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Shin-ichi Yoshimura

Publications and source records attributed to Shin-ichi Yoshimura.

11 recordsLinked to original sources
PubMed2005

Two cases of dissecting aneurysm of the distal posterior inferior cerebellar artery: possible involvement of segmental mediolytic arteriopathy in the pathogenesis.

BACKGROUND: Dissecting aneurysm of the posterior inferior cerebellar artery (PICA) uninvolved with the vertebral artery is rare. The exact pathohistological diagnosis might result in 'unknown' because the underlying pathoanatomical features are, for a variety of reasons, not always identified. CASE DESCRIPTION: We report herein two cases of dissecting aneurysm harbored in different segments of the distal posterior inferior cerebellar artery. In our cases, after trapping the PICA at both just proximal and distal to the aneurysm, the abnormal portion was successfully resected with/without an end-to-end anastomosis. The first patient made a good recovery, while the other died 2 days after the surgery. Although its pathogenetic etiology was unidentified in the second case, the formation of dissecting aneurysm had resulted from a segmental mediolytic arteriopathy in the first case. CONCLUSION: This is the first report of a segmental mediolytic arteriopathy possibly being identified as causing an isolated dissecting aneurysm at this site.

Aortic Dissection↗
PubMed2005

Protective effects of statins involving both eNOS and tPA in focal cerebral ischemia.

Previous studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) protect the brain against ischemic injury by upregulating endothelial nitric oxide synthase (eNOS). Here, we tested the hypothesis that statins provide additional beneficial effects by also upregulating endogenous tissue plasminogen activator (tPA) and enhancing clot lysis in a mouse model of embolic focal ischemia. Heterologous blood clots (0.2 mm) were injected into the distal internal carotid artery to occlude blood flow in the middle cerebral artery territory after long-term (14 days) simvastatin, atorvastatin or vehicle treatment. Ischemic lesion volume, neurologic deficits, as well as residual blood clots were measured at 22 h. Reverse transcription-polymerase chain reaction assessed mRNA levels of eNOS, tPA, and the endogenous plasminogen activator inhibitor PAI-1. Ischemic lesion volumes and neurologic deficits were significantly reduced in wild-type mice by both simvastatin and atorvastatin. Statins increased eNOS and tPA mRNA levels but did not change mRNA levels of PAI-1. In eNOS knockout mice, atorvastatin reduced the volume of ischemic tissue and improved neurologic outcomes after arterial occlusion by blood clot emboli. In contrast, statins did not have protective effects in tPA knockout mice after embolic focal ischemia, but only in a filament model where focal ischemia was achieved via mechanical occlusion. These results suggest that statins protect against stroke by multiple mechanisms involving both eNOS and tPA. The involvement of each pathway may be revealed depending on the choice of experimental stroke model.

Animals↗
PubMed2004

Surgery for carotid dural ring aneurysms.

BACKGROUND: Carotid aneurysms of the paraclinoid segment are usually located in the intradural space, but can infrequently straddle the intra- and extradural space. CASE DESCRIPTION: We present 2 cases of unruptured carotid dural ring aneurysms with an aneurysmal sac that straddled the distal dural ring. Each paraclinoid aneurysm projected superiorly from the anterior surface of the internal carotid artery with a relatively flattened dome and central indentation on angiography. The aneurysmal domes were circumscribed by the distal dural ring and straddled the intra- and extradural space. After broad opening of the distal dural ring, aneurysms were successfully obliterated by clip application in parallel with the internal carotid artery. CONCLUSION: These cases underscore the significance of an aneurysmal dome indentation on angiographic images as a reflection of aneurysmal circumscription by the distal dural ring. Aneurysms that straddle the intra- and extradural space may require broad opening of the distal dural ring for adequate control and clipping.

Aged↗
PubMed2004

Hypoxia-induced renal epithelial cell death through caspase-dependent pathway: role of Bcl-2, Bcl-xL and Bax in tubular injury.

Although injury of epithelial cells has been reported to be responsible for renal disease such as acute renal failure, its molecular mechanisms are largely unknown. As hypoxia has been postulated as the initial trigger of epithelial injury, we studied the molecular mechanisms of apoptosis induced by hypoxia in human renal epithelial cells. Severe hypoxia caused epithelial cell death, accompanied by a significant increase in LDH release (p<0.01). In addition, hypoxic treatment of epithelial cells resulted in a significant increase in apoptotic cells as assessed by cell morphology (p<0.01). The apoptotic change in epithelial cells under hypoxic condition was also confirmed by a significant increase in caspase-3-like activity and release of cytochrome c (p<0.01). The decrease in epithelial cell number was completely abolished by addition of a wide-spectrum caspase inhibitor, Z-VAD, rather than Z-DEVD, a specific caspase-3 inhibitor (p<0.01). Thus, we further studied the molecular mechanisms of apoptosis induced by hypoxia. Anti-apoptotic factors, Bcl-2 and Bcl-xL, were significantly decreased in epithelial cells under a hypoxic condition as assessed by Western blotting (p<0.01). In contrast, hypoxia did not alter their location. Of particular importance, translocation of a proapoptotic factor, Bax, from the cytoplasm to the mitochondrial membrane was observed in response to hypoxia, whereas total Bax protein was not changed by hypoxia. Overall, this study demonstrated that hypoxia caused epithelial cell death induced by caspase-3-like activity-dependent apoptosis. The pro-apoptotic mechanisms of hypoxia in epithelial cells largely depend on a significant decrease in Bcl-2 and Bcl-xL. In addition, the present results demonstrate that translocation of Bax from the cytosol to the mitochondrial membrane occurred under hypoxia, thereby leading to pathological tissue destruction.

Apoptosis↗
PubMed2004

Factors predictive of cerebral hyperperfusion after carotid angioplasty and stent placement.

BACKGROUND AND PURPOSE: Cerebral hyperperfusion syndrome has been increasingly reported as a complication of carotid angioplasty and stent placement. The aim of the present study was to determine significant predictors of hyperperfusion phenomenon after carotid angioplasty and stent placement. METHODS: We retrospectively reviewed 30 consecutive patients with unilateral severe carotid stenosis who underwent angioplasty and stent placement. Resting cerebral blood flow (CBF) and cerebral vasoreactivity (CVR) to acetazolamide challenge were quantitatively measured to evaluate cerebral hemodynamic reserve. Split-dose [(123)I] iodoamphetamine single photon emission CT (SPECT) was performed before and 7 days after carotid angioplasty and stent placement. Technetium-99m hexamethylpropyleneamine oxime (HMPAO) SPECT was performed immediately after the procedure. RESULTS: Three patients had cerebral hyperperfusion phenomenon immediately after angioplasty and stent placement, as shown by HMPAO SPECT: One developed status epilepticus 2 weeks after the procedure. Significant predictors of hyperperfusion included patient age, pretreatment CVR, and pretreatment asymmetry index ([ipsilateral resting CBF/contralateral resting CBF] x 100). Variables determined not to be significant risk factors included pretreatment resting CBF value, degree of carotid stenosis, and interval from the onset of ischemic symptoms. CONCLUSION: Significant predictors of hyperperfusion phenomenon after carotid angioplasty and stent placement included patient age, pretreatment CVR, and pretreatment asymmetry index. Pretreatment CBF measurements, including those obtained by quantifying CVR and performing SPECT immediately after the procedure may aid in identifying patients at risk and in initiating careful monitoring and control of blood pressure to prevent hyperperfusion syndrome.

Acetazolamide↗
PubMed2003

S1P3 receptors mediate the potent constriction of cerebral arteries by sphingosine-1-phosphate.

We characterized the effect of Sphingosine-1-phosphate (S1P) on vascular tone. S1P selectively constricted isolated cerebral, but not peripheral arteries, despite ubiquitous expression of S1P(1), S1P(2), S1P(3) and S1P(5) receptor mRNA. Clostridium B and C3 toxins and the rho-kinase inhibitor Y27632 (trans-N-(4-pyridyl)-4-(l-aminoethyl)-cyclohexane carboxamide) reduced this vasoconstriction to S1P, indicating that the response was mediated through Rho. Pertussis toxin displayed only weak inhibition, suggesting minor involvement of G(i/o) protein. The S1P effect was specifically reduced by adenovirus bearing a s1p(3) but not s1p(2), antisense construct. Furthermore, suramin, which selectively blocks S1P(3) receptors, inhibited the vasoconstrictor effect of S1P, indicating that S1P(3) receptors account for at least part of S1P-mediated vasoconstriction in cerebral arteries. In vivo, intracarotid injection of S1P decreased cerebral blood flow, an effect prevented by suramin treatment. Because S1P constricts cerebral blood vessels and is released from platelets during clotting, the S1P/S1P(3) system constitutes a novel potential target for cerebrovascular disease therapy.

Animals↗
PubMed2003

High 123I-IMP retention on SPECT image in primary central nervous system lymphoma.

The purpose of this study is to characterize the time course of N-isopropyl-p-[123I]-iodoamphetamine (123I-IMP) uptake of primary central nervous system lymphomas (PCNSL) comparing with those of other common brain tumors such as malignant gliomas and meningioma. Ten patients with PCNSL, 14 with malignant gliomas and 7 with meningioma underwent 123I-IMP single photon emission computerized tomography (SPECT). Four (40%), 7 (70%) and 9 cases (90%) of PCNSL showed IMP index more than 1 on early (15 min), delayed (6 h) and extra-delayed (24 h) SPECT images, respectively. In contrast with those IMP index was less than 1 on any image of both malignant gliomas and meningioma. The PCNSL cases with IMP index more than 1 could be distinguished from malignant gliomas and meningioma visually. The mean value of IMP index of PCNSL was increased time-dependently and was higher than those of the other two brain tumor groups on SPECT images of any time phases, and statistically different from those of malignant gliomas, however, not from those of meningioma. Interestingly, the retention rates of 123I-IMP from early to extra-delayed image and delayed to extra-delayed image in PCNSL were significantly higher than those of both malignant gliomas and meningioma. The high 123I-IMP retention on SPECT image is regarded as characteristic in PCNSL and the evaluation of this character is suggested to be more useful for diagnosis of this tumor than that of 123I-IMP up-take on a single SPECT image.

Adolescent↗
PubMed2002

N141I mutant presenilin-2 gene enhances neuronal cell death and decreases bcl-2 expression.

A missense mutation (N1411) in Presenilin-2 (PS-2) gene is associated with early-onset familial Alzheimer's disease. In this study, SK-N-SH human neuroblastoma cells were transfected with wild-type and mutant PS-2 gene to examine presenilin-2 effects on apoptosis. Serum deprivation resulted in enhanced apoptosis in mutant PS-2 comparing with wild-type PS-2. Similarly, mutant PS-2 induced lactate dehydrogenase release to greater extent than wild-type PS-2. Time course experiment demonstrated that the increase in caspase-3-like activity was more pronounced and accelerated in mutant PS-2, compared to wild-type PS-2. While a significant decrease in bcl-2, an anti-apoptotic molecule, occurred in the cells overexpressing mutant PS-2, no significant change was observed in bax, a pro-apoptotic molecule, as compared with the cells overexpressing wild-type PS-2. Our study demonstrated that mutant PS-2 induces apoptosis accompanied by increased caspase-3-like activity and decreased bcl-2 expression in neuronal cells after serum-deprivation.

Apoptosis↗
PubMed2002

Nestin immunoreactivity in local neurons of the adult rat striatum after remote cortical injury.

Nestin is a marker for the neuronal and glial precursor cells and is expressed in reactive astrocytes after brain injury. Following restricted neocortical injury, we found that cells with neuronal morphology in the adult rat striatum became immunoreactive for both nestin and the neuronal marker, microtubule-associated protein 2 (MAP-2), but not for the astroglial marker, glial fibrillary acidic protein (GFAP). The number of nestin-positive cells transiently increased in the striatum. Continuous administration of 5-bromo-2'-deoxyuridine (BrdU) after cortical injury did not reveal any newly generated neurons in the striatum. Double-labeling fluorescent immunocytochemistry revealed that the nestin-positive striatal cells were also substance-P-positive. These findings suggest that some factors released from the injured cortex may induce nestin immunoreactivity in striatal neurons.

Animals↗
PubMed2002

B7.1 immunogene therapy effectively activates CD(4+) tumor-infiltrating lymphocytes in the central nervous system in comparison with B7.2 gene therapy.

The B7 gene utilizing immunogene therapy is one of the most common methods against tumor growth. However, there is no known study that investigated the difference between B7.1 and B7.2 with regard to B7 gene therapy in the central nervous system (CNS). Therefore, to clarify the difference, we established B7.1 or B7.2 gene transduced tumor cells originating from the murine T cell lymphoma cell line EL4 (EL4-B7.1 or EL4-B7.2). First, we observed the survival time after intracranial inoculation of parent (IC-wt) or genetically modified tumor cells. All mice in control groups (IC-wt or IC-mock) were dead within 16 days. While there was significant survival elongation in the B7.2 modified group (IC-B7.2, p=0.0002), all mice in this group were dead of tumor growth within 22 days. On the other hand, 60% of mice inoculated with EL4-B7.1 (IC-B7.1) survived more than 120 days (p<0.0001). Second, to shed light on the anti-tumor immune response in situ, we tried to analyze CD(4+) tumor-infiltrating T lymphocytes (CD(4+) TIL). To purify and analyze CD(4+) TIL, we had to deplete F4/80(+) microglia because of the CD4 expression. In terms of activation marker expression in CD(4+) TIL, a small population was activated (CD25, 9.8%; CD69, 15.8%) in the control group (IC-wt). In contrast, the activation marker positive CD4+ TIL percentage both in IC-B7.1 (CD25, 25.1%; CD69, 40.1%) and IC-B7.2 (CD25, 16.2%; CD69, 28.3%) appeared to reflect the survival curve in both groups. These findings strongly suggest that, in the CNS, B7.1 gene therapy could effectively introduce CD(4+) TIL activation compared with B7.2 gene therapy. This is the first study clearly describing the difference between B7.1 gene therapy and B7.2 gene therapy in the CNS in terms of the activation status of CD(4+) TIL in situ.

Animals↗