anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Postoperative delirium (POD) is a common surgical complication. However, the incidence and risk factors associated with postoperative delirium after revision total knee arthroplasty (rTKA) have not been comprehensively explored through extensive national databases.
METHODS: Utilizing the National Inpatient Sample (NIS), the largest comprehensive U.S. hospital healthcare database, we undertook a retrospective investigation involving 127,400 patients who underwent rTKA between 2010 and 2019. We assessed various aspects, including patient demographics, hospital characteristics, pre-existing medical conditions, and perioperative complications.
RESULTS: The overall incidence of postoperative delirium (POD) in patients undergoing rTKA between 2010 and 2019 was 0.97%. The highest incidence rate of 1.31% was recorded in 2013. Notably, this patient cohort demonstrated advanced age, increased burden of co-morbidities, prolonged hospital stays, increased hospitalization costs, and elevated in-hospital mortality rates (P < 0.001). Moreover, non-elective admissions, non-private insurance payments, and a preference for teaching hospitals were commonly observed among these patients. During their hospitalization, individuals who developed delirium subsequent to rTKA were more prone to experiencing certain perioperative complications. These complications encompassed medical issues like acute myocardial infarction, continuous invasive mechanical ventilation, postoperative shock, sepsis, stroke and other medical problems. Additionally, surgical complications including hemorrhage / seroma / hematoma, irrigation and debridement, prosthetic joint infection, periprosthetic fracture, and wound dehiscence / nonunion were noted. Several risk factors were found to be linked with the development of POD. These included advanced age (≥ 75 years), alcohol abuse, coagulation disorders, congestive heart failure, depression, fluid and electrolyte imbalances, and more. Conversely, female sex, having private insurance, and undergoing elective hospitalization emerged as protective factors against POD.
CONCLUSION: Our findings suggest that the general prevalence of POD in rTKA is relatively low according to NIS. There was a significant connection between the POD of rTKA and advanced age, prolonged length of stay (LOS), more in-patients' costs, higher in-hospital mortality rate, increased comorbidities, postoperative medical complications and postoperative surgical complications. This study helps to understand the risk factors associated with POD to improve poor outcomes.
A system for determining an alertness level of a subject is provided that uses a physiological sensor to provide a physiological sensor signal that distinguishes between a sleep state and an awake state of the subject. The sleep period and its associated time to fall asleep and wake up are identified. A single representative sleep interim time is obtained from a plurality of sleep sessions within a 24-hour period, and the circadian phase is estimated using the single representative sleep interim time. The alertness level is then obtained from the circadian phase. The system avoids the need to use a default circadian phase when determining the level of alertness. The system can more accurately estimate drowsiness of individuals with irregular sleep patterns, such as shift workers or people with sleep disorders. A single representative mid-sleep period can also take into account multiple sleep sessions, i.e., snooze or restless sleep periods.
Disclosed herein is a chewable article for oral mucosa delivery of a composition. The chewable system comprises a chewable base with the composition embedded, coated, integrated or dispersed therein. The composition may be pressurized, oxygenated, and/or atomized. The composition may be released as an aerosol. In one embodiment, the chewable system comprises a pressurized capsule that dissolves or ruptures in the mouth to release a burst of the composition. The chewable system may be configured to allow the composition facing to the buccal mucosa.
In this study, reporters just like researchers were in charge of the low-sodium salt intervention. Reporters are responsible for recommended objects and measure their blood pressure personally. By observing personally the change of blood pressure pre and post low-sodium salt intervention, reporters will increase their confidence and come to the conclusion that the low salt diet is an economical way to reduce blood pressure. Those reporters would share their experiment with other people including their colleagues, Hopefully, those reporters that took part in the trial would consciously keep a sustained focus to this topic, thereby retaining a long-time education in mass media.There were two interventions. One is low-sodium salt intervention and the other is informational intervention. Low-sodium salt intervention was carried out on those family members recommended by reporters, and informational intervention. Low-sodium salt intervention was only on the reporters. The evaluation criteria of low-sodium salt intervention is the blood pressure value, and the evaluation criteria of informational intervention are the numbers of related articles in certain newspaper and the awareness of related knowledges in local population.
Homozygous Familial Hypercholesterolemia (HoFH) is a rare genetic metabolic disorder characterized by markedly elevated LDL-cholesterol (LDL-C) levels, resulting in severe atherosclerosis often leading to early onset of cardiovascular disease. The most frequent cause is mutation in the LDL receptor gene (LDLR). LDL-C levels remain frequently above acceptable levels despite treatment with multiple existing lipid lowering drugs and/or LDL apheresis. Thus, the functional replacement of the defective LDLR via AAV-based liver-directed gene therapy may be a viable approach to treat this disease and improve response to current lipid-lowering treatments. The purpose of this protocol is to identify and screen potential candidates for future enrollment in a gene therapy clinical trial. No study drug will be administered in this screening study.
Negative pressure wound therapy (NPWT) is effective in repairing serious skin injury. The dressing used in the NPWT is important for wound healing. In this paper, we develop biodegradable amphiphilic polyurethanes (PUs) and fabricate the PUs into sponges as wound dressings (Bi@e) with Janus pore architectures for NPWT. The Bi@e is adaptive to all the stages of the wound healing process. The Janus Bi@e sponge consists of two layers: the dense hydrophobic upper layer with small pores provides protection and support during negative pressure drainage, and the loose hydrophilic lower layer with large pores absorbs large amounts of wound exudate and maintains a moist environment. Additionally, antibacterial agent silver sulfadiazine (SSD) is loaded into the sponge against Escherichia coli and Staphylococcus aureus with a concentration of 0.50 wt%. The Janus sponge exhibits a super absorbent capacity of 19.53 times its own water weight and remarkable resistance to compression. In a rat skin defect model, the Janus Bi@e sponge not only prevents the conglutination between regenerative skin and dressing but also accelerates wound healing compared to commercially available NPWT dressing. The Janus Bi@e sponge is a promising dressing for the NPWT.
Children are highly vulnerable to the neurotoxic effects of organophosphates (OPs), which can cause neuronal developmental defects, including intellectual disability, autism, epilepsy, and related comorbidities. Unfortunately, no specific pediatric OP neurotoxicity model currently exists. In this study, we developed and characterized a pediatric rat model of status epilepticus (SE) induced by the OP diisopropylfluorophosphate (DFP) and examined its impact on long-term neurological outcomes. Postnatal day 21 rats were exposed to a DFP regimen with standard antidotes. Progressive behavioral deteriorations were assessed over a three-month period. Development of epileptic seizures, ictal discharges, high-frequency oscillations (HFOs), and interictal spikes were monitored by video-electroencephalography recordings. Histology-stereology analysis was performed to assess neurodegeneration, neuroinflammation, and morphologic abnormalities. DFP-exposed, post-SE animals exhibited significantly elevated levels of anxiety and depression than age-matched controls at 1, 2, and 3 months post-exposure. DFP-exposed animals displayed aggressive behavior and a marked decline in object recognition memory, as well as prominent impairment in spatial learning and memory. DFP-exposed animals had striking electrographic abnormalities with the occurrence of displayed epileptic seizures, ictal discharges, HFOs, and interictal spikes, suggesting chronic epilepsy. Neuropathological analysis showed substantially fewer principal neurons and inhibitory interneurons with a marked increase in reactive microglia and neuroinflammation in the hippocampus and other brain regions. DFP-exposed animals also exhibited mossy fiber sprouting indicating impaired network formations. Long-term epileptic seizures and neuropsychiatric functional deficits induced by DFP were consistent with neuropathological defects. Collectively, this pediatric model displays many hallmarks of chronic sequelae reminiscent of children exposed to OPs, suggesting that it will be a valuable tool for investigating pathologic mechanisms and potential treatment strategies to attenuate long-term OP neurotoxicity. SIGNIFICANCE STATEMENT: Millions of children are exposed to organophosphates (OPs) used in agriculture or chemical incidents. This study investigated the long-term impact of neonatal exposure to the OP chemical diisopropylfluorophosphate (DFP) on neurobehavioral and neurodevelopmental outcomes in adulthood. DFP exposure caused long-lasting behavioral abnormalities, epileptic seizures, and bilateral brain defects with an array of neurological sequelae seen in children's OP neurotoxicity. Thus, this model provides a novel tool to explore therapeutic interventions that mitigate long-term neurotoxic effects of children exposed to OP-induced seizures and status epilepticus.
Human insulin (I) was produced by transplanting a human cell capable of producing (I) into any warm-blooded animal other than a human or in a device, esp., a diffusion chamber, which supplies them with the nutrient body fluid directly from warm-blooded animals. The grown cells are then treated with an insulin inducer. Pref. cells which are recommended for use include human Langerhans β- cells, viral trasformed cells, human insuloma cells, lung tumor cells or cell lines established from the latter and lymphoblastoid leukemia hybridomas. Inducers are saccarides, amino acids, peptide hormones, and metal ions. The amt. of (I) prod. per cell under these conditions is 2 - 50 times greater than possible by in vitro tissue cultures.
In 2016/17, the self-management program for cancer survivors, the Cancer Thriving and Surviving Program (CTS) was translated into German. The content of the CTS was adapted to breast cancer specific needs in three interdisciplinary workshops based on a participatory approach including active patient engagement. Additional disease-specific topics were developed and confirmed applying a multi-stakeholder e-rating approach. After a consensus meeting with the participation of breast cancer survivors, health care professional and international experts in the field of self-management, consensus on the program was reached in June 2017, resulting in the CTS-BC-CH program, i.e. a standardized manual for course leaders.

This pilot study aims to explore the reach of the CTS-BC-CH program (integrated into the clinical pathway) and to investigate its preliminary effectiveness for female Swiss breast cancer patients. The CTS-BC-CH is delivered in two breast cancer centers in in the German-speaking part of Switzerland as a group-based program with seven weekly sessions of 2.5 - 3 hours led by trained peer-leaders. Course leaders have to complete a 4-days training provided by certified master trainers. First, participants are enrolled for usual care, followed by participants who will attend the CTS-BC-CH course. Participants will complete self-reported questionnaires at three time points over a period of 6 months.
Marrubium vulgare L. (Lamiaceae) has a long history of use in traditional herbal medicine for the treatment of respiratory tract infections, inflammatory conditions, and pain. This study aimed to investigate the chemical composition, acute toxicity, and antinociceptive effects of the aqueous extract from M. vulgare leaves (AEMV). Antioxidant activity was evaluated using DPPH and reducing power assays. The chemical composition of AEMV was determined through LC-MS/MS, and the levels of total phenolics, flavonoids, and condensed tannins were quantified. Acute oral toxicity was assessed in male Swiss mice with a single oral dose of AEMV (1, 2, 5 g/kg). The analgesic impact was examined through writhing, hot plate, and formalin tests. Our findings not only confirmed the safety of the extract in animal models but also revealed significant antioxidant activity in AEMV. High-performance liquid chromatography (HPLC) analysis identified important bioactive compounds, with marrubiin being a major component. Furthermore, AEMV demonstrated robust antinociceptive properties in all conducted tests, highlighting its potential as a valuable natural source of bioactive compounds suitable for a wide range of therapeutic applications.
The usual care group will receive usual care alone. Usual care will be limited to physical therapy and conventional medication in this study. Usual care will be provided with reference to a list of most frequently used treatments in neck pain-related patients from Korean Health Insurance Review and Assessment (HIRA) 2014 statistics. Frequency and types of physical therapy used will be recorded in a separate electronic case report form for outcome assessor blinding purposes.
Recent studies demonstrate an important role for sub-acute, chronic inflammation in the development of insulin resistance, type 2 diabetes mellitus (T2 DM) and cardiovascular disease (CVD). A broad body of data indicate that obesity and high fat or "Western" diets activate sub-acute inflammatory processes in fat and liver tissue as well as in mononuclear cells. The inflammatory mediators produced by these tissues and cells promote the development of insulin resistance both locally and at distant sites such as skeletal muscle. These same inflammatory mediators may also increase the risk for CVD. Work from our labs indicate that Nuclear Factor-kappa B (NF-kB), an inflammatory master switch for a multitude of proinflammatory genes and pathways, is activated in fat and liver by obesity and high fat diets. We have also noted similar NF-kB activation in monocytes and macrophages in similar conditions of nutritional excess. It has become evident that salicylates inhibit the NF-kB regulatory protein IKKB (inhibitor of Kappa B Kinase) and we have subsequently demonstrated their ability to downregulate NF-kB activation in each of these above tissues in animals. Moreover, by inhibiting the IKKB/NF-kB pathway, salicylates appear to ameliorate insulin resistance and its associated metabolic abnormalities and potentially provide a new approach for pharmacologic treatment of T2 DM as well as individuals with conditions such as impaired glucose intolerance (IGT) to prevent their progression to diabetes. Preliminary results from a two-week trail is T2 DM patients indicated that high-dose aspirin(ASA,\~7g/day) improved glucose metabolism and associated risk factors. While this was as important first step towards proof-of-principle, the risk of severe gastrointestinal bleeding associated with high-dose ASA precludes broader use. Salicylate in its prodrug form of salsalate(Disalcid), is much safer than ASA(as it does not irritate the gastric mucosa nor alter bleeding times). We have now conducted several preliminary short-term in individuals with IGT or T2 DM as well in obese insulin resistant subjects and have demonstrated that salsalate in doses of 3.5-4.5g/d provides similar blood salicylate levels as high dose ASA and induces similar clinical and metabolic benefits over the 2-4 weeks study duration. Therefore, in vitro, animal and human clinical studies all support the concept that inhibiting the IKKB/NF-kB pathway with salsalate is a feasible approach to reducing insulin resistance. This study will more fully characterize the metabolic benefits of high dose salsalate therapy.
Inflammatory bowel disease, a disease featured by intestinal epithelial barrier destruction and dysfunction, has been a constant threat to animal health. The primary objective of this research was to assess the impact of the extract derived from lotus leaves (LLE) on lipopolysaccharide (LPS) induced damage to the intestines in mice, as well as to investigate the fundamental mechanism involved. The LLE was prepared using ultrasonic extraction in this experiment, and the LLE total flavonoid content was 117.02 ± 10.73 mg/g. The LLE had strong antioxidant activity in vitro, as assessed by 2, 2-diphenyl-1-picrylhydrazyl, ferric reducing antioxidant power, and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) methods. In the vivo experiment, different doses of LLE (50, 100, and 200 mg/kg) were administered for 2 weeks before LPS treatment in mice. The results revealed that LLE alleviates intestinal tissue damage in LPS-induced mice. In the jejunum tissue, LLE significantly upregulated mRNA and protein expression levels of tight junction proteins, such as ZO-1, occludin, and claudin-1, and decreased the contents of the inflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. Furthermore, the malondialdehyde and lactate dehydrogenase contents increased by LPS in the liver were significantly reduced after administration of LLE, and the total antioxidant capacity, superoxide dismutase, and reduced glutathione decreased by LPS were remarkably increased by LLE. It was found that LLE could relieve LPS-induced oxidative stress by upregulating mRNA and protein expression of Nrf2 and HO-1 in jejunum tissue. In conclusion, LLE alleviates LPS-induced intestinal damage through regulation of the Nrf2/HO-1 signal pathway to alleviate oxidative stress, reducing inflammatory factors and increasing the expression of tight junction proteins in mice.
A computer-implemented method of training an artificial neural network is provided. The artificial neural network comprises a feedforward autoencoder and a classification layer, the feedforward autoencoder comprising an input layer of neurons, an output layer of neurons, an embedding layer of neurons between the input and output layers, one or more non-linear intermediate layers of neurons between the input and embedding layer, one or more further non-linear intermediate layers of neurons between the embedding and output layer and respective network weights for each layer, wherein the number of neurons in the embedding layer is less than the number of neurons in the input layer. Data units are defined within a data space to have a data value for each dimension of the data space and a classification label associated with each data unit indicating one of a plurality of groups to which each data sample belongs. The network is trained using a combination of unsupervised learning to reduce a reconstruction loss of the autoencoder and supervised learning to reduce a classification loss of the classification layer. The resulting network finds application in providing embeddings for classification or clustering, for example in the context of analysing phenotypical data, such as physiological data, which may be obtained from electronic health records. The classification or clustering may be used to predict or identify pathologies or to analyse patient subgroups to analyse, for example treatment efficacy, outcomes or survival rates or to triage patients in accordance with relevant criteria.
PURPOSE: Temporal lobe epilepsy (TLE) has a high risk of developing drug resistant and cognitive comorbidities. Adenosine has potential anticonvulsant effects as an inhibitory neurotransmitter, but drugs targeting its receptors and metabolic enzyme has inevitable side effects. Therefore, we investigated adenosine augmentation therapy for seizure control and cognitive comorbidities in TLE animals.
METHODS: Using lentiviral vectors coexpressing miRNA inhibiting the expression of adenosine kinase (ADK), we produced ADK--rMSC (ADK knockdown rat mesenchymal stem cell). ADK--rMSC and LV-con-rMSC (rMSC transduced by randomized scrambled control sequence) were transplanted into the hippocampus of TLE rat respectively. ADK-+DPCPX group was transplanted with ADK--rMSC and intraperitoneally injected with DPCPX (adenosine A1 receptor antagonist). Seizure behavior, EEG, CA1 pyramidal neuron apoptosis, and behavior in Morris water maze and novel object recognition test were studied RESULTS: Adenosine concentration in the supernatants of 105 ADK--rMSCs was 13.8 ng/ml but not detectable in LV-con-rMSCs. ADK--rMSC (n = 11) transplantation decreased spontaneous recurrent seizure (SRS) duration compared to LV-con-rMSC (n = 11, P < 0.05). CA1 neuron apoptosis was decreased in ADK--rMSC (n = 3, P < 0.05). ADK--rMSC (n = 11) improved the Morris water maze performance of TLE rats compared to LV-con-rMSC (n = 11, escape latency, P < 0.01; entries in target quadrant, P < 0.05). The effect of ADK--rMSC on neuron apoptosis and spatial memory were counteracted by DPCPX. However, ADK--rMSC didn't improve the performance in novel object recognition test.
CONCLUSION: Adenosine augmentation-based ADK--rMSC transplantation is a promising therapeutic candidate for TLE and related cognitive comorbidities.
Patients receive atezolizumab IV over 30-60 minutes on days 1 and 15. Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity. Patients also undergo CT or MRI and collection of blood samples throughout the trial and undergo tumor biopsy on study.
While changes in RNA splicing have been extensively studied in hepatocellular carcinoma (HCC), no studies have systematically investigated changes in RNA splicing during earlier liver disease. Mouse studies have shown that disruption of RNA splicing can trigger liver disease and we have shown that the splicing factor SRSF3 is decreased in the diseased human liver, so we profiled RNA splicing in liver samples from twenty-nine individuals with no-history of liver disease or varying degrees of non-alcoholic fatty liver disease (NAFLD). We compared our results with three publicly available transcriptome datasets that we re-analyzed for splicing events (SEs). We found many changes in SEs occurred during early liver disease, with fewer events occurring with the onset of inflammation and fibrosis. Many of these early SEs were enriched for SRSF3-dependent events and were associated with SRSF3 binding sites. Mapping the early and late changes to gene ontologies and pathways showed that the genes harboring these early SEs were involved in normal liver metabolism, whereas those harboring late SEs were involved in inflammation, fibrosis and proliferation. We compared the SEs with HCC data from the TCGA and observed that many of these early disease SEs are found in HCC samples and, furthermore, are correlated with disease survival. Changes in splicing factor expression are also observed, which may be associated with distinct subsets of the SEs. The maintenance of these SEs through the multi-year oncogenic process suggests that they may be causative. Understanding the role of these splice variants in metabolic liver disease progression may shed light on the triggers of liver disease progression and the pathogenesis of HCC.