anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
NEW MATERIAL:A lectin separated from the extracted liquid of human placenta and having the following properties. Molecular weight, 30,000+ or -3,000 (gel- filtration) and 15,000+ or -1,500 (SDS-PAGE method); pH stability, stable at pH >=9; thermal stability, stable at 56 deg.C for 30min; enzyme stability, unstable to trypsin; activity to bind with concanavalin, negative; sugar-binding specificity, positive to galactose; physiological activity, positive to hemagglutination activity; amino acid composition, shown in the table. USE:Biochemical or pharmacological reagent and medicine. PREPARATION:Minced human placenta is homogenated in a buffer solution and the obtained extract liquid is subjected e.g. to gel-filtration. The objective fraction is made to contact with an immobilized lactose and the eluted objective fraction is purified by high-performance liquid chromatography.
This investigational new drug application describes a proposed phase I/II study designed to assess the safety and efficacy of AdV-tk gene therapy in combination with standard brachytherapy for patients with locally recurrent prostate cancer after having failed radiation as a primary treatment with or without minimal metastasis. These patients do not have any standard treatment that has been demonstrated to have a high degree of efficacy in eradicating the tumor with a reasonable degree of safety. Thus, the potential risks associated with the use of gene therapy in this group would appear reasonable. This application is for use of a replication defective adenovirus vector (ADV/RSV-tk) delivering the HSV-tk gene as a biologic vector for gene therapy.

Direct introduction of therapeutic genes into malignant cells in vivo may provide an effective treatment of solid tumors such as prostate cancer. The herpes simplex virus thymidine kinase (HSV-tk) gene codes for an enzyme which phosphorylates the nucleoside analog ganciclovir (GCV) into an intermediate that is incorporated into newly synthesized DNA and terminates further replication, leading to cell death. Since normal mammalian cells do not possess this enzyme, cytotoxicity depends on the successful introduction and expression of the HSV-tk gene, phosphorylation of ganciclovir and synthesis of DNA. Non-dividing cells may express HSV-tk and phosphorylate ganciclovir but are not harmed since they do not synthesize DNA. This approach is especially suitable for the treatment of tumors where rapidly dividing tumor cells are adjacent to tissues made up largely of non-proliferating cells. Using human and animal models for prostate cancer we have demonstrated that adenovirus-mediated transfer of the HSV-tk gene resulted in sensitivity to ganciclovir in vitro and growth suppression of mouse prostate cancer in vivo.
Adverse reactions observed with terbutaline sulfate injection are similar to those commonly seen with other sympathomimetic agents. All these reactions are transient in nature and usually do not require treatment.

The following table compares adverse reactions seen in patients treated with terbutaline sulfate injection (0.25 mg and 0.5 mg), with those seen in patients treated with epinephrine injection (0.25 mg and 0.5 mg), during eight double-blind crossover studies involving a total of 214 patients. 

Note: Some patients received more than one dosage strength of terbutaline sulfate and epinephrine. In addition, there were reports of anxiety, muscle cramps, and dry mouth (< 0.5%). There have been rare reports of elevations in liver enzymes and of hypersensitivity vasculitis with terbutaline administration.

To report SUSPECTED ADVERSE REACTIONS, contact Hikma Pharmaceuticals USA Inc.. at 1-877-233-2001, or the FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
Valsartan can cause fetal harm when administered to a pregnant woman. Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue valsartan as soon as possible. [see Use in Specific Populations (8.1)].
Cryoglobulinemia are responsible for systemic vasculitis, and the most frequently targeted organs are the skin, joints, kidneys and peripheral nervous system. Cryoglobulinemia vasculitis are associated with significant morbidity and mortality, and require therapeutic intervention. Management of non-infectious mixed cryoglobulinemia vasculitis is based on corticosteroids, plasma exchange, and/or immunosuppressants. These treatments are associated with frequent side effects. To date, no study has evaluated the efficacy and safety of these different therapeutic options, explaining the lack of recommendations.

Rituximab, a monoclonal antibody directed against CD20, has emerged as a novel therapeutic option in B-cell related disorders. Data from the French AutoImmunity and Rituximab (AIR) registry recently reported the positive effect of rituximab in non-infectious mixed cryoglobulinemia vasculitis. More recently, the multidisciplinary national French CryoVas survey also suggested a significant superiority of the combination corticosteroid plus rituximab compared to the corticosteroids alone in terms of complete clinical and immunological responses and corticosteroid sparing. However, no randomized controlled data addressing this issue has been published to date.
Abstract of the disclosure:        The invention relates to a non-toxic conjugate vaccine against infections by Gram-negative bacteria, composed of a species-specific polysaccharide and a protein which are covalently linked together, it being characteristic of the vaccine that the polysaccharide originates from the endotoxin of the bacterium and the protein is an exoprotein.   The vaccines according to the invention are, in particular, vaccines against infections by Pseudomonas aeruginosa or Escherichia coli.        The exoprotein is, in particular, an exotoxin or exotoxoid, preferably toxin A from Pseudomonas aeru-ginosa, but also a tetanus toxoid or diphtheria toxoid.        The process for the preparation of the new con-jugate vaccine against infections by Gram-negative bacteria comprises covalent linkage of an appropriate polysaccharide from the endotoxin of the bacterium with an exoprotein.        However, the invention also relates to a con-jugate vaccine composed of a mixture of 3-15 conjugates whose polysaccharide have (sic) been obtained from 3-15 different serotypes of the same species of bacteria.        The invention further relates to a polyvalent vaccine composed of a mixture of conjugate vaccines, each of whose individual components raises antibodies against a particular species of bacteria. The invention further relates to the use of the new conjugate vaccines for the preparation of hyper-immune sera which in turn are used for the preparation of immunoglobulin which can be administered intra-venously or intramuscularly.
Penicillin G is bactericidal against penicillin-susceptible microorganisms during the stage of active multiplication. It acts by inhibiting biosynthesis of cell-wall mucopeptide. It is not active against the penicillinase-producing bacteria, which include many strains of staphylococci. Penicillin G is highly active in vitro against staphylococci (except penicillinase-producing strains), streptococci (groups A, B, C, G, H, L and M), pneumococci and Nelsseria meningitidis. Other organisms susceptible in vitro to penicillin G are Nelsseria gonorrhoeae, Corynebacterium diphtheriae, Bacillus anthracis, clostridia, Actinomyces species, Spirillum minus, Streptobacillus monillformis, Listeria monocytogenes, and leptospira; Treponema pallidum is extremely susceptible.

Some species of gram-negative bacilli were previously considered susceptible to very high intravenous doses of penicillin G (up to 80 million units/day) including some strains of Escherichia coli, Proteus mirabilis, salmonella, shigella, Enterobacter aerogenes (formerly Aerobacter aerogenes) and Alcaligenes faecalis. Penicillin G is no longer considered a drug of choice for infections caused by these organisms.

Susceptibility Testing

For specific information regarding susceptibility test interpretive criteria and associated test methods and quality control standards recognized by FDA for this drug, please see: https://www.fda.gov/STIC.
Maternal sleep deprivation (MSD) has emerged as a significant public health concern, yet its effects on offspring metabolism remain poorly understood. This study investigated the metabolomic implications of MSD on offspring cognitive development, with a particular focus on alterations in glutamate metabolism. Pregnant rats were subjected to sleep deprivation during late gestation. Plasma and brain samples from their offspring were collected at different postnatal days (P1, P7, P14, and P56) and analyzed using untargeted metabolomics with liquid chromatography-mass spectrometry. Metabolomic analysis revealed significant differences in various amino acids, including L-glutamate, L-phenylalanine, L-tyrosine, and L-tryptophan, which are crucial for cognitive function. Subsequent differential analysis and partial least squares discriminant analysis (sPLS-DA) demonstrated a gradual reduction in these metabolic differences in the brain as the offspring underwent growth and development. KEGG pathway analysis revealed differential regulation of several pathways, including alanine, aspartate, and glutamate metabolism, glutathione metabolism, arginine biosynthesis, aminoacyl-tRNA biosynthesis, histidine metabolism, and taurine and hypotaurine metabolism, at different developmental stages. Mantel and Spearman analyses indicated that the observed changes in metabolites in MSD progeny may be related to various gut microbes, Ruminococcus_1, Ruminococcaceae_UCG-005, and Eubacterium_coprostanoligenes_group. Biochemical assays further demonstrated developmental changes in the L-glutamate metabolic pathway. Collectively, these findings suggest that MSD not only affects maternal well-being but also has enduring metabolic consequences for offspring, particularly impacting pathways linked to cognitive function. This highlights the importance of addressing maternal sleep health to mitigate potential long-term consequences for offspring.
This study will test the effectiveness of an emotional processing intervention in individuals with MS in a double blind placebo controlled randomized clinical trial RCT). We will utilize an intervention which has been successfully used in other populations, including Schizophrenia and Traumatic Brain Injury. Our pilot data shows that this intervention is effective in individuals with MS, as well.

All participants will undergo a baseline evaluation assessing emotional processing abilities, cognitive functioning, and psychological functioning. Participants will then be randomized into two groups. During the treatment phase, the experimental group will receive the proposed intervention while the control group will receive a "placebo" treatment. Neuropsychological assessment will be repeated at the end of the intervention.
Prednisolone is a synthetic adrenocortical steroid drug with predominantly glucocorticoid properties. Some of these properties reproduce the physiological actions of endogenous glucocorticosteroids, but others do not necessarily reflect any of the adrenal hormones' normal functions; they are seen only after administration of large therapeutic doses of the drug. The pharmacological effects of prednisolone which are due to its glucocorticoid properties include: promotion of gluconeogenesis; increased deposition of glycogen in the liver; inhibition of the utilization of glucose; anti-insulin activity; increased catabolism of protein; increased lipolysis; stimulation of fat synthesis and storage; increased glomerular filtration rate and resulting increase in urinary excretion of urate (creatinine excretion remains unchanged); and increased calcium excretion. Depressed production of eosinophils and lymphocytes occurs, but erythropoiesis and production of polymorphonuclear leukocytes are stimulated. Inflammatory processes (edema, fibrin deposition, capillary dilatation, migration of leukocytes and phagocytosis) and the later stages of wound healing (capillary proliferation, deposition of collagen, cicatrization) are inhibited. Prednisolone can stimulate secretion of various components of gastric juice. Suppression of the production of corticotropin may lead to suppression of endogenous corticosteroids. Prednisolone has slight mineralocorticoid activity, whereby entry of sodium into cells and loss of intracellular potassium is stimulated. This is particularly evident in the kidney, where rapid ion exchange leads to sodium retention and hypertension.
PURPOSE:To obtain a bile extract-containing composition containing soft anhydrous silicic anhydride or water-containing silicon dioxide, reduced in fishy taste and bitter taste and capable of readily orally administering. CONSTITUTION:1 pts.wt. of a bile extract is blended with 1-5 pts.wt. soft silicic anhydride or water-containing silicon dioxide. A solvent (e.g. ethanol) is added thereto and kneaded, and then the solvent is removed to provide the objective product. The solvent is added to an amount of 1.5-5 pts.wt. based on 1 pt.wt. soft silicic anhydride or water-containing silicon dioxide. The composition is useful as a cholagogue drug and gallstone-dissolving agent and can be prepared in powery preparation, tablet, capsule, etc., by adding vehicles, disintegrators, binders, lubricants, etc., to the composition according to ordinary method.
Reduced glutathione (GSH) is widely used as an antioxidant in clinical practice, but whether GSH affects the development of early lung cancer remains unclear. Herein, we investigated the mechanism underlying the anticancer effect of GSH in patients with pulmonary nodules. Thirty patients with pulmonary nodules were treated with GSH intravenously for 10 days at a dose of 1.8 g/d, followed by oral administration of the drug at a dose of 0.4 g three times daily for 6 months. The results showed that GSH treatment promoted nodule absorption and reduced the IL-6 level in the peripheral blood of the patients. GSH reduced IL-6 expression in inflammatory BEAS-2B and lung cancer cells and inhibited the proliferation of lung cancer cell lines in vitro. In addition, GSH reduced IL-6 expression by decreasing ROS via down-regulating PI3K/AKT/FoxO pathways. Finally, GSH reversed the Warburg effect, restored mitochondrial function, and reduced the IL-6 expression via PI3K/AKT/FoxO pathways. The in vivo experiment confirmed that GSH inhibited lung cancer growth, improved mitochondrial function, and reduced the IL-6 expression by regulating key enzymes via the PI3K/AKT/FoxO pathway. In conclusion, we uncovered that GSH exerts an unprecedentedly potent anti-cancer effect to prevent the transformation of lung nodules to lung cancer by improving the mitochondrial function and suppressing inflammation via PI3K/AKT/FoxO pathway. This investigation innovatively positions GSH as a potentially safe and efficacious old drug with new uses, inhibiting inflammation and early lung cancer. The use of the drug offers a promising preventive strategy when administered during the early stages of lung cancer.
BACKGROUND AND AIMS: Mast cell-derived heparin proteoglycans (HEP-PG) can be mimicked by bioconjugates carrying antithrombotic and anti-inflammatory properties. The dual antiplatelet and anticoagulant (APAC) construct administered, either locally or intravenously (i.v.), targets activated endothelium, its adhesion molecules, and subendothelial matrix proteins, all relevant to atherogenesis. We hypothesized that APAC influences cellular interactions in atherosclerotic lesion development and studied APAC treatment during the initiation and progression of experimental atherosclerosis.
METHODS: Male western-type diet-fed Apoe-/- mice were equipped with perivascular carotid artery collars to induce local atherosclerosis. In this model, mRNA expression of adhesion molecules including ICAM-1, VCAM-1, P-Selectin, and Platelet Factor 4 (PF4) are upregulated upon lesion development. From day 1 (prevention) or from 2.5 weeks after lesion initiation (treatment), mice were administered 0.2 mg/kg APAC i.v. or control vehicle three times weekly for 2.5 weeks. At week 5 after collar placement, mice were sacrificed, and lesion morphology was microscopically assessed.
RESULTS: APAC treatment did not affect body weight or plasma total cholesterol levels during the experiments. In the prevention setting, APAC reduced carotid artery plaque size and volume by over 50 %, aligning with decreased plaque macrophage area and collagen content. During the treatment setting, APAC reduced macrophage accumulation and necrotic core content, and improved markers of plaque stability.
CONCLUSIONS: APAC effectively reduced early atherosclerotic lesion development and improved markers of plaque inflammation in advanced atherosclerosis. Thus, APAC may have potential to alleviate the progression of atherosclerosis.
A monofocal IOL (TECNIS ZCB00, ZCT150 or ZCT225 or AcrySof IQ SA60WF, SA6AT3 or SA6AT4) implanted in the first eye. The AcuFocus IC-8 IOL implanted in the second eye.
The present invention relates to anti-adhesion hyaluronic acid gel with iron ions and medicines after an operation and belongs to a novel anti-adhesion agent. The present invention has very wide application to the field of preventing tissue adhesion after a surgical operation. The present invention is characterized in that under an acid condition, hyaluronic acid and iron chloride are mixed so that iron ions and the hyaluronic acid are sufficiently crosslinked; by forming ferrum-crosslinked transparent acid derivate, the molecular weight of the hyaluronic acid is increased and the degradation period of the hyaluronic acid is prolonged. Then, organic macromolecules for eliminating collagen synthesis are added to further reinforce the anti-adhesion effect of material. The anti-adhesion agent prepared by the present invention has good biocompatibility and long residence time in a body, can effectively prevent adhesion after a surgical operation and can be automatically degraded in a body without the need of taking the anti-adhesion agent out. A product after degradation has no harm to a human body.
The ARX mutations encompass a nearly continuous spectrum of neurodevelopmental disorders (NDDs), ranging from lissencephaly to Proud syndrome, as well as infantile spasms without brain malformations, and including both syndromic and non-syndromic intellectual disabilities (IDs). We describe worsening neuropsychiatric symptoms in the offspring of a Korean family with ID/developmental delay (DD) caused by a novel ARX p.Lys385Ter variant. Sequential genetic testing was performed to investigate the ID, DD, agenesis of the corpus callosum (ACC), and developmental epileptic encephalopathy (DEE) observed in the proband. A comprehensive trio clinical exome sequencing approach using a Celemics G-Mendeliome Clinical Exome Sequencing Panel was employed. Given the clinical manifestations observed in the proband, gene panel sequencing identified a heterozygous ARX variant, c.1153A>T/p.Lys385Ter (Reference transcript ID: NM_139058.3), as the most likely cause of ID, DD, ACC, and DEE in the proband. Sanger sequencing confirmed the segregation of the ARX variant, c.1153A>T/p.Lys385Ter, with the phenotype and established the maternally inherited dominant status of the heterozygous variant in the patient, as well as in her grandmother, mother, and aunt. Our case report adds to the understanding of the female phenotype in ARX-related disorders caused by loss-of-function variants in the ARX gene. Genetic counseling for ARX families should proceed with caution, as female carriers can exhibit a wide range of phenotypes, from normal cognitive development to ID/DD, ACC, and DEE.
The purpose of this study is to measure blood levels of proglumide after a single oral dose (400 mg) over a period of time and compare the blood levels to those with normal hepatic function (N=4) to determine if there is delayed metabolism and clearance of proglumide in those with hepatic impairment (HI) (N=8). Eligible subjects will provide a baseline blood and urine sample prior to ingesting proglumide 400 mg po. Blood will be collected from an intravenous catheter after ingestion at the following intervals: 1 hr, 3 hrs, 5 hrs, 7 hrs and 24 hr (± 4-5 hours). After 3 hrs and 5 hrs subjects will provide a urine sample. Samples will be analyzed by Mass Spectometry. Proglumide blood and urine levels in ng/ml will be plotted over time and the Cmax (peak plasma concentration), Tmax (time to reach Cmax) and T1/2 (elimination half time) calculated for each subject and compared to that of 4 healthy controls.
Skeletal muscle atrophy impairs quality of life and increases the risk of disease, but current methods for assessment of muscle mass have several limitations. We here investigated the urinary concentration of a fragment of the muscle protein titin as a potential biomarker for the early detection of skeletal muscle atrophy. Four mouse models with different atrophy pathways were studied: those of cardiotoxin-induced acute muscle injury, cast-induced muscle immobilization, lipopolysaccharide-induced sepsis, and streptozotocin-induced diabetes. In all four models, urinary titin levels increased early, concurrent with or preceding upregulation of the atrophy-related genes for atrogin-1 and MuRF-1. The increase in the urinary titin concentration was thus associated with initial muscle damage and the onset of proteolysis, rather than with late-stage muscle wasting. Our findings suggest that urinary titin is a promising biomarker for detection of the onset of skeletal muscle catabolism and prediction of the subsequent development of atrophy in different catabolic states. Noninvasive measurement of urinary titin may therefore allow the earlier detection of skeletal muscle proteolysis compared with conventional techniques.
The present study is designed to evaluate the nanotherapeutic efficacy of prepared PLGA-loaded Nedaplatin (PLGA-NDP) against 7,12-dimethyl benz(a)anthracene (DMBA)-induced experimental oral carcinogenesis in hamster buccal pouch (HBP) model. The buccal pouch of golden Syrian hamsters was painted with 0.5% DMBA in liquid paraffin three times a week for 14 weeks, ultimately leading to the development of oral squamous cell carcinoma (OSCC). Oral administration of PLGA-NDP (preinitiation) and Cisplatin delivery (5 mg/kg b.wt) started 1 week before the carcinogen exposure and continued on alternative days. Post-administration of PLGA-NDP (5 mg/kg b.wt) started 2 days after carcinogen (DMBA) induction until the end of the experiment. After the 14th week, we observed that DMBA-painted hamsters exhibited tumor formation, morphological alterations, and well-differentiated OSSC in addition to the responsive molecular proteins during oral carcinogenesis. Furthermore, immunoblotting analysis demonstrated that PLGA-NDP inhibits Notch signaling, as evidenced by downregulation of Bcl-Xl, Bcl-2, p21, PGE2, HGF, and CXCL12 proteins, and upregulation of p53 and Bax. This apoptotic response is crucial for PLGA-NDP to induce apoptosis. In addition, RT-PCR results showed that PLGA-NDP nanoparticles play a downregulatory role in the therapeutic action of the notch signaling gene (Notch1, Notch 2, Hes1, Hey1, and Jagged1) at the mRNA transcription level in HBP carcinoma. Taken together, these data indicate that PLGA-NDP is a potent inhibitor of oral carcinogenesis and the expansion of cells that specifically target the Notch signaling pathway indicates that obstructing Notch signaling could potentially serve as a new and innovative therapeutic approach for oral squamous cell carcinoma (OSCC).