anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
The invention belongs to the field of biotechnology and medicine, and discloses a new human epididymis specific expression sperm binding protein HEL-81 as well as preparation and application thereof. The invention discloses an amino acid sequence of the HEL-81 protein and provides a recombination expression carrier carrying the DNA sequence for encoding the protein. The protein is located in the rear area of the head of a mature sperm. A RT-PCR result shows that the gene is weakly expressed in the epididymis and heart. A band of about 44 KD is detected in the corpus epididymidis part with Western blot. The HEL-81 protein can be used as a target protein for researching and developing immunity contraceptive as well as clinical diagnosis and treatment for male sterility. A method for detecting a corresponding gene or protein based on development of the HEL-81 protein can be widely used for the research field of reproductive medicine.
Fluticasone Furoate/Vilanterol ELLIPTA contains both fluticasone furoate and vilanterol; therefore, the risks associated with overdosage for the individual components described below apply to Fluticasone Furoate/Vilanterol ELLIPTA. Treatment of overdosage consists of discontinuation of Fluticasone Furoate/Vilanterol ELLIPTA together with institution of appropriate symptomatic and/or supportive therapy. The judicious use of a cardioselective beta‑receptor blocker may be considered, bearing in mind that such medicine can produce bronchospasm. Cardiac monitoring is recommended in cases of overdosage.

Fluticasone Furoate

Because of low systemic bioavailability (15.2%) and an absence of acute drug-related systemic findings in clinical trials, overdosage of fluticasone furoate is unlikely to require any treatment other than observation. If used at excessive doses for prolonged periods, systemic effects such as hypercorticism may occur [see Warnings and Precautions (5.8)].

Vilanterol

The expected signs and symptoms with overdosage of vilanterol are those of excessive beta‑adrenergic stimulation and/or occurrence or exaggeration of any of the signs and symptoms of beta-adrenergic stimulation (e.g., seizures, angina, hypertension or hypotension, tachycardia with rates up to 200 beats/min, arrhythmias, nervousness, headache, tremor, muscle cramps, dry mouth, palpitation, nausea, dizziness, fatigue, malaise, insomnia, hyperglycemia, hypokalemia, metabolic acidosis). As with all inhaled sympathomimetic medicines, cardiac arrest and even death may be associated with an overdose of vilanterol.
Corneal ectasia as a complication from refractive (LASIK) surgery as well as keratoconus is a slowly progressive condition that results in high patient morbidity. Treatment options aim to stabilize the shape of the cornea using rigid contact lenses, surgical insertion of stiff plastic intrastromal rings, corneal cross linking, and ultimately corneal transplant in severe patients. The recently FDA approved "Dresden Protocol" involves painful cornea scraping followed by application of concentrated Riboflavin, followed by immediate collagen cross linking with UV light exposure which results in shortening and thickening of the collagen fibrils, and therefore a stronger, stiffer cornea. Avedro has demonstrated an average cornea flattening (K max reduction) of 1.4 diopters and 1.7diopters in two different studies. The current cost of Avedro therapy is between $2500 -$3500 per treatment. This is considered to be an accepted medical procedure at this time and therefore is beginning to be covered by several insurance companies.To spare the patient the severe pain involved in the current procedure, and to avoid the high cost (Avedro is not covered by any medical insurance), the investigator started 7 patients with keratoconus from 2011-2015 in his private practice in Seattle on a trial of oral riboflavin (100 mg or 400 mg daily) and 15 minutes of sunlight exposure daily. No adverse effects have ever been reported with high-dose dietary riboflavin supplements. The results of this preliminary trial are remarkable. During follow-up from 6 months to 5 years, all 7 patients have had corneal stabilization and/or corneal flattening. One patient experienced flattening of the cornea by 1.5 Diopters, comparable to the best results of the Avedro system. A limited animal study was recently completed and published in Switzerland by Dr. Farhad Hafezi , M.D., PhD which was published in the Journal of Cataract \& Refractive Surgery that confirmed corneal cross-linking occurs in response to riboflavin and UV exposure from the sun and proven to successfully crosslink. Our current clinical study would expand the promising preliminary findings to a larger sample size. This has the potential to save millions of dollars in health care costs and ease the burden of treatment in patients who require therapy to induce corneal cross-linking to stabilize the cornea's shape.

To date eye specialists in Brazil, Texas and other locations are beginning to treat patients with our protocol and finding similar successful results using 400 to 800mg dietary riboflavin and 15 to 45 minutes of sunlight exposure for a period of 3 to 6 months with successful results.
Pain, nerve trunk inflammation, and neuronal injury are hallmarks of acute herpes zoster (AHZ). We hypothesize that the development of post-herpetic neuralgia (PHN) strongly depends on two factors: 1) the severity of the initial neural injury and 2) the ability to recover from the initial neural injury. To test this hypothesis, we will prospectively follow 150 patients at high risk for development of PHN. Evolution of pain and neural injury will be evaluated at 2-6 weeks, 6 weeks, 3 months, 6 months and at 2 years or longer after the onset of AHZ by multiple measures. Assessments at 2 years or longer will be compared to those collected during the first 6 months after HZ in order to test whether or not sensory function and cutaneous innervation continues to normalize beyond 6 months in subjects who recover from HZ without severe PHN.

Preliminary analysis of study data showed reduced innervation in HZ skin, mirror image skin and distant control skin in the acute phase of HZ that was not specific to the persistence of pain at 3 months. The innervation appeared to recover more fully by 6 months in distant control skin than in mirror-image skin and HZ skin, despite the fact that the subjects were continuing to experience a further reduction in their zoster-associated pain. This suggests that the symptoms of pain and sensory dysfunction are not due to a mere loss in overall innervation density. The proposed subsequent ≥ 2 year study visit and analysis will allow us to directly correlate pain resolution with resolution of sensory and innervation abnormalities.
Anthropogenic stressors such as agriculture and urbanization can increase river turbidity, which can negatively impact fish gill morphology and growth due to reduced oxygen in the benthic environment. We assessed the gill morphology, field metabolic rate (FMR), and two hypoxia tolerance metrics (oxygen partial pressure at loss of equilibrium, PO2 at LOE, and critical oxygen tension, Pcrit) of eastern sand darter (Ammocrypta pellucida), a small benthic fish listed as threatened under the Species at Risk Act in Canada, from rivers in southern Ontario. Field trials were conducted streamside in the Grand River (August 2019; mean NTU 8) and in the comparatively more turbid Thames River (August 2020; mean NTU 94) to test the effect of turbidity on each physiological endpoint. Gills were collected from incidental mortalities and museum specimens, and were assessed using hematoxylin and eosin and immunofluorescent staining. The between-river comparison indicated that turbidity significantly increased interlamellar space and filament width but had no significant influence on other gill morphometrics or FMR. Turbidity significantly increased PO2 at LOE (i.e., fish had a lower hypoxia tolerance) but did not significantly impact Pcrit. Therefore, although turbidity influences hypoxia tolerance through LOE, turbidity levels were not sufficiently high in the study rivers to contribute to measurable changes in gill morphology or metabolism in the wild. Determining whether changes in gill morphology or metabolism occur under higherturbidity levels would help resolve the ecological importance of turbidity on species physiology in urban and agricultural ecosystems.
Participants will receive JNJ-75348780. The dose levels will be escalated sequentially based on the decisions of the Study Evaluation Team (SET), along with the potential exploration of other routes of administration and schedules, until one or more recommended Phase 2 Doses (RP2D) have been identified.
The present invention discloses an antagonist peptide of the Interleukin-15 (IL-15) activity, which is characterized in that it comprises an amino acid sequence identified as SEQ ID No. 5 or SEQ ID No. 12, or a homodimer of these peptides, as well as a nucleic acid that encodes for the peptide with the sequence identified as SEQ ID No. 5 or SEQ ID No. 12. Pharmaceutical compositions comprising said peptides or nucleic acids encoding said sequences are part of the invention. In addition, it provides the use of an IL-15 antagonist peptide comprising the amino acid sequence identified as SEQ ID No. 5 or SEQ ID No. 12, or a homodimer of these peptides, for the manufacture of a medicament. The invention contemplates a method for the treatment of a disease related to the IL-15 overexpression, prostate and kidney cancer.
PURPOSE:To obtain a transcutaneous absorbefacient having excellent absorbefacient effect of drug active component and good safety and feeling to the skin, by using a nonionic surfactant, etc., containing N in the molecule and a nonionic surfactant free from nitrogen atom in the molecule as active components. CONSTITUTION:The objective agent contains (A) an N-containing nonionic surfactant (e.g. fatty acid alkanolamide or polyoxyethylene fatty acid alkanolamide), ampholytic surfactant (e.g. N,N-dimethyl-N-lauryl-N- carboxymethylammonium betaine), semi-polar surfactant (e.g. lauryl dimethylamine oxide) and cationic surfactant (e.g. fatty acid amine salt) and (B) a nonionic surfactant free from N in the molecule (e.g. sorbitan monooleate) as active components. The effect of the drug-active component such as predonisolone can be promoted by the use of the absorbefacient.
Olodaterol is a long-acting beta2-adrenergic agonist (LABA). The compound exerts its pharmacological effects by binding and activation of beta2-adrenoceptors after topical administration by inhalation. Activation of these receptors in the airways results in a stimulation of intracellular adenyl cyclase, an enzyme that mediates the synthesis of cyclic-3', 5' adenosine monophosphate (cAMP). Elevated levels of cAMP induce bronchodilation by relaxation of airway smooth muscle cells. In vitro studies have shown that olodaterol has 241-fold greater agonist activity at beta2-adrenoceptors compared to beta1-adrenoceptors and 2,299-fold greater agonist activity compared to beta3-adrenoceptors. The clinical significance of these findings is unknown.

Beta-adrenoceptors are divided into three subtypes: beta1-adrenoceptors predominantly expressed on cardiac smooth muscle, beta2-adrenoceptors predominantly expressed on airway smooth muscle, and beta3-adrenoceptors predominantly expressed on adipose tissue. Beta2-agonists cause bronchodilation. Although the beta2-adrenoceptor is the predominant adrenergic receptor in the airway smooth muscle, it is also present on the surface of a variety of other cells, including lung epithelial and endothelial cells and in the heart. The precise function of beta2-receptors in the heart is not known, but their presence raises the possibility that even highly selective beta2-agonists may have cardiac effects.
This Disease Registry is designed to capture the patient characteristics, practice patterns, and therapeutic strategies evaluated in community and academic centers when treating relapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL), and R/R follicular lymphoma (FL). The data collected in this Registry will facilitate the evaluation of the current treatment landscape for non-Hodgkin lymphoma (NHL), including the clinical effectiveness, safety. No investigational product or drug will be administered as part of this study. Enrolled patients will receive treatment and evaluations for their disease according to the standard of care and routine clinical practice at each study site. All treatments that patients receive for their disease will be recorded, including any previous lymphoma treatments. Clinical outcomes will be documented as part of an objective clinical assessment. In addition, patient-reported health-related quality of life (HRQoL) outcomes data will be collected from patients using various validated instruments. Social support data will also be collected.
OBJECTIVES: I. Evaluate oral topotecan and paclitaxel in terms of toxicity and complete and partial response rate in patients with previously untreated extensive stage small cell lung cancer. II. Determine preliminary estimates of survival in this patient population in response to this regimen.

OUTLINE: Patients receive oral topotecan on days 1-5 followed by paclitaxel IV over 3 hours on day 5. Beginning 24-48 hours after chemotherapy, patients receive filgrastim (G-CSF) subcutaneously daily for up to 10 days until blood counts recover. Treatment repeats every 4 weeks for 6 courses in the absence of disease progression. Patients who develop CNS progressive disease only should receive whole brain radiotherapy before continuing study treatment.
The invention belongs to the technical field of biological medicines, and particularly relates to application of ATXN7L3 in diagnosis, treatment and prognosis of liver cancer. The invention provides a molecular marker ATXN7L3 related to the occurrence and development of liver cancer, a liver cancer diagnosis product and means, and whether a patient has the risk of liver cancer is judged by detecting the expression level of the molecular marker. Also provides a drug combination or a method for treating liver cancer, which treats liver cancer through specific up-regulation molecular markers. Experiments show that the expression of ATXN7L3 is compared in cancer tissues and para-cancer tissues of HCC clinical patients, and ATXN7L3 is found to be remarkably low expressed in the HCC tissues of the cancer tissues. In addition, the expression of ATXN7L3 is positively correlated with the differentiation degree of HCC tissues, namely, the expression level of ATXN7L3 is higher in HCC tissues with high differentiation degree. And the expression of ATXN7L3 is in negative correlation with the prognosis of patients, namely, the patients with low expression of ATXN7L3 have low overall survival rate and short survival period. In addition, the ATXN7L3 finds that the reduction of the expression of the ATXN7L3 protein can promote the proliferative capacity of HCC cells through in vivo and in vitro functional experiments.
A coated implantable medical device 10 includes a structure 12 adapted for introduction into the vascular system, esophagus, trachea, colon, biliary tract, or urinary tract; at least one layer 18 of a bioactive material positioned over the structure 12; and at least one porous layer 20 positioned over the bioactive material layer 18. Preferably, the structure 12 is a coronary stent, and the bioactive material is at least one of heparin, dexamethasone or a dexamethasone derivative. The device 10 includes layers 18 and 22 of heparin and dexamethasone, the layer 22 of dexamethasone being positioned above the layer 18 of heparin. The layers of bioactive material also can be individual materials or a combination of different materials. Unexpectedly, the more soluble heparin markedly promotes the release of the less soluble dexamethasone above it. The porous layer 20 is composed of a polymer applied by vapor or plasma deposition and provides a controlled release of the bioactive material. It is particularly preferred that the polymer is a polyimide, parylene or a parylene derivative, which is deposited without solvents, heat or catalysts, merely by condensation of a monomer vapor.
Subject will be randomized to either test product/active comparator/placebo comparator. Test product is Ketoconazole 2% cream manufactured by Douglas Pharmaceuticals America Ltd.
* Tramadol hydrochloride and acetaminophen tablets are not approved for use for more than 5 days.
  * Do not exceed the recommended dose of tramadol hydrochloride and acetaminophen tablets. Do not co-administer tramadol hydrochloride and acetaminophen tablets with other tramadol or acetaminophen containing products [see Warnings and Precautions (5.20)].
  * Tramadol hydrochloride and acetaminophen tablets should be prescribed only by healthcare professionals who are knowledgeable about the use of opioids and how to mitigate the associated risks.
  * Use the lowest effective dosage for the shortest duration of time consistent with individual patient treatment goals [see Warnings and Precautions (5)]. Because the risk of overdose increases as opioid doses increase, reserve titration to higher doses of tramadol hydrochloride and acetaminophen tablets for patients in whom lower doses are insufficiently effective and in whom the expected benefits of using a higher dose opioid clearly outweigh the substantial risks.
  * Many acute pain conditions (e.g., the pain that occurs with a number of surgical procedures or acute musculoskeletal injuries) require no more than a few days of an opioid analgesic. Clinical guidelines on opioid prescribing for some acute pain conditions are available.
  * There is variability in the opioid analgesic dose and duration needed to adequately manage pain due both to the cause of pain and to individual patient factors. Initiate the dosing regimen for each patient individually, taking into account the patient’s underlying cause and severity of pain, prior analgesic treatment and response, and risk factors for addiction, abuse, and misuse [see Warnings and Precautions (5.1)].
  * Respiratory depression can occur at any time during opioid therapy, especially when initiating and following dosage increases with tramadol hydrochloride and acetaminophen tablets. Consider this risk when selecting an initial dose and when making dose adjustments [see Warnings and Precautions (5)].
* Do not prescribe propoxyphene for patients who are suicidal or addiction-prone.
  * Prescribe propoxyphene with caution for patients taking tranquilizers or antidepressant drugs and patients who use alcohol in excess.
  * Tell your patients not to exceed the recommended dose and to limit their intake of alcohol.



Propoxyphene products, in excessive doses, either alone or in combination with other CNS depressants, including alcohol, are a major cause of drug related deaths. Fatalities within the first hour of overdosage are not uncommon. In a survey of deaths due to overdosage conducted in 1975, in approximately 20% of the fatal cases, death occurred within the first hour (5% occurred within 15 minutes). Propoxyphene should not be taken in doses higher than those recommended by the physician. The judicious prescribing of propoxyphene is essential to the safe use of this drug. With patients who are depressed or suicidal, consideration should be given to the use of non-narcotic analgesics. Patients should be cautioned about the concomitant use of propoxyphene products and alcohol because of potentially serious CNS-additive effects of these agents. Because of its added depressant effects, propoxyphene should be prescribed with caution for those patients whose medical condition requires the concomitant administration of sedatives, tranquilizers, muscle relaxants, antidepressants, or other CNS-depressant drugs. Patients should be advised of the additive depressant effects of these combinations.

Many of the propoxyphene-related deaths have occurred in patients with previous histories of emotional disturbances or suicidal ideation or attempts as well as histories of misuse of tranquilizers, alcohol, and other CNS-active drugs. Some deaths have occurred as a consequence of the accidental ingestion of excessive quantities of propoxyphene alone or in combination with other drugs. Patients taking propoxyphene should be warned not to exceed the dosage recommended by the physician.
This invention provides a therapeutic agent capable of specifically forming a complex with human immunodeficiency virus envelope glycoprotein which comprises a polypeptide. In one embodiment of the invention, the amino acid sequence of the polypeptide comprises the amino acid sequence shown in FIG. 6 from about +1 to about +185 fused to the amino acid sequence from about +353 to about +371. In another embodiment of the invention, the amino acid sequence of the polypeptide comprises the amino acid sequence shown in FIG. 6 from about +1 to about +106 fused to the amino acid sequence from about +353 to about +371. In yet a further embodiment of the invention, the amino acid sequence of the polypeptide comprises the amino acid sequence shown in FIG. 6 from about +1 to about +185. This invention also provides a method for treating a subject infected with a human immunodeficiency virus. The method comprises administering to the subject an effective amount of a pharmaceutical composition comprising an effective amount of a therapeutic agent of the invention and a pharmaceutically acceptable carrier.
Pregnancy Exposure Registry

There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to TALTZ during pregnancy. Pregnant women exposed to TALTZ are encouraged to enroll in the TALTZ Pregnancy Registry by calling 1-800-284-1695. Contact information for the registry is also available on http://www.pregnancyregistry.lilly.com.

Risk Summary

Available data from the published literature and the pharmacovigilance database with TALTZ use in pregnant women are insufficient to evaluate for a drug-associated risk of major birth defects, miscarriage or other adverse maternal or fetal outcomes. 

Human IgG is known to cross the placental barrier; therefore, TALTZ may be transmitted from the mother to the developing fetus. An embryofetal development study conducted in pregnant monkeys during organogenesis at doses up to 19 times the maximum recommended human dose (MRHD) revealed no evidence of harm to the developing fetus. When dosing was continued until parturition, neonatal deaths were observed at 1.9 times the MRHD [see Data]. The clinical significance of these nonclinical findings is unknown. 

The background risk of major birth defects and miscarriage for the indicated population is unknown. All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. 

Data

Animal Data

An embryofetal development study was conducted in cynomolgus monkeys administered ixekizumab. No malformations or embryofetal toxicity were observed in fetuses from pregnant monkeys administered ixekizumab weekly by subcutaneous injection during organogenesis to near parturition at doses up to 19 times the MRHD (on a mg/kg basis of 50 mg/kg/week). Ixekizumab crossed the placenta in monkeys. 

In a pre- and post-natal development toxicity study, pregnant cynomolgus monkeys were administered weekly subcutaneous doses of ixekizumab up to 19 times the MRHD from the beginning of organogenesis to parturition. Neonatal deaths occurred in the offspring of two monkeys administered ixekizumab at 1.9 times the MRHD (on a mg/kg basis of 5 mg/kg/week) and two monkeys administered ixekizumab at 19 times the MRHD (on a mg/kg basis of 50 mg/kg/week). These neonatal deaths were attributed to early delivery, trauma, or congenital defect. The clinical significance of these findings is unknown. No ixekizumab-related effects on functional or immunological development were observed in the surviving infants from birth through 6 months of age.