anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
SEZABY is a barbiturate and a CNS depressant with a potential for misuse, abuse, and addiction with unapproved use in adolescents and adults. 

Abuse is the intentional, non-therapeutic use of a drug, even once, for its desirable psychological or physiological effects. Misuse is the intentional use, for therapeutic purposes, of a drug by an individual in a way other than prescribed by a health care provider or for whom it was not prescribed. Drug addiction is a cluster of behavioral, cognitive, and physiological phenomena that may include a strong desire to take the drug, difficulties in controlling drug use (e.g., continuing drug use despite harmful consequences, giving a higher priority to drug use than other activities and obligations), and possible tolerance or physical dependence. Even taking barbiturates as prescribed may put patients at risk for abuse and misuse of their medication. Abuse and misuse of barbiturates, including phenobarbital, may lead to addiction.

Abuse and misuse of barbiturates often (but not always) involve the use of doses exceeding the doses used in clinical practice and commonly involve concomitant use of other medications, alcohol, and/or illicit substances, which is associated with an increased frequency of serious adverse outcomes, including respiratory depression, overdose, or death. Barbiturates, including phenobarbital, are often sought by individuals who abuse drugs and other substances, and by individuals with addictive disorders [see Warnings and Precautions (5.3)].

Symptoms of acute intoxication with barbiturates include unsteady gait, slurred speech, and sustained nystagmus. Mental signs of chronic intoxication include confusion, poor judgment, irritability, insomnia, and somatic complaints. The use of phenobarbital alone can result in death; however, death is more often associated with phenobarbital use in the context of polysubstance use (especially with other CNS depressants, such as opioids and alcohol).
One-time Salbutamol (8 mg) and Propranolol (40mg) administered orally. During two bronchoscopic procedures two pre-specified lung tissue sites (middle lobe and lingula) will be sampled. Bronchoadsorption sample, bronchial brushing, mucosal biopsy, and BAL samples will be taken from each site.
Patients with Cancer Receiving Myelosuppressive Chemotherapy

White blood cell counts of 100‚000/mm3 or greater were observed in approximately 2% of patients receiving filgrastim at dosages above 5 mcg/kg/day. In patients with cancer receiving ZARXIO as an adjunct to myelosuppressive chemotherapy‚ to avoid the potential risks of excessive leukocytosis‚ it is recommended that ZARXIO therapy be discontinued if the ANC surpasses 10‚000/mm3 after the chemotherapy-induced ANC nadir has occurred. Monitor CBCs at least twice weekly during therapy. Dosages of ZARXIO that increase the ANC beyond 10‚000/mm3 may not result in any additional clinical benefit. In patients with cancer receiving myelosuppressive chemotherapy‚ discontinuation of filgrastim therapy usually resulted in a 50% decrease in circulating neutrophils within 1 to 2 days‚ with a return to pretreatment levels in 1 to 7 days.

Peripheral Blood Progenitor Cell Collection and Therapy

During the period of administration of ZARXIO for PBPC mobilization in patients with cancer, discontinue ZARXIO if the leukocyte count rises to > 100,000/mm3.
The invention relates to the use of corticotropin-releasing hormone (CRH) receptor-1 (RI) antagonists and/or CRH-R2 receptor agonists for the treatment of inflammatory diseases via regulation of monocyte / macrophage cell activation, proliferation, differentiation, apoptosis, and inflammatory cytokine production. As CRH system we define natural and synthetic CRH and urocortin (UCN) agonists and antagonists for the CRH-R1 and CRH-R2 receptors and their subtypes as well as the CRH-binding protein (BP), a CRH pseudo receptor. The invention is directed towards pharmacological intervention for the amelioration or treatment of inflammatory diseases using the CR. system-mediated control of monocyte / macrophage cells which play a key role in initiating and maintaining the inflammatory response via production of pro-inflammatory cytokines such as is the interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF)-alpha. By the term inflammation we define the response of an organism to noxious endogenous or exogenous stimuli causing tissue injury. Inflammation is a host defence mechanism, which might harm the de­fending organism. The invention also provides methods for the in vitro and in vivo evaluation of natural and synthetic CRH system modulators for the control of the monocyte / macrophage system.
This is a multicenter, double-blind, parallel, placebo-controlled, randomized phase 2 study to evaluate the safety and efficacy of Gleevec (imatinib mesylate) in the treatment of Idiopathic Pulmonary Fibrosis (IPF). One-hundred- twenty patients will be enrolled in the trial in total. Subjects must have a diagnosis made by HRCT showing definite or probable IPF and clinical symptoms consistent with IPF with onset between 3 and 36 months prior to screening. Subjects will be randomly assigned to receive either Gleevec 600 mg orally or placebo, once per day for approximately 2 years. The primary efficacy will be progression defined as a greater than 10% decline in the forced vital capacity or death. Measures of safety will include all randomized patients who receive at least one dose of study medication. All adverse events and serious adverse events will be separately tabulated and mapped to a standard classification system and grouped by body system. Any serious adverse events that occur during the trial and 30 days after the end of therapy will be reported to the FDA within 24 hours and followed to outcome.
Participants will be instructed to wear the wristwatch for a minimum of 3 hours per day, 5 days per week and engage in telerehabilitation, 1 hour per day 5 times per week over 4 weeks. Weekly, there will be a 45-minute therapy consultation.
The invention relates to a compound preparation for reducing blood sugar and belongs to the technical field of oral preparation. The product is characterized in that the compound preparation is prepared from the following traditional Chinese medicine materials in weight portion: 5 to 25 portions of polygonatum, 5 to 25 portions of herba lophatheri and 3 to 12 portions of balsam pear. Oral liquid is the preferred preparation form; and the compound preparation can also be prepared into different preparation forms. The product has a refined formula, can effectively reduce blood sugar of diabetic patients without causing hypoglycemia reaction, has prevention function, and is mainly used for diabetic prevention and treatment. A safety test, a pharmacodynamic test, an acute toxicity test and a clinical test prove that the product can improve the activity of insulin and reduce the production of mutant insulin so that the product realizes physiological action with higher efficiency, promotes the ingestion and utilization of glucose by tissues and cells, and balances the energy metabolism of organism, thereby removing the symptoms of the diabetic patients. The product has remarkable effect, stability, safety, no toxicity, no side effect and can be taken for a long time.
A drum (1) which acts as roasting chamber is rotatably mounted by means of a hollow shaft (4) and set in rotation by a motor (11). The drum (1) can be heated by means of gas burners (15). Glass beads or similar particles which act as heat-transfer medium are introduced into the drum (1) via a ball valve (3). While the drum (1) is rotated, the heat transfer medium is brought to the desired temperature by means of the gas burners (15). Once the desired temperature is reached, the heat supply is interrupted, and the green coffee beans are added to the heated heat transfer medium. Coffee beans and heat transfer medium are brought into intimate contact by rotating the drum (1). When the roasting procedure is ended, the drum (1) is emptied, and the roasted coffee beans are separated from the heat transfer medium, which is recycled. The process allows organoleptic effects to be achieved, which improve the quality. However, in many cases, this improvement is linked to an increase in titratable acid. The improved quality is particularly obvious in the case of robusta coffee. <IMAGE>
Novel quaternary 5-ammonium-methyl-4-amino-2-R-pyrimidine salts, in which R represents a cycloaliphatic group and the ammonium nitrogen atom is part of a monocyclic or bicyclic heterocyclic radical containing one or more double bonds, one of which extends from the ammonium nitrogen atom, are prepared by reacting a reactive ester or ether of a 4-amino-5-hydroxymethyl - 2 - R - pyrimidine with a monocyclic or bicyclic heterocyclic compound containing at least one ring nitrogen atom and one or more double bonds, one of which extends from the ring nitrogen atom.  4 - Amino - 5 - hydroxymethyl - 2 - R - pyrimidines are prepared by reacting an R-halide with sodium cyanide to form the corresponding R-cyanide, reacting this an alkanol to form the corresponding alkyl R-carboximidate, reacting this with ammonia to form the corresponding R-carboxylic acid amidine, reacting this with a C1- 7 alkoxymethylene-malonitrile to form a 4-amino - 5 - cyano - 2 - R - pyrimidine, hydrogenating this to the corresponding 5-aminomethyl compound and converting this into the corresponding 5-hydroxymethyl compound by treatment with nitrous acid. Alternatively, the 5-cyano compound may be hydrogenated in the presence of hydrochloric acid to form the 5-hydroxymethyl compound directly.  Cyclobutylmethyl bromide is prepared by treating cyclobutane carboxylic acid with lithium aluminium hydride to form cyclobutylmethanol and treating this with phosphorus tribromide. Cyclopropylmethyl bromide is similarly prepared via cyclopropylmethanol.  4 - Amino - 5 - chloromethyl - 2 - cyclopropylmethyl-pyrimidine hydrochloride is prepared by reacting 4-amino-5-hydroxymethyl-2-cyclopropylmethyl-pyrimidine with thionyl chloride.
During period 1, participants were uptitrated daily from BAF312 0.25 mg to 0.5 mg over a 10 day period. After, participants continued on 0.5 mg daily for up to 24 weeks. During period 2, participants were uptitrated daily from BAF312 0.25 mg to 2.0 mg over a 10 day period. After, participants continued on 2.0 mg daily for up to 24 weeks.
BACKGROUND: Postoperative cognitive dysfunction (POCD) is one of the major complications after surgery, with devastating clinical outcomes. Although POCD is a condition with a multifactorial pathophysiology, blood-brain barrier (BBB) dysfunction and neuronal injury have been shown to play a critical role, especially in the elderly. Previous studies have demonstrated that the choice of anesthetics affect BBB permeability and neuroinflammation. However, most studies are carried out on animals, with limited research undertaken on humans. Therefore, we will compare the effect of intravenous anesthetics and inhaled anesthetics on BBB dysfunction and the change of inflammatory markers after surgery.
METHODS: One hundred and fifty-four patients who are 60 years of age or older undergoing major surgery for more than 2 h will be randomly allocated to two anesthetics groups (intravenous, inhaled) in a 1:1 ratio. In the intravenous anesthetics group (group P), propofol will be infused with a target-controlled infusion (TCI) system throughout the entire surgery. In the inhaled anesthetics group (group G), bolus injection of propofol will be administered for loss of consciousness, and simultaneously sevoflurane will be initiated for the maintenance of anesthesia. The primary outcome is the change in serum S100 calcium binding protein β (S100β) at four time points: before induction of anesthesia, at the end of surgery, 4 h after surgery, postoperative day 1. Secondary outcomes include changes in the inflammatory markers, serum interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-α, and C-reactive protein; the incidence of delirium; and the change in the cognitive function between groups. In patients pre-scheduled for postoperative intensive care unit admission, the cerebrospinal fluid/serum albumin quotient (Qalb) between the two groups will be compared before and after surgery, and change in inflammatory markers in serum and CSF will be analyzed in relation to the Qalb.
DISCUSSION: The current study will compare the effect of intravenous versus inhaled anesthetics on blood-brain barrier permeability and, as a result, the difference in neuroinflammation in elderly patients. Also, the study results will provide additional information to develop intraoperative anesthetic strategies to reduce POCD.
TRIAL REGISTRATION: The trial was prospectively registered at Clinical Trials protocol registration with identifier 2310-117-126 on April 9, 2024.
The initial dose of Cyclosporine Capsules USP MODIFIED should be 2.5 mg/kg/day. Cyclosporine Capsules USP MODIFIED should be taken twice daily, as a divided (1.25 mg/kg BID) oral dose. Patients should be kept at that dose for at least 4 weeks, barring adverse events. If significant clinical improvement has not occurred in patients by that time, the patient’s dosage should be increased at 2 week intervals. Based on patient response, dose increases of approximately 0.5 mg/kg/day should be made to a maximum of 4 mg/kg/day.

Dose decreases by 25% to 50% should be made at any time to control adverse events, e.g., hypertension, elevations in serum creatinine (≥ 25% above the patient’s pretreatment level), or clinically significant laboratory abnormalities. If dose reduction is not effective in controlling abnormalities, or if the adverse event or abnormality is severe, Cyclosporine Capsules USP MODIFIED should be discontinued (see Special Monitoring of Psoriasis Patients).

Patients generally show some improvement in the clinical manifestations of psoriasis in 2 weeks. Satisfactory control and stabilization of the disease may take 12 to 16 weeks to achieve. Results of a dose-titration clinical trial with Cyclosporine Capsules USP MODIFIED indicate that an improvement of psoriasis by 75% or more (based on PASI) was achieved in 51% of the patients after 8 weeks and in 79% of the patients after 16 weeks. Treatment should be discontinued if satisfactory response cannot be achieved after 6 weeks at 4 mg/kg/day or the patient’s maximum tolerated dose. Once a patient is adequately controlled and appears stable the dose of Cyclosporine Capsules USP MODIFIED should be lowered, and the patient treated with the lowest dose that maintains an adequate response (this should not necessarily be total clearing of the patient). In clinical trials, cyclosporine doses at the lower end of the recommended dosage range were effective in maintaining a satisfactory response in 60% of the patients. Doses below 2.5 mg/kg/day may also be equally effective.

Upon stopping treatment with cyclosporine, relapse will occur in approximately 6 weeks (50% of the patients) to 16 weeks (75% of the patients). In the majority of patients rebound does not occur after cessation of treatment with cyclosporine. Thirteen cases of transformation of chronic plaque psoriasis to more severe forms of psoriasis have been reported. There were 9 cases of pustular and 4 cases of erythrodermic psoriasis. Long-term experience with Cyclosporine Capsules USP MODIFIED in psoriasis patients is limited and continuous treatment for extended periods greater than one year is not recommended. Alternation with other forms of treatment should be considered in the long-term management of patients with this life long disease.
MYBL1 is a strong transcriptional activator involved in the cell signaling. However, there is no systematic study on the role of MYBL1 in atherosclerosis. The aim of this study is to elucidate the role and mechanism of MYBL1 in atherosclerosis. GSE28829, GSE43292 and GSE41571 were downloaded from NCBI for differentially expressed analysis. The expression levels of MYBL1 in atherosclerotic plaque tissue and normal vessels were detected by qRT-PCR, Western blot and Immunohistochemistry. Transwell and CCK-8 were used to detect the migration and proliferation of HUVECs after silencing MYBL1. RNA-seq, Western blot, qRT-PCR, Luciferase reporter system, Immunofluorescence, Flow cytometry, ChIP and CO-IP were used to study the role and mechanism of MYBL1 in atherosclerosis. The microarray data of GSE28829, GSE43292, and GSE41571 were analyzed and intersected, and then MYBL1 were verified. MYBL1 was down-regulated in atherosclerotic plaque tissue. After silencing of MYBL1, HUVECs were damaged, and their migration and proliferation abilities were weakened. Overexpression of MYBL1 significantly enhanced the migration and proliferation of HUVECs. MYBL1 knockdown induced abnormal autophagy in HUVEC cells, suggesting that MYBL1 was involved in the regulation of HUVECs through autophagy. Mechanistic studies showed that MYBL1 knockdown inhibited autophagosome and lysosomal fusion in HUVECs by inhibiting PLEKHM1, thereby exacerbating atherosclerosis. Furthermore, MYBL1 was found to repress lipid accumulation in HUVECs after oxLDL treatment. MYBL1 knockdown in HUVECs was involved in atherosclerosis by inhibiting PLEKHM1-induced autophagy, which provided a novel target of therapy for atherosclerosis.
This Phase 1b study was designed to evaluate the safety and efficacy of pravibismane, a novel broad-spectrum topical anti-infective, in managing moderate or severe chronic diabetic foot ulcer (DFU) infections. This randomized, double-blind, placebo-controlled, multicenter study consisted of 39 individuals undergoing pravibismane treatment and 13 individuals in the placebo group. Assessment of safety parameters included clinical observations of tolerability and pharmacokinetics from whole blood samples. Pravibismane was well-tolerated and exhibited minimal systemic absorption, as confirmed by blood concentrations that were below the lower limit of quantitation (0.5 ng/mL) or in the low nanomolar range, which is orders of magnitude below the threshold of pharmacological relevance for pravibismane. Pravibismane treated subjects showed approximately 3-fold decrease in ulcer size compared to the placebo group (85% vs. 30%, p = 0.27). Furthermore, the incidence of ulcer-related lower limb amputations was approximately 6-fold lower (2.6%) in the pooled pravibismane group versus 15.4% in the placebo group (p = 0.15). There were no treatment emergent or serious adverse events related to study drug. The initial findings indicate that topical pravibismane was safe and potentially effective treatment for improving recovery from infected chronic ulcers by reducing ulcer size and facilitating wound healing in infected DFUs (ClinicalTrials.gov Identifier NCT02723539).
The recommended dosages for adults and pediatric patients 1 month of age and older are included in Table 1. Administer the total daily dosage orally in two or three divided doses as indicated in Table 1. In pediatric patients, the recommended dosing regimen is dependent upon body weight. Based on clinical response and tolerability, dosage may be increased, approximately weekly.

Table 1. Recommended Dosage for Adults and Pediatric Patients 1 Month and Older 

Both the efficacy and adverse event profiles of pregabalin capsules have been shown to be dose-related. The effect of dose escalation rate on the tolerability of pregabalin capsules has not been formally studied.

The efficacy of adjunctive pregabalin capsules in patients taking gabapentin has not been evaluated in controlled trials. Consequently, dosing recommendations for the use of pregabalin capsules with gabapentin cannot be offered.
The present invention addresses the problem of providing the induction of antibodies against a target protein using a peptide as an antigen.　The present invention relates to a method for preparing a partial peptide that is from within a target protein and induces antibodies specific to the target protein, wherein 1.) a plurality of partial peptides with 5-30 amino acid residues are prepared, 2.) a mixture containing the obtained partial peptides is created, 3.) a non-human mammal is immunized using the obtained mixture, 4.) it is determined whether antibodies specific to the target protein are induced in the mixture as a result of the immunization, and 5.) a partial peptide that induces the specific antibodies is identified from within a mixture determined to induce antibodies.
Prodn. of a pollen complex by extracting the pollen with a mixt. of an aqs. liquid (L) and a weak organic base (B) (esp. a heterocyclic tertiary amine), adding an alum soln. to the extract to ppt. the pollen complex, and recovering the complex. Claims restricted to above process wherein extractant comprises about 50% each of L and B, B being pyridine, lutidine or quinoline and L being distilled water, 0.3% NaHCO3, 0.9% NaCl, 5% dextrose or N/10 NaOH. Therapy and prophylaxis of pollen allergies e.g. hay fever and asthma. Administration is by injection, as a suspension of the above pollen complex in isotonic saline.
Part I - Dose-Ranging. Part I will evaluate the (1) safety and tolerability and (2) efficacy (antiretroviral activity) of 4 doses of doravirine compared with efavirenz, when each is given in combination with TRUVADA® for at least 24 weeks in approximately 200 participants. A single dose of doravirine will be selected for further study after all participants complete the Week 24 visit in Part I. Participants receiving any dose of doravirine in Part I will be switched to the selected doravirine dose and continue in the study for up to 96 weeks, but will not be randomized to Part II.

Part II - Selected Dose. Part II will be initiated after the doravirine dose has been selected as indicated above for Part 1. Approximately 120 additional participants will be randomized in 1:1 ratio to the selected dose of doravirine or efavirenz, each in combination with TRUVADA® for 96 weeks of blinded treatment. Part II will evaluate the safety of the selected dose compared with efavirenz, particularly with regard to central nervous system (CNS) adverse events.
Ten healthy, normal-weight adults after 10-14 hours of fasting, consumed 50g available carbohydrates from D-glucose, tested three times, in different visits as reference food; and 50g available carbohydrates from orange juice and mixed fruit juice (consisted of apple, orange, grape, and pomegranate), each tested once, in different visits, along with 300mL water. There was a washout period of at least two days between visits. Fingertip capillary blood glucose samples were taken at baseline, 15, 30, 45, 60, 90 and 120min after beverage consumption. The first glucose sample was taken exactly 15min after the first sip of drink.
Thrombotic thrombocytopenic purpura (TTP) is a life-threatening, often immune-mediated disease that affects 2-13 persons per million per year. Hemolytic anemia, thrombocytopenia, and end-organ damage due to the formation of microthrombi are characteristic of TTP. ADAMTS13 is a disintegrin, metalloproteinase, cleaving protein of von Willebrand factor (VWF) that processes the VWF multimers to prevent them from interacting with platelets and, in turn, to microvascular thrombosis. Prompt diagnosis of TTP is critical yet challenging. Thrombotic microangiopathies have similar clinical presentation. Measurement of ADAMTS13 activity helps in the differential diagnosis. Less than 10% ADAMTS13 activity is indicative of TTP. Laboratory ADAMTS13 activity assays include incubating the test plasma with the substrate (full-length VWM multimers) and detection with direct or indirect measurement of the cleavage product. The purpose of this study is to examine the diagnostic potential, advantages, and weaknesses of the ADAMTS13 potency in TTP.