anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Primary percutaneous coronary intervention (pPCI) has improved clinical outcomes in patients with ST-segment-elevation myocardial infarction. However, as many as 50% of patients still have suboptimal myocardial reperfusion and experience extensive myocardial necrosis. The PiCSO-AMI-I trial (Pressure-Controlled Intermittent Coronary Sinus Occlusion-Acute Myocardial Infarction-I) evaluated whether PiCSO therapy can further reduce myocardial infarct size (IS) in patients undergoing pPCI.
METHODS: Patients with anterior ST-segment-elevation myocardial infarction and Thrombolysis in Myocardial Infarction flow 0-1 were randomized at 16 European centers to PiCSO-assisted pPCI or conventional pPCI. The PiCSO Impulse Catheter (8Fr balloon-tipped catheter) was inserted via femoral venous access after antegrade flow restoration of the culprit vessel and before proceeding with stenting. The primary end point was the difference in IS (expressed as a percentage of left ventricular mass) at 5 days by cardiac magnetic resonance. Secondary end points were the extent of microvascular obstruction and intramyocardial hemorrhage at 5 days and IS at 6 months.
RESULTS: Among 145 randomized patients, 72 received PiCSO-assisted pPCI and 73 conventional pPCI. No differences were observed in IS at 5 days (27.2%±12.4% versus 28.3%±11.45%; P=0.59) and 6 months (19.2%±10.1% versus 18.8%±7.7%; P=0.83), nor were differences between PiCSO-treated and control patients noted in terms of the occurrence of microvascular obstruction (67.2% versus 64.6%; P=0.85) or intramyocardial hemorrhage (55.7% versus 60%; P=0.72). The study was prematurely discontinued by the sponsor with no further clinical follow-up beyond 6 months. However, up to 6 months of PiCSO use appeared safe with no device-related adverse events.
CONCLUSIONS: In this prematurely discontinued randomized trial, PiCSO therapy as an adjunct to pPCI did not reduce IS when compared with conventional pPCI in patients with anterior ST-segment-elevation myocardial infarction. PiCSO use was associated with increased procedural time and contrast but no increase in adverse events up to 6 months.
REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03625869.
Eligible participant will be administered RO0503821 (methoxy polyethylene glycol-epoetin beta \[Mircera\]) intravenously (IV) using a dose conversion factor of 0.25/150 microgram (mcg)/kilogram (kg) of the previous weekly erythropoiesis stimulating agents (ESA) dose, (equal to 62.50% assumed equi-effective dose) once weekly up to 19 weeks. After 19 weeks of core treatment period, participants will be followed-up for two optional treatment extension periods (54 weeks each).
Malignant hyperthermia (MH) is a pharmacogenetic condition of skeletal muscle that manifests in hypermetabolic responses upon exposure to volatile anaesthetics. This condition is caused primarily by pathogenic variants in the calcium-release channel RYR1, which disrupts calcium signalling in skeletal muscle. However, our understanding of MH genetics is incomplete, with no variant identified in a significant number of cases and considerable phenotype diversity. In this study, we applied a transcriptomic approach to investigate the genome-wide gene expression in MH-susceptible cases using muscle biopsies taken for diagnostic testing. Baseline comparisons between muscle from MH-susceptible individuals (MHS, n = 8) and non-susceptible controls (MHN, n = 4) identified 822 differentially expressed genes (203 upregulated and 619 downregulated) with significant enrichment in genes associated with oxidative phosphorylation (OXPHOS) and fatty acid metabolism. Investigations of 10 OXPHOS target genes in a larger cohort (MHN: n = 36; MHS: n = 36) validated the reduced expression of ATP5MD and COQ6 in MHS samples, but the remaining 8 selected were not statistically significant. Further analysis also identified evidence of a sex-linked effect in SDHB and UQCC3 expression, and a difference in ATP5MD expression across individuals with MH sub-phenotypes (trigger from in vitro halothane exposure only, MHSh (n = 4); trigger to both in vitro halothane and caffeine exposure, MHShc (n = 4)). Our data support a link between MH-susceptibility and dysregulated gene expression associated with mitochondrial bioenergetics, which we speculate plays a role in the phenotypic variability observed within MH.
The present invention relates to a medical pattern patch capable of being painted on a body and a method for manufacturing same. More particularly, a member made of fiber or the like having been used as a medium for fixating and transferring a medication is excluded from an existing medical patch; a printing surface layer, instead of the member, can fixate and transmit a medication; and a unique color of the medication is hidden behind a pattern. The medical pattern patch can provide a body paining effect or a tattoo effect as various patterns are printed on a transfer paper. The medical pattern patch capable of being painted on a body is formed as an adhesive patch to be attached to a portion of a human body and comprises: a transfer paper (100) formed to have a certain image (110); a medication layer (200) comprising a medication mixed with a sticky agent on the surface of the transfer paper (100); an adhesive (300) formed to be attached to an upper side of the medication layer (200); and a release film formed on an upper side of the adhesive layer to protect the adhesive (300). The medical pattern patch capable of being painted on a body is attached to a lesion and transfers a medical effect. As an external appearance of the medical pattern patch has the image (110) and the pattern, and thus the medical pattern patch capable of being painted on a body can be used for body painting and increase preference when attached outside a garment. An external appearance of the medical pattern patch capable of being painted on a body is different from an external appearance of an existing patch. Therefore, the medical pattern patch capable of being painted on a body has various designs and can be used by people regardless of gender and age without hesitation.
PROBLEM TO BE SOLVED: To provide systems and methods for navigation and review regarding items of clinical data within a large data set via a handheld device.SOLUTION: A clinical data set divided into a plurality of portions is provided. Each portion includes a plurality of sub-portions (405) associated with a graphical representation. User navigation is facilitated at various levels of granularity among the plurality of portions (415, 420, 425, 430). User access is allowed to one or more sub-portions within a portion to locate an item of clinical data within a sub-portion (430, 435). User selection of an item of clinical data within a sub-portion is enabled (435, 440, 445, 455). A selected item of clinical data is loaded via a user interface (460).
The composition of encapsulated carbinyl iron salt and a process for preparation thereof. The composition comprises high density particles of carbonyl iron salt in combination with lipids and/or emulsifiers. The invention also relates to composition may additionally contain other minerals or combination of minerals. The composition prevents side effects of the iron and masks metallic taste. Further, the composition provides an improved bioavailability and formulated into various oral delivery forms. This composition is useful in the prevention of iron deficiency anemia.
Small doses of local anesthetics (e.g., bupivacaine hydrochloride injection) injected into the head and neck area, including retrobulbar, dental, and stellate ganglion blocks, may produce adverse reactions similar to systemic toxicity seen with unintentional intravascular injections of larger doses. The injection procedures require the utmost care. Confusion, convulsions, respiratory depression, and/or respiratory arrest, and cardiovascular stimulation or depression have been reported. These reactions may be due to intra-arterial injection of the local anesthetic with retrograde flow to the cerebral circulation. They may also be due to puncture of the dural sheath of the optic nerve during retrobulbar block with diffusion of any local anesthetic along the subdural space to the midbrain. Monitor circulation and respiration and constantly observe patients receiving bupivacaine hydrochloride injection blocks. Resuscitative equipment and drugs, and personnel for treating adverse reactions should be immediately available. Dosage recommendations should not be exceeded [see Dosage and Administration (2.2)].
Each 5 mL ampule of Cromolyn Sodium Oral Solution, Concentrate contains 100 mg cromolyn sodium, USP, in purified water. Cromolyn sodium is a hygroscopic, white powder having little odor. It may leave a slightly bitter aftertaste. Cromolyn Sodium Oral Solution, Concentrate is clear, colorless, and sterile. It is intended for oral use.

Chemically, cromolyn sodium is disodium 5,5’-[(2-hydroxy-trimethylene) dioxy]bis[4-oxo-4H-1-benzopyran-2-carboxylate] The empirical formula is C23H14Na2O11; the molecular weight is 512.34. Its chemical structure is:

Pharmacologic Category: Mast cell stabilizer

Therapeutic Category: Antiallergic
In SARS-CoV-2 infection, it has been observed that viral replication lasts longer in the nasal mucosa than in the lungs, despite the presence of a high viral load at both sites. In hamsters, we found that the nasal mucosa exhibited a mild inflammatory response and minimal pathological injuries, whereas the lungs displayed a significant inflammatory response and severe injuries. The underlying cellular events may be induced by viral infection in three types of cell death: apoptosis, pyroptosis, and necroptosis. Our findings indicate that apoptosis was consistently activated during infection in the nasal mucosa, and the levels of apoptosis were consistent with the viral load. On the other hand, pyroptosis and a few instances of necroptosis were observed only on 7 dpi in the nasal mucosa. In the lungs, however, both pyroptosis and apoptosis were prominently activated on 3 dpi, with lower levels of apoptosis compared to the nasal mucosa. Interestingly, in reinfection, obvious viral load and apoptosis in the nasal mucosa were detected on 3 dpi, while no other forms of cell death were detected. We noted that the inflammatory reactions and pathological injuries in the nasal mucosa were milder, indicating that apoptosis may play a role in promoting lower inflammatory reactions and milder pathological injuries and contribute to the generation of long-term viral replication in the nasal mucosa. Our study provides valuable insights into the differences in cellular mechanisms during SARS-CoV-2 infection and highlights the potential significance of apoptosis regulation in the respiratory mucosa for controlling viral replication.
We will provide current "best practice" to the control arm. Patients with a BMI greater than or equal to the 85th percentile will be flagged in the electronic health record. Clinicians are also provided with clinical decision support tools for pediatric weight management. We will encourage providers to schedule a follow up visit for weight management or make a referral to Harvard Vanguard Medical Associates nutritionists for children in this arm. We will also provide this group with a community resource guide and educational text messages.
Treatment group- liraglutide daily use of drug. Titrated up from 0.6mg/day to 1.8mg/day or highest tolerated dose.
Vascular remodeling to match arterial diameter to tissue requirements commonly fails in ischemic disease. Endothelial cells sense fluid shear stress (FSS) from blood flow to maintain FSS within a narrow range in healthy vessels. Thus, high FSS induces vessel outward remodeling, but mechanisms are poorly understood. We previously reported that Smad1/5 is maximally activated at physiological FSS. Smad1/5 limits Akt activation, suggesting that inhibiting Smad1/5 may facilitate outward remodeling. Here we report that high FSS suppresses Smad1/5 by elevating KLF2, which induces the bone morphogenetic protein (BMP) pathway inhibitor, BMP-binding endothelial regulator (BMPER), thereby de-inhibiting Akt. In mice, surgically induced high FSS elevated BMPER expression, inactivated Smad1/5 and induced vessel outward remodeling. Endothelial BMPER deletion impaired blood flow recovery and vascular remodeling. Blocking endothelial cell Smad1/5 activation with BMP9/10 blocking antibodies improved vascular remodeling in mouse models of type 1 and type 2 diabetes. Suppression of Smad1/5 is thus a potential therapeutic approach for ischemic disease.
The present invention relates to: a composition for relieving stress or preventing, ameliorating or treating stress diseases, the composition comprising a fermented Perilla frutescens L. Britton var. acuta Kudo extract; and use thereof. The fermented Perilla frutescens L. Britton var. acuta Kudo extract of the present invention significantly relieves stress as compared to an unfermented Perilla frutescens L. Britton var. acuta Kudo extract, and thus is effective as a composition for relieving depression, anxiety, tension or stress, and furthermore as a composition for preventing, ameliorating or treating stress diseases. In addition, the fermented Perilla frutescens L. Britton var. acuta Kudo extract can also be used in a method for preventing or treating stress diseases through administration to patients with stress diseases.
This group will consist of 78 women ages 18 to 30 who have received two doses of the HPV vaccine. The second dose must have been received six or more months ago.
Placebo QHS (blinded) and sildenafil 100mgs (open-label) as required for sexual relations. The placebo will be omitted on nights that 100mgs is used. Placebo will start within 24-48 hours post-surgery.
BACKGROUND: Cardiac hypertrophy is an adaptive response to pressure overload aimed at maintaining cardiac function. However, prolonged hypertrophy significantly increases the risk of maladaptive cardiac remodeling and heart failure. Recent studies have implicated long noncoding RNAs in cardiac hypertrophy and cardiomyopathy, but their significance and mechanism(s) of action are not well understood.
METHODS: We measured lincRNA-p21 RNA and H3K27ac levels in the hearts of dilated cardiomyopathy patients. We assessed the functional role of lincRNA-p21 in basal and surgical pressure-overload conditions using loss-of-function mice. Genome-wide transcriptome analysis revealed dysregulated genes and pathways. We labeled proteins in proximity to full-length lincRNA-p21 using a novel BioID2-based system. We immunoprecipitated lincRNA-p21-interacting proteins and performed cell fractionation, ChIP-seq (chromatin immunoprecipitation followed by sequencing), and co-immunoprecipitation to investigate molecular interactions and underlying mechanisms. We used GapmeR antisense oligonucleotides to evaluate the therapeutic potential of lincRNA-p21 inhibition in cardiac hypertrophy and associated heart failure.
RESULTS: lincRNA-p21 was induced in mice and humans with cardiomyopathy. Global and cardiac-specific lincRNA-p21 knockout significantly suppressed pressure overload-induced ventricular wall thickening, stress marker elevation, and deterioration of cardiac function. Genome-wide transcriptome analysis and transcriptional network analysis revealed that lincRNA-p21 acts in trans to stimulate the NFAT/MEF2 (nuclear factor of activated T cells/myocyte enhancer factor-2) pathway. Mechanistically, lincRNA-p21 is bound to the scaffold protein KAP1 (KRAB-associated protein-1). lincRNA-p21 cardiac-specific knockout suppressed stress-induced nuclear accumulation of KAP1, and KAP1 knockdown attenuated cardiac hypertrophy and NFAT activation. KAP1 positively regulates pathological hypertrophy by physically interacting with NFATC4 to promote the overactive status of NFAT/MEF2 signaling. GapmeR antisense oligonucleotide depletion of lincRNA-p21 similarly inhibited cardiac hypertrophy and adverse remodeling, highlighting the therapeutic potential of inhibiting lincRNA-p21.
CONCLUSIONS: These findings advance our understanding of the functional significance of stress-induced long noncoding RNA in cardiac hypertrophy and demonstrate the potential of lincRNA-p21 as a novel therapeutic target for cardiac hypertrophy and subsequent heart failure.
BACKGROUND: Endocrine therapy is the mainstay treatment for breast cancer (BC) to reduce BC recurrence risk. During the first year of endocrine therapy use, nearly 30% of BC survivors are nonadherent, which may increase BC recurrence risk. This study is to examine the association between endocrine therapy adherence trajectories and BC recurrence risk in nonmetastatic BC survivors.
METHODS: This retrospective cohort study included Medicare beneficiaries in the United States (US) with incident nonmetastatic BC followed by endocrine therapy initiation in 2010-2019 US Surveillance, Epidemiology, and End Results linked Medicare data. We calculated monthly fill-based proportion of days covered in the first year of endocrine therapy. We applied group-based trajectory models to identify distinct endocrine therapy adherence patterns. After the end of the first-year endocrine therapy trajectory measurement period, we estimated the risk of time to first treated BC recurrence within 4 years using Cox proportional hazards models.
RESULTS: We identified 5 trajectories of adherence to endocrine therapy in BC Stages 0-I subgroup (n = 28,042) and in Stages II-III subgroup (n = 7781). A trajectory of discontinuation before 6 months accounted for 7.0% in Stages 0-I and 5.8% in Stages II-III subgroups, and this trajectory was associated with an increased treated BC recurrence risk compared to nearly perfect adherence (Stages 0-I: adjusted hazard [aHR] = 1.84, 95% CI = 1.46-2.33; Stages II-III: aHR = 1.38, 95% CI = 1.07-1.77).
CONCLUSIONS: Nearly 7% of BC survivors who discontinued before completing 6 months of treatment was associated with an increased treated BC recurrence risk compared to those with nearly perfect adherence among Medicare nonmetastatic BC survivors.
The invention discloses a consciousness-restoring and epilepsy-relieving pill, which relates to a pill for treating epilepsy, has a short treatment period and is free from toxic and side effects. The consciousness-restoring and epilepsy-relieving pill has a short treatment period and is free from toxic and side effects, and relapse is avoided according to follow-up of healed cases. Phlegm blinds the capacity for clear thinking, so that dysfunction of heart control over mental activities and insanity are caused. According to the pill, costus root is used for flavoring, ventilating, smoothening channels and removing impurities; honey is used for adjusting the lung, dredging intestinal tracts and draining; and millet is derived from essences of grains, and is used for nourishing spleen, protecting stomach, and improving the clearness-ascending and turbidity-descending effects of other medicaments. In the formula, tabasheer, pearl, magnet, ruddle and lapis chloriti are mainly used for clearing heat, reducing phlegm and opening stagnation; stone is used for adding weight and reducing chronic phlegm in chest; calamus is used as an auxiliary ingredient and used for guiding qi downward, reducing phlegm, opening stagnation and inducing resuscitation; and scorpio, centipede and fructus gardenia are used for removing fire of three warmers. A plurality of medicaments are blended, so that both principal and secondary aspects of a disease are treated, the effects of guiding qi downward, clearing heat, reducing phlegm, opening stagnation and recovering consciousness are achieved, and therefore the consciousness-restoring and epilepsy-relieving pill  has a rapid and remarkable curative effect on epilepsy.
AIM: We aimed at creating and validating a prognostic model incorporating easily accessible clinical and laboratory parameters to forecast the likelihood of short-term progression of carotid atherosclerosis.
METHODS: A prediction model was developed and validated for carotid plaque progression within 2 years in an early middle-age population in China. Progression was defined as the new appearance of carotid plaque or stenosis among participants who had normal carotid status at baseline. Leveraging data from a health check-up chain, predictors were identified using statistical methods including stepwise logistic regression, Markov Chain Monte Carlo (MCMC) simulation, random forest analysis and least absolute shrinkage selection operator (Lasso). Model performance was assessed. Bootstrap internal validation, validation on another check-up population and subgroup analysis were also conducted.
RESULTS: Among 7765 participants, predictors including age, diastolic blood pressure, uric acid levels, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were identified for carotid plaque progression in 2 years. The developed prediction model demonstrated good discrimination (AUC = 0.755, 95%CI:0.736-0.774) and calibration ability (slope = 0.922 and interception = 0.007) among development data, as well as among validation data (AUC = 0.759, 95%CI:0.674-0.770; slope = 1.076 and intercept = -0.014). Internal validation using bootstrap method yielded an adjusted AUC of 0.753. The model's performance remained consistent across different subgroups.
CONCLUSIONS: Our study presents a validated risk prediction model for carotid plaque progression in an early middle age population, offering a valuable tool for early identification and monitoring of cardiovascular risks. The model's robustness and applicability across different subgroups highlight its potential utility in preemptive cerebrovascular and cardiovascular disease management.
Aims: Part of hypothalamic (mediobasal hypothalamus [MBH]) neurons detect changes in blood glucose levels that in turn coordinate the vagal control of insulin secretion. This control cascade requires the production of mitochondrial reactive oxygen species (mROS), which is altered in models of obesity and insulin resistance. Obese, insulin-resistant Zücker rats are characterized by hypothalamic hypersensitivity to glucose. This initiates an abnormal vagus-induced insulin secretion, associated with an overproduction of mROS in response to a low glucose dose. Here, we hypothesized that ghrelin, known to buffer reactive oxygen species (ROS) via mitochondrial function, may be a major component of the hypothalamic glucose hypersensitivity in the hypoghrelinemic obese Zücker rat. Results: Hypothalamic glucose hypersensitivity-induced insulin secretion of Zücker obese rats was reversed by ghrelin pretreatment. The overproduction of MBH mROS in response to a low glucose load no longer occurred in obese rats that had previously received the cerebral ghrelin infusion. This decrease in mROS production was accompanied by a normalization of oxidative phosphorylation (OXPHOS). Conversely, blocking the action of ghrelin with a growth hormone secretagogue receptor antagonist in a model of hyperghrelinemia (fasted rats) completely restored hypothalamic glucose sensing-induced insulin secretion that was almost absent in this physiological situation. Accordingly, ROS signaling and mitochondrial activity were increased by the ghrelin receptor antagonist. Innovation: These results demonstrate for the first time that ghrelin addressed only to the brain could have a protective effect on the defective control of insulin secretion in the insulin-resistant, hypoghrelinemic obese subject. Conclusions: Ghrelin, through its action on OXPHOS, modulates mROS signaling in response to cerebral hyperglycemia and the consequent vagal control of insulin secretion. In insulin-resistant obese states, brain hypoghrelinemia could be responsible for the nervous defect in insulin secretion.
Participants in this group will be randomize to no post-operative antibiotic. They will be evaluated for infection, fistula formation, and dehiscence upon discharge and at 30-day follow-up based on standards of care.