Biomedical subjects

N Watanabe

Publications and source records attributed to N Watanabe.

At least 901 records · Page 50Linked to original sources

PubMed1989

Signalling pathway of tumor necrosis factor in normal and tumor cells.

Several aspects of the activity and effects of tumor necrosis factor (TNF) were investigated to gain further insight into its cytotoxic mechanism. The relation between number of TNF receptors and TNF susceptibility of both tumor cells and normal cells was studied, utilizing a specific binding assay. Among the tumor cells, a fairly close correlation (r = 0.855) was observed between receptor number and sensitivity to TNF. No cytotoxic effect by TNF was observed on any of the normal cells tested, even though TNF receptors were shown to be present, and cell proliferation was apparently stimulated by TNF in some cases. TNF internalization and intracellular distribution were studied by pulse-labelling and Percoll density gradient centrifugation. In L-M (murine tumorigenic fibroblasts, highly sensitive to TNF cytotoxicity) cells and HEL (human embryonic lung cells, non-sensitive to TNF cytotoxicity) cells, receptor-bound 125I-labelled recombinant human TNF was rapidly internalized and delivered to lysosomes within 15-30 min, and this was followed by degradation and release into the culture medium. The presence of either a cytoskeletal disrupting agent or a lysosomotropic agent was observed to inhibit the cytotoxic effect of TNF, thus also indicating that TNF internalization, followed by delivery to lysosomes, is essential in the cytolytic mechanism of TNF. As observed by [3H]uridine incorporation, TNF did not affect RNA synthesis in L-R cells (TNF-resistant cell lines derived from L-M cells) and HEL cells, but markedly stimulated (by 3.5 times) RNA synthesis in L-M cells.

Animals↗

PubMed1989

De Vega's annuloplasty for acquired tricuspid disease: early and late results in 110 patients.

From January 1978 through February 1989, 110 tricuspid annuloplasties (De Vega's procedure) were performed in association with mitral and combined mitral and aortic valve disease. Preoperatively, 106 (96%) of 110 patients were in New York Heart Association functional class III or IV. There were seven early deaths (6.3%), and 3 patients, 2 with mitral lesions and 1 with a combined lesion, died during a follow-up period of 3 to 52 months (mean follow-up, 22 months). Four patients (3.6%) required reoperation because of biological mitral valve failure at 5 to 8 years after tricuspid annuloplasty (mean period, 6.6 years). Twenty-three (62%) of 37 randomly selected patients evaluated by echocardiography and 14 (70%) of 20 patients evaluated by right ventriculography showed complete disappearance of tricuspid regurgitation after tricuspid annuloplasty in 1 to 18 months (mean period, 3.3 months). Seventy-seven (96%) of the survivors were in functional class I or II after tricuspid annuloplasty. The actuarial survival rate for the TAP series including early deaths was 85.8% +/- 7.4% at 10 years and the actuarial rate of freedom from reoperation on the tricuspid valve was 96.7% +/- 1.4%. Our surgical experience indicates that the De Vega's annuloplasty, as the method of first choice, is a simple, reliable procedure and resulted in improvement in 90% of patients with moderate to severe functional tricuspid regurgitation.

Adolescent↗

PubMed1989

Nippostrongylus brasiliensis: radioresistant IgE antibody-forming cells in infected rats.

In Nippostrongylus brasiliensis-infected rats, anti-N. brasiliensis IgE antibody production was observed at 20 weeks postinfection, long after the worms, as a source of antigen, had been expelled. The persistent IgE production was not abrogated after whole body irradiation (800 R) administered at 12 or 20 weeks, suggesting the participation of radioresistant IgE-forming cells. Help of T cells and recruitment of B memory cells in the irradiated rats seems to be ruled out by the findings that the irradiation completely inhibited the initiation of anti-N. brasiliensis IgE production in rats shortly after the infection with N. brasiliensis or after primary and secondary immunization with N. brasiliensis-antigen. Moreover, clearance of anti-N. brasiliensis IgE antibody from circulation did not seem to be crucially affected by the irradiation. The radioresistant cells forming anti-N. brasiliensis IgE were most productive in mesenteric lymph nodes as compared to other lymph nodes. The recognition of antigens fractionated by chromatography on Sephadex G-200 was the same for IgE-forming cells from rats 12 weeks after infection as for those from 3 weeks after infection. Based on these results, one of the mechanisms of persistent elevation of IgE antibody in the host infected with helminth parasites might be explained by the participation of radioresistant IgE-forming cells.

Animals↗

PubMed1989

Effect of glucagon-(1-21)-peptide on secretin-stimulated pancreatic exocrine secretion in anesthetized dogs.

The effects of glucagon-(1-21)-peptide on pancreatic exocrine secretion and plasma glucose levels were studied and compared with those of native glucagon in anesthetized dogs. Intravenous bolus administration of 1 nmol or 10 nmol/kg of glucagon-(1-21)-peptide evoked a significant inhibition of secretin-stimulated pancreatic juice secretion and protein output in a dose-dependent manner, as equimolar doses of glucagon did. Native glucagon induced an immediate and transient increase in pancreatic juice volume, which was followed by a significant inhibition. However, glucagon-(1-21)-peptide showed only the inhibitory action. Glucagon-(1-21)-peptide had no effect on plasma glucose levels even when a dose of 10 nmol/kg was given. The results suggest that the N-terminal amino-acid residues of glucagon play an important role in the inhibition of pancreatic exocrine secretion.

Animals↗

PubMed1989

Removal of an arteriovenous malformation in the optic chiasm. A case of Bonnet-Dechaume-Blanc syndrome without retinal involvement.

A rare case of an arteriovenous malformation involving the optic chiasm associated with vascular anomaly in the left maxillary region is presented. The angiogram demonstrated an arteriovenous malformation arising from the anterior circle of Willis (internal carotid, posterior communicating, and proximal anterior cerebral arteries), and located in the region of the optic chiasm and hypothalamus. The case was diagnosed as the Bonnet-Dechaume-Blanc syndrome without intraorbital and retinal arteriovenous malformations. The suprasellar arteriovenous malformation was removed, except for a small portion in the hypothalamus, with satisfactory results.

Adolescent↗

PubMed1989

New hepatoprotective triterpenes from Canarium album.

Canarium album has yielded seven triterpenes of which two appear to be novel. The new triterpenes, which were identified on the basis of spectral characteristics, are urs-12-ene-3 alpha, 16 beta-diol and olean-12-ene-3 alpha, 16 beta-diol. Both compounds exhibited hepatoprotective activity in primary cultured rat hepatocytes intoxicated with D-galactosamine.

Animals↗

PubMed1989

Induction of the transcription factor IRF-1 and interferon-beta mRNAs by cytokines and activators of second-messenger pathways.

Nuclear protein IRF-1 (interferon regulatory factor 1) was earlier shown to bind to cis-acting regulatory elements present on interferon (IFN)-alpha/beta genes and some IFN-inducible genes. Here we show that in both human FS-4 and murine L929 cells, steady-state levels of IRF-1 mRNA were increased by treatment with tumor necrosis factor (TNF), interleukin 1 (IL-1), poly(I).poly(C), or IFN-beta. IRF-1 mRNA induction was also demonstrated in cells treated with calcium ionophore A23187 or with phorbol 12-myristate 13-acetate, but not with epidermal growth factor, dibutyryl-cAMP, or the adenylate cyclase activator forskolin. To determine whether stimulation of IRF-1 mRNA levels correlates with IFN-beta induction, we compared IRF-1 and IFN-beta mRNA levels in cells exposed to various stimuli. In L929 cells, treatment with poly(I).poly(C) under conditions that failed to induce significant levels of IFN-beta mRNA led to a very low induction of IRF-1 mRNA, but "priming" cells with IFN prior to the addition of poly(I).poly(C) greatly increased both IRF-1 and IFN-beta mRNAs. In FS-4 cells an increase in IFN-beta mRNA (examined by the polymerase chain reaction) was seen after treatment with TNF, IL-1, A23187, or poly(I).poly(C), but not with IFN-beta, epidermal growth factor, dibutyryl-cAMP, or forskolin. Thus, all treatments that increased steady-state levels of IFN-beta mRNA also enhanced IRF-1 mRNA levels. However, treatment with IFN-beta, which caused a marked stimulation in IRF-1 mRNA, failed to produce a detectable increase in IFN-beta mRNA. It appears that IRF-1 may be necessary but not sufficient for IFN-beta induction. The ability of TNF and IL-1 to increase both IRF-1 and IFN-beta mRNAs may be responsible for some similarities in the actions of TNF, IL-1, and the IFNs.

Animals↗

PubMed1989

Crystal structure analysis of omega-amino acid:pyruvate aminotransferase with a newly developed Weissenberg camera and an imaging plate using synchrotron radiation.

The three-dimensional structure of omega-amino acid:pyruvate aminotransferase from Pseudomonas sp. F-126, an isologous alpha 4 tetramer containing pyridoxal 5'-phosphate (PLP) as a cofactor, has been determined at 2.0 A resolution. The diffraction data were collected with a newly developed Weissenberg camera with a Fuji Imaging Plate, using synchrotron radiation. The mean figure-of-merit was 0.57. The subunit is rich in secondary structure and comprises two domains. PLP is located in the large domain. The high homology in the secondary structure between this enzyme and aspartate aminotransferase strongly indicates that these two types of enzymes have evolved from a common ancestor.

Aspartate Aminotransferases↗

PubMed1989

The configuration of the laminas and facet joints in degenerative spondylolisthesis. A clinicoradiologic study.

The configuratory variation of laminas and facet joints was discussed with reference to development of degenerative spondylolisthesis and its clinical symptoms. The authors have classified the configuration of laminas in the lower lumbar spine into three different types, (WI, W2, and N), based on the two characteristic features of the lamina: 1) whether or not the inferior articular processes are wider than the waist part of the lamina, and 2) whether or not the facet joint spaces can be recognized on plain anteroposterior (AP) radiographs. Types W1 and W2 laminas have the laterally prominent inferior articular processes, but the facet joint spaces are not visible on AP view in Type W1. Type N lamina has narrow inferior articular processes and its facet joint spaces can be recognized on AP view. Computed tomography (CT) scanning revealed that the direction of facet joints of Types W2 and N laminas was more sagittal than that of Type W1, and that all of Type N laminas with the narrow inferior articular processes have a sagittal facet. Type N lamina was rarely seen in the 257 controls, but was quite frequent in degenerative spondylolisthesis, 3.5% and 45.8%, respectively. Patients with Type N laminas were likely to show more severe clinical symptoms such as difficulty walking and neurologic deficits.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1989

Does peripheral collateralization also cause collateralization in the canine heart?

1. Experiments were conducted in chronically prepared dogs to determine if gradual obstruction of the proximal femoral arteries would also cause collateralization in the coronary circulation. 2. Peripheral coronary pressure was measured before and after peripheral collateralization as an index of coronary collateral function. Coronary collateral blood flow was measured with radioactive microspheres after peripheral collateralization. 3. Peripheral coronary pressure was not significantly altered by peripheral collateralization. Coronary collateral blood flow measured after peripheral collateralization was similar to that reported in non-collateralized hearts. 4. Results indicated that the mechanism(s) responsible for peripheral collateralization do not act systemically, at least not on the coronary circulation.

Animals↗

PubMed1989

Regulation of immunoglobulin E production in mice immunized with an extract of Toxoplasma gondii.

Repeated infection with Toxoplasma gondii could not induce immunoglobulin E (IgE) antibody production. When mice were injected intraperitoneally twice over a 3-week interval with an extract of tachyzoites of T. gondii and Al(OH)3 as adjuvant, antitoxoplasma IgE antibody was produced. Antitoxoplasma IgE antibody titers were low and diminished after a short time in B10.S, BALB/c, C3H, and C57BL/6 mice. This tendency was more evident in IgE low-responder SJL mice. IgE-inducing activity of Toxoplasma antigen was weaker than those of keyhole limpet hemocyanin, ovalbumin, and an extract from Nippostrongylus brasiliensis. The antitoxoplasma IgE antibody production was enhanced by and persisted after whole-body irradiation (150 R) following secondary immunization. The enhanced antitoxoplasma IgE antibody production was suppressed by transferring spleen cells from Toxoplasma antigen-immunized mice. The suppressive effect of the spleen cells was Toxoplasma antigen specific and was removed by treatment with anti-Thy-1.2 and complement. These results indicate that the low IgE production induced by Toxoplasma antigen is the result of irradiation-sensitive and antigen-specific suppressor T cells. These findings might explain the lack of IgE antibody response in mice with Toxoplasma infection.

Animals↗

PubMed1989

Requirement of the single base insertion at the 3' end of the env-related gene of Friend spleen focus-forming virus for pathogenic activity and its effect on localization of the glycoprotein product (gp55).

In order to obtain evidence for the essential role of the single base insertion occurring at the 3' end of the env-related gene of Friend spleen focus-forming virus (SFFV) encoding the leukemogenic glycoprotein (gp55) a mutant SFFV genome was constructed in which the segment of the gp55 gene of the polycythemia-inducing strain of SFFV containing the single base insertion and the 6-base-pair duplication was replaced by the corresponding sequence of the Friend murine leukemia virus env gene. The mutant SFFV-Friend murine leukemia virus complex did not induce symptoms of the erythroproliferative disease in adult DBA/2 mice. During passage through newborn DBA/2 mice, the mutant virus complex invariably gave rise to weakly pathogenic variant SFFVs. All of the variant SFFVs induced in adult DBA/2 mice a transient mild splenomegaly associated with normal or slightly low hematocrit value, and they produced gp55 with a molecular weight similar to that of gp55 of the wild-type SFFV. For the two isolates of variant SFFV, the 3' portion of the viral DNA intermediate containing the 3' portion of the gp55 gene was molecularly cloned. Nucleotide sequences of these biologically active cloned DNAs were determined and showed that the variant SFFV genomes arose from the mutant SFFV genome by regaining the single base insertion, indicating that the single base insertion is essential for the biological activity of gp55. Evidence is presented indicating that the single base insertion which causes a loss of the cytoplasmic domain of the env-related protein is not related to the localization of the further-glycosylated form of gp55 in the plasma membrane but is involved with the release of gp55 from cells.

Amino Acid Sequence↗

PubMed1989

Experimental drug-induced allergic nephritis mediated by antihapten antibody.

Experimental drug-induced allergic nephritis (DIAN) was mediated by an antihapten antibody. It has been postulated that DIAN is induced by cellular and humoral mechanisms. We tried to induce DIAN in mice, where the mechanism depends on humoral immunity. The first attempt was made in mice actively producing antibodies against cephem antibiotics, i.e. cephalothin (CET). Acute interstitial nephritis (AIN), morphologically similar to human disease, was obtained by injection of a CET-protein conjugate into the renal cortex in mice producing anti-CET-IgE and IgG antibodies. AIN could also be induced when normal mice, passively given anti-CET IgG antibody, received a subsequent intrarenal challenge with CET-protein conjugate. These preliminary results indicate that IgG antibody has an important role in the genesis of DIAN. Further experiments were performed with monoclonal antibodies directed against haptens instead of antibiotics in order to clarify the Ig isotype concerned. In mice passively given anti-Dansyl-IgG2a or anti-NP-IgG2a monoclonal antibodies, a challenge with an appropriate hapten-protein conjugate into the renal cortex resulted in AIN. However, transfer of anti-Dansyl-IgE or anti-DNP-IgE monoclonal antibodies, followed by challenge, did not induce AIN. In the experimental systems described, the involvement of a cellular immune mechanism is excluded. The results suggest that IgG, but not IgE antibody, is essential for the induction of DIAN by humoral immune mechanism.

Animals↗

PubMed1989

Fc-epsilon-receptor-bearing lymphocytes in patients with clonorchiasis.

Expression of Fc-epsilon-receptors (Fc epsilon R) on peripheral blood lymphocytes was examined in patients with clonorchiasis. Mean serum IgE levels in these patients was 2,518 IU/ml. Fc epsilon R was detected by flow cytometry analysis with monoclonal antibody. The frequency of Fc epsilon R+ lymphocytes and the density of Fc epsilon R on the cells in the patients were similar to those in normal subjects. Most of the Fc epsilon R+ lymphocytes were B cells. The number of Fc epsilon R+ cells decreased after incubation in serum-free medium at 37 degrees C for 3 h. The amount of regulatory molecules of IgE production, IgE binding factor, was not significantly different between the patients and normal subjects. The number of Fc gamma R bearing T or B cells in the patients was also similar to that of normal subjects. These results indicate that the mechanisms of elevated serum IgE in patients with clonorchiasis might be different from other diseases with hyperglobulinemia E.

Adolescent↗

PubMed1989

Detection and characterization of IgE-producing cells in patients with clonorchiasis.

The ability of peripheral B cells of patients with Clonorchis sinensis infections to secrete IgE spontaneously was investigated in vitro. The de novo synthesis of IgE was observed in unstimulated B-cell cultures of patients. There was a significant relationship between the serum IgE level and the amount of IgE spontaneously secreted by B cells. Pretreatment of patients' B cells with 10 micrograms/ml of rabbit anti-human IgE resulted in the clear suppression of spontaneous IgE synthesis without affecting the IgG synthesis. Their B cells capable of spontaneously secreting IgE were partially sensitive to irradiation with 1,000 rad. The results obtained suggest that such IgE-forming cells may be responsible for at least part of the persistent IgE formation in patients with helminthic infections as well as in those with atopic disease.

Animals↗

PubMed1989

Granulomatous response in selective IgE-deficient SJA/9 mice infected with Schistosoma japonicum.

Granulomatous response was examined in selective IgE-deficient SJA/9 mice infected with Schistosoma japonicum. The average size of granulomas formed around newly deposited eggs in SJA/9 mice was significantly smaller than that in control C57BL/6 or SJL/J mice, although the numbers of adult worms recovered from each strain were comparable among them. Thus, IgE antibody specific to allergenic components of S. japonicum eggs seems to act as an amplifier for the formation of granulomatous lesions.

Animals↗

PubMed1989

Effects of instillation of fly ash in the lung: physiochemical properties and immune responses.

In this study, we examined physiochemical properties of fly ash and aluminum silicate and investigated the effects of these compounds on IgE antibody production and macrophage response in the lung. Fly ash was round in shape, and aluminum silicate was indefinite in shape with respirable size. Both compounds consisted of alumina and silica as the main elements with respirable size. Enhanced IgE and IgG antiovalbumin (OA) antibody production was observed in mice first instilled intratracheally with the aluminum compounds and then given OA aerosol exposure. Histopathologic observations after instillation of fly ash and aluminum silicate showed that a large number of macrophages had ingested the compounds. However, the amount of free compound and the distribution of macrophages were different in mice given fly ash from those given aluminum silicate. These data indicate that particles of fly ash and aluminum silicate instilled into lung act as adjuvant for the production of IgE and IgG antibodies.

Administration, Inhalation↗

PubMed1989

Induction of antigen-specific IgA-forming cells in the upper respiratory mucosa.

We investigated the actual processes for activating respiratory mucosal immunity. Hartley guinea pigs were immunized with particulate antigen of dinitrophenylated ovalbumin into the duodenum (group A), trachea (group B), and nasal cavity (group C) 1 week after systemic priming with the soluble antigen. The control animals (group D) received only systemic priming. Immunoglobulin A antibody titers in nasal secretions and saliva from groups A and B significantly exceeded those of groups C and D (p less than .01). Many antigen-specific IgA-forming cells were detected in the respiratory and gastrointestinal mucosae of groups A and B. Following duodenal immunization, the appearance of antigen-specific IgA-forming cells in Peyer's patches preceded those in mesenteric and hilar lymph nodes, while they simultaneously appeared in the lymphoid tissues after tracheal immunization. These findings suggest that intratracheal immunization mainly stimulates bronchus-associated lymphoid tissue as a source of IgA precursors, as intraduodenal immunization stimulates gut-associated lymphoid tissue.

Animals↗