anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
All participants will get the Erector Spinae Plane (ESP) catheters. Prior to transfer to the operating room, participants will receive bilateral ESP catheters at T7 level under ultrasound guidance. This arm is the treatment group and will receive lidocaine via alternating side automated infusion pump bolus dosing, continued until chest tube removal or postoperative day 5 (whichever occurs earliest).
FMS predominantly affects women and is characterized by chronic widespread musculoskeletal pain, fatigue, sleep disturbance, and multiple tender points on physical examination. The pathophysiological mechanisms underlying FMS are not clearly understood, but neuroendocrine factors seem to be of major importance. Studies of familial association suggest that genetic factors play a role in FMS. This study will establish patterns of genetic linkage in families with FMS.

Participating family members will undergo a brief physical exam (including tender point exam), donate a blood sample, and complete a detailed questionnaire that includes experience with pain, fatigue, depression, bowel symptoms, headache, anxiety, and physical limitations. Measurements of serum serotonin and related compounds will also be obtained. To detect genetic factors, a genome-wide linkage scan using 405 microsatellite markers will be performed.
Patients have baseline data collected two weeks pre-intervention by assessing patient symptomatology using the dizziness handicap inventory, activities specific balance confidence questionnaires and a simulator sickness questionnaire remotely. Next, an interview will be conducted to collect information including age, sex, ethnicity, physical activity level and VR experience. Next patients will undergo 4 or 8 weeks of vestibular rehabilitation if diagnosed with unilateral or bilateral vestibular hypofunction respectively. This involves weekly 40-45 minute in-person sessions with a physiotherapist and three 20 minute sessions a day of at-home independent exercises. In addition, they will undergo an at-home regime that consists of auditory stimulation while wearing a VR headset for 20 minutes daily.
Treatment phase is divided into the "Induction Phase" and "Maintenance Phase". During the induction phase patients are treated with 1 mg/kg nivolumab and 3 mg/kg ipilimumab, during the maintenance phase with nivolumab 3 mg/kg only .
Mutations in the KCNT1 potassium channel cause severe forms of epilepsy which are poorly controlled with current treatments. In vitro studies have shown that KCNT1-epilepsy mutations are gain of function, significantly increasing K+ current amplitudes. To investigate if Drosophila can be used to model human KCNT1 epilepsy, we generated Drosophila melanogaster lines carrying human KCNT1 with the patient mutation G288S, R398Q or R928C. Expression of each mutant channel in GABAergic neurons gave a seizure phenotype which responded either positively or negatively to 5 frontline epilepsy drugs most commonly administered to patients with KCNT1-epilepsy, often with little or no improvement of seizures. Cannabidiol showed the greatest reduction of the seizure phenotype while some drugs increased the seizure phenotype. Our study shows that Drosophila has the potential to model human KCNT1- epilepsy and can be used as a tool to assess new treatments for KCNT1- epilepsy.
The study aimed to investigate the predictive value of clinical characteristics, major computed tomography angiography (CTA) indexes of carotid AS (carotid lumen stenosis and plaque burden), and inflammatory pericarotid adipose tissue for acute stroke risk in patients with a moderate or higher degree of carotid stenosis. In all, 119 patients with unilateral carotid stenosis who underwent head and neck computed tomography angiography were included and assigned to the stroke group or non-stroke group according to magnetic resonance imaging. Pericarotid adipose tissue attenuation value, net enhancement value in the base phase and the enhancement phase, and atherosclerotic features (plaque burden and lumen stenosis) were recorded. Multivariate logistic regression analysis and the operating characteristic curve (ROC) were performed to establish a predictive model for the presence of acute ischemic stroke. ROC analysis showed that pericarotid adipose tissue attenuation value and lumen stenosis were predictive factors for stroke. The AUC of pericarotid adipose tissue attenuation (PCAT) attenuation, lumen stenosis, the novel prediction model independently constructed based on PCAT attenuation, and lumen stenosis resulted in 0.838 (95% CI 0.759-0.899), 0.700 (95% CI 0.826-0.944), and 0.942 (95% CI 0.884-0.977), respectively. The model had a sensitivity and specificity of 0.909 and 0.893, respectively, when the cutoff value was 0.388. We found that the risk model combining pericarotid adipose tissue attenuation value and lumen stenosis has significant predictive values for the presence of symptomatic stroke among patients with a moderate or higher degree of carotid stenosis.
In a recent mechanistic study, octopamine was shown to promote proton transport over the branchial epithelium in green crabs, Carcinus maenas. Here, we follow up on this finding by investigating the involvement of octopamine in an environmental and physiological context that challenges acid-base homeostasis, the response to short-term high pCO2 exposure (400 Pa) in a brackish water environment. We show that hyperregulating green crabs experienced a respiratory acidosis as early as 6 h of exposure to hypercapnia, with a rise in hemolymph pCO2 accompanied by a simultaneous drop of hemolymph pH. The slightly delayed increase in hemolymph HCO3- observed after 24 h helped to restore hemolymph pH to initial values by 48 h. Circulating levels of the biogenic amine octopamine were significantly higher in short-term high pCO2 exposed crabs compared to control crabs after 48 h. Whole animal metabolic rates, intracellular levels of octopamine and cAMP, as well as branchial mitochondrial enzyme activities for complex I + III and citrate synthase were unchanged in posterior gill #7 after 48 h of hypercapnia. However, application of octopamine in gill respirometry experiments suppressed branchial metabolic rate in posterior gills of short-term high pCO2 exposed animals. Furthermore, branchial enzyme activity of cytochrome C oxidase decreased in high pCO2 exposed crabs after 48 h. Our results indicate that hyperregulating green crabs are capable of quickly counteracting a hypercapnia-induced respiratory acidosis. The role of octopamine in the acclimation of green crabs to short-term hypercapnia seems to entail the alteration of branchial metabolic pathways, possibly targeting mitochondrial cytochrome C in the gill. Our findings help advancing our current limited understanding of endocrine components in hypercapnia acclimation. SUMMARY STATEMENT: Acid-base compensation upon short-term high pCO2 exposure in hyperregulating green crabs started after 6 h and was accomplished by 48 h with the involvement of the biogenic amine octopamine, accumulation of hemolymph HCO3-, and regulation of mitochondrial complex IV (cytochrome C oxidase).
A general method is described for the design and production of a multiplicity of novel proteins. The method entails constructing a degenerate family of synthetic genes wherein each codon is chosen to specify either a polar or a non-polar amino acid, but the exact identity of the amino acid at each particular position is not specified explicitly. Thus a huge collection of different proteins can be encoded using a simple binary code of polar versus non-polar amino acids. The periodicity of the polar and non-polar amino acids in the sequence is constrained to match the natural repeat of 3.6 residues/turn in α-helices. Thus all the novel proteins are explicitly designed to have only hydrophobic amino acids in their interiors, and only hydrophilic amino acids on their surfaces. The synthetic genes encoding these novel proteins are cloned and expressed in vivo, thus giving rise to a library of novel proteins, each of which is easily purified in large quantities.
PURPOSE:To obtain the subject treating agent having low side effect on human body and high preventing effect on cystine calculus by using bucillamine or its salt known as an antirheumatic agent, a phlegm-dissolving agent, a hepatopathy suppressing agent and an anticataractous agent as an active component. CONSTITUTION:The objective agent for treating cystinuria contains bucillamine of formula or its salt (e.g. pharmacologically allowable salt of Na, K, etc.) as an active component. The compound can be administered by oral administration as well as parenteral administration. The daily dose for oral administration is usually 10-3,000mg, especially about 100-1,200mg. The compound is highly useful as an agent for treating cystinurea.
The present invention provides multimeric IL-15 soluble fusion molecules and methods of making and using the same. The present invention provides soluble fusion protein complexes having at least two soluble fusion proteins. The first fusion protein is a biologically active polypeptide covalently linked to interleukin-15 (IL-15) or a functional fragment thereof. The second fusion protein is a second biologically active polypeptide covalently linked to a soluble interleukin-15 receptor alpha (IL-15 Ra) polypeptide or a functional fragment thereof. In the complexes of the invention, one or both of the first and second fusion proteins further comprises an immunoglobulin Fc domain or a functional fragment thereof; and the first fusion protein binds to the soluble IL-15 ra domain of the second fusion protein to form a soluble fusion protein complex. The invention further provides methods of making and using the composites of the invention.
Thallium Tl-201, with a physical half-life of 72.9 hours, decays by electron capture to mercury Hg-201. Photons that are useful for detection and imaging are listed in Table 3. The lower energy x-rays obtained from the mercury Hg-201 daughter of thallium Tl-201 are recommended for myocardial imaging, because the mean percent disintegration at 68.9 to 80.3 keV is much greater than the combination of gamma-4 and gamma-6 mean percent disintegration.

Table 3. Principal Radiation Emission Data

From: Stabin MG, da Luz CQPL. New Decay Data for Internal and External Dose Assessment, 2002, Health Phys. 83(4):471-475 3.
The Erb-B2 receptor tyrosine kinase 3 (ERBB3) gene was first identified as a cause of lethal congenital contracture syndrome (OMIM 607598), while a recent study reported six additional patients carrying ERBB3 variants which exhibited distinct clinical features with evident intestinal dysmotility (OMIM 243180). The potential connection between these phenotypes remains unknown, and the ERBB3-related phenotype spectrum needs to be better characterized. Here, we described a patient presenting with a multisystemic syndrome including skip segment Hirschsprung disease, bilateral clubfoot deformity, and cardiac defect. Trio-whole exome sequencing revealed a novel compound heterozygous variant (c.1914-7C>G; c.2942_2945del) in the patient's ERBB3 gene. RT-PCR and in vitro minigene analysis demonstrated that variant c.1914-7C>G caused aberrant mRNA splicing. Both variants resulted in premature termination codon and complete loss of ERBB3 function. erbb3b knockdown in zebrafish simultaneously caused a reduction in enteric neurons in the distal intestine, craniofacial cartilage defects, and micrognathia, which phenotypically mimics ERBB3-related intestinal dysmotility and some features of lethal congenital contracture syndrome in human patients. These findings provide further patient and animal evidence supporting that ERBB3 deficiency causes a complex syndrome involving multiple systems with phenotypic variability among distinct individuals.
According to standard clinical practice related to medically assisted procreation treatments, for controlled ovarian stimulation aimed at oocyte recovery, patients underwent therapy with recombinant, biosimilar, or purified human gonadotropins and eventual suppression of spontaneous ovulation with gonadotropin-releasing hormone stimulating antagonist (gnRH-antagonist), and this information will therefore be recorded. The subsequent final induction of oocyte maturity can be by purified human chorionic gonadotropin (hCG), by gonadotropin-releasing hormone stimulating hormone analog (GnRHa), or by the combination of the two, and this information will therefore also be recorded. Similarly, therapies routinely administered for endometrial preparation and luteal support during embryo transfer procedures will also be recorded (transdermal estradiol, oral estradiol; transvaginal micronized progesterone; subcutaneous progesterone). With regard to the types of PMA used, patients may have undergone homologous or heterologous procedures based on the patient's own choice and specialist indications. The IVF technique is an in vitro fertilization that consists of the union of the egg with the sperm in the laboratory -in vitro- for the purpose of obtaining already fertilized embryos to be transferred into the maternal uterus. The ICSI technique consists of intracytoplasmic sperm injection and involves the insemination of an oocyte by micro-injection of a single sperm directly into it.
BACKGROUND: Recent evidence has demonstrated the vital roles of circular RNAs (circRNAs) in the progression of colorectal cancer (CRC); however, their functions and mechanisms in CRC need to be further explored. This study aimed to uncover the biological function of circXPO1 in CRC progression.
METHODS: CircXPO1 was identified by Sanger sequencing, RNase R, and actinomycin D treatment assays. Colony formation, scratch, transwell assays, and mouse xenograft models were adopted to evaluate CRC cell growth and metastasis in vitro and in vivo. Subcellular expression of circXPO1 was detected by FISH and nuclear-cytoplasmic separation assays. Molecular mechanisms were investigated by MeRIP, RIP, and RNA pull-down assays. Target molecular expression was detected by RT-qPCR, Western blotting and immunohistochemical staining.
RESULTS: circXPO1 was up-regulated in CRC tissues and cells, which indicated a poor prognosis of CRC patients. circXPO1 deficiency delayed the growth, EMT, and metastasis of CRC cells. Mechanistical experiments indicated that down-regulation of ALKBH5 enhanced IGF2BP2-mediated m6A modification of circXPO1 to increase circXPO1 expression. Furthermore, circXPO1 interacted with FMRP to reduce the mRNA stability of WWC2, which consequently resulted in Hippo-YAP pathway activation. Rescue experiments suggested that WWC2 overexpression abrogated circXPO1-mediated malignant capacities of CRC cells. The in vivo growth and liver metastasis of CRC cells were restrained by circXPO1 depletion or WWC2 overexpression.
CONCLUSIONS: m6A-modified circXPO1 by ALKBH5/IGF2BP2 axis destabilized WWC2 via interaction with FMRP to activate Hippo-YAP pathway, thereby facilitating CRC growth and metastasis. Targeting circXPO1 might be a potential therapeutic strategy for CRC.
all participants will be administered panss, sans, esrs, calgary, progesterom, sexual functioning scale, ham-a, covy, hamilton depression scale, and cgi and cgi improved rating on the first visit, as well as blood tests, ecg and weight. they will then be tested using a computer cognitive test (cogscan test) that lasts about 45 minutes. next, they will be given either a two week dose of placebo or treatment (2 mg \* 2 daily for first week, then 4 mg. day, 2 mg. night for the second week). after two weeks they the dose is increased to 4 mg. \* 2 daily. at four weeks all tests are readministered, as well as at six weeks. the study is concluded at 6 weeks, following a readministration of tests. physical examination is also administered at the conclusion.
There continues to be great interest and public health relevance with regard to understanding the neurobiological systems that underlie the comorbidity of substance use disorders and other psychiatric conditions. In a previous award, efforts were focused upon characterizing the neural circuitry underlying moral decision making in incarcerated men with varying levels of two frequently co-occurring conditions: stimulant abuse and psychopathy. Here this work will be extended to incarcerated women, to examine longitudinal outcomes and apply state-of-the-art network analyses for predictive models. Prior studies have demonstrated sex differences in the degree and expression of psychopathic traits, patterns of stimulant abuse, and moral decision-making. However, the neural circuitry that underlies these sex differences is not well understood. Substantial sex differences in regional gray matter volume and density in extant samples have also been identified. Collectively, sex differences in pathophysiology could have significant implications for treatment strategies and differential biomarkers of treatment prediction and outcome in men and women. The investigators will implement the research strategy with a large incarcerated population by deploying a unique mobile MRI scanner to the regional women's prison. Participants will be stratified by level of lifetime stimulant (cocaine, amphetamine) use severity and psychopathic traits (high, medium, low) and will undergo anatomical and functional MRI scanning while completing multi-modal (i.e., linguistic and picture) decision-making tasks. Results will be compared to those obtained in a prior award (incarcerated men, n\>300). Functional network and dynamic network connectivity will also be examined in women using a new multiband echo planar imaging (EPI) pulse sequence, and longitudinal outcomes after release to the community will be collected to test behavioral and neuropredictive models of relapse and future antisocial behavior. This work is expected to generate a large, robust dataset that characterizes the overlapping and unique aspects of neural circuitry underlying stimulant use and psychopathy in females and males. The proposed research is in line with recent priorities emphasized by the National Institute on Drug Abuse (NIDA) for projects aimed at examining male-female differences, and effects specific to females, to improve understanding of the nature and etiology of drug abuse.
Unhealthy behaviors such as overeating and a sedentary lifestyle are largely responsible for overweight and obesity which substantially increase risk for chronic conditions such as heart disease, high blood pressure, stroke, diabetes, arthritis and certain cancers. The rapid rise in obesity threatens to reverse recent gains in life expectancy and account for a large percentage of premature deaths in the U.S. Although there is evidence for the short-term efficacy of a number of methods for initiating health behavior change to lose weight, these interventions have shown only limited ability to affect significant, long-term behavioral changes in the majority of adults. In part this may be because they fail to adequately address how psychological factors that lead to relapse to unhealthy behaviors and failure to maintain long-term behavior change.

The purpose of the study is to understand brain changes that accompany participation in programs that foster healthy behaviors in people seeking to maintain weight loss. We will use MRI scans to study brain function in men and women 25-60 years old who have lost weight in the last year without surgery. Participants will be assigned to one of two programs to help them maintain weight loss and will be compensated for their time. Our goal is to gain a better understanding of the brain changes that lead to long-term success in keeping weight off, in the hope that this knowledge will assist in the development of improved treatments.
DS-5565 10mg/day, administered in 2 doses. Treatment period: 1 week titration and 6 weeks of fixed dose.
A first embodiment is a specific plasmid vector, pDIP/PyCSP.1, into which nucleotides encoding the targets of specific immune responses are inserted. These targets include, but are not limited to proteins and peptides. These plasmid constructs are incorporated in a composition comprising a suitable and acceptable art recognized pharmaceutical reagent that is benign (non-reactive with) to the plasmid construct. The plasmid construct provides protective immune responses to the disease associated with the selected targets. A second embodiment is a construct having, at a minimum, the nucleotide sequences encoding one or more Plasmodium species proteins in a pharmaceutically acceptable vector. a third embodiment is a method of controlling malaria in mammals comprising injecting a polynucleotide delivery vector into a mammal.
The invention relates to a medicine for aversion to cold, body pain, vomiting and dysentery, in particular to an oral liquid for vomiting and diarrhea. Provides a medicine for treating dysentery by inducing sweat to relieve exterior syndrome and promoting the production of body fluid. The oral liquid for treating vomiting and diarrhea comprises Glycyrrhrizae radix, Zingiberis rhizoma, ramulus Cinnamomi, fructus Jujubae, radix Puerariae, herba Ephedrae, radix Paeoniae, semen Armeniacae amarum, fructus forsythiae, and radix Aconiti lateralis. 9 g of liquorice, 9 g of dried ginger, 3 g of peeled cassia twig, 12 Chinese dates, 12 g of kudzu root, 2 g of Chinese ephedra without knots, 6 g of Chinese herbaceous peony, 3 g of almond without peel tips, and 3 g of forsythia and monkshood respectively. The preparation method comprises the steps of boiling ephedra and kudzuvine root with 2000 ml of water, reducing the volume to 400 ml, removing white foam, adding other medicines, boiling to 600 ml, and removing residues. The liquid medicine is vacuum-packed for 15 milliliters each time, 15 milliliters each time and three times a day. By adopting the method, the vomiting and diarrhea dysentery can be effectively treated by inducing sweat to relieve exterior syndrome and promoting the production of body fluid.
Parkinson's disease (PD) is associated with the development of psychosis (PDP), including hallucinations and delusions, in more than half of the patient population. Optimal PD management must therefore involve considerations about both motor and non-motor symptoms. Often, clinicians fail to diagnosis psychosis in patients with PD and, when it is recognized, treat it suboptimally, despite the availability of multiple interventions. In this paper, we provide a summary of the current guidelines and clinical evidence for treating PDP with antipsychotics. We also provide recommendations for diagnosis and follow-up. Finally, an updated treatment algorithm for PDP that incorporates the use of pimavanserin, the only US FDA-approved drug for the treatment of PDP, was developed by extrapolating from a limited evidence base to bridge to clinical practice using expert opinion and experience. Because pimavanserin is only approved for the treatment of PDP in the US, in other parts of the world other recommendations and algorithms must be considered.