anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Diabetic retinopathy (DR) is one of the most prevalent secondary complications associated with diabetes. Specifically, Type 1 Diabetes Mellitus (T1D) has an immune component that may determine the evolution of DR by compromising the immune response of the retina, which is mediated by microglia. In the early stages of DR, the permeabilization of the blood-retinal barrier allows immune cells from the peripheral system to interact with the retinal immune system. The use of new bioactive molecules, such as 3-(2,4-dihydroxyphenyl)phthalide (M9), with powerful anti-inflammatory activity, might represent an advance in the treatment of diseases like DR by targeting the immune systems responsible for its onset and progression. Our research aimed to investigate the molecular mechanisms involved in the interaction of specific cells of the innate immune system during the progression of DR and the reduction in inflammatory processes contributing to the pathology. In vitro studies were conducted exposing Bv.2 microglial and Raw264.7 macrophage cells to proinflammatory stimuli for 24 h, in the presence or absence of M9. Ex vivo and in vivo approaches were performed in BB rats, an animal model for T1D. Retinal explants from BB rats were cultured with M9. Retinas from BB rats treated for 15 days with M9 via intraperitoneal injection were analyzed to determine survival, cellular signaling, and inflammatory markers using qPCR, Western blot, or immunofluorescence approaches. Retinal structure images were acquired via Spectral-Domain-Optical Coherence Tomography (SD-OCT). Our results show that the treatment with M9 significantly reduces inflammatory processes in in vitro, ex vivo, and in vivo models of DR. M9 works by inhibiting the proinflammatory responses during DR progression mainly affecting immune cell responses. It also induces an anti-inflammatory response, primarily mediated by microglial cells, leading to the synthesis of Arginase-1 and Hemeoxygenase-1(HO-1). Ultimately, in vivo administration of M9 preserves the retinal integrity from the degeneration associated with DR progression. Our findings demonstrate a specific interaction between both retinal and systemic immune cells in the progression of DR, with a differential response to treatment, mainly driven by microglia in the anti-inflammatory action. In vivo treatment with M9 induces a switch in immune cell phenotypes and functions that contributes to delaying the DR progression, positioning microglial cells as a new and specific therapeutic target in DR.
Subjects will be provided a placebo, given once daily as a softgel or liquid. Subjects will be instructed to take the supplement daily for 8 weeks.
The endoscopist will perform biopsy until a macroscopic visible core (MVC) will be obtained and specimen will be placed in a container (Container A-MOSE). If the needle passes performed are less than 3 (1 or 2 passes) the specimens acquired in the remnant passes to join standard care of 3 passes, according to ESGE guidelines, will be placed in a second container (Container B).
PURPOSE: The purpose of this review is to discuss important considerations when prescribing buprenorphine for opioid use disorder (OUD) in the intensive care unit (ICU) setting, recognizing the challenges of providing detailed recommendations in the setting of limited available evidence.
SUMMARY: Buprenorphine is a partial mu-opioid receptor agonist that is likely to be increasingly prescribed for OUD in the ICU setting due to the relaxation of prescribing regulations. The pharmacology and pharmacokinetics of buprenorphine are complicated by the availability of several formulations that can be given by different administration routes. There is no single optimal dosing strategy for buprenorphine induction, with regimens ranging from very low-dose to high dose regimens. Faster induction with higher doses of buprenorphine has been studied and is frequently utilized in the emergency department. In patients admitted to the ICU who were receiving opioids either medically or illicitly, analgesia will not occur until their baseline opioid requirements are covered when their preadmission opioid is either reversed or interrupted. For patients in the ICU who are not on buprenorphine at the time of admission but have possible OUD, there are no validated tools to diagnose OUD or the severity of opioid withdrawal in critically ill patients unable to provide the subjective components of instruments validated in outpatient settings. When prescribing buprenorphine in the ICU, important issues to consider include dosing, monitoring, pain management, use of adjunctive medications, and considerations to transition to outpatient therapy. Ideally, addiction and pain management specialists would be available when buprenorphine is prescribed for critically ill patients.
CONCLUSION: There are unique challenges when prescribing buprenorphine for OUD in critically ill patients, regardless of whether they were receiving buprenorphine when admitted to the ICU setting for OUD or are under consideration for buprenorphine initiation. There is a critical need for more research in this area.
Participants will receive fixed dose combination of tramadol hydrochloride 37.5 milligram (mg) plus acetaminophen 325 mg, 1 to 3 tablets per day along with meloxicam (7.5 mg or 15 mg once daily) or aceclofenac (100 mg twice daily) from Day 1 to Day 28. Participants who will have the numeric rating scale score 4 or less on Day 29 will be randomly assigned to the treatment of NSAIDs to receive either meloxicam (7.5 mg or 15 mg once daily) or aceclofenac (100 mg twice daily) from Day 29 to Day 85.
This is a multicenter, randomized (2 PiCSO :1 Control), controlled, pilot study to evaluate safety and feasibility of Pressure-controlled intermittent Coronary Sinus Occlusion (PiCSO) therapy in patients with extensive ST elevation inferior wall myocardial infarction presenting with TIMI 0 or 1 and symptom duration ≤ 12 hours treated adjunct to percutaneous coronary intervention (PCI) compared to standard PCI. Patients with an ST-segment elevated inferior infarct eligible for PCI will be invited to participate in the PiCSO-AMI-V Inferior STEMI study. After consent as per approved ethics committee requirements, baseline assessments will be performed. PCI of the culprit vessel should be performed per standard practices. After TIMI flow restoration, the subjects meeting all eligibility criteria will be enrolled into the study and randomized either to PiCSO Group or Control Group. If the subject is randomized to PiCSO Group, the coronary sinus (CS) will be cannulated through the femoral vein and the PiCSO Impulse Catheter will be placed in the CS. In the event the PiCSO Impulse Catheter cannot be placed in the CS within 30 minutes, the physician should proceed with the regular PCI and the PiCSO treatment will be considered a failure. Once PiCSO Impulse Catheter is placed into CS, PiCSO treatment is started followed by stenting. The physician shall target a PiCSO treatment of 45 minutes whereas the treatment should be continued during and post stent insertion. At the end of the PiCSO treatment, the PiCSO Impulse Console is stopped and the PiCSO Impulse Catheter is removed. The patient is seen for a FU visit at 12-36 hours, 30 days, 6 months and 1 year post index procedure. 12-36 hours and 6 months post index the patient will get a echocardiogram. At every FU visit safety data and health status will be documented.
Microparticles with adsorbent surfaces, methods of making such microparticles, and uses thereof, are disclosed. The microparticles comprise a polymer, such as a poly(.alpha.-hydroxy acid), a polyhydroxy butyric acid, a polycaprolactone, a polyorthoester, a polyanhydride, and the like, and are formed using cationic, anionic, or nonionic detergents. The surface of the microparticles efficiently adsorb biologically active macromolecules, such as DNA, polypeptides, antigens, and adjuvants. Also provided are compositions of an oil droplet emulsion having a metabolizable oil and an emulsifying agent.  Immunogenic compositions having an immunostimulating amount of an antigenic substance, and an immunostimulating amount of an adjuvant composition are also provided. Methods of stimulating an immune response, methods of immunizing a host animal against a viral, bacterial, or parasitic infection, and methods of increasing a Th1 immune response in a host animal by administering to the animal an immunogenic composition of the microparticles, and/or microemulsions of the invention, are also provided.
Carcinogenesis

Lifetime carcinogenicity studies were performed in CD-1 mice and Sprague-Dawley rats. There was no evidence of a carcinogenic effect in mice administered varenicline by oral gavage for 2 years at doses up to 20 mg/kg/day (810 times the maximum recommended human dose [MRHD], on a mg/m2 basis). Rats were administered varenicline (1, 5, and 15 mg/kg/day) by oral gavage for 2 years. In male rats (n = 65 per sex per dose group), incidences of hibernoma (tumor of the brown fat) were increased at the mid dose (1 tumor, 5 mg/kg/day, 405 times the MRHD on a mg/m2 basis) and maximum dose (2 tumors, 15 mg/kg/day, 1216 times the MRHD on a mg/m2 basis). The clinical relevance of this finding to humans has not been established. There was no evidence of carcinogenicity in female rats. 

Mutagenesis

Varenicline was not genotoxic, with or without metabolic activation, in the following assays: Ames bacterial mutation assay; mammalian CHO/HGPRT assay; and tests for cytogenetic aberrations in vivo in rat bone marrow and in vitro in human lymphocytes.

Impairment of Fertility

There was no evidence of impairment of fertility in either male or female Sprague-Dawley rats administered varenicline succinate up to 15 mg/kg/day (1216 times the MRHD on a mg/m2 basis). Maternal toxicity, characterized by a decrease in body weight gain, was observed at 15 mg/kg/day. A decrease in fertility was noted in the offspring of pregnant rats administered varenicline succinate at an oral dose of 15 mg/kg/day. The decrease in fertility in the offspring of treated female rats was not evident at an oral dose of 3 mg/kg/day (243 times the MRHD, on a mg/m2 basis).
Methods and compositions for inhibiting the foreign body response to implanted materials are described herein. The methods include inhibiting the formation of foreign body giant cells by administering an effective amount of an antagonist of Rho GTPase activity. In a preferred embodiment, the methods include contacting an implanted material or the adjacent tissue or bodily fluids with an effective amount of a Rho GTPase antagonist to prevent formation of multinucleated foreign body giant cells at the implantation site. Inhibitors of Rho GTPase activity may be provided separately from the implanted material, or alternatively, may be provided as a component of the external surface of the implanted material. The methods include contacting monocytes or macrophages with inhibitors of Rho family GTPase activity in amounts effective to inhibit fusion of these cells to form multinucleated foreign body giant cells. Inhibitors of Rho GTPase activity are preferably inhibitors of Rac family GTPase activity. In a preferred embodiment, the small molecule Rac inhibitor NSC23766 is used.
The invention relates to a magnetic nano enzyme Fc-MBL @ rGO @ Fe  3  O  4  The preparation method constructs an antibacterial platform combining PTT and CDT of targeted bacteria. The broad spectrum bacterial affinity of Fc-MBL and the physical properties of graphene improve the ability of the material to capture bacteria. Using Fe  3  O  4  Excellent peroxidase-like activity and good photothermal conversion performance of rGO, and PTT and CDT synergy is realizedAnd performing antibacterial treatment. Fc-MBL @ rGO @ Fe  3  O  4  Can realize the rapid enrichment of bacteria within 5min and catalyze low-concentration H  2  O  2  Converted into OH which is toxic to bacteria. Under NIR irradiation, fc-MBL @ rGO @ Fe  3  O  4  The photothermal effect produced has the ability to kill bacteria and enhance the antimicrobial effect of CDT, enabling more effective antimicrobial treatment at low concentrations (40. Mu.g/mL) and milder temperatures (47 ℃). Furthermore, fc-MBL @ rGO @ Fe  3  O  4  Shows good biocompatibility and broad-spectrum antibacterial capability, and provides a potential choice for quick and effective in-vivo antibacterial treatment.
The diet intervention is a partial meal replacement program using the commercially available OPTAVIA® Optimal Weight 4\&2\&1 Plan™. In the OPTAVIA program, subjects are asked to eat 6 times each day, once every 2 to 3 hours.
Walking to school is associated with higher levels of physical activity, which is an objective of Healthy People 2010. However, parents' concerns about safety have been identified as a barrier that prevents their children from walking to school. A walking school bus (WSB) addresses these concerns by providing a supervised period of physical activity on the way to school. A WSB is a group of children led to and from school by responsible adults who walk together along a set route. The peer-reviewed literature on active travel to school is sparse. We evaluated a WSB program, to test the hypothesis that it would increase the proportion of children walking and decrease the proportion of children driven by car to school.

Comparison: We conducted an 18-month controlled, quasi-experimental trial at three public elementary schools in Seattle, Washington. The intervention school was assigned a WSB coordinator who dedicated 10-15 hours/week establishing WSB routes and implementing school activities on pedestrian safety. Each "bus" had its own set route to school from different locations in the surrounding neighborhoods and was staffed by several parent leaders. The two control schools received standard Seattle Public Schools resources on walking to school including "Safe Route Maps," a traffic and safety committee, and school safety patrols. The primary outcomes were the proportions of children who walked with and without an adult or were driven by car to school. We used the test for independent proportions to compare the proportion of children transported to school at the intervention versus control schools.
Coronary heart disease (CHD) is the leading cause of death in the United States; more than 600,000 Americans suffer a fatal cardiac event each year. Traditional CHD risk factors such as high blood pressure, smoking, and elevated cholesterol do not fully account for the timing and occurrence of CHD events. The term "cardiovascular vulnerable patient" has been used to describe patients susceptible to acute coronary events based upon plaque, blood, or myocardial characteristics. Psychosocial factors also have been shown to be associated with increased adverse health outcomes and increased cardiovascular vulnerability. For example, clinical depression and elevated depressive symptoms are associated with increased morbidity and mortality, and as a result, the American Heart Association has recommended that clinicians should routinely assess depression in CHD patients. Although much research and clinical recommendations have focused on depression, the significance of anxiety has been largely ignored, despite the fact that anxiety disorders are as prevalent as depression in the general population and are associated with similar levels of disability.

Despite the prevalence and prognostic significance of anxiety in CHD populations, there have been few randomized clinical trials (RCTs) specifically targeting anxious CHD patients. Anxiolytic medications, including selective serotonin reuptake inhibitors (SSRIs), have been shown to be effective in treating anxiety. SSRIs have been evaluated for the treatment of clinical depression in cardiac patients, with equivocal results. Surprisingly, to our knowledge, there have been no RCTs examining the efficacy of medications for treating anxiety in CHD patients. Moreover, because many cardiac patients are reluctant to take additional medications and psychotropic medications may not be effective for everyone or may produce unwanted side effects, there continue to be a need to identify alternative approaches for treating anxiety in cardiac patients. The investigators believe that exercise may be one such approach.

The purpose of this study is to evaluate the following hypotheses in a population of CHD patients with elevated symptoms of anxiety. The present study will examine the impact of a 3-month intervention of either exercise, Lexapro, or placebo on anxiety symptoms and CHD biomarkers among individuals with cardiac disease and elevated anxiety. The investigators hypothesize that: (1) Both exercise training and medication will reduce anxiety symptoms to a greater extent than placebo; (2) Exercise training will improve CHD biomarkers of risk including autonomic regulation, vascular endothelial function, and inflammation more than either medication or placebo; and (3) Improvements in CHD biomarkers will be mediated by reductions in symptoms of anxiety. The investigators also will explore potential moderators of treatment (e.g., anxiety diagnoses, CHD severity) as well as the longer-term benefits of treatment by documenting medical events and health care costs over a follow-up period of up to 4 years.
OBJECTIVES: I. Evaluate the safety of multiantigen loaded dendritic cells (DC) vaccine in patients with advanced renal cell carcinoma. II. Evaluate the immunologic response to this regimen in this patient population. III. Evaluate the clinical response to this regimen in this patient population.

OUTLINE: This is a sequential cohort study. All patients undergo total nephrectomy to harvest primary tumor for vaccine preparation. Patients without primary tumor undergo surgical resection of the accessible metastatic site for vaccine preparation. Patients are assigned to 1 of 4 treatment arms. Arm I: Patients receive vaccination with irradiated autologous tumor lysate (TuLy) intradermally (ID) on day 0 followed by vaccination with multiantigen liposome loaded dendritic cells (DC) ID on days 7, 14, and 21. Arm II: Patients receive vaccinations as in arm I, except DC are pulsed with tumor cells. Arm III: Patients receive vaccination with irradiated autologous tumor lysate (TuLy) IV on day 0 followed by vaccination with multiantigen liposome loaded DC IV on days 7, 14, and 21. Arm IV: Patients receive vaccinations as in arm III, except DC are treated as in arm II. Patients are followed on days 28, 42, 70, and 112.

PROJECTED ACCRUAL: A total of 24 patients will be accrued for this study.
Sepsis is a life-threatening condition induced by a deregulated host response to infection. Post-sepsis injury includes long-term cognitive impairment, whose neurobiological mechanisms and effective treatment remain unknown. The present study was designed to determine the potential effects of cannabidiol (CBD) in a sepsis-associated encephalopathy (SAE) model and explore if peroxisome proliferator activated receptor gamma (PPARγ) is the putative mechanism underpinning the beneficial effects. SAE was induced in Wistar rats by cecal ligation and puncture (CLP) or sham (control). CLP rats received vehicle, CBD (10 mg/kg), PPARγ inhibitor (GW9662 - 1 mg/kg), or GW9662 (1 mg/kg) + CBD (10 mg/kg) intraperitoneally for ten days. During this period, the survival rate was recorded, and at the end of 10 days, a memory test was performed, and the prefrontal cortex and hippocampus were removed to verify brain-derived neurotrophic factor (BDNF), cytokines (IL-1β, IL-6 and IL-10), myeloperoxidase activity, nitrite nitrate concentration, and lipid and protein carbonylation and catalase activity. Septic rats presented cognitive decline and an increase in mortality following CLP. Only CBD alone improved the cognitive impairment, which was accompanied by restoration of BDNF, reduced neuroinflammation, and oxidative stress, mainly in the hippocampus. This study shows that CLP induces an increase in brain damage and CBD has neuroprotective effects on memory impairment and neurotrophins, as well as against neuroinflammation and oxidative stress, and is mediated by PPARγ activation.
Stress ulcer bleeding is a serious complication after acute ischemic stroke, with a prevalence of 1%-5%, of which only 0.5%-1% require blood transfusion or result in hypotension. Stress ulcer bleeding after ischemic stroke has been shown to be associated with poor outcomes, such as mortality, and basilar artery occlusion and middle cerebral artery cerebral infarction are independent risk factors for stress ulcer bleeding after acute ischemic stroke. Guidelines or consensus on the prevention of stress ulcers after acute ischemic stroke do not advocate the routine use of histamine receptor antagonists or proton pump inhibitors for stress ulcer prevention.

However, stress ulcer prophylaxis is initiated in most patients admitted to the neurological intensive care unit after mechanical embolization of acute anterior circulation large vessel occlusion. With advances such as diagnosis and early initiation of enteral nutrition, the rate of stress ulcer bleeding in patients with mechanical embolization of acute anterior circulation large vessel occlusion is significantly reduced. The relationship between the risk and benefit of SUP in patients undergoing mechanical embolization for acute anterior circulation large vessel occlusion is not yet supported by evidence-based medical evidence. Therefore, the purpose of this study was to investigate the correlation between pharmacological stress ulcer prophylaxis and clinical outcomes in patients undergoing mechanical thrombectomy for acute anterior circulation large vessel occlusion.
Degenerative disc disease is the most prevalent indication for spine surgery and the major source of back pain in afflicted patients. Age related degeneration of the intervertebral discs is not the exception, but the rule. Degenerative changes are associated with weakening of the disc and hypertrophy of the ligamentum flavum in the spine. The aim of this study is to determine if there are any local or systemic biomarkers that correlate with the severity of degeneration as indicated by radiological examination. To date, Imaging (XRay, MRI, CT scans) are the most widely used diagnostic tools for identifying degenerated discs. Physical changes in the disc are also associated with increased secretion and expression of inflammatory mediators in the tissue. The investigators are interested in measuring both gene and protein level changes of inflammatory mediators in degenerated discs in order to correlate these levels with imaging based indicators of degeneration. Protein level changes in the disc and ligamentum flavum have yet to be correlated with MRI-derived disc modic changes classification system. The investigators hypothesize that as the image characteristics of advancing degenerative disease increase, a corresponding change will be present in the secretion (or expression) of specific markers related to inflammatory processes in the disc. Cytokines found to be upregulated in disc tissue or ligamentum flavum will also be measured in patient's serum levels to begin developing a systemic diagnostic method for detecting disc degeneration.