Robleslambertsen6083

The purpose of this study was to clarify the contamination and cleaning of touch panels used in everyday life and the awareness of persons in charge and users of devices about contamination.

Samples from touch panels were cultured to detect viable bacteria (n=132), Staphylococcus aureus (n=66) and Escherichia coli (n=64). A questionnaire survey was conducted on persons in charge and users of the devices on the day of sampling.

Viable bacterial cells were detected in more than 90% of the automatic teller machines (ATMs) at banks, the ticket machines at stations, and the copy machines at convenience stores. S. aureus and E. coli were detected in more than one-half of such devices examined. The detection rate of viable bacterial cells in smartphones was 57.5% and was lower than those in other devices. More than 65% of the ATMs, ticket machines, and copy machines were cleaned once or twice a day. More than one-half of the users of smartphones or button-type mobile phones did not clean their devices. Those who did not aware about the contamination of touch panels were 46.6% of the persons in charge and 38.2% of the users.

It is necessary to examine the suitable number of times and methods of cleaning of touch panels and to raise the awareness of persons in charge or users of such devices about contamination.

It is necessary to examine the suitable number of times and methods of cleaning of touch panels and to raise the awareness of persons in charge or users of such devices about contamination.

A difference in the medical treatment situation between the first group and the second group of the hospital group in the DPC system was clarified using Diagnosis Procedure Combination (DPC) survey data according to Major Diagnostic Category (MDC). Furthermore, the division between the first group and the second group was examined.

DPC survey data collected in 2012 was used. According to MDC, significant differences in the patient ratio of hospitalization, the number of planned hospitalizations, the number of emergency hospitalizations, the number of ambulance conveyances, and the number of treatments were considered. Then, by the Mahalanobis-Taguchi method, distributions of the Mahalanobis distance and item choice according to MDC were considered.

Many items according to MDC showed significant differences between the first group and the second group. The Mahalanobis distance was increased by MDC 16 disease when divided by the Mahalanobis distance of 1.0 between the first group and the second group. The item, which contributed to the calculation of the Mahalanobis distance by item choice, varied and showed a difference between the first group and the second group.

The second group was authorized by the hospital followed by the first group. However, the results showed significant differences in the number of DPC survey data and the Mahalanobis distance of many items.

The second group was authorized by the hospital followed by the first group. However, the results showed significant differences in the number of DPC survey data and the Mahalanobis distance of many items.Traffic-related air pollution is a major contributor to urban air pollution. Diesel exhaust (DE) is its most important component of near-road and urban air pollutions and is commonly used as a surrogate model of air pollution in health effects studies. In particular, diesel exhaust particles (DEPs) and nanoparticles in DEPs are the components considered hazardous for health. It is widely known that exposure to DEPs is associated with mortality caused by respiratory and cardiovascular diseases. Recently, evidence has been accumulating showing that DEPs and nanoparticles may cause neurodegenerative disorders. Selleckchem Pyrvinium Here, we introduce evidence suggesting their association with these disorders. The chemical components and the translocation of DEPs and nanoparticles to the brain are described in part 1. In part 2, we introduce the mechanism of development of neurodegenerative diseases such as stroke, Alzheimer's disease, and Parkinson's disease via oxidative stress and inflammatory events. Furthermore, there are many lines of epidemiological evidence showing that the particulates impair cognitive function and ability of memory through oxidative and inflammatory events in the brain. These lines of evidences are supported by many animal experiments on neurological disorders.Peripheral arterial disease (PAD) is an atherosclerotic obstructive disease of the arteries in lower extremities. Patients with PAD show high rates of mortality from coronary artery disease (CAD) and stroke. Smoking as well as diabetes is an important risk factor for PAD. A lesion of PAD in the lower extremities tends to be more proximal in smokers than in nonsmokers and to be more distal in patients with diabetes than in nondiabetics. By a systematic review, the odds ratio for PAD of smokers vs nonsmokers has been reported to be in the range of 1.7-7.4. Previous epidemiological studies suggest a stronger association of smoking with PAD than that with CAD. Nitric oxide (NO) is an important molecule suppressing the progression of atherosclerosis, but this function is compromised by smoking. Smoking decreases the bioactivity of NO and the expression level of NO synthase. In addition, smoking results in deteriorations of risk factors for atherosclerosis such as decreases in blood HDL (high-density lipoprotein) cholesterol and tissue plasminogen activator levels and increases in the levels of blood triglycerides, LDL (low-density lipoprotein) cholesterol, fibrinogen and the von Willebrand factor. Thus, smoking increases blood coagulability and deteriorates the blood lipid profile, resulting in thrombogenetic proneness and dyslipidemia. Smoking also increases the generation of atherogenic oxidized LDL in blood and decreases antiatherogenic prostacyclin production in the vascular endothelium. Smoking cessation is important for the prevention and therapy of PAD, and to this end, counseling by physicians and nicotine replacement therapy are useful and strongly recommended for patients with PAD.During my academic career for more than 40 years, I was involved in 18 epidemiological field studies, partially or fully. Among these field studies, four (1. Medical services in remote rural areas in Okinawa, 2. Yusho episode, 3. JICA Onchocerciasis Control Project in Guatemala, and 4. Miyako cohort study in Fukuoka) are introduced in this paper, including the latest situation after the presentation. Through these field works experienced by the author, the following lessons were gained. 1. Strong human reliance between researchers and the targeted population is essential in carrying out epidemiological surveys successfully in the field. 2. Data obtained from the survey should be carefully examined and analyzed so that those data may reflect the real situation.Nonalcoholic fatty liver disease (NAFLD) is a common disease in humans having a broad spectrum of liver histology from simple fatty liver to mixed inflammatory cell infiltration and fibrosis (nonalcoholic steatohepatitis, NASH), which is a more severe and progressing form. NASH/NAFLD is significantly associated with lifestyle such as diet and exercise, obesity, insulin resistance, type 2 diabetes, dyslipidemia and hypertension. Age and gender are also associated with the development. On the other hand, NAFLD has been found in a high percentage of nonobese individuals in the Asia-Pacific area. Some characteristic animal models of NAFLD/NASH have been developed to clarify the pathogenesis of human NAFLD/NASH. We have recently developed a novel NASH rat model (stroke-prone spontaneously hypertensive rats, SHRSP5/Dmcr), which showed hepatic steatosis and inflammation at 2 weeks, ballooning, macrovesicular steatosis and fibrosis at 8 weeks, and bridging fibrosis at 14 weeks by feeding of high-fat and -cholesterol (HFC) diet alone. This animal model does not have obesity, insulin resistance or diabetes. Therefore, this may be an excellent animal model of human NASH/NAFLD without obesity and diabetes. Sex and strain differences observed in fibrogenesis by the HFC diet in SHRSP5/Dmcr may be associated with the sensitivity to detoxification enzymes in the liver, because the levels of UGP-glucuronosyltransferase and sulfotransferase and their regulating nuclear receptors only decreased in male SHRSP5/Dmcr rats, but not in female and SHRSP rats. This suggests the importance of phase II reactions of drug-metabolizing enzymes in NASH progression. Importantly, SHRSP5/Dmcr rats are spontaneously hypertensive; therefore, when we use the original strain Wistar Kyoto, which has normal blood pressure, the involvement of blood pressure in the development of human NASH/NAFLD may also be clarified.Arsenic metabolism affects the susceptibility of humans to arsenic toxicity; therefore, clarification of the factors associated with individual variations in arsenic metabolism is an important task. Genetic polymorphisms such as single nucleotide polymorphisms (SNPs) in arsenic (+3 oxidation state) methyltransferase (AS3MT), which can methylate arsenic compounds using S-adenosyl-l-methionine (AdoMet), have been reported to modify arsenic methylation. In this review, we summarize studies conducted by us in Vietnam and by others on the association of AS3MT genetic polymorphisms with arsenic metabolism as well as human health effects. Most of the SNPs in AS3MT showed inconsistent results in terms of genotype-dependent differences in arsenic metabolism among the studies. However, AS3MT 12390 (rs3740393) and 14458 (rs11191439) were consistently related to arsenic methylation regardless of the study population AS3MT 12390 (rs3740393) affected the second step of methylation of arsenic, whereas 14458 (rs11191439) affected the first methylation step.Naturally occurring inorganic arsenic is known to increase the risk of cancers of the skin and several other organs, including the urinary bladder, lung, and liver. Epidemiological studies have also indicated that gestational arsenic exposure is associated with increased incidences of cancers in several organs, including the bladder and liver, in adulthood. Previous studies have shown that epigenetic changes are involved in arsenic-induced carcinogenesis. Among epigenetic changes, DNA methylation changes that are specific to arsenic-induced tumors would be useful for distinguishing such tumors from tumors induced by other factors and for clarifying arsenic carcinogenesis. It has been reported that gestational arsenic exposure of C3H mice, whose males tend to spontaneously develop liver tumors, increases the incidence of tumors in the male offspring. Using the same experimental protocol, we found a number of regions where the DNA methylation status was altered in the liver tumors compared with the normal liver tissues by the methylated DNA immunoprecipitation (MeDIP)-CpG island microarray method. Among such regions, we demonstrated using real-time methylation-specific PCR and bisulfite sequencing that a gene body region of the oncogene Fosb underwent alteration in DNA methylation following gestational arsenic exposure. We also showed that the Fosb expression level significantly increased following gestational arsenic exposure. These findings suggest that the DNA methylation status of the Fosb region is implicated in tumor augmentation and can also be utilized for characterizing tumors induced by gestational arsenic exposure.