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Biomedical subjects

H Ito

Publications and source records attributed to H Ito.

At least 667 records · Page 37Linked to original sources
PubMed1999

Extended thymectomy for myasthenia gravis in an octogenarian. A case report.

An 86-year-old woman with myasthenia gravis successfully underwent an extended thymectomy. The patient had a 2-year history of generalized myasthenia and had limited response to anticholinesterases and steroids. An extended thymectomy was successfully performed in the usual fashion. The postoperative course was uneventful except for an episode of psychosis probably due to postoperative steroid therapy. The steroid dosage was gradually reduced to 5 mg/day over seven months after the operation, during which she became fully asymptomatic. No symptoms due to myasthenia have surfaced for over 2 years after surgery. Although elderly patients are usually considered to be less responsive to an operation, thymectomy may sometimes be the treatment of choice for myasthenia gravis even in octogenarians.

Aged↗
PubMed1999

Role of androgen receptor in prostate cancer.

The growth of prostate cancer is sensitive to androgen, and hormonal therapy has been used for treatment of advanced cancer. About 80% of prostate cancers initially respond to hormonal therapy, however, more than half of the responders gradually become resistant to this therapy. Changes in tumors from an androgen-responsive to an androgen-unresponsive state have been widely discussed. Since androgen action is mediated by androgen receptor (AR), abnormalities of AR is believed to play an important role of the loss of androgen responsiveness in prostate cancer. This article focused on the role of AR in the progression of prostate cancer.

Down-Regulation↗
PubMed1999

Localization of 5-HT1A receptors in the living human brain using [carbonyl-11C]WAY-100635: PET with anatomic standardization technique.

UNLABELLED: Serotonergic 5-hydroxytryptamine-1A (5-HT1A) receptors are of interest in the pathophysiology of several neuropsychiatric disorders such as anxiety, depression and schizophrenia. [Carbonyl-11C]WAY-100635 has recently been shown to be suitable for quantitative determination of 5-HT1A receptors in the human brain using PET. For group comparisons of neuroreceptor distribution on a pixel-by-pixel basis, an anatomic standardization technique is required. In the current study, we have built a database of normal 5-HT1A receptor distribution using [carbonyl-11C]WAY-100635 and an anatomic standardization technique. METHOD: A PET examination lasting 63 min was performed on six subjects after intravenous injection of [carbonyl-11C]WAY-100635. The radioactivity of the PET images were integrated in the interval 12-63 min and normalized by the radioactivity of the cerebellum, providing a measure of the binding potential (BP) in each pixel. Each PET image was transformed into a standard brain anatomy using a computerized brain atlas system. From the standardized PET images, the sample mean and the SD of the BP were calculated in each pixel. RESULT: On the anatomically standardized average image, high BP was observed in the cerebral cortices, hippocampus and raphe nucleus, whereas low BP was observed in the basal ganglia and thalamus. This regional distribution is in good agreement with the distribution of 5-HT1A receptors known from in vitro studies. CONCLUSION: The anatomic standardization technique permits building of a database of the normal 5-HT1A receptor distribution in the living human brain. This technique can be applied for group comparisons of neuroreceptor distribution on a pixel-by-pixel basis.

Adult↗
PubMed1999

Prognosis of early stage avascular necrosis of the femoral head.

Seventy-two femoral heads in 63 patients in whom avascular necrosis of the femoral head was in the early stage were followed up prospectively for a mean period of 6 years 1 month. All of the necrotic lesions were confirmed by magnetic resonance imaging. At the time of final outcome, 46 (64%) of the 72 hips were symptomatic. Necrotic lesions greater than 2/3 of the weightbearing portion on T1 weighted central coronal images indicated a high risk of clinical deterioration. Fifty-nine of the 72 hips initially had necrotic lesions greater than 2/3 of the weightbearing portion, and 44 (75%) of these 59 hips were symptomatic at the final outcome. However, in the radiographic assessment of 15 (25%) asymptomatic hips, even when the necrotic lesions were greater than 2/3 of the weightbearing portion as shown by magnetic resonance imaging, the continuous absence of any radiographic abnormality indicated the possibility of a continuous asymptomatic stage for at least several years.

Adult↗
PubMed1998

Analysis of the role of variation of major histocompatibility complex class II expression on nonobese diabetic (NOD) peripheral T cell response.

The current paradigm of major histocompatibility complex (MHC) and disease association suggests that efficient binding of autoantigens by disease-associated MHC molecules leads to a T cell-mediated immune response and resultant autoimmune sequelae. The data presented below offer a different model for this association of MHC with autoimmune diabetes. We used several mouse lines expressing different levels of I-Ag7 and I-Ak on the nonobese diabetic (NOD) background to evaluate the role of MHC class II in the previously described NOD T cell autoproliferation. The ratio of I-Ag7 to I-Ak expression correlated with the peripheral T cell autoproliferative phenotype in the mice studied. T cells from the NOD, [NOD x NOD. I-Anull]F1, and NOD I-Ak transgenic mice demonstrated autoproliferative responses (after priming with self-peptides), whereas the NOD.H2(h4) (containing I-Ak) congenic and [NOD x NOD. H2(h4) congenic]F1 mice did not. Analysis of CD4(+) NOD I-Ak transgenic primed lymph node cells showed that autoreactive CD4(+) T cells in the NOD I-Ak transgenic mice were restricted exclusively by I-Ag7. Considered in the context of the avidity theory of T cell activation and selection, the reported poor peptide binding capacity of NOD I-Ag7 suggested a new hypothesis to explain the effects of MHC class II expression on the peripheral autoimmune repertoire in NOD mice. This new explanation suggests that the association of MHC with diabetes results from "altered" thymic selection in which high affinity self-reactive (potentially autoreactive) T cells escape negative selection. This model offers an explanation for the requirement of homozygous MHC class II expression in NOD mice (and in humans) in susceptibility to insulin-dependent diabetes mellitus.

Animals↗
PubMed1998

hTERT is a critical determinant of telomerase activity in renal-cell carcinoma.

Telomerase is a ribonucleoprotein enzyme which stabilizes chromosomal structure, thereby inducing cellular immortality. Three major subunits composing telomerase complex have been cloned, designated hTR (human telomerase RNA), TPI (telomerase-associated protein I), and hTERT (human telomerase reverse transcriptase). In the present study, a total of 36 renal-cell carcinomas (RCC) and adjacent normal tissues, as well as cell lines derived from RCC or normal kidney, were examined for the expression of each telomerase subunit and telomerase activity. RT-PCR analyses revealed that hTR and TP I mRNA were constitutively expressed both in tumor and in normal tissues. In contrast, hTERT mRNA was expressed in most tumors, but not in normal tissues. Telomeric-repeat-amplification-protocol (TRAP) assay revealed that more than 80% of RCC tumor tissue exhibited telomerase activity, while none of the adjacent normal tissue did. There was a significant association of telomerase activity with expression of hTERT mRNA, but not with TPI mRNA or hTR expression. Two cell lines, derived from RCC and cervical cancer, expressed telomerase activity and hTERT mRNA, while normal renal cortical epithelial cells expressed neither of them. These findings suggest that hTERT plays a critical role in determining the enzymatic activity of human telomerase, and that up-regulation of hTERT probably plays a role in the progression of human cancers.

Adult↗
PubMed1998

The Fas/Fas ligand system is involved in the pathogenesis of autoimmune myocarditis in rats.

The mechanisms responsible for myocardial injury and cell death in myocarditis are still unclear. We examined whether myocardial cell death occurs via apoptosis in myosin-induced autoimmune myocarditis in rats and whether the Fas/Fas ligand (FasL) system plays a role in this apoptosis. On days 14, 17, 21, and 35 after immunization with porcine heart myosin, some cardiomyocytes and infiltrating lymphocytes were found to be apoptotic on in situ terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling (TUNEL) assay, but none was on day 60 and in control rats. Apoptotic indices peaked at day 17, and laddering of genomic DNA from the affected myocardium was observed on days 17 and 21 on agarose gel electrophoresis. The expression of Fas mRNA and protein was detected on days 17 and 21 in some cardiomyocytes and infiltrating lymphocytes by Northern blot analysis and immunohistochemistry, respectively. In addition, FasL was detected in some infiltrating lymphocytes on days 14, 17, and 21 by both in situ hybridization and immunostaining, and FasL-positive lymphocytes were mainly CD4+ cells. Some rats were injected with anti-Fas Ab (0.1 mg/kg) or anti-FasL Ab (0.1 mg/kg), and subsequently, inflammatory lesions exhibited less severe than did untreated rats with myocarditis. These findings suggest that cell death via apoptosis of cardiomyocytes and lymphocytes is one of the mechanisms of myocardial injury in autoimmune myocarditis, and that the Fas/FasL system might play a role in the induction of this apoptosis.

Acute Disease↗
PubMed1998

Phosphorylation of alphaB-crystallin in mitotic cells and identification of enzymatic activities responsible for phosphorylation.

The immunofluorescence localization of alphaB-crystallin in U373 MG human glioma cells with an antibody specific for alphaB-crystallin that had been phosphorylated at Ser-45 revealed an intense staining of cells in the mitotic phase of the cell cycle. Phosphorylated forms of alphaB-crystallin in mitotic cells were detected in all cell lines examined and in tissue sections of mouse embryos. Increases in the levels of alphaB-crystallin that had been phosphorylated at Ser-45 and Ser-19, but not at Ser-59, were detected biochemically by isoelectric focusing or SDS-polyacrylamide gel electrophoresis and a subsequent Western blot analysis of extracts of cells collected at the mitotic phase. When we estimated the phosphorylation activity specific for alphaB-crystallin in extracts of mitotic U373 MG cells, using the amino-terminal 72-amino acid peptide derived from unphosphorylated alphaB2-crystallin as the substrate, we found that the activities responsible for the phosphorylation of Ser-45 and Ser-19 were markedly enhanced but that the activity responsible for the phosphorylation of Ser-59 was suppressed. The protein kinases responsible for the phosphorylation of Ser-45 and Ser-59 in the amino-terminal 72-amino acid peptide were partially purified from extracts of cells that had been stimulated by exposure to H2O2 in the presence of calyculin A. The activities responsible for the phosphorylation of Ser-45 and Ser-59 were eluted separately from a column of Superdex 200 at fractions corresponding to about 40 and 60 kDa, respectively, while the kinase for Ser-19 was unstable. p44/42 mitogen-activated protein (MAP) kinase and MAP kinase-activated protein (MAPKAP) kinase-2 were concentrated in the Ser-45 kinase fraction and Ser-59 kinase fraction, respectively. Recombinant human p44 MAP kinase and MAPKAP kinase-2 purified from rabbit muscle selectively phosphorylated Ser-45 and -59, respectively. The Ser-45 kinase fraction and Ser-59 kinase fraction phosphorylated myelin basic protein and hsp27, respectively. These results suggest that the phosphorylations of Ser-45 and Ser-59 in alphaB-crystallin are catalyzed by p44/42 MAP kinase and MAPKAP kinase-2, respectively, in cells and that the phosphorylation of Ser-45 by p44/42 MAP kinase is enhanced while the phosphorylation of Ser-59 by MAPKAP kinase-2 is suppressed during cell division.

Animals↗
PubMed1998

Site-specific hydroxylation at polyguanosine in double-stranded DNA by UVA radiation with nalidixic acid.

Nalidixic acid (NA) has been used for urinary tract infections and has been reported to be photocarcinogenic. We examined the mechanism of damage to 32P-labeled DNA fragments obtained from the human c-Ha-ras-1 proto-oncogene and the p53 tumor suppressor gene exposed to 365-nm UVA light in the presence of NA. NA plus UVA light caused damage to the double-stranded DNA fragment at consecutive guanine residues, whereas damage to the single-stranded DNA fragment was caused at single guanines and thymines. The formation of 8-oxo-7, 8-dihydro-2'-deoxyguanosine in native DNA exceeded that in denatured DNA at high NA concentrations. The ESR spin destruction method suggested that DNA damage was caused through electron transfer from guanine residues to photoexcited NA. On the basis of these findings, it is concluded that NA can cause skin cancer through DNA damage mediated by its photoactivation.

Base Sequence↗
PubMed1998

Demonstration of the third antigenically distinct outer membrane lipoprotein (OmlA) in Actinobacillus pleuropneumoniae serotype 7.

The gene encoding an outer membrane lipoprotein (OmlA) of Actinobacillus pleuropneumoniae strain WF83 (serotype 7 reference strain), designated omlA7, was sequenced. The amino acid sequence of OmlA7 showed 64.5 and 71.6% identity to that of OmlA from serotypes 1 (OmlA1) and 5 (OmlA5), respectively. The first 134 amino acids of OmlA7 were identical to those of OmlA5. A Southern blot analysis revealed the presence of a gene highly homologous to the omlA7 in the reference strains of serotypes 3, 4, 6, and 7. A Western blot analysis using a specific antiserum against a recombinant OmlA7 detected expression of the homologous proteins in the serotypes 4, 6, and 7 reference strains and a serotype 3 field strain, but not in a serotype 3 reference strain. The data demonstrate the third antigenically distinct OmlA is expressed in A. pleuropneumoniae.

Actinobacillus Infections↗
PubMed1998

Intratumoral cytogenetic heterogeneity detected by comparative genomic hybridization and laser scanning cytometry in human gliomas.

Although it is well-known that cancers show intratumoral phenotypic heterogeneity, genotypic studies have been scarce. Using comparative genomic hybridization and laser scanning cytometric analyses, we investigated intratumoral cytogenetic heterogeneity in 21 surgically removed gliomas including 11 glioblastomas (GBMs), 8 anaplastic astrocytomas (AAs) and 2 low-grade astrocytomas. Comparative genomic hybridization analysis revealed gain or amplification of 7p in 63%, gain of 7q in 73%, loss of 9p in 53%, loss of 10p in 47%, loss of 10q in 47%, loss of 13q in 53%, and loss of 22q in 37% of high-grade astrocytomas. Because these aberrations were region-independent within the same tumor, they did not contribute to intratumoral cytogenetic heterogeneity. Such heterogeneity was due to cytogenetic changes other than the above region-independent aberrations. Intratumoral cytogenetic heterogeneity was detected in 8 of 11 GBMs, 4 of 8 AAs, and none of the 2 low-grade astrocytomas. These observations suggest that cytogenetic changes at chromosomes 7, 9p, 10, 13, and 22 are primary events in high-grade astrocytomas and that subsequent cytogenetic changes involving increases in copy number provide intratumoral heterogeneity. DNA aneuploidy was detected by laser scanning cytometry in 5 of 11 GBMs and 1 of 8 AAs. All tumors with DNA aneuploidy exhibited intratumoral cytogenetic heterogeneity, and there was a significant correlation between DNA aneuploidy and intratumoral cytogenetic heterogeneity. These results support the notion that cytogenetic heterogeneity results from genetic instability within a tumor.

Adult↗
PubMed1998

Chlorophyll a oxygenase (CAO) is involved in chlorophyll b formation from chlorophyll a.

Chlorophyll b is an ubiquitous accessory pigment in land plants, green algae, and prochlorophytes. Its biosynthesis plays a key role in the adaptation to various light environments. We isolated six chlorophyll b-less mutants by insertional mutagenesis by using the nitrate reductase or argininosuccinate lyase genes as tags and examined the rearrangement of mutant genomes. We found that an overlapping region of a nuclear genome was deleted in all mutants and that this encodes a protein whose sequence is similar to those of methyl monooxygenases. This coding sequence also contains putative binding domains for a [2Fe-2S] Rieske center and for a mononuclear iron. The results demonstrate that a chlorophyll a oxygenase is involved in chlorophyll b formation. The reaction mechanism of chlorophyll b formation is discussed.

Amino Acid Sequence↗