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Biomedical subjects

M Yoshimura

Publications and source records attributed to M Yoshimura.

At least 505 records · Page 28Linked to original sources
PubMed1992

Thyrotropin and triiodothyronine regulate iodothyronine 5'-deiodinase messenger ribonucleic acid levels in FRTL-5 rat thyroid cells.

We investigated the regulation of type I iodothyronine 5'-deiodinase (5'-D) gene expression by TSH and T3 in FRTL-5 rat thyroid cells. Northern blot analysis revealed that these cells express a 5'-D messenger RNA (mRNA) species of 2.1 kilobases. Readdition of TSH to FRTL-5 cells, precultured in both thyroid hormones and TSH-depleted medium for 4 days, increased 5'-D mRNA levels, reaching a maximum (2.8-fold compared to control) after 12 h of TSH (10 microU/ml) stimulation. Dibutyryl cAMP (DBC) and forskolin mimicked this stimulatory effect of TSH on 5'-D mRNA levels. T3 also increased the 5'-D mRNA levels, reaching a maximum (2-fold compared to control) after 8 h of T3 (10(-9) M) stimulation. Addition of TSH (10 microU/ml) or DBC (1 mM) together with T3 (10(-9) M) further increased 5'-D mRNA levels, reaching a maximum (5-fold compared to control) after 12 h of stimulation. Examination of the rate of disappearance of 5'-D mRNA levels after inhibition of mRNA transcription by actinomycin-D revealed that neither TSH nor T3 significantly affected the rate of disappearance. Cycloheximide, a protein synthesis inhibitor, almost completely blocked the induction of 5'-D mRNA by TSH and DBC, but did not block the induction by T3. These results suggest that both TSH and T3 increase 5'-D mRNA levels probably by increasing transcription rate, and that TSH regulates it, in part via the second messenger cAMP, for which cycloheximide-sensitive de novo protein synthesis is required, whereas T3 does without requiring it.

Animals↗
PubMed1992

Identification of a 27-kilodalton protein with the properties of type I iodothyronine 5'-deiodinase in human thyroid gland.

N-Bromoacetyl-[125I]T4(BrAc[125I]T4) was used as affinity label to identify type I 5'-deiodinase (5'-D) in human thyroid glands. Affinity labeled proteins were analyzed by autoradiography after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Human thyroid microsomes labeled with BrAc[125I]T4 showed the most prominent radiolabeled band of protein at a mol wt of approximately 27,000 (p27). BrAc[125I]T4 incorporations into p27 were significantly higher in both Graves' and follicular adenomas than in normal thyroids. On the other hand, four cases out of five carcinomas were lower than the least value of normal thyroids. Furthermore, an excellent correlation was observed between 5'-D activities and quantities of p27 in all cases (r = 0.96; P less than 0.001). Labeling of p27 was strongly inhibited by preferred type I 5'-D substrate rT3, but to a lesser extent by poor substrate T4 or T3, and the type I 5'-D inhibitor, propylthiouracil and iopanoic acid, also inhibited the p27 labeling in normal and various diseases. In addition, the rate of enzyme inactivation by BrAcT4 equaled the rate of p27 labeling. These data suggest that p27 may be a type I 5'-D itself or at These data suggest that p27 may be a type I 5'-D itself or at least the substrate-binding subunit of this enzyme in human thyroid, and that both Graves' and follicular adenoma thyroids contain larger amounts of it, and papillary adenocarcinoma thyroids smaller than normal amounts.

Adenocarcinoma, Papillary↗
PubMed1992

3,3',5'-Triiodothyronine inhibits collagen-induced human platelet aggregation.

To clarify further the activity of rT3, we examined the effect of rT3 on collagen-induced platelet activation as reflected by aggregation, serotonin release, and protein phosphorylation. rT3, T4, T3, and triiodothyroacetic acid inhibited collagen-induced platelet aggregation and serotonin release from platelets in a dose-dependent manner. However, thyronine did not inhibit collagen-induced platelet aggregation. The concentration at which rT3 inhibited by 50% collagen-induced platelet aggregation was 30 +/- 4 (mean +/- SE) mumol/L. rT3, T4, and T3 did not differ significantly in their abilities to inhibit platelet aggregation. Moreover, rT3 inhibited collagen-induced phosphorylation of the 20-kilodalton protein (myosin light chain) in platelets. In contrast, rT3 did not inhibit 12-O-tetradecanoylphorbol 13-acetate (TPA)- or thrombin-induced platelet aggregation and inhibited only minimally TPA-induced 40-kilodalton protein phosphorylation. These results suggest that rT3 inhibits collagen-induced platelet activation by inhibiting the activity of myosin light chain kinase and that it may be interesting to investigate some kinds of activity of rT3.

Blood Platelets↗
PubMed1992

Beta-3 adrenergic agonist, BRL-26830A, and alpha/beta blocker, arotinolol, markedly increase regional blood flow in the brown adipose tissue in anesthetized rats.

Regional vascular effects of some adrenergic agents, focussing on brown adipose tissue (BAT), were investigated using tracer microspheres with a reference sample method in the anesthetized rat. Intravenous injections of 0.5 mg/kg BRL-26830A, a beta 3-adrenergic agonist, increased heart rate, but changes in blood pressure and cardiac output were not significant. The drug decreased blood flow in the brain, the spleen and the kidneys, but markedly increased it in BAT. At 2 mg/kg, arotinolol, an alpha/beta-adrenergic blocker, decreased blood pressure by 20 mmHg and increased cardiac output by 95 ml/min/kg. It slightly but significantly decreased blood flow in the liver and the spleen, but markedly increased the flow in BAT. Acebutolol, a beta 1-adrenergic blocker, decreased blood flow in the liver, the spleen, the pancreas, the kidneys, the adrenals, the skeletal muscle and the skin. Bunazosin, an alpha 1-adrenergic blocker, decreased it in all organs and tissue expect the brain and BAT. The pattern of redistribution of blood flow by arotinolol was very similar to that caused by BRL-26830A. Acebutolol and bunazosin rather decreased the blood flow in the BAT. These results indicate that stimulation of beta 3-adrenergic receptors, in BAT results in vasodilation, and that arotinolol may bind to those beta 3-adrenergic receptors.

Adipose Tissue, Brown↗
PubMed1992

[Coagulation and fibrinolysis in pregnancy].

We studied on coagulation and fibrinolysis systems during pregnancy by measuring plasma levels of thrombin-antithrombin III complex (TAT), plasmin-alpha 2 plasmin inhibitor complex (PIC), fibrinogen/fibrin degradation products (FDP), plasminogen (PLG) and antithrombin III (AT-III). Ninety seven pregnant, 5 post-delivery and 32 nonpregnant women aged from 20 to 52 years old were included in this study. Plasma concentrations of TAT and PIC in nonpregnant women were 3.38 +/- 1.02 micrograms/l and 0.65 +/- 0.24 micrograms/ml, respectively. TAT gradually increased with the progression of pregnancy and rapidly decreased after the delivery. Whereas PIC and AT-III concentrations did not change significantly during pregnancy. Fibrinogen, PLG and FDP concentrations changed similarly as TAT. Eight pregnants whose plasma PIC concentrations elevated more than 1.0 micrograms/l were further examined. In 6 women out of them (71.5%), FDP concentrations were elevated. In this particular group of subjects, however, they delivered normally without complications such as toxemia. These observations suggest that, at least, a hypercoagulative state progresses with pregnancy, being normalized after the delivery. Although we could not find the relationship between the hypercoagulation and clinical complications such as thrombosis and toxemia of pregnancy, present findings suggest that special caution should be paid on the pregnants whose TAT and FDP levels are elevated.

Adult↗
PubMed1992

["Left unilateral agraphia with right hemiparesis" after occlusion of the left middle cerebral artery].

This paper presented a case of a right-handed male who showed a right hemiplegia without aphasia and apraxia. He lost the ability to write with the left hand. A 56-year-old right-handed man, who had a daughter of left-handedness, was sent to our hospital with a homonymous hemianopsia, facial weakness, spastic hemiparesis and sensory disturbance in the right side. CT scan revealed an infarction in the territory of the left middle cerebral artery. On a month after the onset, he was alert and oriented. His speech was normal and verbal comprehension was intact. Although he neglected the right side of the page, he could read and comprehend it correctly. In contrast with his normal abilities to speak, comprehend, and read, difficulties in writing were prominent. Spontaneous writing with the left hand was extremely poor, and he even had difficulty writing his own name. His dictation was also poor, but his writing improved with copying letters. Agraphia had seen even after USN was recovered. Analysis of this case suggested the presence of the dominance for speech, comprehension, and praxis in the intact right hemisphere, and writing center in the damaged left hemisphere.

Agraphia↗
PubMed1992

[Steroid pulse therapy in rapidly progressive glomerulonephritis].

In an attempt to clarify the indication and efficacy of the methylprednisolone pulse therapy (1000 mg x 3 times) for rapidly progressive glomerulonephritis (RPGN), 3 patients with the disease were carefully followed and the clinical course during and after the treatment were precisely analysed. According to the declination rate of reciprocals of serum creatinine (1/Cr), one patient were divided into the acute type (-1.00 x 10(-2) dl/mg/day or less) and the others into the subacute type (more than -1.00 x 10(-2) dl/mg/day). In the patient of acute type, renal biopsy revealed cellular crescent formation in 93.8% of glomeruli observed. One course of the pulse therapy resulted in a decrease in Cr from 3.0 mg/dl to 1.3 mg/dl and transformation of cellular crescents to fibrocellular or fibrous crescents. In the other two patients of subacute type, crescents were observed in 72.7% and 72.0% of glomeruli observed, and 87.5% and 38.9% of them were composed of cellular crescents respectively. Initial courses of the pulse therapy resulted in decreases of Cr from 3.5 mg/dl to 2.4 mg/dl and from 3.0 mg/dl to 1.4 mg/dl respectively. Additional courses, given because of insufficient reduction of Cr in the former, induced a further lowering to 1.3 mg/dl, and because of re-elevation of Cr to 2.2 mg/dl and remaining of cellular crescents in 20% in the latter, induced a decrease of Cr to 1.5 mg/dl and disappearance of cellular crescents.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Slow releasing anticancer drug containing CDDP for intraoperative use in residual cancer cells].

We have already reported the slow releasing property and anticancer effect of Plachitin, which is reconstituted by combination of CDDP and chitin. This study deals in more detail with the slow releasing property, and the renal complications and the effectiveness for solid tumor were examined. After implantation of Plachitin subcutaneously in the abdominal wall, the platinum concentration in the different organs was measured. In the abdominal muscle around the implanted Plachitin, a high concentration of platinum was maintained until 8 weeks and the peak was 4 weeks after implantation. At the same time, the serum concentration of platinum remained low. In kidney, the platinum concentration resembled the levels in the abdominal muscle, but no renal dysfunction was found serologically or histologically. When Plachitin was implanted around the solid tumor, the survival rates were improved and the gain in tumor weight was suppressed as compared with the controls. From these findings, Plachitin seemed to be effective as a slow releasing anticancer drug for topical application.

Animals↗
PubMed1992

[Anticoagulants preventing pseudo-thrombocytopenia].

It is well known that some anticoagulants, especially EDTA (ethylene diamine tetraacetic acid), sometimes lead to pseudo-thrombocytopenia due to the aggregation of thrombocytes. We evaluated appropriate anticoagulants that prevent pseudo-thrombocytopenia without affecting other hematological data. In this study, 10 mg EDTA-2K and 1 mg citric acid were added to 1 ml of blood as anticoagulants. Using these anticoagulants (EC method), an aggregation of thrombocytes was clearly inhibited and the platelet counts remained stable in 10 cases with pseudo-thrombocytopenia. This method did not affect the other blood cell counts, the stainability and the morphology of the cells. Since the addition of citric acid to EDTA could prevent the cell volume change induced by the high concentration of EDTA, the micro-hematocrit values were remained unchanged. Hematological data in 20 cases which did not show any pseudo-thrombocytopenia, correlated significantly between the EDTA method and the EC method, and did not change significantly 24 hours after blood sampling. It is concluded that EDTA and citric acid may be a useful combination of anticoagulants for the prevention of pseudo-thrombocytopenia.

Anticoagulants↗
PubMed1991

Augmented secretion of brain natriuretic peptide in acute myocardial infarction.

In order to elucidate biosynthesis and secretion of natriuretic peptides in the early phase of acute myocardial infarction (AMI), we measured the plasma level of brain natriuretic peptide (BNP), a novel cardiac hormone secreted from the ventricle, in patients with AMI and compared with that of atrial natriuretic peptide (ANP). The plasma level of BNP increased rapidly (within hours from the onset of AMI) and markedly (greater than 100 times the normal level) as compared to that of ANP. The plasma ANP level correlated with pulmonary capillary wedge pressure (PCWP), whereas the plasma BNP level did not correlate with PCWP but highly correlated inversely with cardiac index. These results indicate that BNP is secreted from the heart much more acutely and prominently than ANP in the early phase of AMI, in association with left ventricular dysfunction.

Adult↗
PubMed1991

Inhibition by thyrotropin-releasing hormone of epileptic seizures in spontaneously epileptic rats.

The effects of thyrotropin-releasing hormone (TRH) were investigated on absence-like seizures, which are characterized by the sudden appearance of 5-7 Hz spike-wave-like complexes in the cortical and hippocampal EEG, and on tonic convulsions of spontaneously epileptic rats (SER; zi/zi, tm/tm), a double mutant obtained by mating zitter homozygote (zi/zi) with tremor heterozygote rats (tm/+). TRH (5 and 10 mg/kg i.v.) inhibited the appearance of both absence-like seizures and tonic convulsions of SER without inducing obvious changes in the background EEG. The inhibitory effects were seen 5-20 min after injection of 10 mg/kg TRH and were antagonized by pretreatment with haloperidol (0.5 and 1.0/kg i.p.), although haloperidol alone did not affect the seizures. These results suggest that TRH has an antiepileptic effect in the genetically defined animal model, SER, and that the effect is mediated by the central dopaminergic system.

Animals↗
PubMed1991

Demonstration of an active component of inter-alpha-trypsin inhibitor in the brains of Alzheimer type dementia.

The putative precursor of A4 amyloid protein associated with Alzheimer's disease is known to have a domain with an amino acid sequence characteristic of a Kunitz-type serine protease inhibitor. Human serum inter-alpha-trypsin inhibitor (ITI) is the most similar inhibitor. We screened brain tissues with senile dementia of the Alzheimer type in an attempt to detect ITI immunoreactivity employing immunohistochemical methods. For this purpose, we used the antibody raised against acid-stable proteinase inhibitor (ASPI) which is an active component of ITI. ASPI immunoreactivity was found to be localized in diffuse type senile plaques, the perivascular area and subpial layer. Reactive astrocytes with intense ASPI immunoreactivity were present in the pyramidal layer of the parahippocampus, where loss of neurons was observed. These findings suggest that ITI may be related to the pathogenesis of Alzheimer type dementia.

Aged↗