Transformation and Control of Crystal Structures on Electronic Thin Films

The deposition of Ni film on the Si substrate is important due to its broad applications in electronics, especially at the nanoscale. In this study, we applied molecular dynamics simulations to perform a subatomic observation simultaneously during the process of sputtering Ni on crystalline Si, and a model according to the Thompson formula was developed to simulate the energy distribution of ejected atoms during sputtering. We found the critical parameters controlling interdiffusion behavior were substrate temperature and incident flux of Ni. The substrate temperature significantly leads the crystallinity of the Ni film, where they exhibit amorphous, FCC, and BCC structures at substrate temperatures below 400, 500–600, and beyond 700 K, respectively. The incident flux dominates the crystallinity of the deposited Ni film. Only amorphous Ni forms with 10 atom/ps flux, and fewer defects in the FCC Ni film were observed with 2.5 atom/ps flux. To balance the throughputs and film quality, an incident flux of 2.5 atom/ps is the optimized choice. The detailed understanding enables the control of thin films during electronic fabrication

The amino acids sequences alignment of mutliple 6-phosohate ascorbic acid lactonase amino acid from different <i>Streptococcus</i> species, including <i>S</i>. <i>pneumoniae</i> ATCC 49136, <i>S</i>. <i>agalactiae</i> A909, <i>S</i>. <i>equi</i> 2329, <i>S</i>. <i>mitis</i> 21/39, <i>S</i>. <i>mutans</i> UA159, <i>S</i>. <i>porcinus</i> Str. Jelinkova 176, <i>S</i>. <i>pyogenes</i> GA40634, <i>S</i>. <i>suis</i> R61, <i>S</i>. <i>sanguinis</i> SK353, and, <i>S</i>. <i>uberis</i> B362.

<p>The amino acids sequences alignment of mutliple 6-phosohate ascorbic acid lactonase amino acid from different <i>Streptococcus</i> species, including <i>S</i>. <i>pneumoniae</i> ATCC 49136, <i>S</i>. <i>agalactiae</i> A909, <i>S</i>. <i>equi</i> 2329, <i>S</i>. <i>mitis</i> 21/39, <i>S</i>. <i>mutans</i> UA159, <i>S</i>. <i>porcinus</i> Str. Jelinkova 176, <i>S</i>. <i>pyogenes</i> GA40634, <i>S</i>. <i>suis</i> R61, <i>S</i>. <i>sanguinis</i> SK353, and, <i>S</i>. <i>uberis</i> B362.</p

Schemematic illustration of the mechanism of ampicillin resistance of MBL in <i>S</i>. <i>pneumonia</i> cells.

<p>Schemematic illustration of the mechanism of ampicillin resistance of MBL in <i>S</i>. <i>pneumonia</i> cells.</p

Localization of MBL.

<p>(A) Fluorescence microscopic detection of GFP (i) and MBL-GFP (ii) in <i>E</i>.<i>coli</i>. (B) Upper panel illustrates the immunoprecipitation of bacteria cells with antibody-conjugated magnetic nanoparticles (MNP). Lower panel reveal the PCR products of varied amount of bacteria immunoprecipitated with MBL specific antibody-conjugated magnetic Fe₃O₄ nanoparticles (MNP) and subsequent PCR using streptococci-specific primers that recognize the lytA gene.</p

MOESM1 of Dipeptidyl peptidase-4 inhibitor decreases the risk of atrial fibrillation in patients with type 2 diabetes: a nationwide cohort study in Taiwan

Additional file 1: Table S1. International Classification of Disease (9th edition) Clinical Modification (ICD 9-CM) codes used to define the co-morbidities and clinical outcome in the study cohort

Risk of Shingles in Adults with Primary Sjogren’s Syndrome and Treatments: A Nationwide Population-Based Cohort Study

<div><p>Background</p><p>Primary Sjögren's syndrome (pSS) is associated with immunological dysfunctions—a well-known risk factor of shingles. This study aimed to examine the incidence and risk of shingles in adults with pSS and pharmacological treatments.</p><p>Methods</p><p>This retrospective population-based cohort study was conducted using National Health Insurance claims data. Using propensity scores, 4,287 pSS adult patients and 25,722-matched cohorts by age, gender, selected comorbidities and Charlson comorbidity index scores were identified. Kaplan-Meier analysis and Cox regression were conducted to compare the differences in developing shingles. In pSS, oral and eye dryness are treated with substitute agents. Extraglandular features are often treated with pharmacological drugs including steroids and immunosuppressants. pSS patients were grouped as follows: no pharmacological drugs, steroids alone; immunosuppressants alone; combined therapies.</p><p>Results</p><p>During the follow-up, 463 adults with pSS (10.80%) and 1,345 control cohorts (5.23%) developed shingles. The cumulative incidence of shingles in pSS patients (18.74/1,000 patient-years) was significantly higher than controls (8.55/1,000 patient-years). The adjusted hazard ratio (HR) of shingles was 1.69 (95% confidence interval (CI) 1.50–1.90). In age-subgroup analyses, incidences of shingles in pSS increased with age and peaked in pSS patients aged ≧60; however, adjusted HRs decreased with age. Compared to control cohorts with no drugs, adjusted HRs for shingles in pSS patients were ranked from high to low as: combined therapies (4.14; 95% CI 3.14–5.45) > immunosuppressants alone (3.24; 95% CI 2.36–4.45) > steroids alone (2.54; 95% CI 2.16–2.97) > no pharmacological drugs (2.06; 95% CI 1.76–2.41). Rates of shingles-associated hospitalization and postherpetic neuralgia were 5.62% and 24.41%, both of which were significantly higher than those (2.60%; 13.01%) in the control cohorts.</p><p>Conclusions</p><p>Adults with pSS were at greater risk for shingles than control cohorts. Drug exposures significantly increased the risk of shingles in pSS.</p></div

JEV infection in vimentin-expressing cells.

<p>(A, B) Vimentin expression was observed in most Sox1⁺ NPC cells and GFAP⁺ cells. (C, D) Most TuJ1⁺ expressing cells (matured neurons) did not express the vimentin. Panel C and D, low magnification and high magnification, respectively. (E, F, G) JEV-infected cells (JEV NS1⁺ cells, blue) were colocalized with the vimentin-expressing cells (green), but not the human mature neurons (TuJ1⁺, arrow head, red). Scar bar in each panel, 10 µm.</p

Viral replication and cytopathic effect of JEV-infected NPCs.

<p>(A) The viral growth curve in JEV-infected NPCs at MOI 0.1 is illustrated. (B, C) The infected NPCs expressed the viral NS1 and NS1′ proteins (B) and exhibited a depleted cell population (C) at MOI 0.1. (D) The degree of membrane externalization on the infected cells, detected by Annexin V staining, was quantified by flow cytometry analysis.</p

Demographic characteristics for pSS adults and the control cohorts in Taiwan between 2001 and 2008.

<p>pSS: primary Sjogren’s syndrome; SD: standard deviation.</p><p>Categorical variable was estimated by chi-square test and continuous variable was estimated by student’s t-test.</p><p><i>P</i> < 0.05, statistical significance.</p><p>Demographic characteristics for pSS adults and the control cohorts in Taiwan between 2001 and 2008.</p

JEV infection in hESC-derived glial cells and neurons.

<p>(A) The JEV NS1 proteins were detected in GFAP-expressing glial cells at MOI 1 on 1 d.p.i.. (B–D) The expression of JEV NS1 proteins in mature neurons (TuJ1⁺) is illustrated at MOI 1 on 1 d.p.i. (B) and at MOI 10 on 1 d.p.i. (C) or 3 d.p.i. (D). (E–H) The infectivity of JEV was determined in GABAnergic (E), glutaminergic (F), dopaminergic (G) and serotonergic neurons (H) at MOI 10 on 3 d.p.i. TuJ1 antibody, anti-βIII tubulin. TH, tyrosine hydroxylase. Scale bar, 20 µm.</p