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Biomedical subjects

K Oikawa

Publications and source records attributed to K Oikawa.

At least 127 records · Page 7Linked to original sources
PubMed1985

Familial Creutzfeldt-Jakob disease in Japan. Three cases in a family with white matter involvement.

Three cases of Creutzfeldt-Jakob disease occurring in one family have been clinicopathologically examined. Although the age at onset, duration, and age at death differed for each case, pathological findings, including diffuse neuronal loss, astrocytosis, spongiform changes and patchy and/or diffuse white matter involvement were similar. Life histories and inheritance patterns of the present 3 cases and 2 other families previously reported in Japan are compared with the general findings for familial cases in western countries.

Aged↗
PubMed1985

Studies on the delayed neurotoxicity of organophosphorus compounds--(III).

TOCP (Tri-orthocresyl phosphate), an organophosphorus compound, has been implicated in producing neuropathy in the male S. D. rats. Repeated subcutaneous doses of TOCP (600 mg/kg) for up to 6 weeks produced ataxia, most striking at 50 days after final injection, followed by gradual recovery. Ultrastructurally, the internal structure of affected nerve fibers was primarily composed of altered smooth endoplasmic reticulum, tubular membrane system, and mitochondria, although myelin sheath was found to be essentially normal. In the histopathological examination, axonal and myelin degeneration was disclosed in the gracile nucleus and in the gracile fasciculus of the cords as well as in the sciatic nerves. The localization and degree of these changes were considered to be "dying back", showing systemic neuropathy. In addition, muscular lesion showed small group atrophy, corresponding to Type I fiber atrophy.

Animals↗
PubMed1985

Formation of ester forms of riboflavin in the pituitary gland of rat.

We studied the formation of ester forms of riboflavin in the pituitary gland of rats using 14C-riboflavin labeling and a gel filtration technique. The active formation of ester fraction of riboflavin suggests that two synthesizing enzymes of ester forms, flavokinase and FAD pyrophosphorylase, exist in this organ. A minor peak containing a lesser amount of radioactivity contained protein as measured by UV absorption at 280 nm was found when supernatant from incubated homogenate was chromatographed on a Sephadex G-15 column. This suggests the presence of a riboflavin-binding protein; the amount of 14C-riboflavin bound to pituitary proteins was expressed as the binding capacity of riboflavin. No changes were found in the binding capacity or esterification of riboflavin in the pituitary gland of rats treated with ACTH, dexamethasone phosphate, or subjected to liver impairment by CC14 injection. However, esterification was increased at 24 and 48 h after adrenalectomy. We posit that the riboflavin turnover in the pituitary gland may not be subject to marked changes in order to maintain the function of this organ. In aged rats, esterification was lower than in young rats suggesting that the turnover of pituitary riboflavin is related to senescent phenomena.

Adrenalectomy↗
PubMed1984

Characterization of skeletal muscle calsequestrin by 1H NMR spectroscopy.

Calsequestrin (Mr = 44,000) is a calcium-binding (KD congruent to 1 mM, congruent to 50 sites/molecule) protein found in the lumen of the sarcoplasmic reticulum of skeletal muscle. The 1H NMR spectrum of calsequestrin in the calcium-free form is presented and is characteristic of a protein largely in the random coil configuration. A number of peaks in the aromatic region have been assigned based on their chemical shifts and sensitivity to pH. The interaction of this protein with Ca2+ and K+ was studied by 1H NMR. Potassium ion binding to calsequestrin caused broadening and concomitant loss of intensity in both the aromatic and aliphatic regions of the spectrum. Calcium ion binding caused similar effects but at much lower metal ion concentrations. It was found that the binding of Ca2+ to calsequestrin was cooperative (Hill coefficient n = 2.9 +/- 0.2) with a dissociation constant of 0.25 +/- 0.06 mM in the absence of K+. In contrast, K+ showed binding to a single class of independent sites (KD = 0.20 +/- 0.04 M). Calcium binding was also studied by circular dichroism at protein concentrations similar to the NMR experiments. The binding profile and cooperativity (n = 2.0 +/- 0.1, KD = 0.19 +/- 0.04 mM) were in agreement with the 1H NMR results. Circular dichroism studies performed at low protein concentrations to reduce the possible effect of calcium binding on the concentration of free calcium gave similar values of n = 2.42 +/- 0.14 and KD = 0.21 +/- 0.005 mM. This cooperativity was also observed in the presence of 100 mM KCl although the affinity for calcium has been significantly reduced (n = 1.65 +/- 0.09, KD = 0.87 +/- 0.036 mM). In view of the large number of calcium binding sites in calsequestrin, these small Hill coefficients show that calcium binding to calsequestrin is only mildly cooperative.

Animals↗
PubMed1984

Studies on the delayed neurotoxicity of organophosphorus compounds--(II).

Delayed neurotoxicity experiment was carried out on an organophosphorus compound (TOCP) in hens. Fifteen hens, 1.9 kg of their average body weight and 20 months of age, were orally administered with TOCP in a dose of 400 mg/kg body weight. Two animals out of 15 were sacrificed after 7 days to examine alterations in the nervous system under electron microscope. On the remaining 13 animals, histopathological examinations were carried out after 35 days. During the course of the experiment, progressive neuropathy developed in the animals at 10 to 12 days after the exposure to TOCP. Examinations of the sciatic nerve under electron microscope revealed slight axonal degeneration while the myelin sheath was found to be rather intact. On the animals after the observations periods of 35 days, marked axonal and myelin degeneration was observed in the anterior and posterior funiculus, and in the spinocerebellar tracts of the spinal cord as well as in the cerebellar peduncle and in the white matter of the cerebellum associated with glial proliferation. The localization and degree of these changes were considered to be "Dying Back", showing systemic neuropathy. Moreover, the morphological alterations of the nerve cells were observed in the Purkinje cells, in the cerebellar nucleus, gracilis nucleus, and anterior horn cells of the lumbar spinal cords, characterized by loss of nerve cells and/or tigrolysis. Muscular lesions showed small group atrophy, corresponding to Type I fiber atrophy.

Animals↗
PubMed1984

Cancer-associated alteration of beta-glucuronidase in human lung cancer: elevated activity and increased phosphorylation.

beta-Glucuronidase from human lung neoplasms of various histological types and from uninvolved tissues was studied. A significant elevation of beta-glucuronidase activity was observed in adenocarcinoma and squamous cell carcinoma of the lung as compared with the corresponding uninvolved tissues (P less than 0.01). Saccharo-1,4-lactone, a strong inhibitor of the enzyme, exhibited a substantially greater stabilizing effect on the adenocarcinoma enzyme than on the other enzymes. However, removal of the carbohydrate moiety from the adenocarcinoma enzyme by treatment with endo-beta-N-acetylglucosamidase H (endoglycosidase H) brought about a decrease in the stabilizing effect. Tumor beta-glucuronidase showed considerable negative charge heterogeneity in the pI range from 4.2 to 6.2 in isoelectric focusing on polyacrylamide gel. Upon treatment with exogenous alkaline phosphatase or endoglycosidase H, the heterogenous variant forms of the tumor enzyme appeared to partly or completely lose their negative charge and to be converted into forms similar to those of the normal lung enzyme. These data strongly suggest that the variants are highly phosphorylated on the oligosaccharide chains of the enzyme. An experiment on the labelling of beta-glucuronidase with [32P]-phosphoric acid provided further evidence that the acidic variants found in lung cancers are extensively phosphorylated forms of the enzyme.

Adenocarcinoma↗
PubMed1983

RT1-linked Ir and Is genes control the immune response to bovine insulin in the rat.

The immune response to bovine or pork insulin (BI or PI, respectively) was studied in the rat using the in vitro insulin-induced lymphocyte-proliferation assay. Results indicated that 11 inbred rat strains were divided into categories of high and low responders. Two high responders, SDJ (RT1u) and BN(RT1n) inbred rat strains, appeared to recognize different antigenic determinant(s) on the insulin molecule. The results of linkage and segregation analyses in F1, F2, backcross, and partially congenic rats showed that the Ir gene (Ir-BI), which encodes the high responsiveness in the SDJ rats, is inherited associated with RT1u, whereas the immune suppression gene (Is-BI), which encodes the low responsiveness in the WKA(RT1k) rats, is inherited together with RT1k. The Is-BI is the first major histocompatibility complex (MHC)-linked Is gene reported in the rat. The LEJ(RT1-AuBb) inbred rat strain showed a low response to BI, indicating that Ir-BI is closer to RT1-B/RT1-D region than to RT1-A.

Animals↗
PubMed1983

Elevated activity of beta-hexosaminidase and sulfhydryl modification in the B-variant of human lung cancer.

Activities of beta-hexosaminidase A and beta-hexosaminidase B (Hex B) were measured both in human lung carcinoma and the adjacent normal tissues of 47 patients. The specific activity of total beta-hexosaminidase in the tumors was considerably higher than in the adjacent normal tissues, irrespective of histological types. In isoelectric focusing experiments, Hex B purified from normal lung exhibited a single peak with an isoelectric point (pI) of 7.9, while Hex B purified from adenocarcinoma contained two forms with pI 7.6 and 7.9. With respect to heat stability, Hex B from the normal lung was very stable at 52 degrees, while the tumor Hex B (mixture of pI 7.6 and 7.9 forms) was unstable. After treatment of the tumor enzyme with dithiothreitol, heat stability was restored. When the tumor pI 7.6 form was treated with dithiothreitol and subjected to polyacrylamide gel electrophoresis, the enzyme converted to a pI 7.9 form similar to that of the normal lung. Determination of the sulfhydryl group of the tumor pI 7.6 form under nondenaturing conditions showed that the enzyme had some easily reducible disulfide bonds on its surface. These findings indicate that the formation of mixed disulfide bonds in the tumor Hex B increases the net negative charge and results in the appearance of a heat-labile form.

Chemical Phenomena↗