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Biomedical subjects

K Hirano

Publications and source records attributed to K Hirano.

At least 109 records · Page 6Linked to original sources
PubMed2001

Clinical outcome of stent implantation in small coronary arteries using different types of coronary stents.

PURPOSE: We evaluated the results of stent placement in small coronary arteries. SUBJECTS: The subjects were divided into 2 groups: the first contained 911 lesions treated with stenting in the coronary arteries (stent group), and the second contained 1,203 background- and patient-matched lesions treated with balloon angioplasty (POBA group). There was no significant difference in the background of patients or lesions between the groups. A "small coronary artery" was defined as a coronary artery with a reference vessel diameter < 3.0 mm. RESULTS: There was no significant difference in incidence of acute myocardial infarction (AMI), coronary artery bypass grafting, or death between the groups. In the stent group, acute occlusion (0.8%) and subacute thrombosis (2.1%) occurred. The restenosis rate of 29.8% in the stent group was significantly lower than in the POBA group (38.2%; p < 0.01). The restenosis rate of 19.4% in stented vessels 3.0 mm diameter was significantly lower than in vessels < 3.0 mm diameter (29.8%; p < 0.01). The rate of restenosis was 22.9% for the Multi-Link stent, 24.4% for the NIR stent, 34.1% for the GFX stent, and 35.3% for the PS stent. The restenosis rate of 23.8% in stented vessels > 2.5 mm diameter and < or = 20 mm length was significantly lower than in vessels , < or = 2.5 mm diameter and > 20 mm length (32.7%; p < 0.01). Factors associated with restenosis, analyzed using a stepwise multivariate logistic regression model, included ostial lesions and post-procedural minimum lumen diameter. CONCLUSIONS: Stent implantation in vessels < 3.0 mm diameter using a newly designed coronary stent yielded favorable clinical results, while there was a high prevalence of restenosis, leading to diffused stenotic lesions, in vessels < 2.5 mm diameter.

Aged↗
PubMed2001

[Percutaneous cryosurgery for liver tumors].

A new cryoprobe developed in our department makes it possible to perform percutaneous cryoablation for small liver tumors. This cryoprobe is placed into each lesion using an ultrasonic guidance technique. In this study there were 10 patients with hepatocellular carcinoma and 5 patients with liver metastases from colorectal carcinoma. In 6 cases the tumor size was below 2 cm, in 6 cases between 2 and 3 cm, and in 3 cases over 3 cm. Using a cryoprobe of 3 mm in diameter, each lesion was frozen using liquid nitrogen for 15 or 20 minutes then thawed for 10 minutes, and repeated. The ice ball was found to enlarge to 3 cm in 20 minutes and 5 cm in 60 minutes experimentally. Six cases were CR, 5 PR, 2 NC and 2 PD. After cryoablation, liver function did not change and there were no complications. However, as the size of the ice ball was small (about 3 cm), this method was insufficiently effective in some cases. Percutaneous cryoablation using this probe should be performed for tumors smaller than 3 cm.

Aged↗
PubMed2001

[Evaluation of the BACTEC MGIT 960 system for drug susceptibility testing of Mycobacterium tuberculosis isolates compared with the proportion method on solid media].

The methods most widely used for susceptibility testing against anti-tuberculosis drug (AST) are the proportion method on Löwenstein-Jensen egg (L-J), Ogawa egg or Middle-brook agar media, and BACTEC TB 460 system. Recently, drug concentrations have been established for AST using the automated BACTEC MGIT 960 system (aMGIT). We have evaluated the BACTEC MGIT 960 SIRE kit for AST of Mycobacterium tuberculosis to isoniazid, rifampin, streptomycin and ethambutol. Also we compared the results with the proportion methods on Middlebrook 7H10 agar (7H10), L-J and Ogawa egg, and the manual MGIT system (mMGIT). Overall concordance rates among aMGIT and the proportion method on 7H10 or Ogawa media were 98.3% and 96.9% for 4 first-line drugs, respectively. Rates were particularly high for isoniazid and rifampin between aMGIT and 7H10 (efficiency of 100%). On the other hand, overall concordance rates among two egg media, L-J and Ogawa were 99.9%. Agreement between aMGIT and mMGIT was high for the AST to isoniazid and rifampin, but lower for the AST to ethambutol (90.9%), which relates to a lower specificity of mMGIT. The mean times to aMGIT and mMGIT results of susceptibility were 7 and 6 days, respectively, contrasted with 3 weeks in 7H10 and 4 weeks in L-J and Ogawa, indicating that both MGIT systems have the potential to consistently meet the turnaround time suggested by Centers for Disease Control and Prevention (CDC) of the United States. These results demonstrate that the fully automated BACTEC MGIT 960 SIRE system for AST is useful for rapid diagnosis of drug resistant tuberculosis.

Antitubercular Agents↗
PubMed2001

[Diffusion-weighted imaging of brain death: study of apparent diffusion coefficient].

DWI(Diffusion-weighted images) of the brain has been revealed to be useful in diagnosis of several clinical conditions. However, little is known about DWI with regard to brain death. We had opportunities to study patients with brain death. Case 1. A 34-year-old woman experienced cardiopulmonary arrest due to severe ventricular fibrillation, and resuscitated after about 120 minutes. After brain death, DWI showed high signals in the cerebral cortex, putamen, thalamus, brain stem and cerebellum, and ADC(apparent diffusion coefficient) values were 30-40% lower than those of normal volunteers. Case 2. A 45-year-old woman experienced cardiopulmonary arrest due to pontine hemorrhage, and was resuscitated after about 20 minutes. Before brain death, DWI showed high signals in the cerebral cortex, putamen, thalamus, brain stem and cerebellum, and ADC values were the same as those of normal volunteers. After brain death, DWI showed more clearly defined in these areas, but ADC values were 30-40% lower than the first values. DWI and ADC mapping shows areas corresponding to edema of a cytotoxic nature and to ischemic tissue. The characteristic views of high signals in the whole area of the brain were present, and an objective evaluation was possible with DWI after the brain death diagnosis by measuring ADC values.

Adult↗
PubMed2000

Molecular biology and pathophysiological aspects of plasma cholesteryl ester transfer protein.

Plasma cholesteryl ester transfer protein (CETP) facilitates the transfer of cholesteryl ester (CE) from high density lipoprotein (HDL) to apolipoprotein B-containing lipoproteins. Since CETP regulates the plasma levels of HDL cholesterol and the size of HDL particles, CETP is considered to be a key protein in reverse cholesterol transport, a protective system against atherosclerosis. CETP, as well as plasma phospholipid transfer protein, belongs to members of the lipid transfer/lipopolysaccharide-binding protein (LBP) gene family, which also includes the lipopolysaccharide-binding protein (LBP) and bactericidal/permeability-increasing protein. Although these four proteins possess different physiological functions, they share marked biochemical and structural similarities. The importance of plasma CETP in lipoprotein metabolism was demonstrated by the discovery of CETP-deficient subjects with a marked hyperalphalipoproteinemia (HALP). Two common mutations in the CETP gene, intron 14 splicing defect and exon 15 missense mutation (D442G), have been identified in Japanese HALP patients with CETP deficiency. The deficiency of CETP causes various abnormalities in the concentration, composition, and functions of both HDL and low density lipoprotein. Although the pathophysiological significance of CETP in terms of atherosclerosis has been controversial, the in vitro experiments showed that large CE-rich HDL particles in CETP deficiency are defective in cholesterol efflux. Epidemiological studies in Japanese-Americans and in the Omagari area where HALP subjects with the intron 14 splicing defect of CETP gene are markedly frequent, have shown an increased incidence of coronary atherosclerosis in CETP-deficient patients. The current review will focus on the recent findings on the molecular biology and pathophysiological aspects of plasma CETP, a key protein in reverse cholesterol transport.

Animals↗
PubMed2000

Differential effects of progesterone and 17beta-estradiol on the Ca(2+) entry induced by thapsigargin and endothelin-1 in in situ endothelial cells.

The effects of progesterone and 17beta-estradiol on Ca(2+) signaling in in situ endothelial cells were investigated using front-surface fluorometry of fura-2-loaded strips of porcine aortic valve. Progesterone inhibited the thapsigargin-induced sustained [Ca(2+)](i) elevation (IC(50)=33.9 microM, n=4), while 17beta-estradiol added a transient [Ca(2+)](i) elevation. Progesterone and 17beta-estradiol had no significant effect on the thapsigargin-induced [Ca(2+)](i) elevations in the absence of extracellular Ca(2+). A Mn(2+)-induced decline of fluorescent intensity at 360 nm excitation was accelerated by thapsigargin. This acceleration was completely reversed by progesterone, but not by 17beta-estradiol. Progesterone inhibited, and 17beta-estradiol enhanced the endothelin-1 (ET-1)-induced [Ca(2+)](i) elevation, while both had no effect on the ET-1-induced Ca(2+) release observed in the absence of extracellular Ca(2+) or in the pertussis toxin-treated strips. Progesterone and 17beta-estradiol thus had different effects on Ca(2+) signaling, especially on Ca(2+) influx, in endothelial cells.

Animals↗
PubMed2000

p41 as a possible marker for cell death is generated by caspase cleavage of p42/SETbeta in irradiated MOLT-4 cells.

We have reported previously that X-irradiated MOLT-4 cells during their rapid cell death exhibited dose and time dependently a new protein named p41 detected by two-dimensional polyacrylamide gel electrophoresis (2-D PAGE). An antibody, AM-1, raised against partial peptide of p41 stained two spots, p41 and p42, unexpectedly. Amino acid sequence analysis of partial peptides showed homology between p41 and a putative oncogene, set. In the present study, N-terminal amino acid sequencing of p41 and p42, and polyclonal antibodies newly prepared against different partial peptide sequences revealed that p41 was a N-terminal truncation form of p42, and p42 was identified as SETbeta. The cleavage site was at carboxyl end of SNHD 18 of p42. Radiation-induced p42 cleavage as well as apoptotic cell death was suppressed by a caspase-specific inhibitor Ac-DEVD-CHO but not by Ac-YVAD-CHO. Further in vitro cleavage experiments with recombinant p42 and either irradiated cell extracts or recombinant caspases concluded that the cleavage of p42 into p41 was catalyzed by caspase(s) mainly by caspase-7. One of newly raised antibodies, AM-4, specific to p41 or specific to cleavage site of p42, was found useful enabling simple detection of p41 by 1-D PAGE instead of laborious 2-D PAGE. p41 may serve as a marker of apoptotic cell death.

Amino Acid Sequence↗
PubMed2000

Decreased expression of a member of the Rho GTPase family, Cdc42Hs, in cells from Tangier disease - the small G protein may play a role in cholesterol efflux.

Cholesterol efflux (CE) is the initial and important step of reverse cholesterol transport (RCT), a major protective system against atherosclerosis. However, most of the molecular mechanism for CE still remains to be clarified. In the present study, cDNA subtraction revealed that the expression of a member of the Rho GTPase family, Cdc42Hs, was markedly decreased in both passaged fibroblasts and macrophages (M&phi;) from patients with Tangier disease (TD), a rare lipoprotein disorder with reduced CE. This small G protein is known to have many cell biological activities such as rearrangement of actin cytoskeleton and vesicular transport, however the association between this molecule and lipid transport has never been reported. We demonstrate that MDCK cells expressing the dominant negative form of Cdc42Hs had reduced CE, inversely ones expressing the dominant active form had increased CE. From these observations, we would like to raise a novel hypothesis that this type of small G protein may play a role in some steps of CE. To our knowledge, the present study is the first demonstration that the expression of this molecule is altered in cells from human disease.

Animals↗
PubMed2000

Neovascular Maculopathy Associated with Rubella Retinopathy.

Background: We report three eyes of two patients with rubella retinopathy which were associated with choroidal neovascularization in the macula.Cases: A 7-year-old girl (case 1) and a 12-year-old girl (case 2) whose mothers had suffered rubella during their pregnancy revealed typical rubella retinopathy in both eyes and neovascular maculopathy in one eye at their initial visit to our clinic. Neovascular maculopathy developed in another eye of case 1 after a follow-up of 10 months.Results: The clinical characteristics indicated that (1) sudden visual loss occurs in children, (2) there is no external trigger such as eye injury, and (3) the visual prognosis appears relatively good.Conclusion: Although neovascular maculopathy is rare in pediatric disease, the rubella retinopathy may have the potential to cause neovascular maculopathy.

Journal Article↗
PubMed2000

Mitogen-induced up-regulation of non-smooth muscle isoform of alpha-tropomyosin in rat aortic smooth muscle cells.

Correlation between the expression of the alpha-tropomyosin isoforms and cell growth was investigated in rat aortic smooth muscle cells. The levels of exon 1a, exons 1a+2a (smooth muscle type) and exons 1a+2b (non-smooth muscle type) were determined by reverse transcription-polymerase chain reaction (RT-PCR). When the cells were cultured, the level of exons 1a+2b transiently increased while reaching a maximum at 3-5 days. When the serum-deprived confluent cells were stimulated with 3-20% serum for 1.5 h, the level of exons 1a+2b increased by about twofold. The 1-(5-isoquinolinesulphonyl)-2-methylpiperazine (H-7) but not 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimi de (GF 109203X) inhibited this up-regulation. Phorbol-12, 13-dibutyrate (PDB) mimicked the effect of serum. The DNA synthesis as determined by the incorporation of 5-bromo-2'-deoxy-uridine (BrdU) was not enhanced by the 1.5 h stimulation with serum or phorbol ester. The up-regulation of non-smooth muscle isoform of alpha-tropomyosin occurred during G(0)/G(1) transition before entering S phase. Protein phosphorylation is suggested to be involved in the up-regulation. However, the responsible kinase(s) remain to be elucidated.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2000

Peroxisome proliferator-activated receptor gamma activators downregulate angiotensin II type 1 receptor in vascular smooth muscle cells.

BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) activators, such as troglitazone (Tro), not only improve insulin resistance but also suppress the neointimal formation after balloon injury. However, the precise mechanisms have not been determined. Angiotensin II (Ang II) plays crucial roles in the pathogenesis of atherosclerosis, hypertension, and neointimal formation after angioplasty. We examined the effect of PPARgamma activators on the expression of Ang II type 1 receptor (AT(1)-R) in cultured vascular smooth muscle cells (VSMCs). METHODS AND RESULTS: AT(1)-R mRNA and AT(1)-R protein levels were determined by Northern blot analysis and radioligand binding assay, respectively. Natural PPARgamma ligand 15-deoxy-Delta(12,14)-prostaglandin J(2), as well as Tro, reduced the AT(1)-R mRNA expression and the AT(1)-R protein level. The PPARgamma activators also reduced the calcium response of VSMCs to Ang II. PPARgamma activators suppressed the AT(1)-R promoter activity measured by luciferase assay but did not affect the AT(1)-R mRNA stability, suggesting that the suppression occurs at the transcriptional level. CONCLUSIONS: PPARgamma activators reduced the AT(1)-R expression and calcium response to Ang II in VSMCs. Downregulation of AT(1)-R may contribute to the inhibition of neointimal formation by PPARgamma activators.

Angiotensin II↗
PubMed2000

Early molecular and cellular events of oxidant-induced pulmonary fibrosis in rats.

To evaluate the early molecular events of oxidant-induced pulmonary fibrosis, rats were continuously exposed to 0.4 ppm ozone and 7 ppm nitrogen dioxide. The early responses to the combined gases could be divided into three phases. Acute pulmonary inflammation indicated by an increase in pulmonary edema as well as an influx of neutrophils into the airspaces first occurred on days 1 to 3 of the exposure. The pulmonary inflammation was reversed by day 8, and no biochemical or morphologic aspects of tissue responses were detected from days 15 to 45, suggesting that rats adapted to the stimuli during that period. Pulmonary fibrosis could be detected by an increase in the biomarker of lung collagen content at day 60 and by histopathologic evaluation by day 90. Enhanced expression of macrophage inflammatory protein-2 was observed only at day 1, whereas the pulmonary expression of transforming growth factor-beta was upregulated on days 60 and 90 of the exposure. Macrophage expressions of interleukin-1beta and interleukin-6 were enhanced during acute pulmonary inflammation; however, macrophage expression of tumor necrosis factor-alpha was elevated at both day 1 and days 60-90. Activation of nuclear factor-kappa B and increased expression of thioredoxin in the lungs was also observed at day 1 and days 60-90. The expression of antioxidant enzymes, such as manganeous superoxide dismutase and glutathione peroxidase, was not altered during exposure. These results indicate that macrophage activation and the expression of macrophage-derived cytokines may play an important role in the early pulmonary responses against the combined gases.

Administration, Inhalation↗
PubMed2000

Involvement of SAPK/JNK pathway in X-ray-induced rapid cell death of human T-cell leukemia cell line MOLT-4.

We found that SAPK/JNK was phosphorylated during X-ray-induced rapid cell death of MOLT-4 cells and that acid Sphingomyelinase inhibitor D609 suppressed the rapid cell death as well as phosphorylation of SAPK/JNK. Also C2-ceramide caused phosphorylation of SAPK/JNK, followed by rapid cell death. Further we isolated X-ray-resistant radiation-hybrid clones from MOLT-4 and 50 Gy irradiated mouse FM3A cells by repeated selections with 3 Gy irradiation. One of them named Rh-1a was found resistant to X-ray- as well as C2-ceramide-induced rapid cell death. Rh-1a cells had mouse DNA but no increase in either mouse or human Bcl-2 determined by Western blotting. Accumulation of p53 after X-irradiation was similarly observed in both parental MOLT-4 and Rh-1a cells. However, contrasting to prolonged and prominent phosphorylated status of SAPK/JNK in MOLT-4 cells, Rh-1a cells exhibited short transient increase and FM3A cells showed no increase of phosphorylated status SAPK/JNK after X-irradiation. Therefore, SAPK/JNK activation is considered important in X-ray-induced rapid cell death or apoptosis of MOLT-4 cells.

Animals↗
PubMed2000

Cleavage and phosphorylation of XRCC4 protein induced by X-irradiation.

We report the p35 and p60 forms of XRCC4 protein, appearing in human leukemia MOLT-4 or U937 cells following X-irradiation or hyperthermia. p35 appeared in conjunction with the cleavage of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and the fragmentation of internucleosomal DNA, and was suppressed by Ac-DEVD-CHO. p35 was also produced in vitro by treating MOLT-4 cell lysate with recombinant caspases, suggesting that p35 was a caspase-cleaved fragment of XRCC4 in apoptotic cell death. p60 was sensitive to treatment with phosphatase or wortmannin and was undetectable in M059J cells deficient in DNA-PKcs. However, p60 was found in ataxia-telangiectasia cells after irradiation. These results indicated p60 as a phosphorylated form of XRCC4, requiring DNA-PKcs but not ataxia-telangiectasia mutated (ATM).

Androstadienes↗
PubMed2000

Minimal requirements for the nuclear localization of p27(Kip1), a cyclin-dependent kinase inhibitor.

p27(Kip1) is a cyclin-dependent kinase inhibitor, and its nuclear localization is a prerequisite for it to function as a cell cycle regulator. In the present study, the minimal requirement for the nuclear localization signal (NLS) of p27(Kip1) was determined by analyzing the localization of various mutants of p27(Kip1) tagged with green fluorescent protein (GFP) in HeLa cells and porcine aortic endothelial cells. Wild-type p27(Kip1) exclusively localized into nucleus, while GFP alone localized in both cytosol and nucleus. A comparison of various truncation mutants revealed residues 153-166 to be the minimal region necessary for nuclear localization. However, a fusion of this region to GFP showed cytoplasmic retention in addition to nuclear localization, thus suggesting that some extension flanking this region is required to achieve a full function of NLS. The site-directed mutation of the full-length p27(Kip1) therefore showed that four basic residues (K153, R154, K165, R166), especially R166, play a critical role in the nuclear localization of p27(Kip1).

Amino Acid Sequence↗
PubMed2000

Phase-contrast X-ray imaging with a large monolithic X-ray interferometer.

To increase the field of view for large objects in phase-contrast X-ray imaging, a large monolithic X-ray interferometer has been fabricated using an available silicon ingot of diameter 10 cm. A performance study of this interferometer has been carried out using a synchrotron X-ray source. The view size of the interference pattern obtained with this interferometer was 25 mm wide and 15 mm high and its visibility was 79%. Various structures of a sliced human hepatocellular carcinoma were identified as necrosis, hemorrhagic necrosis, normal liver tissue and blood vessel. The performance of this interferometer was sufficient for phase-contrast X-ray imaging.

Journal Article↗
PubMed2000

Identification of a GPI-anchored type HDL-binding protein on human macrophages.

To identify the HDL3-binding proteins on human macrophages, we examined the involvement of GPI-anchored protein in the binding of HDL3, and tried to purify HDL3-binding protein. From membrane fractions of macrophages, we obtained 80- and 130-kDa HDL3-binding proteins by ligand blotting. Treatment of macrophages with phosphatidylinositol-specific phospholipase C (PI-PLC) significantly decreased the specific HDL3-binding in a dose-dependent manner. Furthermore, treatment with mannosamine, which blocks GPI-anchor formation, decreased specific HDL3-binding in a dose-dependent manner. PI-PLC treatment released from the cells the proteins with an M(r) of 80 kDa, which could also bind HDL3. PI-PLC as well as mannosamine treatment markedly reduced cholesterol efflux from macrophages in association with the decreased HDL-binding. Using HDL3-affinity chromatography, we purified 80-kDa GPI-anchored type HDL3-binding protein. In summary, we demonstrate the implication of 80-kDa GPI-anchored protein in the binding of HDL3 to human macrophages, which might have some role in reverse cholesterol transport.

Binding Sites↗