intracerebroventricularly) 10 min before ischemia and those given saline. The histologic outcome was evaluated 7 days after ischemia by assessing delayed neuronal death in hippocampal CA1 pyramidal cells in these animals. In a second study, hypoxia-induced intracellular Ca2+ increases were evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effects of lidocaine (10, 50, and 100 microM) on the Ca2+ accumulation were examined. In addition, the effect of lidocaine (100 microM) drug perfusion with a Ca2+-free ischemia-like medium was investigated. RESULTS: The preischemic administration of lidocaine delayed the onset of the ischemia-induced membrane depolarization (anoxic depolarization) and reduced its maximal amplitude. The histologic outcome was improved by the preischemic treatment with lidocaine. The in vitro hypoxia-induced increase in the intracellular concentration of Ca2+ was suppressed by the perfusion with lidocaine-containing mediums (50 and 100 microM), regarding the initiation and the extent of the increase. The hypoxia-induced intracellular Ca2+ elevation in the Ca2+-free condition was similar to that in the Ca2+-containing condition. Perfusion with lidocaine (100 microM) inhibited this elevation in the Ca2+-free condition. CONCLUSIONS: Lidocaine helps protect neurons from ischemia by suppressing the direct-current potential shift, by inhibiting the release of Ca2+ from the intracellular Ca2+ stores, and by inhibiting the influx from the extracellular space.

Anesthetics, Local↗
PubMed1997

Ion transport systems in the uptake of 99Tcm-tetrofosmin, 99Tcm-MIBI and 201Tl in a tumour cell line.

The kinetics, intracellular distribution and effects of ion transport inhibitors on the uptake of 99Tcm-tetrofosmin, 99Tcm-methoxyisobutyl isonitrile (99Tcm-MIBI) and 201Tl were investigated in a tumour cell line. Both uptake and washout of the tracers were measured at specific intervals. Cells were treated with ouabain, dimethyl amiloride (DMA) and bumetanide to observe the effects on uptake, while carbonyl cyanide m-chlorophenylhydrazone (CCCP) was used to study the release of the tracers. The tracers showed similar uptake and washout kinetics. Ouabain inhibited 55-67% of 201Tl, 16-22% of 99Tcm-tetrofosmin and 8-14% of 99Tcm-MIBI. DMA inhibited the uptake of both 99Tcm-tetrofosmin (30%) and 99Tcm-MIBI (21%). Bumetanide stimulated the uptake of 99Tcm-tetrofosmin and 99Tcm-MIBI but inhibited that of 201Tl (37%). When cells were pretreated with various combinations of these ion transport inhibitors, the uptake of 201Tl was related to Na+,K+ pump, Na+,K+, 2Cl- co-transport systems, whereas the uptake of both 99Tcm-tetrofosmin and 99Tcm-MIBI was related to the Na+,K+ pump, Na+/H+ antiport systems. Addition of CCCP released 55% and 90% of accumulated 99Tcm-tetrofosmin and 99Tcm-MIBI respectively, indicating that the percentage released was related to mitochondrial uptake.

Amiloride↗
PubMed1997

Molecular genetics of plasma cholesteryl ester transfer protein.

Plasma cholesteryl ester transfer protein facilitates the transfer of cholesteryl ester from HDL to apolipoprotein B-containing lipoproteins, and is a key protein in the reverse cholesterol transport system. The importance of plasma cholesteryl ester transfer protein in lipoprotein metabolism was highlighted by the discovery of deficient individuals with a marked hyper-HDL-cholesterolemia. Cholesteryl ester transfer protein deficiency causes various abnormalities in the concentration, composition, and functions of both HDL and LDL. Its significance in atherosclerosis is still controversial. However, in-vitro evidence shows large cholesteryl ester-rich HDL particles in cholesteryl ester transfer protein deficiency are defective in cholesterol efflux. Recent epidemiological studies have demonstrated an increased incidence of coronary atherosclerosis in deficient patients. The current review will also focus on the molecular genetics of the protein.

Animals↗
PubMed1997

Bactericidal activity of a fermented hot-water extract from Stevia rebaudiana Bertoni towards enterohemorrhagic Escherichia coli O157:H7 and other food-borne pathogenic bacteria.

A fermented aqueous extract from Stevia rebaudiana Bertoni showed strong bactericidal activity towards a wide range of food-borne pathogenic bacteria including enterohemorrhagic Escherichia coli O157:H7. The colony-forming ability of the food-borne pathogenic bacteria tested so far was reduced to < 10(-7) when exposed to > or = 40% (v/v) solutions of the fermented extract at 37 C for 2 hr. Secretion of verocytotoxin 1 and 2 by enterohemorrhagic E. coli was also diminished by fermented extract at a concentration of > or = 10% (v/v). In contrast, the fermented extract did not significantly kill Bifidobacteria or Lactobacilli. The active principle(s) of the fermented Stevia extract were bactericidal under acidic conditions.

Bacterial Toxins↗
PubMed1997

Regression of metastatic liver tumors in rats treated with angiogenesis inhibitor TNP-470: occurrence of apoptosis and necrosis.

To clarify the mechanism of the reduction of metastatic liver tumors in rats treated with angiogenesis inhibitor TNP-470, the death of tumor cells was examined pathologically and ultrastructurally. Liver metastases were developed by intravenous injection of AH-130 cells. TNP-470 was given subcutaneously after tumor cell injection. Alterations in the size and number of metastatic tumors were examined at various time points, in association with the analysis of cell death pattern. The metastatic nodules were divided into 4 groups according to the morphological patterns of cell death; no cell death, scattered apoptosis, central necrosis, and diffuse necrosis. The number and size of the metastatic tumors at 2 weeks in untreated rats were larger than those in treated rats. The number of tumors in untreated rats decreased, but the tumor size increased. All rats treated with TNP-470 were alive and free from tumors after 4 weeks, whereas all the untreated rats died of liver metastases. The percentages of the tumors with necrosis in untreated rats (61.2% at 2 weeks and 100% at 4 weeks) were significantly higher than that (31.8% at 2 weeks) in treated rats (P < 0.01). The percentage of the tumors containing apoptotic cells in treated rats was significantly higher than that in untreated rats (54.5% vs. 30.6%; P < 0.05). The growth of metastatic tumors without treatment might be faster than the growth of vessels in untreated tumors, resulting in central necrosis due to ischemia. On the other hand, the reduction of metastatic liver tumors treated with TNP-470 might be caused by inhibition of angiogenesis, providing a weak ischemic stimulus which triggers apoptosis, rather than by a direct cytotoxic effect on tumor cells, because previous in vivo experiments demonstrated that TNP-470 affected endothelial cells but not tumor cells.

Animals↗
PubMed1997

Origin of intraepithelial apoptotic cells in human colorectal adenomas.

The origin of intraepithelial apoptotic cells in human colorectal adenomas was examined using immunohistochemistry. Tissue sections of human colorectal adenomas obtained during surgery or endoscopy were stained by the streptavidinbiotin method using antibodies against carcinoembryonic antigen (CEA) and leukocyte common antigen (LCA). Approximately 15.7% of apoptotic bodies stained positive for CEA with immunoreactivity on the cytoplasm, whereas all cells stained negative for LCA. These findings suggest that intraepithelial apoptosis in human colorectal adenomas originates from adenoma cells rather than infiltrating lymphocytes as previously proposed, and that apoptotic cells maintained their cytoplasmic antigenicity in the early stages of apoptosis.

Adenoma↗
PubMed1997

Prospective study of nesidioblastosis in newborns and infants: hypoglycemic seizures, epileptogenesis and the significance of the C-peptide suppression test in pancreatectomy.

The long-term follow-up of chronic hyperinsulinemic seizures, epileptogenesis and other neurological complications in five patients who were treated with conservative therapy followed by pancreatectomy during the neonatal period and infancy, who were confirmed to have diffuse nesidioblastosis are described. The reaction pattern of the C-peptide (CPR) suppression test and its relation to the final extent of pancreatectomy was examined in four patients. The chronological change in electro-encephalography (EEG) and its epileptogenesis was also examined in each patient during hyperinsulinemic hypoglycemia, and during normoglycemia in a long-term post-pancreatectomy follow-up. All patients demonstrated several types of hypoglycemic seizures, ranging from apnea, erratic seizures, evolving to generalized/unilateral tonic-clonic or tonic seizures, myoclonic seizures and EEG abnormalities. Four of five patients still suffered from epilepsy at the age of 4-22 years. The reaction pattern of the CPR suppression test showed dichotomy, with a hyper-reactive pattern in two patients who required total pancreatectomy to control hypoglycemia, and a suppression pattern in two other patients treated with 90-95% pancreatectomy. Neonatal onset and subsequent myoclonic seizures were ominous signs of epileptogenesis to various types of intractable epilepsy and other neurological sequelae. A prompt diagnosis and pancreatectomy of a sufficient extent at the first operation are essential. The CPR suppression test may be useful for a prompt diagnosis and selection of the extent of pancreatectomy.

Blood Chemical Analysis↗
PubMed1997

A purified protein from Salmonella typhimurium inhibits high-affinity interleukin-2 receptor expression on CTLL-2 cells.

Previously, we have demonstrated that the immunosuppression induced by the purified substance Salmonella typhimurium-derived inhibitor of T-cell proliferation (STI) involves T-cell non-responsiveness to interleukin-2 (IL-2). In the present study, it was found that STI inhibited the growth of CTLL-2 cells, which are an IL-2-dependent cytotoxic T-cell line. Analysis of IL-2 receptor (IL-2R) function showed that STI inhibited high-affinity receptor expression and internalization by CTLL-2 cells. Furthermore, FACS analysis demonstrated that STI inhibited both beta chain and gamma chain expression of IL-2R on the cells. These results suggest that the suppression of T-cell proliferation induced by STI results from a defect in IL-2R function.

Animals↗
PubMed1997

[Anti-bacterial activities of a sulfonated human immunoglobulin preparation against penicillin resistant Streptococcus pneumoniae and Pseudomonas aeruginosa].

Anti-bacterial activities of a sulfonated human immunoglobulin preparation against penicillin resistant Streptococcus pneumoniae and Pseudomonas aeruginosa were examined. Five week old CBA/J mice were challenged by 10 times of 50% lethal doses of penicillin sensitive (SP1) and resistant (SP2) strains of Streptococcus pneumniae serotype 19, and were treated with a sulfonated human immunoglobulin preparation (hIg). Fifty % protective dose (ED50) were 2-4 mg hIg/ mouse. These doses were parallel with the challenged doses despite of the challenged bacteria, and it was calculated that 6 x 10(6) bacteria were killed by one mg of hIg in both bacteria. Minimal inhibitory concentrations (MIC) of piperacillin, flomoxef, imipenem, amikacin and ofloxacin against SP1 and SP2 were estimated under the presence of various concentrations of hIg. It was found that under the presence of over 10-20 mg/ml of hIg, SP1 and SP2 were not grown even without any antibiotic. That is, MIC of hIg itself against penicillin sensitive and resistant Streptococcus pneumoniae serotype 19 were 10-20 mg/ml. Since about 10(6) bacteria/ml were used for this test, it was calculated that 5-10 x 10(4) bacteria were killed by one mg of hIg in vitro. This result suggested that in vivo anti-bacterial activities of hIg could be 100 times higher than that in vitro. Synergistic or at least additive effects between hIg and all antibiotics tested were seen by the MIC. If hIg was 100 times effective in in vivo, these results suggested that hIg could improve the effect of chemotherapy in clinical cases. Similar in vitro test were carried out for Pseudomonas aeruginosa, and synergistic or at least additive effects between hIg and all antibiotics tested were also confirmed in Pseudomonas aeruginosa. This result suggested that hIg could be effective for clinical pseudomonas infection.

Animals↗