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Y Nishida

Publications and source records attributed to Y Nishida.

At least 181 records · Page 10Linked to original sources
PubMed1996

cDNA cloning of a 20-kDa protein (p20) highly homologous to small heat shock proteins: developmental and physiological changes in rat hindlimb muscles.

A cDNA clone encoding p20, a novel member of the small heat-shock protein family in mammals, was isolated from a rat soleus cDNA library. The clone contained an insert of 1.3 kb with an open reading frame specifying a polypeptide of 162 amino-acid residues. Southern blot analysis suggested that the p20 gene is a single gene in rat genome. Developmental changes and a sciatic nerve denervation experiment suggested that the expression of p20 in rat hindlimb muscle is related to muscle contraction, and specifically in slow-twitch muscles.

Animals↗
PubMed1996

Transcriptional regulation of the Drosophila CycA gene by the DNA replication-related element (DRE) and DRE binding factor (DREF).

The Drosophila gene for cyclin A is expressed in dividing cells throughout development. This expression pattern is similar to those of genes related to DNA replication, suggesting involvement of some common control mechanism(s). In the upstream region (-71 to -64 with respect to the transcription initiation site) of the CycA gene, we found a sequence identical to the DNA replication-related element (DRE; 5'-TATCGATA), which is important for high level expression of replication-related genes such as those encoding DNA polymerase alpha and proliferating cell nuclear antigen. Transient expression assays with chloramphenicol acetyltransferase (CAT) were carried out to examine the function of the DRE sequence of the CycA gene. Deletion or base substitution mutations resulted in an extensive reduction in CAT expression. Furthermore, monoclonal antibodies against DRE binding factor (DREF) diminished or supershifted the complex of the DREF and DRE-containing fragment. The results indicate that the Drosophila CycA gene is under the control of a DRE/DREF system, as are DNA replication-related genes.

Animals↗
PubMed1996

The Drosophila secreted protein Argos regulates signal transduction in the Ras/MAPK pathway.

The Drosophila argos gene encodes a secreted protein with an EGF motif which acts as an inhibitor of cellular differentiation in multiple developmental processes. To investigate the cellular pathways regulated by Argos, we screened for mutations which could modify the phenotype caused by overexpression of argos. We show that the effects of argos overexpression on the eye and wing vein development are suppressed by gain-of-function mutations of the MAPKK/D-MEK gene (Dsor1/D-mek) and the MAPK/ERK-A gene (rolled) and were enhanced by loss-of-function mutations of Star. Loss-of-function mutations in components of the Ras/MAPK signaling cascade act as dominant suppressors of the phenotype caused by the argos null mutations. A loss-of-function argos mutation enhanced the overproduction of R7 neurons caused by gain-of-function alleles of Son of sevenless and Dsor1. Conversely, overexpression of argos inhibited formation of the extra R7 cells that was caused by high-level MAPK/ERK-A activity. A phenotype of the sev; argos double mutants revealed that sev is epistatic to argos. These results provide evidence that Argos negatively regulates signal transduction events in the Ras/MAPK cascade.

Animals↗
PubMed1996

Intravenously-injected naloxone reverses the decrease in renal sympathetic nerve activity seen during hypotensive hemorrhage in conscious rabbits by acting through central mechanisms.

The response of renal sympathetic nerve activity (RNA) to hemorrhage was examined in chronically-instrumented conscious rabbits. Hemorrhage was induced at a rate of 5 ml/kg per min until the mean arterial pressure fell below 40 mmHg. The mean arterial pressure then remained at around 80 mmHg until 10 ml/kg of hemorrhage (normotensive hemorrhage) before falling to below the pre-hemorrhagic control level (hypotensive hemorrhage). The RNA response showed a biphasic pattern, i.e., it increased during normotensive hemorrhage, then fell below the control level during hypotensive hemorrhage. To examine the mechanism involved in this decrease in RNA, naloxone (7.5 mumol/kg), an opioidergic receptor antagonist, was intravenously injected 1 min after the end of hemorrhage. Intravenous injection of naloxone caused an increase in mean arterial pressure and RNA to the level seen during normotensive hemorrhage. These results indicate that the decrease in RNA induced by hypotensive hemorrhage is mediated by opioidergic receptors. To determine whether the effects of naloxone are mediated via central or peripheral opioidergic receptors, naloxone was replaced by an equimolar solution of methylnaloxone, a form unable to cross the blood-brain barrier. Neither the mean arterial pressure nor RNA was significantly altered by administration of methyl naloxone. These results suggest that the effects of naloxone on both the RNA and the mean arterial pressure are mediated via central opioidergic receptors, i.e., the sympathoinhibition induced by hypotensive hemorrhage is mediated via the stimulation of central opioidergic receptors.

Animals↗
PubMed1996

Evaluation of functional recovery of regenerating rat liver after partial hepatectomy using 31P-NMR spectroscopy.

Using 31P-NMR spectroscopy, we studied the process of the functional recovery of the regenerating rat liver at 1-5 weeks after a 65% partial hepatectomy from the viewpoint of phosphate metabolism. Portal vein clamping (20 min) or fructose administration (250 mg/kg body weight) was performed to temporarily reduce adenosine triphosphate (ATP) content in the remnant liver. Changes in ATP level were observed for 60 min after declamping the portal vein or after fructose administration. Significant differences in the increased ATP levels after declamping the portal vein or after fructose administration were observed in each hepatectomized group. Until 3 weeks after hepatectomy, ATP levels during 60 min after declamping the portal vein or after fructose administration were significantly lower than those in the nonresected control rats. However, the increase in ATP in the 4-week group was almost identical to the increase in the control group throughout the 60 min. Remnant liver weight already returned to the nonresected control level 1 week after hepatectomy, and remained constant thereafter. On the other hand, the final ATP levels 60 min after declamping the portal vein or after fructose administration returned to the nonresected control level only after 4 weeks following hepatectomy. These results demonstrate that from the viewpoint of ATP synthesis, functional recovery of the regenerating liver to normal can be observed within 4 weeks after partial hepatectomy.

Adenosine Triphosphate↗
PubMed1996

Acute neurotoxicity of L-glutamate induced by impairment of the glutamate uptake system.

We examined the effect of the glutamate uptake inhibitor L-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) on the neurotoxicity of L-glutamate in organotypic cultures of rat spinal cord. Eighteen-day-old cultures were incubated with 500 microM L-glutamate, 1 mM PDC, or both. After 72 hours, the tissues were stained for acetylcholinesterase (AChE), and the ventral horn AChE-positive neurons (VHANs) analyzed using morphometry. Neither L-glutamate nor PDC affected AChE staining, but in combination they produced markedly reduced AChE staining in the dorsal horn and a significant decrease in the number of VHANs (especially the smaller VHANs) as compared with the control. Moreover, treatment with 200 microM PDC for 2 weeks preferentially affected the smaller VHANs. The neurotoxicity of L-glutamate plus PDC was blocked by the N-methyl-D-aspartate (NMDA) antagonist 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP). Results suggest that glutamate uptake system has an important protective function in the aggravation of acute neuronal damage.

Acetylcholinesterase↗
PubMed1996

Cardiac dysfunction with Becker muscular dystrophy.

Cardiac function was examined in 21 patients with Becker muscular dystrophy (BMD) and compared with 43 patients with Duchenne muscular dystrophy (DMD) and 37 healthy control subjects. Electrocardiography showed myocardial damage was most frequently found in the lateral wall, compatible with autopsy findings. The ratio of the preejection period to the ejection time was higher in patients with BMD (0.37 +/- 0.07, mean +/- SD) than in patients with DMD (0.28 +/- 0.05) and healthy controls (0.23 +/- 0.04). Left ventricular dimension and mitral annular size at end diastole in patients with BMD increased to 52.3 +/- 7.7 mm and 28.8 +/- 5.3 mm with age, respectively. In patients with cardiac failure and BMD, mitral regurgitation was observed at a rate of 66.7%. No definite relation between the deleted locus of the dystrophin gene and cardiac failure was found. Because motor dysfunction progresses more slowly in BMD than in DMD, a prolonged work load on the morbid myocardium may lead to dilated cardiomyopathy with mitral regurgitation.

Adolescent↗
PubMed1996

IFN-gamma in combination with IL-3 accelerates platelet recovery in mice with 5-fluorouracil-induced marrow aplasia.

The effects of interferon-gamma (IFN-gamma) on platelet recovery were examined in mice with marrow aplasia induced by i.p. injection of 250 mg/kg of 5-fluorouracil (5-FU). The cytokine was administrated by microosmotic pump, with an ability to deliver a consistent intact dose of cytokine for 7 consecutive days. Administration of 250 IU/kg/day of IFN-gamma in combination with 10(3) U/kg/day of IL-3, which alone had no effect on platelet counts, diminished the nadir for platelet count and shortened the duration of thrombocytopenia. The effect was comparable to that of higher doses of IL-3 (10(5) U/kg/day). The administration of 250 IU/kg/day of IFN-gamma in combination with 10(3) U/kg/day of IL-3 also induced megakaryocyte proliferation in bone marrow cell cultures. Single administration of either 250 IU/kg/day of IFN-gamma or 10(3) U/kg/day of IL-3 had no significant effects. The effect of this combination was also comparable to that of a higher dose of IL-3 (10(5) U/kg/day). We suggest that IFN-gamma accelerates megakaryocyte development, which leads to platelet production in chemotherapy-induced marrow aplasia. The administration of IFN-gamma in combination with IL-3 might be useful for the management of marrow aplasia.

Anemia, Aplastic↗
PubMed1996

Interferon-gamma enhances megakaryocyte colony-stimulating activity in murine bone marrow cells.

We have demonstrated previously that interferon-gamma (IFN-gamma) accelerates platelet recovery in mice with 5-FU induced-marrow aplasia in vivo. However, the mechanism for the regulation of megakaryocyte development induced by IFN-gamma in bone marrow cells in vivo remains unknown. To further study the effects of IFN-gamma on megakaryocyte development, various steps during IFN-gamma-mediated accelerated differentiation of the megakaryocytes were investigated in serum-free cultures of murine bone marrow cells in vitro. IFN-gamma markedly induced acetylcholine esterase (AChE) activity, a marker of murine megakaryocytic cells, accompanied by increased colony formation of the megakaryocyte lineage. A prominent increase in megakaryocyte number was observed after IFN-gamma treatment. All of these effects were dependent on the presence of IL-3, and, therefore, these results suggest that IFN-gamma acts as a megakaryocyte potentiator (Meg-POT). However, IFN-gamma did not enhance megakaryocyte maturation with respect to increase in cell size. The effects of IFN-gamma on megakaryocyte maturation were similar to those observed after treatment with higher doses of IL-3 alone. Meg-POT is defined as a factor that induces megakaryocyte maturation. Since IFN-gamma enhanced IL-3-dependent megakaryocyte colony formation and proliferation rather than megakaryocyte maturation, the effects on megakaryocyte development, which were induced by IFN-gamma treatment, seem to be different from the effects of a Meg-POT. We, therefore, propose a new function for IFN-gamma as an enhancer of megakaryocyte colony-stimulating factor activity. The effect of IFN-gamma in vitro appears to correlate well with the acceleration of platelet recovery in vivo.

Acetylcholinesterase↗
PubMed1996

Treatment of children with congenital heart disease and growth retardation with recombinant human growth hormone.

Seven prepubertal short children with congenital heart disease were treated with recombinant human growth hormone (GH). Although complete surgical correction was performed for their heart disease at least 2 years before the start of GH therapy, improvement in growth was less than expected in these children. They received 0.5 IU kg-1 week-1 of GH daily for 2 years or more. The growth rate increased from a mean of 4.3 cm year-1 before treatment to a mean of 7.8 cm year-1 in the first year and to a mean of 6.3 cm year-1 in the second year of treatment. Their mean standardized height improved from -3.41 +/- 0.78 to -2.54 +/- 0.62 after 2 years. The mean height age difference minus the bone age difference became positive in these children. We conclude that recombinant GH increases the growth rate in children with congenital heart disease and prepubertal growth retardation.

Child↗
PubMed1996

The effect of reflex closure of the esophageal groove on bioavailability of oral sulfamethoxazole-trimethoprim in ruminating calves.

The effect of reflex closure of the esophageal groove induced by the accustomed milking procedure on absorption of sulfamethoxazole (SMX)-trimethoprim (TMP) combination was examined, using calves trained to suck through a nipple-bucket. The experiment was carried out with a two-way cross-over design in which 2 groups of 5 calves of 6 weeks old were used. SMX-TMP combination was administered to the calves in each group through a nipple-bucket or an esophageal catheter. Tmax of SMX after nipple-bucket dosing was about 40 min shorter than that after catheter dosing. Cmax and AUC of SMX after the nipple-bucket dosing were 7.5 times greater and 6.9 times larger than those after the catheter dosing, respectively. Plasma TMP concentration was measurable only after the nipple-bucket dosing. These results suggest that a large portion of the drugs administered by the nipple-bucket dosing, which induces closure of the esophageal groove, were transferred directly into the abomasum resulting in higher bioavailabilities of the drugs.

Administration, Oral↗
PubMed1996

[A case of leiomyomatosis in pelvic lymph nodes].

We report a rare case of leiomyomatosis in iliac lymph nodes, which was found in a woman operated with a diagnosis as keratinizing epidermoid carcinoma of the cervix. A 39-year-old Japanese female, married, who had received hormonal therapy in her past history, visited the Department of Obstetrics and Gynecology at Kinki University Hospital, with a chief complaint of bloody discharge. Colposcopy and biopsy suggested a diagnosis of keratinizing epidermoid carcinoma of the cervix. A radical hysterectomy and bilateral salpingo-oophorectomy with pelvic lymph nodes dissection was performed. Histopathological examination showed a keratinizing epidermoid carcinoma of the cervix. An intramural leiomyoma nodule (0.5cm in diameter) was detected in the fundus of the uterus. Histopathologically, this was a typical benign leiomyoma. The lymph nodes were free of neoplasms. But bilateral iliac lymph nodes were enlarged up to soybean size. Microscopically, the iliac lymph nodes contained a large amount of well differentiated smooth muscle tissue (11/30). Immunohistochemical investigation showed a positive reaction for smooth muscle actin and desmins in the spindle cells proliferated in the lymph nodes; no cytokeratin positivity was detected. Leiomyomatosis of lymph node may rise through metaplasia of intranodal decidua or endometriosis by myofibroblasts or smooth muscle cells, reflecting the multipotentiality of the pelvic subcoelomic mesenchyme that can be found in the peripheral sinus of lymph nodes.

Adenocarcinoma, Papillary↗
PubMed1996

Urinary albumin excretion in short children treated with recombinant human growth hormone.

The urinary levels of albumin, beta 2-microglobulin (BMG) and beta-D-N-acetyl glucosaminidase (NAG) were studied in 30 children with short stature due to partial or complete growth hormone (GH) deficiency under treatment. All 30 children had a normal urinalysis and no clinical evidence of renal disease. They were treated with recombinant GH in a dose of 0.5 IU/kg/week given subcutaneously. The mean albumin excretion rate (9.13 +/- 8.33 micrograms/min/1.73 m2) of these children was significantly higher than that (4.2 +/- 2.27 micrograms/min/1.73 m2) of 30 age-, sex- and pubertal status-matched normal children (p < 0.01). BMG and NAG excretion was normal in both groups. There was no correlation between the urinary albumin excretion rate and the duration of GH treatment. Among the GH-treated children, the urinary albumin excretion rate was correlated significantly with circulatory insulin-like growth factor I (IGF-I) (r = 0.65, p < 0.01). In 7 other children analyzed before and three months after start of GH treatment, the mean urinary albumin excretion rate increased significantly from 4.71 +/- 3.95 micrograms/min/1.73 m2 to 8.29 +/- 2.70 micrograms/min/1.73 m2 (p < 0.03). These results suggest the possibility of functional glomerular alterations during GH therapy.

Acetylglucosaminidase↗