959 research outputs found

    Quasi-particle interference and superconducting gap in a high-temperature superconductor Ca2-xNaxCuO2Cl2

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    High-transition-temperature (high-Tc) superconductivity is ubiquitous in the cuprates containing CuO2 planes but each cuprate has its own character. The study of the material dependence of the d-wave superconducting gap (SG) should provide important insights into the mechanism of high-Tc. However, because of the 'pseudogap' phenomenon, it is often unclear whether the energy gaps observed by spectroscopic techniques really represent the SG. Here, we report spectroscopic imaging scanning tunneling microscopy (SI-STM) studies of nearly-optimally-doped Ca2-xNaxCuO2Cl2 (Na-CCOC) with Tc = 25 ~ 28 K. They enable us to observe the quasi-particle interference (QPI) effect in this material, through which unambiguous new information on the SG is obtained. The analysis of QPI in Na-CCOC reveals that the SG dispersion near the gap node is almost identical to that of Bi2Sr2CaCu2Oy (Bi2212) at the same doping level, while Tc of Bi2212 is 3 times higher than that of Na-CCOC. We also find that SG in Na-CCOC is confined in narrower energy and momentum ranges than Bi2212. This explains at least in part the remarkable material dependence of TcComment: 13pages, 4fig

    Health and Sickness Absence in Denmark: A Study of Elderly-Care Immigrant Workers

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    The objective of this study is to investigate patterns of sickness absence in light of health status among immigrants. Cross-sectional data from 2005 was used and the study population consisted of 3,121 healthcare assistants and healthcare helpers working in the elderly-care sector in Denmark. A multinomial logistic regression was employed to investigate the relationship between health indicator, sickness absence and being an immigrant. Our findings show that, on one hand, immigrants have worse health status, but on the other, they have significantly lower sickness absence than their Danish counterparts, even after factors such as age and gender are controlled for. The results show that the relationship between being an immigrant and sickness absence differs according to health status. Our findings are in line with Steer and Rhode’s theoretical framework, according to which attendance to work is a function of ability and motivation to be at work

    HIGH PREVALENCE OF Blastocystis spp. INFECTION IN CHILDREN AND STAFF MEMBERS ATTENDING PUBLIC URBAN SCHOOLS IN SÃO PAULO STATE, BRAZIL

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    After a gastroenteritis outbreak of unknown etiology in the municipality ofSebastião da Grama, SãoPaulo, Brazil, we conducted a parasitological survey to establish the epidemiological profile of enteroparasitosis in children and staff members attending the public urban schools in operation in town. The cross-sectional study evaluated 172 children aged 11 months to 6 years old and 33 staff members aged 19 to 58 years old. Overall, 96 (55.81%) children and 20 (60.61%) staff members were mono-parasitized, while 58 (33.72%) children and 4 (12.12%) workers were poly-parasitized. Protozoa (88.37%; 72.73%) was more prevalent than helminthes (3.48%; 0%) in children and staff members respectively.Blastocystis spp. was the most prevalent parasite in children (86.63%) and staff members (66.67%). The age of 1 year old or less was found to be associated with increased prevalence of giardiasis [OR = 13.04; 95%CI 2.89-58.91; p = 0.00] and public garbage collection was identified as a protective factor against intestinal helminth infections [OR = 0.06; 95%CI 0.00-0.79; p = 0.03]. Although most of the children tested positive for Blastocystis spp. and also presented clinical signs/symptoms (62.2%), this association was not statistically significant [OR = 1.35; 95%CI 0.53-3.44; p = 0.51]. Intestinal parasites still represent a public health concern and this study underscores the importance of further investigations to better understand the pathogenic role ofBlastocystis spp

    Expression of MuRF1 or MuRF2 is essential for the induction of skeletal muscle atrophy and dysfunction in a murine pulmonary hypertension model

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    Background Pulmonary hypertension leads to right ventricular heart failure and ultimately to cardiac cachexia. Cardiac cachexia induces skeletal muscles atrophy and contractile dysfunction. MAFbx and MuRF1 are two key proteins that have been implicated in chronic muscle atrophy of several wasting states. Methods Monocrotaline (MCT) was injected over eight weeks into mice to establish pulmonary hypertension as a murine model for cardiac cachexia. The effects on skeletal muscle atrophy, myofiber force, and selected muscle proteins were evaluated in wild-type (WT), MuRF1, and MuRF2-KO mice by determining muscle weights, in vitro muscle force and enzyme activities in soleus and tibialis anterior (TA) muscle. Results In WT, MCT treatment induced wasting of soleus and TA mass, loss of myofiber force, and depletion of citrate synthase (CS), creatine kinase (CK), and malate dehydrogenase (MDH) (all key metabolic enzymes). This suggests that the murine MCT model is useful to mimic peripheral myopathies as found in human cardiac cachexia. In MuRF1 and MuRF2-KO mice, soleus and TA muscles were protected from atrophy, contractile dysfunction, while metabolic enzymes were not lowered in MuRF1 or MuRF2-KO mice. Furthermore, MuRF2 expression was lower in MuRF1KO mice when compared to C57BL/6 mice. Conclusions In addition to MuRF1, inactivation of MuRF2 also provides a potent protection from peripheral myopathy in cardiac cachexia. The protection of metabolic enzymes in both MuRF1KO and MuRF2KO mice as well as the dependence of MuRF2 expression on MuRF1 suggests intimate relationships between MuRF1 and MuRF2 during muscle atrophy signaling

    Genetic variation in autophagy-related genes influences the risk and phenotype of Buruli ulcer

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    Introduction Buruli ulcer (BU) is a severe necrotizing human skin disease caused by Mycobacterium ulcerans. Clinically, presentation is a sum of these diverse pathogenic hits subjected to critical immune-regulatory mechanisms. Among them, autophagy has been demonstrated as a cellular process of critical importance. Since microtubules and dynein are affected by mycolactone, the critical pathogenic exotoxin produced by M. ulcerans, cytoskeleton-related changes might potentially impair the autophagic process and impact the risk and progression of infection. Objective Genetic variants in the autophagy-related genes NOD2, PARK2 and ATG16L1 has been associated with susceptibility to mycobacterial diseases. Here, we investigated their association with BU risk, its severe phenotypes and its progression to an ulcerative form. Methods Genetic variants were genotyped using KASPar chemistry in 208 BU patients (70.2% with an ulcerative form and 28% in severe WHO category 3 phenotype) and 300 healthy endemic controls. Results The rs1333955 SNP in PARK2 was significantly associated with increased susceptibility to BU [odds ratio (OR), 1.43; P = 0.05]. In addition, both the rs9302752 and rs2066842 SNPs in NOD2 gee significantly increased the predisposition of patients to develop category 3 (OR, 2.23; P = 0.02; and OR 12.7; P = 0.03, respectively, whereas the rs2241880 SNP in ATG16L1 was found to significantly protect patients from presenting the ulcer phenotype (OR, 0.35; P = 0.02). Conclusion Our findings indicate that specific genetic variants in autophagy-related genes influence susceptibility to the development of BU and its progression to severe phenotypes.The research leading to these results received funding from the Health Services of the Fundação Calouste Gulbenkian under the grant Proc.N°94776 LJ; from the Fundação para a Ciência e Tecnologia (FCT), cofunded by Programa Operacional Regional do Norte (ON.2—O Novo 267 Norte); from the Quadro de Referência Estratégico Nacional (QREN) through the Fundo Europeu de Desenvolvimento Regional (FEDER) and from the Projeto Estratégico – LA 26 – 2013–2014 (PEst-C/SAU/LA0026/2013). JFM received an individual QREN fellowship (UMINHO/BPD/14/2014); CCu and AGF received an individual FCT fellowship (SFRH/BPD/96176/2013 and SFRH/BPD/68547/2010, respectively); and AC received an FCT contract (IF/00735/2014). The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript

    Prevalence of putative virulence factors and antimicrobial susceptibility of Enterococcus faecalis isolates from patients with dental Diseases

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    <p>Abstract</p> <p>Background</p> <p>This study investigated the prevalence of <it>Enterococcus faecalis</it>, its putative virulence factors and antimicrobial susceptibility in individuals with and without dental diseases. A total of 159 oral rinse specimens were collected from patients (n = 109) suffering from dental diseases and healthy controls (n = 50).</p> <p>Results</p> <p><it>E. faecalis </it>was detected using only culture in 8/109 (7.3%) of the patients with various types of dental diseases, whereas no <it>E. faecalis </it>was found in the healthy controls weather using both culture and PCR. Phenotype characterizations of the 8 <it>E. faecalis </it>isolates indicated that 25% of the isolates produced haemolysin and 37.5% produced gelatinase. Most important virulence genes; collagen binding protein (<it>ace</it>) and endocarditis antigen (<it>efaA</it>) were present in all 8 <it>E. faecalis </it>isolates, while haemolysin activator gene (<it>cylA</it>) was detected only in 25% of isolates, and all isolates were negative for <it>esp </it>gene. All <it>E. faecalis </it>isolates were 100% susceptible to ampicillin, chloramphenicol, ciprofloxacin, vancomycin, and teicoplanin, and to less extent to erythromycin (62.5%).</p> <p>Conclusion</p> <p>This study shows that all <it>E. faecalis </it>isolates were recovered only from patients with dental diseases especially necrotic pulps, and all isolates carried both collagen binding protein and endocarditis antigen genes and highly susceptible to frequently used antimicrobial drugs in Jordan.</p
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