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T Nishida

Publications and source records attributed to T Nishida.

At least 361 records · Page 20Linked to original sources

Association of nbl gene expression and glucocorticoid-induced apoptosis in mouse thymus in vivo.

A gene of unknown biological function, nbl, was originally isolated by virtue of its abundance in a Namalwa Burkitt Lymphoma cDNA library. nbl expression was initially found to be higher in tissues which exhibited internucleosomal DNA cleavage characteristic of apoptosis, than in tissues which did not exhibit a 'DNA ladder'. nbl expression was therefore examined in mouse thymus in vivo, in which apoptosis is induced by the glucocorticoid, dexamethasone. nbl expression was markedly enhanced by dexamethasone treatment and then sharply decreased prior to the occurrence of maximal 'DNA ladder' formation. In contrast, expression of myc, which is believed to be involved in apoptosis in other cell systems, declined as thymic apoptosis increased. Thymic apoptosis was blocked by the transcriptional inhibitor actinomycin D, if administered when nbl expression was enhanced, but not before or after the peak of nbl expression. These results suggest that nbl expression is associated with thymic apoptosis.

Animals↗

[The criteria for the prediction of paroxysmal atrial fibrillation by time domain analysis of the P wave-triggered signal-averaged electrocardiogram].

In order to determine the criteria for definition of atrial late potentials in patients with paroxysmal atrial fibrillation (Paf), the P wave-triggered signal-averaged electrocardiogram (SAE) was recorded in 88 patients with Paf (Paf group) and in 216 normal subjects (Normal group). Three SAE variables, duration of the filtered P wave (FPD), root-mean-square voltage of the last 20 msec (V20) and duration of under 5 microV (D5) of the vector magnitude were measured. FPD and D5 were significantly longer in the Paf than in the Normal group (FPD; 137 +/- 13 vs. 115 +/- 7 msec, D5; 27 +/- 12 vs. 16 +/- 5 msec, p < 0.001, respectively). V20 was also significantly lower in the Paf than in the Normal group (2.5 +/- 1.1 vs. 3.9 +/- 1.1 microV, p < 0.001). The sensitivity and specificity for the prediction of Paf was computed (for all dichotomy points) and compared with various criteria for atrial late potentials based on the three SAE variables. Analysis showed that 1) FPD was a better predictor of Paf than the other two variables, 2) the criteria of [FPD > 125 msec and V20 = 3.0 microV or less] as defining "atrial late potentials" gave a sensitivity of 68%, a specificity of 99% and a predictive accuracy of 90%. These findings suggest that the SAE is useful to predict Paf. Additionally, prospective studies are needed with a larger number of patients to compare the different criteria of "atrial late potentials" by time domain analysis of the SAE.

Adolescent↗

Structure-specific inhibition by bile acids of adenosine triphosphate-dependent taurocholate transport in rat canalicular membrane vesicles.

The adenosine triphosphate (ATP)-dependent transport system is a major determinant of canalicular bile acid secretion. The system transports bile acids and neither organic cations nor non-bile acid organic anions, such as glucuronides or glutathione adducts. To define the structural specificity of the ATP-dependent system, the authors examined the ability of various bile acids to inhibit ATP-dependent taurocholate transport by rat liver canalicular membrane vesicles. Only bile acids with a negative charge inhibited transport, which was unaffected by side chain length. Conjugated, but not unconjugated, mono- and di-hydroxy bile acids inhibited transport. The presence of 7 alpha- and 12 alpha-hydroxylation also influenced inhibition of ATP-dependent taurocholate transport. Inhibition of transport by bile acids was kinetically competitive. These results suggest that the canalicular ATP-dependent bile acid transport system depends on bile acid side chain charge, conjugation, and hydroxylation.

Adenosine Triphosphate↗

Differences in lymphocyte proliferative responses to food antigens and specific IgE antibodies to foods with age among food-sensitive patients with atopic dermatitis.

BACKGROUND: Clinical symptoms of patients with food-sensitive atopic dermatitis often improve with increasing age. OBJECTIVE: To investigate this tendency and the underlying mechanism. METHODS: We selected and divided 194 food-sensitive atopic dermatitis patients into three age groups. The proliferative responses of peripheral blood mononuclear cells (PBMCs) to food antigens and specific IgE antibodies to foods then were evaluated with respect to age. We also followed up 55 food-sensitive patients with atopic dermatitis and examined their improvement ratio after 1 year. Further, we investigated changes in lymphocyte proliferative responses to food antigens and specific IgE antibodies to foods in food-sensitive patients with atopic dermatitis during elimination diets. RESULTS: Proliferative responses of PBMCs to ovalbumin of patients in the over 6-years-old group were significantly (P < .05) lower than those of the less than 1-year-old group. Proliferative responses of PBMCs to bovine serum albumin of patients in the over 6-years-old group were significantly (P < .05) lower than those in the 1 to 5-year-old group and in the less than 1-year-old group. RAST values for hen egg in the over 6-years-old group were significantly (P < .05) lower than those for the less than 1-year-old group. Improvement was shown by 13 of the 33 hen egg-sensitive patients with atopic dermatitis, an improvement ratio of 39%, and by 9 of the 22 cow milk-sensitive patients with atopic dermatitis, an improvement ratio of 41%. Proliferative responses of PBMCs to food antigens in food-sensitive patients with atopic dermatitis decreased rapidly after patients were placed on elimination diets. CONCLUSION: The PBMC proliferative responses to food antigens and RAST values were higher for young children and lower for older ones who suffered from food-sensitive atopic dermatitis. Oral tolerance, in addition to the development of digestive and absorptive functions, may be responsible for these immunologic changes.

Adolescent↗

[A case of remarkable response of colon cancer with multiple liver and bone metastasis treated with tegafur and cisplatin].

A 47-year-old man with ascending colon cancer with multiple liver metastases and bone metastasis (VII thoracic vertebra) showed a remarkable response to the combination therapy of tegafur and cisplatin. Tegafur (1,200 mg/day) was administered through continuous intravenous infusion mixed with IVH, and cisplatin was given every two weeks at a dose of 100 mg. The total dose of tegafur was 39.6g and that of cisplatin was 300mg. After therapy, primary and metastatic lesions were remarkably reduced according to various imaging techniques, and the serum CEA level of 34ng/ml at diagnosis decreased 3.7 ng/ml. Various tumor-related symptoms were improved. Drug toxicity caused slight nausea and leucopenia. Right hemicolectomy with R2 lymph node dissection was performed after chemotherapy. Histologically, primary lesion and regional lymph nodes showed diffuse fibrosis and necrosis, and only a few cancer cells remained some vessels. These results suggested that the combination chemotherapy of tegafur and cisplatin is useful for the treatment of colon cancer.

Adenocarcinoma↗

[Role of neutrophils in lung injury after intestinal ischemia and reperfusion in dogs].

We studied the role of neutrophils in lung injury after intestinal ischemia and reperfusion (I/R) in anesthetized dogs with lung lymph fistulae. One group was subjected to 2.5 hours of balloon occlusion of the superior mesenteric artery without laparotomy, followed by 3 hours of reperfusion (I/R group, n = 7). The other group was subjected to the same procedures, except for intestinal I/R (sham operation group, n = 6). In the sham operation group, lung fluid balance, hemodynamics, extravascular water volume (Qw 1: ml/g BFDW), myeloperoxidase activity in the lung (MPO: unit/g DW), H2O2 production by neutrophils in blood (mean DCF/cell), and migration of neutrophils into the lung lymphatic system did not significantly change. In the I/R group, both lung lymph flow (Jv) and protein clearance (Qp) increased more than 2.5 fold as compared with the baseline values, while capillary pressure (Ppc) and the ratio of lymph to plasma protein concentration (CL/Cp) remained almost the same as the baseline values. Qw1 also moderately increased. MPO activity, H2O2 production, and migration of neutrophils into the lung lymphatic system increased after I/R, and were more remarkable than in the sham operation group. These results suggest that activation and migration of primed neutrophils contributes to lung injury after intestinal ischemia and reperfusion.

Animals↗

[The role of interstitial hyaluronan in acute lung injury].

The pulmonary interstitium may affect the movement of water, macromolecules, and inflammatory cells between capillaries and lymphatics. Hyaluronan (hyaluronic acid), a glycosaminoglycan of the interstitial matrix, helps to retain water in the lung interstitium and to exclude proteins. Marked reduction of interstitial hyaluronan by infusion of hyaluronidase decreased the resistance to fluid transport and decreased water retention in the interstitium, and thus accelerated lymphatic removal of fluid filtered across capillary walls. However, reduction of hyaluronan increased the accumulation of neutrophils in the lung and exacerbated acute lung injury caused by pancreatic elastase. Interstitial hyaluronan may protect against acute inflammatory changes in elastase-induced lung injury.

Acute Disease↗

Characterization of a novel muscarinic receptor agonist, YM796: comparison with cholinesterase inhibitors in in vivo pharmacological studies.

Previous reports have shown that (+/-)-YM796 (2,8-dimethyl-3-methylene-1-oxa-8-azaspiro[4.5]decane) exhibits M1 agonistic activity and ameliorates cognitive impairment, and that the (-)-S isomer is active in in vitro studies. We report here the characterization of the (-)-S isomer, YM796 ((-)-(S)-2,8-dimethyl-3-methylene-1-oxa-8-azaspiro[4.5]decane L-tartrate monohydrate), and its (+)-R isomer in in vivo pharmacological studies in comparison with the cholinesterase inhibitors tacrine, amiridine and E-2020. YM796 (0.031-0.5 mg/kg p.o.), like the racemate, reversed the cognitive impairment in passive avoidance tasks of rats with nucleus basalis magnocellularis lesions, whereas (+)-R-YM796 was ineffective in this experimental amnesia. YM796 exhibited only weak effects on mouse salivation and hypothermia, a peripheral cholinergic response and a central cholinergic response, respectively. The (+)-R isomer, however, failed to induce these cholinergic responses. YM796 also ameliorated the memory deficits induced by scopolamine in rats and electroconvulsive shock in mice. The potency of YM796 in these experimental amnesia models was over a 100 times greater than that of tacrine, over 10 times greater than that of E-2020, and 6 times greater than that of amiridine. In salivary secretion and hypothermia, YM796 was 2-4 times weaker than tacrine and E-2020, and 1-2 times stronger than amiridine. Thus, YM796's ratio of anti-amnesic effects to salivary secretion and hypothermia was much greater than that of the cholinesterase inhibitors tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Transcriptional activation of a cycloheximide-inducible gene encoding laccase is mediated by cpc-1, the cross-pathway control gene, in Neurospora crassa.

Expression of the laccase gene (lacc) of Neurospora crassa is transcriptionally inducible by the protein synthesis inhibitor cycloheximide. A lni-1 mutation, conferring the laccase non-inducible phenotype, was found to be a cpc-1 allele. Northern blots probed with plasmid pLA1, which carries the lacc gene revealed that the cpc-1 mutation abolishes the induced transcription of the lacc gene, indicating requirement of the cpc-1 gene for transcriptional activation of the lacc gene. In Northern blots probed with plasmid pAB1, which bears arg-2 a gene whose transcription is under the control of CPC1, the level of the arg-2 transcript was shown to increase several-fold in wild-type mycelia but remained low in cpc-1 mycelia, after treatment with cycloheximide. This suggests that inhibition of protein synthesis with cycloheximide, as well as amino acid limitation, elicits the CPC1-mediated cross-pathway control. Characterization of the lacc upstream region using a series of 5'-deletion plasmids led to the identification of a 170 bp DNA region required for the induced lacc expression. Sequence analysis of this DNA region demonstrated that it includes a 9 bp sequence with dyad symmetry, ATGAATCAT, which differs only by a central base pair from ATGA(C/G)TCAT, the recognition sequence characteristic of CPC1 and GCN4 binding sites. Possible mechanisms by which CPC1 mediates transcriptional activation of the lacc gene are discussed.

Alleles↗

Characterization of a testis specific protein localized to endoplasmic reticulum of spermatogenic cells.

BACKGROUND: In order to understand the mechanism of spermiogenesis, it is important to characterize germ cell specific genes and proteins expressed during spermatogenesis. We previously reported that a mouse monoclonal antibody, 1C9, raised against golden hamster testis homogenate, recognized a 103 kDa protein in hamster spermatogenic cells (Ohsako et al.; J. Vet. Med. Sci., 53:969-974, 1991). In the present study, we have determined the precise stage and intracellular localization of this protein. MATERIALS AND METHODS: Hamster, mouse, and rat tissues were used for immunocytochemistry, SDS-PAGE, and immunoblotting. Immunoelectron microscopy was performed using Lowicryl K4M embedded hamster testis and colloidal gold conjugated second antibody. Furthermore, immuno-affinity purification was carried out using a 1C9-Sepharose column. RESULTS: In immunoblot analysis, 1C9 also recognized a 103 kDa protein and a 101 kDa protein in the rat and the mouse testes, respectively. Ten different hamster tissues other than testis did not show reactivity against 1C9. In immunostained paraffin sections of hamster testis, the initial staining appeared in middle pachytene spermatocytes and persisted until maturation phase spermatids (step 15). However, it was no longer detectable in the subsequent steps of spermatids. In addition, strong staining was observed in the post-nuclear region of elongated spermatids. Immunoelectron microscopic analysis showed that the protein was localized to the endoplasmic reticulum (ER) and nuclear envelope of spermatogenic cells, but not in the other organelles, such as Golgi apparatus and acrosome of the spermatids. This protein appears to be associated with ER membrane. Furthermore, this protein is found exclusively in the testicular microsomal fraction, not in the cytosol. By affinity purification, approximately 320 micrograms of the 103 kDa protein was obtained from 10 hamster testes. The purified 103 kDa protein was unaffected by N-glycanase, indicating it does not have asparagine-linked glycoconjugates. CONCLUSIONS: These results indicate that the protein recognized by 1C9 appears to be a unique protein that is localized in the ER and nuclear envelope of spermatogenic cells.

Animals↗

Binding of hyaluronan to plasma fibronectin increases the attachment of corneal epithelial cells to a fibronectin matrix.

We wished to determine whether hyaluronan would affect the attachment of epithelial cells to extracellular matrix proteins. Multiwell tissue culture plates were coated with human plasma fibronectin, laminin, or collagen type IV (0.01-10.0 micrograms/ml). Single-cell suspensions of rabbit corneal epithelial cells were placed in the wells, and after 45 minutes incubation the cells adhering to the matrix proteins were stained and counted. Cells attached to all three types of proteins. Preincubation of the matrix proteins with hyaluronan (0.1-1.0 mg/ml) significantly increased the number of cells attached to the fibronectin matrix, but it did not increase the numbers of cells attached to laminin or collagen type IV. Hyaluronidase inhibited this stimulatory effect. Glycosaminoglcyans other than hyaluronan (chondroitin sulfate, keratan sulfate, or heparan sulfate) failed to increase the numbers of attached cells. Treatment of the fibronectin matrix with monoclonal antibodies against the cell-binding domain of fibronectin (FN12-8 or FN30-8, 0.03-0.3 mg/ml, for 1 hour), before or after hyaluronan treatment, significantly decreased the numbers of attached cells. Monoclonal antibody against the fibrin- and heparin-binding domain at the N-terminal (FN9-1), however, significantly decreased the number of attached cells only when this antibody treatment preceded the hyaluronan treatment. Preincubation of the cells with hyaluronan had no effect; preincubation with GRGDSP (1 mg/ml), a synthetic peptide that blocks the cell surface receptor for fibronectin, significantly decreased cell attachment whether the fibronectin matrix was treated with hyaluronan or not. Further studies demonstrated that monoclonal antibody against the fibrin- and heparin-binding domain at the N-terminal of plasma fibronectin prevented radiolabeled hyaluronan from binding to fibronectin; likewise, the isolated N-terminal fragment, coupled with Sepharose 4B, bound to hyaluronan in columns. We conclude that hyaluronan binds to a fibrin- and heparin-binding domain at the N-terminal of plasma fibronectin and facilitates the attachment of epithelial cells.

Animals↗

Tissue distribution of ERp61 and association of its increased expression with IgG production in hybridoma cells.

A protein of molecular weight 60 kDa was purified from the culture medium of a murine colon carcinoma cell line, colon26, and its partial amino-acid sequence determined. Extremely high homology was found with the deduced sequence from cDNA of rat ERp61, earlier found to be an endoplasmic reticulum (ER)-resident protein with redox activity and a similar structure to protein disulfide isomerase (PDI). Western blotting analysis showed that colon26 cells secrete a significant amount of ERp61 into culture medium, although most remains intracellular. The thiol:protein disulfide oxidoreductase activity of the purified mouse ERp61 was demonstrated by insulin-reduction assay. The ER location of the protein in fibroblasts was immunocytochemically confirmed by double staining for ERp61 and another ER-resident protein, PDI or Hsp47. Immunohistochemical studies of murine tissues showed a ubiquitous distribution of ERp61 in a wide variety of cell types. However, it was particularly abundant in plasma cells, mucus-secreting cells in various tissues, neuroendocrine cells including neurons, and follicular epithelia of thyroid gland that actively synthesize and secrete proteins containing cysteine residues. Furthermore, a high correlation was observed between intracellular amounts of ERp61 and immunoglobulin production by hybridoma cells. These results indicate that ERp61 may be involved in disulfide bond formation for such proteins.

Amino Acid Sequence↗

The efficacy of fluconazole in treating prosthetic valve endocarditis caused by Candida glabrata: report of a case.

A case of active prosthetic valve infective endocarditis (PVE) due to Candida glabrata was successfully treated by the systemic administration of fluconazole. A 66-year-old Japanese man with infective endocarditis of unknown etiology underwent aortic and mitral valve replacement to treat severe aortic and mitral regurgitation associated with multiple organ failure. Postsurgical cultures of arterial blood were repeatedly positive for C. glabrata, and therefore fluconazole was administered either intravenously or orally at a dose of 400 mg/day for 46 days. During that time the signs of inflammation including fever such as an elevated white blood cell count and the presence of C-reactive protein (CRP) all improved while the blood cultures became negative. Fluconazole is thus considered to be effective in treating PVE caused by C. glabrata. When administering this treatment, it is also important to monitor the patient's renal and liver function.

Aged↗

Proliferative responses towards native, heat-denatured and pepsin-treated ovalbumin by peripheral blood mononuclear cells from patients with hen's egg-sensitive atopic dermatitis.

In order to clarify the mechanism of food-antigen recognition, the proliferative responses of peripheral blood mononuclear cells (PBMCs) to native, heat-denatured or pepsin-treated ovalbumin (OA) were investigated in 16 hen's egg-sensitive patients with atopic dermatitis (AD). Seven of them had hypersensitivity to boiled hen's egg and others had not. The responses of PBMCs to heat-denatured OA were lower than those to native OA in the patients without hypersensitivity to boiled hen's egg. However, there were no differences of the responses of PBMCs between heat-denatured OA and native OA in the patients with hypersensitivity to boiled hen's egg. Moreover, the reduction of the responses of PBMCs to pepsin-treated OA was recognized in six out of seven patients. The primary structure of OA did not change by heating or pepsin treatment according to sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). These results suggested that the secondary structure of OA changed in connection with the reduction of the responses of PBMCs to denatured OA. In addition, we demonstrated the suppressive effect of anti-HLA-DR and anti-HLA-DQ monoclonal antibodies on the proliferative response of PBMCs to OA. The results suggested that the proliferative responses of PBMCs to OA were restricted by HLA-DR or HLA-DQ in hen's egg-sensitive patients with AD.

Antibodies, Monoclonal↗