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Biomedical subjects

Tetsuya Nagayama

Publications and source records attributed to Tetsuya Nagayama.

8 recordsLinked to original sources
PubMed2006

Primary squamous cell carcinoma of the frontal sinus.

We report a 74-year-old Japanese man with squamous cell carcinoma (SCC) originating in the frontal sinus. It presented as a cutaneous nodule on his right forehead. Magnetic resonance imaging (MRI) revealed invasion of the anterior wall of the ethmoid sinus, the frontal bone, and possibly the meninx by a frontal sinus carcinoma. Despite right fronto craniotomy with en bloc resection followed by two courses of radiation therapy and chemotherapy with 5-fluorouracil and nedaplatin or TS-1 he died of disease-related causes 20 months later. Herein, we present a detailed description of this patient and a review of the published work.

Aged↗
PubMed2005

The environment of increased concentration of docosahexaenoic acid in glioblastoma may suppress the anti-tumor effect of macrophages.

Regarding glioblastoma, there has been controversy over whether a large number of infiltrating macrophages act as anti-tumor effectors or not. It has been exhibited that intratumoral lipid environments have a possible influence on anti-tumor immunity. Necrosis of glioblastoma and non-necrotic tissues of astrocytic tumors were analyzed to compare the amount of free docosahexaenoic acid (DHA) content. The apoptosis inducible effects of DHA on macrophages derived from peripheral blood monocytes and cultured glioma cells were evaluated by flow cytometry. The influence of DHA on the anti-tumor effects of macrophages was assessed at 0, 30, 60, and 90 mM of DHA by (51)Cr releasing assay and MTT assay. The mean concentration of free DHA in necrotic tissues (757.6 mmol/kg) was 5 times higher than that in non-necrotic tissues (147.2 mmol/kg). The DHA concentration of 30 mM induced apoptosis in macrophages, however, glioma cells were not affected even at a DHA concentration of 60 mM. Macrophages pre-exposed to DHA for 24 h decreased the cytotoxicity to U251MG cells as shown by (51)Cr releasing assay. Total viability of co-cultured macrophages and U251MG cells showed an increase at high concentrations of DHA (60 and 90 mM) according to 24 h MTT assay, although each separate culture did not. The DHA concentration in necrosis of glioblastoma was sufficient for macrophages to cause apoptosis and suppress their anti-tumor effects. The results suggest that liberated DHA in necrosis can induce apoptosis in macrophages and inhibit their functions.

Apoptosis↗
PubMed2004

Intractable hiccups as a presenting symptom of cerebellar hemangioblastoma. Case report.

The authors report on a 52-year-old woman with a cerebellar hemangioblastoma who presented with a 2-year history of intractable hiccups. Computerized tomography scans and magnetic resonance images revealed a cerebellar hemangioblastoma with compression of the brainstem at the level of the medulla oblongata. The patient has been free of hiccups and has been neurologically intact since the day after total removal of the tumor. A review of the literature on medullary lesions presenting with intractable hiccups is provided.

Brain Stem↗
PubMed2003

Inducible repair of oxidative DNA lesions in the rat brain after transient focal ischemia and reperfusion.

To determine the role of oxidative DNA damage and repair in brain injury after focal ischemia and reperfusion, the authors investigated DNA base damage and DNA base excision repair (BER) capacity, the predominant repair mechanism for oxidative DNA lesions, in the rat model of temporary middle cerebral artery occlusion. Contents of 8-hydroxyl-2'-deoxyguanosine (8-oxodG) and apurinic/apyrimidinic abasic site (AP site), hallmarks of oxidative DNA damage, were quantitatively measured in nuclear DNA extracts from brains 0.25 to 72 hours after 1 hour of middle cerebral artery occlusion. In parallel to the detection of DNA lesions, the capacity for 8-oxodG- or AP site-dependent DNA repair synthesis was measured in nuclear protein extracts using specific in vitro DNA repair assays. After postischemic reperfusion, the levels of 8-oxodG and AP sites were markedly increased in ischemic tissues. In frontal/parietal cortex, regions that survived ischemia, 8-oxodG and AP sites were efficiently repaired during reperfusion. However, in the caudate, a region that was destined to infarct, the DNA lesions were poorly repaired. In consistent with the patterns of endogenous lesion repair, a markedly induced and long-lasting (at least 72 hours) BER activity was detected in the cortex but not in the caudate after ischemia. The induced BER activity in ischemic cortex was attributed to the upregulation of gene expression and activation of selective BER enzymes, particularly DNA polymerase-beta and OGG1. These results strongly suggest that inducible DNA BER constitutes an important endogenous mechanism that protects brain against ischemia-induced oxidative neuronal injury.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2003

Tumefactive myelinoclastic diffuse sclerosis--case report.

A 6-year-old boy presented with mental disturbance and progressive left hemiparesis. Magnetic resonance imaging demonstrated large intracranial mass lesions with ring-like enhancement. His neurological condition deteriorated rapidly. Open biopsy via craniotomy was performed under the suspicion of tumor. Histological examination showed massive demyelination and axon preservation, but no tumor cells. The diagnosis was myelinoclastic diffuse sclerosis (MDS). He was treated with high-dose methylprednisolone and improved dramatically. MDS is a rare demyelinating disorder of the central nervous system that affects mainly children and may mimic a brain tumor. MDS must be included in the differential diagnosis in young patients with a brain tumor with atypical radiological appearance.

Brain Neoplasms↗
PubMed2002

Two caspase-2 transcripts are expressed in rat hippocampus after global cerebral ischemia.

Caspase family genes play a critical role in the initiation and execution of programmed cell death. Programmed cell death is an important contributor to neuronal loss following cerebral ischemia. We have performed a series of experiments to investigate the role of a specific caspase, caspase-2, in the development of delayed neuronal death following transient global ischemia in the rat. A rat ischemic brain cDNA library was screened, and two splice-variants of caspase-2 mRNA were identified, caspase-2S and caspase-2L, which were highly homologous with the sequences of human and mouse caspase-2S and caspase-2L genes, respectively. RT-PCR demonstrated an increase in expression of both caspase-2S and caspase-2L mRNA at 8, 24 and 72 h of reperfusion after global ischemia. The ratio of the two PCR fragments did not change significantly throughout the time course of reperfusion. Western blot with monoclonal antibody specific to the pro-apoptotic caspase-2L splice variant revealed an increase in procaspase-2 (51 kDa) protein from 4 to 72 h following ischemia compared with sham-operated controls. Furthermore, an approximately 30-kDa cleavage product appeared at 8 h and increased with increasing duration of reperfusion. Thus, caspase-2L is both translated and activated following transient global ischemia. Finally, intraventricular administration of the caspase-2-like inhibitor (VDVAD-FMK) 30 min before induction of ischemia decreased the number of CA1 neurons staining positively for DNA damage (Klenow-labeling assay) and increased the number of healthy-appearing CA1 neurons (cresyl violet) compared with vehicle-treated controls. Taken together, the data suggest that caspase-2 induction and activation are important mediators of delayed neuronal death following transient global ischemia.

Alternative Splicing↗
PubMed2002

Cloning and characterization of rat caspase-9: implications for a role in mediating caspase-3 activation and hippocampal cell death after transient cerebral ischemia.

Delayed hippocampal neurodegeneration after transient global ischemia is mediated, at least in part, through the activation of terminal caspases, particularly caspase-3, and the subsequent proteolytic degradation of critical cellular proteins. Caspase-3 may be activated by the membrane receptor-initiated caspase-8-dependent extrinsic pathway and the mitochondria-initiated caspase-9-dependent intrinsic pathway; however, the precise role of these deduced apoptosis-signaling pathways in activating caspase-3 in ischemic neurons remains elusive. The authors cloned the caspase-9 gene from the rat brain and investigated its potential role in mediating ischemic neuronal death in a rat model of transient global ischemia. Caspase-9 gene expression and protease activity were extremely low in the adult brain, whereas they were developmentally upregulated in newborn rats, especially at postnatal 12 weeks, a finding consistent with the theory of an essential role for caspase-9 in neuronal apoptosis during brain development. After 15-minute transient global ischemia, caspase-9 was overexpressed and proteolytically activated in the hippocampal CA1 neurons at 8 to 72 hours of reperfusion. The temporal profile of caspase-9 activation coincided with that of cytochrome c release and caspase-3 activation, but preceded CA1 neuronal death. Immunoprecipitation experiments revealed that there was enhanced formation of Apaf-1/caspase-9 complex in the hippocampus 8 and 24 hours after ischemia. Furthermore, intracerebral ventricular infusion of the relatively specific caspase-9 inhibitor N-benzyloxycarbonyl-Leu-Glu-His-Asp-fluoro-methylketone before ischemia attenuated caspase-3-like activity and significantly enhanced neuronal survival in the CA1 sector. In contrast, inhibition of caspase-8 activity had no significant effect on caspase-3 activation or neuronal survival. These results suggest that the caspase-9-dependent intrinsic pathway may be the primary mechanism responsible for the activation of caspase-3 in ischemic hippocampal neurons.

Amino Acid Sequence↗