Miracle-dz/UniFAR-FTUs huggingface dataset:
Incidence and risk factors of hospitalisations for respiratory syncytial virus among children aged less than 2 years

Abstract The study aim was to examine the incidence and risk factors of respiratory syncytial virus (RSV) bronchiolitis hospitalisations and disease severity among infants. We compared demographic and health characteristics of children aged 0–23 hospitalised for RSV bronchiolitis (cases, n = 1227) during 2008–2018 and control children (n = 554) of the same age admitted for non-respiratory disease. RSV antigen was detected in nasal swabs by immunochromatography. Multiple logistic regression models were applied. The average annual incidence of hospitalisation for RSV bronchiolitis was 12.6 per 1000 and 1.7 per 1000 (P < 0.001) among infants and toddlers, respectively, with winter seasonality (November–March). The risk of hospitalisation for RSV bronchiolitis increased among children aged 0–5 months (OR 7.66; 95% CI 5.61–10.45) and 6–11 months (OR 12.88, 95% CI 8.48–19.55), compared to those aged 12–23 months. Additional risk factors were living in low vs. higher socio-economic status towns (OR 1.49; 95% CI 1.14–1.95), having chronic medical conditions (OR 2.75; 95% CI 1.61–4.70), birth month (October–January vs. June–September) (OR 2.19; 95% CI 1.60–2.99) and history of stay in neonatal intensive care unit at birth (OR 2.37; 95% CI 1.27–4.41). Male children and those who had pneumonia were more likely to have severe RSV bronchiolitis. In conclusion, the burden of hospitalisations for RSV bronchiolitis is high, especially in young infants. Effective preventive measures such as RSV active vaccines can reduce the risk of hospitalisations for RSV bronchiolitis among these vulnerable groups.
Heterojunction Annealing Enabling Record Open‐Circuit Voltage in Antimony Triselenide Solar Cells

Despite the fact that antimony triselenide (Sb2Se3) thin‐film solar cells have undergone rapid development in recent years, the large open‐circuit voltage (VOC) deficit still remains as the biggest bottleneck, as even the world‐record device suffers from a large VOC deficit of 0.59 V. Here, an effective interface engineering approach is reported where the Sb2Se3/CdS heterojunction (HTJ) is subjected to a post‐annealing treatment using a rapid thermal process. It is found that nonradiative recombination near the Sb2Se3/CdS HTJ, including interface recombination and space charge region recombination, is greatly suppressed after the HTJ annealing treatment. Ultimately, a substrate Sb2Se3/CdS thin‐film solar cell with a competitive power conversion efficiency of 8.64% and a record VOC of 0.52 V is successfully fabricated. The device exhibits a much mitigated VOC deficit of 0.49 V, which is lower than that of any other reported efficient antimony chalcogenide solar cell.
Pharmacometabonomic association of cyclophosphamide 4‐hydroxylation in hematopoietic cell transplant recipients

The widely used alkylating agent cyclophosphamide (CY) has substantive interpatient variability in the area under the curve (AUC) of it and its metabolites. Numerous factors may influence the drug‐metabolizing enzymes that metabolize CY to 4‐hydroxycyclophosphamide (4HCY), the principal precursor to CY’s cytotoxic metabolite. We sought to identify endogenous metabolomics compounds (EMCs) associated with 4HCY formation clearance (ratio of 4HCY/CY AUC) using global metabolomics. Patients who undergo hematopoietic cell transplantation receiving post‐transplant CY (PT‐CY) were enrolled, cohort 1 (n = 26) and cohort 2 (n = 25) donating longitudinal blood samples before they started HCT (pre‐HCT), before infusion of the donor allograft (pre‐graft), before the first dose of PT‐CY (pre‐CY), and 24 h after the first dose of PT‐CY (24‐h post‐CY), which is also immediately before the second dose of CY. A total of 512 and 498 EMCs were quantitated in two cohorts, respectively. Both univariate linear regression with false discovery rate (FDR), and pathway enrichment analyses using a global association test were performed. At the pre‐CY time point, no EMCs were associated at FDR less than 0.1. At pre‐HCT, cohort 1 had one EMC (levoglucosan) survive the FDR threshold. At pre‐graft, cohort 1 and cohort 2 had 20 and 13 EMCs, respectively, exhibiting unadjusted p values less than 0.05, with the only EMCs having an FDR less than 0.1 being two unknown EMCs. At 24‐h post‐CY, there were three EMCs, two ketones, and threitol, at FDR less than 0.1 in cohort 2. These results demonstrate the potential of pharmacometabonomics, but future studies in larger samples are needed to optimize CY.
The vascular impact of dapagliflozin, liraglutide, and atorvastatin alone or in combinations in type 2 diabetic rat model

Diabetic dyslipidemia is a significant contributor in the pathogenesis of type 2 diabetes (T2D). The study aimed at comparing the effect of dapagliflozin, liraglutide, and atorvastatin alone or their combinations on lipids and inflammatory markers and their vascular impact in T2D rats. There were 56 male albino rats included in the study and divided into two main groups. Group A (8 rats) served as normal control. Group B (48 rats) were streptozotocin–nicotinamide‐induced diabetic rats. Subgroups (B‐1, B‐2, B‐3, B‐4, B‐5, and B‐6) received (no medications, dapagliflozin, liraglutide, atorvastatin, dapagliflozin + atorvastatin, and liraglutide + atorvastatin), respectively. Urine albumin/creatinine ratio (UACR), glycosylated hemoglobin (HBA1c), fasting serum glucose (FSG), serum low‐density lipoprotein‐cholesterol (LDL‐C), high‐density lipoprotein‐cholesterol (HDL‐C), TGs, lipoprotein(a) Lp (a), serum thyrotropin (TSH), highly sensitive C‐reactive protein (hs‐CRP) and advanced glycation end products (AGEs), were assessed. Qualitative and quantitative histological examination of kidneys focused on renal corpuscles. Dapagliflozin improved the studied parameters but with statistically insignificant increase in LDL‐C, Lp (a) and significant increase in UACR. Atorvastatin improved the studied parameters but with statistically insignificant increase in FSG and HbA1C. Liraglutide and the combination groups significantly improved all studied parameters. Histologically, liraglutide and atorvastatin produced therapeutic effect, while dapagliflozin depicted nephrotoxic effect. Combination groups resulted in better effects with normalization of most of renal corpuscles. There were positive correlations between LDL‐C and hs‐CRP, AGEs, TSH and mesangial expansion. Combination of atorvastatin with liraglutide can improve its vasculoprotective effect. Moreover, combination of atorvastatin with dapagliflozin can ameliorate its possible nephrotoxic effect.
Examining Technology-Facilitated Intimate Partner Violence: A Systematic Review of Journal Articles

As intimate partner violence in a cyber world is increasing, scholars have started to pay attention to this phenomenon. This study aims to provide a systematic review of empirical studies in the technology-facilitated intimate partner violence (TFIPV) field. We analyzed 31 studies that examined direct TFIPV perpetration and/or victimization experiences identified from four of the largest databases (i.e., Web of Science, PsyInfo, PubMed, and SCOPUS). We found that most studies recruited adolescents or young adults (i.e., college students) and used a very diverse range of terminologies that describe similar phenomena but are not based on validated instruments. We discuss the implications of our findings and suggestions that can enhance the field’s rigor and guide future research.
Restriction of Viral Replication, Rather than T Cell Immunopathology, Drives Lethality in Murine Norovirus CR6-Infected STAT1-Deficient Mice

The intestinal microbiota is a collection of bacteria, archaea, fungi, and viruses that colonize the mammalian gut. Coevolution of the host and microbiota has required development of immunological tolerance to prevent ongoing inflammatory responses against intestinal microbes. ABSTRACT Recent evidence indicates that viral components of the microbiota can contribute to intestinal homeostasis and protection from local inflammatory or infectious insults. However, host-derived mechanisms that regulate the virome remain largely unknown. In this study, we used colonization with the model commensal murine norovirus (MNV; strain CR6) to interrogate host-directed mechanisms of viral regulation, and we show that STAT1 is a central coordinator of both viral replication and antiviral T cell responses. In addition to restricting CR6 replication to the intestinal tract, we show that STAT1 regulates antiviral CD4+ and CD8+ T cell responses and prevents systemic viral-induced tissue damage and disease. Despite altered T cell responses that resemble those that mediate lethal immunopathology in systemic viral infections in STAT1-deficient mice, depletion of adaptive immune cells and their associated effector functions had no effect on CR6-induced disease. However, therapeutic administration of an antiviral compound limited viral replication, preventing virus-induced tissue damage and death without impacting the generation of inflammatory antiviral T cell responses. Collectively, our data show that STAT1 restricts MNV CR6 replication within the intestinal mucosa and that uncontrolled viral replication mediates disease rather than the concomitant development of dysregulated antiviral T cell responses in STAT1-deficient mice. IMPORTANCE The intestinal microbiota is a collection of bacteria, archaea, fungi, and viruses that colonize the mammalian gut. Coevolution of the host and microbiota has required development of immunological tolerance to prevent ongoing inflammatory responses against intestinal microbes. Breakdown of tolerance to bacterial components of the microbiota can contribute to immune activation and inflammatory disease. However, the mechanisms that are necessary to maintain tolerance to viral components of the microbiome, and the consequences of loss of tolerance, are less well understood. Here, we show that STAT1 is integral for preventing escape of a commensal-like virus, murine norovirus CR6 (MNV CR6), from the gut and that in the absence of STAT1, mice succumb to infection-induced disease. In contrast to the case with other systemic viral infections, mortality of STAT1-deficient mice is not driven by immune-mediated pathology. Our data demonstrate the importance of host-mediated geographical restriction of commensal-like viruses.
Present and future bright and dark spots for coral reefs through climate change

Marine heatwaves can cause coral bleaching and reduce coral cover on reefs, yet few studies have identified “bright spots,” where corals have recently shown a capacity to survive such pressures. We analyzed 7714 worldwide surveys from 1997 to 2018 along with 14 environmental and temperature metrics in a hierarchical Bayesian model to identify conditions that contribute to present‐day coral cover. We also identified locations with significantly higher (i.e., “bright spots”) and lower coral cover (i.e., “dark spots”) than regionally expected. In addition, using 4‐km downscaled data of Representative Concentration Pathways (RCPs) 4.5 and 8.5, we projected coral cover on reefs for the years 2050 and 2100. Coral cover on modern reefs was positively associated with historically high maximum sea‐surface temperatures (SSTs), and negatively associated with high contemporary SSTs, tropical‐cyclone frequencies, and human‐population densities. By 2100, under RCP8.5, we projected relative decreases in coral cover of >40% on most reefs globally but projected less decline on reefs in Indonesia, Malaysia, the central Philippines, New Caledonia, Fiji, and French Polynesia, which should be focal localities for multinational networks of protected areas.
Effects of acute ethanol and/or diazepam exposure on immediate and delayed hippocampal metabolite levels in rats anesthetized with isoflurane

Alcohol and benzodiazepines are psychoactive substances frequently associated in voluntary drug intoxications that share common mechanisms of action, including facilitation of GABAergic transmission. This study aimed to assess the separate and combined effects of ethanol and diazepam acute exposure on hippocampal metabolite levels, as well as on delayed cognitive performance, in rats anesthetized with isoflurane. Adult male Wistar rats received one intraperitoneal injection containing either saline solution (“CTL” group, N = 15), a 5‐mg/kg dose of diazepam (“DIA” group, N = 16), a 2‐g/kg dose of ethanol (“EtOH” group, N = 18), or a 5‐mg/kg dose of diazepam + a 2‐g/kg dose of ethanol (“DIA + EtOH” group, N = 24). The levels of brain metabolites in the hippocampal region were assessed using in vivo magnetic resonance spectroscopy (MRS) before and after injection. Behavioral testing, including working memory and visual recognition memory assessment, was performed at week 3, while a new MRS acquisition was conducted 4 weeks after the injection. In the hour following acute exposure, a decrease in glutamate levels was found in the DIA + EtOH group only. Four weeks after injection, a decrease in GABA and glutamate levels and an increase in NAA levels were found in the EtOH group only. No significant between‐group differences were found in the behavioral assessment. While the initial decrease in glutamate levels in the DIA + EtOH group suggests an early potentiation effect between ethanol and diazepam, the long‐term modifications found only in the EtOH group suggest a possible downregulation of ethanol's effect by diazepam at 4 weeks.
Microtubule cytoskeleton and mycorrhizal roots

ABSTRACT For the establishment of the Arbuscular Mycorrhiza (AM) symbiosis it is essential that epidermis and cortical cells from plant roots suffer a strong reorganization to allow the penetration of intracellular fungal hyphae. In the same manner, the new formation of a periarbuscular membrane and a symbiotic interface with specific compositions are required for a functional symbiosis. It is believed that the cytoskeleton of the plant host plays an essential role in these processes, particularly the microtubule (MT) cytoskeleton, as huge modifications have been observed in the MT array of root cells accompanying the establishment of the AM symbiosis. Recent research has established a link between microtubule rearrangements and arbuscule functioning. However, further research is required to elucidate the specific functions of MT cytoskeleton along the different stages of the arbuscule life cycle and to unravel the signals triggering these changes.
Structure of the Mon1-Ccz1 complex reveals molecular basis of membrane binding for Rab7 activation

Significance Rab GTPases are central regulators of intracellular trafficking and serve as markers of organelle identity. They act as molecular switches, and their activation requires precise spatiotemporal control. Members of the family of the Tri Longin domain (TLD) Rab-GEFs (guanine nucleotide exchange factors) act as activators of a subset of Rabs that play a critical role in late endosomal biogenesis. Genetic defects associated with TLD Rab-GEFs cause developmental diseases, but the underlying mechanisms are only partly understood. The determination of the structure of the TLD Rab-GEF Mon1-Ccz1 presented here provides a molecular basis for understanding the function and regulation of these proteins. Activation of the GTPase Rab7/Ypt7 by its cognate guanine nucleotide exchange factor (GEF) Mon1-Ccz1 marks organelles such as endosomes and autophagosomes for fusion with lysosomes/vacuoles and degradation of their content. Here, we present a high-resolution cryogenic electron microscopy structure of the Mon1-Ccz1 complex that reveals its architecture in atomic detail. Mon1 and Ccz1 are arranged side by side in a pseudo-twofold symmetrical heterodimer. The three Longin domains of each Mon1 and Ccz1 are triangularly arranged, providing a strong scaffold for the catalytic center of the GEF. At the opposite side of the Ypt7-binding site, a positively charged and relatively flat patch stretches the Longin domains 2/3 of Mon1 and functions as a phosphatidylinositol phosphate–binding site, explaining how the GEF is targeted to membranes. Our work provides molecular insight into the mechanisms of endosomal Rab activation and serves as a blueprint for understanding the function of members of the Tri Longin domain Rab-GEF family.
Neuronal GPR81 regulates developmental brain angiogenesis and promotes brain recovery after a hypoxic ischemic insult

Perinatal hypoxic/ischemic (HI) brain injury is a major clinical problem with devastating neurodevelopmental outcomes in neonates. During HI brain injury, dysregulated factor production contributes to microvascular impairment. Glycolysis-derived lactate accumulated during ischemia has been proposed to protect against ischemic injury, but its mechanism of action is poorly understood. Herein, we hypothesize that lactate via its G-protein coupled receptor (GPR81) controls postnatal brain angiogenesis and plays a protective role after HI injury. We show that GPR81 is predominantly expressed in neurons of the cerebral cortex and hippocampus. GPR81-null mice displayed a delay in cerebral microvascular development linked to reduced levels of various major angiogenic factors and augmented expression of anti-angiogenic Thrombospondin-1 (TSP-1) in comparison to their WT littermates. Coherently, lactate stimulation induced an increase in growth factors (VEGF, Ang1 and 2, PDGF) and reduced TSP-1 expression in neurons, which contributed to accelerating angiogenesis. HI injury in GPR81-null animals curtailed vascular density and consequently increased infarct size compared to changes seen in WT mice; conversely intracerebroventricular lactate injection increased vascular density and diminished infarct size in WT but not in GPR81-null mice. Collectively, we show that lactate acting via GPR81 participates in developmental brain angiogenesis, and attenuates HI injury by restoring compromised microvasculature.
Perinatal exposure to synergistic multiple stressors leads to cellular and behavioral deficits mimicking Schizophrenia-like pathology

ABSTRACT Protein malnourishment and immune stress are potent perinatal stressors, encountered by children born under poor socioeconomic conditions. Thus, it is necessary to investigate how such stressors synergistically contribute towards developing neurological disorders in affected individuals. Pups from Wistar females, maintained on normal (high-protein, HP:20%) and low-protein (LP:8%) diets were used. Single and combined exposures of Poly I:C (viral mimetic: 5 mg/kg body weight) and Lipopolysaccharide (LPS; bacterial endotoxin: 0.3 mg/kg body weight) were injected to both HP and LP pups at postnatal days (PND) 3 and 9 respectively, creating eight groups: HP (control); HP+Poly I:C; HP+LPS; HP+Poly I:C+LPS; LP; LP+Poly I:C; LP+LPS; LP+Poly I:C+LPS (multi-hit). The effects of stressors on hippocampal cytoarchitecture and behavioral abilities were studied at PND 180. LP animals were found to be more vulnerable to immune stressors than HP animals and symptoms like neuronal damage, spine loss, downregulation of Egr 1 and Arc proteins, gliosis and behavioral deficits were maximum in the multi-hit group. Thus, from these findings it is outlined that cellular and behavioral changes that occur following multi-hit exposure may predispose individuals to developing Schizophrenia-like pathologies during adulthood.
Distinct Neural Signatures of Outcome Monitoring following Selection and Execution Errors

Losing a point in tennis could result from poor shot selection or faulty stroke execution. To explore how the brain responds to these different types of errors, we examined feedback-locked EEG activity while participants completed a modified version of a standard three-armed bandit probabilistic reward task. Our task framed unrewarded outcomes as either the result of errors of selection or errors of execution. We examined whether amplitude of a medial frontal negativity (the Feedback-Related Negativity; FRN) was sensitive to the different forms of error attribution. Consistent with previous reports, selection errors elicited a large FRN relative to rewards and amplitude of this signal correlated behavioral adjustment following these errors. A different pattern was observed in response to execution errors. These outcomes produced a larger FRN, a frontocentral attenuation in activity preceding this component, and a subsequent enhanced error positivity in parietal sites. Notably, the only correlations with behavioral adjustment were with the early frontocentral attenuation and amplitude of the parietal signal; FRN differences between execution errors and rewarded trials did not correlate with subsequent changes in behavior. Our findings highlight distinct neural correlates of selection and execution error processing, providing insight into how the brain responds to the different classes of error that determine future action.
Optimization of physician and specialty pharmacy clinical workflow in assessment of risk category and symptom burden in patients with myelofibrosis (MF)

Aleksander L. Chojecki , Kristyn Y. DiSogra, Justin Arnall, Nicole Cowgill, Amy Soni, Charles H. Packman, Srinivasa Reddy Sanikommu, Nilay A. Shah, Brittany K. Ragon, Thomas G. Knight, Jing Ai, Belinda R. Avalos, Edward A. Copelan and Michael R. Grunwald Department of Hematologic Oncology and Blood Disorders, Levine Cancer Institute, Atrium Health, Charlotte, NC, USA; Atrium Health Specialty Pharmacy Service, Atrium Health, Charlotte, NC, USA
Are brand names special words? Letter visual‐similarity affects the identification of brand names, but not common words

Abstract Brand names are often considered a special type of words of special relevance to examine the role of visual codes during reading: unlike common words, brand names are typically presented with the same letter‐case configuration (e.g., IKEA, adidas). Recently, Pathak et al. (European Journal of Marketing, 2019, 53, 2109) found an effect of visual similarity for misspelled brand names when the participants had to decide whether the brand name was spelled correctly or not (e.g., tacebook [baseword: facebook] was responded more slowly and less accurately than xacebook). This finding is at odds with both orthographically based visual‐word recognition models and prior experiments using misspelled common words (e.g., viotin [baseword: violin] is identified as fast as viocin). To solve this puzzle, we designed two experiments in which the participants had to decide whether the presented item was written correctly. In Experiment 1, following a procedure similar to Pathak et al. (European Journal of Marketing, 2019, 53, 2109), we examined the effect of visual similarity on misspelled brand names with/without graphical information (e.g., anazon vs. atazon [baseword: amazon]). Experiment 2 was parallel to Experiment 1, but we focused on misspelled common words (e.g., anarillo vs. atarillo; baseword: amarillo [yellow in Spanish]). Results showed a sizeable effect of visual similarity on misspelled brand names – regardless of their graphical information, but not on misspelled common words. These findings suggest that visual codes play a greater role when identifying brand names than common words. We examined how models of visual‐word recognition can account for this dissociation.