anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Simulect® (basiliximab) is used as part of an immunosuppressive regimen that includes cyclosporine, USP (MODIFIED) and corticosteroids. Simulect is for central or peripheral intravenous administration only. Reconstituted Simulect should be given either as a bolus injection or diluted to a volume of 25 mL (10-mg vial) or 50 mL (20-mg vial) with 0.9% Sodium Chloride Injection, USP or 5% Dextrose Injection, USP and administered as an intravenous infusion over 20 to 30 minutes. Bolus administration may be associated with nausea, vomiting and local reactions, including pain. 

Simulect should only be administered once it has been determined that the patient will receive the graft and concomitant immunosuppression. Patients previously administered Simulect should only be re-exposed to a subsequent course of therapy with extreme caution due to the potential risk of hypersensitivity (see WARNINGS).

Parenteral drug products should be inspected visually for particulate matter and discoloration before administration. After reconstitution, Simulect should be a clear-to-opalescent, colorless solution. If particulate matter is present or the solution is colored, do not use. 

Care must be taken to assure sterility of the prepared solution because the drug product does not contain any antimicrobial preservatives or bacteriostatic agents.

It is recommended that after reconstitution, the solution should be used immediately. If not used immediately, it can be stored at 2ºC to 8ºC (36ºF to 46ºF) for 24 hours or at room temperature for 4 hours. Discard the reconstituted solution if not used within 24 hours.

No incompatibility between Simulect and polyvinyl chloride bags or infusion sets has been observed. No data are available on the compatibility of Simulect with other intravenous substances. Other drug substances should not be added or infused simultaneously through the same intravenous line.
BACKGROUND: Hypoxic microenvironment is a common feature of most solid tumors including hepatocellular carcinoma (HCC). Vasculogenic mimicry (VM) formation by tumor cells could provide blood supply to tumor cells under hypoxia. NFE2 like basic leucine zipper (bZIP) transcription factor 2 (Nrf2), a regulator of cellular homeostasis, may promote tumor progression in the hypoxic conditions. However, the role and regulatory mechanisms of Nrf2 in HCC are not fully elucidated.
METHODS: Nrf2 and assembly factor for spindle microtubules (ASPM) expression modulations were conducted by lentiviral transfections. Western blot, immunofluorescence, ChIP-qPCR, dual-luciferase reporter gene assay, flow cytometry, RNA sequencing, multiple bioinformatics databases analysis, cell function assays in vitro, mouse model in vivo and human HCC tissues were employed to assess the effect of Nrf2/ASPM axis on HCC progression under hypoxia.
RESULTS: Nrf2 and ASPM expression facilitated epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs) feature, and VM formation of HCC cells under hypoxia. Furthermore, Nrf2-regulated ASPM expression, via binding directly to the promoter region of ASPM and transcriptionally promoting ASPM expression. ASPM re-expression in Nrf2 knockdown cells or ASPM knockdown in Nrf2 overexpression cells reversed the cellular function caused by Nrf2. Meantime, retinol metabolism pathway was disrupted following abnormal ASPM expression. Nrf2/ASPM axis in murine models accelerated tumor growth and VM, corroborating in vitro findings. All-trans retinoic acid treatment reversed stemness and VM of HCC cells in vitro and in vivo. Clinically, Nrf2 and ASPM expressions were related to poor prognosis of HCC patients.
CONCLUSIONS: Nrf2 drives EMT, CSCs characteristics and VM in HCC under hypoxia through the modulation of ASPM. Retinol metabolism pathway was dysregulated in HCC cells with ASPM overexpression. Nrf2/ASPM axis and related pathway provided potential therapeutic target for HCC.
A method for manufacturing a composition for inhibiting diabetes mellitus is provided. In the method, at firstly, prepares a cinnamon extract containing a first organic solution and at least one solute. A second organic solution is used to dissolve 1 part by weight of soybean oil, 1 part by weight of lecithin, 1 part by weight of emulsifier and 1 part by weight of polyethylene glycol to form an emulsifier mixed solution. Then, mixing 200 parts by weight of the cinnamon extract and the emulsifier mixed solution to form a cinnamaldehyde-containing mixed solution containing a cinnamaldehyde-containing galactose mixture. Then, removing the first organic solution and the second organic solution from the cinnamaldehyde-containing mixed solution to remains the cinnamaldehyde-containing galactose mixture. Finally, mixing the cinnamaldehyde-containing galactemulsion mixture and 91 parts by weight of deionized water to form a cinnamaldehyde nano-emulsion, which can be used as the above-mentioned composition for inhibiting diabetes mellitus.
The objective of the current study is to investigate the efficacy and safety of IDegAsp twice daily compared to basal insulin once or twice daily plus pre-prandial insulin for 16 weeks in patients with type 1 diabetes mellitus. The primary endpoint in this study is the change from baseline in HbA1c. Patients with type 1 diabetes who meet the entry criteria are planned for inclusion in this trial. Approximately 40 patients will be enrolled in the study. Patients who qualify will be randomized to IDegAsp group or basal plus pre-prandial insulin group. Duration of treatment includes 2-week screening period, 16-week treatment observation period and 1-week follow-up.
Planned 8 cycles of CyBorD-Dara SC, treatment will be left to the discretion of the treating physician. It is recommended that patients eligible for ASCT undergo ASCT after 8 cycles of induction and that patient ineligible for ASCT, continue maintenance Bortezomib/Dexamethasone administered every other week with daratumumab SC administered every 4 weeks, for a period of 2 years from start of treatment.
Young people assigned to the intervention arm will receive \~9 weeks of daily text messages that talk about healthy sexuality and ways to reduce HIV risk. After a 3 month 'quiet' period, they will receive a week of review messages. Messages are based upon the information-motivation-behavioral model of preventive behavior.
The intervention will be the stimulation with sham transcranial Direct Current Stimulation (sham tDCS). The device will be set by staff member not involved with data collection analysis to ensure the blinding of assessors. The device will be set to give a weak amperage for the first and the last 20 second of stimulation to ensure the blinding of participant giving them a similar sensation experienced by the active tDCS participants without stimulate brain tissues. Device: tDCS device (E.M.S. Electromedical Systems, Bologna, Italy) with a maximum output of 5 mA and administered by two 25-cm2 sponge electrodes of rectangular shape.
SCG101 will be given via Intravenous (IV) infusion. The PD-1/PD-L1 checkpoint inhibitor will be given per product label.
Based on very limited published data, warfarin has not been detected in the breast milk of mothers treated with warfarin. The same limited published data report that some breast-fed infants, whose mothers were treated with warfarin, had prolonged prothrombin times, although not as prolonged as those of the mothers. The decision to breast-feed should be undertaken only after careful consideration of the available alternatives. Women who are breast-feeding and anticoagulated with warfarin should be very carefully monitored so that recommended PT/INR values are not exceeded. It is prudent to perform coagulation tests and to evaluate vitamin K status in infants before advising women taking warfarin to breast-feed. Effects in premature infants have not been evaluated.
Title cpds. of formula (I) are prepd. by esterification of (II): (where RCO = an organoacyl gp.; R2 is an organic residue; R3 is H, alkali metal or a gp. which is easily removed in the blood stream; M is H or alkali metal), to protect the carboxyl gp. with a gp. which is chemically removed under gentle conditions which do not destroy the ring or is easily removable in the blood. This ester is reacted with a phosphorus halide in an inert solvent to give the imino-halide which is reacted with a lower alkanol to produce the imino-ether. The imino-ether is condensed with R2COOH or its active deriv. and this product treated with water or an alkanol with optional removal of the protecting ester gp.
Cognitive decline in Parkinson's disease (PD) varies widely. While models to predict cognitive progression exist, comparing traditional probabilistic models to deep learning methods remains understudied. This study compares sequential modeling techniques to identify cognitive progression in individuals with and without PD. Using data from the Parkinson's Progression Marker Initiative, shallow Markov, deep recurrent (long short-term memory [LSTM]), and nonrecurrent (temporal fusion transformer [TFT]) models were compared to predict cognitive status over time. Cognitive status was categorized into normal cognition (NC), mild cognitive impairment (MCI), and dementia. Predictions were made annually for up to 3 years using clinical data, including demographics, cognitive assessments, PD severity, and medical history. Each approach was evaluated using inverse probability weighted (IPW-) F1 scores. An ensemble method combined outputs from the Markov, LSTM, and TFT models. The dataset included 917 individuals (53% PD; 30% at risk for PD; 17% Healthy Controls). The TFT model outperformed others across all annual periods (IPW-F1 = 0.468) compared to the Markov (IPW-F1 = 0.349) and LSTM (IPW-F1 = 0.414) models, with improved performance using an ensemble approach (IPW-F1 = 0.502). For MCI and dementia predictions, which were rarer occurrences compared to NC status (ratios: 50:8:1), the TFT model consistently outperformed competing models, achieving IPW-F1 scores of 0.496 and 0.533 for MCI and dementia, respectively. In conclusion, sequential deep learning models like TFT, which mitigate long-term memory loss and can interpret complex, high-dimensional data, perform best overall in predicting clinically important cognitive transitions. These methods should be further explored for predicting degenerative conditions.
Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease. Combination therapy is anticipated to surpass monotherapy by targeting multiple pathways involved in RA progression. The present aim is to develop a combination of Teriflunomide (TFD) and Quercetin (QCN) loaded transferosomal gel to enhance permeability and achieve localized delivery to joint tissues. TFD or QCN transferosomes were optimized employing a 3-level, 3-factorial design Box-Behnken design (BBD). The transferosomes exhibited sustained in-vitro drug release. The topical combination gel underwent thorough evaluation of rheology, and also ex-vivo studies showed enhanced permeability through rat skin. The synergistic combination of TFD and QCN effectively suppressed NO, TNF-α and IL-6 levels in in-vitro RAW 264.7 cells. The cytotoxicity in HaCaT cell lines indicates non-toxicity of the gel, further confirmed by skin irritation study conducted in rats. The in-vivo anti-arthritic activity was evaluated in complete freund's adjuvant induced rat paw edema model illustrates the effectiveness of the combination transferosomal gel compared to other treatment groups. In conclusion, the topical delivery of TFD and QCN combination transferosomal gel demonstrated anti-arthritic activity through localized delivery whichallows for dose reduction, thereby may reduce the systemic drug exposure and mitigate the side effects associated with oral administration of TFD.
The safety and effectiveness of AIRDUO RESPICLICK have been established for the treatment of asthma in pediatric patients aged 12 years and older whose asthma (1) is inadequately controlled on a long term asthma control medication or (2) warrants initiation of treatment with both an ICS and a LABA.

Use of AIRDUO RESPICLICK in pediatric patients aged 12 to 17 years for this indication is supported by evidence from two adequate and well-controlled trials in pediatric patients 12 years old and older with persistent symptomatic asthma despite ICS or ICS/LABA therapy (Trials 1 and 2) [see Clinical Studies (14)]. In these trials, 58 adolescents received AIRDUO RESPICLICK one inhalation twice daily.

The safety and effectiveness of AIRDUO RESPICLICK have not been established in pediatric patients younger than 12 years of age for the treatment of asthma. Effectiveness was not demonstrated in one adequate and well-controlled study conducted in 211 patients aged 4 to 11 years with persistent asthma on a stable asthma regimen who were treated with AIRDUO RESPICLICK 55 mcg/14 mcg one inhalation twice daily.

Effect on Growth

Inhaled corticosteroids, including fluticasone propionate, a component of AIRDUO RESPICLICK, may cause a reduction in growth velocity in adolescents [see Warning and Precautions (5.13)]. The growth of pediatric patients receiving ICS, including AIRDUO RESPICLICK, should be monitored.

If an adolescent on any corticosteroid appears to have growth suppression, the possibility that he/she is particularly sensitive to this effect of corticosteroids should be considered. In such patients, the potential growth effects of prolonged ICS treatment should be weighed against the clinical benefits obtained. To minimize the systemic effects of ICS, including AIRDUO RESPICLICK, each patient should be titrated to the lowest strength that effectively controls his/her asthma [see Dosage and Administration (2)].
A modified pigment that may include a polymer. The pigment may be directly attached to a nitrogen atom. The nitrogen atom may be attached directly or indirectly to a group that may include —S-Z. S may be a substituted or unsubstituted alkyl group, substituted or unsubstituted aromatic group, or polymer chain having a molecular weight range from about 300 to about 20000. Z may be a hydrogen, carboxyl, sulfonyl, phenolic, phosphoryl, ammonium, trimethylammonium, or tributylammonium group. Also, a modified pigment that may include a polymer. The pigment may be attached to an organic group through a carbon atom that is part of a N—C═N bond. A cosmetic formulation that may include a pigment covalently bonded to an organic group.
The safety and effectiveness of NALOXONE HYDROCHLORIDE injection, 10 mg, in an auto-injector have been established in pediatric patients 12 years of age and older for emergency treatment where use of high-potency opioids such as fentanyl analogues as a chemical weapon is suspected.

Use of NALOXONE HYDROCHLORIDE injection in this age group is supported by evidence from adult bioavailability studies, adult PK/PD modeling and simulation analysis supporting an effective dose, along with additional evidence from the reported safe and effective use of other naloxone HCl products [see Clinical Pharmacology (12.2)]. No pediatric studies were conducted for NALOXONE HYDROCHLORIDE injection.

The safety and effectiveness of NALOXONE HYDROCHLORIDE injection for intramuscular and subcutaneous use have not been established for pediatric patients less than 12 years old. Absorption of naloxone HCl following subcutaneous or intramuscular administration in pediatric patients may be erratic or delayed. Even when the opiate-intoxicated pediatric patient responds appropriately to naloxone HCl injection, the patient must be carefully monitored for at least 24 hours as a relapse may occur as naloxone is metabolized.

In opioid-dependent pediatric patients, administration of naloxone HCl may result in an abrupt and complete reversal of opioid effects, precipitating an acute opioid withdrawal syndrome. In these settings where it may be preferable to avoid the abrupt precipitation of acute opioid withdrawal symptoms, consider use of an alternative naloxone HCl product that can be dosed according to weight and titrated to effect [see  Warnings and Precautions (5.1)].
Exercise is a first-line treatment for type 2 diabetes, and exerts its beneficial effects not only by burning off energy but also by causing prolonged metabolic changes through changing gene expression. Genes are our genetic materials and the expression of genes determines our biology. In our previous study in animals, we identified some factors that drive exercise-induced gene expression changes. Here we would like to address whether the result is also true in human. This work will provide molecular insights into how exercise remodels our metabolism and will potentially find a way to maximize the benefit we get from physical exercise.

The purpose of this study is to determine whether acute exercise activate certain molecular factors in human skeletal muscle. Participants will be asked to undergo an acute bout of aerobic exercise at \~ moderate intensity for about 2 hours. Before and after the exercise, the participants will undergo a muscle biopsy. The muscle tissues will be used for total RNA extraction and RT-qPCR analysis of genes that include but are not limited to de facto JunD/AP-1 target genes and will also be analyzed by Jun D Chip-qPCT to assess binding of Jun D on its de facto target genes.
The first arm uses mindful walking through a 2km forest trail in Singapore. All Interventional and Control arms will conduct their walk between 8 am to 11 am for five occasions weekly. At the T1, participants will attend a Zoom orientation session to familiarize themselves with the route. During this session, participants will need to answer the self-report questionnaire and provide the first saliva sample for the baseline measurement. In T2, a pre-intervention and post-intervention saliva sample will be taken before the walk. This will follow by T3 the following week. At T4, participants will attend a 60 mins reflection session and answer the self-report questionnaire. On T5 and T6, the participants will continue with the therapeutic rainforest mindfulness walk. On T7, a pre-intervention and post-intervention saliva sample will be taken. On T8, participants will attend a 60 mins reflection session and answer the self-report questionnaire.
Metabolic bone diseases cover a broad spectrum of disorders that share alterations in bone metabolism that lead to a defective skeleton, which is associated with increasing morbidity, disability, and mortality. There is a close connection between the etiology of metabolic bone diseases and genetic factors, with TP53 being one of the genes associated therewith. The single nucleotide polymorphism (SNP) Arg72Pro of TP53 is a genetic factor associated with several pathologies, including cancer, stroke, and osteoporosis. Here, we aim to analyze the influence of the TP53 Arg72Pro SNP on bone mass in humanized Tp53 Arg72Pro knock-in mice. This work reports on the influence of the TP53 Arg72Pro polymorphism in bone microarchitecture, OPG expression, and apoptosis bone status. The results show that the proline variant of the TP53 Arg72Pro polymorphism (Pro72-p53) is associated with deteriorated bone tissue, lower OPG/RANK ratio, and lower apoptosis in bone tissue. In conclusion, the TP53 Arg72Pro polymorphism modulates bone microarchitecture and may be a genetic biomarker that can be used to identify individuals with an increased risk of suffering metabolic bone alterations.
1. A stabilized pharmaceutical composition based on quinupristine and dalfopristine, wherein said composition further comprises an at least stoichiometric amount of methanesulphonic acid and hydrochloric acid, wherein the pH of said composition ranges from 3.5 to 5.0. 2. A stabilized pharmaceutical composition according to claim 1, wherein, if desired, said composition comprises an additional amount of methanesulphonic acid or hydrochloric acid to bring the pH to 3.5 to5 and additionally water 3. A stabilized pharmaceutical composition according to claim 2, wherein said composition further comprises an isotonizing agent and/or pharmaceutically acceptable adjuvants. 4. A stabilized pharmaceutical composition according to claims 1 to 3, wherein said composition is frozen, or in the liquid state. 5. A stabilized pharmaceutical composition according to claims 1 to 3, wherein said composition presents a lyophilizated product. 6. A stabilized pharmaceutical composition according to claims 1 to 4, wherein the concentration of the active substance ranges from about 5 to about 250 mg/ml. 7. A stabilized pharmaceutical composition according to claim 5, wherein the concentration of the active substance ranges from 5 to 95%. 8. A stabilized pharmaceutical composition according to claim 7, wherein the concentration of the active substance ranges from 20 to 95%. 9. A stabilized pharmaceutical composition according to claims 3, 4 and 6, wherein the pH ranges from 3.5 to 4.5. 10. A stabilized pharmaceutical composition according to claim 9, wherein the pH is 3.5. 11. A stabilized pharmaceutical composition according to any of claims 1 to 7, wherein the pH ranges from 4.5 to 5. 12. A preparation of a stabilized ready-for-use solution obtained from a lyophilized or frozen pharmaceutical composition according to claims 1, 4 or 5. 13. A process for the preparation of a pharmaceutical composition according to claim 1, wherein quinupristine, dalfopristine and methanesulphonic acid or hydrochloric acid are simultaneously or successively dissolved in water and then the pH is adjusted in the range of 3.5 to 5. 14. A process according to claim 1, wherein quinupristine and then dalfopristine are disssiolved successively in water acidified by methanesulphonic acid or hydrochloric acid and then the pH is adjusted in the range of 3.5 to 5. 15. A process according to claim 13 or 14 for the preparation of a pharmaceutical composition wherein the composition obtained is subsequently lyophilized and/or frozen. 16. Use of methanesulphonic acid or hydrochloric acid for the preparation of stabilized pharmaceutical composition according to any one of claims 1 to11.
The invention discloses a traditional Chinese medicine composition. The traditional Chinese medicine composition comprises, by mass, 30% of sarcandra glabra, 20% of ligusticum wallichii, 15% of radix angelicae pubescentis, 15% of bark of himalayan coralbean, 15% of clematis root, and 5% of borneol. The above traditional Chinese medicines are processed into super-fine powder according to the mass part ratio and are sealed for next use. The traditional Chinese medicine composition realizes simultaneous treatment of principal and subordinate symptoms, has effects of warming channel, expelling cold, relieving pain, activating blood circulation, dredging channels and relieving swelling and has good treatment effects on knee osteoarthritis. The invention also discloses a preparation method of the traditional Chinese medicine composition and a use of the traditional Chinese medicine composition in treatment on knee osteoarthritis. Through acupoint application, in knee osteoarthritis treatment, the traditional Chinese medicine composition has a low price, good treatment effects and less dosage, is simple and feasible, has safety and no side effects and is worth being deeply researched and popularized.