Miracle-dz/UniFAR-FTUs huggingface dataset:
The association between subjective caregiver burden and depressive symptoms in carers of older relatives: A systematic review and meta-analysis

Background Family carers are an important source of care for older people. Although several studies have reported that subjective caregiver burden is related to depressive symptoms there are no systematic reviews quantifying this association. Objective To establish the extent to which subjective caregiver burden is associated with depressive symptoms and whether this association would vary by study or care characteristics. Methods We searched major databases such as PubMed, CINAHL, PsycINFO, Scopus and ISI Proceedings up to March 2018, and conducted a meta-analysis of included studies. Summary estimates of the association were obtained using a random-effects model to improve generalisation of findings. Results After screening of 4,688 articles, 55 studies were included providing a total of 56 independent comparisons with a total of 9,847 carers from data across 20 countries. There was a large, positive association between subjective caregiver burden and depressive symptoms (r¯ = 0.514; 95% CI = 0.486, 0.541), with very low heterogeneity amongst individual studies (I2 = 8.6%). Sensitivity analyses showed no differences between cross-sectional or repeated measures (r¯ = 0.521; 95% CI = 0.491, 0.550; 51 samples) and longitudinal studies (r¯ = 0.454; 95% CI = 0.398, 0.508; 6 samples). We found a higher effect size for those caring for people living with dementia compared to those caring for frail older people, and stroke survivors. Carer sex, age and kinship did not change the estimate of the effect. Conclusions Subjective caregiver burden is a significant risk factor for depressive symptoms in carers of older people and may precipitate clinical depression. Those caring for people with dementia experience greater burden. There is a need for longitudinal evaluations examining the effects of potential mediators of the association of subjective burden and depressive symptoms. Future interventions should test whether minimizing subjective burden may modify the risk of developing depression in carers of older relatives.
Potential Stem Cell Therapy of Radiation Induced Salivary Gland Dysfunction ( A Review )

Salivary glands play an important role in the maintenance of healthy oral cavity through the production of saliva. Hyposalivation, frequently experienced in certain patients specially those receiving radiation therapy for head and neck cancers. Radiotherapy treatment often results in unavoidable co-irradiation of normal tissues surrounding the tumor, such as the salivary glands . The ability to speak, swallow, masticate, taste food, and maintain a healthy oral cavity is heavily reliant on the presence of saliva. Reduction in saliva results in many symptoms whose combined effect can drastically reduce quality of life. Although artificial lubricants and drugs are available to ameliorate the consequences of hyposalivation, their effects are at best transient. Such management techniques do not address the source of the problem resulting from radiation-induced stem cell sterilization. Therefore, recent reseach work paid attention to stem cell replacement therapy to treat radiationinduced hyposalivation. Substantial progress has been made lately in the understanding of cell turnover in the salivary glands and the recent identification of stem and progenitor cell populations provides a basis for studies toward development of a stem cell-based therapy for xerostomia. Knowledge on the embryonic development, homeostasis and regeneration after atrophy of the salivary glands has provided important knowledge on the location of the salivary gland as well as on the factors that influence proliferation and differentiation. This knowledge has helped to locate, isolate and characterize the salivary gland stem cell in an attempt to be mobilized and transplanted in salivary glands. Hence, this review aims to survey the current state of knowledge of salivary gland stem cells and their potential in prevention or treatment of radiation induced salivary gland damage and hyposalivation in patients .
Inactivation of Escherichia coli O157:H7 by High Hydrostatic Pressure Combined with Gas Packaging

The inactivation of Escherichia coli O157:H7 (E. coli) in physiological saline and lotus roots by high hydrostatic pressure (HHP) in combination with CO2 or N2 was studied. Changes in the morphology, cellular structure, and membrane permeability of the cells in physiological saline after treatments were investigated using scanning electron microscopy, transmission electron microscopy, and flow cytometry, respectively. It was shown that after HHP treatments at 150–550 MPa, CO2-packed E. coli cells had higher inactivation than the N2-packed and vacuum-packed cells, and no significant difference was observed in the latter two groups. Further, both the morphology and intracellular structure of CO2-packed E.coli cells were strongly destroyed by high hydrostatic pressure. However, serious damage to the intracellular structures occurred in only the N2-packed E. coli cells. During HHP treatments, the presence of CO2 caused more disruptions in the membrane of E. coli cells than in the N2-packed and vacuum-packed cells. These results indicate that the combined treatment of HHP and CO2 had a strong synergistic bactericidal effect, whereas N2 did not have synergistic effects with HHP. Although these two combined treatments had different effects on the inactivation of E. coli cells, the inactivation mechanisms might be similar. During both treatments, E. coli cells were inactivated by cell damage induced to the cellular structure through the membrane components and the extracellular morphology, unlike the independent HHP treatment.
The C79G Polymorphism of the β2-Adrenergic Receptor Gene, ADRB2, and Susceptibility to Pediatric Asthma: Meta-Analysis from Review of the Literature

Background The ADRB2 gene encodes the β2-adrenergic receptor (β2-AR). This study aimed to determine the association between the C79G polymorphism of the ADRB2 gene and its association with pediatric asthma using a meta-analysis of the published data. Material/Methods Review of publications up to May 2018 was from the PubMed, EMBASE, China National Knowledge Infrastructure (CNKI), and WanFang databases. The odds ratio (ORs) with 95% confidence interval (CI) were used in evaluating the strength of the reported association between the C79G polymorphism of the ADRB2 gene and pediatric asthma. Results There were 18 controlled studies that included 2,982 pediatric cases of asthma and 2,651 controls. Expression of the C79G polymorphism of the ADRB2 gene was significantly associated with risk of pediatric asthma associated with the C or G allele with comparison of the co-dominant model (GG vs. CC: OR, 0.69; 95% CI, 0.55–0.88) and the recessive model (GG vs. CC+CG: OR, 0.65; 95% CI, 0.53–0.81). Subgroup analysis by ethnicity showed a significantly reduced risk of pediatric asthma in Asian patients for comparison of the co-dominant model (GG vs. CC: OR, 0.59; 95% CI, 0.45–0.78), the recessive model (GG vs. CC+CG: OR, 0.58; 95% CI, 0.45–0.76), and the allelic model (G vs. C: OR, 0.89; 95% CI, 0.79–0.99). Conclusions The C79G polymorphism of the ADRB2 gene encoding β2-AR was associated with a reduced risk for the development of pediatric asthma, particularly in the Asian population.
Risk Factors and Emerging Therapies in Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disease characterized by a permanent degeneration of both upper and lower motor neurons. Many different genes and pathophysiological processes contribute to this disease, however its exact cause remains unclear. Therefore, it is necessary to understand this heterogeneity to find effective treatments. In this review, we focus on selected environmental and genetic risk factors predisposing to ALS and highlight emerging treatments in ALS therapy. Of numerous defective genes associated with ALS, we focus on four principal genes that have been identified as definite causes of ALS: the SOD1 gene, C9orf72, TDP-43, as well as the recently identified TBK1. We also provide up-to-date information on selected environmental factors that have historically been considered as key players in ALS development and pathogenesis. In parallel to our survey of known risk factors, we also discuss emerging ALS stem cell therapies and experimental medicines currently undergoing phase II and III clinical trials.
FusionAtt: Deep Fusional Attention Networks for Multi-Channel Biomedical Signals

Recently, pervasive sensing technologies have been widely applied to comprehensive patient monitoring in order to improve clinical treatment. Various types of biomedical signals collected by different sensing channels provide different aspects of patient health information. However, due to the uncertainty and variability in clinical observation, not all the channels are relevant and important to the target task. Thus, in order to extract informative representations from multi-channel biosignals, channel awareness has become a key enabler for deep learning in biosignal processing and has attracted increasing research interest in health informatics. Towards this end, we propose FusionAtt—a deep fusional attention network that can learn channel-aware representations of multi-channel biosignals, while preserving complex correlations among all the channels. FusionAtt is able to dynamically quantify the importance of each biomedical channel, and relies on more informative ones to enhance feature representation in an end-to-end manner. We empirically evaluated FusionAtt in two clinical tasks: multi-channel seizure detection and multivariate sleep stage classification. Experimental results showed that FusionAtt consistently outperformed the state-of-the-art models in four different evaluation measurements, demonstrating the effectiveness of the proposed fusional attention mechanism.
Contralateral fatigue during severe-intensity single-leg exercise: influence of acute acetaminophen ingestion

Exhaustive single-leg exercise has been suggested to reduce time to task failure (Tlim) during subsequent exercise in the contralateral leg by exacerbating central fatigue development. We investigated the influence of acetaminophen (ACT), an analgesic that may blunt central fatigue development, on Tlim during single-leg exercise completed with and without prior fatiguing exercise of the contralateral leg. Fourteen recreationally active men performed single-leg severe-intensity knee-extensor exercise to Tlim on the left (Leg1) and right (Leg2) legs without prior contralateral fatigue and on Leg2 immediately following Leg1 (Leg2-CONTRA). The tests were completed following ingestion of 1-g ACT or maltodextrin [placebo (PL)] capsules. Intramuscular phosphorus-containing metabolites and substrates and muscle activation were assessed using 31P-MRS and electromyography, respectively. Tlim was not different between Leg1ACT and Leg1PL conditions (402 ± 101 vs. 390 ± 106 s, P = 0.11). There was also no difference in Tlim between Leg2ACT-CONTRA and Leg2PL-CONTRA (324 ± 85 vs. 311 ± 92 s, P = 0.10), but Tlim was shorter in Leg2ACT-CONTRA and Leg2PL-CONTRA than in Leg2CON (385 ± 104 s, both P < 0.05). There were no differences in intramuscular phosphorus-containing metabolites and substrates or muscle activation between Leg1ACT and Leg1PL and between Leg2ACT-CONTRA and Leg2PL-CONTRA (all P > 0.05). These findings suggest that levels of metabolic perturbation and muscle activation at Tlim are not different during single-leg severe-intensity knee-extensor exercise completed with or without prior fatiguing exercise of the contralateral leg. Despite contralateral fatigue, ACT ingestion did not alter neuromuscular responses, muscle metabolites, or exercise performance.
Extreme differences in recombination rate between the genomes of a solitary and a social bee.

Social insect genomes exhibit the highest rates of crossing over observed in plants and animals. The evolutionary causes of these extreme rates are unknown. Insight can be gained by comparing recombination rate variation across the genomes of related social and solitary insects. Here we compare the genomic recombination landscape of the highly social honey bee, Apis mellifera, with the solitary alfalfa leafcutter bee, Megachile rotundata, by analysing patterns of linkage disequilibrium in population-scale genome sequencing data. We infer that average recombination rates are extremely elevated in A. mellifera compared to M. rotundata. However, our results indicate that similar factors control the distribution of crossovers in the genomes of both species. Recombination rate is significantly reduced in coding regions in both species, with genes inferred to be germline-methylated having particularly low rates. Genes with worker-biased patterns of expression in A. mellifera and their orthologues in M. rotundata have higher than average recombination rates in both species, suggesting that selection for higher diversity in genes involved in worker caste functions in social taxa is not the explanation for these elevated rates. Furthermore, we find no evidence that recombination has modulated the efficacy of selection among genes during bee evolution, which does not support the hypothesis that high recombination rates facilitated positive selection for new functions in social insects. Our results indicate that the evolution of sociality in insects likely entailed selection on modifiers that increased recombination rates genome-wide, but that the genomic recombination landscape is determined by the same factors.
Expression and Localization of RGS9-2/Gβ5/R7BP Complex In Vivo Is Set by Dynamic Control of Its Constitutive Degradation by Cellular Cysteine Proteases

A member of regulator of G-protein signaling family, RGS9-2, is an essential modulator of signaling through neuronal dopamine and opioid G-protein-coupled receptors. Recent findings indicate that the abundance of RGS9-2 determines sensitivity of signaling in the locomotor and reward systems in the striatum. In this study we report the mechanism that sets the concentration of RGS9-2 in vivo, thus controlling G-protein signaling sensitivity in the region. We found that RGS9-2 possesses specific degradation determinants which target it for constitutive destruction by lysosomal cysteine proteases. Shielding of these determinants by the binding partner R7 binding-protein (R7BP) controls RGS9-2 expression at the posttranslational level. In addition, binding to R7BP in neurons targets RGS9-2 to the specific intracellular compartment, the postsynaptic density. Implementation of this mechanism throughout ontogenetic development ensures expression of RGS9-2/type 5 G-protein β subunit/R7BP complexes at postsynaptic sites in unison with increased signaling demands at mature synapses.
On Cyclic Behaviour of Unbounded Petri Nets

Cycles in state spaces represent repetitive behaviour of system models. Runs reproducing some state have important interpretations, for example rounds in distributed algorithms. In case of unbounded system models with infinite state space, cycles cannot be found in a straightforward way. For Petri nets, transition invariants provide necessary conditions for cyclic behaviour, but not for every transition invariant there is a corresponding cycle. Another approach to deal with infinite state behaviour is to consider finite coverability graphs which generalize reachability graphs by adding the value "arbitrary many" for unbounded places. Unfortunately, a cycle in the coverability graph does not necessarily represent a cyclic behaviour. This paper combines the concepts transition invariant and coverability graph in such a way that cyclic behaviour can be found in a combined graph. This implies a way to decide whether a sequence constitutes a cycle. A finite representation of all (infinitely many) cycles is implied by a result stating that the set of cycles is semi-linear. We also discuss an application of this concept: schedulability of Petri nets, i.e., control of transition occurrences such that the controlled behaviour does not lead to arbitrary token growth on any place.
Evidential diversity increases generalisation in predictive learning

In property induction tasks, encountering a diverse range of instances (e.g., hippos and hamsters) with a given property usually increases our willingness to generalise that property to a novel instance, relative to non-diverse evidence (e.g., hippos and rhinos). Although generalisation in property induction and predictive learning tasks share conceptual similarities, it is unknown whether this diversity principle applies to generalisation of a predictive association. We tested this hypothesis in two predictive learning experiments using differential training where one category of stimuli (e.g., fruits) predicted an outcome and another category (e.g., vegetables) predicted no outcome. We compared generalisation between a Non-Diverse group who were presented with non-diverse evidence in both positive (predicted the outcome) and negative (predicted no outcome) categories, and two groups who received the same training as the Non-Diverse group but with a more diverse range of exemplars in the positive (Diverse+ group) or negative (Diverse– group) category. Diversity effects were found for both positive and negative categories, in that learning about a diverse range of exemplars increased generalisation of a predictive association to novel exemplars from that same category. The results suggest that diversity, a key principle describing how we reason inductively, also applies to generalisation in associative learning tasks.
Derepression of HMGA2 via Removal of ZBRK1/BRCA1/CtIP Complex Enhances Mammary Tumorigenesis*

The high mobility group AT-hook 2 (HMGA2), a DNA architectural protein, is highly regulated during development and plays an important role in tumorigenesis. Indeed, HMGA2 was overexpressed in many different kinds of tumors. However, the mechanisms regulating HMGA2 expression remain elusive. Using microarray analysis, we found that HMGA2, along with a dozen of other genes, was co-repressed by ZBRK1, BRCA1, and CtIP. BRCA1 exerts its transcriptional repression activity through interaction with the transcriptional repressor ZBRK1 in the central domain, and with CtIP in the C-terminal BRCT domain. Here, we show that ZBRK1, BRCA1, and CtIP form a repression complex that coordinately regulates HMGA2 expression via a ZBRK1 recognition site in the HMGA2 promoter. Depletion of any of the proteins in this complex via adenoviral RNA interference in MCF10A mammary epithelial cells activates HMGA2 expression, resulting in increased colony formation in soft agar. Similarly, depletion of ZBRK1, or ectopic overexpression of HMGA2, in MCF10A cells induces abnormal acinar size with increased cell number and inhibits normal acinar formation. Consistently, many BRCA1-deficient mouse breast tumors express higher levels of HMGA2 than BRCA1-proficient tumors. These results suggest that activation of HMGA2 gene expression through derepression of the ZBRK1/BRCA1/CtIP complex is a significant step in accelerating breast tumorigenesis.
Conserved Genetic Architecture Underlying Individual Recombination Rate Variation in a Wild Population of Soay Sheep (Ovis aries)

Meiotic recombination breaks down linkage disequilibrium (LD) and forms new haplotypes, meaning that it is an important driver of diversity in eukaryotic genomes. Understanding the causes of variation in recombination rate is important in interpreting and predicting evolutionary phenomena and in understanding the potential of a population to respond to selection. However, despite attention in model systems, there remains little data on how recombination rate varies at the individual level in natural populations. Here we used extensive pedigree and high-density SNP information in a wild population of Soay sheep (Ovis aries) to investigate the genetic architecture of individual autosomal recombination rates. Individual rates were high relative to other mammal systems and were higher in males than in females (autosomal map lengths of 3748 and 2860 cM, respectively). The heritability of autosomal recombination rate was low but significant in both sexes (h2 = 0.16 and 0.12 in females and males, respectively). In females, 46.7% of the heritable variation was explained by a subtelomeric region on chromosome 6; a genome-wide association study showed the strongest associations at locus RNF212, with further associations observed at a nearby ∼374-kb region of complete LD containing three additional candidate loci, CPLX1, GAK, and PCGF3. A second region on chromosome 7 containing REC8 and RNF212B explained 26.2% of the heritable variation in recombination rate in both sexes. Comparative analyses with 40 other sheep breeds showed that haplotypes associated with recombination rates are both old and globally distributed. Both regions have been implicated in rate variation in mice, cattle, and humans, suggesting a common genetic architecture of recombination rate variation in mammals.
Thrombose veineuse cérébrale de l’enfant: à propos d’une série de 12 cas

La thrombose veineuse cérébrale (TVC) est rare chez l'enfant. Sa présentation clinique et ses étiologies sont variables. Le pronostic des patients reste redoutable devant le risque de décès et des séquelles neurosensorielles. L'objectif était d'étudier le profil clinique, radiologique et étiologique des TVC de l'enfant, et évaluer l'intérêt du traitement anti thrombotique. L'étude rétrospective menée au service de pédiatrie et de réanimation pédiatrique au CHU Med VI de Marrakech, Maroc, sur une période de 9 ans 10 mois (janvier 2008 à octobre 2018), colligeant tous les cas de TVC confirmés à l'imagerie, ayant un âge entre 1 mois et 15 ans. Nous avons recensé 12 cas. L'âge moyen était de 6,4 ans. Le sexe ratio était de 1.4. Le mode de début était aigu dans 7 cas. Les principales présentations cliniques étaient les convulsions (7 cas), les signes neurologiques focaux (7 cas), et les signes d'hypertension intracrânienne (HTIC) (6 cas). La tomodensitométrie (TDM) et / ou l'imagerie par résonance magnétique (IRM), ont révélé une atteinte du réseau veineux superficiel dans 8 cas, étendue dans 3 cas. L'étiologie était infectieuse chez 6 patients avec un cas de déshydratation, deux cas de maladie de système et une homocystinurie. Cependant, l'étiologie restait inconnue chez deux patients. Le traitement anti-thrombotique instaurait chez 7 enfants, avait permis une bonne évolution clinico-radiologique dans 5 cas. Le décès était survenu chez 2 enfants, et 3 autres avaient des séquelles neurologiques. Les TVCs chez l'enfant sont caractérisées par la grande diversité de leur présentation clinique et de leurs étiologies. L'impact des anticoagulants a été prouvé malgré l'absence de protocole thérapeutique standardisé.