Biomedical subjects

S Kanematsu

Publications and source records attributed to S Kanematsu.

At least 19 recordsLinked to original sources

PubMed2006

Evidence for involvement of glial cell activity in the control of extracellular D-serine contents in the rat brain.

The continuous intra-cortical infusion of a glia toxin, fluorocitrate, at the concentration of 1 mM caused a decrease in the cortical extracellular contents of an intrinsic coagonist for the N-methyl-D-aspartate (NMDA) type glutamate receptor, D-serine, by peaking at 40 min by -25% but produced an increase in those of glycine and L-serine. The attenuated glial activity by fluorocitrate was verified by a marked reduction in the extracellular glutamine contents. The present findings suggest that a group of glial cells such as a population of the protoplasmic astrocytes could, at least in part, participate differently in the regulation of the extracellular release of D-serine and another NMDA coagonist glycine in the medial frontal cortex of the rat.

Animals↗

PubMed2005

Infection of Rosellinia necatrix with purified viral particles of a member of Partitiviridae (RnPV1-W8).

Isolate W8 of the white root rot fungus, Rosellinia necatrix, harbors three dsRNA segments, L1-, L2- and M-dsRNAs, and showed an irregular colony margin, slow growth, and moderate virulence. The M-dsRNA was previously shown to be the genome of a partitivirus, RnPV1-W8. Here a transfection protocol was developed for RnPV1-W8. Protoplasts of two virus-free isolates of R. necatrix were inoculated with purified viral particles using a polyethylene glycol-mediated method. Virus infection was confirmed by electrophoresis and Northern analysis. RnPV1-W8 introduced into the new host isolates was transmissible via hyphal anastomosis. However, the infection had no effect on the morphology and virulence of infected isolates of R. necatrix. This is the first report on the transfection of a partitivirus for R. necatrix.

Ascomycota↗

PubMed2003

Characterization of the small subgenomic RNA of Soybean dwarf virus.

We have characterized a small subgenomic RNA of Japanese strains of Soybean dwarf virus (SbDV). Northern blot analyses of SbDV-infected plants showed that the small RNA contained the 3' terminal sequence of the genome and was detected in four typical Japanese SbDV strains, YS, YP, DS and DP. In the case of SbDV-DS, the RNA was 220 nucleotides in length and was transcribed from the 3' terminal region of the genome. This RNA appeared at a similar time to genomic RNA and a large sgRNA, and thereafter persisted in the infected plant. Since no conserved open reading frame (ORF) among the strains was postulated in the 3' terminal region, the small subgenomic RNA may have some regulatory roles in SbDV infections.

Luteovirus↗

PubMed2001

Comparison of complete nucleotide sequences of genomic RNAs of four Soybean dwarf virus strains that differ in their vector specificity and symptom production.

Soybean dwarf virus (SbDV) is divided into four strains, namely YS, YP, DS and DP. YS and YP cause yellowing in soybeans, while DS and DP cause dwarfing. YS and DS are transmitted by Aulacorthum solani, while YP and DP are transmitted by Acyrthosiphon pisum. To clarify the taxonomic relationship between the four strains and to classify SbDV into an appropriate genus in the Luteoviridae, we determined the complete nucleotide sequences of genomic RNAs of four isolates belonging to each of the strains. The genomes of the four isolates had a chimeric form between Barley yellow dwarf virus-PAV and poleroviruses, and the genome organizations were similar to the Australian isolate SbDV Tas-1. In all of the non-coding regions and ORFs, nucleotide and deduced amino acid sequence identity between the same symptom-type strains was higher than that between the different symptom-type strains. However, in the N-terminal half of the readthrough domain (RTD) the deduced amino acid identity between the same aphid transmissibility-type strains was higher than that between the different aphid transmissibility-type strains. These data suggest that the N-terminal half of the RTD is closely related to the aphid transmission specificity, and that the present strains were generated from ancestral Y and D strains by mutations and strong selection pressures of efficient aphid transmission. Therefore, we propose that SbDV should be classified into a new genus in the family Luteoviridae and that the four strains described should be regarded as different strains of the same virus, rather than as distinct virus species.

Amino Acid Sequence↗

PubMed2001

The Japanese Study Group of Insulin Therapy for Childhood and Adolescent Diabetes (JSGIT): initial aims and impact of the family history of type 1 diabetes mellitus in Japanese children.

The Japanese Study Group of Insulin Therapy for Childhood and Adolescent Diabetes (JSGIT) was established in July 1994 with the chief aim to improve the quality of therapy for type 1 diabetes in children, an entity far less common in Japan than in Europe. We proposed four initial research topics: (i) to determine the current status of medical care and glycemic control in Japanese children with type 1 diabetes mellitus; (ii) to standardize the measurement of hemoglobin A1c; (iii) to establish a registry of a large cohort of patients in order to enable prospective studies to improve the quality of therapy for children with type 1 diabetes in Japan; and (iv) to enable participants of the JSGIT to hold a workshop twice annually. We registered a total of 736 patients from 45 hospitals throughout Japan. Intervention via insulin treatment was instituted after 2 yr for those patients whose hemoglobin A1c level was more than 8.1%. The proportion of patients receiving multiple insulin injections increased after intervention; however, average hemoglobin A1c in females remained significantly higher than in males. We identified two forms of diabetes in Japanese children: a rapidly progressive form and a more slowly progressive form. There was a significantly higher prevalence of a family history of diabetes in first-degree relatives in the slowly progressive form. These preliminary findings are the result of the first collaborative study of childhood diabetes in Japan.

Journal Article↗

PubMed2001

Vesicular prurigo pigmentosa cured by minocycline.

We present a case of prurigo pigmentosa associated with vesicles that we call 'vesicular prurigo pigmentosa'. The subject was treated using minocycline with good results and no recurrence of the lesions over a 2-year period.

Adult↗

PubMed2000

Serum parathyroid hormone and calcitonin levels in racehorses with fracture.

Serum parathyroid hormone (PTH) and calcitonin (CT) levels in fractured racehorses were measured by radioimmunoassay. Racehorses with fracture of large bone such as the radius, third metacarpus, third carpus, digital bone or tibia, showed normal PTH level and elevated CT level in the serum. Serum PTH level was slightly higher in racehorses with sesamoid bone fracture compared to that of healthy racehorses, but not statistically significant. Moreover, serum CT level of racehorses with sesamoid bone fracture was significantly higher than that of healthy racehorses. Racehorses with sesamoid bone fracture and large bone fracture might be in different conditions of calcium regulation.

Animals↗

PubMed1997

Effects of growth hormone (GH)-releasing hormone and its analogs on GH secretion from cultured adenohypophysial cells in cattle.

The effects of the human growth hormone (GH)-releasing hormone (hGRF(1-44)-NH2: hGRF-44), bovine GRF (bGRF(1-44)-NH2: bGRF-44), and their analogs (hGRF(1-29)-NH2, [D-Ala2]- hGRF(1-29)-NH2, bGRF(1-29)-NH2,[D-Ala2,Ala15]-bGRF(1-29)-NH2) as well as rat GRF(rGRF) on bovine GH release from anterior pituitary (AP) cells were studied in vitro in steers. The AP cells were incubated for 2 hr with the GRFs after preincubation for 3.5 d. Both of the hGRF-44 and hGRF(1-29)-NH2 (hGRF-29) significantly stimulated GH release from cultured cells at doses from 10(-14) to 10(-8)M (P < 0.01). The analog [D-Ala2]-hGRF-29 significantly induced GH release in media at doses from 10(-18) to 10(-8) M (P < 0.01). The bGRF-44, bGRF(1-29)-NH2 (bGRF-29), and [D-Ala2, Ala15]-bGRF-29 significantly induced GH release in media at doses as low as 10(-18), 10(-17), and 10(-16)M, respectively (P < 0.01). At doses from 10(-11) to 10(-8)M, there were no significant differences in GH-releasing potency between the hGRFs and bGRFs. The rGRF significantly stimulated GH release at doses ranging from 10(-14) to 10(-8) M (P < 0.01). The linear regression tests showed that the hGRFs, bGRFs, and rGRF, at doses from 10(-14) to 10(-8)M, induced GH release in a dose-related manner (P < 0.01). These results suggest that the hGRF, bGRF, and their analogs, as well as rGRF, are potent secretagogues of GH release from adenohypophysial cells in vitro in cattle.

Animals↗

PubMed1997

Generation of superoxide anion and localization of CuZn-superoxide dismutase in the vascular tissue of spinach hypocotyls: their association with lignification.

The sites of generations of superoxide anions and hydrogen peroxide in cross sections of hypocotyls from spinach seedlings were located by staining with nitroblue tetrazolium (NBT) and with starch-iodide, respectively. Formazan, produced upon the reduction of NBT by superoxide, was observed mainly in the vascular tissue only in the presence of inhibitors of CuZn-superoxide dismutase (CuZn-SOD), and its formation was suppressed under anaerobic conditions. Thus, NBT was reduced to formazan specifically by the superoxide anions generated in vascular tissue. The reduction of NBT was suppressed by inhibitors of NAD(P)H oxidase, but neither by cyanide nor azide, indicating the involvement of NAD(P)H oxidase in the generation of superoxide anions in the vascular tissue. Starch-I2 complex also was formed in the vascular tissue, but not in the presence of either the CuZn-SOD inhibitor or the NAD(P)H oxidase inhibitor, indicating that the hydrogen peroxide is produced via the catalytic disproportionation with CuZn-SOD of the superoxide generated by NAD(P)H oxidase. Generations of superoxide anions and hydrogen peroxide in the vascular tissue were particularly apparent in the xylem and associated with the sites of distribution of CuZn-SOD as determined by an immunohistochemical method, and also with the location of lignin as determined by the phloroglucin-HCl reaction.

Enzyme Inhibitors↗

PubMed1997

Mutations in the hepatocyte nuclear factor-1alpha/MODY3 gene in Japanese subjects with early- and late-onset NIDDM.

Recent studies have shown that mutations in the hepatocyte nuclear factor (HNF)-1alpha gene are the cause of maturity-onset diabetes of the young type 3 (MODY3). We have screened 193 unrelated Japanese subjects with NIDDM for mutations in this gene: 83 with early-onset NIDDM (diagnosis at <30 years of age) and 110 with late-onset NIDDM (diagnosis > or = 30 years of age). All of the members of the latter group also had at least one sibling with NIDDM. The 10 exons, flanking introns, and promoter region were amplified using polymerase chain reaction and were sequenced directly. Mutations were found in 7 of the 83 (8%) unrelated subjects with early-onset NIDDM. The mutations were each different and included four missense mutations (L12H, R131Q, K205Q, and R263C) and three frameshift mutations (P379fsdelCT, T392fsdelA, and L584S585fsinsTC). One of the 110 subjects with late-onset NIDDM was heterozygous for the missense mutation G191D. This subject, who was diagnosed with NIDDM at 64 years of age, also had a brother with NIDDM (age at diagnosis, 54 years) who carried the same mutation, suggesting that this mutation contributed to the development of NIDDM in these two siblings. None of these mutations were present in 50 unrelated subjects with normal glucose tolerance (100 normal chromosomes). Mutations in the HNF-1alpha gene occur in Japanese subjects with NIDDM and appear to be an important cause of early-onset NIDDM in this population. In addition, they are present in about 1% of subjects with late-onset NIDDM.

Age Factors↗

PubMed1996

The effects of xylazine on plasma concentrations of growth hormone, insulin-like growth factor-I, glucose and insulin in calves.

The purpose of the present study was to examine the responses of plasma growth hormone (GH) and insulin-like growth factor-I (IGF-I) levels to intravenous injection of xylazine in female dairy calves. Xylazine (0.05, 0.15 and 0.30 mg/kg body wt., i.v.) injections induced a significant dose-dependent increase in plasma GH level within 30 min. After plasma GH levels reached peaks, GH concentrations began to decrease immediately and they returned to control levels 1 h after xylazine injection. Plasma IGF-I concentration tended to be suppressed by xylazine treatment. Xylazine induced a significant dose-dependent increase in plasma glucose for 3.5 to 5.5 h after the treatments. Xylazine also induced a significant decrease in plasma insulin level within 30 min after treatments. The present data suggested that xylazine stimulates GH release in cattle.

Analgesics↗

PubMed1996

Effects of atipamezole, an alpha 2-adrenergic antagonist, and somatostatin on xylazine-induced growth hormone release in calves.

In order to clarify the mechanism of xylazine-induced GH release, we investigated the effects of atipamezole, a selective alpha 2-adrenergic antagonist, and somatostatin (SRIF) on xylazine-stimulated GH release in calves. Xylazine injection (0.30 mg/kg BW, iv) induced a rapid increase in the GH concentration. When atipamezole was used in combination with xylazine, it blunted the increase in the plasma GH concentration induced by the xylazine injection. The GH levels at 15-50 min after the simultaneous injection of xylazine and atipamezole were significantly (P < 0.05) lower than the corresponding values in the animals given xylazine alone. The area under the GH response curve for 120 min after the simultaneous injection of xylazine and atipamezole was significantly (P < 0.05) smaller than that for the xylazine alone. A series of five intravenous injections of 1 mg of SRIF at 10-min intervals also blunted xylazine-stimulated GH release. Atipamezole partially suppressed xylazine-induced hyperglycemia, but SRIF completely suppressed the hyperglycemia for the first 60 min after the xylazine injection and the suppression by SRIF was stronger than that by atipamezole. On the other hand, both atipamezole and SRIF failed to blunt xylazine-induced hypoinsulinemia. The present results suggest that xylazine stimulates GH release via the alpha 2-adrenergic pathway in cattle, but the mechanism of xylazine-induced hyperglycemia remains to be determined.

Adrenergic alpha-Antagonists↗

PubMed1995

Microdialysis measurement of intracerebral somatostatin in the goat.

A microdialysis sampling technique for the intracerebral measurement of somatostatin (SS) in extracellular fluid was examined in the goat. The microdialysis probe (70-mm shaft, 0.5 mm outer diameter) contained at its tip a 4-mm length of copolymer dialysis membrane (20 kDa cut-off). Artificial cerebrospinal fluid (artificial CSF) was pumped through the probe tip at a rate of 4 microliters/min with a batter-driven syringe pump, and effluent fractions of dialysate (120 microliters) were collected every 30 min. An in vitro recovery test showed that changes in the SS concentration in dialysate were highly correlated (r = 0.95, P < 0.01) with those in the external medium, and the relative recovery averaged 2.0%. As a validation for in vivo microdialysis, trails were conducted with conscious behaving goats wherein the inflow dialysate was changed transiently from artificial CSF with low potassium (2.5 mM) to a solution of 300 mM KCl. Potassium-induced depolarization around the probe tip located in the preoptic area and in the hypothalamus induced an increase in SS concentrations in dialysate at each location. In the most remarkable response, the concentrations of SS were increased 6-fold and 11-fold in the first and second 30-min fractions, respectively, compared with prepotassium concentrations. These results suggest that intracerebral SS levels in extracellular fluid could be estimated from conscious behaving goats by the use of our intracerebral microdialysis system.

Animals↗

PubMed1995

The interactive effects of VIP, PHI, GHRH, and SRIF on the release of growth hormone from cultured adenohypophysial cells in cattle.

The effects of hypothalamic peptides [vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI), growth hormone (GH)-releasing hormone (GHRH) and somatostatin (SRIF) on GH release from cultured bovine adenohypophysial cells were studied. The cells were incubated for 2 h with the peptides after preincubation for 3.5 days. At doses from 10(-9) to 10(-7)M VIP, the amount of GH released was significantly greater than in the controls (P < 0.05 to P < 0.001). PHI (10(-10 to 10(-7)M did not alter the bovine GH concentration in the media. Incubation with the media containing 10(-7)M GHRH, 10(-7)M VIP, and combined treatment with the VIP plus GHRH increased GH by 186, 40 and 182%, respectively (P < 0.001). Furthermore, although VIP-induced GH release was significantly decreased by SRIF compared with the treatment with VIP alone (P<0.001), the VIP significantly blunted the inhibitory effect of the SRIF on GH release by 24% when compared with that of the SRIF plus GHRH without the VIP (P < 0.05). GH release in combined treatments with VIP, GHRH and SRIF was significantly less than that of the VIP plus GHRH (P < 0.001), but it was significant 29% increase compared with the SRIF plus GHRH (P < 0.05). The combined effects of the VIP (10(-7)M) with GHRH (10(-7), 10(-8) and 10(-10)M significantly induced GH release compared with the controls (P < 0.001), but no additive effect was not observed when compared with the GHRH alone. The results indicate that VIP, but not PHI, acts directly on cultured adenohypophysial cells to induce GH release in cattle.

Animals↗

PubMed1994

Effects of pituitary adenylate cyclase-activating polypeptide (PACAP), prostaglandin E2 (PGE2) and growth hormone releasing factor (GRF) on the release of growth hormone from cultured bovine anterior pituitary cells in vitro.

The effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on growth hormone (GH) release was compared with that of prostaglandin E2 (PGE2) and growth hormone releasing factor (GRF) from cultured bovine anterior pituitary cells in vitro. Both PACAP and PGE2 stimulated GH release at concentrations as low as 10(-9) and 10(-8) M, respectively, (P < 0.01). However, GRF released GH at a concentration as low as 10(-13) M (P < 0.01). Percent increases of GH compared with controls were not significantly different among GRF, PACAP, and PGE2 at 10(-7) M; however, the increases of GH by the 10(-8) M GRF, PACAP and PGE2 were 196, 118, and 27%, respectively, (P < 0.01), and 124, 65, and 1% in the 10(-9) M media, respectively, (P < 0.01). When GRF and somatostatin (SS) were added together, the GH releasing effect of GRF was blunted (P < 0.01). Similar bluntness were observed in PACAP and PGE2, when SS was added. The stimulatory effects of GRF and PGE2 together were similar to that by either GRF or PGE2 alone. When GRF and PACAP were added together, the GH released by both secretagogues was greater than that by PACAP alone (P < 0.01); however, a synergistic effect was not clear when compared with GRF alone. These findings suggest that PACAP and PGE2 may modulate the release of GH in cattle.

Animals↗

PubMed1994

Effect of growth hormone (GH)-releasing peptide (GHRP) on the release of GH from cultured anterior pituitary cells in cattle.

The effect of His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP) on growth hormone (GH) release from cultured bovine anterior pituitary (AP) cells was studied in vitro with the interactive effects of GH-releasing factor (GRF: hpGRF (1-29)-NH2) and somatostatin (SRIF). The AP cells (5 x 10(4) cells per well) were incubated with media, and the media were changed 3 days after plating. After 3.5 days in culture, cells were incubated for 2 h with the peptides. GHRP stimulated GH release from cultured cells in a dose-related manner. At doses from 10(-11) to 10(-7) M GHRP, the amount of GH released was significantly greater than the controls (P < 0.05 to P < 0.001). The amounts of GH released at lower doses of GHRP (10(-14) to 10(-12) M) were not significantly different from the controls. GH concentrations after treatment with 10(-11) and 10(-7) M GHRP were 3.98 +/- 0.27 and 4.81 +/- 0.16 ng/ml, respectively. In experiments performed similarly, the 10(-7) M GHRH, GHRP, and combined treatment with GHRP plus GHRH increased GH 126, 57, and 139%, respectively (P < 0.001). The GH releasing effects of either GHRH alone or GHRP plus GHRH were significantly more potent than that of GHRP alone (P < 0.001). The additive effect was not significant when compared with GHRH alone. GH release induced by either GHRH or GHRP was significantly inhibited by SRIF (P < 0.01) compared with the untreated control. The inhibitory effect of SRIF in combined treatment with GHRP plus GHRH was significantly less than that of SRIF with GHRH or with GHRP (P < 0.01). The present study suggests that GH-releasing peptide (GHRP) induced GH release in cattle via a direct action on anterior pituitary cells in vitro.

Animals↗

PubMed1992

Temporal bone findings in keratitis, ichthyosis, and deafness syndrome. Case report.

In 1981, the term KID syndrome was suggested for patients with congenital ichthyosis associated with deafness and keratitis. We had a chance to examine the temporal bone of an infant with this syndrome. This patient showed no auditory brain stem response in either ear. Temporal bone studies revealed cochleosaccular abnormality. These findings are offered as a possible explanation for the patient's deafness. The pathologic inner ear findings of congenital deafness syndromes associated with ichthyosis have been heretofore reported in Refsum's syndrome and in a case with universal alopecia. In these cases, the temporal bone pathologic findings were a result of cochleosaccular abnormality. From our case and previous reports, it is suggested that the deafness associated with congenital ichthyosis might be the result of cochleosaccular abnormality.

Cochlea↗

PubMed1991

Effect of vasoactive intestinal peptide on the release of growth hormone in perifused pituitary and hypothalamus of the goat.

The effect of vasoactive intestinal peptide (VIP) on the release of growth hormone (GH) from the adenohypophysis of the goat was studied in vitro using the perifusion system. Two perifusion systems were employed to differentiate potential direct effects of VIP on the pituitary from indirect effects mediated through the hypothalamus. The first perifusion system used single chambers housing only pituitary fragments. The second system used two chambers in tandem, one containing hypothalamus and the second the pituitary fragments, the flow passing through the hypothalamic chamber first. VIP (10(-6), 10(-7), 10(-8)M) stimulated significant GH release in both perifusion systems (P less than 0.05, P less than 0.01) in a concentration related fashion. The quantity of GH release induced by the 10(-9)M and 10(-10)M VIP groups were not significant. Further, the GH released from the system that perifused the pituitary alone (10(-8)M VIP) was significantly higher than that containing both the hypothalamus and the pituitary fragments (P less than 0.05). The relative lower GH secretory response to the same dose of VIP applied to the hypothalamus-pituitary suggests that the perifused caprine hypothalamus may release an inhibitory factor, such as somatostatin in vitro. These results suggest that VIP stimulates GH release by acting directly on the adenohypophysis of the goat.

Animals↗