Miracle-dz/UniFAR-FTUs huggingface dataset:
Cognition in the First Year After a Minor Stroke, Transient Ischemic Attack, or Mimic Event and the Role of Vascular Risk Factors

Background: Cognitive impairment following a minor stroke or transient ischemic attack (TIA) is common; however, due to diagnostic difficulties, the prevalence and underlying cause of impairment remain poorly defined. We compared cognition in patients after a minor stroke, TIA, or mimic event at three time points in the first year following the event. We examine whether cognitive impairment occurs following these events and whether this impairment differs based on the event type. Further, we measure whether these findings persist after controlling for age, education, and the presence of vascular risk factors and whether the presence of vascular risk factors, independent of event etiology, is associated with cognitive impairment. Lastly, we investigate whether increased stroke risk, as assessed by the ABCD2, is associated with reduced cognition. Methods: Medical information, a cognitive screening test, and a measure of executive functioning were collected from 613 patients (123 minor stroke, 175 TIA, and 315 mimics) using phone interviews at three time points in the first year following the event. Linear mixed models were used to determine the effect of event type, vascular risk factors, and predicted stroke risk on cognitive performance while controlling for confounders. Results: There was no relationship between event type and performance on either cognitive measure. When all confounders are controlled for, performance on the cognitive screening test was uniquely accounted for by the presence of heart failure, myocardial infarction, angina, and hypertension (all p < 0.047), whereas the measure of executive functioning was uniquely accounted for by the presence of hypertension and angina (all p < 0.032). Increased stroke risk also predicted performance on the cognitive screening test and the measure of executive functioning (all p < 0.002). Conclusions: Our findings indicate that cognitive impairment following a minor stroke or TIA may be attributed to the high prevalence of chronic vascular risk factors in these patients. This highlights the importance of long-term management of vascular risk factors beyond event recovery to reduce the risk of cognitive impairment. Increased stroke risk (i.e., ABCD2 score) was also associated with reduced cognition, suggesting that it may be helpful in signaling the need for further cognitive evaluation and intervention post-event.
Authoritarian-Benevolent Leadership, Moral Disengagement, and Follower Unethical Pro-organizational Behavior: An Investigation of the Effects of Ambidextrous Leadership

Drawing on the social cognitive theory of moral disengagement, this study examined the influence of the authoritarian-benevolent style of ambidextrous leadership on follower unethical pro-organizational behavior (UPB), mediated via moral disengagement. We tested the hypotheses using a sample of 175 participants at two time points. The results indicated that authoritarian-benevolent leadership affects moral disengagement. In addition, followers in congruent dyads with low authoritarian-benevolent leadership perceived higher levels of moral disengagement than those in congruent dyads with high authoritarian-benevolent leadership. Furthermore, high authoritarian-benevolent leadership had an indirect effect on follower UPB via moral disengagement. Theoretical and practical implications and future research directions are suggested.
De novo Assembly and Genome-Wide SNP Discovery in Rohu Carp, Labeo rohita

Citation: Das P, Sahoo L, Das SP, Bit A, Joshi CG, Kushwaha B, Kumar D, Shah TM, Hinsu AT, Patel N, Patnaik S, Agarwal S, Pandey M, Srivastava S, Meher PK, Jayasankar P, Koringa PG, Nagpure NS, Kumar R, Singh M, Iquebal MA, Jaiswal S, Kumar N, Raza M, Das Mahapatra K and Jena J (2020) De novo Assembly and Genome-Wide SNP Discovery in Rohu Carp, Labeo rohita. Front. Genet. 11:386. doi: 10.3389/fgene.2020. 00386 De novo Assembly and Genome-Wide SNP Discovery in Rohu Carp, Labeo rohita
Neural Dynamic Responses of Monetary and Social Reward Processes in Adolescents

Adolescence is an essential developmental period characterized by reward-related processes. The current study investigated the development of monetary and social reward processes in adolescents compared with that in children and adults; furthermore, it assessed whether adolescents had different levels of sensitivity to various types of rewards. Two adapted incentive delay tasks were employed for each participant, and event-related potentials (ERPs) were recorded. The behavioral results showed that both monetary and social rewards could motivate response speed, and participants were more accurate under the monetary reward condition than under the social reward condition. The behavioral performances of individuals increased with age. For the ERP data, the cue-P3, target-P2, target-P3 and feedback-related negativity (FRN) components were investigated to identify reward motivation, emotional arousal, attention allocation and feedback processing. Children and adolescents showed higher motivation (larger cue-P3) to rewards than adults. Adolescents showed larger emotional responses to rewards; that is, they had larger target-P2 amplitudes than adults and shorter target-P2 latencies than children. Children showed stronger emotional reactivity for monetary rewards than for social rewards. All age groups had stronger attentional control (larger target-P3) under the monetary reward condition than under the social reward condition. The present study sheds light on the neurodevelopment of reward processes in children, adolescents and adults and shows that various reward process stages demonstrate different age-related and reward-type-related characteristics.
A Novel Computational Approach for Identifying Essential Proteins From Multiplex Biological Networks

The identification of essential proteins can help in understanding the minimum requirements for cell survival and development. Ever-increasing amounts of high-throughput data provide us with opportunities to detect essential proteins from protein interaction networks (PINs). Existing network-based approaches are limited by the poor quality of the underlying PIN data, which exhibits high rates of false positive and false negative results. To overcome this problem, researchers have focused on the prediction of essential proteins by combining PINs with other biological data, which has led to the emergence of various interactions between proteins. It remains challenging, however, to use aggregated multiplex interactions within a single analysis framework to identify essential proteins. In this study, we created a multiplex biological network (MON) by initially integrating PINs, protein domains, and gene expression profiles. Next, we proposed a new approach to discover essential proteins by extending the random walk with restart algorithm to the tensor, which provides a data model representation of the MON. In contrast to existing approaches, the proposed MON approach considers for the importance of nodes and the different types of interactions between proteins during the iteration. MON was implemented to identify essential proteins within two yeast PINs. Our comprehensive experimental results demonstrated that MON outperformed 11 other state-of-the-art approaches in terms of precision-recall curve, jackknife curve, and other criteria.
Altered Time Awareness in Dementia

Our awareness of time, specifically of longer intervals spanning hours, days, months, and years, is critical for ensuring our sense of self-continuity. Disrupted time awareness over such intervals is a clinical feature in a number of frontotemporal dementia syndromes and Alzheimer's disease, but has not been studied and compared systematically in these diseases. We used a semi-structured caregiver survey to capture time-related behavioral alterations in 71 patients representing all major sporadic and genetic syndromes of frontotemporal dementia, in comparison to 28 patients with typical Alzheimer's disease and nine with logopenic aphasia, and 32 healthy older individuals. Survey items pertained to apparent difficulties ordering past personal events or estimating time intervals between events, temporal rigidity and clockwatching, and propensity to relive past events. We used a logistic regression model including diagnosis, age, gender, and disease severity as regressors to compare the proportions of individuals exhibiting each temporal awareness symptom between diagnostic groups. Gray matter associations of altered time awareness were assessed using voxel-based morphometry. All patient groups were significantly more prone to exhibit temporal awareness symptoms than healthy older individuals. Clinical syndromic signatures were identified. While patients with typical and logopenic Alzheimer's disease most frequently exhibited disturbed event ordering or interval estimation, patients with semantic dementia were most prone to temporal rigidity and clockwatching and those with behavioral variant frontotemporal dementia commonly exhibited all these temporal symptoms as well as a propensity to relive past events. On voxel-based morphometry, the tendency to relive past events was associated with relative preservation of a distributed left-sided temporo-parietal gray matter network including hippocampus. These findings reveal a rich and complex picture of disturbed temporal awareness in major dementia syndromes, with stratification of frontotemporal dementia syndromes from Alzheimer's disease. This is the first study to assess symptoms of altered temporal awareness across frontotemporal dementia syndromes and provides a motivation for future work directed to the development of validated clinical questionnaires, analysis of underlying neurobiological mechanisms and design of interventions.
Prematurity With Extrauterine Growth Restriction Increases the Risk of Higher Levels of Glucose, Low-Grade of Inflammation and Hypertension in Prepubertal Children

Introduction: An adipose tissue programming mechanism could be implicated in the extrauterine growth restriction (EUGR) of very preterm infants with morbidity in the cardiometabolic status later in life, as has been reported in intrauterine growth restriction. The aim of this study was to assess whether children with a history of prematurity and EUGR, but also with an adequate growth, showed alterations in the metabolic and inflammatory status. Methods: This was a case–control study. A total of 88 prepubertal children with prematurity antecedents were selected: 38 with EUGR and 50 with an adequate growth pattern (PREM group). They were compared with 123 healthy children born at term. Anthropometry, metabolic parameters, blood pressure (BP), C-reactive protein, hepatocyte growth factor (HGF), interleukin-6 (IL-6), IL-8, monocyte chemotactic protein type 1 (MCP-1), neural growth factor, tumour necrosis factor-alpha (TNF-α) and plasminogen activator inhibitor type-1 were analysed at the prepubertal age. Results: EUGR children exhibited higher BP levels and a higher prevalence of hypertension (46%) compared with both PREM (10%) and control (2.5%) groups. Moreover, there was a positive relationship between BP levels and values for glucose, insulin and HOMA-IR only in children with a EUGR history. The EUGR group showed higher concentrations of most of the cytokines analysed, markedly higher TNF-α, HGF and MCP-1 levels compared with the other two groups. Conclusion: EUGR status leads to cardiometabolic changes and a low-grade inflammatory status in children with a history of prematurity, and that could be related with cardiovascular risk later in life.
Glucocerebrosidase Defects as a Major Risk Factor for Parkinson’s Disease

Heterozygous mutations of the GBA1 gene, encoding for lysosomal enzyme glucocerebrosidase (GCase), occur in a considerable percentage of all patients with sporadic Parkinson’s disease (PD), varying between 8% and 12% across the world. Genome wide association studies have confirmed the strong correlation between PD and GBA1 mutations, pointing to this element as a major risk factor for PD, possibly the most important one after age. The pathobiological mechanisms underlying the link between a defective function of GCase and the development of PD are still unknown and are currently the focus of intense investigation in the community of pre-clinical and clinical researchers in the PD field. A major controversy regards the fact that, despite the unequivocal correlation between the presence of GBA1 mutations and the risk of developing PD, only a minority of asymptomatic carriers with GBA1 mutations convert to PD in their lifetime. GBA1 mutations reduce the enzymatic function of GCase, impairing lysosomal efficiency and the cellular ability to dispose of pathological alpha-synuclein. Changes in the cellular lipidic content resulting from the accumulation of glycosphingolipids, triggered by lysosomal dysfunction, may contribute to the pathological modification of alpha-synuclein, due to its ability to interact with cell membrane lipids. Mutant GCase can impair mitochondrial function and cause endoplasmic reticulum stress, thereby impacting on cellular energy production and proteostasis. Importantly, reduced GCase activity is associated with clear activation of microglia, a major mediator of neuroinflammatory response within the brain parenchyma, which points to neuroinflammation as a major consequence of GCase dysfunction. In this present review article, we summarize the current knowledge on the role of GBA1 mutations in PD development and their phenotypic correlations. We also discuss the potential role of the GCase pathway in the search for PD biomarkers that may enable the development of disease modifying therapies. Answering these questions will aid clinicians in offering more appropriate counseling to the patients and their caregivers and provide future directions for PD preclinical research.
Pathogenic Escherichia coli in Dogs Reveals the Predominance of ST372 and the Human-Associated ST73 Extra-Intestinal Lineages

Escherichia coli is a ubiquitous commensal and pathogen that has also been recognized as a multi-sectoral indicator of antimicrobial resistance (AMR). Given that latter focus, such as on resistances to extended-spectrum cephalosporins (ESC) and carbapenems, the reported population structure of E. coli is generally biased toward resistant isolates, with sequence type (ST)131 being widely reported in humans, and ST410 and ST648 being reported in animals. In this study, we characterized 618 non-duplicate E. coli isolates collected throughout France independently of their resistance phenotype. The B2 phylogroup was over-represented (79.6%) and positively associated with the presence of numerous virulence factors (VFs), including those defining the extra-intestinal pathogenic E. coli isolates (presence of ≥2 VFs: papA, sfaS, focG, afaD, iutA, and kpsMTII) and those more specifically related to uropathogenic E. coli (cnf1, hlyD). The major STs associated with clinical isolates from dogs were by far the dog-associated ST372 (20.7%) and ST73 (20.1%), a lineage that had commonly been considered until now as human-associated. Resistance to ESC was found in 33 isolates (5.3%), along with one carbapenemase-producing isolate, and was mostly restricted to non-B2 isolates. In conclusion, the presence of virulent E. coli lineages may be the issue, rather than the presence of ESC-resistant isolates, and the risk of transmission of such virulent isolates to humans needs to be further studied.
The Peripheral Immune System and Amyotrophic Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease that is defined by loss of upper and lower motor neurons, associated with accumulation of protein aggregates in cells. There is also pathology in extra-motor areas of the brain, Possible causes of cell death include failure to deal with the aggregated proteins, glutamate toxicity and mitochondrial failure. ALS also involves abnormalities of metabolism and the immune system, including neuroinflammation in the brain and spinal cord. Strikingly, there are also abnormalities of the peripheral immune system, with alterations of T lymphocytes, monocytes, complement and cytokines in the peripheral blood of patients with ALS. The precise contribution of the peripheral immune system in ALS pathogenesis is an active area of research. Although some trials of immunomodulatory agents have been negative, there is strong preclinical evidence of benefit from immune modulation and further trials are currently underway. Here, we review the emerging evidence implicating peripheral immune alterations contributing to ALS, and their potential as future therapeutic targets for clinical intervention.
Mitochondrial Genome Polymorphisms in the Human Pathogenic Fungus Cryptococcus neoformans

The Cryptococcus complex consists of at least seven evolutionary divergent lineages and causes ∼200,000 fatal human infections each year worldwide. The dominant lineage is Cryptococcus neoformans which consists of three haploid clades VNI, VNII, and VNB, their haploid hybrids, and various diploids derived from intra- and inter-clade mating events. In this study, we analyzed the mitogenomes of 184 strains of C. neoformans. Our analyses revealed that all 184 mitogenomes contained the same 15 protein-coding genes in the same gene order. However, their mitogenome sizes varied between 24,740 and 31,327 bp, primarily due to differences in the number and size of mitochondrial introns. Twelve nucleotide sites within five mitochondrial genes were found to contain introns in at least one of the 184 strains, ranging from 2 to 7 introns within each mitogenome. The concatenated mitochondrial exon sequences of the 15 protein-coding genes and two rRNA genes showed that VNI, VNII, and VNB strains were separated into distinct clades or sub-clades, largely consistent with results based on nuclear genome SNPs. However, several novel findings were observed. First, one strain of the VNB clade contained mitogenome exon sequences identical to the main VNI mitogenome type but was distant to other VNB mitogenomes. Second, hybrids among clades VNI, VNII, and VNB identified based on their nuclear genome SNPs contained mitogenomes from different clades, with evidence of their mitogenomes inherited from either the MATa or the MATα parents. Third, the eight diploid VNB (C. neoformans) × VNIV (C. deneoformans) hybrids contained recombinant mitogenomes. Fourth, analyses of intron distribution and the paired exon–intron phylogenies for each of the 12 exon–intron pairs suggested frequent gains and losses of mitochondrial introns during the evolution of C. neoformans. The combined mitogenome exon-based phylogeny and intron distributions suggested that clades VNI, VNII and VNB could be further divided into sub-clades. Together, our results revealed a dynamic evolution of mitochondrial genomes in this important human fungal pathogen.
New Robust Principal Component Analysis for Joint Image Alignment and Recovery via Affine Transformations and Frobenius and L2, 1 Norms

This paper proposes an effective and robust method for image alignment and recovery on a set of linearly correlated data via Frobenius and norms. The most popular and successful approach is to model the robust PCA problem as a low-rank matrix recovery problem in the presence of sparse corruption. The existing algorithms still lack in dealing with the potential impact of outliers and heavy sparse noises for image alignment and recovery. Thus, the new algorithm tackles the potential impact of outliers and heavy sparse noises via using novel ideas of affine transformations and Frobenius and norms. To attain this, affine transformations and Frobenius and norms are incorporated in the decomposition process. As such, the new algorithm is more resilient to errors, outliers, and occlusions. To solve the convex optimization involved, an alternating iterative process is also considered to alleviate the complexity. Conducted simulations on the recovery of face images and handwritten digits demonstrate the effectiveness of the new approach compared with the main state-of-the-art works.
Influence Maximization Revisited: Efficient Reverse Reachable Set Generation with Bound Tightened

Given a social network G with n nodes and m edges, a positive integer k, and a cascade model C, the influence maximization (IM) problem asks for k nodes in G such that the expected number of nodes influenced by the k nodes under cascade model C is maximized. The state-of-the-art approximate solutions run in O(k(n+m)log(n)/ε2) expected time while returning a (1-1/e -ε) approximate solution with at least 1-1/n probability. A key phase of these IM algorithms is the random reverse reachable (RR) set generation, and this phase significantly affects the efficiency and scalability of the state-of-the-art IM algorithms. In this paper, we present a study on this key phase and propose an efficient random RR set generation algorithm under IC model. With the new algorithm, we show that the expected running time of existing IM algorithms under IC model can be improved to O(k· n log(n)/ε2), when for any node v, the total weight of its incoming edges is no larger than a constant. Moreover, existing approximate IM algorithms suffer from scalability issues in high influence networks where the size of random RR sets is usually quite large. We tackle this challenging issue by reducing the average size of random RR sets without sacrificing the approximation guarantee. The proposed solution is orders of magnitude faster than states of the art as shown in our experiment.
Predicting Nocturnal Hypoglycemia from Continuous Glucose Monitoring Data with Extended Prediction Horizon

Nocturnal hypoglycemia is a serious complication of insulin-treated diabetes, which commonly goes undetected. Continuous glucose monitoring (CGM) devices have enabled prediction of impending nocturnal hypoglycemia, however, prior efforts have been limited to a short prediction horizon (~ 30 minutes). To this end, a nocturnal hypoglycemia prediction model with a 6-hour horizon (midnight-6 am) was developed using a random forest machine- learning model based on data from 10,000 users with more than 1 million nights of CGM data. The model demonstrated an overall nighttime hypoglycemia prediction performance of ROC AUC = 0.84, with AUC = 0.90 for early night (midnight-3 am) and AUC = 0.75 for late night (prediction at midnight, looking at 3-6 am window). While instabilities and the absence of late-night blood glucose patterns introduce predictability challenges, this 6-hour horizon model demonstrates good performance in predicting nocturnal hypoglycemia. Additional study and specific patient-specific features will provide refinements that further ensure safe overnight management of glycemia.
MYC and the unfolded protein response in cancer: synthetic lethal partners in crime?

The transcription factors of the MYC family play pivotal roles in the initiation and progression of human cancers. High oncogenic level of MYC invades low‐affinity sites and enhancer sequences, which subsequently alters the transcriptome, causes metabolic imbalance, and induces stress response. The endoplasmic reticulum (ER) not only plays a central role in maintaining proteostasis, but also contributes to other key biological processes, including Ca2+ metabolism and the synthesis of lipids and glucose. Stress conditions, such as shortage in glucose or oxygen and disruption of Ca2+ homeostasis, may perturb proteostasis and induce the unfolded protein response (UPR), which either restores homeostasis or triggers cell death. Crucial roles of ER stress and UPR signaling have been implicated in various cancers, from oncogenesis to treatment response. Here, we summarize the current knowledge on the interaction between MYC and UPR signaling, and its contribution to cancer development. We also discuss the potential of targeting key UPR signaling nodes as novel synthetic lethal strategies in MYC‐driven cancers.