anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND: Yearly influenza vaccination is strongly recommended for older adults and patients with chronic diseases including cardiovascular disease (CVD); however, vaccination rates remain suboptimal, particularly among younger patients. Electronic letters incorporating behavioral nudges are highly scalable public health interventions which can potentially increase vaccination, but further research is needed to determine the most effective strategies and to assess effectiveness across different populations. The purpose of NUDGE-FLU-CHRONIC and NUDGE-FLU-2 are to evaluate the effectiveness of electronic nudges delivered via the Danish governmental electronic letter system in increasing influenza vaccination among patients with chronic diseases and older adults, respectively.
METHODS: Both trials are designed as pragmatic randomized implementation trials enrolling all Danish citizens in their respective target groups and conducted during the 2023/2024 influenza season. NUDGE-FLU-CHRONIC enrolls patients aged 18-64 years with chronic diseases. NUDGE-FLU-2 builds upon the NUDGE-FLU trial conducted in 2022/2023 and aims to expand the evidence by testing both previously successful and new nudges among adults ≥65 years during a subsequent influenza season. Persons with exemptions from the electronic letter system are excluded from both trials. In both trials, participants are randomized in a 2.45:1:1:1:1:1:1 ratio to either receive no electronic letter (usual care) or to receive one of 6 different behaviorally informed electronic letters. NUDGE-FLU-CHRONIC has randomized 299,881 participants with intervention letters delivered on September 24, 2023, while NUDGE-FLU-2 has randomized 881,373 participants and delivered intervention letters on September 13, 2023. Follow-up is currently ongoing. In both trials, the primary endpoint is receipt of influenza vaccination on or before January 1, 2024, and the secondary endpoint is time to vaccination. Clinical outcomes including respiratory and cardiovascular hospitalizations, all-cause hospitalization, and mortality are included as prespecified exploratory endpoints. Prespecified individual-level pooled analyses will be conducted across NUDGE-FLU, NUDGE-FLU-CHRONIC, and NUDGE-FLU-2.
DISCUSSION: NUDGE-FLU-CHRONIC is the first nationwide randomized trial of electronic nudges to increase influenza vaccination conducted among 18-64-year-old high-risk patients with chronic diseases. NUDGE-FLU-2 will provide further evidence on the effectiveness of electronic nudges among older adults ≥65 years. Collectively, the NUDGE-FLU trials will provide an extensive evidence base for future public health communications.
TRIAL REGISTRATION: NUDGE-FLU-CHRONIC: Clinicaltrials.gov: NCT06030739, registered September 11, 2023, https://clinicaltrials.gov/study/NCT06030739. NUDGE-FLU-2: Clinicaltrials.gov: NCT06030726, registered September 11, 2023, https://clinicaltrials.gov/study/NCT06030726.
PURPOSE:To obtain a dental bonding composition useful as a high-performance and high-efficiency type primer and adhesive capable of eliminating the waiting time which is a defect of a dental primer and bonding to a porcelain and a metal by blending a silane coupling agent with a phosphoric monoester. CONSTITUTION:This dental bonding composition is obtained by combining 1 pt.wt. silane coupling agent expressed by formula I [R1 is an organic residue having at least one selected from (meth)acryloyl, vinyl, mercapto and epoxy; R2 is OH, a 1-5C alkyl or a 1-5C alkoxy; R4 and R5 are each OH or a 1-5C alkoxyl with 0.001-50 pts.wt. phosphoric monoester expressed by formula II [R5 is H or methyl; (n) is 8-20]. A volatile solvent or a radical-polymerizable monomer may further be added to the resultant composition. Furthermore, a filler or a polymerization initiator may be added thereto. The polymerization initiator is preferably a ternary initiator comprising a sulfinate, an amine and benzoyl peroxide.
Calcium influx and subsequent elevation of the intracellular calcium concentration ([Ca2+]i) induce contractions of brain pericytes and capillary spasms following subarachnoid hemorrhage. This calcium influx is exerted through cation channels. However, the specific calcium influx pathways in brain pericytes after subarachnoid hemorrhage remain unknown. Transient receptor potential canonical 3 (TRPC3) is the most abundant cation channel potentially involved in calcium influx into brain pericytes and is involved in calcium influx into other cell types either via store-operated calcium entry (SOCE) or receptor-operated calcium entry (ROCE). Therefore, we hypothesized that TRPC3 is associated with [Ca2+]i elevation in brain pericytes, potentially mediating brain pericyte contraction and capillary spasms after subarachnoid hemorrhage. In this study, we isolated rat brain pericytes and demonstrated increased TRPC3 expression and its currents in brain pericytes after subarachnoid hemorrhage. Calcium imaging of brain pericytes revealed that changes in TRPC3 expression mediated a switch from SOCE-dominant to ROCE-dominant calcium influx after subarachnoid hemorrhage, resulting in significantly higher [Ca2+]i levels after SAH. TRPC3 activity in brain pericytes also contributed to capillary spasms and reduction in cerebral blood flow in an in vivo rat model of subarachnoid hemorrhage. Therefore, we suggest that the switch in TRPC3-mediated calcium influx pathways plays a crucial role in the [Ca2+]i elevation in brain pericytes after subarachnoid hemorrhage, ultimately leading to capillary spasms and a reduction in cerebral blood flow.
Three intra-articular injections in total and autologous adipose-derived mesenchymal stem cells (AMSCs) suspended in 3 ml autologous platelet rich plasma (PRP) for each injection. Time-points for intervention: 1) initial injection; 2) 3 months following initial injection; 3) 6 months following initial injection.
PURPOSE:To perpare the titled model animal which keeps its characters stably for a long period, easily, by administering a mammalian animal with a low molecular weight immunocomplex obtained from an antibody derived from a specific synthetic bivalent hapten and a protein antigen having the same hapten group as above. CONSTITUTION:An antibody having a molecular weight of about 150,000 and originated from a synthetic bivalent hapten having hapten groups [e.g. group of formula I (X is halogen, etc.; n is 1-3)] at both ends through a lower alkylene chain (e.g. methylene, ethylene, etc.) [e.g. the compound of formula II (n is 1- 11)] and a protein antigen having the same hapten group as the above hapten, is subjected to the ordinary immune reaction (antigen-antibody reaction). The obtained low molecular weight immunocomplex is used as an active cmponent of an agent for causing nephrities in animals, and the agent is administered to a mammalian animal to obtain the nephritis model animal. Dose: about 1- 200mg/kg as the antibody in the low molecular weight immunocomplex is administered by intravenous injection (or 5-500mg/kg in the case of peritoneal infusion), the same amount is administered 30min- 2 days after the first administration, and the process is repeated with 24-48hr intervals.
For monotherapy and adjunctive therapy for partial-onset seizures in patients 17 years of age and older and for adjunctive therapy for primary generalized tonic-clonic seizures in patients 4 years of age and older, an alternate initial dosing regimen for week 1 (e.g., including a loading dose and/or a higher initial dosage) may be administered in patients for whom achieving the recommended maintenance dosage in a shorter timeframe is clinically indicated (see Table 2). The alternate initial dosage regimen should be continued for one week. Lacosamide oral solution may then be titrated based on clinical response and tolerability, no more frequently than once per week, if needed. The loading dose should be administered with medical supervision because of the possibility of increased incidence of adverse reactions, including central nervous system (CNS) and cardiovascular adverse reactions [see Warnings and Precautions (5.2, 5.3), Adverse Reactions (6.1), and Clinical Pharmacology (12.3)]. Titration increments should not exceed those shown in Table 2.

Table 2: Alternate Initial Dosing Regimen to Achieve the Maintenance Dosage in a Shorter Timeframe if Clinically Indicated*

*when not specified, the dosage is the same for monotherapy for partial-onset seizures and adjunctive therapy for partial-onset seizures.

**Monotherapy for partial-onset seizures only

Additional pediatric use information is approved for UCB, Inc.'s VIMPAT® (lacosamide) oral solution. However, due to UCB, Inc.'s marketing exclusivity rights, this drug product is not labeled with that information.
1. An apoptosis inducing agent containing glycerolipid and/or glyceroglycolipid as effective component which does not have in its molecular structure a phosphate ester or phosphonate ester. 2. An agent as set forth in Claim 1 or 2 wherein said glycerolipid and/or glyceroglycolipid are/is derived from plants, microorganisms or animals. 3. An agent as set forth in Claim 3 wherein said glycerolipid and/or glyceroglycolipid are/is derived from tea, mushrooms, algae or cereal residues. 4. A method for the manufacture of the apoptosis inducing agent containing glycerolipid and/or glyceroglycolipid as effective component which does not have in its molecular structure a phosphate ester or phosphonate ester wherein said method includes a step of extracting glycerolipid and/or glyceroglycolipid derived from plants, microorganisms or animals with an organic solvent. 5. The method as set forth in Claim 4 wherein prior to the step of extracting with an organic solvent said method includes a step of treating glycerolipid and/or glyceroglycolipid with an acid or an alkali. 6. The method as set forth in Claim 4 wherein after the step of extracting said method includes a step of separating glycerolipid and/or glyceroglycolipid by the selected method from hydrophobic, reversed phase, or normal phase chromatography. 7. The method as set forth in any of Claims 4 to 6 wherein said glycerolipid and/or glyceroglycolipid are/is derived from tea, mushrooms, algae or cereal residues. 8. A food product where the apoptosis inducing agent is contained therein, added thereto and/or diluted therein as set forth in any of Claims 1 to 3 which is the glycerolipid and/or glyceroglycolipid and does not have in its molecular structure a phosphate ester or phosphonate ester. 9. A food product as set forth in Claim 8 which is a beverage. 10. A food product as set forth in Clams 8 or 9 in which said glycerolipid and/or glyceroglycolipid are/is derived from natural sources such as plants, microorganisms or animals. 11. A food product as set forth in any of Clams 8 to 10 in which said glycerolipid and/or glyceroglycolipid are/is derived from tea, mushrooms, algae or cereal residues.
<P>PROBLEM TO BE SOLVED: To provide a pharmacokinetic simulation device for reducing a burden on a user, and suppressing an occurrence of errors.  <P>SOLUTION: An arrangement means 2 is for inputting a compartment and arranging it. A type input means 4 is for inputting a type for each compartment. A term determination means 6 is for determining a term that appears in a differential equation of a drug that flows into the compartment or flows out to the compartment based on the type of each compartment. A coefficient input region display means 8 is for displaying an input region for inputting a coefficient and a flow-in source compartment or a flow-out destination compartment for each term determined by the term determination means 6. A coefficient input means 10 is for inputting a coefficient from the input region displayed by the coefficient input region display means 8. In this manner, an equation is determined by selecting a compartment type, and a user has only to input a coefficient for settings with few errors.  <P>COPYRIGHT: (C)2009,JPO&INPIT
Participants will take one bottle (80 ml) of Yakult® drink daily for a period of 4 weeks. Yakult is a branded probiotic drink with 8x10\^9 CFU Lacticaseibacillus paracasei strain Shirota. Subsequently, a two-week follow-up period will follow.
Cisplatin Injection can cause dose-related nephrotoxicity, including acute renal failure that becomes more prolonged and severe with repeated courses of the drug. Renal toxicity typically begins during the second week after a dose of Cisplatin Injection. Patients with baseline renal impairment, geriatric patients, patients who are taking other nephrotoxic drugs, or patients who are not well hydrated may be more susceptible to nephrotoxicity [see Use in Specific Populations (8.5, 8.6)].

Ensure adequate hydration before, during, and after Cisplatin Injection administration [see Dosage and Administration (2.1)]. Measure serum creatinine, blood urea nitrogen, creatinine clearance, and serum electrolytes including magnesium prior to initiating therapy, and as clinically indicated. Consider magnesium supplementation as clinically needed.

Consider alternative treatments or reduce the dose of Cisplatin Injection for patients with baseline renal impairment or who develop significant reductions in creatinine clearance during treatment with Cisplatin Injection according to clinical treatment guidelines [see Dosage and Administration (2.5)].
BACKGROUND: Inflammation serves as our body's immune response to combat infections, pathogens, viruses, and external stimuli. Inflammation can be classified into two types: acute inflammation and chronic inflammation. Non-steroidal anti-inflammatory medications (NSAIDs) are used to treat both acute and chronic inflammatory disorders. However, these treatments have various side effects such as reduced healing efficiency, peptic ulcers, gastrointestinal toxicities, etc. METHOD: This review assesses the potential of anti-inflammatory peptides (AIPs) derived from various natural sources, such as algae, fungi, plants, animals, and marine organisms. Focusing on peptides rich in cysteines and methionine, sulphur-containing amino acids known for their role in suppression of inflammation.
RESULT: Due to their varied biological activity, ability to penetrate cells, and low cytotoxicity, bioactive peptides have garnered interest as possible therapeutic agents. The utilisation of AIPs has shown great potential in the treatment of disorders associated with inflammation. AIPs can be obtained from diverse natural sources such as algae, fungi, plants, and animals. Cysteine and methionine are sulphur-containing amino acids that aid in the elimination of free radicals, hence assisting in the treatment of inflammatory diseases.
CONCLUSION: This review specifically examines several sources of AIPs including peptides that contain numerous cysteines and methionine. In addition, the biological characteristics of these amino acids and advancements in peptide delivery are also discussed.
Sweetpotato, Ipomoea batatas (L.) Lam. (2n = 6x = 90), is among the world's most important food crops and is North Carolina's most important vegetable crop. The recent introduction of Meloidogyne enterolobii poses a significant economic threat to North Carolina's sweetpotato industry and breeding resistance into new varieties has become a high priority for the US sweetpotato industry. Previous studies have shown that 'Tanzania', a released African landrace, is resistant to M. enterolobii. We screened the biparental sweetpotato mapping population, 'Tanzania' x 'Beauregard', for resistance to M. enterolobii by inoculating 246 full-sibs with 10,000 eggs each under greenhouse conditions. 'Tanzania', the female parent, was highly resistant, while 'Beauregard' was highly susceptible. Our bioassays exhibited strong skewing toward resistance for three measures of resistance: reproductive factor, eggs per gram of root tissue, and root gall severity ratings. A 1:1 segregation for resistance suggested a major gene conferred M. enterolobii resistance. Using a random-effect multiple interval mapping model, we identified a single major QTL, herein designated as qIbMe-4.1, on linkage group 4 that explained 70% of variation in resistance to M. enterolobii. This study provides a new understanding of the genetic basis of M. enterolobii resistance in sweetpotato and represents a major step towards the identification of selectable markers for nematode resistance breeding.
The precise mechanism(s) by which zonisamide exerts its anticonvulsant effects is unknown. Zonisamide may produce these effects through action at sodium and calcium channels. In vitro pharmacological studies suggest that zonisamide blocks sodium channels and reduces voltage-dependent, transient inward currents (T-type Ca2+ currents), consequently stabilizing neuronal membranes. Other in vitro studies have demonstrated that zonisamide (10–30 µg/mL) suppresses synaptically-driven electrical activity without affecting postsynaptic GABA or glutamate responses (cultured mouse spinal cord neurons) or neuronal or glial uptake of [3H]-GABA (rat hippocampal slices). Thus, zonisamide does not appear to potentiate the synaptic activity of GABA. Zonisamide is a carbonic anhydrase inhibitor. The contribution of this pharmacological action to the therapeutic effects of zonisamide is unknown.
Acute rejection (AR) occurs within the first 6 months after transplantation in 20 percent of heart transplant patients and in 50 percent of lung-transplant patients. Given the often silent clinical presentation of AR, these patients require monitoring with repeated invasive and costly endomyocardial (EMB) or transbronchial biopsies (TBBx). Since organ transplantation is essentially genomic transplantation, our prior studies leveraged the use of distinctive graft and recipient genotype single-nuclear polymorphisms (SNPs) to barcode donor DNA circulating in recipient serum. We have shown that levels of donor DNA measured as the percentage of circulating donor-derived cell-free DNA (%dd-cfDNA) correlate with AR diagnosis and severity as detected by biopsy.

The performance receiver operator curve (ROC) of %dd-cfDNA yielded an area under the curve (AUC) of 0.83. Using this technique, we can diagnose AR by measuring elevations in %dd-cfDNA up to 5 months before EMB-detected pathology. While these findings suggest that monitoring %dd-cfDNA may offer a high-performing, non-invasive, and early diagnostic tool of AR, further validation studies are required to determine its clinical utility. The ability to diagnose AR earlier than is possible with a biopsy offers an opportunity to investigate the pathogenesis of rejection as well as to identify potential AR biomarkers. Thus, the primary objective of this study is to validate the predictive accuracy and ROC characteristics of %dd-cfDNA for AR in a multicenter, prospective cohort study of heart and lung transplant patients, recruited through a consortium of 5 transplant centers in Washington, DC metropolitan area. The secondary objective is to determine the association between early graft injury caused by acute rejection and infection and the development of chronic rejection, i.e., chronic lung allograft dysfunction (CLAD) or chronic allograft vasculopathy (CAV). The exploratory objectives are: 1) to compare %dd-cfDNA characteristics in AMR (antibody-mediated rejection) and ACR (acute cellular rejection), 2) to study early immunological changes associated with a significant rise in %dd-cfDNA, and 3) to examine changes in microbiome architecture and other cell-free nucleic acids in rejection.
System and methods for providing laboratory-based authorization of genetic testing are disclosed. An order for genetic testing is received from an electronic health record (“EHR”) system at a laboratory information system (“LIS”). A prior authorization request is automatically generated at the LIS from data parsed from the order and retrieved from the EHR and sent to a prior authorization provider. If a patient responsibility amount returned to the LIS is below a threshold, testing proceeds. If the patient responsibility amount is above the threshold, an electronic call center request is generated and the patient is contacted to obtain payment. If a billing consent is not obtained, the specimen for the order is destroyed.
Vaginismus is the recurrent or persistent involuntary contraction of the perineal muscles surrounding the outer third of the vagina when penile, finger, tampon, or speculum penetration is attempted . Vaginismus can be primary, in which the women has never been able to have intercourse, or secondary, which is often due to acquired dyspareunia. It is relatively rare, affecting about 1% of women . Treatment of vaginismus is directed toward extinguishing the conditioned involuntary vaginal spasm. This can be accomplished by teaching Kegel exercises to acquaint the patient with voluntary control of her levator muscles. Medications such as lubricants, anesthetic creams, propranolol, or alprazolam to reduce anxiety have been used effectively, but approximately 10% of patients do not respond. Botulinum toxin type A has been successfully used to treat a wide range of muscular disorders such as strabismus, blepharospasm, and cervical dystonia. It is also been used to reduce facial lines and wrinkles.The extent of paralysis depends on the amount of toxin to which there is exposure relative to muscle bulk.In our previous study, one week after injecting botulinum toxin in 23 patients (95.8%) had a vaginal exam, which showed no or little resistance; 18 (75%) achieved satisfactory intercourse after the first injection. Now we are to make comparison between different doses of toxin injection and record the patient sexual satisfaction.
The expression of large conductance calcium-activated potassium channels (BK channels) in adipose tissue has been identified for years. BK channel deletion can improve metabolism in vivo, but the relative mechanisms remain unclear. Here, we examined the effects of BK channels on the differentiation of adipose-derived stem cells (ADSCs) and the related mechanisms. BKα and β1 subunits were expressed on adipocytes. We found that both deletion of the KCNMA1 gene, encoding the pore forming α subunit of BK channels, and the BK channel inhibitor paxilline increased the expression of key genes in the peroxisome proliferator activated receptor (PPAR) pathway and promoted adipogenetic differentiation of ADSCs. We also observed that the MAPK-ERK pathway participates in BK channel deficiency-promoted adipogenic differentiation of ADSCs and that ERK inhibitors blocked the differentiation-promoting effect of BK channel deficiency. Hyperplasia of adipocytes is considered beneficial for metabolic health. These results indicate that BK channels play an important role in adipose hyperplasia by regulating the differentiation of ADSCs and may become an important target for studying the pathogenesis and treatment strategies of metabolic disorder-related diseases.