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T Murase

Publications and source records attributed to T Murase.

At least 73 records · Page 4Linked to original sources
PubMed2000

Analysis of the vasopressin system and water regulation in genetically polydipsic mice.

Polydipsic mice, STR/N, which show extreme polydipsia and polyuria, were discovered in 1958. In the STR/N, urine outputs are much higher than in control mice. The possibility of an abnormal regulation of the arginine vasopressin (AVP) system, or an abnormality in the renal susceptibility to AVP, should be considered. In this study we investigated the AVP system and water regulation in STR/N. We sequenced the AVP and the AVP V(2)-receptor genes of the STR/N by direct sequencing. No mutation was found in either of them. AVP gene expression examined by in situ hybridization and plasma sodium in 8-wk-old STR/N was significantly lower than in control mice, whereas it was significantly higher at 20 wk. Renal sensitivity to injected AVP was attenuated in 20-wk-old STR/N. The suppression of AVP synthesis due to excessive water retention in 8-wk-old STR/N suggests that polydipsia may be the primary cause in this strain. The 20-wk-old STR/N became dehydrated with the acceleration of AVP synthesis, which might have resulted from secondary desensitization to AVP.

Amino Acid Sequence↗
PubMed2000

Effects of acute hypotensive stimuli on arginine vasopressin gene transcription in the rat hypothalamus.

We investigated the baroregulation of arginine vasopressin (AVP) gene transcription in the supraoptic (SON) and paraventricular nuclei (PVN) in conscious rats by use of intronic in situ hybridization. Hemorrhage of 16 ml/kg body wt decreased mean arterial pressure (MAP) by 57% and increased both plasma AVP (control, 1.2 +/- 0.3 pg/ml; 16 ml/kg body wt, 38.9 +/- 3.2 pg/ml) at 10 min and AVP heteronuclear (hn)RNA levels (SON, 150%; PVN, 140% of control values) at 20 min. On the other hand, hemorrhage of 7 ml/kg body wt had no significant effect on MAP, plasma AVP, or the AVP hnRNA levels. To better understand the baroregulation, we also examined the effects of sodium nitroprusside (SNP), which induces hypotension without a change in blood volume. The subcutaneous injection of 2 mg/kg body wt SNP, which decreased the MAP by 60%, increased both plasma AVP (control, 1.6 +/- 0.4 pg/ml; 2 mg/kg body wt, 8.1 +/- 0.4 pg/ml) at 10 min and AVP hnRNA levels (SON, 150%; PVN, 140% of control values) at 30 min. The injection of 0.1 mg/kg body wt SNP, which reduced the MAP by 10%, failed to increase either the plasma AVP or AVP hnRNA levels. These results indicate that AVP gene transcription increases rapidly after both hypotensive hemorrhage and normovolemic hypotension. In addition, it is suggested that the set point for AVP synthesis in the baroregulation is similar to that for AVP release.

Animals↗
PubMed2000

Gene expression in the rat supraoptic nucleus induced by chronic hyperosmolality versus hyposmolality.

Magnocellular neurons of the hypothalamo-neurohypophysial system play a fundamental role in the maintenance of body homeostasis by secreting vasopressin and oxytocin in response to systemic osmotic perturbations. During chronic hyperosmolality, vasopressin and oxytocin mRNA levels increase twofold, whereas, during chronic hyposmolality, these mRNA levels decrease to 10-20% of that of normoosmolar control animals. To determine what other genes respond to these osmotic perturbations, we have analyzed gene expression during chronic hyper- versus hyponatremia. Thirty-seven cDNA clones were isolated by differentially screening cDNA libraries that were generated from supraoptic nucleus tissue punches from hyper- or hyponatremic rats. Further analysis of 12 of these cDNAs by in situ hybridization histochemistry confirmed that they are osmotically regulated. These cDNAs represent a variety of functional classes and include cytochrome oxidase, tubulin, Na(+)-K(+)-ATPase, spectrin, PEP-19, calmodulin, GTPase, DnaJ-like, clathrin-associated, synaptic glycoprotein, regulator of GTPase stimulation, and gene for oligodendrocyte lineage-myelin basic proteins. This analysis therefore suggests that adaptation to chronic osmotic stress results in global changes in gene expression in the magnocellular neurons of the supraoptic nucleus.

Animals↗
PubMed2000

Identification of soluble forms of lectin-like oxidized LDL receptor-1.

Lectin-like oxidized LDL receptor-1 (LOX-1) is a type II membrane protein belonging to the C-type lectin family molecules, which can act as a cell-surface endocytosis receptor for atherogenic oxidized LDL. In this study, we show that soluble forms of LOX-1 are present in conditioned media of cultured bovine aortic endothelial cells (BAECs) and CHO-K1 cells stably transfected with LOX-1 cDNA. Immunoblot analysis of conditioned media from TNF-alpha-activated BAECs and CHO-K1 cells stably expressing LOX-1 revealed that soluble LOX-1 has an approximate molecular mass of 35 kDa. In TNF-alpha-activated BAECs, cell-surface expression of LOX-1 precedes soluble LOX-1 production. Cell-surface biotinylation followed by immunoprecipitation and immunoblotting showed that soluble LOX-1 in cell-conditioned media is derived from LOX-1 expressed on the cell surface. Production of soluble LOX-1 was inhibited by PMSF, suggesting that PMSF-sensitive proteases may be involved in this process. Purification of soluble LOX-1 by high-performance liquid chromatography and N-terminal amino acid sequencing of soluble LOX-1 identified the 2 cleavage sites between Arg(86)-Ser(87) and Lys(89)-Ser(90), which were located in the membrane proximal extracellular domain of LOX-1. The data demonstrate that cell-surface LOX-1 can be cleaved at 2 different sites and transformed into soluble forms. Further studies may explore therapeutic and diagnostic applications of soluble LOX-1 in atherosclerotic diseases.

Amino Acid Sequence↗
PubMed2000

Foods and nutrients in relation to bladder cancer risk: a case-control study in Aichi Prefecture, Central Japan.

To elucidate the role of diet in the etiology of bladder cancer, we conducted a case-control study from 1996 to 1999 in Aichi Prefecture, Central Japan. Cases were patients newly diagnosed with bladder cancer, and one hospital control was selected for each case, matching gender, age, and hospital. A well-validated food frequency questionnaire was adopted to estimate intakes of nutrients and food groups. Odds ratios (ORs) adjusted for smoking and occupational history were computed using conditional logistic models. The analyses based on 297 cases and 295 controls revealed the following. 1) The more the intake of milk and dairy products, the lower the OR; the ORs across quartiles in all subjects were 1.02, 0.73, and 0.52. Fruit intake was negatively associated with the risk, particularly in men (ORs across quartiles = 0.76, 0.77, and 0.52). Green-yellow vegetables were associated with a decreased risk in the highest quartile of consumption in men (OR = 0.57). 2) Dietary intakes of retinol and saturated fatty acids were related to a reduced risk in all subjects (ORs across quartiles = 0.75, 0.54, and 0.66 and 0.55, 0.54, and 0.60, respectively). Monounsaturated fatty acids had an inverse association with bladder cancer risk in men.

Adult↗
PubMed2000

Vasopressin V2 receptor binding is down-regulated during renal escape from vasopressin-induced antidiuresis.

This study evaluated whether renal escape from vasopressin-induced antidiuresis is associated with alterations of vasopressin V2 receptor binding in the kidney inner medulla. A radioligand binding assay was developed using a novel iodinated vasopressin V2 receptor antagonist to analyze vasopressin V2 receptor binding in kidney inner medullary tissue from three groups of rats: normal rats maintained on ad libitum water intake, rats treated with 1-deamino-[8-D-arginine]vasopressin (DDAVP), and rats treated with DDAVP that were also water loaded to induce renal escape from antidiuresis. Analysis of the binding data showed that DDAVP treatment reduced vasopressin V2 receptor binding to 72% of normal levels. Water loading induced a marked further down-regulation of vasopressin V2 receptor binding. This receptor down-regulation began by day 2 of water loading, which correlated with the initiation of renal vasopressin escape; by day 3 of water loading, vasopressin V2 receptor expression fell to 43% of DDAVP-treated levels. No differences in vasopressin V2 receptor binding affinities were found among the three groups. This study demonstrates that vasopressin V2 receptor binding capacity is down-regulated during renal escape from vasopressin-induced antidiuresis and suggests that both vasopressin-dependent mechanisms as well as vasopressin-independent mechanisms associated with water loading are involved in this receptor down-regulation.

Animals↗
PubMed2000

Role of endogenous nociceptin in the regulation of arginine vasopressin release in conscious rats.

The effects of central administration of the opioid-like peptide nociceptin (also known as orphanin FQ) were investigated on the secretion of arginine vasopressin (AVP) in response to dehydration and hyperosmolar or hypovolemic stimulation in conscious rats. Intracerebroventricular (i.c.v.) administration of nociceptin suppressed plasma AVP concentration in a dose-dependent manner (0.1-10 microg/rat) in dehydrated rats, and the maximum effect was obtained 10 min after the administration (dehydration with 10 microg/rat nociceptin, 3.11 +/- 0.27 pg/ml vs. control, 10.32 +/- 0.96 pg/ml). The plasma AVP increase in response to either hyperosmolality [i.p. injection of hypertonic saline (HS) (600 mosml/kg)] or hypovolemia [i.p. injection of polyethylene glycol (PEG)] was also significantly blunted when nociceptin was injected i.c.v. (HS with 10 microg/rat nociceptin, 1.16 +/- 0.09 pg/ml vs. control, 1.82 +/- 0.30 pg/ml; PEG with 10 microg/rat nociceptin, 0.91 +/- 0.16 pg/ml vs. control, 2.41 +/- 0.26 pg/ml). Pretreatment with a selective opioid kappa-receptor antagonist, nor-binaltorphimine (1 microg/ rat, i.c.v.) or naloxone (2.5 mg/rat, s.c. injection) did not reverse the inhibitory effects of nociceptin on AVP release. Moreover, when plasma AVP was suppressed by acute water loading, immunoneutralization of endogenous nociceptin by antinociceptin-antiserum i.c.v. significantly reversed the suppression (0.57 +/- 0.12 pg/ml vs. control, 0.25 +/- 0.04 pg/ml). These results suggest that central nociceptin is physiologically involved in the control of AVP release through an inhibitory action.

Animals↗
PubMed2000

A Japanese patient with lipoprotein lipase deficiency homozygous for the Gly188Glu mutation prevalent worldwide.

We studied the molecular basis of familial lipoprotein lipase (LPL) deficiency in a new Japanese kindred. The proband was a four-month-old infant with severe hyperchylomicronemia. In postheparin plasma, LPL activity was virtually absent, although LPL mass was detectable. Single strand conformational polymorphism (SSCP) analysis showed an abnormal band with exon 5 of the LPL gene that was amplified by PCR from the proband's genomic DNA. DNA sequence analysis of the amplified fragment demonstrated that the proband was homozygous for a G-to-A change at nucleotide position 818 resulting in the substitution of glutamic acid for glycine at codon 188. Although this is among the first Gly188Glu mutations identified in Japanese, the missense mutation has previously been reported as a prevalent cause of familial LPL deficiency worldwide and has been proposed to have a common origin. However, DNA haplotype analysis with either restriction fragment length polymorphism (RFLP) or microsatellite markers revealed that the DNA haplotype of the proband was not identical to the haplotype previously reported as common to the other patients with the Gly188Glu mutation. These results add the Gly188Glu mutation to the growing list of LPL gene mutations underlying familial LPL deficiency in Japanese and indicate that the origin of the Gly188Glu mutation is not necessarily common but would be multicentric at least in part.

Adult↗
PubMed2000

[A case of malignant lymphoma of the epididymis].

A 17-year-old man visited our hospital with the chief complaint of painless swelling of the left scrotal content. An elastic hard mass was palpable at the upper pole of the left testis. Left radical orchiectomy was performed. The tumor originated from the epididymis and did not involve the testis or the spermatic cord. Histologically, the tumor was diagnosed as a malignant lymphoma (non-Hodgkin's lymphoma, diffuse mixed cell type, B-cell type). No abnormalities were found in other organs. After establishment of the diagnosis of primary epididymal malignant lymphoma, 3 courses of chemotherapy (adriamycin, vincristine, cyclophosphamide, prednisolone) were performed. No evidence of recurrence or metastasis was found 26 months after surgery.

Adolescent↗
PubMed2000

[A case of paravesical foreign body granuloma due to surgical sponge retained for 40 years].

A 67-year-old man complained of vague pain in the lower abdomen persisting over 10 years. A hard mass was palpable just under an operative scar (right Gibson incision for ureterolithotomy performed 40 years previously). In addition to the patient's history and physical examination, abdominal echography, computerized tomography and nuclear magnetic resonance imaging (MRI) were performed and resulted in a preoperative diagnosis of retroperitoneal gauzeoma. The paravesical mass, 7 x 6 x 6 cm in size, was surgically removed, which was an encapsulated granuloma surrounding a surgical sponge. The possibility of foreign body granulomas due to a retained surgical sponge (so-called gauzeomas) should be considered in patients who have a previous history of abdominal operations.

Aged↗
PubMed2000

An Asian variant of intravascular large B-cell lymphoma: clinical, pathological and cytogenetic approaches to diffuse large B-cell lymphoma associated with haemophagocytic syndrome.

Diffuse large B-cell lymphoma with haemophagocytic syndrome (BCL-HS) has been reported mainly in Asia and is regarded as a distinct variant of intravascular lymphoma (IVL). However, it is unclear whether all cases of BCL-HS fall within the framework of IVL and available clinical information is limited. We analysed 25 cases with BCL-HS, including 11 autopsied cases (median, 66 years; male-female ratio, 1.1:1). The patients presented with fever, anaemia, thrombocytopenia, hepatosplenomegaly, haemophagocytosis, bone marrow invasion, respiratory disturbance and disseminated intravascular coagulopathy, but usually lacked lymphadenopathy, mass formation, neurological abnormalities and skin lesions. The clinical course was aggressive with a median survival of 7 months. The morphological findings were uniform: large lymphoid cells infiltrated vessels and/or sinusoids of the liver, marrow, lung, kidney and other organs. They were positive for CD19, CD20, CD79a and HLA-DR, but negative for CD10, CD23 and CD30. CD5 was positive in five out of 17 cases. Our critical review indicates that BCL-HS is the equivalent of the Asian variant of IVL.

Adult↗
PubMed1999

Expression of lectinlike oxidized low-density lipoprotein receptor-1 in human atherosclerotic lesions.

BACKGROUND: Oxidized LDL (Ox-LDL) seems to play key roles in atherogenesis. Lectinlike Ox-LDL receptor-1 (LOX-1) is a recently identified cell-surface receptor for Ox-LDL. The relationship of this novel receptor for Ox-LDL to atherogenesis, however, has not yet been clarified. In this study, we explored the expression of LOX-1 in the atherosclerotic lesions of human carotid arteries. METHODS AND RESULTS: Using carotid endarterectomy specimens obtained from 21 patients and 2 samples of normal human aortas, we examined LOX-1 expression by reverse transcription-polymerase chain reaction and immunohistochemistry. In aortas without atherosclerosis, LOX-1 expression was undetectable by immunohistochemistry and negligible by reverse transcription-polymerase chain reaction. In carotid arteries, luminal endothelial cells covering early atherosclerotic lesions were more frequently positive for LOX-1 expression than those in advanced atherosclerotic lesions. Endothelial cells in the intimal neovasculature of advanced lesions also expressed LOX-1. In addition, macrophages and smooth muscle cells in the intima of advanced atherosclerotic plaques were positive for LOX-1 expression. CONCLUSIONS: LOX-1 may play important roles in Ox-LDL uptake and subsequent functional alteration in the luminal endothelium in early atherosclerotic lesions and in intimal neovascular endothelial cells in advanced plaques. Furthermore, LOX-1 may also be involved in Ox-LDL uptake and subsequent foam cell transformation in macrophages and smooth muscle cells in the atherosclerotic intima.

Aged↗
PubMed1999

Kinetic analysis on nitric oxide binding of recombinant Prolixin-S, a nitric oxide transport protein from the bloodsucking bug, Rhodnius prolixus.

Kinetics of the NO binding and removal reaction of recombinant Prolixin-S (rProlixin-S) were analyzed using stopped-flow spectrophotometry. The reaction was observed as a biphasic process. The rate constant of the fast phase increased linearly as NO concentration increased. The rate constant at the slow phase increased as NO concentrations increased at low NO concentration, then reached a plateau at high NO concentration. These NO dependencies of the reaction are characteristic of a bimolecular two-step consecutive reaction. The reaction consisted of the fast NO binding reaction of rProlixin-S and the following slow structural change of NO-protein complex. Kinetic studies revealed that the NO binding rate constant was independent of pH, but the rate constant of the NO removal reaction increased as pH increased. The apparent NO dissociation constant (Kd) of rProlixin-S was also calculated from the values of the kinetic parameters obtained in this work. The Kd value increased as pH and temperature increased. The Kd value of rProlixin-S and NO was 10-300 nM in regular physiological condition, which is 103 higher and 103 lower than those of the other ferric and ferrous hemoproteins and NO, respectively. These results indicate that Prolixin-S is one of NO transport proteins regulating blood pressure.

Animals↗
PubMed1999

Glycogen storage disease type IIIa: first report of a causative missense mutation (G1448R) of the glycogen debranching enzyme gene found in a homozygous patient.

Several different mutations in the glycogen-debranching enzyme gene AGL have been found in patients with glycogen storage disease type III (GSD III) to date, but no missense mutations have been reported for GSD III, only nonsense, splicing, and deletion/insertion lesions. Here we describe a novel G1448R missense mutation in a Japanese GSD IIIa patient from a consanguineous family. Sequence analysis of cDNA from the patient' liver specimen revealed two separate nucleotide changes: a G-to-A transition at nucleotide 3737 in exon 26 (3737G>A) and a G-to-C transversion at nucleotide 4742 in exon 33 (4742G>C), both of which result in substitution of glycine by arginine (G1115R and G1448R). Because homo-zygotes for G1115R were found in healthy controls, G1115R seems to be a polymorphism. Restriction fragment length polymorphism analysis with Bsa JI showed that the patient was homozygous for G1448R and that none of the normal controls had the mutation. This missense mutation is located at a putative glycogen-binding site that is indispensable for enzyme activity. Thus, G1448R is likely to be the causative mutation in this patient. This is the first report of a missense mutation associated with GSD III.

Amino Acid Substitution↗
PubMed1999

Changes in pulsed-field gel electrophoresis patterns in clinical isolates of enterohemorrhagic Escherichia coli O157:H7 associated with loss of Shiga toxin genes.

Pulsed-field gel electrophoresis (PFGE) of XbaI-digested DNA fragments of enterohemorrhagic Escherichia coli (EHEC) O157:H7 strains showed disappearance of a 70- or 80-kb fragment in their patterns associated with loss of Shiga toxin genes during maintenance or subcultivation. Hybridization experiments with a DNA probe complementary to Shiga toxin sequences revealed that the Shiga toxin genes in the parental strain were located on fragments the same size as the lost fragments from the toxin-negative derivatives. The evidence indicates that PFGE pattern of EHEC O157:H7 may change due to loss of Shiga toxin genes, which is likely to be associated with curing of Shiga toxin gene carrying phages in vitro.

Bacterial Toxins↗
PubMed1999

Thymic neuroendocrine tumor (thymic carcinoid): a clinicopathologic study in 15 patients.

BACKGROUND: Thymic neuroendocrine tumor (carcinoid tumor) is rare, and prognosis for patients with this tumor has been difficult to predict. METHODS: The medical records of 15 patients were reviewed, and the patients were classified according to tentative TNM classification and histologic grade. RESULTS: Ten (66.7%) of 15 patients were male. Lymph node metastases were identified in 9 (60%) of 15 patients at the time of resection. There were one grade 1, nine grade 2, and five grade 3 tumors. Total resection was possible in 13 patients. Distant metastases developed in 10 (76.9%) of these 13 patients, although no local recurrence developed. Of these 10 patients, 6 died of distant metastases 5 to 25 months after the recurrence. Three patients are still alive, with metastases to the bone, spleen, and pleura 1 to 24 months after the diagnosis of recurrence. Two patients are presently tumor free (T1N0, grade 3 and T3N2, grade 2), but only 1 has survived beyond 5 years. CONCLUSIONS: Thymic neuroendocrine tumor must be regarded as a malignant neoplasm that is prone to metastasize to mediastinal lymph nodes and to distant sites, even after total excision. Neither T and N classification nor histologic grade has been successful in predicting the outcome of a patient with this tumor. More aggressive management, including adjuvant therapies and reexcision of subsequent tumors, may result in increased survival.

Adult↗