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Yasuhiko Kaku

Publications and source records attributed to Yasuhiko Kaku.

17 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

Thrombosed unruptured cerebral aneurysm causing brain infarction followed by subarachnoid hemorrhage--case report--.

A 71-year-old man presented with right hemiparesis and aphasia due to cerebral infarction in the frontal lobe. Computed tomography (CT) revealed a high-density mass, 12 mm in diameter, in the stem of the left sylvian fissure. Carotid angiography demonstrated occlusion of the left ascending frontal artery complex and retention of contrast medium at the bifurcation of the left middle cerebral artery (MCA). The diagnosis was cerebral infarction caused by occlusion of the ascending frontal artery complex resulting from thrombosed left MCA aneurysm. The patient was managed conservatively and his neurological symptoms gradually improved. One month later, he lapsed into a coma. CT revealed subarachnoid hemorrhage. Carotid angiography showed a large left MCA aneurysm with branch occlusion of the left ascending frontal artery complex. A left frontotemporal craniotomy was performed. The MCA aneurysm was opened and the intramural thrombi removed, and finally neck clipping was performed. The patient made a good postoperative recovery.

Aged↗
PubMed2005

Antegrade recanalization of a completely embolized vertebral artery after endovascular treatment of a ruptured intracranial dissecting aneurysm. Report of two cases.

Occlusion of the parent artery is a traditional method of treatment of unclippable cerebral aneurysms. Surgical or endovascular occlusion of the parent artery proximal to the aneurysm has been recommended for the treatment of dissecting aneurysms located in the vertebrobasilar circulation. Nevertheless, occlusion of the parent artery may not result in permanent exclusion of the aneurysm from the systemic circulation because, occasionally, postoperative rebleeding occurs after proximal occlusion. Alternatively, endovascular occlusion of the affected site, including the aneurysmal dilation, and parent artery, is a safe and reliable treatment for dissecting aneurysms. The authors present two rare cases of ruptured vertebral artery (VA) dissecting aneurysms that were treated by endovascular occlusion of the affected site including the aneurysm and parent artery by using Guglielmi detachable coils. In both cases the VA recanalized in an antegrade fashion during the follow-up period. Based on these unique cases, the authors suggest that a careful angiographic follow up of dissecting aneurysms is required, even in patients successfully treated with endovascular occlusion of the affected artery and aneurysm.

Aortic Dissection↗
PubMed2004

Hepatocyte growth factor promotes neuronal differentiation of neural stem cells derived from embryonic stem cells.

We previously reported that hepatocyte growth factor (HGF) promoted proliferation of neurospheres and neuronal differentiation of neural stem cells (NSCs) derived from mouse embryonic brain. In this study, spheres from mouse embryonic stem (ES) cells were generated by floating culture following co-culture on PA6 stromal cells. In contrast to the behavior of the neurospheres derived from embryonic brain, addition of HGF to the growth medium of the floating cultures decreased the number of spheres derived from ES cells. When spheres were stained using a MAP-2 antibody, more MAP-2-positive cells were observed in spheres cultured with HGF. When HGF was added to the growth and/or differentiation medium, more MAP-2-positive cells were also obtained. These results suggest that HGF promotes neuronal differentiation of NSCs derived from ES cells.

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

Prediction of neurologic deterioration in patients with lacunar infarction in the territory of the lenticulostriate artery using perfusion CT.

BACKGROUND AND PURPOSE: A significant proportion of patients with lacunar infarctions experience neurologic deterioration after onset. However, no clinical examination has been established for prediction of the progress of symptoms. To determine the hemodynamic predictors of such progression, we performed perfusion CT to quantitatively assess cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) of patients with lacunar infarctions in the territory of the lenticulostriate artery. METHODS: We performed MR imaging and perfusion CT of 26 patients with lacunar infarction within 24 hr after onset. On the CBF map on perfusion CT scans, a round small region of interest was set at the region, with decreased CBF in the territory of the lenticulostriate artery (region of interest 1). Another region of interest was set in the mirror position to region of interest 1 in the contralateral hemisphere (region of interest 2). Using these two regions of interest, CBF, CBV, and MTT were measured. All patients underwent neurologic and MR imaging follow-up while receiving equivalent medical treatment. RESULTS: Neurologic deterioration after onset was shown in 13 patients (progress group), whereas no neurologic deterioration was shown in the other 13 patients (control group). In the progress group, lacunar infarctions were enlarged on follow-up MR images. The ratio of region of interest 1/region of interest 2 showed significantly lower CBF and higher MTT in the progress group than in the control group. CONCLUSIONS: These results suggest that progressive lacunar infarction in the territory of the lenticulostriate artery could be predicted with a higher MTT ratio (>1.26) and a lower CBF ratio (<0.76) on perfusion CT scans obtained within 24 hr after onset.

Aged↗
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

Preoperative construction of an extracranial arterial shunt for resection of an aortic arch aneurysm with occluded left carotid artery.

A 68-year-old man with aortic arch aneurysm was referred to our department. Preoperative carotid echography and magnetic resonance angiography revealed occlusion of the left internal carotid artery. Single-photon emission computed tomography scanning indicated that cerebral blood flow was decreased and reactivity to acetazolamide was reduced in the left temporal lobe. A successful superficial temporal artery-middle cerebral artery anastomosis was first made by neurosurgeons. A postoperative single-photon emission computed tomography scan showed that cerebral blood flow and reactivity to acetazolamide were remarkably improved. Two months after the anastomosis, the aortic arch aneurysm was successfully repaired.

Acetazolamide↗
PubMed2003

Cell permeable ROS scavengers, Tiron and Tempol, rescue PC12 cell death caused by pyrogallol or hypoxia/reoxygenation.

The role of superoxide anion (O(2)*-) in neuronal cell injury induced by reactive oxygen species (ROS) was examined in PC12 cells using pyrogallol (1,2,3-benzenetrior), a donor to release O(2)*-. Pyrogallol induced PC12 cell death at concentrations, which evidently increased intracellular O(2)*-, as assessed by O(2)(*-)-sensitive fluorescent precursor hydroethidine (HEt). Caspase inhibitors, Z-VAD-FMK and Z-Asp-CH(2)-DCB, failed to protect cells from injury caused by elevation of intracellular O(2)*-, although these inhibitors had effects on hypoxia- or hydrogen peroxide (H(2)O(2))-induced PC12 cell death. Two known O(2)*- scavengers, Tiron (4,5-dihydroxy-1,3-benzenedisulfonic acid) and Tempol (4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxyl) rescued PC12 cells from pyrogallol-induced cell death. Hypoxia/reoxygenation injury of PC12 cells was also blocked by Tiron and Tempol. Further understanding of the underlying mechanism of the protective effects of these radical scavengers reducing intracellular O(2)*- on neuronal cell death may lead to development of new therapeutic treatments for hypoxic/ischemic brain injury.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗
PubMed2003

Hepatocyte growth factor promotes proliferation and neuronal differentiation of neural stem cells from mouse embryos.

Hepatocyte growth factor (HGF), originally cloned as a hepatocyte mitogen, has recently been reported to exhibit neurotrophic activity in addition to being expressed in different parts of the nervous system. At present, the effects of HGF on neural stem cells (NSCs) are not known. In this study, we first report the promoting effect of HGF on the proliferation of neurospheres and neuronal differentiation of NSCs. Medium containing only HGF was capable of inducing neurosphere formation. Addition of HGF to medium containing fibroblast growth factor 2 or epidermal growth factor increased both the size and number of newly formed neurospheres. More neurons were also obtained when HGF was added in differentiation medium. In contrast, neurosphere numbers were reduced after repeated subculture by mechanical dissociation, suggesting that HGF-formed neurospheres comprised predominantly progenitor cells committed to neuronal or glial lines. Together, these results suggest that HGF promotes proliferation of neurospheres and neuronal differentiation of NSCs derived from mouse embyos.

Animals↗
PubMed2003

Fluorescence-guided resection of glioblastoma multiforme by using high-dose fluorescein sodium. Technical note.

The authors have recently performed a fluorescence-guided tumor resection procedure by using high-dose fluorescein sodium without any special surgical microscopes for the intraoperative visualization of glioblastoma multiforme (GBM), and they report on the actual procedure and clinicopathological findings. Thirty-two patients with GBMs underwent tumor resection during which this fluorescence-guided procedure was used. Fluorescein sodium (20 mg/kg) was intravenously injected after dural opening at the craniotomy site. The tumor was stained almost homogeneously yellow and the color was intense enough to be readily perceived for resection. The center of the solid lesion was stained a deep yellow and surrounded by a transition zone that was faintly stained. The colored lesion was clearly distinguishable from the unstained zone outside the GBM, particularly in the white matter. Both the deeply and faintly stained regions included endothelial proliferation and dense tumor cells. In the unstained region, less dense tumor cells were consistently revealed; however, no endothelial proliferation could be seen. Gross-total resection (GTR) was successful in 84.4% of the patients who received an injection of fluorescein sodium, which accounted for 100% of those in whom all the visible yellow color (both the deeply and faintly stained regions) was judged to have been resected during operation. Gross-total resection was performed in 100% of the patients who underwent the fluorescence-guided procedure and assigned to Stage I, a GBM stage in which, as a therapeutic policy, the tumor should be resected as radically as possible. The GTR rates in patients who received fluorescein sodium were significantly higher than those in patients who did not (73 patients with GBMs who underwent tumor resection without the fluorescence-guided procedure). Although the extent of surgery was revealed to be one of the significant and independent prognostic factors for GBM, the fluorescein sodium-guided resection procedure was not a significant or independent prognostic factor in this series. This surgical procedure does not require any special surgical microscopic equipment and is simple, safe, useful, readily accomplished, and universally available for resection of GBMs. Its efficacy simplifies the surgical procedure of navigating the stained lesion from the unstained area to achieve GTR of GBMs, which can be demonstrated on magnetic resonance images.

Adult↗
PubMed2003

In situ detection of O6-methylguanine-DNA methyltransferase messenger RNA in paraffin-embedded human astrocytic tumor tissues by nested in situ RT-PCR is useful in predicting chemotherapy-resistance of tumors.

O6-methylguanine-DNA methyltransferase (MGMT) is an enzyme that interferes with chemotherapeutic effect of alkylating agents. We performed in situ detection of MGMT mRNA utilizing the nested RT-PCR method in tissue sections (nested in situ RT-PCR). We analyzed 34 samples of paraffin-embedded astrocytic tumor tissue sections with this method [3 astrocytomas, 14 anaplastic astrocytomas (AA), and 17 glioblastoma multiformes (GBM)]. Twenty-five cases (73.5% of all cases) were positive for MGMT either with our method or immunohistochemistry (IHC). Moreover, with our method >25% of the cells in the tumor tissue expressed MGMT in contrast to >4% with IHC among the population of MGMT positive cases. Our method was significantly more sensitive than IHC (p=0.0004). The present results suggest that potentially there is a greater population of MGMT positive cells in astrocytic tumor tissues than the one evaluated with IHC. These findings suggest that the >25% of the MGMT positive cells are involved in the interference with the chemotherapeutic effect of alkylating agents. The MGMT expressing cell population was markedly decreased in GBM compared with AA (26.1% vs 62.1%). The main reason for this marked decrease was that MGMT was expressed in only 9 of 17 cases of GBM in contrast to all AA cases that expressed MGMT. This result suggests that there are potentially two populations of GBM on the basis of MGMT expression, in which the negative population might be mainly composed of de novo GBM. Therefore, it is suggested that our method is practically useful to detect any drug resistance gene product with high sensitivity and would provide a chance to evaluate the chemotherapeutic effect of any agents in an individual patient based manner.

Astrocytoma↗
PubMed2002

Increased expression and secretion of r-Gsp protein, rat counterpart of complement C1s precursor, during cyclic AMP-induced differentiation in rat C6 glioma cells.

The gene, termed r-gsp, was originally isolated during identification of differentiation-associated molecules in rat C6 glial cells. Its mRNA expression was markedly increased during cAMP-induced glial cell differentiation. The deduced amino acid sequence of r-gsp was homologous to those of complement C1s precursors of hamsters and humans. In the present study, we raised anti-peptide antibody against r-Gsp protein and analyzed its change during cAMP-induced differentiation. The 90-kDa r-Gsp protein increased time-dependently and reached the maximal level ( approximately 7.6-fold increase) at 24 h in response to dibutyryl cyclic AMP (dbcAMP) and theophylline. Moreover, it was secreted into the medium and then was cleaved to form disulfide-linked fragments, one of which was 30 kDa, similar to C1s, suggesting its processing in the extracellular space. In fact, the partially purified r-Gsp from culture medium was cleaved by active human C1r to form a 30-kDa polypeptide. Moreover, secreted r-Gsp protein cleaved human C4alpha to yield C4alpha' and associated with human serum C1-esterase inhibitor, strongly suggesting that r-Gsp protein is rat C1s. However, in C6 cells overexpressing r-Gsp, their morphology and proliferation rate were similar to those in parent C6 cells. These results suggest that r-Gsp protein could not induce glial differentiation alone, and suggest that r-Gsp protein was secreted as a proenzyme and processed in culture medium. Its possible role in glial cell differentiation will be discussed.

Animals↗
PubMed2002

Failure of B7.1-modified tumor to evoke full activation of CD8+ tumor-infiltrating lymphocytes in the central nervous system: prevention of parental tumor growth in the subcutaneous environment.

OBJECT: It is well known that the central nervous system (CNS) is an immunologically privileged site. To characterize CD8+ tumor-infiltrating lymphocytes (TILs) recovered from the CNS, the authors compared these cells with TILs recovered from subcutaneous tissue by using a B7.1 gene-modified tumor implantation model. METHODS: The authors established a B7.1 gene-modified EL4 murine lymphoma cell line (EL4-B7.1) and implanted the cells into the CNS to observe the duration of tumor-free survival. Although EL4-B7.1 cells were completely rejected in a subcutaneous implantation model, 40% of animals died after the CNS implantation (all animals in which the parent tumor was implanted died within 16 days). Therefore, the authors isolated TILs from each implantation site and analyzed the expressions of activation antigens CD25 and CD69 by performing the anti-CD8 magnetic beads separation method and flow cytometric analysis. After implantation of the parent tumor, there was no difference in the number of TILs from each site (CD25 1.7-3.2%, CD69 21.9-34.3%). After implantation of the B7.1-modified tumor, the CD25-expressing TIL population from the subcutaneous site was 4.68 times higher than that from the CNS site (17.8% compared with 3.8%). Based on these findings, the authors used a mitomycin C-treated EL4-B7.1 subcutaneous vaccination with various protocols. Vaccination before tumor challenge was sufficient to prevent the development of the tumor. For animals with established tumor, the vaccination protocol was able to prolong host survival (p = 0.0053). CONCLUSIONS: The data clearly demonstrate that the CNS environment fails to activate CD8+ TILs fully. These are the first data indicating in detail a difference between CD8+ TILs from the CNS and those from other sites based on a B7.1-modified tumor model.

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↗