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Biomedical subjects

H Kato

Publications and source records attributed to H Kato.

At least 433 records · Page 24Linked to original sources
PubMed2000

Decreased cerebrospinal fluid levels of beta-phenylethylamine in patients with Rett syndrome.

To clarify the mechanism of brain impairment in Rett syndrome, we measured the cerebrospinal fluid levels of beta-phenylethylamine (PEA) in 17 patients with Rett syndrome. Findings were compared with those obtained in age-matched controls and diseased controls. The cerebrospinal fluid level of PEA was significantly lower in patients with Rett syndrome than in the controls (31% of control values). The alteration in the cerebrospinal fluid level of PEA may reflect dopamine system impairment in Rett syndrome.

Adult↗
PubMed2000

Injury-specific expression of activating transcription factor-3 in retinal ganglion cells and its colocalized expression with phosphorylated c-Jun.

PURPOSE: To ascribe activating transcription factor (ATF)-3 as a specifically induced transcription factor after ON injury and to describe its putative role as a modulator of c-Jun transactivation. METHODS: The adult rat optic nerve was crushed intraorbitally, and expression profiles of ATF-3, ATF-2, and phosphorylated c-Jun (p-c-Jun) were examined by immunohistochemistry and ISH. Western blot analysis for ATF-3 and -2 were also performed. Furthermore, colocalized detection of c-Jun mRNA with ATF-2 or -3 was attempted with a combined method of simultaneous immunohistochemistry and in situ hybridization. RESULTS: In response to optic nerve injury, substantial expression of ATF-3 as well as that of p-c-Jun was observed in the retinal ganglion cells, whereas no expression of ATF-3 was seen in other noninjured retinal cells. In contrast, ATF-2 was normally expressed abundantly in both retinal ganglion cells and displaced amacrine cells, but expression dropped in retinal ganglion cells after nerve injury. The expression profiles of ATF-2 and -3 after optic nerve injury were confirmed by Western blot analysis. A higher degree of colocalization was observed for ATF-3 and c-Jun than the modest codetection for ATF-2 and c-Jun. CONCLUSIONS: The transcription factor ATF-3 is specifically induced upon optic nerve injury and colocalizes with p-c-Jun in surviving ganglion cells. These findings suggest that both ATF-3 and c-Jun are crucial to trigger various transcriptional responses and may act synergistically during the survival phase of the optic nerve in the injury model.

Activating Transcription Factor 2↗
PubMed2000

[Preoperative photodynamic therapy for lung cancer].

In Japan, photodynamic therapy (PDT) for locally superficial hilar lung cancer is common and its indications have already been determined. In order to improve the survival rate for lung cancer patients, it is necessary to increase the number of operable cases and preserve pulmonary function, and it thus would be beneficial to reduce the extent of resection. In our institution, preoperative PDT has been employed as one option to reduce the extent of resection. Nineteen patients who were initially planned to undergo pneumonectomy underwent successful lobectomy. For multiple primary lung cancer lesions, combined use of PDT was carried out in 29 cases. For early-stage lung cancer, PDT was performed and for advanced lesions surgery was selected. These new options may contribute to the management of advanced lung cancer.

Aged↗
PubMed2000

Complement mediated vascular endothelial injury in rheumatoid nodules: a histopathological and immunohistochemical study.

OBJECTIVE: To evaluate morphologically and immunohistochemically the role of IgM rheumatoid factor (RF) immune complexes and complement activation in rheumatoid nodule vascular injury, a typical extraarticular manifestation of rheumatoid arthritis. METHODS: Histological features such as cellular infiltration, endothelial alteration, fibrinoid degeneration, and basement membrane alterations were observed in the small vessels in rheumatoid nodules. An immunohistochemical study was also carried out. RESULTS: Distinct colocalization of IgM RF and terminal complement complexes (TCC: C5b-9) was observed on the luminal surface in some of the damaged endothelial cells. Immuno-electron microscopy revealed endothelial vesiculation, typical of the in vitro protective mechanism against complement attack, with deposition of not only TCC but also IgM RF. Most TCC positive endothelial cells simultaneously expressed the major complement regulatory factor, CD59. CONCLUSION: These data suggest that, in rheumatoid nodules, vascular injury mediated by complement activation involves the assembly of IgM RF on the endothelial cell surface.

Aged↗
PubMed2000

The usefulness of rabbits as an animal model for the neuropathological assessment of neurotoxicity following the administration of vincristine.

Vincristine is an effective chemotherapeutic agent for a variety of human neoplasms, but has dose-limiting neurotoxicity. Since laboratory rodents have proven to be refractive in such neurotoxicological studies, we conducted a neuropathological and behavioral assessment in rabbits treated with vincristine at doses known to be both chemotherapeutically effective and neurotoxic in humans. Rabbits (Kbl: NZW) were given vincristine intravenously at doses of 0 (saline), 200, 250 or 300 microg/kg once a week for 6 weeks, 500 microg/kg once a week for 3 weeks, or a single 500 microg/kg administration. Detailed periodic neurologic examination revealed ataxia in a few animals. Pathologically, axonal injury progressing to fiber degeneration was observed in sensory tracts such as the posterior spinocerebellar tract and posterior funiculus, and in peripheral nerves after treatment with vincristine. These alterations were observed even after a single dose of 500 microg/kg. In the group given weekly doses of 500 microg/kg, neuronal chromatolysis was also found in the spinal cord. These results suggest the rabbit is responsive to vincristine neurotoxicity producing a predominantly sensory neuropathy and confirming earlier studies.

Animals↗
PubMed2000

Schedule dependency of paclitaxel-induced neuropathy in mice: a morphological study.

Paclitaxel, which is known to induce peripheral neuropathy in humans, was administered to BDF1 mice, and a neuropathological examination was then conducted. Paclitaxel was administered at a dose of 30 mg/kg once or several times at different intervals, 3 times, every 3 hours (q3hx3), every day (q1dx3), every 2 days (q2dx3) and 4 times, once a week (q7dx4). The spinal cord, spinal ganglion and peripheral nerves (sciatic and tibial) were then processed for neuropathological examination following perfusion of the anesthetized mice. The effect on the peripheral nerves was evaluated by counting the number of abnormal nerve fibers in the preparations of teased nerve fibers and in the epoxy resin 1-microm-thick sections. The drug-induced degeneration, such as axonal and myelin fragmentations and phagocytosis in the nerve fibers, was detected in the dorsal funiculus, the dorsal spinal roots and the peripheral nerves (sciatic and tibial). No drug-related degeneration was observed in the motor neurons in the spinal cord nor in the ventral spinal roots. The single treatment did not induce any changes. The severity of the degeneration was as follows: q2dx3>q1dx3>>q3hx3 and q7dx4. The degeneration in the mice treated on q3hx3 and q7dx4 was very slight, but it was clear that paclitaxel also induced degeneration on these schedules. These results suggest that paclitaxel induces a predominantly sensory neuropathy in mice and the severity is obviously dependent on the treatment schedule.

Action Potentials↗
PubMed2000

Functional evaluation of p53 and PTEN gene mutations in gliomas.

We screened mutations of two major tumor suppressor genes, p53 and PTEN, in 66 human brain tumors using a yeast-based functional assay and cDNA-based direct sequencing, respectively. The frequency of p53 mutations was 28.8% (19 of 66) and was higher in anaplastic astrocytoma (9 of 14, 64.3%,) than in glioblastoma multiforme (GBM; 7 of 27, 25.9%,), supporting previous speculation that there are at least two genetic pathways leading to GBM, a de novo pathway without p53 mutation and a "progressive" pathway with p53 mutation. PTEN mutation was observed in 8 of 64 tumors (12.5%), mainly GBMs (7 of 26, 26.9%), both with and without p53 mutation. These results suggest that mutation of the PTEN gene is a later event than that of the p53 gene in glioma progression and is associated with both the genetic pathways. All of the detected PTEN missense mutations and an in-frame small deletion inactivated PTEN phosphoinositide phosphatase activity in vitro. Because the tumors containing PTEN mutations also showed loss of heterozygosity in the chromosome 10q23 region flanking the PTEN gene, our data clearly indicate that inactivation of both PTEN alleles occurs in a subset of high-grade gliomas, therefore confirming the previous idea that PTEN acts as a tumor suppressor gene.

Adolescent↗
PubMed2000

[Postoperative adjuvant therapies for esophageal carcinoma].

Recent studies have focused on biochemical modulation with the combined use of CDDP and 5-FU for esophageal cancer. The combination of chemo- and radiotherapy is one of the most effective regimens for esophageal carcinoma. This combination therapy led to complete clinical remission in up to 30% of the cases in a prospective randomized study. We introduce many trials about postoperative adjuvant therapy after surgical treatment for esophageal carcinoma. The development and investigation of more effective chemotherapy regimens, as well as precise assessments of the response to preoperative treatment, is the challenge for randomized trials in the future.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2000

[Correlation between expression of metastasis-related genes and lymph node metastasis in testicular cancer].

To investigate the factors related to lymph node metastasis of testicular germ cell tumors, we first established a seminoma orthotopic model with lymph node metastasis in SCID mice by inoculating small fragments from subcutaneous xenografts. Second, we compared the expression patterns of metastasis-related genes of the seminoma xenografts and of the TCam-2 cells which were established as a seminoma cell line from a primary testicular seminoma. Third, we immunohistochemically analyzed human germ cell tumors (25 seminomas, 17 nonseminomas) using monoclonal antibodies to CD34, VEGF, VEGF-C, Flt-4, MMP-2 and E-cadherin. Testicular seminoma xenografts grew in 32/32 (100%) of the inoculated mice, of which 15 (47%) developed macroscopic metastasis to the renal hilar lymph node. Circulating tumor cells were detectable by using a PCR assay for the human beta-globin gene in 25/32 (78%) mice, although metastatic foci were not histologically evident in the visceral organs, including lungs, liver, kidneys and spleen. This may reflect the lymphophilic characteristics of the seminoma cells used. Regarding mRNA expression of metastasis-related genes, an increased expression of MMP-2 and VEGF compared with that in the s.c. xenografts was demonstrated by RT-PCR assay in the testicular seminoma xenografts. In addition, uPAR, MMP-1, MMP-2, MT1-MMP and MT3-MMP showed a a stronger expression and PAI-2 a weaker expression in the seminoma xenografts than did TCam-2 cells. These results suggest a higher metastatic potential of the seminoma xenografts, especially testicular xenografts, as compared with TCam-2 cells. In the immunohistochemical study, a significant correlation was found between MMP-2 expression and lymph node metastasis, which is compatible with the results for the metastasis-related gene expression from the seminoma xenografts.

Animals↗
PubMed2000

[Vascular and metabolic reserve in a case of hypoplasia of bilateral internal carotid arteries].

We report a 64-year-old right-handed man who presented with a hypoplasia of bilateral internal carotid arteries (ICAs). The patient complained of a vertigo and was diagnosed as having a benign paroxysmal positional vertigo. Upon neurological examination, he was completely free from neurological deficits. MR angiogram revealed an occlusion of both ICAs. On conventional angiogram, the right ICA was occluded about 3 cm distal from its origin, and the left ICA was occluded at the precavernous portion. There was an abundant collateral blood flow to the frontal, temporal and parietal lobes through the posterior communicating arteries. Both carotid canals were hypoplastic on 3D-CT. The patient was then diagnosed as having a hypoplasia of both ICAs. Using a positron emission tomography (PET), cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and vascular transit time (VTT) were measured during resting state, and the vascular reactivities to carbon dioxide inhalation (VRCO2), and to the intravenous administration of Acetazolamide (VRACZ) were also evaluated. There was no global or focal reduction in CBF and VTT was within normal limit, whereas a global reduction of CMRO2 caused mild decrease in OEF. Moreover, VRACZ was significantly decreased and an intracerebral steal phenomenon was observed in the parietal cortical areas, whereas VRCO2 was preserved. The discrepancy between VRACZ and VRCO2 observed could be related to the differences in the mechanisms underlying the vasodilating effects of carbon dioxide and ACZ.

Arterial Occlusive Diseases↗
PubMed1999

Cloning and characterization of a novel human gene encoding a zinc finger protein with 25 fingers.

This study reports cloning and characterization of a human cDNA encoding a novel human zinc finger protein, ZFD25. ZFD25 cDNA is 6118 bp long and has an open reading frame of 2352 bp that encodes a 783 amino acid protein with 25 C2H2-type zinc fingers. The ZFD25 cDNA also contains a region with high sequence similarity to the Krüppel-associated box A and B domain in the 5'-untranslated region, suggesting that ZFD25 belongs to the Krüppel-associated box zinc finger protein family. The ZFD25 gene was localized to chromosome 7q11.2. Northern blot analysis showed that ZFD25 was expressed in a wide range of human organs. In cultured endothelial cells, the mRNA level was decreased upon serum starvation.

Amino Acid Sequence↗
PubMed1999

Effects of the 5-HT(3) receptor antagonist ondansetron on the ketamine- and dizocilpine-induced place preferences in mice.

The effects of the 5-HT(3) receptor antagonist ondansetron on the ketamine- and dizocilpine-induced place preferences in mice were examined. The non-competitive NMDA receptor antagonists ketamine (1. 0-10 mg/kg, i.p.) and dizocilpine (0.1 and 0.2 mg/kg, i.p.) each produced a place preference in a dose-dependent manner. The ketamine (10 mg/kg)- and dizocilpine (0.2 mg/kg)-induced place preferences were dose-dependently blocked by pretreatment with ondansetron (0. 03-0.1 mg/kg, s.c.). These results suggest that 5-HT(3) receptor may be involved in the development of the place preferences produced by ketamine and dizocilpine.

Animals↗
PubMed1999

Effects of adenosine receptors on the synaptic and EPSP-spike components of long-term potentiation and depotentiation in the guinea-pig hippocampus.

1. Long-term potentiation (LTP) of synaptic efficacy comprises two components: a synaptic component consisting of increased field excitatory postsynaptic potentials (EPSPs), and a component consisting of a larger population spike amplitude for a given EPSP size (E-S potentiation). In hippocampal CA1 neurons, delivery of three weak bursts (5 pulses at 100 Hz, 20 min intervals) induced LTP in both the EPSP and E-S components. In the same cells, reversal of LTP (depotentiation, DP) in the field EPSP and the E-S component was achieved by delivering three trains of low-frequency stimuli (LFS; 200 pulses at 1 Hz, 20 min intervals). 2. The effects of adenosine A1 and A2 receptor antagonists on the synaptic and E-S components of LTP and DP in CA1 neurons were studied by perfusing guinea-pig hippocampal slices with either 8-cyclopentyltheophylline (8-CPT) or CP-66713. 3. When bursts or LFS were applied to CA1 inputs in the presence of the A1 receptor antagonist 8-CPT, the field EPSP was enhanced in LTP and attenuated in DP, while the E-S relationship was not significantly affected in either LTP or DP. 4. When similar experiments were performed using the A2 receptor antagonist CP-66713, the field EPSP was blocked in LTP, but facilitated in DP, while E-S potentiation was enhanced during both LTP and DP. 5. The results show that A1 and A2 adenosine receptors modulate both the synaptic and E-S components of the induction and reversal of LTP. Based on these results, we discuss the key issue of the contribution of these receptors to the dynamics of neuronal plasticity modification in hippocampal CA1 neurons.

Action Potentials↗