Miracle-dz/UniFAR-FTUs huggingface dataset:
Tropism of the Chikungunya Virus

Chikungunya virus (CHIKV) is a re-emerging mosquito-borne virus that displays a large cell and organ tropism, and causes a broad range of clinical symptoms in humans. It is maintained in nature through both urban and sylvatic cycles, involving mosquito vectors and human or vertebrate animal hosts. Although CHIKV was first isolated in 1953, its pathogenesis was only more extensively studied after its re-emergence in 2004. The unexpected spread of CHIKV to novel tropical and non-tropical areas, in some instances driven by newly competent vectors, evidenced the vulnerability of new territories to this infectious agent and its associated diseases. The comprehension of the exact CHIKV target cells and organs, mechanisms of pathogenesis, and spectrum of both competitive vectors and animal hosts is pivotal for the design of effective therapeutic strategies, vector control measures, and eradication actions.
Use of Folic Acid-Fortified Milk in the Elderly Population

Folic acid deficiency is common in the elderly population, resulting in anaemia, dementia, many neurological sequelae and an indirect role in atheromatous disease. An increase in natural food folate is relatively ineffective at increasing folate status and the use of folate fortification of foodstuffs is recommended. The aim of our study was to assess the benefits of folic acid-fortified milk to the folate status of an elderly institutionalised population. 49 subjects received fortified milk as part of their daily diet for at least 6 months (active group) and 40 subjects received unfortified milk (control group). Our results showed a mean serum folate level in the active group of 5.81 (1.1–17.6) µg/l compared to the control group mean of 2.16 (0.5–9.4) µg/l (p < 0.001; normal range for serum folate 2.7–20 µg/l). Similarly the mean red cell folate level in the active group of 316.5 (130–905) µg/l was significantly higher than the control group mean of 196.1 (95–490) µg/l (p < 0.001; normal range for red cell folate 150–1,000 µg/l). Our results suggest that folic acid-fortified milk is an efficacious and acceptable method of administration of folic acid in the elderly population and we recommend the use of folic acid-fortified milk in the regular daily diet of the elderly population.
Effect of bilateral carotid occlusion on cerebral hemodynamics and perivascular innervation: An experimental rat model

We aimed to investigate the effect of chronic cerebral hypoperfusion on cerebral hemodynamics and perivascular nerve density in a rat model. Bilateral common carotid artery (CCA) ligation (n = 24) or sham‐operation (n = 24) was performed with a 1‐week interval. A subgroup (ligated n = 6; sham‐operated n = 3) underwent magnetic resonance imaging (MRI) before the procedures and 2 and 4 weeks after the second procedure. After termination, carotids were harvested for assessment of complete ligation and nerve density in cerebral arteries that were stained for the general neural marker PGP 9.5 and sympathetic marker TH by computerized image analysis. Five rats were excluded because of incomplete ligation. MRI‐based tortuosity of the posterior communicating artery (Pcom), first part of the posterior cerebral artery (P1) and basilar artery was observed in the ligated group, as well as an increased volume (p = 0.05) and relative signal intensity in the basilar artery (p = 0.04; sham‐group unchanged). Immunohistochemical analysis revealed that compared to sham‐operated rats, ligated rats had increased diameters of all intracircular segments and the extracircular part of the internal carotid artery (p < 0.05). Ligated rats showed a higher general nerve density compared to controls in P1 (10%, IQR:8.7–10.5 vs. 6.6%, IQR:5.5–7.4, p = 0.003) and Pcom segments (6.4%, IQR:5.8–6.5 vs. 3.2%, IQR:2.4–4.3, p = 0.003) and higher sympathetic nerve density in Pcom segments (3.7%, IQR:2.8–4.8 vs. 1.7%, IQR:1.3–2.2, p = 0.02). Bilateral CCA occlusion resulted in redistribution of blood flow to posteriorly located cerebral arteries with remarkable changes in morphology and perivascular nerve density, suggesting a functional role for perivascular nerves in cerebral autoregulation.
Gastrocnemius Medialis Architectural Properties at Rest and During Stretching in Female Athletes with Different Flexibility Training Background

Background: This study examined gastrocnemius medialis (GM) architectural properties and ankle joint range of motion (ROM) between female athletes with different flexibility training background. Methods: Elite rhythmic gymnasts (n = 10) were compared to national level volleyball athletes (n = 10). Fascicle length, pennation angle and muscle thickness at the medial and the distal part of GM, and ankle ROM were measured at rest and during 1 min of static stretching. Results: At rest, rhythmic gymnasts displayed longer fascicles compared to volleyball athletes, at the medial (5.93 ± 0.27 vs. 4.74 ± 0.33 mm, respectively, p = 0.001) and the distal part of GM (5.63 ± 0.52 vs. 4.57 ± 0.51 mm, respectively, p = 0.001), smaller pennation angle at the medial part (22.4 ± 2.5 vs. 25.8 ± 2.4°; respectively, p = 0.001) and greater ankle angle (121.7 ± 4.1 vs. 113.2 ± 3.7°, respectively, p = 0.001). During the 1 min of static stretching, gymnasts displayed greater fascicle elongation at the distal part (p = 0.026), greater maximal ankle dorsiflexion (p < 0.001) and muscle tendon junction displacement (p < 0.001) with no difference between groups in pennation angles (p > 0.145), muscle thickness (p > 0.105), and fascicle elongation at mid-belly (p = 0.063). Conclusions: Longer muscle fascicles at rest and greater fascicle elongation at the distal part of GM may contribute to the greater ankle ROM observed in rhythmic gymnasts.
Cognitive Assessment of Older People: Do Sensory Function and Frailty Matter?

Background: To examine the associations of visual and hearing functions, and frailty with subjective memory complaints (SMCs) in a community primary care pilot project of older people aged 60 years and over. Methods: The study was conducted in 24 community centers. A total of 1949 community-dwelling older people aged between 60–97 years were evaluated for which detailed information regarding socio-demographics, lifestyle, and clinical factors were documented at baseline and an average of 12 months later. SMCs were assessed using the 5-item Abbreviated Memory Inventory for the Chinese (AMIC). Visual and hearing functions were measured with two separate single questions. Frailty was assessed using a simple frailty question (FRAIL). Results: At baseline, 1685 (74.6%) participants had reported at least 3 SMCs (AMIC score ≥ 3). Of the 573 participants without / with 1–2 SMCs (AMIC score = 0–2) at baseline, 75 had incomplete data regarding SMCs and 190 developed at least 3 SMCs after 12 months. After adjustments for age, sex, marital status, educational level, hypertension, and diabetes at baseline, poor vision (OR 2.2 95% CI 1.8–2.7), poor hearing (OR 2.2 95% CI 1.8–2.8), and frailty (OR 4.6 95% CI 3.1–6.7) at baseline were each significantly associated with an increased risk of at least 3 SMCs at follow-up. After a further adjustment for baseline SMCs, the associations remained significant. Similar results were obtained when incident SMCs and improvement in subjective memory were used as the outcome variables; and Conclusions: In the care of older people, detection of sensory impairment and frailty through screening may allow formulation of strategies to prevent or delay the onset of cognitive decline.
Dioscin Attenuates Myocardial Damages in Diabetic Rats maybe by Regulating NO-sGC-cGMP-PKG Pathway.

PURPOSE The objective of this research was to explore the effect of dioscin on myocardium in streptozotocin (STZ)-induced diabetic rats and the underlying mechanisms. METHODS Diabetic rat model was established by a single intravenous injection of streptozocin (STZ). The rats were divided into 5 groups: control group, control+dioscin group, model group (diabetes), DDL group (diabetic rats treated with 100 μg/kg/day dioscin) and DDH group (diabetic rats treated with 200 μg/kg/day dioscin). Each group was continuously intervened for 6 weeks. Hemodynamic parameters were detected and pathological alterations of myocardium were observed by hematoxylin-eosin (HE) staining. Inflammatory response and related proteins in the NO-sGC-cGMP-PKG pathway were detected by western blot. RESULTS Dioscin treatment can increase ejection fraction (EF) and decrease left ventricular end-diastolic pressure (LVEDP) as well as time constant of left ventricular pressure decay (Tau) parameters in diabetic rats, suggesting the improvement of left ventricular function. By histopathology observation, we found that dioscin treatment can also improve myocardial histological lesions caused by diabetes. In addition, the levels of inflammatory cytokines TGF-β1, TNF-α and IL-1β of the model group were remarkably higher than those in the control group (p<0.01), while after being treated with dioscin these cytokines were obviously decreased (p<0.05). The levels of PDE-5, PKG and p-VASP in the diabetic rats were significantly declined after being treated by dioscin in a dose-dependent manner (p<0.05). CONCLUSION Dioscin may prevent the myocardial injury in diabetic rats by up-regulating NO-sGC-cGMP-PKG pathway.
Updates of Recent Aortic Aneurysm Research.

Aortic aneurysms in both abdominal and thoracic aortic regions have complex pathophysiological features. In recent years, a considerable increase in research on aneurysm pathogenesis has resulted in the discovery of novel mechanisms and implementation of clinical trials that seek to assess strategies for preventing aneurysm expansion. Despite progress on our understanding of aortic aneurysms, there are still many unanswered questions and conflicting findings requiring clarification. This uncertainty highlights the importance of continual cooperation between preclinical and clinical researchers in validating findings from preclinical studies to the human disease, in order to discover medical treatments that prevent or halt the progression of aortic aneurysmal disease. We hope that this brief review prompts interest in reading these highlighted articles and spurs further investigation into this complex and devastating disease.
Research and molecular characteristic of Shiga toxin‐producing Escherichia coli isolated from sheep carcasses

Domestic ruminants are regarded as the major reservoir of Shiga toxin‐producing Escherichia coli (STEC) closely related to human infection. A total of 363 ovine carcasses were swabbed in an Algiers city slaughterhouse for research on STEC. First of all, screening of the STECs was carried out by a multiplex PCR searching for the genes coding for the virulence factors stx1, stx2 and eae. This step was followed by STEC isolation and serotyping. The presence of stx+/stx+eae+ genes was shown in 116 sheep carcasses (31·95%). From the 116 positive samples, 20 bacterial strains (17·24%) were isolated. Nineteen strains belonged to the species E. coli (STEC), and 1 belonged to Citrobacter braakii (eae+ stx1+). During this study, the presence of potentially pathogenic STEC for humans on the surface of sheep carcasses was confirmed. Corrective measures should be considered at the slaughterhouse level to avoid outbreaks of STEC in Algeria.
Cardiovascular risk, myocardial injury, and exacerbations of chronic obstructive pulmonary disease.

RATIONALE Patients with chronic obstructive pulmonary disease (COPD) have elevated cardiovascular risk, and myocardial injury is common during severe exacerbations. Little is known about the prevalence, magnitude, and underlying mechanisms of cardiovascular risk in community-treated exacerbations. OBJECTIVES To investigate how COPD exacerbations and exacerbation frequency impact cardiovascular risk and myocardial injury, and whether this is related to airway infection and inflammation. METHODS We prospectively measured arterial stiffness (aortic pulse wave velocity [aPWV]) and cardiac biomarkers in 98 patients with stable COPD. Fifty-five patients had paired stable and exacerbation assessments, repeated at Days 3, 7, 14, and 35 during recovery. Airway infection was identified using polymerase chain reaction. MEASUREMENTS AND MAIN RESULTS COPD exacerbation frequency was related to stable-state arterial stiffness (rho = 0.209; P = 0.040). Frequent exacerbators had greater aPWV than infrequent exacerbators (mean ± SD aPWV, 11.4 ± 2.1 vs. 10.3 ± 2.0 ms(-1); P = 0.025). Arterial stiffness rose by an average of 1.2 ms(-1) (11.1%) from stable state to exacerbation (n = 55) and fell slowly during recovery. In those with airway infection at exacerbation (n = 24) this rise was greater (1.4 ± 1.6 vs. 0.7 ± 1.3 ms(-1); P = 0.048); prolonged; and related to sputum IL-6 (rho = 0.753; P < 0.001). Increases in cardiac biomarkers at exacerbation were higher in those with ischemic heart disease (n = 12) than those without (n = 43) (mean ± SD increase in troponin T, 0.011 ± 0.009 vs. 0.003 ± 0.006 μg/L, P = 0.003; N-terminal pro-brain natriuretic peptide, 38.1 ± 37.7 vs. 5.9 ± 12.3 pg/ml, P < 0.001). CONCLUSIONS Frequent COPD exacerbators have greater arterial stiffness than infrequent exacerbators. Arterial stiffness rises acutely during COPD exacerbations, particularly with airway infection. Increases in arterial stiffness are related to inflammation, and are slow to recover. Myocardial injury is common and clinically significant during COPD exacerbations, particularly in those with underlying ischemic heart disease.
Free radical-mediated targeting and immobilization of coupled payloads

Abstract Targeted drug delivery is a promising approach to enhance the accumulation of therapies in diseased tissues while limiting off-site effects. Ligand-receptor interactions are traditionally identified to deliver therapies, and although specific, this can be costly and often suffers from limited sensitivity. An emerging approach is to target intermediary species that modulate disease progression. Here, we propose novel methods of targeting therapies by using native free radicals as a homing signal. Elevated concentrations of free radicals are a characteristic comorbidity of many different diseases. In polymer chemistry, free radicals are frequently used to initiate crosslinking reactions. We proposed that free radicals elevated in injury sites are capable of inducing crosslinking of acrylate groups on polymer chains. Coupling payloads to the polymer then allow for specific targeting of therapies to areas with elevated free radicals. We demonstrate in vitro proof-of-principle of this approach. Reactive oxygen species (ROS) initiated crosslinking of acrylated PEGs, which immobilized a fluorescent payload within tissue mimics. The cross-linking efficiency and immobilization potential varied with the polymer chain length, suggesting that a tuneable platform can be achieved. Together these results provide promising proof-of-concept for using free radicals to specifically target and sustain nearly endless payloads to disease sites.
Going beyond SNPs: The role of structural genomic variants in adaptive evolution and species diversification

Although single-nucleotide polymorphism (SNPs) were initially thought to make-up the majority of selectable variation (Morin et al. 2004; Sachidanandam et al. 2001), it is becoming increasingly recognized that structural variation represents a significant, yet often poorly understood, source of genetic variation. It is only within the past 10 years, aided by the development of genomic technologies such as high-throughput and later 3rd generation sequencing, that the extent of intra-and interspecific structural variation has been investigated in a number of non-model species (Chain & Feulner 2014; Fan & Meyer 2014). This article is protected by copyright. All rights reserved.
Preparation of Self-Assembled Composite Films Constructed by Chemically-Modified MXene and Dyes with Surface-Enhanced Raman Scattering Characterization

The effective functionalization and self-assembly of MXene are of crucial importance for a broad range of nanomaterial applications. In this work, we investigated the aggregates of sulfanilic acid-modified MXene (abbreviated as MXene-SO3H) with three model dyes at the air–water interface and demonstrated the morphological and aggregation changes of composite films, using Langmuir-Blodgett (LB) technology, as well as excellent uniformity and reproducibility by using surface-enhanced Raman scattering (SERS) spectra. This research has found that cationic dye molecules were adsorbed onto negatively charged MXene-SO3H particles mainly through electrostatic interaction and the particles induced dyes to form highly ordered nanostructures including H- and/or J-aggregates corresponding to monomers in bulk solution. The surface pressure-area isotherms from different dye sub phases confirmed that the stable composite films have been successfully formed. And the spectral results reveal that different dyes have different types of aggregations. In addition, the SERS spectra indicated that the optimal layers of MXene-SO3H/methylene blue (MB) films was 50 layers using rhodamine 6G (R6G) as probe molecule. And the formed 50 layers of MXene-SO3H/MB films (MXene-SO3H/MB-50) as SERS substrate were proved to possess excellent uniformity and repeatability.
Epithelial barrier repair and prevention of allergy

Allergic diseases have in common a dysfunctional epithelial barrier, which allows the penetration of allergens and microbes, leading to the release of type 2 cytokines that drive allergic inflammation. The accessibility of skin, compared with lung or gastrointestinal tissue, has facilitated detailed investigations into mechanisms underlying epithelial barrier dysfunction in atopic dermatitis (AD). This Review describes the formation of the skin barrier and analyzes the link between altered skin barrier formation and the pathogenesis of AD. The keratinocyte differentiation process is under tight regulation. During epidermal differentiation, keratinocytes sequentially switch gene expression programs, resulting in terminal differentiation and the formation of a mature stratum corneum, which is essential for the skin to prevent allergen or microbial invasion. Abnormalities in keratinocyte differentiation in AD skin result in hyperproliferation of the basal layer of epidermis, inhibition of markers of terminal differentiation, and barrier lipid abnormalities, compromising skin barrier and antimicrobial function. There is also compelling evidence for epithelial dysregulation in asthma, food allergy, eosinophilic esophagitis, and allergic rhinosinusitis. This Review examines current epithelial barrier repair strategies as an approach for allergy prevention or intervention.
A longer duration of red blood cell storage is associated with a lower hemoglobin increase after blood transfusion: a cohort study

RBC concentrates are commonly stored for up to 42 days but there has been conflicting evidence on the effect of storage duration and clinical outcomes. Most clinical studies have focused on possible associations between duration of storage time and risk for adverse outcomes, including mortality. Recent clinical trials did not find any such associations, but fewer studies have addressed whether storage time affects component efficacy. The main aim of this study was to determine the effect of RBC storage time on hemoglobin increment in transfused patients.
Behavior of Metalloproteinases in Adipose Tissue, Liver and Arterial Wall: An Update of Extracellular Matrix Remodeling

Extracellular matrix (ECM) remodeling is required for many physiological and pathological processes. Metalloproteinases (MMPs) are endopeptidases which are able to degrade different components of the ECM and nucleus matrix and to cleave numerous non-ECM proteins. Among pathological processes, MMPs are involved in adipose tissue expansion, liver fibrosis, and atherosclerotic plaque development and vulnerability. The expression and the activity of these enzymes are regulated by different hormones and growth factors, such as insulin, leptin, and adiponectin. The controversial results reported up to this moment regarding MMPs behavior in ECM biology could be consequence of the different expression patterns among species and the stage of the studied pathology. The aim of the present review was to update the knowledge of the role of MMPs and its inhibitors in ECM remodeling in high incidence pathologies such as obesity, liver fibrosis, and cardiovascular disease.
Self-Perceived Mate Value Is Poorly Predicted by Demographic Variables

Mate value is a construct that can be measured in various ways, ranging from complex but difficult-to-obtain ratings all the way to single-item self-report measures. Due to low sample sizes in previous studies, little is known about the relationship between mate value and demographic variables. In this article, we tested the Mate Value Scale, a relatively new, short, 4-item self-report measure in two large samples. In the first sample of over 1,000, mostly college-age participants, the scale was found to be reliable and correlated with criterion variables in expected ways. In the second, larger sample, which included over 21,000 participants, we have tested for differences across demographics. Contrary to theoretical expectations and previous findings with smaller samples, the differences were either very small (sexual orientation, age, education) or small (sex, socioeconomic status, relationship status) in terms of their effect size. This suggests that the scale is not measuring “objective” mate value (as understood either in terms of fitness or actual mating decisions by potential partners on the “market”), but a self-perception of it, open to social comparison, relative standards, possibly even biases, raising questions about measuring self-perceived versus objective mate value.
Vascular and non‐vascular contributors to memory reduction during traumatic brain injury

Traumatic brain injury (TBI) is an increasing health problem. It is a complex, progressive disease that consists of many factors affecting memory. Studies have shown that increased blood‐brain barrier (BBB) permeability initiates pathological changes in neuro‐vascular network but the role of cerebrovascular dysfunction and its mediated mechanisms associated with memory reduction during TBI are still not well understood. Changes in BBB, inflammation, extravasation of blood plasma components, activation of neuroglia lead to neurodegeneration. Extravasated proteins such as amyloid‐beta, fibrinogen, and cellular prion protein may form degradation resistant complexes that can lead to neuronal dysfunction and degeneration. They also have the ability to activate astrocytes, and thus, can be involved in memory impairment. Understanding the triggering mechanisms and the places they originate in vasculature or in extravascular tissue may help to identify potential therapeutic targets to ameliorate memory reduction during TBI. The goal of this review is to discuss conceptual mechanisms that lead to short‐term memory reduction during non‐severe TBI considering distinction between vascular and non‐vascular effects on neurons. Some aspects of these mechanisms need to be confirmed further. Therefore, we hope that the discussion presented bellow may lead to experiments that may clarify the triggering mechanisms of memory reduction after head trauma.