anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PURPOSE: Glaucoma, a leading cause of blindness worldwide, is suspected to exhibit a notable association with psychological disturbances. This study aimed to investigate epidemiological associations and explore shared genetic architecture between glaucoma and mental traits, including depression and anxiety.
METHODS: Multivariable logistic regression and Cox proportional hazards regression models were employed to investigate longitudinal associations based on UK Biobank. A stepwise approach was used to explore the shared genetic architecture. First, linkage disequilibrium score regression inferred global genetic correlations. Second, MiXeR analysis quantified the number of shared causal variants. Third, specific shared loci were detected through conditional/conjunctional false discovery rate (condFDR/conjFDR) analysis and characterized for biological insights. Finally, two-sample Mendelian randomization (MR) was conducted to investigate bidirectional causal associations.
RESULTS: Glaucoma was significantly associated with elevated risks of hospitalized depression (hazard ratio [HR] = 1.54; 95% confidence interval [CI], 1.01-2.34) and anxiety (HR = 2.61; 95% CI, 1.70-4.01) compared to healthy controls. Despite the absence of global genetic correlations, MiXeR analysis revealed 300 variants shared between glaucoma and depression, and 500 variants shared between glaucoma and anxiety. Subsequent condFDR/conjFDR analysis discovered 906 single-nucleotide polymorphisms (SNPs) jointly associated with glaucoma and depression and two associated with glaucoma and anxiety. The MR analysis did not support robust causal associations but indicated the existence of pleiotropic genetic variants influencing both glaucoma and depression.
CONCLUSIONS: Our study enhances the existing epidemiological evidence and underscores the polygenic overlap between glaucoma and mental traits. This observation suggests a correlation shaped by pleiotropic genetic variants rather than being indicative of direct causal relationships.
At W0, if the serum ADA concentration is ≥ 8 μg/mL, ADA administration will be spaced every 21 days. At W24, if the ADA concentration is \< 3.3 μg/mL (having a serum ADA concentration above this threshold was associated with a complete therapeutic response according to one study), administrations will be repeated every 14 days. If the ADA concentration is ≥ 3.3 and \< 8μg/mL, administrations will be left every 21 days. If ADA concentration is still ≥8μg/mL, ADA administrations will be spaced every 28 days.
We present a system for simultaneous recording of the electrocardiogram and the magnetocardiogram. The measurement system contained of printed carbon electrodes and SERF magnetometer. The use of this system confirms that the position of the end of the magnetic T wave extends further than the electric T wave, which is an important indicator for the diagnosis of cardiological patients and for drug arrhythmogenicity. We analyze this phenomenon in depth, and demonstrate, that it originates from the fundamental difference between electric and magnetic measurements. The measured value is always bipolar since the electric measurements require two electrodes. We demonstrate how the dual electric and magnetic measuring system adds a new information to the commonly used electrocardiographic diagnosis. The ECG should be interpreted as the spatial asymmetry of the electric cardiac potential, and not as the potential itself. The results seem to prove, that the relation between the magnetic and the electric imaging of neural activities may be broadly applied for the benefit of medical diagnosis in cardiology and many other fields, where the neural activity is measured. This is a pilot study which requires further confirmation at the clinical level.
OBJECTIVES: I. Compare the sequential chemotherapy with doxorubicin, paclitaxel and cyclophosphamide to combined doxorubicin and cyclophosphamide followed by paclitaxel for disease free and overall survival in women with node positive stage II or IIIA breast cancer. II. Determine whether increasing the dose density of adjuvant chemotherapy will improve disease free and overall survival. III. Compare the toxicity in patients treated with these regimens.

OUTLINE: This is a randomized study. Patients are randomized into one of four arms (sequential chemotherapy every 2 weeks vs every 3 weeks vs concurrent chemotherapy followed by paclitaxel every 2 weeks vs every 3 weeks). All tumor should be removed by either a modified radical mastectomy or a segmental mastectomy plus axillary node dissection. Adjuvant chemotherapy is started within 84 days following the last surgical procedure. Arm I: Patients receive sequential chemotherapy every 3 weeks. Doxorubicin IV is administered once every 3 weeks for 4 doses. Paclitaxel IV is then administered over 3 hours once every 3 weeks for 4 doses. Cyclophosphamide IV is administered once every 3 weeks for 4 doses following paclitaxel. Arm II: Patients receive sequential chemotherapy every 2 weeks. Doxorubicin IV is administered once every 2 weeks for 4 doses. Paclitaxel IV is then administered over 3 hours once every 2 weeks for 4 doses. Cyclophosphamide IV is administered once every 2 weeks for 4 doses following paclitaxel. Filgrastim (G-CSF) is administered by subcutaneous injection on days 3-10 after each dose of doxorubicin, paclitaxel, and cyclophosphamide. Arm III: Patients receive combination chemotherapy every 3 weeks. Combination doxorubicin IV and cyclophosphamide IV is administered once every 3 weeks for 4 doses. Paclitaxel IV is administered over 3 hours once every 3 weeks for 4 doses following combination chemotherapy. Arm IV: Patients receive combination chemotherapy every 2 weeks. Combination doxorubicin IV and cyclophosphamide IV is administered once every 2 weeks for 4 doses. Paclitaxel IV is administered over 3 hours once every 2 weeks for 4 doses following combination chemotherapy. G-CSF is administered by subcutaneous injection on days 3-10 after each dose of doxorubicin/cyclophophamide and after each dose of paclitaxel. After completion of all chemotherapy, patients receive tamoxifen orally for 5 years. Patients undergo radiotherapy 4-6 weeks after the completion of chemotherapy. Patients are followed every 6 months for 5 years, then annually until death.

PROJECTED ACCRUAL: A total of 2,000 patients will be accrued for this study within 22 months.
Provided are a dental implant body and a dental implant body manufacturing method capable of improving the strength of joint to a jawbone, reducing dropping and detachment from the jawbone, and improving a prognosis. Ceramic powder is dispersed in gelatable liquid, and slurry is produced accordingly. The slurry is gelated, and a gel body is produced accordingly. The produced gel body is frozen, dried, and sintered, and accordingly, a porous body including a ceramics sintered body, having blind/continuous holes formed from a surface of the ceramics sintered body, and having walls formed by the blind/continuous holes. In this manner, the dental implant body is manufactured. Further, the concentration of the ceramic powder dispersed in the liquid is set to equal to or higher than 5% and equal to or lower than 65%, the gel body is frozen at a range of equal to or higher than -40°C and equal to or lower than -10°C, the porosity of the blind/continuous holes is 50 ± 10%, and the diameter of the blind/continuous hole is equal to or greater than 50 µm and equal to or smaller than 190 µm.
The invention relates to the technical field of medical image analysis, in particular to a medical image classification method based on a biased label learning model. The gastric cancer pathology image is collected to form a first pathology data set, and a third pathology data set is obtained through data preprocessing and image enhancement. And constructing a first partial label learning model, and training through a third pathological data set to generate a second partial label learning model. Training set samples are separated into trusted and untrusted samples by an improved loss function. And obtaining a second integrated output value through integrated output value calculation and rule filtering, and integrating the second integrated output value with the trusted sample to form a third integrated data set. And constructing a self-adaptive class attention model to train the third integrated data set to obtain a third partial label learning model. Finally, a prediction is made using the fourth set of pathological data based on the model. According to the invention, more accurate image classification is realized under the condition of missing accurate labeling, and powerful support is provided for teaching practice in the medical field.
Leaf rust (LR) caused by Puccinia hordei is a serious disease of barley worldwide, causing significant yield losses and reduced grain quality. Discovery and incorporation of new sources of resistance from gene bank accessions into barley breeding programs is essential for the development of leaf rust resistant varieties. To identify Quantitative Trait Loci (QTL) conferring LR resistance in the two barley subsets, the Generation Challenge Program (GCP) reference set of 142 accessions and the leaf rust subset constructed using the Focused Identification of Germplasm Strategy (FIGS) of 76 barley accessions, were genotyped to conduct a genome-wide association study (GWAS). The results revealed a total of 59 QTL in the 218 accessions phenotyped against barley leaf rust at the seedling stage using two P. hordei isolates (ISO-SAT and ISO-MRC), and at the adult plant stage in four environments in Morocco. Out of these 59 QTL, 10 QTL were associated with the seedling resistance (SR) and 49 QTL were associated with the adult plant resistance (APR). Four QTL showed stable effects in at least two environments for APR, whereas two common QTL associated with SR and APR were detected on chromosomes 2H and 7H. Furthermore, 39 QTL identified in this study were potentially novel. Interestingly, the sequences of 27 SNP markers encoded the candidate genes (CGs) with predicted protein functions in plant disease resistance. These results will provide new perspectives on the diversity of leaf rust resistance loci for fine mapping, isolation of resistance genes, and for marker-assisted selection for the LR resistance in barley breeding programs worldwide.
Retinitis pigmentosa (RP) is a group of inherited retinal degenerations with a worldwide prevalence of approximately 1 in 4,000. Patients typically report night blindness and difficulty with midperipheral visual field in adolescence. As the condition progresses, they lose far peripheral visual field. Most patients have reductions in central vision by age 50 to 80 years. Based on electroretinograms (ERGs), the course of the disease can be slowed on average among adults on 15,000 IU/day of vitamin A palmitate. While conducting the trial on the effects of vitamin A on RP, it became apparent that another substance in the diet could be affecting the course of the disease. This prompted the present randomized, controlled trial.

This study is a randomized, controlled, double-masked trial with a planned duration of 5 years. Patients with the common forms of RP are assigned to either a test or a control group. All receive 15,000 IU/day of vitamin A palmitate in addition to either 1200 mg/d of docosahexaenoic acid or control capsules. Participants will not know the contents of the supplement or the group to which they have been assigned until the end of the trial. The main outcome measurement is the total point score on the Humphrey Field Analyzer (HFA). In addition, computer-averaged 30-Hz cone ERG amplitudes and visual acuity are measured annually.
Use of a compound (I) interacting with brain-derived nerve growth factor (BDNF)-signal transduction cascade for the production of a medicament to treat phantom phenomena of acute tinnitus and/or phantom pain in human or animal. Independent claims are also included for: (1) diagnosing phantom phenomena of the acute tinnitus and/or phantom pain in human or animal, comprising supplying a biological sample, determining the level of the expression of BDNF in the biological sample, comparing the level with a reference value from a healthy organism, and correlating a level lying over the healthy organism with a positive diagnosis; and (2) treating phantom phenomena of the acute tinnitus and/or phantom pain in human or animal, comprising supplying a medicament that exhibits a substance interacting with BDNF signal transduction cascade, and applying the medicament locally to the organism, and optionally repeating the method. ACTIVITY : Auditory; Analgesic. MECHANISM OF ACTION : Brain-derived nerve growth factor (BDNF)-signal transduction cascade blocker; BDNF-signal transduction cascade inhibitor; Gamma aminobutyric acid receptor agonist; L-type-Ca ++>-channel antagonist; Cyclic adenosine monophosphate response element binding protein (CREP) antagonist; Glutamate antagonist; Mitogen activated protein-kinase-inhibitor; Calmodulin-dependent kinase-inhibitor; Tyrosine kinase linked receptor (trkB) antagonist. The ability of (I) to inhibit BDNF-signal transduction cascade was tested in cochlea. (I) Significantly removed the expressions of BNDF Exon-IV.
Analgesic therapies; such as interferential current (IFC) and transcutaneous electrical nerve stimulation (TENS) have been applied solo or combined with exercise for management of neck pain (NP), however, the efficacy of these combinations are unclear. In this study, our objective were to determine if TENS or IFC increase the effectiveness of neck stabilization exercises on pain, disability, mood, and quality of life for chronic NP. 81 patients with chronic NP were included in the study. Patients were randomly assigned into 3 groups; Group I: neck stabilization exercise, Group II: TENS+ neck stabilization exercise and Group III: IFC+ neck stabilization exercise. Patients' pain levels (visual analogue scale (VAS)), quality of life (short form- 36), mood (Beck depression inventory (BDI)), levels of disability (Neck Pain and Disability Index) and the need for analgesics were evaluated prior to treatment, at 6th and 12th week follow-up. All participants had group exercise accompanied by a physiotherapist for 3 weeks and an additional 3 weeks of home exercise program.
Persistently elevated glycolysis in kidney has been demonstrated to promote chronic kidney disease (CKD). However, the underlying mechanism remains largely unclear. Here, we observed that 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a key glycolytic enzyme, was remarkably induced in kidney proximal tubular cells (PTCs) following ischemia-reperfusion injury (IRI) in mice, as well as in multiple etiologies of patients with CKD. PFKFB3 expression was positively correlated with the severity of kidney fibrosis. Moreover, patients with CKD and mice exhibited increased urinary lactate/creatine levels and kidney lactate, respectively. PTC-specific deletion of PFKFB3 significantly reduced kidney lactate levels, mitigated inflammation and fibrosis, and preserved kidney function in the IRI mouse model. Similar protective effects were observed in mice with heterozygous deficiency of PFKFB3 or those treated with a PFKFB3 inhibitor. Mechanistically, lactate derived from PFKFB3-mediated tubular glycolytic reprogramming markedly enhanced histone lactylation, particularly H4K12la, which was enriched at the promoter of NF-κB signaling genes like Ikbkb, Rela, and Relb, activating their transcription and facilitating the inflammatory response. Further, PTC-specific deletion of PFKFB3 inhibited the activation of IKKβ, I κ B α, and p65 in the IRI kidneys. Moreover, increased H4K12la levels were positively correlated with kidney inflammation and fibrosis in patients with CKD. These findings suggest that tubular PFKFB3 may play a dual role in enhancing NF-κB signaling by promoting both H4K12la-mediated gene transcription and its activation. Thus, targeting the PFKFB3-mediated NF-κB signaling pathway in kidney tubular cells could be a novel strategy for CKD therapy.
BACKGROUND: Mechanical spinal cord injury (SCI) is a deteriorative neurological disorder, causing secondary neuroinflammation and neuropathy. ADAM8 is thought to be an extracellular metalloproteinase, which regulates proteolysis and cell adherence, but whether its intracellular region is involved in regulating neuroinflammation in microglia after SCI is unclear.
METHODS: Using animal tissue RNA-Seq and clinical blood sample examinations, we found that a specific up-regulation of ADAM8 in microglia was associated with inflammation after SCI. In vitro, microglia stimulated by HMGB1, the tail region of ADAM8, promoted microglial inflammation, migration and proliferation by directly interacting with ERKs and Fra-1 to promote activation, then further activated Map3k4/JNKs/p38. Using SCI mice, we used BK-1361, a specific inhibitor of ADAM8, to treat these mice.
RESULTS: The results showed that administration of BK-1361 attenuated the level of neuroinflammation and reduced microglial activation and recruitment by inhibiting the ADAM8/Fra-1 axis. Furthermore, treatment with BK-1361 alleviated glial scar formation, and also preserved myelin and axonal structures. The locomotor recovery of SCI mice treated with BK-1361 was therefore better than those without treatment.
CONCLUSIONS: Taken together, the results showed that ADAM8 was a critical molecule, which positively regulated neuroinflammatory development and secondary pathogenesis by promoting microglial activation and migration. Mechanically, ADAM8 formed a complex with ERK and Fra-1 to further activate the Map3k4/JNK/p38 axis in microglia. Inhibition of ADAM8 by treatment with BK-1361 decreased the levels of neuroinflammation, glial formation, and neurohistological loss, leading to favorable improvement in locomotor functional recovery in SCI mice.
Posttraumatic stress disorder (PTSD) is one of the most common mental health diagnoses among Veterans. Cognitive processing therapy (CPT) and prolonged exposure therapy (PE) were widely disseminated in the Veterans Health Administration (VHA) as recommended PTSD treatments. Despite these efforts, few post-9/11 Veterans diagnosed with PTSD initiate CPT or PE. In the small percentage of Veterans who receive these therapies, CPT and PE are rarely the first treatment a Veteran receives. A common treatment sequence identified in implementation research, begins with "stabilization treatment," combinations of psychosocial and medication treatments that prepare Veterans for CPT or PE. Despite consistently identifying stabilization treatment as a common VHA practice, little research has investigated this treatment sequence. A novel approach to solving existing limitations in PTSD treatment delivery involves developing an intervention that both acknowledges the ubiquitous presence and benefits of stabilization treatment, while facilitating timely transition from stabilization treatment to CPT or PE. This CDA-2 aims to improve delivery of PTSD services in the VHA. The proposed research aims are: (1) To qualitatively understand Veterans' and clinicians' perspectives on selecting stabilization treatments and how stabilization treatment serves as a barrier or facilitator of transition to CPT or PE; (2) To develop and conduct a randomized, pragmatic pilot trial of a brief, Veteran-centered intervention to support transition from stabilization treatment to CPT or PE; and (3) To identify sociodemographic disparities in treatment sequences and to determine how treatment sequences influence time to CPT or PE initiation across the VHA.
PROBLEM TO BE SOLVED: To simply and efficiently carry out the perfume compounding of a well- balanced perfume composition by setting specific numerical values related to blended amounts of the respective perfume ingredients on a linear function. SOLUTION: The blended amounts of perfume ingredients are set so as to form a straight line from the logarithm of the blended amounts of the respective perfume ingredients and the descending order obtained by arranging the respective perfume ingredients in the order of the blended amounts. A series comprising Ys calculated by changing (n) as a variable in the formula [A and (b) are each an optional positive constant; (n) is an optional number] or their neighboring values are allotted as blended amounts of the perfumes. Furthermore, a matrix of N groups of the perfumes and M constituent ingredients thereof is prepared to allot the series obtained by the formula as the blended amounts to the matrix of N*M (M and N are each an independent natural number).  This method is carried out by previously dividing, e.g. the perfume ingredients into several groups, forming the matrix, allotting the series comprising the Ys or their neighboring values successively calculated from the formula to the matrix, then calculating the blended amounts in the columns and rows, converting the calculated blended amount into percentages and mixing the perfume ingredients.
C3 glomerulopathy (C3G) is characterized by evidence of alternative complement activation based on C3 deposition in the glomeruli. There are two forms of the disease: dense deposit disease (DDD) and C3 glomerulonephritis (C3GN). There is no approved treatment for patients with C3G.

This is a randomized, double blind, placebo controlled Phase 2 study to evaluate the safety and efficacy of avacopan (CCX168) in patients with C3G. Patients receive avacopan 30mg or matching placebo orally twice-daily. The placebo-controlled treatment period is 26 weeks (182 days). This will be followed by 26 weeks during which time all patients will receive avacopan (results for this second period will be reported in due course in a follow-up publication). Thereafter, all patients will be followed for eight weeks (56 days) without study drug treatment. The primary objective is to evaluate the efficacy of avacopan compared to placebo based on histologic changes in kidney biopsies taken at baseline and after 26 weeks of treatment. The primary endpoint will be based on the percent change from baseline in the C3G Histologic Index for disease activity.
Advances in the field of human genetics have led to an accumulating understanding of the genetic basis of distinct nonischemic cardiomyopathies associated with ventricular tachycardias (VTs) and sudden cardiac death. To date, there is an increasing proportion of patients with inherited cardiomyopathies requiring catheter ablation for VTs. This review provides an overview of disease-causing gene mutations frequently encountered and relevant for clinical electrophysiologists. Available data on VT ablation in patients with an inherited etiology and a phenotype of a nondilated left ventricular cardiomyopathy, dilated cardiomyopathy, or hypertrophic cardiomyopathy are summarized. VTs amenable to catheter ablation are related to nonischemic fibrosis. Recent insights into genotype-phenotype relations of subtype and location of fibrosis have important implications for treatment planning. Current strategies to delineate nonischemic fibrosis and related arrhythmogenic substrates using multimodal imaging, image integration, and electroanatomical mapping are provided. The ablation approach depends on substrate location and extension. Related procedural aspects including patient-tailored (enhanced) ablation strategies and outcomes are outlined. Challenging substrates for VT and the underlying inherited etiologies with a high risk for rapid progressive heart failure contribute to poor outcomes after catheter ablation. Electroanatomical data obtained during ablation may allow the identification of patients at particular risk who need to be considered for early work-up for left ventricular assist device implantation or heart transplantation.