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Biomedical subjects

Y Mimura

Publications and source records attributed to Y Mimura.

At least 37 records · Page 2Linked to original sources
PubMed1998

Renal AT1 receptor: computerized quantification in spontaneously hypertensive rats and DOCA-salt rats.

To assess the involvement of angiotensin II (Ang II) in the regulation of blood pressure, we investigated the alterations of renal Ang II type 1 (AT1) receptors in two different models of hypertension; i.e., in spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats by using the method for quantification of in vitro macro-autoradiography (ARG). In the SHR model, although the number of cortical AT1 receptors equaled that of Wistar Kyoto (WKY) rats at 4 and 12 weeks of age, the number of medullary AT1 receptors in the 4-week-old SHR animals was significantly lower than that in age-matched WKY rats, and increased by 12 weeks of age. The renal AT1 receptor number in DOCA-salt hypertensive rats was significantly higher than that in control rats. The amount of these receptors also increased with age in both DOCA-salt hypertensive rats and control rats. These findings indicate that the development of medullary AT1 receptors in early stages of hypertension in the SHR model differs from that in WKY rats or DOCA-salt hypertensive rats. This suggests that renal AT1 receptors may contribute to the hypertension seen in the SHR group. The renal AT1 receptors appear to be up-regulated in early stages of DOCA-salt-induced hypertension as well.

Age Factors↗
PubMed1997

Effects of OPC-21268, a vasopressin V1-receptor antagonist, on expression of growth factors from glomeruli in spontaneously hypertensive rats.

To assess the chronic in vivo effects of OPC-21268, a vasopressin-V1 receptor antagonist, on renal injury, we investigated the mRNA expressions of platelet-derived growth factor (PDGF) B-chain, transforming growth factor (TGF)-beta1 and proliferating cell nuclear antigen (PCNA) in the glomeruli of spontaneously hypertensive rats (SHR) treated with OPC-21268 for 3 weeks. SHR aged 10 weeks were given 2% NaCl in drinking water for 3 weeks. The OPC group was fed a 0.5% OPC-21268-containing diet for 3 weeks and the control group was given a normal diet. There were no significant changes in the time course of systolic blood pressure, heart rate, urine volume, or urinary sodium, protein and N-acetyl-beta-glucosaminidase (NAG) excretion between the two groups. Serum electrolytes, protein and creatinine levels also did not differ between the groups. The mRNA expressions of PDGF B-chain, TGF-beta1 and PCNA in the glomerulus were examined using reverse transcriptase-polymerase chain reaction (RT-PCR) methods. The mRNA expressions of PDGF B-chain and PCNA among these were significantly suppressed in the OPC group. No significant differences in renal histology including the organ weights were found between the two groups; however, the glomerular size tended to be enlarged in the OPC group. These findings suggest that chronic V1-receptor blockade directly inhibits the glomerular proliferative injury of salt-loaded SHR at the established hypertension stage.

Acetylglucosaminidase↗
PubMed1997

Prenatal nicotine exposure affects the development of the central serotonergic system as well as the dopaminergic system in rat offspring: involvement of route of drug administrations.

The present study was undertaken to examine the effects of prenatal nicotine exposure by two different routes of drug administration, injection and infusion, on the development of monoaminergic systems and open field behavior in the neonatal and juvenile rat. The nicotine administration to pregnant Sprague-Dawley rats was carried out by subcutaneous injection (3 mg/kg twice daily) or infusion via implanted osmotic minipumps (6 mg/kg/day) from gestational day 4 (GD4) until GD20. At postnatal day 7 (PD7), 15 and 22, the contents of the neurotransmitters and their metabolites including noradrenaline (NA), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanilic acid (HVA), serotonin (5-HT) and 5-hydroxy-3-indolacetic acid (5-HIAA) were measured in the midbrain+pons - medulla (M + P - M), forebrain and cerebellum. Prenatal nicotine exposure caused a persistent reduction of DA turnover in the forebrain at PD15 and PD22. In addition, the 5-HT system was also affected by prenatal nicotine, and reductions of 5-HT turnover in the M + P - M at PD15 and in the forebrain and the cerebellum at PD22 were found. Although there was no effect of prenatal nicotine on NE contents, the involvement of this system remains uncertain since we measured only NE contents without metabolites. In the present study, we also found significant route-related changes in the contents of the monoamines and metabolites in the NA, DA and 5-HT systems in all brain regions in rat offspring besides the effects of prenatal nicotine. In addition, the difference in administration route reflected the results of the open field test and the number of ambulations in the injection-group was less than that in the infusion-groups with no relation to nicotine administration. Therefore, such effects of "prenatal stress" accompanied by drug administration are not negligible in considering the risk assessment of prenatal nicotine exposure.

Analysis of Variance↗
PubMed1997

Detection of numeric abnormalities of chromosome 17 and p53 deletions by fluorescence in situ hybridization in pleomorphic adenomas and carcinomas in pleomorphic adenoma. Correlation with p53 expression.

BACKGROUND: A fluorescence in situ hybridization (FISH) technique using specific DNA probes allows for the detection of chromosomal aberrations and gene deletions and gains, even in interphase nuclei in human solid tumors. A high frequency of aberrations of chromosome 17 and mutation of the p53 gene have been reported in some human tumors. The correlation of p53 expression with abnormalities of chromosome 17 and p53 gene deletion in salivary gland tumors has not yet been investigated. METHODS: The authors analyzed the numeric aberrations of chromosome 17 and p53 gene deletions in 11 paraffin embedded pleomorphic adenomas (PA) and 9 carcinomas in pleomorphic adenoma (CIPA), using FISH techniques. The centromere specific DNA probe for chromosome 17 and p53 cosmid DNA probe was used. The aberrations of chromosome 17 and p53 deletion were correlated with immunohistochemical detection of p53 protein. RESULTS: Monosomy 17 was detected in 30.8% of CIPA cells and 29.6% of PA cells, and polysomy 17 was detected in 19.6% of CIPA cells and 9.6% of PA cells. p53 protein expression was observed in 6 of 9 CIPA specimens (66.7%) and 2 of 75 PA specimens (2.7%). Deletion of the p53 gene was frequent in p53 protein positive specimens. A statistically significant correlation existed between p53 protein expression and polysomy 17 (P = 0.0417). CONCLUSIONS: It was observed that loss of chromosome 17 may occur in PA before its transformation to carcinoma. p53 expression was frequently associated with deletion of the p53 gene as detected by FISH. Polysomy 17 was more frequent in CIPA than PA and was associated with mutation of p53.

Adenocarcinoma↗
PubMed1997

Metabolism of anandamide, an endogenous cannabinoid receptor ligand, in porcine ocular tissues.

Anandamide (arachidonylethanolamide) is an endogenous ligand for cannabinoid receptors, and exerts various cannabimimetic activities. Since cannabinoids and anandamide were pharmacologically active with the eye, we examined metabolism of anandamide in a variety of porcine ocular tissues. In the presence of ethanolamine, [14C]arachidonic acid was converted to [14C]anandamide by a homogenate of retina, choroid, iris, optic nerve and lacrimal gland with a specific enzyme activity of 1.9-4.2 nmol min-1 mg-1 protein at 37 degrees C. On the other hand, [14C]anandamide was hydrolysed to [14C]arachidonic acid by a homogenate of each tissue with a specific enzyme activity of 1.2-3.5 nmol min-1 mg-1 protein. Thus, both activities of anandamide synthase and hydrolase were found in these ocular tissues. As for the subcellular distribution, the two enzyme activities were mostly recovered in particulate fractions rather than the cytosol. With the retina microsome palmitic acid was converted to its ethanolamide at a lower rate than arachidonic acid, and palmitoylethanolamide was less active than anandamide as a substrate for the hydrolase.

Animals↗
PubMed1997

Efficacy of amino acid infusion for improving protein metabolism after surgery: a prospective randomized study in patients undergoing subtotal gastrectomy.

BACKGROUND: Appropriate regimens of peripheral parenteral nutrition (PPN) have been proposed for the improvement of protein metabolism after surgery. When evaluating the efficacy of administered nutrients, it is vital to consider the severity of surgical stresses to avoid confounding effects of the trauma on the postoperative metabolism. This study was designed to evaluate protein-sparing regimens through PPN in patients who had undergone subtotal gastrectomy. STUDY DESIGN: Patients hospitalized at our institutes for gastric cancer were randomly divided into the following five groups and received PPN for 7 days after surgery: 1. G group (n = 9), 200 g glucose (per day); 2. AG group (n = 10), 54 g amino acids + 150 g glucose; 3. AGG group (n = 9), AG + 110 g glucose; 4. AGF group (n = 10), AG + 40 g fat; and 5. AGL group (n = 7), 58 g amino acids + 60 g glycerol. Biochemical studies were done before and after surgery. RESULTS: In comparison to G group patients, AG group patients showed less negative cumulative nitrogen balances. No significant differences in cumulative nitrogen balances were observed between AGG, AGF, and AGL groups. Restoration of the reduced serum rapid turnover protein occurred earlier in the AGL group than in either the AGG or the AGF groups. Hyperglycemia, glucosuria, and hyperinsulinemia were prominent in the AGG group, and less prominent in the AGL group. Marked ketosis together with an increase in serum-free fatty acid levels was found in the AGL group. CONCLUSIONS: These results suggest that in patients who have undergone major elective surgery, infusion of amino acid solutions is advantageous for improving protein metabolism after surgery, and nonprotein energy source and intake are not essential when combined with amino acid solutions for improving nitrogen balance after surgery.

Adult↗
PubMed1997

Renal regulation of phosphate excretion in endotoxaemic rats.

1. Maintenance of phosphate homeostasis is essential for energy producing and oxygen delivery systems, particularly, when the energy requirements are increased in certain conditions, such as septicaemia. We investigated the phosphaturic response to parathyroid hormone (PTH) in endotoxin (ETx)-treated rats in order to clarify the renal regulation of phosphate excretion during endotoxaemia. 2. Wistar rats that had undergone thyroparathyroidectomy were challenged with either Escherichia coli ETx (n = 8) or saline vehicle (n = 9). Thirty-minute renal clearance tests were done before and after PTH infusion. Rats infused with saline instead of PTH served as time controls for the ETx- (n = 7) and saline-treated (n = 8) rats. 3. In time control rats, ETx administration enhanced phosphate excretion progressively and this was associated with an obvious increase in the level of kidney adenosine 3', 5'-cyclic mono-phosphate (P < 0.005) compared with levels following saline vehicle administration. However, this phosphaturia in late-phase endotoxaemia was not observed in rats infused with PTH; ETx, but not saline vehicle, blunted the PTH-mediated increase in phosphate excretion (P < 0.005). Increased urinary noradrenaline and constant dopamine excretion were observed in endotoxaemic rats. Endotoxin administration produced marked metabolic acidosis and hypocapnia in comparison with the administration of the saline vehicle. 4. To test whether renal tubular sensitivity to parathyroid hormone related-protein (PTHrP) was enhanced during endotoxaemia, phosphaturic response to PTHrP in ETx- (n = 7) and saline-treated rats (n = 7) was examined. Parathyroid hormone related-protein infusion produced phosphaturia in both groups. However, the severity of the phosphaturia after PTHrP infusion was less in ETx-than in saline-treated rats. 5. In summary, although ETx administration causes a progressive increase in phosphate excretion in the absence of PTH, this is overcome by the antiphosphaturic effect of ETx, attenuating PTH-mediated phosphaturia after PTH infusion.

Animals↗
PubMed1997

Adrenalectomy overcomes the blunted natriuretic response to atrial natriuretic peptide during hypocapnia in rats.

1. Hypocapnia has been shown to blunt the natriuretic effect of atrial natriuretic peptide (ANP) independently of the renal nerves. In order to examine whether the adrenal glands are a limiting factor for the natriuretic effect of ANP, we evaluated the natriuretic responses of adrenalectomized rats to ANP infusion during hypocapnia. 2. Rats subjected to total adrenalectomy (ADX) or sham-operation (sham) were divided into hypocapnic and normocapnic groups depending on their arterial PCO2 levels. 3. In sham rats, ANP infusion at a rate of 12 micrograms/kg per h resulted in a smaller increase in the fractional excretion of sodium during hypocapnia (mean +/- SEM: 1.02 +/- 0.40%, n = 10) than normocapnia (3.95 +/- 0.64%, n = 9; P < 0.001). The level of fractional excretion of sodium with ANP infusion during hypocapnia was not significantly different from the level in saline-infused hypocapnic sham rats (0.93 +/- 0.62%, n = 10). In hypocapnic ADX rats (n = 11), ANP induced greater increases in the fractional excretion of sodium (5.59 +/- 1.35%) than did saline infusion (1.04 +/- 1.02%, n = 10; P < 0.002). In the absence of adrenal glands, the magnitude of natriuresis after ANP infusion during hypocapnia and normocapnia (3.32 +/- 1.07%, n = 9) were the same. 4. We conclude that the natriuretic effect of ANP is blunted during hypocapnia in the presence, but not in the absence, of adrenal glands. Our data suggest that the adrenal glands have an important role in limiting the natriuretic effect of ANP.

Adrenal Glands↗
PubMed1997

In vitro macro- and microautoradiographic localization of V1 and V2 receptors in the rat kidney using OPC-21268 and OPC-31260.

To elucidate the precise localization of vasopressin (VP) V1 and V2 receptors in the kidney, we utilized in vitro macroautoradiography (macro-ARG) and microautoradiography (micro-ARG) of these receptors in Wistar rat kidneys. This was done by using OPC-21268 and OPC-31260, two newly developed selective V1 (OPC-21268) and V2 (OPC-31260) receptor antagonists. For macro-ARG, 10-microm kidney sections were incubated with Tris-HCl buffer containing [3H]-VP with or without unlabeled ligand (VP, OPC-21268, or OPC-31260) at 20 degrees C for 40 min. These sections were then loaded into X-ray cassettes with Hyperfilm-[3H] and exposed in the dark for 2 months. The autoradiograms were quantitatively analyzed by using the research analysis system RAS 1,000; the V1 and V2 receptors were quantitated by subtracting the nonspecific binding (incubated with OPC-21268 and OPC-31260, respectively) from the total binding. To assess a more precise localization of the V1 and V2 receptors, we also investigated the micro-ARG of the renal V1 and V2 receptors by dipping the kidney section slides used for macro-ARG into a photographic emulsion and observing the receptors under light microscopy. [3H]-VP binding to the rat kidney was completely displaced by unlabeled excess VP, but not by unlabeled angiotensin II, indicating that [3H]-VP binding was specific for VP receptors. Computerized quantification showed that V2 receptors, visualized by OPC-31260, were the predominant type of VP receptor in the kidney. Conversely, V1 receptors, visualized by OPC-21268, were fewer in number. V1 receptors were partly localized to the glomerulus, cortical vessels, interstitial cells, and the medullary vessels. The V2 receptors localized to the collecting ducts and medullary tubules. Our findings indicated that renal V1 and V2 receptors can be detected by in vitro macro- and micro-ARG by using OPC-21268 and OPC-31260.

Animals↗
PubMed1997

A case of primary hyperparathyroidism accompanying multiple myeloma.

We report a case of 77-year-old woman who presented with lumbago and hypercalcemia. Multiple myeloma (MM) was first diagnosed by serum protein electrophoresis and bone marrow aspiration, but intact parathyroid hormone (intactPTH) was also found to be high in the presence of persistent hypercalcemia with anorexia and nausea. After lowering serum calcium with bisphosphonate administration, parathyroidectomy was performed. Upon histologic examination, the tumor was determined to be parathyroidal chief-cell hyperplasia and the patient was treated with melphalan and prednisolone. The relationship between MM and primary hyperparathyroidism (I degree HPT) remains unknown. Although the co-existence of MM and I degree HPT was reported in 12 reports from various parts of the world, there was only 1 report in Japan. The present case is an example of successful treatment for a complicated disorder, and suggests that patients suffering from bone pain or hypercalcemia need to be examined both endocrinologically and hematologically.

Aged↗
PubMed1997

Gestational thyrotoxicosis manifesting as wernicke encephalopathy: a case report.

The thyroid gland is physiologically stimulated in normal early pregnancy. This stimulated thyroid function is occasionally termed "gestational transient thyrotoxicosis". The cause of this thyrotoxicosis has been clarified to closely it associate with human chorionic gonadotropin (hCG). We encountered a pregnant patient with hyperemesis and thyrotoxicosis, who manifested symptoms of Wernicke encephalopathy. Although her serum hCG concentration transiently increased in accordance with the thyrotoxicosis, it was within normal limits for the gestational week. Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy. This case suggests that pregnant patients with hyperemesis should undergo careful endocrinological and neurological evaluations.

Adult↗
PubMed1997

Effect of renal denervation on phosphate excretion in endotoxemic rats.

Our previous studies showed that endotoxin (Et) administration causes hypophosphaturia in the presence of PTH. In this study, we tested the hypothesis that enhanced renal nerve activity during endotoxemia is responsible for hypophosphaturia. Two weeks after bilateral renal denervation, phosphate excretion was examined in endotoxemic Wistar rats (300 g body weight). Renal clearance studies were performed before and after 4 mg/kg body weight Escherichia coli Et administration. Et administration resulted in a marked fall in glomerular filtration rates of innervated rats (n=12, from 2.09 +/- 0.11 ml/min to 0.89 +/- 0.15 ml/min, P<0.005) compared to saline-treated innervated rats (n=7, from 1.98 +/- 0.19 ml/min to 1.76 +/- 0.16 ml/min). The glomerular filtration rate of renal denervated rats was the same for saline-treated rats (n=9, from 2.67 +/- 0.92 ml/min to 1.69 +/- 0.12 ml/min) and Et-treated rats (n=10, from 2.37 +/- 0.19 ml/min to 1.52 +/- 0.07 ml/min). Fractional phosphate excretion was significantly reduced after Et challenge in innervated rats (from 24.0 +/- 3.3% to 11.8 +/- 2.2%, P<0.0001) compared to saline injection in innervated rats (from 26.9 +/- 3.9% to 33.0 +/- 1.6%). Although renal denervation improved the hypophosphaturia in comparison to the innervated rats, fractional phosphate excretion was still lower in Et-treated rats (from 28.8 +/- 5.0% to 18.0 +/- 4.7%, P<0.005) than in saline-treated rats (from 30.2 +/- 6.1% to 38.7 +/- 4.2%). In conclusion, our data did not support the hypothesis that renal nerves have an important role in reducing renal phosphate excretion during acute endotoxemia.

Animals↗
PubMed1997

Manifestation of primary hyperthyroidism after pituitary adenomectomy: a case report.

We report a 47-year-old Japanese man who presented with visual disturbance due to a pituitary tumor with suprasellar extension. The patient had mild secondary hypothyroidism preoperatively, and was started on administration of levothyroxine sodium immediately before transsphenoidal surgery. After the operation, levothyroxine sodium was continued for several months. Pathological examination of the surgical specimen, together with endocrinological investigation revealed that the suprasellar tumor was a FSH-producing pituitary adenoma. Since 3 months after the operation, he has developed muscle weakness and finger tremor. He was found to be thyrotoxicosis, and levothyroxine sodium was discontinued. Seven weeks after levothyroxine sodium was discontinued, thyrotoxicosis continued, with a positive thyrotropin binding inhibitory immunoglobulin (TBII) and a high diffuse 123I-uptake by the thyroid. He was started on thiamazole 30 mg/day. Although his thyroid dysfunction improved within 2 months, hyperthyroidism worsened repeatedly on attempts to discontinue thiamazole, and he required continuous treatment at 2.5 mg/day. Patients with occult autoimmune thyroiditis rarely progress to thyrotoxicosis after operations on other endocrine organs such as the adrenal or parathyroid gland. In patients with pituitary adenoma, thyroid function and thyroid-associated autoantibodies should be investigated pre- and post-operatively.

Adenoma↗
PubMed1997

Systemic sclerosis associated with diabetes insipidus.

A rare case of systemic sclerosis that preceded the development of diabetes insipidus is reported. This 25-year-old man presented with Raynaud's phenomenon and ulceration of the tip of the right thumb. The diagnosis of systemic sclerosis was based on findings of proximal scleroderma, sclerodactyly, serological abnormalities, and skin abnormalities verified histologically. Partial central diabetes insipidus was later diagnosed after the sudden appearance of polyuria and polydipsia. Coexistence of systemic sclerosis with diabetes insipidus suggests that diabetes insipidus in this patient might have occurred via an autoimmune mechanism.

Adult↗
PubMed1997

Alterations of renal V1 and V2 receptors in spontaneously hypertensive rats and DOCA-salt hypertensive rats using computerized quantification for macro-autoradiogram.

We previously examined the precise localization of vasopressin (VP) V1 and V2 receptors in the rat kidney using in vitro macro- and micro-autoradiography (ARG), and established the methodology of quantification for macro-ARG. In this study, to elucidate the role of VP in hypertension, we investigated the change within V1 and V2 receptors in the kidney of spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats at different hypertensive stages. In SHR, although medullary V1 and V2 receptors decreased compared with age-matched Wistar-Kyoto (WKY) rats at the developmental hypertensive stage, these receptors increased once hypertension was established. Conversely, in DOCA-salt hypertensive rats, both renal V1 and V2 receptors decreased with elevated blood pressure. Therefore, expression of renal V1 and V2 receptors proved to be different between two models of hypertension, SHR and DOCA-salt hypertensive rats, when their blood pressure increases. In DOCA-salt hypertensive rats, renal V1 and V2 receptors may be down-regulated secondary to the high blood VP level. In SHR, the increase in renal V1 and V2 receptors may have a role in the development of high blood pressure in this strain of rats.

Animals↗
PubMed1996

Mechanism of the development of autoimmune dacryodenitis in the mouse model for primary Sjögren's syndrome.

To elucidate the mechanism of development in autoimmune lacrimal gland disease, we analyzed different aspects of autoimmune dacryoadenitis in a newly established mouse model for primary Sjögren's syndrome, focusing on the local expressions of cytokine genes, and the repertoire of T cell receptor (TCR) V beta genes transcribed within the inflammatory infiltration in the lacrimal glands. We found that the vast majority of inflammatory infiltration into the lacrimal glands were CD4+ V beta 8+ T cells. We detected the up-regulation of local cytokine genes (IL-1 beta, TNF-alpha, IL-2, IFN-gamma, IL-10, IL-12p40) in the lacrimal glands with very early inflammatory lesions by reverse transcriptase (RT)-PCR analysis. The predominant expression of the V beta 8 gene segment was detected from a very early stage, while extensive age-related diversity of TCR V beta gene usage was observed. Single-strand conformation polymorphism (SSCP) analysis demonstrated a distinct and a common binding pattern in the PCR product of the V beta 8 gene on the infiltrating cells during the course of the disease. These data suggest that in autoimmune dacryoadenitis of the mouse model for primary Sjögren's syndrome there may be a restricted usage of TCR V beta elements on a very early stage of the autoimmune lesion to recognize unknown self-antigen, and the autoreactive CD4+ T cells constitute a unique cytokine profile in the autoimmune lacrimal gland disease.

Animals↗