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A Yamauchi

Publications and source records attributed to A Yamauchi.

At least 163 records · Page 9Linked to original sources
PubMed1995

Association of angiotensin I-converting enzyme gene polymorphism with susceptibility to antiproteinuric effect of angiotensin I-converting enzyme inhibitors in patients with proteinuria.

The antiproteinuric effect of angiotensin I-converting enzyme (ACE) inhibitors in patients with renal diseases of various origins has been well recognized. However, individual responses regarding the degree of decrease in urinary protein excretion appear to vary considerably. The mechanism underlying this variable response to ACE inhibitors has not been clarified yet. A possible role of ACE gene insertion/deletion (I/D) polymorphism in the responsiveness to antiproteinuric effect of ACE inhibitors is examined. Thirty-six patients with proteinuria (23 men and 13 woman; mean age, 47 +/- 13 yr) were studied. These patients were classified into two groups on the basis of the percent decrease in their urinary protein excretion: the effective group, those with a decrease in proteinuria (18 patients, -64 +/- 19%) and the noneffective group (18 patients, +13 +/- 40%). A 287-base pair (bp) I/D polymorphism in the ACE gene was examined by polymerase chain reaction. The allelic frequencies of the ACE gene were I/D = 0.53/0.47 in the effective group and I/D = 0.81/0.19 in the noneffective group. The difference in the allelic frequencies between the two groups was significant (chi 2 = 6.25, P = 0.0114 < 0.05). Furthermore, the difference in the responsiveness of proteinuria to ACE inhibition between genotype II versus genotype ID + DD was statistically significant (chi 2 = 4.05, P = 0.0442 < 0.05). There was no significant difference between the two groups with regard to initial urinary protein level, blood pressure, renal function, and daily sodium intake. The genetic susceptibility to the antihypertensive effect of ACE inhibitors was also studied, but no significant relation was observed. This study suggests the association of ACE gene I/D polymorphism with the antiproteinuric efficacy of ACE inhibitors in patients with proteinuria.

Adult↗
PubMed1995

Amino acids and glucose differentially increased extracellular 5-hydroxyindoleacetic acid in the rat brain.

To reveal the role of serotonergic neurons in the regulation of feeding, the levels of 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin, in the striatum and the hypothalamus were continuously monitored by an in vivo microdialysis technique. Intake of 20% casein diet did not induce significant changes in the 5-HIAA level in these regions. When rats were fed on 5% casein diet (83.5% carbohydrate diet) for 2 h, the level of 5-HIAA in the striatum gradually increased and reached a maximum (226 +/- 44% of basal level, M +/- SEM, n = 7) at 4 h after stopping the diet. In the medial hypothalamus, its level also increased to 183 +/- 19% (n = 10) at 2 h after starting the diet. On the other hand, a 60% casein diet increased the level of 5-HIAA in the lateral hypothalamus to 138 +/- 19% (n = 10) at 2 h after starting the diet. The intravenous infusion of each of these nutrients, glucose, amino acid mixture or lipid, produced more rapid elevation of the 5-HIAA level than oral intake of the diets. When rats were infused with glucose, its level in the striatum continued to be elevated. In the medial hypothalamus, glucose infusion increased 5-HIAA to the maximum (189 +/- 38%, n = 7) at 4 h after starting infusion. In contrast, serotonergic neurons in the lateral hypothalamus seemed to respond only to infusion of the amino acid mixture, and the level of 5-HIAA reached 163 +/- 14% (n = 5) of the basal level at 1 h after starting the infusion. These results suggest that rapid elevation of glucose or amino acids may independently stimulate serotonin metabolism in these brain areas, participating in the feedback regulation of nutrient intake.

Amino Acids↗
PubMed1995

[Significance of prostate fluid carcinoembryonic antigen in the diagnosis of prostate cancer].

Clinical studies of carcinoembryonic antigen (CEA) in prostate fluid were performed on 121 men; 29 patients with prostate cancer, 65 with benign prostatic hypertrophy, 10 with prostatitis and 17 without any prostatic diseases. The CEA level in prostate fluid in the prostate cancer group was significantly higher than that in any other group. However, it could not demonstrate any particular advantage when compared with the prostate specific antigen (PSA) in serum. Additional research was done comparing the sensitivity and specificity of CEA level in prostate fluid in the population with slightly elevated PSA level (3.0-14.9 ng/ml). The sensitivity and the specificity were 82% and 83%, respectively. These findings suggest the usefulness of the measurement of prostate fluid CEA as an adjunctive tool in the diagnosis of prostate cancer in the population with a slightly elevated PSA level.

Carcinoembryonic Antigen↗
PubMed1995

[Pre-Cushing's syndrome with intermittent hypokalemia: report of a case].

An adrenal tumor was discovered in a patient with intermittent hypokalemia for 8 years. She had no clinical features of Cushing's syndrome. The case was regarded as pre-Cushing's syndrome by endocrinological evaluation. Our findings suggest that intermittent hypokalemia is a sign of drifting hormonal activities and may appear in a premature status of pre-Cushing's syndrome.

Adrenal Gland Neoplasms↗
PubMed1994

Response to osmotic stimuli in mesangial cells: role of system A transporter.

It has been suggested that mesangial cells have an osmoregulatory mechanism like that of renal medullary cells, such as intracellular accumulation of polyols in response to hypertonicity. We examined osmoregulatory role of neutral amino acids transported by system A in cultured mesangial cells. The contents of almost all amino acids increased under hypertonic conditions to more than twice the value in isotonic cells. In hypertonic cells, the system A transport activity, measured by Na(+)-dependent 2-(methylamino)isobutyric acid (MeAIB) uptake, was 3.8-fold the uptake in isotonic cells, reaching a maximum 16 h after the switch to hypertonic medium. The response to hypertonicity was the result of an increase in maximal velocity without change in Michaelis constant and was dependent on RNA and protein synthesis. When medium osmolality decreased from hypertonic to isotonic, MeAIB uptake reverted to the isotonic level within 16 h and a large transient efflux of L-proline occurred within 10 min. These results suggest that mesangial cells respond to extracellular hypertonicity by increasing system A transport activity and neutral amino acids can function as compatible osmolytes in mesangial cells.

Amino Acids↗
PubMed1994

Organic osmolytes in rat renal inner medulla are modulated by vasopressin V1 and/or V2 antagonists.

For the purpose of clarifying the role of vasopressin V1 and V2 receptors in osmolyte accumulation, we determined the effects on the inner medullary osmolyte content of the administration of orally active vasopressin V1 and/or V2 receptor antagonists OPC-21268 (i.e., 1-(1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl)- 3,4-dihydro-2(1H)-quinolinone) and OPC-31260 (i.e., 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tet rah ydro-1H- benzazepine] under a condition of maximal urine concentration achieved by water deprivation for 4 days. Taurine content increased significantly with the use of the V2 antagonist, irrespective of the use of the V1 antagonist. Inner medullary betaine content decreased with the administration of the V1 antagonist, irrespective of the administration of V2 antagonist. The administration of either the V1 or V2 antagonist alone did not affect sorbitol content, aldose reductase activity, or aldose reductase mRNA abundance in renal inner medulla. However, the combined administration of the V1 and V2 antagonists decreased all of these significantly. Myo-inositol content was not affected by the administration of the V1 or V2 antagonists. Glycerophosphorylcholine content was decreased with the use of the V2 antagonist, irrespective of the use of the V1 antagonist, and this effect paralleled urine osmolality. In conclusion, the individual organic osmolytes responded differently to the antagonists of vasopressin V1 and/or V2 receptors. The mechanisms linked to vasopressin V1 and/or V2 receptors appeared to modulate the accumulation of some organic osmolytes in the inner medulla. Aldose reductase mRNA abundance and sorbitol accumulation in the inner medulla appeared to be mediated through either V1 or V2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehyde Reductase↗
PubMed1994

Mitogen-activated protein kinase and its activator are regulated by hypertonic stress in Madin-Darby canine kidney cells.

Madin-Darby canine kidney cells behave like the renal medulla and accumulate small organic solutes (osmolytes) in a hypertonic environment. The accumulation of osmolytes is primarily dependent on changes in gene expression of enzymes that synthesize osmolytes (sorbitol) or transporters that uptake them (myo-inositol, betaine, and taurine). The mechanism by which hypertonicity increases the transcription of these genes, however, remains unclear. Recently, it has been reported that yeast mitogen-activated protein (MAP) kinase and its activator, MAP kinase-kinase, are involved in osmosensing signal transduction and that mutants in these kinases fail to accumulate glycerol, a yeast osmolyte. No information is available in mammals regarding the role of MAP kinase in the cellular response to hypertonicity. We have examined whether MAP kinase and MAP kinase-kinase are regulated by extracellular osmolarity in Madin-Darby canine kidney cells. Both kinases were activated by hypertonic stress in a time- and osmolarity-dependent manner and reached their maximal activity within 10 min. Additionally, it was suggested that MAP kinase was activated in a protein kinase C-dependent manner. These results indicate that MAP kinase and MAP kinase-kinase(s) are regulated by extracellular osmolarity.

Animals↗
PubMed1994

In vivo osmoregulation of Na/myo-inositol cotransporter mRNA in rat kidney medulla.

myo-Inositol, a major compatible osmolyte in renal medulla, is accumulated in kidney-derived epithelial cells cultured in hypertonic media via Na/myoinositol cotransporter (SMIT). The altered medium osmolality of Madin-Darby canine kidney cells leads to changes in the transcription of the SMIT gene and mRNA abundance. To investigate whether SMIT is regulated by tonicity in vivo, renal medullary myoinositol and SMIT mRNA was measured in rats in hydrated and dehydrated states. Rats were divided into two groups: (1) hydrated rats, free access to 3% sucrose water; (2) dehydrated rats, 3 days of water deprivation. Urine sodium, potassium, urea, and osmolality in dehydrated rats were significantly higher than in hydrated rats. Renal medullary sodium, urea, and myo-inositol in dehydrated rats were significantly higher than in hydrated rats. Northern analysis revealed that there was a message hybridized to SMIT cDNA in the cortex and outer and inner medulla of the kidney. Compared with hydrated rats, SMIT mRNA in dehydrated rats was 2.6-fold higher in the outer medulla and 2.5-fold higher in the inner medulla. These results indicate that there is osmoregulatory SMIT in the outer and inner medulla of the kidney and that myo-inositol accumulation in this region is probably due to the increased expression of the SMIT gene.

Animals↗
PubMed1994

[Evaluation of the method of treating non-Hodgkin's lymphoma].

Forty-two patients with non-Hodgkin's lymphoma were treated between October 1983 and December 1992 in the department of Otolaryngology, Kagawa Medical School Hospital. The twenty-six of these patients whose tumor originated in Waldeyer's ring and who were diagnosed as Stage I or II have been reviewed. In principle, method of treatment was a combination of chemotherapy and radiotherapy. Between 1983 to 1987, COP was primarily used (9 cases) as combination chemotherapy, and after 1988 CHOP was used (17 cases). VAMA was used to treat the poor response and recurring cases. The five-year estimated overall survival rates calculated by the Kaplan-Meier method were 33.3% and 94.1% in the COP and CHOP groups, respectively. We investigated age, stage, cell type and grade, as factors related to recovery, but except for cell type, there were no significant differences in overall survival. The most serious side effect was decreased leucocyte count, but we prescribed G-CSF and were able to continue treatment.

Adult↗
PubMed1994

[Dawn hypertension in pre-Cushing's syndrome: report of two cases].

Two adrenal tumors were incidentally discovered in the patients with dawn hypertension. They had no clinical features of Cushing's syndrome. These cases were regarded as pre-Cushing's syndrome by endocrinological evaluation. After adrenalectomy, the adrenal hormone regulation was normalized and dawn hypertension disappeared. Our findings suggest that dawn hypertension is a typical clinical sign of pre-Cushing's syndrome and this syndrome may represent a premature status of Cushing's syndrome.

Adrenalectomy↗
PubMed1993

Requirement of thiol compounds as reducing agents for IL-2-mediated induction of LAK activity and proliferation of human NK cells.

Thiol-related compounds, such as L-cystine, 2-ME or reduced glutathione (GSH), are important in many lymphoid cell activation pathways. We investigated their role in IL-2-generated lymphokine-activated killer (LAK) activity in human NK (CD16+ and/or CD56+) cells. Depletion of GSH and L-cystine, but not L-leucine or glycine, from medium used during culture of NK cells with IL-2 inhibited LAK and proliferative activities, whereas IL-2-independent lytic function of NK cells remained intact. Addition of L-cysteine, 2-ME or GSH, but not methylated analogs of these compounds (which cannot function as proton donors) to L-cystine/GSH-depleted medium restored proliferative response of NK cells and LAK generation. In the presence of L-buthionine-(S,R)-sulfoximine, an inhibitor of GSH synthesis, IL-2-induced LAK activity and proliferation of NK cells in medium without L-cystine and GSH, could be restored, at least in part, by addition of GSH, but not 2-ME or L-cystine. Furthermore, intracellular GSH levels were depressed in cells cultured in L-cystine/GSH-depleted medium but could be restored by the addition of 2-ME. The results suggest that (1) L-cystine or thiol containing compounds such as L-cysteine, 2-ME, or GSH are necessary for effective IL-2-activation of human NK cells, (2) these compounds must be functional proton-donors, i.e., reducing agents, implying regulation of the IL-2 activation pathway by oxidation-reduction, and (3) GSH synthesis is necessary for the activation. Experiments were performed to begin to dissect the redox-sensitive step(s) in LAK development. Depletion of reducing agents had no effect on internalization of rIL-2. In contrast, intracellular granzyme A activity was significantly depressed in NK cells cultured with rIL-2 in L-cystine/GSH-depleted medium compared with those cultured in medium in which L-cystine levels had been replenished. The findings suggest that step(s) in the transduction of the IL-2 signal in NK cells, between the internalization of IL-2 and the maturation of the lytic mechanism, are subject to regulation by oxidation-reduction.

Animals↗
PubMed1993

Inhibition of epidermal growth factor-stimulated hepatocytes proliferation by autologous sinusoidal mononuclear cells in rat liver.

Mononuclear cells isolated from sinusoid of rat liver by collagenase perfusion method showed a strong inhibitory effect on epidermal growth factor-stimulated proliferation of cocultured autologous hepatocytes, while mononuclear cells from peripheral blood and spleen did not. This inhibitory effect depended on the effector/target ratio. In a single-color flow cytometric analysis, about 25% of sinusoidal mononuclear cells consisted of asialo GM1+ natural killer cells, and there were relatively small numbers of CD3+ T cells and a few leukocyte common antigen-positive B cells compared to peripheral blood mononuclear cells. The natural killer cell activity of sinusoidal mononuclear cells was much stronger than that of peripheral blood mononuclear cells and splenic mononuclear cells. This activity was completely suppressed by the treatment with anti-asialo GM1 antibody plus complement. However, their inhibitory activity on proliferation of autologous hepatocytes was not affected by this treatment. These results suggest that the sinusoidal mononuclear cells, probably CD3+ T cells, play a role in regulation of autologous hepatocyte proliferation.

Animals↗
PubMed1993

Purification of glutamine transaminase K/cysteine conjugate beta-lyase from rat renal cytosol based on hydrophobic interaction HPLC and gel permeation FPLC.

Cysteine conjugate beta-lyase (beta-lyase, EC 4.4.1.13) was purified to homogeneity from rat renal cytosol using a new and highly efficient method, based on C3-hydrophobic interaction (HI) high-performance liquid chromatography (HPLC) in combination with gel permeation fast protein liquid chromatography. The purity of the enzyme was judged from SDS-PAGE and C18-reversed-phase HPLC. The beta-lyase was estimated to be a homodimer consisting of a 47,400-Da subunit with absorption maxima at 280 and 420-430 nm. The specific activity of the purified beta-lyase toward S-(1,2-dichlorovinyl)-L-cysteine (1,2-DCVC) in the presence of alpha-keto-gamma-methiolbutyric acid (KMB) was 6.4 mumol/min/mg protein, which is by far the highest value so far reported. Kinetic analysis of 1,2-DCVC metabolism by the enzyme in the presence of KMB gave Km and Vmax values of 0.33 mM and 8.4 mumol/min/mg protein, respectively. No significant activity of the purified enzyme was detectable with S-2-benzothiazolyl-L-cysteine up to 2 mM. The purified enzyme also had glutamine transaminase K activity (EC 2.6.1.64) as assayed with phenylalanine and KMB as substrates. This specific activity was 16.0 mumol/min/mg. Amino acid analysis of the purified beta-lyase was carried out and was found to be closely similar to the amino acid composition of five other pyridoxal phosphate (PLP)-containing amino acid amino-transferases. This suggests that glutamine transaminase K/cysteine conjugate beta-lyase is a typical member of the PLP-containing aminotransferase group.

Amino Acids↗
PubMed1993

Hypertonicity stimulates transcription of gene for Na(+)-myo-inositol cotransporter in MDCK cells.

Myo-inositol is a major compatible osmolyte accumulated in the hypertonic renal medulla and in Madin-Darby canine kidney (MDCK) cells cultured in hypertonic media. Myo-inositol is taken up by MDCK cells on a Na(+)-coupled transporter whose activity increases sixfold 24 h after cells are switched to hypertonic medium. To investigate the mechanism of regulation of the cotransporter by hypertonicity, we used the cDNA encoding the canine Na(+)-myo-inositol cotransporter that we recently cloned to measure the abundance of the mRNA for the cotransporter and its rate of transcription after changes in osmolality. When MDCK cells were switched from isotonic to hypertonic medium, cotransporter mRNA abundance rose 10-fold in 16 h. Transcription of the cotransporter gene also rose and 16 h after the switch reached a peak approximately 15-fold that in isotonic cells. When cells were switched back to isotonic medium, mRNA abundance and transcription of the gene returned to isotonic levels in 8 h and transport rate reached isotonic levels in 48 h. Thus transcription appears to be the primary step in regulation of myo-inositol transport by hypertonicity.

Animals↗
PubMed1993

Medium tonicity regulates expression of the Na(+)- and Cl(-)-dependent betaine transporter in Madin-Darby canine kidney cells by increasing transcription of the transporter gene.

Betaine is one of the major compatible osmolytes accumulated by kidney derived Madin-Darby canine kidney cells cultured in hypertonic medium. Betaine is accumulated by Na(+)- and Cl(-)-dependent uptake from the medium. To gain insight into the mechanism by which hypertonicity evokes an increase in the Vmax of the betaine transporter in Madin-Darby canine kidney cells, we measured the relative abundance of mRNA for the transporter in cells shifted to a hypertonic medium and found parallel increases in mRNA abundance and cotransporter activity. The increase in mRNA levels preceded the increase in transporter activity slightly. Transcription of the gene for the transporter rose rapidly and to the same relative extent as mRNA abundance in cells shifted to hypertonic medium, indicating that transcription of the gene for the cotransporter plays a major role in regulating the accumulation of betaine in response to hypertonicity.

Animals↗
PubMed1993

Thyrotropin-producing microadenoma associated with pituitary resistance to thyroid hormone.

A 21-yr-old female with hyperthyroidism is described. Though her serum-free T3 was 17.8 pmol/L and free T4 was 60.2 pmol/L, TSH was as high as 10.7 mU/L. TRH stimulated an increase in TSH from 10.7-91.7 mU/L. T3 administration in gradually increasing doses of 100, 200, and 400 mg/day resulted in gradual reduction in serum TSH. Cranial computed tomography and magnetic resonance imaging revealed a microadenoma of the pituitary gland. Histology of the surgical specimen showed a TSH-producing adenoma with TSH cell cluster islets and decreased numbers of TSH cells in the nonneoplastic pituitary. Cultured cells from the adenoma secreted TSH spontaneously and in response to TRH. This TRH-stimulated TSH secretion was suppressed by T3 in a dose-dependent manner. One year postoperatively, neither residual tumor nor recurrence were seen by computed tomography and magnetic resonance imaging. However TSH, as well as free T3 or T4, was still high and overresponsive to TRH.

Adenoma↗
PubMed1993

[Clinical significance of dystrophin test for patients with various neuromuscular diseases--immunofluorescence and immunoblot analyses of dystrophin abnormalities].

The dystrophin test was performed on skeletal muscle specimens from 81 cases with various neuromuscular diseases by using two new monoclonal antibodies. The results were compared with those obtained by using four polyclonal antibodies. These monoclonal and polyclonal antibodies were raised against various portions of the dystrophin molecule. On immunohistochemical analysis, the two new monoclonal antibodies showed the same staining pattern as the four polyclonal antibodies. Non-specific immunostaining of the cytoplasm, often seen with polyclonal antibodies, was not observed with monoclonal antibodies. With the application of monoclonal antibodies, the connective tissue sometimes showed non-specific immunostaining which originated from the second fluorescent antibody. On immunoblot analysis, one of the two monoclonal antibodies, antibody 4-4 C 5, showed weak immunoreactivity, and the 400 kDa dystrophin band was not detected. Three cases out of 15 with Duchenne muscular dystrophy (DMD), and one case out of 3 with limb-girdle type muscular dystrophy which had previously been diagnosed on the basis of clinical data, were found to have non-dystrophin-related muscular dystrophy, and Becker muscular dystrophy (BMD), respectively. Three and two of five cases were diagnosed as DMD and BMD, respectively, though clinical diagnosis had not been possible because they were too young. Clinical diagnosis of congenital muscular dystrophy was confirmed in 9 patients by the dystrophin test. Only one of three certain DMD carriers had a so-called mosaic staining pattern. We conclude that all six antibodies are useful tools for the diagnosis of neuromuscular diseases, because of their high specificity for dystrophin.

Adolescent↗