anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Spontaneous pneumomediastinum is an uncommon condition described in veterinary medicine with concurrent respiratory disease. It can be caused by the Macklin effect, which is when gas leaks from the alveoli into the surrounding interstitial lung tissue. Pulmonary interstitial emphysema (PIE) is the presence of gas within the pulmonary vascular sheaths and indicates the presence of the Macklin effect. In the authors' experience, spontaneous pneumomediastinum and PIE are more prevalent in sighthound dogs than in other breeds and are often considered incidental findings. This retrospective, observational, cross-sectional study compared the prevalence of PIE and subsequent pneumomediastinum in sighthound with other purebred dogs. It characterized the appearance of PIE in CT and analyzed a possible association with concomitant pulmonary pathologies or with the use of general anesthesia. Medical records and thoracic CTs of sighthounds and nonsighthound dogs from two institutions were reviewed. A total of 256 dogs, comprising 127 sighthounds and 129 other purebred dogs, were included. The prevalence of PIE and pneumomediastinum was statistically higher in sighthound (14.2%) compared with other nonsighthound dogs (2.2%). There was no statistical association between the presence of PIE and pneumomediastinum with different age and weight groups or with sex. There was no statistical difference in the prevalence of PIE and pneumomediastinum between dogs with and without pulmonary pathology or in dogs undergoing CT with sedation or general anesthesia. Spontaneous pneumomediastinum in sighthounds is more prevalent than in other breeds, and its prevalence is not associated with the presence of pulmonary pathology or the use of general anesthesia.
Patients receive porfimer sodium IV over 3-5 minutes and undergo irradiation with red light 48 hours later. Patients receive 2 more treatments at 2-day intervals.
Described is a spray-on hydrogel comprising water-soluble PEG polymers that cross-link in situ to form a hydrogel such that the cross-links are reversible. The hydrogel can be useful as a drug delivery composition, wound dressing or surgery adjuvant. Polyethylene glycol polymer and cross-linker solutions are sprayed simultaneously through a common orifice. Cross-linking via formation of thioether or disulfide bonds is initiated upon mixing, providing rapid gelation. The hydrogel components can be derivatized with RGD peptides or analogs thereof to promote retention in/on a body compartment such as the skin, surface of the eye, or a mucosa such as the vaginal mucosa. The cross-links are reversed using a reducing solution enabling easy removal of the hydrogel by dissolution. Processes for preparation of the cross-linker, RGD derivatized PEG and RGD-linked agents are also disclosed.
This group will begin the family wellness program first; approximately, 5 weeks before group 2. The family wellness program consists of 8 parent-child workshops and text message reminders.
After the Lead-in study, in the Phase 2 portion, patients will be randomized 1:1 to standard of care chemotherapy using gemcitabine (GEM) and nab-paclitaxel (NAB-P) (GEM 1000 mg/m2 IV and NAB-P 125 mg/m2 given days 1, 8, and 15 every 28 days) plus placebo or proglumide at the recommended phase 2 dose (RP2D) for proglumide determined in the Lead-in study. Patients will be monitored for safety and toxicity by laboratory blood testing, physical examinations, neurological check, and cardiac monitoring in the Lead-in study. Dosing of chemotherapy will be managed following USPI recommendations. If dose-related toxicity occurs with proglumide, the medication will be held until the AE resolves. Proglumide will then be re-administered at the prior lower dose.

A research tumor biopsy will be performed before starting therapy. Every 8 weeks radiographic imaging will be done for assess tumor burden according to Standard of Care (SOC). Blood work for safety analysis will be done at 2 weeks, then every 4 weeks, interim vital signs and history is done every 4 weeks. Radiographic imaging and CA19-9 tumor marker will be done every 8 weeks according to SOC. A repeat tumor biopsy will be done at week 8 only for research purposes to examine the tumor microenvironment. A blood sample for research Biomarkers will be collected before starting therapy and every 8 weeks. Patients will be treated for 24 weeks or until progression is documented, unacceptable toxicities develop, or treatment is no longer required
Participants will receive coformulated pembrolizumab/vibostolimab via an IV infusion Q3W for up to 35 cycles. Each cycle is 21 days.
Multisystem Inflammatory Syndrome in Children (MIS-C) is a potentially life-threatening complication of COVID-19. The pathophysiological mechanisms leading to severe disease are poorly understood. This study leveraged clinical samples from a well-characterized cohort of children hospitalized with COVID-19 or MIS-C to compare immune-mediated biomarkers. Our objective was to identify selected immune molecules that could explain, in part, why certain SARS-CoV-2-infected children developed MIS-C. We hypothesized that type-2 helper T cell-mediated inflammation can elicit autoantibodies, which may account for some of the differences observed between the moderate-severe COVID-19 (COVID+) and MIS-C cohort. We enumerated blood leukocytes and measured levels of selected serum cytokines, chemokines, antibodies to COVID-19 antigens, and autoantibodies in children presenting to an academic medical center in Connecticut, United States. The neutrophil/lymphocyte and eosinophil/lymphocyte ratios were significantly higher in those in the MIS-C versus COVID+ cohort. IgM and IgA, but not IgG antibodies to SARS-CoV-2 receptor binding domain were significantly higher in the MIS-C cohort than the COVID+ cohort. The serum levels of certain type-2 cytokines (interleukin (IL)-4, IL-5, IL-6, IL-8, IL-10, IL-13, and IL-33) were significantly higher in children with MIS-C compared to the COVID+ and SARS-CoV-2-negative cohorts. IgG autoantibodies to brain antigens and pentraxin were higher in children with MIS-C compared to SARS-CoV-19-negative controls, and children with MIS-C had higher levels of IgG anti-contactin-associated protein-like 2 (caspr2) compared to the COVID+ and SARS-CoV-19-negative controls. We speculate that autoimmune responses in certain COVID-19 patients may induce pathophysiological changes that lead to MIS-C. The triggers of autoimmunity and factors accounting for type-2 inflammation require further investigation.
We have previously demonstrated that exposure to cobalt nanoparticles (Nano-Co) caused extensive interstitial fibrosis and inflammatory cell infiltration in mouse lungs. However, the underlying mechanisms of Nano-Co-induced pulmonary fibrosis remain unclear. In this study, we investigated the role of high-mobility group box 1 (HMGB1) in the epithelial cell-fibroblast crosstalk in Nano-Co-induced pulmonary fibrosis. Our results showed that Nano-Co exposure caused remarkable production and release of HMGB1, as well as nuclear accumulation of HIF-1α in human bronchial epithelial cells (BEAS-2B) in a dose- and a time-dependent manner. Pretreatment with CAY10585, an inhibitor against HIF-1α, significantly blocked the overexpression of HMGB1 in cell lysate and the release of HMGB1 in the supernatant of BEAS-2B cells induced by Nano-Co exposure, indicating that Nano-Co exposure induces HIF-1α-dependent HMGB1 overexpression and release. In addition, treatment of lung fibroblasts (MRC-5) with conditioned media from Nano-Co-exposed BEAS-2B cells caused increased RAGE expression, MAPK signaling activation, and enhanced expression of fibrosis-associated proteins, such as fibronectin, collagen 1, and α-SMA. However, conditioned media from Nano-Co-exposed BEAS-2B cells with HMGB1 knockdown had no effects on the activation of MRC-5 fibroblasts. Finally, inhibition of ERK1/2, p38, and JNK all abolished MRC-5 activation induced by conditioned media from Nano-Co-exposed BEAS-2B cells, suggesting that MAPK signaling might be a key downstream signal of HMGB1/RAGE to promote MRC-5 fibroblast activation. These findings have important implications for understanding the pro-fibrotic potential of Nano-Co.
Innate immune cells are important in the initiation and potentiation of alloimmunity in transplantation. Immediately upon organ anastomosis and reperfusion, recipient monocytes enter the graft from circulation and differentiate to inflammatory macrophages to promote allograft inflammation. However, factors that drive their differentiation to inflammatory macrophages are not understood. Here, we show that the receptor tyrosine kinase AXL was a key driver of early intragraft differentiation of recipient infiltrating monocytes to inflammatory macrophages in the presence of allogeneic stimulation and cell-to-cell contact. In this context, the differentiated inflammatory macrophages were capable of efficient alloantigen presentation and allostimulation of T cells of the indirect pathway. Consequently, early and transient AXL inhibition with the pharmacological inhibitor bemcentinib resulted in a profound reduction of initial allograft inflammation and a significant prolongation of allograft survival in a murine heart transplant model. Our results support further investigation of AXL inhibition as part of an induction regimen for transplantation.
WARNINGS

This product is intended for use by physicians who are experienced in the administration of allergens extracts or for use under the guidance of an allergy specialist. The initial dose must be based on skin testing as described in the dosage and administration section of this insert. Patients being switched from alum-absorbed or other types of precipitated extracts or non-standardized extracts to this extract should be started as though they were coming under treatment for the first time. Patients should be instructed to recognize adverse reaction symptoms and cautioned to contact the physician's office if symptoms occur. As with all allergenic extracts, severe systemic reactions may occur and in certain individuals these reactions may be life-threatening or cause death. Patients should be observed for at least 20 minutes following treatment. Emergency measures as well as personnel trained in their use should be immediately available in the event of a life-threatening reaction. Patients being switched from one lot of extract to another from the same manufacturer should have the dose reduced to 25 percent. Patients receiving beta-blocking drugs may be refractive to the usual dose of epinephrine, in the event that epinephrine is required to control an adverse allergic reaction to this product. This product should never be injected intravenously. See also the WARNINGS, and ADVERSE REACTIONS Sections below.
A Phase 1/2 study to evaluate the safety, tolerability, and efficacy of an antibody conditioning regimen, known as JSP191, in patients with SCID undergoing blood stem cell transplantation. Blood Stem Cell transplantation offers the only potentially curative therapy for SCID.

The biological conditioning regimen, JSP191, is an antibody that binds to CD117. CD117 is the receptor for Stem Cell Factor on blood forming cells. CD117 binding to Stem Cell Factor is critical for survival and maintenance of blood forming stem cells. The binding of JSP191 to CD117 blocks CD117 from binding to Stem Cell Factor on blood forming stem cells. In the absence of CD117/Stem Cell Factor binding, hematopoietic stem cells that are currently occupying the bone marrow niches in SCID patients exit from the bone marrow.
This is the only arm of the study. It will be comprised of 154 inpatients who had a renal ultrasound ordered or performed within the past 4 hours. The intervention will be performing hand-carried ultrasound to evaluate for presence and degree of hydronephrosis.
Participants will undergo a previously validated, half-day first responder training course, taught live in-person by local instructors in each study location. Participant knowledge acquisition will be measured via a 23-question pre/post-training assessment, administered in person. Participant skill performance will be measured via direct observation grading of a standardized patient encounter, performed in person.
BACKGROUND: Liver dysfunction is a known risk factor in the cardiovascular field. It specifically increases perioperative risk in patients undergoing coronary bypass surgery. Since percutaneous coronary intervention (PCI) is the much less invasive procedure for the treatment of coronary artery disease, we aimed to assess the relationship of liver dysfunction with outcomes in patients undergoing PCI.
METHODS: Three libraries were searched (MEDLINE, Web of Science and The Cochrane Library). We performed a meta-analysis of all studies in patients who underwent PCI that provided information on the presence or absence of liver dysfunction. Primary outcome was short-term mortality. Secondary outcomes were major adverse cardio- and cerebrovascular events (MACCE), bleeding and acute kidney injury. Random-effects model was applied.
RESULTS: Five studies were selected and the data from 10,710,317 patients were included in the final analysis. In comparison with the absence of liver dysfunction, patients with liver dysfunction were associated with higher short-term mortality (OR 2.97, 95%CI 1.23-7.18, p = 0.02), higher MACCE (OR 1.42, 95%CI 1.08-1.87, p = 0.01), and higher bleeding (OR 2.23, 95%CI 1.65-3.00, p < 0.01). There was no significant difference regarding acute kidney injury (OR 1.20, 95%CI 0.50-2.87, p = 0.69).
CONCLUSIONS: The analysis suggests that liver dysfunction in patients undergoing PCI is independently associated with higher risk of short-term mortality and increased occurrence of MACCE and bleeding. However, there appears to be no association to acute kidney injury.
Pregnancy Category D

Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue captopril as soon as possible. These adverse outcomes are usually associated with use of these drugs in the second and third trimester of pregnancy. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. Appropriate management of maternal hypertension during pregnancy is important to optimize outcomes for both mothers and fetus. 

In the unusual case that there is no appropriate alternative to therapy with drugs affecting the renin-angiotensin system for a particular patient, apprise the mother of the potential risk to the fetus. Perform serial ultrasound examinations to assess the intra-amniotic environment. If oligohydramnios is observed, discontinue captopril, unless it is considered lifesaving for the mother. Fetal testing may be appropriate, based on the week of pregnancy. Patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury. Closely observe infants with histories of in utero exposure to captopril for hypotension, oliguria, and hyperkalemia. [See PRECAUTIONS, Pediatric Use]. 

When captopril was given to rabbits at doses about 0.8 to 70 times (on a mg/kg basis) the maximum recommended human dose, low incidences of craniofacial malformations were seen. No teratogenic effects of captopril were seen in studies of pregnant rats and hamsters. On a mg/kg basis, the doses used were up to 150 times (in hamsters) and 625 times (in rats) the maximum recommended human dose.
The prevalence of obesity and its associated comorbidities has surged dramatically in recent decades. Especially concerning is the increased rate of childhood obesity, resulting in diseases traditionally associated only with adulthood. While obesity fundamentally arises from energy imbalance, emerging evidence over the past decade has revealed the involvement of additional factors. Epidemiological and murine studies have provided extensive evidence linking parental obesity to increased offspring weight and subsequent cardiometabolic complications in adulthood. Offspring exposed to an obese environment during conception, pregnancy, and/or lactation often exhibit increased body weight and long-term metabolic health issues, suggesting a transgenerational inheritance of disease susceptibility through epigenetic mechanisms rather than solely classic genetic mutations. In this review, we explore the current understanding of the mechanisms mediating transgenerational and intergenerational transmission of obesity. We delve into recent findings regarding both paternal and maternal obesity, shedding light on the underlying mechanisms and potential sex differences in offspring outcomes. A deeper understanding of the mechanisms behind obesity inheritance holds promise for enhancing clinical management strategies in offspring and breaking the cycle of increased metabolic risk across generations.
PURPOSE:To obtain a skin-beautifying bathing agent without destructing the vitamins, proteins and enzymes in cow's milk and preventing the lowering of quality by subjecting whole milk, skim milk, natural calcium, natural minerals and natural vitamin E to vacuum freeze-drying treatment. CONSTITUTION:Whole milk, skim milk, natural calcium, natural minerals and natural vitamin E are compounded at proper ratios, the mixture is stirred at room temperature until the mixture becomes a homogeneous solution and the solution is preparatorily frozen under prescribed condition. The objective bathing agent containing cow's milk can be prepared by freeze-drying the frozen solution in vacuum under prescribed condition. The agent may be incorporated with a proper amount of chemically synthesized additives. A natural substances such as rice or starch may be used as a substitute for the calcium and natural minerals. The use of the vacuum freeze drying is effective in preventing the destruction of proteins and enzymes and the lowering of the quality of the active components. Furthermore, vitamins and other natural substances can be easily added to the agent and a frozen product can be advantageously prepared without causing degradation of the substance.
Severe acute respiratory syndrome is treated with a natural human alpha interferon, a dsRNA or both natural human alpha interferon and a dsRNA. Avian influenza is treated with natural human alpha interferon, neuraminidase inhibitor(s) and ribavirin. Effects of influenza virus are mitigated with a dsRNA in combination with a neuraminidase influenza virus inhibitor. These two products, dsRNA, and alpha interferon, have therapeutic utility either given preventively (prophylactically) or in treatment of active disease. These unique immunological/antiviral actions, operating through immunological “cascades” ameliorates the lethal effects of viral mutation which, by causing resistance to commonly available drugs, greatly accelerates the death rate. For example, in 1918-1920, Avian Influenza caused the death of approximately 40 million people worldwide (ref.  National Geographic,  September 2005).
Colorectal cancer (CRC) is one of the most common malignant carcinoma worldwide. DNA polymerase epsilon 2, accessory subunit (POLE2) participates in DNA replication, repair, and cell cycle control, but its association with CRC development remains unclear. In the present study, the differentially expressed genes (DEGs) in CRC were screened from bioinformatics analysis based on GEO database. RT-qPCR was used to assess mRNA expression. CCK-8 and colony formation assays were applied for the evaluation of cell proliferation. Wound healing and transwell assays were used to detect cell migration and invasion. Protein levels were determined by Western blotting assay. We found that POLE2 was highly expressed in CRC tissues and cell lines. Inhibition of POLE2 suppressed the proliferation, migration and invasion of CRC cells. Mechanistically, Wnt/β-catenin signaling pathway was inactivated by inhibition of POLE2. Activation of Wnt/β-catenin pathway can reverse the function of POLE2 knockdown on CRC cells. In vivo studies demonstrated that POLE2 silencing could notably inhibit the growth of tumors, which was consistent with the results in vitro. In conclusion, we found POLE2 as a novel oncogene in CRC, providing a potential therapeutic or diagnostic target in CRC.
INTRODUCTION: Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, and it significantly increases the risk of cardiovascular complications and morbidity, even with appropriate treatment. Tissue remodeling has been a significant topic, while its systematic transcriptional signature remains unclear in AF.
OBJECTIVES: Our study aims to systematically investigate the molecular characteristics of AF at the cellular-level.
METHODS: We conducted single-nuclei RNA-sequencig (snRNA-seq) analysis using nuclei isolated from the left atrial appendage (LAA) of AF patients and sinus rhythm. Pathological staining was performed to validate the key findings of snRNA-seq.
RESULTS: A total of 30 cell subtypes were identified among 80, 592 nuclei. Within the LAA of AF, we observed a specific subtype of dedifferentiated cardiomyocytes (CMs) characterized by reduced expression of cardiac contractile proteins (TTN and TRDN) and heightened expression of extracellular-matrix related genes (COL1A2 and FBN1). Transcription factor prediction analysis revealed that gene expression patterns in dedifferentiated CMs were primarily regulated by CEBPG and GISLI. Additionally, we identified a distinct subtype of endothelial progenitor cells (EPCs) demonstrating elevated expression of PROM1 and KDR, a population decreased within the LAA of AF. Epicardial adipocytes disclosed a reduced release of the anti-inflammatory and anti-fibrotic factor PRG4, and an augmented secretion of VEGF signals targeting CMs. Additionally, we noted accumulation of M2-like macrophages and CD8+ T cells with high pro-inflammatory score in LAA of AF. Furthermore, the analysis of intercellular communication revealed specific pathways related to AF, such as inflammation, extracellular matrix, and vascular remodeling signals.
CONCLUSIONS: This study has discovered the presence of dedifferentiated CMs, a decrease in endothelial progenitor cells, a shift in the secretion profile of adipocytes, and an amplified inflammatory response in AF. These findings could offer crucial insights for future research on AF and serve as valuable references for investigating novel therapeutic approaches for AF.
The CR microintervention (session 1) is drawn from Barlow \& colleagues empirically supported treatment for emotional disorders (the Unified Protocol for Transdiagnostic Treatment of Emotional Disorders). The microintervention consist of four sections: (1) Introduction to cognitive appraisal; (2) Introducing the idea of "thinking traps" that prevent reappraisal and maintain negative emotion; (3) Describing cognitive reappraisal as a strategy that can help the participant "get out" of such thinking traps; (4) Providing an example of this process (situation\> negative appraisal \> negative emotion \> thinking trap \> opportunity for cognitive reappraisal) and have participants provide a personalized example.