anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
To conduct a double-blinded, placebo-controlled trial to determine the effects of TSEC therapy on the progression of subclinical atherosclerosis in healthy postmenopausal women. A total of 360 postmenopausal women with a uterus who are within 6 years of menopause and 45-59 years of age and without clinical cardiovascular disease and diabetes mellitus will be randomized to Bazedoxifene/Conjugated Equine Estrogen (BZA 20 mg/CE 0.45 mg) or placebo. Recruitment will occur over 3 years and the treatment period will be up to 3 years depending on when an individual is randomized. Rate of change in carotid artery intima-media thickness (CIMT) determined from the distal common carotid artery (CCA) far wall intima-media thickness (IMT) in computer image processed B mode ultrasonograms will be the primary trial endpoint. Arterial stiffness measured from the CCA (same location as CIMT) in computer image processed B mode ultrasonograms will be the secondary trial endpoint. Three composite cognitive measures will be used to test for randomized treatment group differences in cognition; each composite will be considered as co-endpoints.
Despite the notion that human CD8 +  T cells are the final mediators of autoimmune β-cell destruction in type 1 diabetes (TID), none of their target epitopes has been demonstrated to be naturally processed and presented by β cells. The inventors therefore performed an epitope discovery study combining HLA Class I peptidomics and transcriptomics strategies. Inflammatory cytokines increased β-cell peptide presentation  in vitro , paralleling upregulation of HLA Class I expression. Peptide sources included known β-cell antigens and several insulin granule proteins. Secretogranin V (SCG5/7B2) was identified as a novel β-cell antigen, which was processed into HLA-A2- and HLA- A3-restricted epitopes recognized by circulating naïve CD8 +  T cells in type 1 diabetic and healthy donors. HLA-A2-bound neo-epitopes were also represented and originated from an alternative SCG5-009 mRNA splice isoform. Accordingly, the present invention relates to antigenic peptides derived from secretogranin V and uses thereof for the diagnosis and treatment of T1D.
During pre-marketing controlled clinical trials, infusion reactions were reported in 26% of patients treated with KRYSTEXXA 8 mg every 2 weeks, and 41% of patients treated with KRYSTEXXA 8 mg every 4 weeks, compared to 5% of patients treated with placebo. These infusion reactions occurred in patients being pre-treated with an oral antihistamine, intravenous corticosteroid and/or acetaminophen. This pre-treatment may have blunted or obscured symptoms or signs of infusion reactions and therefore the reported frequency may be an underestimate. [See Adverse Reactions (6)]

KRYSTEXXA should be administered in a healthcare setting by healthcare providers prepared to manage infusion reactions. Patients should be pre-treated with antihistamines and corticosteroids. KRYSTEXXA should be infused slowly over no less than 120 minutes. In the event of an infusion reaction, the infusion should be slowed, or stopped and restarted at a slower rate.

The risk of infusion reaction is higher in patients whose uric acid level increases to above 6 mg/dL, particularly when 2 consecutive levels above 6 mg/dL are observed. Monitor serum uric acid levels prior to infusions and consider discontinuing treatment if levels increase to above 6 mg/dL. Because of the possibility that concomitant use of oral urate-lowering therapy and KRYSTEXXA may potentially blunt the rise of serum uric acid levels, it is recommended that before starting KRYSTEXXA patients discontinue oral urate-lowering medications and not institute therapy with oral urate-lowering agents while taking KRYSTEXXA.
This study will be conducted in 15 healthy volunteers at a clinical research unit located in Daytona Beach, Florida. Screening will be done within 35 days prior to the first dose of study drug (first Dosing Period). Each subject will complete two 10-day Dosing Periods, one using once daily dosing and the other twice daily dosing. The interval between the Dosing Periods will be 7 to 17 days. Patients will be randomly assigned to which regimen is administered the first Dosing Period. Safety laboratory tests will be performed at screening, and prior to and after each Dosing Period. End-of-Study (EOS) visit, the final study event, will be performed 14 to 21 days after the last dose of study drug.
Patients receive docetaxel IV over 1 hour on day 1. Patients also receive oral atrasentan and oral prednisone once daily on days 1-21. Treatment repeats every 21 days for up to 12 courses. Patients with stable or responding disease after course 12 may register for continued oral atrasentan treatment for up to 52 weeks.
The present application relates to a composition comprising, notably in a physiologically acceptable medium: •a. water; and•b. at least one cellulosic cationic polymer (CP); and•c. at least one anionic polymer (AP) chosen from methacrylic acid homopolymer salts; and•d. at least one anionic surfactant comprising at least one cationic counterion; and•e. a fatty phase; and•f. at least one pigment; the weight ratio of the total amount of cellulosic cationic polymer(s)/the sum of the total amount of cellulosic cationic polymer(s) and of the total amount of anionic polymer(s) ranging from 40% to 80%, preferably from 60% to 70%; the weight ratio of the sum of the total amount of cellulosic cationic polymer(s) and of the total amount of anionic polymer(s)/the amount of water ranging from 5% to 20%. The invention also relates to a process for coating keratin materials, in particular the skin, notably the contour of the eyes, eyelashes or eyebrows, and keratin fibers, such as the eyelashes and/or the eyebrows, comprising a step of applying to said keratin materials at least one composition as defined above.
Participants will be enrolled at the recommended phase 2 dose (RP2D) of CM-24 (MK-6018), determined by escalation studies, minus 1 dose level of MK-6018 in combination with a fixed dose of 200 mg pembrolizumab. Participants will be escalated to the RP2D of MK-6018 + 200 mg pembrolizumab. If the RP2D of MK-6018 + 200 mg pembrolizumab is not tolerated, the dose of MK-6018 will be de-escalated but will not fall below 1 mg/kg. Participants will be treated for 6 weeks during Cycle 1 and 2. Afterwards participants with clinical benefit and no DLTs are treated for up to 35 cycles.
Sepsis, a severe condition instigated by infections, continues to be a primary global cause of death, typified by systemic inflammation and advancing immune dysfunction. Comprehending the complex pathological processes that underlie sepsis is integral to the creation of efficacious treatments. Despite the inability of animal models to entirely reproduce the clinical intricacies related to sepsis, they are invaluable instruments for the exploration and development of therapeutic approaches. Within this context, the zebrafish model is particularly noteworthy due to its genetic tractability, transparency, and appropriateness for high-throughput screening of genetic mutants and therapeutic compounds. This scholarly review emphasizes the crucial role that the zebrafish disease model plays in enhancing our comprehension of sepsis, by exploring its applications in deciphering immune and inflammatory responses, evaluating the consequences of genetic alterations, and examining novel therapeutic agents. The Insights derived from zebrafish research not only augment our understanding of the underlying mechanisms of sepsis, but also possess considerable potential for the transference of these discoveries into clinical therapies, thus potentially transforming the approach to sepsis management. The objective of this scholarly article is to underscore the importance of zebrafish in the realm of biomedical research pertaining to sepsis, and to delineate forthcoming opportunities for utilizing this model in clinical applications.
Patients undergo radiotherapy once daily on days 1-5, 8-12, 15-19, 22-26, 29-33, and 36-40. Beginning the night before the first dose of radiotherapy and ending the night before the last dose of radiotherapy, patients receive concurrent oral temozolomide once daily on days 0-39. Patients also receive MGd IV over 30 minutes prior to radiotherapy once daily on days 1-5 and 8-12 and then on days 15, 17, 19, 22, 24, 26, 29, 31, 33, 36, 38, and 40. Beginning 28 days after the completion of radiotherapy, patients receive oral temozolomide once daily on days 1-5. Treatment repeats every 28 days for up to 12 courses in the absence of disease progression or unacceptable toxicity.
OBJECTIVE: To determine the intracranial ictal onset and early spread patterns in pediatric patients with Temporal lobe epilepsy and its possible association with histopathology, temporal structure involved, mesial structural pathology, and possible implication in postsurgical outcome.
METHODS: A descriptive, retrospective, cross-sectional study was carried out in a group of children from Children's Wisconsin between 2016 and 2022.
RESULTS: This study showed a strong association between ictal onset patterns and underlying histology (p < 0.05). Low-Frequency High Amplitude periodic spikes were seen only in patients with HS (20.6 %). A strong statistically significant association was found between different ictal onset patterns and the temporal lobe structure involved in the ictal onset (p < 0.001). Seizures with ictal onset consisting of Slow Potential Shift with superimposed Low Voltage Fast Activity arise from the Inferior Temporal Lobe or Middle Temporal Gyrus in a more significant proportion of seizures than those that originated from mesial temporal structures (Difference of proportion; p < 0.05). Low Voltage Fast Activity periodic spikes as an ictal pattern were seen in a patient with seizures arising outside the mesial temporal structure. The most frequent early spread pattern observed was Low Voltage Fast Activity (89.4 %); this pattern did not depend on the type of mesial structure pathology. Ictal onset patterns were associated with postsurgical outcomes (p < 0.001). The ictal onset pattern depends on the histopathology in the ictal onset zone and the temporal lobe structure involved in the ictal onset (p = 0.001).
CONCLUSIONS: Intracranial ictal onset patterns in TEMPORAL LOBE EPILEPSY depend on underlying histology and the temporal lobe structure involved in its onset.
The present invention discloses a method for producing a prostaglandin E1 freeze-dried powder injection preparation encapsulated by cyclodextrin. The present invention adopts a beta-cyclodextrin derivative and alpha-cyclodextrin to clathrate an alkyl side chain structure of a five carbon ring structure of PGE1, and cyclodextrin water solution is prepared from injection water solution with proper amount. Anhydrous alcohol with PGE1 of 5 to 50 ml per gram is dissolved to prepare anhydrous alcohol solution of PGE1. The cyclodextrin water solution and the anhydrous alcohol solution are clathrated by an ultrasonic instrument after being mixed, are added with low molecular dextran and mannitol which are used as excipients, and are prepared into a white crystalline and block PGE1-CYD preparation by a conventional refrigerating device. The PGE1 of the preparation can not be devitalized after being stored for two years at normal temperature. The present invention enhances the chemical stability and the physiological activity of the PGE1 preparation, and avoids the adverse reaction of partial reddish swelling and pain in the injection process.
In one aspect, the invention relates to methods for treating muscle atrophy by providing to an animal in need thereof an effective amount of a compound. The compound can modulate the expression levels of multiple mRNA of a muscle atrophy signature. This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention. The disclosed compounds can treat muscle atrophy when administered in an effective amount to an animal, such as a mammal, fish or bird. For example, human. Also disclosed in a method of lowering blood glucose in an animal by administering ursolic acid or ursolic acid analogs, such as betulininc acid analogs, and narigenin analogs, such as naringenin, in an effective amount to an animal. Also disclosed in a method of lowering blood glucose in an animal by administering ungerine/hippeastrine analogs, such as hippeastrine, in an effective amount to an animal. The disclosed compounds can also promote muscle health, promote normal muscle function, and/or promote healthy aging muscles by providing to a subject in need thereof an effective amount of a disclosed compound.
The safety of ipratropium bromide nasal solution, 0.06% at a dose of two sprays (84 mcg) per nostril three times a day (total dose 504 mcg/day) for two to four days has been demonstrated in two clinical trials involving 362 pediatric patients 5 to 11 years of age with naturally acquired common colds. In this pediatric population ipratropium bromide nasal solution, 0.06% had an adverse event profile similar to that observed in adolescent and adult patients. When ipratropium bromide nasal solution, 0.06% was concomitantly administered with an oral decongestant (pseudoephedrine HCI) in 122 children ages 5 to 12 years, and concomitantly administered with an oral decongestant/antihistamine combination (pseudoephedrine HCI/chlorpheniramine maleate) in 123 children ages 5 to 12 years, adverse event profiles were similar to ipratropium bromide nasal solution, 0.06% alone. The safety of ipratropium bromide nasal solution, 0.06% at a dose of two sprays (84 mcg) per nostril four times a day (total dose 672 mcg/day) for three weeks in pediatric seasonal allergic rhinitis patients down to 5 years is based upon the safety demonstrated in the pediatric common cold trials and the trial in adult and adolescent patients 12 to 75 years of age with seasonal allergic rhinitis. The effectiveness of ipratropium bromide nasal solution, 0.06% for the treatment of rhinorrhea associated with the common cold and seasonal allergic rhinitis in this pediatric age group is based on extrapolation of the demonstrated efficacy of ipratropium bromide nasal solution, 0.06% in adolescents and adults with the conditions and the likelihood that the disease course, pathophysiology, and the drug’s effects are substantially similar to that of adults. The recommended dose for common cold for the pediatric population is based on cross-study comparisons of the efficacy of ipratropium bromide nasal solution, 0.06% in adult and pediatric patients and on its safety profile in both adults and pediatric common cold patients. The recommended dose for seasonal allergic rhinitis for the pediatric population down to 5 years is based upon the efficacy and safety of ipratropium bromide nasal solution, 0.06% in adults and adolescents 12 years of age and above with seasonal allergic rhinitis and the safety profile of this dose in both adult and pediatric common cold patients. The safety and effectiveness of ipratropium bromide nasal solution, 0.06% in pediatric patients under 5 years of age have not been established.
Mannitol Injection, USP is a sterile, nonpyrogenic solution of mannitol in water for injection available in a concentration of 20% in flexible plastic containers.

The content and characteristics of the available concentration is as follows:

The solution contains no bacteriostat, antimicrobial agent or added buffer (except for pH adjustment) and is intended only as a single-dose injection. When smaller doses are required the unused portion should be discarded.

Mannitol Injection, USP is an osmotic diuretic for intravenous administration.

Mannitol, USP is chemically designated D-mannitol (C6H14O6), a white crystalline powder or free-flowing granules freely soluble in water. It has the following structural formula:

Water for Injection, USP is chemically designated H2O.

The flexible plastic container is fabricated from a specially formulated polyvinylchloride. Water can permeate from inside the container into the overwrap, but not in amounts sufficient to affect the solution significantly. Solutions in contact with the plastic container may leach out certain chemical components from the plastic in very small amounts; however, biological testing was supportive of the safety of the plastic container materials. Exposure to temperatures above 25°C/77°F during transport and storage will lead to minor losses in moisture content. Higher temperatures lead to greater losses. It is unlikely that these minor losses will lead to clinically significant changes within the expiration period.
Therapeutic compounds and compositions for the treatment of infectious diseases are disclosed. The compounds are xanthones and xanthone derivatives, such as 3,5-bis-ε-(N,N-diethylamino)amyloxyxanthone. The described compositions include such compounds and a pharmaceutical carrier. These compositions also can include additional materials conventionally used to form therapeutic compositions. 3,5-bis-ε-(N,N-diethylamino)amyloxyxanthone has an IC 50  for Plasmodium falciparum of about 0.15 μM, and an IC 50  for Leishmania mexicana of <<0.5 μM. These compositions are additionally useful for forming soluble complexes with heme and porphyrins.
Premature Closure of Fetal Ductus Arteriosus:

Avoid use of NSAIDs, including ibuprofen tablets, in pregnant women at about 30 weeks gestation and later. NSAIDs including ibuprofen tablets, increase the risk of premature closure of the fetal ductus arteriosus at approximately this gestational age.

Oligohydramnios/Neonatal Renal Impairment:

Use of NSAIDs, including ibuprofen tablets, at about 20 weeks gestation or later in pregnancy may cause fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. These adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after NSAID initiation. Oligohydramnios is often, but not always, reversible with treatment discontinuation. Complications of prolonged oligohydramnios may, for example, include limb contractures and delayed lung maturation. In some postmarketing cases of impaired neonatal renal function, invasive procedures such as exchange transfusion or dialysis were required.

If NSAID treatment is necessary between about 20 weeks and 30 weeks gestation, limit ibuprofen tablets use to the lowest effective dose and shortest duration possible. Consider ultrasound monitoring of amniotic fluid if ibuprofen tablets treatment extends beyond 48 hours. Discontinue ibuprofen tablets if oligohydramnios occurs and follow up according to clinical practice [see PRECAUTIONS; Pregnancy].
The device comprises a case database (5), in which the known case data are stored. An examination is performed depending on the database case content. New data expands respectively the content of the case database and forms the basis for determining a next examination step. An adaptive control of the examination is performed through interpretation of the content of the case database with the help of a medical knowledge base (6). The device comprises preferably an interface (9) to an external data processor (10) for transferring physiological data. The measurement of physiological data is preferably performed automatically.
BACKGROUND: Pain is a significant burden for children with neurodevelopmental disabilities but is difficult for clinicians to identify. No pain assessment tools for children with neurodevelopmental disabilities have been validated for use in pediatric intensive care units. The Individualized Numeric Rating Scale (INRS) is an adapted 0-to-10 rating that includes parents' input on their child's pain indicators.
OBJECTIVES: To evaluate the reliability, validity, and feasibility and acceptability of use of the INRS for assessing pain in critically ill children with neurodevelopmental disabilities.
METHODS: This observational study enrolled critically ill patients with neurodevelopmental disabilities aged 3 to 17 years in 2 pediatric intensive care units at a children's hospital using a prospective repeated-measures cohort design. Structured parent interviews were used to populate each patient's INRS. Bedside nurses assessed pain using the INRS throughout the study. The research team completed independent INRS ratings using video clips. Participating parents and nurses completed feasibility and acceptability surveys. Psychometric properties of the INRS and survey responses were evaluated with appropriate statistical methods.
RESULTS: For 481 paired INRS pain ratings in 34 patients, interrater reliability between nurse and research team ratings was moderate (weighted κ = 0.56). Parents said that creating the INRS was easy, made them feel more involved in care, and helped them communicate with nurses.
CONCLUSIONS: The INRS has adequate measurement properties for assessing pain in critically ill children with neurodevelopmental disabilities. It furthers goals of patient- and family-centered care but may have implementation barriers.
Malignant melanomas (MMs) are the abnormal proliferation of melanocytes and are one of the lethal skin cancers in humans, equines, and canines. Accordingly, MMs in companion animals can serve as naturally occurring animal models, completing conventional cancer models. The common constitutive activation of the MAPK and PI3K pathways in MMs has been described in all three species. Targeting the related pathways is considered a potential option in comparative oncologic approaches. Herein, we present a cross-species comparative analysis exposing a set of ten melanoma cell lines (one human, three equine, and six canine) derived from primary tumors or metastasis to a pan-RAF and RAF dimer inhibitor (LY3009120). Cellular response (proliferation, biomass, metabolism, early and late apoptosis/necrosis, and morphology) and the presence of pathogenic single-nucleotide variants (SNVs) within the mutational hotspot genes BRAF exon 11 and 15, NRAS exon 2 and 3, KRAS exon 2, and KIT exon 11 were analyzed. This study showed that equine malignant melanoma (EMM) cells (MelDuWi) harbor the KRAS p.Q61H mutation, while canine malignant melanoma (CMM) cells (cRGO1 and cRGO1.2) carry NRAS p.G13R. Except for EMM metastasis cells eRGO6 (wild type of the above-mentioned hotspot genes), all melanoma cell lines exhibited a decrease in dose dependence after 48 and 72 h of exposure to LY3009120, independent of the mutation hotspot landscape. Furthermore, LY3009120 caused significant early apoptosis and late apoptosis/necrosis in all melanoma cell lines except for eRGO6. The anti-tumor effects of LY3009120 were observed in nine melanoma cell lines, indicating the potential feasibility of experimental trials with LY3009120. The present study reveals that the irradiation-resistant canine metastasis cells (cRGO1.2) harboring the NRAS p.G13R mutation are significantly LY3009120-sensitive, while the equine metastases-derived eRGO6 cells show significant resistance to LY3009120, which make them both valuable tools for studying resistance mechanisms in comparative oncology.
<P>PROBLEM TO BE SOLVED: To provide an affected-part patch which can relieve or remove pain or stiffness of shoulder or waist of human being, and to provide a method for using the same.  <P>SOLUTION: The affected-part patch having analgesic action is prepared by filling a bag of a required size with a mixture of each powder of the loquat leaf, the mulberry leaf, the mugwort leaf, and the Saururaceae leaf, followed by sealing the bag. A body warmer is adhered to the back side of the bag of the affected-part patch. The surface of the bag is applied to the affected part of a human body, and the periphery of the affected part is covered and held with a holding member such as a plaster and a tape from the body warmer side. Thus, the patch is used in the state of warming.  <P>COPYRIGHT: (C)2011,JPO&INPIT