anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
This is a multi-center (more than one clinical site will work on a medical research study), randomized (study medication assigned to participants by chance), double-blind (neither investigator nor participant knows which treatment the participant receives), placebo-controlled (placebo is an inactive substance that is compared with a drug to test whether the drug has a real effect in a clinical trial) study to determine the efficacy and safety of guselkumab in participants with PsA. The study will consist of 4 parts: Screening period (6 weeks), a double-blind treatment period (consists of guselkumab and placebo treatment for 24 weeks), an active treatment period (guselkumab for 20 weeks), and follow-up period (12 weeks). The maximal study duration for a participant will not exceed 62 weeks including the Screening period. Eligible participants will be randomly assigned to one of two groups in a 2:1 ratio to either receive Guselkumab 100 milligram (mg) at Weeks 0, 4 then every 8 weeks or Placebo at Weeks 0, 4 then every 8 weeks until Week 24. At week 24, participants remaining in the placebo group will start to receive guselkumab 100 mg at Weeks 24, 28, 36 and 44. Participants in both treatment groups who have less than (\<) 5 percent (%) improvement from baseline in both tender and swollen joint counts at Week 16 will qualify for early escape and will switch to open-label therapy with ustekinumab 45 mg or 90 mg at Weeks 16, 20, 32, and 44 based on the approved dosage for the PsA indication in the particular country of study. The efficacy will be assessed primarily by measuring percentage of participants who achieve an American College of Rheumatology (ACR) 20 Response at Week 24. Participants' safety will be monitored throughout the study.
<P>PROBLEM TO BE SOLVED: To provide a molecular marker useful for earlier diagnosing disorders in patients in a hypophosphatemic state and in a hyperphosphatemic state, classifying malignancy and classifying a stage of a disease and to provide a method for similarly and effectively treating patients of hypophosphatemic and hyperphosphatemic disorders.  <P>SOLUTION: The new nucleic acid encodes a fibroblast growth factor-23 (FGF23) in which mutations are associated with autosomal dominant hypophosphatemic rickets (ADHR). The protein is encoded thereby. The method for diagnosing and treating hypophosphatemic and hyperphosphatemic disorders comprises inhibiting or stimulating, respectively, the biological activity of FGF23 in a patient. The method for treating osteoporosis, dermatomyositis and coronary artery disease comprises stimulating the biological activity of FGF23 in a patient.  <P>COPYRIGHT: (C)2008,JPO&INPIT
BACKGROUND: Apical papilla stem cells (SCAPs) exhibit significant potential for tissue repair, characterized by their anti-inflammatory and pro-angiogenic properties. Exosomes derived from stem cells have emerged as safer alternatives that retain comparable physiological functions. This study explores the therapeutic potential of exosomes sourced from SCAPs in the treatment of non-alcoholic steatohepatitis (NASH).
METHODS: A NASH mouse model was established through the administration of a high-fat diet (HFD), and SCAPs were subsequently isolated for experimental purposes. A cell model of NASH was established in vitro by treating hepatocellular carcinoma cells with oleic acid (OA) and palmitic acid (PA). Exosomes were isolated via differential centrifugation. The mice were treated with exosomes injected into the tail vein, and the hepatocytes were incubated with exosomes in vitro. After the experiment, physiological and biochemical markers were analyzed to assess the effects of exosomes derived from SCAPs on the progression of NASH in both NASH mouse models and NASH cell models.
RESULTS: After exosomes treatment, the weight gain and liver damage induced by HFD were significantly reduced. Additionally, hepatic fat accumulation was markedly alleviated. Mechanistically, exosomes treatment promoted the expression of genes involved in hepatic fatty acid oxidation and transport, while simultaneously suppressing genes associated with fatty acid synthesis. Furthermore, the levels of serum inflammatory cytokines and the mRNA expression of inflammatory markers in liver tissue were significantly decreased. In vitro cell experiments produced similar results.
The present invention relates to a newly identified human ubiquitin protease belonging to the family of mammalian deubiquitinating enzymes. The invention also relates to polynucleotides encoding the ubiquitin protease. The invention further relates to methods using the ubiquitin protease polypeptides and polynucleotides as a target for diagnosis and treatment in ubiquitin-mediated or -related disorders. The invention further relates to drug-screening methods using the ubiquitin protease polypeptides and polynucleotides to identify agonists and antagonists for diagnosis and treatment. The invention further encompasses agonists and antagonists based on the ubiquitin protease polypeptides and polynucleotides. The invention further relates to procedures for producing the ubiquitin protease polypeptides and polynucleotides.
The invention discloses a probiotic human injection, and relates to an injection for treating high-risk diseases of cancers, phthisis and AIDS (Acquired Immune Deficiency Syndrome). Only a part of focus of infection can be cut off by employing a western medicine surgery; human cells, and tissues and organs are damaged, probiotic bacteria in the body are killed, and the human immunity is damaged when germs and viruses are killed by the Chinese-western drugs. The incubation periods of the cancers and AIDS are 7-8 years, and the cancers and AIDS cannot be cured within a day, so that the Chinese-western drugs are theories and basis in fact for the incurable high-risk diseases. The probiotic human injection is injected all over a human body, and directly achieves the focus of infection; the human cells, and tissues and organs are not damaged; the injured cells are repaired; the probiotic bacteria in the body are not damaged. The human immune function is enhanced by probiotics; the germs and viruses are treated by bacteria; the sufferer inevitably quickly recovers along with gradual reduction of the germs and viruses in the body. Therefore, the probiotic human injection is the theory of curing the high-risk diseases.
A pace lead is mounted on the stomach, and exteriorized trough the skin and connected to an external pacemaker. The pacemaker is set to the following settings: 10,5 Volt, 14 hz, 330 Micro sec, Cycling 5 seconds off 0,1 sec on. The pacemaker is turned on.
Use of divalproex sodium extended-release tablets during pregnancy can cause congenital malformations including neural tube defects. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus. Divalproex sodium extended-release tablets should be considered for women of childbearing potential only after the risks have been thoroughly discussed with the patient and weighed against the potential benefits of treatment.   
Data suggest that there is an increased incidence of congenital malformations associated with the use of valproate by women with seizure disorders during pregnancy when compared to the incidence in women with seizure disorders who do not use antiepileptic drugs during pregnancy, the incidence in women with seizure disorders who use other antiepileptic drugs, and the background incidence for the general population.   
The data described below were gained almost exclusively from women who received valproate to treat epilepsy. There are multiple reports in the clinical literature that indicate the use of antiepileptic drugs during pregnancy results in an increased incidence of congenital malformations in offspring. Antiepileptic drugs, including valproate, should be administered to women of childbearing potential only if they are clearly shown to be essential in the management of their medical condition.   
Antiepileptic drugs should not be discontinued abruptly in patients in whom the drug is administered to prevent major seizures because of the strong possibility of precipitating status epilepticus with attendant hypoxia and threat to life. In individual cases where the severity and frequency of the seizure disorder are such that the removal of medication does not pose a serious threat to the patient, discontinuation of the drug may be considered prior to and during pregnancy, although it cannot be said with any confidence that even minor seizures do not pose some hazard to the developing embryo or fetus. [see Boxed Warning and Use in Specific Populations(8.1)].
Maternal ZDV treatment starting at 28 weeks Gestational Age (GA) and continuing through labor and delivery, and six weeks of infant ZDV treatment starting at birth (Lmother-Linfant). This study arm was the reference regimen.
Reducing hypoglycemia is an important aspect of management of T1D in older adults, many of whom have hypoglycemic unawareness, cognitive impairment, or both. CGM offers the opportunity to reduce hypoglycemia and its related complications such as fractures from falls and hospitalizations and improve quality of life including reducing hypoglycemic fear and diabetes distress. Despite these potential benefits, CGM is used by only a small proportion of older adults with T1D. Previous studies assessing CGM efficacy have included only a small number of adults ≥ 60 years of age, excluded patients most prone to severe hypoglycemia, focused on improving HbA1c rather than hypoglycemia, and used older generation CGM sensors. These studies are not generalizable to the population of older adults with T1D. The potential benefit of CGM in reducing hypoglycemia in the older adult population has not been well studied. The goal of this study is to assess the potential benefits and risks of CGM in older adults with T1D.
The invention relates to a product comprised of specific combinations of cell lines intended for use as an allogeneic immunotherapy agent for the treatment of cancer in humans. The heterogeneity of the immunotherapeutic matches the heterogeneity of the antigenic profile in the target cancer and immunises the recipients with many of the potential TAA and TSA which are expressed at various stages of the disease. The invention discloses a two part product comprising as first part: a single cell line used for the first two to five administrations; and a second part which is a mixture of three different of the cell lines which may or may not include the single cell line used in the first part, used for subsequent vaccinations. Cell lines may be prepared from cancer biopsy material using techniques known to those skilled in the art. In the case of prostate cancer, for example, cell lines may be prepared from primary or metastatic prostate cancer biopsy material. The cell lines are lethally irradiated utilising gamma irradiation at 50-300 Gy to ensure that they are replication incompetent.
This intervention consists of 6, 50-60-minute online individual sessions delivered via video conference. Content will include a CBT-I based program adapted to the specific needs of spousally bereaved individuals.
OBJECTIVES: I. Determine the maximum tolerated dose of LY231514 followed by irinotecan in patients with metastatic cancer. II. Determine the quantitative and qualitative toxicity of LY231514 in combination with irinotecan in these patients. III. Assess plasma pharmacokinetics in these patients treated with this regimen. IV. Document any antitumor activity of this regimen in these patients.

OUTLINE: This is a dose escalation study. Patients receive LY231514 IV over 10 minutes followed by irinotecan IV over 90 minutes on day 1. Courses repeat every 3 weeks in the absence of disease progression and unacceptable toxicity. Cohorts of 3-6 patients each receive escalating doses of LY231514 and irinotecan. If escalation of one drug in the combination results in unacceptable dose limiting toxicity (DLT), the drug is not escalated further. Instead, the dose of that drug is decreased to its safe dose, and the second drug is escalated until unacceptable DLT results. If DLT occurs in 2 of up to 6 patients at any level, dose escalation is stopped. The maximum tolerated dose is defined as the highest dose at which fewer than 2 of 6 patients experience DLT during courses 1 or 2.

PROJECTED ACCRUAL: Up to 42 patients will be accrued for this study.
BACKGROUND AND PURPOSE: CSF leaks of the skull base and spine share a common process of CSF volume loss, and yet only the latter has been associated with spontaneous intracranial hypotension (SIH). Despite published claims that only spinal leaks cause SIH, no prior studies have evaluated brain MR imaging in patients with skull base leaks for findings associated with SIH, such as dural enhancement. The purpose of our study was to use a validated brain MR imaging scoring system to evaluate patients with skull base CSF leaks for findings associated with SIH.
MATERIALS AND METHODS: We included patients with confirmed skull base CSF leaks and contrast-enhanced preoperative brain MRI. The preoperative MR images were reviewed for findings associated with SIH by using the Bern score. Patient age, presenting symptoms and their duration, and leak site were also recorded.
RESULTS: Thirty-one patients with skull base CSF leaks were included. Mean Bern score was 0.9 (range 0-4, standard deviation 1.1), and only 1 patient (3%) had dural enhancement. Mean age was 53 years (range 18-76). Mean symptom duration was 1.3 years, with 22 patients presenting within 1 year of symptom onset. Twenty-three patients (74.2%) had intraoperative confirmation of leak from the middle cranial fossa, involving the temporal bone, while 7 (22.6%) had leaks from the anterior skull base. One patient, who had dural enhancement, had an infratentorial CSF leak along the petrous segment of the internal carotid artery.
CONCLUSIONS: Our study provides further evidence that skull base and spinal CSF leaks represent distinct pathophysiologies and present with different brain MRI findings.
PURPOSE:To obtain an anticarious agent, containing an ingredient of green tea or an extract therefrom soluble in chloroform as an active ingredient, capable of sterilizing Streptococcus mutans which is a bacterium causing the dental caries or suppressing the proliferation thereof and having ultrahigh practicality without any side effects on the human body. CONSTITUTION:This anticarious agent contains an ingredient of green tea or an extract therefrom soluble in chloroform as an active ingredient. The ingredient soluble in chloroform is preferably obtained by a method for extracting a drinkable tea leaf such as green tea or oolong tea with water or an organic solvent such as ethanol, then distilling away the solvent from the resultant extract solution, subsequently dissolving or suspending its residue in water, then carrying out the partition with chloroform and further distilling away the chloroform, etc., from the chloroform layer. Furthermore, the anticarious agent is used by mixing in, e.g. a dentifrice, a gargle, a chewing gum, etc.; however, the amount thereof used therein is preferably 100-500ppm.
The present inventions relates to substances which are capable of controlling the inclusion of exon (10) of the tau gene. The substances can reverse "wrong"  tau splicing pattern and. Since "wrong" tau splicing patterns are associated with tauopathies that cause dementia, the substances can be used as therapeutic agents. The invention also provides a method for testing substances that control tau exon (10) inclusion. The method is suitable for a high throughput screening. Additional products which are useful for changing tau exon (10) expression or for performing the test method are described as well.
Participants will receive anodal TDCS over the left inferior frontal cortex. TDCS will be delivered at 1milliampere (mA) intensity for 20 minutes during speech fluency training (5 consecutive days).
<P>PROBLEM TO BE SOLVED: To provide a new photosensitizer which allows photodynamic therapy to more effectively adapt to the therapy of acne and psoriasis.  <P>SOLUTION: An acne therapeutic agent and a sebum secretion inhibitor comprise an indole-3-alkylcarboxylic acid (IAA) or its derivative as a new application. More specifically, the photosensitizer for photodynamic therapy (PDT) comprises IAA having a property of being activated by rays. A kit for photodynamic therapy and a composition for photodynamic therapy comprise the same, and a new application as an acne therapeutic agent and a sebum secretion inhibitor is disclosed. As a light source for activating IAA, ultraviolet rays and visible rays can be used and particularly, blue rays or green rays are preferably utilized.  <P>COPYRIGHT: (C)2009,JPO&INPIT
There is widespread empirical evidence that the COVID-19 pandemic contributed to elevated risk of mental and physical health symptoms and decreased quality of life. The present investigation sought to examine if individual differences in anxiety sensitivity was associated with mental health, psychosomatic, and well-being among a sample of US adults during a 6-month period early in the COVID-19 pandemic. Employing longitudinal research methodology, we tested the hypothesis that the anxiety sensitivity global factor would be related to increased risk of anxiety, depression, fatigue, and lower well-being. Secondary analyses evaluated the lower order anxiety sensitivity factors for the same criterion variables. The sample consisted of 778 participants with an average age of 37.96 (SD = 11.81; range 18-73). Results indicated that, as hypothesized, anxiety sensitivity was associated with increased risk for more severe anxiety, depression, fatigue, and lesser well-being; the observed effects of anxiety sensitivity were relatively robust and evident in adjusted models that controlled for numerous theoretically and clinically relevant factors (e.g. perceived health status). Overall, these results suggest that pandemic functioning could likely be improved via interventions that target elevated anxiety sensitivity as a vulnerability factor for a broad range of aversive psychosomatic symptoms and personal well-being.
Uncontrolled TLR signaling can cause inflammatory immunopathology and trigger autoimmune diseases. For example, TLR7 promotes pathogenesis of systemic lupus erythematosus. However, whether RNA structural changes affect nucleic acids-sensing TLRs signaling and impact disease progression is unclear. Here by iCLIP-seq we identify a TLR7-binding long non-coding RNA, Lnc-Atg16l1, and find that it promotes TLR7 and other MyD88-dependent TLRs signaling in various types of immune cells. Depletion of Lnc-Atg16l1 attenuates development of TLR7-linked autoimmune phenotypes in the mouse SLE model. Mechanistically, we find that Lnc-Atg16l1 binds to TLR7 at bases near U84 and MyD88 at bases around A129. The analysis of Lnc-Atg16l1 in situ structures show that it strengthens the interaction between TIR domain of TLR7 and MyD88 through specific stem-loop structure changes as a molecular scaffold after TLR7 activation to promote TLR7 downstream signaling. Therefore, we discover a mechanism for host RNA regulation of innate signaling and autoimmune disease through its structural changes. These findings provide insights into the pro-inflammatory function of self RNA in a structure-dependent manner and suggest a potential target for TLR-related autoimmune disorders.
Participants performed an intervention for 3 sessions/week, over 3 weeks and a cycle ergometer was used. The workout regimen consisted of a structured warm-up lasting 2 minutes. The main exercise phase comprised an 8-minute cycling session performed at 75% of HRmax. Finally, a cool down phase lasting 2 minutes.
Participants complete an overnight fast of ≥ 10 hours and then receive a single dose of oral SR13668 in a PEG400/Labrasol® liquid formulation with 8 ounces of water. Participants may not eat for ≥ 4 hours after study drug administration.
The present disclosure provides a film for biological application, which contains regenerated cellulose and is advantageous in shortening the time required to wear the film to a biological tissue. The disclosed film (10) for biological application contains regenerated cellulose and an accelerator. The promoter promotes the wearing of regenerated cellulose to the body tissue. The film (10) for biological adhesion is a self-supporting film having a thickness of 20 to 5000 nm. The accelerator is represented by the following formula (a). Wherein a and c are integers of 0 or more, b and d are integers of 1 or more, and R is 1 Is a hydrogen atom, an acyl group, or an alkyl group, R 2 Is a hydrogen atom, a hydroxyl group, an acyl group, or an alkyl group.
An apparatus for anonymizing user data is disclosed. The apparatus includes at least a processor and a memory communicatively connected to the at least a processor. The memory instructs the processor to receive, from a first database, a plurality of user data comprising a plurality of metadata. The memory instructs the processor to detach the plurality of metadata for the plurality of user data. The memory instructs the processor to identify a plurality of patient identifiers within the plurality of user data and the plurality of metadata. The memory instructs the processor to generate a plurality of anonymized data and anonymized metadata as a function of the plurality of patient identifiers and the plurality of metadata using an anonymization machine learning model. The memory instructs the processor to construct a plurality of anonymized user records as a function of the plurality of anonymized data.
Chronic limb-threatening ischaemia (CLTI), the most severe manifestation of peripheral arterial disease (PAD), is associated with a poor prognosis and high amputation rates. Despite novel therapeutic approaches being investigated, no significant clinical benefits have been observed yet. Understanding the molecular pathways of skeletal muscle dysfunction in CLTI is crucial for designing successful treatments. This study aimed to identify miRNAs dysregulated in muscle biopsies from PAD cohorts. Using MIcroRNA ENrichment TURned NETwork (MIENTURNET) on a publicly accessible RNA-sequencing dataset of PAD cohorts, we identified a list of miRNAs that were over-represented among the upregulated differentially expressed genes (DEGs) in CLTI. Next, we validated the altered expression of these miRNAs and their targets in mice with hindlimb ischaemia (HLI). Our results showed a significant downregulation of miR-1, miR-133a, and miR-29b levels in the ischaemic limbs versus the contralateral non-ischaemic limb. A miRNA target protein-protein interaction network identified extracellular matrix components, including collagen-1a1, -3a1, and -4a1, fibronectin-1, fibrin-1, matrix metalloproteinase-2 and -14, and Sparc, which were upregulated in the ischaemic muscle of mice. This is the first study to identify miR-1, miR-133a, and miR-29b as potential contributors to fibrosis and vascular pathology in CLTI muscle, which supports their potential as novel therapeutic agents for this condition.
The control arm will not receive vitamin D replacement, but patients in both study arms will receive care consistent with best care practices for stone disease. All patients will be evaluated by the stone clinic clinical nutritionist and full nutritional evaluation will be performed. All patients will be advised to maintain adequate hydration (\>2L/day), no-added salt diet (Na 80-100mmol/day), low protein diet (1 g/kg/day). Patients with hyperoxaluria will be advised to follow low-oxalate diet. All patients will be advised to maintain moderate calcium intake; 800-1200mg/day.