anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
PEMFEXY is a hazardous drug. Follow applicable special handling and disposal procedures.1

Calculate the dose of PEMFEXY and determine the number of vials needed. Withdraw the calculated dose of PEMFEXY from the vial(s). Store unused portion in vial refrigerated at 2°C to 8°C (36°F to 46°F) for up to 28 days. Each vial contains 500 mg pemetrexed per 20 mL (25 mg/mL). The vial contains an excess of pemetrexed to facilitate delivery of labeled amount.

  * Dilute PEMFEXY with 5% Dextrose in Water, USP or Normal Saline to achieve a total volume of 100 mL for intravenous infusion. Do not use other diluents, such as Lactated Ringer’s Injection, USP or Ringer’s Injection, USP.
  * Visually inspect for particulate matter and discoloration prior to administration, whenever solution and container permit. Discard if particulate matter or discoloration is observed.
  * Administer PEMFEXY as an intravenous infusion over 10 minutes.
  * Store diluted PEMFEXY refrigerated at 2°C to 8°C (36 °F to 46°F) for no more than 48 hours. PEMFEXY diluted with 5% Dextrose in Water, USP can also be stored at ambient room temperature and room light for no more than 48 hours. When prepared as directed, infusion solutions of PEMFEXY contain no antimicrobial preservatives. Discard after 48 hours.



PEMFEXY is compatible with polyolefin infusion bags with polyvinyl chloride (PVC) ports.
Sex chromosome aneuploidies (SCAs) are collectively common conditions caused by carriage of a sex chromosome dosage other than XX for females and XY for males. Increases in sex chromosome dosage (SCD) have been shown to have an inverted-U association with height, but we lack combined studies of SCA effects on height and weight, and it is not known if any such effects vary with age. Here, we study norm-derived height and weight z-scores in 177 youth spanning 8 SCA karyotypes (XXX, XXY, XYY, XXXX, XXXY, XXYY, XXXXX, and XXXXY). We replicate a previously described inverted-U association between mounting SCD and height, and further show that there is also a muted version of this effect for weight: both phenotypes are elevated until SCD reaches 4 for females and 5 for males but decrease thereafter. We next use 266 longitudinal measures available from a subset of karyotypes (XXX, XXY, XYY, and XXYY) to show that mean height in these SCAs diverges further from norms with increasing age. As weight does not diverge from norms with increasing age, BMI decreases with increasing age. These findings extend our understanding of growth as an important clinical outcome in SCA, and as a key context for known effects of SCA on diverse organ systems that scale with body size.
To provide a liquid composition which can inhibit the polymerization of 3-hydroxybutyric acid even if containing 3-hydroxybutyric acid.SOLUTION: There is provided a liquid composition containing 3-hydroxybutyric acid and water, wherein the pH of the liquid composition is adjusted to inhibit the polymerization of 3-hydroxybutyric acid. In this method, a basic compound may be added to partially neutralize the 3-hydroxybutyric acid and adjust the pH higher. In the liquid composition after pH adjustment, the total ratio of 3-hydroxybutyric acid and a salt of 3-hydroxybutyric acid may be adjusted to 15 mass% or more in the liquid composition in terms of 3-hydroxybutyric acid in a free form. Further, in the liquid composition after pH adjustment, the total ratio of 3-hydroxybutyric acid and a salt of 3-hydroxybutyric acid may be adjusted to less than 15 mass% in the liquid composition in terms of 3-hydroxybutyric acid in a free form. The 3-hydroxybutyric acid may be R-3-hydroxybutyric acid. The pH of the liquid composition may be adjusted to 2.2 or more.SELECTED DRAWING: None
<P>PROBLEM TO BE SOLVED: To provide a method for making comb-type anti-thrombotic conjugate wherein substantially all side chains of water soluble PVA are extended by ring-opening polymerization to form a copolymer wherein substantially all terminals are conjugated to an anti-thrombotic molecule.  <P>SOLUTION: A method for applying a coating comprising a comb-type anti-thrombotic conjugate to at least a portion of an implantable device to prevent or reduce the formation of thrombosis on the surface of the device is also provided. A first or sub-layer of the coating is prepared by mixing a polymeric material and a biologically active agent with a solvent, thereby forming a homogeneous solution. A second or outer layer comprising a comb-type anti-thrombotic conjugate may be applied over the inner drug-containing layers using a dip coating or spray coating process. The comb-type anti-thrombotic conjugate may be used as a matrix material to encapsulate a pharmaceutical agent to form microspheres or nanospheres before depositing the microspheres or nanospheres onto a medical device.  <P>COPYRIGHT: (C)2009,JPO&INPIT
Patients who are not currently taking any pharmacological treatment for their depression. Patients will be administered a single dose of SPL026 by intravenous infusion.
All participants received lenalidomide and prednisone therapy for 6 cycles (24 weeks). Each cycle is 28 days (4 weeks).
This is a Prospective, multi-center, open label, randomized controlled comparative safety and effectiveness trial with objectives: 1. To determine the effectiveness of enoxaparin and apixaban in patients hospitalized (but not yet intubated) with confirmed COVID-19 and 2. To determine the safety of enoxaparin and apixaban in patients hospitalized (but not yet intubated) with confirmed COVID-19. Observational analyses have suggested potential benefit for in-hospital use of anticoagulation. Yet, due to a lack of rigorous evidence for optimal anticoagulation regimens, practice patterns among hospitalized patients with COVID-19 vary significantly. Specifically, the choice of anticoagulant, dosing, and duration of treatment are not well understood. A preliminary analysis of approximately 2700 patients admitted to the Mount Sinai Health System (MSHS) in New York, demonstrated an association between in-hospital administration of therapeutic Anticoagulation (AC) and improved survival compared to no or prophylactic dose AC. A subsequent analysis under review of a larger 4400 patient cohort with longer follow up demonstrated similar associations with reduction in the risk of mortality and risk of intubation. Further analyses suggest more pronounced benefit with therapeutic as opposed to prophylactic doses. Bleeding rates were generally low overall, but higher among patients on therapeutic anticoagulation. Finally, though exploratory in nature, a potential signal for benefit was observed for patients on novel oral anticoagulant therapy (primarily apixaban) at therapeutic doses compared to low molecular weight heparin. Ultimately, randomized controlled trials are needed to elucidate the optimal anticoagulation regimen to improve outcomes in patients hospitalized with COVID-19.
Data on cholestasis and biliary injury in patients with COVID-19 are scarce. The primary aim of this study was to evaluate the prevalence of cholestasis and factors associated with its development and outcome in critically ill patients with COVID-19 associated acute respiratory distress syndrome (ARDS). In this retrospective exploratory study, COVID-19 patients with ARDS admitted to an intensive care unit (ICU) at the Medical University of Vienna were evaluated for the development of cholestasis defined as an alkaline phosphatase level of 1.67x upper limit of normal for at least three consecutive days. Simple and multiple logistic regression analysis was used to evaluate parameters associated with development of cholestasis and survival. Of 225 included patients 119 (53%) developed cholestasis during ICU stay. Patients with cholestasis had higher peak levels of alkaline phosphatase, gamma-glutamyl transferase, bilirubin and inflammation parameters. Factors independently associated with cholestasis were extracorporeal membrane oxygenation support, ketamine use, high levels of inflammation parameters and disease severity. Presence of cholestasis and peak ALP levels were independently associated with worse ICU and 6-month survival. Development of cholestasis is a common complication in critically ill COVID-19 patients and represents a negative prognostic marker for survival. It is associated with disease severity and specific treatment modalities of intensive care.
Testosterone gel 1.62% for topical use is a clear, colorless gel containing testosterone, USP. Testosterone is an androgen. Testosterone gel 1.62% is available in a metered-dose pump or unit dose packets.

The active pharmacologic ingredient in testosterone gel 1.62% is testosterone. Testosterone, USP is a white to almost white powder chemically described as 17-beta hydroxyandrost-4-en-3-one. The structural formula is:

The inactive ingredients in testosterone gel 1.62% are: carbomer homopolymer type C (carbopol 980), ethyl alcohol, isopropyl myristate, purified water, and sodium hydroxide.
Participants received Octreotide long-acting release (LAR) 30 mg intramuscular injection every 28 days for 3 months beginning on Day 1. Participants also received immediate-release Octreotide 600 µg/day (administered subcutaneously 2 or 3 times a day or via continuous intravenous (IV) or subcutaneous injection over a 24 hour period) and methlylpredinisolone 3-4 mg/kg per day (IV bolus for 1 hour or 2 subcutaneous injections) for the first 6 days.
This group consists of individuals who are in the highest quartile of the genetic risk score (GRS) and will ingest one sugar drink (equal to 2 soft drinks) per day for 3 weeks. The GRS is computed by adding the number of alleles that increase the risk for liver lipogenesis or fatty liver.
These will receive a total of 6 sessions with a week's interval of radial shockwaves that will be performed using a (Storz Medical) device with the following manufacturer's parameters: 0.57mJ/mm2 (intensity 1.5 bar) applied as low energy, pulses 2000, frequency 15 Hz. The D20 transmitter (Ø 20 mm) headpiece will be used. Total treatment time including standard PT stretches and exercises would be 30 minutes). The radial shockwave will be delivered by designated physiotherapist, who will evaluate the participants before the treatment. Before the treatment, the treating physical therapist would ensure aseptic techniques, they would ensure the participants skin is intact and clean coupling gel will be used during the treatment. Furthermore prior to treatment, the myofascial triggers would be specifically confirmed by twitching response induced by a localized probe using a digital algometer.
Risk Summary

There are no data regarding the presence of ramelteon or its metabolites in human milk, the effects on the breastfed infant, or the effects on milk production. Ramelteon and/or its metabolites are present in rat milk. When a drug is present in animal milk, it is likely that the drug will be present in human milk. Because of the mechanism of action of ramelteon, there is a potential risk for somnolence in a breastfed infant (see Clinical Considerations). The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for ramelteon and any potential adverse effects on the breastfed infant from ramelteon tablets or from the underlying maternal condition.

Clinical Considerations

Infants exposed to ramelteon through breastmilk should be monitored for somnolence and feeding problems. A lactating woman may consider interrupting breastfeeding and pumping and discarding breast milk during treatment and for 25 hours (approximately 5 elimination half-lives) after ramelteon tablets administration in order to minimize drug exposure to a breastfed infant.
In the intercostal block (ICB) group, liposomal bupivacaine 1.3% (4 ml) will injected by the surgeon under direct vision into the proximal intercostal space at the level of the thoracotomy and one interspace above and below. In addition, liposomal bupivacaine 1.3 % (4 ml) will be injected at each of the chest tube exit sites. Thus, a total of 20 ml liposomal bupivacaine 1.3% (260 mg) will be administered.
BACKGROUND: Parkinson's disease (PD) is a debilitating neurodegenerative condition characterized by the loss of dopaminergic neurons and neuroinflammation. Previous research has identified the involvement of Poly (rC)-binding protein 1 (PCBP1) in certain degenerative diseases; however, its specific mechanisms in PD remain incompletely understood.
METHODS: In this study, 6-OHDA-induced neurotoxicity in the cell lines SH-SY5Y, BV-2 and HA, was used to evaluate the protective effects of PCBP1. We assessed alterations in BDNF levels in SY5Y cells, changes in GDNF expression in glial cells, as well as variations in HSP70 and NF-κB activation. Additionally, glial cells were used as the in vitro model for neuroinflammation mechanisms.
RESULTS: The results indicate that the overexpression of PCBP1 significantly enhances cell growth compared to the control plasmid pEGFP/N1 group. Overexpression of PCBP1 leads to a substantial reduction in early apoptosis rates in SH-SY5Y, HA, and BV-2 cells, with statistically significant differences (p < 0.05). Furthermore, the overexpression of PCBP1 in cells results in a marked increase in the expression of HSP70, GDNF, and BDNF, while reducing NF-κB expression. Additionally, in SH-SY5Y, HA, and BV-2 cells overexpressing PCBP1, there is a decrease in the inflammatory factor IL-6 compared to the control plasmid pEGFP/N1 group, while BV-2 cells exhibit a significant increase in the anti-inflammatory factor IL-10.
CONCLUSION: Our findings suggest that PCBP1 plays a substantial role in promoting cell growth and modulating the balance of neuroprotective and inflammatory factors. These results offer valuable insights into the potential therapeutic utility of PCBP1 in mitigating neuroinflammation and enhancing neuronal survival in PD.
TP53, functioning as the keeper of the genome, assumes a pivotal function in the inhibition of tumorigenesis. Recent studies have revealed that p53 regulates ferroptosis pathways within tumor cells and is closely related to tumorigenesis. Therefore, we summarize the pathways and mechanisms by which p53 regulates ferroptosis and identify a series of upstream and downstream molecules involved in this process. Furthermore, we construct a p53-ferroptosis network centered on p53. Finally, we present the progress of drugs to prevent wild-type p53 (wtp53) degeneration and restore wtp53, highlighting the deficiencies of drug development and the prospects for p53 in cancer treatment. These findings provide novel strategies and directions for future cancer therapy.
Neovascularization is implicated in the pathology of retinopathy of prematurity (ROP), diabetic retinopathy (DR), and age-related macular degeneration (AMD), which are the leading causes of blindness worldwide. In our work, we analyzed how heme released during hemorrhage affects hypoxic response and neovascularization. Our retrospective clinical analysis demonstrated, that hemorrhage was associated with more severe retinal neovascularization in ROP patients. Our heme-stimulated human retinal pigment epithelial (ARPE-19) cell studies demonstrated increased expression of positive regulators of angiogenesis, including vascular endothelial growth factor-A (VEGFA), a key player of ROP, DR and AMD, and highlighted the activation of the PI3K/AKT/mTOR/VEGFA pathway involved in angiogenesis in response to heme. Furthermore, heme decreased oxidative phosphorylation in the mitochondria, augmented glycolysis, facilitated HIF-1α nuclear translocation, and increased VEGFA/GLUT1/PDK1 expression suggesting HIF-1α-driven hypoxic response in ARPE-19 cells without effecting the metabolism of reactive oxygen species. Inhibitors of HIF-1α, PI3K and suppression of mTOR pathway by clinically promising drug, rapamycin, mitigated heme-provoked cellular response. Our data proved that oxidatively modified forms of hemoglobin can be sources of heme to induce VEGFA during retinal hemorrhage. We propose that hemorrhage is involved in the pathology of ROP, DR, and AMD.
INTRODUCTION: People living with HIV (PLWH) have higher rates of non-infectious comorbid diseases (NCDs) than individuals without HIV. We characterized the risk of NCDs among PLWH with undetectable viral load and persistent low-level viraemia (pLLV) in the African Cohort Study (AFRICOS). We secondarily quantified the role of immune activation in the association between LLV and NCDs.
METHODS: AFRICOS enrols participants in 12 clinics in Uganda, Kenya, Tanzania and Nigeria. Participants on antiretroviral therapy ≥ 6 months without an NCD at enrolment were included. PLLV was defined as at least two consecutive visits with a detectable viral load <1000 copies/ml. We examined elevated blood pressure, hypercholesterolemia, hyperglycaemia, renal insufficiency and a composite variable of any NCD. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard modelling. Among a subset of participants with biomarker data, we assessed the interaction between viral load and 13 biomarkers in the association with any NCD.
RESULTS: From 23 January 2013 to 1 December 2022, 1755 participants met the inclusion criteria for these analyses. At the first eligible visit, the majority of participants had an undetectable viral load (n = 1375, 78.35%). Participants with pLLV had an increased rate of developing any NCD (aHR: 1.22, 95% CI: 1.02-1.47) compared to participants with an undetectable viral load. There was a statistically significant interaction between LLV and TNF-α, CCL2/MCP-1 and TNF-RII in the association with any NCD.
CONCLUSIONS: PLLV was significantly associated with NCDs and immune inflammation in this population. Aggressive management of LLV may positively impact NCDs in PLWH.
Seizures are a concerning adverse event frequently associated with the use of psychedelics, and hence, studies involving these substances tend to exclude patients with past history of epilepsy. This is especially relevant because epileptic seizures are markedly increased in the population suffering from mental disorders, and psychedelic assisted therapy is being researched as a promising treatment for several of them. To determine the extent of the current literature on the relationship between classic psychedelics and seizures, a scoping review was performed using the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews). The search was conducted in PubMed, Web of Science, Google scholar, LILACS and Scielo, and both animal and human models were included. A total of 16 publications on humans, and 11 on animals, were found. The results are heterogeneous, but globally suggest that psychedelics may not increase the risk of seizures in healthy individuals or animals in the absence of other drugs. However, concomitant use of other substances or drugs, such as kambo or lithium, could increase the risk of seizures. Additionally, these conclusions are drawn from data lacking sufficient external validity, so they should be interpreted with caution. Future paths for research and a summary on possible neurobiological underpinnings that might clarify the relationship between classical psychedelics and seizures are also provided.
Patients with clinical stage IIIA N2 non-small cell lung cancer (NSCLC) have a 5-year survival rate of 10% to 15%, much worse than those of earlier stages of disease. The use of pre-operative (neo-adjuvant) chemotherapy has been shown to be beneficial in several studies.1 However, the precise chemotherapeutic regimen for neoadjuvant therapy remains an open question.

The treatment response and toxicity of chemotherapy vary widely among and within individuals, and races. Recently, molecular predictive markers may help to identify who may benefit from individual therapy. Many evidence shows that the level of ERCC1 (an excision nuclease within the nucleotide excision repair pathway) is important for the repair of platinum-DNA adducts and the response to platinum-based chemotherapy.2-5 Not only by measuring protein and mRNA expression, studies addressed on the polymorphism of ERCC1(118 C/T and C8092A) had demonstrated impact on survival of chemotherapy-treated NSCLC patients6,7. XPD/ERCC2 (xeroderma pigmentosum group D/excision repair cross-complementing group 2) 8, XRCC1 (X-ray repair cross-complementing group 1) and XRCC3 (X-ray repair cross-complementing group 3) are another three proteins involving NER, serving as prognostic factor of survival.9 BRCA1 is a protein participating in recombinant repair (RR) and is stronge predictive marker of chemotherapy response. BRCA1 functions as a differential modulator of survival with cisplatin and antimicrotubule drugs (paclitaxel, docetaxel and vinorelbine). Low level of BRCA1 enhance cisplatin activity but lead to resistance to paclitaxel, docetaxel and vinorelbine, whereas the opposite phenomenon is observed in the presence of normal or high levels of BRCA1. In contract, BRCA1 levels do not influence the effect of gemcitabine10. On the contrary, RRM1 (ribonucleotid reductase subunit M1) is involved in gemcitabine metabolism and DNA repair after chemotherapy damage, and increased RRM1 mRNA expression has been related to gemcitabine resistance in NSCLC11. All these DNA repair genes participate the pathogenesis, mechanism of chemotherapeutic resistance and outcome of lung cancer patients.

Previously, a joint study done by NTUH and VGH Taipei used gemcitabine and cisplatin as induction chemotherapy to treat 52 patient with stage III NSCLC, 36 were operable and 18 were completely resected.12 From 2004 till now, a prospective study has been performed in NTUH using docetaxel and cisplatin as neoadjuvant regimen to treat patients with stage IIIA (N2) non-small cell lung cancer. Up to now, more than 40 patients were enrolled, all of them have received tumor sampling before chemotherapy and more 90% received operation with their tumor resected. The tissue specimens are valuable as all these patients had received protocolized treatment, with filed detailed clinical information collected systematically. All the peroperative biopsied and operatively resected tumor tissues are available in paffin-embedded block, some in frozen tissue stock, we plan to study the DNA polymorphism, protein and RNA expression of the above-mentioned DNA repair genes in these two series of patients.
FIELD: pharmacy. SUBSTANCE: preparation is hydrophilic-adsorption melt of components prepared by mixing essential or turpentine oil preliminary dissolved in heated dimexide (at 45-50 C) with hot solution of synthetic high-molecular and low-molecular polyethylene oxides. Ratio of components, wt. -%: essential or turpentine oil 40-50; dimexide 5-15; high-molecular polyethylene oxide 20-30; low-molecular polyethylene oxide up to 100. Preparation is melted at 35 C and above, essential (or turpentine) oil is released from the melt and contacts with body surface where it is applied. Preparation shows high penetrating capability and accelerates effect of active components. EFFECT: improved method of preparing, enhanced effectiveness of preparation. 4 cl, 10 ex