anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Inflammation and oxidative stress are critical to pregnancy, but most human study has focused on downstream, non-causal indicators. Oxylipins are lipid mediators of inflammation and oxidative stress that act through many biological pathways. Our aim was to characterize predictors of circulating oxylipin concentrations based on maternal characteristics.
METHODS: Our study was conducted among 901 singleton pregnancies in the LIFECODES Fetal Growth Study, a nested case-cohort with recruitment from 2007 to 2018. We measured a targeted panel of oxylipins in early pregnancy plasma and urine samples from several biosynthetic pathways, defined by the polyunsaturated fatty acid (PUFA) precursor and enzyme group. We evaluated levels across predictors, including characteristics of participants' pregnancy, socioeconomic determinants, and obstetric and medical history.
RESULTS: Current pregnancy and sociodemographic characteristics were the most important predictors of circulating oxylipins concentrations. Plasma oxylipins were lower and urinary oxylipins higher for participants with a later gestational age at sampling (13-23 weeks), higher prepregnancy BMI (obesity class I, II, or III), Black or Hispanic race and ethnicity, and lower socioeconomic status (younger age, lower education, and uninsured). For example, compared to those with normal or underweight prepregnancy BMI, participants with class III prepregnancy obesity had 45-46% lower plasma epoxy-eicosatrienoic acids, the anti-inflammatory oxylipins produced from arachidonic acid (AA) by cytochrome P450, and had 81% higher urinary 15-series F2-isoprostanes, an indicator of oxidative stress produced from non-enzymatic AA oxidation. Similarly, in urine, Black participants had 92% higher prostaglandin E2 metabolite, a pro-inflammatory oxylipin, and 41% higher 5-series F2-isoprostane, an oxidative stress indicator.
CONCLUSIONS: In this large pregnancy study, we found that circulating levels of oxylipins were different for participants of lower socioeconomic status or of a systematically marginalized racial and ethnic groups. Given associations differed along biosynthetic pathways, results provide insight into etiologic links between maternal predictors and inflammation and oxidative stress.
This is a 4-session individual workshop using behavioral activation techniques. Emphasis is placed upon understanding the individuals values and increasing the number of pleasurable activities aligned with the individuals values.
Prazosin capsules beginning at 1 mg orally at bedtime. Titrate over 5 weeks to maximum dose of 5 mg in the morning and 20 mg at bedtime.
1. An intraoral or intranasal transmucosal preparation comprising levosimendan or a pharmaceutically acceptable salt thereof as a therapeutically active ingredient, together with one or more pharmaceutically acceptable excipients. 2. A preparation according to Claim 1, which is a buccal, sublingual or sinuidal transmucosal preparation. 3. A preparation according to Claim 1 or 2, which is in the form of a mucoadhesive preparation. 4. A preparation according to any of Claims 1-3, which comprises mucoadhesive matrix. 5. A preparation according to any of Claims 1-4, which is in the form of a patch. 6. Use of levosimendan or a pharmaceutically acceptable salt thereof in the manufacture of a medicament for transmucosal administration to oral or nasal mucosa of levosimendan or a pharmaceutically acceptable salt thereof. 7. A method for treating heart failure comprising administering transmucosally, particularly to oral or nasal mucosa, a therapeutically effective amount of levosimendan or a pharmaceutically acceptable salt thereof to a subject in need of such treatment. 8. A method of administering transmucosally, particularly to oral or nasal mucosa, levosimendan or a pharmaceutically acceptable salt thereof to a patient, wherein the method comprises contacting an intact mucous membrane with a source of levosimendan or a pharmaceutically acceptable salt thereof, and maintaining said source in contact with said mucous membrane for a sufficient time period to deliver said levosimendan or a pharmaceutically acceptable salt thereof to the patient.
Activation of immune cells requires the remodeling of cell metabolism in order to support immune function. We study these metabolic changes through the infection of Drosophila larvae by parasitoid wasp. The parasitoid egg is neutralized by differentiating lamellocytes, which encapsulate the egg. A melanization cascade is initiated, producing toxic molecules to destroy the egg while the capsule also protects the host from the toxic reaction. We combined transcriptomics and metabolomics, including 13C-labeled glucose and trehalose tracing, as well as genetic manipulation of sugar metabolism to study changes in metabolism, specifically in Drosophila hemocytes. We found that hemocytes increase the expression of several carbohydrate transporters and accordingly uptake more sugar during infection. These carbohydrates are metabolized by increased glycolysis, associated with lactate production, and cyclic pentose phosphate pathway (PPP), in which glucose-6-phosphate is re-oxidized to maximize NADPH yield. Oxidative PPP is required for lamellocyte differentiation and resistance, as is systemic trehalose metabolism. In addition, fully differentiated lamellocytes use a cytoplasmic form of trehalase to cleave trehalose to glucose and fuel cyclic PPP. Intracellular trehalose metabolism is not required for lamellocyte differentiation, but its down-regulation elevates levels of reactive oxygen species, associated with increased resistance and reduced fitness. Our results suggest that sugar metabolism, and specifically cyclic PPP, within immune cells is important not only to fight infection but also to protect the host from its own immune response and for ensuring fitness of the survivor.
Participants will be offered the opportunity to join one of two weekly meeting times. Participants will be sent a link to join a Zoom videoconference session at the outset of each week, allowing them to log in at their chosen timeslot. These meeting times will be arranged based on discussions with the PAC around optimal timeslots for their shift workers. Sessions will be 90 minutes in length and will be facilitated by a minimum of 2 trained clinician facilitators and 1 research assistant. The session will include a PowerPoint presentation of the CBTm material in a lecture format. Participants will be invited and encouraged to discuss, comment and ask questions of the facilitators about the material throughout the presentation. Homework will be assigned each session relating to the material that was covered. Participants will have 1 week to work through and practice the skills learned, and this homework will be discussed at the next session.
This is a single center study. All participants will be recruited from the USA. The study intends to recruit pre-pubertal children for inclusion in the 1 year growth hormone treatment trial. The study also plans to collect the following detailed phenotypic data at the first study visit: height, weight, musculoskeletal evaluation, photographs, radiographs (knees, left hand), MRI of the knees. The participants will be required to return to Cincinnati Childrens Hospital Medical Center (CCHMC) for 3 study visits over the 12 month period. At the follow up visits participants will receive a routine physical/pubertal exam, joint exam, have vitals sign checked, height/weight taken, and labs drawn. A funduscopic exam will be performed to look for signs of intracranial pressure. Study participants are also required to complete phone check ins at scheduled intervals, and a locally drawn blood sample to check insulin-like growth factor (IGF1) levels approximately 3 months after treatment start date. Concomitant medications, adverse events will be recorded and updated at all study visits and phone check ins. Medication will be resupplied and shipped to the participant as needed at every point of follow up contact. If the subjects grow well enough in the first 12 months per study protocol, they are eligible to continue treatment through the study for an additional 2 years. They will continue to come to CCHMC every 6 months for follow up study visits. Study procedures will remain the same as the initial 1 year trial with the following additions: (1) local labs may need to be obtained for dose adjustment purposes, (2) repeat knee MRI may be completed for participants that are found to have early signs of joint disease on their baseline knee MRI scan.

The study will enroll interested and affected relatives of the participant in the joint phenotyping protocol as well. These participants will come to CCHMC only one time to complete the phenotyping visit. This is not an outcome of the study but the information gathered from the imaging will provide insight into the effects of ACAN mutation on the joint cartilage.
Patients in (G1) will be treated by a designed physiotherapy program consisted of aerobic exercise on treadmill, stretching exercise, Proprioceptive neuromuscular facilitation (PNF) techniques, Graduated active exercises, gait training, Reciprocal and weight shifting exercises. The treatment will be conducted three sessions per week, day after day for successive four weeks. The session duration was 40min to 1 hour.
This is a combination of the above two arms. The participants who randomly assigned to this arm will received two acupuncture sessions and two sessions on lifestyle management every week, and the intervention duration is 8 weeks.
OBJECTIVE: This study aims to establish an effective predictive model for predicting Xp11.2 translocation/TFE3 gene fusion renal cell carcinoma (TFE3-RCC) and develop optimal therapeutic strategies.
METHODS: Data from 4961 patients diagnosed with renal cell carcinoma at two medical centers in China were retrospectively analyzed. A cohort of 1571 patients from Zhejiang Provincial People's Hospital (Ra cohort) was selected to construct the model. Another cohort of 1124 patients from the Second Affiliated Hospital of Zhejiang Chinese Medical University was used for external validation (the Ha cohort). All patients with TFE3-RCC in both cohorts were included in the Ta cohort for the prognostic analysis. Univariate and multivariate binary logistic regression analyses were performed to identify independent predictors of the predictive nomogram. The apparent performance of the model was validated. Decision curve analysis was also performed to assess the clinical utility of the developed model. Factors associated with progression and prognosis in the Ta cohort were analyzed using the log-rank method, and Cox regression analysis and Kaplan-Meier survival curves were used to describe the effects of factors on prognosis and progression.
RESULTS: Univariate and multivariate logistic regression analyses demonstrated that age, sex, BMI, smoking, eosinophils, and LDL were independent predictors of TFE3-RCC. Therefore, a predictive nomogram for TFE3-RCC, which had good discriminatory power (AUC = 0.796), was constructed. External validation (AUC = 0.806) also revealed good predictive ability. The calibration curves displayed good consistency between the predicted and observed incidences of TFE3-RCC. Invasion of regional lymph nodes, tyrosine kinase inhibitors, and surgical methods were independent factors associated with progression. Tyrosine kinase inhibitors are independent prognostic factors.
CONCLUSION: This study not only proposed a high-precision clinical prediction model composed of various variables for the early diagnosis of Xp11.2 translocation/TFE3 gene fusion renal cell carcinoma but also optimized therapeutic strategies through prognostic analysis.
In recent years there has been a great interest in analyzing the relationship between smoking and depression due to the high smoking rates in this population. Smokers with depression are more likely to smoke heavily, show greater tobacco dependence, suffer more severe withdrawal, experience lower quit rates and have more relapse than smokers without depression. Some studies propose the inclusion of behavioural activation techniques to standard cognitive-behavioural therapy for quitting smoking, arguing that the loss of the ability to experience pleasure in response to daily activities after quitting smoking is a significant barrier to achieving and maintaining abstinence. With this type of intervention, the exposure to positive reinforcers alternative to cigarettes increases and the resulting distress of withdrawal syndrome it is also reduced. Therefore, behavioural activation may improve smoking abstinence rates and depressive symptomatology. This project aims to assess the effectiveness of a psychological intervention for smoking cessation with components of behavioural activation for managing depressed mood. We will use a single blind controlled randomized design. Two hundred and fifty daily (≥ 10 cigarettes/day) smokers will be randomized to one of three conditions: 1) standard cognitive-behavioural smoking cessation treatment (n=100); 2) standard cognitive-behavioural smoking cessation treatment plus behavioural activation (n=100); or 3) a control group of three months delayed treatment (n=50). Both active treatments will be administered in eight weekly 60 minute sessions. The primary outcomes will be carbon monoxide (CO) verified at 24-hours point prevalence abstinence at the end of the treatment, a 7-day point prevalence abstinence at 3 months follow-up, a 30-days point prevalence abstinence at 6-, and 12-months follow-ups; and depressive symptomatology through BDI-II and Hamilton Depression Rating Scale scores at the end of treatment, and at 3-, 6-, and 12-months follow-ups. Additional aims include assessing others activation-related variables, craving, self-efficacy and withdrawal syndrome. This randomized controlled trial will be the first trial of Behavioural Activation and Smoking Cessation psychological treatment in a Spanish sample of seeking treatment smokers.
We aimed to assess the association of tramadol use with the risk of dementia. This population-based retrospective cohort study using the Korean National Health Insurance Service database included a total of 1,865,827 older adult patients aged 60 years or older with common musculoskeletal pain between January 1, 2003, and December 31, 2007. Individuals who were newly dispensed tramadol (N = 41,963) were identified and propensity score-matched with those who were not (N = 41,963). Over a maximum of 14-year follow-up, the incidence rates (events per 1000 person-years) of all-cause dementia were 6.1 for nonusers, 6.2 for those with cumulative tramadol use of 1-14 days, 7.7 for those with 15-90 days of use, and 8.0 for those with > 90 days of use. Longer cumulative duration of tramadol use was associated with an increased risk of all-cause dementia compared with nonuse (1 to 14 days: aHR 1.06, 95% CI 0.96-1.17; 15 to 90 days: aHR 1.14, 95% CI 1.10-1.35; and more than 90 days: aHR 1.18, 95% CI 1.00-1.39; test for trend: P < 0.001). The results showed a similar pattern for Alzheimer's disease and were robust across subgroup and sensitivity analyses, but not for vascular dementia. This study found that exposure to tramadol was associated with an increased risk of dementia. Taking this potential risk into consideration, clinicians should carefully weigh potential benefits and risks when prescribing tramadol to older adults with musculoskeletal pain.
The present invention is directed to a method for treating cystic fibrosis. The method comprises the steps of: identifying a patient suffering from cystic fibrosis, and administering to the patient an effective amount of denufosol or a pharmaceutically acceptable salt thereof and an effective amount of a macrolide. In one method, denufosol and the macrolide are administered by inhalation, preferably in a single formulation. In another method, denufosol is administered by inhalation and the macrolide is administered orally. The present invention is also directed to a pharmaceutical formulation comprising denufosol or a pharmaceutically acceptable salt thereof, a macrolide, and a pharmaceutically acceptable carrier. Preferred denufosol is denufosol tetrasodium and preferred macrolide is azithromycin. The pharmaceutical formulation preferably is in a form of an inhalable dry powder or in a liquid form.
For a majority of patients with advanced heart failure, medical treatment is only partially effective in relieving heart failure symptoms. Therefore, it is recommended that palliative care be initiated soon after diagnosis. There is a need for complementary, nonpharmacologic interventions that could be easily implemented by health care providers to provide palliative care. Three major pathologic pathways underlying heart failure symptoms have been identified: fluid overload, inflammation, and oxidative stress. Prior research has demonstrated that three nutrients-sodium, omega-3 fatty acids, and lycopene-can alter these pathologic pathways. Clinical trials to date have only tested each nutrient individually. There is strong theoretical rationale that a combined intervention targeting all three nutrients would have substantial benefit in relieving symptoms in advanced heart failure. Therefore, the purposes of this study are to test the effects of a 6-month nutrition intervention of dietary sodium reduction combined with supplementation of lycopene and omega-3 fatty acids on heart failure symptoms, health-related quality of life, and time to heart failure rehospitalization or all-cause death. The aims of this placebo controlled study are 1) to determine the effects of a 6-month nutrition intervention on symptom burden (edema, shortness of air, and fatigue) and health related quality of life at 3 and 6 months, and time to heart failure rehospitalization or all-cause death over 12 months from baseline; 2) compare dietary sodium intake, inflammation, and markers of oxidative stress between the nutrition intervention group and a placebo group at 3 and 6 months; and 3) compare body weight, serum lycopene, and erythrocyte omega-3 index between the nutrition intervention group and a placebo group at 3 and 6 months. A total of 150 patients with advanced heart failure will be randomized to either the nutrition intervention or placebo group (75 per group). The nutrition intervention group will receive a theory based education and skill building intervention designed to decrease dietary sodium intake to \~2 g per day. A research nurse will make 4 home visits and one follow-up telephone call over 6 months to provide the education-skill building intervention. The intervention group will take 3 omega-3 fatty acid capsules (350 mg eicosapentaenoic acid and 50 mg docosahexaenoic acid) and consume tomato juice or other tomato-based products containing 20-25 mg of lycopene daily for six months. The placebo group will receive the same number of visits and phone calls but only general nutrition information will be provided. They will take 3 placebo capsules containing rice oil (500 mg/capsule) and consume their choice of fruit juices that do not contain lycopene daily for six months. Data will be collected in person at baseline, 3 months, and 6 months by a research assistant blinded to the group assignment. Patients will be followed for an additional 6 months by telephone to collect longer term data on symptom burden and quality of life as well as heart failure hospitalization and all-cause mortality at 9 and 12 months.
The household participants will be analyzed alongside the index participants to determine household-level effects from the intervention. Household participants must live in an index participant's household. Index participants are allowed to have up to 3 household participants.
Omeza® OCM™ is an FDA cleared 510(K) medical combination drug/device which is applied directly to the wound bed. Treatment, followed by compression management, is applied on a weekly basis.
100 volunteers will be recruited for a 6 week intervention. The study group will be divided into 3 arms, each with approximately. 33 participants; one arm will receive a placebo capsule, one arm will receive a capsule with 400mg of curcumin (corresponding to two teaspoons of turmeric powder). These treatments are done double-blind. A third arm is 'open label', these volunteers will receive a bag with at least 135g turmeric and be asked to add two teaspoon to their food. Participants will be asked to supplement their diet with turmeric (powder, capsule or placebo) every other day for six weeks.

Participants will be asked to attend the NU-Food research facility on 3 occasions. The first will be a screening session where participants will be given the option to discuss the project with a researcher. Participants will complete a screening questionnaire and sign an informed consent form. On the next visit, participants will arrive at the research facility at a pre-arranged time and firstly have their height and weight measured. Participants will then give 10ml of blood via venepuncture and asked to provide a 10ml spot urine sample. After this participants will be randomly allocated a treatment group (placebo, turmeric capsule or turmeric powder) and given instructions on dosage. After a 6 week treatment period, participants will return to the research facility, have their height and weight measured then give a second 10ml venous blood sample and provide a final spot urine sample. Each visit will take around 20 minutes.

The main outcomes of the trial are oxidative stress and inflammation tests which will be conducted by PB bioscience and an assessment of DNA methylation by University College London. Proteomics analysis will be conducted on Urine samples.
MicroRNAs play crucial roles in plant defense responses. However, the underlying mechanism by which miR398b contributes to soybean responses to soybean cyst nematode (Heterodera glycines) remains elusive. In this study, by using Agrobacterium rhizogenes-mediated transformation of soybean hairy roots, we observed that miR398b and target genes GmCCS and GmCSD1b played vital functions in soybean-H. glycines interaction. The study revealed that the abundance of miR398b was downregulated by H. glycines infection, and overexpression of miR398b enhanced the susceptibility of soybean to H. glycines. Conversely, silencing of miR398b improved soybean resistance to H. glycines. Detection assays revealed that miR398b rapidly senses stress-induced reactive oxygen species, leading to the repression of target genes GmCCS and GmCSD1b and regulating the accumulation of plant defense genes against nematode infection. Moreover, exogenous synthetic ds-miR398b enhanced soybean sensitivity to H. glycines by modulating H2O2 and O2- levels. Functional analysis demonstrated that overexpression of GmCCS and GmCSD1b in soybean enhanced resistance to H. glycines. RNA interference-mediated repression of GmCCS and GmCSD1b in soybean increased susceptibility to H. glycines. RNA sequencing revealed that a majority of differentially expressed genes in overexpressed GmCCS were associated with oxidative stress. Overall, the results indicate that miR398b targets superoxide dismutase genes, which negatively regulate soybean resistance to H. glycines via modulating reactive oxygen species levels and defense signals.