anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Endogenous androgens are responsible for normal growth and development of the male sex organs and for maintenance of secondary sex characteristics. These effects include growth and maturation of the prostate, seminal vesicles, penis, and scrotum; development of male hair distribution, such as beard, pubic, chest, and axillary hair; laryngeal enlargement, vocal cord thickening, and alterations in body musculature and fat distribution. Drugs in this class also cause retention of nitrogen, sodium, potassium, and phosphorus, and decreased urinary excretion of calcium. Androgens have been reported to increase protein anabolism and decrease protein catabolism. Nitrogen balance is improved only when there is sufficient intake of calories and protein.

Androgens are responsible for the growth spurt of adolescence and for eventual termination of linear growth, brought about by fusion of the epiphyseal growth centers. In children, exogenous androgens accelerate linear growth rates, but may cause disproportionate advancement in bone maturation. Use over long periods may result in fusion of the epiphyseal growth centers and termination of the growth process. Androgens have been reported to stimulate production of red blood cells by enhancing production of erythropoietic stimulation factor.

During exogenous administration of androgens, endogenous testosterone release is inhibited through feedback inhibition of pituitary luteinizing hormone (LH). At large doses of exogenous androgens, spermatogenesis may also be suppressed through feedback inhibition of pituitary follicle stimulating hormone (FSH).

There is a lack of substantial evidence that androgens are effective in fractures, surgery, convalescence, and functional uterine bleeding.
BACKGROUND: Breast cancer (BC) ranks as the third most fatal malignant tumor worldwide, with a strong reliance on fatty acid metabolism. CLDN6, a candidate BC suppressor gene, was previously identified as a regulator of fatty acid biosynthesis; however, the underlying mechanism remains elusive. In this research, we aim to clarify the specific mechanism through which CLDN6 modulates fatty acid anabolism and its impact on BC growth and metastasis.
METHODS: Cell function assays, tumor xenograft mouse models, and lung metastasis mouse models were conducted to evaluate BC growth and metastasis. Human palmitic acid assay, triglyceride assay, Nile red staining, and oil red O staining were employed to investigate fatty acid anabolism. Reverse transcription polymerase chain reaction (RT-PCR), western blot, immunohistochemistry (IHC) assay, nuclear fractionation, immunofluorescence (IF), immunoprecipitation and acyl-biotin exchange (IP-ABE), chromatin immunoprecipitation (ChIP), dual luciferase reporter assay, and co-immunoprecipitation (Co-IP) were applied to elucidate the underlying molecular mechanism. Moreover, tissue microarrays of BC were analyzed to explore the clinical implications.
RESULTS: We identified that CLDN6 inhibited BC growth and metastasis by impeding RAS palmitoylation both in vitro and in vivo. We proposed a unique theory suggesting that CLDN6 suppressed RAS palmitoylation through SREBP1-modulated de novo palmitic acid synthesis. Mechanistically, CLDN6 interacted with MAGI2 to prevent KLF5 from entering the nucleus, thereby restraining SREBF1 transcription. The downregulation of SREBP1 reduced de novo palmitic acid synthesis, hindering RAS palmitoylation and subsequent endosomal sorting complex required for transport (ESCRT)-mediated plasma membrane localization required for RAS oncogenic activation. Besides, targeting inhibition of RAS palmitoylation synergized with CLDN6 to repress BC progression.
CONCLUSIONS: Our findings provide compelling evidence that CLDN6 suppresses the palmitic acid-induced RAS palmitoylation through the MAGI2/KLF5/SREBP1 axis, thereby impeding BC malignant progression. These results propose a new insight that monitoring CLDN6 expression alongside targeting inhibition of palmitic acid-mediated palmitoylation could be a viable strategy for treating oncogenic RAS-driven BC.
Major depressive disorder (MDD) is a leading cause of global disability, and approximately 30% of MDD patients are resistant to antidepressant pharmacotherapy. Repetitive transcranial magnetic stimulation (rTMS) of the left dorsolateral prefrontal cortex (DLPFC) is an FDA-cleared intervention with proven efficacy in treatment-resistant depression, but only 30-40% of these patients achieve remission after a single course. Other studies have shown that rTMS targeting the dorsomedial prefrontal cortex (DMPFC) is comparably effective, but biomarkers for informing target site selection do not exist. Diagnostic heterogeneity has been an obstacle to biomarker discovery efforts. Recently, we developed and validated an approach to diagnose four novel MDD subtypes or "biotypes' defined by resting state functional connectivity (RSFC) patterns and predicting differing antidepressant responses at the individual level to rTMS. This pivotal trial will test a novel, biotype-guided treatment selection strategy motivated by the hypothesis that an individual patient's likelihood of responding to left DLFPC vs.DMPFC rTMS is determined in part by individual differences in 1) the degree to which their symptoms are driven by dysfunction in specific cerebral network targets comprising Valence Systems; and 2) the degree to which dysfunction in those targets can be modulated by stimulating the left DLPFC or DMPFC. Subjects (N=348; 174 from this site) will be randomized to receive a) biotype-guided rTMS targeting the DMPFC or left DLPFC; b) to a disconfirmation arm receiving rTMS targeting the opposite site; and c) to a third arm receiving FDA-cleared, standard-of-care rTMS targeting the left DLFPC, regardless of biotype. The dosage and method of delivery of rTMS for all arms are as follows: intermittent theta burst stimulation (iTBS) will be delivered at 120% of the resting motor threshold. It will be administered in triplet 50 Hz bursts, repeated at 5 Hz with a duty cycle of 2 s on and 8 s off, for a total of 600 pulses per session and a total duration of 3 min 9 s. All patients will be assessed before and after treatment on a battery of fMRI, behavioral, and clinical assessments. The primary goal is to confirm the efficacy of a novel RSFC biomarker-guided approach to differential treatment selection in treatment resistant depression.
Pregnancy-onset thrombotic thrombocytopenic purpura (TTP) is a rare and life-threatening disease of which diagnosis and management requires experienced multidisciplinary teams. The mechanisms responsible for a deficiency in the disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13 (ADAMTS13) leading to pregnancy-onset TTP may be congenital or acquired, and studying ADAMTS13 conformation could be of interest. The differential diagnosis between TTP and other pregnancy-associated thrombotic microangiopathies (TMA) is often challenging. Our retrospective multicenter study highlights the significance and the challenges associated with pregnancy-onset TTP and childbirth in terms of diagnosis, obstetric management, and follow-up aspects. Among 1174 pregnancy-onset TMA enrolled in the French Registry for TMA from 2000 to 2020, we identified 108 pregnancy-onset TTP: 52 immune-mediated TTP (iTTP, 48.1%), 27 acquired TTP of unidentified mechanism (uTTP, 25%), and 29 congenital TTP (cTTP, 26.9%). Data show that maternal outcome is good (survival rate: 95%) and fetal outcome is linked to the gestational age at the onset of the disease (survival rate: 75.5%). Three distinct entities with different natural histories emerged: pregnancy-onset iTTP appears similar to idiopathic iTTP, with an open ADAMTS13 conformation, and is marked by a relapse risk independent of subsequent pregnancies; pregnancy-onset uTTP appears to have a different pathophysiology with an unexpected open ADAMTS13 conformation and a very low relapse risk independent of subsequent pregnancies; finally, pregnancy-onset cTTP is characterized by the necessity of pregnancy as a systematic and specific trigger and a need for prophylactic plasmatherapy for subsequent pregnancies. This trial was registered at www.clinicaltrials.gov as #NCT00426686, and at the Health Authority and the French Ministry of Health (P051064/PHRC AOM05012).
A reusable, custom-made forced-air warming mattress was made of a light to medium weight water resistant canvas, sewn like mattress with 2 arms placed underneath the patient. An open hole at proximal part of one arm was designed to attach with a hose of warm air delivery device. Small holes (2-3 mm2), 5 inches apart were punched on the upper surface of this mattress around the patient except for the area underneath the patient that the holes were 9 inches apart. The weight of the patient will obstruct the air flow and prevent direct blowing of warm air onto the underside of patients. There is a special appendage connected to the upper part of mattress which can connect warm air to cover the patient's chest. There is a special appendage connected to the upper part of mattress which can convect warm air to cover the patient's chest. The mattress is 97 inches x 97 inches, with 2 arms of 25 inches x 16 inches and a special appendage of 45 inches x 12 inches for covering the chest with warm air delivery. This size is proper for patient of 170 cm. height. In order to reuse it, the mattress can be washed, dried and sterilized by gas or autoclaved for more than 50 times. A sterile sheet well enhance the sterile environment of the operating field.
* Stop Tri Femynor if an arterial thrombotic event or venous thromboembolic (VTE) event occurs.
  * Stop Tri Femynor if there is unexplained loss of vision, proptosis, diplopia, papilledema, or retinal vascular lesions. Evaluate for retinal vein thrombosis immediately [see Adverse Reactions (6.2)].
  * If feasible, stop Tri Femynor at least 4 weeks before and through 2 weeks after major surgery or other surgeries known to have an elevated risk of VTE as well as during and following prolonged immobilization.
  * Start Tri Femynor no earlier than 4 weeks after delivery, in women who are not breastfeeding. The risk of postpartum VTE decreases after the third postpartum week, whereas the risk of ovulation increases after the third postpartum week.
  * The use of COCs increases the risk of VTE. However, pregnancy increases the risk of VTE as much or more than the use of COCs. The risk of VTE in women using COCs is 3 to 9 cases per 10,000 woman-years. The risk of VTE is highest during the first year of use of COCs and when restarting hormonal contraception after a break of 4 weeks or longer. The risk of thromboembolic disease due to COCs gradually disappears after use is discontinued.
  * Use of COCs also increases the risk of arterial thromboses such as strokes and myocardial infarctions, especially in women with other risk factors for these events. COCs have been shown to increase both the relative and attributable risks of cerebrovascular events (thrombotic and hemorrhagic strokes). This risk increases with age, particularly in women over 35 years of age who smoke.
  * Use COCs with caution in women with cardiovascular disease risk factors.
BACKGROUND: A series of qualitative studies conducted by the OMERACT Myositis Working Group identified pain interference, fatigue, and physical function as highly important life impact domains for adults with idiopathic inflammatory myositis (IIM). In this study, our goal was to assess the responsiveness and minimal important difference of PROMIS pain interference (6a), fatigue (7a), and physical function (8b).
METHODS: Adults with IIM from USA, Netherlands, Korea, Sweden, and Australia with two "clinical" visits were enrolled in this prospective study. Anchor questions on a Likert scale were collected at baseline, and manual muscle testing (MMT), physician and patient reported global disease activity, and PROMIS instruments were collected at both visits. Responsiveness was assessed with i) ANOVA, ii) paired t-test, effect size and standardized response mean, and iii) Pearson correlation. Minimal important difference (MID), minimal important change (MIC) and minimal detectable change (MDC) values were calculated.
RESULTS: 114 patients with IIM (median age 60, 60 % female) completed both visits. Changes in PROMIS instruments were significantly different among anchor categories. Patients who reported improvement had a significant improvement in their PROMIS scores with at least medium effect size, while patients who reported worsening and stability did not show a significant change with weak effect size. PROMIS instruments had weak to moderate correlations with MMT, patient and physician global disease activity. MID was approximately 2-3 points for Pain Interference and 3-4 points for Fatigue and Physical Function forms based on the method used. MIC was approximately 4-5 for improvement of all the instruments, while MDC was 1.7-2 points for Pain Interference and Physical Function and 3.2-3.9 for Fatigue.
CONCLUSION: This study provides evidence towards the responsiveness of the PROMIS instruments in a large international prospective cohort of adults with IIM supporting their use as PROMs in adult myositis.
FIELD: pharmacy, pharmacology. SUBSTANCE: invention proposes the novel method and pharmaceutical preparation exhibiting sensory blockade and minimal motor blockade. Preparation is pharmaceutically acceptable ropivacaine salt at concentration less 0.5 wt.-% in solution and used for epidural infusion. Method relates to some specificities of this preparation using also. Invention is useful especially for patients suffering with pains after surgery operations and in delivery. EFFECT: valuable analgetic properties of preparation. 11 cl
FIELD: medicine.SUBSTANCE: invention relates to medicine, namely to functional diagnostics, somnology, public health and health care, labor physiology, chronobiology, can be used to predict the adjusted average sleep phase according to the Munich test in persons aged 18 to 22 years inclusive with increasing screen time (ST). The ST increases in minutes are detected. Next, the time of daylight exposure (DE) is determined. The corrected mean sleep phase according to the Munich test (MSP) is calculated. Next, the predicted shift of the MSP to a later time is determined. Then the predicted MSP shift is added to the time of the calculated MSP value and the predicted MSP is obtained with an increase in ST.EFFECT: method makes it possible to predict the corrected mean sleep phase according to the Munich Chrono-Type Questionnaire test in persons aged 18 to 22 years, inclusive, with an increase in screen time.1 cl, 1 tbl, 4 ex
The invention discloses a device for quickly predicting liver cancer risk level, which mainly comprises a data acquisition module, a database, a data processing module and a risk evaluation module. The data acquisition module acquires basic data of a tester and stores the basic data of the tester into a preliminary data matrix P of the database. And the data processing module calls and processes the preliminary data matrix P in the database to obtain a sample data matrix P 'and inputs the sample data matrix P' into the risk assessment module. The risk evaluation module stores a liver cancer risk evaluation model. And the liver cancer risk evaluation model processes the sample data matrix P' and outputs a risk evaluation result y. The invention ensures the reliability of liver cancer risk prediction.
The invention belongs to the field of biological medicine, and in particular relates to a design and application of novel thrombolytic agent citPA5 with high efficiency and safety. The novel thrombolytic agent citPA5 is obtained by mutating self-cleavage cyclic Tyr141-Tyr151, plasmin cleavage site Arg15-Ile16 and activated pocket hydrophobic region Ile21-Phe21-His143-His144-Lys156 of human tissue type plasminogen activator tPA2, and the amino acid sequence is shown as SEQ ID NO. 4. The thrombolytic agent citPA5 thrombolytic activity is regulated by fibrin, has thrombolytic activity only in the presence of thrombus, and has the ability to escape the endogenous inhibitor PAI-1. The experimental result of mice with cerebral infarction in vivo shows that the citPA5 has good treatment effect. Multiple bleeding risk assessments demonstrated that citPA5 neither resulted in systemic fibrinolysis nor aggravated local cerebral hemorrhage. The novel thrombolytic agent citPA5 is expected to be used before stroke classification in the future, and the pre-screening time is saved. In addition, it can be used for treating thrombotic diseases including myocardial infarction, ischemic cerebral apoplexy, pulmonary embolism, etc.
The invention discloses application of a short chain VE analogue. The molecular structure of the short chain VE analogue is shown in the formula (I). The analogue can be used for preparing feed additives or immunoenhancers. Experiments verify that the short chain VE analogue further has the antioxidant characteristic. Compared to natural VE, the analogue can achieve same biological activity just by using 50% amount. As the feed additive, the analogue can be used for effectively promoting growth of raised animals and improving the immunity and biological activity of the raised animals, and has a huge application potential in the field of feeds. The formula is shown in the description.
Local tissue damage following snakebite envenoming remains a poorly researched area. To develop better strategies to treat snakebites, it is critical to understand the mechanisms through which venom toxins induce envenomation effects including local tissue damage. Here, we demonstrate how the venoms of two medically important Indian snakes (Russell's viper and cobra) affect human skeletal muscle using a cultured human myoblast cell line. The data suggest that both venoms affect the viability of myoblasts. Russell's viper venom reduced the total number of cells, their migration, and the area of focal adhesions. It also suppressed myogenic differentiation and induced muscle atrophy. While cobra venom decreased the viability, it did not largely affect cell migration and focal adhesions. Cobra venom affected the formation of myotubes and induced atrophy. Cobra venom-induced atrophy could not be reversed by small molecule inhibitors such as varespladib (a phospholipase A2 inhibitor) and prinomastat (a metalloprotease inhibitor), and soluble activin type IIb receptor (a molecule used to promote regeneration of skeletal muscle), although the antivenom (raised against the Indian 'Big Four' snakes) has attenuated the effects. However, all these molecules rescued the myotubes from Russell's viper venom-induced atrophy. This study demonstrates key steps in the muscle regeneration process that are affected by both Indian Russell's viper and cobra venoms and offers insights into the potential causes of clinical features displayed in envenomed victims. Further research is required to investigate the molecular mechanisms of venom-induced myotoxicity under in vivo settings and develop better therapies for snakebite-induced muscle damage.
Evidence shows the effectiveness of Osteopathic Manipulative Treatment (OMT) for various headache types, with limited evidence of its use for headaches related to mild traumatic brain injury (MTBI). No studies were found regarding OMT for headaches in patients with post-concussion syndrome (PCS), defined as symptom persistence \>3 months after MTBI.

Objective: To evaluate OMT for headaches in patients with PCS. Methods: A controlled pilot study was conducted of patients with PCS who presented to an outpatient interdisciplinary rehabilitation clinic. Twenty-six subjects with symptoms lasting \>3 months were enrolled and were randomly assigned to a treatment group (n = 13) and a control group (n = 13). Primary outcome measures were 1) immediate change in headache scores with a visual analog scale (VAS) and 2) change in the 6-item Headache Impact Test (HIT-6) between baseline and follow-up visits. 10 control participants completed HIT-6 between baseline and follow-up visits but did not receive OMT and did not complete VAS. After OMT, immediate VAS changes in treatment group and the improvements in HIT-6 scores for both groups between baseline and follow-up were analyzed for statistical significance.
Initial injection must be given on the day of randomization. Follow-up injections will be performed as often as every 4 weeks unless criteria for deferral are met.
Procedure will consist in 1 team performing laparoscopic TME. Following stapled closure of the rectum below the tumor, and complete mobilization of the rectosigmoid, the specimen is extracted using a Pfannenstiel incision . A stapled (knight-Griffen) colorectal anastomosis or coloanal anastomosis will be created and a temporary diverting stoma will be fashioned which is standard of care following surgery for this type of cancer.
Cardiovascular disease (CVD) is the leading cause of death and disability for women in the United States. Posttraumatic Stress Disorder (PTSD) affects 1 in 20 reproductive aged women and significantly increases risk CVD. In the perinatal period, cardiovascular complications account for one third of maternal deaths, and emerging evidence indicates that PTSD increases risk for pregnancy-related CVD. As well, exposure to cardiovascular complications in pregnancy increases risk for CVD later in life. Therefore, effective treatment of PTSD in reproductive aged women, prior to disease, holds significant potential to decrease risk for CVD onset across the life course. Repetitive transcranial magnetic stimulation (TMS) is a safe, non-invasive, promising novel approach to treat PTSD and reduce risk for CVD. TMS dramatically reduces PTSD symptoms, and a single session of non-invasive brain stimulation methods, including TMS, reduce heart rate and blood pressure, and increase heart rate variability. However, lack of knowledge on the long-term autonomic benefits of TMS prevents utilization of this intervention for patients at risk for CVD. In this COBRE Center for Neuromodulation pilot study, we aim to determine the acute and longer-term effects of TMS on blood pressure in women at risk for CVD. We propose a single arm trial of TMS among 20 women with elevated PTSD symptoms who also have a diagnosis of hypertension. All participants will receive 30 sessions (5 days/week, 6 consecutive weeks) of active TMS to the left dorsolateral prefrontal cortex (DLPFC) administered at 10Hz, 120% of motor threshold, 3000 pulses per session. At the first TMS session, blood pressure, heart rate, and heart rate variability will be monitored for 20 minutes before, during, and after TMS to evaluate acute cardiovascular changes to TMS. Throughout the intervention and at 1-month post intervention, participants will complete 24-hour blood pressure monitoring and PTSD symptom assessments to enable examination of longer-term effects of TMS on blood pressure, as well as test the temporal associations between change in PTSD symptoms and blood pressure. The specific aims of the study are to: examine safety and acute effects of TMS on autonomic function (Aim 1), examine change in 24-hour blood pressure following a standard course of TMS (Aim 2), and examine if change in PTSD symptoms is associated with changes in 24-hour blood pressure among reproductive aged women with elevated PTSD symptoms (Aim 3). The current proposal is closely aligned with the research priorities described by the NHBLI working group on hypertension to 1) support clinical trials for early intervention for high blood pressure, particularly in younger populations, and 2) support studies related to the role of sex differences in the complications of hypertension and hypertension in pregnancy. Results from this pilot project will establish a new line of inquiry in neuromodulation for PI Bublitz and will provide essential pilot data for a future R01 application to conduct a mechanistic sham-controlled clinical trial of TMS for treatment of PTSD and hypertension in at-risk women.