Analisa Pengaruh Putaran Spindel 800 Rpm Dan 1250 Rpm Pada Sambungan Fe-Cu Dengan Menggunakan Metode FSW (Friction Stir Welding) Single Track

This study aims to determine the tensile strength, hardness of steel joints with copper using the FSW method. Material used st37 steel, copper. in the welding process using a conventional milling machine with rotational rotation of 800 rpm and 1250 rpm, feed rate 12.5 mm / min, slope angle 10 and 1.8 mm plunge dept. using the ASTM E8M testing standard for tensile testing and ASTM E384 standard for violent testing. From the tensile strength test of Fe-Cu connections round 800 rpm has an average voltage of 320.63 Mpa and an average strain of 2.07%, while the 1250 rpm Fe-Cu connection has an average voltage of 165.28 MPa and an average strain - average 1.33%. For base metal at Fe-Cu 800 rpm Fe material has an average stress of 318.01 Mpa and an average strain of 7.62%, while Cu material has an average voltage of 388.26 MPa and an average strain of 13, 27%. For base metal at 1250 rpm Fe-Cu connection Cu material has an average voltage of 388.26 MPa and an average strain of 13.27%, while Fe material has an average voltage of 303.36 Mpa and an average strain of 9 , 46%. From the results of testing the hardness of Fe-Cu connection of rotation of 800 rpm at the stir zone area showed 270,8 HVN value and HAZ area showed 296,2 HVN value, while at 1250 rpm Fe-Cu connection at stir zone area showed 250,3 HVN and the HAZ area shows a value of 270.1 HVN. For base metal Fe-Cu 800 rpm connection in Fe material showed value of 162,4 HVN and Cu material showed 73,1 HVN value, while for base metal connection at Fe-Cu 1250 rpm Fe material showed 162,2 HVN value and material Cu shows a value of 74.2 HVN. Keywords: friction stir welding, st37 steel, copper, tensile, hardness. Spindle

Retrospective cohort study evaluating clinical, biochemical and pharmacological prognostic factors for prostate cancer progression using primary care data

This is the final version. Available on open access from BMJ Publishing group via the DOI in this recordObjectives – To confirm the association of previously reported prognostic factors with future progression of localised prostate cancer using primary care data and identify new potential prognostic factors for further assessment in prognostic model development and validation. Design – Retrospective cohort study, employing Cox proportional hazards regression controlling for age, PSA, and Gleason score, stratified by diagnostic stage. Setting – Primary care in England Participants – Males with localised prostate cancer diagnosed between 01/01/1987 and 31/12/2016 within the Clinical Practice Research Datalink database, with linked data from the National Cancer Registration and Analysis Service and Office for National Statistics. Primary and Secondary outcomes – Primary outcome measure was prostate cancer mortality. Secondary outcomes measures were all-cause mortality and commencing systematic therapy. Up13 staging after diagnosis was not used as a secondary outcome owing to significant missing data. Results 10,901 males (mean age 74.38 +/- 9.03 years) with localised prostate cancer were followed up for a mean of 14.12 (+/- 6.36) years. 2,331 (21.38%) men underwent systemic therapy and 3,250 (31.65%) died, including 1,250 (11.47%) from prostate cancer. Factors associated with an increased risk of prostate cancer mortality included age; high PSA; current or ex-smoker; ischaemic heart disease; high C-Reactive Protein; high ferritin; low haemoglobin; high blood glucose; and low albumin. Conclusions This study identified several new potential prognostic factors for prostate cancer progression, as well as confirming some known prognostic factors, in an independent primary care data set. Further research is needed to develop and validate a prognostic model for prostate cancer progression.Can Test Collaborative/CRU

Role of common human TRIM5α variants in HIV-1 disease progression

BACKGROUND: The retroviral restriction factor tripartite motif protein (TRIM)5α, is characterized by marked amino acid diversity among primates, including specific clusters of residues under positive selection. The identification of multiple non-synonymous changes in humans suggests that TRIM5α variants might be relevant to retroviral pathogenesis. Previous studies have shown that such variants are unlikely to modify susceptibility to HIV-1 infection, or the course of early infection. However, the longterm effect of carrying Trim5α variants on disease progression in individuals infected with HIV-1 has not previously been investigated. METHODS: In a cohort of 979 untreated individuals infected with HIV-1 with median follow up 3.2 years and 9,828 CD4 T cell measurements, we analysed common amino acid variations: H43Y, V112F, R136Q, G249D, and H419Y. The rate of CD4 T cell decline before treatment was used as the phenotype. In addition, we extended previous work on the in vitro susceptibility of purified donor CD4 T cells (n = 125) to HIV-1 infection, and on the susceptibility of HeLa cells that were stably transduced with the different TRIM5 variants. Haplotypes were analysed according to the most parsimonious evolutionary structure, where two main human TRIM5α groups can be defined according to the residue at amino acid 136. Humans present both Q136 and R136 at similar frequency, and additional TRIM5α amino acid variants are almost exclusively derived from R136-carrying haplotypes. RESULTS: We observed modest differences in disease progression for evolutionary branches carrying R136-derived haplotypes, and with the non-synonymous polymorphisms G249D and H419Y. In vitro analysis of susceptibility of donor CD4 T cells, and of the various transduced HeLa cell lines supported the absence of significant differential restriction of HIV-1 infection by the various huTRIM5α alleles. CONCLUSION: Common human variants of TRIM5α have no effect or modest effect on HIV-1 disease progression. These variants occur at sites conserved throughout evolution, and are remote from clusters of positive selection in the primate lineage. The evolutionary value of the substitutions remains unclear

Bariatric surgery in morbidly obese insulin resistant humans normalises insulin signalling but not insulin-stimulated glucose disposal.

This is the final published version. Available from PLoS via the DOI in this record.All relevant data are available from Figshare, under the DOI http://dx.doi. org/10.6084/m9.figshare.1292883.AIMS: Weight-loss after bariatric surgery improves insulin sensitivity, but the underlying molecular mechanism is not clear. To ascertain the effect of bariatric surgery on insulin signalling, we examined glucose disposal and Akt activation in morbidly obese volunteers before and after Roux-en-Y gastric bypass surgery (RYGB), and compared this to lean volunteers. MATERIALS AND METHODS: The hyperinsulinaemic euglycaemic clamp, at five infusion rates, was used to determine glucose disposal rates (GDR) in eight morbidly obese (body mass index, BMI=47.3 ± 2.2 kg/m(2)) patients, before and after RYGB, and in eight lean volunteers (BMI=20.7 ± 0.7 kg/m2). Biopsies of brachioradialis muscle, taken at fasting and insulin concentrations that induced half-maximal (GDR50) and maximal (GDR100) GDR in each subject, were used to examine the phosphorylation of Akt-Thr308, Akt-473, and pras40, in vivo biomarkers for Akt activity. RESULTS: Pre-operatively, insulin-stimulated GDR was lower in the obese compared to the lean individuals (P<0.001). Weight-loss of 29.9 ± 4 kg after surgery significantly improved GDR50 (P=0.004) but not GDR100 (P=0.3). These subjects still remained significantly more insulin resistant than the lean individuals (p<0.001). Weight loss increased insulin-stimulated skeletal muscle Akt-Thr308 and Akt-Ser473 phosphorylation, P=0.02 and P=0.03 respectively (MANCOVA), and Akt activity towards the substrate PRAS40 (P=0.003, MANCOVA), and in contrast to GDR, were fully normalised after the surgery (obese vs lean, P=0.6, P=0.35, P=0.46, respectively). CONCLUSIONS: Our data show that although Akt activity substantially improved after surgery, it did not lead to a full restoration of insulin-stimulated glucose disposal. This suggests that a major defect downstream of, or parallel to, Akt signalling remains after significant weight-loss.Diabetes Research and Wellness FoundatioMedical Research Council (MRC)Astra Zenec

Equating scores of the University of Pennsylvania Smell Identification Test and Sniffin' Sticks test in patients with Parkinson's disease

BACKGROUND: Impaired olfaction is an important feature in Parkinson's disease (PD) and other neurological diseases. A variety of smell identification tests exist such as "Sniffin' Sticks" and the University of Pennsylvania Smell Identification Test (UPSIT). An important part of research is being able to replicate findings or combining studies in a meta-analysis. This is difficult if olfaction has been measured using different metrics. We present conversion methods between the: UPSIT, Sniffin' 16, and Brief-SIT (B-SIT); and Sniffin' 12 and Sniffin' 16 odour identification tests. METHODS: We used two incident cohorts of patients with PD who were tested with either the Sniffin' 16 (n = 1131) or UPSIT (n = 980) and a validation dataset of 128 individuals who took both tests. We used the equipercentile and Item Response Theory (IRT) methods to equate the olfaction scales. RESULTS: The equipercentile conversion suggested some bias between UPSIT and Sniffin' 16 tests across the two groups. The IRT method shows very good characteristics between the true and converted Sniffin' 16 (delta mean = 0.14, median = 0) based on UPSIT. The equipercentile conversion between the Sniffin' 12 and 16 item worked well (delta mean = 0.01, median = 0). The UPSIT to B-SIT conversion showed evidence of bias but amongst PD cases worked well (mean delta = -0.08, median = 0). CONCLUSION: We have demonstrated that one can convert UPSIT to B-SIT or Sniffin' 16, and Sniffin' 12 to 16 scores in a valid way. This can facilitate direct comparison between tests aiding future collaborative analyses and evidence synthesis

Control of magnetic anisotropy by orbital hybridization in (La0.67Sr0.33MnO3)n/(SrTiO3)n superlattice

The asymmetry of chemical nature at the hetero-structural interface offers an unique opportunity to design desirable electronic structure by controlling charge transfer and orbital hybridization across the interface. However, the control of hetero-interface remains a daunting task. Here, we report the modulation of interfacial coupling of (La0.67Sr0.33MnO3)n/(SrTiO3)n superlattices by manipulating the periodic thickness with n unit cells of SrTiO3 and n unit cells La0.67Sr0.33MnO3. The easy axis of magnetic anisotropy rotates from in-plane (n = 10) to out-of-plane (n = 2) orientation at 150 K. Transmission electron microscopy reveals enlarged tetragonal ratio > 1 with breaking of volume conservation around the (La0.67Sr0.33MnO3)n/(SrTiO3)n interface, and electronic charge transfer from Mn to Ti 3d orbitals across the interface. Orbital hybridization accompanying the charge transfer results in preferred occupancy of 3d3z2-r2 orbital at the interface, which induces a stronger electronic hopping integral along the out-of-plane direction and corresponding out-of-plane magnetic easy axis for n = 2. We demonstrate that interfacial orbital hybridization in superlattices of strongly correlated oxides may be a promising approach to tailor electronic and magnetic properties in device applications

Stochastic population growth in spatially heterogeneous environments

Classical ecological theory predicts that environmental stochasticity increases extinction risk by reducing the average per-capita growth rate of populations. To understand the interactive effects of environmental stochasticity, spatial heterogeneity, and dispersal on population growth, we study the following model for population abundances in $n$ patches: the conditional law of $X_{t+dt}$ given $X_t=x$ is such that when $dt$ is small the conditional mean of $X_{t+dt}^i-X_t^i$ is approximately $[x^i\mu_i+\sum_j(x^j D_{ji}-x^i D_{ij})]dt$, where $X_t^i$ and $\mu_i$ are the abundance and per capita growth rate in the $i$-th patch respectivly, and $D_{ij}$ is the dispersal rate from the $i$-th to the $j$-th patch, and the conditional covariance of $X_{t+dt}^i-X_t^i$ and $X_{t+dt}^j-X_t^j$ is approximately $x^i x^j \sigma_{ij}dt$. We show for such a spatially extended population that if $S_t=(X_t^1+...+X_t^n)$ is the total population abundance, then $Y_t=X_t/S_t$, the vector of patch proportions, converges in law to a random vector $Y_\infty$ as $t\to\infty$, and the stochastic growth rate $\lim_{t\to\infty}t^{-1}\log S_t$ equals the space-time average per-capita growth rate \sum_i\mu_i\E[Y_\infty^i] experienced by the population minus half of the space-time average temporal variation \E[\sum_{i,j}\sigma_{ij}Y_\infty^i Y_\infty^j] experienced by the population. We derive analytic results for the law of $Y_\infty$, find which choice of the dispersal mechanism $D$ produces an optimal stochastic growth rate for a freely dispersing population, and investigate the effect on the stochastic growth rate of constraints on dispersal rates. Our results provide fundamental insights into "ideal free" movement in the face of uncertainty, the persistence of coupled sink populations, the evolution of dispersal rates, and the single large or several small (SLOSS) debate in conservation biology.Comment: 47 pages, 4 figure

An epidemiological study on anemia among institutionalized people with intellectual and/or motor disability with special reference to its frequency, severity and predictors

BACKGROUND: To examine the type, frequency, severity, and predictors of anemia and its relationship with co-morbid conditions among institutionalized people with intellectual and/or motor disability. METHODS: We conducted a cross-sectional study at a public facility for people with intellectual and/or motor disability in Ibaraki prefecture, Japan. Health checkup data obtained in 2001 from 477 people with intellectual disability (male: 286, average age 40.6 ± 12.3; female: 191, average age 45.1 ± 11.6) were retrospectively reviewed. RESULTS: The prevalence of anemia among male participants was higher than in female participants for each disability category (intellectual disability, 41.1%, 4.2%; cerebral palsy, 37.5%, 4.8%; Down's syndrome, 15.0%, 0%; severe motor and intellectual disabilities, 61.9%, 16.7%). Most participants with anemia (93.8 – 100%) showed a normocytic normochromic anemia pattern. Multivariate analysis revealed that factors related to an increase in frequency included sex (male), low body mass index (BMI), use of anticonvulsants or major tranquilizers, and a high zinc sulfate turbidity test (ZTT) value. No clinically diagnosed co-morbid condition was found to be related to the presence of anemia. CONCLUSION: A high frequency of mild normocytic normochromic anemia in institutionalized people with intellectual and/or motor disability was observed, particularly among males. Medications and chronic inflammation may increase the risk of anemia