anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
If eligible, assigned to this arm and without contraindications to prasugrel administration, patients will receive a loading dose of prasugrel (60 mg) via nasogastric tube as soon as possible after arrival at the emergency department. Afterwards a 30 micrograms (mcg)/kg iv bolus of cangrelor followed immediately by a 4 mcg/kg/min iv infusion (lasting for at least 2 hours or for the duration of the revascularization procedure, whichever is longer) will be administered.
FIELD: cosmetology. SUBSTANCE: pomade has perfume and castor oil, lanolin, beeswax, paraffin, ceresine and perfume agent and, additionally, olive oil, butyl stearate, terlan, carnauba and candellil waxes, candy fat, Tween-60 or Tween-80 or sorbitanoleate, antal "СУ", larch galipot, and bioactive addition that involves sodium foscarnet, or acyclovir, or enzyme RNAase and pot-marigold or celandine oily extract. Oil is heated to 70-80 C and waxes, ceresine, paraffin, terlan, lanolin, fat, butyl stearate, antal "СУ" were added at stirring. Stirring is carried out before additional substance mixture formation. Then temperature is decreased to 40-50 C and larch galipot and bioactive addition were added to mixture but preliminary bioactive addition is activated: dry sodium foscarnet milled up to particle size 0.1-3 mc; or acyclovir or enzyme RNAase were mixed with surface-active substance and medicinal plants oily extract. Mixture is stirred thoroughly up to formation of homogeneous substance as microcapsules, then beeswax is added, stirred repeatedly and heated gradually to 80 C. Dry antiviral substance and sodium foscarnet were milled by ultrasonic oscillation at power 200 db for 5 min. Antiviral substance, surface-active substances and medicinal plant oily extracts were mixed for 1-2 h. Pomade can be used for influenza A prophylaxis. EFFECT: improved method of preparing, prolonged antiviral and antiherpetic activity.
The present invention is concerned with the use of a compound of formula (I): Ar-Y-Q, wherein Ar is either (i) furyl, thienyl, thienyl 1,1-dioxide, pyrryl, pyridyl, benzofuryl, benzothienyl, benzothienyl 1,1-dioxide, indolyl, naphthyl, quinolyl, or tetrahydronaphthyl, any of which is optionally substituted by one or more substituents independently selected from C1-4 alkyl (which may itself optionally be substituted by one or more halogen atoms), C1-4 alkoxy, halo, nitro, amino, carboxy, C1-4 alkoxycarbonyl and hydroxy, or (ii) phenyl optionally substituted by one or more substituents independently selected from phenyl (which is itself optionally substituted by one or more substituents independently selected from those optional substituents specified in (i) above) and those specified as optional substituents in (i) above; Y is C1-10 alkylene or C2-10 alkenylene; Q is formula (II), where R1 is hydrogen, C¿1-4? alkyl, a group as defined for Ar above, or a group of formula -N(R?4)R5¿ wherein R4 is hydrogen or C¿1-4? alkyl and R?5¿ is hydrogen, C¿1-4? alkyl, or phenyl optionally substituted by one or more substituents independently selected from those specified as optional substituents in (i) above; and R?2¿ is hydrogen, C¿1-4? alkyl, amino, C1-4 alkylamino, di-C1-4 alkylamino, C5-7 cycloalkylamino, C5-7 cycloalkyl(C1-4 alkyl)-amino, anilino, N-C1-4 alkylanilino, or a group as defined for Ar above; or a physiologically acceptable base salt or physiologically functional derivative thereof; in the manufacture of a medicament for the prophylaxis and treatment of conditions for which inhibition of the oxidative modification of lipids is indicated, for example, atherosclerosis. The medicaments obtained thereby and their preparation and use in the prophylaxis and treatment of the aforementioned conditions are also within the scope of the invention.
A drug-formulating method, a drug commercial-distribution method, and a drug formulation improve safety of a drug that is at risk for abuse—such as methylphenidate, or amphetamine, or an amphetamine-like central-nervous-system stimulant. The drug is formulated into a form (not a transdermal patch) that tends to deter conversion to powder; and in this form commercially distributed, e. g. wholesale or retail. Preferably that form is enclosed in a nontoxic capsule. Preferably the formulating includes dissolving or dispersing the drug into or onto a nontoxic carrier—for example a gel, e. g., methylcellulose, hydroxymethylcellulose, carbomer polymer, or other gelatinous pharmaceutical agent that is FDA-acceptable. Preferably the carrier is water-insoluble, to deter dissolving in water for injection. The carrier may be an oil or a solid—for example paper or other thin medium broadly extended in two dimensions, or a sponge or other medium having generally coarse cellular structure.
BACKGROUND: Gastric cancer (GC) is difficult to treat with currently available treatments. Securinine (SCR) has a lengthy history of use in the treatment of disorders of the nervous system, and its anticancer potential has been gaining attention in recent years. The aim of this study was to explore the repressive effect of SCR on GC and its fundamental mechanism.
METHODS: The efficacy of SCR in GC cells was detected by MTT assays. Colony formation, flow cytometry and Transwell assays were used to assess the changes in the proliferation, apoptosis, cell cycle distribution, migration and invasion of GC cells after treatment. AGS (human gastric carcinoma cell)-derived xenografts were used to observe the effect of SCR on tumor growth in vivo. The molecular mechanism of action of SCR in GC was explored via RNA sequencing, bioinformatics analysis, Western blotting, molecular docking, and immunohistochemistry.
RESULTS: SCR was first discovered to inhibit the proliferation, migration, and invasion of GC cells while initiating apoptosis and cell cycle arrest in vitro. It was also established that SCR has excellent anticancer effects in vivo. Interestingly, AURKA acts as a crucial target of SCR, and AURKA expression can be blocked by SCR. Moreover, this study revealed that SCR suppresses the cell cycle and the β-catenin/Akt/STAT3 pathways, which were previously reported to be regulated by AURKA.
CONCLUSION: SCR exerts a notable anticancer effect on GC by targeting AURKA and blocking the cell cycle and β-catenin/Akt/STAT3 pathway. Thus, SCR is a promising pharmacological option for the treatment of GC.
Precision nutrition leverages the specificity of molecular and phenotypic differences in personalizing diet and lifestyle interventions. Specific Aims: 1) Examine the effectiveness of gene-based nutrition counseling on health-related behavior change in service members as measured by body weight, body mass index (BMI), blood glucose, lipids, 25-hydroxyvitamin (OH) D, %body fat (BF), waist circumference, and blood pressure; 2) Evaluate the feasibility of a digital application to accurately capture diet, activity, and sleep behaviors; and 3) Describe military-unique characteristics in demographics, diet, and lifestyle for northwest Army and southwest Air Force cohorts.

A baseline genomic profile will be created from 70 diet-responsive genes and 80 variants following amplicon sequencing on an Illumina MiSeq platform and will be informed by serum biomarkers specific to diet-related chronic disease risk (i.e. metabolic syndrome, vitamin D deficiency) for each subject. Risk variants were selected if minor allele frequency \> 5% and at least two published papers verified the link to the phenotype of interest. Treatment group receives gene-based nutrition counseling for six weekly sessions; Controls receive evidence-based nutrition pamphlets, all content directed at preventing metabolic syndrome. A digital app provides real-time health data capture with continuous feedback and is verified by in-person dietitian interviews. Both groups will also use study resources independently for six weeks, returning for final body composition and serum biomarkers after the twelve-week intervention. The control group receives the genomic profile with dietary recommendations upon study completion. Data analysis will examine between-group and by-cohort differences on primary anthropometric and biomarker outcomes.
One potential candidate for a new approach to advanced cancer therapy is hyperthermia because cancer cells are thermo-sensitive, with significantly reduced heat shock protein (HSP) expression. Moreover, hyperthermia (42°C) causes repression of genes involved in the cell cycle and cellular growth and proliferation. Upon exposure to hyperthermic conditions, HSP expression is increased in normal cells. However, when cancer cells are exposed to hyperthermia, they initially express significantly less HSPs than normal cells, which sensitizes them to hyperthermia. Mild hyperthermia (43°C for less than two hours) induces extensive double-stranded DNA fragmentation and, at a later time, apoptosis in murine thymocytes. In cells with irreparable levels of DNA damage, apoptosis is the means of elimination.
BACKGROUND: Silicosis is an irreversible fibrotic disease of the lung caused by chronic exposure to silica dust, which manifests as infiltration of inflammatory cells, excessive secretion of pro-inflammatory cytokines, and pulmonary diffuse fibrosis. As the disease progresses, lung function further deteriorates, leading to poorer quality of life of patients. Currently, few effective drugs are available for the treatment of silicosis. Bicyclol (BIC) is a compound widely employed to treat chronic viral hepatitis and drug-induced liver injury. While recent studies have demonstrated anti-fibrosis effects of BIC on multiple organs, including liver, lung, and kidney, its therapeutic benefit against silicosis remains unclear. In this study, we established a rat model of silicosis, with the aim of evaluating the potential therapeutic effects of BIC.
METHODS: We constructed a silicotic rat model and administered BIC after injury. The FlexiVent instrument with a forced oscillation system was used to detect the pulmonary function of rats. HE and Masson staining were used to assess the effect of BIC on silica-induced rats. Macrophages-inflammatory model of RAW264.7 cells, fibroblast-myofibroblast transition (FMT) model of NIH-3T3 cells, and epithelial-mesenchymal transition (EMT) model of TC-1 cells were established in vitro. And the levels of inflammatory mediators and fibrosis-related proteins were evaluated in vivo and in vitro after BIC treatment by Western Blot analysis, RT-PCR, ELISA, and flow cytometry experiments.
RESULTS: BIC significantly improved static compliance of lung and expiratory and inspiratory capacity of silica-induced rats. Moreover, BIC reduced number of inflammatory cells and cytokines as well as collagen deposition in lungs, leading to delayed fibrosis progression in the silicosis rat model. Further exploration of the underlying molecular mechanisms revealed that BIC suppressed the activation, polarization, and apoptosis of RAW264.7 macrophages induced by SiO2. Additionally, BIC inhibited SiO2-mediated secretion of the inflammatory cytokines IL-1β, IL-6, TNF-α, and TGF-β1 in macrophages. BIC inhibited FMT of NIH-3T3 as well as EMT of TC-1 in the in vitro silicosis model, resulting in reduced proliferation and migration capability of NIH-3T3 cells. Further investigation of the cytokines secreted by macrophages revealed suppression of both FMT and EMT by BIC through targeting of TGF-β1. Notably, BIC blocked the activation of JAK2/STAT3 in NIH-3T3 cells required for FMT while preventing both phosphorylation and nuclear translocation of SMAD2/3 in TC-1 cells necessary for the EMT process.
CONCLUSION: The collective data suggest that BIC prevents both FMT and EMT processes, in turn, reducing aberrant collagen deposition. Our findings demonstrate for the first time that BIC ameliorates inflammatory cytokine secretion, in particular, TGF-β1, and consequently inhibits FMT and EMT via TGF-β1 canonical and non-canonical pathways, ultimately resulting in reduction of aberrant collagen deposition and slower progression of silicosis, supporting its potential as a novel therapeutic agent.
On the day of the patient's admission, the total calories required for the diabetic diet during the hospitalization period were calculated according to "ideal weight \* 25/kcal" (BMI \> 28, 80% of this value). Carbohydrates, fats, and proteins accounted for 50%, 30%, and 20% of the energy supply, respectively, and the calories of the three meals were distributed according to 1:2:2. The meal replacement intervention group replaced the daily meal with meal replacement on the basis of the conventional diabetic diet. About 400kcal calories in carbohydrates.
Hyponatremia may occur as a result of treatment with SSRIs and SNRIs, including FETZIMA. In many cases, hyponatremia appears to be the result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Cases with serum sodium lower than 110 mmol/L have been reported. Elderly patients may be at greater risk of developing hyponatremia with SSRIs and SNRIs. Also, patients taking diuretics or who are otherwise volume depleted can be at greater risk. FETZIMA should be discontinued in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted. Signs and symptoms of hyponatremia include headache, difficulty concentrating, memory impairment, confusion, weakness, and unsteadiness, which can lead to falls. Signs and symptoms associated with more severe and/or acute cases have included hallucination, syncope, seizure, coma, respiratory arrest, and death.
Tourniquet would be tied to left upper limb of Patients who undergoing laparotomy for 30 minutes after the induction of anesthesia,but put no press on it. Other processes are consistent with conventional methods.
OBJECTIVE: To explore the mechanism underlying the therapeutic effect of Bufei Yishen Formula III combined with exercise rehabilitation (ECC-BYF III + ER) on chronic obstructive pulmonary disease (COPD) and further identify hub genes.
MATERIALS AND METHODS: Gene Set Enrichment Analysis was used to identify the COPD-associated pathways and reversal pathways after ECC-BYF III + ER treatment. Protein-protein interaction network analysis and cytoHubba were used to identify the hub genes. These genes were verified using independent datasets, molecular docking and quantitative real-time polymerase chain reaction experiment.
RESULTS: Using the high-throughput sequencing data of COPD rats from our laboratory, 49 significantly disturbed pathways were identified in COPD model compared with control group via gene set enrichment analysis (false discovery rate < 0.05). The 34 pathways were reversed after ECC-BYF III + ER treatment. In the 2306 genes of these 34 pathways, 121 of them were differentially expressed in COPD rats compared with control samples. A protein-protein interaction network comprising 111 nodes and 274 edges was created, and 34 candidate genes were identified. Finally, seven COPD hub genes (Il1b, Ccl2, Cxcl1, Apoe, Ccl7, Ccl12, and Ccl4) were well identified and verified in independent COPD rat data from our laboratory and the public dataset GSE178513. The area under the receiver operating characteristic curve values ranged from 0.86 to 1 and from 0.67 to 1, respectively. The reliability of the mentioned genes, which can bind to the active ingredients of ECC-BYF III through molecular docking, were further verified through qRT-PCR experiments.
CONCLUSION: Thirty-four COPD-related pathways and seven hub genes that may be regulated by ECC-BYF III + ER were identified and well verified. The findings of this study may provide insights into the treatment and mechanism underlying COPD.
A pharmaceutical formulation comprises amoxycillin and clavulanate in a ratio of n:1, where n = 1-16, and consists of: a first set of granulates comprising amoxycillin and clavulanate in a ratio of from m:1 to 1:1, where m  n; and a second set of granulates comprising amoxycillin and no clavulanate; and the ratio of the sets of granulates gives an overall ratio between amoxycillin and clavulanate of n:1. The ratio of amoxycillin to clavulanate in the first granulates is 1:1 or 2:1; alternatively, n = 2, 4, 6, 7, 8 or 14. The amoxycillin is the trihydrate, and the clavulanate is the potassium salt. The granulates comprise an intragranular disintegrant, preferably cross-linked N-vinyl-2-pyrrolidone (CLPVP) or sodium starch glycollate, and an extra-granular excipient, preferably low-substituted hydroxypropyl cellulose. The first set also includes silica gel. The formulation is in the form of a tablet, sachet, capsule or a powder for reconstitution as an aqueous syrup. The combined weight of all excipients is  20% of the uncoated weight of the tablet.
PURPOSE:To provide a curable composition containing a vinyl monomer containing an acidic group having a specific structure, a specific ion-releasing filler and a polymerization initiator, surely bonding to tooth even by curing in moist state, resistant to discoloration and giving a cured material having sufficiently high strength. CONSTITUTION:The objective curable composition contains (A) 100 pts.wt. of a vinyl monomer containing >=30wt.% of a vinyl monomer (e.g. compound of formula II or formula III) having an acidic group and expressed by formula I (R1 and R4 are H or methyl; R2 and R3 are 1-4C alkylene), (B) 30-500 pts.wt. of an ion-releasing filler capable of releasing 2-60mgeq/g of polyvalent metal ion (e.g. ion of Ca, Sr, Ba, Al, Zn, etc., and the filler is preferably calcium hydroxide, zinc oxide or especially a fluoroaluminosilicate glass) and (C) 0.1-3 pts.wt. of a polymerization initiator (e.g. benzoyl peroxide). Since the curable composition exhibits high bonding power even in the presence of water, high bonding strength can be surely developed even in the clinical application such as the mending of tooth.
PROBLEM TO BE SOLVED: To obtain a safe and stable carrier for gene transfer formed of a polymer substance obtained by binding a hydrophilic polymer to a polymer containing a residue having a positive electron charge in a physiologically pH range and combining the polymer with a specific amount of gene in a cell or in vivo. SOLUTION: This carrier for carrying gene is formed of a polymer substance obtained by binding a hydrophilic polymer (e.g. polyethylene glycol) to a polymer (e.g. polylysine) such as a polyamino acid comprising a basic amino acid containing a residue having a positive electron charge in a physiological pH range. In the carrier, the polymer substance is combined with a carrying gene in a ratio of a value obtained by dividing weight parts of a polymer part having a positive electron charge in the polymer substance by molecular weight of the residue to 1/300 of weight parts of the carrying gene. The carrier for carrying gene is safe and stable in a cell or in vivo and is useful for gene therapy for carrying out treatment of diseases, means, etc., for obtaining organisms such as new bacteria or animals and plants which have extremely useful properties.
We assessed the feasibility of implementing a virtually guided Neuromuscular Electrical Stimulation (NMES) protocol over the tibialis anterior (TA) muscle while collecting heart rate (HR), Numeric Pain Rating Scale (NPRS), and quality of contraction (QoC) data. We investigated if HR, NPRS, and QoC differ ON and OFF the TA motor point and explored potential relationships between heart rate variability (HRV) and the NPRS. Twelve healthy adults participated in this cross-sectional study. Three NMES trials were delivered ON and OFF the TA motor point. HR, QoC, and NPRS data were collected. There was no significant difference in HRV ON and OFF the motor point (p > 0.05). The NPRS was significantly greater OFF the motor point (p < 0.05). The QoC was significantly different between motor point configurations (p < 0.05). There was no correlation between the NPRS and HRV (p > 0.05, r = -0.129). We recommend non-electrical methods of measuring muscle activity for future studies. The NPRS and QoC can be administered virtually. Time-domain HRV measures could increase the validity of the protocol. The variables should be explored further virtually to enhance the protocol before eventual ICU studies.
Aicardi syndrome is a sporadic X-linked dominant, presumably male-lethal, neurodevelopmental disorder. It was initially characterized by agenesis of the corpus callosum, neuronal migration defects, eye abnormalities (chorioretinal lacunae, colobomas of the optic nerve and microphthalmia) and severe early-onset seizures and neurodevelopmental delay. It is now well recognized that other brain abnormalities, such as polymicrogyria, agyria, cysts and heterotopias are common features of Aicardi syndrome. The investigators previously hypothesized that the gene causing Aicardi syndrome and possibly additional phenotypically similar disorders with X-linked inheritance, such as Goltz syndrome or Focal Dermal Hypoplasia, are in or near the region on chromosome Xp22 that is deleted in another condition named microphthalmia with linear skin defects syndrome (MLS), because all three have some clinical similarities. However, interim studies have shown that this is likely not the case because no mutations were found in Aicardi syndrome in human holocytochrome c-type synthetase (HCCS) , the gene that is deleted or mutated in MLS. In addition, a mouse model for MLS has no features of Aicardi syndrome. Furthermore, the ivnestigators identified mutations in PORCN (Xp11.3) in Goltz syndrome patients, but not in Aicardi syndrome patients. Therefore, it is likely that the mutated gene is elsewhere on the X-chromosome.

For this study the investigators are collecting information on patients with clinical findings suggesting a diagnosis of Aicardi syndrome, MLS syndrome or a condition that phenotypically overlaps with these disorders. A detailed family history will be obtained, when indicated, and additional family members will be evaluated after appropriately obtained written voluntary consent. A detailed report of the history or physical findings will be obtained from referring physicians for patients identified at outside facilities, or the participants may be evaluated by the study collaborators. Blood and skin biopsy will be obtained from affected individuals, unaffected parents and from other affected or unaffected family members where indicated. It is anticipated that some severely affected patients will expire; in that case, (post mortem) pathological specimens may be obtained. Occasionally, affected individuals may undergo surgical procedures with removal of tissues; in this case we may obtain tissues that would be otherwise discarded or that are not essential for further diagnostic studies or clinical care of the patient. It is anticipated that these specimens will be extremely valuable for understanding the pathogenesis of the investigated conditions. DNA, RNA or protein will be prepared from leukocytes and from tissues and used for sequencing and mutation analysis and other molecular studies of the identified genes. Permanent lymphoblastoid cell lines will be prepared and stored in the laboratory as a permanent source of DNA for the molecular studies. Cell lines may be made from skin biopsies
PURPOSE:To provide the titled promoting agent containing a tetracyclo compound as an active component, exhibiting extremely strong antitumor action, effective in remarkably promoting the antitumor effect of other antitumor agent and free from side effects. CONSTITUTION:The objective agent contains a tetracyclo compound of formula (R<1>, R<2> and R<3> are lower alkanoyl) as an active component. If is converted into a drug preparation by using various carriers e.g. an excipient (e.g. sucrose or calcium carbonate), a binder (e.g. cellulose or starch), a disintegrant and a lubricant. The antitumor agent to promote its activity by the titled promoting agent is preferably a drug having a drug mechanism different from the mechanism of the antitumor action of the tetracyclo compound, e.g. 5-Fu or Ara-C. The administration ratio of the antitumor agent to the promoting agent is (0.01-500):1, preferably (0.1-50):1 by weight.