anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Sleep is a physiological process that preserves the integrity of the neuro-immune-endocrine network to maintain homeostasis. Sleep regulates the production and secretion of hormones, neurotransmitters, cytokines and other inflammatory mediators, both at the central nervous system (CNS) and at the periphery. Sleep promotes the removal of potentially toxic metabolites out of the brain through specialized systems such as the glymphatic system, as well as the expression of specific transporters in the blood-brain barrier. The blood-brain barrier maintains CNS homeostasis by selectively transporting metabolic substrates and nutrients into the brain, by regulating the efflux of metabolic waste products, and maintaining bidirectional communication between the periphery and the CNS. All those processes are disrupted during sleep loss. Brain endothelial cells express the blood-brain barrier phenotype, which arises after cell-to-cell interactions with mural cells, like pericytes, and after the release of soluble factors by astroglial endfeet. Astroglia, pericytes and brain endothelial cells respond differently to sleep loss; evidence has shown that sleep loss induces a chronic low-grade inflammatory state at the CNS, which is associated with blood-brain barrier dysfunction. In animal models, blood-brain barrier dysfunction is characterized by increased blood-brain barrier permeability, decreased tight junction protein expression and pericyte detachment from the capillary wall. Blood-brain barrier dysfunction may promote defects in brain clearance of potentially neurotoxic metabolites and byproducts of neural physiology, which may eventually contribute to neurodegenerative diseases. This chapter aims to describe the cellular and molecular mechanisms by which sleep loss modifies the function of the blood-brain barrier.
Participants from the hospital randomized to the experimental group will be first to receive an invitation to complete the web-based educational program. The program will be open for one month. Thirty days after a participant completes the program, they will be sent a link to a follow up survey (web-based). At 60 days, participants who completed the program and the first follow up survey will be randomized to complete a second follow up survey or participate in a 1:1 interview.
The concomitant use of benzodiazepines and opioids increases the risk of respiratory depression because of actions at different receptor sites in the CNS that control respiration. Benzodiazepines interact at GABAA sites and opioids interact primarily at mµ receptors. When benzodiazepines and opioids are combined, the potential for benzodiazepines to significantly worsen opioid-related respiratory depression exists. Limit dosage and duration of concomitant use of benzodiazepines and opioids, and monitor patients closely for respiratory depression and sedation.  
If diazepam is to be combined with other psychotropic agents or anticonvulsant drugs, careful consideration should be given to the pharmacology of the agents to be employed, particularly with known compounds which may potentiate the action of diazepam, such as phenothiazines, narcotics, barbiturates, MAO inhibitors, and other antidepressants. In highly anxious patients with evidence of accompanying depression, particularly those who may have suicidal tendencies, protective measures may be necessary.  
Diazepam injection has produced hypotension or muscular weakness in some patients particularly when used with narcotics, barbiturates, or alcohol.  
The clearance of diazepam and certain other benzodiazepines can be delayed in association with cimetidine administration. The clinical significance of this is unclear.
DYT-TOR1A (DYT1) dystonia, characterized by reduced penetrance and suspected environmental triggers, is explored using a "second hit" DYT-TOR1A rat model. We aim to investigate the biological mechanisms driving the conversion into a dystonic phenotype, focusing on the striatum's role in dystonia pathophysiology. Sciatic nerve crush injury was induced in ∆ETorA rats, lacking spontaneous motor abnormalities, and wild-type (wt) rats. Twelve weeks post-injury, unbiased RNA-sequencing was performed on the striatum to identify differentially expressed genes (DEGs) and pathways. Fenofibrate, a PPARα agonist, was introduced to assess its effects on gene expression. 18F-FDG autoradiography explored metabolic alterations in brain networks. Low transcriptomic variability existed between naïve wt and ∆ETorA rats (17 DEGs). Sciatic nerve injury significantly impacted ∆ETorA rats (1009 DEGs) compared to wt rats (216 DEGs). Pathway analyses revealed disruptions in energy metabolism, specifically in fatty acid β-oxidation and glucose metabolism. Fenofibrate induced gene expression changes in wt rats but failed in ∆ETorA rats. Fenofibrate increased dystonia-like movements in wt rats but reduced them in ∆ETorA rats. 18F-FDG autoradiography indicated modified glucose metabolism in motor and somatosensory cortices and striatum in both ∆ETorA and wt rats post-injury. Our findings highlight perturbed energy metabolism pathways in DYT-TOR1A dystonia, emphasizing compromised PPARα agonist efficacy in the striatum. Furthermore, we identify impaired glucose metabolism in the brain network, suggesting a potential shift in energy substrate utilization in dystonic DYT-TOR1A rats. These results contribute to understanding the pathophysiology and potential therapeutic targets for DYT-TOR1A dystonia.
Fibrotic scar tissue formation occurs in humans and mice. The fibrotic scar impairs tissue regeneration and functional recovery. However, the origin of scar-forming fibroblasts is unclear. Here, we show that stromal fibroblasts forming the fibrotic scar derive from two populations of perivascular cells after spinal cord injury (SCI) in adult mice of both sexes. We anatomically and transcriptionally identify the two cell populations as pericytes and perivascular fibroblasts. Fibroblasts and pericytes are enriched in the white and gray matter regions of the spinal cord, respectively. Both cell populations are recruited in response to SCI and inflammation. However, their contribution to fibrotic scar tissue depends on the location of the lesion. Upon injury, pericytes and perivascular fibroblasts become activated and transcriptionally converge on the generation of stromal myofibroblasts. Our results show that pericytes and perivascular fibroblasts contribute to the fibrotic scar in a region-dependent manner.
BACKGROUND: Upper gastrointestinal bleeding (UGIB) in older patients is associated with substantial in-hospital morbidity and mortality. This study aimed to develop and validate a simplified risk score for predicting 30-day in-hospital mortality in this population.
METHODS: A retrospective analysis was conducted on data from 1899 UGIB patients aged ≥ 65 years admitted to a single medical center between January 2010 and December 2019. An additional cohort of 330 patients admitted from January 2020 to October 2021 was used for external validation. Variable selection was performed using five distinct methods, and models were generated using generalized linear models, random forest, support vector machine, and k-nearest neighbors approaches. The developed score, "ABCAP," incorporated Albumin < 30 g/L, Blood Urea Nitrogen (BUN) > 7.5 mmol/L, Cancer presence, Altered mental status, and Pulse rate > 100/min, each assigned a score of 1. Internal and external validation procedures compared the ABCAP score with the AIMS65 score.
RESULTS: In internal validation, the ABCAP score demonstrated robust predictive capability with an area under the curve (AUC) of 0.878 (95% CI: 0.824-0.932), which was significantly better than the AIMS65 score (AUC: 0.827, 95% CI: 0.751-0.904), as revealed by the DeLong test (p = 0.048). External validation of the ABCAP score resulted in an AUC of 0.799 (95% CI: 0.709-0.889), while the AIMS65 score yielded an AUC of 0.743 (95% CI: 0.647-0.838), with no significant difference between the two scores based on the DeLong test (p = 0.16). However, the ABCAP score at the 3-5 score level demonstrated superior performance in identifying high-risk patients compared to the AIMS65 score. This score exhibited consistent predictive accuracy across variceal and non-variceal UGIB subgroups.
CONCLUSIONS: The ABCAP score incorporates easily obtained clinical variables and demonstrates promising predictive ability for 30-day in-hospital mortality in older UGIB patients. It allows effective mortality risk stratification and showed slightly better performance than the AIMS65 score. Further cohort validation is required to confirm generalizability.
12.1 Mechanism of Action

Phenylephrine hydrochloride is an α-1 adrenergic receptor agonist.

12.2 Pharmacodynamics

Interaction of phenylephrine with α1-adrenergic receptors on vascular smooth muscle cells causes activation of the cells and results in vasoconstriction. Following phenylephrine hydrochloride intravenous administration, increases in systolic and diastolic blood pressures, mean arterial blood pressure, and total peripheral vascular resistance are observed. The onset of blood pressure increase following an intravenous bolus phenylephrine hydrochloride administration is rapid, typically within minutes. As blood pressure increases following intravenous administration, vagal activity also increases, resulting in reflex bradycardia. Phenylephrine has activity on most vascular beds, including renal, pulmonary, and splanchnic arteries.

12.3 Pharmacokinetics

Following an intravenous infusion of phenylephrine hydrochloride, the observed effective half-life was approximately 5 minutes. The steady-state volume of distribution of approximately 340 L suggests a high distribution into organs and peripheral tissues. The average total serum clearance is approximately 2100 mL/min. The observed phenylephrine plasma terminal elimination half-life was 2.5 hours.

Phenylephrine is metabolized primarily by monoamine oxidase and sulfotransferase. After intravenous administration of radiolabeled phenylephrine, approximately 80% of the total dose was eliminated within first 12 hours; and approximately 86% of the total dose was recovered in the urine within 48 hours. The excreted unchanged parent drug was 16% of the total dose in the urine at 48 hours post intravenous administration. There are two major metabolites, with approximately 57 and 8% of the total dose excreted as m-hydroxymandelic acid and sulfate conjugates, respectively. The metabolites are considered not pharmacologically active.
We designed and implemented the kneeling stool to perform CPR with the kneeling posture for a patient on a bed. The frame is constructed of an aluminum alloy. The size is 570 mm (width) x 598 mm (depth) x 600 mm (height). The weight is 9.3 kg, which is easily moved as needed. For easy rotation between rescuers, a step plate was inserted. To prevent pain to the knees of the kneeling CC performer, a 40mmthick sponge cushion was placed on the top plate and fixed to the frame.

A standard hospital bed frame (Transport stretcher®, 760 x2110 mm, 228 kg, Stryker Co., Kalamazoo, Michigan, USA), a foam mattress (660 x 920 x 80 mm, soft foam with polyurethane coverage, Stryker Co., USA), a backboard (450 ×600 ×10 mm, 3 kg Lifeline Plastic, Sung Shim Medical Co., Bucheon, Korea), and a step stool (395 x 450 x 410 mm, Gunica Co., Gyeongsangnam-do, Korea) were used in the experiment. A Resusci Annie Modular System Skill Reporter® manikin (Laerdal Medical, Orpington, UK) was used to perform CPR in the evaluations. We added weight to the manikin to equal 34 kg for simulating the upper body weight of an adult human as in a previous study.

Data collection The participants were divided into two groups by random drawing. Each performer in the first group knelt on the kneeling stool beside the manikin on a bed and compressed the chest of the manikin (CCs with a kneeling posture, PK).Each performer in the second group stood on a step stool beside the manikin on a bed and compressed the chest of the manikin (CCs with a standing posture, PS). When the performer stood beside the manikin on a bed, the height of the manikin's back was adjusted in height to the knee level of the provider using the step stool and the bed height adjustment mechanism. All the participants performed continuous CCs for 5 minutes without audio-visual feedback. After 2 weeks, the posture used for the CCs by each group was changed. Each participant recorded his/her fatigue and pain levels on a visual analogue scale (VAS, score 0 indicates "no pain and fatigue" and score 10 indicates "unbearable pain and fatigue") for each minute during 5 minutes of CCs. After conclusion of the experiment, the participants selected a preferred CC posture in terms of the safety and the quality of the CCs.
A process for producing substantially radio-impurity-free Bi-212 is disclosed. An acidic feed solution containing Pb-212 is contacted with an extraction medium to bind the Pb-212 thereto. The extraction medium is rinsed with a second acid solution to remove impurities therefrom, leaving a substantially impurity-free Pb-212-laden extraction medium. The Pb-212 grows on the extraction medium to form Bi-212 by radioactive decay. The Bi-212 is then eluted from the extraction medium with an acid solution to form a substantially radio-impurity-free Bi-212 acid solution. An apparatus for carrying out this process and a process for the therapeutic use thereof are also disclosed.
The neuroinflammatory response promotes secondary brain injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 1 (TREM1) is a key regulator of inflammation. However, the role of TREM1 in TBI is poorly studied. The purpose of this study was to investigate the role of TREM1 in TBI and the possible underlying mechanism. We found that the protein expression of TREM1 significantly increased after TBI in rats, and the TREM1 protein localized to microglia. Inhibition of the TREM1 protein with LP17 significantly blocked ERK phosphorylation and reduced cytoplasmic phospholipase A2 (cPLA2) protein expression and phosphorylation. In addition, LP17-mediated TREM1 inhibition significantly reduced the protein expression of iNOS and increased the protein expression of Arg1. Moreover, after TREM1 was inhibited, the secretion of the proinflammatory factors TNF-α and IL-1β was significantly reduced, while the secretion of the anti-inflammatory factors IL-4 and IL-10 was significantly increased. Additionally, inhibition of TREM1 by LP17 significantly reduced neuronal apoptosis and ameliorated nerve dysfunction in TBI model rats. In conclusion, our findings suggest that TREM1 enhances neuroinflammation and promotes neuronal apoptosis after TBI, and these effects may be partly mediated via the ERK/cPLA2 signalling pathway.
FIELD: virology, biotechnology. SUBSTANCE: method involves two- or three-stage immunization of monkey Cercopithecus aethiops with the purified inactivated viral antigen with Freund's adjuvant to obtain the necessary antibody level in animal blood to Marburg virus at titer by "ИФА" 1:640 (not less) and the following infection that is carried out once or twice. The first dose at infection is 1-10 LD 50  and at the second one - 10-100 LD 50 . Method can be used for preparing diagnostic agents and sera for Marburg virus control. EFFECT: improved method of preparing. 1 tbl
Control group: patient group (n = 34) receiving placebo compounded to look similar to the caffeine treatment, taken twice daily. This will be an adjuvant to their standard pain control.
BACKGROUND: Reduction mammoplasty (RM) remains one of the most common plastic surgeries worldwide. Many different techniques have been described in the literature, each with its advantages and limitations. Nipple-areolar complex necrosis remains a daunting complication, regardless of the chosen surgical approach.
OBJECTIVE: We describe the senior author's (HYK) unique reduction mammoplasty technique, employing the infero-central (IC) pedicle throughout the last two decades.
PATIENTS AND METHODS: A retrospective chart review of 520 patients undergoing breast reduction was performed. After exclusion criteria, 360 were included in the study. These patients underwent RM with the IC technique, with stabilization of the breast mound and plication of the inferior pole dermis to prevent bottoming out. Demographics, operative data, and complications were recorded. Pre- and postoperative photographs were evaluated by a specialists' panel. The BREAST-Q questionnaire was utilized to assess satisfaction rates.
RESULTS: BREAST-Q questionnaire-satisfaction with breast score was 84.19, and outcome score was 91.67. Aesthetic outcome evaluation, reviewed by four plastic surgeons, yielded a high score in all parameters (1.64-2; range 0-2). On a per-breast basis for all patients, the following complications were analyzed: dehiscence (3.61%), infection (2.22%), hematoma (1.66%), superficial wound healing problems (1.38%), seroma (0.83%), skin flap ischemia (1.52%), hypertrophic scar (1.38%), fat necrosis (0.97%), and partial nipple ischemia (0.27%).
CONCLUSION: Infero-central mound technique can be applied to breast reductions of nearly all sizes, allowing for consistently satisfactory aesthetic outcomes for most patients. Due to robust vascularity of the pedicle, complication rates are kept at a minimum. IC mound technique is an essential tool in the plastic surgeon's armamentarium.
LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .
This is an open label study to determine the efficacy and mechanism(s) of the proprietary DPCP gel composition as a topical immunotherapeutic agent for the treatment of cutaneous metastases. This study is investigator initiated, carried out only at Rockefeller University and the Sponsor holds the IND and is providing the test agent. The products to be evaluated are 0.4% DPCP, in a non-volatile gel vehicle, and 0.04% DPCP in the same gel vehicle applied to the target lesions biweekly for 14 weeks. It is our goal to apply the study drug to all cutaneous metastatic lesions, but at the Investigator's discretion, certain lesions will be avoided if they are in particularly difficult locations such as around the eyes or on the lips. The estimated duration of the study is 142 days with 112 days of treatment followed by subject examination on Day 142. If DPCP is shown to cause resolution of lesions by this visit, there will be the possibility of continuing DPCP use as long as study medication continues to be provided to The Rockefeller University.
Nerve-calming baijiu is disclosed. The nerve-calming baijiu is prepared from 500-510 parts by weight of rice, 20-21 parts by weight of pea, 6-7 parts by weight of honey, 1-2 parts by weight of spine date seeds, 3-4 parts by weight of silktree albizia bark, 2-3 parts by weight of poria sclerotium with hostwood, 1-2 parts by weight of dwarf lilyturf tuber, 5-6 parts by weight of baking soda, 0.25-0.3 part by weight of glucoamylase, 0.1-0.2 part by weight of amylase, a proper amount of lactic acid, 5-6 parts by weight of jiuqu, 0.8-0.9 part by weight of chitosan and 1-1.2 parts by weight of carrageenan. The rice which is a raw material is puffed after being baked and is porous and loose in structure, thus facilitating glucoamylase catalytic hydrolysis. The heat transfer coefficient of superheated steam fed is high, thus accelerating rice temperature rising. After the baking soda is dissolved by adding water, hydroxyl ions are formed through ionization in the solution, and therefore association among water molecules is weakened, the degree of freedom of the water molecules is increased, water is liable to enter the insides of the molecules of rice starch to swell the rice, and the degree of gelatinization is increased. The added chitosan and the added carrageenan can neutralize gastric acid generated through alcohol irritation, thus reducing irritation. The nerve-calming baijiu can calm nerves.
Patients in the drug treatment group will be followed-up at 3, 6, 9 and 12 months after randomization. All the patients in this group will take their baseline antihypertensive medication at the original doses, without any changes except when medically required. Antiarrhythmic drugs treatment is consistent in both arms.
Signs, Symptoms and Laboratory Findings of Acute Overdosage in Humans

The highest known dose of oral LEVETIRACETAM received in the clinical development program was 6000 mg/day. Other than drowsiness, there were no adverse reactions in the few known cases of overdose in clinical trials. Cases of somnolence, agitation, aggression, depressed level of consciousness, respiratory depression and coma were observed with LEVETIRACETAM overdoses in postmarketing use.

Treatment or Management of Overdose \- There is no specific antidote for overdose with LEVETIRACETAM. If indicated, elimination of unabsorbed drug should be attempted by emesis or gastric lavage; usual precautions should be observed to maintain airway. General supportive care of the patient is indicated including monitoring of vital signs and observation of the patient’s clinical status. A Certified Poison Control Center should be contacted for up to date information on the management of overdose with LEVETIRACETAM.

Hemodialysis \- Standard hemodialysis procedures result in significant clearance of levetiracetam (approximately 50% in 4 hours) and should be considered in cases of overdose. Although hemodialysis has not been performed in the few known cases of overdose, it may be indicated by the patient's clinical state or in patients with significant renal impairment.
Atrial fibrillation (AF) refers to the orderly loss of atrial electrical activity, replaced by rapid and disorderly atrial fibrillation wave, is the most acute atrial electrical activity disorders, is also one of the common tachyarrhythmias. So far, the mechanism of atrial fibrillation has not yet been completely clarified. At present, there are various mechanisms to participate in the occurrence and maintenance of atrial fibrillation, which mainly involves two aspects. One is the triggering factor of atrial fibrillation, and the other is the occurrence and maintenance of atrial fibrillation (substrate). Trigger factors are varied, including sympathetic and parasympathetic stimulation, bradycardia, atrial premature beats or tachycardia, atrioventricular bypass and acute atrial pull, etc, which pulmonary vein electrical activity triggered the most common, but also is an most important theoretical Basis for the Radiofrequency Catheter Ablation of Atrial Fibrillation . Substrate is a necessary condition for the onset and maintenance of atrial fibrillation. Electrical remodeling and structural remodeling are by shortening the atrial effective refractory period. Atrial dilatation and atrial fibrosis play a major role in the formation of atrial fibrillation reentry.Circumferential pulmonary Vein Isolation (CPVI) is considered to be the cornerstone of paroxysmal atrial fibrillation ablation, but recently reported in the literature that pure CPVI treatment for paroxysmal atrial fibrillation the 5-year success rate as low as 46.6%, and the incidence of atrial reentry tachycardia is also high in the follow-up period. Therefore it is necessary for us to explore whether the success rate of CPVI combined with Leftatrium Roofline Ablation (CPVI + LARA) for paroxysmal atrial fibrillation is higher than the pure CPVI.