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Biomedical subjects

K Higashino

Publications and source records attributed to K Higashino.

At least 199 records · Page 11Linked to original sources
PubMed1990

Purification and some properties of the fast migrating alkaline phosphatase in FL-amnion cells (the Kasahara isoenzyme) and its cDNA cloning.

One of two main FL-amnion cell alkaline phosphatase (AP), the fast migrating one (FL-APF) has been reported to be identical to Kasahara isoenzyme (K.I.), which occurs preferentially in sera of patients with primary hepatoma. We purified FL-APF of which the apparent molecular weight was 135,000 by gel filtration, and that of the subunit was 62,000 on SDS/PAGE, indicating homodimeric structure of FL-AL-APF. FL-APF was found to react with monoclonal antibody against adult intestinal AP, but not with monoclonal antibody to placental AP. We isolated FL-APF cDNA clone from FL-amnion cells, of which cDNA was 2525 base pairs in length. Nucleotide sequence of the coding region and the 3' untranslated region was identical to the sequence of human adult intestinal AP cDNA. But the untranslated region of the 5' end of the isolated clone was slightly longer than that of intestinal AP. Hence, FL-APF (K.I.) may occur by altered glycosylation of intestinal AP.

Alkaline Phosphatase↗
PubMed1990

IL-5 up-regulates but IL-4 down-regulates IL-2R expression on a cloned B lymphoma line.

Both IL-4 and IL-5 demonstrate B cell growth activity. IL-5 can render a cloned neoplastic B cell line, BCL1-CL-3 cells, responsive to IL-2, whereas IL-4 has no such activity. The response to IL-5 and IL-2 proceeds in two phases: the first phase which clearly depends upon IL-5 is the obvious increase in number of high affinity IL-2R (3.1-fold) with modest increase of low affinity IL-2R (1.2-fold) and gain of the ability of facilitated IL-2-binding and internalization of IL-2, and the second phase which is induced by IL-2 in the IL-5-stimulated CL-3 cells comprises the striking increase of low affinity IL-2R (8.5-fold). Kinetic study has revealed that high affinity IL-2R expressed on CL-3 cells begins to increase at 6 h and reaches to maximum at 12 h after stimulation with IL-5 or IL-5 plus IL-2, whereas low affinity IL-2R expression increases at 18 h and becomes maximal at 24 h after stimulation of CL-3 cells with IL-5 and IL-2. However, in the presence of IL-4, IL-5 cannot induce an increase in number of high affinity IL-2R on CL-3 cells. Thus, CL-3 cells stimulated with the mixture of IL-5 and IL-4 cannot respond to IL-2, and fail to show up-regulated expression of low affinity IL-2R. IL-4 also has a capacity to modestly interfere with the action of IL-2 to up-regulate low affinity IL-2R expression on IL-5-pretreated CL-3 cells. Thus, this monoclonal B cell system provides an excellent model system to define the roles of IL-5 and IL-4 involved in the B cell differentiation and to characterize the properties of B cells competent to IL-2 stimulation and the signal transduction mechanism which operates through IL-2/IL-2R system.

Animals↗
PubMed1990

Monoclonal antibody to pseudouridine used to develop a radioimmunoassay.

Pseudouridine, a component of tRNA, was modified to yield the derivatives: succinyl, palmitoyl pseudouridine, and protein conjugates. These derivatives were used in preparation of monoclonal antibodies specifically directed to pseudouridine. MAbs from three hybridomas (OAL 881, 812 and 814) were established and shown to be directed to pseudouridine, uridine and uracil. OAL 881 was equally reactive with the three substrates, OAL 812 showed the same reactivity for pseudouridine and uracil, while OAL 814 showed a reactivity mainly for pseudouridine. MAb OAL 814 was used in a radioimmunoassay (RIA) system unique for pseudouridine. A good dose-response curve was observed in the range between 31.3 and 2000 nmol/ml. Intra- and inter-assay CV values were below 4.1% and 7.4% respectively, and good results were obtained from recovery of added material and dilution tests. The ratio of pseudouridine/creatinin in urine was significantly higher in patients with cancer than in normal subjects.

Antibodies, Monoclonal↗
PubMed1990

Effects of transforming growth factor-beta 1 on murine clonal osteoblastic cells (MC3T3-E1).

Transforming growth factor (TGF)-beta family is considered to be an important local factor that greatly regulates bone metabolism. However, the effects of this polypeptide on osteoblasts have been divergent under various experimental conditions. Moreover, three forms of TGF-beta have been recently described. Therefore, we reexamined the effects of TGF-beta 1 on clonal murine osteoblastic MC3T3-E1 cells. TGF-beta 1 dose- and time-dependently depressed alkaline phosphatase activity in the cells supported by low concentration of serum. On the contrary, in the same range of concentrations, TGF-beta 1 stimulated DNA synthesis in the cells. These effects of TGF-beta 1 were observed in the cells cultured in the media without or with a high concentration of serum. These effects of TGF-beta 1 are not mediated by endogenous production of prostaglandin, since the basal level of prostaglandin E2 was very low and rather inhibited by TGF-beta 1; and, further, indomethacin did not modify the effects of TGF-beta 1 on the cells under the present conditions. Furthermore, TGF-beta 1 greatly stimulated not only type I but also type III collagen production. Hydroxyurea completely blocked the stimulation of DNA synthesis by TGF-beta 1, but partially inhibited the collagen synthesis, suggesting that the TGF-beta 1-stimulated collagen synthesis is at least in part linked to the proliferation. However, the stimulation of collagen synthesis by TGF-beta 1 was greater than that of DNA synthesis, and further, the amount of hydroxyproline in the cell was evidently augmented by TGF-beta 1. Our data presented here thus suggest that TGF-beta 1 may act on preosteoblasts to increase the number of osteoblasts and the amount of bone organic matrix.

Alkaline Phosphatase↗
PubMed1990

[A case report of high plasma renin activity in chronic pulmonary disease and the effect of angiotensin-II-analogue (1-sarcosine, 8-isoleucine-angiotensin-II)].

Five patients with chronic pulmonary diseases (3 pulmonary emphysema, 1 chronic respiratory failure caused by old tuberculosis, 1 diffuse panbronchiolitis) showed a marked increase of plasma angiotensin-I and PRA level, which was accompanied by an increase of angiotensin-II level, however, whose systemic blood pressure was not elevated. The intravenous infusion of angiotensin-II-analogue (1-Sarcosine, 8-Isoleucine-Angiotensin-II) elicited an antagonistic blood pressure response resembling Bartter's syndrome.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1990

The effect of completely purine-free diet of low sodium content on purine intermediates and end-product.

Intake of completely purine-free foods of low sodium content increased the plasma concentrations of both hypoxanthine and inosine and the urinary excretion of hypoxanthine, while it decreased the urinary excretion of uric acid and the fractional clearance of uric acid. However, this diet affects neither nucleotides (inosine monophosphate, adenosine monophosphate, adenosine diphosphate and adenosine triphosphate) in red blood cells, enzymes (purine nucleoside phosphorylase, adenosine deaminase and hypoxanthine guanine phosphoribosyl transferase) in red blood cells nor the fractional clearance of oxypurines. These results suggest that the salvage of purines becomes more effective by limiting the conversion of hypoxanthine to xanthine and limiting the loss of uric acid during intake of completely purine-free foods of low sodium content; also that a decrease in the fractional clearance of uric acid due to completely purine-free foods of low sodium content may be an additional mechanism associated with the conservation of purines but is more likely to be a response to the low sodium diet on the renal handling of uric acid.

Adult↗
PubMed1990

Analysis of uric acid transport in renal tubules using benzbromarone and pyrazinamide.

Both the benzbromarone loading test alone and the pyrazinamide suppression test combined with the benzbromarone loading test were performed in four healthy male volunteers to examine the renal handling of uric acid and to demonstrate whether benzbromarone selectively blocks postsecretory reabsorption. On the basis of the four-component theory, equations of four states of fractional uric acid clearance were constructed: 1) the control state, the states of 2) benzbromarone loading, 3) pyrazinamide suppression and 4) both pyrazinamide suppression and benzbromarone loading. As a result, presecretory reabsorption, tubular secretion and postsecretory reabsorption of uric acid were calculated to be about 93-98%, 30-44% and 79-92%, respectively. In addition, it was calculated that benzbromarone inhibited postsecretory reabsorption selectively. Because of the selectivity of the action site of benzbromarone in renal tubules, this loading test is considered to reflect uric acid transport more precisely than tests using probenecid.

Benzbromarone↗
PubMed1989

B cell response pathways regulated by IL-5 and IL-2. Secretory microH chain-mRNA and J chain mRNA expression are separately controlled events.

We have examined the effect of IL-5 and/or IL-2 on the expression of the secretory form of microH chain (microsecond) and J chain mRNA in a homogeneous neoplastic B cell clone, in which proliferation, IL-2R up-regulation and entry into the IgM secretory state are separately controlled events. The IL-5 signal triggers a partial induction of CL-3 cells into the IgM secretory state, characterized by a striking increase of microsecond mRNA expression and an increase in the ratio of the secretory to membrane forms of microH chain mRNA, with a modest increase of J chain mRNA. In contrast, amplification of J chain mRNA is accomplished by the late-acting B cell differentiation stimulus, IL-2, acting on IL-5-pretreated CL-3 cells or acting simultaneously with IL-5 on CL-3 cells. Such dually stimulated cells now are fully induced into IgM secreting cells. These results define the relative roles of IL-5 and IL-2 in B cell differentiation by showing important regulatory effects at the mRNA level. In addition, these results substantiate that appearance of mRNA for J chain, a molecule key to the formation of pentameric IgM, is a limiting factor for high level IgM secretion. The separate control of microsecond and J chain mRNA found in CL-3 cells stimulated with IL-5 and IL-2 elucidates a molecular mechanism by which these two lymphokines synergize in the development of CL-3 cells into IgM secreting cells.

B-Lymphocytes↗
PubMed1989

Metabolism of pyrazinamide and allopurinol in hereditary xanthine oxidase deficiency.

The metabolism of pyrazinamide and allopurinol was studied in three xanthinuric patients from two families with hereditary xanthinuria to determine whether both substrates were oxidized only by xanthine oxidase or by other oxidases as well. One xanthinuric patient could neither metabolize pyrazinamide into 5-hydroxypyrazinamide nor allopurinol into oxypurinol. Two xanthinuric patients could metabolize both pyrazinamide into 5-hydroxypyrazinamide and allopurinol into oxypurinol but could not oxidize pyrazinoic acid to 5-hydroxypyrazinoic acid. These findings suggest that xanthinuria comprises at least two subgroups.

Adult↗
PubMed1989

Reduction of 7-ketolithocholic acid by human liver enzyme preparations in vitro.

The formation of chenodeoxycholic and ursodeoxycholic acids from 7-ketolithocholic acid by human liver preparations was examined in vitro. Liver preparations were incubated with 7-ketolithocholic acid at pH 5.5 in a sodium-potassium-phosphate buffer containing NADPH or NADH. The products formed were analyzed by gas chromatography and gas chromatography-mass spectrometry. Results showed that chenodeoxycholic and ursodeoxycholic acids could be formed from 7-ketolithocholic acid by human liver enzyme(s). The enzyme(s) required NADPH but not NADH as coenzyme and was localized largely in the microsomes. The conjugated 7-ketolithocholic acid, especially the taurine conjugated, was predominantly reduced to chenodeoxycholic acid, whereas the unconjugated 7-ketolithocholic acid was not reduced well to either chenodeoxycholic acid or ursodeoxycholic acid. Thus the reduction of 7-ketolithocholic acid by human liver enzyme(s) was found to be dependent on whether the substrate was conjugated or not.

Chenodeoxycholic Acid↗
PubMed1989

Effect of probenecid on oxypurines in plasma.

Probenecid decreased the plasma concentration of oxypurines (hypoxanthine and xanthine) but did not increase the renal excretion of oxypurines. However, the concentrations of hypoxanthine and nucleotides (inosine monophosphate, adenosine monophosphate, adenosine diphosphate, adenosine triphosphate, guanosine diphosphate and guanosine triphosphate) in red blood cells did not change after the administration of probenecid. In addition, the drug did not inhibit adenosine deaminase, purine nucleoside phosphorylase, hypoxanthine guanine phosphoribosyl transferase and xanthine oxidase in vitro. These results suggested that the rapid fall of plasma concentration of uric acid due to the potent uricosuric action of probenecid resulted in the fall of plasma concentration of oxypurines.

Adenosine Deaminase↗
PubMed1989

[A case of multiple cavities on chest film with high titer of serum cryptococcal antigen].

A 26-year-old man admitted to Nishinomiya Municipal Hospital for further evaluation for abnormal shadows on the chest film in a mass examination. He had no subjective complaints; for example, cough, sputum or dyspnea. His past history and physical examinations yielded no significant findings. The chest film revealed the multiple cavities accompanied with a little infiltration throughout several lobes bilaterally. The inflammatory reactions; such as, CRP and ESR, were all intact, but the titer of the serum cryptococcal antigen was high. He was not immunocompromised. Although bronchoscopy and transbronchial lung biopsy were performed twice during admission, they revealed no pathogenic findings both bacteriologically and histologically. The elevation of the serum cryptococcal antigen titer suggested that this disease is the primary pulmonary cryptococcosis. The titer decreased with spontaneous disappearance of the abnormal shadows on the chest film. This test has a sensitivity of 90% for cryptococcal infection, but in rheumatoid arthritis, a small percentage of false positive results have been reported. Therefore, if the rheumatoid factor is eliminated, the test is more specific for cryptococcal infection. On the other hand, some authors have reported the false positive results in Trichosporon beigelii infection by this method. But this disease is negligible for its frequency in clinical features in our country. We emphasized that this non-invasive test is more useful for the diagnosis of the primary pulmonary cryptococcosis.

Adult↗
PubMed1989

The effect of phenobarbital on human plasma lipids.

The effect of phenobarbital to increase the activity of hepatic microsomal enzyme system, resulting in an increase in high density lipoprotein (HDL)-cholesterol, is well known. However, it remains uncertain whether phenobarbital increases plasma concentrations of cholesterol and triglyceride, and which subfractions of the high density lipoprotein fractions phenobarbital increases. The present study was therefore, conducted to investigate these points. Long-term treatment of phenobarbital increased the plasma concentrations of HDL2-cholesterol, HDL3-cholesterol and HDL3-phospholipid, and decreased the plasma concentrations of low density lipoprotein + very low density lipoprotein-cholesterol. On the other hand, its long-term treatment did not affect the plasma concentrations of cholesterol, triglyceride and phospholipid. In addition, phenobarbital increased the plasma concentration of apolipoprotein A-I, decreased the plasma concentration of apolipoprotein B, but did not affect the plasma concentration of apolipoprotein A-II. These results indicate the possibility that phenobarbital has an antiatherogenic effect.

Adult↗