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Biomedical subjects

Y Kataoka

Publications and source records attributed to Y Kataoka.

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

Imbalance production between interleukin-1beta (IL-1beta) and IL-1 receptor antagonist (IL-1Ra) in bronchial asthma.

Genes of the IL-1 family encode three different peptides, IL-1alpha, IL-1beta, and IL-1Ra, respectively. IL-1 operates through IL-1RI, and is involved in airway inflammation in asthmatic subjects, whereas IL-1Ra appears to be a specific competitive inhibitor of IL-1. All genes are on chromosome 2q12-21 where genomewide searches have identified linkage for asthma. To test whether variants of IL-1 relate to asthma, we conducted a genetic association study in a Japanese population. We show that the A2 allele of IL1RN (encoding IL-1Ra) associates with nonatopic asthma [OR = 5.71, 95% CI: 1.63-19. 8, Pc = 0.007]. Both atopic and nonatopic asthmatics with the A2 allele had significantly lower serum IL-1Ra levels in both types of asthmatics. Peripheral blood cells from asthmatics with A2 alleles, however, produced as much IL-1 as did those with A1 homozygotes. Since Th1 and Th2 cytokines differentially regulate the ratio between IL-1beta and IL-1Ra, these findings suggest that dysregulation of IL-1beta/IL-1Ra, probably due to interaction between epithelium and immuno-competent cells in the airway, is important in asthma inflammation.

Adult↗
PubMed2000

Neovascularization with blood-brain barrier breakdown in delayed neuronal death.

Various kinds of acute pathological events in the central nervous system, such as ischemia, hemorrhage, and trauma, often cause brain edema. The edema may advance for days or weeks while inducing extensive damage in neural function, regardless of the extent of the original damage, and often results in death. Delayed edema is thought to be vasogenic; however, the mechanism underlying edema induction remains unknown. We found delayed vascular cell proliferation with a blood-brain barrier breakdown in and around the gerbil CA1 hippocampus, a region known to be involved in delayed apoptotic neuronal death 2-6 days after transient ischemia. Vascular cell proliferation, assessed by (3)H-thymidine incorporation, was most prominent 4-6 days after ischemia, and extravasation of exogenously applied dye or endogenous serum albumin from blood vessels was observed concomitantly. We propose neovascularization in delayed neuronal death as a cause of brain edema advancing days after neurological events.

Animals↗
PubMed2000

Rifampicin-associated pseudomembranous colitis.

We report a case of pseudomembranous colitis that developed in a patient with liver cirrhosis during anti-tuberculosis therapy with rifampicin and isoniazid. The association between rifampicin and pseudomembranous colitis has been controversial; this report, however, supports the association. Colonoscopy performed 3 days after the onset of the pseudomembranous colitis revealed only reddish patches and a few aphthoid lesions, but 4 days later pseudomembranes were apparent. The pseudomembranous colitis was successfully controlled by discontinuation of the anti-tuberculosis agents, along with the administration of lactic acid bacteria, without vancomycin or metronidazole. Possible predisposing factors for the development of pseudomembranous colitis in this patient are also discussed.

Antibiotics, Antitubercular↗
PubMed2000

Morphological survey of prolactin-releasing peptide and its receptor with special reference to their functional roles in the brain.

The gene of prolactin-releasing peptide (PrRP) was first cloned in 1998 and preproproteins encoded by cDNAs produced at least two isoforms of PrRP with different lengths; PrRP31 and PrRP20. PrRP has been shown to release prolactin from the anterior pituitary at least in vitro (Hinuma, Y.S., Habata, Y., Fuji, R., Hosoya, M., Fukusumi, S., Kitada, C., Masuo, Y., Asano, T., Matsumoto, H., Sekiguchi, M., Kurokawa, T., Nishimura, O., Onda, H., and Fujino, A., 1998. A prolactin-releasing peptide in the brain. Nature 393, 272-6). PrRP receptor has also been detected by quantitive reverse transcription polymerase chain reaction, and in situ hybridization histochernistry revealed that expression of PrRP receptor mRNA was found in the broad areas of the brain and in the anterior pituitary of the rat. This review surveys morphological studies on PrRP, PrRP mRNA and PrRP receptor mRNA in the rat brain and discusses the possible functional significance of PrRP in the brain. PrRP immunoreactive neuronal perikarya showed a similar distributional pattern to those with PrRP mRNA signals. However, distribution of nerve processes and terminals with PrRP immunoreactivity was broadly expanded in the forebrain and brainstem. They were hardly detected in the median eminence particularly in its external layer. PrRP receptor mRNA signals were distributed in the preoptic area, and the hypothalamic area, where PrRP immunoreactive nerve processes and terminals were also detected. The strongest signal of PrRP receptor mRNA was detected in the reticular nucleus of the thalamus where neither PrRP immunoreactive nerve processes nor axon terminals were distributed. From the distribution pattern of PrRP and its receptor, it is suggested that PrRP is involved in control of secretion of oxytocin, corticotropin releasing hormone and somatostatin.

Animals↗
PubMed2000

Involvement of glial endothelin/nitric oxide in delayed neuronal death of rat hippocampus after transient forebrain ischemia.

1. We examined time- and cell-type-dependent changes in endothelin (ET)-1-like immunoreactivity, ET receptors binding and nitric oxide (NO) synthase (NOS) activity in CA1 subfields of the hippocampus of stroke-prone spontaneously hypertensive rats subjected to a 10-min bilateral carotid occlusion and reperfusion. 2. Microglia aggregated in accord with neuronal death and expressed a high density of ET(B) receptors and an intense NOS activity in the damaged CA1 pyramidal cell layer, 7 days after the induced transient forebrain ischemia. The increased NOS activity and ET(B) receptor in microglia disappeared 28 days after this transient ischemia. 3. In contrast to microglia, astrocytes presented a moderate level of ET-1-like immunoreactivity, ET(B) receptors, and NOS activity in all areas of the damaged CA1 subfields, 7 days after the ischemia. These events were further enhanced 28 days after the ischemia. 4. In light of these findings, the possibility that the microglial and the astrocytic ET(B)/NO system largely contributes to development of the neuronal death and to reconstitution of the damaged neuronal tissue, respectively, in the hippocampus subjected to a transient forebrain ischemia would have to be considered.

Animals↗
PubMed2000

Involvement of glial cells in cyclosporine-increased permeability of brain endothelial cells.

1. To test whether astrocytes participate in cyclosporine-induced dysfunction of the blood-brain barrier, we examined the effects of cyclosporine on the permeability of the mouse brain endothelial (MBEC4) cells cocultured with C6 glioma cells, each cell layer placed on the top and bottom of the insert membrane, respectively. 2. The presence of C6 cells remarkably aggravated cyclosporine-increased permeability of MBEC4 cells to sodium fluorescein. 3. In light of these findings, the possibility that astroglial cells could contribute to the occurrence of cyclosporine-induced dysfunction of the blood-brain barrier triggering neurotoxicity should be considered.

Animals↗
PubMed2000

Role of synaptophysin in exocytotic release of dopamine from Xenopus oocytes injected with rat brain mRNA.

1. The role of synaptophysin in the exocytotic release of dopamine (DA) was examined in Xenopus laevis oocytes injected with rat brain mRNA. 2. The mRNA-injected oocytes showed DA uptake which depended on the incubation time and external DA concentrations. 3. Stimulation with KCl (10-50 mM) of mRNA-injected oocytes preloaded with DA evoked external Ca2+ -dependent release of DA. The noninjected and water-injected oocytes did not produce uptake of DA and stimulation-evoked release of DA. 4. The high-KCl (50 mM)-stimulated release of DA decreased in the oocytes injected with rat brain mRNA together with antibody to synaptophysin. 5. Immunoblot analysis demonstrated that synaptophysin was expressed in the brain mRNA-injected oocytes but not in the noninjected and water-injected oocytes. 6. Thus, uptake and release machinery similar to native dopaminergic nerve terminals was expressed in Xenopus oocytes by injecting mRNA-extracted from the rat brain, and synaptophysin may play a role in the exocytotic release of DA.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Control of neurotransmission, behaviour and development, by photo-dynamic manipulation of tissue redox state of brain targets.

Reversible manipulation of local neurotransmission in brain areas, using controlled spatial and temporal resolution, is one of the powerful techniques used to investigate integrative aspects of brain function. We have developed a novel technique for rapidly inactivating local synaptic transmission, from outside the brain, within seconds or minutes via oxidation of target tissue using a photosensitive dye followed by photoirradiation (photo-dynamic tissue oxidation; PDTO). PDTO applied through a defined slit, sharply suppressed excitatory synaptic transmission in rat hippocampal slices and also suppressed in vivo hippocampal neurotransmission reversibly. Furthermore, we manipulated the voluntary movement of gerbils in free-field activity by application of PDTO to the striatum. Also, in freely moving kittens, the development of the visual cortex was manipulated by long-lasting application of PDTO to the eye. Thus, PDTO enables external manipulation of in vivo or in vitro neurotransmission in various clearly defined regions on the submillimeter scale. Suppression of neurotransmission occurred only within the photo-oxidized area which can be histochemically visualized.

Animals↗
PubMed2000

Graft-versus-host-disease-associated donor cell engraftment in an F1 hybrid model is dependent upon the Fas pathway.

The graft-versus-host disease (GVHD) generated in BDF1 mice by the injection of spleen cells from the C57BL/6 parental strain induces a direct cell-mediated attack on host lymphohaematopoietic populations, resulting in the reconstitution of the host with donor cells. We examined Fas-Fas ligand (FasL) interactions in donor and host haematopoietic cells over a prolonged period of parental-induced GVHD. Fas expression on bone marrow cells of both donor and host origin increased at 2 weeks. Host cell incubation with anti-Fas antibody induced apoptosis, and the number of haematopoietic progenitor cells decreased. Fas-induced apoptosis by the repopulating donor cells, however, did not increase until 12 weeks, when more than 90% of the cells were donor cells. The expression of various cytokines, such as interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha), and FasL gene expression in the bone marrow increased concomitantly. To examine directly whether FasL has a major role in the development of donor cell engraftment, FasL-deficient (gld) mice were used as donors. Injection of B6/gld spleen cells induced significantly less host lymphohaematopoietic depletion, resulting in a failure of donor cell engraftment. Furthermore, injection of IFN-gamma gene knockout (gko) B6 spleen cells failed to augment Fas and FasL expression in recipient mice, resulting in a failure of donor cell engraftment. This suggests that the induction of apoptosis by Fas-FasL interactions in host cells may contribute to a reconstitution of the host with donor cells and that donor-derived IFN-gamma plays a significant role for Fas-FasL interactions in host cells during parental-induced GVHD.

Animals↗
PubMed2000

Cytoprotection by WR-1065, the active form of amifostine, is independent of p53 status in human malignant glioma cell lines.

PURPOSE: This study tests the hypothesis that p53 status, i.e. wild type versus mutant form, is a determinant in radiation protection of human glioma cells by WR-1065, the active thiol form of amifostine (WR-2721). MATERIALS AND METHODS: The cytoprotective effectiveness of WR-1065 when present during irradiation was investigated using four well-characterized human glioma cell lines. The p53 positive lines were U87 and D54, and the mutant p53 lines were U251 (mutant at codon 273; CGT/CAT; Arg/His) and A172 (mutant at codon 242; TGC/TTC; Cys/Phe). Treatment conditions included exposure of cells to a range of doses (0-10Gy) alone or in combination with 4mM of WR-1065 added 30min prior to irradiation. Resultant survival curves were obtained using a clonogenic assay and protection factors, the ratio of terminal slopes +/- WR-1065, were determined for each glioma cell line. RESULTS: The Do values of wild-type U87 and D54 were 1.62 and 1.89Gy while those of p53 mutants U251 and A172 were 1.64 and 1.68 Gy, respectively. Protection factors were determined to be 2.4 and 1.9 for U87 and D54, and 2.6 and 2.8 for U251 and A172, respectively. CONCLUSIONS: The p53 status of the four human glioma cell lines tested was not a predictor for either their relative sensitivity to ionizing radiation or ability to be protected by WR-1065. It is concluded that cytoprotection exhibited by cells exposed to WR-1065 during irradiation is independent of their p53 status.

Amifostine↗
PubMed2000

Protein binding and the metabolism of thiamylal enantiomers in vitro.

UNLABELLED: Thiamylal, a chiral thiobarbiturate, is marketed as a racemic product. We studied the serum protein binding and microsomal metabolism of thiamylal enantiomers in vitro. The unbound fraction of R(+)-thiamylal was greater than that of S(-)-thiamylal. The analysis of binding data revealed that both enantiomers bound to human serum albumin through only one site. In displacement studies with site-specific probes, dansylsarcosine, but not warfarin, significantly decreased the binding of both enantiomers. The bindings of enantiomers were also decreased by octanoate and a large concentration of oleate. These findings suggest that both enantiomers bind to Site II of albumin with higher affinity for S(-)-enantiomer. R(+)-thiamylal was metabolized more rapidly than S(-)-enantiomer by human liver microsomes. An experiment with isoform-selective inhibitors and cytochrome P-450 (CYP) isoforms showed that CYP2C9 had the highest activity for the metabolism of both enantiomers, the activity being 7 to 10 times that of CYP2E1 and CYP3A4. CYP2C9 showed a significantly rapid metabolism of R(+)-enantiomer, suggesting that CYP2C9 is mainly involved in the enantioselective metabolism of thiamylal. IMPLICATIONS: Because clinically marketed thiamylal is a racemic compound, a pharmacokinetic study of each enantiomer may be beneficial. We found that the enantioselectivity of thiamylal existed in protein binding and metabolism. This may be caused by the differences in the affinities of enantiomers for albumin and cytochrome P-450 isoform.

Adult↗
PubMed2000

Nitric oxide protects against contrast media-increased pulmonary vascular permeability in rats.

RATIONALE AND OBJECTIVES: Nitric oxide (NO) regulation of endothelial function is involved in the development of acute lung injury. The role of NO in contrast media-induced increases in pulmonary vascular permeability was investigated in a rat model. METHODS: Nonionic (iohexol) and ionic (ioxaglate) contrast media were intravenously injected at 1.5 mL/min in rats. Pulmonary vascular permeability was evaluated by measuring the amount of Evans blue dye uptake as a quantitative marker of albumin extravasation in lung tissue. RESULTS: Intravenous injections of contrast media at doses of 4 and 6 g I/kg induced a dose-dependent increase in pulmonary vascular permeability. L-Arginine (an NO synthase substrate) and N(G)-nitro-L-arginine (L-NNA) (an NO synthase inhibitor) prevented and aggravated, respectively, the increase in pulmonary vascular permeability induced by the contrast medium. An aggravating action of L-NNA was confirmed by morphological and histological observations, this action being blocked by L-arginine (300 mg/kg) but not by D-arginine. Isosorbide dinitrate (1-20 mg/kg), an NO donor, had a dose-dependent protective effect on ioxaglate-increased vascular permeability. CONCLUSIONS: Our experimental findings suggest that contrast media at high doses produce pulmonary edema by inhibiting endothelial NO production, and nitrovasodilators protect against this adverse effect in rats.

Animals↗
PubMed2000

Pancreatographic classification of pancreatic ductal injuries caused by blunt injury to the pancreas.

BACKGROUND: In the treatment of patients with pancreatic injury, the focus of attention is usually on main ductal injuries. METHODS: To develop a classification system for pancreatic ductal injuries, we retrospectively analyzed blunt pancreatic injuries in 40 patients. We assessed the relationships between findings on pancreatography (36 endoscopic retrograde procedures and 4 transduodenal procedures), the treatment modality, and the clinical course. RESULTS: Patients with class 1 injuries (radiographically normal ducts, n = 13) could be treated nonsurgically without major complications. Patients with class 2 injuries (branch injuries, n = 7), in whom contrast medium from ductal branches did not leak from the pancreatic parenchyma (class 2a, n = 3), could be treated nonsurgically. Patients with leaks into the retroperitoneal space (class 2b, n = 4) required at least a drainage laparotomy. Patients with class 3 injuries (main duct injuries, n = 20), including two patients in whom conservative treatment resulted in severe complications, required laparotomy. CONCLUSION: This classification system for pancreatic ductal injuries may facilitate the selection of appropriate therapeutic modalities for patients with blunt pancreatic injury.

Adult↗
PubMed2000

A 10-year survey of antimicrobial susceptibility of streptococcus suis isolates from swine in Japan.

A number of 689 Streptococcus suis isolates collected nationwide from diseased and healthy pigs from 1987 to 1996 were surveyed for antibiotic susceptibilities to 11 drugs. No isolates resistant to amoxicillin, chloramphenicol, and sulfamethoxazole/trimethoprim were found. Isolates were highly susceptible to penicillins (penicillin G, ampicillin, and amoxicillin) except cloxacillin. They were not susceptible to tetracycline, streptomycin, and kanamaycin (MIC90 50 microg/ml, > or = 100 microg/ml, and > or = 100 microg/ml, respectively). Multiple-resistant isolates (> or = 3 antimicrobial agents) were found in 20.3% of all isolates tested.

Animals↗
PubMed2000

Amifostine: mechanisms of action underlying cytoprotection and chemoprevention.

Amifostine is an important drug in the new field of cytoprotection. It was developed by the Antiradiation Drug Development Program of the US Army Medical Research and Development Command as a radioprotective compound and was the first drug from that Program to be approved for clinical use in the protection of dose limiting normal tissues in patients against the damaging effects of radiation and chemotherapy. Its unique polyamine-like structure and attached sulfhydryl group give it the potential to participate in a range of cellular processes that make it an exciting candidate for use in both cytoprotection and chemoprevention. Amifostine protects against the DNA damaging effects of ionizing radiation and chemotherapy drug associated reactive species. It possesses anti-mutagenic and anti-carcinogenic properties. At the molecular level, it has been demonstrated to affect redox sensitive transcription factors, gene expression, chromatin stability, and enzymatic activity. At the cellular level it has important effects on growth and cell cycle progression. This review focuses on relating its unique chemical design to mechanisms of action that underlie its broad usefulness as both a cytoprotective and chemopreventive agent for use in cancer therapy.

Adolescent↗
PubMed2000

Transient hypoxia/hypoglycemia upregulates endothelin B receptors in cultured rat astrocytes.

Endothelins are potent vasoactive peptides that bind to their specific receptors, playing an important role in the CNS under physiological and pathophysiological conditions. Astrocytes, which have been shown to express these receptors, also have a considerable role to play under physiological and pathophysiological conditions, particularly those involved in delayed neuronal death. We carried out in vitro receptor autoradiographic binding experiments using specific ligands for endothelin receptors on cultured rat astrocytes. On astrocytes, the specific binding sites for (125)I-PD151242 (a selective endothelin A receptor antagonist) and (125)I-IRL 1620 (a selective endothelin B receptor agonist) were detected. We also characterized the qualitative and quantitative changes of endothelin receptors 24 h after subjecting cultured rat astrocytes to a transient 4-h hypoxia/hypoglycemia insult, used as a model of delayed neuronal death. After transient hypoxia/hypoglycemia, the number of endothelin B receptors increased significantly on cultured astrocytes, but this did not occur among the endothelin A receptors. These findings suggest that the astrocytic effects associated with endothelin in delayed neuronal death include gliosis or the repair process or both, manifested primarily by an increase in the number of endothelin B receptors. This rise does not require interaction with other types of CNS cells. Endothelin A receptors might have a role taking their number into consideration on rat astrocytes under both physiological and pathophysiological conditions.

Animals↗
PubMed2000

[A study of institutional medical care of female victims of sexual assault and violence].

OBJECTIVE: The purpose of the study is to clarify the present situation of medical care for victims of sexual assault and violence. Medical facilities in two wards in Tokyo were studied in order to know what problems regarding medical care exist and how to support female victims. METHODS: In April 1998, we distributed questionnaires to 338 medical facilities covering all the clinics and hospitals, that had more than only otorhinolaryngology and ophthalmology, in Kouto-ku and Sumida-ku, Tokyo. The questionnaire included questions about individual experience of consulting with sexual assault and violence against women, the number of victims in the last year, and their understandings for victims. RESULT: 1) 76 of the respondents completed the answer sheet by themselves. The mean age of the subjects was 57.4 years old, 16.3% of them had seen sexual assault victims, and about 36.8% had cared for victims of violence. 2) 67 victims of sexual assault and violence were reported in the previous year. 36% of victims of sexual assault were reported by facilities related to obstetrics, and 85% of victims of violence were reported by general medical facilities. 3) As for understandings for victims, those who thought the victims were responsible for the sexual assault also regarded violence as caused by carelessness of victims. CONCLUSION: Medical facilities may be an important place to care for victims of sexual assault and violence against women. There are few data available as to how many women suffer from sexual violence. This study showed for the first time the reality of sexual assault and violence from the viewpoints of medical facilities in Japan, although it had some limitations. It is necessary for more discussion about roles of medical care for female victims of sexual assault and violence.

Adolescent↗