Experimental investigation of radiation heat waves driven by laser-induced Planck radiation.
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Journal Article↗
Biomedical subjects
M Murakami
Publications and source records attributed to M Murakami.
Growth hormone deficiency and empty sella syndrome in a boy with dup(X) (q13.3----q21.2).
A 2 8/12-year-old boy with severe growth failure and mental retardation was found to have a maternally derived tandem duplication of the long arm of X chromosome, dup(X) (q13.3----q21.2). Karyotypic interpretation was further confirmed in this patient by a double gene dose for red blood cell phosphoglycerate kinase. DNA replication study showed that the duplicated X chromosome was always late replicating in peripheral blood lymphocytes as well as in skin fibroblasts from the mother. Endocrine studies in the patient demonstrated growth hormone deficiency. Magnetic resonance imaging of the head then disclosed the empty sella syndrome. This appears to be the first report of a dup(Xq) patient associated with a growth hormone deficiency and the empty sella syndrome. We emphasize that duplication of the proximal Xq in males represents another microduplication syndrome (Thode-Leonard syndrome).
Child, Preschool↗
Unique karyotypes in two patients with Prader-Willi syndrome.
A physical disruption of the Prader-Willi syndrome (PWS) chromosome region is thought to cause PWS. We describe 2 girls with PWS phenotype, who had unique chromosome 15 abnormalities. The first patient showed mosaicism: 45,XX,t(15;15)(qter----p11.1::q11.200----qter)/46,XX,t(15;15)(qter----p1 1.1::q 11.200----qter), +mar. The band 15q11.2 apparently remained intact in the t(15;15) chromosome, and the mar chromosome was considered as r(15) (p11.1q11.1). The second patient had a karyotype of 47,XX,del(15)(q11.200----q11.207), +idic (15)(pter----q11.1::q11.1----pter). The complex breakage and reunion involving the 15q11.2 regions of the father's homologous chromosomes 15 at meiosis appeared to have resulted in the idic(15) and the del(15) chromosomes. These cytogenetic findings suggest that the PWS chromosome region may be localized on the very proximal portion of band 15q11.2.
Child↗
Change in phospholipid composition of mouse bone marrow-derived mast cells during cultivation with fibroblasts.
A mouse bone marrow-derived mast cell (BMMC) clone, designated as MC-MKM, was established. MC-MKM cells released histamine and generated lipid chemical mediators such as prostaglandin D2 or platelet-activating factor upon stimulation with IgE and antigen. It is known that BMMCs acquired the characteristics of connective tissue mast cells (CTMCs) during coculture with fibroblasts. In the present study, we found that cellular phospholipid composition changed drastically when MC-MKM cells were cultured for 2 weeks in the presence of mouse 3T3 fibroblasts. In MC-MKM cells, phosphatidylcholine was the predominant phospholipid class, followed by phosphatidylethanolamine. During coculture with fibroblasts for 2 weeks, total phospholipid content in MC-MKM cells increased 2.5-fold. Among major phospholipid classes, a percentage of phosphatidylethanolamine increased most dramatically in accordance with a decrease in that of phosphatidylcholine, while no appreciable change in composition of other phospholipids was observed. The phospholipid composition of cocultured MC-MKM cells was closer to that of rat peritoneal CTMCs than that of the starting MC-MKM cells. The present findings that BMMCs converted their phenotype into CTMC-like cells by the interaction with fibroblasts in terms of phospholipid composition are not contradictory to the previous observations that BMMCs changed into CTMC-like cells.
3T3 Cells↗
Restoration of superconducting properties of proton-implanted ceramic YBa2Cu3O7-x by annealing in oxygen.
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Journal Article↗
Thyroid hormone affects the hydrolysis of inositol phospholipids in the rat hypothalamus.
We have attempted to elucidate the effect of thyroid hormone on phospholipase C-linked inositol phospholipid hydrolysis in the rat hypothalamus. Hypothalamic slices of each animal, euthyroid control, hypothyroid, and thyroxine (T4)-supplemented hypothyroid rats were labeled with [3H]myoinositol in the presence of 5 mM LiCl, and then incubated for 60 min in KHG buffer containing either vehicle or 1 mM ouabain, a Na-K ATPase inhibitor. Hypothyroidism caused a significant increase in both basal and ouabain-stimulated accumulation of [3H]inositol phosphate ([3H]IP) in hypothalamic slices, whereas supplement with T4 to hypothyroid rats resulted in a complete restoration of hypothalamic [3H]IP formation to the value of euthyroid control. The present results indicate that thyroid hormone affects phospholipase C-linked inositol phospholipid hydrolysis in the hypothalamus, suggesting that negative feedback action of thyroid hormone may occur at a post-receptor site in the hypothalamus.
Animals↗
A transgenic model of autoimmune hemolytic anemia.
We made double transgenic mice bearing immunoglobulin heavy and light chain genes encoding an autoantibody against the mouse erythrocyte by the cross of C57BL/6 mice carrying the transgene for each chain of the immunoglobulin. Although no obvious disorders were found in the single-chain transgenic mice, severely anemic symptoms were found in some of the double transgenic mice, in which most B cells express, at least on their surface, the autoantibody reactive to self-antigens on the erythrocyte. Individual double-transgenic mice showed a wide variation of phenotypes between severe anemia and no symptoms. Both deletion and anergy of autoreactive B cells were seen in each individual mouse, but their relative contribution to self-tolerance was variable and not directly related to the severity of anemia or the amount of the autoantibody produced. This transgenic system provides a good autoimmune disease model for exploring its onset mechanism, and means of its treatment and prevention.
Anemia, Hemolytic↗
The molecular biology of interleukin 6 and its receptor.
Functional pleiotropy and redundancy are characteristic features of cytokines. Interleukin 6 (IL-6) is a typical example: IL-6 induces cellular differentiation or expression of tissue-specific genes; it is involved in processes such as antibody production in B cells, acute-phase protein synthesis in hepatocytes, megakaryocyte maturation, cytotoxic T cell differentiation, and neural differentiation of PC12 (pheochromocytoma) cells. It promotes growth of myeloma/plasmacytoma cells, T cells, keratinocytes and renal mesangial cells, and it inhibits growth of myeloid leukaemic cell lines and certain carcinoma cell lines. The IL-6 receptor consists of two polypeptide chains, a ligand-binding chain (IL-6R) and a non-ligand-binding, signal-transducing chain (gp130). Interaction of IL-6 with IL-6R triggers the association of gp130 and IL-6R, and the signal can be transduced through gp130. Association of gp130 with IL-6R is involved in the formation of high affinity binding sites. This two-chain model has been shown to be applicable to receptor systems for several other cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3, IL-5 and nerve growth factor (NGF). The pleiotropy and redundancy of cytokines may be explained on the basis of this unique receptor system.
Animals↗
Interleukin-5 in eosinophilic gastroenteritis.
During a 4-year period a 28-year-old female had 4 episodes of eosinophilia of over 10,000/mu 1; these episodes were associated with nausea, vomiting, diarrhea, and abdominal pain. On one occasion, she had ascites and pleural effusion which contained numerous mature eosinophils. On each occasion, these attacks disappeared within several weeks without any specific treatment. A diagnosis of eosinophilic gastroenteritis was made. A plasma sample obtained during the eosinophilia generated in vitro eosinophilic colonies when added to granulocyte/macrophage-progenitor (CFU-GM) cultures without exogenous growth factors. Colony formation was inhibited by anti-interleukin-5 (IL-5) antibody but not by antibodies toward IL-3, granulocyte colony-stimulating factor (G-CSF) or GM-CSF. A high plasma interleukin-5 (IL-5) level was noted when measured by enzyme-linked immunosorbent assay, while IL-3, G-CSF, and GM-CSF were undetectable. During remission the plasma gave negative results both for colony formation and IL-5 level. These results indicate that the eosinophilia of this disease is mediated by IL-5.
Adult↗
Characteristics and possible functions of mast cell phospholipases A2.
Phospholipase A2 activity in lysates of mast cells and their related cells [mouse bone marrow-derived IL-3 dependent mast cells (BMMC), rat connective tissue mast cells (CTMC), and rat mastocytoma RBL-2H3 cells] was measured using phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidylcholine (PC) as exogenous substrates. Both BMMC and RBL cells showed rather high phospholipase A2 activity, whereas CTMC showed only weak activity. These cells contained at least three types of phospholipase A2. Type 1 enzyme showed no appreciable affinity to heparin, and preferentially hydrolyzed either PC or PE, both of which have an arachidonic acid at the sn-2 position. The activity was absorbed by monoclonal antibody against rabbit platelet cytosolic 85-kDa phospholipase A2. Type 2 enzyme had an affinity to heparin, and was completely inhibited by anti-rat platelet 14-kDa secretory phospholipase A2. This enzyme could be expressed as an "ecto-type" enzyme on the cell surface and might be secreted from cells when mast cells are activated. Type 3 enzyme also had an affinity to heparin, but was separated from type 2 enzyme on reverse-phase HPLC. This enzyme did not interact with anti-14-kDa secretory enzyme antibody. Purified type 3 enzyme (30-kDa) specifically hydrolyzed PS. p-Bromophenacylbromide inhibited all types of phospholipase A2, whereas mepacrine inhibited type 2 and type 3 enzymes, but not type 1 enzyme. Type 2 enzyme was also inhibited by the specific antibody, complement degradation product, and a small-molecular-weight inhibitor. Histamine release was inhibited by all these inhibitors, whereas PGD2 production was inhibited only by p-bromophenacylbromide. Possible roles for these phospholipases A2 in mast cell function are proposed.
Animals↗
Pharmacological analysis of positive chronotropic and inotropic responses to etilefrine in isolated dog heart preparations.
Positive chronotropic and inotropic responses to etilefrine (alpha-[(ethylamino)methyl]-m-hydroxybenzyl alcohol), an orally active cardiovascular agent, were investigated in isolated dog right atrial and left ventricular preparations. Intravenous administration of etilefrine to a support dog increased heart rate and mean systemic blood pressure, and increased sinus rate and atrial contractile force in the isolated right atrium perfused with blood from the support dog. Etilefrine injected intra-arterially to isolated atria and ventricles induced dose-dependent positive chronotropic and inotropic effects. Etilefrine was about 100 times less potent than isoproterenol. The effects of etilefrine in isolated atria were significantly inhibited by treatment with atenolol, but were not significantly inhibited by ICI 118,551. The effects of etilefrine were partially inhibited by imipramine. These results indicate that etilefrine is a highly selective beta-1 adrenoceptor agonist and suggest a moderate catecholamine-releasing activity by tyramine-like action in the blood-perfused dog heart.
Adrenergic beta-Antagonists↗
Inhibition of pancreatic adenocarcinoma cell growth by lovastatin.
RAS protein (p21 ras) requires farnesyl (an intermediate of cholesterol synthesis) for activation. Activating mutations of K-ras gene have been detected in most human pancreatic adenocarcinomas. In the present study, the effect of lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, the rate-limiting enzyme of cholesterol synthesis, on the growth of five pancreatic cancer cell lines (human-CAV, MIA Paca2, CAPAN2 and PANC1, and hamster-H2T) in vitro and of two cell lines (CAV and H2T) in vivo was examined. Inhibition of cell growth was observed with lovastatin doses at or above 2.5 micrograms/mL for H2T, CAV, MIA Paca2, and CAPAN2 or 10 micrograms/mL in PANC1. The H2T cell line was studied further to determine the reversibility of growth inhibition. Mevalonic acid (1 mmol/L) reversed lovastatin-induced inhibition of cell growth if it was added with lovastatin (2.5 micrograms/mL). Similarly, removal of lovastatin from the medium within 24 hours after treatment allowed recovery of cell growth. The effect of lovastatin on cell growth was irreversible after 48 hours of exposure. The survival fraction of H2T cells was markedly decreased by 1- or 24-hour exposure to 75 micrograms/mL but not to doses ranging from 0.5 to 60 micrograms/mL of lovastatin. Growth of pancreatic carcinoma xenografts (CAV and H2T) in nude mice was inhibited by a subcutaneous infusion of lovastatin (50 micrograms/h). These results indicate that mevalonic acid or a metabolite in the cholesterol synthesis pathway is necessary for growth of pancreatic cancer cells and suggest that lovastatin should be further examined as a potential therapeutic agent for pancreatic cancer.
Animals↗
Inhibitory effects of okadaic acid on thyrotropin and prolactin secretion from rat anterior pituitaries.
The present study was undertaken to elucidate the effects of okadaic acid, a potent inhibitor of protein phosphatases, on thyrotropin (TSH) and prolactin (PRL) secretion, and on the hydrolysis of inositol phospholipids in rat anterior pituitaries. Preincubation of anterior pituitaries with okadaic acid caused a dose dependent decrease in TRH- and K(+)-induced TSH secretion, whereas basal secretion of TSH was not affected by pretreatment with okadaic acid. In contrast, okadaic acid resulted in a marked inhibition in both basal, and TRH- and K(+)-stimulated PRL release from anterior pituitaries. In addition, pretreatment with okadaic acid caused a slight, but significant decrease in the formation of [3H]inositol phosphate ([3H]IP) in rat anterior pituitaries. The present study suggests that okadaic acid blocks the release of TSH and PRL by inhibiting Ca2+ influx and that inhibitory effects of okadaic acid on PRL release are, at least in part, due to the inhibition of inositol phospholipid hydrolysis.
Animals↗
Thyroid hormones regulate the formation of inositol phosphate in response to thyrotropin-releasing hormone in rat anterior pituitaries.
The effects of thyroid hormones on TSH secretion and inositol phospholipid hydrolysis in response to thyrotropin-releasing hormone (TRH) in rat anterior pituitaries were examined. Experimental hypothyroidism caused a significant increase in [3H]inositol phosphate ([3H]IP) formation in response to TRH in rat anterior pituitaries with a concomitant elevation of blood TSH. In contrast, administration of thyroxine (T4) to hypothyroid rats resulted in a complete restoration of blood TSH and TRH-stimulated [3H]IP formation to the euthyroid control value. Furthermore, in vitro pre-treatment of anterior pituitaries with triiodothyronine (T3) produced a dose-dependent decrease in both TSH secretion and the formation of [3H]IP in response to TRH. These results indicate that thyroid hormones regulate TRH receptor-linked inositol phospholipid hydrolysis in the rat anterior pituitary, suggesting that negative feedback action of thyroid hormone occurs at post receptor event in the rat anterior pituitary, which may, to a certain extent, be responsible for the underlying mechanism of T3 inhibition of TSH secretion.
Animals↗
The effects of amylin on insulin secretion from Rin m5F cells and glycogen synthesis and lipogenesis in rat primary cultured hepatocytes.
The purpose of the study was to determine the physiological actions of amylin, a novel 37-amino acid peptide isolated from pancreatic islet amyloid deposits. Our results showed that an infusion of amylin reduced fasting plasma insulin levels and impaired glucose tolerance in mice. Amylin significantly reduced insulin secretion in rat insulinoma cell lines (Rin m5F cells) that were stimulated by either isoproterenol and forskolin, but it did not affect insulin secretion stimulated by isobutyl-methylxanthine (IBMX) or dibutyryl cyclic-adenosine monophosphate (db-cAMP). Amylin also reduced cAMP levels in Rin m5F cells in response to isoproterenol, but did not affect cAMP levels in cells pretreated with pertussis toxin. These results suggest that the reduction of cAMP by amylin may be mediated through pertussis toxin-sensitive Gi proteins. Amylin significantly reduced basal and insulin-stimulated glycogen synthesis in rat primary cultured hepatocytes. Amylin stimulated basal and insulin-stimulated lipogenesis in hepatocytes. Amylin did not affect DNA synthesis in hepatocytes. These results suggest that amylin conducts dispersion actions on in vivo glucose metabolism in rat, and in vitro insulin secretion from Rin m5F cells and metabolism in rat hepatocytes.
Acetates↗
A convenient method for regional monoamine oxidase-A determination by [14C]clorgyline autoradiography.
The availability of clorgyline for regional monoamine oxidase-A (MAO-A) determination was examined using [14C]clorgyline in rat. [14C]Clorgyline was synthesized by the methylation reaction of N-desmethyl-clorgyline and [14C]methyliodide in dimethylformamide with high radiochemical yield. The MAO-A distribution map by autoradiography correlated with that by histochemical technique and its quantity was consistent with the calculated MAO-A amount based on previous reports. The combination of labeled clorgyline and autoradiographic technique will promise the quantitative measurement of regional MAO-A distribution.
Animals↗
Regulation of IL-6 receptor and gp130 expression on human cell lines of lymphoid and myeloid origin.
The expression of 80 kDa interleukin-6 receptor (IL-6R) and the associated molecule gp130 has been studied on human cell lines by FACS- and Northern blot analysis. The effects of dexamethasone, dibutyric-(DB)-cAMP and phorbol-12-myristate-13-acetate (TPA) have been studied on plasmacytoma cell line U266, B cell line BMNH and monocytoid cell line U937. Our data show a definite downregulation of IL-6R and gp130 expression by TPA in U266 and BMNH at both mRNA and cell surface protein levels. In U937 TPA inhibits only the IL-6R expression, without affecting that of gp130. DB-cAMP decreases the expression of both proteins in U937, slightly inhibits the IL-6R expression in U266, but is uneffective in BMNH. Dexamethasone induces considerable upregulation of gp130 only in U266. Our findings suggest separate regulation of IL-6R and gp130 on U266, BMNH and U937 cell lines.
Antigens, CD↗
Immunohistochemical evaluation with Ki-67: an application to salivary gland tumours.
Using Ki-67, a monoclonal antibody, the proliferating capacity of 15 salivary gland tumours, including nine pleomorphic adenomas, four adenoid cystic carcinomas, one mucoepidermoid carcinoma and one acinic cell carcinoma was determined immunohistochemically, using normal salivary gland tissue as a control. The frequency of Ki-67 positive cells was 4.7 percent in the normal salivary gland and one percent in pleomorphic adenomas, whereas the average frequency in malignant tumours was 18.3 percent. Among adenoid cystic carcinomas, the frequency was related to the morphological type; the solid sub-type had the highest frequency of Ki-67-positive cells. As this sub-type is recognized as the most aggressive of these tumours, this technique has the potential of providing an early indication of the clinical behaviour of a tumour.
Carcinoma, Adenoid Cystic↗