anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The invention discloses a preparation technology of Gu Chisan for treating periodontitis. Gu Chisan comprises tortoise shell, halitum, Ligusticum wallichii, Cyperus Rotundus L, lotus leaf, Chinese prickly ash, hibiscus syriacus linn and dahurian angelica root. The process includes: A. pretreating raw medicinal materials; B. pulverizing the medicinal materials, i.e. pulverizing the dried net medicinal materials that are cooled to room temperature respectively in a rough grinding machine into rough powder, and sieving the powder through a sieve of 80 meshes; C. disinfecting the rough powder of all medicinal materials with oxirane; D. due to a high water content of the disinfected medicinal rough powder, drying the rough powder of all medicinal materials in a baking oven to a water content of 5.0-6.0%; E. pulverizing and sieving, i.e. pulverizing the dried rough powder of all medicinal materials respectively into finest powder in a fine grinding machine, and sieving through a sieve of 120 meshes so as to obtain finest powder of each medicinal materials; F. weighing, proportioning and packaging: weighing and charging the finest powder of each medicinal material based on a mass ratio of the components, mixing the finest powder overall; charging separately and packaging hermetically the mixed finest powder, thus obtaining a finished product. The preparation technology is characterized by high degree of mechanical automation, further guaranteed quality, low labor intensity and high production efficiency.
Heart failure with preserved ejection fraction (HFpEF) comprises approximately 50% of all heart failure. The effectively therapeutic approaches for HFpEF remain limited. The PARAGON-HF trial found that Angiotensin Receptor-Neprilysin Inhibition (ARNI) has potential benefits for the management of HFpEF. Nevertheless, the role of ARNI in cardiac fibrosis in HFpEF are still unclear. We will conduct a prospective randomized controlled trial to evaluate the effect of ARNI on cardiac fibrosis in patients with HFpEF by cardiac magnetic resonance (CMR). We will randomly assign 60 patients with HFpEF (NYHA II-IV) class, ejection fraction ≥ 50% and elevated level of natriuretic peptides to receive sacubitril-valsartan (target 100mg bid) or placebo (100mg bid). The primary endpoint is change in extracellular volume \[ECV\] measured by CMR. The secondary endpoints were 6-minute walking distance(6-WMD), KCCQ, hospitalizations for heart failure, myocardial infarction and death.
Disruption of SYNGAP1 directly causes a genetically identifiable neurodevelopmental disorder (NDD) called SYNGAP1-related intellectual disability (SRID). Without functional SynGAP1 protein, individuals are developmentally delayed and have prominent features of intellectual disability (ID), motor impairments, and epilepsy. Over the past two decades, there have been numerous discoveries indicating the critical role of Syngap1. Several rodent models with a loss of Syngap1 have been engineered, identifying precise roles in neuronal structure and function, as well as key biochemical pathways key for synapse integrity. Homozygous loss of SYNGAP1/Syngap1 is lethal. Heterozygous mutations of Syngap1 result in a broad range of behavioral phenotypes. Our in vivo functional data, using the original mouse model from the Huganir laboratory, corroborated behaviors including robust hyperactivity and deficits in learning and memory in young adults. Furthermore, we described impairments in the domain of sleep, characterized using neurophysiological data that was collected with wireless, telemetric electroencephalography (EEG). Syngap1+/- mice exhibited elevated spiking events and spike trains, in addition to elevated power, most notably in the delta power frequency. For the first time, we illustrated that primary neurons from Syngap1+/- mice displayed: 1) increased network firing activity, 2) greater bursts, 3) and shorter inter-burst intervals between peaks, by utilizing high density microelectrode arrays (HD-MEA). Our work bridges in vitro electrophysiological neuronal activity and function with in vivo neurophysiological brain activity and function. These data elucidate quantitative, translational biomarkers in vivo and in vitro that can be utilized for the development and efficacy assessment of targeted treatments for SRID.
Store MYXREDLIN in the refrigerator (36°F to 46°F [2°C to 8°C]) in the original carton to protect from light. Do not use after the expiration date printed on the carton and container label.

If needed, MYXREDLIN may be removed from the original carton and stored at room temperature up to 77°F (25°C) for up to 30 days. Once stored at room temperature, do not place back in the refrigerator. Discard MYXREDLIN after 30 days if stored at room temperature.

Do not freeze and do not use MYXREDLIN if it has been frozen. Do not shake.
PURPOSE: Patients with anterior cutaneous nerve entrapment syndrome (ACNES) often require a step-up treatment strategy including abdominal wall injections, pulsed radiofrequency (PRF) or a neurectomy. Long-term success rates of PRF and surgery are largely unknown. The aim of the current study was to report on the long-term efficacy of PRF and neurectomy in ACNES patients who earlier participated in the randomized controlled PULSE trial.
METHODS: Patients who completed the PULSE trial were contacted about pain status and additional treatments in the following years. Treatment success was based on numerical rating scale (NRS) following IMMPACT recommendations and Patient Global Impression of Change (PGIC) scores.
RESULTS: A total of 44 of the original 60 patients were eligible for analysis (73.3%). Median follow-up was 71.5 months. One patient (4.3%) was still free of pain after a single PRF session, and five additional patients (21.7%) were free of pain by repetitive PRF treatments. By contrast, 13 patients (61.9%) in the neurectomy group were still free of pain without additional treatments. All pain recurrences and therefore primary re-interventions occurred in the first 2 years after the initial treatment.
CONCLUSION: Approximately one in five ACNES patients undergoing PRF treatment reports long-term success obviating the need of surgical intervention. Surgery for ACNES is long-term effective in approximately two of three operated patients. Recurrent ACNES beyond 2 years after either intervention is rare.
The study population consists of 30 patients with unstable angina pectoris (UAP, n = 30). They will all undergo coronary angiography for the diagnosis of acute coronary syndrome. The diagnosis is made according to the criteria of the American Heart Association (AHA, 2014 and 2015). Patients who had autoimmune diseases, malignancies, chronic or acute infections, asthma, severe heart failure (NYHA class 3 and 4) and advanced liver or renal diseases are excluded.
###  Pregnancy Category C:

There are no adequate and well controlled studies in pregnant women; therefore, zolmitriptan should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

In reproductive toxicity studies in rats and rabbits, oral administration of zolmitriptan to pregnant animals was associated with embryolethality and fetal abnormalities. When pregnant rats were administered oral zolmitriptan during the period of organogenesis at doses of 100, 400, and 1200 mg/kg/day, there was a dose-related increase in embryolethality which became statistically significant at the high dose. The maternal plasma exposures at these doses were approximately 280, 1100, and 5000 times the exposure in humans receiving the maximum recommended total daily dose of 10 mg. The high dose was maternally toxic, as evidenced by a decreased maternal body weight gain during gestation. In a similar study in rabbits, embryolethality was increased at the maternally toxic doses of 10 and 30 mg/kg/day (maternal plasma exposures equivalent to 11 and 42 times exposure in humans receiving the maximum recommended total daily dose of 10 mg), and increased incidences of fetal malformations (fused sternebrae, rib anomalies) and variations (major blood vessel variations, irregular ossification pattern of ribs) were observed at 30 mg/kg/day. Three mg/kg/day was a no effect dose (equivalent to human exposure at a dose of 10 mg). When female rats were given zolmitriptan during gestation, parturition, and lactation, an increased incidence of hydronephrosis was found in the offspring at the maternally toxic dose of 400 mg/kg/day (1100 times human exposure).
PURPOSE: To prepare the subject composition, comprising a thromboxane A2 receptor antagonist as an active ingredient and capable of promoting the curing of skin injuries and/or limiting the degree of the injuries. CONSTITUTION: This composition comprises a thromboxane A2 antagonist, e.g. 7-oxabicycloheptane-substituted diamidoprostaglandin analog, a phenoxyalkylcarboxylic acid, a sulfonamidophenylcarboxylic acid or an arylthioalkylphenylcarboxylic acid as an active ingredient. The resultant composition is systemically or locally administered to skin during or after suffering thereof from a heat burn or a trauma or before or during or after suffering thereof from pressure injuries (e.g. a decubitus) when the skin suffers therefrom. The daily dose thereof is 5-2,500mg, preferably 10-2,000mg in the case of a systemic dosage form.
The Cleerly Stage-Based Care group will receive personalized care centrally managed by a remote cardiologist-led team. They will also receive an initial pre-randomization assessment of current treatment by a centralized cardiology team to optimize care relative to primary prevention guidelines. Cleerly CAD Staging System results will be discussed with participants and serve as the basis for standardized algorithm-supported pharmacotherapy \& education, which will be intensified if plaque burden has progressed at 24 months.
ACE inhibitors, Angiotensin II receptor antagonists, aldosterone blockers, potassium supplements, heparin, low molecular weight heparin, and other drugs known to cause hyperkalemia: Concomitant administration may lead to severe hyperkalemia. 

Alcohol, barbiturates, or narcotics: Potentiation of orthostatic hypotension may occur. 

Antidiabetic drugs (e.g., oral agents, insulin): Dosage adjustment of the antidiabetic drug may be required (see Precautions). 

Corticosteroids, ACTH: Intensified electrolyte depletion, particularly hypokalemia, may occur. 

Pressor amines (e.g., norepinephrine): Both spironolactone and hydrochlorothiazide reduce the vascular responsiveness to norepinephrine. Therefore, caution should be exercised in the management of patients subjected to regional or general anesthesia while they are being treated with spironolactone and hydrochlorothiazide tablets. 

Skeletal muscle relaxants, nondepolarizing (e.g., tubocurarine): Possible increased responsiveness to the muscle relaxant may result. 

Lithium: Lithium generally should not be given with diuretics. Diuretic agents reduce the renal clearance of lithium and add a high risk of lithium toxicity. 

Nonsteroidal anti-inflammatory drugs (NSAIDs): In some patients, the administration of an NSAID can reduce the diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing, and thiazide diuretics. Combination of NSAIDs, e.g., indomethacin, with potassium-sparing diuretics has been associated with severe hyperkalemia. Therefore, when spironolactone and hydrochlorothiazide tablets and NSAIDs are used concomitantly, the patient should be observed closely to determine if the desired effect of the diuretic is obtained. 

Acetylsalicylic acid: Acetylsalicylic acid may reduce the efficacy of spironolactone. Therefore, when spironolactone and hydrochlorothiazide tablets and acetylsalicylic acid are used concomitantly, spironolactone and hydrochlorothiazide tablets may need to be titrated to higher maintenance dose and the patient should be observed closely to determine if the desired effect is obtained.

Digoxin: Spironolactone has been shown to increase the half-life of digoxin. This may result in increased serum digoxin levels and subsequent digitalis toxicity. Monitor serum digoxin levels and adjust dose accordingly. Thiazide-induced electrolyte disturbances, i.e. hypokalemia, hypomagnesemia, increase the risk of digoxin toxicity, which may lead to fatal arrhythmic events (see Precautions). 

Cholestyramine: Hyperkalemic metabolic acidosis has been reported in patients given spironolactone concurrently with cholestyramine. 

Drug/Laboratory test interactions: Thiazides should be discontinued before carrying out tests for parathyroid function (see Precautions: General ). Thiazides may also decrease serum PBI levels without evidence of alteration of thyroid function. 

Several reports of possible interference with digoxin radioimmunoassays by spironolactone or its metabolites have appeared in the literature. Neither the extent nor the potential clinical significance of its interference (which may be assay specific) has been fully established.
Patients will undergo a 50 min manual lymphatic drainage (MLD) therapy session by a certified lymphedema therapist. MLD therapy is performed routinely for standard of care in these patients and consists of light massage to facilitate lymphatic fluid mobility.
1. A method for prevention of diabetic vascular dysfunction, said method comprising administering to a mammal in need of said prevention an effective amount of a COMT inhibitor or its pharmaceutically acceptable salt or ester. 2. The method of claim 1, wherein said dysfunction is microangiopathy. 3. The method of claim 2, wherein said dysfunction is nephropathy and/or retinopathy. 4. The method of any one of claims 1-3, wherein said COMT inhibitor is nitecapone. 5. A method for prevention of neuropathy by administering to a mammal in need of said prevention an effective amount of a COMT inhibitor or its pharmaceutically acceptable salt or ester to prevent said neuropathy. 6. The method of claim 5, wherein said COMT inhibitor is nitecapone.
Subjects will perform a lung ultrasound in order to determine the ability of patients to take an ultrasound from their homes. The lung ultrasound will be coupled with telehealth clinical support to monitor the severity of COVID-19 patients and provide standard of care. All subjects will receive the lung ultrasound technology and daily calls for teleguidance through the ultrasound and standard of care to monitor symptoms.
GLYDO (lidocaine HCl jelly, USP) 2% is a sterile aqueous product that contains a local anesthetic agent and is administered topically (see INDICATIONS AND USAGE for specific uses). 

GLYDO (lidocaine HCl jelly, USP) 2% contains lidocaine HCl which is chemically designated as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl)-, monohydrochloride and has the following structural formula: 

GLYDO (lidocaine HCl jelly, USP) 2% also contains hypromellose, and the resulting mixture maximizes contact with mucosa and provides lubrication for instrumentation. The unused portion should be discarded after initial use. 

GLYDO (lidocaine HCl jelly, USP) 2% is available in 6 mL and 11 mL single-dose prefilled syringes. Each mL contains 20 mg of lidocaine HCl. The formulation also contains hypromellose, and sodium hydroxide to adjust pH to 6.0 to 7.0.
Liver fibrosis is commonly occurred in chronic liver diseases, but there is no approved drug for clinical use. The nuclear receptor peroxisome proliferator-activated receptors (PPARs) could not only regulate metabolic homeostasis but also possess anti-inflammatory and antifibrotic effects, and pan-PPARs agonist was considered as a potential anti-liver fibrosis agent. In this study, a series of novel piperazine pan-PPARs agonists were developed, and the preferred compound 12 displayed potent and well-balanced pan-PPARs agonistic activity. Moreover, compound 12 could dose-dependently stimulate the PPARs target genes expression and showed high selectivity over other related nuclear receptors. Importantly, compound 12 exhibited excellent pharmacokinetic profiles and good anti-liver fibrosis effects in vivo. Collectively, compound 12 holds promise for developing an anti-liver fibrosis agent.
Participants receive grazoprevir 100 mg/elbasvir 50 mg FDC tablets q.d. by mouth, along with RBV capsules twice daily (b.i.d.) by mouth (weight-based dosing; 800 to 1400 mg total daily dose), for 12 weeks.
The present invention discloses medicine for treating coronary disease, which is powder preparation formed by reasonably matching notoginseng, red sage root, lignum dalbergiae odoriferae, chuanxiong rhizome, sauted peach kernel, sauted apricot kernel, black plum, safflower, goat blood, red peony root, musk and Chinese date. Meanwhile, rhizoma pinelliae or fructus trichosanthis mongolian snakegourd, tuber onion bulb, prepared licorice root and pseudostellaria root can be added to the raw materials on the basis of the basic formulation based on different symptoms of patients. All of the components of the medicine of the present invention are consistent with rules of pharmaceutical administration legislation. The medicine is in a powder type and can be loaded in a capsule to be taken orally. The present invention doesn't need to be decocted and can be taken easily. Moreover, the cost of the medicine is low, and a therapeutic effect is good. An effective rate reaches 90%.
Subjects who received 2 doses of Gardasil vaccine at Day 0 and Month 6 and 1 dose of placebo at Month 2. The vaccines were administered intramuscularly, in the deltoid muscle of the non-dominant upper arm.
Sudden cardiac death (SCD) has been the leading cause of on-duty death (ODD) in the fire service over the past several decades, accounting for 51.6% of all ODDs in 2019. The primary factors that contribute to SCD among firefighters are overexertion and stress, and SCD is most likely to occur during fire suppression and alarm response. When an emergency occurs, firefighters are alerted/awoken by loud mechanical bells. This high noise level may induce a stress response triggering a cardiovascular event. In fact, "high levels of environmental noise fuel cardiac risk" by stimulating the amygdala and inflaming the arteries. While other companies have attempted to modernize alerting systems, they failed to address the problem of stressful alarms because they focus on alerting "stations" not individual firefighters. A significant need exists to develop a less stressful alerting system for firefighters. The objective of this SBIR Phase I R43 research study is to develop a commercially viable Fire Fighter Alerting System (FFAS) comprised of proprietary wearables and optional bed shakers called BunkAlerts. Collectively "personal alerting devices," the wearables and BunkAlerts enhance the alerting process for firefighters by replacing jarring audible alarms with tactile alerts delivered to the firefighter's wrist. This alternative approach is designed to significantly decrease tachycardic responses associated with legacy alerting systems. Meeting this need has the potential to reduce firefighter ODDs and improve the quality of life for the 15.4 million firefighters around the world. The feasibility of EaseAlert's FFAS is reinforced by preliminary data collected during field testing with six (6) fire departments in three (3) states where EaseAlert's prototype FFAS ("Gen 1") successfully delivered over 10,000 alerts to firefighters called to an emergency with no calls missed. The potential for the FFAS to reduce stress and SCD risk among firefighters is supported by preliminary data which shows that: 1) noise triggers a startle response and 2) tactile alerts are associated with positive valence and high arousal. The proposed research will be accomplished with two aims: Aim 1 - develop a commercially viable FFAS and Aim 2 - determine the effectiveness of the FFAS in reducing cardiac reactivity and improving sleep. EaseAlert will leverage the Gen 1 FFAS as a foundation for developing its Gen 2 FFAS outlined in Aim 1. Aim 2 will test two study hypotheses in a within-subjects pilot clinical trial design: (H2.1) that EaseAlert will result in a significant reduction in the stress response to alarms compared to traditional auditory alerting systems, and (H2.2) EaseAlert will result in a significant improvement in sleep efficiency.
Death from positional asphyxia is often an accidental event occurring when the victim's body assumes a position which can compromise an effective respiration. Its diagnosis is usually not simple, because it needs to know the exact circumstance in which the body was found and the original positioning of all the body segments. In this case, a 41-year-old man with a history of opioid drugs abuse was found dead in a knee-chest position; the head was down on the floor with the face resting on a plastic bag. Pictures of the scene of death was taken while the body was still in its original position. At first, the main suspicion was that of a fatal overdose. Following the autopsy examination, completed by histological and toxicological examinations, the cause of death was determined as postural asphyxia secondary to intoxication by methadone, in the presence of ischemic heart disease. Some features, moreover, were typical of the death in head down position, and the prolonged knee-chest position was also associated with the obstruction of mouth and nose by the plastic bag, which may have contributed to the asphyxiation. These cases of "combined" asphyxia represent a challenge for the current classifications of asphyxia, which are very variable and not standardized, as we observe from a brief review of the literature. The elaboration of new systems of classification for asphyxias, which must be clear, simple and shareable, is necessary to avoid confusion in categorizing cases that present overlapping between several types of asphyxiation modalities.
Cellular senescence assumes pivotal roles in various diseases through the secretion of proinflammatory factors. Despite extensive investigations into vascular senescence associated with aging and degenerative diseases, the molecular mechanisms governing microvascular endothelial cell senescence induced by traumatic stress, particularly its involvement in senescence-induced inflammation, remain insufficiently elucidated. In this study, we present a comprehensive demonstration and characterization of microvascular endothelial cell senescence induced by spinal cord injury (SCI). Lysine demethylase 6A (Kdm6a), commonly known as UTX, emerges as a crucial regulator of cell senescence in injured spinal cord microvascular endothelial cells (SCMECs). Upregulation of UTX induces senescence in SCMECs, leading to an amplified release of proinflammatory factors, specifically the senescence-associated secretory phenotype (SASP) components, thereby modulating the inflammatory microenvironment. Conversely, the deletion of UTX in endothelial cells shields SCMECs against senescence, mitigates the release of proinflammatory SASP factors, and promotes neurological functional recovery after SCI. UTX forms an epigenetic regulatory axis by binding to calponin 1 (CNN1), orchestrating trauma-induced SCMECs senescence and SASP secretion, thereby influencing neuroinflammation and neurological functional repair. Furthermore, local delivery of a senolytic drug reduces senescent SCMECs and suppresses proinflammatory SASP secretion, reinstating a local regenerative microenvironment and enhancing functional repair after SCI. In conclusion, targeting the UTX-CNN1 epigenetic axis to prevent trauma-induced SCMECs senescence holds the potential to inhibit SASP secretion, alleviate neuroinflammation, and provide a novel treatment strategy for SCI repair.
Participants will remain in a waiting list. After 12 weeks, they will be offered the same intervention.