Miracle-dz/UniFAR-FTUs huggingface dataset:
Occupational exposure to vinyl chloride and cancer risk: a review of the epidemiologic literature

Occupational exposure to vinyl chloride (VC) is causally related to liver angiosarcoma, whereas there is inconsistent epidemiologic evidence for other neoplasms. Two pooled analyses of worker cohorts from 56 plants in North America and Europe provide the most comprehensive and updated data on cancer risk among workers exposed to VC. These included over 22 000 workers, with a total of 640 000 person-years of observation, followed-up for up to 50 years. Overall, a total of 1 778 cancer deaths were observed versus 1 829.46 expected, corresponding to a standardized mortality ratio (SMR) of 0.97 (95% confidence interval (CI)=0.93–1.02). Excluding 71 confirmed angiosarcomas, there were 60 deaths from liver cancers versus 44.35 expected (SMR=1.35, 95% CI=1.03–1.74). Lung and laryngeal cancer mortality were significantly lower than expected (SMR=0.88 and 0.59, respectively). The SMRs for soft tissue sarcoma, brain, lymphoid and haematopoietic system cancers were not materially different from unity. Thus, the aggregate data from over 20 000 VC workers in North America and Europe exclude any excess mortality from lung, laryngeal, soft tissue sarcoma, brain, lymphoid and haematopoietic neoplasms. There appears to be a slight excess of liver cancer other than angiosarcoma, which is difficult to interpret and is likely due to residual misclassification of angiosarcomas.
Cognitive impairments in Parkinson's disease

Objective: Dementia and cognitive impairment (CI) are common in Parkinson's disease (PD) and have important clinical consequences. We explored the prognostic factors for CI in patients with PD. Methods: A total of 102 patients with PD in Xuan wu hospital and Qian dongnan People's Hospital from 2005 to 2010 were included in this study. All patients underwent clinical and neurological assessments. Relevant demographic and performance parameters were analysed to determine variables that may be independently associated with the progression of CI. Results: In the 6-month follow-up group, CI progressed in three out of 58 cases (5%): two cases progressed from mild CI (MiCI) to moderate CI (MoCI), and one case from MoCI to dementia. In the six-month-to-two-year follow-up group, seven out of 46 cases (15%) worsened: one case developed MiCI, three cases progressed from MiCI to MoCI and three other cases from MoCI to dementia. In the two-to-five-year group, 20 out of 44 cases (45%) worsened with one case developing MiCI, 14 cases progressing from MiCi to MoCI and five cases from MoCI to dementia. Compared with other patients, those with worsening of CI symptoms were significantly older in the two-to-five-year group. Progression of CI was also associated with age at onset and initial staging of PD. Conclusions: Advanced age, late onset of disease and severity of PD are the predictive factors for the progression of CI in PD. The highest probability of progression of CI is in patients with initial severe impairments of visuospatial function.
CALL PAPERS Translational Research in Acute Lung Injury and Pulmonary Fibrosis 14-3-3 isoforms bind directly exon B of the 5 = -UTR of human surfactant protein A2 mRNA

14-3-3 isoforms bind directly exon B of the 5 = -UTR of human surfactant protein A2 mRNA. Am J Physiol Lung Cell Mol Physiol 309: L147–L157, 2015. Human surfactant protein (SP) A (SP-A), an innate immunity molecule, is encoded by two genes, SFTPA1 and SFTPA2. The 5 = untranslated splice variant of SP-A2 (ABD), but not SP-A1 (AD), contains exon B (eB). eB is an enhancer for transcription and translation and contains cis -regulatory elements. Speciﬁc trans -acting factors, including 14-3-3, bind eB. The 14-3-3 protein family contains seven isoforms that have been found by mass spectrometry in eB electromobility shift assays (Noutsios et al. Am J Physiol Lung Cell Mol Physiol 304: L722–L735, 2013). We used four different approaches to investigate whether 14-3-3 isoforms bind directly to eB. puriﬁed 14-3-3 isoforms (cid:2) , (cid:3) , ε , (cid:4) , (cid:5) , and (cid:6) , but not isoform (cid:7) , with wild-type eB RNA. 3 and 4 ) RNA afﬁnity chromatography assays and surface plasmon resonance analysis showed that 14-3-3 isoforms (cid:2) , (cid:3) , ε , (cid:4) , (cid:5) , and (cid:6) , but not isoform (cid:7) , speciﬁcally and directly bind eB. Inhibition of 14-3-3 isoforms (cid:3) , ε , (cid:4) , and (cid:6) / (cid:8) with shRNAs in NCI-H441 cells resulted in downregulation of SP-A2 levels but did not affect SP-A1 levels. However, inhibition of 14-3-3 isoform (cid:5) was correlated with lower levels of SP-A1 and SP-A2. Inhibition of 14-3-3 isoform (cid:7) / (cid:9) , which does not bind eB, had no effect on expression levels of SP-A1 and SP-A2. In conclusion, the 14-3-3 protein family affects differential regulation of SP-A1 and SP-A2 by binding directly to SP-A2 5 = -UTR mRNA.
Phenotype Microarray Profiling of Staphylococcus aureus menD and hemB Mutants with the Small-Colony-Variant Phenotype

ABSTRACT Standard biochemical tests have revealed that hemin and menadione auxotrophic Staphylococcus aureus small-colony variants (SCVs) exhibit multiple phenotypic changes. To provide a more complete analysis of the SCV phenotype, two genetically defined mutants with a stable SCV phenotype were comprehensively tested. These mutants, generated via mutations in menD or hemB that yielded menadione and hemin auxotrophs, were subjected to phenotype microarray (PM) analysis of over 1,500 phenotypes (including utilization of different carbon, nitrogen, phosphate, and sulfur sources; growth stimulation or inhibition by amino acids and other nutrients, osmolytes, and metabolic inhibitors; and susceptibility to antibiotics). Compared to parent strain COL, the hemB mutant was defective in utilization of a variety of carbon sources, including Krebs cycle intermediates and compounds that ultimately generate ATP via electron transport. The phenotype of the menD mutant was similar to that of the hemB mutant, but the defects in carbon metabolism were more pronounced than those seen with the hemB mutant. In both mutant strains, hexose phosphates and other carbohydrates that provide ATP in the absence of electron transport stimulated growth. Other phenotypes of SCV mutants, such as hypersensitivity to sodium selenite, sodium tellurite, and sodium nitrite, were also uncovered by the PM analysis. Key results of the PM analysis were confirmed in independent growth studies and by using Etest strips for susceptibility testing. PM technology is a new and efficient technology for assessing cellular phenotypes in S. aureus.
Assessing the Effective Stance of Monetary Policy: A Factor-Based Approach

We present an empirical approach to derive the implicit stance of monetary policy. The indicator can be interpreted as an implied short-term interest rate that is not restricted by the effective lower bound. Factor analysis is used to extract an expectations and term premium component from fitted yield curve data. Based on this, an implied short-term interest rate is constructed, which reflects how much the short-term rate should have fallen to achieve observed drop in long-term yields, assuming it could not have been caused by a fall in the term premium. Following Lombardi and Zhu (2014), we study how the implied rate performs as instrument for monetary policy analysis. Regression analyses suggests that the implied rate provides a good gauge for the identification of non-standard monetary policy shocks, and has responded significantly to financial stress as opposed to the output and inflation gap.
Abeta(1-40) prevents heparanase-catalyzed degradation of heparan sulfate glycosaminoglycans and proteoglycans in vitro. A role for heparan sulfate proteoglycan turnover in Alzheimer's disease.

Alzheimer's disease is characterized by senile plaques composed of polymeric fibrils of beta amyloid (Abeta), a 39-42-amino acid peptide formed after proteolytic processing of the amyloid precursor protein (betaAPP). Heparan sulfate proteoglycans have been shown to colocalize with Abeta in Alzheimer's disease brain, and experimental evidence indicates that the interactions between the proteoglycan and the peptide are important for the promotion, deposition, and/or persistence of the senile plaques. Studies in rat brain indicated that both the core protein and the heparan sulfate glycosaminoglycan chains are required for amyloid fiber formation and deposition in vivo (Snow, A. D., Sekiguchi, R., Nochlin, D., Fraser, P., Kimata, K. , Mizutani, A., Arai, M., Schreier, W. A., and Morgan, D. G. (1994) Neuron 12, 219-234), suggesting that one mechanism to prevent the formation of Abeta-heparan sulfate proteoglycan complexes that lead to deposition of amyloid would be to degrade the proteoglycan. Normally, heparan sulfate proteoglycans are internalized and degraded to short glycosaminoglycans by intracellular heparanases. These reactions occur in the endosomal-lysosomal pathway, which is the same intracellular location where betaAPP is processed to Abeta. Using partially purified heparanase activities from Chinese hamster ovary cells we examined whether Abeta(1-40) affects the catabolism of Chinese hamster ovary heparan sulfate glycosaminoglycans and proteoglycans in vitro. Abeta(1-40) binds to both the long heparan sulfate glycosaminoglycans attached to core proteins and the short, heparanase-derived chains in a concentration-dependent and pH-dependent manner. When Abeta(1-40) is added to heparanase assays, it prevents the partially purified activities from releasing heparan sulfate chains from core proteins and degrading them to short glycosaminoglycans; however, a large molar excess of the peptide to heparan sulfate is required to see the effect. Our results suggest that normally the levels of Abeta in the endosomal pathway are not sufficient to interfere with heparanase activity in vivo. However, once the level of Abeta-peptides are elevated, as they are in Alzheimer's disease, they could interact with heparan sulfate proteoglycans and prevent their catabolism. This could promote the formation and deposition of amyloid, since the binding of Abeta to the proteoglycan species will predominate.
Acetylcholine Activates an α-Bungarotoxin-Sensitive Nicotinic Current in Rat Hippocampal Interneurons, But Not Pyramidal Cells

The effects of acetylcholine on both pyramidal neurons and interneurons in the area CA1 of the rat hippocampus were examined, using intracellular recording techniques in an in vitroslice preparation. In current-clamp mode, fast local application of acetylcholine (ACh) to the soma of inhibitory interneurons in stratum radiatum resulted in depolarization and rapid firing of action potentials. Under voltage-clamp, ACh produced fast, rapidly desensitizing inward currents that were insensitive to atropine but that were blocked by nanomolar concentrations of the nicotinic α7 receptor-selective antagonists α-bungarotoxin (αBgTx) and methyllycaconitine. Nicotinic receptor antagonists that are not selective for α7-containing receptors had little (mecamylamine) or no effect (dihydro-β-erythroidine) on the ACh-induced currents. Glutamate receptor antagonists had no effect on the ACh-evoked response, indicating that the current was not mediated by presynaptic facilitation of glutamate release. However, the current could be desensitized almost completely by bath superfusion with 100 nm nicotine. In contrast to those actions on interneurons, application of ACh to the soma of CA1 pyramidal cells did not produce a detectable current. Radioligand-binding experiments with [125I]-αBgTx demonstrated that stratum radiatum interneurons express α7-containing nAChRs, and in situhybridization revealed significant amounts of α7 mRNA. CA1 pyramidal cells did not show specific binding of [125I]-αBgTx and only low levels of α7 mRNA. These results suggest that, in addition to their proposed presynaptic role in modulating transmitter release, α7-containing nAChRs also may play a postsynaptic role in the excitation of hippocampal interneurons. By desensitizing these receptors, nicotine may disrupt this action and indirectly excite pyramidal neurons by reducing GABAergic inhibition.
Global dynamic FET model for GaN transistors: DynaFET model validation and comparison to locally tuned models

Extensive results are presented validating a recently enhanced large signal FET model, DynaFET, applied to an advanced 6×75um periphery, 0.5um gate-length GaN HFET transistor, manufactured by RFMD. Excellent results are achieved for DC (including leakage current), S-parameters versus frequency and temperature, harmonic and intermodulation distortion, as well as load-pull figures of merit, over a very wide range of bias conditions, complex loads, powers, and frequencies. The DynaFET model features detailed dynamic trapping and de-trapping mechanisms for gate and drain lag, and dynamic self-heating. The multi-variate constitutive relations are represented by artificial neural networks (ANNs) trained from large-signal waveform data obtained using an active source injection NVNA-based characterization procedure. The new model is compared with two empirical models, each independently extracted from pulsed I-V data from different quiescent bias points and tuned for specific applications. The DynaFET model is demonstrated to have a much better fit than each of the individually tuned models, even at the tuned conditions. The new global model is sufficiently accurate over the entire operating range of the device that no tuning of model parameters is required for different operating points or amplifier classes of operation. The model runs in transient, harmonic balance, envelope, and all other simulation modes.
Clinical outcomes following primary percutaneous coronary intervention for ST-elevation myocardial infarction according to sex and race

Background: Female sex and South Asian race have been associated with poor clinical outcomes following primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) but remain understudied in large real-world series. We therefore investigated the association of sex and race with clinical outcomes following PPCI. Methods: We conducted a prospective study of all patients undergoing PPCI for STEMI between January 2009 and December 2011 at a large UK cardiac centre. Clinical characteristics and outcomes were compared according to sex and race using Chi-square test, independent samples Student’s t-test and Mann–Whitney U-test. Primary and secondary outcomes were 12-month major adverse cardiovascular events (MACEs) – defined as all-cause mortality, myocardial infarction and unplanned revascularization, analysed using Cox proportional hazard models adjusting for cardiovascular risk factors. Results: Three thousand and forty-nine patients were included. Women (n=826) were older than men (n=2223) (median age 69 vs. 60 years, p <0.01). Mortality (hazard ratio 1.48 (1.15–1.90)) and MACE (hazard ratio 1.40 (1.14–1.72)) were higher in women in univariable analysis. However, there were no significant sex-differences in mortality or MACE after age-stratification alone. Multivariable analysis also showed no significant differences in outcomes between sexes. South Asians (n=297) were younger but had a higher prevalence of most risk factors than White patients (n=2570). Mortality and MACE did not differ significantly between South Asian and White patients in univariable or multivariable analysis. Conclusion: MACE and mortality was not greater in women, or in South Asian patients following PPCI after adjustment for cardiovascular risk factors including age, which was most strongly associated with both outcomes.
Neutrophil gelatinase‐associated lipocalin as an early biomarker of acute kidney injury in liver transplantation

Acute kidney injury (AKI) is a common complication and a significant prognostic factor of long‐term outcome in patients undergoing liver transplantation. We evaluated the utility of urine and plasma neutrophil gelatinase‐associated lipocalin (NGAL) concentrations as biomarkers of AKI during and after liver transplantation.
Functional polymorphisms in pre-miR146a and pre-miR499 are associated with systemic lupus erythematosus but not with rheumatoid arthritis or Graves’ disease in Mexican patients

Recently, different microRNA (miRNA) gene polymorphisms have been evaluated in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Graves’ disease (GD). In the present study, we examined three single-nucleotide polymorphisms (SNPs) located in the pre-miR-146a (rs2910164G/C), pre-miR-196a-2 (rs11614913C/T), and pre-miR-499 (rs3746444A/G) genes. Our study population included 900 Mexican patients with RA, SLE, or GD, as well as 486 healthy control individuals with no family history of inflammatory or autoimmune diseases. Genotyping was performed using TaqMan probes and a 5′ exonuclease assay. None of the investigated SNPs were associated with RA or GD susceptibility under any genetic model (co-dominant, recessive, or dominant). Genotype and allele frequencies of the miR-196a-2 rs11614913C/T polymorphism were similar between SLE cases and controls. In contrast, the miR-146a rs2910164G/C and miR-499 rs3746444A/G polymorphisms were associated with SLE susceptibility. These SNPs were not associated with lupus nephritis (LN). Our results suggest that polymorphisms in miR-146a, miR-196a-2, and miR-499 are not associated with RA or GD susceptibility. This is the first report documenting that the miR-146a rs2910164G/C and miR-499 rs3746444 polymorphisms are associated with SLE susceptibility but not with LN.
Fibrinolytic function after dietary supplementation with omega3 polyunsaturated fatty acids.

Hypertension is associated with derangements in glucose and lipid metabolism. Increased levels of plasminogen activator inhibitor type 1 (PAI-1) are thought to potentiate the development of coronary events in this condition. Fish oil (omega3 polyunsaturated fatty acids [PUFAs]) have lipid-lowering effects, but the cardioprotective potential has been questioned because fish oil has been found to increase PAI-1 activity. This study was performed to determine the effects of omega3 PUFAs on the fibrinolytic function in hypertension. Seventy-eight persons with untreated hypertension were included in a 16-week, double-blind, randomized, controlled intervention study with 4 g/d of eicosapentaenoic and docosahexaenoic acids or corn oil placebo. Plasma PAI-1 activity, tissue plasminogen activator (tPA) activity, levels of fibrinogen and factor VII(c), and platelet count were measured before and after intervention (mean+/-SE). PAI-1 activity changed similarly in the fish oil and corn oil groups (1.8+/-1.0 U/mL versus 3.5+/-1.2 U/mL, P=.25), as did tPA (-0.02+/-0.02 IU/mL versus -0.13+/-0.03 IU/mL, P=.28), levels of factor VII(c) (6+/-5% versus 5+/-4%, P>.3), and platelet count (2+/-7x10(9)/L versus 3+/-5x10(9)/L, P>. 3). None of these variables changed from pretreatment levels during fish oil intake. Fibrinogen levels increased significantly both during fish oil (0.6+/-0.1 g/L, P=.0001) and corn oil (0.4+/-0.1 g/L, P=.002) intake. There was no between-group difference (P>.3). In conclusion, a daily intake of 4 g omega3 PUFAs does not affect PAI-1 and tPA activity in persons with hypertension. A modest increase in fibrinogen levels was observed after both fish oil and corn oil intake.
Sporulation of a Cortexless Mutant of a Variant of Bacillus cereus

A stage 4 sporulation mutant of a strain of Bacillus cereus var. alesti fails to synthesize a cortex although all other structural components appear normal. With terminal lysis the spore core as well as the sporangium is lysed. Both the uptake of 45Ca and the synthesis of dipicolinic acid (DPA) are similar to these activities in the parent strain, but these components (DPA and Ca) are lost to the medium with the drastic lysis. The first stage of diaminopimelic acid incorporation, that into germ cell wall mucopeptide, is intact in the mutant; the second stage, that into cortical mucopeptide, is absent. These biochemical studies as well as phospholipid metabolism and freeze-etch analysis suggest the lesion lies in the outer forespore membrane.
Export Product Range and Economic Growth in the EU Countries

We analyse the number of different HS8 products in the EU countries’ exports in 1995–2015. We review what share, or coverage, of the total possible number of these products the countries have exported each year. The EU15 countries have typically witnessed a slow rise in this coverage rate, that is, a widening of their extensive margins. The exception is Finland where the share has declined considerably. On the other hand, Ireland, Greece, Portugal and the new member countries have seen a dramatic increase in their export product coverage. We analyse how the development in the coverage rate and, as a comparison, the diversification of exports as measured by the Herfindahl–Hirschman index are associated with GDP per capita growth. We find that changes in the former measure are positively associated with economic growth after we have controlled for GDP per capita catching‐up as well as investment and export activity. We also find that smaller EU economies do not specialise more than large ones in their exports as could perhaps be assumed.
Effects of Quantitative Easing on Financial Market Integration and Hedging Efficacy

This thesis consists of three essays. The first essay (chapter 2) examines the correlations between bond markets, stock markets and currency forwards during the quantitative easing (QE) programs launched by the U.S. Federal Reserve. Using DCC-GARCH models, we document a spillover impact of QE on the international financial markets and find that these correlations differ by QE period across developed and emerging countries. Our findings provide new insights into the impact of unconventional monetary policy regimes on the relationships between various international financial asset markets. The second essay (chapter 3) examines the effectiveness and performance (E&P) of hedging international portfolios of bonds from developed and emerging countries. The excess returns and the variances of these portfolios are significantly lower during the QE versus pre-QE period. During the QE period, excess return and variance sensitivities are positive and negative with the Fed’s MBS holdings and become less positive and less negative with the Fed’s holdings of Treasuries. Hedging E&P during the QEs depend on the chosen hedging strategy and level of economic development. Results are robust using other hedging E&P measures and excluding countries with their own QEs. The third essay (chapter 4) finds that the integration of international bond and stock markets in 31 countries are affected significantly by U.S. quantitative easing (QE). After conceptually linking variations in the QE effects on bond and stock market integration to six transmission channels, we find that the actual effects depend upon the Fed holdings (MBS or Treasuries), channel considered, asset type (bond or stock), and the economic development categorization of the countries (developed or emerging). Cross-border banking flows as our proxy for the risk-taking channel significantly increase bond and stock market integration during each QE period for both developed and emerging countries.
Swarming of mobile router networks

A decentralized method for mobile router net works is proposed in this paper. A group of mobile routers moves in a cluttered environment maintaining connectivity between a base station and multiple exploring users. The network is seen as a switched system in which virtual spring mass interactions create and destroy the links between agents. We prove static (i.e., fixed graph topology) and dynamic (i.e., switching graph topology) stability using Lyapunov theory. To demonstrate the applicability of this method, we offer simulations for a self-healing case and for a non-isotropic environment.