Miracle-dz/UniFAR-FTUs huggingface dataset:
Specific effect of hypobaria on cerebrovascular hypercapnic responses in hypoxia

It remains unknown whether hypobaria plays a role on cerebrovascular reactivity to CO2 (CVR). The present study evaluated the putative effect of hypobaria on CVR and its influence on cerebral oxygen delivery (cDO2) in five randomized conditions (i.e., normobaric normoxia, NN, altitude level of 440 m; hypobaric hypoxia, HH at altitude levels of 3,000 m and 5,500 m; normobaric hypoxia, NH, altitude simulation of 5,500 m; and hypobaric normoxia, HN). CVR was assessed in nine healthy participants (either students in aviation or pilots) during a hypercapnic test (i.e., 5% CO2). We obtained CVR by plotting middle cerebral artery velocity versus end‐tidal CO2 pressure (PETCO2) using a sigmoid model. Hypobaria induced an increased slope in HH (0.66 ± 0.33) compared to NH (0.35 ± 0.19) with a trend in HN (0.46 ± 0.12) compared to NN (0.23 ± 0.12, p = .069). PETCO2 was decreased (22.3 ± 2.4 vs. 34.5 ± 2.8 mmHg and 19.9 ± 1.3 vs. 30.8 ± 2.2 mmHg, for HN vs. NN and HH vs. NH, respectively, p < .05) in hypobaric conditions when compared to normobaric conditions with comparable inspired oxygen pressure (141 ± 1 vs. 133 ± 3 mmHg and 74 ± 1 vs. 70 ± 2 mmHg, for NN vs. HN and NH vs. HH, respectively) During hypercapnia, cDO2 was decreased in 5,500 m HH (p = .046), but maintained in NH when compared to NN. To conclude, CVR seems more sensitive (i.e., slope increase) in hypobaric than in normobaric conditions. Moreover, hypobaria potentially affected vasodilation reserve (i.e., MCAv autoregulation) and brain oxygen delivery during hypercapnia. These results are relevant for populations (i.e., aviation pilots; high‐altitude residents as miners; mountaineers) occasionally exposed to hypobaric normoxia.
The unidentified hormonal defense against weight gain

Human biology has evolved to keep body fat within a range that supports survival. During the last 25 years, obesity biologists have uncovered key aspects of physiology that prevent fat mass from becoming too low. In contrast, the mechanisms that counteract excessive adipose expansion are largely unknown. Evidence dating back to the 1950s suggests the existence of a blood-borne molecule that defends against weight gain. In this article, we discuss the research supporting an “unidentified factor of overfeeding” and models that explain its role in body weight control. If it exists, revealing the identity of this factor could end a long-lasting enigma of energy balance regulation and facilitate a much-needed breakthrough in the pharmacological treatment of obesity.
Effects of a 12-Week Cycling Intervention on Successful Aging Measures in Mid-Aged Adults

ABSTRACT Purpose: To compare the effect of 12-weeks of cycling training and competition versus recreational cycling on successful aging across physical, psychological, cognitive, and social functioning domains in mid-aged adults. Methods: Recreational cyclists were randomly assigned to an intervention (n = 13, M age = 47.18 years) and comparison (n = 13, M age = 46.91 years) group. Analysis of Covariance was used on self-reported pre-post data to determine changes across time and differences between groups on outcomes. Results: The intervention group scored higher on the role limitation due to physical problems measure of physical functioning (p = .045) and the social activity measure of social functioning (p = .008) with large effect sizes (ηp 2 > .14). The remaining physical, psychological, cognitive, and social functioning measures were not significantly different (p > .05) between groups with small to medium effect sizes (ηp 2 > .01 to ≤ .06). Conclusion: Cycling training and competition promotes better physical and social functioning than recreational cycling. This finding indicates that an intervention that incorporates the training and competition aspects of sport may promote positive outcomes that are above and beyond those that can be gained from participation in recreational physical activity. Objective measurements on larger samples across a broader range of sports are required to confirm and extend these findings.
Effect of Improved Water Quality, Sanitation, Hygiene and Nutrition Interventions on Respiratory Illness in Young Children in Rural Bangladesh: A Multi-Arm Cluster-Randomized Controlled Trial

Abstract. Acute respiratory infections cause mortality in young children. We assessed the effects of water, sanitation, hygiene (WASH) and nutritional interventions on childhood ARI. Geographic clusters of pregnant women from rural Bangladesh were randomly assigned to receive 1) chlorinated drinking water and safe storage (W); 2) upgraded sanitation (S); 3) handwashing promotion (H); 4) combined water, sanitation, and handwashing (WSH); 5) nutrition intervention including lipid-based nutrient supplements; 6) combined WSH plus nutrition (WSHN); or 7) no intervention (control). Masking of participants was not possible. Acute respiratory illness was defined as caregiver-reported persistent cough, panting, wheezing, or difficulty breathing in the past 7 days among index children, those born to enrolled women. We assessed outcomes at 12 and 24 months of intervention using intention to treat. Compared with children in the control group (ARI prevalence, P: 8.9%), caregivers of index children reported significantly lower ARI in the water (P: 6.3%, prevalence ratio (PR): 0.71; 95% CI: 0.53, 0.96), sanitation (P: 6.4%, PR: 0.75, 95% CI: 0.58, 0.96), handwashing (P: 6.4%, PR: 0.68, 95% CI: 0.50, 0.93), and the combined WSH+N arms (P: 5.9%, PR: 0.67, 95% CI: 0.50, 0.90). Those in the nutrition (P: 7.4%, PR: 0.84, 95% CI: 0.63, 1.10) or the WSH arm (P: 8.9%, PR: 0.99, 95% CI: 0.76, 1.28) reported similar ARI prevalence compared with control children. Single targeted water, sanitation, and hygiene interventions reduced reported respiratory illness in young children. There was no apparent respiratory health benefit from combining WASH interventions.
Race May Not Impact Endocrine Therapy–Related Changes in Breast Density

Background: Reduction in breast density may be a biomarker of endocrine therapy (ET) efficacy. Our objective was to assess the impact of race on ET-related changes in volumetric breast density (VBD). Methods: This retrospective cohort study assessed longitudinal changes in VBD measures in women with estrogen receptor–positive invasive breast cancer treated with ET. VBD, the ratio of fibroglandular volume (FGV) to breast volume (BV), was measured using Volpara software. Changes in measurements were evaluated using a multivariable linear mixed effects model. Results: Compared with white women (n = 191), black women (n = 107) had higher rates of obesity [mean ± SD body mass index (BMI) 34.5 ± 9.1 kg/m2 vs. 30.6 ± 7.0 kg/m2, P < 0.001] and premenopausal status (32.7% vs. 16.7%, P = 0.002). Age- and BMI-adjusted baseline FGV, BV, and VBD were similar between groups. Modeled longitudinal changes were also similar: During a follow-up of 30.7 ± 15.0 months (mean ± SD), FGV decreased over time in premenopausal women (slope = −0.323 cm3; SE = 0.093; P = 0.001), BV increased overall (slope = 2.475 cm3; SE = 0.483; P < 0.0001), and VBD decreased (premenopausal slope = −0.063%, SE = 0.011; postmenopausal slope = −0.016%, SE = 0.004; P < 0.0001). Race was not significantly associated with these longitudinal changes, nor did race modify the effect of time on these changes. Higher BMI was associated with lower baseline VBD (P < 0.0001). Among premenopausal women, VBD declined more steeply for women with lower BMI (time × BMI, P = 0.0098). Conclusions: Race does not appear to impact ET-related longitudinal changes in VBD. Impact: Racial disparities in estrogen receptor–positive breast cancer recurrence and mortality may not be explained by differential declines in breast density due to ET.
Cell-associated HIV-1 RNA predicts viral rebound and disease progression after discontinuation of temporary early ART.

Plasma viral load (VL) and CD4+ T-cell count are widely used as biomarkers of HIV-1 replication, pathogenesis, and response to antiretroviral therapy (ART). However, the clinical potential of cell-associated (CA) HIV-1 molecular markers is much less understood. Here, we measured CA HIV-1 RNA and DNA in HIV-infected individuals treated with temporary ART initiated during primary HIV-1 infection. We demonstrate significant predictive value of CA RNA for: (a) the virological and immunological response to early ART, (b) the magnitude and time to viral rebound after discontinuation of early ART, and (c) the disease progression in the absence of treatment. Remarkably, when adjusted for CA RNA, plasma VL no longer appeared as an independent predictor of any clinical endpoint in this cohort. The potential of CA RNA as an HIV-1 clinical marker, in particular as a predictive biomarker of virological control after stopping ART, should be explored in the context of HIV-1 curative interventions.
Root Response to Drought Stress in Rice (Oryza sativa L.)

The current unpredictable climate changes are causing frequent and severe droughts. Such circumstances emphasize the need to understand the response of plants to drought stress, especially in rice, one of the most important grain crops. Knowledge of the drought stress response components is especially important in plant roots, the major organ for the absorption of water and nutrients from the soil. Thus, this article reviews the root response to drought stress in rice. It is presented to provide readers with information of use for their own research and breeding program for tolerance to drought stress in rice.
Effect of Antimicrobial Peptide Microcin J25 on Growth Performance, Immune Regulation, and Intestinal Microbiota in Broiler Chickens Challenged with Escherichia coli and Salmonella

Simple Summary Antimicrobial peptides are thought to be ideal candidates, owing to their antimicrobial properties, broad spectrum of activity, and low propensity for development of bacterial resistance. Microcin J25 (MccJ25) is an antimicrobial peptide produced by a fecal strain of Escherichia coli (E. coli) containing 21 Arbor Acres (AA) broilers, and has a strong inhibition on E. coli and Salmonella. This study was performed primarily to evaluate the effects of MccJ25 on growth performance and gut health in broilers challenged with E. coli and Salmonella, as a potential substitute for antibiotics. The results showed that MccJ25 promoted growth performance, improved intestinal morphology, and influenced fecal microbiota composition. Abstract The purpose of this study was to investigate the effects of antimicrobial peptide microcin J25 (MccJ25) on growth performance, immune regulation, and intestinal microbiota in broilers. A total of 3120 one-day-old male Arbor Acres (AA) broilers were randomly allocated to five groups (12 replicates, 52 chickens per replicate). The treatments were control, challenge (0 mg/kg MccJ25), different dosages of antimicrobial peptide (AMP) (0.5 and 1mg/kg MccJ25), and antibiotic groups (20 mg/kg colistin sulfate). The MccJ25 groups increased the body weight gain (starter and overall) that was reduced in the challenge group. The overall (day 1 to day 42) feed-to-gain ratio (G:F) was significantly decreased in AMP groups compared with the challenge group. Birds fed AMP had a decreased population of total anaerobic bacteria (day 21 and day 42) and E. coli (day 21 and day 42) in feces, as well as a lower Salmonella infection rate (day 21 and day 42) compared with birds in the challenge group. The villus height of the duodenum, jejunum, and ileum, as well as the villus height/crypt depth of the duodenum and jejunum were greater in AMP groups than birds in the challenge group. Moreover, MccJ25 linearly improved the villus height of the duodenum and jejunum. The addition of MccJ25 decreased the concentration of TNF-α, IL-1β, and IL-6 compared with challenge group. At d 21, MccJ25 linearly reduced the level of IL-6. In conclusion, dietary supplemented MccJ25 effectively improved performance, systematic inflammation, and improved fecal microbiota composition of the broilers.
Influence of Benz[a]anthracene on Bone Metabolism and on Liver Metabolism in Nibbler Fish, Girella punctata

It has been reported that spinal deformity was induced in developing fish by the addition of polycyclic aromatic hydrocarbons (PAHs). To examine the mechanism of the disruption of fish bone metabolism, the effect of benz[a]anthracene (BaA), a kind of PAH, on plasma calcium, inorganic phosphorus, osteoblasts, and osteoclasts was investigated in this study. We also measured several plasma components to analyze the toxicity of BaA on other metabolisms. BaA (1 or 10 ng/g body weight) was intraperitoneally injected (four times) into nibbler fish during breeding, for 10 days, and it was indicated, for the first time, that injecting high doses of BaA to nibbler fish induced both hypocalcemia and hypophosphatemia. Furthermore, in the scales of nibbler fish treated with high doses of BaA, both osteoclastic and osteoblastic marker messengerRNA (mRNA) expressions decreased. These results are a cause of disruption of bone metabolism and, perhaps, the induction of spinal deformities. In addition, we found that total protein, metabolic enzymes in the liver, total cholesterol, free cholesterol, and high-density lipoprotein cholesterol levels significantly decreased in BaA-injected fish. These results indicate that BaA may affect liver diseases and emphasize the importance of prevention of aquatic PAH pollution.
Viability and Stimulation of Human Stem Cells from the Apical Papilla (hSCAPs) Induced by Silicate-Based Materials for Their Potential Use in Regenerative Endodontics: A Systematic Review

Blood clot formation in the apical third of the root canal system has been shown to promote further root development and reinforcement of dentinal walls by the deposition of mineralized tissue, resulting in an advancement from traditional apexification procedures to a regenerative endodontic treatment (RET) for non-vital immature permanent teeth. Silicate-based hydraulic biomaterials, categorized as bioactive endodontic cements, emerged as bright candidates for their use in RET as coronal barriers, sealing the previously induced blood clot scaffold. Human stem cells from the apical papilla (hSCAPs) surviving the infection may induce or at least be partially responsible for the regeneration or repair shown in RET. The aim of this study is to present a qualitative synthesis of available literature consisting of in vitro assays which analyzed the viability and stimulation of hSCAPs induced by silicate-based hydraulic biomaterials. A systematic electronic search was carried out in Medline, Scopus, Embase, Web of Science, Cochrane and SciELO databases, followed by a study selection, data extraction, and quality assessment following the PRISMA protocol. In vitro studies assessing the viability, proliferation, and/or differentiation of hSCAPs as well as their mineralization potential and/or osteogenic, odontogenic, cementogenic and/or angiogenic marker expression in contact with commercially available silicate-based materials were included in the present review. The search identified 73 preliminary references, of which 10 resulted to be eligible for qualitative synthesis. The modal materials studied were ProRoot MTA and Biodentine. Both bioceramic materials showed significant positive results when compared to a control for hSCAP cell viability, migration, and proliferation assays; a significant up-regulation of hSCAP odontogenic/osteogenic marker (ALP, DSPP, BSP, Runx2, OCN, OSX), angiogenic growth factor (VEGFA, FIGF) and pro-inflammatory cytokine (IL-1α, IL-1β, IL-6, TNF-α) expression; and a significant increase in hSCAP mineralized nodule formation assessed by Alizarin Red staining. Commercially available silicate-based materials considered in the present review can potentially induce mineralization and odontogenic/osteogenic differentiation of hSCAPs, thus prompting their use in regenerative endodontic procedures.
Prevalence of the metabolic syndrome among US middle-aged and older adults with and without diabetes--a preliminary analysis of the NHANES 1999-2002 data.

OBJECTIVE This study examined the racial differences in the distribution of the individual and clustered metabolic syndrome components among diabetics and nondiabetics and the presence of inflammatory markers. STUDY DESIGN AND METHOD This is a secondary data analysis of the National Health and Nutrition Examination Survey (NHANES) from 1999-2002. The analysis only included adults aged > or = 40 years who were White, Black, and Mexican American. Differences in the rate of metabolic syndrome, each of its components, and inflammation markers among the three racial groups were examined by using chi-square tests. RESULTS An estimated 12 million adults > or = 40 years of age have diagnosed and undiagnosed diabetes. Most diabetics have metabolic syndrome (69.9% for Whites, 64.8% for Blacks, and 62.4% for Mexican Americans). Abdominal obesity is more prevalent among Whites with diabetes than Mexican Americans (80.6% vs 67.8%, P = .008). Hypertension is significantly greater among Blacks with diabetes (73.1%) as compared to Whites (58.6%) and Mexican Americans (50.8%); hypertension in those without diabetes was 47.5% among Blacks, 32.4% among Whites, and 23.4% among Mexican Americans. Among nondiabetics, Blacks have higher prevalence of elevated serum C-reactive protein (17.4%) and high plasma fibrinogen (49.7%) than Whites (9.7% and 36%, respectively). CONCLUSION These data demonstrate racial differences in the prevalence of components of the metabolic syndrome among diabetics and nondiabetics. They raise questions about the current definition of the metabolic syndrome, which weights each component equally. Further research is necessary to more precisely quantify the characteristics of metabolic syndrome in different racial and ethnic groups.
Micro RNA Molecules as Modulators of Treatment Resistance, Immune Checkpoints Controllers and Sensitive Biomarkers in Glioblastoma Multiforme

Based on genome sequencing, it is estimated that over 90% of genes stored in human genetic material are transcribed, but only 3% of them contain the information needed for the production of body proteins. This group also includes micro RNAs representing about 1%–3% of the human genome. Recent studies confirmed the hypothesis that targeting molecules called Immune Checkpoint (IC) open new opportunities to take control over glioblastoma multiforme (GBM). Detection of markers that indicate the presence of the cancer occupies a very important place in modern oncology. This function can be performed by both the cancer cells themselves as well as their components and other substances detected in the patients’ bodies. Efforts have been made for many years to find a suitable marker useful in the diagnosis and monitoring of gliomas, including glioblastoma.
Drying of the Natural Fibers as A Solvent-Free Way to Improve the Cellulose-Filled Polymer Composite Performance

When considering cellulose (UFC100) modification, most of the processes employ various solvents in the role of the reaction environment. The following article addresses a solvent-free method, thermal drying, which causes a moisture content decrease in cellulose fibers. Herein, the moisture content in UFC100 was analyzed with spectroscopic methods, thermogravimetric analysis, and differential scanning calorimetry. During water desorption, a moisture content drop from approximately 6% to 1% was evidenced. Moreover, drying may bring about a specific variation in cellulose’s chemical structure. These changes affected the cellulose-filled polymer composite’s properties, e.g., an increase in tensile strength from 17 MPa for the not-dried UFC100 to approximately 30 MPa (dried cellulose; 24 h, 100 °C) was observed. Furthermore, the obtained tensile test results were in good correspondence with Payne effect values, which changed from 0.82 MPa (not-dried UFC100) to 1.21 MPa (dried fibers). This raise proves the reinforcing nature of dried UFC100, as the Payne effect is dependent on the filler structure’s development within a polymer matrix. This finding paves new opportunities for natural fiber applications in polymer composites by enabling a solvent-free and efficient cellulose modification approach that fulfils the sustainable development rules.
Detection of live attenuated influenza vaccine virus and evidence of reassortment in the U.S. swine population

Influenza vaccines historically have been multivalent, whole virus inactivated products. The first bivalent, intranasal, live attenuated influenza vaccine (LAIV; Ingelvac Provenza), with H1N1 and H3N2 subtypes, has been approved for use in swine. We investigated the LAIV hemagglutinin (HA) sequences in diagnostic cases submitted to the Iowa State University Veterinary Diagnostic Laboratory and potential vaccine virus reassortment with endemic influenza A virus (IAV) in swine. From January 3 to October 11, 2018, IAV HA sequences demonstrating 99.5–99.9% nucleotide homology to the H1 HA or 99.4–100% nucleotide homology to the H3 HA parental strains in the LAIV were detected in 58 of 1,116 (5.2%) porcine respiratory cases (H1 HA A/swine/Minnesota/37866/1999[H1N1; MN99]; H3 HA A/swine/Texas/4199-2/1998[H3N2; TX98]). Nine cases had co-detection of HA genes from LAIV and wild-type IAV in the same specimen. Thirty-five cases had associated epidemiologic information that indicated they were submitted from 11 states representing 31 individual sites and 17 production systems in the United States. Whole genome sequences from 11 cases and another subset of 2 plaque-purified IAV were included in our study. Ten whole genome sequences, including 1 plaque-purified IAV, contained at least one internal gene from endemic IAV detected within the past 3 y. Phylogenetic analysis of whole genome sequences indicated that reassortment occurred between vaccine virus and endemic field strains circulating in U.S. swine. Our data highlight the need and importance of continued IAV surveillance to detect emerging IAV with LAIV genes in the swine population.
Mitochondrial Mechanisms in Diabetic Cardiomyopathy

Mitochondrial medicine is increasingly discussed as a promising therapeutic approach, given that mitochondrial defects are thought to contribute to many prevalent diseases and their complications. In individuals with diabetes mellitus (DM), defects in mitochondrial structure and function occur in many organs throughout the body, contributing both to the pathogenesis of DM and complications of DM. Diabetic cardiomyopathy (DbCM) is increasingly recognized as an underlying cause of increased heart failure in DM, and several mitochondrial mechanisms have been proposed to contribute to the development of DbCM. Well established mechanisms include myocardial energy depletion due to impaired adenosine triphosphate (ATP) synthesis and mitochondrial uncoupling, and increased mitochondrial oxidative stress. A variety of upstream mechanisms of impaired ATP regeneration and increased mitochondrial reactive oxygen species have been proposed, and recent studies now also suggest alterations in mitochondrial dynamics and autophagy, impaired mitochondrial Ca2+ uptake, decreased cardiac adiponectin action, increased O-GlcNAcylation, and impaired activity of sirtuins to contribute to mitochondrial defects in DbCM, among others. In the current review, we present and discuss the evidence that underlies both established and recently proposed mechanisms that are thought to contribute to mitochondrial dysfunction in DbCM.