anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
A system and method determines priorities and presents heterogeneous medical data. The method includes retrieving medical data of a patient, the medical data including data from a plurality of data sources. The method includes phenotyping the medical data to generate inference cues and inference results including one or more codes, the inference cues including a basis for determining the inference results. The method includes assigning a relevance score to each code of the one or more codes. The method includes ranking the codes based on the relevance score for each code of the one or more codes. The method includes displaying the codes in a sorted order.
The study is a multicenter, open label Phase I/II trial. Phase I, dose-escalation: This portion of the overall study uses a 3+3 design to estimate the maximum tolerated dose (MTD). The starting dose level will be 1.0 μCi/Kg of Lintuzumab-Ac225 and 15 μg/Kg unlabeled HuM195 divided into 2 equal fractionated doses (0.5 μCi/Kg and 7.5 μg /Kg + 0.5 μCi/Kg and 7.5 μg /Kg) with the first fraction administered approximately 4 - 7 days after 1 cycle of LDAC (20 mg subQ every 12 h x 10 days administered for cytoreduction) and the second fraction administered 4-7 days after the first fraction. Subjects will then go on to receive up to 11 additional cycles of LDAC or until progression of disease. Three to six patients will be treated at each dose level, and dose escalation will proceed if less than 33% of patients in a cohort experience dose-limiting toxicity.

Phase II, efficacy component. The study was designed as a 2- stage minimax design. Patients will be given two infusions of Lintuzumab-Ac225, 4-8 days apart (Day 5-Day 9), initially at the dose level determined to be the MTD in the Phase I portion. The second dose of Lintuzumab-Ac225 may be delayed up to 14 days after the first dose for clinical or scheduling reasons. Response will be initially assessed on or around days 28-42 after the final study drug administration. The primary endpoint (CR+CRp + CRi) will be determined on day 42. Best response will be evaluated from Day 1, Dose 1 until the end of the study.
In 2020, Denmark buried approximately four million culled, farmed mink in mass graves treated with slaked lime due to widespread SARS-CoV-2 infections. After six months, environmental concerns prompted the exhumation of these cadavers. Our analysis encompassed visual inspections, soil pH measurements, and gas emission assessments of the grave environment. Additionally, we evaluated carcasses for decay status, cadaverine content, and the presence of various pathogens, including SARS-CoV-2 and mink coronavirus. Our findings revealed minimal microbial activity and limited carcass decomposition. Although viral RNA from SARS-CoV-2 and mink coronavirus, along with DNA from Aleutian mink disease virus, were detected, the absence of infectious SARS-CoV-2 in cell culture assays suggests slow natural degradation processes. This study provides critical insights for future considerations in managing mass burial scenarios during outbreaks of livestock-associated zoonotic pathogens.
The objective of this study is to explore whether sodium valproate (VPA) alleviates epileptic seizures via suppressing lysyl oxidase (Lox)-mediated ferroptosis. Epileptic seizure mouse model was prepared via intrahippocampal injection of kainic acid (250 ng/μl). After treatment with kainic acid, VPA was injected intraperitoneally by the dose of 250 mg/kg twice daily for 4 days. Ferroptosis-associated indices including lipid peroxides (LPO) level and Ptgs2 mRNA in hippocampal tissue samples were detected. Additionally, effects of VPA on Lox mRNA and enzymatic activity were assessed by quantitative real-time PCR and a commercial kit, respectively. Neuronal survival was assessed by Nissl staining. In kainic acid-induced epileptic seizure mouse model, VPA significantly suppressed LPO level and Ptgs2 mRNA and the suppression of ferroptosis was positively correlated with its anti-seizure effect. Lox mRNA and enzymatic activity were also found to decrease in hippocampus of epileptic seizure mice after VPA treatment. Furthermore, overexpression of Lox via adeno-associated virus infection remarkably abrogated the inhibitory effect of VPA on ferroptosis and neuronal impairment together with its anti-seizure effect. VPA suppresses Lox-mediated ferroptosis process, which can provide the explanation for its anti-seizure property.
The invention provides a glucosamine derivative ligand compound and a preparing method thereof. The invention further provides a tricarbonyl Tc-99m labeled complex, wherein the tricarbonyl Tc-99m labeled complex is of the structure shown in the general formula (B). The invention further provides a preparing method and application of the tricarbonyl Tc-99m labeled complex. According to the glucosamine derivative ligand compound, 3-Aminoalanine is used for being coupled with glucosamine, the raw materials are easy to obtain, and the preparing method is easy and convenient to implement. The tricarbonyl Tc-99m labeled complex is formed by the glucosamine derivative ligand compound and the radioactive tc-carbonyl-99m, and is high in chemical stability, simple in preparation, high in chemical purity, good in biological property and capable of being used for preparing a novel tumor SPECT developer. The structure is shown in the specification.
BACKGROUND AND AIMS: A complete understanding of disease pathophysiology in advanced liver disease is hampered by the challenges posed by clinical specimen collection. Notably, in these patients, a transjugular liver biopsy (TJB) is the only safe way to obtain liver tissue. However, it remains unclear whether successful sequencing of this extremely small and fragile tissue can be achieved for downstream characterization of the hepatic landscape.
METHODS: Here we leveraged in-house available single-cell RNA-sequencing (scRNA-seq) and single-nucleus (snRNA-seq) technologies and accompanying tissue processing protocols and performed an in-patient comparison on TJB's from decompensated cirrhosis patients (n = 3).
RESULTS: We confirmed a high concordance between nuclear and whole cell transcriptomes and captured 31,410 single nuclei and 6,152 single cells, respectively. The two platforms revealed similar diversity since all 8 major cell types could be identified, albeit with different cellular proportions thereof. Most importantly, hepatocytes were most abundant in snRNA-seq, while lymphocyte frequencies were elevated in scRNA-seq. We next focused our attention on hepatic myeloid cells due to their key role in injury and repair during chronic liver disease. Comparison of their transcriptional signatures indicated that these were largely overlapping between the two platforms. However, the scRNA-seq platform failed to recover sufficient Kupffer cell numbers, and other monocytes/macrophages featured elevated expression of stress-related parameters.
CONCLUSION: Our results indicate that single-nucleus transcriptome sequencing provides an effective means to overcome complications associated with clinical specimen collection and could sufficiently profile all major hepatic cell types including all myeloid cell subsets.
<P>PROBLEM TO BE SOLVED: To provide a vaccine protective against meningococcal serogroup W135 and H. influenzae b type diseases.  <P>SOLUTION: Conjugated capsular saccharides derived from meningococcal serogroup C, serogroup W135 and serogroup Y are safe and immunogenic in humans when combined in a single dose. The conjugated antigens can stably be combined in a single aqueous dose without the need for lyophilization. Broad protection against serogroup B infection can be achieved by using a small number of defined polypeptide antigens. The polypeptide antigens can be combined with the saccharide antigens without losing the protective efficacy for any of the five serogroups. The efficacy of a serogroup W135 conjugate is enhanced by addition of protein antigens derived from a serogroup B strain. Addition of Hib (H. influenzae B type) conjugate to meningococcal conjugates enhances the overall activity against the meningococcal serogroup W135.  <P>COPYRIGHT: (C)2011,JPO&INPIT
PURPOSE: To provide a safe intravenous administration method of fatty acids. CONSTITUTION: At the time of safe intravenous administration of fatty acids or the salts or other derivatives of the fatty acids or conjugate fatty acids, a patient is subcutaneously or intravenuosly dosed with heparin or associated compds. in the amt. of 1,000 to 20,000 IU, more preferably 3,000 to 10,000 IU or haparin-like protein or peptide in an equiv. anticoagulation amt. prior to the injection of the fatty acids or the heparin or associated compds. in the amt. of 1 to 100 IU/ml, more preferably 10 to 20 IU/ml the haparin-like protein or peptide in the equiv. anticoagulation amt. is added to an injection liquid carrying the fatty acids or both of the preliminary procedure of the patient by the heparin and the addition of the heparin to the injection liquid are combined.  This method is effective for treatment of cancers, virus infectious diseases and other disorders requiring the maintenance of the high plasma fatty acid level.
A web-based audio recording tool will be used to record voice sample answering the prompt, "How are you feeling today?" Participants are asked to speak for 1-minute. Following the recording, participants are asked to complete the Patient Health Questionnaire-9 and Generalized Anxiety Disorder-7 questions.
Patients will be asked to spend about six months in this study. There will be 4 different phases in this study as follows: (1) Loading Phase: This is the first week (week 1) of the study, when patients receive their first (loading) dose of cetuximab only, in the vein. (2) Concurrent Phase: During this phase patients will be treated simultaneously (concurrently) with radiation therapy to their chest and cetuximab. Radiation is delivered 5 days a week, Monday to Friday for a total of 7 weeks (weeks 2-8). Cetuximab is delivered in the vein, weekly, during the weeks of radiation. (3) Recovery Phase: Patients receive no treatment during these next 3 weeks (weeks 9-11). This phase is designed to allow patients to recover from side effects before they start the last phase. (4) Consolidation Phase: The last phase. Patients will receive 3 doses of chemotherapy with docetaxel during this phase. Docetaxel is given intravenously every 21 days. Patients also receive weekly cetuximab during this phase. Cetuximab is delivered in a similar way as it was during the concurrent (second) phase of this study. In total, this phase lasts 6 weeks (weeks 12-18). Once the therapy treatment is completed, and if the patient's cancer did not get worse, follow up visits will include visits to their physician every three months for 2 years, then every 4 months for 2 years or more, as long as their cancer doesn't get worse (at which time they will be removed from the study).
The investigators will conduct a randomized controlled trial in which physicians prescribe time in nature as an intervention to the study group. In total a goal of 240 patients will be recruited, including both children (13+) and adults. 120 of them will be assigned to the study group and 120 to the assigned to the control group. All study participants will be provided with a Global Positioning System (GPS)-enabled wearable device (Garmin Vivosmart 5) that is able to measure their activity levels, location, and additional health-related metrics, such as heart rate. All participants will be asked to provide information about their health and well-being through survey instruments and electronic health records. Both groups (intervention and control) will receive regular health advice targeting lifestyle factors associated with risk of chronic diseases. The treatment group will additionally receive a park prescription with information about the benefits of spending time in nature. They will also received a specified target amount of time to spend in nature, along with frequency of visits and recommended locations (e.g., specific parks), and information about parks and programming in the study area. Participants will also be asked to answer brief questions regarding their mental and physical health, as well as their physical excercise patterns every 72-hours through a research-grade smartphone app called Urban Mind over the course of this study. At baseline and end of study at 6-months the participants will also answer questionnaires that will assess their mental and physical health, as well as lifestyle factors such as physical activity, sleep, stress and exposure to nature. These questionnaires will be administered through the REDCap survey system.
Disruption of the intestinal microbiome is observed with acute graft-versus-host disease (GVHD) of the lower gastrointestinal (LGI) tract, and fecal microbiota transplantation (FMT) has successfully cured steroid-refractory cases. In this open-label, single-arm, pilot study, third-party, single-donor FMT was administered in combination with systemic corticosteroids to participants with high-risk acute LGI GVHD, with a focus on treatment-naïve cases. Participants were scheduled to receive 1 induction dose (15 capsules per day for 2 consecutive days), followed by 3 weekly maintenance doses, consisting of 15 capsules per dose. The primary end point of the study was feasibility, which would be achieved if ≥80% of participants able to swallow ≥40 of the 75 scheduled capsules. Ten participants (9 treatment-naïve; 1 steroid-refractory) were enrolled and treated. The study met the primary end point, with 9 of 10 participants completing all eligible doses. Organ-specific LGI complete response rate at day 28 was 70%. Initial clinical response was observed within 1 week for all responders, and clinical responses were durable without recurrent LGI GVHD in complete responders. Exploratory analyses suggest that alpha diversity increased after FMT. Although recipient microbiome composition never achieved a high degree of donor similarity, expansion of donor-derived species and increases in tryptophan metabolites and short-chain fatty acids were observed within the first 7 days after FMT. Investigation into the use of microbiome-targeted interventions earlier in the treatment paradigm for acute LGI GVHD is warranted. This trial was registered at www.ClinicalTrials.gov as #NCT04139577.
Meta-analysis of genome-wide association study data has implicated PDE4B in the pathogenesis of Alzheimer's disease (AD), the leading cause of senile dementia. PDE4B encodes one of four subtypes of cyclic adenosine monophosphate (cAMP)-specific phosphodiesterase-4 (PDE4A-D). To interrogate the involvement of PDE4B in the manifestation of AD-related phenotypes, the effects of a hypomorphic mutation (Pde4bY358C) that decreases PDE4B's cAMP hydrolytic activity were evaluated in the AppNL-G-F knock-in mouse model of AD using the Barnes maze test of spatial memory, 14C-2-deoxyglucose autoradiography, thioflavin-S staining of β-amyloid (Aβ) plaques, and inflammatory marker assay and transcriptomic analysis (RNA sequencing) of cerebral cortical tissue. At 12 months of age, AppNL-G-F mice exhibited spatial memory and brain metabolism deficits, which were prevented by the hypomorphic PDE4B in AppNL-G-F/Pde4bY358C mice, without a decrease in Aβ plaque burden. RNA sequencing revealed that, among the 531 transcripts differentially expressed in AppNL-G-F versus wild-type mice, only 13 transcripts from four genes - Ide, Btaf1, Padi2, and C1qb - were differentially expressed in AppNL-G-F/Pde4bY358C versus AppNL-G-F mice, identifying their potential involvement in the protective effect of hypomorphic PDE4B. Our data demonstrate that spatial memory and cerebral glucose metabolism deficits exhibited by 12-month-old AppNL-G-F mice are prevented by targeted inhibition of PDE4B. To our knowledge, this is the first demonstration of a protective effect of PDE4B subtype-specific inhibition in a preclinical model of AD. It thus identifies PDE4B as a key regulator of disease manifestation in the AppNL-G-F model and a promising therapeutic target for AD.
The present invention relates to a double-coated Lactic acid bacteria powder with a high survival rate of Lactic acid bacteria cell in the body by doubly coating Lactic acid bacteria with a protein and a polysaccharide and a method for preparing the Lactic acid bacteria powder. <??>The double-coated lactic acid bacteria powders according to the present invention show improved heat-resistance, acid-resistance, bile-resistance and storage stability, as well as excellent survival rate until reaching the intestines. <??>The present invention further relates to a method for manufacturing a dosage form containing the Lactic acid bacteria powder, which can minimize the death of the viable cell during manufacture of the dosage form. <IMAGE>
Cohort 1 (Aim 1) - 6 participants Cohort 1 will be comprised of 6 neonates (≤28 days of age) admitted to the CICU or NICU who are neither undergoing ECMO nor CPB. Cohort 1 will receive a single dose of ATIII by short 15 minute infusion.
Participants will receive plain white rice (75g of available carbohydrate) alongside a snack with crackers and cheese. The meal is similar in energy and macronutrients to the test meal.
Approval of the study was obtained from the hospital's ethical committee. The study design and methodology followed the tenets of Declaration of Helsinki. All patients were provided with written informed consent and received a thorough explanation of the study design, aims, benefits and potential risks. This is a prospective non-comparative interventional study.

Aqueous humor samples were collected from participants to virus detection. Participants will take oral acyclovir 100 mg three times a day and data will be collected prospectively with regard to ophthalmologic outcomes. Study participants will be followed for up to 12 months to determine efficacy, and an additional 30 days for safety reports. Descriptive statistics will be gathered on participant demographics, uveitis characteristics, change in immunosuppressive medications, number of responders, ophthalmologic measures and change in corticosteroid dose during the study period.
The patients received 13 administrations of a placebo, as per the following schedule: For the first five doses: 1 dose every 3 weeks. For the remaining 8 doses: 1 dose every 12 weeks.
FIELD: genetic engineering, molecular biology. SUBSTANCE: invention relates to vectors comprising defective viral genome that expresses antigen useful for induction of secretory and systemic immune responses and antibody providing protection against infectious agent. The presented defective viral genome is prepared from the parental genome of porcine virus of transmissive gastroenteritis (TGEV) by deleting part of parental genome and retains 3'- and 5'-ends of parental genome with localized recognition signals by viral replicase and at least a promoter. Indicated vectors are useful for design of recombinant system that comprises the indicated expression vector and helper virus. Such system is used for preparing mono- and polyvalent vaccines against infectious agents of animals of different species. Invention proposes also vectors of expression of heterologous genes with high level of safety and capacity of cloning and their construction provides species specificity and tropism that can be controlled easily. EFFECT: valuable properties of vector. 14 cl, 2 tbl, 30 dwg, 5 ex
CARNEXIV is a replacement therapy for oral carbamazepine. Carbamazepine treatment should generally be initiated with an oral carbamazepine formulation. 

The total daily dose of CARNEXIV is 70% of the total daily oral carbamazepine dose from which patients are being switched (see Table 1). The total daily dose of CARNEXIV should be equally divided in four 30-minute infusions, separated by 6 hours.

Patients should be switched back to oral carbamazepine administration at their previous total daily oral dose and frequency of administration as soon as clinically appropriate. The use of CARNEXIV for periods of more than 7 days has not been studied.

Table 1\. Determination of Total Daily Dose for CARNEXIV Infusion
Deposition of amyloid beta (Aβ) into plaques is a major hallmark of Alzheimer's disease (AD). Different amyloid precursor protein (APP) mutations cause early-onset AD by altering the production or aggregation properties of Aβ. We recently identified the Uppsala APP mutation (APPUpp), which causes Aβ pathology by a triple mechanism: increased β-secretase and altered α-secretase APP cleavage, leading to increased formation of a unique Aβ conformer that rapidly aggregates and deposits in the brain. The aim of this study was to further explore the effects of APPUpp in a transgenic mouse model (tg-UppSwe), expressing human APP with the APPUpp mutation together with the APPSwe mutation. Aβ pathology was studied in tg-UppSwe brains at different ages, using ELISA and immunohistochemistry. In vivo PET imaging with three different PET radioligands was conducted in aged tg-UppSwe mice and two other mouse models; tg-ArcSwe and tg-Swe. Finally, glial responses to Aβ pathology were studied in cell culture models and mouse brain tissue, using ELISA and immunohistochemistry. Tg-UppSwe mice displayed increased β-secretase cleavage and suppressed α-secretase cleavage, resulting in AβUpp42 dominated diffuse plaque pathology appearing from the age of 5-6 months. The γ-secretase cleavage was not affected. Contrary to tg-ArcSwe and tg-Swe mice, tg-UppSwe mice were [11C]PiB-PET negative. Antibody-based PET with the 3D6 ligand visualized Aβ pathology in all models, whereas the Aβ protofibril selective mAb158 ligand did not give any signals in tg-UppSwe mice. Moreover, unlike the other two models, tg-UppSwe mice displayed a very faint glial response to the Aβ pathology. The tg-UppSwe mouse model thus recapitulates several pathological features of the Uppsala APP mutation carriers. The presumed unique structural features of AβUpp42 aggregates were found to affect their interaction with anti-Aβ antibodies and profoundly modify the Aβ-mediated glial response, which may be important aspects to consider for further development of AD therapies.
Patients receive dexamethasone IV on days 1, 8, 15, and 22 of cycles 1-2 and IV on day 1 and PO on days 8, 15, and 22 of subsequent cycles and elotuzumab IV on days 1, 8, 15, and 22 of cycles 1-2 and day 1 of subsequent cycles. Patients also receive pomalidomide PO on days 1-21. Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity.
The hallmark of heart failure (HF) is structural myocardial remodeling including cardiomyocyte hypertrophy, fibrosis, cardiomyocyte cell death, and a low-grade aseptic inflammation. The initiation and maintenance of persistent chronic low-grade inflammation in HF are not fully understood. Oxidative stress-mediated neutrophil extracellular traps (NETs) are the main immune defense mechanism against external bacterial infections. Furthermore, NETs play important roles in noninfectious diseases. In the settings of myocardial infarction, myocarditis, or cardiomyopathies, neutrophils infiltrate the cardiac tissue and undergo NETosis that further aggravate the inflammation. A number of stimuli may cause NETosis that is a form of programmed cell death of neutrophils that is different from apoptosis of these cells. Whether NETosis is directly involved in the pathogenesis and development of HF is still unclear. In this review, we analyzed the mechanisms and markers of NETosis, especially placing the accent on the activation of the neutrophil-specific myeloperoxidase (MPO), elastase (NE), and peptidylarginine deiminase 4 (PAD4). These conclusions are supported by the recent genetic and pharmacological studies which demonstrated that MPO, NE, and PAD4 inhibitors are effective at least in the settings of post-myocardial infarction adverse remodeling, cardiac valve diseases, cardiomyopathies, and decompensated left ventricular hypertrophy whose deterioration can lead to HF. This is essential for understanding NETosis as a contributor to pathophysiology of HF and developments of new therapies of HF.