anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
An exposure monitoring system comprises at least one camera, a plurality of beacons, and a video analytics system. The camera captures 710 video of a monitoring area. The beacons comprise at least one light emitting element and a controller to provide an actuation sequence to the light emitting element. The captured video is transmitted 720 to a video analytics system which analyses the video for the presence of light emissions from the beacons and decodes the actuation sequence of the light emissions to identify 730 the beacons. The analytics system further compiles 740 and stores 745 a location history for each beacon in the monitoring area and determines 750 an exposure risk associated with each beacon. The analytics system may use the location history to determine 760 proximity to an exposure source, the proximity being used in the risk calculation. This proximity may be with respect to time. The exposure source may be one of the plurality of beacons. The system may be applied to monitoring of exposure to pathogens such as the SARS-Cov-2 virus.
AIMS: Current evidence suggests that there is no completely effective method for endometriosis (EMS) without trauma due to diverse adverse effects. Reliable evidence illustrates that inhibiting ferroptosis is a potential strategy for EMS. We sufficiently verified that the expression of endogenous protein PDZ and LIM domain 3 (PDLIM3) was significantly increased in EMS.
METHODS: PDLIM3 knockdown reduced primary ectopic endometrial stromal cells' (EESCs) viability and migration, and elevated ferroptosis signaling indicators including Fe2+, malondialdehyde (MDA), and reactive oxygen species (ROS) in EESCs.
RESULTS: Mechanistic studies revealed that inhibition of PDLIM3 accelerated glioma-associated oncogene-1 (Gli1) degradation and further deactivated Hedgehog signaling. Gli1 inhibitor, GANT61, abrogated the impact of PDLIM3 deletion on EESC growth, migration, and ferroptosis. In vivo experiments suggested that PDLIM3 reduction repressed the growth of endometrial lesions. Likewise, repression of PDLIM3 promoted ferroptosis and attenuated Hedgehog signaling in endometrial lesions.
CONCLUSIONS: Collectively, silencing of PDLIM3 facilitates ferroptosis in EMS by inducing Gli1 degradation and blocking Hedgehog signaling. It may provide an alternative strategy for developing therapeutic agents of EMS in the future.
BACKGROUND: OTUD7B, a member of the ovarian tumor (OTU) protein superfamily, functions as a deubiquitinating enzyme and is associated with various biological processes and disease conditions, including tumors. In this study, we aimed to explore the expression patterns, prognostic significance, and the functional roles and underlying mechanisms of OTUD7B in gastric cancer (GC).
MATERIALS AND METHODS: Using a blend of bioinformatics, clinical case reviews, and molecular experiments, we evaluated the expression of OTUD7B in GC at both mRNA and protein levels. We examined the relationship between OTUD7B expression and clinicopathological characteristics of GC patients. Additionally, in vitro assays were utilized to assess the effects of OTUD7B on the migratory and invasive capabilities of GC cells. RNA sequencing analysis was conducted to identify critical genes and pathways linked to OTUD7B in GC.
RESULTS: OTUD7B was found to be significantly overexpressed in GC, both at mRNA and protein levels. Higher levels of OTUD7B were positively associated with advanced tumor TNM stage, higher histological grade, and presence of lymph/vein invasion. These correlations were indicative of poorer overall survival (OS) and disease-free survival (DFS) in GC patients. In vitro assays revealed that genetic knockout of OTUD7B markedly reduced the migration and invasion of GC cells, while overexpression of OTUD7B led to enhanced cellular migration and invasion. Furthermore, RNA sequencing and bioinformatic analyses indicated that the absence of OTUD7B suppressed signaling pathways related to cancer progression, metastasis, and metabolism. Mechanistically, OTUD7B likely promotes GC metastasis through the WNT signaling pathway, specifically targeting β-catenin.
CONCLUSIONS: OTUD7B serves as a novel marker for poor prognosis in GC and actively promotes tumor metastasis. Our results shed light on the signaling pathways regulated by OTUD7B and highlight potential targets for therapeutic intervention.
Bone Mineral Density   
In clinical trials in HIV-1 infected adults and in a clinical trial of HIV-1 uninfected individuals, TDF (a component of emtricitabine and tenofovir disoproxil fumarate) was associated with slightly greater decreases in bone mineral density (BMD) and increases in biochemical markers of bone metabolism, suggesting increased bone turnover relative to comparators [see Adverse Reactions (6.1)].  Serum parathyroid hormone levels and 1,25 Vitamin D levels were also higher in subjects receiving TDF. 

Clinical trials evaluating TDF in pediatric and adolescent subjects were conducted. Under normal circumstances, BMD increases rapidly in pediatric patients. In HIV-1 infected subjects aged 2 years to less than 18 years, bone effects were similar to those observed in adult subjects and suggest increased bone turnover. Total body BMD gain was less in the TDF-treated HIV-1 infected pediatric subjects as compared to the control groups. Similar trends were observed in adolescent subjects aged 12 years to less than 18 years treated for chronic hepatitis B. In all pediatric trials, skeletal growth (height) appeared to be unaffected.

The effects of TDF-associated changes in BMD and biochemical markers on long-term bone health and future fracture risk are unknown. Assessment of BMD should be considered for adult and pediatric patients who have a history of pathologic bone fracture or other risk factors for osteoporosis or bone loss. Although the effect of supplementation with calcium and vitamin D was not studied, such supplementation may be beneficial. If bone abnormalities are suspected, appropriate consultation should be obtained.

Mineralization Defects   
Cases of osteomalacia associated with proximal renal tubulopathy, manifested as bone pain or pain in extremities and which may contribute to fractures, have been reported in association with TDF use [see Adverse Reactions (6.1)].  Arthralgia and muscle pain or weakness have also been reported in cases of proximal renal tubulopathy. Hypophosphatemia and osteomalacia secondary to proximal renal tubulopathy should be considered in patients at risk of renal dysfunction who present with persistent or worsening bone or muscle symptoms while receiving TDF-containing products [see Warnings and Precautions (5.3)].
PCT No. PCT/JP95/01734 Sec. 371 Date May 21, 1997 Sec. 102(e) Date May 21, 1997 PCT Filed Aug. 31, 1995 PCT Pub. No. WO96/11713 PCT Pub. Date Apr. 25, 1996The present invention provides a gene-containing composition including a gene and a transporter, the transporter being capable of transporting the gene from a pregnant body to fetal cells. When this composition is administered to a pregnant body, birth of offsprings with gene deficiency can be prevented, and gene deficiency can be treated during pregnancy. In animal experiments, when an unknown gene is introduced to animals during their embryogenic stage, the function of the gene in ontogenesis can be elucidated. Moreover, the composition can be used for breeding animals such as pets, industrial animals and cattle.
Streptococcus anginosus (S. anginosus) was enriched in the gastric mucosa of patients with gastric cancer (GC). Here, we show that S. anginosus colonized the mouse stomach and induced acute gastritis. S. anginosus infection spontaneously induced progressive chronic gastritis, parietal cell atrophy, mucinous metaplasia, and dysplasia in conventional mice, and the findings were confirmed in germ-free mice. In addition, S. anginosus accelerated GC progression in carcinogen-induced gastric tumorigenesis and YTN16 GC cell allografts. Consistently, S. anginosus disrupted gastric barrier function, promoted cell proliferation, and inhibited apoptosis. Mechanistically, we identified an S. anginosus surface protein, TMPC, that interacts with Annexin A2 (ANXA2) receptor on gastric epithelial cells. Interaction of TMPC with ANXA2 mediated attachment and colonization of S. anginosus and induced mitogen-activated protein kinase (MAPK) activation. ANXA2 knockout abrogated the induction of MAPK by S. anginosus. Thus, this study reveals S. anginosus as a pathogen that promotes gastric tumorigenesis via direct interactions with gastric epithelial cells in the TMPC-ANXA2-MAPK axis.
The patients in the remifentanil group will receive remifentanil hydrochloride (Ultiva, GlaxoSmithKline, Oslo, Norway) diluted in physiologic saline to a concentration of 40µg/ml and administered using PCA pump with a bolus duration of 20 sec. A stepwise bolus doses from 15 to 30 µg, maximum 40 per 2 min will be applied with no background infusion.
P-OM3 (4 g/d) for the first six weeks of treatment. Placebo (soy oil) for the second six weeks of treatment.
Disclosed are compounds of Formula I, Formula II, and Formula III. Also disclosed are salts of the compounds, pharmaceutical composition comprising the compounds or salts, and methods for treating HCV infection by administration of the compounds or salts. In another aspect, the present invention discloses pharmaceutical compositions comprising a compound of Formula I or a pharmaceutically acceptable salt thereof. In another aspect, the present invention discloses pharmaceutically acceptable salts of the compounds of Formula II or Formula III. In another aspect, the present invention discloses pharmaceutical compositions comprising a compound of Formula II or Formula III or a pharmaceutically acceptable salt thereof. In another aspect, the present invention discloses a method for treating a viral infection, for example infection with HCV, in a human, comprising administration of a pharmaceutical composition of the invention.
Probiotic 2: A dietary probiotic supplement which contains Lactobacillus acidophilus. Dose: \> 10 billion CFU, Frequency: 1 capsule/day, duration: 6 weeks.
OBJECTIVES: This study investigates the influence of normal cohort (NC) size and the impact of different NCs on automated MRI-based brain atrophy estimation.
METHODS: A pooled NC of 3945 subjects (NCpool) was retrospectively created from five publicly available cohorts. Voxel-wise gray matter volume atrophy maps were calculated for 48 Alzheimer's disease (AD) patients (55-82 years) using veganbagel and dynamic normal templates with an increasing number of healthy subjects randomly drawn from NCpool (initially three, and finally 100 subjects). Over 100 repeats of the process, the mean over a voxel-wise standard deviation of gray matter z-scores was established and plotted against the number of subjects in the templates. The knee point of these curves was defined as the minimum number of subjects required for consistent brain atrophy estimation. Atrophy maps were calculated using each NC for AD patients and matched healthy controls (HC). Two readers rated the extent of mesiotemporal atrophy to discriminate AD/HC.
RESULTS: The maximum knee point was at 15 subjects. For 21 AD/21 HC, a sufficient number of subjects were available in each NC for validation. Readers agreed on the AD diagnosis in all cases (Kappa for the extent of atrophy, 0.98). No differences in diagnoses between NCs were observed (intraclass correlation coefficient, 0.91; Cochran's Q, p = 0.19).
CONCLUSION: At least 15 subjects should be included in age- and sex-specific normal templates for consistent brain atrophy estimation. In the study's context, qualitative interpretation of regional atrophy allows reliable AD diagnosis with a high inter-reader agreement, irrespective of the NC used.
CLINICAL RELEVANCE STATEMENT: The influence of normal cohorts (NCs) on automated brain atrophy estimation, typically comparing individual scans to NCs, remains largely unexplored. Our study establishes the minimum number of NC-subjects needed and demonstrates minimal impact of different NCs on regional atrophy estimation.
KEY POINTS: • Software-based brain atrophy estimation often relies on normal cohorts for comparisons. • At least 15 subjects must be included in an age- and sex-specific normal cohort. • Using different normal cohorts does not influence regional atrophy estimation.
Lazertinib 240 milligrams (mg) will be administered orally once daily. Participants will receive amivantamab subcutaneous and co-formulated with recombinant human hyaluronidase (SC-CF), 1600 mg/ 2240 mg depending on the body weight by manual injection. Participants benefiting from study treatment after primary analysis may continue to receive access to study treatment within the study by transferring to the long-term extension (LTE) Phase.
Participants received GLPG0634 50 mg capsules, orally, QD during Weeks 1 to 12. Participants who were responders (having at least 20% improvement on TJC68 and SJC66) remained on 50 mg QD while nonresponders were re-randomized to 100 mg QD during Weeks 13 to 24.
The present invention provides a method of using a physiologically-based pharmacokinetic model to select a prodrug molecule (NO-X) comprising a therapeutic agent X (e.g. nonsteroidal anti-inflammatory drug, (NSAID)) and an appropriate nitric oxide donor NO. The NSAID can be a non-selective or selective cyclooxygenase inhibitor or other biocompatible compound comprising a carboxyl group. The pharmacokinetic model uses in vitro and/or in silico data to estimate an optimal set of parameters that can predict whether a particular NO-X candidate is capable of producing desirable therapeutic effects, e.g. enhanced antiiflammatory activity, reduced intestinal, cardiac and renal toxicity. Accordingly, the present invention may help with proper selection of an appropriate candidate for drug development, with less development time and at lower cost.
The Standard of Care therapy in this study is multi-layer compression therapy. A number of compression bandaging systems are commercially available. The trial will utilize Coban-2 (3M, Minneapolis, MN).
INTRODUCTION: The prevalence of gestational diabetes mellitus (GDM) is rising in the UK and is associated with maternal and neonatal complications. National Institute for Health and Care Excellence guidance advises first-line management with healthy eating and physical activity which is only moderately effective for achieving glycaemic targets. Approximately 30% of women require medication with metformin and/or insulin. There is currently no strong evidence base for any particular dietary regimen to improve outcomes in GDM. Intermittent low-energy diets (ILEDs) are associated with improved glycaemic control and reduced insulin resistance in type 2 diabetes and could be a viable option in the management of GDM. This study aims to test the safety, feasibility and acceptability of an ILED intervention among women with GDM compared with best National Health Service (NHS) care.
METHOD AND ANALYSIS: We aim to recruit 48 women with GDM diagnosed between 24 and 30 weeks gestation from antenatal clinics at Wythenshawe and St Mary's hospitals, Manchester Foundation Trust, over 13 months starting in November 2022. Participants will be randomised (1:1) to ILED (2 low-energy diet days/week of 1000 kcal and 5 days/week of the best NHS care healthy diet and physical activity advice) or best NHS care 7 days/week until delivery of their baby. Primary outcomes include uptake and retention of participants to the trial and adherence to both dietary interventions. Safety outcomes will include birth weight, gestational age at delivery, neonatal hypoglycaemic episodes requiring intervention, neonatal hyperbilirubinaemia, admission to special care baby unit or neonatal intensive care unit, stillbirths, the percentage of women with hypoglycaemic episodes requiring third-party assistance, and significant maternal ketonaemia (defined as ≥1.0 mmol/L). Secondary outcomes will assess the fidelity of delivery of the interventions, and qualitative analysis of participant and healthcare professionals' experiences of the diet. Exploratory outcomes include the number of women requiring metformin and/or insulin.
ETHICS AND DISSEMINATION: Ethical approval has been granted by the Cambridge East Research Ethics Committee (22/EE/0119). Findings will be disseminated via publication in peer-reviewed journals, conference presentations and shared with diabetes charitable bodies and organisations in the UK, such as Diabetes UK and the Association of British Clinical Diabetologists.
TRIAL REGISTRATION NUMBER: NCT05344066.
For IDH1 mutated AML patients randomized to first-line therapy with IDHi+aza, patients will receive Ivosidenib 500mg po orally daily on Days 1-28 of each 28 day cycle. For IDH2 mutated AML patients randomized to first-line therapy with IDHi+aza, patients will receive Enasidenib 100mg po orally daily on Days 1-28 of each 28 day cycle. Azacitidine will be given to both groups intravenously or subcutaneously at 75mg/m2 daily on days 1-7 or 1-5/8-9 of each 28 day cycle. Subsequent cycles after CR/CRi/CRh/MLFS achievement may be adjusted in timing and dosing.
Participants with a history of prescription opioid use, but who did not abuse them. Participants in this arm received the 3 interventions (0, 15, and 30 mg) at random.
THYMOGLOBULIN® (anti-thymocyte globulin [rabbit]) is a purified, pasteurized, immunoglobulin G, obtained by immunization of rabbits with human thymocytes. This immunosuppressive product contains cytotoxic antibodies directed against antigens expressed on human T-lymphocytes.

THYMOGLOBULIN is a sterile, lyophilized powder for intravenous administration after reconstitution with sterile Water for Injection, USP (SWFI). Each single-dose 10 mL vial contains 25 mg of anti-thymocyte globulin (rabbit), 50 mg glycine, 10 mg sodium chloride, and 50 mg mannitol.

After reconstitution with 5 mL SWFI, each vial of reconstituted product contains approximately 5 mg/mL of THYMOGLOBULIN, of which >90% is rabbit gamma immune globulin (IgG). The reconstituted solution has a pH of 6.5 to 7.2.

Human red blood cells are used in the manufacturing process to deplete cross-reactive antibodies to non–T-cell antigens. The manufacturing process is validated to remove or inactivate potential exogenous viruses. All human red blood cells are from U.S.-registered or FDA-licensed blood banks. A virus removal step (nanofiltration, using a 20 nm filter) and a viral inactivation step (pasteurization, i.e., heat treatment of active ingredient at 60°C/10 hr) are performed for each lot. Each THYMOGLOBULIN lot is released following potency testing (lymphocytotoxicity and anti-CD2 binding inhibition), and cross-reactive antibody testing (hemagglutination, platelet agglutination, and fibroblast toxicity assays on every lot).
Therapeutic compositions for the treatment of tropical phagedenic ulcers and infected wounds comprise (a) an antibiotic component active against gram-positive and gram-negative organisms consisting of reomycin and polymixin B, or reomycin and bacitracin, or reomycin, polymixin B and bacitracin; (b) a proteolytic enzyme component comprising hyaluronidase and trypsin or chymotrypsin; and (c) a film-forming agent as a carrier, e.g. polyvinyl pyrrolidone or dextran.  The compositions which are preferably used in the form of dry, free-flowing dusting powders should contain less than 2 per cent of moisture, and in the method of preparation steps are taken to ensure this low moisture content.  In a preferred method, the antibiotic component and the trypsin or chymotrypsin are dried preferably to a moisture content of about 0.5 per cent, the hyaluronidase and polyvinyl pyrrolidone are dissolved in water and the solution lyophilized to a substantially anhydrous powder and said powder is mixed with the antibiotic and enzyme mixture.  In this way, a thorough distribution of the hyaluronidase throughout the mixture is ensured also.  In one gm. of the composition there are: from 3.5 to 25 mg of reomycin, 1,000 to 10,000 units of polymixin, 50 to 3,000 units of bacitracin, 12 to 200 turbidity; reducing units of hyaluronidase and 4 to 500 mg. of trypsin or chymotrypsin, and the remainder is made of of polyvinyl pyrrolidone or dextran.
The present invention relates to novel specifically-substituted phenyl compounds, especially substituted di-tert-butyl phenol derivatives, which are effective as anti-inflammatory, analgesic and/or antipyretic agents. These phenyl compounds are substituted with a low molecular weight alkyl chain which terminates in a specific unsaturated functional group. These unsaturated functionalities are -C=CH, C=CH2, C=C=CH2, and aldehydes in the form of their acetals. The present invention further relates to pharmaceutical compositions which contain an anti-inflammatory agent of the present invention and a pharmaceutically-acceptable carrier. Finally, the present invention relates to methods for treating diseases characterized by inflammation, such as rheumatoid arthritis and osteoarthritis, in humans or lower animals. Such methods comprise administering to a human or lower animal in need of such treatment a safe and effective amount of an anti-inflammatory agent or composition of the present invention.
[EP0251408A1]
* Wash hands before and after applying FILSUVEZ or wear gloves for application.
  * Apply a 1 mm layer of FILSUVEZ to the affected wound surface only. Do not rub in the gel. Cover the wound with a sterile non-adhesive wound dressing. Alternatively, apply FILSUVEZ directly to the dressing so that the topical gel is in direct contact with the wound.
  * Apply FILSUVEZ to cleansed wounds with wound dressing changes until the wound is healed.
  * If a FILSUVEZ-treated wound becomes infected, discontinue treatment to that wound until the infection has resolved.
  * Each tube of FILSUVEZ is for one-time use only. Once the tube is opened, use the product immediately. Discard the tube after use in household trash or through a drug take back site, if available.
  * Avoid contact of FILSUVEZ with eyes and mucous membranes (e.g., mouth, vagina, anus). In case of accidental contact, irrigate the area with water.
  * FILSUVEZ is for topical use only. Not for use on mucous membranes (oral, intravaginal, or intra-anal). Not for ophthalmic use.
Treatment with PROGLYCEM should be initiated under close clinical supervision, with careful monitoring of blood glucose and clinical response until the patient’s condition has stabilized. This usually requires several days. If not effective in 2 to 3 weeks, discontinue PROGLYCEM.

Prolonged treatment requires regular monitoring of urine glucose and ketones, especially under stress conditions. Advise patients to promptly report any abnormalities to their healthcare provider. Periodically monitor blood glucose to determine the need for dosage adjustment.

Consider the effects of PROGLYCEM on the hematopoietic system and the level of serum uric acid; the latter should be considered particularly in patients with hyperuricemia or a history of gout.

Since the plasma half-life of diazoxide is prolonged in patients with impaired renal function, a reduced dosage should be considered. Serum electrolyte levels should also be evaluated for such patients.

The antihypertensive effect of other drugs may be enhanced by PROGLYCEM, and this should be kept in mind when administering it concomitantly with antihypertensive agents.

Because of the protein binding, administration of PROGLYCEM with coumarin anticoagulants or its derivatives may require reduction in the dosage of the anticoagulant, although there has been no reported evidence of excessive anticoagulant effect. In addition, PROGLYCEM may displace bilirubin from albumin; consider this when treating newborns with increased bilirubinemia.

Pulmonary hypertension has been reported in neonates and young infants treated with diazoxide (see WARNINGS).