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Biomedical subjects

Y Wakabayashi

Publications and source records attributed to Y Wakabayashi.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Efficacy and safety of cefozopran (CZOP) monotherapy and combination therapy with CZOP and amikacin (AMK) for infections accompanying hematological diseases].

We evaluated efficacy and safety of monotherapy with CZOP (1-2 g x 2/day) and combination therapy with CZOP (1-2 g x 2/day) and AMK (200 mg x 2/day) for infections in patients with hematological diseases. Efficacy was evaluated in 71 patients of monotherapy group and 70 patients of combination therapy group. Underlying diseases were mostly leukemia and lymphoma. Infections included sepsis, suspected sepsis, pneumonia and so on. Efficacy in CZOP monotherapy was excellent in 21 patients (31.3%), good in 23 patients (34.3%), fair in 5 patients (7.5%) and the efficacy rate was 65.7%. On the other hand, in combination therapy, each was 14 patients (21.2%), 23 patients (34.8%), 12 patients (18.2%) and the efficacy rate was 56.1%. Side effects such as eruption were noted in 2 patients. Abnormal laboratory findings were noted in 9 patients. All side effects as well as abnormal laboratory findings were minimal. It was concluded that CZOP monotherapy was effective in the treatment of various infections accompanying hematological diseases.

Adolescent↗
PubMed2000

Cellular expressions and serum concentrations of Fas ligand and Fas receptor in patients with infectious mononucleosis.

Although lymphocytosis and neutropenia are commonly associated with infectious mononucleosis (IM), the precise mechanisms involved remain unclear. Accumulated evidence has revealed that the apoptosis-mediating system, Fas receptor/Fas ligand (Fas-R/Fas-L), plays an important role in this disease. Recently, lymphocytes, monocytes, and neutrophils have been reported to constitutively express Fas-R, and the Epstein-Barr virus (EBV) has been shown to activate, in addition to B cells, peripheral blood CD8+ T cells, monocytes, and neutrophils. We elucidated cell surface expression and serum concentrations of Fas-R and Fas-L in patients with IM in an effort to more clearly define the role and contribution of apoptosis in this disease. The expression of lymphocyte surface Fas-L and Fas-R was significantly increased in patients with IM (P < .005 and P < .001, respectively), and among lymphocytes, CD4+ or CD8+ populations contained Fas-R+ as well as Fas-R- subpopulations. The constitutive Fas-R expression levels of monocytes and neutrophils were also increased in IM. Moreover, serum levels of both soluble Fas-L and Fas-R were significantly higher in patients with IM than in healthy volunteers (P < .001 and P < .0001, respectively). Positive relationships between the number of peripheral blood CD95+ lymphocytes and white blood cell count, number of lymphocytes, or number of CD4+ or CD8+ lymphocytes were observed. Our results suggest that the Fas-R/Fas-L system might play a role in eliminating EBV-infected or -activated peripheral blood cells by cell-to-cell contact or in an autocrine and/or paracrine fashion in patients with IM.

Adult↗
PubMed1999

Usefulness of measurement of plasma atrial natriuretic peptide levels in exercise testing of patients with coronary heart disease.

Atrial natriuretic peptide secretion on exercise testing may be exaggerated by left ventricular dysfunction due to multivessel coronary disease rather than by scintigraphically detectable myocardial ischemia. The measurement of plasma atrial natriuretic peptide levels during exercise test may provide additional information regarding the severity of coronary heart disease.

Aged↗
PubMed1999

Effect of red wine consumption on low-density lipoprotein oxidation and atherosclerosis in aorta and coronary artery in Watanabe heritable hyperlipidemic rabbits.

Red wine was given to Watanabe heritable hyperlipidemic (WHHL) rabbits (7 mL/kg/day, approximately 23 mg total polyphenol/kg/day) from the age of 4 months for 14 months. With WHHL rabbits given a comparable dose of alcohol used as references, the effect of wine phenolics on the morphology of atherosclerotic lesions in the coronary artery and aorta was investigated in light of the susceptibility of plasma intermediate and low-density protein (ILDL) to oxidation. ILDL of animals consuming red wine showed reduced susceptibility to oxidation, but atherosclerotic lesion progression was not prevented. In WHHL rabbits, a dose of wine phenolics sufficient to inhibit ILDL oxidation might not be adequate to prevent the progression of atherosclerosis morphologically.

Alcohol Drinking↗
PubMed1999

Carbon monoxide overproduced by heme oxygenase-1 causes a reduction of vascular resistance in perfused rat liver.

This study aimed to examine whether livers overexpressing heme oxygenase (HO)-1 could alter the vascular resistance through the vasorelaxing action of carbon monoxide (CO). The relationship among HO-1 expression, CO generation, and the vascular resistance was assessed in perfused rat livers pretreated with hemin, an inducer of HO-1. At 18 h after the hemin treatment, livers displayed marked increases in HO-1 expression in hepatocytes and venous CO flux and a reduction of the basal resistance. The reduction of the resistance in hemin-treated livers was canceled by administration of oxyhemoglobin, a reagent trapping both CO and nitric oxide (NO), but not by methemoglobin, which captures NO but not CO. Liposome-encapsulated oxyhemoglobin, which cannot access the space of Disse, did not cause vasoconstriction. Furthermore, these livers became less sensitive to endothelin-1, a vasoconstrictive peptide, than the untreated controls through mechanisms involving CO. On the other hand, at 12 or 24 h after the treatment when the HO-1 induction was not accompanied by CO overproduction, neither a decrease in the basal resistance nor vascular hyporeactivity to endothelin-1 was observed. These results suggest that CO overproduced in the extrasinusoidal compartment is a determinant of the HO-1-mediated vasorelaxation in the liver.

Animals↗
PubMed1999

[Cortical deafness due to bilateral temporal subcortical hemorrhages associated with moyamoya disease: report of a case].

A 51-year-old male with moyamoya disease had experienced a left putaminal hemorrhage 14 years previously, in 1983. Left encephalo-duro-arterio-synangiosis (EDAS) was performed in that year. The left putaminal hemorrhage reoccurred in 1990 and in 1994. Left superficial temporal artery-middle cerebral artery anastomosis (STA-MCA anastomosis) was performed. He was symptom free after the surgery. However, he suddenly suffered from deafness in 1997, when computerized tomography (CT) revealed the right temporal subcortical hemorrhage. Deafness continued for three days. It gradually improved and completely disappeared in two months. The damage to the bilateral auditory radiation was suggested as the cause of deafness in this patient. Cortical deafness is a rare symptom that is most often associated with cerebral infarction. This may be the first report of moyamoya disease which developed cortical deafness.

Cerebral Angiography↗
PubMed1999

[Changes in 24-hour urinary excretion of sodium and potassium in a community-based heath education program on salt reduction].

PURPOSE: To examine changes in urinary excretion of sodium, potassium and sodium/potassium ratio in a community-based health education program on salt reduction. SUBJECTS AND METHODS: The surveyed community was Kyowa town (census population in 1985 = 16,792) where we have conducted a community-based blood pressure control program since 1981 and health education on reduction of salt intake since 1983 for primary prevention of hypertension. A 24-hour urine collection was conducted for systematically selected samples of the participants aged 40-69 in cardiovascular risk surveys in 1982-86 (early period) and in 1990-94 (later period) to estimate changes in urine excretion of sodium, potassium, and sodium/potassium ratio. RESULTS: A 24-hour urine collection was available for 565 persons (410 men and 155 women) in 1982-86 and 1,461 persons (571 men and 890 women) in 1990-94. A decline in mean sodium excretion was larger in ages 40-49 than in other age groups, and for ages 40-69 combined, the decline was 0.9-1.1 g per day for men and women. Mean sodium excretion declined to 10 g or less per day for men and women aged 60-69. Mean potassium excretion did not change except for men aged 60-69 with an increase in potassium. Sodium/potassium ratio tended to decline for women aged 40-49, and declined significantly for other sex-age groups. A larger reduction in sodium excretion was seen among persons with a history of hypertension compared to those without it. CONCLUSIONS: A significant reduction in urinary excretion of sodium and sodium/potassium ratio was observed in a community-based health education program. Men and women aged 60-69 reached a recommended level of 10 g or less in sodium intake.

Adult↗
PubMed1999

[Diaminodiphenyl sulfone therapy for refractory idiopathic thrombocytopenic purpura--long-term effectiveness and possible mechanisms].

Eight patients with idiopathic thrombocytopenic purpura (ITP) refractory to corticosteroids were given oral diaminodiphenyl sulfone (DDS) (75 mg to 150 mg/day). Responses to DDS were observed in 5 patients, and their platelet counts significantly increased to more than 10 x 10(4)/microliter. The duration of treatment required to obtain platelet counts of more than 10 x 10(4)/microliter ranged from 35 to 64 days. In 3 of the 5 responsive patients, platelet counts stabilized at over 10 x 10(4)/microliter during DDS therapy for 3 to 6 years. Although adverse effects including local skin rash and itching were observed in 3 patients, they disappeared after suspension of DDS or in response to medication with antihistamines. Although the exact mechanism by which it increases the platelet counts in ITP patients is still obscure, DDS may inhibit the reticuloendothelial system by excessive red blood cell destruction. We concluded that DDS therapy is well-tolerated and seems to be an effective alternative treatment for patients with ITP that is refractory to other conventional therapies.

Administration, Oral↗
PubMed1999

Effects of extrinsically elevated plasma norepinephrine concentration on myocardial 123I-MIBG kinetics in rats.

UNLABELLED: Rapid 123I-metaiodobenzylguanidine (MIBG) washout and high plasma norepinephrine (NE) levels are frequently observed in patients with congestive heart failure, and high plasma NE levels are not necessarily induced by increased cardiac NE spillover. The purpose of this study was to assess the effect of extrinsically elevated plasma NE levels on myocardial MIBG kinetics. METHODS: MIBG was injected into the femoral vein in 47 adult male Wister rats. In the first study, normal saline solution or NE (0.3, 1.0 and 3.0 microg/kg/min) was administered to each group of 6 or 7 rats continuously from 30 min before to 30 min after MIBG injection. In the second study, NE was administered at 3.0 microg/kg/min to each group of 7 rats continuously from 30 min before to 2 h after or from 30 to 60 min after MIBG injection, and NE was not administered to a control group of 7 rats. For 2 or 4 h after MIBG injection, scintigrams were acquired using a gamma camera with a pinhole collimator, after which myocardial MIBG uptake (percentage injected dose normalized for the difference in rat weight per tissue weight) was determined in isolated heart with a gamma counter. RESULTS: In the first study, the MIBG washout rate from the heart was significantly increased during high-dose NE infusion (1.0 and 3.0 microg/kg/min) compared with that during saline infusion, whereas the washout rate was not increased during low-dose NE infusion. In the second study, the MIBG washout rate from the heart during NE infusion was significantly increased compared with that of the control but was not increased during discontinuation of NE infusion. CONCLUSION: Extrinsically induced high levels of plasma NE may accelerate MIBG washout from the heart.

3-Iodobenzylguanidine↗
PubMed1998

A novel type of myosin encoded by the mouse deafness gene shaker-2.

The mouse recessive deafness mutation, shaker-2(sh-2), represents a plausible model for an autosomal recessive form of human non-syndromic genetic deafness, DFNB3. Here we report the use of a positional cloning approach to show that the gene mutated in sh-2 mice encodes a novel type of unconventional myosin. A G-to-A transition changing cysteine to tyrosine in the conserved actin binding domain is detected in sh-2 but absent in laboratory strains and wild mice belonging to different mouse subspecies and species. This suggests that the novel myosin gene is a strong candidate for DFNB3.

Actins↗
PubMed1998

Allelic loss analysis of gamma-ray-induced mouse thymic lymphomas: two candidate tumor suppressor gene loci on chromosomes 12 and 16.

A total of 429 gamma-ray-induced thymic lymphomas were obtained from F1 and backcross mice between BALB/c and MSM strains, about a half of which carried a p53-deficient allele. A genome-wide allelic loss analysis has revealed two loci exhibiting frequent allelic losses but no allelic preference, one is localized within a 2.9 cM region between D12Mit53 and D12Mit279 loci on chromosome 12, and the other is near the D16Mit122/D16Mit162 loci on chromosome 16. The frequency of allelic loss in the D12Mit279 region is 62% and does not differ in tumors between the presence and absence of the p53-deficient allele. In contrast, the loss frequency of D16Mit122 is raised by the existence of p53-deficient allele: 62% for p63(-/+) and 13% for p53(+/+), suggesting co-operative function of the two losses. The D12Mit279 and D16Mit122 regions probably harbor different types of tumor suppressor gene that play key roles in lymphoma development.

Animals↗
PubMed1998

Increase of growth-associated protein-43 immunoreactivity following cyclophosphamide-induced cystitis in rats.

We examined the effect of inflammation on immunoreactivity of growth-associated protein (GAP-43) in the rat urinary bladder in which acute cystitis was induced with cyclophosphamide (CPA). Following CPA injection, the number of GAP-43 labeled nerves was significantly increased in the muscle layer. Immunoreactivity of PGP9.5, which was used as an axonal marker, was not augmented following CPA injection. Double fluorescence immunohistochemistry revealed that substance P immunoreactivity was present in most GAP-43 immunoreactive fibers (90.2%) in the inflamed bladder. Electron microscopic examination showed that GAP-43 immunoreactivity was localized on axons. Some GAP-43 positive axons showed degeneration. Possible significance of the increase of GAP-43 immunoreactive afferent nerve fibers in the muscle layer of acutely inflamed bladder was discussed.

Administration, Intravesical↗
PubMed1998

Nitric oxide suppression reversibly attenuates mitochondrial dysfunction and cholestasis in endotoxemic rat liver.

This study aimed to examine whether nitric oxide (NO) plays a causal role in endotoxin-induced dysfunction of biliary transport. Rats were treated with intraperitoneal injection of endotoxin (O111B4, 4 mg/kg). At 2 hours, the liver was excised and perfused ex vivo with taurocholate (TC)-containing Krebs-Ringer solution under monitoring bile output and NO2 in the perfusate and tissue cyclic guanosine monophosphate (cGMP) levels as indices of NO production. The endotoxin treatment evoked a marked decrease in the bile acid-dependent bile formation concurrent with the increasing NO2 output, cGMP elevation, and a reduction of hepatic adenosine triphosphate (ATP) contents and oxygen consumption. Perfusion with 1 mmol/L aminoguanidine (AG), an inhibitor of inducible NO synthase, but not with L-nitroarginine methyl ester, an inhibitor of the constitutive form of the enzyme, significantly reversed the endotoxin-induced increment of the bile formation in concert with the recovery of oxygen consumption and ATP levels. Laser confocal microfluorography of the liver lobules using rhodamine 123 (Rh), a fluoroprobe sensitive to mitochondrial membrane potential, revealed that endotoxin elicited a significant mitochondrial dysfunction panlobularly. The AG administration reversed the endotoxin-induced decrease in mitochondrial membrane potential. Collectively, up-regulation of NO by inducible NO synthase accounts for a mechanism through which endotoxin impairs the bile formation, and its suppression serves as a therapeutic strategy for improvement of hepatobiliary function.

Animals↗
PubMed1998

Carbon monoxide as a regulator of bile canalicular contractility in cultured rat hepatocytes.

This study aimed to examine the mechanism(s) by which carbon monoxide (CO), a product of heme oxygenase reaction, controls the contractility of bile canaliculus (BC) in hepatocytes. When BCs associated with the couplet cells in cultured rat hepatocyte suspension were observed using time-lapse video microscopy, they exhibited periodical contractions with a most-probable interval of 6 minutes under our experimental conditions. The addition of 1 micromol/L zinc protoporphyrin IX (ZnPP), a potent inhibitor of heme oxygenase, to the culture medium elicited a 40% shortening of the interval time together with an increase in intracellular calcium concentrations, while the same concentration of iron protoporphyrin IX did not induce such changes. The production of CO, which was 0.5 nmol/h/10(8) cells in the absence of ZnPP, diminished to less than 0.1 nmol/h/10(8) cells upon application of ZnPP. The ZnPP-elicited increases in both contractile frequency and intracellular calcium concentrations were attenuated by the addition of 1 micromol/L CO or 50 micromol/L 1,2-bis(2-aminophenoxy) ethane-tetraacetate, a calcium chelator. Clotrimazole or metyrapone, inhibitors of cytochrome P450-dependent monooxygenase activities, also attenuated the ZnPP-induced elevation of the contractile frequency. On the other hand, intracellular cyclic guanosine monophosphate (cGMP) contents were not altered significantly by the application of ZnPP or by CO. These results indicate that CO generated by heme oxygenase controls the BC function by changing intracellular calcium concentrations presumably through a mechanism involving the cytochrome P450 reaction.

Animals↗
PubMed1998

Expression of multidrug resistance protein gene in patients with glioma after chemotherapy.

Two different ATP-binding membrane glycoproteins, the 170 kDa P-glycoprotein (P-gp) and the 190 kDa multidrug resistance protein (MRP), are involved in the acquisition of multidrug resistance phenotypes in cancer cells. Overexpression of P-gp is often observed in various human tumors when treated with anticancer agents. In this study, we asked whether MRP was overexpressed in human gliomas after cancer chemotherapy. We investigated expression of MRP and P-gp before and after chemotherapy in tumor samples from patients with glioma. MRP expression was observed in 16 (70%) of 23 untreated patients, and the proportion of MRP-positive cells in the whole cell population ranged from 3 to 32% in the 16 MRP-positive patients. P-gp-positive tumors were observed in 4 (18%) of 23 patients, and the proportional rates of P-gp-positive cells in the whole cell population ranged from 4 to 23%. The proportional rate of MRP-positive or P-gp-positive glioma cells increased after chemotherapy when compared with that before chemotherapy in all patients examined. We could observe no statistically significant correlation between expression of MRP or P-gp and tumor grade. These results suggest that MRP as well as P-gp may be involved in acquired or intrinsic drug resistance in human glioma.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Tissue-selective expression of enzymes of arginine synthesis.

Arginine is a non-essential amino acid in mammals as judged from nitrogen balance study. Citrulline is synthesized from glutamate in the small intestine, whilst kidneys and some other tissues convert citrulline to arginine. Ornithine transcarbamylase and carbamylphosphate synthetase are expressed in liver and small intestine. Tissue-selective expression depends on the regulatory elements in the promoter, or far 5', region of these genes to which tissue-selective transcription factors bind and activate transcription. Argininosuccinate synthetase and argininosuccinate lyase do not appear to have such elements, therefore their expression is more or less ubiquitous. The selective expression of pyrroline-5-carboxylate synthase activity in the intestine remains to be clarified.

Animals↗
PubMed1998

beta 3-Adrenergic agonist induces a functionally active uncoupling protein in fat and slow-twitch muscle fibers.

The mitochondrial uncoupling protein (UCP) has usually been found only in brown adipose tissue. We recently observed that a chronic administration of the beta 3-adrenergic agonist CL-316,243 (CL) induced the ectopic expression of UCP in white fat and skeletal muscle in genetic obese yellow KK mice. The aim of the present study was to examine whether UCP could be induced in nongenetic obese animals produced by neonatal injections of monosodium L-glutamate (MSG). The daily subcutaneous injection of CL (0.1 mg/kg) to MSG-induced obese mice for 2 wk caused significant reductions of body weight (15%) and white fat pad weight (58%). Northern and Western blot analyses showed that CL induced significant expressions of UCP in the white fat and muscle, as well as in brown fat. Immunohistochemical observations revealed that the UCP stains in white fat were localized on multilocular cells and that those in muscle were localized on slow-twitch fibers rich in mitochondria. Immunoelectron microscopy confirmed the mitochondrial localization of UCP in the myocytes. The guanosine 5'-diphosphate (GDP) binding to mitochondria in brown fat doubled after the CL treatment. Moreover, significant GDP binding was detected in the white fat and muscle of the CL-treated mice, at about one-fourth and one-thirteenth the activity of brown fat, respectively, suggesting that ectopically expressed UCP is functionally active. We concluded that the beta 3-adrenergic agonist CL can induce functionally active UCP in white fat and slow-twitch muscle fibers of obese mice.

Adipose Tissue↗