Search PubMed⌕ Search

Biomedical subjects

M Shibuya

Publications and source records attributed to M Shibuya.

At least 253 records · Page 14Linked to original sources
PubMed1994

Meningiomas: correlation between MRI characteristics and operative findings including consistency.

The findings on magnetic resonance imaging (MRI) in 73 surgically verified intracranial meningiomas were correlated with their histology and consistency during resection. T 1-weighted imaging was least useful since most of the tumours were iso-intense, similar to cortical grey matter regardless of histology or tumour consistency. The signal intensity on T2-weighted images was found to best correlate with both the histology and consistency of the meningioma. Generally, the low intensity portion of the tumour on T2-weighted images indicated a more fibrous and harder character, while the higher intensity portions indicated a more soft character. Most of the fibroblastic meningiomas showed the features of a hard tumour while angioblastic tumours showed the features of soft tumours. Tumours predicted to be harder on MR imaging generally took longer to resect than softer ones, and this relationship was shown best for the larger tumours. Using linear regression analysis, it appears that operative time for soft tumours is more affected by factors other than tumour consistency. Blood loss during surgery was also unrelated to the consistency of the tumour. These results suggest that the histology and consistency of meningiomas may be predictable from findings on T2-weighted imaging, and this may also predict the difficulty and time required for resection.

Adolescent↗
PubMed1994

Effects of prophylactic intrathecal administrations of nicardipine on vasospasm in patients with severe aneurysmal subarachnoid haemorrhage.

Calcium antagonists are currently most widely used for chronic cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH). However, the vasodilatory effects of systemically administered calcium antagonists can be limited secondary to hypotension. We previously compared intrathecal and intravenous routes of administration of nicardipine. Intrathecal administration of nicardipine significantly dilated spastic basilar arteries on day 7 in a two-haemorrhage canine model of vasospasm. In the present communication, the effects of prophylactic, serial administration of intrathecal nicardipine on vasospasm was examined in 50 patients. Patients were classified as Fisher SAH group 3 and all had their aneurysms clipped within 3 days of SAH. Following placement of a cisternal drain, 2 mg of nicardipine was injected, three times each day for an average of 10 days. The control group consisted of 91 similar patients with cisternal drainage not treated with nicardipine. Intrathecal administration of nicardipine decreased the incidence of symptomatic vasospasm by 26%, angiographic vasospasm by 20% and increased good clinical outcome at one month after the haemorrhage by 15%. Postoperative angiograms revealed that patients in the nicardipine group showed less vasospasm of major cerebral arteries, near the tip of a drain in the basal cistern, but vasospasm in the A2 and M2 segments was not decreased. Radio-isotope cisternography suggested that nicardipine might not reach the subarachnoid space around A2 and M2 segments. Nine patients complained of headache probably secondary to nicardipine induced vasodilation. Two patients suffered from meningitis, both were successfully treated. Intrathecal administration nicardipine appears to be effective in the treatment of vasospasm, but side effects were significant.

Adult↗
PubMed1994

Differing effects of vasopressin on regional cerebral blood flow of dogs following intracisternal vs. intra-arterial administration.

We investigated the differential effect of the intracisternal and intraarterial administration of vasopressin on the regional cerebral blood flow (rCBF) in the parietal cortex of dogs. Regional CBF, velocity and blood volume were assayed by laser flowmetry. The intracisternal injection of 1 nmol vasopressin significantly increased the rCBF and velocity, without affecting blood volume. However, the intravertebral arterial injection of 1 nmol vasopressin significantly decreased the rCBF and velocity. This discrepancy can be explained by a difference in the affected vasculature; large blood vessels in the subarachnoid space vs. whole cerebral vascular system. The intracisternal and intraarterial injection of the nitric oxide inhibitor NG-monomethyl-L-arginine reduced the rCBF from the base line, and significantly suppressed the rCBF elevation induced by vasopressin. The effect of vasopressin may be considered as the summation of the increased flow from the dilated large vessels via the release of nitric oxide from the endothelium, and of the decreased flow from the contracted small vessels.

Animals↗
PubMed1994

A role of nitric oxide in vasomotor control of cerebral parenchymal arterioles in rats.

The present study was undertaken to determine the role of nitric oxide (NO) in the regulation of vasomotor tone in rat cerebral parenchymal arterioles under physiological and pathological conditions. Cerebral arterioles, about 60 microns in diameter, were isolated from rats and cannulated with glass pipettes. Changes in the arteriolar diameter secondary to extraluminal application of drugs were monitored continuously through a videodimension analysis system. The arterioles were dilated by L-arginine (12.2 +/- 2.2% at 10(-3) M) and were constricted by NG-monomethyl-L-arginine (L-NMMA) (13.8 +/- 1.5% at 10(-4) M) in a dose-dependent manner. Pretreatment with superoxide dismutase (600 U) increased sensitivity to L-arginine. These results suggest that NO plays an important role in regulation of basal vasomotor tone of cerebral parenchymal arterioles under physiological conditions. Next, NO-modification of vasomotor responses to an endogenous vasoactive substance, arginine vasopressin (AVP) was studied in cerebral parenchymal arterioles. Increasing concentrations of AVP produced biphasic responses of vasodilation (10(-11) M) and vasoconstriction (10(-10)-10(-8) M). Inhibition of NO by pretreatment with L-NMMA (10(-4) M) or oxyhemoglobin (10(-5) M) abolished the vasodilation and enhanced the vasoconstriction by AVP. Therefore, under pathological conditions in which NO function was suppressed, such endogenous substances may produce contraction in parenchymal arterioles instead of dilation with aggravation of cerebral ischemia.

Animals↗
PubMed1994

Dysfunction of nitric oxide in the spastic basilar arteries after subarachnoid hemorrhage.

The function of nitric oxide in spastic cerebral arteries after subarachnoid hemorrhage (SAH) was angiographically investigated in dogs. On days 4 and 7, after two intracisternal injections of autologous blood, higher concentrations of L-arginine than those of endogenous L-arginine in the cerebrospinal fluid produced a transient vasodilation of the spastic basilar artery, whereas NG-monomethyl-L-arginine (L-NMMA) produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on day 4 than day 7, but less than that in intact dogs. Vasopressin, which is known to activate the endothelial L-arginine pathway, could induce a vasodilation only after the treatment with L-arginine. Intracisternal injection of superoxide dismutase (SOD), which caused no effect by itself, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on day 4 and both the magnitude and duration of that effect on day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. Enhancement of L-arginine's effect by SOD suggested that the inactivation of nitric oxide by superoxide anion contributed to the development of vasospasm.

Animals↗
PubMed1994

Vasopressin mediated vasodilation of cerebral arteries.

The bolus injection of vasopressin into the vertebral artery produced a dose-dependent vasodilation in the major cerebral arteries, detected angiographically, while it elicited a decrease in vertebral blood flow. One nanomol of vasopressin was the optimal dose for producing maximal vasodilation. The basilar, posterior communicating, and internal carotid arteries showed the most dilatation, followed by the middle cerebral, the intracranial portion of the vertebral artery and the anterior spinal artery. The extracranial portion of the vertebral artery was less sensitive to vasopressin. The vasodilation was inhibited by a V1-antagonist and NG-monomethyl-L-arginine. These results suggest that the arteries of the circle of Willis at the base of the brain are more sensitive to nitric oxide release induced by vasopressin compared with other intracranial and extracranial arteries.

Anesthesia↗
PubMed1994

Effects of vasopressin on regional cerebral blood flow in dogs.

Vasopressin may regulate the regional cerebral blood flow (rCBF) via two balancing effects: increased flow from the vessels dilated by nitric oxide from the endothelium, and decreased flow from the vessels contracted by direct stimulation of smooth muscle. The effect on the rCBF in anesthetized dogs following the intracisternal or intraarterial administration of vasopressin was investigated by laser flowmetry with the device placed on the dura over the parietal cortex. The intracisternal injection of 1 nmol vasopressin significantly increased the rCBF to 145.3 +/- 27.3% of base line. In contrast, the intravertebral arterial injection of vasopressin had no significant effect on the rCBF. This can be explained by a difference in the affected vasculature; mainly large vessels in the subarachnoid space vs. whole vascular system supplied by the vertebral artery. The intracisternal injection of 10 mumol of NG-monomethyl-L-arginine (L-NMMA) reduced the rCBF; pretreatment with this agent significantly suppressed the elevation in rCBF induced by vasopressin. The intraarterial injection of L-NMMA reduced the rCBF more than its intracisternal administration. It also suppressed the rCBF induced by vasopressin.

Animals↗
PubMed1994

Functional role of charybdotoxin-sensitive K+ channels in the resting state of dog basilar artery.

To determine the possible role of Ca(2+)-activated K+ (KCa) channels in the regulation of resting tone of cerebral arteries, the effect of agents which interact with these channels on tension and 86Rb efflux was examined in endothelium-denuded strips of dog basilar artery, and data were compared with findings in the mesenteric artery. The basilar artery maintained a myogenic tone; that is, the resting tone decreased when nifedipine was added. The addition of charybdotoxin, a blocker of large conductance KCa channels, caused a concentration-dependent contraction in the basilar artery but not in the mesenteric artery. In strips preloaded with 86Rb, the basal 86Rb efflux rate constant was significantly greater in the basilar artery than in the mesenteric artery. Nifedipine decreased the basal 86Rb efflux rate constant only in the basilar artery. The basal 45Ca influx in the resting state of the basilar artery was significantly increased when compared with the mesenteric artery and this increase in the basilar artery was reduced by nifedipine. The results suggest that the charybdotoxin-sensitive KCa channels regulate the myogenic tone in the resting state of the basilar artery. The activation of KCa channels in the basilar artery appears to be secondary to the increased transmembrane Ca2+ influx probably via the activation of L-type voltage-dependent Ca2+ channels in the resting state of this artery.

Animals↗
PubMed1994

D-type cyclin-dependent kinase activity in mammalian cells.

D-type cyclin-dependent kinase activities have not so far been detected in mammalian cells. Lysis of rodent fibroblasts, mouse macrophages, or myeloid cells with Tween 20 followed by precipitation with antibodies to cyclins D1, D2, and D3 or to their major catalytic partner, cyclin-dependent kinase 4 (cdk4), yielded kinase activities in immune complexes which readily phosphorylated the retinoblastoma protein (pRb) but not histone H1 or casein. Virtually all cyclin D1-dependent kinase activity in proliferating macrophages and fibroblasts could be attributed to cdk4. When quiescent cells were stimulated by growth factors to enter the cell cycle, cyclin D1-dependent kinase activity was first detected in mid G1, reached a maximum near the G1/S transition, and remained elevated in proliferating cells. The rate of appearance of kinase activity during G1 phase lagged significantly behind cyclin induction and correlated with the more delayed accumulation of cdk4 and formation of cyclin D1-cdk4 complexes. Thus, cyclin D1-associated kinase activity was not detected during the G0-to-G1 transition, which occurs within the first few hours following growth factor stimulation. Rodent fibroblasts engineered to constitutively overexpress either cyclin D1 alone or cyclin D3 together with cdk4 exhibited greatly elevated cyclin D-dependent kinase activity, which remained absent in quiescent cells but rose to supraphysiologic levels as cells progressed through G1. Therefore, despite continued enforced overproduction of cyclins and cdk4, the assembly of cyclin D-cdk4 complexes and the appearance of their kinase activities remained dependent upon serum stimulation, indicating that upstream regulators must govern formation of the active enzymes.

3T3 Cells↗
PubMed1994

Combined effect of L-arginine and superoxide dismutase on the spastic basilar artery after subarachnoid hemorrhage in dogs.

To investigate the function of nitric oxide (a major endothelium-derived relaxing factor) in cerebral arteries after subarachnoid hemorrhage (SAH) in vivo, several nitric oxide-related substances were administered to dogs that had undergone double SAH. These included L-arginine (a substrate for the formation of nitric oxide), NG-monomethyl-L-arginine (L-NMMA, an analog of L-arginine that inhibits the formation of nitric oxide from L-arginine), and superoxide dismutase (SOD, which protects nitric oxide from oxidation by superoxide anion), which were given via intracisternal injection. The diameter of the basilar artery was assessed angiographically. In intact dogs, intracisternal bolus injections of L-arginine (1, 10, or 100 mumol) produced a dose-dependent increase in the internal diameter of the basilar artery; conversely, L-NMMA reduced the diameter of the basilar artery from baseline in a dose-dependent manner. On Days 4 and 7, after two intracisternal injections of autologous blood, L-arginine produced transient vasodilation of the spastic basilar artery, whereas L-NMMA produced no significant vasoconstriction. The vasodilator effect of L-arginine after SAH was stronger on Day 4 than on Day 7, but less than in intact dogs. Intracisternal injection of SOD, which caused no effect per se, enhanced the duration of the vasodilator effect of L-arginine on the basilar artery on Day 4 and both the magnitude and duration of that effect on Day 7. Thus, the basal release of nitric oxide was impaired after SAH, but the ability to synthesize nitric oxide in the vascular wall was not abolished. The finding that the simultaneous injection of SOD enhanced and prolonged the vasodilation induced by sufficient exogenous L-arginine suggests that the inactivation of nitric oxide by superoxide anion contributes to the development of vasospasm.

Animals↗
PubMed1994

[Deep sylvian meningioma: a case report of a child].

A case of deep sylvian meningioma without dural attachment in a 12-year-old boy was reported. He had been suffering from severe headache for a month. Neurological examination was normal. CT scan and MR images showed a well-enhanced 7 cm mass lesion with small cysts, located in the left sylvian fissure. Peritumoral edema was slight and the midline structures were minimally shifted in spite of its large size. A fronto-temporal craniotomy was made and the tumor was grossly totally removed. The tumor had no dural attachment and existed in the left sylvian fissure, involving the middle cerebral artery and its branches. The histological diagnosis was transitional meningioma without malignancy. The postoperative course was uneventful except for transient mild left oculomotor palsy for several days. He is doing well now one year after the surgery and follow-up MR images showed no recurrence. Intracranial meningioma is rare in children. According to the literature, meningioma in children is slightly more frequent in males. There is a higher incidence of lack of dural attachment and cystic tumors than in adults. Deep sylvian meningioma without dural attachment is also very rare. Including our case, 13 cases of deep sylvian meningioma were reported in the literature. Four of them were under 20 years old. We report this case in detail with other cases reported previously.

Age of Onset↗
PubMed1994

[The usefulness of the bayesian method for the prediction of plasma theophylline levels in asthmatic children during RTC therapy by the sustained preparation of theophylline].

Pharmacokinetic prediction of plasma theophylline levels during RTC therapy by the sustained release preparation of theophylline was studied with a one compartment model in children aged 1-6 years old showing comparatively long sleeping time. Using the parameters measured from the population of 1-17 year olds, the accuracy of the prediction was studied by the Bayesian method. Absolute error (A.E.) and estimation error (E.E.) were about 2.0. The prediction values of E.E. seemed to be rather higher if the measured values of the absorption phase were used, and the values seemed to be rather lower if the values of the elimination phase were used. From these results it might be concluded that the Bayesian method seems to be useful for RTC therapy in children under 6 years old.

Adolescent↗
PubMed1994

A new communication system between hepatocytes and sinusoidal endothelial cells in liver through vascular endothelial growth factor and Flt tyrosine kinase receptor family (Flt-1 and KDR/Flk-1).

Hepatocyte Growth Factor (HGF)/Scatter Factor secreted from sinusoidal endothelial cells and Kupffer cells in liver activates the c-Met tyrosine kinase receptor expressed on hepatocytes. Here we report yet another possible communication system through a different ligand and tyrosine kinase receptor in an opposite direction. We isolated and determined the primary structure of the entire coding region of rat flt-1 (fms-like tyrosine kinase), a receptor for Vascular Endothelial Growth Factor (VEGF). Using rat flt-1 cDNA as a probe we found that the flt-1 mRNA was expressed at very high levels in sinusoidal endothelial cells in normal rat liver, but was hardly detectable in hepatocytes. The transcripts of another VEGF receptor KDR/Flk-1 structurally related to Flt-1 was also expressed specifically in sinusoidal endothelial cells. On the other hand, VEGF mRNA was expressed weakly in hepatocytes, but not in the nonparenchymal cell fraction. Furthermore, in an in vitro culture system, VEGF demonstrated a remarkably specific growth-stimulatory activity as well as maintenance activity on the sinusoidal endothelial cells. These results suggest that hepatocytes regulate the proliferation and survival of the sinusoidal endothelial cells in liver in a paracrine manner. Therefore two reciprocal communication systems, VEGF-Flt receptor family and HGF-Met receptor, may exist in hepatic tissue.

Amino Acid Sequence↗
PubMed1994

Allele loss on chromosome 17 in ovarian cystic teratomas.

We examined the DNA from 12 patients with ovarian tumors (four benign germ cell tumors, one malignant germ cell tumor, one benign common epithelial tumor and six common epithelial carcinomas) for the allele loss on chromosome 17 using 12 probes for hypervariable loci. At THH59 loss of heterozygosity (LOH) was detected in three benign germ cell tumors and two epithelial carcinomas. At a more distal locus, KKA35, LOH was detected in three benign germ cell tumors and one epithelial carcinoma.

Alleles↗
PubMed1994

Possible involvement of VEGF-FLT tyrosine kinase receptor system in normal and tumor angiogenesis.

A novel receptor-type tyrosine kinase gene flt (fms-like tyrosine kinase, flt-1) was isolated from human placenta cDNA library. Flt-1 receptor carries a ligand binding domain which contains seven immunoglobulin-like stretches. Further, Flt-1 tyrosine kinase domain is separated by an approximately 70 amino acid-insert region similar to the cases of Fms/Kit/PDGF-R (fms family). However, unlike the fms family members, Flt-1 insert region does not contain "Tyr-X-X-Met" motif, which is known to be important for signal transduction and for the binding of P13 kinase to the receptor. Thus, a unique structure of Flt-1 suggests that a signal transduction pathway from Flt receptor is different from that in the fms family. The expression of flt-1 gene is detectable in a variety of normal tissues, and cell fractionation studies indicate that the flt-1 mRNA is highly expressed in endothelial cell-enriched fraction. VEGF, which has recently been reported as a ligand for Flt-1 receptor, dramatically stimulated growth of endothelial cells in culture. Many human tumors were found to express VEGF mRNA but not Flt-1 message, suggesting a paracrine mechanism for tumor angiogenesis. Interestingly, VEGF could not stimulate proliferation of Flt-1-overexpressing NIH3T3 fibroblast cells. These results suggest that Flt-1 is an endothel-specific growth factor receptor and that the signal transducing pathway through Flt-1 receptor is inactive in the fibroblast background.

3T3 Cells↗