Search PubMed⌕ Search

Biomedical subjects

T Matsuzaki

Publications and source records attributed to T Matsuzaki.

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

Effect of 1-week treatment with erythropoietin on the vascular endothelial function in anaesthetized rabbits.

Chronic administration of erythropoietin (EPO) is often associated with hypertension in animals and humans. The aim of this study was to estimate whether 1-week treatment with EPO can affect the vascular endothelial function. Rabbits were given with EPO (400 iu kg(-1) s.c.) or saline each other day for 1 week. Hypotensive responses to intravenously given acetylcholine (ACh), endothelium-independent nitric oxide donors (NOC7, nitroprusside and nitroglycerin) and prostaglandin I2 were tested before and after administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a specific nitric oxide synthase inhibitor, under pentobarbitone anaesthesia. Blood haemoglobin concentration in EPO group was significantly higher than that in control group, whereas baseline values of aortic pressure, heart rate and femoral vascular resistance were similar. The dose of ACh (172 ng kg(-1)) requiring for a 15 mmHg hypotension from the baseline in EPO group was apparently higher than that (55 ng kg(-1)) in control group. On the contrary, hypotensive responses to NOC7, nitroprusside, nitroglycerin and prostaglandin I2 were comparable between two groups. The extent of ACh-induced hypotension did not correlate with haemoglobin concentration. L-NAME significantly inhibited the ACh-induced vasodilating response in control group but did not in EPO group. In another set of rabbits, the same treatment with EPO also decreased vasodilating responses to carbachol, bradykinin and substance P besides ACh as compared with control group. These results indicate that 1-week treatment with EPO selectively attenuates depressor responses to endothelium-dependent vasodilators in anaesthetized rabbits, most likely due to inhibition of endothelial nitric oxide synthase.

Acetylcholine↗
PubMed2001

beta-Adrenoceptor blocking activities of nipradilol and its optical isomers in pig coronary artery.

1. beta-Adrenoceptor blocking activities of nipradilol, its four optical isomers (RR, RS, SR, SS) and denitro nipradilol were evaluated using pig isolated coronary arteries. 2. (-)-Isoprenaline produced concentration-dependent relaxations of the arteries, which were antagonized by nipradilol, its four optical isomers or denitro nipradilol under KCl-induced contracture. 3. The order of pA2 values for beta-adrenoceptor blocking activities was SR > nipradilol > SS > or = denitro nipradilol > RR > RS. 4. The nitroxy group in nipradilol appears to enhance its beta-adrenoceptor blocking activity, because the beta-adrenoceptor blocking activity of nipradilol was more potent than that of denitro nipradilol. 5. Isomers that have the S configuration (SR, SS) at the 2' position (having a hydroxyl group) in the aryloxypropanolamine showed more potent beta-adrenoceptor blocking activity than isomers that have the R configuration (RR, RS). 6. Isomers that have the R configuration (SR, RR) at the 3 position (having a nitroxy group) in the benzopyran ring showed more potent beta-adrenoceptor blocking activity than those with the S configuration (SS, RS). 7. It is suggested that the difference in configuration of the chemical structure of nipradilol may result in variations of binding affinity for the beta-adrenoceptor.

Adrenergic beta-Agonists↗
PubMed2001

The apical localization of SGLT1 glucose transporter is determined by the short amino acid sequence in its N-terminal domain.

SGLT1, an isoform of Na+-dependent glucose cotransporters, is localized at the apical plasma membrane in the epithelial cells of the small intestine and the kidney, where it plays a pivotal role in the absorption and reabsorption of sugars, respectively. To search the domain responsible for the apical localization of SGLT1, we constructed an N-terminal deletion clone series of rat SGLT1 and analyzed the localization of the respective products in Madin-Darby canine kidney (MDCK) cells. The products of N-terminal deletion clones up to the 19th amino acid were localized at the apical plasma membrane, whereas the products of N-terminal 20- and 23-amino-acid deletion clones were localized along the entire plasma membrane. Since single-amino-acid mutations of either D28N or D28G in the N-terminal domain give rise to glucose/galactose malabsorption disease, we examined the localization of these mutants. The products of D28N and D28G clones were localized in the cytoplasm, showing that the aspartic acid-28 may be essential for the delivery of SGLT1 to the plasma membrane. These results suggest that a short amino acid sequence of the N-terminal domain of SGLT1 plays important roles in plasma membrane targeting and specific apical localization of the protein.

Amino Acid Sequence↗
PubMed2001

Muscle plasma membrane changes in dystrophin gene exon 52 knockout mouse.

Changes in muscle plasma membranes in mice lacking exon 52 of the dystrophin gene (mdx52 mouse) were studied using the freeze-fracture technique. The extensor digitorum longus (EDL) muscle plasma membrane of the mdx52 mouse at 8 weeks of age showed significantly increased caveola density (p < 0.05 by two-tailed t-test) and significantly decreased densities of intramembranous particles (IMPs), orthogonal arrays (OAs) and orthogonal array subunit particles (OASPs) (p < 0.05 by two-tailed t-test, p < 0.01 by Wilcoxon rank-sum test, p < 0.05 by two-tailed t-test, respectively) on the protoplasmic face when compared with those of control EDL muscles. These changes are more similar to those seen in DMD than those in the mdx mouse at the same age as reported previously. Thus, the gene abnormality in the different exon of the mouse dystrophin gene seems to induce somewhat different changes in the muscle plasma membrane.

Animals↗
PubMed2001

HTLV-I proviral load correlates with progression of motor disability in HAM/TSP: analysis of 239 HAM/TSP patients including 64 patients followed up for 10 years.

To clarify clinical and laboratory findings that may be related to the pathomechanism of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), we analyzed these findings in 239 patients with HAM/TSP, including 64 patients followed up for 10 years after their first examinations, with special interest in the HTLV-I proviral load in peripheral blood mononuclear cells (PBMCs). The proviral load in PBMCs did not differ in terms of modes of HTLV-I transmission. However, the proviral load in patients with age of disease onset greater than 65 years tended to be higher than those with a younger age of onset. In the 64 patients followed up for 10 years, the clinical symptoms deteriorated in 36 patients (56%), unchanged in 26 patients (41%), and improved in 2 patients (3%). HTLV-I proviral load also appeared to be related to the deterioration of motor disability in these patients. To our knowledge, the present study is the first longitudinal study concerning the relationship between the clinical course of HAM/TSP and HTLV-I proviral load. It is suggested that HTLV-I proviral load is related to the progression of motor disability and is an important factor to predict prognosis of patients with HAM/TSP.

Age of Onset↗
PubMed2001

Enhancement of natural killer cytotoxicity delayed murine carcinogenesis by a probiotic microorganism.

Regulation of innate immunity may be an effective means of cancer control. Delaying cancer onset is regarded as an important mode of action in cancer prevention. We have been investigating the chemopreventive mechanisms of Lactobacillus casei Shirota (LcS), a probiotic strain. In this study, we evaluated the effect of LcS on tumor onset and the involvement of natural killer (NK) cells using a 3-methylcholanthrene-induced carcinogenesis model. C3H/HeN mice were divided into three groups, according to treatment: vehicle-treated, treated with vehicle only; control, 3-methylcholanthrene treated; LcS, 3-methylcholanthrene and LcS treated. 3-Methylcholanthrene was injected intradermally at 7 weeks of age. LcS was mixed into the diet (0.05%, w/w), which the mice were fed from the day of 3-methylcholanthrene injection onward. Tumor incidence was observed weekly. Profiles of splenic NK cells, in vitro cytotoxicity and the proportion, in the early stage of carcinogenesis were analyzed at 5 weeks after the injection. The tumor suppressive effect of LcS was also evaluated in a beige mouse model that is genetically deficient in NK cells. LcS delayed tumor onset and reduced tumor incidence in the results with C3H/HeN mice (P< 0.05). More specifically, tumor incidence in the control group was 33% at 6 weeks after the injection and 83% at 11 weeks as opposed to 0 and 42%, respectively, in the LcS group. NK cell cytotoxicity was significantly higher than in the control group, and the number of NK cells also increased in the LcS group of C3H/HeN mice. However, LcS failed to suppress tumorigenesis in the beige mouse. These findings suggest that enhancement of the cytotoxicity of NK cells by LcS delays tumor onset.

Animals↗
PubMed2001

Hypertonicity-induced expression of aquaporin 3 in MDCK cells.

Aquaporins (AQPs) are water channel proteins that participate in water transport. In the principal cells of the kidney collecting duct, water reabsorption is mediated by the combined action of AQP2 in the apical membrane and both AQP3 and AQP4 in the basolateral membrane, and the expression of AQP2 and AQP3 is regulated by antidiuretic hormone and water restriction. The effect of hypertonicity on AQP3 expression in Madin-Darby canine kidney (MDCK) epithelial cells was investigated by exposing the cells to hypertonic medium containing raffinose or NaCl. Northern blot and immunoblot analyses revealed that the amounts of AQP3 mRNA and AQP3 protein, respectively, were markedly increased by exposure of cells to hypertonicity. These effects were maximal at 12 and 24 h, respectively. Immunofluorescence and immunoelectron microscopy also demonstrated that the abundance of AQP3 protein was increased in cells incubated in hypertonic medium and that the protein was localized at the basolateral plasma membrane. These results indicate that the expression of AQP3 is upregulated by hypertonicity.

Animals↗
PubMed2001

Resting ultrasonic tissue characterization and dobutamine stress echocardiography for prediction of functional recovery in chronic left ventricular ischemic dysfunction.

This study was designed to assess the diagnostic accuracy of the percentage of resting systolic wall thickening (WT), dobutamine stress echocardiography (DSE), resting cyclic variation of integrated backscatter (IBS-CV), and low-dose dobutamine stress IBS-CV (DSE-IB) for the prediction of regional function recovery (RFR) in patients with chronic left ventricular (LV) ischemic dysfunction. The study also evaluated whether or not global LV function affected the diagnostic accuracy. All studies were conducted before percutaneous transluminal coronary angioplasty (PTCA) and RFR was assessed after PTCA (mean interval, 10 months) in 30 patients with chronic LV ischemic dysfunction. Patients were divided into 2 groups according to the LV ejection fraction (LVEF): group A, LVEF<40%, n=14; group B, LVEF> or =40%, n=16. Of a total of 480 segments, 37 initially demonstrating akinetic wall motion before PTCA were analyzed. The wall motion of 24 of the 37 segments improved on visual analysis after PTCA. In the prediction of RFR, resting WT, DSE, resting IBS-CV and DSE-IB had sensitivities of 79%, 79%, 92% and 62%, and specificities of 54%, 84%, 83% and 69%, respectively. In particular, the resting IBS-CV in group A, as well as DSE, was an excellent predictor of RFR (sensitivity, 100%; specificity, 86%; vs sensitivity, 82%; specificity, 78%; respectively). Therefore, both resting IBS-CV and DSE are useful predictors for RFR in patients with chronic LV ischemic dysfunction.

Aged↗
PubMed2001

Effects of leptin on secretion of LH and FSH from primary cultured female rat pituitary cells.

BACKGROUND: Leptin, which is the product of the obese gene, is believed to play important roles in pubertal development and reproductive function in females. In a study using adult male rats, it was found that leptin stimulated secretion of gonadotropin from the pituitary in a dose-related manner. However, there has been no such study in female rats. OBJECTIVE: To investigate the effects of leptin on the production of LH and FSH from the pituitary in female rats, using primary cultured pituitary cells. METHODS: In this study, we determined body weight, serum leptin concentration and serum estradiol (E(2)) concentration in female Wistar rats at 3, 5, 6, 7, 9 and 11 weeks of age, and cultured pituitary cells from 6-week-old female Wistar rats with leptin (0--10(-7) mol/l) and GnRH (0 or 10(-8) mol/l). Then basal and GnRH-stimulated extra- and intracellular LH and FSH were assayed by RIA. RESULTS: Serum leptin concentration increased with increases in body weight and E(2) concentration. The pubertal serum leptin concentration was about 10(-10) mol/l. At a lower or moderate concentration, leptin produced dose-related increases in both basal and GnRH-stimulated extra- and intracellular LH and FSH in pituitary cells. At a concentration of 10 mol/l, leptin significantly (P<0.05) stimulated both basal and GnRH-stimulated extra- and intracellular LH and FSH. However, at greater concentrations, these effects diminished. CONCLUSIONS: These results indicated that leptin induced pituitary cells to produce and secrete both LH and FSH, with or without GnRH. The concentration of leptin that induced the greatest production of gonadotropins by pituitary cells was 10(-10) mol/l, which was the same as the physiological pubertal concentration. Leptin may be involved in the onset of puberty. It is also conceivable that leptin may be a cause of ovulatory failure, not only in weight loss but also in weight gain.

Animals↗
PubMed2000

Kdap, a novel gene associated with the stratification of the epithelium.

The skin develops and differentiates during embryogenesis, which is concertedly regulated by a variety of genes. The present study isolated from the rat embryonic skin a novel differentiation-associated gene named Kdap (keratinocyte differentiation-associated protein) by suppression subtractive hybridization between the skin of 14day postcoitus (dpc) embryo (the prehair-germ stage) and that of 17dpc embryo (the hair-germ stage). Its mRNA contained four spliced forms in these tissues. The gene encoded a protein of total 98 amino acids with a calculated molecular mass of 11kDa and an isoelectric point of 6.1 as an unspliced form. The two splicing zones were well conserved among rat, mouse, and human. This protein had a high hydrophobic N-terminal region, a possible signal sequence, and contained two putative N-myristoylation sites and two casein kinase II phosphorylation sites. In situ hybridization experiments detected Kdap transcripts exclusively in the suprabasal cell layers of the embryonic epidermis. Intense expression was also seen in suprabasal cells in regions of infundibulum of the hair follicle. These results indicated that Kdap provides a new insight into the mechanism of differentiation and the maintenance of stratified epithelia.

Amino Acid Sequence↗
PubMed2000

Diarylheptanoids suppress expression of leukocyte adhesion molecules on human vascular endothelial cells.

Diarylheptanoids possess potent anti-inflammatory properties. However, the mechanism of their action is not fully understood. In this study, we found that three diarylheptanoids, 1-(3, 5-dimethoxy-4-hydroxyphenyl)-7-phenylhept-1-en-3-one (YPE-01), yakuchinone B and demethyl-yakuchinone B, reduced the adhesion of both human monocytic cell line U937 and human eosinophilic cell line EoL-1 cells to tumor necrosis factor-alpha (TNF-alpha)-treated human umbilical vein endothelial cells. In addition, they suppressed interleukin-1beta- or TNF-alpha-induced expression of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on the surface of the endothelial cells. Since YPE-01 reduced both VCAM-1 and ICAM-1 mRNA induction in TNF-alpha-stimulated endothelial cells, diarylheptanoids appeared to suppress adhesion molecule expression at the transcriptional level. Furthermore, YPE-01 suppressed both VCAM-1 and ICAM-1 mRNA induction as well as edema in 12-O-tetradecanoylphorbol 13-acetate (TPA)-inflamed mice ears in vivo. These results suggest that the anti-inflammatory action of diarylheptanoids is, at least in part, due to their suppressive effect on the surface expression of inducible adhesion molecules in endothelial cells, and subsequent leukocyte adhesion.

Animals↗
PubMed2000

Induction of erythroid differentiation by inhibition of Ras/ERK pathway in a friend murine leukemia cell line.

The role of Ras and MAP kinases (MAPKs) in the regulation of erythroid differentiation was studied using a cell line (SKT6) derived from Friend virus (Anemic strain)-induced murine erythroleukemia. This cell line undergoes differentiation in vitro in response to erythropoietin (EPO) or other chemical inducers such as dimethylsulfoxide (DMSO). When a constitutively active ras mutant (ras12V) was expressed in SKT6 cells, EPO-induced differentiation was inhibited. Conversely, a dominant negative ras mutant (ras17N) induced differentiation even in the absence of EPO, suggesting that the basal Ras activity is essential for the maintenance of the undifferentiated phenotype and proliferative potential in this cell line. Rapid inactivation of ERK was observed after expression of ras17N. Slow but significant inactivation of ERK was also observed during EPO-induced differentiation. Furthermore, overexpression of a constitutively active mutant of ERK-activating kinase (MAPKK) was found to suppress erythroid differentiation, while pharmacological inhibition of MAPKK induced differentiation. These findings suggest that down-regulation of Ras/ERK signaling pathway may be an essential event in EPO-induced erythroid differentiation in this system.

Androstadienes↗
PubMed2000

Identification and characterization of a PDZ protein that interacts with activin type II receptors.

We have identified a mouse PDZ protein that interacts with the activin type IIA receptor (ActRIIA), which we named activin receptor-interacting protein 1 (ARIP1). By using yeast two-hybrid screening, we isolated a cDNA clone of ARIP1 from a mouse brain cDNA library. We detected two forms of ARIP1, ARIP1-long and ARIP1-short, which may be produced by alternative splicing. ARIP1-long had one guanylate kinase domain in the NH(2)-terminal region, followed by two WW domains and five PDZ domains (PDZ1-5). ARIP1-short had a deletion in the NH(2)-terminal region and lacked the guanylate kinase domain. Both forms interacted with ActRIIA through PDZ5. The COOH-terminal residues of ActRIIA (ESSL) agree with a PDZ-binding consensus motif, and ARIP1 recognized the consensus sequence. ARIP1 interacts specifically with ActRIIA among the receptors for the transforming growth factor beta family. Interestingly, ARIP1 also interacted with Smad3, which is an activin/transforming growth factor beta intracellular signaling molecule. The mRNA of ARIP1 was more abundant in the brain than in other tissues. Overexpression of ARIP1 controls activin-induced and Smad3-induced transcription in activin-responsive cell lines. These findings suggest that ARIP1 has a significant role in assembling activin signaling molecules at specific subcellular sites and in regulating signal transduction in neuronal cells.

Activin Receptors↗
PubMed2000

Proteomic analysis of Epstein-Barr virus-transformed human B-lymphoblastoid cell lines before and after immortalization.

Infection of human B lymphocytes with Epstein-Barr virus (EBV) induces proliferative B-lymphoblastoid cell lines (LCLs). However, the majority of EBV-transformed LCLs are mortal and unable to avoid cellular senescence. In our previous experiment, three immortalized LCLs were established by passages of EBV-transformed LCLs for nearly five years accompanied by strong telomerase activity. In the present study, proteomic profiles of these three LCLs were analyzed comparatively at the early and the late passages of cell culture, and a protein spot was found which most significantly decreased with the immortalization in two LCLs. The expression of the protein in the third LCL was suppressed at 17 population doubling level (PDL), already suggesting that part of the immortalization process had been initiated before 17 PDL. The protein was assigned to ssp7001 (16.3 kDa, pI 6.0) by referring to our TMIG-2DPAGE proteome database. The protein was transferred onto a polyvinylidene difluoride (PVDF) membrane and digested with lysilendopeptidase to perform peptide mass fingerprinting by nanoelectrospray ionization mass spectrometry (nano-ESI-MS). Subsequent MS-Fit database search indicated that ssp7001 is a phosphoprotein stathmin. This speculation was confirmed by the tandem MS (MS/MS) analysis in a Q-Tof system and by Edman degradation microsequencing.

Amino Acid Sequence↗
PubMed2000

Development of invasive adenocarcinoma in a long-standing diverted ileal J-pouch for ulcerative colitis: report of a case.

We report a case of a 50-year-old male with ulcerative colitis who developed well-differentiated adenocarcinoma in the ileal J-pouch, which had been defunctioning for 18 years. The extension of the carcinoma in the pouch suggested that it had recently appeared in the pouch. Monitoring by endoscopic examination and biopsy or pouch excision seems to be an appropriate action if a pouch is out of the fecal stream.

Adenocarcinoma↗
PubMed2000

A major metabolite of aceclofenac, 4'-hydroxy aceclofenac, suppresses the production of interstitial pro-collagenase/proMMP-1 and pro-stromelysin-1/proMMP-3 by human rheumatoid synovial cells.

OBJECTIVE AND DESIGN: We examined the effects of aceclofenac and its metabolites on the production of pro-collagenase-1/pro-matrix metalloproteinase-1 (proMMP-1), pro-gelatinase A/proMMP-2, pro-stromelysin-1/proMMP-3 and tissue inhibitor of metalloproteinases-1 (TIMP-1) by rheumatoid synovial cells. MATERIALS: Synovial cells were obtained from patients with rheumatoid arthritis. TREATMENT: Cultures of confluent cells were treated with interleukin-1beta (IL-1beta)(1 ng/ml) and/or test drugs (0.3-30 microM) for 48 h. METHODS: Production of proMMPs and TIMP-1 was monitored by Western blotting or gelatin zymography. Prostaglandin E2 (PGE2) was measured by an enzyme immunoassay. RESULTS: 4'-Hydroxy aceclofenac, a major metabolite of aceclofenac, down-regulated both basal and IL-1beta-induced production of proMMP-1 and proMMP-3 at a concentration sufficient to suppress PGE2 production without modulating proMMP-2 or TIMP-1, whereas aceclofenac itself had no marked effect on the production of proMMPs. CONCLUSIONS: Down-regulation of proMMP-1 and proMMP-3 production by 4'-hydroxy aceclofenac may contribute to the therapeutic effect of aceclofenac on rheumatoid arthritis and osteoarthritis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Reference data of forearm bone mineral density in healthy Japanese male and female subjects in the second decade based on calendar age and puberty onset: Japanese Population Based Osteoporosis (JPOS) study.

Osteoporosis is a major public health problem in Japan. The second decade is an important period in which to attain a high peak bone mass. However, normal values of forearm bone mineral density (BMD) are not well known in children and adolescents. BMD at one-third of forearm length proximal to the ulnar end plate (BMD1/3) and the ultradistal forearm (BMDud) was measured using dual-energy X-ray absorptiometry (DXA) in 1207 (631 males, 576 females) Japanese subjects aged 9-18 years. Puberty onset was assessed by questionnaire, by obtaining the time that pubic hair appeared in males and the time that menstruation started in females. BMD1/3 and BMDud increased steadily with age in males. In relation to puberty development, these parameters also increased after puberty onset although the increase in BMD1/3 was not statistically significant after the fifth year from puberty onset and that of BMDud was not significant after the sixth year from puberty onset. BMD1/3 and BMDud increased with age and then plateaued in females. The increase in BMD1/3 was not statistically significant after 15-16 years of age and that of BMDud was not significant after 13-14 years of age. In relation to puberty development, the increase in BMD1/3 leveled out after the fourth year from puberty onset and that of BMDud also plateaued after the third year from puberty onset. We provide reference values of forearm BMD in Japanese children and adolescents by DXA according to calendar age and puberty development. Peak bone mass of the forearm may be in the late second decade in Japanese females.

Absorptiometry, Photon↗