anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Participants will receive 2 treatments of intermittent Theta Burst Stimulation, each two weeks apart. First session will be iTBS alone, the second session will be combined iTBS with APT (Attention processing training).
The present invention relates to novel therapeutic or prophylactic treatment in human subjects. The present invention results in part from the discovery that antagonists of IL-18R.alpha. are effective in vivo for treating diseases.  Accordingly, the invention provides a method of treating, preventing or ameliorating the symptoms of an autoimmune or demyelinating disease (such as multiple sclerosis) in a subject, preferably a human subject, said method comprising administering to the subject a therapeutically effective amount of an antagonist of IL-18R.alpha.. The invention also pertains to the use of an antagonist of IL-18R.alpha. in the manufacture of a medicament for the treatment of an autoimmune or demyelinating diseases (such as multiple sclerosis).
Colorectal cancer is the third largest cause of cancer mortality in the United States. The treatment of metastatic colorectal cancer is undergoing rapid improvement. Currently, there are two major chemotherapy regimens, which can both be combined with anti-angiogenesis treatment. These regimens are 5-Fluorouracil (5-FU) + irinotecan and 5-FU + oxaliplatin. Each therapy has roughly similar rates of response, but it is unclear which specific therapy would benefit which patients. The advent of genome wide expression analysis provides a tool to analyze these differences. In the microarray analysis of colon cancer outcome trial, sponsored by the National Institutes of Health (NIH) and Moffitt Cancer Center, patients with newly diagnosed metastatic colon cancer are biopsied and samples are preserved in ribonucleic acid (RNA) later. Patients are then randomized to either one of two state of the art regimens: capecitabine + irinotecan + avastin (bevacizumab) or capecitabine + oxaliplatin + avastin. Response to chemotherapy, time to progression, and overall survival are end points of this trial. Once accrual of patients has been met, the investigators will compare genome wide expression patterns for each group.
PURPOSE: To produce a cross-linked polysaccharide free of unreacted substances, high in safety and biocompatibility, and useful as a medical material by irradiating an ionizing radiation-reactive polysaccharide with an ionizing radiation. CONSTITUTION: An ionizing radiation-reactive polysaccharide having a polysaccharide (biocompatible polysaccharide such as glycosaminoglycan is pref.) bonded to at least 1 ionizing radiation-reactive compd. (compd. low in toxicity and little in side effect even when used as a medical material is pref., examples of which include cinnamic acid and coumarin) via covalent bonds is irradiated with an ionizing radiation to bring about a mutual cross-linking reaction of ionizing radiation-reactive compd. residues to produce a cross-linked polysaccharide. The cross-linked polysaccharide free of unreacted substances causative of a side effect, etc., high in safety and biocompatibility, and useful as a medical material is obtd. according to the foregoing procedure.
This invention is an anti-allergy composition comprising the distillation solution of wood vinegar as the effective component. It is preferable to use the distillation solution of bamboo vinegar by using bamboo materials as the wood materials. Also, it is preferable that the composition substantially not comprises benzopyrene, dibenzanthracene, and methylcholanthrene. The anti-allergic composition can express anti-allergy function by oral administration of effective amount of the composition. Specifically, The composition can be applied in the inhibition of type I allergy such as allergic rhinitis, pollinosis, allergic conjunctivitis, atopic dermatitis, allergic asthma, urticaria, food allergy, anaphylaxis and the like. Further, the composition can be applied to skin. The distillation solution of wood vinegar is obtained by smoke treatment which is to smoke the wood materials at 130 to 170 DEG C and dry; then by carbonization treatment at 350 to 450 DEG C; the smoke discharged from the carbonization treatment is condensed resulting in a crude wood vinegar; the crude wood vinegar is distilled under reduced pressure and low temperature at 50 to 60 DEG C.
PURPOSE: A method for preparing apipiprazole crystal form II is provided to improve the purity of apipiprazole and to lower preparation cost. CONSTITUTION: A method for preparing apipiprazole crystal form II comprises: a step of introducing apipiprazole crystal in a mixture solvent of acetone and 1-methoxy-2-propanol or 1-methoxy-2-propanol single solvent; a step of heating in the mixture solvent at 45-60 Deg. C. or in the single solvent at 70-90 Deg. C. and stirring; a step of seeding the apipiprazole crystal form II at 35-65 Deg. C.; and a step of isolating the crystal from the solution. The method additionally comprises a step of washing and drying.
PROBLEM TO BE SOLVED: To obtain the subject pharmaceutical preparation rapidly dissolving and disintegrating by saliva and capable of readily taking into a human body without using water thereby. SOLUTION: This pharmaceutical preparation contains an active ingredient, erythritol and a solid organic acid having a small acidity. Furthermore, the total content of erythritol in the pharmaceutical preparation and the solid organic acid is 50-99.9wt.%. The content of the solid organic acid is 0.0001 to 5wt.% based on the content of erythritol and the solid organic acid in the pharmaceutical preparation. Since the pharmaceutical preparation uses erythritol as a sugar alcohol, the preparation does not react with the active ingredient and since the erythritol hardly exhibits hygroscopic property, the active ingredient is good in stability. Since the preparation contains the solid organic acid having a small acidity, the preparation has good drinking feeling and can readily be taken by children and aged persons.
BACKGROUND: Determining which patients benefit from a serious illness conversation (SIC) is challenging. The authors sought to determine whether Epic's Risk of Readmission Score (RRS), could be combined with a simple, validated, one-question mortality prognostic screen (the surprise question: Would you be surprised if the patient died in the next 12 months?) to identify hospitalized patients with SIC needs.
METHODS: In this retrospective study, the authors randomly selected encounters for patients ≥ 18 years of age to a general medicine service from January 2019 to October 2021 who had an RRS > 28%. Two adjudicators independently performed chart reviews for each encounter to answer the surprise question to create two distinct prognostic groups (yes vs. no). Fisher's exact test was used to assess for statistically significant differences in standardized documentation of SICs between groups.
RESULTS: Out of 2,879 encounters, 202 patient encounters were randomly selected. Adjudicators answered "no" to the surprise question for 156 (77.2%) patients. Patients for whom adjudicators answered "no" were generally older with higher comorbidity and more often had standardized documentation of a SIC (14 [9.0%] vs. 0.[0.0%], p = 0.042) compared to patients for whom adjudicators answered "yes."
CONCLUSION: Approximately three quarters of patients with a high RRS were predicted to have a lifespan of less than a year. Although these patients were significantly more likely to have a SIC, rates of SICs were extremely low. Combining available electronic health record (EHR) data with a simple one-question screening tool may help identify hospitalized patients who require a SIC in quality improvement initiatives.
INTRODUCTION: LncRNA LBX2-AS1 drives the development of various cancers, but the exact mechanism whereby LBX2-AS1 affects glioblastoma (GBM) progression is unaddressed. This study intended to delineate the regulatory mechanism of LBX2-AS1 in GBM metastasis and angiogenesis.
MATERIAL AND METHODS: LBX2-AS1 level in GBM was assessed by bioinformatics methods. The lncRNA-transcription factor (TF)-mRNA trios were predicted using the lncMAP database. Correlation between genes was predicted by Pearson analysis. The binding relationship was predicted by JASPAR. Levels of LBX2-AS1 and its downstream genes were assayed via qRT-PCR. Changes in expressions of VEGF-A, IL4R, and epithelial-mesenchymal transition (EMT)-associated proteins were assessed through western blot. GBM cell proliferation, migration, and invasion were assayed through CCK8, colony formation, and Transwell experiments. In vitro angiogenesis capacity was evaluated via a HUVEC tube formation experiment. The regulatory relationship between various genes was verified through radioimmunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), and dual-luciferase assays.
RESULTS: LBX2-AS1 was elevated in GBM, and in vitro experiments demonstrated the stimulatory effect of LBX2-AS1 on GBM cell proliferation, invasion, migration, and angiogenesis. We observed that LBX2-AS1 activated IL4R expression by binding the transcription factor NFKB1, thus promoting the progression of GBM. Rescue experiments illustrated that silencing IL4R or NFKB1 reversed the impact of forced LBX2-AS1 expression on GBM cells.
CONCLUSIONS: This study revealed the mechanism of the LBX2-AS1/NFKB1/IL4R axis in driving GBM metastasis and angiogenesis, which may help to improve the regulatory network of GBM malignant progression and provide potential targets for GBM treatment.
F(ab) fragments are isolated from an antibody containing source by contacting the antibody containing source with a papain-polyacrylamide matrix to produce F(ab) and F(c) fragments which are then passed through an antigen-polyacrylamide gel capable of attracting the F(ab) fragments. F(ab)2 fragments are obtained by contacting the antibody containing source with a pepsin-polyacrylamide matrix to produce F(ab)2 and F(c) fragments which are then passed through an antigen-polyacrylamide gel capable of attracting the F(ab)2 fragments. IgG antibodies are obtained by passing an antibody containing source through an antigen-polyacrylamide gel. These processes can be used to purifiy a wide variety of antibodies which can be used as therapeutic agents and as diagnostic agents. Antivenins produced by these processes have substantially reduced foreign protein levels and hence are less likely to produce immunogenic reactions. Bulk, unprocessed antibody sources may be utilized and, for reasons of process simplification, are preferred.
The present invention relates to a traditional Chinese medicine compound preparation for treating asthma, which belongs to the field of medical preparation of traditional Chinese medicine. The present invention is made from liquorice extract, magnolia bark extract, common cnidium fruit P. E and medicine supplementary material, and is a safe, controllable, stable and effective traditional Chinese medicine compound preparation for treating asthma. The present invention has the efficacy of promoting Qi circulation and relieving asthma, and mainly treats the symptoms of phlegm dampness, essential resistance, inhibited lung energy, chest distress, cough with dyspnea, etc. Action mechanisms are specific. The present invention can be made into tablets, micro drop pills, granules and preparations of controlled slow release. Administration ways are oral administration, perfusion, etc., which is favorable to the clinic treatment of asthma diseases.
BACKGROUND: Lymph node metastasis (LNM) is a critical factor affecting the outcomes of head and neck squamous cell carcinoma (HNSCC) and the main reason for treatment failure. This study was designed to examine the effects of the key genes involved in the LNM of HNSCC.
METHODS: Tissue samples (HNSCC) were examined by transcriptome sequencing, and the core genes associated with LNM were detected via bioinformatics analysis. The functions of these core genes were then validated using the TCGA biological database and their effects on the propagation, invasion, and metastasis of HNSCC cells were evaluated through cell culture experiments. Moreover, the effect of core gene expression on the LNM capability of HNSCC was confirmed via a footpad xenograft mice model.
RESULTS: In the findings, a key gene involved in the LNM of HNSCC was identified as SLC7A2. It was correlated with adverse clinical prognosis and expressed with low expression in HNSCC tissues. As shown in cell culture experiments, FaDu and SCC15 cell growth, invasion, and migration were inhibited when SLC7A2 was overexpressed. Further, cell apoptosis was stimulated, and lymphangiogenesis was suppressed through the downregulation of CPB2 expression. Animal studies demonstrated that the growth and LNM of HNSCC cells were inhibited by SLC7A2 overexpression.
CONCLUSION: It is concluded that SLC7A2 is involved in HNSCC lymphatic metastasis by controlling CPB2 function. The results are anticipated to offer new directions for the effective treatment of HNSCC.
Retrospective and prospective data will be collected about patients who participated in the Scleroderma Lung Study (SLS). An attempt will be made to include all of the participants of the Scleroderma Lung Study, who were reported as alive at the end of that study.

A total of 158 subjects (79 per treatment arm) were randomized on the original Scleroderma Lung Study. Of those, 109 subjects completed the study. A single telephone interview with the participants to assess the occurrence of severe events and a review of the participant's medical records may be conducted. The outcome information will be combined with information collected about all participants in the SLS study. The data being collected includes information on mortality, development of cancers, development of organ failure, and performance status.
Retinal pigment epithelium (RPE) structure and function are essential to normal vision, and alterations in the RPE can impair function and lead to retinopathy. Gene therapy is currently investigated for the treatment of retinal pigment epithelial diseases but there is a need for identifying promoter polynucleotides that will allow specific expression of polynucleotides of interest in said tissue. The SLC16A8 gene encodes for a RPE-specific lactate transporter MCT3. The inventors aimed at defining the sequence sufficient to drive specific expression of SLC16A8 in the RPE. To identify the promoter region of SLC16A8, different candidate fragments were then cloned into plasmids expressing a reporter gene to test the ability of each of these regions to activate the expression of this reporter. They also chose to exploit the restricted expression of SLC16A8 and to perform this experiment by a new in vivo approach using recombinant adenovirus associated virus (rAAV). By combining the methods, the inventors succeed in identifying the promoter region of SLC16A8.
Participants with CAD and a BRS greater than 0 who are randomized to the Optimization Group have treatment goals that include achieving LDL-C\<70 mg/dL, hemoglobin A1c \<7%, blood pressure \<130/80 mmHg, smoking cessation, at least 30 minutes of moderate-intensity aerobic activity 5 days a week and weight loss to body mass index \<30 kg/m2. To achieve these goals, both pharmacological and lifestyle interventions will be considered and individualized for each patient.
After randomization, participants received a single daily oral dose of 5 mg amlodipine and 160 mg valsartan free combination therapy, taken in the morning between 6-10 am. At week 4, uncontrolled patients (msSBP \>= 140 mmHg and/or msDBP \>= 90 mmHg or msSBP \>= 130 mmHg and/or msDBP \>= 80 mmHg in the case of diabetes or renal insufficiency measured by using conventional methods) received amlodipine/valsartan 10/160 mg for 4 additional weeks. Patients who were controlled at Week 4 (msSBP \< 140 mmHg and msDBP \< 90 mmHg or msSBP \< 130 mmHg and msDBP \< 80 mmHg in the case of diabetes or renal insufficiency) continued their amlodipine/valsartan 5/160 mg treatment for the remaining 4 weeks of the study.
A variety of clinical studies have demonstrated that elevated levels of Total-C, LDL-C, and Apo B promote human atherosclerosis. Similarly, decreased levels of HDL-C are associated with the development of atherosclerosis. Epidemiological investigations have established that cardiovascular morbidity and mortality vary directly with the level of Total-C and LDL-C, and inversely with the level of HDL-C.

Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including VLDL, intermediate-density lipoprotein (IDL), and their remnants, can also promote atherosclerosis. Elevated plasma TG are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with non-lipid metabolic risk factors for coronary heart disease (CHD). As such, total plasma TG has not consistently been shown to be an independent risk factor for CHD. Furthermore, the independent effect of raising HDL-C or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined.

SIMCOR

SIMCOR reduces total-C, LDL-C, non-HDL-C, Apo B, TG, and Lp(a) levels and increases HDL-C in patients with primary hyperlipidemia, mixed dyslipidemia, or hypertriglyceridemia.

Niacin

Niacin (but not nicotinamide) in gram doses reduces LDL-C, Apo B, Lp(a), TG, and Total-C, and increases HDL-C. The magnitude of individual lipid and lipoprotein responses may be influenced by the severity and type of underlying lipid abnormality. The increase in HDL-C is associated with an increase in apolipoprotein A-I (Apo A-I) and a shift in the distribution of HDL subfractions. These shifts include an increase in the HDL2:HDL3 ratio, and an elevation in lipoprotein A-I (Lp A-I, an HDL-C particle containing only Apo A-I). Niacin treatment also decreases serum levels of apolipoprotein B-100 (Apo B), the major protein component of the very low-density lipoprotein (VLDL) and LDL fractions, and of Lp(a), a variant form of LDL independently associated with coronary risk. In addition, preliminary reports suggest that niacin causes favorable LDL particle size transformations, although the clinical relevance of this effect requires further investigation.

Simvastatin

Simvastatin reduces elevated total-C, LDL-C, Apo B, and TG, and increases HDL-C in patients with primary heterozygous familial and nonfamilial hypercholesterolemia and mixed dyslipidemia. Simvastatin reduces total-C and LDL-C in patients with homozygous familial hypercholesterolemia. Simvastatin decreases VLDL, total-C/HDL-C ratio, and LDL-C/HDL-C ratio.
Participants enrolling from study 001B, received lumasiran, SC injection, at a starting dose of 3.0 mg/kg, QM, from Day 1 up to a maximum of Month 21. By Month 21, all participants were approved to change dosing regimen to receive lumasiran, SC injection, at a dose of 3.0 mg/kg, Q3M, up to Month 51 of the treatment period.
1. A Salmonella microorganism having an attenuating mutation which disrupts the expression of ssaV gene and mutation which disrupts the expression of aroC gene. 2. A microorganism according to claim 1, wherein the microorganism further comprises a heterologous antigen or a therapeutic protein. 3. A microorganism according to claim 2, wherein the antigen is a hepatitis A, B or C antigen. 4. A microorganism according to any preceding claim, wherein the microorganism is Salmonella typhi Ty2. 5. A microorganism according to any preceding claim, for use in therapy of bacterial or virus infection. 6. A vaccine composition comprising a microorganism according to any of claims 1 to 4, and an adjuvant and a physiologically acceptable diluent. 7. A composition according to claim 6, comprising from 10<7>-10<10> CFUs in a single dosage unit. 8. A composition according to claim 7, comprising 10<8>-10<9> CFUs. 9. Use of a microorganism as defined in any of claims 1 to 4, in the manufacture of a medicament for intravenous administration for the treatment of systemic bacterial infection. 10. Use of a microorganism as defined in any of claims 1 to 4, in the manufacture of a medicament for oral delivery for the treatment of systemic bacterial infection. 11. Use according to claim 9 or claim 10, for the treatment of typhoid.
BACKGROUND: Hardware removal (HR) is one of the most common surgical procedures in pediatric orthopaedics. Surgeons advocate for HR for a variety of reasons, including to limit peri-implant fracture risk, restore native anatomy for adult reconstruction surgery, permit bone growth and development, and mitigate implant-related pain/irritation. To our knowledge, no recent study has investigated the characteristics and complications of HR in pediatric orthopaedics. The goal of this study is to report the prevalence and complications of hardware removals across all of pediatric orthopaedic surgery.
METHODS: A retrospective case series was conducted of all hardware removals from 2012 to 2023 performed at a single urban tertiary-care children's hospital. Cases were identified using CPT codes/billing records. Spinal hardware and cases for which hardware was either implanted or explanted at an outside hospital were excluded. Patient demographic and clinical data were recorded. For patients with multiple hardware removals, each case was recorded independently.
RESULTS: A total of 2585 HR cases for 2176 children met study criteria (57.7% male; mean age 12.3±4.4 y). The median postoperative follow-up time was 1.7 months (interquartile range: 0.6 to 6.9). The most common sites of hardware removal were the femur/knee (32.7%), tibia/fibula/ankle (19.3%), and pelvis/hip (18.5%). The most common complications included sustained, new-onset postoperative pain (2.6%), incomplete hardware removal (1.6%), and perioperative fracture (1.4%). The overall complication rate of hardware removal was 9.5%. Eighty-eight percent of patients who underwent hardware removal for pain experienced pain relief postoperatively. HR >18 months after insertion had a 1.2x higher odds of overall complication ( P =0.002) and 3x higher odds of incomplete removal/breakage ( P <0.001) than hardware removed 9 to 18 months after insertion.
CONCLUSIONS: The overall complication rate of hardware removal across a large series in the pediatric population was 9.5%. Despite hardware removal being one of the most common and often routine procedures in pediatric orthopaedics, the complication rate is not benign. Surgeons should inform patients and families about the likelihood of success and the risks of incomplete removal during the informed consent process.
LEVEL OF EVIDENCE: IV.
A composition for improving sleep. In one embodiment, the composition comprises L-Tryptophan, L-Theanine, Reishi mushroom extract, Uridine, a polyphenol, and paeoniflorin. In certain embodiments, the composition further comprises citrus bioflavonoid extract, γ-Oryzanol, holy basil extract, saffron extract, Schisandra chinensis extract, sesamin extract, blueberry extract, quercetin, Polygala tenufolia root extract, gotu kola extract, ashwagandha extract, betaine, magnesium, or combinations thereof. In other embodiments, the composition further comprises astaxanthin, lycopene, hawthorne extract, or combinations thereof. In certain embodiments, the composition is incorporated into pills. A method for promoting the brain pathways involved in sleep, relaxation, and calmness comprising: ingesting a composition comprising L-Tryptophan, L-Theanine, Reishi mushroom extract, Uridine, a polyphenol, and paeoniflorin. In one method, the composition is ingested at least one and a half hours before bedtime.