anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Background and Objectives: Neurodevelopment is a fragile brain process necessary for learning from the beginning of childhood to adulthood. During the procedure, several risks could affect it, including environmental factors such as neurotoxic chemicals or environmental pollutants and, within them, exposure to pesticides. Materials and Methods: This ecological descriptive study attempted to assess the association between environmental exposure to pesticides and neurodevelopmental disorders. This study was conducted on 4830 children diagnosed for 11 years in a total population of 119,897 children in three areas: high, medium, and low greenhouse concentrations. Results: Chromosomal abnormalities were the most common prenatal disorder (28.6%), while intrauterine physical factors were the least common (0.5%). Among perinatal diagnoses, gestational age less than 32 weeks was the most common (25%), while hyperbilirubinemia requiring exchange transfusion and birth complications was the least common (0.4%). Brain damage was the most common problem detected in postnatal diagnosis (36.7%), while unspecified postnatal abnormalities were the least common (3.1%). Conclusions: The areas with the highest greenhouse concentration had higher incidences of neurodevelopmental disorders, particularly in boys, and lower age of referral. Chromosomal abnormalities were prevalent for prenatal diagnoses, gestational age below thirty-two weeks for perinatal diagnoses, and brain damage for postnatal diagnoses. Future studies should analyze the connection between pesticide exposure and neurodevelopmental disorders using spatial point pattern analysis.
Successful intervention to support a child with congenital hearing loss requires early identification and consistent access to frequent professional services. In the early 2000s, the United States implemented an initiative, Early Hearing Detection and Intervention (EHDI), to provide timely identification and treatment of congenital hearing loss. This national program aims to screen hearing by 1 month of age, diagnose hearing loss by 3 months of age, and provide intervention to infants with hearing loss by 6 months of age. To date, the United States is successfully implementing hearing screening by 1 month of age but continually struggling to diagnose and treat congenital hearing loss promptly for many infants. This article begins by exploring the current state of American children and families, focusing on social determinants of health, specifically race and poverty. The objective is to understand how race affects social determinants of health, and ultimately hearing healthcare access for children. A narrative literature review spanning public health, sociology, and hearing research was completed to inform this work. The current body of literature supports the conclusion that race and racism, separate from poverty, lead to decreased access to pediatric hearing healthcare. Interventions targeting these issues are necessary to improve timely access to hearing loss diagnosis and treatment for American children.
FIELD: veterinary, agriculture. SUBSTANCE: composition for encapsulation of biologically active compounds for ruminant animals contains zein and stearic acid or if it is necessary it contains also ethyl cellulose as water insoluble polymer. Proposed composition contains (mass): zein 10.0-70.0, stearic acid 30.0-90.0, or it may contains (mass): zein 13.0-60.0, stearic acid 30.0-80.0, ethyl cellulose 7.0-20.0. Said composition is stable in rumen and in abomasum of animal. EFFECT: improves quality of composition. 2 cl, 2 tbl
There is currently only one method of having one's own hair on one's head. This method is the implantation of individual hair on bald skin on a person's head. My method consists of using bryophyilum pinnatum juice rubbed into the scalp, in this method, a person should rub the juice obtained from the lower leaves of bryophyilum pinnatum once a day. Effects should be visible after a month, i.e. after 30-45 days. The lower leaves of bryophyilum pinnatum can be cut and smashed into the pulp, and subsequently rubbed on the hairless scalp, and one should continue to apply this treatment every other day after the appearance of the hair. I would like to note that the juice may be rubbed into the scalp when hair starts to fall out for some reason, or when we want to have dense hair. Moreover, after each massage, the residue of bryophyilum pinnatum should be combed out and head should be washed with soap or shampoo after three hours. In this way the green hair will have its original color.
Spreading depolarizations (SDs) occur frequently in patients with malignant hemispheric stroke. In animal-based experiments, SDs have been shown to cause secondary neuronal damage and infarct expansion during the initial period of infarct progression. In contrast, the influence of SDs during the delayed period is not well characterized yet. Here, we analyzed the impact of SDs in the delayed phase after cerebral ischemia and the potential protective effect of ketamine. Focal ischemia was induced by distal occlusion of the left middle cerebral artery in C57BL6/J mice. 24 h after occlusion, SDs were measured using electrocorticography and laser-speckle imaging in three different study groups: control group without SD induction, SD induction with potassium chloride, and SD induction with potassium chloride and ketamine administration. Infarct progression was evaluated by sequential MRI scans. 24 h after occlusion, we observed spontaneous SDs with a rate of 0.33 SDs/hour which increased during potassium chloride application (3.37 SDs/hour). The analysis of the neurovascular coupling revealed prolonged hypoemic and hyperemic responses in this group. Stroke volume increased even 24 h after stroke onset in the SD-group. Ketamine treatment caused a lesser pronounced hypoemic response and prevented infarct growth in the delayed phase after experimental ischemia. Induction of SDs with potassium chloride was significantly associated with stroke progression even 24 h after stroke onset. Therefore, SD might be a significant contributor to delayed stroke progression. Ketamine might be a possible drug to prevent SD-induced delayed stroke progression.
Persistent congenital hyperinsulinism (HI) is a rare genetically heterogeneous condition characterised by dysregulated insulin secretion leading to life-threatening hypoglycaemia. For up to 50% of affected individuals screening of the known HI genes does not identify a disease-causing variant. Large deletions have previously been used to identify novel regulatory regions causing HI. Here, we used genome sequencing to search for novel large (>1 Mb) deletions in 180 probands with HI of unknown cause and replicated our findings in a large cohort of 883 genetically unsolved individuals with HI using off-target copy number variant calling from targeted gene panels. We identified overlapping heterozygous deletions in five individuals (range 3-8 Mb) spanning chromosome 20p11.2. The pancreatic beta-cell transcription factor gene, FOXA2, a known cause of HI was deleted in two of the five individuals. In the remaining three, we found a minimal deleted region of 2.4 Mb adjacent to FOXA2 that encompasses multiple non-coding regulatory elements that are in conformational contact with FOXA2. Our data suggests that the deletions in these three children may cause disease through the dysregulation of FOXA2 expression. These findings provide new insights into the regulation of FOXA2 in the beta-cell and confirm an aetiological role for chromosome 20p11.2 deletions in syndromic HI.
The invention describes a coordination polymer construct for multimodal imaging and therapy. The construct consists of a core particle made of a novel coordination polymer. The core is coated with a biocompatible coating that stabilizes the particles in a physiological environment. The biocompatible coating can contain attached targeting agents, imaging agents and therapeutic agents or combinations one or more of the targeting, imaging and therapeutic agents. When administered to a subject or a subject-derived specimen, the resulting coordination polymer core-shell construct enables multimodal imaging and therapy, which improves the diagnostic and treatment outcomes of the conditions or diseases where it is administered. The invention describes the novel material, base for the construct, methods for the preparation of the said construct and its use as a multimodal imaging and therapy agent.
Diflunisal is 2',4'-difluoro-4-hydroxy-3-biphenylcarboxylic acid. Its structural formula is:

C13H8F2O3 M.W. 250.20

Diflunisal is a stable, white to off-white, crystalline compound with a melting point of 211° to 213°C. It is practically insoluble in hexane and water. It is soluble in most organic solvents including acetone and ethyl acetate and it is slightly soluble in chloroform, carbon tetrachloride and methylene chloride.

Each diflunisal tablet intended for oral administration contains 500 mg of diflunisal. In addition, each tablet contains the following inactive ingredients: colloidal silicon dioxide, croscarmellose sodium, hypromellose, microcrystalline cellulose, pregelatinised starch and sodium stearyl fumarate. Additionally, each diflunisal tablets contain opadry blue 03B505010 which contains FD&C blue #2, FD&C yellow #6, hypromellose, polyethylene glycol and titanium dioxide.
Products and methods for treating or preventing muscular dystrophies in patients with mutations in the 5′ end of their DMD gene are provided. In some aspects, oligonucleotides, antisense phosphorodiamidate morpholino oligomers (PMO), and antisense cell penetrating peptide-conjugated PMOs (PPMOs) are provided for skipping exon 2 of the DMD gene. These oligonucleotides and oligomers can selectively suppress mutant forms of the dystrophin protein while allowing a functional form of the dystrophin protein to be expressed in sufficient quantity to retain its function in the cell. The oligonucleotides or oligomers can regulate or restore expression of transcripts of the DMD gene and a functional form of the dystrophin protein. Methods comprising administering the oligonucleotides. PMO, and PPMO targeting the DMD gene are provided. The products and methods are used for treating, ameliorating and/or preventing muscular dystrophies, such as Duchenne Muscular Dystrophy or Becker Muscular Dystrophy.
Chronic kidney disease (CKD) has reached epidemic proportions worldwide, partly due to the increasing population of elderly and obesity. Macroautophagy/autophagy counteracts CKD progression, whereas autophagy is stagnated owing to lysosomal overburden during aging and obesity, which promotes CKD progression. Therefore, for preventing CKD progression during aging and obesity, it is important to elucidate the compensation mechanisms of autophagy stagnation. We recently showed that FGF21 (fibroblast growth factor 21), which is a prolongevity and metabolic hormone, is induced by autophagy deficiency in kidney proximal tubular epithelial cells (PTECs); however, its pathophysiological role remains uncertain. Here, we investigated the interplay between FGF21 and autophagy and the direct contribution of endogenous FGF21 in the kidney during aging and obesity using PTEC-specific fgf21- and/or atg5-deficient mice at 24 months (aged) or under high-fat diet (obese) conditions. PTEC-specific FGF21 deficiency in young mice increased autophagic flux due to increased demand of autophagy, whereas fgf21-deficient aged or obese mice exacerbated autophagy stagnation due to severer lysosomal overburden caused by aberrant autophagy. FGF21 was robustly induced by autophagy deficiency, and aged or obese PTEC-specific fgf21- and atg5-double deficient mice deteriorated renal histology compared with atg5-deficient mice. Mitochondrial function was severely disturbed concomitant with exacerbated oxidative stress and downregulated TFAM (transcription factor A, mitochondrial) in double-deficient mice. These results indicate that FGF21 is robustly induced by autophagy disturbance and protects against CKD progression during aging and obesity by alleviating autophagy stagnation and maintaining mitochondrial homeostasis, which will pave the way to a novel treatment for CKD.
Patients in the KCCQ-12 arm will undergo KCCQ-12 assessment of patient-reported heart failure health status in the electronic health record at each heart failure clinic visit beginning at the start of the trial. Assessment results will be available to clinicians in the electronic health record when making treatment decisions during each clinic visit.
Microglia, resident brain immune cells, is critical in inflammation, apoptosis, neurogenesis and neurological recovery during cerebral ischemia/reperfusion (I/R) injury. Mesencephalic astrocyte-derived neurotrophic factor (MANF), a novel identified endoplasmic reticulum stress-inducible neurotrophic factor, can alleviate I/R injury by reducing the inflammatory reaction, but its specific regulatory mechanism on microglia after ischemic stroke has not been fully clarified. To mimic the process of ischemia/reperfusion in vivo and in vitro, middle cerebral artery occlusion/reperfusion (MCAO/R) was induced in C57BL/6J mice and oxygen glucose deprivation/reoxygenation (OGD/R) model was established in BV-2 cells. Moreover, MANF small interfering RNA (siRNA) was used to silence the expression of endogenous MANF, while recombination human MANF protein (rhMANF) acted as an exogenous supplement. Seventy-two hours after MCAO/R, 2,3,5-triphenyltetrazolium staining, neurological scores, brain water content, immunohistochemical staining, immunofluorescent staining, flow cytometry, hematoxylin and eosin staining, quantitative real-time PCR and western blot are applied to evaluate the protective effect and possible mechanism of MANF on cerebral I/R injury. In vitro, cell viability, inflammatory cytokines and the expression of MANF, A20, NF-κB and the markers of microglia were analyzed. The results showed that MANF decreased brain infarct volume, neurological scores, and brain water content. In addition, MANF promoted the polarization of microglia to an anti-inflammatory phenotype both in vivo and in vitro, which are related to A20/NF-κB pathway. In summary, MANF may offer novel therapeutic approaches for ischemic stroke in the process of microglia polarization.
Long non-coding RNAs (lncRNAs), defined as RNA molecules exceeding 200 nucleotides in length, have been implicated in the regulation of various biological processes and the progression of tumors. Among them, LINC00518, a recently identified lncRNA encoded by a gene located on chromosome 6p24.3, consists of three exons and is predicted to positively regulate the expression of specific genes. LINC00518 has emerged as a key oncogenic lncRNA in multiple cancer types. It exerts its tumor-promoting effects by modulating the expression of several target genes, primarily through acting as a sponge for microRNAs (miRNAs). Additionally, LINC00518 influences critical signaling pathways, including the Wnt/β-catenin, JAK/STAT, and integrin β3/FAK pathways. Elevated levels of LINC00518 in tumor tissues are associated with increased tumor size, advanced clinical stage, metastasis, and poor survival prognosis. This review provides a comprehensive summary of the genetic characteristics, expression patterns, biological functions, and underlying mechanisms of LINC00518 in human diseases.
Subjects assigned to this arm will receive 4 intravenous infusions of placebo (saline solution). Infusions will occur at day 0, 3, 7, and 10.
Multiple peptide resistance factor (MprF) confers resistance to cationic antimicrobial peptides (AMPs) in several pathogens, thereby enabling evasion of the host immune response. The role of MprF in commensals remains, however, uncharacterized. To close this knowledge gap, we used a common gut commensal of animals, Lactiplantibacillus plantarum, and its natural host, the fruit fly Drosophila melanogaster, as an experimental model to investigate the role of MprF in commensal-host interactions. The L. plantarum ΔmprF mutant that we generated exhibited deficiency in the synthesis of lysyl-phosphatidylglycerol (Lys-PG), resulting in increased negative cell surface charge and increased susceptibility to AMPs. Susceptibility to AMPs had no effect on ΔmprF mutant's ability to colonize guts of uninfected flies. However, we observed significantly reduced abundance of the ΔmprF mutant after infection-induced inflammation in the guts of wild-type flies but not of flies lacking AMPs. Additionally, we found that the ΔmprF mutant compared to wild-type L. plantarum induces a stronger intestinal immune response in flies due to the increased release of immunostimulatory peptidoglycan fragments, indicating an important role of MprF in promoting host tolerance to commensals. Our further analysis suggests that MprF-mediated lipoteichoic acid modifications are involved in host immunomodulation. Overall, our results demonstrate that MprF, besides its well-characterized role in pathogen immune evasion and virulence, is also an important commensal resilience factor.
Participants with MF regardless of spliceosome mutation status or presence of ring sideroblasts received imetelstat 9.4 mg/kg, IV as 2-hour infusion on Days 1, 8, and 15 of 21-day cycle in Cycle 1 followed by 9.4 mg/kg on Day 1 of each 21-day cycle up to 9 cycles in the Core Phase. Participants could receive imetelstat beyond Cycle 9 in the Extension Phase if they did not meet any of the withdrawal criteria, did not have disease progression and were receiving clinical benefit from treatment as determined by the investigator. Following treatment discontinuation, participants entered the Event Monitoring Phase for collection of survival status, disease status, and subsequent treatment information (Up to approximately 5.7 years).
Children will be given yogurt twice a day for four weeks. The dose for an adult is 8 ounces of yogurt twice a day. The dose will be scaled to the children based upon surface area dosing charts, but will not exceed a resistant starch load of 1 gram per year of age plus 10 grams10.
Subjects were orally administered a microdose of midazolam 75 microgram (75 μg) solution for injection, orally on Day -1, and prior receiving BI 730357 on Days 3, and 14. Subjects were orally administered BI 730357 400 mg, film-coated tablet once daily over 28 days after the intake of a standard continental breakfast.
No specific information on emergency treatment of overdosage is available for Sectral. However, overdosage with other β-blocking agents has been accompanied by extreme bradycardia, advanced atrioventricular block, intraventricular conduction defects, hypotension, severe congestive heart failure, seizures, and in susceptible patients, bronchospasm and hypoglycemia. Although specific information on the emergency treatment of Sectral overdose is not available, on the basis of the pharmacological actions and the observations in treating overdoses with other β-blockers, the following general measures should be considered:  


  1. Empty stomach by emesis or lavage.
  2. Bradycardia: IV atropine (1 to 3 mg in divided doses). If antivagal response is inadequate, administer isoproterenol cautiously since larger than usual doses of isoproterenol may be required. 
  3. Persistent hypotension in spite of correction of bradycardia: Administer vasopressor (e.g., epinephrine, levarterenol, dopamine, or dobutamine) with frequent monitoring of blood pressure and pulse rate. 
  4. Bronchospasm: A theophylline derivative, such as aminophylline and/or parenteral β2-stimulant, such as terbutaline. 
  5. Cardiac failure: Digitalize the patient and/or administer a diuretic. It has been reported that glucagon is useful in this situation. 



Sectral is dialyzable.
Group supplemented with omega-3 (4g/day) and whey protein (40g/day). All groups will undergo a training program with strength exercises for 12 weeks.
Uncontrolled hemorrhage results in various complications and is currently the leading cause of death in the general population. Traditional hemostatic methods have drawbacks that may lead to ineffective hemostasis and even the risk of secondary injury. Therefore, there is an urgent need for more effective hemostatic techniques. Polymeric hemostatic materials, particularly hydrogels, are ideal due to their biocompatibility, flexibility, absorption, and versatility. Functional hemostatic hydrogels can enhance hemostasis by creating physical circumstances conducive to hemostasis or by directly interfering with the physiological processes of hemostasis. The procoagulant principles include increasing the concentration of localized hemostatic substances or establishing a physical barrier at the physical level and intervention in blood cells or the coagulation cascade at the physiological level. Moreover, synergistic hemostasis can combine these functions. However, some hydrogels are ineffective in promoting hemostasis or have a limited application scope. These defects have impeded the advancement of hemostatic hydrogels. To provide inspiration and resources for new designs, this review provides an overview of the procoagulant principles of hemostatic hydrogels. We also discuss the challenges in developing effective hemostatic hydrogels and provide viewpoints.
A trisiloxane having at least one carbinol functional group comprises the reaction product of (A) an initial trisiloxane and (B) an organic compound. Component (A) has a pendant silicon-bonded functional group selected from a hydrogen atom, an epoxy-containing group, an ethylenically unsaturated group, and an amine group. Typically, component (A) is free of certain terminal silicon-bonded functional groups and is free of polyoxyalkylene groups. Component (B) has a functional group reactive with the pendant silicon-bonded functional group of component (A), and has at least one hydroxyl functional group. The trisiloxane is useful for a number of applications including use as a detergent additive. The trisiloxane may be of the following general formula (I): (R13SiO1/2)(R1R3SiO2/2)(R13SiO1/2) (I). In formula (I), each R1 is an independently selected hydrocarbyl group. R3 may be selected from the groups (i) to (iv) described herein. Typically, the trisiloxane has 1-6 carbinol groups.
Substantially odourless dimethyl sulphoxide (D.M.S.O.) having a U.V. absorbence at a wavelength of 290 millimicrons less than 0.10 using air as a standard is obtained by treating impure D.M.S.O. with an organic solvent selected from halogenated paraffin hydrocarbons, aromatic hydrocarbons, halogenated aromatic hydrocarbons, C1- 4 alkyl derivatives of aromatic hydrocarbons, esters and ethers, to form an organic solvent solution of D.M.S.O.; intimately contacting said organic solvent solution with water to form a uniform mixture, whereby D.M.S.O. is extracted from the organic solvent solution into the water, thereby forming an aqueous extract solution of D.M.S.O.; allowing the mixture to settle into a distinct organic solvent phase and a distinct aqueous extract phase containing D.M.S.O.; separating the aqueous extract phase from the organic solvent phase, and fractionally distilling the aqueous extract phase under conditions such that the liquid bottoms temperature does not exceed 108 DEG  C. The organic solvent is preferably employed in an amount of 1 to 10 volumes per volume of D.M.S.O. and the preferred amount of water employed is 0.25 to 3 volumes per volume of D.M.S.O. being extracted.