Biomedical subjects

S Shibata

Publications and source records attributed to S Shibata.

At least 325 records · Page 18Linked to original sources

PubMed1996

[A case of virus-associated hemophagocytic syndrome (VAHS) complicated by rhabdomyolysis which were associated with herpes-simplex virus infection].

A 60-year-old male was admitted to our hospital complaining abdominal pain and fatigue. Complete blood count showed as follows; WBC 3,900/microliters (48% of monocytes), Hb 11.5 g/dl, Plt 0.9 x 10(4)/microliters. Marrow smears showed the presence of phagocytic histiocytes that consist 22.4% of total nuclear cells. Laboratory findings showed as follows; BUN 109.5 mg/dl, Creatinine 7.4 mg/dl, CPK 1,259 IU/l, Aldolase 195 IU/l, Myoglobin 4,200 mg/dl. Serological studies showed a 16-fold increase in herpes-simplex virus (HSV) antibody titers 4 weeks after admission. So we diagnosed his illness as virus-associated hemophagocytic syndrome (VAHS) and rhabdomyolysis that were associated with HSV. We performed three times of hemodialysis for acute renal failure and used prednisolone for VAHS. These treatments were successful, and he made a complete recovery from illness. VAHS complicated by rhabdomyolysis is very rare, and we think this case is full of suggestions.

Acute Kidney Injury↗

PubMed1996

[Preventive effect of intracisternal methylprednisolone on symptomatic vasospasm after aneurysmal subarachnoid hemorrhage].

A series of 103 patients with ruptured cerebral aneurysms were treated by intracranial irrigation, after aneurysmal clipping, with pH 8.0 Hartmann solution containing 1 mg/ml of methylprednisolone sodium succinate, during operation. Postoperatively, 5 ml/day of the solution was also injected until day 14, percutaneously through an Ommaya reservoir into the cisterns around the clipped aneurysm. Six (5.7%) of the 103 patients suffered symptomatic vasospasm postoperatively. The Glasgow Outcome Scale at discharge of all patients indicated good recovery, Moderately disabled, Severely disabled and Vegetative state in 74 (72%), 18 (17%), 9 (9%) and 2 (2%) patients respectively. As a complication, subdural effusion was noticed in 17 (17%) patients, without any influence on outcome at all.

Female↗

PubMed1996

[A case of embryonal carcinoma successfully treated by neoadjuvant chemotherapy: report of a case].

A 20-year-old man was admitted with a complaint of cough and dyspnea. Chest X-ray revealed a large anterior mediastinal tumor. On chest CT scan, the inferior vena cava was found to be enclosed, and tumor invasion to the right pulmonary artery and left atrium was observed. The serum alpha-fetoprotein (AFP) level was increased. A diagnosis of primary mediastinal embryonal carcinoma was made by the needle biopsy. After three courses of chemotherapy, consisting of cisplatin, etoposide and bleomycin, the tumor became smaller and the serum AFP level became normal. Complete resection of the tumor was performed successfully. The resected tumor showed no evidence of active disease. The patient has been free of the disease for 3 years.

Adult↗

PubMed1996

[IgM antibody against sulfated glucuronyl paragloboside in a case of Guillain-Barré syndrome].

High-titer IgM antibody against sulfated glucuronyl paragloboside (SGPG) was detected in a case of Guillain-Barré syndrome. The patient recovered rapidly by the treatment with double filtration plasmapheresis and the anti-SGPG antibody was not detected on the 40th day of illness. Facial nerve palsy, however, lasted until the 6th month of illness. Anti-SGPG antibody might have the important role in the pathologic mechanisms of Guillain-Barré syndrome in this case.

Adult↗

PubMed1996

Reliability of inferred age, and coincidence between inferred age and chronological age.

Outdoor research is restricted by many factors. The age inference was one of the biggest problems for the outdoor researchers. We have investigated the reliability of inferred age for the Japanese people, and took out the estimation formula for the age, even if it was based on the inferred age. The age classification was the most popular method for this purpose, and there were many classifications. We took the classification of young, middle aged, and elderly groups, in which classification of the SDs were rather small, that is, 4, 5, and 7 years for the young, middle aged, and elderly age groups, respectively.

Adult↗

PubMed1995

Circadian rhythm of spontaneous neuronal activity in the suprachiasmatic nucleus of old hamster in vitro.

The effects of aging on neuronal activity in the suprachiasmatic nucleus (SCN) were examined in hamsters kept under light-dark (LD) or constant light (LL) conditions. The free-running period in wheel-running rhythm of 24-month-old hamsters (24.2 +/- 0.04) was shorter than that of the 2-month-old hamsters (24.4 +/- 0.057). There was a significant difference in the mean firing rates of SCN neuron activity between old and young hamsters during subjective day (6.58 +/- 0.36 spikes/s in young and 5.63 +/- 0.24 in old hamsters), but not during subjective night (4.33 +/- 0.47 in young and 4.05 +/- 0.39 in old). Similar to LL condition, the firing activity during zeitgeber time 3-11 (4.33 +/- 0.27) in old hamsters kept under LD condition, was significantly lower than that of young hamsters (6.22 +/- 0.32). These results suggest that deterioration of SCN neuronal activity in old hamsters assessed as reduction of daytime activity may reflect changes in the interaction between SCN clocks and the overt behaviors and/or pacemaking properties of SCN cells.

Aging↗

PubMed1995

Circadian changes in long-term potentiation of rat suprachiasmatic field potentials elicited by optic nerve stimulation in vitro.

Optic nerve stimulation caused a postsynaptic field potential in the rat suprachiasmatic nucleus (SCN) of hypothalamic slices. In the present experiment, we demonstrated whether tetanic stimulation of optic nerve can produce a long-term potentiation (LTP) in the SCN postsynaptic field potential. The amplitude of SCN field potential was higher in the subjective day animals than that in the subjective night animals. Tetanic stimulation of optic nerve (100 Hz, 1 s) at subjective daytime (projected zeitgeber time: ZT 0-8) produced a LTP in this field potential, although the onset of LTP was slow. When tetanic stimulation was applied at ZT4, the percent increase of amplitude was 116.6% immediately after, 159.8% 30 min after and 215.4% 120 min after tetanic stimulation, whereas tetanic stimulation of optic nerve at subjective night-time caused a weak LTP in the SCN. Although tetanic stimulation of Schaffer collaterals induced a LTP formation in the CA1 region of rat hippocampal slices, there were no obvious circadian changes in this LTP formation. The present results demonstrated that excitatory influence on the SCN caused a synaptic plasticity such as LTP. Although the physiological meaning of this LTP is uncertain at present, LTP may be related to adaptation mechanism to photic stimulation.

Animals↗

PubMed1995

Increase in the septal vasopressin content by prolyl endopeptidase inhibitors in rats.

Prolyl endopeptidase (PEP; EC 3.4.21.26) cleaves the Pro-Arg bond of arginine-vasopressin (AVP). This study investigated the effects of PEP inhibitors, 1-[1-(benzyloxycarbonyl)-L-prolyl]prolinal (Z-Pro-prolinal) and 1-[3-(2-indanylacetyl)-L-thioprolyl]pyrrolidine (Z-321), on the AVP content in the septum of rats. Oral administration of Z-Pro-prolinal (100 mg/kg) and Z-321 (100 mg/kg) significantly increased the septal AVP content. At 10 mg/kg, Z-321 slightly increased the content. In contrast, the D-thioprolyl form of Z-321 (100 mg/kg), which lacks an inhibitory effect on the enzyme, failed to affect the AVP content. These results indicate that PEP inhibitors increase the content of AVP through inhibition of the enzyme activity in vivo. Therefore, it is suggested that PEP may contribute to the degradation of endogenous AVP in the brain.

Administration, Oral↗

PubMed1995

Methylcobalamin attenuates the hypoxia/hypoglycemia- or glutamate-induced reduction in hippocampal fiber spikes in vitro.

The effects of methylcobalamin, a vitamin B12 analogue, on the hypoxia/hypoglycemia- or glutamate-induced reduction in hippocampal CA1 presynaptic fiber spikes elicited by Schaffer collateral stimulation in rat brain slices were evaluated. Hippocampal slices were exposed to 15 min of hypoxia/hypoglycemia, and then these slices were returned to oxygenated and glucose-containing buffer for 3 h. Hypoxia/hypoglycemia reduced CA1 presynaptic potentials in vitro. Treatment with 10 microM methylcobalamin attenuated the impairment of CA1 presynaptic potentials induced by hypoxia/hypoglycemia or glutamate application (10 mM). Daily injection of methylcobalamin (0.5 mg/kg i.p./day) for 3 days in vivo also attenuated the hypoxia/hypoglycemia- or glutamate-induced reduction in presynaptic potentials in hippocampal slices. Pretreatment with cyanocobalamin at 10 microM failed to attenuate the impairment of CA1 presynaptic potentials. However, daily injection of cyanocobalamin (0.5 mg/kg i.p./day) for 3 days caused a protective action against the hypoxia/hypoglycemia- or glutamate-induced functional deficit. Furthermore, co-treatment of L-arginine (100 microM), a substrate for nitric oxide synthase, with methylcobalamin in vitro reversed the methylcobalamin-induced functional recovery. The present results demonstrate that methylcobalamin application in vivo or in vitro leads to functional recovery from hypoxia/hypoglycemia- or glutamate-induced impairment of CA1 presynaptic potentials. Neuroprotection was obtained by in vivo application of cyanocobalamin, but not by its in vitro application. It is reported that in vivo injected cyanocobalamin converted to methylcobalamin in the hepatic cells. Therefore, the results suggest that a transmethylation reaction in the hippocampal regions may be involved in the methylcobalamin-induced functional recovery from ischemic impairment.

Animals↗

PubMed1995

kappa-Opioid receptor agonist protects against ischemic reduction of 2-deoxyglucose uptake in morphine-tolerant rats.

We examined the effects of mu-opioid receptor agonist and antagonists, and kappa-opioid receptor agonist on the hypoxia/hypoglycemia-induced reduction in 2-deoxyglucose uptake of rat hippocampal slices. Naloxone, a mu-opioid receptor antagonist and (5,7,8)-(+)-3,4-dichloro-N-methyl-N-(7,8,1-pyrrolidinyl)-1-oxaspirol+ ++ (4,5)dec-8-yl)-benzeneacetamide methanesulfonate, U-62,066E, a kappa-opioid receptor receptor agonist, showed neuroprotective actions against the hypoxia/hypoglycemia-induced deficit in glucose uptake. In contrast, morphine exhibited an exacerbating action. These results suggest that blockade of mu-opioid receptor- and stimulation of kappa-opioid receptor-mediated functions has a protective role against the hypoxia/hypoglycemia-induced decreases in glucose metabolism in hippocampal slices. Chronic administration of morphine (10 mg/kg) for 9 days affected neither the basal nor the hypoxia/hypoglycemia-induced reduction in 2-deoxyglucose uptake. Rats treated with morphine chronically exhibited not only tolerance to the analgesic effect but also tolerance to the exacerbating action. However, chronic morphine did not modify U-62,066E-induced neuroprotection. These findings indicate that the receptor mechanisms of neuroprotection produced by the activation of kappa-opioid receptors may not be involved in mu-opioid receptor function.

Analgesics↗

PubMed1995

HNK-1-reactive novel oligosaccharide, sulfate-O-3GlcA beta 1-4Xyl beta 1-(4-methylumbelliferone), synthesized by cultured human skin fibroblasts.

4-Methylumbelliferyl-beta-D-xyloside (Xyl-MU) was added to the medium of cultured human skin fibroblasts. After incubation, the culture medium was pooled, and the Xyl-MU-induced oligosaccharides in the medium were purified by gel filtration chromatography. A novel Xyl-MU derivative was obtained, in addition to the previously reported Xyl-MU derivatives such as Gal-Gal-Xyl-MU, Gal-Xyl-MU, Sia-Gal-Xyl-MU, GlcA-Xyl-MU, and Xyl-Xyl-MU. The novel Xyl-MU derivative was purified using gel-filtration chromatography and high performance liquid chromatography and then subjected to carbohydrate composition analysis, enzymic digestion, Smith degradation, and ion spray mass spectrometric analysis. The results indicated that it was sulfate-O-3GlcA beta 1-4Xyl beta 1-MU. The structure of the nonreducing terminal of this Xyl-MU-induced oligosaccharide was the same as that of the oligosaccharide chain of a human peripheral nerve-derived glycolipid, reactive with the mouse monoclonal antibody HNK-1, and this Xyl-MU-induced oligosaccharide also reacted with HNK-1. These results suggest that the oligosaccharide, which is structurally identical to that of human peripheral nerve-derived glycolipid synthesized by nervous tissue and related to cell adhesion, is synthesized also by mesenchymal cells.

Antigens, CD↗

PubMed1995

Effect of a nitric oxide synthase inhibitor, N-nitro-L-arginine methylester, on light-induced phase delay of circadian rhythm of wheel-running activity in golden hamsters.

Under constant darkness hamsters demonstrate free-running activity rhythms and light exposure during the early subjective night results in permanent phase delays of the activity rhythm. Recently, we reported that application of glutamate receptor agonists such as N-methyl-D-aspartate could reset the phase of the circadian rhythm of suprachiasmatic nucleus firing activity in vitro via nitric oxide production. In order to confirm this result by in vivo experiment, we examined the effect of nitric oxide synthesis inhibitor on the light-induced phase delay of circadian rhythms of wheel-running activity in hamsters. In vehicle-treated animals, light stimulation at circadian time 13.5 resulted in stable phase delays (1.3 +/- 0.63 h), whereas pre-treatment with 150 mg/kg of N-nitro-L-arginine methylester (L-NAME) significantly attenuated light-induced phase delays (0.72 +/- 0.18 h). L-NAME administration alone without light exposure, did not cause phase changes. The L-NAME-induced attenuating effect was reversed by co-administration of L-arginine (300 mg/kg). The present results suggest that nitric oxide production is involved in the light-induced phase delay of the hamster's circadian system.

Animals↗

PubMed1995

Immunohistochemical expression of the estrogen receptor-related antigen (ER-D5) in human intracranial tumors.

BACKGROUND: Expression of the estrogen receptor-related antigen (ER-D5) has been reported in some normal and neoplastic tissues. The authors evaluated the expression of ER-D5 in 143 intracranial tumors of different histologic types. METHODS: Formalin fixed, paraffin embedded tumor sections were stained with the monoclonal D5 antibody by avidin-biotin complex immunohistochemistry. RESULTS: Eighty-eight (62%) of the 143 brain tumors showed positive ER-D5 immunoreactivity. ER-D5 expression was observed in 9/30 low grade astrocytomas, in 6/13 anaplastic astrocytomas, in 16/27 glioblastomas, in 2/5 ependymomas, in 5/8 medulloblastomas, in 10/15 meningiomas, in 20/23 schwannomas, in 11/11 hemangioblastomas, in 9/9 germ cell tumors, in 0/2 oligodendrogliomas, and in 17/28 pediatric and childhood brain tumors. The mean percentage of ER-D5-positive cells varied in different tumor types, was lowest in the meningotheliomatous meningiomas, and was highest in the hemangioblastomas. ER-D5 immunoreactivity was also observed in the microvascular endothelial proliferations and in tumor blood vessels. ER-D5 expression in tumors was not related to the overall tumor grades, but a statistically significant higher percentage of ER-D5-positive cells was noted in the glioblastomas compared with the low grade astrocytomas (P < 0.05) and in the combined high grade tumors compared with the low grade tumors (P < 0.005) if vascular-origin tumor hemangioblastomas are considered a separate entity from other brain tumors. CONCLUSION: The current study suggests that the ER-D5 antigen may participate in the growth of the intracranial tumors and tumor angiogenesis. ER-D5 in embryonal and germ cell brain tumors suggests that ER-D5 may be a developmentally regulated protein.

Adolescent↗

PubMed1995

Hyaluronic-acid-deficient extracellular matrix induced by addition of 4-methylumbelliferone to the medium of cultured human skin fibroblasts.

The effects of xylosyl-beta-D-(4-methylumbelliferone) and its aglycone, 4-methylumbelliferone, on hyaluronic acid synthesis were investigated in cultured human skin fibroblasts. Xylosyl-beta-D-(4-methylumbelliferone) added to the medium of cultured cell reduced the synthesis of hyaluronic acid. Furthermore, 4-methylumbelliferone reduced the production of hyaluronic acid markedly. In addition, 4-methylumbelliferone had hardly any effect on proteoglycan synthesis, whereas xylosyl-beta-D-(4-methylumbelliferone) produced a large amount of glycosaminoglycan chains. The present results indicate that cells cultured with 4-methylumbelliferone produce a hyaluronic-acid-deficient extracellular matrix, which will be useful for functional studies of hyaluronic acid.

Cells, Cultured↗

PubMed1995

Calcium channel blockers improve hypoxia/hypoglycemia-induced impairment of rat hippocampal 2-deoxyglucose uptake in vitro after ethanol withdrawal.

The aim of the present study was to determine whether calcium channel antagonists attenuated hypoxia/hypoglycemia- or glutamate-induced reduction in 2-deoxyglucose (2-DG) uptake of hippocampal slices obtained from ethanol withdrawal rats. Ethanol withdrawal significantly potentiated the hypoxia/hypoglycemia- and glutamate-induced reductions in 2-DG uptake of hippocampal slices. Both nifedipine and flunarizine exhibited attenuating effects on ethanol withdrawal-induced potentiation of impairment of 2-DG uptake caused by hypoxia/hypoglycemia or glutamate. Hypoxia/hypoglycemia-induced deficit of 2-DG uptake was prevented by ethanol, but chronic consumption of ethanol resulted in the development of tolerance to neuroprotective effect. These findings suggest that the increased sensitivity of neurons to ischemic damage by ischemia may involve in the increased activity of calcium channels in the hippocampus.

Animals↗

PubMed1995

Effects of transient forebrain ischemia on long-term enhancement of dopamine release in rat striatal slices.

We studied the effects of transient forebrain ischemia in vivo on long-term enhancement of dopamine (DA) release from rat striatal slices. One hour after the high-frequency tetanic stimulation (HFTS) or L-glutamate (10(-6) M) application in Mg(2+)-free medium to striatal slices, the high concentration of KCl (high K+)-evoked DA release was measured. Tetanic stimulation or L-glutamate application significantly potentiated the high-K(+)-evoked DA release. When striatal slices were prepared from rats exposed to 3 min of ischemia followed by 24-h survival, the enhancement of DA release by HFTS was unaffected by ischemia. In contrast, the enhancement of DA release by HFTS was impaired in rats exposed to 5 min or 10 min of ischemia. In addition, high K(+)-evoked DA release per se was significantly impaired by 10 min of ischemia. The enhancement of DA release elicited by pretreatment with L-glutamate was also impaired in the rats exposed to 5 min of ischemia. When striatal slices were prepared from rats exposed to 5 min of ischemia with 7-day survival, the enhancement of DA release by HFTS was still impaired. The present results indicate that the neuronal mechanisms of the enhancement of DA release may be more sensitive to impairment from short periods of ischemia. Furthermore, the results suggest that an impairment of long-term enhancement of DA release by ischemia may be related the dysfunction of motor performance in rats exposed to ischemia.

Animals↗

PubMed1995

NG-nitro-L-arginine protects against hypoxia/hypoglycemia-induced decrease in CA1 presynaptic spikes in rat hippocampal slices.

The effects of nitric oxide (NO) synthase inhibitors on the hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes elicited by stimulation of the Schaffer collaterals were investigated using rat hippocampal slices. Drugs were added to normal medium for 10 min before incubation under hypoxic/hypoglycemic conditions (15 min), and after a 3-h washout, the CA1 presynaptic potential was measured. Treatment with NG-nitro-L-arginine methyl ester but not with NG-nitro-D-arginine methyl ester produced a concentration-dependent attenuation of the hypoxia/hypoglycemia-induced decrease in presynaptic fiber spikes. In contrast, treatment with precursors of NO in the arginine-to-NO pathway, such as sodium nitroprusside, S-nitro-N-acetylpenicillamine and N-morpholino sydnonimine exacerbated the 15-min hypoxia/hypoglycemia-induced decrease in the CA1 presynaptic potential. The neuroprotective effect of NG-nitro-L-arginine methyl aster was significantly attenuated by co-treatment with L-arginine. The present results suggest a facilitatory role of NO production in hypoxia/hypoglycemia-induced presynaptic dysfunction in CA1 regions of hippocampal slices.

Amino Acid Oxidoreductases↗

PubMed1995

A role of sigma receptors on hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes in rat hippocampal slices.

Effects of sigma receptor agonists or antagonists on hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes elicited by the stimulation of Schaffer collaterals were investigated using rat hippocampal slices. Treatment with sigma receptor antagonists such as haloperidol, NE-100 and rimcazole produced a concentration-dependent attenuation of the hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes. The order of potency of protection against hypoxia/hypoglycemia-induced reduction in CA1 presynaptic potential was: NE-100 = haloperidol > rimcazole. Treatment with sigma receptor agonist DTG potentiated the hypoxia/hypoglycemia-induced decrease in the CA1 presynaptic potential, whereas SKF10047 which possesses an affinity for phencyclidine site attenuated the decrease of potential. NE-100 antagonized a functional deficit induced by DTG, but unaffected the improving effect induced by SKF10047. The present results suggest a facilitatory role of sigma receptor stimulation in hypoxia/hypoglycemia-induced an impairment of neurophysiological functions in CA1 presynaptic regions of hippocampal slices.

Action Potentials↗