anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
BACKGROUND AND AIMS: Cancer cells reprogram their metabolic pathways to support bioenergetic and biosynthetic needs and to maintain their redox balance. In several human tumors, the Keap1-Nrf2 system controls proliferation and metabolic reprogramming by regulating the pentose phosphate pathway (PPP). However, whether this metabolic reprogramming also occurs in normal proliferating cells is unclear.
APPROACH AND RESULTS: To define the metabolic phenotype in normal proliferating hepatocytes, we induced cell proliferation in the liver by 3 distinct stimuli: liver regeneration by partial hepatectomy and hepatic hyperplasia induced by 2 direct mitogens: lead nitrate (LN) or triiodothyronine. Following LN treatment, well-established features of cancer metabolic reprogramming, including enhanced glycolysis, oxidative PPP, nucleic acid synthesis, NAD + /NADH synthesis, and altered amino acid content, as well as downregulated oxidative phosphorylation, occurred in normal proliferating hepatocytes displaying Nrf2 activation. Genetic deletion of Nrf2 blunted LN-induced PPP activation and suppressed hepatocyte proliferation. Moreover, Nrf2 activation and following metabolic reprogramming did not occur when hepatocyte proliferation was induced by partial hepatectomy or triiodothyronine.
CONCLUSIONS: Many metabolic changes in cancer cells are shared by proliferating normal hepatocytes in response to a hostile environment. Nrf2 activation is essential for bridging metabolic changes with crucial components of cancer metabolic reprogramming, including the activation of oxidative PPP. Our study demonstrates that matured hepatocytes exposed to LN undergo cancer-like metabolic reprogramming and offers a rapid and useful in vivo model to study the molecular alterations underpinning the differences/similarities of metabolic changes in normal and neoplastic hepatocytes.
Titanium-nitride-oxide coated cobalt-chromium OPTIMAX™ bio-active stent (BAS). Patients will have OCT follow-up 1 month after the index procedure.
As with other NSAIDs, anaphylactoid reactions may occur in patients without known prior exposure to naproxen tablets. Naproxen tablets should not be given to patients with the aspirin triad. This symptom complex typically occurs in asthmatic patients who experience rhinitis with or without nasal polyps, or who exhibit severe, potentially fatal bronchospasm after taking aspirin or other NSAIDs (see CONTRAINDICATIONS and PRECAUTIONS: Preexisting Asthma). Emergency help should be sought in cases where an anaphylactoid reaction occurs. Anaphylactoid reactions, like anaphylaxis, may have a fatal outcome. 

Skin Reactions

NSAIDs, including naproxen tablets, can cause serious skin adverse events such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events may occur without warning. Patients should be informed about the signs and symptoms of serious skin manifestations and use of the drug should be discontinued at the first appearance of skin rash or any other sign of hypersensitivity.

Pregnancy

In late pregnancy, as with other NSAIDs, naproxen tablets should be avoided because it may cause premature closure of the ductus arteriosus.
A method and apparatus converts host cells of a first type into cells of a second type. The host cells are placed in intimate contact with donor cells of the second type. The intimate contact is under predetermined conditions that transport a sufficient number of mRNA molecules from the donor cells into the host cells to reprogram the host cells into the second type. The conditions may include the application of an electromagnetic force, using a media that enables the electromagnetic force to produce an electrophoresis effect that acts on the mRNA molecules from the donor cells to transport them through an outer cell membrane into the hosts cells. The host and donor cells may be subjected to while in intimate contact to a transporting force that enables the mRNA molecules of the donor cells to penetrate an outer membrane wall of host cells without damaging the membrane wall. The transporting force may include an electric field, a magnetic field, or a combined electric field and magnetic field.
AVINZA capsules are a modified-release formulation of morphine sulfate intended for once daily administration indicated for the relief of moderate to severe pain requiring continuous, around-the-clock opioid therapy for an extended period of time.

AVINZA is NOT intended for use as a prn analgesic.

The safety and efficacy of using AVINZA in the postoperative setting has not been evaluated. AVINZA is not indicated for postoperative use. If the patient has been receiving the drug prior to surgery, resumption of the pre-surgical dose may be appropriate once the patient is able to take the drug by mouth. Physicians should individualize treatment, moving from parenteral to oral analgesics as appropriate. (see American Pain Society guidelines)
<P>PROBLEM TO BE SOLVED: To provide an emulsifier composition for an organopolysiloxane causing a small impact on the environment and having an excellent emulsifying ability and an organopolysiloxane emulsion composition emulsified with the emulsifier composition.  <P>SOLUTION: The emulsifier composition for an organopolysiloxane is a mixture of a polyoxyethylene alkyl ether expressed by general formula (I). In the formula, the median of the number of the carbons of the alkyl group is 10. The polyoxyethylene alkyl ether comprises component A whose n is 3, component B whose n is 5 and/or component C whose n is 6 and component D whose n is 8. The weight ratio among these components is component A:(component B+component C):component D=0.9-1.1:0.9-1.1:0.9-1.1. The emulsified composition is obtained by emulsifying an organopolysiloxane in water using the emulsifier composition.  <P>COPYRIGHT: (C)2005,JPO&NCIPI
Recruitment of patients will be achieved in the department of digestive surgery. It will involve 122 patients with severe obesity undergoing bariatric surgery scheduled within the digestive surgery department. Patients recruited will be examined for evaluating the presence and severity of periodontitis, and separated into either group 1: for patients with moderate or severe periodontitis, and or group 2: for patients without or with mild periodontitis. The day before the surgery, blood sample will be collected for the analysis of circulating metabolic and inflammatory markers. Collection of stimulated saliva, periodontal sample and faeces samples (50 g) will also be carried out for bacteria determination. During the surgical procedure, a sample of visceral adipose tissue (50 g) will be collected and used for periodontal bacteria detection and inflammatory markers analyses.
INTRODUCTION: Early salvage radiotherapy is indicated for patients with biochemical recurrence after radical prostatectomy. However, for various reasons, certain patients do not benefit from this treatment (OBS) or only at a late stage (LSR). There are few studies on this subject and none on a "high-risk" population, such as patients of African descent. Our objective was to estimate the metastasis-free (MFS) and overall survival (OS) of patients who did not receive salvage radiotherapy, and to identify risk factors of disease progression.
PATIENTS AND METHODS: This was a single-center retrospective study that included 154 patients, 99 in the OBS group and 55 in the LSR group. All were treated by total prostatectomy for localized prostate cancer between January 2000 and December 2020 and none received early salvage radiotherapy after biochemical recurrence.
RESULTS: Baseline characteristics were similar between groups, except for the time to biochemical recurrence. The median follow-up was 10.0 and 11.8 years for the OBS and LSR groups, respectively. The median time from surgery to LSR was 5.1 years. The two groups did not show a significant difference in MFS: 90.6% at 10 years for the OBS group and 93.3% for the LSR group. The median MFS was 19.8 and 19.6 years for the OBS and LSR groups respectively. OS for the OBS group was significantly higher than that for the LSR group (HR: 2.14 [1.07-4.29]; p = 0.03), with 10-year OS of 95.9% for the OBS group and 76.1% for the LSR group. Median OS was 16 and 15.6 years for the OBS and LSR groups, respectively.
CONCLUSION: In this study, we observed satisfactory metastasis-free and OS rates relative to those reported in the scientific literature. The challenge is not to question the benefit of early salvage radiotherapy, but to improve the identification of patients at risk of progression through the development of molecular and genomic tests for more highly personalized medicine.
FIELD: pharmacology. SUBSTANCE: agent exhibiting analgesic and wound-healing activity and preventing formation of hypertrophic cicatrices and facilitating restoration of skin contains non-refined sunflower oil, burdock root, and camomile flower. Agent is prepared by infusion of dried vegetable stock with non-refined sunflower oil. Root is preliminarily peeled and ground. EFFECT: increased therapeutic activity. 3 cl, 2 ex
PROBLEM TO BE SOLVED: To obtain the subject polymer having excellent moisture retaining properties in application to skin and hair, continuing its effects for many hours, having excellent touch, useful as a humectant for various cosmetics and detergent compositions, by including a specific structural unit. SOLUTION: This hydrophilic polymer comprises structural units of formula I and formula II [R<1> and R<4> are each H or methyl; R<2> and R<3> are each a (substituted) 1-10C alkyl; Y and Z are each NH or 0; Y is a (substituted) 1-10C bifunctional saturated hydrocarbon; (p) is 2-5; A is a 2-4C alkylene] and has 500-500,000 weight-average molecular weight. The ratio of the composition of the structural units of formula I and formula II by weight is preferably 10:90 to 90:10. The polymer is obtained by polymerizing monomers of formula III and formula IV in the presence of a polymerization solvent (e.g. water, methanol, ethanol, etc.), by using a radical polymerization initiator (e.g. an azo-based radical initiator) preferably at 40-80 deg.C.
A two-coat cosmetic product, uses thereof and a make-up kit containing the same product are provided, which two-coat cosmetic product is glossy, has no taste, does not migrate and does not transfer, and gives comfort such as, no drying and no tightening to a user when it is applied on the skin of the user and the application time is passed. The two-coat cosmetic product comprises a first and second compositions, wherein the first composition comprises at least one film-forming linear ethylene block polymer in a cosmetically acceptable organic liquid medium; and the second composition comprises a different cosmetically acceptable organic liquid medium; the block polymer is free from styrene; the block polymer is not elastomer; the block polymer is ethylene polymer derived from aliphatic ethylene monomer containing carbon-carbon double bond and at least one ester group(-COO-) or amide group(-CON-); the block polymer comprises a first block and a second block having different vitreous transition temperature(Tg); the first and second blocks are connected between them by an intermediate segment having the vitreous transition temperature(Tg) between the vitreous transition temperatures(Tg) of the first and second blocks; and the first block has a Tg temperature selected from 40 deg. C or more, 20 deg. C or less, and between 20 deg. C to 40 deg. C.
Celecoxib capsule is a nonsteroidal anti-inflammatory drug, available as capsules containing 50 mg, 100 mg, 200 mg and 400 mg celecoxib for oral administration. The chemical name is 4-[5-(4-methylphenyl)- 3-(trifluoromethyl)-1H-pyrazol-1-yl] benzenesulfonamide and is a diaryl-substituted pyrazole. The molecular weight is 381.38. Its molecular formula is C 17H 14F 3N 3O 2S, and it has the following chemical structure:   


  


Celecoxib USP is a white or almost white crystalline powder with a pKa of 11.1 (sulfonamide moiety). Celecoxib USP is hydrophobic (log P is 3.5) and is soluble in ethanol and in methylene chloride, practically insoluble in water.

  


The inactive ingredients in celecoxib capsules include: croscarmellose sodium, lactose monohydrate, magnesium stearate, povidone and sodium lauryl sulfate. The empty hard gelatin capsule shell contains gelatin and titanium dioxide. The capsules are printed with ink containing black iron oxide, potassium hydroxide, propylene glycol and shellac.
The present invention provides pharmaceutically acceptable salts having local anesthetic and anti-inflammatory activities. The preferred pharmaceutically acceptable salt is a diclofenac salt of lidocaine. Diclofenac is a non-steroidal anti-inflammatory drug ("NSAID"). Lidocaine is a local anesthetic. Other NSAID (except the salicylic acid derivatives of NSAID) can be used to replace diclofenac and/or other local anesthetics can be used to replace lidocaine. The pharmaceutically acceptable salts are crystalline compounds, which are distinctively different from either the NSAID alone or the local anesthetic alone, as indicated by differential scanning calorimetry (DSC), thermogravimetric analysis (TGA), High Performance Liquid Chromatography (HPLC) and Fourier-Transformed Infrared Spectroscopy (FTIR) analyses. These pharmaceutically acceptable salts are suitable for use in topical treatment or parenteral injection to treat patients with localized pain, including muscle pain, joint pain, pain associated with herpes infection, and wound pain (such as surgical wound, burn wound etc.).
PURPOSE: The Pediatric Normal Tissue Effects in the Clinic (PENTEC) hearing loss (HL) task force reviewed investigations on cochlear radiation dose-response relationships and risk factors for developing HL. Evidence-based dose-response data are quantified to guide treatment planning.
METHODS AND MATERIALS: A systematic review of the literature was performed to correlate HL with cochlear dosimetry. HL was considered present if a threshold exceeded 20 dB at any frequency. Radiation dose, ototoxic chemotherapy exposure, hearing profile including frequency spectra, interval to HL, and age at radiation therapy (RT) were analyzed.
RESULTS: Literature was systematically reviewed from 1970 to 2021. This resulted in 739 abstracts; 19 met inclusion for meta-analysis, and 4 included data amenable to statistical modeling. These 4 studies included 457 cochleas at risk in patients treated with RT without chemotherapy, and 398 cochlea treated with chemotherapy. The incidence and severity of cochlear HL from RT exposure alone is related to dose and age. Risk of HL was <5% in cochlea receiving a mean dose ≤35 Gy but increased to 30% at 50 Gy. HL risk ranged from 25% to 40% in children under the age of 5 years at diagnosis, declining to 10% in older children for any radiation dose. Probability of similar severe HL occurred at doses 18.3 Gy higher for children <3 versus >3 years of age. High-frequency HL was most common, with average onset occurring 3.6 years (range, 0.4-13.2 years) after RT. Exposure to platinum-based chemotherapies added to the rates of HL at a given cochlear dose level, with 300 mg/m2 shifting the dose response by 7 Gy.
CONCLUSIONS: In children treated with RT alone, risk of HL was low for cochlear dose <35 Gy and rose when dose exceeded 35 Gy without clear RT dose dependence. High-frequency HL was most prevalent, but all frequencies were affected. Children younger than 5 years were at highest risk of developing HL, although independent effects of dose and age were not fully elucidated. Future reports with more granular data are needed to better delineate time to onset of HL and the effects of chemoradiotherapy.
Apply a thin film of Mometasone Furoate Cream USP, 0.1% to the affected skin areas once daily. Mometasone furoate cream may be used in pediatric patients 2 years of age or older. Since safety and efficacy of mometasone furoate cream have not been established in pediatric patients below 2 years of age; use in this age group is not recommended [see Warnings and Precautions (5.1) and Use in Specific Populations (8.4)].

Therapy should be discontinued when control is achieved. If no improvement is seen within 2 weeks, reassessment of diagnosis may be necessary. Safety and efficacy of mometasone furoate cream in pediatric patients for more than 3 weeks of use have not been established.

Mometasone furoate cream should not be used with occlusive dressings unless directed by a physician. Mometasone furoate cream should not be applied in the diaper area if the child still requires diapers or plastic pants, as these garments may constitute occlusive dressing.

Mometasone furoate cream is for topical use only. It is not for oral, ophthalmic, or intravaginal use.

Avoid use on the face, groin, or axillae.
The colon is the largest compartment of the immune system, with innate immune cells exposed to antigens in the environment. However, the mechanisms by which the innate immune system is instigated are poorly defined in colorectal cancer (CRC). Here, a population of CD16+ neutrophils that specifically accumulate in CRC tumor tissues by imaging mass cytometry (IMC), immune fluorescence, and flow cytometry, which demonstrated pro-tumor activity by disturbing natural killer (NK) cells are identified. It is found that these CD16+ neutrophils possess abnormal cholesterol accumulation due to activation of the CD16/TAK1/NF-κB axis, which upregulates scavenger receptors for cholesterol intake including CD36 and LRP1. Consequently, these region-specific CD16+ neutrophils not only competitively inhibit cholesterol intake of NK cells, which interrupts NK lipid raft formation and blocks their antitumor signaling but also release neutrophil extracellular traps (NETs) to induce the death of NK cells. Furthermore, CD16-knockout reverses the pro-tumor activity of neutrophils and restored NK cell cytotoxicity. Collectively, the findings suggest that CRC region-specific CD16+ neutrophils can be a diagnostic marker and potential therapeutic target for CRC.
Background: Sleep disturbances, which are common problems in older adults, often lead to cognitive decline and depression and may even increase mortality risk. Foot thermal therapy is a simple and safe approach for improving sleep and is associated with relatively few side effects. However, the effect of different operations of foot thermal therapy on sleep quality in older adults is inconclusive. This study aimed to access the effects of temperature, duration, and heating height of foot thermal therapy (administered through a footbath) on the subjective and objective sleep quality of older adults. Methods: Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline, eight databases were searched for all relevant articles published up to July 2023, and a rigorous systematic review and meta-analysis was conducted. This study was registered in the PROSPERO database (CRD42022383460). Inclusion criteria were: (1) participants with a mean age ≥60 years; (2) interventions that included foot thermal therapy; (3) a control group that received routine care but no thermal therapy; (4) outcome measurements that assessed sleep quality; and (5) the studies that utilized randomized controlled trials or quasi-experimental studies. Methodological quality was assessed using the Joanna Briggs Institute critical appraisal tools. The meta-analysis was performed using RevMan version 5.4. Results: A total of 11 studies were included. Foot thermal therapy before bedtime improved subjective sleep quality in older adults, with optimal parameters of 40°C temperature (standardized mean difference [SMD] = 0.66, 95% confidence interval [CI]: 0.33 to 0.99), ≤20-min duration (SMD = 0.66, 95% CI: 0.39 to 0.93), and 10 cm heating height (SMD = 0.78, 95% CI: 0.45 to 1.11). Subgroup analyses revealed that a temperature of 41°C-42°C can improve objective sleep latency (SMD = 0.54, 95% CI: 0.09 to 0.99). Conclusions: It is recommended to administer foot thermal therapy (40°C; ≤20 min; 10 cm above the ankle) to older adults 1 h before their bedtime. If they have trouble falling asleep, the temperature can be increased to 41°C-42°C.
Fenofibric acid delayed-release capsules (fenofibric acid) are a lipid regulating agent available as delayed release capsules for oral administration. Each delayed release capsule contains choline fenofibrate, equivalent to 45 mg or 135 mg of fenofibric acid. The chemical name for choline fenofibrate is ethanaminium, 2-­hydroxy-N,N,N-trimethyl, 2-{4-(4-chlorobenzoyl)phenoxy] -2-methylpropanoate (1:1) with the following structural formula:   
  
The molecular formula is C 22H 28ClNO 5 and the molecular weight is 421.91. Choline fenofibrate is freely soluble in methanol, sparingly soluble in ethanol and water, slightly soluble in DMSO and practically insoluble in dichloromethane. The melting point is approximately 210°C. Choline fenofibrate is a white to off white crystalline powder, which is stable under ordinary conditions. 

  


Each delayed release capsule contains enteric coated mini-tablets comprised of choline fenofibrate and the following inactive ingredients: hypromellose, hydroxypropyl cellulose, methacrylic acid - ethyl acrylate copolymer (1:1) type A , microcrystalline cellulose, povidone K30, silicon dioxide, sodium stearyl fumarate, talc, triethyl citrate. The capsule shell of the 45 mg capsule contains the following inactive ingredients: ferrosoferric oxide, ferric oxide red, gelatin and titanium dioxide. The capsule shell of the 135 mg capsule contains the following inactive ingredients: FD&C blue no.1, FD&C red no.3, FD&C red no. 40, gelatin and titanium dioxide.
The present invention provides means to identify functional CD8+ T-cell epitopes in any protein of interest. The present invention further provides CD8+ T-cell epitopes of various proteins. In additional embodiments, the present invention provides epitopes suitable for use in prophylactic and/or therapeutic vaccines. In particularly preferred embodiments, the present invention provides modified epitopes suitable for use in prophylactic and/or therapeutic vaccines.  In some preferred embodiments, the present invention provides means for the development of HPV vaccines, in particular multivalent vaccines for the prevention of infection with high-risk HPV strains. In particular, the present invention provides means to identify CD8+ T-cell epitopes in HPV strains such as HPV 16 and HPV 18. In additional embodiments, the present invention provides means for the development of therapeutic vaccines against high-risk HPV types that prevent the development of benign and/or malignant tumors in infected individuals. The present invention further provides epitopes suitable for use in prophylactic and therapeutic vaccines.
Endometriosis (EMS) is known to be closely associated with inflammation. We evaluate the possible mechanism linking the PI3K/AKT signaling pathway with pyroptosis and inflammation in EMS. We collected 30 patients undergoing laparoscopic for endometriosis as the EMS group and those undergoing surgery for uterine fibroids as the control group, from whom we collected serum, normal endometrium, eutopic endometrium and ectopic endometrium. Transmission electron microscopy (TEM) was used to observe the internal structure of endometrial cells. Western Blot was used to detect the protein expression of PI3K, P-PI3K, AKT, P-AKT, NLRP3, Caspase-1, GSDMD, and GSDMD-N. Immunohistochemistry (IHC) staining was used to detect the expression of PI3K, AKT, NLRP3, Caspase-1, GSDMD, and GSDMD-N proteins. Immunofluorescence (IF) staining was used to observe the expression of GSDMD-N. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze the mRNA levels of PI3K, AKT, NLRP3, Caspase-1, GSDMD, and GSDMD-N. ELISA was used to detect serum levels of IL-1β, IL-18, TLR4, and NF-κB. We found that activation of PI3K/AKT signaling pathway in endometriosis significantly increased the level of cellular pyroptosis and inflammatory factors. Our results suggest that there is a positive correlation between the PI3K/AKT signaling pathway and pyroptosisas well as inflammation in EMS patients.