Miracle-dz/UniFAR-FTUs huggingface dataset:
The impact of human resources practices and labor relations on organizational performance in Uruguay : an empirical test 1 Cassoni

The present paper analyzes the impact of Human Resources Management Practices on Organizational Performance under different contexts of industrial relations that have taken place in Uruguay starting in 2005. Using the CRANET Survey multivariate models are used to estimate the effects of union variables on performance in different sectors and the impact and complementarities of calculative or collaborative HRM practices on the firm's performance, as meassured by, gross benefits, productivity and quality. The differential impact of these HRM practices under the changing conditions of union influence are finally examined. Results indicate a variety of different arrangements (bundles) and different complementarities under different regimes and the relevance of introducing the destination between calculative and collaborative practices.
Exact permutational tests for group sequential clinical trials.

An efficient numerical algorithm is developed for computing stopping boundaries for group sequential clinical trials. Patients arrive in sequence, and are randomized to one of two treatments. The data are monitored at interim time points, with a fresh block of patients entering the study from one monitoring point to the next. The stopping boundaries are derived from the exact joint permutational distribution of the linear rank statistics observed across all the monitoring times. Specifically, the algorithm yields the exact boundary generating function, Pr(W1 < b1, W2 < b2, ., Wi-1 < bi-1, Wi = wi), where Wj is the linear rank statistic at the jth interim time point. The distribution theory is based on assigning ranks after pooling all the patients who have entered the study, and then permuting the patients to the two treatments independently within each block of newly arrived patients. The methods are applicable for an arbitrary number of monitoring times, which need not be specified at the start of the study. The data may be continuous or categorical, and censored or uncensored. The randomization rule for treatment allocation can be adaptive. The algorithm is especially useful during the early stages of a clinical trial, when very little data have been gathered, and stopping boundaries are based on the extreme tails of the relevant boundary generating function. In that case the corresponding large-sample theory is not very reliable. To illustrate the techniques we present a group sequential analysis of a recently completed study by the Eastern Cooperative Oncology Group.
Tristetraprolin Is Required for Full Anti-Inflammatory Response of Murine Macrophages to IL-101

IL-10 is essential for inhibiting chronic and acute inflammation by decreasing the amounts of proinflammatory cytokines made by activated macrophages. IL-10 controls proinflammatory cytokine and chemokine production indirectly via the transcription factor Stat3. One of the most physiologically significant IL-10 targets is TNF-α, a potent proinflammatory mediator that is the target for multiple anti-TNF-α clinical strategies in Crohn’s disease and rheumatoid arthritis. The anti-inflammatory effects of IL-10 seem to be mediated by several incompletely understood transcriptional and posttranscriptional mechanisms. In this study, we show that in LPS-activated bone marrow-derived murine macrophages, IL-10 reduces the mRNA and protein levels of TNF-α and IL-1α in part through the RNA destabilizing factor tristetraprolin (TTP). TTP is known for its central role in destabilizing mRNA molecules containing class II AU-rich elements in 3′ untranslated regions. We found that IL-10 initiates a Stat3-dependent increase of TTP expression accompanied by a delayed decrease of p38 MAPK activity. The reduction of p38 MAPK activity releases TTP from the p38 MAPK-mediated inhibition, thereby resulting in diminished mRNA and protein levels of proinflammatory cytokines. These findings establish that TTP is required for full responses of bone marrow-derived murine macrophages to IL-10.
Up-regulation and functional effect of cardiac β3-adrenoreceptors in alcoholic monkeys.

BACKGROUND Recent studies link altered cardiac beta-adrenergic receptor (AR) signaling to the pathology of alcoholic cardiomyopathy (ACM). However, the alteration and functional effect of beta(3)-AR activation in ACM are unknown. We tested the hypothesis that chronic alcohol intake causes an up-regulation of cardiac beta(3)-AR, which exacerbates myocyte dysfunction and impairs calcium regulation, thereby directly contributing to the progression of ACM. METHODS We compared myocyte beta(3)- and beta(1)-AR expression and myocyte contractile ([Ca(2+)](i)), transient ([Ca(2+)](iT)), and Ca(2+) current (I(Ca,L)) responses to beta- and beta(3)-AR stimulation in myocytes obtained from left ventricle (LV) tissue samples obtained from 10 normal control (C) and 16 monkeys with self-administered alcohol for 12 months prior to necropsy: 6 moderate (M) and 10 heavy (H) drinkers with group average alcohol intakes of 1.5 +/- 0.2 and 3.3 +/- 0.2 g/kg/d, respectively. RESULTS Compared with control myocytes (C), in alcoholic cardiomyocytes, basal cell contraction (dL/dt(max), -39%, H: 69.8 vs. C: 114.6 microm/s), relaxation (dR/dt(max), -37%, 58.2 vs. 92.9 microm/s), [Ca(2+)](iT) (-34%, 0.23 vs. 0.35), and I(Ca,L) (-25%, 4.8 vs. 6.4pA/pF) were all significantly reduced. Compared with controls, in moderate and heavy drinkers, beta(1)-AR protein levels decreased by 23% and 42%, but beta(3)-AR protein increased by 46% and 85%, respectively. These changes were associated with altered myocyte functional responses to beta-AR agonist, isoproterenol (ISO), and beta(3)-AR agonist, BRL-37344 (BRL). Compared with controls, in alcoholic myocytes, ISO (10(-8) M) produced significantly smaller increases in dL/dt(max) (H: 40% vs. C: 71%), dR/dt(max) (37% vs. 52%), [Ca(2+)](iT) (17% vs. 37%), and I(Ca,L) (17% vs. 27%), but BRL (10(-8) M) produced a significantly greater decrease in dL/dt(max) (H: -23% vs. C: -11%), [Ca(2+)](iT) (-30% vs. -11%), and I(Ca,L) (-28% vs. -17%). CONCLUSIONS Chronic alcohol consumption down-regulates cardiac beta(1)- and up-regulates beta(3)-ARs, contributing to the abnormal response to catecholamines in ACM. The up-regulation of cardiac beta(3)-AR signaling enhances inhibition of LV myocyte contraction and relaxation and exacerbates the dysfunctional [Ca(2+)](i) regulation and, thus, may precede the development of ACM.
Mortality in psychiatric patients, with a specific focus on cancer mortality associated with schizophrenia.

BACKGROUND Higher mortality rates among psychiatric patients compared with the general population have been widely reported. On the other hand, lower cancer mortality for schizophrenics has been occasionally pointed out. Few studies from Japan have investigated mortality among psychiatric patients, and this study is the first large-scale follow-up in this country. METHODS A total of 4980 patients admitted to a national mental hospital from 1948 through 1982 were followed up until 31 August 1985. The standardized mortality ratios (SMR) were calculated in comparison to the general population, using the person-years method. RESULTS The SMR for total deaths and those for malignancy were as follows for males/females respectively: 2.55/3.02 and 0.84/1.37 for schizophrenia, 1.76/2.37 and 1.44/2.10 for depression, 2.45/3.04 and 1.18/1.82 for mania, 1.81/1.90 and 0.27/1.07 for neurosis, 5.55/4.33 and 1.85/3.34 for alcohol/drug abuse, and 3.65/3.57 and 1.01/0.72 for organic brain syndrome. CONCLUSIONS The SMR for total deaths were significantly elevated in schizophrenia, depression, mania, neurosis, alcohol/drug abuse, and organic brain syndrome, respectively. The SMR for malignancy were not elevated nor lowered significantly in any of these disease categories. The SMR for stomach cancer in male schizophrenics was significantly lower (0.27; P < 0.05).
Randomised controlled trial of bariatric surgery versus a community weight loss programme for the sustained treatment of idiopathic intracranial hypertension: the Idiopathic Intracranial Hypertension Weight Trial (IIH:WT) protocol

Introduction Effective treatments are lacking for idiopathic intracranial hypertension (IIH), a condition characterised by raised intracranial pressure (ICP) and papilloedema, and found primarily in obese women. Weight loss and lowering body mass index (BMI) have been shown to lower ICP and improve symptoms in IIH; however, weight loss is typically not maintained, meaning IIH symptoms return. The Idiopathic Intracranial Hypertension Weight Trial (IIH:WT) will assess whether bariatric surgery is an effective long-term treatment for patients with IIH with a BMI over 35 kg/m2. The National Institute for Health and Care Excellence recommends bariatric surgery in people with a BMI over 35 kg/m2 and a qualifying comorbidity; currently IIH does not qualify as a comorbidity. Methods and analysis IIH:WT is a multicentre, open-label, randomised controlled clinical trial of 64 participants with active IIH and a BMI over 35 kg/m2. Participants will be randomised in a 1:1 ratio to bariatric surgery or a dietary weight loss programme and followed up for 5 years. The primary outcome measure is ICP at 12 months. Secondary outcome measures include ICP at 24 and 60 months, and IIH symptoms, visual function, papilloedema, headache, quality of life and cost-effectiveness at 12, 24 and 60 months. Trial registration number IIH:WT is registered as ISRCTN40152829 and on ClinicalTrials.gov as NCT02124486 and is in the pre-results stage.
FDG PET reimbursement.

Today, PET is increasingly accepted as a crucial imaging modality for early detection of disease, precise staging of disease progression, and accurate assessment of the effects of therapy. As the role of PET continues to emerge, so do questions regarding PET reimbursement. Understanding the complexities and complying with reimbursement policies, procedures, and interpretation of payer programs is key to receiving appropriate reimbursement for services performed. Therefore, it is imperative that facilities stay current on reimbursement issues—especially for a fast-evolving modality like PET, where indications and policies for reimbursement are continually being updated by the Centers for Medicare and Medicaid Services (CMS).
THE ASSOCIATION OF THYROID HORMONES AND TSH WITH THE METABOLIC SYNDROME IN EUTHYROID TAIWANESE INDIVIDUALS.

OBJECTIVE There are conflicting studies in euthyroid males and females regarding associations between thyroidrelated hormones and parameters of the metabolic syndrome (MetS). We investigated the association between serum thyroid hormones and thyroid-stimulating hormone (TSH) concentrations and MetS in euthyroid men and women. METHODS Taiwanese subjects aged 20 to 65 years who had undergone a voluntary health examination at a preventive examination agency in Taipei were enrolled in this cross-sectional study. The definition of MetS was suggested by the Bureau of Health Promotion, Department of Health, Taiwan. Euthyroidism was defined as TSH and free thyroxine (FT4) levels within the normal reference ranges while not taking any thyroid medication. We conducted multiple logistic regression to identify the ability of serum triiodothyronine (T3), FT4, and TSH concentrations to identify the relative risk for the presence of MetS and components of the MetS in euthyroid Taiwanese individuals. RESULTS A total of 8,207 Taiwanese subjects (mean age: men, 45.3 ± 9.9 years; women, 43.5 ± 9.3 years) were enrolled in this study. A total of 1,672 subjects (20.4%) were defined as having MetS; these subjects had significantly higher (P<.0001) mean age (48.4 ± 9.1 years vs. 43.6 ± 10.7 years), prevalence of men (78.7% vs. 53.4%), and smoking (16.8% vs. 11.6%) than those without MetS. The median TSH, FT4, and T3 levels in all subjects were 1.70 mIU/L, 1.41 ng/dL, and 1.20 ng/mL, respectively. Higher T3 and lower FT4 values rather than TSH increased the odds ratio for MetS in men and women after adjusting for smoking and age, particularly for the association of T3 and MetS in women (uppermost quartile versus lowermost quartile: odds ratio, 2.4; 95% confidence interval, 1.6 to 3.5; P for trend <.0001). CONCLUSION In euthyroid Taiwanese men and women, relatively high serum T3 concentrations was most strongly associated with the presence of the MetS; relatively low serum T4 was less strongly related, and serum TSH levels were not associated with the MetS. It is not known if the relationship of serum T3 and T4 to the MetS is causal. ABBREVIATIONS BMI = body mass index FT4 = free thyroxine MetS = metabolic syndrome OR = odds ratio T3 = triiodothyronine TSH = thyroid-stimulating hormone WC = waist circumference.
Identification and Analysis of Genomic Regions with Large Between‐Population Differentiation in Humans

The primary aim of genetic association and linkage studies is to identify genetic variants that contribute to phenotypic variation within human populations. Since the overwhelming majority of human genetic variation is found within populations, these methods are expected to be effective and can likely be extrapolated from one human population to another. However, they may lack power in detecting the genetic variants that contribute to phenotypes that differ greatly between human populations. Phenotypes that show large differences between populations are expected to be associated with genomic regions exhibiting large allele frequency differences between populations. Thus, from genome‐wide polymorphism data genomic regions with large allele frequency differences between populations can be identified, and evaluated as candidates for large between‐population phenotypic differences. Here we use allele frequency data from ∼1.5 million SNPs from three human populations, and present an algorithm that identifies genomic regions containing SNPs with extreme Fst. We demonstrate that our candidate regions have reduced heterozygosity in Europeans and Chinese relative to African‐Americans, and are likely enriched with genes that have experienced positive natural selection. We identify genes that are likely responsible for phenotypes known to differ dramatically between human populations and present several candidates worthy of future investigation. Our list of high Fst genomic regions is a first step in identifying the genetic variants that contribute to large phenotypic differences between populations, many of which have likely experienced positive natural selection. Our approach based on between population differences can compliment traditional within population linkage and association studies to uncover novel genotype‐phenotype relationships.
Early Retirement and Post Retirement Health

This paper studies empirically the consequences of retirement on health. We make use of a targeted retirement offer to army employees 55 years of age or older. Before the offer was implemented in the Swedish defense, the normal retirement age was 60 years of age. Estimating the effect of the offer on individuals' health within the age range 56-70, we find support for a reduction in both mortality and in inpatient care as a consequence of the early retirement offer. Increasing the mandatory retirement age may thus not only have positive government income effects but also negative effects on increasing government health care expenditures.
Therapeutic effect of transplanting β2m−/Thy1+ bone marrow‐derived hepatocyte stem cells transduced with lentiviral‐mediated HGF gene into CCl4‐injured rats

β2m−/Thy1+ bone marrow‐derived hepatocyte stem cells (BDHSCs) isolated from the bone marrow of cholestatic rats by magnetic bead cell sorting consistently express characteristics of both stem and liver cells. These stem cells may be good vehicles for gene transfer. Administration of exogenous hepatocyte growth factor (HGF) may be potentially useful for the treatment of liver fibrosis. Because lentiviral vectors integrate stably into the host‐cell genome of nondividing and dividing cells, it may efficiently transfect β2m−/Thy1+ BDHSCs in vitro and secrete high‐level HGF consistently. Transplantation of β2m−/Thy1+ BDHSCs transduced with lentiviral vectors containing the HGF gene may reduce liver fibrosis in rats.
The common invariant subspace problem and Tarski’s theorem

This article presents a computable criterion for the existence of a common invariant subspace of n×n complex matrices A1, . , As of a fixed dimension 1 ≤ d ≤ n. The approach taken in the paper is model-theoretic. Namely, the criterion is based on a constructive proof of the renowned Tarski’s theorem on quantifier elimination in the theory ACF of algebraically closed fields. This means that for an arbitrary formula φ of the language of fields, a quantifier-free formula φ′ such that φ↔φ′ in ACF is given explicitly. The construction of φ′ is elementary and based on the effective Nullstellensatz. The existence of a common invariant subspace of A1, . , As of dimension d can be expressed in the first-order language of fields, and hence, the constructive version of Tarski’s theorem yields the criterion. In addition, some applications of this criterion in quantum information theory are discussed.
Mechanisms Underlying Midazolam-Induced Peripheral Nerve Block and Neurotoxicity

Background and Objectives The benzodiazepine midazolam has been reported to facilitate the actions of spinally administrated local anesthetics. Interestingly, despite the lack of convincing evidence for the presence of &ggr;-aminobutyric acid type A (GABAA) receptors along peripheral nerve axons, midazolam also has been shown to have analgesic efficacy when applied alone to peripheral nerves. These observations suggest midazolam-induced nerve block is due to another site of action. Furthermore, because of evidence indicating that midazolam has equal potency at the benzodiazepine site on the GABAA receptor and the 18-kd translocator protein (TSPO), it is possible that at least the nerve-blocking actions of midazolam are mediated by this alternative site of action. Methods We used the benzodiazepine receptor antagonist flumazenil, and the TSPO antagonist PK11195, with midazolam on rat sciatic nerves and isolated sensory neurons to determine if either receptor mediates midazolam-induced nerve block and/or neurotoxicity. Results Midazolam (300 &mgr;M)–induced block of nerve conduction was reversed by PK11195 (3 &mgr;M), but not flumazenil (30 &mgr;M). Midazolam-induced neurotoxicity was blocked by neither PK11195 nor flumazenil. Midazolam also causes the release of Ca2+ from internal stores in sensory neurons, and there was a small but significant attenuation of midazolam-induced neurotoxicity by the Ca2+ chelator, BAPTA. BAPTA (30 &mgr;M) significantly attenuated midazolam-induced nerve block. Conclusions Our results indicate that processes underlying midazolam-induced nerve block and neurotoxicity are separable, and suggest that selective activation of TSPO may facilitate modality-selective nerve block while minimizing the potential for neurotoxicity.
Exchangeable magnesium pool masses in spontaneously hypertensive rats.

We explored magnesium (Mg) metabolism by determination of exchangeable Mg pool masses and Mg kinetic parameters using stable Mg isotopes in spontaneously hypertensive rats (SHRs). Classical intracellular and extracellular Mg status biomarkers were also measured. Male SHRs and their male Wistar Kyoto (WKY) controls were fed a semipurified diet containing Mg 550 mg /kg for 2 weeks. Each rat received then an intravenous injection of 1.37 mg (25)Mg. The plasma (25)Mg disappearance curve over the next 7 days was used to measure the mass and fractional transport rate of 3 rapidly exchanging Mg metabolic pools, M1, M2, and M3. In the SHRs, plasma and erythrocyte Mg levels and urinary Mg excretion were not modified compared with their control WKYs, but tibia Mg level was significantly lower in the SHRs. Pool M3, the deep tissue pool, was significantly lower in SHRs compared with WKYs, but pools M1 and M2, the extracellular Mg pools, were statistically similar. The fractional transport rate of Mg from M1 to M2 and from M2 to M1 in the SHRs was higher than in the controls. The half-life of M1 was significantly decreased in SHRs compared with WKYs. In conclusion, this work demonstrates a decrease in intracellular Mg stores in SHRs compared with WKYs and disturbance of Mg exchanges in extracellular Mg, confirming a Mg metabolism disturbance in spontaneously hypertensive rats. Further work is now needed to elucidate the origin of the Mg depletion in SHRs and to explore Mg pools in hypertensive patients.
Different types of synapses with different spectral types of cones underlie color opponency in a bipolar cell of the turtle retina

Electrophysiologically, color-opponent retinal bipolar cells respond with opposite polarities to stimulation with different wavelengths of light. The origin of these different polarities in the same bipolar cell has always been a mystery. Here we show that an intracellularly recorded and HRP-injected, red-ON, blue/green-OFF bipolar cell of the turtle retina made invaginating (ribbon associated) synapses exclusively with L-cones. Non-invaginating synapses resembling wide-cleft basal junctions were made exclusively with M-cones. Input from S-cones was not seen. From these results we suggest sign-inverting transmission from L-cones at invaginating synapses via metabotropic glutamate receptors, and sign-conserving transmission from M-cones at wide-cleft basal junctions via ionotropic receptors. To explain the pronounced blue sensitivity of the bipolar cell, computer simulations were performed using a sign-conserving input from a yellow/blue chromaticity-type (H3) horizontal cell. The response properties of the red-ON, blue/green-OFF bipolar cell could be quantitatively reproduced by this means. The simulation also explained the asymmetry in L- and M-cone inputs to the bipolar cell as found in the ultrastructural analysis and assigned a putative role to H3 horizontal cells in color processing in the turtle retina.
Lung Cancer Incidence and Survival in England: An Analysis by Socioeconomic Deprivation and Urbanization

Introduction: Most previous studies have investigated either socioeconomic deprivation or urbanization in relationship to lung cancer incidence or survival. We investigated the association between socioeconomic deprivation, urbanization, and lung cancer incidence and survival in England. Methods: We extracted data on patients diagnosed with lung cancer (ICD-10 C33-C34) between 2003 and 2007 and who were resident in England. We assigned each patient to an urbanization score and to a socioeconomic quintile based on their postcode of residence. We calculated age-specific and age-standardized incidence rates (per 100,000 European standard population) by urbanization, sex, and socioeconomic deprivation group. We used Kaplan-Meier survival analysis to compare the survival of patients from urban and rural areas by socioeconomic deprivation. Results: A high proportion of urban areas in England were classified as deprived and rural areas were mostly affluent. The incidence of lung cancer was higher in urban areas than in rural areas. In the more affluent areas, the incidence of lung cancer in urban and rural areas was very similar. Survival from lung cancer was slightly higher in affluent areas than in deprived areas. Survival from lung cancer in urban and rural areas was similar across all socioeconomic deprivation quintiles. Conclusions: The difference in incidence between urban and rural areas can be explained by the differences in the distribution of socioeconomic deprivation quintiles in the two urbanization categories. When socioeconomic deprivation is taken into account, little difference is seen between both the incidence and survival of lung cancer in urban and rural areas.