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Biomedical subjects

K Hara

Publications and source records attributed to K Hara.

At least 91 records · Page 5Linked to original sources
PubMed2001

Characterization of two genes, Sig1 and Sig2, encoding distinct plastid sigma factors(1) in the moss Physcomitrella patens: phylogenetic relationships to plastid sigma factors in higher plants.

We isolated the cDNA for a sigma factor from the moss Physcomitrella patens, which possesses unusually large N-terminal extension and the conserved subdomains 1.2-4.2. Phylogenetic analyses indicated that this novel sigma factor and PpSIG1*(2), a plastid sigma factor previously identified from Physcomitrella, were classified into SigA and SigB groups, two major classes of higher plant plastid sigma factors, respectively. According to the nomenclature recently proposed, we renamed PpSIG1* into PpSIG2, and named the novel sigma factor PpSIG1. A transient expression assay using a green fluorescent protein showed that the N-terminal region of PpSIG1 acts as a chloroplast-targeting signal. Reverse transcription-PCR experiments showed that light induces the expression of the Sig1 and Sig2 genes encoding PpSIG1 and PpSIG2, respectively. Thus, PpSIG1 and PpSIG2 are likely plastid sigma factors regulating plastid gene expression in response to light signals.

Amino Acid Sequence↗
PubMed2001

Measurement of B(0)(d)-B_(0)(d) mixing rate from the time evolution of dilepton events at the upsilon(4S).

We report a determination of the B(0)(d)-&B_(0)(d) mixing parameter Deltam(d) based on the time evolution of dilepton yields in Upsilon(4S) decays. The measurement is based on a 5.9 fb(-1) data sample collected by the Belle detector at KEKB. The proper-time difference distributions for same-sign and opposite-sign dilepton events are simultaneously fitted to an expression containing Deltam(d) as a free parameter. Using both muons and electrons, we obtain Deltam(d) = 0.463+/-0.008 (stat)+/-0.016 (syst) ps(-1). This is the first determination of Deltam(d) from time evolution measurements at the Upsilon(4S). We also place limits on possible CPT violations.

Journal Article↗
PubMed2001

Measurement of the CP violation parameter sin2 phi(1) in B(0)(d) meson decays.

We present a measurement of the standard model CP violation parameter sin2 phi(1) (also known as sin2beta) based on a 10.5 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric e(+)e(-) collider. One neutral B meson is reconstructed in the J/psiK(S), psi(2S)K(S), chi(c1)K(S), eta(c)K(S), J/psiK(L), or J/psipi(0) CP-eigenstate decay channel and the flavor of the accompanying B meson is identified from its charged particle decay products. From the asymmetry in the distribution of the time interval between the two B-meson decay points, we determine sin2 phi(1) = 0.58(+0.32)(-0.34)(stat)+0.09-0.10(syst).

Journal Article↗
PubMed2001

Cloning and characterization of the cDNA for a plastid sigma factor from the moss Physcomitrella patens.

We isolated a cDNA PpSig1 encoding a plastid sigma factor from the moss Physcomitrella patens. The PpSIG1 protein is composed of the conserved subdomains for recognition of -10 and -35 promoter elements, core complex binding and DNA melting. Southern blot analysis showed that the moss sig1 gene is likely a member of a small gene family. Transient expression assay using green fluorescent protein demonstrated that the N-terminal region of PpSIG1 functions as a chloroplast-targeting signal peptide. These observations suggest that multiple nuclear-encoded sigma factors regulate chloroplast gene expression in P. patens.

Amino Acid Sequence↗
PubMed2001

Cloning and functional expression of a degradation-resistant novel isoform of p27Kip1.

p27(Kip1) is an inhibitor of cyclin-dependent kinases. It has been implicated as having a role in the induction of growth arrest at the G(1) phase of the cell cycle in response to anti-mitogenic signals such as cell contact and serum starvation. Proteasome-mediated degradation plays an important role in the rapid inactivation of p27(Kip1), causing quiescent cells to re-enter the cell cycle. Although the existence of a second isoform has been suggested, no such isoform was isolated. Through screening of a cDNA library derived from growth-arrested confluent porcine endothelial cells, we obtained clones for a novel isoform of p27(Kip1) in addition to the original isoform. The novel isoform differed from the original isoform at the C-terminus. The tissue-specific expression of the original and novel isoforms was demonstrated at the mRNA and protein levels. An in vitro degradation assay demonstrated this novel isoform to be resistant to proteasome-mediated destruction. The expression as a fusion protein with green fluorescent protein revealed this isoform to be targeted to the nucleus by a bipartite nuclear-localization signal with a C-terminal part different from that of the original isoform. The expression of the novel isoform caused the growth arrest of HeLa cells and an accumulation of cells in the G(0)/G(1) phase, and this effect was similar to that seen with the original isoform. The present study suggests that the novel isoform functions as a negative regulator of the cell cycle, and may play a distinct role. The novel isoform was named p27(Kip1R) because of its resistance to degradation.

Alternative Splicing↗
PubMed2001

Variants of neurogenin 3 gene are not associated with Type II diabetes in Japanese subjects.

AIMS/HYPOTHESIS: Neurogenin 3 (ngn3) is a transcription factor expressed in the endocrine precursor cells of the pancreas. It has recently been reported that ngn3-deficient mice show absence of pancreatic endocrine cells and die of postnatal diabetes. The purpose of this investigation was to screen for polymorphisms of the ngn3 gene and to test whether these polymorphisms are associated with Type II (non-insulin-dependent) diabetes mellitus in the Japanese subjects. METHODS: We screened ngn3 gene and upstream region by direct sequencing and estimated the prevalence of polymorphisms in 197 patients with Type II (non-insulin-dependent) diabetes mellitus and 216 control subjects. RESULTS: We identified four novel polymorphisms, Ser199Phe (596C/T), -43insCA, -983C/T and -1822G/A. In an association study the allelic frequencies of the major allele of these four polymorphisms were 0.721, 0.914, 0.912 and 0.530 in diabetic patients, respectively, and 0.694, 0.905, 0.917 and 0.537 in control subjects, respectively. CONCLUSION/INTERPRETATION: Mutations and polymorphisms of ngn3 gene are not significantly associated with Type II (non-insulin-dependent) diabetes mellitus in the Japanese subjects.

Aged↗
PubMed2001

Inhibitory role of eosinophils on cell surface plasmin generation by bronchial epithelial cells: inhibitory effects of transforming growth factor beta.

Eosinophilic bronchitis is an essential component of bronchial asthma, and eosinophils play an important role. We studied the effect of eosinophils on cell surface plasmin generation by bronchial epithelial cells, because plasmin is thought to be involved in bronchial tissue repair/remodeling by means of fibrinolysis and the activation of proteases such as matrix metalloproteases. Plasmin was generated from exogenous plasminogen on the cell surface of cultured bronchial epithelial cells, NCI-H292. Transforming growth factor beta (TGF-beta) treatment resulted in reduced cell surface plasmin generation and a large increase in plasminogen activator inhibitor-type 1 (PAI-1) antigen production in NCI-H292 cells, whereas no conspicuous effects were observed with IL-1 beta and TNF alpha treatment (regulators in pulmonary epithelial cells). On the other hand, this cell surface plasmin generation was reduced by co-incubation with Eol-1, an eosinophil cell line. The addition of TGF-beta antisense and anti-TGF-beta antibodies attenuated this adverse effect of Eol-1 cell co-incubation. These data suggest that eosinophils play an inhibitory role on cell surface plasmin generation by bronchial epithelial cells by means of the up-regulation of PAI-1 expression induced by TGF-beta. Therefore, the accumulation of eosinophils in bronchial walls is thought to be involved in bronchial tissue repair/remodeling in asthma through this protease network.

Asthma↗
PubMed2001

Evidence for infection with Helicobacter pylori in patients with acute myocardial infarction.

BACKGROUND: Anti-Helicobacter pylori (HP) IgA and IgG antibody titers were measured in patients with ischemic heart diseases. METHODS: There were 60 healthy individuals that served as control subjects, and 21 patients with acute myocardial infarction (AMI), 34 with old myocardial infarctions (OMI), 35 with effort angina (AP) and 41 with vasospastic angina (VSA). RESULTS: In the control group, the IgA and IgG anti-HP antibody titers were positively correlated with age. When the IgA and IgG antibody titers were compared among patient groups, IgG did not significantly differ between each patient group and the control group, whereas IgA was significantly higher in the AMI group (5.10+/-1.25 EV) than in the OMI (p<0.01), AP, or the control (p<0.05). Moreover, the positivity rate for IgA anti-HP antibody was the highest in the AMI group (90%), with an odds ratio to the age-matched control group of 4.09, whereas the positivity rate for IgG did not significantly differ between the groups when either the 10 or 55 U/ml cut-off value was used. CONCLUSIONS: These results suggest that an increased IgA antibody titer, which is an index of the active phase of HP infection, should be an etiological marker for acute myocardial infarction.

Antibodies, Bacterial↗
PubMed2001

A giant internal carotid-posterior communicating artery aneurysm presenting with atypical trigeminal neuralgia and facial nerve palsy in a patient with autosomal dominant polycystic kidney disease: a case report.

BACKGROUND: In cases of internal carotid-posterior communicating artery (IC-PC) aneurysm, involvement of the trigeminal nerve at its root is rare, and facial nerve palsy is even more unusual. CASE REPORT: A large, unruptured IC-PC aneurysm was detected in a 56-year-old man with autosomal dominant polycystic kidney disease (ADPKD), but surgery was not performed because of mild renal dysfunction. Two months later, a sudden, severe headache suggested a subarachnoid hemorrhage, which was ruled out by computed tomography and lumbar puncture. Neurological examination revealed complete oculomotor palsy, atypical trigeminal neuralgia, and facial palsy with gustatory disturbance. Magnetic resonance (MR) imaging revealed a partially thrombosed giant aneurysm that directly compressed the trigeminal nerve root, reached the internal auditory canal, and was adjacent to the facial nerve. The neck of the aneurysm was successfully clipped via a subtemporal transtentorial approach. The postoperative course was uneventful, and all neurological symptoms had resolved within 3 months. CONCLUSIONS: We believe that the prosopalgia in this case was atypical trigeminal neuralgia due to direct compression of the trigeminal nerve root by the aneurysmal sac. A contributory cause was stretching of the oculomotor nerve, which contains sensory afferent inhibitory fibers derived from the ophthalmic branch of the trigeminal nerve. The facial palsy was of peripheral type and was accompanied by gustatory disturbance. This is the first reported case of facial palsy caused by an IC-PC aneurysm and also a very rare case of an IC-PC aneurysm clipped by a subtemporal transtentorial approach.

Carotid Artery Diseases↗
PubMed2001

Effects of quinapril on expression of eNOS, ACE, and AT1 receptor in deoxycorticosterone acetate-salt hypertensive rats.

Angiotensin II and nitric oxide (NO) may play a role in hypertensive cardiovascular remodeling. We evaluated the effects of long-term treatment with quinapril, an angiotensin converting enzyme (ACE) inhibitor, on expression of endothelial NO synthase (eNOS), ACE, and angiotensin II type 1 (AT1) receptor in the left ventricle and evaluated these relations to myocardial remodeling in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Deoxycorticosterone acetate-salt rats were induced with weekly injections of DOCA (30 mg/kg) and 1% saline in drinking water after right nephrectomy. Quinapril (DOCA-QUI, 10 mg/kg/day, subdepressor dose) or AT1 receptor antagonist TCV-116 (DOCA-TCV, 5 mg/kg/day, subdepressor dose) or vehicle (DOCA-V) were given after induction of DOCA-salt hypertension for 5 weeks, and age-matched sham-operated rats (ShC) served as a control group. The eNOS expression in the left ventricle were significantly decreased in DOCA-V compared with ShC, and were significantly increased in DOCA-QUI and DOCA-TCV compared with ShC and DOCA-V. The gene expression of ACE, AT1 receptor, and type I collagen mRNA were significantly increased in DOCA-V compared with ShC, and significantly suppressed in DOCA-QUI compared with DOCA-V. The DOCA-V rats demonstrated a significant increase of the wall-to-lumen ratio, perivascular fibrosis, and myocardial fibrosis, with all these parameters being significantly improved by quinapril. Myocardial remodeling in DOCA-salt hypertensive rats was significantly ameliorated by a subdepressor dose of quinapril, which may be due to an increase in eNOS mRNA and protein expression and a decrease in ACE and AT1 receptor mRNA expression in the left ventricle.

Angiotensin Receptor Antagonists↗
PubMed2001

Purification of a novel myofibril-bound serine proteinase inhibitor (MBSPI) from the skeletal muscle of lizard fish.

A novel myofibril-bound serine proteinase inhibitor (MBSPI) was purified to homogeneity from the skeletal muscle of lizard fish (Saurida wanieso). Purification was carried out by ammonium sulfate fractionation, followed by column chromatographies on DEAE-Sephacel, SP-Sepharose and Sephadex G-150. MBSPI was purified 7.7-fold starting from the DEAE-Sephacel fraction, with a yield of 0.2%. It is a monomeric protein with the molecular mass of 50 kDa as estimated by SDS-PAGE and gel filtration. MBSPI reveals high inhibition specificity toward a myofibril-bound serine proteinase (MBSP) purified from lizard fish muscle. No inhibition is detected toward bovine trypsin, bovine chymotrypsin, two trypsins from carp hepatopancreas and a serine proteinase isolated from the sarcoplasmic fraction of white croaker muscle. It does not exert any inhibitory activity toward a myofibril-bound serine proteinase from carp muscle.

Ammonium Sulfate↗
PubMed2001

Purification, N-terminal amino acid sequence, and some properties of Cu, Zn-superoxide dismutase from Japanese flounder (Paralichthys olivaceus) hepato-pancreas.

Cu, Zn-superoxide dismutase (SOD) has been purified to homogeneity from Japanese flounder Paralichthys olivaceus hepato-pancreas. The purification of the enzyme was carried out by an ethanol/chloroform treatment and acetone precipitation, and then followed by column chromatographies on Q-Sepharose, S-Sepharose and Ultrogel AcA 54. On SDS-PAGE, the purified enzyme gave a single protein band with molecular mass of 17.8 kDa under reducing conditions, and showed approximately equal proportions of 17.8 and 36 kDa molecular mass under non-reducing conditions. Three bands were obtained when the purified enzyme was subjected to native-PAGE, both on protein and activity staining, but the electrophoretic mobility of the purified enzyme differed from that of bovine erythrocyte Cu, Zn-SOD. Isoelectric point values of 5.9, 6.0 and 6.2, respectively, were obtained for the three components. The N-terminal amino acid sequence of the purified enzyme was determined for 25 amino acid residues, and the sequence was compared with other Cu, Zn-SODs. The N-terminal alanine residue was unacetylated, as in the case of swordfish SOD. Above 60 degrees C, the thermostability of the enzyme was much lower than that of bovine Cu, Zn-SOD.

Amino Acid Sequence↗
PubMed2001

Effect of salt and heating on a mesoscopic structure composed of ovalbumin globules in aqueous solution.

Mesoscopic structural changes of an ovalbumin solution by heating and adding NaCl have been investigated with a small-angle neutron scattering method. In the natural solution, a broad peak at q = 0.057 A(-1), which disappeared by adding NaCl, indicates the existence of an electrostatic long-range interaction between the ovalbumin globules. Along with the broad peak, a prominent intensity increase in a very small q region was observed on heating except for the initial and final stages, indicating the coexistence of a disordered structure of the denatured ovalbumin and a regular-interspacing structure of the natural ovalbumin globules. Though the macroscopic feature in the final stage, whether the solution forms a gel (10 wt %) or not (5 wt %), strongly depended on the concentration of the ovalbumin, the scattering profiles showed a common characteristic feature: the appearance of a new peak around q = 0.023 A(-1), which indicates the emergence of another regular structure.

Animals↗
PubMed2001

The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity.

Adiponectin is an adipocyte-derived hormone. Recent genome-wide scans have mapped a susceptibility locus for type 2 diabetes and metabolic syndrome to chromosome 3q27, where the gene encoding adiponectin is located. Here we show that decreased expression of adiponectin correlates with insulin resistance in mouse models of altered insulin sensitivity. Adiponectin decreases insulin resistance by decreasing triglyceride content in muscle and liver in obese mice. This effect results from increased expression of molecules involved in both fatty-acid combustion and energy dissipation in muscle. Moreover, insulin resistance in lipoatrophic mice was completely reversed by the combination of physiological doses of adiponectin and leptin, but only partially by either adiponectin or leptin alone. We conclude that decreased adiponectin is implicated in the development of insulin resistance in mouse models of both obesity and lipoatrophy. These data also indicate that the replenishment of adiponectin might provide a novel treatment modality for insulin resistance and type 2 diabetes.

Adiponectin↗