anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Gastroesophageal reflux disease (GERD) and Chronic Obstructive Pulmonary Disease (COPD) often coexist and have been associated in observational studies. However, the real potential causal relationship between GERD and COPD is unknown and not well established.
METHODS: In this study, we conducted a bidirectional two-sample Mendelian randomization(MR) to estimate whether GERD and COPD are causal. The GERD genetic data is from summary level data of a genome-wide association (GWAS) meta-analysis (Ncases = 71,522, Ncontrol=26,079). The COPD GWAS are available from the FinnGen (Ncases=16,410, Ncontrol=283,589). MR-Egger regression, Weighted Median, and Inverse-variance weighted (IVW) were used for MR analysis from the R package "TwoSampleMR", and IVW was the dominant estimation method. Additionally, the MR pleiotropy residual sum and outlier (MR-PRESSO), Cochran Q statistic, and leave-one-out analysis were used to detect and correct for the effect of heterogeneity and horizontal pleiotropy.
RESULTS: MR analysis indicated that GERD was causally associated with an increased risk of COPD (IVW odds ratio (OR): 1.3760, 95% confidence interval (CI): 1.1565-1.6371, P=0.0003), and vice versa (IVW OR: 1.1728, 95% CI:1.0613-1.2961, P=0.0018). The analyses did not reveal any pleiotropy or heterogeneity.
CONCLUSION: Our study revealed possible evidence for a bidirectional causal relationship between GERD and COPD. Implementing screening and preventive strategies for GERD in individuals with COPD, and vice versa, will be crucial in future healthcare management. Further studies are needed to elucidate the mechanisms underlying the causal relationship between GERD and COPD.
1,263,873. Glycol methacrylate polymer hydrogels. CESKOSLOVENSKA AKADEMIE VED. 9 Jan., 1970 [14 Jan., 1969], No. 1152/70. Headings C3C and C3P. Glycol methacrylate polymer hydrogels are prepared by polymerizing a monomer mixture containing a glycol monomethacrylate and less than 2% by weight of a cross-linking comonomer in the presence of up to 35% by weight, based on the monomer mixture, of a filler which is a glycol methacrylate polymer crosslinked with at least 2%, by weight of the polymer, of a cross-linking comonomer component and which consists of rounded discrete particles having grain size of 0À1-100 Á. The monomer mixture may optionally be prepolymerized or thickened with a soluble non-cross-linked glycol monomethacrylate polymer. Polymerization of the mixture may be effected with initiators such as diisopropyl percarbonate, t-butyl peroctoate, dibenzoyl peroxide, ammonium persulphate, azobisisobutyronitrile, and redox (e.g. peroxide-cobalt naphthenate) systems. In examples mixtures of (a) ethylene glycol mono- and di-methacrylates and (b) diethylene glycol mono- and di-methacrylates are polymerized with corresponding polymers of higher diester content as filler. Polymerization in some cases is effected in the presence of magnesium sulphate crystals, which are subsequently washed out with water to produce a spongy polymer product having pores 300-400 Á in diameter. The hydrogel polymers are suitable for the production of contact lenses and dialysis membranes.
Lidocaine Hydrochloride Injection, USP is a sterile, nonpyrogenic solution of lidocaine hydrochloride in water for injection for parenteral administration in various concentrations with characteristics as follows:

May contain sodium hydroxide and/or hydrochloric acid for pH adjustment. The pH is 6.5 (5.0 to 7.0).

Lidocaine is a local anesthetic of the amide type.

Lidocaine Hydrochloride, USP is chemically designated 2-(diethylamino)-N-(2,6-dimethylphenyl)-acetamide monohydrochloride monohydrate, a white powder freely soluble in water. The molecular weight is 288.82. It has the following structural formula:
Device for controlled release of an active agent (I) comprises (I) dissolved in a non-swollen swellable hydrogel. The concn. of (I) increases from the surface of the device to its core, the conc. gradient being in the form of a continuous sigmoidal curve having a point of inflection. - The device is in the form of a bead with a dia. of O.01-20mm. (I) is a drug. The core of the bead is uniformly loaded with (I) and occupies 1-60% of the radius of the bead. The sigmoidal concn. gradient covers 30-99% of the radius, and the rest (up to 10% of the radius) is at least partially depleted of (I). The concn. of (I) at the surface is no more than 10% of its concn. in the core. The hydrogel is a water-insoluble water-swellable crosslinked polymer.
Participants will have four 20-minute in-lab treatment conditions across two weeks. Within the Attention Bias Modification control sessions, participants will be presented with a fixation cross for 500 ms. The fixation cross will then be replaced with a word pair consisting of either a threat/neutral pair or a neutral/neutral word for 500 ms, followed by a probe in the location of one of the two words (80% threat/neutral pairs, 20% neutral/neutral pairs; the target appears in the location of the neutral word in 50% of the trials. Complete Stroop and 3-back task, etc.
<P>PROBLEM TO BE SOLVED: To provide an extracting means for ensuring a yield very close to 24.2%, the fucose content Nemacystus decipiens naturally has, by increasing extraction efficiency of fucose from the raw material Nemacystus decipiens by leaps and bounds.  <P>SOLUTION: The method comprises extracting fucoidan from powdery products obtained by crushing and processing dried Nemacystus decipiens. The powder Nemacystus decipiens obtained by crushing and processing the dried Nemacystus decipiens is kneaded with water 25 times the weight thereof and the kneadate is boiled with agitation in an agitating hot-water extractor or a high-pressure extraction pot for 60-120 min at 80-90°C after adding an appropriate amount of water (diluted with an alcohol as occasion demands). The boiled product is transferred to an alcohol extraction tank, cleared of the alcohol and subjected to filtration and extraction to give a stock solution. The stock solution is subjected to separative purification by an ultrahigh-speed centrifuge and is subsequently concentrated by 4-8 times by a concentration machine to give a fucoidan-containing concentrated liquid. The fucose content in the fucoidan-containing concentrated liquid manufactured by the method corresponds to the yield of 21.6% based on the weight of the raw material powder Nemacystus decipiens used.  <P>COPYRIGHT: (C)2005,JPO&NCIPI
Excessive neuroinflammation mediated by microglia has a detrimental effect on the progression of ischemic stroke. Eriocalyxin B (EriB) was found with a neuroprotective effect in mice with Parkinson's disease via the suppression of microglial overactivation. This study aimed to investigate the roles of EriB in permanent middle cerebral artery occlusion (pMCAO) mice. The pMCAO was induced in the internal carotid artery of the mice by the intraluminal filament method, and EriB (10 mg/kg) was administered immediately after surgery by intraperitoneal injection. The behavior score, 2,3,5-triphenyltetrazole chloride staining, Nissl staining, TUNEL, immunohistochemistry, immunofluorescence, PCR, ELISA, and immunoblotting revealed that EriB administration reduced brain infarct and neuron death and ameliorated neuroinflammation and microglia overactivation in pMCAO mice, manifested by alterations of TUNEL-positive cell numbers, ionized calcium binding adaptor molecule 1 (Iba-1)-positive cell numbers, and expression of tumor necrosis factor-α, interleukin 6, IL-1β, inducible nitric oxide synthase, and arginase 1. In addition, EriB suppressed ischemia-induced activation of nuclear factor kappa B (NF-κB) signaling in the brain penumbra, suggesting the involvement of NF-κB in EriB function. In conclusion, EriB exerted anti-inflammatory effects in ischemia stroke by regulating the NF-κB signaling pathway, and this may provide insights into the neuroprotective effect of EriB in the treatment of ischemic stroke.
INTRODUCTION: Traumatic cardiac arrest (TCA) is a severe condition with a high mortality rate, and patients who survive from TCA face a poor prognosis due to post-resuscitation injury, including cardiac and cerebral injury, which remains a serious challenge. Sodium octanoate has shown protective effects against various diseases. The present study aims to investigate sodium octanoate's protective effects against cardiac and cerebral injury after TCA in a porcine model.
METHODS: The study included a total of 22 male domestic pigs divided into three groups: Sham group (n = 7), TCA group (n = 7), and sodium octanoate (SO) group (n = 8). Hemorrhage was initiated via the right femoral artery by a blood pump at a rate of 2 ml·kg-1·min-1 to establish TCA model. The Sham group underwent only endotracheal intubation and arteriovenous catheterization, without experiencing the blood loss/cardiac arrest/resuscitation model. At 5 min after resuscitation, the SO group received a continuous sodium octanoate infusion while the TCA group received the same volume of saline. General indicators were monitored, and blood samples were collected at baseline and at different time points after resuscitation. At 24 h after resuscitation, pigs were sacrificed, and heart and brain were obtained for cell apoptosis detection, iron deposition staining, oxidative stress detection, and the expression of ferroptosis-related proteins (ACSL4 and GPX4).
RESULTS: Sodium octanoate significantly improved mean arterial pressure, cardiac output and ejection fraction induced by TCA. Serum biomarkers of cardiac and cerebral injury were found to increase at all time points after resuscitation, while sodium octanoate significantly reduced their levels. The apoptosis rates of cardiomyocytes and cerebral cortex cells in the SO group were significantly lower than in the TCA group, along with a reduced area of iron deposition staining. The sodium octanoate also reduced oxidative stress and down-regulated ferroptosis which was indicated by protein level alteration of ACSL4 and GPX4.
CONCLUSION: Our study's findings suggest that early infusion of sodium octanoate significantly alleviates post-resuscitation cardiac and cerebral injury in a porcine model of TCA, possibly through inhibition of cell apoptosis and GPX4-mediated ferroptosis. Therefore, sodium octanoate could be a potential therapeutic strategy for patients with TCA.
Henoch-Schoenlein purpura nephritis (HSPN) with massive proteinuria,renal insufficiency and crescent formation at onset have high risks of progressing to end stage renal failure. Though clinical studies have shown that steroids in combination with cyclophosphamide could reduce proteinuria and preserve renal function, this protocol is associated with many side effects, and is not effective in some patients.

Recent studies have shown that mycophenolic acid(MPA), the active metabolite of mycophenolate mofetil(MMF),could inhibit multifarious effects on endothelial cells, including adhesion molecular expression, neutrophil attachment,IL-6 secretion, and the process of angiogenesis, which contribute to the efficacy of MMF in the treatment of vasculitis. Clinical studies also showed that MMF was effective in the treatment of lupus nephritis with vasculitic lesions. These findings suggest that MMF might be effective in the treatment of severe HSPN, which is a kind of vasculitic lesion. This prospective open-labeled clinical trial study investigates the efficiency of MMF in the treatment of severe HSPN compared with pulse intravenous cyclophosphamide. After 12 months of treatment, we will assess the efficacy, safety, tolerability and relapse of MMF compared with cyclophosphamide in the treatment of severe HSPN.
As a widespread global issue, protein deficiency hinders development and optimal growth in offspring. Maternal low-protein diet influences the development of age-related diseases, including sarcopenia, by altering the epigenome and organ structure through potential increase in oxidative stress. However, the long-term effects of lactational protein restriction or postnatal lifelong protein restriction on the neuromuscular system have yet to be elucidated. Our results demonstrated that feeding a normal protein diet after lactational protein restriction did not have significant impacts on the neuromuscular system in later life. In contrast, a lifelong low-protein diet induced a denervation phenotype and led to demyelination in the sciatic nerve, along with an increase in the number of centralised nuclei and in the gene expression of atrogenes at 18 months of age, indicating an induced skeletal muscle atrophy. These changes were accompanied by an increase in proteasome activity in skeletal muscle, with no significant alterations in oxidative stress or mitochondrial dynamics markers in skeletal muscle later in life. Thus, lifelong protein restriction may induce skeletal muscle atrophy through changes in peripheral nerves and neuromuscular junctions, potentially contributing to the early onset or exaggeration of sarcopenia.
Accurate delineation of key waveforms in an ECG is a critical step in extracting relevant features to support the diagnosis and treatment of heart conditions. Although deep learning based methods using segmentation models to locate P, QRS, and T waves have shown promising results, their ability to handle arrhythmias has not been studied in any detail. In this paper we investigate the effect of arrhythmias on delineation quality and develop strategies to improve performance in such cases. We introduce a U-Net-like segmentation model for ECG delineation with a particular focus on diverse arrhythmias. This is followed by a post-processing algorithm which removes noise and automatically determines the boundaries of P, QRS, and T waves. Our model has been trained on a diverse dataset and evaluated against the LUDB and QTDB datasets to show strong performance, with F1-scores exceeding 99% for QRS and T waves, and over 97% for P waves in the LUDB dataset. Furthermore, we assess various models across a wide array of arrhythmias and observe that models with a strong performance on standard benchmarks may still perform poorly on arrhythmias that are underrepresented in these benchmarks, such as tachycardias. We propose solutions to address this discrepancy.
BACKGROUND: Dietary patterns and lifestyle factors can influence the intensity of systemic inflammation and, consequently, the development and progression of coronary artery calcification (CAC). This study aimed to explore the relationship between the inflammatory potentials of diet and lifestyle, as captured by novel dietary and lifestyle inflammation scores (DIS and LIS), with CAC incidence and progression.
METHODS: We analyzed data on 5949 Black and White men and women ≥ 45 years old participating in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort. Baseline data on diet and lifestyle factors were collected from 2000 to 2002 and used to construct the DIS and LIS, which reflect the overall inflammatory potential of diet and lifestyle. Cox proportional hazard regression was used to calculate the hazard ratios (HR) and 95% confidence intervals (95% CI) for CAC incidence and progression across quartiles of DIS and LIS, adjusting for potential confounders.
RESULTS: Over a median follow-up of 8.0 years, among 2638 participants with zero CAC score at baseline, 977 individuals developed positive scores, and 1681 out of 2561 participants showed CAC progression. For individuals in the highest (more pro-inflammatory) compared to the lowest (more anti-inflammatory) quartiles of the LIS, the multivariable-adjusted HR for CAC incidence was 1.35 (95% CI, 1.10-1.65; P trend < 0.002). This association was stronger among younger adults aged < 60 years compared to those aged ≥ 60 years, with respective values of 1.76 (1.34-2.30) and 1.02 (0.78-1.35) (P interaction < 0.001). However, the LIS was not significantly associated with the progression of existing CAC. Among the components of the LIS, a body mas index (BMI) ≥ 25 kg/m2 and current smoking were significant predictors for the incidence and progression of CAC, respectively. No significant association was found between DIS and CAC incidence and progression.
CONCLUSIONS: Lifestyle factors, through their impact on systemic inflammation, may be associated with a higher risk of CAC incidence in middle and late adulthood.
Placebo (glucose 5%) will also be administered with a loading dose and continuous infusion (in equal amounts of fluid as in experimental arm) by intravenous or gastro-intestinal infusion. The treatment protocol will be equal to the protocol in the doxapram arm.
Renal hemangioblastoma (HB) is a rare subset of HBs arising outside of the central nervous system (CNS), with its molecular drivers remaining entirely unknown. There were no significant alterations detected in previous studies, including von Hippel-Lindau gene alterations, which are commonly associated with CNS-HB. This study aimed to determine the real molecular identity of renal HB and better understand its relationship with CNS-HB. A cohort of 10 renal HBs was submitted for next-generation sequencing technology. As a control, 5 classic CNS-HBs were similarly analyzed. Based on the molecular results, glycoprotein nonmetastatic B (GPNMB) immunohistochemistry was further performed in the cases of renal HB and CNS-HB. Mutational analysis demonstrated that all 10 renal HBs harbored somatic mutations in tuberous sclerosis complex 1 ( TSC1 , 5 cases), TSC2 (3 cases), and mammalian target of rapamycin (2 cases), with the majority classified as pathogenic or likely pathogenic. The CNS-HB cohort uniformly demonstrated somatic mutations in the von Hippel-Lindau gene. GPNMB was strong and diffuse in all 10 renal HBs and completely negative in CNS-HBs, reinforcing the molecular findings. Our study reveals a specific molecular hallmark in renal HB, characterized by recurrent TSC/mammalian target of rapamycin mutations, which defines it as a unique entity distinct from CNS-HB. This molecular finding potentially expands the therapeutic options for patients with renal HB. GPNMB can be considered for inclusion in immunohistochemical panels to improve renal HB identification.
<P>PROBLEM TO BE SOLVED: To provide a method for preparing a chimeric animal by which a xenogeneic specific binding protein can be produced in a host of a living body other than a human by immunizing the host with a suitable antigen.  <P>SOLUTION: The mammalian host other than the human is characterized by an endogenous Ig locus and a functional human Ig locus inactivated for a response to an antigen and produces a human antibody or its analog. The host is prepared by multi-stage genetic modification of an embryonic cell in conjunction with breeding. Different strategies are adopted for random recombination of a human genetic locus or analogous recombination of the host locus. Thereby, the chimeric and transgenic mammal having a large xenogeneic DNA segment stably incorporated therein, especially a mouse is obtained by fusion of a yeast spheroplast having a YAC (yeast artificial chromosome) having the xenogeneic DNA segment and a selective marker such as HPRT (human hypoxanthine phosphoribosyl transferase) with an embryonic stem cell.  <P>COPYRIGHT: (C)2007,JPO&INPIT
D-peptidic compounds that specifically bind to VEGF are provided. Also provided are multivalent D-peptidic compounds that include two or more of the domains connected via linking components. The multivalent (e.g., bivalent, trivalent, tetravalent, etc.) compounds can include multiple distinct domains that specifically bind to different binding sites on a target protein to provide for high affinity binding to, and potent activity against, the VEGF target protein. D-peptidic GA and Z domains that find use in the multivalent compounds are also provided, which polypeptides have specificity-determining motifs (SDM) for specific binding to VEGF (e.g., VEGF-A). Since the target protein is homodimeric (e.g., VEGF-A), the D-peptidic compounds may be similarly dimeric, and include a dimer of multivalent (e.g., bivalent) D-peptidic compounds. Also provided are methods for treating a disease or condition associated with VEGF or angiogenesis in a subject such as age-related macular degeneration (AMD) or cancer.
OBJECTIVE: To explore the genetic etiology for a child with Progressive external ophthalmoplegia with mitochondrial DNA deletions, autosomal dominant 6 (PEOA6).
METHODS: A child who had attended the Women and Children's Hospital Affiliated to Ningbo University on 7 August, 2023 was selected as the study subject. Clinical data of the child were analyzed retrospectively. The child and her parents were subjected to whole exome sequencing (WES), and candidate variant was verified by Sanger sequencing and bioinformatic analysis. This study was approved by the Women and Children's Hospital Affiliated to Ningbo University (Ethics No. EC2020-048).
RESULTS: The child, a 7-year-old female, had presented with limb muscle pain, amyosthenia, significantly increased creatine kinase, congenital diaphragmatic hernia and recurrent respiratory tract infections. WES revealed that the she has harbored a heterozygous c.1590G>C (p.L530F) variant of the DNA2 gene, which was verified to have a de novo origin by Sanger sequencing. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), the c.1590G>C was rated as a likely pathogenic variant (PS2+PM2_Supporting+PP3).
CONCLUSION: The c.1590G>C (p.L530F) variant of the DNA2 gene probably underlay the PEOA6 in this child.
We investigators have been working on the development of a closed loop (artificial endocrine pancreas) insulin and glucagon infusion system since 2005 and are part of the Juvenile Diabetes Research Foundation Artificial Pancreas Consortium. As part of our studies, we give small doses of glucagon to prevent hypoglycemia. As we assessed the success and failure of glucagon administration during these studies, we found the use of glucagon reduced the frequency of hypoglycemia by about 75%. However, the fact that approximately 25% of administrations of glucagon are ineffective remains a concern.

The primary question to be addressed by this study is, in the setting of low dose subcutaneous glucagon administration, how do plasma glucagon and plasma insulin quantitatively interact? In other words, as the rate of insulin administration is increased, how much more glucagon is necessary to overcome the effect of insulin to prevent hypoglycemia? This study is designed to address this question. Subjects will be brought in to a Legacy Hospital for four 10 hour experiments on each of four separate days. On each study day, there will be a continuous infusion of a different rate of IV Regular insulin in order to achieve different steady state free insulin levels. At each insulin level, there will be four subcutaneous glucagon doses given. Octreotide will be infused by IV at a constant rate to suppress endogenous production of glucagon. A stable glucose isotope will also be infused to allow for measurement of hepatic glucose production and glucose turnover. Arterialized venous blood glucose will be measured by the HemoCue Glucose 201 Analyzer.
The invention relates to an immunological adsorber for treating inflammations, in particular for eliminating complement factors, and, optionally, additional sepsis-mediators, such as, TNF and interleukins from body fluids. The invention also relates to a method for the production and use of said immunological adsorber.  The aim of the invention is to develop a modular immunoadsorption system, in particular for extracorporal detoxification, which enables plasma and tissue levels, which are specific to the patient, to be reduced.  The inventive immunological adsorber consists of organic or synthetic polymer support materials whereon polyclonal and monoclonal antibodies are connected which are oriented counter to the complement factor C3a and/or C5a. In a preferred embodiment, other antibodies which are oriented counter to the additional inflammation mediators, are connected to the support. In a particularly advantageous embodiment, the invention relates to an immunoadsorber provided with antibodies against C5a and IL6.