anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Bigleaf hydrangea (Hydrangea macrophylla) is a widely cultivated ornamental plant species. Leaf spot disease, caused by Corynespora cassiicola, poses a significant threat to the ornamental quality and economic value of hydrangeas. However, the disease resistance breeding of hydrangea is limited due to the lacking of resistant varieties and genes.
RESULTS: This study evaluated ten hydrangea varieties for their resistance to leaf spot disease. Among them, 'White Angel' and 'Ocean Heart' were screened out as representative varieties for resistance and susceptibility, respectively, on the basis of evaluation. Physiological and biochemical indices, phytohormones, and transcriptomic changes were measured in the leaves of both varieties at 0 and 24 h post inoculation with C. cassiicola. The results showed that C. cassiicola infection significantly increased abscisic acid (ABA) contents in both varieties; however, the increase was significantly higher in the susceptible variety 'Ocean Heart' compared to the resistant variety 'White Angel' (p < 0.05). Moreover, exogenous ABA (100 µM) decreased the leaves' resistance to C. cassiicola of both varieties, underscoring its key role in reduced disease resistance. Transcriptome profiling revealed 17,087 differentially expressed genes (DEGs) responding to C. cassiicola between the two varieties. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated significant enrichment of DEGs in "Plant hormone signal transduction", particularly related to ABA signaling (HmPP2C and HmABFs). In addition, the expression of ABA biosynthesis genes (HmZEP3, HmABA2, and HmAAO3) was upregulated in both varieties. Meanwhile, the ABA catabolism gene (HmCYP707A4) exhibited significantly upregulated expression in the resistant variety 'White Angel' and downregulated expression in the susceptible variety 'Ocean Heart'. Intriguingly, the expression of HmCYP707A4 was 15-fold higher in 'White Angel' than in 'Ocean Heart'.
CONCLUSION: In summary, these findings highlight the crucial role of ABA in the resistance of bigleaf hydrangea to leaf spot disease and provide valuable genetic resources for breeding programs to enhance the disease resistance in hydrangeas.
In the study CT coronary angiography-based rapid "rule out" arm (Group B), participants will receive initial cardiac troponin and creatinine tests. Upon return of normal laboratory values (including a calculated creatinine clearance), the participants will receive a CT coronary angiography an estimated 90 minutes or as soon as the CT scanner is available following the initial values assessment. Participants with negative test results will be discharged unless other indications for admission per standard of care and follow up will comprise telephone interviews 30 days and 1 year after triage/presentation. Participants with positive test results will be admitted to the hospital for further management as dictated by the admitting team.
BACKGROUND: Electronic health record (EHR)-based clinical decision support is a scalable way to help standardize clinical care. Clinical decision support systems have not been extensively investigated in cirrhosis management. Human-centered design (HCD) is an approach that engages with potential users in intervention development. In this study, we applied HCD to design the features and interface for a clinical decision support system for cirrhosis management, called CirrhosisRx.
METHODS: We conducted technical feasibility assessments to construct a visual blueprint that outlines the basic features of the interface. We then convened collaborative-design workshops with generalist and specialist clinicians. We elicited current workflows for cirrhosis management, assessed gaps in existing EHR systems, evaluated potential features, and refined the design prototype for CirrhosisRx. At the conclusion of each workshop, we analyzed recordings and transcripts.
RESULTS: Workshop feedback showed that the aggregation of relevant clinical data into 6 cirrhosis decompensation domains (defined as common inpatient clinical scenarios) was the most important feature. Automatic inference of clinical events from EHR data, such as gastrointestinal bleeding from hemoglobin changes, was not accepted due to accuracy concerns. Visualizations for risk stratification scores were deemed not necessary. Lastly, the HCD co-design workshops allowed us to identify the target user population (generalists).
CONCLUSIONS: This is one of the first applications of HCD to design the features and interface for an electronic intervention for cirrhosis management. The HCD process altered features, modified the design interface, and likely improved CirrhosisRx's overall usability. The finalized design for CirrhosisRx proceeded to development and production and will be tested for effectiveness in a pragmatic randomized controlled trial. This work provides a model for the creation of other EHR-based interventions in hepatology care.
Women (n=150) who have failed first-line treatment (TDF/3TC/EFV) based on HIV RNA levels and CD4 count. These women will be switched to second-line treatment (AZT/3TC/ATZ/r) per Malawi Ministry of Health standard of care.
This group will receive reduced visual and auditory stimuli in addition to usual care during venipuncture. Phototherapy goggles and earmuffs will be placed 3 minutes before the venipuncture (leaving the patient in resting state after the manipulation) and will be maintained during the procedure. Monitor alarms and devices will be silenced and will remain silenced and noise in the unit will be minimized during the procedure.
To examine the effects of clomiphene citrate (CC) on follicular fluid metabolites and related metabolic pathways in rats with polycystic ovary syndrome (PCOS) using non-targeted metabolomics and determine how CC treats ovulation disorder in PCOS. The Sprague Dawley rats were randomly divided into control, model, and CC groups. A PCOS model was established with letrozole. Body weight, ovarian weight, estrus cycles, serum hormone levels, and ovary histopathology of the rats were collected for further evaluation. Moreover, through ultra-performance liquid chromatography-mass spectrometry, the study of follicular fluid metabolites revealed the mechanism of action of CC. CC reduced ovarian weight and regulated estrous cycles and serum hormone levels in PCOS rats but did not affect their body weight. Moreover, the metabolomic results showed that CC adjusted 153 metabolites, among which 16 cross metabolites like testosterone, androstenedione, 17α-hydroxyprogesterone, and cholic acid were considered as potential biomarkers for CC to improve ovulation disorders in PCOS rats. Kyoto Encyclopedia of Genes and Genomes pathway enrichment also showed that the CC group mainly engaged in tryptophan metabolism and steroid hormone biosynthesis. CC can improve ovulation disorders in rats, and its mechanism is related to the regulation of the secretion of serum hormone and follicular fluid metabolites and the amelioration of multi-metabolic pathways.
BACKGROUND: Surgical site infections (SSIs) occur frequently and impact patients and health care systems. Remote surveillance of surgical wounds is currently limited by the need for manual assessment by clinicians. Machine learning (ML)-based methods have recently been used to address various aspects of the postoperative wound healing process and may be used to improve the scalability and cost-effectiveness of remote surgical wound assessment.
OBJECTIVE: The objective of this review was to provide an overview of the ML methods that have been used to identify surgical wound infections from images.
METHODS: We conducted a scoping review of ML approaches for visual detection of SSIs following the JBI (Joanna Briggs Institute) methodology. Reports of participants in any postoperative context focusing on identification of surgical wound infections were included. Studies that did not address SSI identification, surgical wounds, or did not use image or video data were excluded. We searched MEDLINE, Embase, CINAHL, CENTRAL, Web of Science Core Collection, IEEE Xplore, Compendex, and arXiv for relevant studies in November 2022. The records retrieved were double screened for eligibility. A data extraction tool was used to chart the relevant data, which was described narratively and presented using tables. Employment of TRIPOD (Transparent Reporting of a Multivariable Prediction Model for Individual Prognosis or Diagnosis) guidelines was evaluated and PROBAST (Prediction Model Risk of Bias Assessment Tool) was used to assess risk of bias (RoB).
RESULTS: In total, 10 of the 715 unique records screened met the eligibility criteria. In these studies, the clinical contexts and surgical procedures were diverse. All papers developed diagnostic models, though none performed external validation. Both traditional ML and deep learning methods were used to identify SSIs from mostly color images, and the volume of images used ranged from under 50 to thousands. Further, 10 TRIPOD items were reported in at least 4 studies, though 15 items were reported in fewer than 4 studies. PROBAST assessment led to 9 studies being identified as having an overall high RoB, with 1 study having overall unclear RoB.
CONCLUSIONS: Research on the image-based identification of surgical wound infections using ML remains novel, and there is a need for standardized reporting. Limitations related to variability in image capture, model building, and data sources should be addressed in the future.
Understanding the mechanisms of geroprotective interventions is central to aging research. We compare four prominent interventions: senolysis, caloric restriction, in vivo partial reprogramming, and heterochronic parabiosis. Using published mice transcriptomic data, we juxtapose these interventions against normal aging. We find a gene expression program common to all four interventions, in which inflammation is reduced and several metabolic processes, especially fatty acid metabolism, are increased. Normal aging exhibits the inverse of this signature across multiple organs and tissues. A similar inverse signature arises in three chronic inflammation disease models in a non-aging context, suggesting that the shift in metabolism occurs downstream of inflammation. Chronic inflammation is also shown to accelerate transcriptomic age. We conclude that a core mechanism of geroprotective interventions acts through the reduction of inflammation with downstream effects that restore fatty acid metabolism. This supports the notion of directly targeting genes associated with these pathways to mitigate age-related deterioration.
A therapeutically effective dose of polymethoxylated flavones, for example in the form of citrus peel extract, is provided for reducing the activity of 11(beta)-HSD1. Reducing the activity of 11(beta)-HSD1 in turn undesirable excess glucocorticoid, e.g. cortisol, levels. Particularly, the PMFs can be effectively used to inhibit a rise in glucocorticoids associated with the stress of weight loss. The polymethoxylated flavones may include one or more of tangeretin, nobiletin, and sinensetin. The PMFs may be administered in any of a variety of known modes of administrations such as oral and topical.
During treatment with RAVICTI, patients should be followed clinically and with plasma ammonia levels to determine the need for dosage titration. Closely monitor plasma ammonia levels during treatment with RAVICTI and when changing the dosage of RAVICTI. 

The methods used for measuring plasma ammonia levels vary among individual laboratories and values obtained using different assay methods may not be interchangeable. Normal ranges and therapeutic target levels for plasma ammonia depend upon the assay method used by the individual laboratory. During treatment with RAVICTI, refer to the assay-specific normal ranges and to the therapeutic target ranges for plasma ammonia. 

Normal Plasma Ammonia

In patients treated with RAVICTI who experience neurologic symptoms (e.g. nausea, vomiting, headache, somnolence or confusion) in the absence of high plasma ammonia or other intercurrent illness to explain these symptoms, consider reducing the RAVICTI dosage and clinically monitor patients for potential neurotoxicity from high phenylacetate (PAA) concentrations. If available, obtain measurements of plasma PAA concentrations and plasma phenylacetylglutamine (PAGN) to calculate the ratio of plasma PAA to PAGN which may help to guide RAVICTI dosing. The PAA to PAGN ratio has generally been less than 1 in patients with UCDs who did not have significant plasma PAA accumulation. In general, a high PAA to PAGN ratio may indicate a slower or less efficient conjugation reaction to form PAGN, which may lead to increases in PAA without further conversion to PAGN [see Warnings and Precautions (5.1), Clinical Pharmacology (12.3)]. 

Elevated Plasma Ammonia

In patients 6 years and older, when plasma ammonia is elevated, increase the RAVICTI dosage to maintain fasting plasma ammonia to less than half the upper limit of normal (ULN). In infants and pediatric patients below 6 years of age, if obtaining fasting ammonia is problematic due to frequent feedings, adjust the RAVICTI dosage to keep the first ammonia of the morning below the ULN for age. If available, the ratio of PAA to PAGN in the same plasma sample may provide additional information to assist in dosage adjustment decisions [see Use in Specific Populations (8.7), Clinical Pharmacology (12.3)]. 

Dietary Protein Intake

If available, urinary phenylacetylglutamine (U-PAGN) measurements may be used to help guide RAVICTI dosage adjustment. Each gram of U-PAGN excreted over 24 hours covers waste nitrogen generated from 1.4 grams of dietary protein. If U-PAGN excretion is insufficient to cover daily dietary protein intake and the fasting ammonia is greater than half the ULN, the RAVICTI dosage should be increased. The amount of dosage adjustment should factor in the amount of dietary protein that has not been covered, as indicated by the 24-hour U-PAGN output, and the estimated RAVICTI dose needed per gram of dietary protein ingested and the maximum total daily dosage (i.e., 17.5 mL). 

Consider a patient's use of concomitant medications, such as probenecid, when making dosage adjustment decisions based on U-PAGN. Probenecid may result in a decrease of the urinary excretion of PAGN [see Drug Interactions (7.2)].
A total of 5 sessions of 1.5 hours of group therapy will be applied to the Intervention Group. Group therapies will be carried out over the internet once a week, after appropriate days and times are determined.
Chronic pain is a debilitating symptom with a significant negative impact on the quality of life and socioeconomic status, particularly among adults and the elderly. Major Depressive Disorder (MDD) stands out as one of the most important comorbid disorders accompanying chronic pain. The kynurenine pathway serves as the primary route for tryptophan degradation and holds critical significance in various biological processes, including the regulation of neurotransmitters, immune responses, cancer development, metabolism, and inflammation. This review encompasses key research studies related to the kynurenine pathway in the context of headache, neuropathic pain, gastrointestinal disorders, fibromyalgia, chronic fatigue syndrome, and MDD. Various metabolites produced in the kynurenine pathway, such as kynurenic acid and quinolinic acid, exhibit neuroprotective and neurotoxic effects, respectively. Recent studies have highlighted the significant involvement of kynurenine and its metabolites in the pathophysiology of pain. Moreover, pharmacological interventions targeting the regulation of the kynurenine pathway have shown therapeutic promise in pain management. Understanding the underlying mechanisms of this pathway presents an opportunity for developing personalized, innovative, and non-opioid approaches to pain treatment. Therefore, this narrative review explores the role of the kynurenine pathway in various chronic pain disorders and its association with depression and chronic pain.
Despite state-of-the-art advances in the treatment of acute myocardial infarction (AMI), including early and prompt reperfusion therapy and advanced pharmaceutical therapy, AMI remains the leading cause of death of patients hospitalized for cardiovascular disease. Loss of myocardium after AMI, resulting in reducing LVEF and ultimately pump failure, are essential for unfavorable clinical outcomes and mortality, highlighting that to protect the myocardium from AMI-induced damage is the principal rule for treatment of the AMI patients. The pathological findings have clearly identified that loss of myocardium after AMI results from first ischemic necrosis, followed by ischemia-reperfusion injury, vigorous inflammatory reaction, generation of oxidative stress, and finally, upregulation of immune reaction. Thus, a phenomenon of "propagation of myocardium from injury to irrepressible death" at the moment just after AMI always occurs. These are the reasons why a satisfactory therapy for AMI is still difficult, highlighting the timing remains the Achilles' heel for salving the jeopardized myocardium. These raise the consideration of urgently to develop a new effective and safe treatment for patients.

Abundant data have shown mesenchymal stromal cells (MSC) pleiotropic capacities of anti-inflammation, immunomodulation, and tissue regeneration. Experimental studies have further demonstrated that MSC therapy effectively protected the organs from ischemic/ischemia-reperfusion injury. However, the therapeutic impact of stem cells on the clinical setting of AMI is still universally controversial. When investigators further look at the clinical trials, delayed time to apply the stem cells on AMI patients is universally consistent. Investigators have demonstrated that early intracoronary administration (i.e., at the time interval of 90 minutes after AMI induction) of OmniMSC-AMI significantly protected the left ventricular myocardium and improved LVEF in the mini-pig AMI model. The aforementioned issues and the results of our experimental study may support our hypothesis that immediate intracoronary administration of OmniMSC-AMI into the infarcted-related vessel in first AMI patients who just yet underwent primary PCI will be safe and may offer benefits in improving LVEF and outcome.
Carbapenem-resistant Acinetobacter baumannii (CRAB) is a persistent nosocomial pathogen that poses a significant threat to global public health, particularly in intensive care units (ICUs). Here we report a three-month longitudinal genomic surveillance study conducted in a Hangzhou ICU in 2021. This followed a three-month study conducted in the same ICU in 2019, and infection prevention and control (IPC) interventions targeting patients, staff and the ICU environment. Most A. baumannii isolated in this ICU in 2021 were CRAB (80.9%; 419/518) with higher-level resistance to carbapenems. This was accompanied by the proportion of global clone 2 (GC2) isolates falling from 99.5% in 2019 to 50.8% (213/419) in 2021. The phylogenetic diversity of GC2 increased, apparently driven by regular introductions of distinct clusters in association with patients. The remaining CRAB (40.2%; 206/419) were a highly clonal population of ST164. Isolates of ST164 carried blaNDM-1 and blaOXA-23 carbapenemase genes, and exhibited higher carbapenem MIC50/MIC90 values than GC2. Comparative analysis of publicly available genomes from 26 countries (five continents) revealed that ST164 has evolved towards carbapenem resistance on multiple independent occasions. Its success in this ICU and global capacity for acquiring resistance determinants indicate that ST164 CRAB is an emerging high-risk lineage of global concern.
Patients randomized to the BUP/NX arm will receive daily doses for 13 days with sublingual administration of 2 mg buprenorphine/0.5 mg naloxone tablet(s) and/or an 8 mg buprenorphine/2.0 mg naloxone tablet(s). The starting dose on day 1 is 4 mg/1 mg BUP/NX with an additional 4 mg/1 mg, if needed, escalating in a step-wise manner to 16 mg/4 mg BUP/NX on day 3 and tapering to 2 mg/ 0.5 mg BUP/NX by days 12 to 13. Patients randomized to the clonidine arm will receive oral clonidine (0.05 to 0.1 mg depending upon weight) every 4 to 6 hours for 24 hours not to exceed 0.6 mg total on day 1. On day 2, a clonidine transdermal patch will be applied (0.1 mg/day/7-day patch with number of patches adjusted by weight). Oral clonidine will continue to be given on the second day of detoxification and increased to 0.2 mg every 6 hours or 0.1 mg every 3 hours not to exceed 0.8 mg over 24 hours. Patches will be worn all 13 days of detoxification. The dose of clonidine will be adjusted according to the proposed detoxification schedule, patient's weight, tolerance, and systolic blood pressure. Patients will receive counseling according to procedures in existence at each CTP throughout the study. Self-help detoxification handbooks will be distributed to all study participants.
Depression is a common neuropsychiatric disease which brings an increasing burden to all countries globally. Baicalin, a flavonoid extracted from the dried roots of Scutellaria, has been reported to exert anti-inflammatory, antioxidant, and neuroprotective effects in the treatment of depression. However, the potential biological mechanisms underlying its antidepressant effect are still unclear. In the present study, we conducted extensive research on the potential mechanisms of baicalin's antidepressant effect using the methods of network pharmacology, including overlapped terms-based analysis, protein-protein interaction (PPI) network topology analysis, and enrichment analysis. Moreover, these results were further verified through molecular docking, weighted gene co-expression network analysis (WGCNA), differential gene expression analysis, and subsequent animal experiments. We identified forty-one genes as the targets of baicalin in the treatment of depression, among which AKT1, IL6, TP53, IL1B, and CASP3 have higher centrality in the more core position. Meanwhile, the roles of peripheral genes derived from direct potential targets were also observed. Our study suggested that biological processes, such as inflammatory reaction, apoptosis, and oxidative stress, may be involved in the therapeutic process of baicalin on depression. These mechanisms were validated at the level of structure, gene, protein, and signaling pathway in the present study. Taken together, these findings propose a new perspective on the potential mechanisms underlying baicalin's antidepressant effect, and also provide a new basis and clarified perspective for its clinical application.