Miracle-dz/UniFAR-FTUs huggingface dataset:
Associations of SF-36 mental health functioning and work and family related factors with intentions to retire early among employees

Objective: To examine the associations of mental health functioning (SF-36) and work and family related psychosocial factors with intentions to retire early. Methods: Cross sectional survey data (n = 5037) from the Helsinki Health Study occupational cohort in 2001 and 2002 were used. Intentions to retire early were inquired with a question: “Have you considered retiring before normal retirement age? ” Mental health functioning was measured by the Short Form 36 (SF-36) mental component summary (MCS). Work and family related psychosocial factors included job demands and job control, procedural and relational justice, conflicts between work and family, and social network size. Multinomial regression models were used to analyse the data. Results: Poor mental health functioning, unfavourable psychosocial working conditions, and conflicts between work and family were individually related to intentions to retire early. After adjustments for all work and family related factors the odds ratio for low mental health functioning was halved (from OR = 6.05 to 3.67), but nevertheless the association between poor mental health functioning and strong intentions to retire early remained strong. Conclusions: These findings highlight not only the importance of low mental health and unfavourable working conditions but also the simultaneous impact of conflicts between work and family to employees’ intentions to retire early.
Correlation of HLA-DP/DQ polymorphisms with transplant etiologies and prognosis in liver transplant recipients

Abstract Previous study has identified that the genetic variants in the human leukocyte antigen (HLA)-DP/DQ region were strongly associated with hepatitis B virus (HBV) infection. But their roles in liver function recovery after hepatic transplantation were still obscure. This study aimed to investigate whether HLA-DP/DQ polymorphisms were associated with post-transplant etiologies and prognosis in Chinese liver transplant recipients. A total of 144 liver transplant recipients were enrolled, which were divided into 2 groups according to the transplant etiology: HBV-related disease and non-HBV-related disease. HBV-related disease includes 3 subgroups: liver cirrhosis, hepatocellular carcinoma, and progressive HBV hepatitis. Three single-nucleotide polymorphisms HLA-DP (rs3077 and rs9277535) and HLA-DQ (rs7453920) were studied in all recipients by high-resolution melting curve analysis. Liver function indices (albumin, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyltranspeptidase, direct bilirubin, total bilirubin) and coagulation indices (prothrombin time, platelet, international normalized ratio, fibrinogen) were routinely tested. After transplant, 10 recipients who were positive for HBsAg or with elevation in HBV virus load were regarded as HBV recurrence. No significant association of HLA-DP/DQ polymorphisms with HBV recurrence or transplant etiology was observed (P < .05). Recipients with HLA-DQ (rs7453920) AG and AA genotype had lower direct bilirubin levels than GG genotype individuals, especially on the 14th day after surgery (17.80 vs. 5.35, P = .038). Patients with A alleles displayed earlier liver function recovery than patients with G alleles (7 vs. 6 months). No significant correlation was shown in HLA-DP rs3077 and rs9277535 with HBV infection or liver function recovery (P < .05). Our study concluded that HLA-DP (rs3077 and rs9277535) and HLA-DQ (rs7453920) were not significantly associated with HBV recurrence or HBV susceptibility, but HLA-DQ rs7453920 was related to prognosis of liver transplant recipients. HLA-DQ rs7453920 A might be used as an indicator of earlier recovery and better prognosis after transplantation.
A Multilayer Negative-Refractive-Index Transmission-Line (NRI-TL) Metamaterial Free-Space Lens at X-Band

A volumetric free-space negative-refractive-index (NRI) transmission-line (TL) metamaterial lens is described that employs fully printed interdigitated capacitors and meandered inductors designed to exhibit NRI properties at X-band (8-12 GHz). The volumetric topology is realized in a layer-by-layer fashion without any vias, which facilitates easy and rapid fabrication. The fabricated lens was tested for its transmission and dispersion properties using a free-space X-band measurement system consisting of an Agilent network analyzer, standard gain horn antennas, and Rexolite dielectric lenses fabricated in-house, and showed good correspondence with simulations. The focusing ability of the multilayer NRI-TL lens was also verified using a free-space field probing system based on small shielded-loop antennas affixed to a computer-controlled xyz-translator apparatus. Arguably, these results represent the first experimental evidence of coupling between TL-based metamaterials and sources in free space.
Integrated pathway and epistasis analysis reveals interactive effect of genetic variants at TERF1 and AFAP1L2 loci on melanoma risk

Genome‐wide association studies (GWASs) have characterized 13 loci associated with melanoma, which only account for a small part of melanoma risk. To identify new genes with too small an effect to be detected individually but which collectively influence melanoma risk and/or show interactive effects, we used a two‐step analysis strategy including pathway analysis of genome‐wide SNP data, in a first step, and epistasis analysis within significant pathways, in a second step. Pathway analysis, using the gene‐set enrichment analysis (GSEA) approach and the gene ontology (GO) database, was applied to the outcomes of MELARISK (3,976 subjects) and MDACC (2,827 subjects) GWASs. Cross‐gene SNP–SNP interaction analysis within melanoma‐associated GOs was performed using the INTERSNP software. Five GO categories were significantly enriched in genes associated with melanoma (false discovery rate ≤ 5% in both studies): response to light stimulus, regulation of mitotic cell cycle, induction of programmed cell death, cytokine activity and oxidative phosphorylation. Epistasis analysis, within each of the five significant GOs, showed significant evidence for interaction for one SNP pair at TERF1 and AFAP1L2 loci (pmeta‐int = 2.0 × 10−7, which met both the pathway and overall multiple‐testing corrected thresholds that are equal to 9.8 × 10−7 and 2.0 × 10−7, respectively) and suggestive evidence for another pair involving correlated SNPs at the same loci (pmeta‐int = 3.6 × 10−6). This interaction has important biological relevance given the key role of TERF1 in telomere biology and the reported physical interaction between TERF1 and AFAP1L2 proteins. This finding brings a novel piece of evidence for the emerging role of telomere dysfunction into melanoma development.
Does the Timing of Auditor Changes Affect Audit Quality? Evidence From the Initial Year of the Audit Engagement

We focus on the first year of the auditor–client relationship and investigate whether audit quality varies with the timing of the new auditor’s appointment. We find that audit quality is not lower for companies that engage new auditors before the end of the third fiscal quarter than for companies that do not change auditors. However, companies that engage new auditors during or after the fourth fiscal quarter are more likely to misstate their audited financial statements than companies that engage new auditors earlier in the year and companies that do not change auditors. In additional tests, we find that the decrease in audit quality associated with late auditor changes is more pronounced for companies with complex operations (i.e., more operating segments). These results suggest that the extent to which audit quality suffers in the first year of audit engagements is affected by both the amount of time required to understand the client’s business, assess risks, and perform the audit (all of which are driven by client complexity), as well as the amount of time available for auditors to perform these tasks.
t(7;11)(p15;p15) chronic myeloid leukaemia  developed into blastic transformation showing a novel  NUP98/HOXA11 fusion

Summary. We encountered a patient with Philadelphia‐negative chronic myeloid leukaemia, witht(7;11)(p15;p15), in whom acute leukaemia phase (acute myeloid leukaemia‐M2 morphology) developed within a short period. We detected a novel gene fusion between NUP98 and HOXA11 both in the chronic phase and in the acute leukaemia phase in this case. Although it is well known that a fusion of NUP98–HOXA9 in myeloid malignancies is created by the t(7;11)(p15;p15), this case suggests the possibility that HOXA11 might be another partner gene for NUP98 in t(7;11)(p15;p15) leukaemia.
Helicobacter pylori occurrence and transmission: A family affair?

About half of the world's population is estimated to be infected with Helicobacter pylori, a gastric bacterium that contributes to the development of peptic ulcer disease and gastric cancer. H. pylori is more prevalent in low-income areas of the world and social and economic development decreases the prevalence as reflected in comparisons both within and between countries. The infection is typically acquired in early childhood and once established commonly persists throughout life unless treated. Person-to-person transmission within the family appears to be the predominant mode of transmission, particularly from mothers to children and among siblings, indicating that intimate contact is important. The route of transmission is uncertain, but the gastro-oral, oral-oral and faecal-oral routes are likely possibilities. Hence, gastroenteritis may facilitate dissemination of the infection. The community and environment may play additional roles for H. pylori transmission in some (low-income) settings. Furthermore, host and bacterial factors may modify the probabilities of acquisition and persistence of the infection. The understanding of H. pylori occurrence and transmission is of practical importance if future study deems prevention of the infection desirable in some high-prevalence populations. The present paper reviews aspects of H. pylori occurrence and transmission with an emphasis on household factors.
Hepatitis C virus infection after liver transplantation is associated with lower levels of activated CD4+CD25+CD45RO+IL‐7rαhigh T cells

The expression of interleukin 7 receptor alphahigh (IL‐7Rαhigh) discriminates between activated CD25+CD45RO+CD4+ T cells [IL‐7Rαhigh and forkhead box P3–negative (FoxP3−)] and regulatory T cells (IL‐7Rαlow and FoxP3+). The IL‐7RαhighCD25+CD45RO+CD4+FoxP3− T cell population has been shown to be expanded in the blood and tissues of patients after kidney transplantation and to contain alloreactive T cells (activated T cells). In the present study, we analyzed the distribution of IL‐7RαhighCD25+CD45RO+CD4+FoxP3− T cells in the blood of 53 patients after liver transplantation. The IL‐7RαhighCD25+CD45RO+CD4+FoxP3− T cell population was significantly expanded (P < 0.0001) in stable transplant recipients versus healthy donors. However, the magnitude of the expansion was significantly higher (P < 0.0001) in liver transplant recipients with no hepatitis C virus (HCV) infection in comparison with those with a preexisting HCV infection. Interestingly, effective suppression of HCV viremia after antiviral therapy was associated with an increase in the IL‐7RαhighCD25+CD45RO+CD4+FoxP3− T cell population to levels comparable to those of liver transplant recipients not infected with HCV. The present results indicate that (1) the IL‐7RαhighCD25+CD45RO+CD4+FoxP3− T cell population is expanded after liver transplantation, (2) it is a valuable immunological marker for monitoring activated and potential alloreactive CD4 T cells in liver transplantation, and (3) a preexisting HCV infection negatively influences the expansion of this population in liver transplant recipients. Liver Transpl 16:49–55, 2010. © 2009 AASLD.
Prolonged exposure to antibiotics and its associations in extremely preterm neonates - the Western Australian experience

Abstract Background: Prolonged exposure to antibiotics (PEA) is associated with increased risk of necrotising enterocolitis (NEC), late onset sepsis (LOS) and death in preterm neonates. Aim: To evaluate PEA (≥4 d) for suspected (blood culture negative) sepsis and its association with NEC, LOS and death in extremely preterm (EP: Gestation <28 weeks) neonates. Methods: Data on demographic characteristics, antibiotic exposure for early onset sepsis (EOS) or LOS and outcomes to discharge/death were collected for 216 EP neonates admitted between 1/1/2009 and 31/12/2010. Results: All 216 neonates received antibiotics for suspected EOS; 120/216 (56%) had PEA. 137/216 who survived first 72 h of life, had suspected LOS [range 1–8 episodes], treated with antibiotics for median (IQR) duration of 8 (5–14) days. 89/216 had proven (blood culture positive) LOS [range 1–3 episodes], treated with antibiotics for median (IQR) duration of 10 (7–18) days. The incidence of and death due to ≥Stage II NEC was 17/216 (7.8%) and 5/17 (29.4%) respectively. PEA for suspected EOS was associated with proven LOS (OR: 2.1, 95% CI: 1.2–3.7, p = 0.013) after adjusting for gestation and IUGR, but not with NEC/death. Conclusion: PEA for ≥4 d for suspected EOS was associated with increased odds for proven LOS.
Revision and validation of the Individual Child Engagement Record: A practitioner‐friendly measure of learning opportunities for children with disabilities in early childhood settings

Abstract Background The purpose of this study was to revise and validate the Individual Child Engagement Record (ICER), an instrument designed to observe and measure the engagement of children with disabilities in early childhood settings.1 Method The ICER was revised with reference to pilot study results and the literature. Inter‐observer reliability of the revised measure (ICER‐R) was examined by calculating levels of agreement between observers coding video‐clips of children with disabilities engaged in three different activity types (mealtime, free play, and structured group time) in an inclusive childcare centre. The E‐Qual III was used as a criterion measure to examine concurrent validity. Results Good overall percentage agreement and kappa coefficients were achieved for the codes recorded. A statistically significant correlation was found between data gathered using the ICER‐R and the E‐Qual III when comparing total engaged behaviours. Conclusions The ICER‐R was found to be a valid and reliable measure of engagement of children with disabilities in early childhood settings. The results support the potential of the ICER‐R as a practitioner‐friendly tool.
Effects of differing insulin levels on response to equivalent hypoglycemia in conscious dogs.

The aim of this study was to determine if differing concentrations of insulin can modify the counterregulatory response to equivalent hypoglycemia. Insulin was infused intraportally into normal 18-h-fasted conscious dogs at 2 (low, n = 6) or 8 mU.kg-1.min-1 (high, n = 7) on separate occasions. This resulted in steady-state arterial insulin levels of 80 +/- 8 and 610 +/- 55 microU/ml, respectively. Glucose was infused during the high dose to maintain plasma glucose similar to low (50 +/- 1 mg/dl). Despite similar plasma glucose levels, epinephrine (2,589 +/- 260, 806 +/- 180 pg/ml), norepinephrine (535 +/- 60, 303 +/- 55 pg/ml), cortisol (12.1 +/- 1.5, 5.8 +/- 1.2 micrograms/dl), and pancreatic polypeptide (1,198 +/- 150, 598 +/- 250 pg/ml) were all increased in the presence of high-dose insulin (P < 0.05). Glucagon levels were similar during both insulin infusions. Hepatic glucose production, measured with [3-3H]-glucose, rose from 2.6 +/- 0.2 to 4.7 +/- 0.3 mg.kg-1.min-1 in response to high insulin (P < 0.01) but remained unchanged, 3.0 +/- 0.5 mg.kg-1.min-1, during low-dose infusions. Six hyperinsulinemic euglycemic control experiments (2 or 8 mU.kg-1.min-1, n = 3 in each) provided baseline data. By the final hour of the high-dose euglycemic clamps, cortisol (2.4 +/- 0.4 to 4.8 +/- 0.8 micrograms/dl) and norepinephrine (125 +/- 34 to 278 +/- 60 pg/ml) had increased (P < 0.05) compared with baseline. Plasma epinephrine levels remained unchanged during both series of euglycemic studies. (ABSTRACT TRUNCATED AT 250 WORDS)
Cell therapy in congestive heart failure

Congestive heart failure (CHF) has emerged as a major worldwide epidemic and its main causes seem to be the aging of the population and the survival of patients with post-myocardial infarction. Cardiomyocyte dropout (necrosis and apoptosis) plays a critical role in the progress of CHF; thus treatment of CHF by exogenous cell implantation will be a promising medical approach. In the acute phase of cardiac damage cardiac stem cells (CSCs) within the heart divide symmetrically and/or asymmetrically in response to the change of heart homeostasis, and at the same time homing of bone marrow stem cells (BMCs) to injured area is thought to occur, which not only reconstitutes CSC population to normal levels but also repairs the heart by differentiation into cardiac tissue. So far, basic studies by using potential sources such as BMCs and CSCs to treat animal CHF have shown improved ventricular remodelling and heart function. Recently, however, a few of randomized, double-blind, placebo-controlled clinical trials demonstrated mixed results in heart failure with BMC therapy during acute myocardial infarction.
Enteroaggregative Escherichia coli associated with persistent diarrhea in a cohort of rural children in India.

A cohort of 452 rural children was followed longitudinally for 13 mo to ascertain the role of HEp-2 cell adherent Escherichia coli and other pathogens in causing acute (less than or equal to 14 d) and persistent (greater than 14 d) diarrhea. Aeromonas, Campylobacter jejuni, E. coli manifesting localized adherence to HEp-2 cells and enterotoxigenic E. coli were significantly associated with acute diarrhea. E. coli strains that exhibit aggregative adherence, so-called enteroaggregative E. coli, a newly-described category of diarrheagenic E. coli distinct from enterotoxigenic, enteroinvasive, enterohemorrhagic, and enteropathogenic E. coli, were found significantly more often in patients with persistent diarrhea (29.5%) than with acute diarrhea (12.8%) (P = .0052) or controls (9.9%) (P = .0006).
Integrated Settings at the Early Childhood Level: The Role of Nonretarded Peers

Recent trends toward early intervention and mainstreaming have resulted in a growing number of preschool programs that integrate retarded and nonretarded children. These programs are generally based on the assumption that nonhandicapped peers function as behavioral models and/or reinforcing agents for handicapped youngsters within the context of positive social interaction. However, a review of relevant empirical literature indicates that such benefits do not necessarily result from integrated programing. This article discusses the implications of recent studies that have investigated procedures for structuring peer imitation and peer reinforcement at the preschool age level. Specific suggestions are offered for maximizing the potential benefits of integrated early childhood programs. Additionally, recommendations are made concerning research needs in this area.
Damage-induced DNA replication stalling relies on MAPK-activated protein kinase 2 activity

Significance Our results imply a direct impact of the p38–MAP kinase-activated protein kinase 2 (MK2) kinase pathway on the cellular response to replicative stress. In this situation, MK2 activity determines the decision between replication fork stalling and translesion synthesis. In the absence of MK2 activity, even the otherwise essential checkpoint kinase Chk1 becomes dispensable for S phase progression and cell survival. Moreover, MK2 represents a determinant of cancer cell sensitivity toward nucleoside analogue treatment. DNA damage can obstruct replication forks, resulting in replicative stress. By siRNA screening, we identified kinases involved in the accumulation of phosphohistone 2AX (γH2AX) upon UV irradiation-induced replication stress. Surprisingly, the strongest reduction of phosphohistone 2AX followed knockdown of the MAP kinase-activated protein kinase 2 (MK2), a kinase currently implicated in p38 stress signaling and G2 arrest. Depletion or inhibition of MK2 also protected cells from DNA damage-induced cell death, and mice deficient for MK2 displayed decreased apoptosis in the skin upon UV irradiation. Moreover, MK2 activity was required for damage response, accumulation of ssDNA, and decreased survival when cells were treated with the nucleoside analogue gemcitabine or when the checkpoint kinase Chk1 was antagonized. By using DNA fiber assays, we found that MK2 inhibition or knockdown rescued DNA replication impaired by gemcitabine or by Chk1 inhibition. This rescue strictly depended on translesion DNA polymerases. In conclusion, instead of being an unavoidable consequence of DNA damage, alterations of replication speed and origin firing depend on MK2-mediated signaling.
Multimodality Strategy for Cardiovascular Risk Assessment: Performance in 2 Population-Based Cohorts

Background: Current strategies for cardiovascular disease (CVD) risk assessment among adults without known CVD are limited by suboptimal performance and a narrow focus on only atherosclerotic CVD (ASCVD). We hypothesized that a strategy combining promising biomarkers across multiple different testing modalities would improve global and atherosclerotic CVD risk assessment among individuals without known CVD. Methods: We included participants from MESA (Multi-Ethnic Study of Atherosclerosis) (n=6621) and the Dallas Heart Study (n=2202) who were free from CVD and underwent measurement of left ventricular hypertrophy by ECG, coronary artery calcium, N-terminal pro B-type natriuretic peptide, high-sensitivity cardiac troponin T, and high-sensitivity C-reactive protein. Associations of test results with the global composite CVD outcome (CVD death, myocardial infarction, stroke, coronary or peripheral revascularization, incident heart failure, or atrial fibrillation) and ASCVD (fatal or nonfatal myocardial infarction or stroke) were assessed over >10 years of follow-up. Multivariable analyses for the primary global CVD end point adjusted for traditional risk factors plus statin use and creatinine (base model). Results: Each test result was independently associated with global composite CVD events in MESA after adjustment for the components of the base model and the other test results (P<0.05 for each). When the 5 tests were added to the base model, the c-statistic improved from 0.74 to 0.79 (P=0.001), significant integrated discrimination improvement (0.07, 95% confidence interval [CI] 0.06–0.08, P<0.001) and category free net reclassification improvement (0.47; 95% CI, 0.38–0.56; P=0.003) were observed, and the model was well calibrated (&khgr;2=12.2, P=0.20). Using a simple integer score counting the number of abnormal tests, compared with those with a score of 0, global CVD risk was increased among participants with a score of 1 (adjusted hazard ratio, 1.9; 95% CI, 1.4–2.6), 2 (hazard ratio, 3.2; 95% CI, 2.3–4.4), 3 (hazard ratio, 4.7; 95% CI, 3.4–6.5), and ≥4 (hazard ratio, 7.5; 95% CI, 5.2–10.6). Findings replicated in the Dallas Health Study were similar for the ASCVD outcome. Conclusions: Among adults without known CVD, a novel multimodality testing strategy using left ventricular hypertrophy by ECG, coronary artery calcium, N-terminal pro B-type natriuretic peptide, high-sensitivity cardiac troponin T, and high-sensitivity C-reactive protein significantly improved global CVD and ASCVD risk assessment.