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Biomedical subjects

Hiroyuki Takano

Publications and source records attributed to Hiroyuki Takano.

At least 19 recordsLinked to original sources
PubMed2006

Feasibility and safety of granulocyte colony-stimulating factor treatment in patients with acute myocardial infarction.

BACKGROUND: This study examined feasibility and safety of granulocyte colony-stimulating factor (G-CSF) treatment for patients with acute myocardial infarction (AMI). METHODS: Forty patients with AMI related with the left anterior descending coronary artery, who underwent successful percutaneous coronary intervention (PCI), were randomized into G-CSF group (n=18) or Control group (n=22). G-CSF treatment was started within 24 h after PCI. 99mTc-tetrofosmin single-photon emission computed tomography (SPECT) was performed at 4 days and 6 months after AMI. SPECT data was analyzed for LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), LV ejection fraction (LVEF) and myocardial perfusion. RESULTS: LVEF at 6 months was significantly better than that at 4 days in G-CSF group (p=0.013), but not changed in Control group (p=0.245). Although no significant difference was observed for LVEDV between the two groups, LVESV tended to be decreased only in G-CSF group. In G-CSF group, defect score (DS) was significantly decreased from 4 days to 6 months after AMI. Restenosis rate at 6 months after AMI was not significantly different between the two groups. CONCLUSIONS: G-CSF treatment for patients with AMI was effective and did not have any clinical and angiographic adverse effects.

Aged↗
PubMed2006

Remediation of cadmium-contaminated paddy soils by washing with calcium chloride: verification of on-site washing.

We developed a new, three-step soil-wash method to remediate Cd-contaminated paddy fields. The method comprises (1) chemically washing the field soil with a CaCl2 solution; (2) washing the treated soil with water to eliminate residual Cd and CaCl2; and (3) on-site treatment of wastewater using a portable wastewater treatment system. Cd concentrations in the treated water were below Japan's environmental quality standard (0.01 mg Cd L-1), and the removal of Cd from the exchangeable fraction was 55% and from the acid-soluble fraction 15%. While soil fertility properties were affected by the soil washing, adverse effects were not crucial and could be corrected. The washing had no affect on rice growth, and reduced the average Cd concentration in rice grains by about two-thirds compared to a control plot. These results confirmed the effectiveness of the soil-wash method in remediating Cd-contaminated paddy fields.

Agriculture↗
PubMed2006

Remediation of cadmium-contaminated paddy soils by washing with chemicals: effect of soil washing on cadmium uptake by soybean.

We conducted a pot experiment to evaluate the effect of soil washing with CaCl(2) on Cd absorption by two soybean cultivars. The results were as follows: (1) Soybean growth was not significantly different in washed and unwashed soils, but the seed Cd concentration for both cultivars decreased significantly, up to 25%, in the washed soils compared with the unwashed soils. (2) In the washed soils, the Cd concentration in the soil solution indicated an obviously lower value from sowing to the flowering stage; however, the change in Cd speciation was not evident in the CaCl(2)-washed soil solution. Consequently, the effect of soil washing using CaCl(2) on Cd-contaminated paddy soils can be expected to continue after a CaCl(2)-washed paddy field is converted to an upland field.

Cadmium↗
PubMed2006

Remarkable thickening of right atrial wall in subjects with cardiac amyloidosis complicated with sick sinus syndrome.

We observed a 63-year old male with cardiac amyloidosis who presented with the clinical symptoms of sick sinus syndrome and dyspnea and abnormal thickening of the right atrial wall, which extended to the junction of the superior vena cava. This may explain the relationship of abnormal thickening of the right atrium which extends to the junction of the superior vena cava and right atrium with amyloid deposits in the sinus node and occurrence of sick sinus syndrome.

Amyloidosis↗
PubMed2006

Remediation of cadmium contamination in paddy soils by washing with chemicals: selection of washing chemicals.

The efficiencies of neutral salts, strong acids, and chelates were tested for extracting cadmium (Cd) from three paddy soils. The higher the selectivity of the cations of the added neutral salts toward soil adsorption sites, the lower the pH in the extracts and the more soil Cd could be extracted. In addition, soil carbon and nitrogen contents and mineral composition were closely associated with the amount of Cd extracted. Calcium chloride and iron(III) chloride were selected as wash chemicals to restore Cd-contaminated paddy soils in situ. Washing with calcium chloride led to the formation of Cd chloride complexes, enhancing Cd extraction from the soils. The washing also substantially decreased soil levels of exchangeable and acid-soluble Cd, which are the major forms of bioavailable Cd for rice (Oryza sativa L.). The optimum conditions for in situ soil washing were also determined for calcium chloride.

Acids↗
PubMed2006

Granulocyte colony stimulating factor directly inhibits myocardial ischemia-reperfusion injury through Akt-endothelial NO synthase pathway.

OBJECTIVE: Granulocyte colony stimulating factor (G-CSF) has been reported recently to prevent cardiac remodeling and dysfunction after acute myocardial infarction through signal transducer and activator of transcription 3 (STAT3). In this study, we examined acute effects of G-CSF on the heart against ischemia-reperfusion injury. METHODS AND RESULTS: Rat hearts were subjected to global 35-minute ischemia and 120-minute reperfusion in Langendorff system with or without G-CSF (300 ng/mL). G-CSF administration was started at the onset of reperfusion. Triphenyltetrazolium chloride staining revealed that G-CSF markedly reduced the infarct size. G-CSF strongly activated Janus kinase 2 (Jak2), STAT3, extracellular signal-regulated kinase (ERK), Akt, and endothelial NO synthase (NOS) in the hearts subjected to ischemia followed by 15-minute reperfusion. The G-CSF-induced reduction in infarct size was abolished by inhibitors of phosphatidylinositol 3-kinase, Jak2, and NOS but not of mitogen-activated protein kinase kinase (MEK). CONCLUSIONS: These results suggest that G-CSF acts directly on the myocardium during ischemia-reperfusion injury and has acute nongenomic cardioprotective effects through the Akt-endothelial NOS pathway.

Animals↗
PubMed2006

G-CSF prevents the progression of atherosclerosis and neointimal formation in rabbits.

Granulocyte colony-stimulating factor (G-CSF) prevents left ventricular remodeling after myocardial infarction, but its effect on atherosclerosis is unknown. We examined two kinds of rabbit atherosclerosis models. Myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHL-MI) rabbits were treated with G-CSF or saline for 7 days from 14 months old. The vascular injury models were created by inflating angioplasty balloon in the iliac artery of rabbits and were divided into G-CSF and saline group. G-CSF significantly reduced the stenosis score of coronary artery and lipid plaque area of thoracic aorta in WHHL-MI rabbits at 4 weeks after the treatment. In the vascular injury model, G-CSF significantly prevented an increase in neointima/media ratio at 4 weeks after the treatment. G-CSF accelerated the reendothelialization of denuded arteries, and the pretreatment with nitric oxide synthase inhibitor significantly inhibited it. These results suggest that G-CSF has a therapeutic potential for the progression of atherosclerosis.

Animals↗
PubMed2006

Cardioprotective effects of granulocyte colony-stimulating factor in swine with chronic myocardial ischemia.

OBJECTIVES: The aim of this study was to investigate the effect of granulocyte colony-stimulating factor (G-CSF) on chronic myocardial ischemia in swine. BACKGROUND: We recently have reported that G-CSF prevents cardiac remodeling and dysfunction after acute myocardial infarction in mice and swine. It remains unclear whether G-CSF has beneficial effects on chronic myocardial ischemia. METHODS: An ameroid constrictor was placed on left circumflex coronary artery of swine. The presence of myocardial ischemia was verified at four weeks after the operation, and the animals were randomly assigned into the following two groups: 1) administration of vehicle (control group, n = 10), and 2) administration of G-CSF (10 microg/kg/day) for seven days (G-CSF group, n = 10). RESULTS: Echocardiographic examination revealed that the G-CSF treatment prevented left ventricular dilation and dysfunction at eight weeks after the operation. Stress echocardiography revealed that G-CSF ameliorated the regional contractility of chronic myocardial ischemia. Morphological analysis revealed that the extent of myocardial fibrosis of the ischemic region was less in the G-CSF group than in control group. There were more vessels and less apoptotic cells at the ischemic region of the heart of the G-CSF group than control group. Moreover, Akt1 was more strongly activated in the heart of the G-CSF group than control group. CONCLUSIONS: These findings suggest that G-CSF improves cardiac function of chronic myocardial ischemia through decreases in fibrosis and apoptotic death and an increase in vascular density in the ischemic region.

Animals↗
PubMed2006

Effects of G-CSF on left ventricular remodeling and heart failure after acute myocardial infarction.

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic cytokine that promotes proliferation and differentiation of neutrophil progenitors. G-CSF also possesses immunomodulatory properties. G-CSF-induced hematopoietic stem cell mobilization is widely used clinically for transplantation. After it was recently reported that G-CSF mobilizes bone marrow stem cells (BMSCs) into the infarcted hearts and accelerates the differentiation into vascular cells and cardiac myocytes, myocardial regeneration utilizing mobilization of BMSCs by G-CSF is attracting the attention of investigators. In animal models, G-CSF prevents left ventricular remodeling and dysfunction after acute myocardial infarction, at least in part, through a decrease in apoptotic cells and an increase in vascular cells. Although it is controversial whether BMSCs mobilized by G-CSF can differentiate into cardiac myocytes, G-CSF-induced angiogenesis is indeed recognized in infarcted heart. The cardioprotective effects of G-CSF are recognized even in isolated perfused heart. In addition, G-CSF activates various signaling pathways such as Akt, extracellular signal-regulated kinase, and Janus kinase 2/signal transducer and activator of transcription 3 through G-CSF receptors in cardiac myocytes. These observations suggest that G-CSF not only induces mobilization of stem cells and progenitor cells but also acts directly on cardiomyocytes. Therefore, G-CSF may be utilized as a novel agent to have protective and regenerative effects on injured myocardium. Although the effects of G-CSF on the progression of atherosclerosis are still unclear, there is a possibility that G-CSF will become a promising therapy for ischemic heart diseases.

Animals↗
PubMed2006

Intracoronary injection of granulocyte colony-stimulating factor ameliorates the progression of left ventricular remodeling after myocardial ischemia/reperfusion in rabbits.

BACKGROUND: Although granulocyte colony-stimulating factor (G-CSF) is known to prevent left ventricular (LV) remodeling after acute myocardial infarction (AMI), the best method of administration is unknown. METHODS AND RESULTS: A rabbit ischemia/reperfusion model was created and G-CSF was administered into the coronary artery immediately after reperfusion. The LV size and contraction were determined by echocardiography, and the extent of infarcted myocardium was measured by Masson-Trichrome staining. The benefits of intracoronary injection of G-CSF on LV remodeling were similar to subcutaneous injection. CONCLUSIONS: Direct intracoronary G-CSF injection may become a new therapy for AMI with lower adverse effects.

Acute Disease↗
PubMed2005

Phosphatidylinositol 3-kinase-Akt pathway plays a critical role in early cardiomyogenesis by regulating canonical Wnt signaling.

We have recently reported that activation of phosphatidylinositol 3-kinase (PI3K) plays a critical role in the early stage of cardiomyocyte differentiation of P19CL6 cells. We here examined molecular mechanisms of how PI3K is involved in cardiomyocyte differentiation. DNA chip analysis revealed that expression levels of Wnt-3a were markedly increased and that the Wnt/beta-catenin pathway was activated temporally during the early stage of cardiomyocyte differentiation of P19CL6 cells. Activation of the Wnt/beta-catenin pathway during this period was required and sufficient for cardiomyocyte differentiation of P19CL6 cells. Inhibition of the PI3K/Akt pathway suppressed the Wnt/beta-catenin pathway by activation of glycogen synthase kinase-3beta (GSK-3beta) and degradation of beta-catenin. Suppression of cardiomyocyte differentiation by inhibiting the PI3K/Akt pathway was rescued by forced expression of a nonphosphorylated, constitutively active form of beta-catenin. These results suggest that the PI3K pathway regulates cardiomyocyte differentiation through suppressing the GSK-3beta activity and maintaining the Wnt/beta-catenin activity.

Animals↗
PubMed2005

The role of PPARgamma-dependent pathway in the development of cardiac hypertrophy.

Peroxisome proliferator-activated receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily. PPARs have three isoforms, alpha, beta (or delta) and gamma. It has been conceived that PPARgamma is expressed predominantly in adipose tissue and promotes adipocyte differentiation and glucose homeostasis. Recently, synthetic antidiabetic thiazolidinediones and natural prostaglandin D2 (PGD2) metabolite, 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2), have been identified as ligands for PPARgamma. Following demonstration that PPARgamma is present in a variety of cell types, further study of PPARgamma has been conducted. Although activation of PPARgamma appears to have beneficial effects on atherosclerosis and heart failure, it is still largely uncertain whether PPARgamma ligands prevent the development of cardiovascular diseases. Recent evidence suggests that some benefit from the antidiabetic agents known as thiazolidinediones may occur through PPARgamma-independent mechanisms. In this review, we report on the latest developments concerning the study of PPARs and summarize the roles of the PPARgamma-dependent pathway in cardiovascular diseases.

Cardiomegaly↗
PubMed2005

G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes.

Granulocyte colony-stimulating factor (G-CSF) was reported to induce myocardial regeneration by promoting mobilization of bone marrow stem cells to the injured heart after myocardial infarction, but the precise mechanisms of the beneficial effects of G-CSF are not fully understood. Here we show that G-CSF acts directly on cardiomyocytes and promotes their survival after myocardial infarction. G-CSF receptor was expressed on cardiomyocytes and G-CSF activated the Jak/Stat pathway in cardiomyocytes. The G-CSF treatment did not affect initial infarct size at 3 d but improved cardiac function as early as 1 week after myocardial infarction. Moreover, the beneficial effects of G-CSF on cardiac function were reduced by delayed start of the treatment. G-CSF induced antiapoptotic proteins and inhibited apoptotic death of cardiomyocytes in the infarcted hearts. G-CSF also reduced apoptosis of endothelial cells and increased vascularization in the infarcted hearts, further protecting against ischemic injury. All these effects of G-CSF on infarcted hearts were abolished by overexpression of a dominant-negative mutant Stat3 protein in cardiomyocytes. These results suggest that G-CSF promotes survival of cardiac myocytes and prevents left ventricular remodeling after myocardial infarction through the functional communication between cardiomyocytes and noncardiomyocytes.

Animals↗
PubMed2005

Pioglitazone, a peroxisome proliferator-activated receptor gamma activator, ameliorates experimental autoimmune myocarditis by modulating Th1/Th2 balance.

OBJECTIVES: The aim of this study is to investigate the effect of Peroxisome proliferator-activated receptor gamma (PPAR gamma) ligand on experimental autoimmune myocarditis (EAM). BACKGROUND: Rat EAM model resembles the giant cell myocarditis in human. Recent studies have suggested that Th1 cytokines are involved in the initiation and progression of EAM, whereas Th2 cytokines are associated with the remission. PPAR gamma, which is a member of nuclear hormone receptor superfamily, has been known to affect not only glucose homeostasis but also immune responses, by regulating the Th1/Th2 balance. METHODS: Lewis rats were immunized with cardiac myosin and divided into three groups: Group N, normal control rats (n = 16); Group E, EAM rats (n = 17); and Group P, EAM rats treated with a PPAR gamma activator pioglitazone (n = 20). RESULTS: Cardiac dysfunction and remodeling were inhibited in Group P compared to Group E. Heart weight/body weight ratio and the degree of inflammation and fibrosis were significantly lower in Group P than in Group E. The mRNA levels of macrophage inflammatory protein-1alpha (MIP-1alpha), which plays an important role in the recruitment of inflammatory cells in the early stage of EAM, were upregulated in the heart of Group E, but not in the heart of Group P. Furthermore, the treatment with pioglitazone decreased the expression levels of proinflamatory cytokine (TNF alpha and IL-1beta) genes and Th1 cytokine (IFN-gamma) genes, and increased the expression levels of Th2 cytokine (IL-4) gene. CONCLUSIONS: PPAR gamma ligands may have beneficial effects on myocarditis by inhibiting MIP-1alpha expression and modulating the Th1/Th2 balance.

Animals↗
PubMed2005

[PPARs and heart diseases].

After it has been reported that activation of PPARalpha or PPARgamma suppresses production of proinflammatory cytokines, medical interest in PPARs have grown and a huge research effort has been concentrated. Synthetic antidiabetic thiazolidinediones (TZDs) and natural prostaglandin D2 (PGD2) metabolite, 15d-PGJ2, are well known as ligands for PPARgamma. Hyperlipidemic drugs (fibrates) are synthetic PPARalpha ligands. Recent studies suggest that ligands of PPAR not only regulate glucose and lipid metabolism but also have pleiotropic effects on many tissues and cell types. Ligands of PPARs may become therapeutic agents useful in the prevention of cardiovascular diseases beyond their effects on glucose and lipid metabolism. This review will focus on the latest developments in the PPARs field and the roles of PPAR-dependent pathway in cardiovascular diseases.

Animals↗
PubMed2004

Effects of G-CSF on cardiac remodeling after acute myocardial infarction in swine.

We examined whether granulocyte colony-stimulating factor (G-CSF) prevents cardiac dysfunction and remodeling after myocardial infarction (MI) in large animals. MI was produced by ligation of left anterior descending coronary artery in swine. G-CSF (10 microg/kg/day, once a day) was injected subcutaneously from 24h after ligation for 7 days. Echocardiographic examination revealed that the G-CSF treatment induced improvement of cardiac function and attenuation of cardiac remodeling at 4 weeks after MI. In the ischemic region, the number of apoptotic endothelial cells was smaller and the number of vessels was larger in the G-CSF treatment group than in control group. Moreover, vascular endothelial growth factor was more abundantly expressed and Akt was more strongly activated in the ischemic region of the G-CSF treatment group than of control group. These findings suggest that G-CSF prevents cardiac dysfunction and remodeling after MI in large animals.

Animals↗