Miracle-dz/UniFAR-FTUs huggingface dataset:
BIOLOGICAL EVALUATION OF PROBIOTIC FERMENTED MILK (RAYEB) ON OBESE RATS

Probiotics have been widely explored in food processing, production, research and disease prevention, therefore, the present study was conducted to evaluate the biological evaluation of probiotic fermented milk (Rayeb) on obese rats for 8 weeks. The rats (n=35) were classified into 5 groups, as follows: Group (1): fed on basal diet and kept as negative control group. While the rats (n= 28) were fed on high fat diet for four weeks to induce obesity then were divided into four groups, group (2) was fed on high fat diet only and served as control positive group. Groups (3 and 4): obese rats were fed on high fat diet and were given orally 1 ml of fermented milk “Rayeb” and Vitamin D at 600 IU/Kg BW respectively. Group (5): was fed on basal diet and was given orally a mixture of (1 ml of Rayeb and Vitamin D at 600 IU/Kg BW). The results indicated that, the supplementation with fermented milk (Rayeb), vitamin D or their mixture significantly decreased (P<0.05) the final body weight compared to the positive control group by 26.27%, 21.84%, 30.03%, respectively due to lowering the feed intake and the feed efficiency ratio of the obese rats. Moreover, the concentration of leptin hormone as well as the percent of peritoneal fat bad were significantly lowered (P<0.05) for all treated groups. It was observed that, the supplementation with the tested food materials improved the liver and kidney functions as well as lipid profile of the obese rats. It could be concluded that, fermented milk (Rayeb), vitamin D or their mixture might be useful in weight reduction.
(Lack of) knowledge of mothers about sickle cell trait and disease: a qualitative study.

OBJECTIVE to analyze the understanding of mothers about sickle cell disease and/or trait of the family from a diagnosed child. METHODS this is a qualitative study, using a semi-structured interview with 23 mothers, at a sickle cell disease outpatient clinic of a public institution, from October to December 2017. Analysis was thematic. RESULTS all participants had sickle cell trait as well as the parents of their children. Twenty children were diagnosed with sickle cell disease by Heel Prick Test, and three, after hospitalization due to the disease. Most did not know how to report the presence of the trait or disease in relatives other than nuclear. FINAL CONSIDERATIONS diagnosis cannot be restricted to the result of neonatal screening, requiring that preventive information on sickle cell crises be reinforced. It is recommended to search for other affected relatives to learn about their genetic condition, reflecting on their reproductive decisions.
Emotional Analysis of Bogus Statistics in Social Media

Fake info or bogus statistics is a new term and it is now considered as a greatest threat to democracy. Since the world is full of surprises and humans have developed their delicate nature to detect unexcepted information. Social media plays a vital role in information spreading, since the impact towards fake information has gained more attention due to the social media platforms. Trending the hot topic without analyzing the information will introduce great impact over millions of people. So, it is essential to analyze the message and its truthfulness. Emotional analysis is an important factor in bogus statistics as the information gets reshared among other based on individual emotions. Considering these facts in social media information analysis, an efficient emotional analysis for bogus statistics in social media is proposed in this research work using recurrent neural network. In an emotional perspective, fake messages are compared with actual message and false messages are identified experimentally using recurrent neural network.
The role of sialic acid-binding immunoglobulin-like-lectin-1 (siglec-1) in immunology and infectious disease

Abstract Siglec-1, also known as Sialoadhesin (Sn) and CD169 is highly conserved among vertebrates and with 17 immunoglobulin-like domains is Siglec-1 the largest member of the Siglec family. Expression of Siglec-1 is found primarily on dendritic cells (DCs), macrophages and interferon induced monocyte. The structure of Siglec-1 is unique among siglecs and its function as a receptor is also different compared to other receptors in this class as it contains the most extracellular domains out of all the siglecs. However, the ability of Siglec-1 to internalize antigens and to pass them on to lymphocytes by allowing dendritic cells and macrophages to act as antigen presenting cells, is the main reason that has granted Siglec-1’s key role in multiple human disease states including atherosclerosis, coronary artery disease, autoimmune diseases, cell-cell signaling, immunology, and more importantly bacterial and viral infections. Enveloped viruses for example have been shown to manipulate Siglec-1 to increase their virulence by binding to sialic acids present on the virus glycoproteins allowing them to spread or evade immune response. Siglec-1 mediates dissemination of HIV-1 in activated tissues enhancing viral spread via infection of DC/T-cell synapses. Overall, the ability of Siglec-1 to bind a variety of target cells within the immune system such as erythrocytes, B-cells, CD8+ granulocytes and NK cells, highlights that Siglec-1 is a unique player in these essential processes. Graphical Abstract
Temporal Alterations to Central Auditory Processing without Synaptopathy after Lifetime Exposure to Environmental Noise.

People are increasingly exposed to environmental noise through the cumulation of occupational and recreational activities, which is considered harmless to the auditory system, if the sound intensity remains <80 dB. However, recent evidence of noise-induced peripheral synaptic damage and central reorganizations in the auditory cortex, despite normal audiometry results, has cast doubt on the innocuousness of lifetime exposure to environmental noise. We addressed this issue by exposing adult rats to realistic and nontraumatic environmental noise, within the daily permissible noise exposure limit for humans (80 dB sound pressure level, 8 h/day) for between 3 and 18 months. We found that temporary hearing loss could be detected after 6 months of daily exposure, without leading to permanent hearing loss or to missing synaptic ribbons in cochlear hair cells. The degraded temporal representation of sounds in the auditory cortex after 18 months of exposure was very different from the effects observed after only 3 months of exposure, suggesting that modifications to the neural code continue throughout a lifetime of exposure to noise.
Two distinct Sertoli cell states are regulated via germ cell crosstalk†

Abstract Sertoli cells are a critical component of the testis environment for their role in maintaining seminiferous tubule structure, establishing the blood-testis barrier, and nourishing maturing germ cells in a specialized niche. This study sought to uncover how Sertoli cells are regulated in the testis environment via germ cell crosstalk in the mouse. We found two major clusters of Sertoli cells as defined by their transcriptomes in Stages VII–VIII of the seminiferous epithelium and a cluster for all other stages. Additionally, we examined transcriptomes of germ cell-deficient testes and found that these existed in a state independent of either of the germ cell-sufficient clusters. Altogether, we highlight two main transcriptional states of Sertoli cells in an unperturbed testis environment, and a germ cell-deficient environment does not allow normal Sertoli cell transcriptome cycling and results in a state unique from either of those seen in Sertoli cells from a germ cell-sufficient environment. Summary sentence Sertoli cells exist in one of two main states and require germ cell crosstalk for normal spermatogenic cycling. Graphical Abstract
Mobile microscopy and telemedicine platform assisted by deep learning for the quantification of Trichuris trichiura infection

Soil-transmitted helminths (STH) are the most prevalent pathogens among the group of neglected tropical diseases (NTDs). Kato-Katz technique is the diagnosis method recommended by WHO and although is generally more sensitive than other microscopic methods in high transmission settings, it often presents a decreased sensitivity in low transmission settings and it is labour intensive. Digitizing the samples could provide a solution which allows to store the samples in a digital database and perform remote analysis. Artificial intelligence methods based on digitized samples can support diagnostics efforts by support diagnostics efforts by performing an automatic and objective quantification of disease infection. In this work, we propose an end-to-end pipeline for microscopy image digitization and automatic analysis of digitized images of soil-transmitted helminths. Our solution includes (1) a digitalization system based on a mobile app that digitizes the microscope samples using a low-cost 3D-printed microscope adapter, (2) a telemedicine platform for remote analysis and labelling and (3) novel deep learning algorithms for automatic assessment and quantification of parasitological infection of STH. This work has been evaluated by comparing the STH quantification using both a manual remote analysis based on the digitized images and the AI-assisted quantification against the reference method based on conventional microscopy. The deep learning algorithm has been trained and tested on 41 slides of stool samples containing 949 eggs from 6 different subjects using a cross-validation strategy obtaining a mean precision of 98,44% and mean recall of 80,94%. The results also proved the potential of generalization capability of the method at identifying different types of helminth eggs. In conclusion, this work has presented a comprehensive pipeline using smartphone-based microscopy integrated with a telemedicine platform for automatic image analysis and quantification of STH infection using artificial intelligence models.
Hallmarks of RET and Co-occuring Genomic Alterations in RET-aberrant Cancers

Activating receptor-tyrosine kinase rearranged during transfection (RET) mutations and fusions are potent drivers of oncogenesis. The recent FDA approvals of highly potent and selective RET inhibitors, selpercatinib and pralsetinib, has altered the therapeutic management of RET aberrant tumors. There is ample evidence of the role of RET signaling in certain cancers. RET aberrations as fusions or mutations occur in multiple cancers, however, there is considerable phenotypic diversity. There is emerging data on the lack of responsiveness of immunotherapy in RET-altered cancers. Herein, we review the registrational data from the selective RET-inhibitor trials, and comprehensively explore RET alterations in pan-cancer adult malignancies and their co-alterations. These co-occuring alterations may define the future of RET inhibition from specific selective targeting to customized combination therapies as data are rapidly emerging on both on-target and off-target acquired resistance mechanisms. Fascinatingly, oncogenic RET fusions have been reported to mediate resistance to EGFR inhibition and KRASG12C inhibition.
Adjunctive Rifampicin Increases Antibiotic Efficacy in Group A Streptococcal Tissue Infection Models

Biofilm has recently been highlighted as a complicating feature of necrotizing soft tissue infections (NSTI) caused by Streptococcus pyogenes (i.e., group A Streptococcus [GAS]) contributing to a persistence of bacteria in tissue despite prolonged antibiotic therapy. Here, we assessed the standard treatment of benzylpenicillin and clindamycin with or without rifampin in a tissue-like setting. ABSTRACT Biofilm has recently been highlighted as a complicating feature of necrotizing soft tissue infections (NSTI) caused by Streptococcus pyogenes (i.e., group A Streptococcus [GAS]) contributing to a persistence of bacteria in tissue despite prolonged antibiotic therapy. Here, we assessed the standard treatment of benzylpenicillin and clindamycin with or without rifampin in a tissue-like setting. Antibiotic efficacy was evaluated by CFU determination in a human organotypic skin model infected for 24 or 48 h with GAS strains isolated from NSTI patients. Antibiotic effect was also evaluated by microcalorimetric metabolic assessment in in vitro infections of cellular monolayers providing continuous measurements over time. Adjunctive rifampin resulted in enhanced antibiotic efficacy of bacterial clearance in an organotypic skin tissue model, 97.5% versus 93.9% (P = 0.006). Through microcalorimetric measurements, adjunctive rifampin resulted in decreased metabolic activity and extended lag phase for all clinical GAS strains tested (P < 0.05). In addition, a case report is presented of adjunctive rifampin treatment in an NSTI case with persistent GAS tissue infection. The findings of this study demonstrate that adjunctive rifampin enhances clearance of GAS biofilm in an in vitro tissue infection model.
Estrogen-related receptor γ2 controls NaCl uptake to maintain ionic homeostasis.

Estrogen-related receptors (ERRs) are known to function in mammalian kidney as key regulators of ion transport-related genes; however, a comprehensive understanding of the physiological functions of ERRs in vertebrate body fluid ionic homeostasis is still elusive. Here, we used medaka (Oryzias melastigma), a euryhaline teleost, to investigate how ERRs are involved in ion regulation. After transferring medaka from hypertonic seawater to hypotonic freshwater (FW), the mRNA expression levels of errγ2 were highly upregulated, suggesting that ERRγ2 may play a crucial role in ion uptake. In situ hybridization and immunofluorescence staining showed that errγ2 was specifically expressed in ionocytes, the cells responsible for Na+/Cl- transport. In normal FW, ERRγ2 morpholino knockdown caused reductions in the mRNA expression of Na+/Cl- cotransporter (NCC), the number of NCC ionocytes, Na+/Cl- influxes of ionocytes, and whole-body Na+/Cl- contents. In FW with low Na+ and low Cl-, the expression levels of mRNA for Na+/H+ exchanger 3 (NHE3) and NCC were both decreased in ERRγ2 morphants. Treating embryos with DY131, an agonist of ERRγ, increased the whole-body Na+/Cl- contents and ncc mRNA expression in ERRγ2 morphants. As such, medaka ERRγ2 may control Na+/Cl- uptake by regulating ncc and/or nhe3 mRNA expression and ionocyte number, and these regulatory actions may be subtly adjusted depending on internal and external ion concentrations. These findings not only provide new insights into the underpinning mechanism of actions of ERRs, but also enhance our understanding of their roles in body fluid ionic homeostasis for adaptation to changing environments during vertebrate evolution.
Atorvastatin inhibited TNF-α induced matrix degradation in rat nucleus pulposus cells by suppressing NLRP3 inflammasome activity and inducing autophagy through NF-κB signaling

ABSTRACT Intervertebral disc degeneration (IDD) is one of the main causes of lower back pain (LBP). It results from an imbalance between the degradation and synthesis of extracellular matrix (ECM) components in nucleus pulposus (NP) cells. Atorvastatin, an HMG-CoA reductase inhibitor, plays a vital role in many diseases, such as cardiovascular disease and osteoarthritis. However, the effect of atorvastatin on IDD is unclear. Herein, we demonstrated that atorvastatin affects matrix degradation induced by TNF-α and demonstrated the mechanism by which TNF-α modulates matrix metabolism in rat NP cells. Real-time PCR, western blotting and immunofluorescence staining were performed to detect the mRNA and protein expression of related genes. mRFP-GFP-LC3 adenovirus plasmid transfection and transmission electron microscopy (TEM) were used to detect cell autophagy. NLRP3 inhibitor and lentiviral vectors containing shRNA-NLRP3 were used to show the effect of NLRP3 on autophagic flux and the NF-κB signaling pathway. The results revealed that atorvastatin might suppress matrix degradation induced by TNF-α by suppressing NLRP3 inflammasome activity and inducing autophagic flux. Moreover, atorvastatin suppressed NF-κB signaling induced by TNF-α. NF-κB signaling inhibition suppressed NLRP3 inflammasome activity, and NLRP3 inhibition suppressed NF-κB signaling activation induced by TNF-α. NLRP3 inhibition or NLRP3 knockdown induced autophagic flux in the presence of TNF-α. Overall, the present study demonstrated that atorvastatin might suppress matrix degradation induced by TNF-α and further revealed the crosstalk among NLRP3 inflammasome activity, autophagy and NF-κB signaling.
The Nt17 domain and its helical conformation regulate the aggregation, cellular properties and neurotoxicity of mutant huntingtin exon 1

Converging evidence points to the N-terminal domain comprising the first 17 amino acids of the Huntingtin protein (Nt17) as a key regulator of its aggregation, cellular properties and toxicity. In this study, we further investigated the interplay between Nt17 and the polyQ domain repeat length in regulating the aggregation and inclusion formation of exon 1 of the Huntingtin protein (Httex1). In addition, we investigated the effect of removing Nt17 or modulating its local structure on the membrane interactions, neuronal uptake, and toxicity of monomeric or fibrillar Httex1. Our results show that the polyQ and Nt17 domains synergistically modulate the aggregation propensity of Httex1 and that the Nt17 domain plays an important role in shaping the surface properties of mutant Httex1 fibrils and regulating their poly-Q-dependent growth, lateral association and neuronal uptake. Removal of Nt17 or disruption of its transient helical conformations slowed the aggregation of monomeric Httex1 in vitro, reduced inclusion formation in cells, enhanced the neuronal uptake and nuclear accumulation of monomeric Httex1 proteins, and was sufficient to prevent cell death induced by Httex1 72Q overexpression. Finally, we demonstrate that the uptake of Httex1 fibrils into primary neurons and the resulting toxicity are strongly influenced by mutations and phosphorylation events that influence the local helical propensity of Nt17. Altogether, our results demonstrate that the Nt17 domain serves as one of the key master regulators of Htt aggregation, internalization, and toxicity and represents an attractive target for inhibiting Htt aggregate formation, inclusion formation, and neuronal toxicity. Highlights The Nt17 and polyQ domains synergistically promote Httex1 aggregation. The Nt17 domain is a key determinant of the lateral association and morphology of fibrils. The Nt17 domain and conformation regulate the nuclear/cytoplasmic distribution and toxicity of Httex1. Nt17 conformation is a key determinant of Httex1 fibril membrane interaction and cellular uptake. Nt17 serves as one of the master regulators of Httex1 aggregation, cellular uptake and toxicity. Graphical abstract The Nt17 domain: A master switch of Httex1 aggregation, uptake, subcellular localization and neurotoxicity. In this paper, we showed that 1) the Nt17 and polyQ domains synergistically promote Httex1 aggregation; 2) the Nt17 domain is a key determinant of the lateral association and morphology of fibrils in vitro, 3) Nt17 conformation is a key determinant of Httex1 fibril membrane interaction and cellular uptake in primary neurons; 4) the Nt17 domain and conformation regulate the nuclear/cytoplasmic distribution and toxicity of Httex1 in primary neurons. The figure was created with Biorender and https://www.vectorstock. com/royalty-free-vector/icon-on-and-off-toggle-switch-button-white-design-vector-30148026
IGSF11 is required for pericentric heterochromatin dissociation during meiotic diplotene

Meiosis initiation and progression are regulated by both germ cells and gonadal somatic cells. However, little is known about what genes or proteins connecting somatic and germ cells are required for this regulation. Our results show that deficiency for adhesion molecule IGSF11, which is expressed in both Sertoli cells and germ cells, leads to male infertility in mice. Combining a new meiotic fluorescent reporter system with testicular cell transplantation, we demonstrated that IGSF11 is required in both somatic cells and spermatogenic cells for primary spermatocyte development. In the absence of IGSF11, spermatocytes proceed through pachytene, but the pericentric heterochromatin of nonhomologous chromosomes remains inappropriately clustered from late pachytene onward, resulting in undissolved interchromosomal interactions. Hi-C analysis reveals elevated levels of interchromosomal interactions occurring mostly at the chromosome ends. Collectively, our data elucidates that IGSF11 in somatic cells and germ cells is required for pericentric heterochromatin dissociation during diplotene in mouse primary spermatocytes.
NEAT1/miR-146a-3p/TrkB/ShcB axis regulates the development and function of chondrocyte

ABSTRACT The current study aimed to explored the regulatory effect of Tropomyosin-related kinases B (TrkB) in the development and function of chondrocyte. Correlation between clinicopathological characteristics and osteoarthritis (OA) were analyzed. The expressions of TrkA, brain-derived neurotrophic factor (BDNF), TrkB, Src homolog and collagen homolog B (ShcB), and ShcC in OA cartilage tissue and IL-1β-stimulated chondrocytes from normal cartilage were determined by Western blot/qRT-PCR. After manipulating the expressions of TrkA, shTrkB, ShcB, miR-146a-3p and nuclear paraspeckle assembly transcript 1 (NEAT1), the differentiation-related molecules, and apoptosis-related molecules were examined by Western blot/qRT-PCR, and migration, invasion, proliferation, tube formation, and apoptosis rate in IL-1β-stimulated chondrocyte were examined by scratch, Transwell, colony formation, and tube formation, and flow cytometry assays, respectively. Bioinformatics, dual-luciferase and Spearman were used to analyze the binding and correlation of target genes. The findings showed that OA was related to body mass Index (BMI). The expressions of TrkA, TrkB and ShcB and NEAT1 were up-regulated in OA and IL-1β-stimulated chondrocytes, while miR-146a-3p was donwnregulated and was negatively correlated with TrkB or NEAT1. NEAT1 competed with TrkB in chondrocytes for miR-146a-3p binding. ShTrkB reversed the decrease in expressions of differentiation-related molecules, migration, invasion and proliferation, and the increase in ShcB expression and tube formation, of IL-1β-stimulated chondrocytes. Overexpressed ShcB reversed effect of shTrkB on the functions of IL-1β-stimulated chondrocytes. MiR-146a-3p inhibitor reversed effects of shTrkB on the function and apoptosis-related molecules on IL-1β-stimulated chondrocytes, while NEAT1 reversed role of miR-146a-3p. This paper demonstrated that NEAT1/miR-146a-3p/TrkB/ShcB axis regulates the development and function of chondrocyte.
Study of the flue gas characteristics and gasification reaction of pulverized coal combustion in O2/CO2/H2O atmosphere

ABSTRACT The impacts of O2 and H2O on the combustion characteristics of pulverized coal in O2/CO2/H2O atmosphere were studied. The gasification reaction ratio was calculated from the components of flue gas. The competition exists between C-CO2 and C-H2O reactions under rich CO2 atmosphere. At various H2O concentrations, the differences were found in generation amounts of CO and H2 in flue gas. At O2 concentrations <10%, C-CO2 reaction decreased while C-H2O reaction increased with increasing H2O concentration; while at O2 concentration >30%, H2O showed no obvious specific patterns of effects. The gasification ratio was reduced as coal ranks increase.