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K Kishida

Publications and source records attributed to K Kishida.

At least 19 recordsLinked to original sources
PubMed2004

A new dynamical approach to auditory evoked magnetic field by blind identification.

A new approach to understand neural dynamics underlying the generation of auditory evoked magnetic field is proposed. MEG time series data are temporally decorrelated by using a blind signal separation method. Two components are selected from their periodical property and a remixing matrix is applied to the two selected components to retrieve MEG signals of auditory evoked magnetic field. After principal component data for each sensor pairs are calculated, a minimum phase innovation model is identified from the viewpoint of statistical inverse problem. By using a blind identification method based on feedback system theory transfer functions can be evaluated to get a dynamical understanding of brain auditory functions. It is reported that all changes of their impulse responses between right and left hemisphere decay within about 40 ms, and that directional differences in transfer functions can be found.

Acoustic Stimulation↗
PubMed2002

Transfer and distribution profiles of dietary sulphonamides in the tissues of the laying hen.

The five sulphonamides, sulphadiazine (SDZ), sulphadimidine (SDD), sulphamethoxazole (SMX), sulphamonomethoxine (SMM) and sulphaquinoxaline (SQ), were fed to laying hens at a dietary concentration of 100 mg kg(-1), respectively. On the 7th day after the start of feeding, the drug concentrations in the plasma, muscle and the main tissues involved in egg formation, the liver, and ovary and oviducts (magnum and isthmus plus shell grand) were determined by high-performance liquid chromatography. Dietary sulphonamides were distributed throughout the above tissues. SQ was found at the highest concentration in all tissues, while the reverse was true for SDD. The ratio of SDD concentrations in the main tissues involved in egg formation to that in the plasma were greater than those for the other drugs.

Animals↗
PubMed2001

Matrix solid-phase dispersion extraction and high-performance liquid chromatographic determination of residual sulfonamides in chicken.

Simultaneous determination of the six sulfonamides (SAs) sulfadiazine, sulfadimidine, sulfamonomethoxine, sulfamethoxazole, sulfadimethoxine and sulfaquinoxaline in chicken using matrix solid-phase dispersion (MSPD) with neutral aluminium oxide as an MSPD sorbent and high-performance liquid chromatography (HPLC) is presented. In the present MSPD, six SAs could be isolated by only one step, elution with a 70% (v/v) aqueous ethanol solution, without the sorbent conditioning and the sorbent-tissue matrix washing. For the HPLC determination, a LiChrospher 100 RP-8 and a mixture of 1% acetic acid solution (pH 3.0, in water)-acetonitrile-N,N-dimethylformamide (78:22:5, v/v/v) as the mobile phase with a photodiode array detector were used. Average recoveries were greater than 87.6% with relative standard deviations between 0.5 and 8.6%. The total time and amount of solvent required for the analysis of one sample were <1.5 h and <12 ml, respectively.

Animals↗
PubMed2001

Enhancement of the aquaporin adipose gene expression by a peroxisome proliferator-activated receptor gamma.

The current study demonstrates that aquaporin adipose (AQPap), an adipose-specific glycerol channel (Kishida, K., Kuriyama, H., Funahashi, T., Shimomura, I., Kihara, S., Ouchi, N., Nishida, M., Nishizawa, H., Matsuda, M., Takahashi, M., Hotta, K., Nakamura, T., Yamashita, S., Tochino, Y., and Matsuzawa, Y. (2000) J. Biol. Chem. 275, 20896-20902), is a target gene of peroxisome proliferator-activated receptor (PPAR) gamma. The AQPap mRNA amounts increased following the induction of PPARgamma in the differentiation of 3T3-L1 adipocytes. The AQPap mRNA in the adipose tissue increased when mice were treated with pioglitazone (PGZ), a synthetic PPARgamma ligand, and decreased in PPARgamma(+/-) heterozygous knockout mice. In 3T3-L1 adipocytes, PGZ augmented the AQPap mRNA expression and its promoter activity. Serial deletion of the promoter revealed the putative peroxisome proliferator-activated receptor response element (PPRE) at -93/-77. In 3T3-L1 preadipocytes, the expression of PPARgamma by transfection and PGZ activated the luciferase activity of the promoter containing the PPRE, whereas the PPRE-deleted mutant was not affected. The gel mobility shift assay showed the direct binding of PPARgamma-retinoid X receptor alpha complex to the PPRE. DeltaPPARgamma, which we generated as the dominant negative PPARgamma lacking the activation function-2 domain, suppressed the promoter activity in 3T3-L1 cells, dose-dependently. We conclude that AQPap is a novel adipose-specific target gene of PPARgamma through the binding of PPARgamma-retinoid X receptor complex to the PPRE region in its promoter.

3T3 Cells↗
PubMed2001

Genomic structure and insulin-mediated repression of the aquaporin adipose (AQPap), adipose-specific glycerol channel.

Aquaporin adipose (AQPap) is a putative glycerol channel in adipocytes (Kishida, K., Kuriyama, H., Funahashi, T., Shimomura, I., Kihara, S., Ouchi, N., Nishida, M., Nishizawa, H., Matsuda, M., Takahashi, M., Hotta, K., Nakamura, T., Yamashita, S., Tochino, Y., and Matsuzawa, Y. (2000) J. Biol. Chem. 275, 20896-20902). In the current study, we examined the genomic structure of the mouse AQPap gene and its regulation by insulin. The mouse AQPap gene spanned 12 kilobase pairs in chromosome 4 and consisted of 8 exons and 7 introns. The first two exons, designated exon 1 and exon 1', are alternatively spliced to common exon 2, and thus the AQPap gene possessed two potential promoters. The exon 1-derived transcript is dominant in both adipose tissues and adipocytes on the basis of RNase protection assay and promoter analysis. The mRNA increased after fasting and decreased with refeeding. Insulin deficiency generated by streptozotocin enhanced the mRNA in adipose tissue. Insulin down-regulated AQPap mRNA in 3T3-L1 adipocytes. The AQPap promoter contained heptanucleotide sequences, TGTTTTT at -443/-437, similar to the insulin-response element identified previously in the promoters of insulin-repressed genes. Deletion and single base pair substitution analysis of the promoter revealed that these sequences were required for insulin-mediated repression of AQPap gene transcription. The phosphatidylinositol 3-kinase pathway was involved in this inhibition. We conclude that insulin represses the transcription of AQPap gene via insulin response element in its promoter. Sustained up-regulation of AQPap mRNA in adipose tissue in the insulin-resistant condition may disturb glucose homeostasis by increasing plasma glycerol.

3T3 Cells↗
PubMed2001

Galectin-12, an Adipose-expressed Galectin-like Molecule Possessing Apoptosis-inducing Activity.

Galectins constitute a family of proteins that bind to beta-galactoside residues and have diverse physiological functions. Here we report on the identification of a galectin-like molecule, galectin-12, in a human adipose tissue cDNA library. The protein contained two potential carbohydrate-recognition domains with the second carbohydrate-recognition domain being less conserved compared with other galectins. In vitro translated galectin-12 bound to a lactosyl-agarose column far less efficiently than galectin-8. Galectin-12 mRNA was predominantly expressed in adipose tissue of human and mouse and in differentiated 3T3-L1 adipocytes. Caloric restriction and treatment of obese animals with troglitazone increased galectin-12 mRNA levels and decreased the average size of the cells in adipose tissue. The induction of galectin-12 expression by the thiazolidinedione, troglitazone, was paralleled by an increase in the number of apoptotic cells in adipose tissue. Immunocytochemical analysis revealed that galectin-12 was localized in the nucleus of adipocytes, and transfection with galectin-12 cDNA induced apoptosis of COS-1 cells. These results suggest that galectin-12, an adipose-expressed galectin-like molecule, may participate in the apoptosis of adipocytes.

3T3 Cells↗
PubMed2001

Adipocyte-derived plasma protein, adiponectin, suppresses lipid accumulation and class A scavenger receptor expression in human monocyte-derived macrophages.

BACKGROUND: Excessive lipid accumulation in macrophages plays an important role in the development of atherosclerosis. Recently, we discovered an adipocyte-specific plasma protein, adiponectin, that is decreased in patients with coronary artery disease. We previously demonstrated that adiponectin acts as a modulator for proinflammatory stimuli and inhibits monocyte adhesion to endothelial cells. The present study investigated the effects of adiponectin on lipid accumulation in human monocyte-derived macrophages. METHODS AND RESULTS: Human monocytes were differentiated into macrophages by incubation in human type AB serum for 7 days, and the effects of adiponectin were investigated at different time intervals. Treatment with physiological concentrations of adiponectin reduced intracellular cholesteryl ester content, as determined using the enzymatic, fluorometric method. The adiponectin-treated macrophages contained fewer lipid droplets stained by oil red O. Adiponectin suppressed the expression of the class A macrophage scavenger receptor (MSR) at both mRNA and protein levels by Northern and immunoblot analyses, respectively, without affecting the expression of CD36, which was quantified by flow cytometry. Adiponectin reduced the class A MSR promoter activity, as measured by luciferase reporter assay. Adiponectin treatment dose-dependently decreased class A MSR ligand binding and uptake activities. The mRNA level of lipoprotein lipase as a marker of macrophage differentiation was decreased by adiponectin treatment, but that of apolipoprotein E was not altered. Adiponectin was detected around macrophages in the human injured aorta by immunohistochemistry. CONCLUSIONS: The adipocyte-derived plasma protein adiponectin suppressed macrophage-to-foam cell transformation, suggesting that adiponectin may act as a modulator for macrophage-to-foam cell transformation.

Adipocytes↗
PubMed2001

Cysteine conjugate of methazolamide is metabolized by beta-lyase.

Bovine kidney and liver homogenates degraded a cysteine conjugate of methazolamide, S-(5-acetylimino-4-methyl-Delta2-1,3,4-thiadiazolin-2-yl)cysteine. We isolated the degradation product following incubation with kidney homogenate by high-performance liquid chromatography on reversed-phase columns. The chemical structure was confirmed by proton and carbon-13 nuclear magnetic resonance spectroscopy (1H NMR and 13C NMR, respectively), and elemental analysis by high-resolution mass spectrometry to be N-(3-methyl-5-mercapto-Delta4-1,3,4-thiadiazol-2-yl)acetamide, a thiol compound. The reaction is thought to be catalyzed by a pyridoxal-dependent enzyme(s) as indicated by an inhibition study using aminooxyacetic acid. Possible involvement of the thiol compound in the development of an adverse effect is discussed.

Animals↗
PubMed2001

High-performance liquid chromatographic procedure for routine residue monitoring of seven sulfonamides in milk.

A simplified method for routine monitoring of 7 residual sulfonamides (SAs) (sulfadiazine (SDZ), sulfamerazine (SMR), sulfadimidine (SDD), sulfamonomethoxine (SMM), sulfamethoxazole (SMX), sulfadimethoxine (SDM), and sulfaquinoxaline (SQ)) in milk using high-performance liquid chromatography (HPLC) with a photodiode array detector is described. The spiked and blank samples were cleaned up by using an Ultrafree-MC/PL centrifugal ultrafiltration unit. For determination/identification, a Mightysil RP-4 GP column and a mobile phase of 25% (v/v) ethanol in water with a photodiode array detector were used. Average recoveries from milk samples spiked with 0.05, 0.1, 0.2, and 0.5 microg mL(-1) of each drug were >82%. The inter- and intra-assay variabilities were 2.0-3.1%. The practical detection limits for 7 SAs were 0.005-0.02 microg mL(-1). The total time and amount of solvent required for the analysis of one sample were <40 min and <6 mL of ethanol, respectively. No toxic solvents were used.

Animals↗
PubMed2001

The expression of SPARC in adipose tissue and its increased plasma concentration in patients with coronary artery disease.

OBJECTIVE: Adipocytes secrete various cytokines and matrix proteins. Several of them precipitate in obesity-associated diseases, including atherosclerosis. In the current study, we have examined the expression of secreted protein, acidic and rich in cysteine (SPARC) in adipose tissue and its significance in obesity and coronary artery disease (CAD). RESEARCH METHODS AND PROCEDURES: The SPARC mRNA expressions both in vivo and in vitro were detected by Northern blot analysis. Plasma SPARC concentrations were measured by enzyme immunosorbent assay. First, we investigated the plasma SPARC levels of 88 unrelated adult Japanese subjects (62 men and 26 women; average age: [+/- SD] 50 +/- 12 years; body mass index [BMI]: 16 to 46 kg/m(2)). Additionally 31 subjects with CAD diagnosed by coronary angiography (20 men and 11 women) were also investigated. RESULTS: Human adipose tissues expressed abundant SPARC mRNA. SPARC expression in adipose tissues was upregulated in obese db/db mice. Markedly enhanced expression of SPARC mRNA was observed in 3T3-L1 fibroblasts during adipocyte differentiation. Consistent with these results, plasma SPARC levels proved a positive correlation with BMI in humans (r = 0.27; p < 0.01). Interestingly, plasma SPARC concentrations were significantly elevated in age- and BMI-matched subjects with CAD (p < 0.05). DISCUSSION: SPARC was expressed in adipose tissues and its expression was enhanced in obese mice. In human, plasma SPARC levels were elevated in obesity and CAD patients. This elevated SPARC may be involved in the progression of CAD.

Adipose Tissue↗
PubMed2001

[Increasing incidence and the mechanism of resistance of nalidixic acid resistant Shigella sonnei].

One hundred and fourteen Shigella sonnei strains obtained in 1991 to 2000 were tested for their susceptibilities to 12 antimicrobial agents. Nalidixic acid (NA) resistance was found in 2 of 15 strains (13.3%) in 1993, 2 of 8 strains (25%) in 1996, one of 5 strains (20%) in 1998, 7 of 21 strains (33.3%) in 1999 and 6 of 12 strains (50%) in 2000. The incidence of resistance to NA in S. sonnei strains increased significantly during this period. Among those 19 NA resistant strains, 11 strains were derived from patients with traveler's diarrhea and 8 strains were derived from patients who had not traveled abroad before the infection, namely domestic patients. PFGE analysis with Xba I revealed that all strains tested differentiated into two major clonal clusters, one cluster consisted of strains derived from patients who had traveled to India after 1993, and another cluster included strains derived from domestic patients. Mechanism of NA resistance was examined by sequencing the quinolone resistance-determining region (QRDR) of gyrA gene. Among 19 NA resistant strains tested, 11 strains presented a change at Ser-83 to Leu and 7 strains presented a change at Asp-87 to Try (5 strains) or Asn (2 strains), whereas 3 NA sensitive strains had no change in the region. These findings indicated that this mutation in gyrA plays an important role in acquisition of Nalidixic-acid resistance in clinical isolates of S. sonnei.

DNA Gyrase↗
PubMed2001

PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein.

Insulin resistance and its dreaded consequence, type 2 diabetes, are major causes of atherosclerosis. Adiponectin is an adipose-specific plasma protein that possesses anti-atherogenic properties, such as the suppression of adhesion molecule expression in vascular endothelial cells and cytokine production from macrophages. Plasma adiponectin concentrations are decreased in obese and type 2 diabetic subjects with insulin resistance. A regimen that normalizes or increases the plasma adiponectin might prevent atherosclerosis in patients with insulin resistance. In this study, we demonstrate the inducing effects of thiazolidinediones (TZDs), which are synthetic PPARgamma ligands, on the expression and secretion of adiponectin in humans and rodents in vivo and in vitro. The administration of TZDs significantly increased the plasma adiponectin concentrations in insulin resistant humans and rodents without affecting their body weight. Adiponectin mRNA expression was normalized or increased by TZDs in the adipose tissues of obese mice. In cultured 3T3-L1 adipocytes, TZD derivatives enhanced the mRNA expression and secretion of adiponectin in a dose- and time-dependent manner. Furthermore, these effects were mediated through the activation of the promoter by the TZDs. On the other hand, TNF-alpha, which is produced more in an insulin-resistant condition, dose-dependently reduced the expression of adiponectin in adipocytes by suppressing its promoter activity. TZDs restored this inhibitory effect by TNF-alpha. TZDs might prevent atherosclerotic vascular disease in insulin-resistant patients by inducing the production of adiponectin through direct effect on its promoter and antagonizing the effect of TNF-alpha on the adiponectin promoter.

3T3 Cells↗
PubMed2001

Visceral fat is a major contributor for multiple risk factor clustering in Japanese men with impaired glucose tolerance.

OBJECTIVE: The significance of abdominal visceral fat accumulation was evaluated in Japanese men with impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: The IGT subjects (n = 123) were aged 55 +/- 9 years with a BMI of 24 +/- 3 kg/m(2). The 148 control subjects with normal glucose tolerance (NGT) were matched for age and BMI. IGT and NGT were classified according to the 1985 World Health Organization criteria. Abdominal fat distribution was analyzed by computed tomography at umbilical level. Plasma lipid, glucose, and insulin concentrations and blood pressure (BP) were measured. RESULTS: In subjects with IGT, the average visceral fat area (VFA) was significantly greater than in subjects with NGT. Fasting insulin, the sum of insulin concentrations during an oral glucose tolerance test, insulin resistance according to a homeostasis model assessment for insulin resistance (HOMA-IR), systolic BP, and serum triglyceride were significantly higher, whereas the DeltaI(30-0)/DeltaG(30-0) was significantly lower, in subjects with IGT. Subjects with IGT and NGT were then divided into three subgroups according to the number of risk factors they possessed (dyslipidemia, hypertension, neither, or both). In both IGT and NGT subjects, BMI, VFA, subcutaneous fat area, fasting insulin, HOMA-IR, and insulin secretion of the homeostasis model assessment were significantly higher in the double-risk factor subgroup than in the no-risk factor subgroup, and VFA was a potent and independent variable in association with the presence of a double risk factor. CONCLUSIONS: Visceral fat accumulation is a major contributor for multiple risk factor clustering in Japanese men with IGT and NGT.

Adipose Tissue↗
PubMed2001

[Evaluation of emergence from total intravenous anesthesia with propofol for long neurosurgery].

In six neurosurgical patients we examined their emergence from more than six hours of total intravenous anesthesia with propofol and fentanyl. The anesthesia was maintained properly with total intravenous anesthesia with propofol and fentanyl without nitrous oxide. We calculated the estimated blood concentration of propofol from the anesthesia record using a three-compartment pharmacokinetic model. The patients were extubated after they had shown good awareness. The average time for extubation was 18 minutes after discontinuation of propofol infusion. The mean estimated concentration of propofol at the extubation was 1.36 micrograms.ml-1 (range: 1.1-1.5 micrograms.ml-1). The estimated emergence times in these cases, also calculated with the pharmacokinetic model, correlated significantly with the time from discontinuation of propofol infusion to the patients' awakening. It was concluded, first, that the estimated concentration of propofol at extubation after long anesthesia was similar to that measured in common cases, and second, that we could reduce the emergence time at the tail end of long-sustained neurosurgery by avoiding the delay in emergence.

Adolescent↗
PubMed2000

Aquaporin adipose, a putative glycerol channel in adipocytes.

Adipose tissue is a major site of glycerol production in response to energy balance. However, molecular basis of glycerol release from adipocytes has not yet been elucidated. We recently cloned a novel member of the aquaporin family, aquaporin adipose (AQPap), which has glycerol permeability. The current study was designed to examine the hypothesis that AQPap serves as a glycerol channel in adipocytes. Adipose tissue expressed AQPap mRNA in high abundance, but not the mRNAs for the other aquaglyceroporins, AQP3 and AQP9, indicating that AQPap is the only known aquaglyceroporin expressed in adipose tissue. Glycerol release from 3T3-L1 cells was increased during differentiation in parallel with AQPap mRNA levels and suppressed by mercury ion, which inhibits the function of AQPs, supporting AQPap functions as a glycerol channel in adipocytes. Fasting increased and refeeding suppressed adipose AQPap mRNA levels in accordance with plasma glycerol levels and oppositely to plasma insulin levels in mice. Insulin dose-dependently suppressed AQPap mRNA expression in 3T3-L1 cells. AQPap mRNA levels and adipose glycerol concentrations measured by the microdialysis technique were increased in obese mice with insulin resistance. Accordingly, negative regulation of AQPap expression by insulin was impaired in the insulin-resistant state. Exposure of epinephrine translocated AQPap protein from perinuclear cytoplasm to the plasma membrane in 3T3-L1 adipocytes. These results strongly suggest that AQPap plays an important role in glycerol release from adipocytes.

3T3 Cells↗
PubMed2000

Multiple "mirror" aneurysms involving intracavernous carotid arteries and vertebral arteries: case report.

BACKGROUND: Bilateral intracavernous carotid artery aneurysms are rare. Moreover, the proportion of vertebrobasilar aneurysms in association with multiple aneurysms is extremely low. We describe a rare case of "mirror" aneurysms on the bilateral intracavernous carotid and bilateral vertebral arteries. CASE DESCRIPTION: A 54-year-old male suffered from ophthalmic pain and oculomotor palsy on the left side. Cerebral angiography disclosed a giant left cavernous aneurysm and large asymptomatic aneurysms on the right intracavernous carotid artery and bilateral vertebral arteries. The cavernous sinus syndrome on the left side was successfully treated by left carotid artery ligation. However, 2 years later, severe subarachnoid hemorrhage (SAH) occurred. Computed tomography revealed thick clots densely distributed in the basal cisterns and third and fourth ventricles, indicating that the SAH originated from one of the vertebral artery aneurysms. Consciousness disturbance progressed rapidly, leading to cardiopulmonary arrest. CONCLUSION: The literature contains no case of mirror intracranial aneurysms involving both intracavernous carotid and vertebral arteries. Multi-staged surgical techniques with optimal combinations of direct clipping, ligation or trapping, and endovascular embolization may be essential for patients with multiple aneurysms to avoid SAH.

Carotid Artery Diseases↗
PubMed2000

Catheter interventional treatment in Kawasaki disease: A report from the Japanese Pediatric Interventional Cardiology Investigation group.

OBJECTIVE: To assess the current status of catheter intervention in Kawasaki disease and to evaluate its efficacy and outcome. STUDY DESIGN: A questionnaire was sent to 55 major institutions in Japan. RESULTS: A total of 58 procedures in 57 patients were reported. The median age at the time of intervention was 12.1 years. The procedures included percutaneous transluminal coronary angioplasty (PTCA; n = 34), percutaneous transluminal coronary rotational ablation (PTCRA; n = 13), directional coronary atherectomy (DCA; n = 4), and stent implantation (n = 7). The immediate success rate was 74% for PTCA, 100% for PTCRA, 100% for DCA, and 86% for stents. The interval from the onset of disease to intervention in successful PTCA (n = 25) was significantly shorter than that in unsuccessful PTCA (n = 9). Restenosis after PTCA was observed in 24%. Development of new coronary aneurysms was reported in 3 patients for PTCA, 2 for PTCRA, 3 for DCA, and 1 for stents. Except for the DCA, all new aneurysms were associated with the use of high-pressure balloon inflation. Two deaths were reported as acute complications. CONCLUSIONS: Catheter intervention is a promising therapeutic strategy in the management of coronary stenosis caused by Kawasaki disease. Care should be paid to avoid acute coronary arterial complications and the development of new coronary aneurysms.

Adolescent↗