anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
An extensive effort has been mounted to understand the neurobiologic mechanisms involved in the development and persistence of cocaine addiction and tendency to relapse. Although the last two decades have resulted in an explosion in our understanding of the biological mechanisms of reward, establishing the relevance of this knowledge to the addictive process has been problematic. Most importantly, this information has been of limited utility in offering new pharmacologic treatment approaches to addicted patients - particularly those with cocaine addiction. Over the past 15 years our laboratory has published multiple studies using pharmacologic probes to explore the biologic underpinnings of cocaine addiction using single photon emissions computerized tomography (SPECT) technology. More recently, however, functional magnetic resonance imaging (fMRI) has offered several advantages over SPECT and is now a favored approach, e.g. fMRI allows the continuous measurement of neural responses rather than a very limited time period with SPECT (1-3 minutes every 48 hours). Using fMRI \[including both ASL (Arterial Spin Labeling) and fcMRI (functional connectivity\], the neural response can be measured throughout the 60 min that follows infusion, allowing identification and capture of the maximal brain response period that may occur at any time during this 60 min. In the proposed study, we will assess the brain response to two of the probes (scopolamine and lidocaine) we have previously studied with SPECT.
Patients receive cemiplimab IV over 30 minutes on day 1. Treatment repeats every 21 days for up to 3 cycles (or up to 4 cycles for patients whose disease is unresectable after 3 cycles) in the absence of disease progression or unacceptable toxicity. Within 6 weeks of last dose of therapy, patients with potentially resectable tumors undergo surgical resection.
The invention relates to a method for measuring and calculating definite gray scale based on disease standard mortality. First, determining a standard mortality rate of a target disease; and collecting the diagnosis cases and death cases reported daily in the target area. And secondly, accumulating the diagnosis cases and the death cases reported every day to obtain accumulated diagnosis cases and accumulated death cases. The regional diagnostic grayscale is then estimated based on the standard mortality, the accumulated diagnostic cases, and the accumulated mortality cases. And finally, estimating the actual cumulative number of infected people in the target area according to the confirmed diagnosis gray level and the cumulative confirmed diagnosis case data. The method mainly explains the situation that the mortality rate of a disease in various areas or countries is greatly different, estimates the actual epidemic situation of the disease through the actual accumulated infection situation, and is convenient for timely and reasonable taking preventive measures.
A system and a method for facilitating payment requests within a health care network are disclosed. The method includes providing a patient interface connected to the health care network. Further, a non-patient interface connected to the health care network is provided. The method further includes receiving a payment request from a payment sender for making a payment to a payment receiver. The payment sender is one and the payment receiver is another of patients and non-patients. Thereafter, the payment request is processed based on at least one of an authentication of the payment receiver and payment details stored in a blockchain database.
Complement component 3 (C3) deficiency has recently been reported as one of the novel causes of constipation. To identify a unique gene specific to constipation caused by C3 deficiency, the total RNA extracted from the mid colon of C3 knockout (C3 KO) mice was hybridized to oligonucleotide microarrays, and the function of the candidate gene was verified in in vitro and in vivo models. C3 KO mice used for microarrays showed definite phenotypes of constipation. Overall, compared to the wild type (WT), 1237 genes were upregulated, and 1292 genes were downregulated in the C3 KO mice. Of these, the major genes included were lysine (K)-specific demethylase 5D (KDM5D), olfactory receptor 870 (Olfr870), pancreatic lipase (PNLIP), and alkaline phosphatase intestinal (ALPI). Specifically, the ALPI gene was selected as a novel gene candidate based on alterations during loperamide (Lop)-induced constipation and intestinal bowel disease (IBD). The upregulation of ALPI expression treated with acetate recovered the expression level of mucin-related genes in primary epithelial cells of C3 KO mice as well as most phenotypes of constipation in C3 KO mice. These results indicate that ALPI plays an important role as the novel gene associated with C3 deficiency-induced constipation.
A method of setting up a wearable user device to allow a user to scan products and obtain product recommendations based on the user's personal biological/genetic data, using a cartridge to perform a test on the user's personal biological/genetic data via a desktop test control system into which the cartridge is plugged. A user account is associated with a cartridge ID read from the cartridge. The cartridge ID is also read using the wearable user device and passed to the server when the wearable user device is coupled to the test control system, associating the test with the user account. The test control system communicates test results to the server which analyses the test results to generate analysis results. The analysis results are then downloaded to the wearable user device. Product codes are also downloaded to the wearable user device, and stored in association with the product codes.
The invention provides a cell tag comprising an extracellular region, a transmembrane region and optionally an intracellular region. The extracellular region comprises an IL5 receptor alpha (IL 5 Ra) sequence linked to a transmembrane domain, and the recombinant polypeptide is unable to play a role in signal transduction. The cell tag can be operably linked to a transgene. The expression of the cell tag allows identification, detection, selection and ablation of cells expressing the transgene and the cell tag. In some embodiments, the genetically modified host cell comprises a transgene comprising a polynucleotide encoding a chimeric antigen receptor comprising a ligand binding domain and a polynucleotide encoding a cell tag. Pharmaceutical formulations produced by the method and methods of using the pharmaceutical formulations are also described.
The present invention relates to novel therapeutic and diagnostic dendrimer based modular platforms (e.g., drug delivery platforms). In particular, the dendrimer based modular platforms are configured such that two or more dendrimers (e.g., PAMAM dendrimers) are coupled together (e.g., via a cycloaddition reaction) wherein each of the coupled dendrimers is functionalized (e.g., functionalized for targeting, imaging, sensing, and/or providing a therapeutic or diagnostic material and/or monitoring response to therapy). In some embodiments, the present invention provides dendrimer based modular platforms having coupled dendrimers (e.g., two or more coupled dendrimers) wherein each dendrimer is conjugated to one or more functional groups (e.g., therapeutic agent, imaging agent, targeting agent, triggering agent) (e.g., for specific targeting and/or therapeutic use of the dendrimer based modular platform). In some embodiments, the functional groups are conjugated to the dendrimers via a linker and/or a triggering agent. In addition, the present invention is directed to methods of synthesizing dendrimer based modular platforms, compositions comprising the dendrimer based modular platforms, as well as systems and methods utilizing the dendrimer based modular platforms (e.g., in diagnostic and/or therapeutic settings (e.g., for the delivery of therapeutics, imaging, and/or targeting agents (e.g., in disease (e.g., cancer) diagnosis and/or therapy, etc.)).
Compositions and methods are provided for the modulation of abnormal expression of beta-amyloid. Oligonucleotides are provided which are specifically hybridizable with RNA or DNA encoding beta-amyloid. Oligonucleotides specifically hybridizable with a translation initiation site, codon 717, codon 670 or codon 671 of betaAPP are provided. Such oligonucleotides can be used for diagnostics as well as for research purposes. Methods are also disclosed for modulating beta-amyloid expression in cells and tissues using the oligonucleotides provided, and for specific modulation of expression of the mutant betaAPP gene. Methods for diagnosis, detection and treatment of diseases associated with abnormal betaAPP expression are also disclosed.
Dosage adjustment for patients taking iloperidone tablets concomitantly with potential CYP2D6 inhibitors: Iloperidone tablet dose should be reduced by one-half when administered concomitantly with strong CYP2D6 inhibitors such as fluoxetine or paroxetine. When the CYP2D6 inhibitor is withdrawn from the combination therapy, iloperidone tablet dose should then be increased to where it was before [see Drug Interactions (7)].

Dosage adjustment for patients taking iloperidone tablets concomitantly with potential CYP3A4 inhibitors: Iloperidone tablet dose should be reduced by one-half when administered concomitantly with strong CYP3A4 inhibitors such as ketoconazole or clarithromycin. When the CYP3A4 inhibitor is withdrawn from the combination therapy, iloperidone tablet dose should be increased to where it was before [see Drug Interactions (7)].

Dosage adjustment for patients taking iloperidone tablets who are poor metabolizers of CYP2D6: Iloperidone tablet dose should be reduced by one-half for poor metabolizers of CYP2D6 [see Clinical Pharmacology (12.3)].

Hepatic Impairment: No dose adjustment to iloperidone tablets is needed in patients with mild hepatic impairment. Patients with moderate hepatic impairment may require dose reduction, if clinically indicated. Iloperidone tablets are not recommended for patients with severe hepatic impairment [see Use in Specific Populations (8.6)].
The goal is to challenge metabolically healthy human subjects with a high-calorie, Western diet for 8 weeks to identify the metabolite(s) responsible for monocyte priming and use redox proteomics, RNAseq and Chipseq to determine the genes and pathways involved in monocyte priming in humans. To reflect some key components of the typical Western intake, the Study Team will compose the diet to be high in saturated fat (15% of total energy intake) and fructose (14% of total energy intake) with excess energy intake that is 25% higher than estimated total energy expenditure. A total of 30 participants, including 15 men and 15 women, will complete a run-in phase where weight stability will be achieved on the control diet. After weight is stabilized during the run-in period, participants will enter the experimental phase of the dietary intervention, where overfeeding will begin with additional calories provided by the key nutrients as noted above. Participants will be monitored throughout the feeding trial. After completion of the 8-week overfeeding period, individuals will be allowed to return to a normal dietary intake. All study participants will be given access to counseling for weight reduction should it be needed following the overfeeding period.
There are epidemiological associations between obesity and type 2 diabetes, cardiovascular disease and Alzheimer's disease. The role of amyloid beta 42 (Aβ42) in these diverse chronic diseases is obscure. Here we show that adipose tissue releases Aβ42, which is increased from adipose tissue of male mice with obesity and is associated with higher plasma Aβ42. Increasing circulating Aβ42 levels in male mice without obesity has no effect on systemic glucose homeostasis but has obesity-like effects on the heart, including reduced cardiac glucose clearance and impaired cardiac function. The closely related Aβ40 isoform does not have these same effects on the heart. Administration of an Aβ-neutralising antibody prevents obesity-induced cardiac dysfunction and hypertrophy. Furthermore, Aβ-neutralising antibody administration in established obesity prevents further deterioration of cardiac function. Multi-contrast transcriptomic analyses reveal that Aβ42 impacts pathways of mitochondrial metabolism and exposure of cardiomyocytes to Aβ42 inhibits mitochondrial complex I. These data reveal a role for systemic Aβ42 in the development of cardiac disease in obesity and suggest that therapeutics designed for Alzheimer's disease could be effective in combating obesity-induced heart failure.
Participants will undergo 10 days of unilateral immobilization whereby a leg will remain in 60 degrees of flexion with the use of a brace. All participants will complete this protocol.
Nostoc formulations, dietary supplements comprising the Nostoc formulations, and food products comprising Nostoc commune, (also known as Nostoc sphaericum, or Nostoc commune var. sphaericum) are disclosed. Nostoc formulations that may additionally comprise a medicinal composition are described. The present invention further relates to processes for producing these Nostoc formulations. In addition, the present invention relates to methods for promoting the health of an individual utilizing the Nostoc formulations, dietary supplements, food products and/or pharmacological compositions of the present invention. Moreover, this invention provides a method for cultivating Nostoc commune comprising (a). isolating and purifying Nostoc commune; (b). culturing the Nostoc commune; and (c). conditions suitable for optimal growth of Nostoc commune.
Uric acid in mammalian subjects is reduced and excretion of uric acid is increased by administering a compound of Formula (I) or a pharmaceutically acceptable salt thereof. In Formula (I) m is 0, 1, 2, 3 or 4; n is 0 or 1; m + n is not more than 4; t is 0 or 1; q is 0 or 1; and r is 0, 1 or 2. R6 is hydrogen, methyl or ethyl and R12 is hydrogen or methyl, or R6 is hydroxy and R12 is hydrogen, or R6 is O and R12 is absent, or R6 and R12 together are -CH2CH2-. R7 is hydrogen or alkyl having from 1 to 3 carbon atoms. One of R8 and R9 is alkyl having from 1 to 3 carbon atoms, and the other is hydrogen or alkyl having from 1 to 3 carbon atoms. R10 is hydrogen, halo, alkyl having from 1 to 3 carbon atoms or alkoxy having from 1 to 3 carbon atoms. X is C(O) and r is 0 and t is 0; or X is NH(R11) wherein R11 is hydrogen or alkyl having from 1 to 3 carbon atoms. A is phenyl, unsubstituted or substituted by 1 or 2 groups selected from halo, hydroxy, methyl, ethyl, perfluoromethyl, methoxy, ethoxy, and perfluoromethoxy; or a 5 or 6 membered heteroaromatic ring having 1 or 2 ring heteroatoms selected from N, S and O and the heteroaromatic ring is covalently bound to the remainder of the compound of Formula (I) by a ring carbon; or cycloalkyl having from 3 to 6 ring carbon atoms wherein the cycloalkyl is unsubstituted or one or two ring carbons are independently monosubstituted by methyl or ethyl. The uric acid-lowering effects of the Compounds of Formula (I) are used to treat or prevent a variety of conditions including gout, hyperuricemia, elevated levels of uric acid that do not meet the levels customarily justifying a diagnosis of hyperuricemia, renal dysfunction, kidney stones, cardiovascular disease, risk for developing cardiovascular disease, tumor-lysis syndrome, and cognitive impairment.
Multi-drug resistant superbugs are a persistent problem in modern health care. This invention provides an antimicrobial endolysin-Lysostaphin triple fusion protein, comprising (1) an endolysin CHAP endopeptidase domain, (2) an endolysin amidase domain, and (3) a Lysostaphin glycyl-glycine endopeptidase domain. The domains are derived from two proteins that show antimicrobial synergy when used in combination. The protein has specificity and exolytic activity for the peptidoglycan cell wall of untreated, live  Staphylococcus aureus  from many growth phases i.e. stationary, logarithmic and biofilm growth. The recombinant triple fusion protein comprising the three functional antimicrobial domains is designed to be refractory to resistance development.
Cancer stem cells (CSCs) represent a small yet pivotal subset of tumor cells endowed with self-renewal capabilities. These cells are intricately linked to tumor progression and are central to drug resistance, metastasis, and recurrence. The tumor microenvironment (TME) encompasses the cancer cells and their surrounding milieu, including immune and inflammatory cells, cancer-associated fibroblasts, adjacent stromal tissues, tumor vasculature, and a variety of cytokines and chemokines. Within the TME, cells such as immune and inflammatory cells, endothelial cells, adipocytes, and fibroblasts release growth factors, cytokines, chemokines, and exosomes, which can either sustain or disrupt CSCs, thereby influencing tumor progression. Conversely, CSCs can also secrete cytokines, chemokines, and exosomes, affecting various components of the TME. Exosomes, a subset of extracellular vesicles (EVs), carry a complex cargo of nucleic acids, proteins, and lipids, playing a crucial role in the communication between CSCs and the TME. This review primarily focuses on the impact of exosomes secreted by CSCs (CSC-exo) on tumor progression, including their roles in maintaining stemness, promoting angiogenesis, facilitating metastasis, inducing immune suppression, and contributing to drug resistance. Additionally, we discuss how exosomes secreted by different cells within the TME affect CSCs. Finally, we explore the potential of utilizing exosomes to mitigate the detrimental effects of CSCs or to target and eliminate them. A thorough understanding of the exosome-mediated crosstalk between CSCs and the TME could provide valuable insights for developing targeted therapies against CSCs.
The investigators have conducted a randomized, triple-blind, cross-over study in 15 healthy human volunteers to investigate the absorption and metabolism of cocoa flavanols from a high-flavanol chocolate made with added sugar and a high-flavanol chocolate containing the sugar substitute maltitol; a nutrient-matched low flavanol control product was also fed. All products were matched for macro-nutrients, as well as for alkaloids (theobromine and caffeine), and were similar in taste and appearance. Both high-flavanol products contained \~259 mg cocoa flavanols, whilst the low-flavanol chocolate contained 48 mg of cocoa flavanols. On each study day, subjects were cannulated and baseline blood samples were collected prior to consumption of any of the test chocolates. Additional blood samples were collected at 1, 2 and 4 hours and plasma levels of flavanols were assessed using HPLC with fluorescence detection. All test products were well-tolerated by study participants.
We present a case of a man in his 70s who presented with worsening rectal and back pain associated with weight loss, dyspnoea and brownish discolouration of urine. Physical examination noted abdominal distention and epigastric tenderness. Laboratory investigations revealed acute kidney injury, hyperkalaemia, hyperphosphataemia and hyperuricaemia. Contrast CT of the abdomen/pelvis showed multiple, low-density masses throughout the liver, suspicious for metastatic disease. Oesophagogastroduodenoscopy demonstrated a large, fungating, infiltrative and ulcerated mass in the gastric body and lesser curvature of the stomach. Surgical pathology confirmed invasive moderately differentiated gastric adenocarcinoma. He met both the laboratory and clinical criteria for spontaneous tumour lysis syndrome (STLS) as per the Cairo-Bishop criteria. He was managed with aggressive fluid hydration, rasburicase and allopurinol, resulting in improvement in his renal function and laboratory findings. STLS of solid organ tumours, especially gastric adenocarcinoma, is rare and requires early detection with timely management to ensure favourable outcomes.
Understanding the molecular underpinnings of neurodegeneration processes is a pressing challenge for medicine and neurobiology. Alzheimer's disease (AD) and Parkinson's disease (PD) represent the most prevalent forms of neurodegeneration. To date, a substantial body of experimental evidence has strongly implicated hypoxia in the pathogenesis of numerous neurological disorders, including AD, PD, and other age-related neurodegenerative conditions. Hypoxia-inducible factor (HIF) is a transcription factor that triggers a cell survival program in conditions of oxygen deprivation. The involvement of HIF-1α in neurodegenerative processes presents a complex and sometimes contradictory picture. This review aims to elucidate the current understanding of the interplay between hypoxia and the development of AD and PD, assess the involvement of HIF-1 in their pathogenesis, and summarize promising therapeutic approaches centered on modulating the activity of the HIF-1 complex.
Sulphamoyl benzoic acid derivs. of formula (I) are prepd. by reacting a sulphamoyl benzoic acid deriv. of formula (II) or its reactive deriv. with a piperazine deriv. of formula (III) in the presence of a condensing agent. In the formulas, R1 is Cl or phonoxy; R2 is H, halogen, lower alkyl, lower alkoxy or methylenedioxy. (I) have a saluretic, uricosuric and hypotensive activity.
Acne vulgaris is one of the most prevalent skin disorders of sebaceous follicles, affecting more than 85% of adolescents in United States. Acne can persist throughout the adulthood, and even a mild form of acne might progress to permanent scarring on the face, chest and back, thereby causing significant physical and psychosocial morbidities. Acne is a multifactorial disease of which etiology has not been fully elucidated, although considerable progress has been made in understanding its pathogenesis during last decade. The major pathogenic features of acne include abnormal ductal keratinization, sebum overproduction, Propionibacterium acnes, and inflammation. Common acne medications such as topical retinoids, antibiotics and isotretinoin are associated with irritation and incomplete responses, increased bacterial resistance or untoward side events, respectively. Thus there is a continuing need for a novel, effective agent targeting different aspects of acne pathogenesis, with minimal side effects.

In the recent decade, epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent in green tea, has attracted much interest on account of its potent anti-carcinogenic, anti-inflammatory, anti-proliferative, and antimicrobial activities. Preclinical, observational, and clinical trial data have indicated that EGCG can inhibit tumor initiation, promotion, progression, and angiogenesis. EGCG also suppresses neutrophil chemotaxis, and has been suggested to improve many diseases that have inflammatory components such as diabetes, kidney injuries, arthritis, allergies, dental caries, cardiovascular, gastrointestinal, and neurodegenerative diseases. In skin, EGCG has been investigated mainly in light of antioxidative, immunopotentiating and anticarcinogenic properties against chemicals or ultraviolet irradiation. Moreover, EGCG has lipid-lowering and antiandrogenic properties, and can downregulate peroxisome proliferator-activated receptor-γ expression. Based on these observations, it can be inferred that EGCG might be effective in the treatment of acne.