anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PURPOSE: A system and method for processing a medical treatment image is provided to process a medical treatment image without a special knowledge with respect to an image processing. CONSTITUTION: A medical treatment image obtaining server(100) stores a digital medical treatment image being supplied from various kinds of medical treatment image photographing devices such as a CT(Computed Tomography) and an MRI(Magnetic Resonance Imaging). An image processing system(200) is connected to the medical treatment image obtaining server(100) and a plurality of client computers by a TCP/IP. A user interface unit(210) converts an intention of a user being supplied from the client computers into a computer signal, and outputs the signal. An image processing processor(220) performs a program having a medical treatment image control algorithm in accordance with a processing control signal supplied through the user interface unit(210), reads a medical treatment image from a medical treatment image database, performs the user control signal, and outputs a calculated result. An output device(230) receives a signal being supplied from the image processing processor(220) and supplies the signal as a form capable of being recognized by the user.
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease of unknown etiology. The emerging evidence demonstrates that metabolic homeostatic imbalance caused by repetitive injuries of the alveolar epithelium is the potential pathogenesis of IPF. Proteomic analysis identified that Acetyl-CoA synthetase short chain family member 3 (ACSS3) expression was decreased in IPF patients and mice with bleomycin-induced fibrosis. ACSS3 participated in lipid and carbohydrate metabolism. Increased expression of ACSS3 downregulated carnitine palmitoyltransferase 1A (CPT-1A) and resulted in the accumulation of lipid droplets, while enhanced glycolysis which led to an increase in extracellular lactic acid levels in A549 cells. ACSS3 increases the production of succinyl-CoA through propionic acid metabolism, and decreases the generation of acetyl-CoA and ATP in alveolar epithelial cells. Overexpression of Acss3 inhibited the excessive deposition of ECM and attenuated the ground-glass opacity which determined by micro-CT in vivo. In a nutshell, our findings demonstrate that ACSS3 decreased the fatty acid oxidation through CPT1A deficiency and enhanced anaerobic glycolysis, this metabolic reprogramming deactivate the alveolar epithelial cells by lessen mitochondrial fission and fusion, increase of ROS production, suppression of mitophagy, promotion of apoptosis, suggesting that ACSS3 might be potential therapeutic target in pulmonary fibrosis.
Eligible subjects will receive the ICS/LAMA/LABA products twice daily and dosing regimens as prescribed by their physician for a period of 24 weeks. Study treatment may be augmented with other prescribed COPD medications such as including rescue medications, which will be prescribed and obtained according to usual practice.
Single arm with Pembrolizumab 200 mg over 30 minutes IV infusion on Day 1 every 3 weeks until disease progression or inacceptable toxicity or end of study treatment. Lenvatinib 8 mg for a body weight \< 60 kg and 12 mg for a body weight ≥ 60 kg orally continuously once daily, starting on Day 1 of every 3 week cycle until disease progression or inacceptable toxicity or end of study treatment.
Despite the fact that ibuprofen appears to minimize the renal side effects seen following bolus indomethacin, other concerns regarding both short and long-term safety remain. Indomethacin, on the other hand, has been used to treat premature neonates for many years. Other than transient vasoconstrictive effects, no significant toxicity has been noted. Thus, if we were to be able to eliminate the differential renal effects, indomethacin would remain, for many, the therapy of choice for the premature neonate with a persistent PDA. We hypothesized that continuous administration of indomethacin would provide this option. Ibuprofen therapy has not, to date, been compared with indomethacin administered by continuous infusion. Hence, in the current study we attempted to determine whether continuous indomethacin administration could potentially offer the same advantages as ibuprofen in treating PDA, specifically in terms of mitigation of renal side effects. Specifically, our primary objective was to show no differences in urine output and/or in serum creatinine between the treatment groups. As a secondary objective, we aimed to show no other potentially vascular-mediated clinical differences, eg. Necrotizing enterocolitis (NEC), intraventricular hemorrhage (IVH), retinopathy of prematurity (ROP) and on bilirubin albumin binding between the groups.

B-type natriuretic peptide (BNP) is released by ventricular myocytes in response to ventricular volume load. It, in turn, mediates vasodilation, natriuresis and diuresis. Serum BNP levels have been shown to be clinically useful in differentiating between respiratory and cardiac disease, in monitoring heart failure therapies and in serving as early diagnostic biomarkers of ductal patency in premature neonates. As secondary objectives we intend to determine whether a decrease in BNP levels would be an equally reliable indicator of therapeutic efficacy in infants treated with ibuprofen as with indomethacin.In addition we will look at comparative effects on other vascular beds which might mediate long term side effects described above.
Targeting tumor angiogenesis is an important approach in advanced tumor therapy. Here we investigated the effect of the suppressor of variegation 3-9 homolog 1 (SUV39H1) on tumor angiogenesis in oral squamous cell carcinoma (OSCC). The GEPIA database was used to analyze the expression of SUV39H1 in various cancer tissues. The expression of SUV39H1 in OSCC was detected by immunohistochemistry, and the correlation between SUV39H1 and Notch1 and microvascular density (MVD) was analyzed. The effect of SUV39H1 inhibition on OSCC was investigated in vivo by chaetocin treatment. The migration and tube formation of vascular endothelial cells by conditioned culture-medium of different treatments of oral squamous cell cells were measured. The transcriptional level of SUV39H1 is elevated in various cancer tissues. The transcription level of SUV39H1 in head and neck squamous cell carcinoma was significantly higher than that in control. Immunohistochemistry result showed increased SUV39H1 expression in OSCC, which was significantly correlated with T staging. The expression of SUV39H1 was significantly correlated with Notch1 and CD31. In vivo experiment chaetocin treatment significantly inhibit the growth of tumor, and reduce SUV39H1, Notch1, CD31 expression. The decreased expression of SUV39H1 in OSCC cells lead to the decreased expression of Notch1 and VEGF proteins, as well as the decreased migration and tube formation ability of vascular endothelial cells. Inhibition of Notch1 further enhance this effect. Our results suggest inhibition of SUV39H1 may affect angiogenesis by regulating Notch1 expression. This study provides a foundation for SUV39H1 as a potential therapeutic target for OSCC.
INTRODUCTION: Sepsis patients experience a complex interplay of host pro- and anti-inflammatory processes which compromise the clinical outcome. Despite considering the latest clinical and scientific research, our comprehension of the immunosuppressive events in septic episodes remains incomplete. Additionally, a lack of data exists regarding the role of epigenetics in modulating immunosuppression, subsequently impacting patient survival.
METHODS: To advance the current understanding of the mechanisms underlying immunosuppression, in this study we explored the dynamics of DNA methylation using the Infinium Methylation EPIC v1.0 BeadChip Kit in leukocytes from patients suffering from sepsis, septic shock, and critically ill patients as controls, within the first 24 h after admission in the Intensive Care Unit of a tertiary hospital.
RESULTS AND DISCUSSION: Employing two distinct analysis approaches (DMRcate and mCSEA) in comparing septic shock and critically ill patients, we identified 1,256 differentially methylated regions (DMRs) intricately linked to critical immune system pathways. The examination of the top 100 differentially methylated positions (DMPs) between septic shock and critically ill patients facilitated a clear demarcation among the three patient groups. Notably, the top 6,657 DMPs exhibited associations with organ dysfunction and lactate levels. Among the individual genes displaying significant differential methylation, IL10, TREM1, IL1B, and TNFAIP8 emerged with the most pronounced methylation alterations across the diverse patient groups when subjected to DNA bisulfite pyrosequencing analysis. These findings underscore the dynamic nature of DNA methylation profiles, highlighting the most pronounced alterations in patients with septic shock, and revealing their close association with the disease.
FIELD: biology, microbiology, medicine, stomatology, biochemistry, pharmacy. SUBSTANCE: invention can be used in medicinal practice. Invention describes recombinant strains of Streptococcus mutans characterizing with deficiency in production of lactic acid and production of recombinant alcohol dehydrogenase. These recombinant strains of S. mutans can be used in prophylactic treatment of dental caries. Invention describes methods for preparing recombinant strain and its using in method for reducing frequency of arising and severity of dental caries disease by oral administration of this strain in different therapeutic forms: as component of chew, dental paste and so on. Invention describes also pharmaceutical composition and strain-base medicinal agent as an active component. Using the invention provides the enhancement of effectiveness of prophylaxis and treatment of dental caries. EFFECT: enhanced effectiveness of strain, valuable medicinal properties. 21 cl, 5 dwg, 10 ex
PURPOSE:To enhance the shelf life of this reagent and to perform immunity analysis highly accurately by adding stabilizer comprising a specified compound into immunity analysis reagent using liposome. CONSTITUTION:The main components of a reagent are a liposome-dispersing- fluid stabilizer containing compounds selected among polyhydric alcohol, saccharides, gelatine, lithium chloride, cesium chloride and polyoxyethylene-based surface-active agent, phospholipid and cholesterol. In liposome, antigen or antibody is bonded at the surface, and a label material is sealed in the inside. Stabilizer is mixed in the liposome dispersion fluid containing liposome. The stabilizer is also sealed in the inside of the liposome. Thus, the shelf life of the reagent is enhanced, and immunity analysis can be performed highly accurately.
Rationale: Patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) have a high short-term mortality rate. Semaphorin-6B (SEMA6B) plays a crucial role in the pathogenesis of HBV-ACLF, but its molecular basis remains unclear. This study aimed to elucidate the mechanisms of SEMA6B in HBV-ACLF progression. Methods: A total of 321 subjects with HBV-ACLF, liver cirrhosis (LC), chronic hepatitis B (CHB), and normal controls (NC) from a prospective multicenter cohort were studied. 84 subjects (HBV-ACLF, n = 50; LC, n = 10; CHB, n = 10; NC, n = 14) among them underwent mRNA sequencing using peripheral blood mononuclear cells (PBMCs) to clarify the mechanisms of SEMA6B in HBV-ACLF. These mechanisms were validated through in vitro studies with hepatocytes and macrophages, as well as in vivo using SEMA6B knockout mice and mice treated with synthetic SEMA6B siRNA. Results: Transcriptome analysis of PBMCs showed that SEMA6B was among the most differentially expressed genes when comparing patients with HBV-ACLF to those with LC, CHB, or NC. ROC analysis demonstrated the reliable diagnostic value of SEMA6B for HBV-ACLF in both the sequencing cohort and an external validation cohort (AUROC = 0.9788 and 0.9026, respectively). SEMA6B levels were significantly higher in the HBV-ACLF patients, especially in non-survivors, with high expression mainly observed in macrophages and hepatocytes in liver tissue. Genes significantly associated with highly expressed SEMA6B were enriched in inflammation and apoptosis pathways in HBV-ACLF non-survivors. Overexpression of SEMA6B in macrophages activated systemic inflammatory responses, while its overexpression in hepatocytes inhibited proliferation through G0/G1 cell cycle arrest and induced apoptosis. Knocking out SEMA6B rescued mice with liver failure by improving liver functions, reducing inflammatory responses, and decreasing hepatocyte apoptosis. Transcriptome analysis of liver tissue showed that SEMA6B knockout significantly ameliorated the liver failure signature, significantly downregulating inflammation-related pathways. Importantly, therapeutic delivery of synthetic SEMA6B siRNA also improved liver function, and reduced both inflammation and hepatocyte apoptosis in mice with liver failure. Conclusion: SEMA6B, a potential diagnostic biomarker for HBV-ACLF, exacerbates liver failure through macrophage-mediated systemic inflammation and hepatocyte apoptosis. These findings highlight SEMA6B as a promising early treatment target for HBV-ACLF patients.
Eligible subjects will be admitted to the clinical site on Day -1. Subjects will receive crushed oxycodone HCl IR 40mg in a randomized, double-blind, crossover manner.
Neutrophils, the most abundant white blood cells in the human circulation, play crucial roles in various diseases, including kidney disease. Traditionally viewed as short-lived pro-inflammatory phagocytes that release reactive oxygen species, cytokines and neutrophil extracellular traps, recent studies have revealed their complexity and heterogeneity, thereby challenging this perception. Neutrophils are now recognized as transcriptionally active cells capable of proliferation and reverse migration, displaying phenotypic and functional heterogeneity. They respond to a wide range of signals and deploy various cargo to influence the activity of other cells in the circulation and in tissues. They can regulate the behavior of multiple immune cell types, exhibit innate immune memory, and contribute to both acute and chronic inflammatory responses while also promoting inflammation resolution in a context-dependent manner. Here, we explore the origin and heterogeneity of neutrophils, their functional diversity, and the cues that regulate their effector functions. We also examine their emerging role in infectious and non-infectious diseases with a particular emphasis on kidney disease. Understanding the complex behavior of neutrophils during tissue injury and inflammation may provide novel insights, thereby paving the way for potential therapeutic strategies to manage acute and chronic conditions. By deciphering their multifaceted role, targeted interventions can be developed to address the intricacies of neutrophil-mediated immune responses and improve disease outcomes.
Since the invention of cardiopulmonary bypass, cardioprotective strategies have been investigated to mitigate ischemic injury to the heart during aortic cross-clamping and reperfusion injury with cross-clamp release. With advances in cardiac surgical and percutaneous techniques and post-operative management strategies including mechanical circulatory support, cardiac surgeons are able to operate on more complex patients. Therefore, there is a growing need for improved cardioprotective strategies to optimize outcomes in these patients. This review provides an overview of the basic principles of cardioprotection in the setting of cardiac surgery, including mechanisms of cardiac injury in the context of cardiopulmonary bypass, followed by a discussion of the specific approaches to optimizing cardioprotection in cardiac surgery, including refinements in cardiopulmonary bypass and cardioplegia, ischemic conditioning, use of specific anesthetic and pharmaceutical agents, and novel mechanical circulatory support technologies. Finally, translational strategies that investigate cardioprotection in the setting of cardiac surgery will be reviewed, with a focus on promising research in the areas of cell-based and gene therapy. Advances in this area will help cardiologists and cardiac surgeons mitigate myocardial ischemic injury, improve functional post-operative recovery, and optimize clinical outcomes in patients undergoing cardiac surgery.
Pain of VOC in sickle-cell patients seen in the emergency department (ED) is severe. Analgesia is a therapeutic emergency based on intravenous (IV) morphine titration. However, for technical reasons (patient flow in ED, difficult venous access) this treatment is often delayed. The Equimolar Mixture of Oxygen-Nitrous Oxide (EMONO), an inhaled analgesic administered, makes it possible to temporarily and very partially compensate for the major analgesic defect. Its efficacy in this indication has never been demonstrated; it is less effective than opiates during labour and is associated with a risk of addiction. The intranasal (IN) route is used to administer strong opiates such as sufentanil. Sufentanil IN has been shown to be rapidly effective in traumatology. Its duration of action is similar to that of morphine IV but its duration of action is far too short to completely replace it. Its ideal place would therefore be the initial phase of the management while waiting for a venous approach.

The strategy is to propose an intranasal administration of an opioid (Sufentanil) at the initial management of vaso-occlusive crisis in sickle-cell patients in the ED waiting to a venous route for morphine.

Follow-up of the study will be carried out in the ED with numeric rating scale (NRS) measurement every 5 minutes until patient relief (defined by NRS ≤ 3/10). Once relieved, NRS will be measured every 15 minutes for at least 2 hours. Treatment-related side effects will be systematically investigated up to 4 hours after starting treatment. In particular, the respiratory rate and level of consciousness will be measured, and all side effects will be recorded: nausea, vomiting, dizziness, behavioural disorders, pruritus.
Neuroendocrine neoplasm (NEN) generally refers to all tumors that originate from peptidergic neurons and neuroendocrine cells. It is a relatively rare tumor, ranging from indolent, slow-growing low-grade malignant tumors to obvious distant metastases. A series of malignant tumors. The most common place for neuroendocrine tumors is in the digestive system, and about two-thirds of neuroendocrine tumors occur in the gastrointestinal pancreas. However, with the change of people's living habits and the improvement of physical examination awareness, the incidence of neuroendocrine tumors increased from 1.09/100,000 in 1973 to 6.98/100,000 in 2012. The incidence has increased by 6 times compared with other tumors. , NENs increase more rapidly. The incidence of people over 65 years of age has increased by 8 times, and the incidence of people younger than 50 years of age has also increased by 3 times, and the incidence has been increasing year by year. It is worth noting that the average age of pancreatic neuroendocrine tumors is only 56.7-13.3 years old, showing a younger trend.

Because most neuroendocrine tumors lack specific manifestations, coupled with unique inert biological characteristics, clinicians often lack understanding, which can easily lead to misdiagnosis and treatment. Taking gastrointestinal pancreatic neuroendocrine tumors (GEP-NEN) as an example, due to the uneven diagnosis and treatment level, GEP-NEN patients may be diagnosed with a delay of up to 7 years. Because of this, as many as 40-95% of GEP-NEN patients have developed distant metastases at the time of diagnosis, and 65-95% of them have liver metastases. Liver metastasis is the most critical prognostic risk factor in GEP-NEN, and it has a decisive impact on the survival of patients. The 5-year survival rate of gastrointestinal neuroendocrine tumors with liver metastasis is 56%-83%, while the 5-year survival rate of pancreatic neuroendocrine tumors is only 48.8%, and the 10-year survival rate is only 30.2%. For limited-stage patients, even if radical surgical resection, up to 94% of cases will still have recurrence and metastasis within 5 years. For inoperable patients, although chemotherapy, targeted therapy, biological therapy and other methods can be used, the effect is still limited. Therefore, the systematic development of basic-clinical translational research on neuroendocrine tumors is very important and imminent.

Based on the above-mentioned problems, this project intends to conduct a systematic and in-depth study of neuroendocrine tumors: 1. Use single-cell sequencing technology to deeply study the molecular biological characteristics of NEN tumors, tumor heterogeneity and cell subtypes. 2. Construct NEN models, including primary cell lines, organoids, and mouse animal models. This study can establish a neuroendocrine tumor research system to find the molecular mechanism and potential intervention targets of NEN recurrence and metastasis, and provide clinicians with safe and effective treatment strategies, thereby improving the therapeutic effect of neuroendocrine tumors.
High mortality has been reported in severe cases of COVID-19. Emerging reports suggested that the severity is not only due to SARS-CoV-2 infection, but also due to coinfections by other pathogens exhibiting symptoms like COVID-19. During the COVID-19 pandemic, simultaneous respiratory coinfections with various viral (Retroviridae, Flaviviridae, Orthomyxoviridae, and Picoviridae) and bacterial (Mycobacteriaceae, Mycoplasmataceae, Enterobacteriaceae and Helicobacteraceae) families have been observed. These pathogens intensify disease severity by potentially augmenting SARSCoV-2 replication, inflammation, and modulation of signaling pathways. Coinfection emerges as a critical determinant of COVID-19 severity, principally instigated by heightened pro-inflammatory cytokine levels, as cytokine storm. Thereby, in co-infection scenario, the severity is also driven by the modulation of inflammatory signaling pathways by both pathogens possibly associated with interleukin, interferon, and cell death exacerbating the severity. In the current review, we attempt to understand the role of co- infections by other pathogens and their involvement in the severity of COVID-19.
Participants with HCV GT1b without cirrhosis received the adult 3-DAA (OBV/PTV/RTV and DSV) regimen: two 12.5 mg ombitasvir /75 mg paritaprevir /50 mg ritonavir tablets taken orally every morning (QD) and one dasabuvir 250 mg tablet taken orally twice a day (BID) for 12 weeks. Participants with HCV GT1a without cirrhosis received 12-week treatment with the adult 3-DAA regimen and ribavirin 200 mg tablets were administered orally per local label.
EMPWR is a two-pronged intervention model comprised of 1) a provider-driven, telemedicine-based behavioral intervention to mitigate anxiety sensitivity and sleep deficiency and enhance peripartum buprenorphine retention, and 2) an adjunctive mobile application to promote patients' buprenorphine adherence and use of therapy skills learned through the behavioral intervention. The EMPWR therapy protocol is comprised of five 30-60-minute sessions delivered weekly or biweekly by a therapist during the second and/or third trimester of pregnancy, and three 30-minute booster sessions delivered months 1-3 postpartum.