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K Hoshino

Publications and source records attributed to K Hoshino.

At least 37 records · Page 2Linked to original sources
PubMed2001

New avenues in dinitrogen fixation research.

The present article focuses on a recent finding concerning dinitrogen fixation by using titanium oxide/conducting polymer composite systems and its comparison with an earlier fixation method (Schrauzer process) that makes use of a powdered titanium oxide. Both processes work under the stimulus of light at room temperature and pressure, but dinitrogen is fixed to a solid ammonium salt crystal in the former and to a gaseous ammonia molecule in the latter process. Differences in the physicochemical concepts between the two processes are discussed.

Animals↗
PubMed2001

Endotoxin-induced maturation of MyD88-deficient dendritic cells.

LPS, a major component of the cell wall of Gram-negative bacteria, can induce a variety of biological responses including cytokine production from macrophages, B cell proliferation, and endotoxin shock. All of them were completely abolished in MyD88-deficient mice, indicating the essential role of MyD88 in LPS signaling. However, MyD88-deficient cells still show activation of NF-kappaB and mitogen-activated protein kinase cascades, although the biological significance of this activation is not clear. In this study, we have examined the effects of LPS on dendritic cells (DCs) from wild-type and several mutant mice. LPS-induced cytokine production from DCs was dependent on MyD88. However, LPS could induce functional maturation of MyD88-deficient DCs, including up-regulation of costimulatory molecules and enhancement of APC activity. MyD88-deficient DCs could not mature in response to bacterial DNA, the ligand for Toll-like receptor (TLR)9, indicating that MyD88 is differentially required for TLR family signaling. MyD88-dependent and -independent pathways originate at the intracytoplasmic region of TLR4, because both cytokine induction and functional maturation were abolished in DCs from C3H/HeJ mice carrying the point mutation in the region. Finally, in vivo analysis revealed that MyD88-, but not TLR4-, deficient splenic CD11c(+) DCs could up-regulate their costimulatory molecule expression in response to LPS. Collectively, the present study provides the first evidence that the MyD88-independent pathway downstream of TLR4 can lead to functional DC maturation, which is critical for a link between innate and adaptive immunity.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Lipopolysaccharide-induced IL-18 secretion from murine Kupffer cells independently of myeloid differentiation factor 88 that is critically involved in induction of production of IL-12 and IL-1beta.

IL-18, produced as biologically inactive precursor, is secreted from LPS-stimulated macrophages after cleavage by caspase-1. In this study, we investigated the mechanism underlying caspase-1-mediated IL-18 secretion. Kupffer cells constantly stored IL-18 and constitutively expressed caspase-1. Inhibition of new protein synthesis only slightly reduced IL-18 secretion, while it decreased and abrogated their IL-1beta and IL-12 secretion, respectively. Kupffer cells deficient in Toll-like receptor (TLR) 4, an LPS-signaling receptor, did not secrete IL-18, IL-1beta, and IL-12 upon LPS stimulation. In contrast, Kupffer cells lacking myeloid differentiation factor 88 (MyD88), an adaptor molecule for TLR-mediated-signaling, secreted IL-18 without IL-1beta and IL-12 production in a caspase-1-dependent and de novo synthesis-independent manner. These results indicate that MyD88 is essential for IL-12 and IL-1beta production from Kupffer cells while their IL-18 secretion is mediated via activation of endogenous caspase-1 without de novo protein synthesis in a MyD88-independent fashion after stimulation with LPS. In addition, infection with Listeria monocytogenes, products of which have the capacity to activate TLR, increased serum levels of IL-18 in wild-type and MyD88-deficient mice but not in caspase-1-deficient mice, whereas it induced elevation of serum levels of IL-12 in both wild-type and caspase-1-deficient mice but not in MyD88-deficient mice. Taken together, these results suggested caspase-1-dependent, MyD88-independent IL-18 release in bacterial infection.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Two hyperandrogenic adolescent girls with congenital portosystemic shunt.

UNLABELLED: We describe two adolescent girls with a congenital portosystemic shunt who exhibited hyperandrogenism in addition to insulin resistant hyperinsulinaemia. Case 1 was referred to our clinic to undergo a routine clinical work-up prior to tonsillectomy at 14 years of age. Mild liver dysfunction was identified and hypogenesis of the portal vein with a congenital portosystemic shunt diagnosed. Primary amenorrhoea and virilization were evident and an endocrinological evaluation revealed hyperandrogenism and insulin resistant hyperinsulinaemia. Case 2 was referred at 15 years of age because of cardiomegaly. Mild liver dysfunction and hyperbilirubinaemia led to a diagnosis of agenesis of the portal vein with a congenital portosystemic shunt. Virilization was evident and an endocrinological evaluation revealed hyperandrogenism and insulin resistant hyperinsulinaemia. The haemodynamics of these patients were similar to those of secondary portosystemic shunt due to liver cirrhosis, which is often associated with hyperinsulinaemia and/or non-insulin dependent diabetes mellitus. On the other hand, hyperandrogenism is associated with certain insulin-resistant conditions with hyperinsulinaemia, including the polycystic ovary syndrome (PCO). Hyperinsulinaemia is believed to cause hyperandrogenism in patients with PCO by stimulating androgen production in both the ovary and adrenal gland. Therefore, in congenital portosystemic shunts, hyperinsulinaemia is also thought to cause hyperandrogenism due to the same mechanism. CONCLUSION: A certain percentage of female patients with hyperandrogenism, likely including those with polycystic ovary syndrome may also have congenital portosystemic shunts. Our results indicate that serum levels of total bile acids and ammonia are prognostic indicators of this hepatic vascular anomaly.

Adolescent↗
PubMed2001

Mineral density and histomorphometric assessment of bone changes in the proximal tibia early after induction of type II collagen-induced arthritis in growing and mature rats.

Bone changes in both actively growing (6-week-old) and mature (6-month-old) rats with collagen-induced arthritis (CIA) were investigated in order to clarify the mechanisms of osteoporosis near inflamed joints in patients with early rheumatoid arthritis (RA) and juvenile RA. In female Sprague-Dawley rats, the proximal tibiae from the CIA and control groups early after immunization, when any influence of immobilization due to joint pain and swelling is minimal, were studied using dual X-ray absorptiometry and histomorphometry after double-labeling with tetracycline. Arthritis developed within 10-14 days after immunization in both growing and mature rats. Physical activity, growth, and body weight continued to resemble that of the control group for at least 10 days. The bone mineral density in the proximal tibia did not differ significantly between the CIA and control groups. In growing rats, a highly significant increase in bone resorption, and decreases in bone formation and trabecular bone volume became evident histomorphometrically before visible signs of arthritis had developed. In mature rats, bone formation was markedly decreased without an increase in bone resorption. The differences in the reaction between growing and mature rats reflected a difference in the number of remodeling sites (units) and an uncoupling between osteoblasts and osteoclasts. We conclude that osteoporosis near inflamed joints results from an imbalance between bone resorption and formation caused by immune reactions in the CIA rats. Moreover, a decrease in bone formation may, in part, precede the clinical onset of arthritis.

Animals↗
PubMed2001

Identification and quantification of chlorinated bisphenol A in wastewater from wastepaper recycling plants.

Chlorinated derivatives of bisphenol A were detected in the final effluents of eight paper manufacturing plants in Shizuoka, Japan, where thermal paper and/or other printed paper is used as the raw material. Their amounts were determined by gas chromatography/mass spectrometry (GC/MS) after treatment with N, O-bis(trimethylsilyl)trifluoroacetamide, and ranged from traces to 2.0 microg/l. They are likely produced by chlorination of bisphenol A, which was released into the effluents from the pulping process of wastepaper, during or after bleaching with chlorine.

Benzhydryl Compounds↗
PubMed2001

Development of language in Rett syndrome.

Ninety-nine cases of Rett syndrome (RTT) diagnosed clinically (age range 3 years 6 months to 29 years 9 months) were evaluated for the ability of language. The presence of meaningful words, vocabularies, and ages at the start and disappearance of speech were assessed. Phenotype/genotype correlation was evaluated in 22 cases in whom mutations of the genes of methyl-CpG-binding protein 2 (MECP2) existed. Fifty-five cases (55.5%) could speak some words, and of them eight cases (14.5%) spoke two-word sentences. No case had more than 40 words. The vocabularies were mainly bilabial words, known as the characteristics of the initial words in normal children. They began to utter a word between 12 and 48 months, and most of them (85.4%) before 20 months. Those who spoke two-word sentence(s) began to utter a word earlier (10.4+/-3.7 months) than others (17.1+/-9.8 months). Thirty-three cases lost their word(s) in 12-36 months. Among 22 gene-proven cases two cases with mutation of R133C and two cases with R294X had word(s), but another two cases with T158M had not. In RTT a delay in the neuronal systems involved in normal speech development was suggested and its severity seemed to depend on the loci of mutation.

Adolescent↗
PubMed2001

Effects of moderate hypothermia on sarcolemmal Na(+)/H(+) exchanger activity and its inhibition by cariporide in cardiac ventricular myocytes.

1. Specific inhibitors of the sarcolemmal Na(+)/H(+) exchanger (NHE) such as cariporide are being evaluated for cardioprotective therapy during cardiac surgery. We determined the effects of moderate hypothermia (25 degrees C), as occurs during cardiac surgery, on (1) sarcolemmal NHE activity and (2) the NHE-inhibitory potency of cariporide, in isolated adult rat ventricular myocytes. 2. As the index of NHE activity, trans-sarcolemmal acid efflux rate (J(H)) was determined by microepifluorescence in single cells (n = 8 to 11 per group), during recovery from intracellular acidosis in bicarbonate-free conditions. 3. Initially, myocytes were subjected to two consecutive acid pulses; these both occurred at 37 degrees C in the normothermic control group but the second pulse was at 25 degrees C in the moderate hypothermia group. J(H) values obtained after the first pulse were superimposed in both groups, indicating comparable cell populations. However, after the second pulse, J(H) values in the moderate hypothermia group were approximately 50% of those in the normothermic control group over the pH(i) range 6.80 - 7.10. 4. Similar results were obtained in cells subjected to a single acid pulse at 37 or 25 degrees C, with J(H) values in the latter group measuring approximately 60% of those in the former over the pH(i) range 6.80-7.10. 5. Cariporide (0.01, 0.03, 0.1, 0.3, 1.0 or 3.0 microM), present during recovery from a single acid pulse, reduced J(H) in a concentration-dependent manner, with IC(50) values of 150 and 130 nM at 37 and 25 degrees C, respectively. 6. We conclude that moderate hypothermia produces (1) a significant, but partial, inhibition of sarcolemmal NHE activity, and (2) no significant effect on the NHE-inhibitory potency of cariporide.

Animals↗
PubMed2001

Immunohistochemical characterisation of Fos-positive cells in brainstem monoaminergic nuclei following intracranial self-stimulation of the medial forebrain bundle in the rat.

Fos immunostaining was used as a marker of neuronal activity following intracranial self-stimulation (ICSS) of the medial forebrain bundle (MFB) in the rat, and was combined with immunostaining for tyrosine hydroxylase (TH), serotonin (5-HT), gamma-aminobutyric acid (GABA), or NR1 (one of the glutamate N-methyl- D-aspartate receptor subunits) for purposes of neurochemical identification. ICSS induced a significant but different degree of increase in the number of Fos-immunopositive (Fos+) cells in the six brainstem monoaminergic nuclei examined, which included the ventral tegmental area (VTA), substantia nigra pars compacta (SNc), dorsal raphe nucleus (DR), median raphe nucleus (MR), locus coeruleus (LC), and A7 noradrenaline cells. Densely labelled Fos+ cells were observed in the LC following ICSS, and many of these Fos+ cells were colocalized with TH. Similarly, many of Fos+ cells in the A7 and DR/MR were colocalized with TH and 5-HT, respectively. By contrast, a smaller number of Fos+ cells was detected in the VTA and SNc following the ICSS, and in these regions the majority of Fos+ cells were not colocalized with TH. Although results among regions quantitatively differed, the ICSS induced a significant increase in the number of double-labelled cells (GABA+/Fos+ or NR1+/Fos+) in all of the VTA, DR, and LC, in which the ICSS produced an ipsilaterally weighted increase in Fos-like immunoreactivity. These results suggest that ICSS of the MFB induces differential Fos expression within monoaminergic and GABAergic neurons in brainstem monoaminergic nuclei under modulation by glutamatergic afferents.

Animals↗
PubMed2001

Sequence heterogeneity of the ten rRNA operons in Clostridium perfringens.

We have cloned and sequenced rRNA operons of Clostridium perfringens strain 13 and analyzed the sequence structure in view of the phylogenesis. The organism had ten copies of rRNA operons all of that comprised of 16S, 23S and 5S rDNAs except for one operon. The operons clustered around the origin of replication, ranging within one-third of the whole genome sequence as it is arranged in a circle. Seven operons were transcribed in clockwise direction, and the remaining three were transcribed in counter clockwise direction assuming that the gyrA was transcribed in clockwise direction. Two of the counter clockwise operons contained tRNA(Ile) genes between the 16S and 23S rDNAs, and the other had a tRNA(Ile) genes between the 16S and 23S rDNAs and a tRNA(Asn) gene in the place of the 5S rDNA. Microheterogeneity was found within the rRNA structural genes and spacer regions. The length of each 16S, 23S and 5S rDNA were almost identical among the ten operons, however, the intergenic spacer region of 16S-23S and 23S-5S were variable in the length depending on loci of the rRNA operons on the chromosome. Nucleotide sequences of the helix 19, helix 19a, helix 20 and helix 21 of 23S rDNA were divergent and the diversity appeared to be correlated with the loci of the rRNA operons on the chromosome.

Base Sequence↗
PubMed2001

Sex-dependent toxicity of a novel acyl-CoA:cholesterol acyltransferase inhibitor, YIC-C8-434, in relation to sex-specific forms of cytochrome P450 in rats.

YIC-C8-434 is a novel inhibitor of acyl coenzyme A:cholesterol acyltransferase (ACAT). To clarify the toxicity of YIC-C8-434, the compound was given orally to Sprague-Dawley rats for 28 days at 0, 4, 20, 100, or 500 mg/kg/day. The toxicity of the drug differed significantly between male and female rats. In female rats treated at 500 mg/kg, many symptoms including moribund condition, suppression of weight gain and food consumption, abnormal blood chemistry, and decreases in organ weights (thymus, ovaries, and uterus) were observed. In male rats by contrast, no significant toxicity was observed at any dose. After a single administration of YIC-C8-434 at 500 mg/kg, female rats had a higher blood concentration of the compound than male rats. Little elimination of YIC-C8-434 was observed in female rats on analysis of drug-elimination kinetics. Furthermore, the metabolism of YIC-C8-434 was analyzed using rat hepatic microsomal preparations from both sexes. Consistent with the observations in vivo, hepatic microsomes from male rats better metabolized YIC-C8-434 than those from females. In addition, the metabolism of YIC-C8-434 by hepatic microsomes from male rats was blocked by SKF525A, a P450 inhibitor. Inhibition experiments using anti-rat CYP1A1, CYP1A2, CYP2B1, CYP2C11, CYP2E1, CYP3A2, and CYP4A1 antisera indicated that CYP3A2 played the predominant role in the metabolism of YIC-C8-434 in rats. Since there is less CYP3A2 in the liver of female than male rats, the involvement of CYP3A2 in YIC-C8-434 metabolism has implications for the sex-related metabolic activity and toxicity of YIC-C8-434.

Administration, Oral↗
PubMed2001

Identification and characterization of inhibitors of multidrug resistance efflux pumps in Pseudomonas aeruginosa: novel agents for combination therapy.

Whole-cell assays were implemented to search for efflux pump inhibitors (EPIs) of the three multidrug resistance efflux pumps (MexAB-OprM, MexCD-OprJ, MexEF-OprN) that contribute to fluoroquinolone resistance in clinical isolates of Pseudomonas aeruginosa. Secondary assays were developed to identify lead compounds with exquisite activities as inhibitors. A broad-spectrum EPI which is active against all three known Mex efflux pumps from P. aeruginosa and their close Escherichia coli efflux pump homolog (AcrAB-TolC) was discovered. When this compound, MC-207,110, was used, the intrinsic resistance of P. aeruginosa to fluoroquinolones was decreased significantly (eightfold for levofloxacin). Acquired resistance due to the overexpression of efflux pumps was also decreased (32- to 64-fold reduction in the MIC of levofloxacin). Similarly, 32- to 64-fold reductions in MICs in the presence of MC-207,110 were observed for strains with overexpressed efflux pumps and various target mutations that confer resistance to levofloxacin (e.g., gyrA and parC). We also compared the frequencies of emergence of levofloxacin-resistant variants in the wild-type strain at four times the MIC of levofloxacin (1 microg/ml) when it was used either alone or in combination with EPI. In the case of levofloxacin alone, the frequency was approximately 10(-7) CFU/ml. In contrast, with an EPI, the frequency was below the level of detection (<10(-11)). In summary, we have demonstrated that inhibition of efflux pumps (i) decreased the level of intrinsic resistance significantly, (ii) reversed acquired resistance, and (iii) resulted in a decreased frequency of emergence of P. aeruginosa strains that are highly resistant to fluoroquinolones.

Anti-Infective Agents↗
PubMed2001

Localization of nitric oxide synthase activity in unfertilized oocytes and fertilized embryos during preimplantation development in mice.

Changes in the activities of nitric oxide synthase (NOS) during embryonic development, and the distribution of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) isoforms were examined in unfertilized mouse oocytes at the second meiotic metaphase (MII) stage and in fertilized mouse embryos during preimplantation development. In addition, the effects of NOS inhibitors on mouse preimplantation development in vitro were investigated. The activities of NOS in MII oocytes and fertilized embryos during the preimplantation period were determined by NADPH-diaphorase staining. Although NOS activity was detected in unfertilized MII oocytes, the intensity of staining was much weaker than that of fertilized embryos at the one-cell stage. There was a decrease in NOS activity in embryos from the four-cell to the eight-cell stage; however, NOS activity increased again in embryos at the morula stage, particularly in the inner cell population. In the expanded blastocysts, staining was confined to the inner cell mass. Immuno-cytochemical staining showed that eNOS and iNOS were expressed in the cytoplasm of oocytes and embryos during the preimplantation period, and eNOS was also distributed in the nuclei of the embryos. When one-cell embryos were treated with 1 mmol N(omega)-nitro-L-arginine methyl ester (L-NAME) l(-1), their development in vitro was arrested at the two-cell stage. This inhibition of development was overcome by the addition of 1 mmol L-arginine l(-1) to the medium. These observations indicate that nitric oxide plays an important role as a diffusible regulator of cell proliferation and differentiation, especially at the developmental transition from the two-cell to the four-cell stage during preimplantation development of mice.

Animals↗
PubMed2001

Fighting by sleep-deprived rats as a possible manifestation of panic: effects of sodium lactate.

Increased fighting is an effect of desynchronized sleep deprivation (DSD) in rats, and recently this behavior has been suggested to be spontaneous panic and equivalent to panic disorder. In the present study we tested this hypothesis by evaluating the effect of sodium lactate on this aggressiveness, because this substance is recognized to induce spontaneous panic attacks in patients. A total of 186 male albino Wistar rats, 250-350 g, 90-120 days of age, were submitted to DSD (multiple platform method) for 0, 4, or 5 days. At the end of the deprivation period the rats were divided into subgroups respectively injected intraperitoneally with 1.86, 2.98 and 3.72 g/kg of 1 M sodium lactate, or 1.86 and 3.72 g/kg of 2 M sodium lactate. The control animals were submitted to the same procedures but received equivalent injections of sodium chloride. Regardless of DSD time, sleep-deprived animals that received sodium lactate presented a significantly higher mean number of fights (0.13 +/- 0.02 fights/min) and a longer mean time spent in confrontation (2.43 +/- 0.66 s/min) than the controls (0.01 +/- 0.006 fights/min and 0.12 +/- 0.07 s/min, respectively; P<0.01, Student t-test). For the sodium lactate group, concentration of the solution and time of deprivation increased the number of fights, with the mean number of fights and mean duration of fighting episodes being greater with the 2.98 g/kg dose using 1 M lactate concentration. These results support the hypothesis that fighting induced by DSD is probably a spontaneous panic manifestation. However, additional investigations are necessary in order to accept this as a promising animal model for studies on panic disorder.

Aggression↗
PubMed2001

Eradication of foot and mouth disease in Japan.

An outbreak of foot and mouth disease (FMD) was recorded in Japan in the spring of 2000, the first for ninety-two years. Between 25 March and 11 May, four farms were infected. However, the disease was eradicated without resorting to vaccination, through a campaign of culling, movement control of cloven-hoofed animals in areas surrounding infected premises, and intensive clinical and serological surveillance. Japan regained FMD-free status by the end of September 2000. The authors describe the nature of the outbreaks, the eradication measures implemented, and the clinical and serological surveillance methods used. The possible sources of infection are also examined. Finally, the direct and indirect economic losses are presented.

Animals↗
PubMed2001

Development of endoscopic surgery for the minimally invasive treatment of digestive and other diseases.

Minimally invasive surgery has rapidly changed the performance of surgical practice in a wide range of surgical specialities in the last decade of the 20th century. The marked progress in endoscopic surgery has been conducted especially in general and digestive surgery. The Department of Surgery, School of Medicine, Keio University has contributed to the development and establishment of endoscopic surgery in every subspeciality of general and digestive surgery. Our achievements include the development of original methods for laparoscopic wedge gastrectomy and endoscopic thyroidectomy, establishment of surgical techniques in endoscopic surgery for esophageal, gastric, colorectal and hepatobiliary diseases, and the introduction of robotics and tele-communicative technologies to endoscopic surgery.

Digestive System Surgical Procedures↗
PubMed2001

Characteristics of improved NOVA magnesium ion-selective electrode: changes of ionized magnesium values and reference interval in healthy children.

Following the report of interference between the thiocyanate ion (SCN-) and NOVA's previous ion-selective electrode (ISE) for ionized magnesium (iMg2+), NOVA has developed a new ISE which eliminates the effect of SCN-. Two hundred and sixty healthy children were divided into two groups; those who had presented when using NOVA's previous ISE (group A; n = 160) and those using NOVA's new ISE (group B; n = 100). The mean iMg2+ value and the mean iMg2+ percent fraction (iMg2+/serum Mg) were significantly higher in group B than in group A (0.59 +/- 0.03 vs 0.54 +/- 0.03 mmol/L for iMg2+; p < 0.001 and 64.8 +/- 3.1 vs 58.2 +/- 4.1 per cent for iMg2+ percent fraction; p < 0.001). The mean serum SCN- level was 0.023 +/- 0.008 mmol/L in group A (n = 8) and 0.0.21 +/- 0.007 mmol/L in group B (n = 12), and was not significantly different between the two groups. The suspected change of iMg2+ value interfered by SCN- was 0.037 mmol/L in group A. The difference of iMg2+ percent fraction between two groups was higher at high serum magnesium (SMg) levels. The reference interval of iMg2+ was 0.56-0.62 mmo/L in healthy children with the NOVA's new ISE, and was constant irrespective of growth. The NOVA's previous iMg2+ ISE may be interfered with mainly by SCN-. The newly designed ISE eliminated these effects especially at higher SMg levels.

Adolescent↗