anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Nowadays, cesarean is one of the most common surgical interventions and its prevalence has increased in most countries in the recent years. Delay in healing of cesarean wound and formation of visible scar are common symptoms of maternal morbidity after cesarean section. These complications affect mother's quality of life due to stress, anxiety, delay in mother's ability and health recovery, and also they are associated with additional cost as a result of the increased need for wide spectrum antibiotics and sometimes hospitalization and repeated repair of wound. Improve the final aspect of would and visible scars, have been a challenge for medicine. Mesenchymal stem cells (MSC) are a population of pluripotent stem cells that are self-renewing and capable of differentiating into canonical cells of the mesenchyme. Recently, stem cells have been applied to regenerative medicine, even for internal organs such as blood vessels, nerves, and heart.

The study is to investigate the efficacy and safety of perinatal tissue mesenchyme stem cells treatment on the appearance of a caesarean scar as compared to a similar untreated scar. This is a randomized, double-blind, placebo-controlled clinical trial designed to investigate the efficacy and safety of perinatal tissue mesenchyme stem cells (MSC) treatment on the appearance of a caesarean scar as compared to a similar untreated scar. A total of ninety (90) participants will be randomized (1:1:1) to receive MSC or placebo. All of participants will be undergoing delivery by lower segment caesarean section through a transverse abdominal incision, and there will be no clear indication for a particular surgical technique or material to be used. In low-dose MSC group, participants will receive transdermal one dose of 1\*10\^6 cells of Perinatal Tissue Mesenchyme Stem Cells in the gel once a day for continuous three days and then receive transdermal placebo without of Perinatal Tissue Mesenchyme Stem Cells in the gel once a day for continuous next three days; In high-dose MSC group, participants will receive transdermal one dose of 1\*10\^6 cells of Perinatal Tissue Mesenchyme Stem Cells in the gel once a day for continuous six days; And in placebo group, participants will receive transdermal placebo without of Perinatal Tissue Mesenchyme Stem Cells in the gel once a day for continuous six days. After randomization, baseline data, and transdermal treatment, participants will be followed up at 1 month, 3 months and 6 months. For the purpose of the endpoint analysis and safety evaluations, the investigators will utilize an "intention-to-treat" study population.
Participants with EGFR ex20ins positive locally advanced or metastatic NSCLC who have received mobocertinib in China's routine clinical practice setting will be observed in this study. The observation period for each participant is planned to be 18 months, starting from the participant who received mobocertinib enrolled in this study and ending at the earliest occurrence of the completion of 18 months of follow-up, death, loss to follow-up, or withdrawal from the study.
Transplant recipients from matched sibling donors and dual cord donors. Subjects will receive plerixafor at 240 ug/kg subcutaneously every other day beginning at day +2 after transplant until day +21 or engraftment occurs.
The use of Protopic® Ointment should be avoided on pre-malignant and malignant skin conditions. Some malignant skin conditions, such as cutaneous T-cell lymphoma (CTCL), may mimic atopic dermatitis.

The use of tacrolimus ointment is not recommended in patients having skin conditions with a skin barrier defect where there is the potential for increased systemic absorption of tacrolimus, including but not limited to, Netherton's syndrome, lamellar ichthyosis, generalized erythroderma or cutaneous Graft Versus Host Disease. Oral application is also not recommended. Post-marketing cases of increased tacrolimus blood level have been reported in these conditions.

The use of Protopic® Ointment may cause local symptoms such as skin burning (burning sensation, stinging, soreness) or pruritus. Localized symptoms are most common during the first few days of Protopic® Ointment application and typically improve as the lesions of atopic dermatitis resolve. With Protopic® Ointment 0.1%, 90% of the skin burning events had a duration between 2 minutes and 3 hours (median 15 minutes). 90% of the pruritus events had a duration between 3 minutes and 10 hours (median 20 minutes) (see ADVERSE REACTIONS).
Participants in the Immediate Treatment Group will receive DTTC Treatment four times per week (45-minute sessions each) for 8 weeks. Total duration will be 180 minutes/week over 32 sessions. Treatment will begin between 1-3 weeks following the diagnostic evaluation.
PegIFN-2b (1.5 µg/kg/week subcutaneously) plus RBV (600-1400 mg/day, orally, divided into two daily doses) for 4 weeks followed by placebo to boceprevir plus PegIFN-2b/RBV for 44 weeks with 24 weeks post-treatment follow-up (Control Arm). Participants who do not achieve HCV-RNA \<9.3 IU/mL by Treatment Week 24 (TW24) are eligible to cross-over and receive boceprevir along with the PegIFN-2b and RBV for up to 44 weeks.
UNLABELLED: Coxsackievirus group B3 (CVB3) belongs to the genus Enteroviruses of the family Picornaviridae and is the main pathogen underlying viral myocarditis (VMC). No specific therapeutic is available for this condition. Argininosuccinate synthase 1 (ASS1) is a key enzyme in the urea cycle that converts citrulline and aspartic acid to argininosuccinate. Here, we found that CVB3 and its capsid protein VP2 inhibit the autophagic degradation of ASS1 and that CVB3 consumes citrulline to upregulate ASS1, triggers urea cycle metabolic reprogramming, and then activates macrophages to develop pro-inflammatory polarization, thereby promoting the occurrence and development of VMC. Conversely, citrulline supplementation to prevent depletion can downregulate ASS1, rescue macrophage polarization, and alleviate the pathogenicity of VMC. These findings provide a new perspective on the occurrence and development of VMC, revealing ASS1 as a potential new target for treating this disease.
IMPORTANCE: Viral myocarditis (VMC) is a common and potentially life-threatening myocardial inflammatory disease, most commonly caused by CVB3 infection. So far, the pathogenesis of VMC caused by CVB3 is mainly focused on two aspects: one is the direct myocardial injury caused by a large number of viral replication in the early stage of infection, and the other is the local immune cell infiltration and inflammatory damage of the myocardium in the adaptive immune response stage. There are few studies on the early innate immunity of CVB3 infection in myocardial tissue, but the appearance of macrophages in the early stage of CVB3 infection suggests that they can play a regulatory role as early innate immune response cells in myocardial tissue. Here, we discovered a possible new mechanism of VMC caused by CVB3, revealed new drug targets for anti-CVB3, and discovered the therapeutic potential of citrulline for VMC.
The HOXA9 transcription factor serves as a molecular orchestrator in cancer stemness, epithelial-mesenchymal transition (EMT), metastasis, and generation of the tumor microenvironment in hematological and solid malignancies. However, the multiple modes of regulation, multifaceted functions, and context-dependent interactions responsible for the dual role of HOXA9 as an oncogene or tumor suppressor in cancer remain obscure. Hence, unravelling its molecular complexities, binding partners, and interacting signaling molecules enables us to comprehend HOXA9-mediated transcriptional programs and molecular crosstalk. However, it is imperative to understand its central role in fundamental biological processes such as embryogenesis, foetus implantation, hematopoiesis, endothelial cell proliferation, and tissue homeostasis before designing targeted therapies. Indeed, it presents an enormous challenge for clinicians to selectively target its oncogenic functions or restore tumor-suppressive role without altering normal cellular functions. In addition to its implications in cancer, the present review also focuses on the clinical applications of HOXA9 in recurrence and drug resistance, which may provide a broader understanding beyond oncology, open new avenues for clinicians for accurate diagnoses, and develop personalized treatment strategies. Furthermore, we have also discussed the existing therapeutic options and accompanying challenges in HOXA9-targeted therapies in different cancer types.
Lidocaine hydrochloride exerts its antiarrhythmic effect by raising the electrical stimulation threshold of the ventricle during diastole. In usual therapeutic doses, lidocaine hydrochloride produces no change in myocardial contractility, systemic arterial pressure or in absolute refractory period.

Onset of action is rapid after an intravenous bolus with a duration of action of approximately 15 to 20 minutes.

Approximately 90% of an administered dose of lidocaine hydrochloride is metabolized in the liver. The remainder (10%) of the drug is excreted unchanged in the urine. Pharmacokinetic data indicate reduced elimination of lidocaine after prolonged (24 hours) infusion with resultant prolongation of the half-life to approximately three times that seen following a single administration.
Dissolve the lyophilized glucagon using the accompanying diluting solution and use immediately. Discard any unused portion.

The doses in the following table may be administered for relaxation of the stomach, duodenum, and small bowel, depending on the onset and duration of effect required for the examination. Since the stomach is less sensitive to the effect of glucagon, 0.5 mg (0.5 units) IV or 2 mg (2 units) IM are recommended.

For examination of the colon, it is recommended that a 2 mg (2 units) dose be administered intramuscularly approximately 10 minutes prior to the procedure. Colon relaxation and reduction of patient discomfort may allow the radiologist to perform a more satisfactory examination.
Sarcopenia is an age-associated loss of skeletal muscle mass, strength, and function, accompanied by severe adverse health outcomes, such as falls and fractures, functional decline, high health costs, and mortality. Hence, its prevention and treatment have become increasingly urgent. However, despite the wide prevalence and extensive research on sarcopenia, no FDA-approved disease-modifying drugs exist. This is probably due to a poor understanding of the mechanisms underlying its pathophysiology. Recent evidence demonstrate that sarcopenia development is characterized by two key elements: (i) epigenetic dysregulation of multiple molecular pathways associated with sarcopenia pathogenesis, such as protein remodeling, insulin resistance, mitochondria impairments, and (ii) the creation of a systemic, chronic, low-grade inflammation (SCLGI). In this review, we focus on the epigenetic regulators that have been implicated in skeletal muscle deterioration, their individual roles, and possible crosstalk. We also discuss epidrugs, which are the pharmaceuticals with the potential to restore the epigenetic mechanisms deregulated in sarcopenia. In addition, we discuss the mechanisms underlying failed SCLGI resolution in sarcopenia and the potential application of pro-resolving molecules, comprising specialized pro-resolving mediators (SPMs) and their stable mimetics and receptor agonists. These compounds, as well as epidrugs, reveal beneficial effects in preclinical studies related to sarcopenia. Based on these encouraging observations, we propose the combination of epidrugs with SCLI-resolving agents as a new therapeutic approach for sarcopenia that can effectively attenuate of its manifestations.
The cytosolic dipeptidyl-aminopeptidase 9 (DPP9) cleaves protein N-termini post-proline or -alanine. Our analysis of DPP9 mRNA expression from the TCGA 'breast cancer' data set revealed that low/intermediate DPP9 levels are associated with poor overall survival of breast cancer patients. To unravel the impact of DPP9 on breast cancer development and progression, the transgenic MMTV-PyMT mouse model of metastasizing breast cancer was used. In addition, tissue- and time-controlled genetic deletion of DPP9 by the Cre-loxP recombination system was done. Despite a delay of tumor onset, a higher number of lung metastases were measured in DPP9-deficient mice compared to controls. In human mammary epithelial cells with oncogenic RAS pathway activation, DPP9 deficiency delayed tumorigenic transformation and accelerated TGF-β1 induced epithelial-to-mesenchymal transition (EMT) of spheroids. For further analysis of the mechanism, primary breast tumor cells were isolated from the MMTV-PyMT model. DPP9 deficiency in these cells caused cancer cell migration and invasion accompanied by EMT. In absence of DPP9, the EMT transcription factor ZEB1 was stabilized due to insufficient degradation by the proteasome. In summary, low expression of DPP9 appears to decelerate mammary tumorigenesis but favors EMT and metastasis, which establishes DPP9 as a novel dynamic regulator of breast cancer initiation and progression.
PURPOSE: Bronchiectasis is predominantly marked by neutrophilic inflammation. The relevance of type 2 biomarkers in disease severity and exacerbation risk is poorly understood. This study explores the clinical significance of these biomarkers in bronchiectasis patients.
METHODS: In a cross-sectional cohort study, bronchiectasis patients, excluding those with asthma or allergic bronchopulmonary aspergillosis, underwent clinical and radiological evaluations. Bronchoalveolar lavage samples were analyzed for cytokines and microbiology. Blood eosinophil count (BEC), serum total immunoglobulin E (IgE), and fractional exhaled nitric oxide (FeNO) were measured during stable disease states. Positive type 2 biomarkers were defined by established thresholds for BEC, total IgE, and FeNO.
RESULTS: Among 130 patients, 15.3% demonstrated BEC ≥ 300 cells/μL, 26.1% showed elevated FeNO ≥ 25 ppb, and 36.9% had high serum total IgE ≥ 75 kU/L. Approximately 60% had at least one positive type 2 biomarker. The impact on clinical characteristics and disease severity was variable, highlighting BEC and FeNO as reflective of different facets of disease severity and exacerbation risk. The combination of low BEC with high FeNO appeared to indicate a lower risk of exacerbation. However, Pseudomonas aeruginosa colonization and a high neutrophil-to-lymphocyte ratio (NLR ≥ 3.0) were identified as more significant predictors of exacerbation frequency, independent of type 2 biomarker presence.
CONCLUSIONS: Our study underscores the distinct roles of type 2 biomarkers, highlighting BEC and FeNO, in bronchiectasis for assessing disease severity and predicting exacerbation risk. It advocates for a multi-biomarker strategy, incorporating these with microbiological and clinical assessments, for comprehensive patient management.
Neurodegenerative diseases are often accompanied by neuroinflammation and impairment of the blood-brain barrier (BBB) mediated by activated glial cells through their release of proinflammatory molecules. To study the effects of glial cells on mouse brain endothelial cells (mBECs), we developed an in vitro BBB model with inflammation by preactivating mixed glial cells (MGCs) with lipopolysaccharide (LPS) before co-culturing with mBECs to study the influence of molecules released by activated MGCs. The response of the mBECs to activated MGCs was compared to direct stimulation with LPS. The cytokine profile of activated MGCs was analyzed together with their effects on the mBEC's integrity, expression of tight junction proteins, adhesion molecules, and BBB-specific transport proteins. Stimulation of MGCs significantly upregulated mRNA expression and secretion of several pro-inflammatory cytokines. Co-culturing mBECs with pre-stimulated MGCs significantly affected the barrier integrity of mBECs similar to direct stimulation with LPS. The gene expression levels of tight junction proteins were unaltered, but tight junction proteins revealed rearrangements with respect to subcellular distribution. Compared to direct stimulation with LPS, the expression of cell-adhesion molecules was significantly increased when mBECs were co-cultured with prestimulated MGCs and thus pre-activating MGCs transforms mBECs into a proinflammatory phenotype.
This is a randomized (study drug assigned by chance), multicenter, double-blind (neither physician nor patient knows the name of the assigned drug), add-on study (NSAIDs or COX-2 medications maintained at pre-study dose.) to investigate the tolerability of titrated doses of tramadol hydrochloride/acetaminophen combination tablet in osteoarthritis patients taking NSAIDS or COX-2 inhibitors (both are drugs used to treat inflammation and pain) compared to non-titrated doses of tramadol hydrochloride/acetaminophen combination tablet. The patients will be randomized into 2 treatment groups. First group (the titration group) receives 1 tablet of tramadol hydrochloride/acetaminophen in the morning, 1 tablet of placebo in the afternoon and evening for 3 days, then 1 tablet of tramadol hydrochloride/acetaminophen in the morning, 1 tablet of placebo in the afternoon and 1 tablet of tramadol hydrochloride/acetaminophen in the evening for 4 days, and the 1 tablet of tramadol hydrochloride/acetaminophen three times daily for next 7 days. The second group (non-titration group) will receive 1 tablet of tramadol hydrochloride/acetaminophen three times daily without titration for 14 days. The study hypothesis is the first group's discontinuation rate due to adverse events is lower than that of second group. Safety assessments include adverse event, vital sign and clinical lab monitoring. First group will receive 1 tablet of tramadol hydrochloride/acetaminophen and 2 tablets of placebo for 3 days, 2 tablets of tramadol hydrochloride/acetaminophen and 1 tablet of placebo for 4 days, and 3 tablets of tramadol hydrochloride/acetaminophen for 7 days. Second group will receive 3 tablets of tramadol hydrochloride/acetaminophen for 14 days.
Stage pIIIA/N2 non-small cell lung cancer (NSCLC) is primarily treated by complete surgical resection combined with neoadjuvant/adjuvant therapies. However, up to 40% of patients experience tumor recurrence. Here, we studied 119 stage pIIIA/N2 NSCLC patients who received complete surgery plus adjuvant chemotherapy (CT) or chemoradiotherapy (CRT). The paired tumor and resection margin samples were analyzed using next-generation sequencing (NGS). Although all patients were classified as negative resection margins by histologic methods, NGS revealed that 47.1% of them had molecularly positive surgical margins. Patients who tested positive for NGS-detected residual tumors had significantly shorter disease-free survival (DFS) (P = 0.002). Additionally, metastatic lymph node ratio, erb-b2 receptor tyrosine kinase 2 (ERBB2) mutations, and SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 4 (SMARCA4) mutations were also independently associated with DFS. We used these four features to construct a COX model that could effectively estimate recurrence risk and prognosis. Notably, mutational profiling through broad-panel NGS could more sensitively detect residual tumors than the conventional histologic methods. Adjuvant CT and adjuvant CRT exhibited no significant difference in eliminating locoregional recurrence risk for stage pIIIA/N2 NSCLC patients with molecularly positive surgical margins.
OBJECTIVE: Paroxysmal, rhythmic, and repetitive events (PRREs) during infancy can be concerning for possible seizures, especially following perinatal brain injuries. The workup for establishing whether a PRRE represents a seizure involves the use of continuous video-electroencephalography (cVEEG) for event characterization. This study aims to determine the diagnostic yield of cVEEG for evaluating events concerning for seizures in children aged 1-24 months.
METHODS: We performed a single-center retrospective chart review (January 1, 2019-December 31, 2020) and included all children aged 1-24 months admitted for PRRE capture and characterization using cVEEG. Chart abstraction included demographics, birth and family history, known brain injury, event semiology, duration, and frequency, as well as interictal electroencephalographic (EEG) features. For each of these variables, odds ratios for seizure prediction were calculated.
RESULTS: A total of 243 patients were identified for this study. On cVEEG, n = 160 (65.4%) had a target event of concern captured during an initial admission with cVEEG. Whereas n = 41 (25.8%) patients with events captured were confirmed to have seizures, most patients (n = 119) were confirmed to have nonepileptic events. Several variables predicted seizure likelihood during the initial admission with cVEEG, including event duration (>1 min), frequency (occurring ≥3 times per week), and presence of abnormal interictal findings on cVEEG. For patients who did not receive a diagnosis at the time of initial admission with cVEEG, the likelihood of a subsequent epilepsy diagnosis was associated with specific PRRE semiology (motor active or motor passive), longer event duration (>1 min duration), and the presence of interictal abnormal EEG features on initial cVEEG admission. Prediction tools utilizing scoring systems to stratify risk in infants with suspected seizures due to PRREs are included.
SIGNIFICANCE: Unique patient attributes and PRRE characteristics, as well as the presence of EEG interictal abnormalities, can provide valuable insights for discerning children with a higher likelihood of epilepsy diagnosis following cVEEG admission.
Insertion of tympanostomy tubes after 3 months observation for chronic otitis media with effusion (OME) according to the National guidelines in Denmark. Sleep measurements with accelerometer 7 nights before and 7 nights after intervention. Caregivers report use of paracetamol during nights with sleep measurements.
An aqueous negative contrast agent for CT imaging of the gastrointestinal tract and the preparation method thereof. The agent is used in biological and pharmaceutical field. Its components and the weight percent are: hydrogel matrix 0.01-1%, micro-/nano-particles of the materials with low densities 5-50%, stabilization agents 0.1-5%, the rest is deionized water. The preparation method is: stabilization agents are added into the hydrogel matrix made of natural or synthetic hydrophilic polymers, then micro-/nano-particles of the materials with low CT densities are added or prepared, and uniformly dispersed in the hydrogel matrix. The CT density of the resulted aqueous negative contrast agent for CT imaging of the gastrointestinal tract is −30 HU to −500 HU. It can decrease the CT density inside the intestine lumen to lower than −30 HU. The intestine wall can be depicted clearly and the CT signals intensities inside lumen are uniform. It is feasible for 3D images processing such as virtual endoscopy reconstruction with the negative contrast agent. The agent is safe, stable and nontoxic. It will not lead to diarrhea after administration. It is of great significance for the improved sensitivity and specificity of CT diagnosis for the diseases on the intestinal wall and lumen.
The invention relates to the use of compounds of the general formula I <IMAGE> where n has the meaning 3 or 4, for controlling dandruff and to compositions for the treatment of the scalp and/or for cleaning, caring for or strengthening the hair with a content of these compounds. The concentration of the compounds of the formula I is 0.02 to 3.0% by weight, preferably 0.05 to 1.5% by weight. The described compositions are intended to come into contact with the scalp on use thereof. Preferred formulations are shampoos and hair lotions. The compounds of the formula I have an excellent activity against dandruff and a pleasant odour. They also act as disinfectants and are readily soluble in customary cosmetic solvents such as water and water/alcohol mixtures.