anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Prenatal exposure to maternal diabetes has been recognized as a significant cardiovascular risk factor, increasing the susceptibility to the emergence of conditions such as high blood pressure, atherosclerosis, and heart disease in later stages of life. However, it is unclear if offspring exposed to diabetes in utero have worse vascular outcomes on a high-salt (HS) diet. To test the hypothesis that in utero exposure to maternal diabetes predisposes to HS-induced vascular dysfunction, we treated adult male wild-type offspring (DM_Exp, 6 mo old) of diabetic Ins2+/C96Y mice (Akita mice) with HS (8% sodium chloride, 10 days) and analyzed endothelial function via wire myograph and cyclooxygenase (COX)-derived prostanoids pathway by ELISA, quantitative PCR, and immunochemistry. On a regular diet, DM_Exp mice did not manifest any vascular dysfunction, remodeling, or inflammation. However, HS increased aortic contractility to phenylephrine and induced endothelial dysfunction (analyzed by acetylcholine-induced endothelium-dependent relaxation), vascular hydrogen peroxide production, COX2 expression, and prostaglandin E2 (PGE2) overproduction. Interestingly, ex vivo antioxidant treatment (tempol) or COX1/2 (indomethacin) or COX2 (NS398) inhibitors improved or reverted the endothelial dysfunction in DM_Exp mice fed a HS diet. Finally, DM_Exp mice fed with HS exhibited greater circulating cytokines and chemokines accompanied by vascular inflammation. In summary, our findings indicate that prenatal exposure to maternal diabetes predisposes to HS-induced vascular dysfunction, primarily through the induction of oxidative stress and the generation of COX2-derived PGE2. This supports the concept that in utero exposure to maternal diabetes is a cardiovascular risk factor in adulthood.NEW & NOTEWORTHY Using a unique mouse model of prenatal exposure to maternal type 1 diabetes, our study demonstrates the novel observation that prenatal exposure to maternal diabetes results in a predisposition to high-salt (HS) dietary-induced vascular dysfunction and inflammation in adulthood. Mechanistically, we demonstrated that in utero exposure to maternal diabetes and HS intake induces vascular oxidative stress, cyclooxygenase-derived prostaglandin E2, and inflammation.
Lymphangioma, a benign mass of lymphatic origin, primarily affects the head, neck, and oral cavity, with the abdomen being an uncommon location. Clinical presentation is defined by site of origin and size. We present the case of a 10-month-old male infant with no previous medical history, admitted to our department with diffuse abdominal pain and distension. Physical examination revealed a huge, palpable mass arising from the left abdomen, abdominal tenderness, guarding, and rigidity. Abdominal ultrasound revealed a multilocular, non-measurable mass with both cystic and solid components that were suggestive of a giant cystic lymphangioma. Multidetector computed tomography and magnetic resonance imaging were performed to estimate the size and extension of the tumor for preoperative planning. Moreover, an elevated alpha-fetoprotein level further supported the neoplastic origin of the tumor. Exploratory laparotomy was performed, and a mass measuring approximately 13.9×16.7×15.4 cm was identified and completely excised in negative margins. Histopathological findings confirmed the initial diagnosis. Our patient had an uncomplicated postoperative course and recovery, with no signs of recurrence on a 6-month follow-up. Giant abdominal lymphangiomas in infants are extremely rare and close attention for complications is vital. Surgical intervention with complete resection is considered the optimal management.
INTRODUCTION: Children presenting to the emergency department (ED) often require procedural sedation and analgesia (PSA) prior to procedures. Although ketamine is used widely for PSA safely, there is a risk of adverse effects. Among them, vomiting is significant as it occurs in about 10% of patients and can potentially endanger the airway. Because there is evidence that post-operative complications might be due to anxiety prior to the operation, this study aims to investigate the association between pre-procedural anxiety and vomiting in the ED.
METHODS: In this cohort study, a convenient sample of children aged 2 to 14 years who were a candidate for PSA with ketamine in the ED were enrolled. Anxiety was evaluated using the short version of the modified Yale preoperative anxiety scale (mYAS). Vomiting was recorded during the period of hospitalization in the ED and 24 h after discharge by a phone call. Association between anxiety level and vomiting was analyzed using the independent samples t-test and multivariable logistic regression was used to control for covariates.
RESULTS: 102 children were enrolled and 93 were included in final analysis. The mean age of participants was 3.95 ± 1.79 years and 55.9% were male. According to the mYAS, the mean score of anxiety was 48.67 ± 21.78 in the waiting room and 59.10 ± 23.86 in the operating room. The mean score of anxiety was 58.3±25.3 and 51.0±20.7 in the vomiting and non-vomiting groups, respectively. At least one episode of vomiting was reported in 23 children of which, 19 took place in the hospital and 4 after discharge. No significant association was observed between pre-procedural anxiety and the occurrence of vomiting. On univariate regression model, the odds ratio of the association between mean anxiety and vomiting was 1.02 (CI 95%: 0.99-1.04) (P-value: 0.16). On the multivariable logistic regression model, after adjusting for all the covariates, the odds ratio was 1.03 (CI 95%: 1.0-1.05) (P-value: 0.05).
CONCLUSION: The present study showed that anxiety before procedural sedation and analgesia with ketamine in children was not associated with the incidence of vomiting.
Participants randomized to this arm will have access to the W-PPMA mobile app throughout the 16-week study. Participants are asked to use the app for at least 5 minutes a day during the treatment phase (first 8 weeks) and then as often as they like during the follow-up phase (last 8 weeks) of the study.
Effective emergency responses are crucial for preventing coal mine accidents and mitigating injuries. This paper aims to investigate the characteristics of emergency psychophysiological reactions to coal mine accidents and to explore the potential of key indicators for identifying emergency behavioral patterns. Initially, virtual reality technology facilitated a simulation experiment for emergency escape during coal mine accidents. Subsequently, the characteristics of emergency reactions were analyzed through correlation analysis, hypothesis testing, and analysis of variance. The significant changes in physiological indicators were then taken as input features and fed into the three classifiers of machine learning algorithms. These classifications ultimately led to the identification of behavioral patterns, including agility, defensiveness, panic, and rigidity, that individuals may exhibit during a coal mine accident emergency. The study results revealed an intricate relationship between the mental activities induced by accident stimuli and the resulting physiological changes and behavioral performances. During the virtual reality simulation of a coal mine accident, subjects were observed to experience significant physiological changes in electrodermal activity, heart rate variability, electromyogram, respiration, and skin temperature. The random forest classification model, based on SCR + RANGE + IBI + SDNN + LF/HF, outperformed all other models, achieving accuracies of up to 92%. These findings hold promising implications for early warning systems targeting abnormal psychophysiological and behavioral reactions to emergency accidents, potentially serving as a life-saving measure in perilous situations and fostering the sustainable growth of the coal mining industry.
As with all therapeutic proteins, there is potential for immunogenicity. The detection of antibody formation is highly dependent on the sensitivity and specificity of the assay. Additionally, the observed incidence of antibody (including neutralizing antibody) positivity in an assay may be influenced by several factors including assay methodology, sample handling, timing of sample collection, concomitant medications, and underlying disease. For these reasons, comparison of the incidence of antibodies to RITUXAN HYCELA and rituximab in the studies described below with the incidence of antibodies in other studies or to other products may be misleading.

In the SABRINA study, where previously untreated patients with follicular lymphoma were treated with RITUXAN HYCELA or rituximab in combination with CVP or CHOP, the incidence of treatment-induced/enhanced anti-rituximab antibodies in the RITUXAN HYCELA group was similar to that observed in the rituximab group (2.0% RITUXAN HYCELA vs. 1.9% rituximab). The incidence of treatment-induced/enhanced anti-recombinant human hyaluronidase antibodies was 15% in the RITUXAN HYCELA group compared with 8% in the rituximab group, and the overall proportion of patients found to have anti-recombinant human hyaluronidase antibodies remained generally constant over the follow-up period in both cohorts. All patients who tested positive for anti-recombinant human hyaluronidase antibodies at any point during the study were negative for neutralizing antibodies.

In the SAWYER study, where previously untreated patients with CLL were treated with RITUXAN HYCELA or rituximab in combination with FC, the incidence of treatment-induced/enhanced anti-rituximab antibodies was 12% in the RITUXAN HYCELA group and 15% in the rituximab group. The incidence of treatment-induced/enhanced anti-recombinant human hyaluronidase antibodies was 11% in the RITUXAN HYCELA treatment arm. None of the patients who tested positive for anti-recombinant human hyaluronidase antibodies tested positive for neutralizing antibodies. 

The clinical relevance of the development of anti-rituximab or anti-recombinant human hyaluronidase antibodies after treatment with RITUXAN HYCELA is not known.
The first part of this study was a phase IIa randomized, double blind, placebo controlled, multi-center study to investigate adding efprezimod alfa to standard of care tacrolimus and methotrexate in acute graft-versus host disease (GVHD) prophylaxis for allogeneic hematopoietic stem cell transplantation (HCT) with matched unrelated donors in treatment of leukemia and myelodysplastic syndrome. The primary objective was to evaluate the safety, tolerability and dose-limiting toxicities (DLTs) of efprezimod alfa in participants undergoing matched unrelated donor myeloablative allogeneic HCT for malignant hematologic disorders. Three dose cohorts were planned with 240 mg at day -1 (one day prior to HCT), 480 mg at day -1, and the multi-dose cohort of 480-240-240 mg at day -1, day 14 and day 28. The efprezimod alfa : placebo randomization ratio was 3:1.

The second part was a prospective open label phase IIa expansion cohort trial investigating the addition of efprezimod alfa to standard acute graft-versus host disease (GVHD) prophylaxis for allogeneic hematopoietic stem cell transplantation (HCT). Based on the first part's safety results and the pharmacokinetic data, the phase IIa expansion dose was the multi-dose 480-240-240 mg regimen administered on day -1, day 14 and day 28, respectively. The primary objective of phase IIa expansion was to determine if the addition of efprezimod alfa to standard GVHD prophylaxis improves 180 days post-HCT grade III-IV acute GVHD-free survival (AGFS) when compared to Center for International Blood and Marrow Transplant Research (CIBMTR) database registered control participants who had standard GVHD prophylaxis alone. Eligible participants were those requiring allogeneic HCT for malignant hematologic conditions and receiving a myeloablative conditioning regimen.
No intervention was given to the control group. After the education given to the intervention group and the reminder text messages sent for 12 weeks, the intervention and control groups were asked to fill out the Cardiovascular Disease Risk Awareness Rating Scale (CDRAAS), Cardiovascular Disease Risk Factor Knowledge Level Scale (CARRF-KL) and EQ-5D Quality of Life Scale again in the same week. After the post-tests were taken, the control group also received training.
NIV must be delivered by full or oronasal mask with any available ventilator. The ventilator settings will be decided according to the usual practice: maximal tolerated inspiratory pressure to obtain a measured or estimated expired tidal volume of 6-8 mL·kg-1 of body weight and a positive end expiratory pressure (PEEP) between 3 and 5 cmH2O. An interface rotational strategy will be allowed among only different types of masks.
As with all therapeutic proteins, there is potential for immunogenicity. The detection of antibody formation is highly dependent on the sensitivity and specificity of the assay. Additionally, the observed incidence of antibody (including neutralizing antibody) positivity in an assay may be influenced by several factors including assay methodology, sample handling, timing of sample collection, concomitant medications, and underlying disease. For these reasons, comparison of the incidence of antibodies to NORDITROPINwith the incidence of antibodies to other products may be misleading. In the case of growth hormone, antibodies with binding capacities lower than 2 mg/mL have not been associated with growth attenuation. In a very small number of patients treated with somatropin, when binding capacity was greater than 2 mg/mL, interference with the growth response was observed.

In clinical trials, GH deficient pediatric patients receiving NORDITROPINfor up to 12 months were tested for induction of antibodies, and 0/358 patients developed antibodies with binding capacities above 2 mg/L. Amongst these patients, 165 had previously been treated with other somatropin formulations, and 193 were previously untreated naive patients. Eighteen of 76 children (~24%) treated with NORDITROPINfor short stature born SGA developed anti-rhGH antibodies.
INTRODUCTION: Identification of liver disease during bariatric operations is an important task given the patients risk for occult fatty liver disease. Surgeon's accuracy of assessing for liver disease during an operation is poorly understood. The objective was to measure surgeons' performance on intra-operative visual assessment of the liver in a simulated environment.
METHODS: Liver images from 100 patients who underwent laparoscopic bariatric surgery and pre-operative ultrasound elastography between July 2020 and July 2021 were retrospectively evaluated. The perception of 15 surgeons regarding the degree of hepatic steatosis and fibrosis was collected in a simulated clinical environment by survey and compared to results determined by ultrasonographic exam.
RESULTS: The surgeons' ability to correctly identify the class of steatosis and fibrosis was poor (accuracy 61% and 59%, respectively) with a very weak correlation between the surgeon's predicted class and its true class (r = 0.17 and r = 0.12, respectively). When liver disease was present, surgeons completely missed its presence in 26% and 51% of steatosis and fibrosis, respectively. Digital image processing demonstrated that surgeons subjectively classified steatosis based on the "yellowness" of the liver and fibrosis based on texture of the liver, despite neither correlating with the true degree of liver disease.
CONCLUSION: Laparoscopic visual assessment of the liver surface for identification of non-cirrhotic liver disease was found to be an inaccurate method during laparoscopic bariatric surgery. While validation studies are needed, the results suggest the clinical need for alternative approaches.
Sickle cell anemia is an autosomal recessive disorder and the most common genetic disease affecting African-Americans. Approximately 0.15% of African-Americans are homozygous for sickle cell disease, and 8% have sickle cell trait. Acute pain crisis, acute chest syndrome (ACS), and secondary pulmonary hypertension are common complications of sickle cell anemia. Pulmonary hypertension has now been identified as a major cause of death in adults with sickle cell disease. Inhaled nitric oxide (NO) has been proposed as a possible therapy for both primary and secondary pulmonary hypertension. Furthermore, a number of recent studies have suggested that NO may have a favorable impact on sickle red cells at the molecular level and could improve the abnormal microvascular perfusion that is characteristic of sickle cell anemia. In addition, chronic exchange transfusion therapy may reduce the progression and/or severity of pulmonary hypertension in these patients.

This clinical trial is designed (1) to determine the pathophysiologic processes that are associated with and potentially contribute to secondary pulmonary hypertension in adult patients with sickle cell anemia, by comparing the cardio-pulmonary status of patients with sickle cell disease with and without pulmonary hypertension (2) to determine the relative acute vasodilatory effects of oxygen, intravenous prostacyclin, and inhaled nitric oxide on pulmonary artery pressures and other hemodynamic parameters in patients with secondary pulmonary hypertension and sickle cell anemia, (3) to determine the effects of two months of inhaled nitric oxide on pulmonary artery pressures, other hemodynamic parameters, exercise tolerance, and symptoms in this patient population, and (4) to determine the effects of three months of exchange transfusion on pulmonary artery pressures, other hemodynamic parameters, exercise tolerance, and symptoms in patients who do not receive or fail to respond to NO therapy.
INTRODUCTION: The development of chronic obstructive pulmonary disease (COPD) is strongly associated with oxidative stress, but it is unclear whether increasing dietary antioxidant intake reduces the risk of COPD. Therefore, this study assessed the association between antioxidant intake and COPD in US adults aged ≥ 40 years and further examined the correlation using the Composite Dietary Antioxidant Index (CDAI).
METHODS: The study included 8,257 US adults aged ≥ 40 years using data from the National Health and Nutrition Examination Survey (NHANES) for three cycles from 2007-2012. Multivariate logistic regression models were used to calculate the correlation between antioxidant intake and CDAI with COPD. Restricted cubic spline was further used to explore the exposure-response relationship. Mediation analysis was used to explore the role of inflammatory factors in the association between CDAI and COPD.
RESULTS: This study included 8257 participants (4111 women [weighted, 50.7%]; mean [SD] age, 58.8 [11.2] years). In a multivariable-adjusted model of single antioxidant intake, a linear downward association between carotenoid intake and the incidence of COPD (P for trend = 0.052; Pnon- linear = 0.961). In a multivariable adjusted model for CDAI, this association is similarly present (P for trend = 0.018; Pnon-linear = 0.360). Multiple linear regression modeling showed that leukocytes (P = 0.002), alkaline phosphatase (P< 0.001), and c-reactive protein (P< 0.001) were negatively associated with CDAI levels. Meanwhile, mediation analysis revealed that alkaline phosphatase and c-reactive protein partially influenced the association between CDAI and COPD prevalence, with mediation ratios of 6.4% (P< 0.01) and 4.68% (P = 0.04), respectively.
CONCLUSION: The risk of COPD decreased with increased carotenoid intake and CDAI. In addition, CDAI has been found to be strongly associated with inflammatory factors and can reduce the incidence of COPD by mediating inflammatory factors.
BACKGROUND AND PURPOSE: Quantification of neurofilament light chain protein in serum (sNfL) enables the neuro-axonal damage in peripheral blood to be reliably assessed and monitored. There is a long-standing debate whether essential tremor represents a 'benign' tremor syndrome or whether it is linked to neurodegeneration. This study aims to investigate sNfL concentrations in essential tremor compared to healthy controls (cross-sectionally and longitudinally) and to assess whether sNfL is associated with motor and nonmotor markers of disease progression.
METHODS: Data of patients with essential tremor from our prospective registry on movement disorders (PROMOVE) were retrospectively analysed. Age-, sex- and body-mass-index-matched healthy controls were recruited from an ongoing community-dwelling aging cohort. sNfL was quantified by an ultra-sensitive single molecule array (Simoa). All participants underwent detailed clinical examination at baseline and after approximately 5 years of follow-up.
RESULTS: Thirty-seven patients with clinically diagnosed essential tremor were included and 37 controls. The essential tremor group showed significantly higher sNfL levels compared to healthy controls at baseline and follow-up. sNfL levels increased over time in both groups, and the slope of sNfL increase was similar in the essential tremor and healthy control groups. Comparing patients with a disease duration under 5 years to those with a longer disease duration, the former group had a significantly greater increase of sNfL over time, which strongly correlated to worsening of tremor and cognition.
CONCLUSION: Our findings indicate that neurodegeneration, possibly happening at an early disease stage, might play a role in the pathophysiology of essential tremor.
Saccharomyces cerevisiae has long been used as a model organism to study genome instability. The SAM1 and SAM2 genes encode AdoMet synthetases, which generate S-AdenosylMethionine (AdoMet) from Methionine (Met) and ATP. Previous work from our group has shown that deletions of the SAM1 and SAM2 genes cause changes to AdoMet levels and impact genome instability in opposite manners. AdoMet is a key product of methionine metabolism and the major methyl donor for methylation events of proteins, RNAs, small molecules, and lipids. The methyl cycle is interrelated to the folate cycle which is involved in de novo synthesis of purine and pyrimidine deoxyribonucleotides (dATP, dTTP, dCTP, and dGTP). AdoMet also plays a role in polyamine production, essential for cell growth and used in detoxification of reactive oxygen species (ROS) and maintenance of the redox status in cells. This is also impacted by the methyl cycle's role in production of glutathione, another ROS scavenger and cellular protectant. We show here that sam2∆/sam2∆ cells, previously characterized with lower levels of AdoMet and higher genome instability, have a higher level of each dNTP (except dTTP), contributing to a higher overall dNTP pool level when compared to wildtype. Unchecked, these increased levels can lead to multiple types of DNA damage which could account for the genome instability increases in these cells.
Surgery for traumatic brain injury is an anaesthetic challenge fraught with complications such as brain bulge, excessive bleeding, hypotension etc. As yet there are no anaesthetic regimen guidelines to follow for induction of anaesthesia in neurotrauma surgeries. Although the functional effect of anaesthetic agents on neuronal tissue is known quite well, there is lack of studies documenting the effect of these anaesthetic agents on head injured patients. It is also not known whether the requirement of anaesthetic agent in the same as a non head injured patient. This study was designed to assess the requirement of anaesthetic thiopentone in head injured patients and compare the anaesthetic usage with and without Bispectral index (BIS) monitoring. We also observed the real time change in neuronal function using Bispectral Index monitoring after craniotomy, i.e. effectively decompression and release of intracranial pressure intraoperatively.