anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
There have been reports of ventricular dysrhythmias, cardiac arrest, and death secondary to acute rhabdomyolysis with hyperkalemia in apparently healthy pediatric patients who received ANECTINE. Many of these pediatric patients were subsequently diagnosed with a skeletal muscle myopathy, such as Duchenne muscular dystrophy 

This syndrome often presents as peaked T-waves and sudden cardiac arrest within minutes after the administration of ANECTINE in healthy appearing pediatric patients (usually, but not exclusively, males, and most frequently 8 years of age or younger). There have also been reports in adolescents. 

Therefore, when a healthy appearing infant or child develops cardiac arrest soon after administration of ANECTINE not felt to be due to inadequate ventilation, oxygenation, or anesthetic overdose, immediate treatment for hyperkalemia should be instituted. This should include administration of intravenous calcium, bicarbonate, and glucose with insulin, with hyperventilation. Due to the abrupt onset of this syndrome, routine resuscitative measures are likely to be unsuccessful. However, extraordinary and prolonged resuscitative efforts have resulted in successful resuscitation in some reported cases. In addition, in the presence of signs of malignant hyperthermia, appropriate treatment should be instituted concurrently [see Warnings and Precautions (5.5)]. 

Since there may be no signs or symptoms to alert the practitioner to which patients are at risk, it is recommended that the use of ANECTINE in pediatric patients should be reserved for emergency intubation or instances where immediate securing of the airway is necessary, e.g., laryngospasm, difficult airway, full stomach, or for intramuscular use when a suitable vein is inaccessible.
This study focuses on an underserved, understudied population: African American and White homebound persons with dementia and their caregivers (CGs). Severe dementia, frailty, multiple disabling co-morbid diseases, lack of transportation, inability to afford or obtain a sitter for the care recipient (CR), and lack of time in a CG's burdened daily schedule may prevent care dyads (caregivers and their family member with dementia) from receiving services in primary care settings and from participating in clinical studies. Homebound issues may be particularly important for African American CGs, yet the minority CG literature has not addressed relevant issues for homebound dyads. Nor are the chronic needs of homebound dementia care dyads adequately attended by the current home health care system, which now focuses on skilled nursing care. This study has been designed to address these research deficits. The study will examine the benefit (through improving depression, anxiety, and health perception) and the cost-effectiveness of home-based dementia caregiving interventions, with attention to both the informal care provided by the CG and the use of formal care services.

Care dyads will be randomized to either Usual Care or Enhanced Care. Both Usual Care and Enhanced Care caregivers will receive usual home health care delivered by home health nurses on the schedule determined by the patient's needs and set by the home care agency. For the Enhanced Care caregivers, to ensure protocol adherence, using the same schedule as the home health visits, trained interventionists from the research staff will deliver the intervention. The interventionists will teach dementia family caregivers to cope with difficult care recipient behaviors and challenges to caregiving and will teach caregivers how to cope with their own responses to caregiving. Following established protocols and using fifth grade level pamphlets and educational material, the interventionists will tailor the intervention sessions to meet the individual needs of each care dyad in their own home environment. Enhanced Care sessions will not exceed 60 minutes. Research specialists will perform data collection visits in the care dyads' homes at baseline, within 2 weeks of home care ending and six months.
The dosage of chloroquine phosphate is often expressed in terms of equivalent chloroquine base. Each 250 mg tablet of chloroquine phosphate contains the equivalent of 150 mg chloroquine base. In infants and children the dosage is preferably calculated by body weight.  
Prophylaxis against chloroquine-sensitive Plasmodium species   
Adult Dose: The dosage for prophylaxis is 250 mg (= 150 mg base) administered once per week on exactly the same day of each week.  
Pediatric Dose: The dosage for prophylaxis is 5 mg calculated as base, per kg of body weight, administered once per week on exactly the same day of each week. The pediatric dose should never exceed the adult dose regardless of weight.  
If circumstances permit, suppressive therapy should begin two weeks prior to exposure. However, failing this in adults, an initial double (loading) dose of 1 g (= 600 mg base), or in children 10 mg base/kg may be taken in two divided doses, six hours apart. The suppressive therapy should be continued for eight weeks after leaving the endemic area.
Bolus of 5-40 mg (0.5 - 4 ml) of furosemide iv at physicians discretion followed by infusion of furosemide. Infusion rate: 0-40 mg/hour. Starting rate: 20 mg/hour. The infusion is adjusted according effect. Target is a negative fluid balance of 1 ml/kg/hour. The fluid balance is calculated 3 times a dag at 6:00 am, 2:00 pm and 10:00 pm. Goal directed fluid removal is stopped when the fluid balance is assessed neutral.
Elevations of one or more hepatic function enzymes and bilirubin may occur during zileuton extended-release tablets therapy. These laboratory abnormalities may progress to clinically significant liver injury, remain unchanged, or resolve with continued treatment, usually within three weeks. The ALT (SGPT) test is considered the most sensitive indicator of liver injury for zileuton extended-release tablets. 

Assess hepatic function enzymes prior to initiation of, and during therapy with, zileuton extended- release tablets. Assess serum ALT before treatment begins, once a month for the first 3 months, every 2 to 3 months for the remainder of the first year, and periodically thereafter for patients receiving long-term zileuton extended-release tablets therapy. If clinical signs and/or symptoms of liver dysfunction develop (e.g., right upper quadrant pain, nausea, fatigue, lethargy, pruritus, jaundice, or "flu-like" symptoms) or transaminase elevations ≥5×ULN occur, discontinue zileuton extended-release tablets and follow hepatic function enzymes until normal. 

In controlled and open-label clinical studies involving more than 5000 patients treated with zileuton immediate-release tablets, the overall rate of ALT elevation ≥3×ULN was 3.2%. In these trials, one patient developed symptomatic hepatitis with jaundice, which resolved upon discontinuation of therapy. An additional 3 patients with transaminase elevations developed mild hyperbilirubinemia that was less than 3×ULN. There was no evidence of hypersensitivity or other alternative etiologies for these findings. 

Since treatment with zileuton extended-release tablets may result in increased hepatic function enzymes and liver injury, zileuton extended-release tablets should be used with caution in patients who consume substantial quantities of alcohol and/or have a past history of liver disease.
Participants will be asked to complete the same 7 validated questionnaires, the brief psychiatric rating scale and a physical health assessment at the start. The will continue to receive standard care from their usual care professionals. The same measures that were completed at the beginning will be re-assessed again at 6 months.
Patients with prior history of coronary artery disease (CAD) (myocardial infarction, cerebrovascular accident, coronary angioplasty, S/p CABG operation) who will be given on the first day either caffeine of placebo tablet and 1-2 hours thereafter a brachial artery endothelial function testing (BRT) will be assessed for measuring the FMD. After 1 week the patients will come for a second BRT on placebo/caffeine tablets. If the patient received caffeine tablet the first BRT, he will be receiving placebo tablet the second week, however, if the patient received placebo the first BRT, a caffeine tablet will be given prior to the second BRT.
Sensorcaine ® (bupivacaine HCl) injections are sterile isotonic solutions that contain a local anesthetic agent with and without epinephrine (as bitartrate) 1:200,000 and are administered parenterally by injection. See INDICATIONS AND USAGE for specific uses. Solutions of bupivacaine HCl may be autoclaved if they do not contain epinephrine. 

Sensorcaine injections contain bupivacaine HCl which is chemically designated as 2- piperidinecarboxamide, 1-butyl- N-(2,6-dimethylphenyl)-, monohydrochloride, monohydrate and has the following structure:

Epinephrine is (-)-3,4-Dihydroxy-α [(methylamino)methyl] benzyl alcohol. It has the following structural formula: 

The pK a of bupivacaine (8.1) is similar to that of lidocaine (7.86). However, bupivacaine possesses a greater degree of lipid solubility and is protein bound to a greater extent than lidocaine.

Bupivacaine is related chemically and pharmacologically to the aminoacyl local anesthetics. It is a homologue of mepivacaine and is chemically related to lidocaine. All three of these anesthetics contain an amide linkage between the aromatic nucleus and the amino, or piperidine group. They differ in this respect from the procaine-type local anesthetics, which have an ester linkage.

Dosage forms listed as Sensorcaine-MPF indicates s ingle dose solutions that are Methyl Paraben Free (MPF).

Sensorcaine-MPF is a sterile isotonic solution containing sodium chloride. Sensorcaine in multiple dose vials, each mL also contains 1 mg methylparaben as antiseptic preservative. The pH of these solutions is adjusted to between 4.0 and 6.5 with sodium hydroxide and/or hydrochloric acid.

Sensorcaine-MPF with Epinephrine 1:200,000 (as bitartrate) is a sterile isotonic solution containing sodium chloride. Each mL contains bupivacaine hydrochloride and 0.005 mg epinephrine, with 0.5 mg sodium metabisulfite as an antioxidant and 0.2 mg citric acid (anhydrous) as stabilizer. Sensorcaine with Epinephrine 1:200,000 (as bitartrate) in multiple dose vials, each mL also contains 1 mg methylparaben as antiseptic preservative. The pH of these solutions is adjusted to between 3.3 to 5.5 with sodium hydroxide and/or hydrochloric acid. Filled under nitrogen.

Note: The user should have an appreciation and awareness of the formulations and their intended uses (see DOSAGE AND ADMINISTRATION).
Participants will receive Treatment A (JNJ-64565111 subcutaneous \[SC\] administration in the upper arm in fasted condition) on Day 1 of Treatment Period 1; followed by Treatment B (JNJ-64565111 SC administration in the thigh in fasted condition) on Day 1 of Treatment Period 2 and then Treatment C (JNJ-64565111 SC administration in the abdomen in fasted condition) on Day 1 of Treatment Period 3. Each treatment period will be separated by a washout Period of at least 7 days between the last pharmacokinetic (PK) sample collection and dosing on Day 1 of subsequent treatment period.
Pregnancy Category C   
Tizanidine has not been studied in pregnant women. Tizanidine should be given to pregnant women only if the benefit outweighs the risk to the unborn fetus. Reproduction studies performed in rats at a dose of 3 mg/kg, equal to the maximum recommended human dose on a mg/m2 basis, and in rabbits at 30 mg/kg, 16 times the maximum recommended human dose on a mg/m 2 basis, did not show evidence of teratogenicity. Tizanidine at doses that are equal to and up to 8 times the maximum recommended human dose on a mg/m2 basis increased gestation duration in rats. Prenatal and postnatal pup loss was increased and developmental retardation occurred. Post-implantation loss was increased in rabbits at doses of 1 mg/kg or greater, equal to or greater than 0.5 times the maximum recommended human dose on a mg/m 2 basis.
Evidence suggests that circulating tumor DNA (ctDNA) analysis can noninvasively identify minimal residual disease (MRD) in clinical oncology. The researches will be sharply increased about ctDNA potential clinical application in the near future. In the early stage of NSCLC, ctDNA has been indicated to identify those at high risk of recurrence after radical surgery. And this study will focus on those patients with advanced NSCLC who have long-term benefit from first-line immunotherapy (PFS 12 months). 10ml plasma will be collected every three months until disease progression to interrogate ctDNA by high-depth panel sequencing, exploring its prediction value about the risk of progression. Meanwhile, the investigators would like to explore the lead time of detectable ctDNA before regular imaging finding.
BACKGROUND: The treatment for papillary thyroid microcarcinoma (PTMC) is controversial. Central lymph node metastasis (CLNM) is one of the main predictors of recurrence and survival, accurate preoperative identification of CLNM is essential for surgical protocol establishment for PTMC. The objective of this study was to establish a nomogram to predict the possibility of CLNM in PTMC patients.
METHODS: A total of 3023 PTMC patients were randomly divided into two groups by a ratio of 7 to 3, the training group (n = 2116) and validation group (n = 907). The LASSO regression model and multivariate logistic regression analysis were performed to examine risk factors associated with CLNM. A nomogram for predicting CLNM was established and internally validated. Meanwhile, we follow-up the serum thyroid function FT3, FT4, TSH, Tg, TGAb and TPOAb in 789 PTMC patients for 4 years after surgery and compared the differences between the CLNM (+) and CLNM (-) groups, respectively.
RESULTS: The LASSO regression model and multivariate logistic regression analysis showed that younger age, lower BMI, being male, location in the lower pole, calcification, 1 ≥ diameter ≥ 0.5 cm, multifocality lesions, extra thyroidal extension (ETE), enlargement of central lymph node (ECLN), lateral lymph node metastasis (LLNM) and higher carcinoembryonic antigen were the ultimate risk factors for determining CLNM. A nomogram for predicting CLNM was constructed based on the influencing factors and internally validated. By establishing the prediction model, the AUC of CLNM in the training and validation groups were 0.73 (95% CI, 0.70-0.76) and 0.75 (95% CI, 0.71-0.79) respectively. Results of the DCA showed that the model is clinically useful when deciding on intervention in the most range of the threshold probability. A 4-year follow-up of thyroid function showed that FT3 and FT4 remained at stable levels after 3 months postoperative and were higher in the CLNM (+) group than in the CLNM (-) group. Hypothyroidism appeared predominantly within 3 months after surgery. The overall incidence of the CLNM (+) group and CLNM (-) groups were 16.46% and 12.04%, respectively.
CONCLUSION: The nomogram model constructed in this study has a good predictive effect on CLNM in PTMC patients and provides a reasonable reference for clinical treatment.
Rationale: The clinical treatment of epilepsy is faced with challenges. On the one hand, the effectiveness of existing antiepileptic drugs (AEDs) is limited by the blood‒brain barrier (BBB); on the other hand, changes in the inflammatory microenvironment during epileptogenesis are often neglected. Methods: The death-associated protein kinase 1 inhibitor TC-DAPK6 and the fluorescent probe rhodamine B were encapsulated in hollow mesoporous silica nanocarriers (HMSNs), which were then coated with a macrophage membrane to prepare macrophage membrane-biomimetic nanoparticles, namely, MA@RT-HMSNs. In vitro biotoxicity, cellular uptake, BBB permeability and inflammatory targeting ability were evaluated in cells. The effects of MA@RT-HMSN treatment were explored by immunohistochemistry, TUNEL assay, Western blot analysis, quantitative real-time polymerase chain reaction, electroencephalogram recording and behavioural tests in kainic acid-induced acute and chronic epilepsy model mice. Results: MA@RT-HMSNs showed excellent biocompatibility both in vitro and in vivo. MA@RT-HMSNs successfully crossed the BBB and exhibited increased efficacy in targeted delivery of TC-DAPK6 to inflammatory lesions in epileptic foci. Macrophage membrane coating conferred MA@RT-HMSNs with higher stability, greater cellular uptake, and enhanced TC-DAPK6 bioavailability. Furthermore, MA@RT-HMSNs exerted beneficial therapeutic effects on acute and chronic epilepsy models by alleviating microenvironment inflammation, preventing neuronal death, and inhibiting neuronal excitability and gliosis. Conclusions: MA@RT-HMSNs target inflammatory foci to inhibit death-related protein kinase 1 and exert antiepileptic effects. This study provides a promising biomimetic nanodelivery system for targeted epilepsy therapy.
Propafenone Hydrochloride Extended-Release Capsules, USP are an antiarrhythmic drug supplied in extended- release capsules of 225, 325, and 425 mg for oral administration.

Chemically, propafenone hydrochloride is 2'-[2-hydroxy-3-(propylamino)-propoxy]-3- phenylpropiophenone hydrochloride, with a molecular weight of 377.92. The molecular formula is C21H27NO3∙HCl.

Propafenone HCl has some structural similarities to beta-blocking agents. The structural formula of propafenone HCl is given below:

Propafenone HCl occurs as colorless crystals or white crystalline powder with a very bitter taste. It is slightly soluble in water (20°C), chloroform, and ethanol. Propafenone Hydrochloride Extended-Release Capsules, USP are filled with white to off white round, biconvex mini tablets containing propafenone and the following inactive ingredients: hypromellose and magnesium stearate. Each capsule contains titanium dioxide and gelatin. In addition, the 225 mg capsule contains D&C Yellow No. 10 and FD&C Red No. 3, the 325 mg capsule contains FD&C Blue No. 2, and the 425 mg capsule contains FD&C Green No. 3. The black imprinting ink consists of black iron oxide (ferrosoferric oxide), propylene glycol, potassium hydroxide, shellac, and ammonium hydroxide.

USP Dissolution Test Pending
Neuroinflammation, mediated by the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3 (NLRP3) inflammasome, is a significant contributor to the pathogenesis of neurodegenerative diseases (NDDs). Reynosin, a natural sesquiterpene lactone (SL), exhibits a broad spectrum of pharmacological effects, suggesting its potential therapeutic value. However, the effects and mechanism of reynosin on neuroinflammation remain elusive. The current study explores the effects and mechanisms of reynosin on neuroinflammation using mice and BV-2 microglial cells treated with lipopolysaccharide (LPS). Our findings reveal that reynosin effectively reduces microglial inflammation in vitro, as demonstrated by decreased CD11b expression and lowered interleukin-1 beta (IL-1β) and interleukin-18 (IL-18) mRNA and protein levels. Correspondingly, in vivo, results showed a reduction in the number of Iba-1 positive cells and alleviation of morphological alterations, alongside decreased expressions of IL-1β and IL-18. Further analysis indicates that reynosin inhibits NLRP3 inflammasome activation, evidenced by reduced transcription of NLRP3 and caspase-1, diminished NLRP3 protein expression, inhibited apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization, and decreased caspase-1 self-cleavage. Additionally, reynosin curtailed the activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, demonstrated by reduced NADP+ and NADPH levels, downregulation of gp91phox mRNA, protein expression, suppression of p47phox expression and translocation to the membrane. Moreover, reynosin exhibited a neuroprotective effect against microglial inflammation in vivo and in vitro. These collective findings underscore reynosin's capacity to mitigate microglial inflammation by inhibiting the NLRP3 inflammasome, thus highlighting its potential as a therapeutic agent for managing neuroinflammation.
In this group, the order of interventions will be randomized. Therefore, the volunteer can start with manual therapy or sham TMS. In manual therapy, patients will be submitted to 45 minutes of a protocol. In addition, with regard to sham TMS, the same parameters will be used, however, it will be performed using two coils, one connected to the magnetic stimulator, away from the patient's scalp and another uncoupled from the stimulator and positioned in the same way as in real stimulation.
The subject invention concerns materials and methods for expansion of stem cells, such as mesenchymal stem cells (MSC), that improve translational success of the cells in the treatment of various conditions. The subject invention utilizes cell self-aggregation as a non-genetic means to enhance their therapeutic potency in a microcarrier bioreactor. In one embodiment of the method cells are cultured in a container or vessel in the presence of thermally responsive microcarriers (TRMs) wherein cells adhere to the surface of the TRMs. After a period of time the cell culture temperature is reduced so that the cells detach from the TRMs. The detached cells are allowed to form 3D aggregates. The 3D aggregates can be collected and treated to dissociate the cells. Dissociated cells can then be used for transplantation in methods of treatment or for in vitro characterization and study.
A method and apparatus to determine body composition of a subject is disclosed. Physical characteristics of a subject and water in a pool is determined. A body of the subject is completely submerged in the pool of water such that a head of the subject is just below a surface of the water in the pool. The subject completely exhales air into an air measuring device as the body of the subject is submerged just below the surface of the water. A semi-rigid strip or tab portion may be coupled to the air measuring device to indicate when air pressure within the air measuring device is between a predetermined range. The body composition is then determined based on the determined subject characteristics, water characteristics and the amount of air exhaled into the air measuring device when the air pressure is between the predetermined range.