Search PubMed⌕ Search

Biomedical subjects

N Yoshimura

Publications and source records attributed to N Yoshimura.

At least 613 records · Page 34Linked to original sources
PubMed1983

B cell growth factors and B cell differentiation factor from human T hybridomas. Two distinct kinds of B cell growth factor and their synergism in B cell proliferation.

Human T hybridomas secreting B cell growth factors (BCGF) and B cell differentiation factor (BCDF) have been established. Hybrid clones 77-A, 94-C, and 98-F secreted BCGF that induced proliferation of anti-IgM-stimulated normal B cells. The culture supernatant from 77-A cells could also maintain continuous proliferation of colony-forming B cells, but the factor from 94-C could not. The addition of the supernatant from 94-C cells to that from 77-A cells, however, synergistically augmented the proliferation of colony-forming B cells, demonstrating the existence of two distinct kinds of BCGF and the synergism between them. These supernatants, however, showed no interleukin 2 (IL-2) or BCDF activity. A hybrid clone, 90-E, secreted BCDF. The culture supernatant induced Ig production in Cowan I-stimulated normal B cells or in a transformed B cell line, CESS. However, the supernatant had no BCGF or IL-2 activity. Anti-Ig-stimulated B cells, but not IL-2-dependent T cells, absorbed BCGF activity and CESS cells absorbed BCDF activity but not BCGF activity in the culture supernatants from T hybridomas. Taken collectively, the results demonstrated that IL-2, BCGF, and BCDF were different molecules and acceptors specific for the each molecule are present on the each target cell.

Absorption↗
PubMed1983

Mitochondrial abnormalities in Menkes' kinky hair disease (MKHD). Electron-microscopic study of the brain from an autopsy case.

The brain of an autopsy case of Menkes' kinky hair disease (MKHD), after routine histological examination, was studied extensively by electron microscopy, particularly the mitochondrial alteration. There were widespread mitochondrial abnormalities, including enlargement with tubulo-vesiculated cristae, swelling, and dense body formation and occasional accumulation of glycogen within mitochondria, in addition to increased numbers of mitochondria in some neurons. These abnormalities of mitochondria were present in decreasing severity in the following: Purkinje cells, neurons of the molecular and granule cell layers of the cerebellum, and neurons of the cerebral cortex, globus pallidus, lateral nuclei of the thalamus, caudate nucleus, and the myelinated axons in the white matter. This distribution and the degree of mitochondrial abnormalities in the various structures of the brain were compared with those of degenerative lesions in the respective structures. The comparison disclosed that there was a positive correlation between the two. The mitochondrial enlargement and swelling as in the present study had been well documented in the brain of the brindled mouse; mitochondrial dense bodies had also been reported in previous case reports of MKHD by other authors. The present study strongly suggests that the mitochondrial disease is an essential abnormality and may be responsible for the progressive degeneration of the CNS in MKHD.

Brain↗
PubMed1983

Similarity and dissimilarity in subunit structures of calpains I and II from various sources as demonstrated by immunological cross-reactivity.

The structural relationship between calpain I (low Ca2+-requiring) and calpain II (high Ca2+-requiring) molecules and their respective larger (80K) and smaller (30K) subunit proteins of several non-muscular tissues and cells was studied by testing immunological cross-reactivities. In addition to qualitative analyses by a conventional double immunodiffusion method, quantitative data were obtained, for the first time, by enzyme-linked immunosorbent assays using affinity-purified anticalpain I and anti-calpain II immunoglobulins. The enzyme sources included rat kidney, porcine kidney and erythrocytes, and human erythrocytes. It was concluded that the 30K subunits are immunologically almost indistinguishable between calpains, either I or II, not only from the same but also from different sources, while the 80K subunits of different origins are immunologically related to variable extents but always with discrimination between calpain I and calpain II. Similarity of the 30K subunit proteins and dissimilarity of the 80K counterparts were further substantiated by their chromatographic and electrophoretic behaviors.

Animals↗
PubMed1983

The retinal toxicity of befunolol and other adrenergic beta-blocking agents: inhibition of phagocytic activity of cultured retinal pigment epithelial cells.

Effects of befunolol and other beta-blocking agents on the phagocytosis of cultured retinal pigment epithelial cells (RPE cells) from the chick embryo were investigated. Toxicity was evaluated as an ability of RPE cell phagocytosis of polystylene latex spheres (PS). After an incubation with beta-blockers, PS was added to the medium. The phagocytic reaction was terminated, and particle numbers in RPE cells were counted under an oil immersion microscope. Incubation with befunolol in a range of concentration of 10(-9)-10(-3) M resulted in a time- and dose-dependent inhibition of phagocytosis. Incubation with 10(-6) M befunolol inhibited phagocytic activity down to 60% of control. The same mode of action was observed in other beta-blockers. The inhibitory effect of befunolol at 10(-4) M or lower concentrations was reversible, while incubation with 10(-3) M for 24 h was irreversible.

Adrenergic beta-Antagonists↗
PubMed1983

Helper and suppressor T-cells regulating killer cells of EB virus infected cells.

Using an in-vitro human lymphocyte system, a study was performed to determine whether helper T-cells and suppressor T-cells control the generation of killer cells against autologous B-cells transformed by Epstein-Barr (EB) virus. When T-cells were treated with mitomycin C and reacted in the presence of macrophages with target cells bearing HLA-DR, helper T-cells were induced but suppressor T-cells were not. In contrast, when T-cells were reacted in the absence of macrophages to target cells lacking HLA-DR, suppressor T-cells but not helper T-cells were induced. The culture supernatant of the T-cells which showed suppressor activity also suppressed the generation of killer cells. The thus-induced suppressor T-cells also suppressed the HLA incompatible allogeneic killer cells which were directed against autologous B-cells transformed by EB virus and also autologous killer cells directed against allogeneic target cells. These observations indicated that there is no HLA restriction between the suppressor T-cells and the killer cells and the suppression is antigen nonspecific.

B-Lymphocytes↗
PubMed1983

Metabolic deterioration in shock state and its modulation.

The initial cellular reaction against the deleterious effects of shock-inducing stimuli apparently elevates the energy-producing capacity so that the cell is able to sustain its normal function. Several endocrine events are fundamentally important as triggering factors for this kind of reaction. As the shock state advances, cellular metabolism deteriorates progressively and cellular energy is exhausted. Depression of intracellular cAMP may induce cellular metabolic unresponsiveness to hormonal stimuli. Consistent degradation of high-energy substances, extreme deviation of the redox state in the NAD+-NADH system, and decrease of endogenous key substances such as L-carnitine ultimately may lead to a standstill of cellular enzymatic reactions (Fig. 13). Methods intended to sustain cellular membrane and enzymatic systems may offer the best contribution to the improvement of shock therapy.

Adenine Nucleotides↗
PubMed1983

Antishock effect of gabexate mesilate (FOY).

The antishock effects of gabexate mesilate (FOY) were investigated in rats subjected to hemorrhagic hypotension, with particular attention focused on the stabilizing effects of hepatic lysosomes. The survival time of rats treated with FOY, infused for 2 hours intravenously at a rate of 50 mg/kg/hr, was significantly prolonged, accompanied by a tendency to decreased activity of plasma lysosomal enzymes. FOY, at a concentration of 10(-3) M, exerted a significant decrease in the extralysosomal release of acid phosphatase (15%, P less than 0.05), beta-glucuronidase (25%, P less than 0.05) and cathepsin D (25%, P less than 0.02) following hyposmotic labilization of lysosomes. Although the release of lysosomal enzymes might be counterbalanced by 50 mg/kg/hr of FOY, favorable cytochemical findings indicating stabilization of lysosomal membranes were consistently observed. The data suggest that FOY has antishock properties, and that these properties are caused, at least partially, by the stabilization of lysosomes.

Acid Phosphatase↗
PubMed1983

[The effect of prostaglandin F2 alpha on the gastrointestinal movement after urological surgery].

To facilitate postoperative flatus, Prostaglandin F2 alpha (PGF2 alpha) was given intravenously to 23 patients who underwent urological operations. The patients were 14 males and 6 females aged from 20 to 77 years old. Patients with hypertension or cardiovascular disease were not included. Twelve operations were performed under general anesthesia, and 8 under epidural anesthesia. Thirteen operations were performed for the upper urinary tract or adrenal gland, and 5 were for the lower urinary tract. In 2 cases, the peritoneal cavity was opened and operations were performed on the intestines. PGF2 alpha 2000 micrograms was added to the postoperative drip infusion and administered in 2 to 3 hours. Until the first flatus was recognized, PGF2 alpha was given once a day in the same manner. Twenty-six patients, 10 of whom were given either vagostigmine or pantothen postoperatively, served as the control group. PGF2 alpha accelerated the postoperative flatus by 8.7 hours (mean) compared with the control group, but it was not significant. The onset of flatus was significantly promoted under epidural anesthesia. Gastrointestinal movement tended to be facilitated in the PGF2 alpha group after lower urinary tract surgery and in the patients over 50 years old. Three patients complained of severe abdominal pain as a side effect; and, injection of PGF2 alpha was stopped. In 7 patients, mild stomachache , vascular pain, nausea, vomiting or elevation of blood pressure were observed.

Adult↗
PubMed1983

[A case of a tumor of the spermatic cord metastatic from cecal cancer].

A 71-year-old man was admitted with the complaint of painless tumor in the right inguinal region, one month after right hemicolectomy for cecal cancer. The tumor seemed to exist in the right spermatic cord, so right radical orchiectomy was done. A tumor was found in the right spermatic cord, but the right spermatic duct, right epididymis and right testicle were intact. Histopathological examination of the tumor revealed metastatic adenocarcinoma from the cecal cancer. Twenty cases of metastatic tumors of the spermatic cord from the gastrointestinal cancers have been reported in Japan including this case.

Adenocarcinoma↗
PubMed1983

Effect of Fluosol-DA on the blood coagulation/fibrinolytic system and the renin-angiotensin system in man.

Either F-DA, Ringer's lactate or HES was given to three groups of six patients each who were undergoing elective gynecologic surgery, and their effects on the blood coagulation/fibrinolytic systems, and the renin-angiotensin systems were evaluated. Platelet counts were found to increase markedly using the Coulter Counter method, but no change was observed when the Rees-Ecker method was used. Platelet aggregation was inhibited and AT-III concentrations were decreased by administration of F-DA. There were no significant changes in PT or a-PTT as a result of F-DA administration. Similarly, there were no significant changes in the concentrations of fbg, FDP, a2-PI, P-FN and renin, angiotensin I, II and angiotensin converting enzyme following F-DA administration. Based upon these findings, it is suggested that a clinical dosage of 20 to 30 ml/kg of F-DA can be safely administered to patients with normal platelet and RES function.

Adult↗
PubMed1982

Acute rubella retinal pigment epitheliitis in an adult.

A 50-year-old man who had been taking betamethasone for 20 days experienced a slight bilateral decrease in visual acuity. There were localized dark-gray atrophic lesions at the posterior pole, accompanied by a diffuse detachment of the sensory retina. The retinal vessels appeared to be normal and only minimal anterior uveitis was present in the more severely affected eye. Fluorescein angiograms showed no masking of choroidal fluorescence in the early phase and late-phase fluorescein angiograms showed multifocal leakage of the dye into the subretinal space. Electro-oculographic findings were abnormal only during the acute stage in the more severely affected eye and returned to normal within three months. The retinal detachment spontaneously resolved within three months; visual acuity returned to normal but some atrophic areas remained in the retinal pigment epithelium. Because the antibody titer to rubella was 1:1,028 during the acute stage but decreased to 1:257 within one month, we believe this patient had rubella retinitis, a rare condition in adults. The betamethasone may have made him more susceptible to the viral infection.

Betamethasone↗
PubMed1982

Infusion of branched-chain enriched amino acid solution in patients with hepatic encephalopathy.

Hospitalized patients with hepatic insufficiency often suffer from severe catabolic states and are in urgent need of nutritional support during their acute illness. Protein intolerence, however, remains a significant problem with respect to the provision of adequate nutrition, either enterally or parenterally. The following report is an anecdotal series of 63 consecutive patients in a large urban hospital treated prospectively with nutritional support using a prototype high branched-chain amino acid solution (FO80) given by technique of total parenteral nutrition by the subclavian or internal jugular route with hypertonic dextrose. Sixty-three patients, of which 42 had chronic liver disease (cirrhosis) with acute decompensation and 17 with acute hepatic injury as well as four with hepatorenal syndrome, are the subject of this report. All required intravenous nutritional support and were either intolerant to commercially available parenteral nutrition solutions or were in hepatic encephalopathy at the time they were initially seen. The cirrhotic patients had been hospitalized for a mean of 14.5 +/- 1.9 days before therapy, had a mean bilirubin of 13 mg/100 ml, and had been in coma for 4.8 +/- 0.7 days despite standard therapy. Patients with acute hepatitis had been in the hospital for 16.2 +/- 4.1 days before therapy, had a mean bilirubin of 25 mg/100 ml, and had been in coma 5.2 +/- 1.6 days before therapy. Routine tests of liver function, blood chemistries, amino acids, EEGs, and complex neurological testing including Reitan trailmaking tests were used in the evaluation of these patients. Up to 120 grams of synthetic amino acid solution with hypertonic dextrose was tolerated in these patients with improvement noted in encephalopathy of at least one grade in 87% of the patients with cirrhosis and 75% of the patients with hepatitis. Nitrogen balance was achieved when 75 to 80 grams of synthetic amino acids were administered. Survival was 45% in the cirrhotic group and 47% in the acute hepatitis group. Encephalopathy appeared to correlate with individual amino acids differentially in the various groups and with the ratio between the aromatic and the branched-chain amino acids. Ammonia did not correlate with either the degree of encephalopathy or improvement therefrom. In 24 Patients therapy for hepatic encephalopathy was limited to infusion of the branched-chain enriched amino acid solution only, with wake-up in 66% of this group. The results strongly suggest that in protein intolerant patients requiring nutritional support, infusion with branchedchain enriched amino acid solutions is well tolerated with either no worsening of or improvement in hepatic encephalopathy coincident with the achievement of nitrogen equilibrium and adequate nutritional support.

2-Hydroxyphenethylamine↗
PubMed1982

A human helper T cell clone secreting both killer helper factor(s) and T cell-replacing factor(s).

A human helper T cell clone (d4), which showed its helper effect on the differentiation of both T and B cells, was established by MLC reaction of normal T cells against a B lymphoblastoid cell line (CESS) followed by cloning in the presence of IL2 and x-irradiated CESS and autologous non-T cells. d4 cells helped the induction of cytotoxic T cells against UV-treated CESS cells. Antigen-stimulated d4 cells secreted helper factor(s) involved in the induction of cytotoxic T cells (killer helper factor(s), KHF), and KHF activity could be separated into two fractions, one with the m.w. of 15,000 to 20,000 and the other with the m.w. of 45,000 to 50,000. The factor with 15,000 to 20,000 m.w. showed IL 2 activity; the other factor showed gamma-interferon activity without IL 2 activity, suggesting that both IL 2 and gamma-interferon exerted KHF activity. d4 cells or their culture supernatant showed helper activity in the induction of IgG in a B cell line (CESS). The helper activity of the supernatant (TRF) was absorbed with CESS cells but not with IL 2-dependent CTLL, whereas KHF activity was absorbed with IL 2-dependent CTLL but not with CESS cells. The results showed that TRF and KHF were distinct molecules and a single helper T cell clone could secrete helper factors for both B and T cells.

B-Lymphocytes↗