Amorphous molybdenum silicon superconducting thin films

Amorphous superconductors have become attractive candidate materials for superconducting nanowire single-photon detectors due to their ease of growth, homogeneity and competitive superconducting properties. To date the majority of devices have been fabricated using WxSi1-x, though other amorphous superconductors such as molybdenum silicide (MoxSi1-x) offer increased transition temperature. This study focuses on the properties of MoSi thin films grown by magnetron sputtering. We examine how the composition and growth conditions affect film properties. For 100 nm film thickness, we report that the superconducting transition temperature (Tc) reaches a maximum of 7.6 K at a composition of Mo83Si17. The transition temperature and amorphous character can be improved by cooling of the substrate during growth which inhibits formation of a crystalline phase. X-ray diffraction and transmission electron microscopy studies confirm the absence of long range order. We observe that for a range of 6 common substrates (silicon, thermally oxidized silicon, R- and C-plane sapphire, x-plane lithium niobate and quartz), there is no variation in superconducting transition temperature, making MoSi an excellent candidate material for SNSPDs.This work was supported by the EPSRC through grant EP/I036303/1. RHH acknowledges a Royal Society of London University Research Fellowship. The data used in this paper can be accessed at https://www.repository.cam.ac.uk/handle/1810/247704.This is the final version of the article. It first appeared from AIP Publishing via http://dx.doi.org/10.1063/1.492828

Quality of private and public ambulatory health care in low and middle income countries: systematic review of comparative studies

Paul Garner and colleagues conducted a systematic review of 80 studies to compare the quality of private versus public ambulatory health care in low- and middle-income countries

A one-year trial of lamivudine for chronic hepatitis B

Background and Methods: In preliminary trials, lamivudine, an oral nucleoside analogue, has shown promise for the treatment of chronic hepatitis B. We conducted a one-year double-blind trial of lamivudine in 358 Chinese patients with chronic hepatitis B. The patients were randomly assigned to receive 25 mg of lamivudine (142 patients), 100 mg of lamivudine (143), or placebo (73) orally once daily. The patients underwent liver biopsies before entering the study and after completing the assigned treatment regimen. The primary end point was a reduction of at least two points in the Knodell necroinflammatory score. Results: Hepatic necroinflammatory activity improved by two points or more in 56 percent of the patients receiving 100 mg of lamivudine, 49 percent of those receiving 25 mg of lamivudine, and 25 percent of those receiving placebo (P<0.001 and P=0.001, respectively, for the comparisons of lamivudine treatment with placebo). Necroinflammatory activity worsened in 7 percent of the patients receiving 100 mg of lamivudine, 8 percent of those receiving 25 mg, and 26 percent of those receiving placebo. The 100mg dose of lamivudine was associated with a reduced progression of fibrosis (P=0.01 for the comparison with placebo) and with the highest rate of hepatitis B e antigen (HBeAg) seroconversion (loss of HBeAg, development of antibody to HBeAg, and undetectable HBV DNA) (16 percent), the greatest suppression of HBV DNA (98 percent reduction at week 52 as compared with the base-line value), and the highest rate of sustained normalization of alanine aminotransferase levels (72 percent). Ninety-six percent of the patients completed the study. The incidence of adverse events was similar in all groups, and there were few serious events. Conclusions: In a one-year study, lamivudine was associated with substantial histologic improvement in many patients with chronic hepatitis B. A daily dose of 100 mg was more effective than a daily dose of 25 mg.published_or_final_versio

Public funding of health at the district level in Indonesia after decentralization – sources, flows and contradictions

<p>Abstract</p> <p>Background</p> <p>During the Suharto era public funding of health in Indonesia was low and the health services were tightly controlled by the central government; district health staff had practically no discretion over expenditure. Following the downfall of President Suharto there was a radical political, administrative and fiscal decentralization with delivery of services becoming the responsibility of district governments. In addition, public funding for health services more than doubled between 2001 and 2006. It was widely expected that services would improve as district governments now had both more adequate funds and the responsibility for services. To date there has been little improvement in services. Understanding why services have not improved requires careful study of what is happening at the district level.</p> <p>Methods</p> <p>We collected information on public expenditure on health services for the fiscal year 2006 in 15 districts in Java, Indonesia from the district health offices and district hospitals. Data obtained in the districts were collected by three teams, one for each province. Information on district government revenues were obtained from district public expenditure databases maintained by the World Bank using data from the Ministry of Finance.</p> <p>Results</p> <p>The public expenditure information collected in 15 districts as part of this study indicates district governments are reliant on the central government for as much as 90% of their revenue; that approximately half public expenditure on health is at the district level; that at least 40% of district level public expenditure on health is for personnel, almost all of them permanent civil servants; and that districts may have discretion over less than one-third of district public expenditure on health; the extent of discretion over spending is much higher in district hospitals than in the district health office and health centers. There is considerable variation between districts.</p> <p>Conclusion</p> <p>In contrast to the promise of decentralization there has been little increase in the potential for discretion at the district level in managing public funds for health – this is likely to be an important reason for the lack of improvement in publicly funded health services. Key decisions about money are still made by the central government, and no one is held accountable for the performance of the sector – the district blames the center and the central ministries (and their ministers) are not accountable to district populations.</p

Adaptive Evolution of the Myo6 Gene in Old World Fruit Bats (Family: Pteropodidae)

PMCID: PMC3631194This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Disease progression in Plasmodium knowlesi malaria is linked to variation in invasion gene family members.

Emerging pathogens undermine initiatives to control the global health impact of infectious diseases. Zoonotic malaria is no exception. Plasmodium knowlesi, a malaria parasite of Southeast Asian macaques, has entered the human population. P. knowlesi, like Plasmodium falciparum, can reach high parasitaemia in human infections, and the World Health Organization guidelines for severe malaria list hyperparasitaemia among the measures of severe malaria in both infections. Not all patients with P. knowlesi infections develop hyperparasitaemia, and it is important to determine why. Between isolate variability in erythrocyte invasion, efficiency seems key. Here we investigate the idea that particular alleles of two P. knowlesi erythrocyte invasion genes, P. knowlesi normocyte binding protein Pknbpxa and Pknbpxb, influence parasitaemia and human disease progression. Pknbpxa and Pknbpxb reference DNA sequences were generated from five geographically and temporally distinct P. knowlesi patient isolates. Polymorphic regions of each gene (approximately 800 bp) were identified by haplotyping 147 patient isolates at each locus. Parasitaemia in the study cohort was associated with markers of disease severity including liver and renal dysfunction, haemoglobin, platelets and lactate, (r = ≥ 0.34, p =  <0.0001 for all). Seventy-five and 51 Pknbpxa and Pknbpxb haplotypes were resolved in 138 (94%) and 134 (92%) patient isolates respectively. The haplotypes formed twelve Pknbpxa and two Pknbpxb allelic groups. Patients infected with parasites with particular Pknbpxa and Pknbpxb alleles within the groups had significantly higher parasitaemia and other markers of disease severity. Our study strongly suggests that P. knowlesi invasion gene variants contribute to parasite virulence. We focused on two invasion genes, and we anticipate that additional virulent loci will be identified in pathogen genome-wide studies. The multiple sustained entries of this diverse pathogen into the human population must give cause for concern to malaria elimination strategists in the Southeast Asian region

Lactoferrin prevents LPS-induced decrease of the iron exporter ferroportin in human monocytes/macrophages.

Iron balance is tightly linked to inflammation and it has been demonstrated that many proteins involved in cellular iron management are up- or down-regulated by inflammatory stimuli, ultimately leading to iron retention in the reticuloendothelial system. Ferroportin is a key player in maintenance of correct iron homeostasis, because it is the only known mammalian cellular iron exporter. In this work we show that incubation of THP-1 monocytes/macrophages with lactoferrin prevents the LPS-induced decrease of ferroportin by reducing secretion of IL-6. © 2014 Springer Science+Business Media New York.Iron balance is tightly linked to inflammation and it has been demonstrated that many proteins involved in cellular iron management are up- or downregulated by inflammatory stimuli, ultimately leading to iron retention in the reticuloendothelial system. Ferroportin is a key player in maintenance of correct iron homeostasis, because it is the only known mammalian cellular iron exporter. In this work we show that incubation of THP-1 monocytes/macrophages with lactoferrin prevents the LPS-induced decrease of ferroportin by reducing secretion of IL-6