anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
It is particularly important to administer bupropion hydrochloride extended-release tablets (SR) in a manner most likely to minimize the risk of seizure (see WARNINGS). Gradual escalation in dosage is also important if agitation, motor restlessness, and insomnia, often seen during the initial days of treatment, are to be minimized. If necessary, these effects may be managed by temporary reduction of dose or the short-term administration of an intermediate to long-acting sedative hypnotic. A sedative hypnotic usually is not required beyond the first week of treatment. Insomnia may also be minimized by avoiding bedtime doses. If distressing, untoward effects supervene, dose escalation should be stopped. Bupropion hydrochloride extended-release tablets (SR) should be swallowed whole and not crushed, divided, or chewed, as this may lead to an increased risk of adverse effects including seizures.
New incretin-based pharmacotherapies provide efficient and safe therapeutic options to curb appetite and produce weight loss in patients with obesity. Delivered systemically, these molecules produce pleiotropic metabolic benefits, but the target sites mediating their weight-suppressive action are located within the brain. Recent research has increased our understanding of the neural circuits and behavioral mechanisms involved in the anorectic and metabolic consequences of glucagon-like peptide 1 (GLP-1)-based weight loss strategies, yet little is known about how these drugs access their functional targets in the brain to produce sustained weight loss. The majority of brain cells expressing incretin receptors are located behind the blood-brain barrier, shielded from the circulation and fluctuations in the availability of peripheral signals, which is a major challenge for the development of CNS-targeted therapeutic peptides. GLP-1 receptor (GLP-1R) agonists with increased half-life and enhanced therapeutic benefit do not cross the blood-brain barrier, yet they manage to access discrete brain sites relevant to the regulation of energy homeostasis. In this review, we give a brief overview of the different routes for peptide hormones to access the brain. We then examine the evidence informing the routes employed by incretins and incretin receptor agonists to access brain targets relevant for their appetite and weight-suppressive actions. We highlight existing controversies and suggest future directions to further establish the functionally relevant access routes for GLP-1-based weight loss compounds, which might guide the development and selection of the future generation of incretin receptor polypharmacologies.
C-reactive protein (CRP) is an acute-phase protein produced by the liver in response to infection and during chronic inflammatory disorders. Systemic inflammation is a major driver of cirrhosis progression from the compensated to the decompensated stage. Previous studies have shown that pentameric CRP (pCRP) to be a weak predictor of disease severity and prognosis in patients with decompensated hepatitis B cirrhosis, with it being only helpful for identifying patients with a higher short-term risk of death under certain conditions. Accumulating evidence indicates that pCRP dissociates to and acts primarily as the monomeric conformation (mCRP) at inflammatory loci, suggesting that mCRP may be a potentially superior disease marker with higher specificity and relevance to pathogenesis. However, it is unknown whether mCRP and anti-mCRP autoantibodies are associated with disease severity, or progression in decompensated hepatitis B cirrhosis. In this study, we evaluated the serum levels of mCRP and anti-mCRP autoantibodies in patients with decompensated cirrhosis of hepatitis B and their association with disease severity and theoretical prognosis. The results showed that patients with high mCRP and anti-mCRP autoantibody levels had more severe liver damage and that coagulation function was worse in patients with high anti-mCRP autoantibodies. Analysis of the correlation between pCRP, mCRP and anti-mCRP autoantibody levels with Model for End-Stage Liver Disease (MELD), Albumin-Bilirubin (ALBI), and Child-Turcotte-Pugh (CTP) prognostic scores showed that mCRP was the most strongly correlated with MELD score, followed by anti-mCRP autoantibodies; conversely, pCRP was not significantly correlated with prognostic score. Therefore, mCRP and anti-mCRP autoantibodies may be more advantageous clinical indicators than pCRP for evaluating the pathological state of decompensated hepatitis B cirrhosis.
Over 1.1 million people in the United States are living with human immunodeficiency virus (HIV). Liver disease is a leading cause of mortality in persons with HIV (PWH), and PWH suffer a disproportionate burden of non-alcoholic fatty liver disease (NAFLD). While the mechanisms underlying this disparity are not well understood, harmful changes in the intestinal microbiome ("dysbiosis") and increased bacterial product movement across the intestinal lining ("leaky gut") are implicated in the pathogenesis of NAFLD in HIV-negative persons. HIV infection has been shown to alter the intestinal microbiome and promote leaky gut; however, there are few data on the microbiome among PWH with NAFLD. Our overarching hypothesis is that intestinal dysbiosis in PWH promotes NAFLD through: 1) impairment of the barrier function of the intestinal lining causing translocation of proinflammatory bacterial products to the bloodstream and 2) alteration of plasma metabolites that promote NAFLD. Specifically, HIV-associated gut dysbiosis leads to reduction in the production of short chain fatty acids, which are essential for the maintenance of a healthy intestinal lining. A reduction in butyrate production leads to breakdown of the intestinal barrier, allowing for translocation of inflammatory bacterial products into the splanchnic vasculature and the liver. These products lead to inflammation and disruption of lipid metabolism in the liver causing lipid deposition in the liver. Additionally, dysbiosis in PWH leads to lower bacterial production of lipids necessary for fat metabolism in the liver leading to NAFLD. We will test these hypotheses in a single arm pre/post feasibility and efficacy trial of an intervention designed to restore a healthy gut microbiome in PWH with NAFLD (n=63). The study will assess the effects of a probiotic containing multiple strains of bacteria supporting butyrate synthesis and prebiotic fiber among PWH at risk of NAFLD (diagnosis of metabolic syndrome, elevated BMI or elevated transaminases) without history of current excessive alcohol use, viral hepatitis or other known liver diseases.
PURPOSE: To explore the impact of a selection of contributing factors on employment in adults with cerebral palsy (CP).
METHOD: Eighty adults with CP (39 male, median age 31, IQ > 70) were evaluated using standardized tests and questionnaires for hand function, gross motor function, pain, depressive symptoms, fatigue, social participation, performing daily activities, supportive materials, and mobility aids. Two separate analyses were performed. Firstly, differences between three subgroups were investigated: employee (n = 43), volunteer/sheltered (n = 14), and unemployed (n = 23). Secondly, multivariable regression analysis was applied to investigate the association between functional factors and employment hours.
RESULTS: Compared to employees, volunteer/sheltered workers performed significantly slower hand function tasks (p < 0.001). Participants in the employee group had primarily MACS I (55.8%) or MACS II (44.9%) scores. The employee group showed significantly (p < 0.001) higher social participation and performance in daily activities. Thirty-eight percent of the variance in working hours could be explained by social participation, daily activities, fatigue, and gross motor function.
INTERPRETATION: Employees are more likely adults with CP with better manual abilities. Sheltered/volunteer workers showed slower execution in hand function and higher limitations in fine motor skills. Social participation, performing daily activities, fatigue, and gross motor function are functional factors associated with hours of employment.
The world is currently experiencing unprecedented challenges caused by the global coronavirus (COVID19) pandemic. Many countries are enforcing measures to restrict movement of people to reduce the spread of the outbreak, including lock-downs, social distancing and self-isolation. These methods, although necessary to slow the spread of disease, will have negative effects on psychological well-being of large populations. Shortage of health care professionals and measures to restrict interpersonal contact means facilitated psychological interventions will not be feasible for many, at least during the height of the pandemic. There is therefore a need for self-directed psychological interventions that can be practically and quickly implemented online.

Emotional disclosure-based therapies, such as expressive writing (EW), hold potential as low-cost, easy to implement means of support, with minimal requirement for facilitation. In its original format, EW involved writing daily for 15-20 minutes for 3-4 days about a traumatic event. Since its development, it has been adapted in many ways, including writing about positive events and writing about stress from a compassionate stance. There is evidence that such interventions can provide significant psychological and physical benefits in healthy populations and reduce the effects of natural disasters on health and well-being. However, to our knowledge this form of psychological intervention has not been tested during a rapidly evolving crisis or pandemic.

The aim of this study is to test whether an online self-compassion and EW based intervention (LIO-C) can reduce the negative effects of the COVID19 pandemic on health and well-being. The intervention is based on an existing intervention, LIO, that we previously developed for use in advanced disease populations, in collaboration with clinical and health psychologists, and patient and public representatives. For this study, we have adapted the intervention for people living through the current COVID19 pandemic by altering the writing prompts, and translating the intervention to an online hub. As this is an unfacilitated intervention, the instructions involve writing from a compassionate stance to minimise any potential short term negative effects associated with writing about difficult experiences.
COMETRIQ can cause hypertension, including hypertensive crisis. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (modified JNC criteria) stage 1 or 2 hypertension was identified in 61% in COMETRIQ-treated patients compared with 30% of placebo-treated patients in the randomized trial [see Adverse Reactions (6.1)].

Do not initiate COMETRIQ in patients with uncontrolled hypertension. Monitor blood pressure regularly during COMETRIQ treatment. Withhold COMETRIQ for hypertension that is not adequately controlled with medical management; when controlled, resume COMETRIQ at a reduced dose. Discontinue COMETRIQ for severe hypertension that cannot be controlled with anti-hypertensive therapy and for hypertensive crisis [see Dosage and Administration (2.2)].
A composition for the prevention, treatment and control of metabolic degenerative diseases in humans and animals comprises a mixture of vitamin E and a selenium compound.  The selenium compound may be sodium selenite (preferred), barium selenate, seleno-methionine, di-seleno di-valeric acid, sodium selenate, potassium selenite, barium selenite, seleno-cystene, selenium oxide and potassium seleno-cyanate.  The vitamin E may be alpha tocopherol, beta tocopherol, gamma tocopherol, delta tocopherol; epsilon-, zeta, eta, d-alpha-, dl-alphatocopherol; dl-alpha tocopheryl acetate; mixed natural tocopherols, disodium salt of al-alpha tocopherol and alpha tocopheryl succinate.  The compositions may be administered orally or parenterally.  Examples are given of capsules and aqueous injections. The injections may contain a suspending or emulsifying agent such as polysorbate and a bacteriostat such as propyl p-hydroxybenzoate or sodium ethylmereurithiosalicylate.  Methods of administering the injections to (a), new born and young lambs, (b) new born calves, (c) pregnant ewes, (d) weaner calves and pregnant cows, in the treatment of white muscle disease, are provided.
OBJECTIVES: The understanding of the impact of tethered cord syndrome (TCS) on the physiology of the colorectal area is limited. Our aim was to describe anorectal and colonic motility in children with TCS and compare the findings to those of children with functional constipation (FC).
METHODS: We conducted a retrospective review of children with TCS who had an anorectal manometry (ARM) performed at our institution from January 2011 to September 2023. We recorded demographics, medical and surgical history, clinical symptoms, and treatment at time of ARM, ARM findings (resting pressure, push maneuver, rectal sensation, rectoanal inhibitory reflex [RAIR], and RAIR duration), and the final interpretation of colonic manometry (CM) if performed. We identified age and sex-matched control groups of children with FC.
RESULTS: We included 24 children with TCS (50% female) who had ARM testing (median age at ARM 6.0 years, interquartile range 4.0-11.8 years). All children had constipation at time of ARM. Nineteen children had detethering surgery before ARM was performed. No significant differences in ARM parameters were found between children who had detethering surgery before ARM and children with FC. Among the 24 children, 14 also had a CM performed (13/14 after detethering surgery). No significant differences in colonic motility were found between children with a history of TCS and children with FC.
CONCLUSIONS: Anorectal physiology and colonic motility are similar between children with a history of TCS and children with FC, suggesting that the underlying pathophysiology of defecatory disorders in children with and without history of TCS is similar.
PURPOSE:To obtain an odorless antiallergic action substance by specifically treating garlic to suppress or deactivate activity of an enzyme related to a smell in garlic. CONSTITUTION:For example, unground garlic is heated or pressurized to deactivate allinase, an enzyme capable of forming aliicine to cause a smell of garlic (the treating condition is such a degree as not to damage antiallergic activity in garlic). Then the treated garlic is ground and an insoluble fraction is removed to give an odorless antiallergic action substance. A fresh garlic is preferable as the garlic used in the treatment and a bulb is especially preferable. Since the odorless antiallergic action substance derived from garlic has no characteristic smell of garlic, the substance can be mixed with various foods such as jelly, tablet cake drink. The substance can be daily administered especially to children as meal or snack without resistance and is expected to reduce allergic symptoms.
Irreversible retinal damage was observed in some patients treated with hydroxychloroquine sulfate and it is related to cumulative dosage and treatment duration. In patients of Asian descent, retinal toxicity may first be noticed outside the macula. 

Risk factors for retinal damage include daily hydroxychloroquine sulfate dosages ≥ 5 mg/kg of actual body weight, durations of use greater than five years, renal impairment, use of concomitant drug products such as tamoxifen citrate, and concurrent macular disease. 

Within the first year of starting hydroxychloroquine sulfate, a baseline ocular examination is recommended including best corrected distance visual acuity (BCVA), an automated threshold visual field (VF) of the central 10 degrees (with retesting if an abnormality is noted), and spectral domain ocular coherence tomography (SD-OCT). For patients at higher risk of retinal damage, monitoring should include annual examinations which include BCVA, VF and SD-OCT. For patients without significant risk factors, annual retinal exams can usually be deferred until five years of treatment. In patients of Asian descent, it is recommended that visual field testing be performed in the central 24 degrees instead of the central 10 degrees.

If ocular toxicity is suspected, discontinue hydroxychloroquine sulfate and monitor the patient closely given that retinal changes and visual disturbances may progress even after cessation of therapy.
This project leverages our expertise in the epidemiology of colorectal cancer (CRC); disparities; obesity; metabolic dysregulation, an important manifestation of inflammation; the microbiome; animal CRC models; and lifestyle intervention trials to address the growing problem of Early-Onset CRC (EOCRC) (i.e., \<50 years). Adiposity and diet drive metabolic dysregulation. So, understanding the interaction between diet and adiposity are key to understanding the genesis of EOCRC - and an array of other obesity-related cancers. This project will address the absence of critical clinical trials and mechanistic studies involving lifestyle interventions for EOCRC. We intend to address this gap; and have the transdisciplinary team representing complementary backgrounds to do so. We focus on dietary modulation of gut microbes to reduce metaflammation and subsequent metabolic dysfunction in obesity, with a goal of preventing EOCRC. We will perform an anti-inflammatory dietary intervention trial in dyads of adults and children at elevated risk for CRC. We also will conduct a complementary mechanistic animal study that builds on and leverages our expertise in mechanistic studies on obesity and CRC. This work is supported by infrastructure that we have built over the past decades in two key centers at the University of South Carolina (USC): (1) Center for Colon Cancer Research (CCCR, 2002 - present - which specializes in mouse models of CRC); and (2) the Cancer Prevention and Control Program (CPCP, 2003 - present - which specializes in the epidemiology of cancer and lifestyle intervention trials for cancer, with a focus on cancer disparities). The two projects that comprise the proposed grant address two Specific Aims that are represented by the human study and laboratory animal experiment: i.e. ,1: To establish the metabolic protective effects of an anti-inflammatory diet in obese, high-risk African-American (AA) and European-American (EA) adults and children in reducing inflammation as indicated by Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), IGF-1, Tumor Necrosis Factor alpha (TNFα), Interleukin 6 (IL-6), and C-Reactive Protein (CRP), and a creating more favorable microbiome signature; 2: To establish gut microbes as mediators between anti-inflammatory dietary input and reversal of metabolic dysfunction and associated CRC risk. This complements the human study by carrying out pre-clinical murine model studies with similar inputs (diet), intermediate endpoints (inflammation, microbiome), and outcomes (CRC-related). We hypothesize that an anti-inflammatory dietary intervention will reduce metabolic dysfunction and metainflammation through regulatory effects on gut microbiota.

Results from this work will address the role of metabolic dysregulation in relation to factors that are known to be important in carcinogenesis, that therefore could have profound effects on EOCRC, have implications for other obesity-related cancers, and have great promise for moving the field forward by addressing mechanisms that drive large health-related disparities that consistently disfavor African Americans.
An exemplary system, method and computer-accessible medium for determining a risk of developing breast cancer for a patient(s) can include, for example receiving an image(s) of an internal portion(s) of a breast of the patient(s), and determining the risk by applying a neural network(s) to the image(s). The neural network can be a convolutional neural network (CNN). The CNN can include a plurality of layers. Each of the layers can have a different number of feature channels. The CNN can include at least four layers. A first layer of the at least four layers can have 256×256×16 feature channels, a second layer of the at least four layers can have 128×128×32 feature channels, a third layer of the at least four layers can have 64×64×64 feature channels, and a fourth layer of the at least four layers can have 32×32×128 feature channels.
Vigabatrin causes edema in adults. Pediatric clinical trials were not designed to assess edema, but observed incidence of edema-based pooled data from controlled pediatric studies appeared similar for pediatric patients on vigabatrin and placebo.   
Pooled data from controlled trials demonstrated increased risk among vigabatrin patients compared to placebo patients for peripheral edema (vigabatrin 2%, placebo 1%), and edema (vigabatrin 1%, placebo 0%). In these studies, one vigabatrin and no placebo patients discontinued for an edema related AE. In adults, there was no apparent association between edema and cardiovascular adverse events such as hypertension or congestive heart failure. Edema was not associated with laboratory changes suggestive of deterioration in renal or hepatic function.
BACKGROUND: Interferon regulatory factor-1 (IRF1) is a transcription factor that plays a significant role in various biological processes, including inflammatory injury, viral infection, cell death, and immune responses, and it has been extensively studied in the context of different lung diseases. However, the mechanism underlying its involvement in lung fibrosis remains largely unknown.
METHODS: Wild type (WT) mice, IRF1 global-null mice (Irf1-/-) were subjected to a bleomycin-induced lung fibrosis model to enable examination of the role of IRF1 in lung fibrosis. Proteomic analysis of lung tissue from WT and Irf1-/- mice treated with saline or bleomycin was performed to explore the mechanism of IRF1 in regulating lung fibrosis.
RESULTS: In the bleomycin-induced fibrosis mouse model, increased expression of IRF1 was observed. Irf1 knockout mice displayed decreased lung fibrosis relative to WT mice following treatment with bleomycin. The protein expression of fibronectin, as assessed by the Western blot analysis of lung tissues, was downregulated in Irf1-/- mice. We observed a similar reduction in collagen content using hydroxyproline detection. Histologically, there was less collagen deposition in the lungs of Irf1-/- mice compared with WT mice. Proteomics data revealed that IRF1 may be involved in lung fibrosis via the regulation of ferroptosis. We determined that paraoxonase 1(PON1), a poorly characterized protein in lung fibrosis, was upregulated in Irf1-/- mice following exposure to bleomycin. In vitro experiments revealed that IRF1 could regulate the level of GSH and MDA through PON1. We also determined that PON1 levels were lower in the plasma of IPF patients compared with healthy controls.
CONCLUSION: Our data highlight the importance of IRF1 in the fibrotic process, and PON1 may be a potential mediator of IRF1 in the progression of lung fibrosis.
Fifty subjects will be randomly assigned to receive 10 μg of PA9159 Nasal Spray for 14 days. Subjects will be administered two vials of drug (spray bottle A and spray bottle B) once daily in the morning, one spray each in the left and right nostril, in the order of first spray A and then spray B. Spray Bottle A: 5 μg/spray; Spray Bottle B: 0 μg/spray.