Miracle-dz/UniFAR-FTUs huggingface dataset:
Sex Differences in Brain Gray and White Matter in Healthy Young Adults: Correlations with Cognitive Performance

Sex-related differences in behavior are extensive, but their neuroanatomic substrate is unclear. Indirect perfusion data have suggested a higher percentage of gray matter (GM) in left hemisphere cortex and in women, but differences in volumes of the major cranial compartments have not been examined for the entire brain in association with cognitive performance. We used volumetric segmentation of dual echo (proton density and T2-weighted) magnetic resonance imaging (MRI) scans in healthy volunteers (40 men, 40 women) age 18–45. Supertentorial volume was segmented into GM, white matter (WM), and CSF. We confirmed that women have a higher percentage of GM, whereas men have a higher percentage of WM and of CSF. These differences sustained a correction for total intracranial volume. In men the slope of the relation between cranial volume and GM paralleled that for WM, whereas in women the increase in WM as a function of cranial volume was at a lower rate. In men the percentage of GM was higher in the left hemisphere, the percentage of WM was symmetric, and the percentage of CSF was higher in the right. Women showed no asymmetries. Both GM and WM volumes correlated moderately with global, verbal, and spatial performance across groups. However, the regression of cognitive performance and WM volume was significantly steeper in women. Because GM consists of the somatodendritic tissue of neurons whereas WM comprises myelinated connecting axons, the higher percentage of GM makes more tissue available for computation relative to transfer across distant regions. This could compensate for smaller intracranial space in women. Sex difference in the percentage and asymmetry of the principal cranial tissue volumes may contribute to differences in cognitive functioning.
Efficient re-use of CRs under deep fading for improving cooperative sensing performance

It is well known in the research field of cooperative spectrum sensing that deeply faded local cognitive sensors need to be eliminated from contributing to the fusion pool at the fusion center in order to improve global detection reliability. Also, most current works on the topic unrealistically assume that the reporting channels between the cognitive sensors and the fusion center are free of loss and fading. This paper proposes an innovative technique to re-use those eliminated sensors by reassigning them to act as cooperative diversity relays to assist the surviving sensors in combatting outages due to Rayleigh fading in the reporting channel.
Cooperative Learning in the Classroom

Cooperative Learning: What Is It And Why Does It Matter? Learning For All? Using Diversity as a Strength Talk, Talk, Talk Cooperative Learning and How It Can Help Putting Cooperative Learning Into Practice APPENDICES Cooperative Learning Professional Development Programme Fulfilling Pupils Needs Cooperative Learning Structures Developing Effective Communication Skills - A Phased Programme Roles in Groups Five Key Steps to Implement Cooperative Learning Action Plan for Teaching and Developing Cooperative Learning Skills Quick Cooperative Learning Starter Activities Cooperative Learning - Common Social Problems Cooperative Learning Peer Observation Proforma Pupil Questionnaire
Encephalomyocarditis virus 3C protease attenuates type I interferon production through disrupting the TANK–TBK1–IKKε–IRF3 complex

TRAF family member-associated NF-κB activator (TANK) is a scaffold protein that assembles into the interferon (IFN) regulator factor 3 (IRF3)-phosphorylating TANK-binding kinase 1 (TBK1)–(IκB) kinase ε (IKKε) complex, where it is involved in regulating phosphorylation of the IRF3 and IFN production. However, the functions of TANK in encephalomyocarditis virus (EMCV) infection-induced type I IFN production are not fully understood. Here, we demonstrated that, instead of stimulating type I IFN production, the EMCV-HB10 strain infection potently inhibited Sendai virus- and polyI:C-induced IRF3 phosphorylation and type I IFN production in HEK293T cells. Mechanistically, EMCV 3C protease (EMCV 3C) cleaved TANK and disrupted the TANK–TBK1–IKKε–IRF3 complex, which resulted in the reduction in IRF3 phosphorylation and type I IFN production. Taken together, our findings demonstrate that EMCV adopts a novel strategy to evade host innate immune responses through cleavage of TANK.
Aproximación conceptual al uso de la integración sensorial en personas con demencia tipo Alzheimer

Background: Due to the increase of the diagnosis of Alzheimer´s disease in the general population and the serious repercussions it has on the person´s performance and autonomy, as well as the consequences it generates at the biological, psychological and social levels, a multidisciplinary approach is necessary to promote actions that improve the quality of life of the affected individual and her family. Objective: To review a theoretical approach of the use of sensorial integration as a means to generate adaptive behaviors in persons with Alzheimer´s disease. Method: The concept of dementia, the epidemiology of the disease, the stages that appear throughout its development, the relation between cerebral function and neuropathology of Alzheimer´s disease as well as the modalities of treatment in occupational therapy emphasizing the use of sensorial integration are considered. Results: The treatment is described involving the therapeutic strategies of sensorial and cognitive stimulation and its benefits according to the stage of the disease and the levels of production of answers for positive effects on the central nervous system. Conclusions: Following a sequential order is important in this kind of approach. The proper stimulus must be favored in order to produce appropriate therapeutic behavior.
New templates for HIV-1 antibody-based vaccine design

A current strategy for the design of neutralizing antibody-based vaccines to prevent HIV-1 transmission is that of reverse engineering, starting from a neutralizing antibody and working back to reconstruct its epitope by structure-based design technology. However, the field has been impeded by a lack of appropriate antibodies for use as templates. Recently, new antibodies have been described that may fulfil this role, invigorating the field.
A Text Categorization Method using Extended Vector Space Model by Frequent Term Sets

Text categorization is one of the most important research topics in Natural Language Processing and Information Retrieval due to the ever-increasing electronic documents. This paper presents a new text categorization method using frequent term sets. A novel constraint measure AD-Sup was introduced to extract discriminative features from frequent term sets for classification task. Then text documents are represented in the global feature space which contains both single terms and frequent term sets. To solve the sparse instance problem, a term weighting strategy is then implemented which assigns estimated weights using feature similarity and highly reduces the sparse rate. Through extensive experiments, the optimal proportion of single features and frequent term set features is empirically determined. Classification results on Reuters-21578 and WebKB corpus demonstrate that AD-Sup constraint is effective to extract useful frequent features and the combination strategy is effective to build better feature space and improve the SVM classifier.
Throwing the Baby Out with the Bathwater: When Can We Trust Self Report with the SMI Inpatient Population?

Throwing the Baby Out with the Bathwater: When Can We Trust Self-Report Outcome Assessment from Inpatient SMI? Jeffrey A. Lee Department of Psychology Doctor of Philosophy Reliability of self-report outcome assessment is often called into question with the severely mentally ill population. In the context of inpatient care, demand characteristics may further complicate self-report measures. Although clinician-completed outcome measures, such as the Brief Psychiatric Rating Scale-Expanded Version (BPRS-E), have become industry standard with this population, self-report assessment may be useful under certain conditions. This study sought to explore the relationship between a clinician-completed, the BPRS-E, and a self-completed measure, the SOQ, within the SMI inpatient population. A total of 357 adult participants with a minimum of three assessment iterations were analyzed. The results of the analysis indicated both measures correlated at all assessment iterations (admission, 90-, 180-, 270-, 360+ days), but when divided into SOQ admission clinical and subclinical groups only the clinical group maintained the correlation at all points. A logistical regression analysis indicated that membership in the subclinical group can be predicted by one subscale (Mood Disturbance) and three items (Hallucinations, Uncooperativeness, and Conceptual Disorganization) from the BPRS-E. The change trajectories of both measures were essentially identical; however, when divided into SOQ admission clinical and subclinical scores the SOQ and BPRS-E change trajectories were significantly different from each other and clinical versus subclinical on the same measure were significantly different. Further examination of the subclinical SOQ group revealed two distinct groups, scores that eventually had reliable change and exceeded the cutoff score and those that never did. A logistical regression analyses revealed that membership in these two groups can be reliably predicted by two BPRS-E items (Somatic Concerns and Suspiciousness), in that as each item increases the likelihood of membership in the group that never exceeds the cutoff score also increases. These results suggest that although the SMI inpatient population present with profound limitations, it may be possible to predict those who will eventually provide reliable self-report outcome assessments and those who will not. Although further research is necessary, these results are promising and may provide decision points for clinicians on when and when not to trust self-report outcome assessment with the SMI inpatient population.
Second-order power corrections in the heavy-quark effective theory. I. Formalism and meson form factors.

In the heavy-quark effective theory, hadronic matrix elements of currents between two hadrons containing a heavy quark are expanded in inverse powers of the heavy-quark masses, with coefficients that are functions of the kinematic variable $v\ifmmode\cdot\else\textperiodcentered\fi{}{v}^{\ensuremath{'}}$. For the ground-state pseudoscalar and vector mesons, this expansion is constructed at order $\frac{1}{{m}_{Q}^{2}}$. A minimal set of universal form factors is defined in terms of matrix elements of higher-dimensional operators in the effective theory. The zero recoil normalization conditions following from vector current conservation are derived. Several phenomenological applications of the general results are discussed in detail. It is argued that at zero recoil the semileptonic decay rates for $B\ensuremath{\rightarrow}D\ensuremath{\ell}\ensuremath{\nu}$ and $B\ensuremath{\rightarrow}{D}^{*}\ensuremath{\ell}\ensuremath{\nu}$ receive only small second-order corrections, which are unlikely to exceed the level of a few percent. This supports the usefulness of the heavy-quark expansion for a reliable determination of ${V}_{\mathrm{cb}}$. g
Genome-Wide mRNA Expression Analysis of Hepatic Adaptation to High-Fat Diets Reveals Switch from an Inflammatory to Steatotic Transcriptional Program

Background Excessive exposure to dietary fats is an important factor in the initiation of obesity and metabolic syndrome associated pathologies. The cellular processes associated with the onset and progression of diet-induced metabolic syndrome are insufficiently understood. Principal Findings To identify the mechanisms underlying the pathological changes associated with short and long-term exposure to excess dietary fat, hepatic gene expression of ApoE3Leiden mice fed chow and two types of high-fat (HF) diets was monitored using microarrays during a 16-week period. A functional characterization of 1663 HF-responsive genes reveals perturbations in lipid, cholesterol and oxidative metabolism, immune and inflammatory responses and stress-related pathways. The major changes in gene expression take place during the early (day 3) and late (week 12) phases of HF feeding. This is also associated with characteristic opposite regulation of many HF-affected pathways between these two phases. The most prominent switch occurs in the expression of inflammatory/immune pathways (early activation, late repression) and lipogenic/adipogenic pathways (early repression, late activation). Transcriptional network analysis identifies NF-κB, NEMO, Akt, PPARγ and SREBP1 as the key controllers of these processes and suggests that direct regulatory interactions between these factors may govern the transition from early (stressed, inflammatory) to late (pathological, steatotic) hepatic adaptation to HF feeding. This transition observed by hepatic gene expression analysis is confirmed by expression of inflammatory proteins in plasma and the late increase in hepatic triglyceride content. In addition, the genes most predictive of fat accumulation in liver during 16-week high-fat feeding period are uncovered by regression analysis of hepatic gene expression and triglyceride levels. Conclusions The transition from an inflammatory to a steatotic transcriptional program, possibly driven by the reciprocal activation of NF-κB and PPARγ regulators, emerges as the principal signature of the hepatic adaptation to excess dietary fat. These findings may be of essential interest for devising new strategies aiming to prevent the progression of high-fat diet induced pathologies.
Targets of MiRNAs in lung cancer related pathways as predictors of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characterized by persistent airflow limitation. The mechanisms underlying COPD remain unclear. Identifying expression patterns of miRNAs and mRNAs in COPD may enhance our understanding of the mechanisms of disease. In the current study, we used miRNA and mRNA expression profiling data of lung tissue from smokers with and without COPD to examine the miRNA-targets regulations and gene expression patterns in enriched lung cancer-related pathways. Firstly, we identified 40 differentially expressed miRNAs that exhibit significant differential expression in the COPD samples compared to normal samples. Then, we conducted target prediction and pathway enrichment analysis with these miRNAs to investigate potential associated genes and pathway targets. From those significant enriched pathways, we specially selected two lung cancer-related pathways: Small cell lung cancer pathway and Non-small cell lung cancer pathway. Finally, we examined the miRNA-targets regulations and gene expression patterns in these two pathways. Our results suggested that the targets of miRNAs in lung cancer-related pathways can be as predictors of COPD. Investigating miRNA-targets relationships may further help our understanding of the mechanisms of lung diseases.
Experimental salmonellosis in the chicken. 2. Fate of a temperature-sensitive filamentous mutant.

A temperature-sensitive filamentous mutant of Salmonella enteritidis administered orally to 1-day-old chicks exhibited the same predilection for the caudal intestine and ceca as the wild type of the organism. Administered intracardially, it was found by 6 hr postinoculation (PI) in the cecal lumen but was unable to proliferate there and by 24 hr PI declined slowly in numbers. Rare fragments of the filaments were seen in the lower intestinal and cecal epithelium and lamina propria, but no true entry into the tissues appeared to occur. By 24 hr following intracardial inoculation in 1-day-old chicks, the blood and liver cultured negative. Clearance was even more rapid in 2-week-old birds inoculated intravenously. The organism produced no observable pathological changes in any tissue of either age group apart from a mild heterophil response in the ceca of 1-day-old chicks following oral administration.
Molecular Pathways Molecular Pathways : Adipose In fl ammation as a Mediator of Obesity-Associated Cancer

The increasing rate of obesity worldwide is predicted to be associated with a surge in diseases. Notably, obesity has been linked to approximately 20% of cancer cases in the United States; obesity is associated with both increased risk and worse outcomes after diagnosis. Altered levels of circulating factors are strongly implicated, including insulin, insulin-like growth factor 1, leptin, adiponectin, and interleukin6 (IL-6). In addition, increasing attention has focused on the consequences of local adipose inflammation. Inflammatory foci characterized by crown-like structures consisting of dead adipocytes encircled by macrophages occur in white adipose depots, including the breast tissue, of most overweight and obese women. Saturated fatty acids, released as a consequence of obesity-associated lipolysis, induce macrophage activation via Toll-like receptor 4, thereby stimulating NF-kB signaling. This, in turn, activates transcription of proinflammatory genes including COX-2, IL-6, IL-1b, and TNFa. Elevated levels of proinflammatory mediators cause both local and systemic effects. Of particular relevance with regard to breast cancer is increased transcription of the CYP19 gene encoding aromatase, the ratelimiting enzyme for estrogen synthesis. Notably, this obesity–inflammation–aromatase axis provides a plausible explanation for increased rates of postmenopausal, hormone receptor–positive breast cancer associated with obesity and hence may offer targets for interventions to attenuate risk or improve prognosis. Potential approaches include weight reduction, exercise, and suppression of obesity-driven signaling pathways using pharmaceutical or dietary agents. A key future goal is to identify biomarkers that accurately report adipose inflammation, both for identification of at-risk individuals and to assess the efficacy of interventions. Clin Cancer Res; 19(22); 1–10. 2013 AACR.
Critical role of PA28γ in hepatitis C virus-associated steatogenesis and hepatocarcinogenesis

Hepatitis C virus (HCV) is a major cause of chronic liver disease that frequently leads to steatosis, cirrhosis, and eventually hepatocellular carcinoma (HCC). HCV core protein is not only a component of viral particles but also a multifunctional protein because liver steatosis and HCC are developed in HCV core gene-transgenic (CoreTg) mice. Proteasome activator PA28γ/REGγ regulates host and viral proteins such as nuclear hormone receptors and HCV core protein. Here we show that a knockout of the PA28γ gene induces the accumulation of HCV core protein in the nucleus of hepatocytes of CoreTg mice and disrupts development of both hepatic steatosis and HCC. Furthermore, the genes related to fatty acid biosynthesis and srebp-1c promoter activity were up-regulated by HCV core protein in the cell line and the mouse liver in a PA28γ-dependent manner. Heterodimer composed of liver X receptor α (LXRα) and retinoid X receptor α (RXRα) is known to up-regulate srebp-1c promoter activity. Our data also show that HCV core protein enhances the binding of LXRα/RXRα to LXR-response element in the presence but not the absence of PA28γ. These findings suggest that PA28γ plays a crucial role in the development of liver pathology induced by HCV infection.
Cutting edge: memory CD8 T cell compartment grows in size with immunological experience but nevertheless can lose function.

The size of the adaptive immune system is considered to be kept constant by the attrition of pre-existing memory. However, recently it was shown that the CD8 memory compartment can grow in size and the number of pre-existing memory is largely preserved, predicting that pre-existing immunity should be maintained (Vezys et al.; Nature 457: 196-199). Experimental proof for this assumption is still lacking. We address this question in the Listeria monocytogenes (L.m.) infection model and confirm the growth of size of the memory compartment by subsequent vaccination with modified vaccinia virus Ankara. We also find only modest attrition of pre-existing L.m. -specific memory CD8 T cells. However, pre-existing protective immunity toward L.m. is not preserved. Pre-existing L.m. -specific effector-memory cells, in contrast to central memory cells, become altered, and this results in a significant loss of pre-existing protective immunity. Our findings are clinically relevant for vaccines introducing new CD8 memory cells in high numbers, as this might influence pre-existing immunity.
WRKY transcription factors: key components in abscisic acid signalling.

WRKY transcription factors (TFs) are key regulators of many plant processes, including the responses to biotic and abiotic stresses, senescence, seed dormancy and seed germination. For over 15 years, limited evidence has been available suggesting that WRKY TFs may play roles in regulating plant responses to the phytohormone abscisic acid (ABA), notably some WRKY TFs are ABA-inducible repressors of seed germination. However, the roles of WRKY TFs in other aspects of ABA signalling, and the mechanisms involved, have remained unclear. Recent significant progress in ABA research has now placed specific WRKY TFs firmly in ABA-responsive signalling pathways, where they act at multiple levels. In Arabidopsis, WRKY TFs appear to act downstream of at least two ABA receptors: the cytoplasmic PYR/PYL/RCAR-protein phosphatase 2C-ABA complex and the chloroplast envelope-located ABAR-ABA complex. In vivo and in vitro promoter-binding studies show that the target genes for WRKY TFs that are involved in ABA signalling include well-known ABA-responsive genes such as ABF2, ABF4, ABI4, ABI5, MYB2, DREB1a, DREB2a and RAB18. Additional well-characterized stress-inducible genes such as RD29A and COR47 are also found in signalling pathways downstream of WRKY TFs. These new insights also reveal that some WRKY TFs are positive regulators of ABA-mediated stomatal closure and hence drought responses. Conversely, many WRKY TFs are negative regulators of seed germination, and controlling seed germination appears a common function of a subset of WRKY TFs in flowering plants. Taken together, these new data demonstrate that WRKY TFs are key nodes in ABA-responsive signalling networks.
Agricultural soil denitrifiers possess extensive nitrite reductase gene diversity

Denitrification transforms nitrogen applied as fertilizer and emits N2 O, which is a potent greenhouse gas. Very little is known about the identities of abundant and active denitrifiers in agricultural soils. We coupled DNA stable-isotope probing (DNA-SIP) with flow-through reactors (FTRs) to detect active agricultural soil denitrifiers. The FTRs were incubated with nitrate and 13 C6 -glucose under anoxic conditions and sampled at multiple time points. Labelled DNA from active microorganisms was analyzed by 16S rRNA gene fingerprinting, amplicon and shotgun metagenomic sequencing. Taxonomic representation of heavy fractions was consistent across sites and time points, including Betaproteobacteria (71%; Janthinobacterium, Acidovorax, Azoarcus and Dechloromonas), Alphaproteobacteria (8%; Rhizobium), Gammaproteobacteria (4%; Pseudomonas) and Actinobacteria (4%; Streptomycetaceae). Most nitrite-reductase reads from heavy DNA annotated to the copper-containing form (nirK). Assigned taxonomies of active denitrifiers based on reads matching the nirK gene were comparable to those obtained through nitric oxide (norB) and RNA polymerase (rpoB) annotations but not the nitrous oxide reductase gene (nosZ). Analysis of recovered metagenomes from heavy DNA demonstrated extensive nirK sequence family diversity, including novel taxonomic groups that are not captured by existing primers.