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Biomedical subjects

M Yoshimura

Publications and source records attributed to M Yoshimura.

At least 289 records · Page 16Linked to original sources
PubMed1997

Quarantine for contaminated pathogens in transplantable human tumors or infections in tumor bearing mice.

To quarantine human tumor samples for transplantation into immune deficient mice or tumor xenograft lines established and introduced from other institutions, we performed isolated implantation and passaging of tumors in a vinyl isolator, and microbiological examinations of sentinel mice kept together with tumor bearing mice. We examined 105 pairs of sentinel mice used to quarantine 907 tumors, and found six cases of contamination or infection with Staphylococcus aureus, 20 cases with Pseudomonas aeruginosa and one case with mouse hepatitis virus (MHV). It was, however, possible that Mycoplasma pulmonis contamination was overlooked because the microbe had been isolated from tumors passaged after quarantine, even though the results of the quarantine of these tumors showed no sign of pathogens. Direct culture of tumors for the microbe was recommended to improve the quarantine system.

Animals↗
PubMed1997

Cardiovascular regulation by L-arginine in the brain of rats: role of the brain renin-angiotensin system and nitric oxide.

The effect of brain L-arginine on arterial pressure was investigated by injecting L- or D-arginine into the cerebral ventricles of male Wistar rats that were anesthetized with urethane. Intracerebroventricular (I.C.V.) injection of 1 micromol L-arginine reduced the arterial pressure and the abdominal sympathetic nervous activity (SNA), whereas the injection of 10 micromol L-arginine induced a transient pressor response and reduced both the heart rate and SNA. Although I.C.V. injection of 1 micromol D-arginine had no effect on cardiovascular function or SNA, injection of 10 micromol of this enantiomer elicited a transient pressor response, similar to that induced by 10 micromol L-arginine, followed by a persistent increase in arterial pressure and a corresponding increase in SNA. I.C.V. pretreatment with the nitric oxide synthase inhibitor N(G)-monomethyl L-arginine abolished the vasodepressor response and reduced the inhibition of SNA induced by I.C.V. injection of 1 micromol L-arginine; such pretreatment increased the arterial pressure, heart rate, and SNA measured 30 min after I.C.V. injection of 10 micromol L-arginine. I.C.V. pretreatment with the angiotensin II type 1 receptor antagonist CV-11974 inhibited the pressor response to 10 micromol L-arginine and the first phase of the pressor response to 10 micromol D-arginine. Intravenous pretreatment with the alpha1-adrenoceptor blocker bunazosin hydrochloride abolished the pressor response to 10 micromol L-arginine and both phases of the pressor response to 10 micromol D-arginine. Brain L-arginine thus appears to exert pressor actions through stimulation of the brain renin-angiotensin system and peripheral SNA. However, these actions may be attenuated by L-arginine-derived nitric oxide.

Animals↗
PubMed1997

Sudden death due to diabetic coma in insulin-department diabetes mellitus: an autopsy report.

Sudden death caused by the acute onset of diabetic coma is reported. A 15-year-old female had been suffering from insulin-dependent diabetes mellitus for the prior 8 years and had a fever and vomiting for the past few days. On the 4th day, after the onset of fever and vomiting, she died suddenly, and was autopsied to clarify the cause of death. Macroscopic examination revealed that the pancreas was atrophic (40 g) whereas the liver was markedly enlarged (2,740 g). Histological findings were: 1) The islets of Langerhans were decreased in size and number. They were not positive for aldehyde-fuchsin staining, 2) There were severe fatty changes in the liver cells. The retained blood in the left ventricle was analyzed: glucose, 1,016 mg/dl; acetone, 345 mg/l; acetoacetate, 5.91 mmol/l: D-3-hydroxybutyrate, 4.17 mmol/l; hemoglobin A1c, 10.2%; fructosamine, 416 mumol/l; total serum cholesterol, 220 mg/dl; triglycerides, 205 mg/dl; free fatty acid, 8.0 mEq/l; urea nitrogen, 40 mg/dl. Although the biochemical estimation of the glucose and ketone levels in post-mortem body fluids was recognized as being unreliable, many of these values were far elevated in comparison with those of normal individuals. Thus, we concluded that the cause of death was diabetic ketoacidosis. We also discuss the diagnostic problems of postmortem blood chemistry.

Adolescent↗
PubMed1997

[Application of urinary free dopamine as a marker of renal function, and comparison with other renal marker].

Urinary free dopamine (U-f-DA) is derived from renal DA synthesized in the renal proximal tubules, and plays an important role for diuresis and natriuresis. We were previously reported that U-f-DA was the superior marker of renal function as compared with ordinary methods including alpha 1-microglobulin (U-alpha 1 MG), beta 2-microglobulin (U-beta 2 MG) and N-acetyl-beta-D-glucosaminidase (U-NAG) in spot urine samples. U-f-DA can be used as index for the evaluation of renal transplantation. In order to evaluate the clinical usefulness of U-f-DA as a marker of renal function, we investigated as follows; firstly, the age related changes of U-f-DA in healthy out-patients, secondly, the correlation between U-f-DA and creatinine clearance (CCr), serum creatinine (S-Cr) in in-patients, and thirdly, the chronological changes of U-f-DA, U-alpha 1 MG, U-beta 2 MG, CCr and S-Cr in patients with chronic renal failure before and after renal transplantation. There is no age-related changes in U-f-DA from patients with 3 years to 88 years old. U-f-DA was positively correlated with CCr and negatively correlated with S-Cr. There are parallel changes of U-f-DA and CCr in increasing direction, on the other hand, parallel changes of U-alpha 1 MG, U-beta 2 MG and S-Cr in decreasing direction after renal transplantation. In patients with post renal transplantation who were not well controlled, S-Cr increased gradually with the decreasing level of U-f-DA. These results suggest that the measurement of U-f-DA in spot urine samples is useful marker for evaluation of the renal function and can be used an index of viability of the transplanted kidney.

Adolescent↗
PubMed1997

[Serum hepatocyte growth factor as a possible indicator of vascular lesions].

To investigate the possible involvement of hepatocyte growth factor (HGF) with vascular lesions, we studied the relationship between serum HGF concentrations and the grades of retinal arteriosclerosis, coronary atherosclerosis, and the proliferative changes in the retina of diabetic subjects. Individuals with more advanced grades of arteriosclerotic change showed higher serum HGF values (grade 0, 0.056 +/- 0.004ng/ml; grade 1, 0.132 +/- 0.026ng/ml; grade 2-3, 0.271 +/- 0.023ng/ml). The serum HGF concentration was increased (p < 0.05) in subjects with double- (0.323 +/- 0.037ng/ml) or triple-(0.345 +/- 0.027ng/ml) vessel coronary heart diseases, as compared to that in subjects with single-vessel coronary heart disease (0.191 +/- 0.027ng/ml). Serum HGF in diabetics without retinopathy was lower than that in nondiabetic subjects (0.041 +/- 0.003ng/ml vs 0.080 +/- 0.010ng/ml, p < 0.05), but did not differ from other diabetic subjects with background retinopathy (0.058 +/- 0.007ng/ml) or preproliferative retinopathy (0.048 +/- 0.010ng/ml). Serum HGF was increased in proliferative retinopathy without photocoagulation (0.138 +/- 0.035ng/ml, p < 0.01), but not with photocoagulation (0.040 +/- 0.008ng/ml). Increased serum HGF may be involved in the pathogenesis of arteriosclerosis/atherosclerosis or retinal neovascularization, and measurement of serum HGF may be a useful test to predict the presence of these vascular lesions.

Arteriosclerosis↗
PubMed1997

[Sleeve lobectomy for tuberculous bronchial stenosis: a case report].

We describe a patient with tuberculous bronchial stenosis who was subjected to bronchoplasty. The patient was a 33-year-old man who had stenosis of the left main bronchus. Because the lesion was associated with bronchomalacia, previous balloon dilatation therapy had failed. At thoracotomy, the left upper lobe was found not to be saved for the tuberculous lesion. Although there were many inflamed nodules in the left lower lobe due to repeated episodes of pneumonia, we decided to save it using bronchoplasty expecting its respiratory functional recovery. He ran uneventful course postoperatively and his lung function improved. We conclude that bronchoplasty may prove effective for patients with tuberculous bronchial stenosis associated with bronchomalacia; and thus, to avoid pneumonectomy, bronchoplasty should be attempted even if the reconstructed lung is mildly inflamed.

Adult↗
PubMed1997

Muscarinic inhibition of basal L-type calcium current in pacemaker cells from the rabbit atrioventricular node.

Effects of acetylcholine (ACh) on the L-type calcium current were examined in isolated atrioventricular nodal cells that exhibited spontaneous contractions. ACh (0.1 to 10 microM) inhibited basal calcium current dose-dependently. This inhibition was eliminated by dialysis with 8Br cAMP or cAMP-dependent kinase inhibitory peptide. Both extracellular N-ethylmaleimide 50 microM and intracellular GDPssS 0.2 mM abolished the ACh effect. Dialysis with cGMP or NG-monomethyl-L-arginine did not significantly affect ACh inhibition of basal calcium current. Similarly, cGMP-dependent protein kinase inhibitor KT5823 (1 microM) and the type II phosphodiesterase inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine (30 microM) did not attenuate the ACh effect. Therefore, ACh inhibits the basal calcium current in the atrioventricular node mainly by suppressing cAMP synthesis through the inhibitory GTP-binding protein.

Acetylcholine↗
PubMed1997

[Diffuse Lewy body disease].

Lewy body disease (LBD) is a progressive neurological disorder with parkinsonism, having many Lewy bodies (LBs) and degenerative changes. LBD is classified into the three types according to the distribution of LBs: "brain-stem type", "transitional type" and "diffuse type". The brain-stem type is identical to classical Parkinson's disease (PD). The diffuse type is nominated as "diffuse Lewy body disease" (DLBD). DLBD is a neuropathological entity, characterized by abundant LBs not only in the basal ganglia and brain-stem but in the cerebral cortex, combined with senile changes. Juvenile onset DLBD is called "pure form" of DLBD because of no or few senile changes. The LBs are present in the amygdala, nucleus basalis of Meynert, hypothalamic nuclei, substantia nigra, nucleus paranigralis, locus caeruleus, dorsal vagal nucleus and reticular nuclei. The cerebral LBs are numerous in the parahippocampal gyrus, cingular gyrus, and insular, frontal and temporal cortices. The LBs show immunoreactivity to ubiquitin and the ubiquitin-immunoreactive neurites in the CA2-3 region appear to be specific for DLBD. The clinical features of DLBD in the senium are progressive dementia, psychotic state, parkinsonism and autonomic signs. In general, progressive dementia is an initial symptom, followed by parkinsonism in the later stage. Some show progressive autonomic failure. A few present respiratory failure or vocal cord palsy resulting in sudden death in DLBD. DLBD is characterized neurochemically by severe affection of multiple neurotransmitters networks. In DLBD an impairment of the innominato-cortical cholinergic and mesocortical dopaminergic system, differentiating from Alzheimer's disease and PD, may play an important role in developing disease process.

Humans↗
PubMed1996

Functional assessment of two vitamin D-responsive elements in the rat 25-hydroxyvitamin D3 24-hydroxylase gene.

Two vitamin D-responsive elements (VDRE-1 and VDRE-2) were recently identified in the 5'-upstream region of the rat 25-hydroxyvitamin D3 24-hydroxylase gene at -151/-137 and -259/-245, respectively. We studied the transcriptional regulation of this gene by vitamin D by means of mutational analysis. Introducing mutations into VDRE-1 and VDRE-2 in the native promoter -291/+9 reduced vitamin D-dependent chloramphenicol acetyltransferase activity by 86 and 41%, respectively. Mutation of the direct repeat -169/-155 located at 3 base pairs upstream of VDRE-1 also caused 50% decrease of chloramphenicol acetyltransferase activity. Connection of the element -169/-155 to VDRE-1 enhanced the vitamin D responsiveness of VDRE-1 5-fold through the heterologous beta-globin promoter. The fragment -291/-102 containing the two VDREs showed two shifted bands in the presence of the vitamin D receptor and retinoid X receptor in gel retardation analysis, and the appearance of the slower migrating band indicates that two sets of receptor complexes bind to this fragment simultaneously. These results demonstrate that VDRE-1 is a stronger mediator of vitamin D function than VDRE-2 due to the presence of the accessory element -169/-155 located adjacent to VDRE-1, although VDRE-2 exhibits a smaller dissociation constant for the vitamin D receptor-retinoid X receptor complex than VDRE-1.

Animals↗
PubMed1996

Functional role of cation-independent mannose 6-phosphate/insulin-like growth factor II receptor in cell adhesion and proliferation of a human myeloma cell line OPM-2.

The molecular mechanism underlying the interaction between myeloma cells and stromal cells was investigated by using a human myeloma cell line (OPM-2) and human umbilical vein endothelial cells (HUVECs). Adhesion of OPM-2 cells to HUVECs was found to be significantly augmented with treatment of OPM-2 cells with an alpha-glycosidase inhibitor, castanospermine (CSP). The treatment of OPM-2 cells with CSP resulted in alteration of oligosaccharide structures of cell surface glycoproteins particularly at molecular weight of 220 kD (GP220). To determine if GP220 was involved in the adhesion of OPM-2 cells to HUVECs, cell surface glycoproteins of HUVECs were labeled by biotin and were incubated with the PVDF membrane to which cell surface glycoproteins of OPM-2 cells were blotted. The biotinylated glycoproteins at the plasma membrane of HUVECs specifically bound to GP220 of OPM-2 cells. Purification and partial amino acid sequencing of GP220 revealed that GP220 had a structure homologous to cation-independent mannose 6-phosphate/insulin-like growth factor-II (CIM6P/IGF-II) receptor. Furthermore, an antibody against CIM6P/IGF-II receptor was reactive with GP220, indicating that GP220 was a CIM6P/IGF-II receptor. The adhesion of OPM-2 cells to HUVECs was inhibited by mannose 6-phosphate. Moreover, M6P was found to suppress the adhesion of human myeloma cell lines, OPM-2 and RPMI 8226, to bone marrow stromal cells that was established from the patients with multiple myeloma. In addition, proliferation of OPM-2 was stimulated in response to IGF-II. These results suggest that CIM6P/IGF-II receptor may be functional in terms of supporting cell adhesion and proliferation of myeloma cells.

Cell Adhesion↗