anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Retinal ischemia/reperfusion (IR) injury is a common pathological process in many ophthalmic diseases. Interleukin-1β (IL-1β) is an important inflammatory factor involved in the pathology of retinal IR injury, but the mechanism by which IL-1β is regulated in such injury remains unclear. Caspase-11 non-canonical inflammasomes can regulate the synthesis and secretion of IL-1β, but its role in retinal IR injury has not been elucidated. This study aimed to evaluate the role of caspase-11 non-canonical inflammasomes in retinal IR injury.
METHODS: Retinal IR injury was induced in C57BL/6J mice by increasing the intraocular pressure to 110 mmHg for 60 min. The post-injury changes in retinal morphology and function and in IL-1β expression were compared between caspase-11 gene knockout (caspase-11-/-) mice and wild-type (WT) mice. Morphological and functional changes were evaluated using hematoxylin-eosin staining and retinal whole mount staining and using electroretinography (ERG), respectively. IL-1β expression in the retina was measured using enzyme-linked immunosorbent assay (ELISA). The levels of caspase-11-related protein were measured using western blot analysis. The location of caspase-11 in the retina was determined via immunofluorescence staining. Mouse type I astrocytes C8-D1A cells were used to validate the effects of caspase-11 simulation via hypoxia in vitro. Small-interfering RNA targeting caspase-11 was constructed. Cell viability was evaluated using the MTT assay. IL-1β expression in supernatant and cell lysate was measured using ELISA. The levels of caspase-11-related protein were measured using western blot analysis.
RESULTS: Retinal ganglion cell death and retinal edema were more ameliorated, and the ERG b-wave amplitude was better after retinal IR injury in caspase-11-/- mice than in WT mice. Further, caspase-11-/- mice showed lower protein expressions of IL-1β, cleaved caspase-1, and gasdermin D (GSDMD) in the retina after retinal IR injury. Caspase-11 protein was expressed in retinal glial cells, and caspase-11 knockdown played a protective role against hypoxia in C8-D1A cells. The expression levels of IL-1β, cleaved caspase-1, and GSDMD were inhibited after hypoxia in the si-caspase-11 constructed cells.
CONCLUSIONS: Retinal IR injury activates caspase-11 non-canonical inflammasomes in glial cells of the retina. This results in increased protein levels of GSDMD and IL-1β and leads to damage in the inner layer of the retina.
BACKGROUND: Epicardial radiofrequency catheter ablation (RFCA) of idiopathic ventricular arrhythmias (VAs) originating from the left ventricular summit (LVS) is challenging because of the anatomic barriers. On the other hand, RFCA at the endocardial sites near the earliest epicardial activation site of LVS-VAs (anatomic approach) has proven successful. The evolving trends in the approaches and outcomes of RFCA of LVS-VAs at a single center were evaluated.
METHODS: We studied 88 consecutive patients with idiopathic LVS-VAs at our institute from 2009 to 2019. These patients were divided into 3 periods: 2009 to 2012 (early), 2013 to 2015 (middle), and 2016 to 2019 (recent). The data were compared among the 3 periods.
RESULTS: The RFCA success rate did not significantly change from the early to middle period but significantly increased from the middle to recent period (P=0.0315). The transpericardial approach usage significantly decreased over the 3 periods. The anatomic approach usage significantly increased over the 3 periods. The use of the transpericardial approach did not affect the RFCA outcomes over the 3 periods. The success rate of the anatomic RFCA tended to increase from the early to middle period and significantly increased from the middle to recent period (P=0.0412). The number of endocardial locations where RFCA was successful increased over the 3 periods.
CONCLUSIONS: Over the 10-year period, the transpericardial approach became decreasingly performed, whereas the anatomic approach became increasingly performed with a satisfactory improvement in the RFCA outcomes of LVS-VAs. The anatomic RFCA became more successful by identifying more and various endocardial locations as target sites.
An aortic aneurysm (thoracic or abdominal) is a permanent dilatation of the aorta caused by weakening in the arterial wall. The feared complication is aortic rupture or dissection, leading to potentially lethal aortic bleeding and associated with mortality rates up to 95%. Diagnosis of the aneurysm and especially its risk of rupture or dissection is highly challenging. If the aneurysm diameter and/or growth rate exceed a specific threshold (respectively 55 mm and 1 cm/year), a highly invasive and dangerous surgery is performed. However, several studies have shown no correlation between the maximum transverse diameter and the risk of rupture or dissection. Since aneurysm rupture is associated with multiple aortic tissue properties, both biomechanics-based and microstructurally-based criteria can be a promising alternative.

The overall goal of this trial is a biomechanical and microstructural analysis of aneurysms to improve the diagnostic criterion for aneurysm rupture risk. Within this goal, two scientific objectives can be distinguished. Firstly, a highly unique dataset with patient data allowing the development of an improved diagnostic tool will be created. This dataset will contain an abundance of relevant parameters such as patient characteristics, geometry, material properties and biomechanical and microstructural characteristics. The biomechanical and microstructural data will be obtained by the analysis of resected aneurysmal tissue and by dynamic imaging (4D CT). 4D CT scans are a series of ECG-gated scans that are taken at specified intervals in the cardiac circle. The second objective is to create a personalized diagnostic tool. An aneurysm rupture risk criteria based on geometry as well as biomechanical and microstructural properties is expected to be significantly more reliable than the current criteria. More specifically, a correlation between patient characteristics that can be measured non-invasively and the aneurysm rupture risk is searched for.
T4RP is a relapse prevention mHealth program text messaging to people who have schizophrenia/SAD. The intervention will include an online interface for clinicians and an automated text messaging program for patients. Firstly, patients and providers will meet in an intake session, to identify the patient's personal early warning signs from a pre-identified list. Using the online interface, providers will enter additional warning signs or personalize the wording of the messages as requested by the patient. The patient also will determine the threshold at which the provider will be alerted about a possible relapse and whether additional contact people should be alerted.
This invention teaches the use of chelating agents to diagnose and treat metal toxins in a patient. Chelation agents are given to the mother for the benefit of the baby. Metal toxins such as lead, arsenic, mercury, tin, antimony, aluminum and others are known to cause miscarriages, birth defects, maldevelopment of the organs and tissues and maldevelopment of the brain. Chelation treatments of the mother can prevent these problems in the embryo, fetus and infant. Removal of lead and mercury and other toxins allows improved development of the offspring, both during the chelation and alter the chelation is discontinued. Determining whether a mother who has just delivered a baby has elevated levels of heavy metals can also be used to identify the elevated metals of the mother as a possible cause of birth defects.
Participants are provided a unique identifier to access the online website. The opening page welcomes them to the study, then directs them to the chunked consent materials and baseline survey. As soon as they have completed this, they receive access to the intervention, which for management is expected to take 1-2 hours and for staff, 30-45 minutes (i.e., the online equivalent of 3-4 and 1 hour, respectively). After completion of the required modules, participants receive access to the optional modules as well as the posttest survey to evaluate the training. Once the post-test is complete, they are thanked for their involvement and informed they will receive an e-mail to access a follow-up survey in six months' time.
Subjects will receive no treatment in this study. Each subject will attend the clinic on 2 occasions, initially for a screening visit and then for further assessments (Visit 1). Subjects will remain in the study for maximum 33 days from the screening visit to follow up.
The present invention relates to a fusion protein (FcsFNDC4) comprising a) a soluble FNDC4 (sFNDC4) or a functional fragment thereof; b) a peptide linker; and c) a Fc-domain. The present invention further relates to a nucleic acid molecule comprising a nucleotide sequence encoding said fusion protein, a vector comprising said nucleic acid molecule, and a host cell comprising the vector or the nucleic add molecule. The present invention also relates to a fusion protein for use in therapy. In particular, the present invention relates to a fusion protein for use in a method of preventing and/or treating diabetes or inflammation in a subject. The invention also relates to a composition comprising at least one fusion protein. Further, the present invention relates to a kit comprising said fusion protein or said composition. The invention also comprises a method of producing the fusion protein and a method of stratifying a subject with diabetes applying the fusion protein of the invention.
At the initial assessment, written informed consent will be obtained before participants will undergo a clinical exam (inspection and palpation of the foot, measurement of bilateral passive ankle range of motion). All participants will complete the Short Form (SF)36 and the Foot Function Index20 to obtain pain and functional scores (approximate duration: 30 minutes). Participants will be able to familiarize with treadmill walking at their preferred walking speed. Surface electrodes will be placed bilaterally over the tibialis anterior, gastrocnemius medialis and lateralis, soleus, and peroneus brevis. Isokinetic muscle strength in ankle plantarflexion/ dorsiflexion and inversion/eversion will be tested using the Biodex system 4 Pro (approximate duration: 45 minutes). Reflective surface markers will be placed bilaterally on anatomic landmarks according to the Plug In Gait model and a specific foot model. These markers are seen by 6 Vicon MX cameras. Participants will be asked to stand on the treadmill (h/p cosmos, Zebris), and data for a standing reference trial will be collected. Single-limb heel rise performance with each leg will be tested on the treadmill while kinematic, electromyography (EMG), and pressure data will be measured. Participants will then walk barefoot for 2 minutes at 0% slope while kinematic, EMG, and pressure data will be recorded. Subsequently, the treadmill incline will be increased to 15%, and data for 2 minutes walking at this slope will be recorded followed by three heel rises (approximate duration: 45 minutes). The estimated total time for each participant is 120 minutes.
Participants will complete 8 training sessions over 4 weeks, in which they walk on a treadmill at their self-selected speed. During training sessions, the magnitude of the vibration applied to the hip abductors will vary randomly (following a normal distribution) on a step-by-step basis.
A delivery method and apparatus for massage oil is provided along with an associated massage oil composition. The massage oil is provided in a solid state at room temperature. The massage oil is heated to a liquid state at a temperature which is skin safe. The massage oil can then be applied to the skin and massaged into the skin. The massage oil can be provided in candle form to facilitate melting of the massage oil from the solid state to the liquid state. Compositions including primarily an oil such as hydrogenated soybean oil, palm kernel oil, coconut oil or cocoa butter, which are solid at room temperature, provide a major constituent for the massage oil composition disclosed. Fragrances, emollients, moisturizers, sweeteners, flavorants or other constituents can also be included.
This is a 2-part, Phase 1/2, open-label (all people know the identity of the intervention), multiple-dose and dose-escalation study of intravenous (directly into a vein) siltuximab in participants with malignant solid tumors. The study tests the safety and effectiveness of the experimental drug, siltuximab, in participants with advanced cancer (abnormal tissue that grows and spreads in the body). This study also tests how siltuximab is cleared from the body and how the body reacts to it. For this reason blood tests will be performed and some characteristics of the tumor will be analyzed. Siltuximab will be given by intravenous infusion (a fluid or a medicine delivered into a vein by way of a needle) over 1 hour. In Phase 1 (Cohort 1-4) doses will be administered in a range of 2.8-15 milligram per kilogram (mg/kg). Cohort 5 of Phase 1 will receive the recommended dose and schedule as determined from Cohort 1-4. Participants in Phase 1 (Cohort 1-4) will receive 4 administrations of siltuximab over a 10-13 week period, while participants in Cohort 5 and Phase 2 will receive 12 administrations over a 33 week period. Follow-up visits up to 12 weeks after last dose will be scheduled. Participants may then be contacted for up to 1 year after the last dose for follow-up survival and disease status information. Efficacy will primarily be evaluated as per response evaluation criteria in solid tumors (RECIST) criteria. Participants' safety will be monitored at every visit.
PURPOSE:To obtain a substance containing dissolved chitosan for use as food or a food material which can be easily mixed with other general foods and is amenable to oral ingestion by adding chitosan to kojic acid and keeping the obtained mixture below a specified temperature. CONSTITUTION:Chitosan is added to kojic acid, and the resulting mixture is kept at about 30 deg.C or below to dissolve the chitosan. It is desirable from the viewpoints of increasing the solubility of chitosan and of making the chitosan nonastringent that the kojic acid to be used is red kojic acid prepared by fermenting red koji. It is more desirable from the same viewpoints that a red kojic acid mixture containing natural mineral spring water, hibiscus extract and ethanol is used as the above kojic acid. When the dissolution temperature is above about 30 deg.C, the dissolved chitosan is fermented and gradually emits a foreign odor undesirably. The obtained substance containing the dissolved chitosan is nonastringent.
There will be a washout of at least 5 days between opevesostat dosing in Period 1 and the first carbamazepine dosing in Period 2. In Period 2, carbamazepine will be administered twice daily (BID) for 17 consecutive days with a single dose of opevesostat coadministered on the morning of Day 14 under fasting conditions. HRT (prednisone and fludrocortisone) will be administered under fed conditions on Day 14, approximately 4.5 hours after opevesostat and/or carbamazepine dosing.
To examine the relationship between in-home continuous measures of tremor, bradykinesia, mobility, and dyskinesia acquired over a 7-day period, from 2 mobile health technologies (Personal Kinetigraph, Kinesia 360) with one-time in-clinic measures of motor functional ability pertaining to the same 7-day period as assessed by Part 2 of the MDS-UPDRS, Part 4 of the MDS-UPDRS, Neuro-QOL, and PDQ-39. This will be examined in n=20 patients (10 patients assigned to each technology with a crossover at 3 months for a total of 20 patients over 6 months, 6 timepoints with data collected every 2 weeks). Patients will then be following for an observational period of an additional 6 months.
BACKGROUND: The severity of pulmonary hypoplasia is a main determinant of outcome for babies with congenital diaphragmatic hernia (CDH). Antenatal administration of extracellular vesicles derived from amniotic fluid stem cells (AFSC-EVs) has been shown to rescue morphological features of lung development in the rat nitrofen model of CDH. Herein, we evaluated whether AFSC-EV administration to fetal rats with CDH is associated with neonatal improvement in lung function.
METHODS: AFSC-EVs were isolated by ultracentrifugation and characterized by size, morphology, and canonical marker expression. At embryonic (E) day 9.5, dams were gavaged with olive oil (control) or nitrofen to induce CDH. At E18.5, fetuses received an intra-amniotic injection of either saline or AFSC-EVs. At E21.5, rats were delivered and subjected to a tracheostomy for mechanical ventilation (flexiVent system). Groups were compared for lung compliance, resistance, Newtonian resistance, tissue damping and elastance. Lungs were evaluated for branching morphogenesis and collagen quantification.
RESULTS: Compared to healthy control, saline-treated pups with CDH had fewer airspaces, more collagen deposition, and functionally exhibited reduced compliance and increased airway resistance, elastance, and tissue damping. Conversely, AFSC-EV administration resulted in improvement of lung mechanics (compliance, resistance, tissue damping, elastance) as well as lung branching morphogenesis and collagen deposition.
CONCLUSIONS: Our studies show that the rat nitrofen model reproduces lung function impairment similar to that of human babies with CDH. Antenatal administration of AFSC-EVs improves lung morphology and function in neonatal rats with CDH.
LEVEL OF EVIDENCE: N/A (animal and laboratory study).
BACKGROUND: Inflammatory macrophage infiltration plays a critical role in acute kidney disease induced by ischemia-reperfusion (IRI-AKI). Calycosin is a natural flavone with multiple bioactivities. This study aimed to investigate the therapeutic role of calycosin in IRI-AKI and its underlying mechanism.
METHODS: The renoprotective and anti-inflammatory effects of calycosin were analyzed in C57BL/6 mice with IRI-AKI and lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. RNA-seq was used for mechanism investigation. The molecular target of calycosin was screened by in silico methods and validated by surface plasmon resonance (SPR). Macrophage chemotaxis was analyzed using Transwell and agarose gel spot assays.
RESULTS: Calycosin treatment significantly reduced serum creatinine and urea nitrogen and attenuated tubular destruction in IRI-AKI mice. Additionally, calycosin markedly suppressed NF-κB signaling activation and the expression of inflammatory mediators IL-1β and TNF-α in IRI-AKI kidneys and LPS-stimulated RAW 264.7 cells. Interestingly, RNA-seq revealed calycosin remarkably downregulated chemotaxis-related pathways in RAW 264.7 cells. Among the differentially expressed genes, Ccl2/MCP-1, a critical chemokine mediating macrophage inflammatory chemotaxis, was downregulated in both LPS-stimulated RAW 264.7 cells and IRI-AKI kidneys. Consistently, calycosin treatment attenuated macrophage infiltration in the IRI-AKI kidneys. Importantly, in silico target prediction, molecular docking, and SPR assay demonstrated that calycosin directly binds to macrophage migration inhibitory factor (MIF). Functionally, calycosin abrogated MIF-stimulated NF-κB signaling activation and Ccl2 expression and MIF-mediated chemotaxis in RAW 264.7 cells.
CONCLUSIONS: In summary, calycosin attenuates IRI-AKI by inhibiting MIF-mediated macrophage inflammatory chemotaxis, suggesting it could be a promising therapeutic agent for the treatment of IRI-AKI.
The increasing prevalence of chronic heart failure (CHF) among older people is a global problem. Despite the success of treatment, the mortality rate of these patients remains high, resulting in the need to search for new mechanisms of the development and progression of cardiovascular system pathologies, as well as to develop innovative branches of therapy. Considerable recent interest has been directed towards studying changes in the composition of the intestinal microbiota in people with age, its role in development, as well as potential directions for the prevention of cardiovascular diseases and their complications. One of these complications, especially in the elderly, where several lines of relationship with the intestinal microbiota can be traced, is CHF. Pathogenetically, the effect is due to chronic systemic inflammation, as well as the effect of intestinal metabolites on its course. The objective of this literature review is to analyse and systematize existing scientific studies on the relationship between microflora, its changes and chronic heart failure, as well as to study methods of dealing with the links of pathogenesis, which in turn can stop the progression of this complication of SSS diseases. The review presents literature sources published mainly in the period 2019-2024 using PubMed, ScienceDirect, eLIBRARY databases, including review articles, meta-analyses, clinical studies.
The kit contains a syringe containing ARISTADA sterile aqueous extended-release injectable suspension and 2 or 3 safety needles depending on dose (a 2-inch 20 gauge needle with yellow needle hub, a 1 ½-inch 20 gauge needle with yellow needle hub, and a 1-inch 21 gauge needle with green needle hub (441 mg kit only)) for intramuscular injection. All materials should be stored at room temperature. 

  


A | 5 mL syringe containing ARISTADA sterile aqueous extended-release injectable suspension 

B | 20 gauge needle, 2-inch with yellow needle hub 

C | 20 gauge needle, 1½-inch with yellow needle hub 

D | 21 gauge needle, 1-inch with green needle hub 

1\. TAP and vigorously SHAKE the syringe. 

1a. Tap the syringe at least 10 times to dislodge any material which may have settled. 

1b. Shake the syringe vigorously for a minimum of 30 seconds to ensure a uniform suspension. If the syringe is not used within 15 minutes, shake again for 30 seconds. 

2\. SELECT the injection needle. 

2a. Select injection site. 

2b. Select needle length based on injection site. For patients with a larger amount of subcutaneous tissue overlaying the injection site muscle, use the longer of the needles provided. 

[see Dosage and Administration (2.1)]

3\. ATTACH the injection needle. 

Attach the appropriate needle securely with a clockwise twisting motion. Do NOT overtighten. Overtightening could lead to needle hub cracking. 

4\. PRIME the syringe to remove air. 

4a. Bring the syringe into upright position and tap the syringe to bring air to the top. 

4b. Depress the plunger rod to remove air until a few drops are released. It is normal to see small air bubbles remaining in the syringe. 

5. Inject in a RAPID and CONTINUOUS manner. Product requires a RAPID injection. Do not hesitate. Administer the entire content intramuscularly. Do not inject by any other route. 

6\. DISPOSE of the needle. Cover the needle by pressing the safety device. Dispose of used and unused items in a proper waste container.