anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
OBJECTIVE: Our research objective was to validate and contribute further evidence to the studies regarding large for gestational age and birthweight percentile by examining oral glucose tolerance test and glycosylated hemoglobin levels in both healthy women and those with gestational diabetes mellitus.
METHODS: This retrospective cohort study was conducted at a tertiary care hospital involving 106 women who delivered at gestational week 36 or later between February 2022 and February 2023. Maternal, obstetric, and neonatal data were collected from the participant's medical records. Large for gestational age and non-large for gestational age groups were compared. Correlation analysis was used to determine associations among oral glucose tolerance test, glycosylated hemoglobin levels, and the birthweight percentile.
RESULTS: Mothers of neonates in the large for gestational age category had higher body mass indexes before pregnancy (p=0.002) and delivery (p=0.003), as well as a higher incidence of gestational diabetes mellitus (p=0.027). Mothers of male large for gestational age infants had higher fasting plasma glucose and glycosylated hemoglobin levels compared to male non-large for gestational age infants (p=0.007 and p=0.004, respectively). There was a weak positive correlation between fasting plasma glucose levels and birthweight percentile in the overall group (r=0.342, p<0.006). Further analysis by gender showed a weak positive correlation between birthweight percentile and fasting plasma glucose and glycosylated hemoglobin values in male newborns (r=0.393, p=0.004 and r=0.373, p=0.006, respectively).
CONCLUSION: Our study has established a clear association between the birthweight percentile in male infants and the levels of glycosylated hemoglobin and fasting plasma glucose measured during oral glucose tolerance test. It is imperative to devise potential strategies aimed at achieving optimal glycosylated hemoglobin and fasting plasma glucose parameters to effectively reduce the frequency of large for gestational age in male infants.
There have been postmarketing reports of acute pancreatitis in patients taking saxagliptin. In a cardiovascular outcomes trial enrolling participants with established atherosclerotic cardiovascular disease (ASCVD) or multiple risk factors for ASCVD (SAVOR trial), cases of definite acute pancreatitis were confirmed in 17 of 8240 (0.2%) patients receiving saxagliptin compared to 9 of 8173 (0.1%) receiving placebo. Preexisting risk factors for pancreatitis were identified in 88% (15/17) of those patients receiving saxagliptin and in 100% (9/9) of those patients receiving placebo.

  


After initiation of saxagliptin, observe patients for signs and symptoms of pancreatitis. If pancreatitis is suspected, promptly discontinue saxagliptin and initiate appropriate management. It is unknown whether patients with a history of pancreatitis are at increased risk for the development of pancreatitis while using saxagliptin.
Patients allocated to the intervention group will receive carvedilol 6.25 mg twice daily, then increased to 12.5 mg twice daily, until maximum dose of 25 mg twice daily according to the patients' tolerance; The dosis increments will occur every 5 days. If after the increment the patient develops bradycardia or hypotension, the dose will be reduced to the maximum tolerated dose. Carvedilol will ideally be maintained for up to 30 days after the end of chemotherapy.
INTRODUCTION: Among children who suffer from acute recurrent pancreatitis (ARP) or chronic pancreatitis (CP), acute pancreatitis (AP) episodes are painful, often require hospitalization, and contribute to disease complications and progression. Despite this recognition, there are currently no interventions to prevent AP episodes. In this retrospective cohort study, we assessed the impact of pancreatic enzyme therapy (PERT) use on clinical outcomes among children with pancreatic-sufficient ARP or CP.
METHODS: Children with pancreatic-sufficient ARP or CP in the INSPPIRE-2 cohort were included. Clinical outcomes were compared for those receiving vs not receiving PERT, as well as frequency of AP before and after PERT. Logistic regression was used to study the association between development of AP episodes after starting PERT and response predictors.
RESULTS: Among 356 pancreatic-sufficient participants, 270 (76%) had ARP, and 60 (17%) received PERT. Among those on PERT, 42% did not have a subsequent AP episode, during a mean 2.1 years of follow-up. Children with a SPINK1 mutation ( P = 0.005) and those with ARP (compared with CP, P = 0.008) were less likely to have an AP episode after starting PERT. After initiation of PERT, the mean AP annual incidence rate decreased from 3.14 down to 0.71 ( P < 0.001).
DISCUSSION: In a retrospective analysis, use of PERT was associated with a reduction in the incidence rate of AP among children with pancreatic-sufficient ARP or CP. These results support the need for a clinical trial to evaluate the efficacy of PERT to improve clinical outcomes among children with ARP or CP.
The neuronal excitotoxicity that follows reoxygenation after a hypoxic period may contribute to epilepsy, Alzheimer's disease, Parkinson's disease and various disorders that are related to inadequate supplement of oxygen in neurons. Therefore, counteracting the deleterious effects of post-hypoxic stress is an interesting strategy to treat a large spectrum of neurodegenerative diseases. Here, we show that the expression of the key telomere protecting protein Trf2 decreases in the brain of mice submitted to a post-hypoxic stress. Moreover, downregulating the expression of Terf2 in hippocampal neural cells of unchallenged mice triggers an excitotoxicity-like phenotype including glutamate overexpression and behavioral alterations while overexpressing Terf2 in hippocampal neural cells of mice subjected to a post-hypoxic treatment prevents brain damages. Moreover, Terf2 overexpression in culture neurons counteracts the oxidative stress triggered by glutamate. Finally, we provide evidence that the effect of Terf2 downregulation on excitotoxicity involves Sirt3 repression leading to mitochondrial dysfunction. We propose that increasing the level of Terf2 expression is a potential strategy to reduce post-hypoxic stress damages.
OBJECTIVE: Approximately 3 million Americans served in the armed forces during the Vietnam War. Veterans have a higher incidence rate of lung cancer compared with the general population, which may be related to exposures sustained during service. Agent Orange, one of the tactical herbicides used by the armed forces as a means of destroying crops and clearing vegetation, has been linked to the development of several cancers including non-small cell lung cancer. However, traditional risk models of lung cancer survival and recurrence often do not include such exposures. We aimed to examine the relationship between Agent Orange exposure and overall survival and disease recurrence for surgically treated stage I non-small cell lung cancer.
METHODS: We performed a retrospective cohort study using a uniquely compiled dataset of US Veterans with pathologic I non-small cell lung cancer. We included adult patients who served in the Vietnam War and underwent surgical resection between 2010 and 2016. Our 2 comparison groups included those with identified Agent Orange exposure and those who were unexposed. We used multivariable Cox proportional hazards and Fine and Gray competing risk analyses to examine overall survival and disease recurrence for patients with pathologic stage I disease, respectively.
RESULTS: A total of 3958 Vietnam Veterans with pathologic stage I disease were identified (994 who had Agent Orange exposure and 2964 who were unexposed). Those who had Agent Orange exposure were more likely to be male, to be White, and to live a further distance from their treatment facility (P < .05). Tumor size distribution, grade, and histology were similar between cohorts. Multivariable Cox proportional hazards modeling identified similar overall survival between cohorts (Agent Orange exposure hazard ratio, 0.97; 95% CI, 0.86-1.09). Patients who had Agent Orange exposure had a 19% increased risk of disease recurrence (hazard ratio, 1.19; 95% CI, 1.02-1.40).
CONCLUSIONS: Veterans with known Agent Orange exposure who undergo surgical treatment for stage I non-small cell lung cancer have an approximately 20% increased risk of disease recurrence compared with their nonexposed counterparts. Agent Orange exposure should be taken into consideration when determining treatment and surveillance regimens for Veteran patients.
Treatment of damaged, diseased, abnormal, obstructive, cancerous or undesired tissue (e.g. a tumor, a benign tumor, a malignant tumor, a cyst, or an area of diseased tissue, etc) is provided by delivering specialized pulsed electric field (PEF) energy to target tissue areas in a specific dose so as to obtain a superior outcome. The PEF energy and delivery has been optimized to provide advanced treatment of target tissue areas, including destruction of undesired tissue and generation of improved inflammatory and immune responses. These various types of treatment are controlled by a variety of factors including the electrode geometry, the dose of PEF energy delivered, the time the energy is delivered over, and the waveform of the PEF energy itself. The PEF energy is delivered in the form a dose which is considered to be one application of the specialized energy. Each dose creates a lesion in the target tissue area.
PURPOSE:To obtain a detergent composition for dentures, capable of changing color tone of a detergent solution in a short time even under neutral condition, informing a user about completion of washing and capable of imparting excellent feeling of use without sliminess, by blending laccaic acid with an oxidizing agent. CONSTITUTION:The aimed substance obtained by using and blending laccaic acid which is one kind of natural anthraquinone derivatives and extracted from a female of an insect Laccifer lacca (lac insect) with a peroxide based oxidizing agent (e.g. potassium monoperhydrogensulfate) and, as necessary, using and blending other coloring matters, alkalinizing agents, neutralizing agents, surfactants, binders, enzymes, perfumes, etc. The laccaic acid is blended in an amount of 30ppm-0.2wt.% based on the total amount of the ingredients in the detergent composition for dentures. The above-mentioned composition is prepared in the form of a solid, such as powder, granule or tablet, and used by dissolving in water in use. The pH of the detergent solution is preferably 5.5-7.5 in aspects of feeling of use.
Iron overload occurs due to excessive iron intake compared to the body's demand, leading to iron deposition and impairment of multiple organ functions. Our previous study demonstrated that chronic oral administration of ferric citrate (FC) caused colonic inflammatory injury. However, the precise mechanism underlying this inflammatory response remains unclear. The current study aims to investigate the mechanism by which iron overload induced by FC exposure leads to colonic inflammation. To accomplish this, mice were orally exposed to three different concentrations of FC (71 mg/kg/bw (L), 143 mg/kg/bw (M) and 286 mg/kg/bw (H)) for continuous 16 weeks, with the control group receiving ultrapure water (C). Exposure to FC caused disturbances in the excretory system, altered colonic flora alpha diversity, and enriched pathogenic bacteria, such as Mucispirillum, Helicobacter, Desulfovibrio, and Shigella. These changes led to structural disorders of the colonic flora and an inflammatory response phenotype characterized by inflammatory cells infiltration, atrophy of intestinal glands, and irregular thickening of the intestinal wall. Mechanistic studies revealed that FC-exposure activated the NF-κB signaling pathway by up-regulating TLR4, MyD88, and NF-κB mRNA levels and protein expression. This activation resulted in increased production of pro-inflammatory cytokines, further contributing to the colonic inflammation. Additionally, in vitro experiments in SW480 cells confirmed the activation of NF-κB signaling pathway by FC exposure, consistent with the in vivo findings. The significance of this study lies in its elucidation of the mechanism by which iron overload caused by FC exposure leads to colonic inflammation. By identifying the role of pathogenic bacteria and the NF-κB signaling pathway, this study could potentially offer a crucial theoretical foundation for the research on iron overload, as well as provide valuable insights for clinical iron supplementation.
Placebo plus gemcitabine ('Placebo') Placebo was administered on Day 1 of Weeks 1 through 7 during the first cycle and on Day 1 of Weeks 1 through 3 of subsequent cycles. Gemcitabine was administered by i.v. infusion at an initial dose of 1000 mg/m2 once weekly for up to 7 weeks (or until toxicity necessitated reducing or holding a dose), followed by a week of rest from treatment. Subsequent cycles consisted of infusions once weekly for 3 consecutive weeks, followed by a week of rest from treatment.
FIELD: medicinal cosmetology, particularly, creams of special purpose. SUBSTANCE: composition for skin treatment contains vegetable and vaseline oils, wax, glycerine, antioxidant, flavoring, conserving agent, and water. Said composition may additionally comprise stearamide ether of carboxylic acid, glycerinemonostearate, cetyl alcohol, polyethylsiloxane, aloe-vera, D-pantenol, allantoin, tocopherol acetate, ethylenediaminetetraacetate disodium salt and sodium hydroxide. The composition does not cause appearance of skin nodules or depigmentation in place of skin treatment after dermabrasion. EFFECT: higher efficiency. 1 cl, 3 ex
This intervention is Individualized Computer Based Cognitive Remediation (ICBCR) and skills development group (SDG). Participants receive 15 weeks of computerized training (with intake, 15 and 30 week assessments). This intervention relies upon intense, frequent, repetition of tasks being made incrementally more challenging. Computer tasks are organized so that the initial trials are easily completed and more challenging levels are then attempted. Parameters such as duration of task, task speed, and intra-task variables all be are manipulated. A trainer will be present at each session to help set up the computer tasks and answer questions. Besides the first two sessions that will be orientation sessions, the trainer has little involvement during the training sessions. The role of the trainer is to help organize, support, and provide feedback to each participant. All subjects randomized to this condition also are receiving the weekly skills group (SDG).
Nearly one third of 700,000 military personnel deployed during Desert Shield and Desert Storm (Aug 2, 1990 to July 31, 1991) in the Kuwaiti War Theater are suffering from Gulf War Illness (GWI), an unexplained chronic illness characterized by multiple symptoms. The illness has taken a heavy toll on deployed Veterans' overall quality of life. Recent research has revealed the host gut microbiome's role in gastrointestinal disturbance, systemic inflammation, and neurotrophic abnormalities in Gulf War Illness mouse models. Also, short-chain fatty acids such as butyrate restored a healthy microbiome and improved gut microbial metabolism apart from attenuating GWI symptom persistence in preclinical studies. Butyrate, a nutraceutical endogenously produced in the host gut following bacterial fermentation, has shown promise in gastrointestinal disturbances such as irritable bowel syndrome (IBS) and Inflammatory bowel disease (IBD).

This is a randomized, two-group, double-blind, placebo-controlled, Phase II clinical trial. The treatment group will receive microencapsulated butyrate capsules (600 mg twice a day for 18 weeks). The placebo group will receive a matching placebo formulation twice a day for 18 weeks. However, after two weeks of the treatment (20 weeks) there will be a follow up virtual visits. The primary outcome measure for this clinical trial is a change from baseline of VSF-36 and CVLT III test scores with respect to physical and mental functioning and symptoms. The secondary outcome measures include changes from baseline of host-microbiome signature, intestinal permeability assessment, peripheral pro-inflammatory biomarkers, and GWI-associated symptoms IBS, chronic pain, fatigue, sleep issues, and cognitive impairment.
These invention relates to metal-complexing, cysteine-free peptides which may be coupled to an organ-specific probe directly or via a linker and are thus enriched as conjugates specifically in tumors, organs, tissues or centers of inflammation. The organ-specific probes used are, for example, antibodies or part-sequences of antibodies against tumor-associated antigens, e.g. the carcino-embryonal antigen (CEA, which are thus specifically enriched in tumors. The invention also relates to processes for producing the metal-complexing cysteine-free peptides and their conjugates. The present invention also relates to the use of the conjugates as components of a kit for in vivo diagnosis or in vivo therapy and radio-pharmaceuticals containing these conjugates together with radio-isotopes. The organ-specific conjugates are used to image tumors, organs or centers of inflammation.
Research participants in the cognitive intervention group will undergo a baseline neuropsychological evaluation. One week later, they will receive the online training program (brainHQ by Posit Science) three times a week for 45 minutes for a total of 12 weeks. This group will return one week after completing the online intervention program for their follow-up neuropsychological evaluation. They will then return again one year later for another follow-up neuropsychological evaluation.
Participants will take Empagliflozin (10 mg OD) and matching placebo to Finerenone (OD). for up to 180 days.
Microdamage and its related inflammation contribute to the development of radiographic axial spondyloarthritis (r-axSpA). Inflammation and cell death in damaged tissues are associated with cell-free DNA (cfDNA) release. Here we investigated whether circulating cfDNA could be a potential biomarker for evaluating disease activity and treatment response in r-axSpA. Circulating cfDNA was detected in the discovery and validation cohort with 79 and 60 newly diagnosed r-axSpA patients respectively and 42 healthy controls using the Quant-iT PicoGreen dsDNA reagent and kit. As a result, cfDNA levels were significantly higher in r-axSpA patients compared with healthy controls in the discovery and validation cohort. Moreover, cfDNA levels were positively correlated with CRP, ASDAS-CRP and neutrophil counts. Additionally, non-steroid anti-inflammatory drugs (NSAIDs) combined with disease-modifying anti-rheumatic drugs or tumor necrosis factor inhibitors but not NSAIDs alone could reduce cfDNA levels. Moreover, a decrease of cfDNA levels after treatment was associated with an effective therapeutic response. Intriguingly, patients with higher levels of cfDNA at diagnosis responded better to combination therapy rather than NSAIDs. However, patients with lower levels of cfDNA displayed similar responses to combination or mono-NSAID treatment. In conclusion, circulating cfDNA levels showed a significant correlation with disease activity as well as treatment efficacy in patients with r-axSpA. Moreover, cfDNA at diagnosis might predict the response to different therapy. Consequently, cfDNA may serve as a useful biomarker of inflammation in r-axSpA.
TNF-α-induced protein 3 (TNFAIP3), commonly referred to as A20, is an integral part of the ubiquitin-editing complex that significantly influences immune regulation, apoptosis, and the initiation of diverse immune responses. The A20 protein is characterized by an N-terminal ovarian tumor (OTU) domain and a series of seven zinc finger (ZNF) domains. Mutations in the TNFAIP3 gene are implicated in various immune-related diseases, such as Behçet's disease, polyarticular juvenile idiopathic arthritis, autoimmune thyroiditis, autoimmune hepatitis, and rheumatoid arthritis. These mutations can lead to a spectrum of symptoms, including, but not limited to, recurrent fever, ulcers, rashes, musculoskeletal and gastrointestinal dysfunctions, cardiovascular issues, and respiratory infections. The majority of these mutations are either nonsense (STOP codon) or frameshift mutations, which are typically associated with immune dysfunctions. Nonetheless, missense mutations have also been identified as contributors to these conditions. These genetic alterations may interfere with several biological pathways, notably abnormal NF-κB signaling and dysregulated ubiquitination. Currently, there is no definitive treatment for A20 haploinsufficiency; however, therapeutic strategies can alleviate the symptoms in patients. This review delves into the mutations reported in the TNFAIP3 gene, the clinical progression in affected individuals, potential disease mechanisms, and a brief overview of the available pharmacological interventions for A20 haploinsufficiency. Mandatory genetic testing of the TNFAIP3 gene should be performed in patients diagnosed with autoinflammatory disorders to better understand the genetic underpinnings and guide treatment decisions.
The application discloses a TOP2A polypeptide ligand, wherein the amino acid sequence of the TOP2A polypeptide ligand is shown as SEQ ID NO. 1. The application also discloses a TOP2A protein degradation agent, which sequentially comprises an E3 ubiquitin ligase ligand, a PEG linker, the TOP2A polypeptide ligand and a membrane penetrating peptide from the N end to the C end. The application also discloses application of the degradation agent in preparing medicines for preventing and/or treating TOP2A mediated diseases. The application also discloses application of the degradation agent in preparing products with any one of the following functions: 1) Degrading TOP2A protein; 2) Inhibit cancer cell proliferation and clonogenic; 3) Inhibit tumor growth. The application also discloses a pharmaceutical composition which comprises the degradation agent and a pharmaceutically acceptable carrier.
Patients with solid tumors receive 17-N-allylamino-17-demethoxygeldanamycin (17-AAG) IV over 60-120 minutes on days 1, 4, 8, and 11. Treatment repeats every 21 days for up to 17 courses in the absence of disease progression or unacceptable toxicity.
The present invention relates to an apparatus, method, and system that provides a personal, portable module that can be used by a pharmacist, pharmacy student, or pharmacy preceptor to more effectively practice. It can be usable by others, including other types of healthcare practitioners. The module is preferably hand-portable and has both input and output features. It can be communicated to another device. It includes software which integrates several practice functions and allows data transfer, both to another device for further use or to the portable module for point of care use. In one aspect of the invention, the system establishes a mechanism to assess the level of cognitive complexity of patient interventions performed by students or practitioners. Another aspect of the invention involves automatic documentation of the intervention. In another aspect of the invention, the system enables data entry and the capture of drug-related problem intervention information, enables treatment guidelines to be incorporated into the point of care.