Miracle-dz/UniFAR-FTUs huggingface dataset:
Under five mortality patterns and associated maternal risk factors in sub-Saharan Africa: A multi-country analysis

Background Under-5 mortality rate in the sub-Saharan region has remained unabated. Worse still, information on the regional trend and associated determinants are not readily available. Knowledge of the trend and determinants of under-5 mortality are essential for effective design of intervention programmes that will enhance their survival. We aimed to examine the mortality patterns in under-5 children and maternal factors associated with under-5 deaths. Methods Demographic and Health Survey (DHS) data from five sub-Sahara Africa countries; Chad, Democratic Republic of Congo, Mali, Niger and Zimbabwe were used in this study. The sample size consisted of 68,085 women aged 15–49 years with at least one history of childbirth. The outcome variable was under-five mortality rate. Relevant information on maternal factors were extracted for analysis. Multivariable Cox proportional hazards regression was used to model maternal factors associated with under-five mortality. Results The current under-5 mortality rate (per 1,000 live births) was; 133 in Republic of Chad, 104 in Democratic Republic of Congo, 95 in Mali, 127 in Niger, and 69 in Zimbabwe. Several maternal and child level factors were found to be significantly associated with under-five mortality. Lack of spousal support (not currently married) resulted to increase in under-five mortality (Chad- Hazard Ratio [HR] = 1.11, 95%CI = 0.97–1.25; DR Congo- HR = 1.24, 95%CI = 1.11–1.40; Mali- HR = 2.43, 95%CI = 1.63–3.64; Niger- HR = 1.59, 95%CI = 1.24–2.03; Zimbabwe- HR = 1.33, 95%CI = 1.06–1.67). Delivery by caesarean section was significantly associated with under-five mortality (Chad- HR = 1.32, 95%CI = 1.00–1.77; DR Congo- HR = 1.20, 95%CI = 1.01–1.43; Mali- HR = 1.42, 95%CI = 1.08–1.85; Niger- HR = 1.43, 95%CI = 1.06–1.92; Zimbabwe- HR = 1.49, 95%CI = 1.03–2.15). Conclusion Despite concerted effort by government and several stakeholders in health to improve childhood survival, the rate of under-5 mortality is still high. Our findings provided evidence on the contribution of maternal age, place of residence, household wealth index, level of education, employment, marital status, religious background, birth type, birth order and interval, sex and size of child, place and mode of delivery, to Under-5 mortality rate in SSA. The position of prominent risk factors for under-five mortality should be addressed through effective design of timely and efficient intervention aimed at reducing childhood mortality.
Exercise ameliorates insulin resistance via regulating TGFβ‐activated kinase 1 (TAK1)‐mediated insulin signaling in liver of high‐fat diet‐induced obese rats

Exercise is an effective therapy for insulin resistance. However, the underlying mechanism remains to be elucidated. Previous research demonstrated that TGFβ‐activated kinase 1 (TAK1)‐dependent signaling plays a crucial character in hepatic insulin resistance. Hepatic ubiquitin specific protease 4 (USP4), USP18, and dual‐specificity phosphatases 14 (DUSP14) can suppress TAK1 phosphorylation, besides tumor necrosis factor receptor‐associated factor 3 (TRAF3) and tripartite motif 8 (TRIM8) promote its phosphorylation. In this study, we tried to verify our hypothesis that exercise improves insulin resistance in high‐fat diet (HFD)‐induced obese (DIO) rats via regulating the TAK1 dependent signaling and TAK1 regulators in liver. Forty male Sprague–Dawley rats were randomized into four groups (n = 10): standard diet and sedentary as normal control; fed on HFD and DIO‐sedentary; fed on HFD and DIO‐chronic exercise; and fed on HFD and DIO‐acute exercise. HFD feeding resulted in increased body weight, visceral fat mass, serum FFAs and hepatic lipid deposition, but decreased hepatic glycogen content and insulin sensitivity. Moreover, hepatic TRAF3 and TRIM8 protein levels increased, whereas USP4, USP18, and DUSP14 protein levels were decreased under obese status, which resulted in enhanced TAK1 phosphorylation and impaired insulin signaling. Exercise training, containing chronic and acute mode, both ameliorated insulin resistance. Meanwhile, decreased TAK1, c‐Jun N‐terminal kinase 1 (JNK1), and insulin receptor substrate 1 (IRS1) phosphorylation enhanced Akt phosphorylation in liver. Moreover, exercise enhanced USP4 and DUSP14 protein levels, whereas decreased TRIM8 protein levels in obese rats’ liver. These results showed that exercise triggered a crucial modulation in TAK1‐dependent signaling and its regulators in obese rats’ liver, and distinct improvement in insulin sensitivity, which provide new insights into the mechanism by which physical exercise improves insulin resistance.
Desensitizing the Attention System to Distraction While Idling: A New Latent Learning Phenomenon in the Visual Attention Domain

For the good and the bad, the world around us is full of distraction. In particular, onset stimuli that appear abruptly in the scene grab attention, thus disrupting the ongoing task. Different cognitive mechanisms for distractor filtering have been proposed, but prevalent accounts share the idea that filtering is accomplished to shield target processing from interference. Here we provide novel evidence that challenges this view, as passive exposure to a repeating visual onset is sufficient to trigger learning-dependent mechanisms to filter the unwanted stimulation. In other words, our study shows that during passive exposure the cognitive system is capable of learning about the characteristics of the salient yet irrelevant stimulation, and to reduce the responsiveness of the attention system to it, thus significantly decreasing the impact of the distractor upon start of an active task. However, despite passive viewing efficiently attenuates the spatial capture of attention, a short-lived performance cost is found when the distractor is initially encountered within the context of the active task. This cost, which dissipates in a few trials, likely reflects the need to familiarize with the distractor, already seen during passive viewing, in the new context of the active task. Although top-down inhibitory signals can be applied to distractors for the successful completion of goal-directed behavior, our results emphasize the role of more automatic habituation mechanisms for distraction exclusion based on a neural model of the history of the irrelevant stimulation.
Learning to Teach with Dynamic Loss Functions

Teaching is critical to human society: it is with teaching that prospective students are educated and human civilization can be inherited and advanced. A good teacher not only provides his/her students with qualified teaching materials (e.g., textbooks), but also sets up appropriate learning objectives (e.g., course projects and exams) considering different situations of a student. When it comes to artificial intelligence, treating machine learning models as students, the loss functions that are optimized act as perfect counterparts of the learning objective set by the teacher. In this work, we explore the possibility of imitating human teaching behaviors by dynamically and automatically outputting appropriate loss functions to train machine learning models. Different from typical learning settings in which the loss function of a machine learning model is predefined and fixed, in our framework, the loss function of a machine learning model (we call it student) is defined by another machine learning model (we call it teacher). The ultimate goal of teacher model is cultivating the student to have better performance measured on development dataset. Towards that end, similar to human teaching, the teacher, a parametric model, dynamically outputs different loss functions that will be used and optimized by its student model at different training stages. We develop an efficient learning method for the teacher model that makes gradient based optimization possible, exempt of the ineffective solutions such as policy optimization. We name our method as "learning to teach with dynamic loss functions" (L2T-DLF for short). Extensive experiments on real world tasks including image classification and neural machine translation demonstrate that our method significantly improves the quality of various student models.
Parkinson's Disease Biomarkers: Where Are We and Where Do We Go Next?

Objective measures of Parkinson's disease (PD) are needed for purposes of diagnosis and prognostication, as well as identification of those at risk of PD. In this qualitative review, we provide an overview of the current state of the field of PD biomarker development, delineate challenges, and discuss how the field is evolving.
Isolation of two novel purple naphthoquinone pigments concomitant with the bioactive red bikaverin and derivates thereof produced by Fusarium oxysporum

Filamentous fungi have gained growing interest as sources of diverse pigmented secondary metabolites. Some specific polyketides from Ascomycetous species have demonstrated a wide range of industrial applications in food, cosmetic, textile, and in the design of pharmaceutical products. The formulation of recipes containing fungal polyketides has increased over recent years. Fusarium strains were proven useful to mankind in a variety of technologies. Nevertheless, there is still need of new isolates of Fusarium for use in emerging and already existing fields. In this article, we report the concomitant production of the bioactive red bikaverin along with two novel purple pigments by the phytopathogenic Fusarium oxysporum LCP531 strain isolated from soil. In literature, the production of purple pigment had only been described in cultures of Fusarium Fujikuroi, Fusarium verticillioides, and Fusarium graminearum. The production of these naphthoquinonic pigments, their distribution (either produced in mycelia or excreted in liquid medium) and their chemical profiles were investigated with respect to nutrient composition. The pigments were extracted by using a pressurized liquid extraction method, monitored by colorimetric analysis and characterized by HPLC‐DAD chromatography. To our knowledge, this is the first report of these two novel wild‐type purple naphtoquinones pigments along with bikaverin, where additionally, the culture conditions were put into perspective to optimize fermentation cultures and extraction process accordingly to the pigment/biomolecule desired. These colored naphthoquinones should be promising fungal functional compounds which could be expected to have a place of choice, along with other antibacterial, antifungal, antiviral, anticancer, and antineoplastic derivatives. © 2018 American Institute of Chemical Engineers Biotechnol. Prog. , 35: e2738, 2019
Deep learning tutorial for denoising

We herein introduce deep learning to seismic noise attenuation. Compared with traditional seismic noise attenuation algorithms that depend on signal models and their corresponding prior assumptions, a deep neural network is trained based on a large training set, where the inputs are the raw datasets and the corresponding outputs are the desired clean data. After the completion of training, the deep learning method achieves adaptive denoising with no requirements of (i) accurate modeling of the signal and noise, and (ii) optimal parameters tuning. We call this intelligent denoising. We use a convolutional neural network as the basic tool for deep learning. The training set is generated with manually added noise in random and linear noise attenuation, and with the wave equation in the multiple attenuation. Stochastic gradient descent is used to solve the optimal parameters for the convolutional neural network. The runtime of deep learning on a graphics processing unit for denoising has the same order as the $f-x$ deconvolutional method. Synthetic and field results show the potential applications of deep learning in the automation of random noise attenuation with unknown variance, linear noise, and multiples.
Vago-Splenic Axis in Signal Transduction of Remote Ischemic Preconditioning in Pigs and Rats

Rationale: The signal transduction of remote ischemic conditioning is still largely unknown. Objective: Characterization of neurohumoral signal transfer and vago-splenic axis in remote ischemic preconditioning (RIPC). Methods and Results: Anesthetized pigs were subjected to 60 minutes of coronary occlusion and 180 minutes of reperfusion (placebo+ischemia/reperfusion [PLA+I/R]). RIPC was induced by 4×5/5 minutes of hindlimb I/R 90 minutes before coronary occlusion (RIPC+I/R). Arterial blood samples were taken after placebo or RIPC before I/R. In subgroups of pigs, bilateral cervical vagotomy, splenectomy, or splenic denervation were performed before PLA+I/R or RIPC+I/R, respectively. In pigs with RIPC+I/R, infarct size (percentage of area at risk) was less than in those with PLA+I/R (23±12% versus 45±8%); splenectomy or splenic denervation abrogated (splenectomy+RIPC+I/R: 38±15%; splenic denervation+RIPC+I/R: 43±5%), and vagotomy attenuated (vagotomy+RIPC+I/R: 36±11%) RIPC protection. RIPC increased phosphorylation of STAT3 (signal transducer and activator of transcription 3) in left ventricular biopsies taken at early reperfusion. Splenectomy or splenic denervation, but not vagotomy, abolished this increased phosphorylation. In rats with vagotomy, splenectomy, or splenic denervation, RIPC (3×5/5 minutes of hindlimb occlusion/reperfusion) or placebo was performed, respectively. Hearts were isolated, saline perfused, and subjected to 30/120-minute global I/R. With RIPC, infarct size (percentage of ventricular mass) was less (20±7%) than with placebo (37±6%), and vagotomy, splenectomy, or splenic denervation abrogated RIPC protection (38±12%, 36±9%, and 36±7%), respectively. Rat spleens were isolated, saline perfused, and splenic effluate (SEff) was sampled after infusion with carbachol (SEffcarbachol) or saline (SEffsaline). Pig plasma or SEff was infused into isolated perfused rat hearts subjected to global I/R. Infarct size was less with infusion of RIPC+I/Rplasma+ (24±6%) than with PLA+I/Rplasma (40±8%), vagotomy+PLA+I/Rplasma (39±11%), splenectomy+PLA+I/Rplasma (35±8%), vagotomy+RIPC+I/Rplasma (40±9%), splenectomy+RIPC+I/Rplasma (33±9%), or splenic denervation+RIPC+I/Rplasma (39±8%), respectively. With infusion of SEffcarbachol, infarct size was less than with infusion of SEffsaline (24 [19–27]% versus 35 [32–38]%). Conclusions: Activation of a vago-splenic axis is causally involved in RIPC cardioprotection.
Effect of selenium enrichment on metabolism of tomato (Solanum lycopersicum) fruit during postharvest ripening.

BACKGROUND Selenium (Se) enrichment of plants seems effective in enhancing the health-related properties of produce and in delaying plant senescence and fruit ripening. The current study investigated the effects of Se on tomato fruit ripening. Tomato (Solanum lycopersicum L.) plants were grown in hydroponics with different Se-enriched nutrient solutions. Se, as sodium selenate, was added at a rate of 0 mg L-1 (control), 1, and 1.5 mg L-1 . RESULTS Selenium was absorbed by roots and translocated to leaves and fruit. Enrichment with Se did not significantly affect the qualitative parameters of fruit at commercial harvest; instead it delayed ripening by affecting specific ripening-related processes (respiration, ethylene production, color evolution) during postharvest. In the current experiment 100 g of tomato hydroponically grown with a 1.5 mg Se L-1 enriched solution provided a total of 23.7 µg Se. Selenium recommended daily intake is 60 µg for women and 70 µg for men; thus the daily consumption of 100 g of enriched tomato would not lead to Se toxicity but would provide a good Se diet supplementation. CONCLUSIONS The cultivation of tomato plants in a Se-enriched solution appeared effective in producing tomato fruit with improved performance during storage and postharvest shelf life, and also with greater potential health-promoting properties. © 2018 Society of Chemical Industry.
Appropriateness of DOAC Prescribing Before and During Hospital Admission and Analysis of Determinants for Inappropriate Prescribing

Background and Objectives: Appropriate dosing of direct oral anticoagulants (DOACs) is required to avoid under- and overdosing that may precipitate strokes or thromboembolic events and bleedings, respectively. Our objective was to analyze the appropriateness of DOAC dosing according to the summaries of product characteristics (SmPC). Furthermore, determinants for inappropriate prescribing were investigated. Methodology: Retrospective cohort study of hospitalized patients aged ≥60 years with at least one DOAC intake during hospital stay. Descriptive analyses were used to summarize the characteristics of the study population. Chi-square test was used to evaluate differences between DOACs. Binary logistic regression analysis was performed to assess determinants for inappropriate prescribing. Results: For the 772 included patients, inappropriate dosing occurred in 25.0% of hospitalizations with 23.4, 21.9, and 29.7% for dabigatran, rivaroxaban, and apixaban, respectively (p = 0.084). Underdosing was most prevalent for apixaban (24.5%) compared to dabigatran (14.0%) and rivaroxaban (12.8%), p < 0.001. In 67.1% (apixaban), 26.7% (dabigatran), and 51.2% (rivaroxaban) of underdosed DOAC cases according to the SmPC, the dose would be considered appropriate according to the European Heart Rhytm Association (EHRA) guidelines. Overdosing was observed in 4.5% (apixaban), 4.7% (dabigatran), and 7.7% (rivaroxaban) of patients. For all DOACs, our analysis showed an age ≥80 years (p = 0.036), use of apixaban (p = 0.026), DOAC use before hospitalization (p = 0.001), intermediate renal function (p = 0.014), and use of narcotic analgesics (p = 0.019) to be associated with a higher rate of inappropriate prescribing. Undergoing surgery was associated with a lower odds of inappropriate prescribing (p = 0.012). For rivaroxaban, use of medication for hypothyroidism (p = 0.027) and the reduced dose (p < 0.001) were determinants for inappropriate prescribing. Treatment of venous thromboembolism was associated with less errors (p = 0.002). For apixaban, severe renal insufficiency (p < 0.001) and initiation in hospital (p = 0.016) were associated with less and the reduced dose (p < 0.001) with more inappropriate prescribing. No determinants were found in the dabigatran subgroup. Conclusions: Inappropriate DOAC prescribing is frequent with underdosing being the most common drug related problem when using the SmPC as reference. More appropriate prescriptions were found when taking the EHRA guidelines into account. Analysis of determinants of inappropriate prescribing yielded insights in the risk factors associated with inappropriate DOAC prescriptions.
Porphyrin‐Based SOD Mimic MnTnBuOE‐2‐PyP5+ Inhibits Mechanisms of Aortic Valve Remodeling in Human and Murine Models of Aortic Valve Sclerosis

Background Aortic valve sclerosis (AVSc), the early asymptomatic presentation of calcific aortic valve (AV) disease, affects 25% to 30% of patients aged >65 years. In vitro and ex vivo experiments with antioxidant strategies and antagonists of osteogenic differentiation revealed that AVSc is reversible. In this study, we characterized the underlying changes in the extracellular matrix architecture and valve interstitial cell activation in AVSc and tested in vitro and in vivo the activity of a clinically approved SOD (superoxide dismutase) mimic and redox‐active drug MnTnBuOE‐2‐PyP5+ (BMX‐001). Methods and Results After receiving informed consent, samples from patients with AVSc, AV stenosis, and controls were collected. Uniaxial mechanical stimulation and in vitro studies on human valve interstitial cells were performed. An angiotensin II chronic infusion model was used to impose AV thickening and remodeling. We characterized extracellular matrix structures by small‐angle light scattering, scanning electron microscopy, histology, and mass spectrometry. Diseased human valves showed altered collagen fiber alignment and ultrastructural changes in AVSc, accumulation of oxidized cross‐linking products in AV stenosis, and reversible expression of extracellular matrix regulators ex vivo. We demonstrated that MnTnBuOE‐2‐PyP5+ inhibits human valve interstitial cell activation and extracellular matrix remodeling in a murine model (C57BL/6J) of AVSc by electron microscopy and histology. Conclusions AVSc is associated with architectural remodeling despite marginal effects on the mechanical properties in both human and mice. MnTnBuOE‐2‐PyP5+ controls AV thickening in a murine model of AVSc. Because this compound has been approved recently for clinical use, this work could shift the focus for the treatment of calcific AV disease, moving from AV stenosis to an earlier presentation (AVSc) that could be more responsive to medical therapies.
The Effect of Gluten Free Diet on Components of Metabolic Syndrome: A Randomized Clinical Trial

Background: This study aimed to assess the effects of Gluten free diet (GFD) on components of metabolic syndrome (MES). Materials and Methods: In this randomized clinical trial, 50 subjects diagnosed with MES were randomly divided into two groups (n=25). The first group received a GFD and the second group continued their regular diet. Biochemical markers of MES and blood pressure were measured before and after 8-week intervention. Results: Forty five subjects completed the study. A post-hoc comparison of the groups showed no effects of the GFD and control diet on LDL cholesterol, total cholesterol, fasting insulin, HOMA-IR, systolic and diastolic blood pressure levels. The GFD reduced fasting blood glucose, waist circumference (WC) and serum triglyceride concentration significantly compared with the control diet (p<0.05). Conclusion: Short-term GFD reduced WC and improved glycemic control and Triglyceride level in subjects with the metabolic syndrome.
Mitochondrial transplantation in humans: “magical” cure or cause for concern?

Mitochondrial transplantation is a therapeutic approach developed by McCully and colleagues that entails the injection of healthy mitochondria harvested from unaffected tissue into an ischemic organ of the same subject (1). It has recently been applied to human pediatric patients with myocardial ischemia (2), receiving widespread media attention accompanied by sensationalistic claims on its mechanism of action, e.g.: (a) after injection into the heart, “mitochondria moved like magnets to the proper places in the cells and began supplying energy;” and (b) after infusion into the coronary arteries, “somehow the organelles will gravitate almost magically to the injured cells that need them and take up residence” (3). According to the purported mechanism of action, the mitochondria must, seemingly, perform three “magic tricks. ” First, the mitochondria must survive transfer from an intracellular environment to an extracellular one with high Ca2+ concentrations. Second, if they survive, mitochondria must produce ATP that is able to enter cardiac myocytes to support contraction. Third, enough mitochondria must pass through the cell membrane to contribute to ATP production by the host cell. A corollary to trick number three is a variation in which the mitochondria are injected into the bloodstream and somehow pass through the endothelial vascular permeability barrier, migrate into the interstitium, and are incorporated into the dysfunctional target tissue. Given the rapid translation of this [. ] Viewpoint