Syndrome of inappropriate secretion of antidiuretic hormone associated with schizophrenia.
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Biomedical subjects
Publications and source records attributed to I Mori.
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Control mechanisms of growth hormone (GH) receptors in the eel liver were examined by following the time course of changes in total (MgCl2-treated membranes) and free (untreated membranes) GH-binding sites after hypophysectomy and replacement therapy with homologous GH. Both total and free binding sites decreased significantly 1 week after hypophysectomy. Scatchard analysis indicated that the reduction in GH receptors was primarily due to a decrease in the number of binding sites, rather than to a change in binding affinity. When recombinant eel GH was injected intramuscularly into hypophysectomized eels (2 micrograms/g body wt), plasma GH concentration increased to a maximal value after 10 hr and decreased to the initial level by 72 hr. Free binding sites decreased to a minimal value 24 hr after the injection and returned to the initial level after 72 hr. The reduction in free binding sites seems to be due to occupation of GH receptors. Total binding sites increased gradually to almost twofold over those of the controls 5 days after the injection, the increase being due to an increase in the binding capacity. GH appears to be importantly involved in inducing and maintaining its own receptors in the eel liver.
The development of antibody against lactic dehydrogenase virus in five strains of mice (NZB x NZWF1, BALB/c, C.B-17, ICR and C.B-17 scid or SCID mice) was examined by indirect immunofluorescence (IIF) of infected liver sections. IIF antibody appeared 1 to 3 weeks and rose progressively 2 to 4 weeks after infection in four strains of mice (NZB x NZWF1, BALB/c, C.B-17 and ICR mice). SCID mice did not develop antibody. These results suggest that IIF may be applicable for detecting LDV infection in many other ordinary strains of mice.
The role of reperfusion injury in the progression to necrosis in pulmonary embolism was evaluated. To simulate this condition, we used a technique that enables occlusion and reopening of the pulmonary arterial branch supplying the right upper lobe in conscious rats. The rats were divided into five groups: the occlusion group (n = 12), in which the pulmonary artery (PA) branch was occluded without reperfusion; the reperfusion group (n = 12), in which the PA branch was reopened after a 2-h period of occlusion; and the reperfusion-SOD (n = 9), reperfusion-IM (n = 8), or reperfusion-IA-SOD (n = 6) groups, in which superoxide dismutase (SOD), indomethacin (IM), or inactivated SOD (IA-SOD), respectively, was administered during reperfusion. The lungs were removed 24 h after the PA occlusion, and histologic examination was performed. In the occlusion group, the alveolar structure of the right upper lobe was well preserved, and there was no erythrocyte or leukocyte accumulation. The only significant changes compared with the control lobe was the appearance of wavy internal elastic lamina of the PA and slight neutrophil adherence to the endothelial cells. In contrast, the right upper lobe of the reperfusion group disclosed numerous foci of hemorrhagic necrosis, with disrupted alveoli and leukocyte accumulation in all cases. With SOD treatment, the changes compatible with hemorrhagic necrosis were attenuated to the level of the control lobes. However, neither IM nor IA-SOD decreased these changes.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of hyaluronan (HA) on the release of arachidonic acid (AA) from phospholipids induced by bradykinin in synovial fibroblasts of osteoarthritic patients were examined. HA inhibited [14C]AA release from prelabeled synovial cells stimulated with and without bradykinin 1 hr after incubation with HA and thereafter. The inhibitory effects of HA on [14C]AA release were dependent on the concentration and molecular weight of HA. However, inhibition of [14C]AA release by HA was not merely due to the viscosity of HA. The [14C]AA release induced by calcium-ionophore A23187 was also inhibited by HA with a high molecular weight. In addition, HA did not affect [14C]AA uptake by the cells. Our results suggest that HA with a high molecular weight elicits anti-inflammatory effects, at least in part, by inhibiting AA release in inflamed joints.
We have demonstrated that biotinylated asparaginase binds to mouse monocytes. Also, asparaginase bound to peritoneal exudate, resident, splenic, bone marrow and pulmonary macrophages, but not to neutrophils or lymphocytes. Labelled asparaginase binding to peritoneal exudate macrophages was inhibited by 20-fold excess of unlabelled asparaginase. The binding of asparaginase to monocytes from mice injected with lactic dehydrogenase virus (LDV) or carrageenan was decreased. This decreased binding following treatment with LDV or carrageenan was reversed when mice were treated with diethylstilboestrol. In-vivo asparaginase clearance in mice infected with LDV was impaired as compared with that in uninfected mice. Neither strain nor age differences affected the binding to monocytes. The results suggest that the ability of asparaginase to bind to monocytes in vitro may reflect clearance function in vivo.
Persistent lactic dehydrogenase virus (LDV) infection prevents the development of antinuclear antibody (ANA) in (NZB x NZW)F1 mice. To assess the suppressive mechanisms, we focused on the role of the E series of prostaglandin(PGE), since previously we have shown enhanced production of PGE by macrophages from chronically LDV-infected mice. Treatment with PGE2 suppressed ANA titres more markedly in non-infected mice than in LDV-infected mice. Indomethacin enhanced ANA titres more markedly in LDV-infected mice than in non-infected mice. The number of Ia antigen positive(Ia+) macrophages was less in LDV-infected mice than in uninfected mice. The number of Ia+ macrophages was decreased in non-infected mice by PGE2 treatment and increased in LDV-infected mice by indomethacin treatment. These results suggest that the low ANA production in LDV-infected (NZB x NZW)F1 mice may be related to the decreased number of Ia+ macrophages and that one of the factors responsible for suppression of Ia+ macrophages may be the enhanced PGE2 production in the LDV-infected mice.
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The lactic dehydrogenase (LDH) level in plasma and the clearance of LDH in C.B-17 scid (severe combined immunodeficiency; SCID) mice were compared with those in C.B-17 or BALB/cCrSlc mice with or without lactic dehydrogenase virus (LDV) infection. The resting enzyme level in SCID mice showed little difference from that in C.B-17 or BALB/cCrSlc mice. The degree of increased plasma LDH level in SCID mice was lower than that in C.B-17 and BALB/cCrSlc mice after LDV infection. To assess the mechanisms of decrease in LDH elevation in SCID mice infected with LDV, virus replication was compared in SCID and BALB/cCrSlc mice. The infectivity titre of plasma in SCID mice was higher (more than 10 times) than that in BALB/cCrSlc mice. Moreover, the percentage of virus antigen positive Kupffer cells was higher in SCID mice than that in BALB/cCrSlc mice. The level of endogenous LDH release as a result of carbon tetrachloride treatment was similar in the SCID and BALB/cCrSlc mice. The clearance rate of endogenous LDH was greater in SCID mice than in BALB/cCrSlc mice with or without LDV infection. The rate of clearance of intravenously injected porcine LDH-5, but not porcine LDH-1, was enhanced in SCID mice as compared with that in BALB/cCrSlc mice. Furthermore, carbon clearance was higher in SCID mice than that in BALB/cCrSlc mice. These results suggest that the smaller increase of plasma LDH after infection might be due, at least in part, to the enhanced LDH-5 clearance function by macrophages in SCID mice.
1) We report 5 cases of aseptic meningitis following vaccination against mumps. Of the 5 cases, 4 cases were diagnosed as mumps meningitis. 2 cases received monovalent mumps vaccine and the other 2 MMR vaccine. They consisted of 2 boys and 2 girls, aged 2 years and 2 months to 4 years and 5 months. The period between vaccination and symptoms ranged from 15 days to 20 days (mean 18 days). Cerebrospinal fluid of the cases contained 507 to 2688 cells/mm3. Eruption was observed in the 2 cases who received MMR vaccine, while parotid swelling was not seen in any case. 2) In all 4 cases, IgM antibody to mumps virus in the cerebrospinal fluid was detected by the ELISA or EIA methods. Causative organism of the fifth case was obscure. 3) PCR (Polymerase Chain Reaction) tests revealed that mumps virus isolated from 2 cases were of vaccine strain origin. 4) To evaluate the frequency of mumps meningitis following vaccination, it seems important to investigate carefully the number of children who received the vaccine and to exclude the cases of aseptic meningitis caused by other agents. On the other hand, cases of young infants tend to be overlooked because of atypical signs.
We report here an unusual activation of the Tc1 transposable element system in Caenorhabditis elegans. Germline Tc1 activity, as measured by reversion of unc-22::Tc1 alleles, is elevated 50- to 100-fold by certain crosses. For example, unc-22::Tc1 reversion is 1 x 10(-3) in a mut-6 IV strain and less than 1 x 10(-6) in a non-mutator strain, but in the unc-22::Tc1 progeny of a cross between mut-6 hermaphrodites and non-mutator males, reversion is 10(-1). The reciprocal cross does not induce this enhancement of reversion. Results similar to those for mut-6 were obtained using a mut-5 II strain. The mutator hermaphrodite by nonmutator male cross per se is not required for the enhancement of reversion, as mut-5 hermaphrodites x mut-6/+ males also induce unc-22 revertants at an elevated frequency. This reversion enhancement appears to depend on a maternal component inherited from a mutator strain, suggesting that the regulation of Tc1 activity may be complex.
A 10-month-old girl with mild developmental delay became hemiplegic after seizures. Cranial CT scan and magnetic resonance imaging (MRI) revealed no lesions related to vascular diseases, but brain atrophy on the right side was remarkable. Digital subtraction angiography showed slightly decreased visualization of peripheral branches of the right medial cerebral artery. Propionic acidaemia was diagnosed on the basis of high plasma levels of propionic acid and its metabolites and the elevated urinary excretion of these acids. With therapy, the levels of these acids fell, and her left hemiplegia disappeared 3 months later.
We report a case of acinic cell carcinoma of the parotid gland with neuroendocrine differentiation. Light microscopically, the tumor appeared as clear cell-type acinic cell carcinoma. In addition, the tumor showed neurosecretory features such as Grimelius positivity and the presence of neurosecretory granules by electron microscopy. We suggest that a tumor cell arising from a stem cell can show simultaneous differentiation to both neuroendocrine and acinic cells.
The concentration and degradation of hyaluronic acid in the synovial fluid of carrageenin-induced arthritic joints of rabbits was studied. A 0.5-ml volume of 1% lambda-carrageenin was intra-articularly injected three times into a right knee joint, and saline into a left. After 5 d from the last injection, inflammatory changes were observed in the synovial membrane and synovial fluid, but not in the articular cartilage. In the inflammatory synovial fluid, lipid peroxide content, phosphatase activity and cell counts were significantly increased, but the copper concentration was not changed. Concentration of polymeric hyaluronic acid and total hyaluronic acid were determined by high-performance liquid chromatography using gel-permeation columns. Total hyaluronic acid was appreciably decreased in the inflammatory fluid. The polymeric hyaluronic acid determined was 38% of the total hyaluronic acid in the inflammatory fluid and 74% in the control fluid. This suggests that in the inflammatory fluid, molecular weights of hyaluronic acid are distributed in the broader range. The concentration of chondroitin sulphates was similar in both the inflammatory fluid and the control fluid, but the content ratio of chondroitin sulphates to hyaluronic acid was higher in the inflammatory fluid. In the inflamed synovial membrane, synthesis of hyaluronic acid as measured by incorporation of [14C]glucosamine into glycoconjugates was increased by about twice that in the control membrane.
A high-performance liquid chromatographic (HPLC) method for quantifying unsaturated hexasaccharide and tetrasaccharide from Streptomyces hyaluronidase enzyme digestion products of hyaluronic acid was developed using a gel-permeation column packed with a sulphated polystyrene-divinylbenzene gel. For the oligosaccharides, the separation was accomplished in less than 7 min with a detection limit of 65 ng. An unsaturated non-sulphated disaccharide prepared from hyaluronic acid (delta Di-HA) and an unsaturated sulphated disaccharide (delta Di-4S) were analyzed by a HPLC method using a combination of two different gel-permeation columns. The separation of the disaccharides required less than 17 min at a flow rate of 0.7 ml/min with detection limits of as little as 4 ng for delta Di-HA and 5 ng for delta Di-4S. Both chromatographic methods were used for assay of a major component of hyaluronic acid and trace amounts of chondroitin sulphates in rabbit synovial fluid. The resulting contents of hyaluronic acid were compared to the values of polymeric hyaluronic acid directly measured by a HPLC method using two gel-permeation columns packed with a poly(hydroxyalkyl methacrylate) gel and the amounts of hyaluronic acid converted from uronic acid content determined by a colorimetric method.