anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
NT-proBNP is a member of the natriuretic hormone family which plays an important role in regulation of extracellular fluid volume and blood pressure.It is secreted from the cardiac ventricle myocytes in response to myocardial stress. This hormone serves as a marker of ventricular dysfunction in adults but its role in newborns and especially preterm infants has not been well studied yet. Following birth of a healthy infant there is a surge in NT-proBNP levels which is then followed by a rapid decrease. One explanation for this surge is the transition in hemodynamics from fetal circulation into postnatal one. Few studies conducted in this area have shown association between NT-proBNP level and patency of ductus arteriosus and with respiratory distress syndrome of the newborn. Cardiac troponin T (cTnT)is a specific cardiac protein which serves as a specific indicator of cardiac damage in adults, it is usually not detected at birth but following myocardial injury its serum levels will slowly rise and generally will not be detectable until at least 4 hours after onset of injury. There is no "gold standard" test for diagnosis of hemodynamic instability in very low birth weight infants. Myocardial dysfunction is thought to be the major cause for this condition in VLBW population. Since this condition is associated with severe short and long term morbidity early recognition and specific treatment may be detrimental. We hypothesized that NT-proBNP and cTnT levels may serve as a more accurate markers for diagnosis, monitoring, and outcome prediction in VLBW infants during the first days of life, than the methods we currently use (blood pressure, urine output etc.)
<P>PROBLEM TO BE SOLVED: To efficiently utilize crustaceans, especially krill, as resources, to efficiently recover fat-soluble effective substances, such as carotenoid, highly unsaturated fatty acid, and phospholipid, which are components of the crustaceans, and to utilize the substances.  <P>SOLUTION: An aggregate is formed by collecting eyeballs of the crustaceans, so that the aggregate is used as a supply source of the carotenoid, the highly unsaturated fatty acid, and/or the phospholipid. A food or a dietary supplement contains the collected eyeballs, as they are, or a powdered product thereof and is used for supplying the carotenoid, the highly unsaturated fatty acid, and/or the phospholipid. The aggregate is produced by reducing a water content of the crustaceans to make the eyeballs bring into a state of being easily separated, and then giving physical impact thereto, so that the eyeballs are isolated and recovered. The krill or mysids are preferably used as the crustaceans.  <P>COPYRIGHT: (C)2005,JPO&NCIPI
Internet-based parenting program with weekly parental support from a family guide (psychologist) via a chat function integrated into the program. The program consists of a brief introducing module and 5 modules conducted over 5-7 weeks. Parents work independently with material online and receive support from the family guide through chat/text messages in the program.
Disease tolerance is an essential defense strategy against pathogens, alleviating tissue damage regardless of pathogen multiplication. However, its genetic and molecular basis remains largely unknown. Here, we discovered that protein condensation at the endoplasmic reticulum (ER) regulates disease tolerance in Arabidopsis against Pseudomonas syringae. During infection, Hematopoietic protein-1 (HEM1) and Bax-inhibitor 1 (BI-1) coalesce into ER-associated condensates facilitated by their phase-separation behaviors. While BI-1 aids in clearing these condensates via autophagy, it also sequesters lipid-metabolic enzymes within condensates, likely disturbing lipid homeostasis. Consequently, mutations in hem1, which hinder condensate formation, or in bi-1, which prevent enzyme entrapment, enhance tissue-damage resilience, and preserve overall plant health during infection. These findings suggest that the ER is a crucial hub for maintaining cellular homeostasis and establishing disease tolerance. They also highlight the potential of engineering disease tolerance as a defense strategy to complement established resistance mechanisms in combating plant diseases.
A system for providing preselected data to a human user who is a patient in a healthcare facility. The data can feature therapeutic audio content, informational content, and instructional content. The system can include a portable cart or other mobile platform on which a computer and touch screen display connected to the computer are installed. The computer can include a memory device capable of storing the therapeutic audio content. The touch screen display can feature control icons sized so as to be easily selected by manual manipulation by a user who is ill, impaired, or at least partially incapacitated. The touch screen display may also include a detachable transparent film affixed over a display surface. A method of the invention can include the step of decreasing audio volume to permit two-way communication between the user and a healthcare professional using the system.
BACKGROUND: In this article we describe an underexposed cause of subgaleal hematoma in the older child. Subgaleal hematomas are well-known in the context of trauma or blood clotting disorders. International literature acknowledges excessive force during hair styling as a possible cause. Here, we present two cases to illustrate the importance of a complete patient work-up.
CASE DESCRIPTION: Recently, two patients presented themselves at Juliana Children's Hospital, the Hague, the Netherlands, with a swelling on the head and headache with no obvious cause. Radiological imaging showed subgaleal hematomas. Upon questioning, both patients mentioned using extensive traction while styling their hair.
CONCLUSION: In conclusion, when analysing an older child with a swelling on the head with no obvious cause, consider the diagnoses subgaleal hematoma due to hair traction. It might be helpful to observe them styling their hair. A proper clinical review can therefore prevent over-testing and overtreatment.
OBJECTIVE: Eradication of hepatitis C virus (HCV) infection has been linked with improvement in neurocognitive function, but few studies have evaluated the effect of antiviral treatment/ response on risk of dementia. Using data from the Chronic Hepatitis Cohort Study (CHeCS), we investigated how antiviral therapy impacts the risk of developing dementia among patients with HCV.
METHODS: A total of 17,485 HCV patients were followed until incidence of dementia, death, or last follow-up. We used an extended landmark modeling approach, which included time-varying covariates and propensity score justification for treatment selection bias, as well as generalized estimating equations (GEE) with a link function as multinominal distribution for a discrete time-to-event data. Death was considered a competing risk.
RESULTS: After 15 years of follow-up, 342 patients were diagnosed with incident dementia. Patients who achieved sustained virological response (SVR) had significantly decreased risk of dementia compared to untreated patients, with hazard ratios (HRs) of 0.32 (95% CI 0.22-0.46) among patients who received direct-acting antiviral (DAA) treatment and 0.41 (95% CI 0.26-0.60) for interferon-based (IFN) treatment. Risk reduction remained even when patients failed antiviral treatment (HR 0.38, 95% CI 0.38-0.51). Patients with cirrhosis, Black/African American patients, and those without private insurance were at significantly higher risk of dementia.
CONCLUSION: Antiviral treatment independently reduced the risk of dementia among HCV patients, regardless of cirrhosis. Our findings support the importance of initiation antiviral therapy in chronic HCV-infected patients.
TBCT (de Oliveira, 2008) is a novel transdiagnostic approach (Wenzel, 2017). It has been shown to be effective for depression (Hemanny et al., 2019), social anxiety disorder (Neufeld et al., 2020; Caetano et al., 2018; de Oliveira et al., 2011; Powell et al., 2013), and PTSD (Duran et al., 2020). TBCT differs from other CBT approaches in that it introduces a new, organized, and systematic approach to change dysfunctional negative core beliefs, and allows cognitive, emotional, and experiential work to be done simultaneously (de Oliveira, 2016). Interestingly, it incorporates a courtroom metaphor to challenge dysfunctional core beliefs conceptualized as self-accusations (de Oliveira, 2016). TBCT is an example of assimilative psychotherapy integration that relies on Beckian CBT (de Oliveira, 2016). It incorporates and integrates components of other psychotherapies (Delavechia et al., 2016).
BACKGROUND: Exposure to postnatal systemic inflammation is associated with increased risk of brain injury in preterm infants, leading to impaired maturation of the cerebral cortex and adverse neurodevelopmental outcomes. However, the optimal method for identifying cortical dysmaturation is unclear. Herein, we compared the utility of electroencephalography (EEG), diffusion tensor imaging (DTI), and neurite orientation dispersion and density imaging (NODDI) at different recovery times after systemic inflammation in newborn rats.
METHODS: Sprague Dawley rat pups of both sexes received single-daily lipopolysaccharide (LPS; 0.3 mg/kg i.p.; n = 51) or saline (n = 55) injections on postnatal days (P)1, 2, and 3. A subset of these animals were implanted with EEG electrodes. Cortical EEG was recorded for 30 min from unanesthetized, unrestrained pups at P7, P14, and P21, and in separate groups, brain tissues were collected at these ages for ex-vivo MRI analysis (9.4 T) and Golgi-Cox staining (to assess neuronal morphology) in the motor cortex.
RESULTS: Postnatal inflammation was associated with reduced cortical pyramidal neuron arborization from P7, P14, and P21. These changes were associated with dysmature EEG features (e.g., persistence of delta waveforms, higher EEG amplitude, reduced spectral edge frequency) at P7 and P14, and higher EEG power in the theta and alpha ranges at P21. By contrast, there were no changes in cortical DTI or NODDI in LPS rats at P7 or P14, while there was an increase in cortical fractional anisotropy (FA) and decrease in orientation dispersion index (ODI) at P21.
CONCLUSIONS: EEG may be useful for identifying the early evolution of impaired cortical development after early life postnatal systemic inflammation, while DTI and NODDI seem to be more suited to assessing established cortical changes.
Participants will receive a 35-hour "dose" of CI therapy. Treatment will consist of 35 therapist/client contact hours in the clinic, 10 weekdays, over 3 weeks. To promote carry-over of motor gains to daily activities, participants will complete: (1) a treatment contract, (2) daily self-report of arm use, and (3) problem-solving to overcome barriers to use of the more affected upper extremity. In addition, the client will agree to wear a padded restraint mitt on the less affected hand for the majority of waking hours to encourage use of the weaker hand for daily activities. Finally, the participant will agree to 30 minutes per day of individualized task-practice outside the clinic (in addition to training in the clinic) focused on functional activities catered towards accomplishing the person's therapeutic goals.
SERIOUS INFECTIONS

Patients treated with HUMIRA are at increased risk for developing serious infections that may lead to hospitalization or death [see Warnings and Precautions (5.1)]. Most patients who developed these infections were taking concomitant immunosuppressants such as methotrexate or corticosteroids.

Discontinue HUMIRA if a patient develops a serious infection or sepsis.

Reported infections include:

  * Active tuberculosis (TB), including reactivation of latent TB. Patients with TB have frequently presented with disseminated or extrapulmonary disease. Test patients for latent TB before HUMIRA use and during therapy. Initiate treatment for latent TB prior to HUMIRA use.   

  * Invasive fungal infections, including histoplasmosis, coccidioidomycosis, candidiasis, aspergillosis, blastomycosis, and pneumocystosis. Patients with histoplasmosis or other invasive fungal infections may present with disseminated, rather than localized, disease. Antigen and antibody testing for histoplasmosis may be negative in some patients with active infection. Consider empiric anti-fungal therapy in patients at risk for invasive fungal infections who develop severe systemic illness.   

  * Bacterial, viral and other infections due to opportunistic pathogens, including Legionella and Listeria.



Carefully consider the risks and benefits of treatment with HUMIRA prior to initiating therapy in patients with chronic or recurrent infection.

Monitor patients closely for the development of signs and symptoms of infection during and after treatment with HUMIRA, including the possible development of TB in patients who tested negative for latent TB infection prior to initiating therapy [see Warnings and Precautions (5.1) and Adverse Reactions (6.1)].

MALIGNANCY

Lymphoma and other malignancies, some fatal, have been reported in children and adolescent patients treated with TNF blockers including HUMIRA [see Warnings and Precautions (5.2)]. Post-marketing cases of hepatosplenic T-cell lymphoma (HSTCL), a rare type of T-cell lymphoma, have been reported in patients treated with TNF blockers including HUMIRA. These cases have had a very aggressive disease course and have been fatal. The majority of reported TNF blocker cases have occurred in patients with Crohn's disease or ulcerative colitis and the majority were in adolescent and young adult males. Almost all these patients had received treatment with azathioprine or 6-mercaptopurine (6–MP) concomitantly with a TNF blocker at or prior to diagnosis. It is uncertain whether the occurrence of HSTCL is related to use of a TNF blocker or a TNF blocker in combination with these other immunosuppressants [see Warnings and Precautions (5.2)].
The waiting-list group will receive the intervention 7 weeks after the intervention group finishes. The intervention group will finish the research in week 7, while the waiting-list group will start to attend the intervention. They will complete the questionnaires and the experiment.
Endometriosis. In moderate to severe disease, or in patients infertile due to endometriosis, a starting dose of 800 mg given in two divided doses is recommended. Amenorrhea and rapid response to painful symptoms is best achieved at this dosage level. Gradual downward titration to a dose sufficient to maintain amenorrhea may be considered depending upon patient response. For mild cases, an initial daily dose of 200 mg to 400 mg given in two divided doses is recommended and may be adjusted depending on patient response. Therapy should begin during menstruation. Otherwise, appropriate tests should be performed to ensure that the patient is not pregnant while on therapy with danazol capsules (see CONTRAINDICATIONS  and WARNINGS). It is essential that therapy continue uninterrupted for 3 to 6 months but may be extended to 9 months if necessary. After termination of therapy, if symptoms recur, treatment can be reinstituted. 

Hereditary Angioedema. The dosage requirements for continuous treatment of hereditary angioedema with danazol capsules should be individualized on the basis of the clinical response of the patient. It is recommended that the patient be started on 200 mg, two or three times a day. After a favorable initial response is obtained in terms of prevention of episodes of edematous attacks, the proper continuing dosage should be determined by decreasing the dosage by 50% or less at intervals of one to three months or longer if frequency of attacks prior to treatment dictates. If an attack occurs, the daily dosage may be increased by up to 200 mg. During the dose adjusting phase, close monitoring of the patient's response is indicated, particularly if the patient has a history of airway involvement.
Although granule cell dispersion (GCD) in the hippocampus is known to be an important feature associated with epileptic seizures in temporal lobe epilepsy (TLE), the endogenous molecules that regulate GCD are largely unknown. In the present study, we have examined whether there is any change in AEG-1 expression in the hippocampus of a kainic acid (KA)-induced mouse model of TLE. In addition, we have investigated whether the modulation of astrocyte elevated gene-1 (AEG-1) expression in the dentate gyrus (DG) by intracranial injection of adeno-associated virus 1 (AAV1) influences pathological phenotypes such as GCD formation and seizure susceptibility in a KA-treated mouse. We have identified that the protein expression of AEG-1 is upregulated in the DG of a KA-induced mouse model of TLE. We further demonstrated that AEG-1 upregulation by AAV1 delivery in the DG-induced anticonvulsant activities such as the delay of seizure onset and inhibition of spontaneous recurrent seizures (SRS) through GCD suppression in the mouse model of TLE, while the inhibition of AEG-1 expression increased susceptibility to seizures. The present observations suggest that AEG-1 is a potent regulator of GCD formation and seizure development associated with TLE, and the significant induction of AEG-1 in the DG may have therapeutic potential against epilepsy.
Co-administration of ivacaftor or tezacaftor/ivacaftor with digoxin, a sensitive P-gp substrate, increased digoxin AUC by 1.3-fold, consistent with weak inhibition of P-gp by ivacaftor. Administration of TRIKAFTA may increase systemic exposure of medicinal products that are sensitive substrates of P-gp, which may increase or prolong their therapeutic effect and adverse reactions. When used concomitantly with digoxin or other substrates of P-gp with a narrow therapeutic index such as cyclosporine, everolimus, sirolimus and tacrolimus, caution and appropriate monitoring should be used [see Clinical Pharmacology (12.3)].

Elexacaftor and M23-ELX inhibit uptake by OATP1B1 and OATP1B3 in vitro. Co-administration of TRIKAFTA may increase exposures of medicinal products that are substrates of these transporters, such as statins, glyburide, nateglinide and repaglinide. When used concomitantly with substrates of OATP1B1 or OATP1B3, caution and appropriate monitoring should be used [see Clinical Pharmacology (12.3)]. Bilirubin is an OATP1B1 and OATP1B3 substrate.
Optimized malaria control interventions as in the control arm. In addition, following identification of microscopy or RDT positive, passively-detected index cases at the health post or health center; individuals who reside within a 100-meter radius of the index case will receive diagnosis for malaria using a conventional RDT. Positive individuals will receive treatment and follow-up as per the national treatment guidelines. 14 days of primaquine (PQ) will only be administered to those found to be normal upon G6PD testing. Additional procedures will include the collection of a dried blood spot.
PURPOSE:To provide a new choline ester derivative of a highly unsaturated fatty acid for imparting a highly unsaturated fatty acid with water-solubility and useful for pharmaceuticals, foods, chemicals, cosmetics, etc. CONSTITUTION:The choline ester compound of a highly unsaturated fatty acid of formula (R is highly unsaturated fatty acid residue; Xis salt-forming anion), e.g. N,N-dimethyl-2-aminoethyl docosahexaenoate. The compound of formula can be produced e.g. by reacting N, N-dimethyl-2-aminoethanol to a highly unsaturated fatty acid or its ester and methylating the obtained N, Ndimethyl-2- aminoethanol fatty acid ester with a methylation agent such as methyl halide and dimethyl sulfate. The compound of formula is easily soluble in organic solvents such as various alcohols and extremely easily soluble in water. It can be formed in the form of flakes by freeze-drying and is applicable widely in various fields.
<P>PROBLEM TO BE SOLVED: To provide a preparation capable of preventing side effects (e.g. peeling, scaling or dryness) that accompany topical and systemic (oral) retinoid therapy without significantly diminishing the desired therapeutic effect, whether by antagonism, competition, or otherwise.  <P>SOLUTION: These side effects can be reduced or eliminated by the topical administration of an inhibitor, especially a natural inhibitor, of the epidermal growth factor receptor (EGFR), administered concomitantly with the retinoid, separately from the retinoid (such as on an as-needed basis), or both. Administration of the two together is facilitated by a composition suitable for topical application and comprising both retinoid and a natural EGFR inhibitor. Preferred natural EGFR inhibitors are genistein and other isoflavones extracted from natural occurring substances, or simple derivatives of such substances.  <P>COPYRIGHT: (C)2009,JPO&INPIT
Here, we describe a minimalist approach to mimic the aggregation-prone modules within tau. We carried out a backbone residue scan and showed that amide N-amination completely abolishes the tendency of these peptides to self-aggregate, rendering them soluble mimics of ordered β-strands from the tau R2 and R3 domains. Several N-amino peptides (NAPs) inhibit tau fibril formation in vitro. We further demonstrate that NAPs 12 and 13 are effective at blocking the cellular seeding of endogenous tau by interacting with monomeric or fibrillar forms of extracellular tau. Peptidomimetic 12 is serum stable, non-toxic to neuronal cells, and selectivity inhibits the fibrilization of tau over Aβ42. Structural analysis of our lead NAPs shows considerable conformational constraint imposed by the N-amino groups. The described backbone N-amination approach provides a rational basis for the mimicry of other aggregation-prone peptides that drive pathogenic protein assembly.
The present disclosure provides hypoglycemic Se—enriched tea polysaccharides and preparation method of buccal tablet thereof. The Se—enriched tea polysaccharide buccal tablet is tableted with the following raw materials (by weight): 5—20 parts of Se—enriched 5 tea polysaccharides, 12—20 parts of Se—enriched tea leaves, 7—12 parts of mint leaves, 3—5 parts of dried, lemons, 3—8 parts of stevia leaves, 45—65 parts of bulking agent, and 0.5—5 parts of lubricant. The Se—enriched, tea polysaccharides are natural Se— enriched, tea polysaccharides extracted from. Se—enriched, tea or 10 artificial Se—enriched, tea polysaccharides synthesized, from inorganic Se. It is found that both natural Se—enriched tea polysaccharides and artificial Se—enriched tea polysaccharides can inhibit d—glucosidase activity effectively, and the inhibitory activity thereof is significantly stronger than that of common tea l5 polysaccharides. The buccal tablet is safe and efficient, supples essential Se to the body, and exhibits hypoglycemic effect, so there are excellent application prospects in patients with hyperglycemia/diabetes. 20 (+ Fig. 3)
The invention discloses a beta-carboline derivative containing hydroximic acid as well as a preparation method and a medical application thereof. The product has the structure as shown in the general formula I. The compound can be combined with other antitumor drugs such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors and DNA intercalating agents and additionally can be combined with radiotherapy. The invention also discloses a pharmaceutical composition containing the compound with the general formula I as well as medical application thereof, particularly application of preparation of antitumor medicines, Alzheimer disease medicines and Parkinson disease medicines. The other antitumor medicines or radiotherapy can be administrated with the compound at the same time or in different times. The combination therapy can generate the synergistic effect, so that the treatment effect is improved.