177 research outputs found

    A lack of classical Cepheids in the inner part of the Galactic disk

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    Recent large-scale infrared surveys have been revealing stellar populations in the inner Galaxy seen through strong interstellar extinction in the disk. In particular, classical Cepheids with their period-luminosity and period-age relations are useful tracers of Galactic structure and evolution. Interesting groups of Cepheids reported recently include four Cepheids in the Nuclear Stellar Disk (NSD), about 200 pc around the Galactic Centre, found by Matsunaga et al. and those spread across the inner part of the disk reported by Dekany and collaborators. We here report our discovery of nearly thirty classical Cepheids towards the bulge region, some of which are common with Dekany et al., and discuss the large impact of the reddening correction on distance estimates for these objects. Assuming that the four Cepheids in the NSD are located at the distance of the Galactic Centre and that the near-infrared extinction law, i.e. wavelength dependency of the interstellar extinction, is not systematically different between the NSD and other bulge lines-of-sight, most of the other Cepheids presented here are located significantly further than the Galactic Centre. This suggests a lack of Cepheids in the inner 2.5 kpc region of the Galactic disk except the NSD. Recent radio observations show a similar distribution of star-forming regions.Comment: 8 pages, 4 figures, accepted for publication in MNRA

    Cepheids and other short-period variables near the Galactic Centre

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    We report the result of our near-infrared survey of short-period variable stars (P<60d) in a field-of-view of 20'x30' towards the Galactic Centre. Forty-five variables are discovered and we classify the variables based on their light curve shapes and other evidence. In addition to 3 classical Cepheids reported previously, we find 16 type II Cepheids, 24 eclipsing binaries, one pulsating star with P=0.265d (RR Lyr or delta Sct) and one Cepheid-like variable whose nature is uncertain. Eclipsing binaries are separated into the foreground objects and those significantly obscured by interstellar extinction. One of the reddened binaries contains an O-type supergiant and its light curve indicates an eccentric orbit. We discuss the nature and distribution of type II Cepheids as well as the distance to the Galactic Centre based on these Cepheids and other distance indicators. The estimates of R0(GC) we obtained based on photometric data agree with previous results obtained with kinematics of objects around the GC. Furthermore, our result gives a support to the reddening law obtained by Nishiyama and collaborators, A(Ks)/E(H-Ks)=1.44, because a different reddening law would result in a rather different distance estimate.Comment: 13 pages, 10 figures, 7tables, accepted for publication in MNRA

    Health effects of immediate telework introduction during the COVID-19 era in Japan: A cross-sectional study

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    [Background] Telework has been widely discussed in several fields; however, there is a lack of research on the health aspects of teleworking. The current study was conducted to determine the health effects of teleworking during an emergency statement as evidence for future policy development. [Method] This was a cross-sectional study in which we administered an online questionnaire to 5, 214 general workers (response rate = 36.4%) from June 2020 to August 2020. Based on working methods during the pandemic, workers were categorized into the office group (n = 86) and telework group (n = 1597), and we characterized their demographics, changes in lifestyle, telework status, physical symptoms, and mental health. [Results] The results showed that the workers’ residence, marital status, management positions, and employee status affected the choice of the work method. During the emergency, teleworkers experienced more changes in their habits than office workers. In terms of exercise habits, 67.0% of the individuals belonging to the office-telework (OT) group exercised less. Approximately half of the teleworkers were satisfied with their telework, and those in the OT group were less satisfied with their telework than those in the telework-telework (TT) group, and they reported an increase in both working hours and meeting hours. Work-family conflict was more pronounced in the TT group than in the two other groups. Only 13.2% of individuals did not experience any stress in the past 30 days, and all three groups showed varying degrees of anxiety and depressive tendencies. In addition, all teleworkers experienced adverse physical symptoms before and after the emergency. [Conclusion] Health issues associated with teleworking should be given adequate attention

    Glucoraphanin: A broccoli sprout extract that ameliorates obesity-induced inflammation and insulin resistance

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    金沢大学医薬保健研究域医学系Obesity is a low-grade sustained inflammatory state that causes oxidative stress in different metabolic tissues, which leads to insulin resistance and nonalcoholic fatty liver disease (NAFLD). Particularly, obesity-induced metabolic endotoxemia plays an important role in the pathogenesis of insulin resistance and inflammation. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of antioxidant signaling that serves as a primary cellular defense against the cytotoxic effects of oxidative stress. Pharmacological stimulation of Nrf2 mitigates obesity and insulin resistance in mice; however, Nrf2 activators are not clinically available due to biosafety concerns. A recent study demonstrated that glucoraphanin, a precursor of the Nrf2 activator sulforaphane, ameliorates obesity by enhancing energy expenditure and browning of white adipose tissue, and attenuates obesity-related inflammation and insulin resistance by polarizing M2 macrophages and reducing metabolic endotoxemia. Thus, this review focuses on the efficiency and safety of glucoraphanin in alleviating obesity, insulin resistance, and NAFLD.Embargo Period 12 month

    Regulation of Gut Microbiota and Metabolic Endotoxemia with Dietary Factors

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    金沢大学医学系細胞分子機能学Metabolic endotoxemia is a condition in which blood lipopolysaccharide (LPS) levels are elevated, regardless of the presence of obvious infection. It has been suggested to lead to chronic inflammation-related diseases such as obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease (NAFLD), pancreatitis, amyotrophic lateral sclerosis, and Alzheimer\u27s disease. In addition, it has attracted attention as a target for the prevention and treatment of these chronic diseases. As metabolic endotoxemia was first reported in mice that were fed a high-fat diet, research regarding its relationship with diets has been actively conducted in humans and animals. In this review, we summarize the relationship between fat intake and induction of metabolic endotoxemia, focusing on gut dysbiosis and the influx, kinetics, and metabolism of LPS. We also summarize the recent findings about dietary factors that attenuate metabolic endotoxemia, focusing on the regulation of gut microbiota. We hope that in the future, control of metabolic endotoxemia using dietary factors will help maintain human health

    Relationship between serum isoflavone concentrations and frequency of soybean products consumption in patients with prostate cancer

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    Dietary consumption of high concentrations of soybean products has been suggested to reduce the risk for prostate cancer (PCa). We conducted a survey using patients with PCa to assess the relationship between serum concentrations of isoflavone aglycones and frequency of soybean products consumption in patients with PCa. We measured the serum concentrations of daidzein, genistein, glycitein, and equol in 99 PCa patients, in addition to conducting a survey using a self administrated questionnaire that included the frequencies of various food item consumptions. If serum concentrations of equol were at a value less than 0.5 ng/mL, they were classified as an equol non producer, and the other patients were classified as equol producers. As a result, serum concentrations of daidzein, genistein, and glycitein were found to be significantly correlated to each other (P<0.001). The frequency of tofu (soybean curd) consumption was significantly correlated with the serum concentration of daidzein (P<0.05). Likewise, the frequency of natto (fermented soybean) consumption was significantly correlated with the serum concentrations of daidzein, genistein, and glycitein (P<0.01). In the study there were 40 equol producers and 59 equol non producers, but none of the food items were significantly different between the equol producers and the equol non producers. We have a plan to perform a similar survey for population based controls in the future. Comparisons between the data of the PCa patients and the controls would give us more information about the role of isoflavones and equol production in regard to the risk of PCa

    Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with Vitamin E

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    Hepatic insulin resistance and nonalcoholic steatohepatitis (NASH) could be caused by excessive hepatic lipid accumulation and peroxidation. Vitamin E has become a standard treatment for NASH. However, astaxanthin, an antioxidant carotenoid, inhibits lipid peroxidation more potently than Vitamin E. Here, we compared the effects of astaxanthin and Vitamin E in NASH. We first demonstrated that astaxanthin ameliorated hepatic steatosis in both genetically (ob/ob) and high-fat-diet-induced obese mice. In a lipotoxic model of NASH: mice fed a high-cholesterol and high-fat diet, astaxanthin alleviated excessive hepatic lipid accumulation and peroxidation, increased the proportion of M1-type macrophages/Kupffer cells, and activated stellate cells to improve hepatic inflammation and fibrosis. Moreover, astaxanthin caused an M2-dominant shift in macrophages/Kupffer cells and a subsequent reduction in CD4+ and CD8+ T cell recruitment in the liver, which contributed to improved insulin resistance and hepatic inflammation. Importantly, astaxanthin reversed insulin resistance, as well as hepatic inflammation and fibrosis, in pre-existing NASH. Overall, astaxanthin was more effective at both preventing and treating NASH compared with Vitamin E in mice. Furthermore, astaxanthin improved hepatic steatosis and tended to ameliorate the progression of NASH in biopsy-proven human subjects. These results suggest that astaxanthin might be a novel and promising treatment for NASH

    L-carnitine prevents lenvatinib-induced muscle toxicity without impairment of the anti-angiogenic efficacy

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    Lenvatinib is an oral tyrosine kinase inhibitor that acts on multiple receptors involved in angiogenesis. Lenvatinib is a standard agent for the treatment of several types of advanced cancers; however, it frequently causes muscle-related adverse reactions. Our previous study revealed that lenvatinib treatment reduced carnitine content and the expression of carnitine-related and oxidative phosphorylation (OXPHOS) proteins in the skeletal muscle of rats. Therefore, this study aimed to evaluate the effects of L-carnitine on myotoxic and anti-angiogenic actions of lenvatinib. Co-administration of L-carnitine in rats treated with lenvatinib for 2 weeks completely prevented the decrease in carnitine content and expression levels of carnitine-related and OXPHOS proteins, including carnitine/organic cation transporter 2, in the skeletal muscle. Moreover, L-carnitine counteracted lenvatinib-induced protein synthesis inhibition, mitochondrial dysfunction, and cell toxicity in C2C12 myocytes. In contrast, L-carnitine had no influence on either lenvatinib-induced inhibition of vascular endothelial growth factor receptor 2 phosphorylation in human umbilical vein endothelial cells or angiogenesis in endothelial tube formation and mouse aortic ring assays. These results suggest that L-carnitine supplementation could prevent lenvatinib-induced muscle toxicity without diminishing its antineoplastic activity, although further clinical studies are needed to validate these findings

    Hepatobiliary cystadenoma exhibiting morphologic changes from simple hepatic cyst shown by 11-year follow up imagings

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    <p>Abstract</p> <p>Background</p> <p>A long-term follow up case of hepatobiliary cystadenoma originating from simple hepatic cyst is rare.</p> <p>Case presentation</p> <p>We report a case of progressive morphologic changes from simple hepatic cyst to hepatobiliary cystadenoma by 11 – year follow up imaging. A 25-year-old man visited our hospital in 1993 for a simple hepatic cyst. The cyst was located in the left lobe of the liver, was 6 cm in diameter, and did not exhibit calcification, septa or papillary projections. No surgical treatment was performed, although the cyst was observed to gradually enlarge upon subsequent examination. The patient was admitted to our hospital in 2004 due to epigastralgia. Re-examination of the simple hepatic cyst revealed mounting calcification and septa. Abdominal CT on admission revealed a hepatic cyst over 10 cm in diameter and a high-density area within the thickened wall. MRI revealed a mass of low intensity and partly high intensity on a T1-weighted image. Abdominal angiography revealed hypovascular tumor. The serum levels of AST and ALT were elevated slightly, but tumor markers were within normal ranges. Left lobectomy of the liver was performed with diagnosis of hepatobiliary cystadenoma or hepatobiliary cystadenocarcinoma. The resected specimen had a solid component with papillary projections and the cyst was filled with liquid-like muddy bile. Histologically, the inner layer of the cyst was lined with columnar epithelium showing mild grade dysplasia. On the basis of these findings, hepatobiliary cystadenoma was diagnosed.</p> <p>Conclusion</p> <p>We believe this case provides evidence of a simple hepatic cyst gradually changing into hepatobiliary cystadenoma.</p

    Increased oxidative stress precedes the onset of high-fat diet-induced insulin resistance and obesity

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    金沢大学医薬保健研究域医学系Insulin resistance is a key pathophysiological feature of metabolic syndrome. However, the initial events triggering the development of insulin resistance and its causal relations with dysregulation of glucose and fatty acids metabolism remain unclear. We investigated biological pathways that have the potential to induce insulin resistance in mice fed a high-fat diet (HFD). We demonstrate that the pathways for reactive oxygen species (ROS) production and oxidative stress are coordinately up-regulated in both the liver and adipose tissue of mice fed an HFD before the onset of insulin resistance through discrete mechanism. In the liver, an HFD up-regulated genes involved in sterol regulatory element binding protein 1c-related fatty acid synthesis and peroxisome proliferator-activated receptor α-related fatty acid oxidation. In the adipose tissue, however, the HFD down-regulated genes involved in fatty acid synthesis and up-regulated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex. Furthermore, increased ROS production preceded the elevation of tumor necrosis factor-α and free fatty acids in the plasma and liver. The ROS may be an initial key event triggering HFD-induced insulin resistance. © 2008 Elsevier Inc. All rights reserved
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