Search PubMed⌕ Search

Biomedical subjects

S Suga

Publications and source records attributed to S Suga.

At least 55 records · Page 3Linked to original sources
PubMed2001

Cerebral microaneurysms found incidentally during aneurysm surgery.

Not uncommonly, cerebral microaneurysms are found incidentally during surgery for another previously diagnosed cerebral aneurysm(s). The frequency and angiographic characteristics of such incidental microaneurysms are retrospectively summarized. Seventeen patients were identified as harboring incidental microaneurysms, comprising 4.9% of the whole series. The middle cerebral artery (MCA) was the most frequent location (seven cases, 41%) of these microaneurysms. There was a tendency for MCA microaneurysms to be contiguous to a previously known, larger aneurysm at the same location. Neurosurgeons as well as interventional neuroradiologists should be aware of the possible presence of these incidental microaneurysms while treating patients with a cerebral aneurysm(s). Although the actual clinical implications of these incidental microaneurysms have not been elucidated, the few additional risks to patients already surgically exposed for the treatment of another aneurysm, along with the possible benefit of preventing their rupture and growth, would justify the surgical treatment of these microaneurysms.

Adult↗
PubMed2001

Directional distribution of radiation around an accident at a uranium fuel factory in Tokai-mura, 1999.

A beta-ray survey was carried out on concrete walls of the boundary and buildings after a criticality accident at a factory of JCO Co. Ltd. at Tokai-mura. A remarkable distribution of beta counts was observed on the walls depending on the complex internal and external structures of buildings surrounding a precipitation vessel containing uranium 23 days after the accident. The directional distribution function, based on the beta counts on the walls, was consistent with data concerning the neutron dose rate measured in several directions during the accident, suggesting an anisotropic neutron distribution to the residential area.

Humans↗
PubMed2001

Rapid contamination of the environments with varicella-zoster virus DNA from a patient with herpes zoster.

Patients with zoster are considered to be less contagious than varicella patients because their infection is localised. It is not known, however, when and for how long a spread of varicella-zoster virus (VZV) from a zoster patient begins and continues and the extent of virus spread from the patient. The polymerase chain reaction (PCR) was used to detect VZV DNA in samples obtained from the hands and throat of a patient with zoster and from her room environments including surfaces of the back of a chair, the door handle, the table and the air conditioner filter. VZV DNA was detected on the surfaces of the back of the seat and the table and in peripheral blood mononuclear cells (PBMCs) and serum on Day 4 of the illness. VZV DNAemia persisted for 4 days until Day 7 of the illness. It was also detected in samples collected from throat and the air conditioner filter on Days 6 and 7 of the illness respectively. All of the surfaces, that were examined in her home environment, were contaminated with VZV DNA by Day 7 of the illness. The present study showed rapid and wide spread of VZV DNA in the environment even from a patient with zoster.

Adult↗
PubMed2001

[Varicella].

Explore the source record for details and available documents.

Age Factors↗
PubMed2001

[A case with cerebral subcortical hemorrhage following the administration of phenylpropanolamine].

A 21-year-old woman experienced severe headache and nausea one hour after taking pills containing 160 mg of phenylpropanolamine for common cold. She had no previous history of drug abuse or hypertension. Physical examination revealed slight left-sided hemiparesis. Her blood pressure was 100/52 mmHg. Subcortical hemorrhage was noted in the right frontal lobe with a cranial computed tomography. On the seventh hospital day, cerebral angiography demonstrated with segmental narrowing of a branch of the right anterior cerebral artery, indicating the presence of focal angitis. This finding disappeared on the 35th hospital day. In the majority of the reported cases of the intracerebal hemorrhage associated with the ingestion of phenylpropanolamine, focal angitis rather than induced hypertension is considered to be a causative factor for hemorrhage. Thus, we would like to emphasize that the administration of phenylpropanolamine should be avoided, even to the patients without hypertention or past history of intracerebral hemorrhage.

Adult↗
PubMed2000

Hexamminecobalt(III) chloride inhibits glucose-induced insulin secretion at the exocytotic process.

Hexamminecobalt(III) (HAC) chloride was found to have a potent inhibitory effect on glucose-induced insulin secretion from pancreatic islets. HAC at 2 mm inhibited the secretion in response to 22.2 mm glucose by 90% in mouse islets. Perifusion experiments revealed that the first phase of insulin secretion was severely suppressed and that the second phase of secretion was completely abrogated. Removal of HAC from the perifusate immediately restored insulin secretion with a transient overshooting above the normal level. However, HAC failed to affect glucose-induced changes in d-[6-(14)C]glucose oxidation, levels of reduced forms of NAD and NADP, mitochondrial membrane potential, ATP content, cytosolic calcium concentration, or calcium influx into mitochondria. Furthermore, HAC inhibited 50 mm potassium-stimulated insulin secretion by 77% and 10 microm mastoparan-stimulated insulin secretion in the absence of extracellular Ca(2+) by 80%. The results of a co-immunoprecipitation study of lysates from insulin-secreting betaHC9 cells using anti-syntaxin and anti-vesicle-associated membrane protein antibodies for immunoprecipitation or Western blotting suggested that HAC inhibited disruption of the SNARE complex, which is normally observed upon glucose challenge. These results suggest that the inhibitory effect of HAC on glucose-induced insulin secretion is exerted at a site(s) distal to the elevation of cytosolic [Ca(2+)], possibly in the exocytotic machinery per se; and thus, HAC may serve as a useful tool for dissecting the molecular mechanism of insulin exocytotic processes.

Adenosine Triphosphate↗
PubMed2000

Post-ischemic hypothermia delayed neutrophil accumulation and microglial activation following transient focal ischemia in rats.

Following ischemia, inflammation has been demonstrated to be involved in the progression of the tissue damage. Intra-ischemic hypothermia has been shown to attenuate the adverse activities of neutrophils and microglia. We investigated whether neutrophil accumulation and/or microglial activation is attenuated in post-ischemic hypothermia following transient focal ischemia in rats. After 1 h of ischemia, the neutrophil accumulation and the microglial activation was evaluated immunohistochemically. Percent infarct area was compared at 1, 2, 3, 5, and 7 days after ischemia/reperfusion. In hypothermia, the neutrophil accumulation was delayed but not attenuated. In normothermia, the accumulation reached the peak at 2 days after ischemia. The peak shifted to 3 days in hypothermia. Similarly, the microglial activation was delayed in hypothermia. Comparison of the infarct area showed significant protection by hypothermia at 1 and 2 days after reperfusion. However, hypothermia failed to show significant protection after 3 days and later. These results show that the delayed neutrophil accumulation and the microglial activation can be responsible for the loss of persistent protection in post-ischemic hypothermia.

Animals↗
PubMed2000

Probing bulk states of correlated electron systems by high-resolution resonance photoemission

Electron correlations are known to play an important role in determining the unusual physical properties of a variety of compounds. Such properties include high-temperature superconductivity, heavy fermion behaviour and metal-to-insulator transitions. High-resolution photoelectron spectroscopy (PES) provides a means of directly probing the electronic states (particularly those near the Fermi level) in these materials, but the short photoelectron mean free paths (< or = 5 A) associated with the low excitation energies conventionally used (< or = 120 eV) make this a surface-sensitive technique. Now that high-resolution PES is possible at much higher energies, with mean free paths as long as 15 A (ref. 6), it should become feasible to probe the bulk electronic states in these materials. Here we demonstrate the power of this technique by applying it to the cerium compounds CeRu2Si2 and CeRu2. Previous PES studies of these compounds revealed very similar spectra for the Ce 4f electronic states, yet it is expected that such states should be different owing to their differing degrees of hybridization with other valence bands. Our determination of the bulk Ce 4f electronic states of these compounds resolves these differences.

Journal Article↗
PubMed2000

Postischemic hypothermia attenuates apoptotic cell death in transient focal ischemia in rats.

Hypothermia confers potent neuroprotection against ischemic injury. Attenuation of apoptosis by hypothermia can be one of the responsible mechanisms. In this study, in situ DNA nick-end labeling (TUNEL) and immunostaining of Bax protein were performed to evaluate the effect of postischemic hypothermia on apoptotic cell death, employing rodent transient focal ischemia. Animals received 1 hour of transient focal ischemia. Brain temperature was maintained at 37.5 +/- 0.5 degrees C during ischemia. Immediately after reperfusion, animals were assigned to either a normothermic or hypothermic group. In hypothermia, animals were cooled and brain temperature was lowered to 34.5 +/- 1.0 degrees C. Prolonged hypothermia was maintained for 16 hours and animals rewarmed. In both groups, TUNEL and immunostaining of Bax was performed. In normothermia, the number of TUNEL positive cells reached the peak at 2 days after ischemia and decreased gradually. In hypothermia, the peak was shifted to 3 days after ischemia. The number of TUNEL positive cells in hypothermia was persistently below that of normothermia. Similarly, in hypothermia, immunostaining of Bax showed attenuated immunoreactivity compared with that in normothermia. In conclusion, postischemic hypothermia reduced both the number of TUNEL positive cells and immunoreactivity of Bax, which may be one of the responsible mechanisms with which hypothermia exerts neuroprotection.

Animals↗
PubMed2000

Purification and properties of a novel azide-sensitive ATPase of Exiguobacterium aurantiacum.

Exiguobacterium aurantiacum BL77/1 possesses at least two distinct membrane-bound ATPases. One of them was solubilized with decanoyl N-methylglucamide, a non-ionic detergent, and purified by successive chromatography on DEAE-Sepharose and hydroxyapatite. The purified ATPase appears to consist of a single polypeptide component with an apparent molecular mass of 54 kDa. Among the triphosphates of various nucleosides tested, ATP was the best substrate. The enzyme exhibited a Km of 0.5 mM for ATP and a Vmax of 109 micromol ATP (mg protein)(-1) min(-1); the optimum pH for activity was near 6.5. The enzyme was sensitive to azide and inactivated by N,N'-dicyclohexylcarbodiimide. Analysis of the inhibition kinetics by N,N'-dicyclohexylcarbodiimide suggested that binding of the drug to a single carboxyl group per ATPase molecule is sufficient for inactivation.

Adenosine Triphosphatases↗
PubMed2000

cAMP-independent decrease of ATP-sensitive K+ channel activity by GLP-1 in rat pancreatic beta-cells.

Using the patch-clamp method, we studied the mechanism of depolarization of rat pancreatic beta-cells induced by glucagon-like peptide 1 (7-36) amide (GLP-1). GLP-1 caused depolarization in a concentration-dependent manner (0.2-100 nM). Exendin (9-39) amide, a GLP-1 receptor antagonist, prevented the GLP-1-induced depolarization. GLP-1 reduced tolbutamide-sensitive membrane currents evoked by voltage ramps from -90 to -50 mV, recorded in the perforated whole-cell configuration, suggesting that GLP-1 decreased the activity of the ATP-sensitive K+ channel (KATP). This GLP-1 effect was prevented by exendin (9-39) amide. In cells treated with Rp-cAMPS, an inhibitor of the cAMP-dependent protein kinase (PKA), GLP-1 still caused depolarization and reduced the whole-cell membrane current through KATP. Examined in the cell-attached configuration, 20 nM GLP-1, applied out of the patch, had little effect on KATP activity. In the inside-out configuration, the open time probability and the single-channel conductance of KATP in the absence of ATP inside the membrane were unaffected by the presence of 20 nM GLP-1 in the pipette. In both conditions, application of ATP to the inside of the membrane reduced KATP activity. The half-maximal concentrations (ki) of ATP were 11.6 microM without and 5.6 microM with 20 nM GLP-1 in the pipette (P<0.05). The values of the Hill coefficient (h) were 1.03 without and 1.01 with GLP-1. We conclude that GLP-1 reduces KATP activity by elevating the sensitivity of KATP to ATP, resulting in depolarization of pancreatic beta-cells. This GLP-1 action is independent of the cAMP signalling pathway.

Action Potentials↗
PubMed2000

Long-term outcome of 17 cases of large-giant posterior fossa aneurysm.

Long-term outcome of 17 patients who harbored a large or giant aneurysm of posterior fossa was summarized. The anatomical distribution of aneurysms included eight cases of basilar artery (BA) bifurcation aneurysms, three cases of BA trunk aneurysms, and six cases of vertebral artery (VA) aneurysms. Eight patients received surgical or endovascular treatment for their lesion. The clinical outcome was good recovery in six, moderate disability in one, and vegetative state in one case, respectively. The other nine patients were followed conservatively. Four of them had fatal aneurysmal rupture, and another two patients suffered from aggravation of pre-existing symptoms related to their aneurysm. Only three patients remain intact. Comparison of the radiographic parameters between those who bled and those who did not bleed revealed that those with subsequent rupture had significantly higher rate of aneurysmal thrombus and had a trend for larger diameter of the aneurysm. Although more aggressive and multidisciplinary measure should be taken to these patients to improve their long-term outcome, our results showed the limitation of treatment for these patients in the present era at the same time. The patients with broad neck BA bifurcation aneurysm in which efferent vessels were incorporated into aneurysmal dome, and those with fusiform, giant BA trunk aneurysm with thrombus were the least amenable to treatment in our series.

Adult↗
PubMed2000

Basilar artery occlusion due to mucormycotic emboli, preceded by acute hydrocephalus.

A rare case of brain stem infarction caused by mucormycotic emboli, preceded by acute hydrocephalus, is reported. The patient, who had suffered from leukemia and had undergone bone marrow transplantation several months before, presented initially with seizure and persistent disturbance of consciousness. A head CT scan revealed marked ventricular dilation and diagnosed as acute hydrocephalus. The patient received emergent ventricular drainage. Despite the aggressive treatment, the patient did not survive. Autopsy revealed systemic mucormycosis occluding and invading various arteries including basilar artery and its branches, causing fatal brainstem infarction. Although early diagnosis remains difficult in the cases of systemic mucormycosis, prompt initiation of treatment is mandatory; one must have in mind the possibility of presence of fungal infection when treating patients with acute neurological deterioration who have underlying debilitating diseases, even though fungi themselves are hard to detect in most cases.

Acute Disease↗
PubMed2000

Involvement of phosphorylation of beta-subunit in cAMP-dependent activation of L-type Ca2+ channel in aortic smooth muscle-derived A7r5 cells.

We investigated the effect of intracellular cAMP on the gating kinetics of L-type Ca2+ channel in an A7r5 smooth muscle-derived cell line using the whole-cell patch-clamp technique. Application of dibutyryl cyclic AMP (db-cAMP) to the cell increased the magnitude of Ca2+ currents through L-type Ca2+ channels (I(Ca)), and shifted the current-voltage relationship (I-V curve) for I(Ca) to the left. The magnitudes of maximum I(Ca) were 14.1 +/- 0.7 before and 16.0 +/- 1.1 pA/pF after application of 1 mM db-cAMP (P < 0.05). The values of the half-activation potential (V(1/2)) of I(Ca), estimated from activation curves, were -7.0 +/- 0.8 mV before and -10.8 +/- 1.0 mV after application of db-cAMP (P < 0.05). In cells pretreated with 10 microM Rp-cAMPS (a specific inhibitor of PKA), db-cAMP affected neither the I-V curve nor the activation curve for I(Ca). In cells pretreated with the antisense oligonucleotide for the beta-subunit of L-type Ca2+ channel, db-cAMP failed to enhance I(Ca) or alter the activation curve. On the other hand, in the cells pretreated with the nonsense oligonucleotide, application of db-cAMP caused an increase in magnitude of I(Ca) and shifted the activation curve to the left. Western blot analysis revealed that the pretreatment of cells with antisense oligonucleotide but nonsense oligonucleotide reduced the expression of the beta-subunit of the L-type Ca2+ channel. We conclude that the cAMP-dependent phosphorylation of the beta-subunit potentiates the voltage dependency of the activation kinetics of the L-type Ca2+ channel in A7r5 cells.

Animals↗
PubMed2000

Effect of neutral endopeptidase inhibitor on endogenous atrial natriuretic peptide as a paracrine factor in cultured cardiac fibroblasts.

1. Cardiac remodelling is a fundamental response to hypertension, myocardial infarction and chronic heart failure, and involves cardiac fibroblast proliferation and production of extracellular matrix components such as collagen. The present study was performed to examine the role of endogenous atrial natriuretic peptide (ANP) as a possible paracrine factor for cardiac fibroblasts, and to examine the effects of three neutral endopeptidase (NEP) inhibitors, thiorphan, phosphoramidon and ONO-BB-039-02 (ONO-BB) on endogenous ANP-induced changes in collagen synthesis by cultured neonatal rat cardiac fibroblasts. 2. Each NEP inhibitor singly had no significant effect on collagen synthesis by cardiac fibroblasts, except for maximum concentration (10(-3) M) of thiorphan. 3. Exogenous ANP inhibited collagen synthesis in a concentration-dependent manner (10(-8) - 10(-6) M). Thiorphan (10(-4) and 10(-3) M) and phosphoramidon (10(-5) and 10(-4) M) enhanced the ANP (10(-7) M)-induced decrease in collagen synthesis. ONO-BB (10(-5) and 10(-4) M) slightly enhanced the ANP-induced decrease in collagen synthesis. 4. Myocyte-conditioned medium (MC-CM), as well as exogenous ANP, inhibited collagen synthesis dose-dependently. The decrease in collagen synthesis at 100% MC-CM was augmented by thiorphan (10(-3) M), phosphoramidon (10(-4) M) and ONO-BB (10(-4) M). 5. HS-142-1, a natriuretic peptide receptor antagonist, significantly reduced the MC-CM plus thiorphan- and MC-CM plus ONO-BB-induced decrease in collagen synthesis, by 92 and 62%, respectively and showed a tendency to attenuate the MC-CM plus phosphoramidon-induced decrease in collagen synthesis by 40%. 6. Our observations suggested that endogenous ANP released from cardiomyocytes inhibited collagen synthesis as a paracrine factor and that NEP inhibitors enhanced the activity of this peptide in cardiac fibroblasts.

Animals↗
PubMed2000

CT scans essential after posttraumatic loss of consciousness.

The frequency of "talk and deteriorate" in the emergency department (ED), subsequent deterioration of patients with seemingly "mild" head injury at the time of presentation, is summarized. Among the 1,073 patients with minor head injury treated in the last 5 years, five patients (0.5%) deteriorated in the ED. All of the five patients had experienced transient loss of consciousness (LOC) before presentation. Deterioration had occurred during treatment of trivial associated injuries in four-fifths of the cases. Computed tomography (CT) scans revealed four acute epidural hematomas and one cerebellar contusion. Retrospectively, immediate brain CT shortly after their arrival may have revealed the presence of traumatic intracranial hematomas before deterioration. Although routine use of CT scans in patients with mild head injury has been controversial, the authors conclude that CT scans should be taken if patients have experienced transient LOC to prevent or reduce the occurrence of deterioration in ED.

Adult↗
PubMed2000

2-Aminoethoxydiphenyl borate modulates kinetics of intracellular Ca(2+) signals mediated by inositol 1,4,5-trisphosphate-sensitive Ca(2+) stores in single pancreatic acinar cells of mouse.

Regulation of the kinetics of intracellular Ca(2+) signals with a novel, membrane-penetrable, inositol 1,4,5-trisphosphate (InsP(3)) receptor/Ca(2+) channel modulator, 2-amino-ethoxydiphenyl borate (2APB), has been investigated using patch-clamp, whole-cell recording to monitor Ca(2+)-activated Cl(-) currents in single isolated pancreatic acinar cells. 2APB itself fails to evoke a detectable current response but it dramatically changes the kinetics of agonist-induced Ca(2+) release from pulsatile spikes to long-lasting, huge Ca(2+) waves, suggesting that 2APB coordinates local Ca(2+) release to generate global Ca(2+) signals. The regulation by 2APB can be elicited by internal perfusion of InsP(3) in a concentration-dependent manner, indicating that this regulation is not mediated through membrane receptors or G protein signal transduction. The InsP(3) receptor blocker heparin, but not the ryanodine-sensitive receptor blockers ruthenium red or ryanodine, abolishes 2APB-mediated regulation of Ca(2+) release. This results also suggest that 2APB effects are mediated through InsP(3) receptors. 2APB substantially modifies single inward Cl(-) current pulse evoked by the photolytic release of caged InsP(3) but not by caged Ca(2+). These data indicate that 2APB-induced regulation is mediated neither by Ca(2+)-induced Ca(2+) release nor by affecting Cl(-) channel activity directly. We conclude that 2APB regulates the kinetics of intracellular Ca(2+) signals, represented as the change in the Ca(2+) oscillation patterns from brief pulsatile spikes to huge, long-lasting Ca(2+) waves. Moreover, this regulation seems to be mediated through InsP(3)-sensitive Ca(2+) pools. 2APB may act as a novel, useful pharmacological tool to study the genesis of intracellular Ca(2+) signals.

Animals↗