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Biomedical subjects

S Chiba

Publications and source records attributed to S Chiba.

At least 91 records · Page 5Linked to original sources
PubMed2001

Molecular analysis of defect healing in rat diaphyseal bone.

Spatial expression of messenger ribonucleic acid (mRNA) for osteoblastic marker in drill hole defect healing of adult male rats was analyzed by in situ hybridization. The defect was filled with hematoma 3 days after surgery, expressing Type I collagen mRNA. Hematoma was replaced with fibrous tissue on day 7, and then with new trabecular bone on day 10, originated from the intra-medullary space, respectively. mRNA for Type I collagen, parathyroid hormone 1 receptor (PTHIR), and alkaline phosphatase (ALP) were expressed in the same cell population of fibrous tissue adjacent to newly-formed trabecular bone, and in osteoblasts lining the newly-formed trabecular bone. Hematopoietic marrow with osteoclasts subsequently invaded the region, also from the intra-medullary space, replacing all the new trabecular bone by day 21, except for a thin sub-periosteal layer. mRNA for Type I collagen, PTH1R and ALP was expressed on the periosteal surface of thin layer. Although cartilage formation was not histologically visible, mRNA for Type II collagen was weakly detected in the majority of osteoblasts lining the newly-formed trabecular bone.

Alkaline Phosphatase↗
PubMed2001

Crow-Fukase syndrome with ischemic cardiomyopathy.

A 31-year-old man was admitted to our hospital for further evaluation of heart failure symptoms. Crow-Fukase syndrome was diagnosed on the basis of findings of polyneuropathy, hepatomegaly, monoclonal hypergammaglobulinemia, and hypertrichosis. Dipyridamole-stress thallium-201 perfusion imaging, contrast left ventriculography, and coronary angiography revealed a markedly dilated and dysfunctioning left ventricle, extensive reversible ischemia with fixed defect, and multiple coronary lesions. Histopathology of myocardial biopsy specimens demonstrated ischemia-induced myocardial necrosis. These findings suggested that ischemic cardiomyopathy, probably due to inflammatory reactions of coronary arteries in Crow-Fukase syndrome, was responsible for the heart failure symptoms and left ventricular dysfunction in this patient.

Adult↗
PubMed2001

Central infusion of histamine reduces fat accumulation and upregulates UCP family in leptin-resistant obese mice.

Leptin resistance has recently been confirmed not only in animal obese models but in human obesity. Evidence is rapidly emerging that suggests that activation of histamine signaling in the hypothalamus may have substantial anti-obesity and antidiabetic actions, particularly in leptin-resistant states. To address this issue, effects of central, chronic treatment with histamine on food intake, adiposity, and energy expenditure were examined using leptin-resistant obese and diabetic mice. Infusion of histamine (0.05 pmol x g body wt(-1) x day(-1)) into the lateral cerebroventricle (i.c.v.) for 7 successive days reduced food intake and body weight significantly in both diet-induced obesity (DIO) and db/db mice. Histamine treatment reduced body fat weight, ob gene expression, and serum leptin concentration more in the model mice than in pair-fed controls. The suppressive effect on fat deposition was significant in visceral fat but not in subcutaneous fat. Serum concentrations of glucose and/or insulin were reduced, and tests for glucose and insulin tolerance showed improvement of insulin sensitivity in those mice treated with histamine compared with pair-fed controls. On the other hand, gene expression of uncoupling protein (UCP)-1 in brown adipose tissue and UCP-3 expression in white adipose tissue were upregulated more in mice with i.c.v. histamine infusion than in the pair-fed controls. These upregulating effects of histamine were attenuated by targeted disruption of the H1-receptor in DIO and db/db mice. Sustained i.c.v. treatment with histamine thus makes it possible to partially restore the distorted energy intake and expenditure in leptin-resistant mice. Together, i.c.v. treatment with histamine contributes to improvement of energy balance even in leptin-resistant DIO and db/db mice.

Adipose Tissue↗
PubMed2001

Targeted disruption of histamine H1-receptor attenuates regulatory effects of leptin on feeding, adiposity, and UCP family in mice.

Histamine neurons are widely distributed in the brain and suppress food intake through the histamine H1 receptor (H1-R) in the hypothalamus. To examine the role of neuronal histamine in leptin signaling pathways, we investigated the effects of H1-R knockout (H1KO) mice on both food intake and mRNA expressions of uncoupling proteins (UCPs) as regulated by leptin, and concomitantly on basal changes in both expression of hypothalamic neuropeptides and diet-induced fat deposition in adipose tissues. H1KO mice showed no change in daily food intake, growth curve, body weight, or adiposity. Reflecting no specificity in these parameters, H1KO mice induced no basal changes in mRNA expression of hypothalamic neuropeptides, ob gene, or peripheral UCPs. Loading H1KO mice with a high-fat diet accelerated fat deposition and ob gene expression compared with the controls. Leptin-induced feeding suppression was partially attenuated in H1KO mice, indicating involvement of histamine neurons in feeding regulation as a downstream signal of leptin. Upregulation of fat UCP mRNA and reduction of body fat induced by central infusion of leptin were attenuated in the H1KO mice. These results show that H1KO mice are a novel leptin-resistant model and that H1-R is a key receptor for downstream signaling of leptin in the brain that contributes to regulation of feeding, fat deposition, and UCP mRNA expression.

Adipose Tissue↗
PubMed2001

Synergistic action of HNF-3 and Brachyury in the notochord differentiation of ascidian embryos.

In vertebrate embryos, the class I subtype forkhead domain gene HNF-3 is essential for the formation of the endoderm, notochord and overlying ventral neural tube. In ascidian embryos, Brachyury is involved in the formation of the notochord. Although the results of previous studies imply a role of HNF-3 in notochord differentiation in ascidian embryos, no experiments have been carried out to address this issue directly. Therefore the present study examined the developmental role of HNF-3 in ascidian notochord differentiation. When embryos were injected with a low dose of HNF-3 mRNA, their tails were shortened and when embryos were injected with a high dose of HNF-3 mRNA, which was enough to inhibit differentiation of epidermis and muscle, no obvious ectopic differentiation of endoderm or notochord cells was observed. However, co-injection of HNF-3 mRNA along with Brachyury mRNA resulted in ectopic differentiation of notochord cells in the animal hemisphere, suggesting that HNF-3 acts synergistically with Brachyury in ascidian notochord differentiation. Notochord differentiation of the A-line precursor cells depends on inducing signal(s) from endodermal cells, which can be mimicked by bFGF treatment. Treatment of notochord precursor cells isolated from the 32-cell stage embryoswith bFGF resulted in upregulation of both the HNF-3 and Brachyury genes.

Amino Acid Sequence↗
PubMed2001

[AAA proteases].

Explore the source record for details and available documents.

Adenosine Triphosphatases↗
PubMed2001

[A case of pulmonary lymphangioleiomyomatosis originally treated as bronchial asthma].

The subject was a 37-year-old woman in whom bronchial asthma had been diagnosed, for which inhaled steroid and theophylline had been prescribed for about nine months. Her symptoms improved temporarily, but there-after she experienced gradually worsening dyspnea on exertion. Chest radiographs showed diffuse reticulonodular shadows, but no evidence of hyperinflation or pleural effusion. Chest CT scans revealed multiple thinwalled cystic lesions in both lung fields. Pulmonary lymphangioleiomyomatosis was confirmed by thoracoscopic lung biopsy, and medroxyprogesterone was prescribed. Her airways appeared to demonstrate hyperresponsiveness to inhaled methacholine and her symptoms resembled those of bronchial asthma. The relationship between pulmonary lymphangioleiomyomatosis and airway hyperresponsiveness should be considered in future.

Adult↗
PubMed2001

[A patient with recurrent breast cancer whose liver metastasis regressed following combined use of weekly docetaxel and MPA.5'-DFUR].

A 28-year-old woman who was 10 months pregnant was diagnosed with left breast cancer. She received preoperative chemotherapy and underwent mastectomy after parturition. Endocrine therapy and adjuvant CMF and CAF was administered, but a bone metastasis appeared 2 years later and a liver metastasis 3 years later. Weekly docetaxel and MPA plus 5'-DFUR combination therapy were successively and simultaneously administered. The liver tumor regressed, and the survival time was prolonged by 1 year and 6 months. This case suggests that the combined use of both therapies was safe for the patient in serious bad condition and had a strong antitumor effect.

Adult↗
PubMed2000

Mutations of the AML1 gene in myelodysplastic syndrome and their functional implications in leukemogenesis.

The AML1 gene encodes a DNA-binding protein that contains the runt domain and is the most frequent target of translocations associated with human leukemias. Here, point mutations of the AML1 gene, V105ter (single-letter amino acid code) and R139G, (single-letter amino acid codes) were identified in 2 cases of myelodysplastic syndrome (MDS) by means of the reverse transcriptase-polymerase chain reaction single-strand conformation polymorphism method. Both mutations are present in the region encoding the runt domain of AML1 and cause loss of the DNA-binding ability of the resultant products. Of these mutants, V105ter has also lost the ability to heterodimerize with polyomavirus enhancer binding protein 2/core binding factor beta (PEBP2beta/CBFbeta). On the other hand, the R139G mutant acts as a dominant negative inhibitor by competing with wild-type AML1 for interaction with PEBP2beta/CBFbeta. This study is the first report that describes mutations of AML1 in patients with MDS and the mechanism whereby the mutant acts as a dominant negative inhibitor of wild-type AML1.

Amino Acid Substitution↗
PubMed2000

Convulsive seizures induced by N-methyl-D-aspartate microinjection into the mesencephalic reticular formation in rats.

Effects of microinjections of a single 2 or 10 nmol dose of N-methyl-D-aspartate (NMDA) into the unilateral mesencephalic reticular formation (MRF) on behavior and electroencephalogram were examined in rats (n=18) during a 15 min period (Exp. 1), and subsequent effects of sound stimulation with key jingling applied at 15, 30, and 45 min after the injections were observed (Exp. 2). The microinjections of 2 nmol dose of NMDA (n=10) induced hyperactivity (9 of 10 rats) and running/circling (8 of 10 rats) in Exp. 1, and hyperactivity (3 of 10 rats) in Exp. 2. Moreover, the microinjections of 10 nmol dose of NMDA (n=8) induced not only hyperactivity (8 of 8 rats) and running/circling (7 of 8 rats) but also generalized tonic-clonic seizures (GTCS) (5 of 8 rats) in Exp. 1; these seizure patterns were also elicited by sound stimulation in Exp. 2. The seizure patterns were accompanied by electroencephalographic seizure discharges in the MRF and the motor cortex. In contrast, the control group rats (n=10) which received a single dose of saline microinjection into the unilateral MRF showed no behavioral or electroencephalographic changes in both Exp. 1 and 2. These findings suggest that the MRF has an important role in the development of GTCS, which follows hyperactivity and running/circling, and that potentiation of excitatory neurotransmission in the MRF participates in the development of audiogenic seizures as well as GTCS.

Acoustic Stimulation↗
PubMed2000

Epstein-Barr virus lacking glycoprotein gp85 cannot infect B cells and epithelial cells.

To evaluate whether the BXLF2 gene of Epstein-Barr virus (EBV), which codes gp85 protein, is essential for infection of B cells and epithelial cells, we analyzed the infectivity of an EBV recombinant lacking gp85. The cells that were infected with the BXLF2-disrupted virus were unable to express gp85 proteins that could be detected by mouse monoclonal antibody E1D1, specific for gp85/gp25 complexes. The BXLF2-disrupted EBV had the ability to attach to, but not infect, B cells. On the other hand, the same virus failed to bind to and infect NU-GC-3, a human gastric adenocarcinoma cell line that is susceptible to EBV infection. The results indicate that the gp85 is used for infection of not only B cells but also epithelial cells and suggest that the gp85 is necessary for attaching the virus to epithelial cells.

Animals↗
PubMed2000

Rat homologue of the human M(r) 110000 antigen is the protein that expresses widely in various tissues.

The rat homologue of the human M(r) 110000 antigen, which cross-reacts with anti-carcinoembryonic antigen antibodies, was isolated from a rat lung cDNA library. The deduced amino acid sequence revealed a signal peptide, cysteine-rich and immunoglobulin-like region, serine-threonine region, and N-glycosylation sites in the extracellular portion. Northern blot analysis demonstrated a wide distribution of the mRNA in adult rat tissues and A10 rat vascular smooth muscle cells. Therefore, the rat homologue of the human M(r) 110000 antigen may be a receptor or a cell adhesion molecule rather than a specific carcinogenic antigen.

Amino Acid Sequence↗
PubMed2000

Physical interaction of Delta1, Jagged1, and Jagged2 with Notch1 and Notch3 receptors.

The Delta/Serrate/LAG-2 (DSL) domain-containing proteins, Delta1, Jagged1, and Jagged2, are considered to be ligands for Notch receptors. However, the physical interaction between the three DSL proteins and respective Notch receptors remained largely unknown. In this study, we investigated this issue through the targeting of Notch1 and Notch3 in two experimental systems using fusion proteins comprising their extracellular portions. Cell-binding assays showed that soluble forms of Notch1 and Notch3 proteins physically bound to the three DSL proteins on the cell surface. In solid-phase binding assays using immobilized soluble Notch1 and Notch3 proteins, it was revealed that each DSL protein directly bound to the soluble Notch proteins with different affinities. All interactions between the DSL proteins and soluble Notch proteins were dependent on Ca(2+). Taken together, these results suggest that Delta1, Jagged1, and Jagged2 are ligands for Notch1 and Notch3 receptors.

Animals↗