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Biomedical subjects

M Yasui

Publications and source records attributed to M Yasui.

At least 91 records · Page 5Linked to original sources
PubMed1996

Glucocorticoids stimulate the maturation of H,K-ATPase in the infant rat stomach.

The development of gastric H,K-ATPase from fetal to adult life was studied in the rat. The alpha and beta H,K-ATPase mRNA abundance, the protein abundance, and the enzyme activity increased postnatally. The sharpest increase in mRNA and enzyme activity was observed in the weaning period. Several intestinal enzymes are known to be stimulated by glucocorticoids at the time of weaning. To study the role of glucocorticoids in the maturation of gastric H,K-ATPase, we treated 10-d-old rats with a single injection of betamethasone. Twenty-four hours after betamethasone injection, the enzyme activity was significantly higher than in the control animals (2.6-fold, p < 0.05). The abundance of catalytic alpha H,K-ATPase protein was also increased (2.5-fold, p < 0.01). The time-dependent effect of betamethasone on alpha H,K-ATPase mRNA was determined from 6 to 24 h after treatment. Glucocorticoids did not significantly alter the mRNA abundance within 18 h. Twenty-four hours after injection, the gastric H,K-ATPase mRNA was significantly increased compared with controls (2.8- and 2.2-fold increase for alpha and beta subunits, respectively, P < 0.01 for both). In conclusion this study indicates that glucocorticoids may regulate the long-term maturation of gastric H,K-ATPase by indirectly stimulating enzyme synthesis.

Animals↗
PubMed1996

[Increased CA19-9 level in serum and bronchoalveolar lavage fluid from a patient with pulmonary tuberculosis].

A 66-year-old woman was admitted to the hospital because of general malaise and loss of appetite. Laboratory examination revealed an abnormally high level of CA19-9 in serum and a chest roentgenogram revealed soft reticular shadows in the right mid-lung field. An extensive examination revealed no malignant disease. Bronchoalveolar lavage fluid obtained from the right B5 contained an abnormally high level of CA19-9. Immunochemical staining for CA19-9 was positive in the epithelial cells of respiratory bronchioles. The level of CA19-9 decreased during anti-tuberculosis therapy. This case suggests that the CA19-9 level can reflect the activity of pulmonary tuberculosis.

Aged↗
PubMed1996

[Diffuse alveolar septal amyloidosis associated with multiple myeloma (IgA lambda type)].

A 75-year-old man with multiple myeloma presented with fever and respiratory symptoms. A chest roentgenogram showed interstitial shadows and transbronchial lung biopsy revealed diffuse infiltration of amyloid in the alveolar walls. Analysis of bronchoalveolar lavage fluid showed the presence of an IgA-lambda paraprotein, and the IgA/albumin ratio was similar to that in serum. However, plasma cells could not be detected in the cells obtained by lavage. We know of no previous case in Japan in which bronchoalveolar lavage fluid was examined in a case of diffuse alveolar septal amyloidosis.

Aged↗
PubMed1996

Results of single and double autografts for high-risk neuroblastoma patients.

Although intensive therapy with autologous bone marrow transplantation (ABMT) has improved the outcome of advanced neuroblastoma, nearly half the patients with this disease still relapse after a single ABMT. In our previous study, 10 of 22 patients relapsed within 16 months post-transplantation. Predictive risk-factors for relapse were the presence of bone lesions at diagnosis, and a minor response or progressive disease at transplantation. In order to improve the outcome of these high-risk patients, we tested the feasibility of double autografts. To date, eight patients have been treated, and no treatment-related deaths were observed. Six remain in CR or with stable disease for 6 to 29 months. Although more cases and longer observation are needed to draw conclusions, these results are encouraging.

Bone Marrow Transplantation↗
PubMed1996

[The clinical significance of minimal residual disease of acute leukemia with t(4;11) (q21;q23)].

Hybrid fusion genes are specific tumor markers of several leukemic subtypes. The use of reverse transcription-polymerase chain reaction (RT-PCR) to amplify chimeric cDNAs allows sensitive detection of the leukemia clone. The clinical relevance of minimal residual disease (MRD) remains controversial. In this report, an infantile acute lymphoblastic leukemia with t(4;11) (q21; q23) was analyzed after each treatment for the presence of MRD by RT-PCR amplification of the MLL/LTG4 fusion gene which became available recently. The patient soon achieved a hematological CR, after induction therapy, and underwent autologous BMT following consolidation chemotherapy for 9 months. However, he relapsed three months after the BMT. MRD was always detectable during his clinical course. These findings suggest that the detection of MRD of the MLL/LTG4 fusion transcript is a useful tool for monitoring MRD and selecting treatment.

Child, Preschool↗
PubMed1996

Comparison of heavy metal concentrations in human umbilical cord in 1980 and 1990.

The well-known Minamata disease was caused by mercury; the Itai-Itai disease by cadmium; and lead poisoning by gasoline additives. Following our previous investigation on heavy metal concentrations in the umbilical cords in 1980, total mercury, cadmium and lead concentrations in the umbilical cords (from 20 males and 20 females) have been measured in 1990 for comparison in the present study. The changes in metal concentrations in 1980 and 1990 were: from 0.007 +/- 0.005 microgram/g to 0.011 +/- 0.008 microgram/g for total mercury; from 0.019 +/- 0.016 microgram/g to 0.006 +/- 0.005 microgram/g, from 0.151 +/- 0.123 microgram/g to 0.046 +/- 0.038 microgram/g for lead. Total mercury accumulated in the umbilical cords increased to approximately 1.6-fold, while cadmium and lead decreased to approximately 1/3-fold during these 10 years.

Adult↗
PubMed1995

CCKB receptor activation protects CA1 neurons from ischemia-induced dysfunction in stroke-prone spontaneously hypertensive rats hippocampal slices.

We examined the effect of cholecystokinin octapeptide sulfated type (CCK-8S) on dysfunction of CA1 pyramidal neurons induced by in vitro ischemic insult in hippocampal slices of stroke-prone spontaneously hypertensive rats (SHRSP). CCK-8S shortened the time required for partial recovery from block of a population spike produced by ischemia. Furthermore, CCK-8S reduced ischemic insult-induced accumulation of K+ in extracellular space. Suppression of the K+ conductance by the CCKB receptor activation is suggested to contribute to neuroprotection by CCK-8S.

Animals↗
PubMed1995

Immunohistochemical staining for endotoxin using horseshoe crab factor C in fecal peritonitis.

The object of the present study was to apply a new immunohistochemical staining method to the in vivo determination of endotoxin localization. The immunohistochemical staining method requires factor C (an initiation factor in the Limulus clotting system which is mediated by endotoxin) as a specific ligand of endotoxin, and a newly developed murine monoclonal antibody to factor C. The blood endotoxin level and endotoxin localization in the rat were determined before and at 6, 12 and 24 h after intraperitoneal injection of 0.25 g/kg of fresh rat feces. The greatest blood endotoxin level was achieved at 12 h after the injection, and uptake of endotoxin was evident in Kupffer cells in the liver at 24 h after the injection. There has been no report on determining endotoxin localization in cases of endotoxemia attributed to fecal peritonitis. This new immunohistochemical staining method for determining endotoxin localization will contribute to the histopathological diagnosis of endotoxemia in humans.

Animals↗
PubMed1995

Differential effects of glucocorticoids and mineralocorticoids on the mRNA expression of colon ion transporters in infant rats.

Several epithelial ion transporters are developmentally regulated in the preweaning period, at the time when the circulating levels of glucocorticoid and mineralocorticoid hormones increase. The specific role of glucocorticoids and mineralocorticoids in the maturation of epithelial ion transport is still disputed. In this study, we investigated the effect of corticosteroids on the mRNA expression of ion transporters in the infant rat colon, a glucocorticoid- and mineralocorticoid-sensitive organ. The expression of the Na,K-ATPase, the H,K-ATPase and the amiloride-sensitive Na+ channel mRNA was investigated in control rats from fetal to adult life. We found that the mRNA of the three transporters is temporarily up-regulated in the preweaning period. Rats were then injected with a single dose of betamethasone or aldosterone at 10 d of age. The main effect was the glucocorticoid stimulation of the Na,K-ATPase mRNA within 6 h (4-fold). Glucocorticoids did not alter H,K-ATPase nor Na+ channel mRNA within 6 h. Aldosterone moderately (1.7-fold) stimulated Na+ channel within 6 h, but dit not alter Na,K-ATPase nor H,K-ATPase mRNA. Twenty-four hours after injection, both glucocorticoids and mineralocorticoids had less pronounced and distinct effects. In tissue with lower aldosterone receptor abundance (renal cortex) or with no aldosterone receptor (stomach), glucocorticoids induce a similarly rapid increases in Na,K-ATPase mRNA (4-fold within 6 h), whereas aldosterone had no effect within 6 h. However, glucocorticoids did not stimulate Na,K-ATPase mRNA in the brain, a tissue rich in glucocorticoid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1995

CCKB-receptor activation augments the long-term potentiation in guinea pig hippocampal slices.

Effects of cholecystokinin octapeptide (CCK-8) on long-term potentiation (LTP) of CA1 synaptic transmission induced by tetanic stimulation of the input fibers were examined in guinea pig hippocampal slices. CCK-8 and a selective agonist for the CCKB receptor, non-sulfated CCK-8, dose-dependently augmented the magnitude of LTP. Concomitant application of a selective antagonist for the CCKB-receptor subtype, L-365,260 (3R(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4- benzodiazepine-3-yl)-N'-(3-methylphenyl)urea), completely blocked the augmentation of LTP induced by CCK-8, whereas a selective CCKA-receptor antagonist, L-364,718 (3S(-)-N-(2,3-dihydro-1-methyl-2- oxo-5-phenyl-1H-1,4-benzodiazepine)), had little effect. Thus, enhancement of LTP by CCK appears to be mediated by CCKB receptors. Furthermore, CCK-8 enhanced paired-pulse facilitation at a concentration of 10(-7) M without affecting the amplitude of the population spike induced by single stimulation. This effect was mimicked by a low dose of tetraethylammonium (TEA), a K+ channel blocker. Moreover, both CCK-8 and TEA reduced the late component of evoked field potentials. This late evoked potential was diminished by increasing the extracellular K+ concentration. It is suggested that CCK-8 reduces the K+ conductance in CA1 pyramidal neurons. This reduction in the K+ conductance might be related to enhancement of the LTP.

Animals↗
PubMed1995

[A case of idiopathic hypoparathyroidism with slurred speech and mild dementia].

A case of idiopathic hypoparathyroidism (IHP) is discussed with reference to a study of rats maintained on various low-calcium diets. A 45-year-old man complained of difficulty speaking, especially an inability to speak loudly and of fine finger tremors over the past 2 or 3 years. His brain MRI showed marked calcification in the bilateral basal ganglia and cerebellum and his in sera findings showed low calcium, extremely low levels in all kinds of examined parathyroid hormones and 1,25 (OH)2D, thus we diagnosed idiopathic hypoparathyroidism. His finger tremors stopped soon after administration of 1 alpha D3 2 microgram/day as verified by calcium, phosphorus and creatinine levels in sera, however, a brain CT one year later showed no changes in calcification. As reported earlier in studies of deposition in the soft tissues, especially central nervous system tissues of rats maintained on low-calcium diets, it is difficult to reduce calcium deposition if symptoms appear in adults. Therefore, it is necessary to start therapy as soon as possible in order to prevent additional calcium deposition in the early stage of IHP.

Brain↗
PubMed1995

Effects of calcium-deficient diets on manganese deposition in the central nervous system and bones of rats.

The presence of both aluminum (Al) and manganese (Mn) in central nervous system tissues (CNS) has been reported in Parkinson's disease and in parkinsonism-dementia (PD) on Guam. Epidemiological surveys on Guam have suggested that low calcium (Ca), magnesium (Mg) and high Al and Mn in river, soil and drinking water may be implicated in the pathogenesis of PD. Experimentally, low Ca-Mg diets with or without added Al have been found to accelerate Al deposition in the CNS of rats and monkeys. Although excessive deposition of Mn produces similar neurotoxic action to Al in CNS tissues, the mechanism of Mn deposition coupled with Al loading in the presence of low Ca-Mg intake is not yet known. In this study, the deposition and mental-metal interaction of both Al and Mn in the CNS, visceral organs and bones of rats fed unbalanced mineral diets were analyzed. Male Wistar rats, weighing 200 g, were maintained for 90 days on the following diets: (A) standard diet, (B) low Ca diet, (C) low Ca-Mg diet, (D) low Ca-Mg diet with high Al. Al and Mn content were determined in the frontal cortex, spinal cord, kidney, muscle, abdominal aorta, femur and lumbar spine using neutron activation analysis (NAA). Our results demonstrate that serum Ca levels were decreased in the following dietary order: C<D<B<A. Serum Mg levels were significantly lower in rats from Groups C and D, compared with those in Groups A and B, reflecting the content of Mg and other interacting minerals in the diet. There was no significant difference in serum Al, zinc and phosphorus levels. Ca and Mg contents in lumbar vertebrae and the femur were significantly lower and Al levels significantly higher in rats maintained on the low Ca-Mg diet with or without added Al. Al content in CNS tissues and visceral organs were highest in rats fed diets deficient in Ca alone or low in Ca-Mg with or without added Al. Bone Mn levels significantly increased in rats fed the low Ca-Mg diet with added Al. Mn content in the frontal cortex significantly increased in rats fed diets low in Ca-Mg with or without added Al. But the Mn content of other tissues including the spinal cord, kidney, muscle and abdominal aorta was unchanged in rats given Ca deficient diets. Intake of low Ca and Mg with added Al in rats led to the high concentrations of Mn and Al in bones and in the frontal cortex. We conclude that unbalanced mineral diets and metal-metal interactions may lead to the unequal distribution of Al and Mn in bones and ultimately in the CNS inducing CNS degeneration.

Aluminum↗
PubMed1994

Vulnerability of CA1 neurons in SHRSP hippocampal slices to ischemia, and its protection by Ca2+ channel blockers.

Vulnerability of CA1 pyramidal neurons to hypoxic and hypoglycemic insult was compared in hippocampal slices between the stroke-prone spontaneously hypertensive rat (SHRSP) and its mother strain, Wistar Kyoto rat (WKY). Stimulation of Schaffer collateral-commissural fibers induced D-2-amino-5-phosphonovalerate sensitive multi-component population spikes in slices from both strains when the external K+ concentration was elevated. The K+ concentration required for this phenomenon was significantly lower in SHRSP slice preparations than in those from WKY. The hypoxic and hypoglycemic insult in slice preparations is assumed to be equivalent to ischemic conditions in vivo. Although the short-term 'ischemic' insult caused a complete loss of population spikes in slices from both strains, a transient hyperexcitability, spreading depression-like depolarization, accumulation of extracellular K+ and reduction of extracellular Ca2+ occurred in SHRSP slices, but not in WKY. Time required for partial recovery of the population spike following the 'ischemic' insult was markedly increased in SHRSP slices compared with WKY. Thus, CA1 pyramidal neurons of SHRSP were more vulnerable to 'ischemic' insult than those of WKY. This vulnerability of pyramidal neurons in the SHRSP strain was independent of its hypertensive phenotype. A novel L-type Ca2+ channel blocker, S-312-d, its stereoisomer, S-312-1, and nimodipine protected the 'ischemic' insult-induced neuronal dysfunction at submicromolar concentrations. It is concluded that hippocampal neurons in SHRSP are innately vulnerable. This vulnerability is suggested to be due, at least in part, to some abnormality in K+ channel channels of hippocampal neurons.

Animals↗
PubMed1994

Effects of hepatic arterial infusion chemotherapy on unresectable or recurrent hepatocellular carcinoma.

We performed hepatic arterial infusion chemotherapy (HAI) on 86 patients with unresectable hepatocellular carcinoma (HCC, 61 patients) or unresectable recurrent HCC after hepatectomy (25 patients). As drug therapy, 250 mg of 5-fluorouracil was injected daily for 14 days using a reservoir embedded in the subcutaneous layer. During this period, 0.4 mg/kg of doxorubicin and 0.12 mg/kg of mitomycin C suspended in Lipiodol Ultra-Fluide were also injected twice intra-arterially. This was defined as one course of HAI, and it was repeated every 3 months. In the patients with unresectable HCC, the 1-, 2-, and 3-year survival rates were 31.5%, 22.4%, and 10.7%, respectively, and the numbers of cases showing a complete response (CR), a partial response (PR), a minor response (MR), no change (NC), and progressive disease (PD) according to the Criteria for the Evaluation of the Clinical Effects of Solid Cancer Chemotherapy established by the Japan Society for Cancer Therapy were 1 (1.6%), 20 (32.8%), 5 (8.2%), 28 (45.9%), and 7 (11.5%), respectively. On the other hand, the 1-, 2-, and 3-year survival rates of the patients with unresectable recurrent HCC were 69.6%, 34.8%, and 14.9%, respectively. The rate of catheter patency after 1 year was 64.1%, and the mean catheter-patency period was 311.9 days. Patients in group A (CR+PR, n = 21) survived significantly longer than those in group B (MR+NC+PD, n = 40; P < 0.05). In conclusion, since responders to HAI achieve longer survival than nonresponders, the selection of effective drugs is important for this therapy.

Adult↗
PubMed1994

New familial nephropathy involving glomerular and tubular basement membranes.

We describe two siblings, an 8-year-old boy and a 9-year-old girl, with severe mental retardation, dwarfism, optic atrophy and nephropathy. Laboratory examination showed beta 2-microglobulinuria, decreased creatinine clearance, hypercholesterolaemia and elevated serum levels of muscle enzymes. Renal biopsy from one of the patients demonstrated characteristic ultrastructural changes involving both the glomerular and tubular basement membrane. This group of symptoms and laboratory findings is quite distinct and differs from those of other reported familial nephropathy syndromes. We conclude that this disorder may represent a new syndrome of autosomal recessive inheritance.

Basement Membrane↗
PubMed1994

Direct expression of a synthetic gene in Escherichia coli: purification and physicochemical properties of human initiation factor 4E.

An artificial synthetic gene coding for human eIF-4E was cloned into an expression vector and direct expression was attempted in Escherichia coli [BL21(DE3) strain] under the control of T7 promoter. The active gene product which was induced in high yield (ca. 4 mg/100 ml) by isopropyl-beta-D-thiogalactopyranoside was purified to homogeneity by a two-step chromatographic procedure with a good yield (ca. 74%), and was confirmed to be recombinant human eIF-4E by amino acid composition and sequence analyses, isoelectric focusing, and absorption spectral measurements. The identity of three-dimensional structures between the recombinant and native human eIF-4Es was confirmed by CD and fluorescence measurements.

Amino Acid Sequence↗
PubMed1994

Glucocorticoids regulate the transcription of Na(+)-K(+)-ATPase genes in the infant rat kidney.

Glucocorticoids modulate the maturation of Na(+)-K(+)-ATPase mRNA in a tissue- and age-dependent manner. In this study, we report the effect of glucocorticoids on Na(+)-K(+)-ATPase gene transcription in the infant rat kidney. Ten-day-old rats were treated with one intraperitoneal injection of betamethasone. In glucocorticoid-treated rats, there was a significant increase in renal cortical alpha 1- and beta 1-mRNAs (3.08 +/- 0.34- and 4.06 +/- 0.10-fold). Pretreatment with cycloheximide, an inhibitor of protein synthesis, did not abolish the increase in alpha 1- and beta 1-mRNA after glucocorticoids. The alpha 1- and beta 1-gene transcription rates were significantly increased in nuclei isolated from kidneys of glucocorticoid-treated rat (2.16 +/- 0.05- and 3.12 +/- 0.50-fold). Interaction between nuclear proteins and Na(+)-K(+)-ATPase alpha 1-promoter was studied by gel retardation assay. Nuclear protein from glucocorticoid-treated rats retarded a fragment of alpha 1-promoter that includes a half-consensus glucocorticoid response element (GRE) at position -750 bp but did not retard a fragment including a half-consensus GRE at position -481. Retardation of alpha 1-promoter was inhibited by incubation with molar excess of GRE or with a monoclonal antibody against glucocorticoid receptor. We conclude that in the infant kidney, glucocorticoids directly stimulate the transcription of alpha 1- and beta 1-Na(+)-K(+)-ATPase subunits. It is likely that the binding of glucocorticoid receptor to alpha 1-Na(+)-K(+)-ATPase promoter requires the presence of an auxiliary factor.

Animals↗