Miracle-dz/UniFAR-FTUs huggingface dataset:
The effects of total knee arthroplasty on physical functioning in the older population.

OBJECTIVE Clinical research provides convincing evidence that total knee arthroplasty (TKA) is safe and improves joint-specific outcomes. However, higher-level functioning associated with self care and independent living has not been studied. Furthermore, most previous studies of the effects of TKA relied on relatively small clinical samples. We undertook this study to estimate the effects of TKA on 3 levels of physical functioning in a national sample of older adults. METHODS Data were obtained from the Medicare Current Beneficiary Survey from 1992 to 2003. Medicare claims data identified participants with osteoarthritis of the knee who received TKA (n=259) or no TKA (n=1,816). Propensity scores were used to match treatment and no-treatment groups according to demographic characteristics, comorbid conditions, and baseline functioning. Three levels of physical functioning were examined as outcomes of TKA. These levels were represented by items on the Nagi Disability Scale, the Instrumental Activities of Daily Living (IADL) Scale, and the Activities of Daily Living (ADL) Scale. These items were measured after TKA and at comparable intervals for the no-treatment group. Average treatment effects were calculated for relevant Nagi Disability Scale, IADL Scale, and ADL Scale tasks. RESULTS Between baseline and outcome assessments, TKA recipients improved on all 3 levels of physical functioning; the no-treatment group declined. Statistically significant average treatment effects for TKA were observed for one or more tasks for each measure of physical functioning. CONCLUSION TKA is associated with sizeable improvements in 3 levels of physical functioning among elderly Medicare beneficiaries.
Do Audit Firm Tenure and Size Moderate Changes in Financial Reporting Quality Due to Mandatory IFRS Adoption?

Regulators have expressed concerns that auditors become less effective external monitors as the length of the auditor-client relationship increases. I examine how audit firm tenure is associated with changes in financial reporting quality due to mandatory adoption of International Financial Reporting Standards. I argue that auditors were integral in proper implementation of IFRS and could have mitigated potential negative consequences associated with IFRS adoption. My findings suggest that short audit firm tenure was associated with a decrease in quality, relative to those with medium length tenure. Differences between clients with medium and long tenure are generally not significant. Other results indicate that companies with a Big 4 auditor had greater improvements, or smaller decreases, in reporting quality relative to non-Big 4 clients. My results do not support concerns that longer tenure impairs audit quality. My study is also relevant to standard setters as they evaluate the results of IFRS adoption.
IP-10 mRNA expression in cultured keratinocytes is suppressed by inhibition of protein kinase-C and tyrosine kinase and elevation of cAMP.

IFN-gamma-inducible protein-10 (IP-10) is a chemokine, which plays an important role in mediating inflammation by attracting activated T cells, and it has been demonstrated in inflammatory skin diseases and cutaneous T cell lymphomas. Keratinocytes can abundantly produce IP-10 mRNA after IFN-gamma treatment. In this study we explored possibilities to downregulate IP-10 expression using human cultured keratinocytes as a model system. Decreased IP-10 mRNA levels were found using specific inhibitors of protein kinase (PK)-C (H-7 and Calphostin C). Moreover, depletion of PK-C by pretreatment of the cells with phorbol myristate (PMA) also down-regulated IP-10 mRNA expression. In addition, elevated cAMP levels were shown to inhibit IP-10 mRNA expression as could be concluded from experiments with forskolin and W-7, substances which, directly or indirectly, raise the intracellular cAMP level. With Genistein, an inhibitor of tyrosine kinase, the IFN-gamma-induced IP-10 mRNA expression was also found to be diminished. These data suggest that inhibitors of the IP-10 mRNA expression in cultured keratinocytes may be potentially of clinical relevance to suppress inflammatory processes in the skin.
Lactobacillus-Mediated Priming of the Respiratory Mucosa Protects against Lethal Pneumovirus Infection

The inflammatory response to respiratory virus infection can be complex and refractory to standard therapy. Lactobacilli, when targeted to the respiratory epithelium, are highly effective at suppressing virus-induced inflammation and protecting against lethal disease. Specifically, wild-type mice primed via intranasal inoculation with live or heat-inactivated Lactobacillus plantarum or Lactobacillus reuteri were completely protected against lethal infection with the virulent rodent pathogen, pneumonia virus of mice; significant protection (60% survival) persisted for at least 13 wk. Protection was not unique to Lactobacillus species, and it was also observed in response to priming with nonpathogenic Gram-positive Listeria innocua. Priming with live lactobacilli resulted in diminished granulocyte recruitment, diminished expression of multiple proinflammatory cytokines (CXCL10, CXCL1, CCL2, and TNF), and reduced virus recovery, although we have demonstrated clearly that absolute virus titer does not predict clinical outcome. Lactobacillus priming also resulted in prolonged survival and protection against the lethal sequelae of pneumonia virus of mice infection in MyD88 gene-deleted (MyD88−/−) mice, suggesting that the protective mechanisms may be TLR-independent. Most intriguing, virus recovery and cytokine expression patterns in Lactobacillus-primed MyD88−/− mice were indistinguishable from those observed in control-primed MyD88−/− counterparts. In summary, we have identified and characterized an effective Lactobacillus-mediated innate immune shield, which may ultimately serve as critical and long-term protection against infection in the absence of specific antiviral vaccines.
Hypothermic or normothermic abdominal regional perfusion in high‐risk donors with extended warm ischemia times: impact on outcomes?

Donation after circulatory determination of death (DCD) has the potential to increase the applicability of transplantation as a treatment for end‐stage organ disease; its use is limited, however, by the warm ischemic damage suffered by potential grafts. Abdominal regional perfusion (ARP) has been employed in this setting to not only curtail the deleterious effects of cardiac arrest by re‐establishing oxygenated flow but also test and even improve the viability of the kidneys and liver prior to transplantation. In the present review article, we discuss experimental and clinical studies that have been published to date on the use of ARP in DCD, differentiating between its application under hypothermic and normothermic conditions. In addition to describing results that have been achieved thus far, we describe the major obstacles limiting the broader implementation of ARP in this context as well as potential means for improving the effectiveness of this modality in the future.
Urotensin II, from fish to human

The cyclic peptide urotensin II (UII) was originally isolated from the urophysis of teleost fish on the basis of its ability to contract intestinal smooth muscle. The UII peptide has subsequently been isolated from frog brain and, later on, the pre‐proUII cDNA has been characterized in mammals, including humans. A UII paralog called urotensin II‐related peptide (URP) has been identified in the rat brain. The UII and URP genes originate from the same ancestral gene as the somatostatin and cortistatin genes. In the central nervous system (CNS) of tetrapods, UII is expressed primarily in motoneurons of the brainstem and spinal cord. The biological actions of UII and URP are mediated through a G protein–coupled receptor, termed UT, that exhibits high sequence similarity with the somatostatin receptors. The UT gene is widely expressed in the CNS and in peripheral organs. Consistent with the broad distribution of UT, UII and URP exert a large array of behavioral effects and regulate endocrine, cardiovascular, renal, and immune functions.
Lower running performance and exacerbated fatigue in soccer played at 1600 m.

PURPOSE This study investigated the decrement in running performance of elite soccer players competing at low altitude and time course for abatement of these decrements. METHODS Twenty elite youth soccer players had their activity profile, in a sea-level (SL) and 2 altitude (Alt, 1600 m, d 4, and d 6) matches, measured with a global positioning system. Measures expressed in meters per minute of match time were total distance, low- and high-velocity running (LoVR, 0.01-4.16 m/s; HiVR, 4.17-10.0 m/s), and frequency of maximal accelerations (>2.78 m/s2). The peak and subsequent stanza for each measure were identified and a transient fatigue index calculated. Mean heart rate (HR) during the final minute of a submaximal running task (5 min, 11 km/h) was recorded at SL and for 10 d at Alt. Differences were determined between SL and Alt using percentage change and effect-size (ES) statistic with 90% confidence intervals. RESULTS Mean HR almost certainly increased on d 1 (5.4%, ES 1.01 ± 0.35) and remained probably elevated on both d 2 (ES 0.42 ± 0.31) and d3 (ES 0.30 ± 0.25), returning to baseline at d 5. Total distance was almost certainly lower than SL (ES -0.76 ± 0.37) at d 4 and remained probably reduced on d 6 (ES -0.42 ± 0.36). HiVR probably decreased at d 4 vs SL (-0.47 ± 0.59), with no clear effect of altitude at d 6 (-0.08 ± 0.41). Transient fatigue in matches was evident at SL and Alt, with a possibly greater decrement at Alt. CONCLUSION Despite some physiological adaptation, match running performance of youth soccer players is compromised for at least 6 d at low altitude.
What Factors Affect Income Inequality and Economic Growth in Middle-Income Countries?

Income inequality in many middle-income countries has increased at an alarming level. While the time series relationship between income inequality and economic growth has been extensively investigated, the causal and dynamic link between them, particularly for the middle-income countries, has been largely ignored in the current literature. This study was conducted to fill in this gap on two different samples for the period from 1960 to 2014: (i) a full sample of 158 countries; and (ii) a sample of 86 middle-income countries. The Granger causality test and a system generalized method of moments (GMM) are utilized in this study. The findings from this study indicate that causality is found from economic growth to income inequality and vice versa in both samples of countries. In addition, this study also finds that income inequality contributes negatively to the economic growth in the middle-income countries in the research period.
Stress Marker Signatures in Lesion Mimic Single and Double Mutants Identify a Crucial Leaf Age-Dependent Salicylic Acid Related Defense Signal

Plants are exposed to abiotic and biotic stress conditions throughout their lifespans that activates various defense programs. Programmed cell death (PCD) is an extreme defense strategy the plant uses to manage unfavorable environments as well as during developmentally induced senescence. Here we investigated the role of leaf age on the regulation of defense gene expression in Arabidopsis thaliana. Two lesion mimic mutants with misregulated cell death, catalase2 (cat2) and defense no death1 (dnd1) were used together with several double mutants to dissect signaling pathways regulating defense gene expression associated with cell death and leaf age. PCD marker genes showed leaf age dependent expression, with the highest expression in old leaves. The salicylic acid (SA) biosynthesis mutant salicylic acid induction deficient2 (sid2) had reduced expression of PCD marker genes in the cat2 sid2 double mutant demonstrating the importance of SA biosynthesis in regulation of defense gene expression. While the auxin- and jasmonic acid (JA)- insensitive auxin resistant1 (axr1) double mutant cat2 axr1 also led to decreased expression of PCD markers; the expression of several marker genes for SA signaling (ISOCHORISMATE SYNTHASE 1, PR1 and PR2) were additionally decreased in cat2 axr1 compared to cat2. The reduced expression of these SA markers genes in cat2 axr1 implicates AXR1 as a regulator of SA signaling in addition to its known role in auxin and JA signaling. Overall, the current study reinforces the important role of SA signaling in regulation of leaf age-related transcript signatures.
Effects of maternal gestational diabetes on offspring adiposity at 4-7 years of age.

OBJECTIVE The purpose of this study was to assess the long-term effects of maternal prenatal factors, including gestational diabetes mellitus (GDM), adiposity, and weight gain during pregnancy, on adiposity of offspring from 4 to 7 years of age. A second purpose was to investigate the relationships among childhood adiposity, blood pressure, and 2-h postprandial glucose level. RESEARCH DESIGN AND METHODS Prospective observational study of four groups of children including large-for-gestational-age (LGA) offspring of mothers with gestational diabetes (OGDM); appropriate-for-gestational-age (AGA) OGDM; LGA control subjects; and AGA control subjects. Anthropometrics including skin-fold measurements, blood pressure measurements, and a 2-h postprandial glucose measurement were obtained at each visit. Repeated measures analysis of variance models were used to detect different patterns of longitudinal change among the groups. RESULTS LGA OGDM were more likely to be heavier, have larger circumferences and skin-fold measurements, and have a higher BMI than AGA OGDM and control subjects, and these findings increased with increasing age. Blood pressures and postprandial glucose values were similar for OGDM and control subjects at 4-7 years. Multivariable analyses showed that infant BMI and maternal prepregnant BMI predicted 7-year BMI for OGDM, whereas for control subjects, maternal prepregnancy BMI and weight gain during pregnancy were positive predictors with a small negative contribution from birth BMI. CONCLUSIONS We conclude that LGA OGDM have evidence of increasing body size and adiposity with increasing age and that maternal GDM and maternal prepregnant adiposity are significant predictors of their unique growth patterns.
A family‐based study of Indian subjects from Kolkata reveals allelic association of the serotonin transporter intron‐2 (STin2) polymorphism and attention‐deficit‐hyperactivity disorder (ADHD)

Serotonin transporter (SLC6A4) polymorphisms are variously implicated in mediating susceptibility to attention‐deficit‐hyperactivity disorder (ADHD), a highly heritable and heterogeneous disorder with onset in childhood. Since there has been no survey in this regard from India, a sample of 56 ADHD cases and 174 healthy individuals from Kolkata were genotyped for the SLC6A4 promoter (5‐HTTLPR) and intron‐2 (STin2) polymorphisms. We report that the observed distribution of allele frequencies is consonant with that expected as per Hardy–Weinberg equilibrium proportions. Pair‐wise combination of alleles comprising the 5‐HTTLPR and STin2 polymorphic systems exhibit significant (χ2 = 14.74, df = 1; P = 0.0001) linkage disequilibrium of low magnitude (D' = 0.269). The estimates of haplotype‐based haplotype relative risk (HHRR) (χ2 = 4.92, P = 0.027; RR = 1.47; 95% CI = 1.01–2.13) and transmission disequilibrium test (TDT) statistics (χ2 = 7.00, P = 0.008; OR = 3.00; 95% CI = 1.53–5.90) using a family‐based study design, indicate significant preferential transmission of the STin2.12 (A12) allele to ADHD cases. Maternal inheritance of the A12 allele is significant in terms of the HHRR (χ2 = 6.53, P = 0.011; RR = 2.00; 95% CI = 1.08–3.72) and TDT (χ2 = 8.07, P = 0.005; OR = 6.50; 95% CI = 1.76–23.98) suggesting a novel role for epigenetic mechanisms in the etiology of ADHD. Similar analyses yielded no evidence of association between the 5‐HTTLPR polymorphism and ADHD. Studies including additional polymorphic markers, ADHD subjects and other ethnic groups are warranted to further substantiate the present findings. © 2006 Wiley‐Liss, Inc.
Red blood cell microparticles show altered inflammatory chemokine binding and release ligand upon interaction with platelets

BACKGROUND: Storage of red blood cells (RBCs) under standard blood bank conditions results in reduced structural integrity leading to membrane budding and release of microparticles. Microparticles express the blood group Duffy antigen known to bind multiple inflammatory chemokines, but the functional chemokine binding properties of microparticles are not known.
Kinase Control Prevents HIV-1 Reactivation in Spite of High Levels of Induced NF-κB Activity

ABSTRACT Despite its clinical importance, the molecular biology of HIV-1 latency control is at best partially understood, and the literature remains conflicting. The most recent description that latent HIV-1 is integrated into actively expressed host genes has further confounded the situation. This lack of molecular understanding complicates our efforts to identify therapeutic compounds or strategies that could reactivate latent HIV-1 infection in patients, a prerequisite for the eradication of HIV-1 infection. Currently, many therapeutic development efforts operate under the assumption that a restrictive histone code could govern latent infection and that either dissipation of the histone-based restrictions or NF-κB activation could be sufficient to trigger HIV-1 reactivation. We here present data that suggest an additional, higher level of molecular control. During a high-content drug screening effort, we identified AS601245 as a potent inhibitor of HIV-1 reactivation in latently infected primary T cells and T cell lines. In either system, AS601245 inhibited HIV-1 reactivation despite high levels of induced NF-κB activation. This finding suggests the presence of a gatekeeper kinase activity that controls latent HIV-1 infection even in the presence of high levels of NF-κB activity. Potential therapeutic stimuli that do not target this gatekeeper kinase will likely fail to trigger efficient system-wide HIV-1 reactivation.
A Friend or a Foe? Detecting Malware using Memory and CPU Features

With an ever-increasing and ever more aggressive proliferation of malware, its detection is of utmost importance. However, due to the fact that IoT devices are resource-constrained, it is difficult to provide effective solutions. The main goal of this paper is the development of lightweight techniques for dynamic malware detection. For this purpose, we identify an optimized set of features to be monitored at runtime on mobile devices as well as detection algorithms that are suitable for battery-operated environments. We propose to use a minimal set of most indicative memory and CPU features reflecting malicious behavior. The performance analysis and validation of features usefulness in detecting malware have been carried out by considering the Android operating system. The results show that memory and CPU related features contain enough information to discriminate between execution traces belonging to malicious and benign applications with significant detection precision and recall. Since the proposed approach requires only a limited number of features and algorithms of low complexity, we believe that it can be used for effective malware detection, not only on mobile devices, but also on other smart elements of IoT.
Nitric oxide donors regulate nitric oxide synthase in bovine pulmonary artery endothelium

This study examined the notion that exogenous generation of nitric oxide (NO) modulates NOS gene expression and activity. Bovine pulmonary artery endothelial cells (BPAEC) were treated with the NO donors, 1 mM SNAP (S‐nitroso‐N‐acetylpenicillamine), 0.5 mM SNP (sodium nitroprusside) or 0.2 μM NONOate (spermine NONOate) in medium 199 containing 2% FBS. Controls included untreated cells and cells exposed to 1 mM NAP (N‐acetyl‐D‐penicillamine). NOS activity was assessed using a fibroblast‐reporter cell assay; intracellular Ca2+ concentrations were assessed by Fura‐2 microfluorometry; and NO release was measured by chemiluminescence. Constitutive endothelial (e) and inducible (i) NOS gene and protein expression were examined by northern and western blot analysis, respectively. Two hours exposure to either SNAP or NONOate caused a significant elevation in NO release from the endothelial cells (SNAP = 51.4 ± 5.9; NONOate = 23.8 ± 4.2; control = 14.5 ± 2.8 μM); but A23187 (3 μM)‐stimulated NO release was attenuated when compared to controls. Treatment with either SNAP or NONOate for 2 h also resulted in a significant increase in NOS activity in endothelial homogenates (SNAP = 23.6 ± 2.5; NONOate = 29.8 ± 7.7; control = 14.5 ± 2.5 fmol cGMP/μg per 106 cells). Exposure to SNAP and SNP, but not NONOate, for 1 h caused an increase in intracellular calcium. Between 4 and 8 h, SNAP and NONOate caused a 2‐ to 3‐fold increase in eNOS, but not iNOS, gene (P < 0.05) and protein expression. NAP had little effect on either eNOS gene expression, activity or NO production. Our data indicate that exogenous generation of NO leads to a biphasic response in BPAEC, an early increase in intracellular Ca2+, and increases in NOS activity and NO release followed by increased expression of the eNOS gene, but not the iNOS gene. We conclude that eNOS gene expression and activity are regulated by a positive‐feedback regulatory action of exogenous NO. J. Cell. Physiol. 186:116–123, 2001. © 2001 Wiley‐Liss, Inc.
DDA1 promotes stage IIB–IIC colon cancer progression by activating NFκB/CSN2/GSK-3β signaling

Conventional high-recurrence risk factors are not sufficient to predict post-operative risk of tumor recurrence or sensitivity to 5-fluorouracil (5-FU)-based chemotherapy for stage II colon cancer. DDA1, an evolutionarily conserved gene located at 19p13.11, may be involved in the activation of nuclear factor kappaB (NFκB). This study aimed to investigate whether DDA1 contributes to tumorigenesis and progression of stage II colon cancer via activation of the NFκB pathway. We found that positive expression of DDA1 alone or in combination with p65 nuclear translocation correlated with increased risk of tumor recurrence in patients with stage IIB–IIC colon cancer. DDA1 overexpression in colon cancer lines promoted cell proliferation, facilitated cell cycle progression, inhibited 5-FU-induced apoptosis, enhanced invasion, and induced the epithelial-mesenchymal transition. Suppression of DDA1 inhibited tumor progression, and reduced tumor growth in vivo. We also demonstrated that DDA1-mediated tumor progression is associated with the activation of the NFκB/COP9 signalosome 2(CSN2)/glycogen synthase kinase3β (GSK3β) pathway. These results indicate that DDA1 promotes colon cancer progression through activation of NFκB/CSN2/GSK3β signaling. DDA1, together with NFκB activation status, may serve as a sensitive biomarker for tumor recurrence risk and prognosis in patients with stage IIB–IIC colon cancers.