Miracle-dz/UniFAR-FTUs huggingface dataset:
Sleep patterns and quality among Nigerian medical students: A cross-sectional study

Adequate sleep is crucial for individuals’ well-being and cognitive functioning. However, medical students face unique challenges that disrupt their sleep patterns, such as a rigorous curriculum, long study hours, and high-stress levels. Understanding the sleep patterns and quality among medical students in Nigeria is important to develop targeted interventions and support their overall well-being. This study involved 802 medical students from 3 medical schools in Southwest Nigeria. Participants completed an online questionnaire that collected data on their demographic characteristics, sleep patterns and self-reported sleep quality. Descriptive statistics and correlation analysis were used to analyze the data and identify patterns and associations. Most participants were female (56.9%), with the highest representation from the UNILORIN (65.5%). The average reported sleep duration was 5.74 hours per night, indicating insufficient sleep. Irregular bedtimes and wake-up times were commonly reported. A significant proportion of students consumed coffee late at night (27.1%) and used medication to induce sleep (24.3%). Sleep patterns and behaviors, such as snoring (36.1%) and nocturnal eating (57.6%), were reported. Overall, participants reported satisfactory (28.3%) or poor (29.7%) sleep quality. Correlation analysis revealed significant associations between sleep patterns, sleep quality, academic performance, and other sleep-related factors. The study identified insufficient sleep duration, irregular bedtimes, late-night coffee consumption, and poor sleep quality. These findings emphasize the need for interventions and strategies to promote healthy sleep habits among medical students, which can positively impact their overall health and academic performance.
Comparison of Sociodemographic and Radiographic Features in Distal Radio Fracture Treatment: Hand Surgeons versus Non-specialists

Objective: This study evaluated sociodemographic and radiographic features of patients with distal radial fractures treated at a trauma hospital in southern Brazil, comparing those treated by hand surgery specialists (group 1) and non-specialists (group 2). Methods: This study consists of a retrospective cohort of 200 patients treated in 2020. After reviewing medical records and radiographs, the following parameters were analyzed: age, gender, trauma mechanism, laterality, associated comorbidities and fractures, fracture classification (AO), radial height, radial inclination, and volar inclination. Comparison of the two groups used the Student t-test, chi-square test, or Fisher exact test. Results: Most subjects were women (54%), sustained low-energy traumas (58%), and were left-handed (53%). Group 1 had a lower mean age (50.2 years); most of their subjects sustained high-energy trauma (54%) and had type C fractures (73%); type A fractures prevailed in group 2 (72%). Radiographs showed a significant difference regarding the mean radial inclination (21.5° in group 1 and 16.5° in group 2 [ p < 0.001] in women, and 21.3° in group 1 and 17° in group 2 [ p < 0.001] in men) and volar inclination (10.1° and 12.8° in groups 1 and 2, respectively [ p < 0.001]). In addition, the absolute number of cases with reestablished anatomical parameters per the three evaluated variables was also significantly different; all parameters were better in group 1. Conclusion: Hand surgeons treated the most severe fractures and had the best radiographic outcomes.
Human tumor necrosis factor alpha gene regulation in phorbol ester stimulated T and B cell lines

The minimal region of the human tumor necrosis factor alpha (TNF-alpha) gene promoter necessary for its transcriptional induction by phorbol esters (PMA) in human T and B lymphocyte cell lines has been localized between -52 and +89 nucleotides (nt) relative to the gene's transcriptional start site. Comparison of these sequences to those required to mediate virus or lipopolysaccharide (LPS) induction of the gene reveal significant differences, and thus, the sequence requirements for PMA induction are distinct from those that mediate induction by virus or LPS. Although three sites in the TNF-alpha promoter (kappa 1, kappa 2, and kappa 3) specifically bind the transcription factor NF-kappa B in lymphoid nuclear extracts, TNF-alpha mRNA induction by PMA does not correlate with NF-kappa B binding activities displayed by different T and B cell lines. Moreover, kappa 1- kappa 3 can each be deleted from the TNF-alpha promoter with little effect on the gene's inducibility by PMA. Therefore, TNF-alpha mRNA induction by PMA, like its induction by virus and LPS, is not primarily mediated by NF-kappa B, but rather is mediated through other sequences and protein factors. Surprisingly, multimers of kappa 1-kappa 3 can confer PMA inducibility on a heterologous promoter in a B (Raji), but not a T (HUT78) cell line. However they are not functional on a truncated TNF-alpha promoter, indicating that promoter context and cell type specificity influence the PMA inducible function of these NF-kappa B binding sites.
Effects of ranolazine with atenolol, amlodipine, or diltiazem on exercise tolerance and angina frequency in patients with severe chronic angina: a randomized controlled trial.

CONTEXT Many patients with chronic angina experience anginal episodes despite revascularization and antianginal medications. In a previous trial, antianginal monotherapy with ranolazine, a drug believed to partially inhibit fatty acid oxidation, increased treadmill exercise performance; however, its long-term efficacy and safety have not been studied in combination with beta-blockers or calcium antagonists in a large patient population with severe chronic angina. OBJECTIVES To determine whether, at trough levels, ranolazine improves the total exercise time of patients who have symptoms of chronic angina and who experience angina and ischemia at low workloads despite taking standard doses of atenolol, amlodipine, or diltiazem and to determine times to angina onset and to electrocardiographic evidence of myocardial ischemia, effect on angina attacks and nitroglycerin use, and effect on long-term survival in an open-label observational study extension. DESIGN, SETTING, AND PATIENTS A randomized, 3-group parallel, double-blind, placebo-controlled trial of 823 eligible adults with symptomatic chronic angina who were randomly assigned to receive placebo or 1 of 2 doses of ranolazine. Patients treated at the 118 participating ambulatory outpatient settings in several countries were enrolled in the Combination Assessment of Ranolazine In Stable Angina (CARISA) trial from July 1999 to August 2001 and followed up through October 31, 2002. INTERVENTION Patients received twice-daily placebo or 750 mg or 1000 mg of ranolazine. Treadmill exercise 12 hours (trough) and 4 hours (peak) after dosing was assessed after 2, 6 (trough only), and 12 weeks of treatment. MAIN OUTCOME MEASURES Change in exercise duration, time to onset of angina, time to onset of ischemia, nitroglycerin use, and number of angina attacks. RESULTS Trough exercise duration increased by 115.6 seconds from baseline in both ranolazine groups (pooled) vs 91.7 seconds in the placebo group (P =.01). The times to angina and to electrocardiographic ischemia also increased in the ranolazine groups, at peak more than at trough. The increases did not depend on changes in blood pressure, heart rate, or background antianginal therapy and persisted throughout 12 weeks. Ranolazine reduced angina attacks and nitroglycerin use by about 1 per week vs placebo (P<.02). Survival of 750 patients taking ranolazine during the CARISA trial or its associated long-term open-label study was 98.4% in the first year and 95.9% in the second year. CONCLUSION Twice-daily doses of ranolazine increased exercise capacity and provided additional antianginal relief to symptomatic patients with severe chronic angina taking standard doses of atenolol, amlodipine, or diltiazem, without evident adverse, long-term survival consequences over 1 to 2 years of therapy.
Selective endosomal microautophagy is starvation-inducible in Drosophila

ABSTRACT Autophagy delivers cytosolic components to lysosomes for degradation and is thus essential for cellular homeostasis and to cope with different stressors. As such, autophagy counteracts various human diseases and its reduction leads to aging-like phenotypes. Macroautophagy (MA) can selectively degrade organelles or aggregated proteins, whereas selective degradation of single proteins has only been described for chaperone-mediated autophagy (CMA) and endosomal microautophagy (eMI). These 2 autophagic pathways are specific for proteins containing KFERQ-related targeting motifs. Using a KFERQ-tagged fluorescent biosensor, we have identified an eMI-like pathway in Drosophila melanogaster. We show that this biosensor localizes to late endosomes and lysosomes upon prolonged starvation in a KFERQ- and Hsc70-4- dependent manner. Furthermore, fly eMI requires endosomal multivesicular body formation mediated by ESCRT complex components. Importantly, induction of Drosophila eMI requires longer starvation than the induction of MA and is independent of the critical MA genes atg5, atg7, and atg12. Furthermore, inhibition of Tor signaling induces eMI in flies under nutrient rich conditions, and, as eMI in Drosophila also requires atg1 and atg13, our data suggest that these genes may have a novel, additional role in regulating eMI in flies. Overall, our data provide the first evidence for a novel, starvation-inducible, catabolic process resembling endosomal microautophagy in the Drosophila fat body.
Human Cardiac Stem Cell Differentiation Is Regulated by a Mircrine Mechanism

Background— Cardiac stem cells (CSCs) delivered to the infarcted heart generate a large number of small fetal-neonatal cardiomyocytes that fail to acquire the differentiated phenotype. However, the interaction of CSCs with postmitotic myocytes results in the formation of cells with adult characteristics. Methods and Results— On the basis of results of in vitro and in vivo assays, we report that the commitment of human CSCs (hCSCs) to the myocyte lineage and the generation of mature working cardiomyocytes are influenced by microRNA-499 (miR-499), which is barely detectable in hCSCs but is highly expressed in postmitotic human cardiomyocytes. miR-499 traverses gap junction channels and translocates to structurally coupled hCSCs favoring their differentiation into functionally competent cells. Expression of miR-499 in hCSCs represses the miR-499 target genes Sox6 and Rod1, enhancing cardiomyogenesis in vitro and after infarction in vivo. Although cardiac repair was detected in all cell-treated infarcted hearts, the aggregate volume of the regenerated myocyte mass and myocyte cell volume were greater in animals injected with hCSCs overexpressing miR-499. Treatment with hCSCs resulted in an improvement in ventricular function, consisting of a better preservation of developed pressure and positive and negative dP/dt after infarction. An additional positive effect on cardiac performance occurred with miR-499, pointing to enhanced myocyte differentiation/hypertrophy as the mechanism by which miR-499 potentiated the restoration of myocardial mass and function in the infarcted heart. Conclusions— The recognition that miR-499 promotes the differentiation of hCSCs into mechanically integrated cardiomyocytes has important clinical implications for the treatment of human heart failure.
Couple of the Variational Iteration Method and Fractional-Order Legendre Functions Method for Fractional Differential Equations

We present a new numerical method to get the approximate solutions of fractional differential equations. A new operational matrix of integration for fractional-order Legendre functions (FLFs) is first derived. Then a modified variational iteration formula which can avoid “noise terms” is constructed. Finally a numerical method based on variational iteration method (VIM) and FLFs is developed for fractional differential equations (FDEs). Block-pulse functions (BPFs) are used to calculate the FLFs coefficient matrices of the nonlinear terms. Five examples are discussed to demonstrate the validity and applicability of the technique.
Multi‐gradient echo with susceptibility inhomogeneity compensation (MGESIC): Demonstration of fMRI in the olfactory cortex at 3.0 T

Short image acquisition times and sensitivity to magnetic susceptibility favor the use of gradient echo imaging methods in functional MRI (fMRI). However, magnetic susceptibility effects attributed to air‐tissue interfaces also lead to severe signal loss in images of the large inferior frontal and lateral temporal cortices of the human brain, which renders these regions inaccessible to fMRI. The signal loss is caused by the local field gradients in the slice selection direction. A multigradient echo with magnetic susceptibility inhomogeneity compensation method (MGESIC) is proposed to overcome this problem. The MGESIC method effectively corrects the susceptibility artifacts and maintains the advantages of gradient echo methods to both BOLD sensitivity and fast image acquisition. The effectiveness of the MGESIC method is demonstrated by fMRI experimental results within the olfactory cortex.
Comprehensive pan-cancer analysis of 33 human cancers reveals immunotherapeutic value of focal adhesion tyrosine kinase

The immune environment in tumors is the key factor affecting the survival and immunotherapeutic response of patients. This research aimed to explore the underlying association between focal adhesion tyrosine kinase (FAK/PTK2) and cancer immunotherapy in 33 human cancers. Gene expression data and clinical features of 33 cancers were retrieved from the Cancer Genome Atlas Database. The immunotherapy cohorts included GSE67501, GSE78220, and IMVIGOR210, which were derived from the comprehensive gene expression database or from previous studies. Clinical parameters including patient age, gender, survival rate, and tumor stage were analyzed to evaluate the prognostic value of FAK/PTK2. FAK/PTK2 activity was detected by single-sample gene set enrichment analysis and used to compare the difference between FAK/PTK2 transcriptome and protein expression levels. To better understand the role of FAK/PTK2 in cancer immunotherapy, we analyzed its correlations with tumor microenvironment and with immune processes/elements (e.g., immune cell infiltration, immunosuppressants, and stimulants) and major histocompatible complexes. Potential pathways associated with FAK/PTK2 signaling in cancers were also explored. Correlations between FAK/PTK2 and 2 immunotherapeutic biomarkers (tumor mutation load and microsatellite instability) were studied. Finally, the 3 independent immunotherapy cohorts were used to study the relationship between FAK/PTK2 and immunotherapeutic response. Although FAK/PTK2 is not closely associated with age (13/33), gender (5/33), or tumor stage (5/33) in any of the studied human cancers, it has potential prognostic value for predicting patient survival. Consistency between FAK/PTK2 activity and expression exists in some cancers (3/33). Generally, FAK/PTK2 is robustly correlated with immune cell infiltration, immune modulators, and immunotherapeutic markers. Moreover, high FAK/PTK2 expression is significantly related to immune-relevant pathways. However, FAK/PTK2 is not significantly correlated with the immunotherapeutic response. Research on the immunotherapeutic value of FAK/PTK2 in 33 human cancers provides evidence regarding the function of FAK/PTK2 and its role in clinical treatment. However, given the use of a bioinformatics approach, our results are preliminary and require further validation.
Human immunodeficiency virus dynamics in secondary lymphoid tissues and the evolution of cytotoxic T lymphocyte escape mutants

Abstract In secondary lymphoid tissues, human immunodeficiency virus (HIV) can replicate in both the follicular and extrafollicular compartments. Yet, virus is concentrated in the follicular compartment in the absence of antiretroviral therapy, in part due to the lack of cytotoxic T lymphocyte (CTL)–mediated activity there. CTLs home to the extrafollicular compartment, where they can suppress virus load to relatively low levels. We use mathematical models to show that this compartmentalization can explain seemingly counter-intuitive observations. First, it can explain the observed constancy of the viral decline slope during antiviral therapy in the peripheral blood, irrespective of the presence of CTL in Simian Immunodeficiency Virus (SIV)-infected macaques, under the assumption that CTL-mediated lysis significantly contributes to virus suppression. Second, it can account for the relatively long times it takes for CTL escape mutants to emerge during chronic infection even if CTL-mediated lysis is responsible for virus suppression. The reason is the heterogeneity in CTL activity and the consequent heterogeneity in selection pressure between the follicular and extrafollicular compartments. Hence, to understand HIV dynamics more thoroughly, this analysis highlights the importance of measuring virus populations separately in the extrafollicular and follicular compartments rather than using virus load in peripheral blood as an observable; this hides the heterogeneity between compartments that might be responsible for the particular patterns seen in the dynamics and evolution of the HIV in vivo.
VoCCN: voice-over content-centric networks

A variety of proposals call for a new Internet architecture focused on retrieving content by name, but it has not been clear that any of these approaches are general enough to support Internet applications like real-time streaming or email. We present a detailed description of a prototype implementation of one such application -- Voice over IP (VoIP) -- in a content-based paradigm. This serves as a good example to show how content-based networking can offer advantages for the full range of Internet applications, if the architecture has certain key properties.
Derandomization Beyond Connectivity: Undirected Laplacian Systems in Nearly Logarithmic Space

We give a deterministic \tilde{O}(\log n)-space algorithm for approximately solving linear systems given by Laplacians of undirected graphs, and consequently also approximating hitting times, commute times, and escape probabilities for undirected graphs. Previously, such systems were known to be solvable by randomized algorithms using O(\log n) space (Doron, Le Gall, and Ta-Shma, 2017) and hence by deterministic algorithms using O(\log^{3/2} n) space (Saks and Zhou, FOCS 1995 and JCSS 1999). Our algorithm combines ideas from time-efficient Laplacian solvers (Spielman and Teng, STOC 04; Peng and Spielman, STOC 14) with ideas used to show that Undirected S-T Connectivity is in deterministic logspace (Reingold, STOC 05 and JACM 08; Rozenman and Vadhan, RANDOM 05).
How rats perform spatial working memory tasks: Limitations in the use of egocentric and idiothetic working memory

Rats of the Dark Agouti strain were trained on delayed alternation under conditions that should encourage egocentric working memory. In two experiments a T-maze was set within a cross-maze so that different arms could be used for the sample and test runs. The maze had high opaque side-walls, and testing was conducted in low light levels so that distal visual cues might be eliminated. By rotating the maze 90° between the sample and choice run and by using two identical mazes set side by side it was possible to nullify other spatial strategies. Experiments 1 and 2 showed that rats preferentially used place information, intramaze cues, and direction cues, even though only egocentric or idiothetic (nonmatch-to-turn) working memory could successfully solve every trial. Rats were able to maintain an accurate sense of location within the maze even though distal cues were not visible and the animal was moved between the sample and choice runs. Experiment 2 confirmed that another rat strain (Long-Evans) shows the same learning profiles. Both experiments indicate that rats are very poor at using either egocentric or idiothetic information to alternate, and that retention delays as short as 10 s can eliminate the use of these forms of memory.
Media and scientific communication: a case of climate change

Abstract This paper explores how media representational practices shape and affect current international science and policy or practice communications, through a focus on climate change. Many complex factors contribute to these interactions. The norms and pressures that guide journalistic decision-making and shape mass-media coverage of anthropogenic climate science critically shape current discourses at the highly politicized climate science–policy interface. This paper investigates the multifarious journalistic, political, cultural and economic norms that dynamically influence media coverage of climate science. It explores the case-study of climate change to also work through factors shaping the translation of uncertainty in climate science. This project demonstrates that mass-media coverage of climate change is not simply a random amalgam of articles and segments; rather, it is a social relationship between scientists, policy actors and the public that is mediated by such news packages. Moreover, this research shows how mass media play a significant role in shaping the construction and maintenance of discourse on climate change at the interface of science and policy.
Neural criticality from effective latent variables

Observations of power laws in neural activity data have raised the intriguing notion that brains may operate in a critical state. One example of this critical state is ‘avalanche criticality’, which has been observed in various systems, including cultured neurons, zebrafish, rodent cortex, and human EEG. More recently, power laws were also observed in neural populations in the mouse under an activity coarse-graining procedure, and they were explained as a consequence of the neural activity being coupled to multiple latent dynamical variables. An intriguing possibility is that avalanche criticality emerges due to a similar mechanism. Here, we determine the conditions under which latent dynamical variables give rise to avalanche criticality. We find that populations coupled to multiple latent variables produce critical behavior across a broader parameter range than those coupled to a single, quasi-static latent variable, but in both cases, avalanche criticality is observed without fine-tuning of model parameters. We identify two regimes of avalanches, both critical but differing in the amount of information carried about the latent variable. Our results suggest that avalanche criticality arises in neural systems in which activity is effectively modeled as a population driven by a few dynamical variables and these variables can be inferred from the population activity.