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Biomedical subjects

Yoichi Katayama

Publications and source records attributed to Yoichi Katayama.

At least 37 records · Page 2Linked to original sources
PubMed2005

Cerebral salt wasting in subarachnoid hemorrhage rats: model, mechanism, and tool.

Cerebral salt wasting (CSW) frequently occurs concomitantly with aneurysmal subarachnoid hemorrhage (SAH). CSW induces excessive natriuresis and osmotic diuresis, and reduces total blood volume. As a result, the risk of symptomatic cerebral vasospasm may be elevated. Therefore, it is important to determine the mechanism of CSW. The purpose of this study was to evaluate whether the rat SAH model exhibits CSW and to investigate the relationship between CSW and natriuretic peptides. A SAH model was produced in 24 rats by perforating a cerebral artery with a nylon thread up through the common carotid artery. To evaluate CSW, urine was cumulatively collected from SAH onset to 12 hours and sodium (Na) excretion was analyzed. Body weight and hematocrit were analyzed before and after SAH onset. Concentrations of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in plasma were also analyzed. Urine volume and total Na excretion of SAH rats were significantly higher than those of sham rats (p<0.05). Body weight of SAH rats significantly decreased and hematocrit significantly increased (p < 0.05). ANP concentration was significantly decreased in SAH rats (p<0.05). However, BNP concentrations did not change. This study demonstrated for the first time that a rat SAH model exhibited CSW. It was suggested that the cause of CSW was neither ANP nor BNP. In addition, this rat SAH model will be useful for study of CSW after SAH.

Animals↗
PubMed2005

Three-dimensional display with a long viewing distance by use of integral photography.

We developed a technique of three-dimensional (3-D) display for distant viewing of a 3-D image without the need for special glasses. The photobased integral photography (IP) method allows precise 3-D images to be displayed at long viewing distances without any influence from deviated or distorted lenses in a lens array. We calculate elemental images from a referential viewing area for each lens and project the corresponding result images to photographic film through each lens. We succeed in creating an image display that appears to have three dimensionality even when viewed from a distance, with an image depth of 5.7 m or more in front of the display and 3.5 m or more behind the display. To the best of our knowledge, the long-distance IP display presented here is technically unique because it is the first report of generation of an image with such a long viewing distance.

Data Display↗
PubMed2005

Promoter hypermethylation of mismatch repair gene hMLH1 predicts the clinical response of malignant astrocytomas to nitrosourea.

PURPOSE: In certain types of human cancers, transcriptional inactivation of hMLH1 by promoter hypermethylation plays a causal role in the loss of mismatch repair functions that modulate cytotoxic pathways in response to DNA-damaging agents. The aim of the present study was to investigate the role of promoter methylation of the hMLH1 gene in malignant astrocytomas. EXPERIMENTAL DESIGN: We examined the hMLH1 promoter methylation in a homogeneous cohort of patients with 41 malignant astrocytomas treated by 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-2(2-chloroethyl)-3-nitrosourea chemotherapy in combination with radiation and interferon therapy, and assessed the correlation of such methylation with clinical outcome. RESULTS: hMLH1 promoter methylation was found in 6 (15%) of the 41 newly diagnosed malignant astrocytomas. Hypermethylation of the hMLH1 promoter corresponded closely with a loss of immunohistochemical staining for hMLH1 protein (P = 0.0013). Patients with hMLH1-methylated tumors displayed a greater chance of responding to adjuvant therapy as compared with those with hMLH1-unmethylated tumors (P = 0.0150). The presence of hMLH1 hypermethylation was significantly associated with a longer progression-free survival on both univariate analysis (P = 0.0340) and multivariate analysis (P = 0.0161). CONCLUSIONS: The present study identified hMLH1 methylation status as a predictor of the clinical response of malignant astrocytomas to chloroethylnitrosourea-based adjuvant therapy. The findings obtained suggest that determination of the methylation status of hMLH1 could provide a potential basis for designing rational chemotherapeutic strategies, as well as for predicting prognosis.

Adaptor Proteins, Signal Transducing↗
PubMed2005

O6-methylguanine-DNA methyltransferase methylation and TP53 mutation in malignant astrocytomas and their relationships with clinical course.

Epigenetic silencing of O(6)-methylguanine-DNA methyltransferase (MGMT) by promoter methylation can confer cancer cells with an increased sensitivity to alkylating chemotherapeutic agents and a higher susceptibility to TP53 transition mutations. The aim of our study was to assess the correlation of promoter methylation of the MGMT gene with TP53 mutations and the clinical characteristics of malignant astrocytomas. We analyzed the MGMT promoter methylation and TP53 mutations in 45 malignant astrocytomas (16 anaplastic astrocytomas and 29 glioblastomas multiforme) treated prospectively with 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-2(2-chloroethyl)-3-nitrosourea, interferon-beta and radiation therapy, and evaluated their clinical usefulness. MGMT promoter methylation was found in 17 (38%) of the 45 newly diagnosed malignant astrocytomas. A clear trend existed between MGMT methylation and G:C to A:T transition mutations of TP53 (p = 0.0596). Patients with MGMT-methylated tumors displayed a greater chance of responding to adjuvant therapy as compared with those with MGMT-unmethylated tumors (p = 0.0393). TP53 mutation was not significantly associated with the clinical response (p = 0.1310). While neither MGMT methylation nor TP53 mutation had a significant effect on prognosis of the whole population, the presence of MGMT methylation emerged as a significant predictor of a longer survival when exclusively analyzing 29 patients with glioblastomas multiforme. These findings highlight the importance of MGMT methylation as a specific predictive factor for responsiveness to nitrosourea chemotherapy.

Adult↗
PubMed2005

Difference in surgical strategies between thalamotomy and thalamic deep brain stimulation for tremor control.

Stereotactic targeting strategies differ between thalamotomy and thalamic deep brain stimulation (DBS) for tremor control. In thalamotomy, a minimal radiofrequency lesion created within the lateral portion of the nucleus ventralis intermedius (Vim) often affords the best control of parkinsonian tremor, supporting the assumption that there is a concentrated cluster of cells within this area which is responsible for tremor. However, this assumption may not always be true; such neural elements sometimes appear to spread out across wide areas. Cells with tremor-frequency activity are widely distributed over the areas extending from the Vim to the nuclei ventralis oralis posterior and anterior (Vop and Voa). All of these cells appear to be more or less involved in tremor generation, especially in patients with essential tremor and post-stroke tremor. In contrast to radiofrequency lesions for thalamotomy, electrodes for DBS can be arranged in such a way that wide areas can be stimulated, if necessary. For this purpose, it is critically important to determine optimal placement and orientation of DBS leads for arranging the electrodes to yield maximal benefits in patients with tremor.

Deep Brain Stimulation↗
PubMed2005

Angiogenesis of glioma: evaluation of ultrastructural characteristics of microvessels and tubular bodies (Weibel-Palade) in endothelial cells and immunohistochemical findings with VEGF and p53 protein.

Capillary endothelial proliferation is often a prominent feature of malignant gliomas. The understanding of structural and functional characteristics of the vascular microenvironment in gliomas is essential for the design of future therapeutic strategies against this tumor. Electron microscopic analysis of the capillary endothelial proliferation in malignant gliomas indicated that the complex vascular structures within the tumor were composed essentially of immature capillaries. Immature capillaries had a narrow slitlike lumen composed of endothelial cells with their high nuclear : cytoplasmic ratio and the relative paucity of organelles. They resembled capillary buds seen in normal repair tissue. Immature microvessels caused by angiogenesis were found more frequently in marginal zone of the tumors with increased microvessels. The tubular body was an organelle observed in vascular endothelial cells and was used frequently as a marker of the endothelial cell. Tubular bodies were evaluated by quantitative measurement of the mean percent (%) ratio of the number of endothelial cells with tubular bodies to all endothelial cells in microvessels of tumors. In glioblastomas it yielded a value of 32.4% in the margin, about two times as high as that in the center of the tumors. However, it was lower in all locations of astrocytomas. Tubular bodies in endothelial cells could be increased in proportion to neovascularization, and they might serve as a marker for increasing microvessels in astrocytic tumors. Tumor angiogenesis may be regulated by growth factors with angiogenic activities that are secreted by tumor cells. Vascular endothelial growth factor (VEGF) may play a critical role in the regulation of vascular endothelial proliferation. We found that 86% of 29 glioblastomas and 79% of 14 anaplastic astrocytomas demonstrated immunoreactivity for VEGF in their tumor cells. There tended to be a correlation between VEGF and vascularity. A correlation existed between the grade of immunoreactivity for VEGF and the grade of p53 protein expression in the malignant gliomas. However, the MIB-1 indices did not increase in correlation with increase in the extent of immunoreactivity for VEGF.

Brain↗
PubMed2005

Human interferon beta, nimustine hydrochloride, and radiation therapy in the treatment of newly diagnosed malignant astrocytomas.

Previous investigators have reported encouraging results for malignant gliomas treated using a combination of human interferon beta (IFN-beta) with nimustine hydrochloride (ACNU) and radiation therapy (termed IAR therapy). This study was undertaken to examine further the efficacy of the IAR regimen followed by maintenance therapy with IFN-beta and ACNU in patients with newly diagnosed malignant astrocytomas. Fifty-eight patients were enrolled onto the trial. IFN-beta (2 x 10(6) IU/m(2)/day x 5 days/week for 8 consecutive weeks) and ACNU (80 mg/m(2) on days 1 and 36) were administered intravenously concomitant with radiation therapy followed by IFN-beta (every 2 weeks) and ACNU (every 6 weeks). Of 33 patients assessable for a response, 11 responded (33%), with 4 complete responses. The estimated median overall survival (OS) was 16 months, with values of 58 and 13 months for anaplastic astrocytoma (AA) and glioblastoma (GB) patients, respectively. The overall progression free survival (PFS) was 11 months, with values of 31 and 7 months for AA and GB patients, respectively. The IAR therapy was safe and well tolerated. Based on a statistical analysis of the factors that affected the PFS and OS, histologic grade, postoperative Karnofsky performance scale (KPS), and extent of surgery were identified as independent predictors. The postoperative KPS stood out as the most powerful prognostic factor, which was also the best predictor for the response to IAR therapy. Our findings suggest a possible benefit for IAR therapy followed by maintenance therapy mainly in AA. In addition, they emphasize the importance of a preserved KPS after cytoreductive surgery, which could produce a potential benefit for adjuvant therapy and could ultimately lead to a prolonged survival.

Adult↗
PubMed2005

Aberrant TP53 protein accumulation in the neuronal component of ganglioglioma.

Gangliogliomas are characterized by their different phenotypic composition of ganglion cells and glial cells. In contrast to the glial cells that are capable of mitotic activity, the ganglion cells are generally considered to lack a neoplastic nature. The authors report here the first unequivocal case of a ganglioglioma harboring aberrant TP53 product that was expressed predominantly in the neuronal component. GeneChip TP53 assay revealed a point mutation resulting in an exchange of amino acid. This case suggests that ganglion cells can participate in the neoplastic process of gangliogliomas.

Brain Neoplasms↗
PubMed2005

Therapeutic implications of interferon regulatory factor (IRF)-1 and IRF-2 in diffusely infiltrating astrocytomas (DIA): response to interferon (IFN)-beta in glioblastoma cells and prognostic value for DIA.

The precise mechanisms governing the direct effect of IFN-beta, including apoptosis induction, are not yet fully understood. To gain a better insight into these mechanisms, we investigated the signaling pathways focusing particularly on interferon regulatory factor 1 (IRF-1) and IRF-2 in glioblastoma cell lines. Furthermore, we attempted to determine whether or not IRF-1 and IRF-2 act as additional prognostic indicators in diffusely infiltrating astrocytomas (DIA). We first assessed the cytotoxic effects of IFN-beta based on a cell growth study and modified MTT assay, and then quantified the apoptosis using a sandwich enzyme immunoassay following IFN-beta treatment in the cell lines, U-87MG, T98G, and A-172. Subsequently, we carried out an analysis of apoptosis-related molecules as evaluated by densitometric analysis of Western blots, focusing on IRF-1 and IRF-2, and two major initiator caspases, caspase-8 and caspase-9. Furthermore, we assessed the expression of type I IFN receptor, IRF-1, and IRF-2 using immunohistochemical techniques in 63 DIA (15 of WHO grade II, 18 of grade III, and 30 of grade IV), and analyzed their impact on prognosis. An increase in apoptosis was apparent after 48 h of IFN-beta treatment (1 x 10(4) IU/ml) in T98G but not in U-87MG or A-172. IFN-beta treatment for 6 h significantly enhanced the expression of IRF-1 in all three cell lines. However, an enhanced expression of IRF-2 was observed only in the not-most-sensitive, non-apoptosis-induced U-87MG and A-172. While minimal processing of caspase-8 was noted in the three cell lines throughout the experiment, caspase-9 activation was observed in the apoptosis-detected T98G after 48 h of treatment, as indicated by a 1.33-fold increase (P=0.037). On the other hand, the IRF-1 LI and IRF-1/IRF-2 LI ratio were greater in low-grade DAI, and were negatively correlated with the histopathological grade in DIA (P=0.017 and P=0.001, respectively). Furthermore, the IRF-1/IRF-2 LI ratio was negatively correlated with the MIB-1 LI in DIA (P=0.004), and represented an independent and most powerful determinant of overall survival compared to other conventional prognostic factors (P=0.018). However, the relation was not statistically significant when only patients with high-grade DIA were assessed. Our findings suggest that up-regulation of IRF-1 and IRF-2 might be an important determinant of susceptibility to IFN-beta mediated cytotoxicity including apoptosis. Furthermore, the IRF-1/IRF-2 LI ratio may reflect the proliferative state of DIA and constitute an important prognostic marker in DIA. Thus, IRF-1 and IRF-2 could represent one of the therapeutic target sites for the regulation of cell growth in DIA.

Adult↗
PubMed2005

Application of multichannel near-infrared spectroscopic topography to physiological monitoring of the cortex during cortical mapping: technical case report.

BACKGROUND: Cortical stimulation via a subdural grid electrode (SGE) is one of the most reliable methods for identifying eloquent areas before surgery. However, the physiological conditions of the cortex during stimulation cannot be monitored electrophysiologically because of electrical artifacts. In the present case, we tested whether or not multichannel near-infrared spectroscopy (NIRS) topography, a noninvasive optical imaging technique, is applicable for monitoring the physiological conditions of the stimulated cortex. CASE DESCRIPTION: The patient (a 27-year-old right-handed man) suffered from glioma in the left frontal lobe. For preoperative cortical mapping, SGEs were implanted over the left motor cortex before tumor resection. Employing NIRS topography, we undertook 2 dimensional imaging of the changes in oxyhemoglobin (Oxy-Hb) and deoxyhemoglobin (Deoxy-Hb) concentration during electrical stimulation. Five-hertz stimulation with 5 mA at the left-hand area produced a localized increase in Oxy-Hb and a decrease in Deoxy-Hb, associated with slight twitching of the right hand. In contrast, 50-Hz stimulation produced significant increases in both Oxy-Hb and Deoxy-Hb at the stimulation site, and the area with such cerebral blood oxygenation (CBO) changes propagated beyond the hand area associated with prominent muscle contractions of the right upper extremity, suggesting that 50-Hz stimulation caused epileptic discharge. CONCLUSION: Near-infrared spectroscopy topography may represent a useful tool for imaging the degree and extent of the physiological effects of electrical stimulation on the cortex, and permits safe and accurate cortical mapping.

Adult↗
PubMed2005

The p15(INK4b)/p16(INK4a)/RB1 pathway is frequently deregulated in human pituitary adenomas.

Pituitary adenomas are common benign intracranial neoplasms. However, their tumorigenesis is not yet clearly defined. Inactivation of genes involved in the negative cell-cycle regulatory p15(INK4b) - p16(INK4a) -cyclin D/CDK4-RB1-mediated pathway (RB1 pathway) is one of the most common and important mechanisms in the growth advantage of tumor cells. Recently, much attention has been focused on the importance of alternative mechanisms of gene inactivation, particularly promoter hypermethylation in the transcriptional silencing of such tumor-suppressor genes. Based on the rare occurrence of inactivation by gene mutations and deletions of the RB1 pathway in pituitary adenomas, we investigated the deregulation of the RB1 pathway in 42 sporadic human pituitary adenomas, especially focusing on the methylation status of this pathway as determined by a methylation-specific polymerase chain reaction assay. Homozygous deletion of the p15(INK4b) or p16(INK4a) gene was detected in one adenoma each. Amplification of the CDK4 gene was not apparent in any of the pituitary adenomas presently examined. Promoter hypermethylation of the p15(INK4b), p16(INK4a), and RB1 genes was detected in 15 (35.7%), 30 (71.4%), and 12 (28.6%) of the adenomas, respectively. Promoter hypermethylation of the p15(INK4b) gene coincided with p16(INK4a) alteration and/or RB1 methylation, whereas p16(INK4a) and RB1 methylations tended to be mutually exclusive (p = 0.019). Thus, the vast majority of the adenomas (38 of 42, 90.5%) displayed alterations of the RB1 pathway. None of the clinicopathologic features, including the proliferation cell index, was significantly correlated with any particular methylation status. Our results suggest that inactivation of the RB1 pathway may play a causal role in pituitary tumorigenesis, with hypermethylation of the p16(INK4a) gene being the most common deregulation, and further provide evidence that RB1 and p16(INK4a) methylations tend to be mutually exclusive but occasionally coincide with p15(INK4b) methylation.

Adenoma↗
PubMed2005

Tissue plasminogen activator extravasated through the cerebral vessels: evaluation using a rat thromboembolic stroke model.

Neurotoxic effects of endogenous tissue plasminogen activator (tPA) have recently been reported. Employing a rat model of thromboembolic stroke, we evaluated the extent and degree of extravasation of exogenous tPA administered for the purpose of fibrinolysis. In a thromboembolic model using Sprague-Dawley rats, focal cerebral ischemia was induced at the territory of the middle cerebral artery (MCA). Early reperfusion was induced by administering tPA (10 mg/kg) intravenously at 30 minutes after the onset of ischemia. Extravasated tPA was evaluated by immunohistochemistry, and the concentration of tPA in the brain tissue was quantified by enzyme-linked immunosorbent assay methods. The integrity of the blood-brain barrier (BBB) was examined electronmicroscopically. In a thread model of transient ischemia, reperfusion was induced without tPA administration at 30 minutes or 2 hours after the onset of ischemia, and the tPA content of the brain was quantified. In the rats with thromboembolic stroke, extravasation of tPA was observed at the territory of the MCA. Both the endogenous and exogenous tPA contents were 3.5 +/- 1.6 ng/ml of homogenized brain in saline. Electronmicroscopically, mild ischemic changes were observed, although the integrity of the BBB was preserved. In the thread model rats, the endogenous tPA contents of the ischemic hemisphere were 0.9 +/- 0.1 and 1.0 +/- 0.2 ng/ml in the 30-minute and 2-hour ischemia groups, respectively, and were significantly lower than the tPA contents in the thromboembolic stroke rats (p<0.01). The present findings indicate that significant extravasation of exogenous tPA occurs through the cerebral vessels even though early reperfusion is induced.

Animals↗
PubMed2005

Attenuation of extravasation of tissue plasminogen activator by the free radical scavenger, edaravone: evaluation in a rat thromboembolic stroke model.

OBJECTIVES AND METHODS: Deleterious effects of tissue plasminogen activator (tPA) have been described recently in experimental studies. For example, tPA can aggravate ischemic neuronal damage through its proteolytic activity. The present study was undertaken to examine whether or not the free radical scavenger, edaravone, could prevent the extravasation of tPA administered for the purpose of fibrinolysis in a rat model of thromboembolic stroke. RESULTS: Significant amounts of tPA were extravasated through the cerebral vessels even when early recanalization was induced by administering tPA at 30 minutes after the onset of schema. Edaravone significantly attenuated such extravasation of tPA. CONCLUSION: In acute ischemic stroke patients, combination therapy using tPA with edaravone appears to be a reasonable strategy for diminishing the negative effects of tPA.

Analysis of Variance↗
PubMed2005

Expression of hard alpha-keratins in pilomatrixoma, craniopharyngioma, and calcifying odontogenic cyst.

To examine the properties of shadow and ghost cells, 3 kinds of antibodies were raised against human hair proteins and their immunoreactivity was examined in tumors expressing those cells: pilomatrixoma, 14 cases; craniopharyngioma, 17 cases; and calcifying odontogenic cyst (COC), 14 cases. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analyses demonstrated that 2 polyclonal antibodies, PA-HP1 and PA-HP 2, reacted strongly with type I acidic and type II neutral/basic hard alpha-keratins. The other monoclonal antibody, MA-HP1, reacted with type II neutral/basic hard alpha-keratins. Immunohistochemical examination revealed that all 3 antibodies reacted only with the hair shaft in sections of normal skin and dermoid cyst. In all pilomatrixoma cases, 3 antibodies reacted with the cytoplasm of transitional and shadow cells but not with that of basophilic cells. Positive reactions were found only in shadow cells of all 13 adamantinomatous craniopharyngiomas. In all COCs, the antibodies reacted only with ghost cells, not with other epithelial components. Immunoreactivity for phosphothreonine, detected in hard alpha-keratins, also was found in transitional, shadow, and ghost cells. The appearance of shadow or ghost cells might represent differentiation into hair in these 3 kinds of tumors.

Animals↗
PubMed2005

Sagittal magnetic resonance imaging of intramural hematoma from non-traumatic dissection of the anterior cerebral artery. Case report.

A 46-year-old woman presented with non-traumatic anterior cerebral artery dissection manifesting as sudden onset of headache and motor weakness of the right lower limb. Angiography revealed luminal narrowing of the left anterior cerebral artery from the A(3) portion to the distal portion. Sagittal T(1)-weighted magnetic resonance imaging showed hyperintensity due to an intramural hematoma around the flow void signal of the affected anterior cerebral artery. Sagittal magnetic resonance imaging should be performed in suspected cases of anterior cerebral artery dissection to detect the diagnostic finding of intramural hematoma.

Aortic Dissection↗
PubMed2005

Traumatic cervical internal carotid artery occlusion in an infant. Case report.

A 10-month-old boy presented with traumatic internal carotid artery (ICA) occlusion caused by blunt injury after falling from a baby carrier attached to a standing bicycle. Physical examination found bruises on the scalp in the right temporal region and the right shoulder, but no wound in the neck. Chest radiography showed a right clavicular fracture. He developed left hemiparesis at 19 hours after the injury. Computed tomography revealed cerebral infarct and angiography showed cervical ICA occlusion. Conservative therapy with hemodilution was given under a diagnosis of cervical ICA occlusion caused by extension and rotational head injury. Traumatic cervical ICA occlusion due to blunt injury is not uncommon in adults, but extremely rare in infants. We would like to emphasize the dangers of leaving a baby unattended in a carrier attached to a standing bicycle.

Accidental Falls↗
PubMed2004

Long-term prognosis of hemangioblastomas of the central nervous system: clinical and immunohistochemical study in relation to recurrence.

The long-term prognosis and immunohistochemical findings for the expression of VEGF (vascular endothelial growth factor), p53 protein, and proliferative potential with MIB-1 were evaluated in six patients with VHL (von Hippel-Lindau) disease and seven patients with sporadic hemangioblastomas in relation to recurrent or new central nervous system (CNS) hemangioblastomas following treatment. Sporadic CNS hemangioblastomas were treated by total removal, and they demonstrated a good long-term prognosis without neurological deficits and no recurrence. However, even if total removal of the CNS hemangioblastomas in patients with VHL disease was performed initially, new lesions, consisting of small multiple hemangioblastomas, recurred in areas remote from the primary region in three of four patients during long-term follow-up. Such newly developed hemangioblastomas in patients with VHL disease could reflect the biological multipotentiality of CNS hemangioblastomas that were not detected during the initial operation. All of the hemangioblastomas displayed extensive overexpression of VEGF protein. The immunohistochemical findings for VEGF protein, p53 protein, and MIB-1 did not differ significantly between the sporadic and VHL disease-associated hemangioblastomas. In conclusion, since patients with VHL disease are at risk of developing new lesions, the management of hemangioblastomas in patients with VHL disease represents a more prolonged and difficult task.

Adolescent↗