Miracle-dz/UniFAR-FTUs huggingface dataset:
Applying Push-Pull-Mooring Framework to Investigate SNSs Switching Behavior

Switching behavior refer to that users often move from one IT product to another. There are complex motivations and reasons to be explained behind the behavior. Understanding the factors that influence users’ switching behavior is important for SNS providers to consolidate existing user base and attract more users. In view of this, this study introduced the migration theory based on human migration studies from the perspective of social network services, and tried to find out the characteristics of SNSs switching. Based on the PPM framework, we had constructed a conceptual model in which we served social network fatigue as the push driver, three types of network externalities as pull drivers, and inertia as the mooring driver, and put forward relevant assumptions. After the reliability and validity test of the questionnaire, the model and related assumptions were tested using SmartPLS 2.0. We found that push effect of social network fatigue has positive impact on switching intention and is influenced by perceived overloads, pull effects of network size positively influenced switching intention as well. However, the positive associations of social network fatigue and network size with switching intention were alleviated by the mooring effect of inertia. And affective commitment and switching costs significantly promoted the inertia. Finally, the switching intention exerted positive impact on actual switching behavior. Our finding helps to further understand SNS users’ switching behavior, provides reference value for information processing and management of SNSs, and deepen theoretically the switching behaviors of conceptual model in the virtual community users.
Brexpiprazole for treatment-resistant major depressive disorder

ABSTRACT Introduction:Treatment-resistant depression (TRD), seldom interchangeably referred to as ‘depression inadequately responding to the standard antidepressant drug,’ carries a significant burden. The atypical antipsychotics represent a popular augmentation strategy for antidepressant-resistant depression, although their efficacy/safety profiles vary across different agents and presentations of depression. Areas covered: This review appraises the evidence supporting the use of brexpiprazole augmentation for major depressive disorder (MDD) adults showing an inadequate response to standard antidepressants, covering the related regulatory affairs, and essential pharmacology. Expert opinion: Brexpiprazole is a ‘third-generation’ antipsychotic featuring dopaminergic D2 and serotonergic 5-HT1A partial agonism approved by the U.S. Food and Drug Administration for the treatment of MDD, besides schizophrenia in adults. The clinical trials leading to the extended approval of brexpiprazole rely on the definition of ‘inadequate response’ to antidepressants, which seems to poorly represent the most severe cases of TRD seen in clinical practice. TRD definitions appraised in the literature are likewise inconsistent and questionable from a clinical-standpoint. Compared to aripiprazole, brexpiprazole has lower D2 intrinsic activity, although the latter features a more potent serotonergic 5-HT2A antagonism. The actual propensity of brexpiprazole to induce akathisia and tardive dyskinesia warrants assessment by ad-hoc designed long-term, controlled trials.
Interface Effects on He Ion Irradiation in Nanostructured Materials

In advanced fission and fusion reactors, structural materials suffer from high dose irradiation by energetic particles and are subject to severe microstructure damage. He atoms, as a byproduct of the (n, α) transmutation reaction, could accumulate to form deleterious cavities, which accelerate radiation-induced embrittlement, swelling and surface deterioration, ultimately degrade the service lifetime of reactor materials. Extensive studies have been performed to explore the strategies that can mitigate He ion irradiation damage. Recently, nanostructured materials have received broad attention because they contain abundant interfaces that are efficient sinks for radiation-induced defects. In this review, we summarize and analyze the current understandings on interface effects on He ion irradiation in nanostructured materials. Some key challenges and research directions are highlighted for studying the interface effects on radiation damage in nanostructured materials.
Immunological Regulation of Vascular Inflammation During Cancer Metastasis

Metastasis is the predominant cause of cancer-related mortality, despite being a highly inefficient process overall. The vasculature is the gatekeeper for tumor cell seeding within the secondary tissue microenvironment—the rate limiting step of the metastatic cascade. Therefore, factors that regulate vascular physiology dramatically influence cancer outcomes. There are a myriad of physiologic circumstances that not only influence the intrinsic capacity of tumor cells to cross the endothelial barrier, but also that regulate vascular inflammation and barrier integrity to enable extravasation into the metastatic niche. These processes are highly dependent on inflammatory cues largely initiated by the innate immune compartment, that are meant to help re-establish tissue homeostasis, but instead become hijacked by cancer cells. Here, we discuss the scientific advances in understanding the interactions between innate immune cells and the endothelium, describe their influence on cancer metastasis, and evaluate potential therapeutic interventions for the alleviation of metastatic disease. By triangulating the relationship between immune cells, endothelial cells, and tumor cells, we will gain greater insight into how to impede the metastatic process by focusing on its most vulnerable phases, thereby reducing metastatic spread and cancer-related mortality.
Attitudes of nurses from a public teaching hospital regarding the nursing process.

OBJECTIVE To measure the attitudes of nurses on nursing process at a public teaching hospital. METHOD A cross-sectional and analytical study conducted with nurses at a tertiary hospital. It was applied an instrument to characterize sample, as well as the Positions on the Nursing Process instrument, which measures nurses' attitudes in relation to the nursing process. There are 20 items to be considered, in which the minimum possible value is 20 and the maximum of 140. The data were submitted to descriptive statistics and the variables of interest were analyzed by the Mann-Whitney, Student's t-test, Chi-square test, Kruskal-Wallis, Spearman's correlation coefficient and hierarchical multiple regression models, as appropriate. RESULTS In a sample of 226 nurses, 80.5% (182) stated that they performed pdaily. The mean score of the instrument was 102.50 (SD = 21.76). The item "routine/creative" had a lower score (3.54), while "unimportant/important" had a higher score (5.81). CONCLUSION The nurses reported being in favor and presented positive attitudes about nursing process, in addition to considering it important, but routine, as well as affirming little or no contact with research, classes or events on the subject.
Goal Preferences, Affect, Activity Patterns and Health Outcomes in Women With Fibromyalgia

Some motivational models understand health behavior as a result of the interaction between goal preferences and mood. However, this perspective has not been explored in fibromyalgia. Furthermore, in chronic pain, it has only been explored with regard to negative affect. Thus, our aims were: (1) to develop a Spanish version of the Goal Pursuit Questionnaire (GPQ); (2) to explore the relationships between goal preferences and health outcomes, testing the moderator role of affect and the mediating role of chronic pain activity patterns. We conducted two cross-sectional studies. In Study 1, after a double translation/back-translation process, we interviewed 94 women attending the Fibromyalgia Unit of the Community of Valencia in order to identify the cultural feasibility and the content validity of the GPQ. Study 2 comprised 260 women. We explored the GPQ structure and performed path analyses to test conditional mediation relationships. Eight activities from the original GPQ were changed while maintaining the conceptual equivalence. Exploratory factor analysis showed two factors: ‘Pain-avoidance goal’ and ‘Mood-management goal’ (37 and 13% of explained variance, respectively). These factors refer to patients’ preference for hedonic goals (pain avoidance or mood-management) over achievement goals. Robust RMSEA fit index of the final models ranged from 0.039 for pain to 0.000 for disability and fibromyalgia impact. Pain avoidance goals and negative affect influenced pain mediated by task-contingent persistence. They also affected disability mediated by task and excessive persistence. Pain avoidance goals and positive affect influenced fibromyalgia impact mediated by activity avoidance. We also found a direct effect of negative and positive affect on health outcomes. Preference for pain avoidance goals was always related to pain, disability and fibromyalgia impact through activity patterns. Affect did not moderate these relationships and showed direct and indirect paths on health outcomes, mainly by increasing persistence and showing positive affect as an asset and not a risk factor. Intervention targets should include flexible reinforcement of achievement goals relative to pain avoidance goals and positive affect in order to promote task-persistence adaptive activity patterns and decreased activity avoidance.
Synovial Tissue Inflammation Mediated by Autoimmune T Cells

In rheumatoid arthritis (RA), various hematopoietic and non-hematopoietic cells present in the synovial tissue secrete numerous inflammatory mediators including pro-inflammatory cytokines critical for the induction of chronic joint inflammation and bone destruction. Fibroblast-like synoviocytes (FLSs) in the non-hematopoietic cell compartment are key inflammatory cells activated in inflamed joints and driving the disease; yet how synovial tissue inflammation is modulated by autoimmune T cells is not fully understood. In this review, mainly based on recent findings with a mouse model of spontaneous autoimmune arthritis, we discuss the mechanism of Th17-mediated synovial tissue inflammation; that is, what environmental stimuli and arthritogenic self-antigens trigger arthritis, how arthritogenic T cells initiate joint inflammation by stimulating FLSs, and how the cellular sources of GM-CSF from lymphoid and tissue stromal cells in the synovium contribute to the development of arthritis. We also highlight possible plasticity of Th17 cells toward pathogenic GM-CSF producers, and the functional instability of regulatory T cells under inflammatory conditions in RA joints.
CRISPR applications in plant virology: virus resistance and beyond.

CRISPR/Cas (Clustered Regularly Interspaced Short Palindromic Repeats/CRISPR-associated genes) is a prokaryotic adaptive immune system which has been reprogrammed into a precise, simple and efficient gene targeting technology. This emerging technology is revolutionizing various areas of life sciences, medicine, biotechnology and has raised significant interest among plant biologists, both in basic science and in plant protection and breeding. In this review, we describe the basic principles of CRISPR/Cas systems, and how they can be deployed to model plants and crops for the control, monitoring and study of the mechanistic aspects of plant virus infections. We discuss how Cas endonucleases can be used to engineer plant virus resistance by directly targeting viral DNA or RNA, as well as how they can inactivate host susceptibility genes. Additionally, other applications of CRISPR/Cas in plant virology such as virus diagnostics and imaging are reviewed. The review also provides a systemic comparison between CRISPR/Cas technology and RNA interference approaches, the latter of which has also been used for development of virus resistant plants. Finally, we outline challenges to be solved before CRISPR/Cas can produce virus-resistant crop plants which can be marketed.
Turning a Collagenesis-Inducing Peptide Into a Potent Antibacterial and Antibiofilm Agent Against Multidrug-Resistant Gram-Negative Bacteria

Antimicrobial resistance is becoming one the most serious health threats worldwide, as it not only hampers effective treatment of infectious diseases using current antibiotics, but also increases the risks of medical procedures like surgery, transplantation, bone and dental implantation, chemotherapy, or chronic wound management. To date, there are no effective measures to tackle life-threatening nosocomial infections caused by multidrug resistant bacterial species, of which Gram-negative species within the so-called “ESKAPE” pathogens are the most worrisome. Many such bacteria are frequently isolated from severely infected skin lesions such as diabetic foot ulcers (DFU). In this connection, we are pursuing new peptide constructs encompassing antimicrobial and collagenesis-inducing motifs, to tackle skin and soft tissue infections by exerting a dual effect: antimicrobial protection and faster healing of the wound. This produced peptide 3.1-PP4 showed MIC values as low as 1.0 and 2.1 μM against Escherichia coli and Pseudomonas aeruginosa, respectively, and low toxicity to HFF-1 human fibroblasts. Remarkably, the peptide was also potent against multidrug-resistant isolates of Klebsiella pneumoniae, E. coli, and P. aeruginosa (MIC values between 0.5 and 4.1 μM), and hampered the formation of/disaggregated K. pneumoniae biofilms of resistant clinical isolates. Moreover, this notable hybrid peptide retained the collagenesis-inducing behavior of the reference cosmeceutical peptide C16-PP4 (“Matrixyl”). In conclusion, 3.1-PP4 is a highly promising lead toward development of a topical treatment for severely infected skin injuries.
General Anesthesia: A Probe to Explore Consciousness

General anesthesia reversibly alters consciousness, without shutting down the brain globally. Depending on the anesthetic agent and dose, it may produce different consciousness states including a complete absence of subjective experience (unconsciousness), a conscious experience without perception of the environment (disconnected consciousness, like during dreaming), or episodes of oriented consciousness with awareness of the environment (connected consciousness). Each consciousness state may potentially be followed by explicit or implicit memories after the procedure. In this respect, anesthesia can be considered as a proxy to explore consciousness. During the recent years, progress in the exploration of brain function has allowed a better understanding of the neural correlates of consciousness, and of their alterations during anesthesia. Several changes in functional and effective between-region brain connectivity, consciousness network topology, and spatio-temporal dynamics of between-region interactions have been evidenced during anesthesia. Despite a set of effects that are common to many anesthetic agents, it is still uneasy to draw a comprehensive picture of the precise cascades during general anesthesia. Several questions remain unsolved, including the exact identification of the neural substrate of consciousness and its components, the detection of specific consciousness states in unresponsive patients and their associated memory processes, the processing of sensory information during anesthesia, the pharmacodynamic interactions between anesthetic agents, the direction-dependent hysteresis phenomenon during the transitions between consciousness states, the mechanisms of cognitive alterations that follow an anesthetic procedure, the identification of an eventual unitary mechanism of anesthesia-induced alteration of consciousness, the relationship between network effects and the biochemical or sleep-wake cycle targets of anesthetic agents, as well as the vast between-studies variations in dose and administration mode, leading to difficulties in between-studies comparisons. In this narrative review, we draw the picture of the current state of knowledge in anesthesia-induced unconsciousness, from insights gathered on propofol, halogenated vapors, ketamine, dexmedetomidine, benzodiazepines and xenon. We also describe how anesthesia can help understanding consciousness, we develop the above-mentioned unresolved questions, and propose tracks for future research.
Clinical profile of hyponatremia in critical care patients in a tertiary care centre in India.

INTRODUCTION: Disorders of sodium and water metabolism are frequently encountered in patients admitted to the Intensive Care Unit (ICU), and may even be acquired there. A systematic approach is needed to evaluate the causes of hyponatremia for better patient care. MATERIAL AND METHODS: 100 adult patients with admission serum sodium levels <135 mEq/L in the ICU were recruited for this study over 18 months. Through history taking and appropriate laboratory investigations, the prevalence, causes, morbidity and mortality of hyponatremia were assessed. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) was diagnosed using Schwartz and Bartter clinical criterion. RESULTS: 23 cases were deemed to have pseudohyponatremia likely caused by dyslipidemia or hyperproteinemia, whereas remaining 77 cases had true hyponatremia. Values of arterial and venous sodium have a positive correlation indicating agreement between the parameters. Majority of subjects were males (61%). Causes of hyponatremia include: neurological causes in 34 cases (44.2%), followed by gastrointestinal cause 18 cases (23.4%), respiratory cause 15 cases (19.5%), cardiac cause 5 cases (6.5%), and other causes 5 cases (6.5%). Most frequently encountered diagnosis included cerebrovascular accident (16 cases), pneumonia (10 cases), metabolic encephalopathy (10 cases), acute gastroenteritis (8 cases) and tubercular meningitis (6 cases). Of 77 cases studied, 18 cases (23.4%) had hypovolemic hyponatremia (due to acute gastroenteritis), 51 cases (66.2%) had euvolemic hyponatremia (due to SIADH, likely caused by cerebrovascular accident, pneumonia or metabolic encephalopathy) and 8 cases (10.4%) had hypervolemic hyponatremia (due to chronic renal failure or congestive cardiac failure). Mortality in this population was 11.7%, and was seen mainly in patients of severe hyponatremia. CONCLUSIONS: Severity of hyponatremia, male gender and neurological symptoms correlated significantly with morbidity and mortality in this cohort and the information from this study can be used to better identify patients at risk of adverse outcomes due to hyponatremia in critical care setting.
CRDS: Consensus Reverse Docking System for target fishing

MOTIVATION Identification of putative drug targets is a critical step for explaining the mechanism of drug action against multiple targets, finding new therapeutic indications for existing drugs, and unveiling the adverse drug reactions. One important approach is to use the molecular docking. However, its widespread utilization has been hindered by the lack of easy-to-use public servers. Therefore, it is vital to develop a streamlined computational tool for target prediction by molecular docking on a large scale. RESULTS We present a fully automated web tool named CRDS (Consensus Reverse Docking System) which predicts potential interaction sites for a given drug. To improve hit rates, we developed a strategy of consensus scoring. CRDS carries out reverse docking against 5,254 candidate protein structures using three different scoring functions (GoldScore, Vina, and LeDock from GOLD version 5.7.1, AutoDock Vina version 1.1.2, and LeDock version 1.0, respectively), and those scores are combined into a single score named CDS (Consensus Docking Score). The web server provides the list of top fifty predicted interaction sites, docking conformations, ten most significant pathways, and the distribution of consensus scores. AVAILABILITY The web server is available at http://pbil.kaist. ac.kr/CRDS. SUPPLEMENTARY INFORMATION Supplementary data are available at Bioinformatics online.
Upregulated microRNA-671-3p promotes tumor progression by suppressing forkhead box P2 expression in non-small-cell lung cancer

In the present study, the expression of microRNA (miR)-671-3p in non-small-cell lung cancer (NSCLC) was detected via reverse transcription-quantitative polymerase chain reaction analysis, and its role in cell proliferation, apoptosis, migration and invasion was investigated via Cell Counting Kit-8, colony formation, flow cytometry, Transwell and scratch assays, respectively. It was observed that the expression of miR-671-3p was upregulated in NSCLC tissues and cell lines (A549 and H1975). Treatment with miR-671-3p inhibitors suppressed cell proliferation, migration and invasion, and increased apoptosis in vitro, suggesting that miR-671-3p functions as an oncogene in NSCLC. In addition, forkhead box P2 (FOXP2) has been reported to be a tumor suppressor that is downregulated in several types of cancer, and its low expression was confirmed in NSCLC tissues and cell lines in the current study via western blotting. The results of the luciferase reporter assay also demonstrated that miR-671-3p targeted directly the 3′-untranslated region of FOXP2. Furthermore, overexpression of FOXP2 in A549 and H1975 cell lines suppressed the growth, migration and invasion, and promoted apoptosis, whereas these effects were reversed by transfection with miR-671-3p mimics, suggesting that miR-671-3p promoted tumor progression via regulating FOXP2. Taken together, the results reported in the present study implied that miR-671-3p may be a potential therapeutic target in NSCLC.
Hypothalamic Fatty Acids and Ketone Bodies Sensing and Role of FAT/CD36 in the Regulation of Food Intake

The obesity and type-2 diabetes epidemic is escalating and represents one of the costliest biomedical challenges confronting modern society. Moreover, the increasing consumption of high fat food is often correlated with an increase in body mass index. In people predisposed to be obese or already obese, the impaired ability of the brain to monitor and respond to alterations in fatty acid (FA) metabolism is increasingly recognized as playing a role in the pathophysiological development of these disorders. The brain senses and regulates metabolism using highly specialized nutrient-sensing neurons located mainly in the hypothalamus. The same neurons are able to detect variation in the extracellular levels of glucose, FA and ketone bodies as a way to monitor nutrient availability and to alter its own activity. In addition, glial cells such as astrocytes create major connections to neurons and form a tight relationship to closely regulate nutrient uptake and metabolism. This review will examine the different pathways by which neurons are able to detect free fatty acids (FFA) to alter its activity and how high fat diet (HFD)-astrocytes induced ketone bodies production interplays with neuronal FA sensing. The role of HFD-induced inflammation and how FA modulate the reward system will also be investigated here.