anthonyyazdaniml/gliner-biomed-curated-corpus huggingface dataset:
Patients with Parkinson's disease treated with entacapone tablets, which increases plasma levodopa levels, or with levodopa have reported suddenly falling asleep without prior warning of sleepiness while engaged in activities of daily living (including the operation of motor vehicles). Some of these episodes resulted in accidents. Although many of these patients reported somnolence while on entacapone tablets, some did not perceive warning signs, such as excessive drowsiness, and believed that they were alert immediately prior to the event. Some of these events have been reported as late as one year after initiation of treatment.

The risk of somnolence was increased (entacapone tablets 2% and placebo 0%) in controlled studies. It has been reported that falling asleep while engaged in activities of daily living always occurs in a setting of preexisting somnolence, although patients may not give such a history. For this reason, prescribers should reassess patients for drowsiness or sleepiness especially since some of the events occur well after the start of treatment. Prescribers should also be aware that patients may not acknowledge drowsiness or sleepiness until directly questioned about drowsiness or sleepiness during specific activities. Patients should be advised to exercise caution while driving, operating machines, or working at heights during treatment with entacapone tablets. Patients who have already experienced somnolence and/or an episode of sudden sleep onset should not participate in these activities during treatment with entacapone tablets.

Before initiating treatment with entacapone tablets, advise patients of the potential to develop drowsiness and specifically ask about factors that may increase this risk such as concomitant use of sedating medications and the presence of sleep disorders. If a patient develops daytime sleepiness or episodes of falling asleep during activities that require active participation (e.g., conversations, eating, etc.), entacapone tablets should ordinarily be discontinued (see DOSAGE AND ADMINISTRATION for guidance on discontinuing entacapone tablets). If the decision is made to continue entacapone tablets, patients should be advised not to drive and to avoid other potentially dangerous activities. There is insufficient information to establish whether dose reduction will eliminate episodes of falling asleep while engaged in activities of daily living.
INCA33890 will be administered at a protocol defined starting regimen intravenously. Subsequent dose regimens will be determined during study conduct.
Polocaine® stabilizes the neuronal membrane and prevents the initiation and transmission of nerve impulses, thereby effecting local anesthesia.

Polocaine® is rapidly metabolized, with only a small percentage of the anesthetic (5 to 10 percent) being excreted unchanged in the urine. Polocaine® because of its amide structure, is not detoxified by the circulating plasma esterases. The liver is the principal site of metabolism, with over 50 percent of the administered dose being excreted into the bile as metabolites. Most of the metabolized mepivacaine is probably resorbed in the intestine and then excreted into the urine since only a small percentage is found in the feces. The principal route of excretion is via the kidney. Most of the anesthetic and its metabolites are eliminated within 30 hours. It has been shown that hydroxylation and N-demethylation, which are detoxification reactions, play important roles in the metabolism of the anesthetic. Three metabolites of mepivacaine have been identified from adult humans: two phenols, which are excreted almost exclusively as their glucuronide conjugates, and the N-demethylated compound (2,' 6' - pipecoloxylidide).

The onset of action is rapid (30 to 120 seconds in the upper jaw; 1 to 4 minutes in the lower jaw) and 3% (30 mg/mL) Polocaine® DENTAL will ordinarily provide operating anesthesia of 20 minutes in the upper jaw and 40 minutes in the lower jaw.

2% (20 mg/mL) Polocaine® DENTAL with Levonordefrin 1:20,000 provides anesthesia of longer duration for more prolonged procedures, 1 hour to 2.5 hours in the upper jaw and 2.5 hours to 5.5 hours in the lower jaw.

Polocaine® does not ordinarily produce irritation or tissue damage.

Levonordefrin is a sympathomimetic amine used as a vasoconstrictor in local anesthetic solutions. It has pharmacologic activity similar to that of Epinephrine but it is more stable than Epinephrine.

In equal concentrations, Levonordefrin is less potent than Epinephrine in raising blood pressure, and as a vasoconstrictor.
This is a multicenter, randomized prospective cohort study to compare the impact of catheter ablation with antiarrhythmic drug therapy for treating patients with sustained ventricular tachycardia (VT) and coronary artery disease. Patients that meet all inclusion criteria and no exclusion criteria will be recruited to the study cohort. After baseline measurements are taken, patients will be randomized in a 2:1 fashion to either undergo radiofrequency catheter ablation or receive antiarrhythmic drug therapy (amiodarone or sotalol). The in-clinic appointments include: enrollment, baseline, intervention, and follow-up every three months for one year post-ablation. At each follow-up visit, electrogram (ECG) and Holter monitoring tests will be performed to measure any episodes of ventricular tachyarrhythmia. Furthermore, interrogation of the patient's implantable cardioverter defibrillator (ICD) will be performed at all follow-up visits to detect any episodes of ventricular tachyarrhythmia that required antitachycardia pacing (ATP) or shocks.
OBJECTIVE: People who sustain joint injuries such as anterior cruciate ligament (ACL) rupture often develop post-traumatic osteoarthritis (PTOA). In human patients, ACL injuries are often treated with ACL reconstruction. However, it is still unclear how effective joint restabilization is for reducing the progression of PTOA. The goal of this study was to determine how surgical restabilization of a mouse knee joint following non-invasive ACL injury affects PTOA progression.
DESIGN: In this study, 187 mice were subjected to non-invasive ACL injury or no injury. After injury, mice underwent restabilization surgery, sham surgery, or no surgery. Mice were then euthanized on day 14 or day 49 after injury/surgery. Functional analyses were performed at multiple time points to assess voluntary movement, gait, and pain. Knees were analyzed ex vivo with micro-computed tomography, RT-PCR, and whole-joint histology to assess articular cartilage degeneration, synovitis, and osteophyte formation.
RESULTS: Both ACL injury and surgery resulted in loss of epiphyseal trabecular bone (-27-32%) and reduced voluntary movement at early time points. Joint restabilization successfully lowered OA score (-78% relative to injured at day 14, p < 0.0001), and synovitis scores (-37% relative to injured at day 14, p = 0.042), and diminished the formation of chondrophytes/osteophytes (-97% relative to injured at day 14, p < 0.001, -78% at day 49, p < 0.001).
CONCLUSIONS: This study confirmed that surgical knee restabilization was effective at reducing articular cartilage degeneration and diminishing chondrophyte/osteophyte formation after ACL injury in mice, suggesting that these processes are largely driven by joint instability in this mouse model. However, restabilization was not able to mitigate the early inflammatory response and the loss of epiphyseal trabecular bone, indicating that these processes are independent of joint instability.
OBJECTIVES: To identify preoperative predictors of postcardiotomy cardiogenic shock in patients with ischemic and nonischemic cardiomyopathy and evaluate trajectory of postoperative ventricular function.
METHODS: From January 2017 to January 2020, 238 patients with ejection fraction <30% (206/238) or 30% to 34% with at least moderately severe mitral regurgitation (32/238) underwent conventional cardiac surgery at Cleveland Clinic, 125 with ischemic and 113 with nonischemic cardiomyopathy. Preoperative ejection fraction was 25 ± 4.5%. The primary outcome was postcardiotomy cardiogenic shock, defined as need for microaxial temporary left ventricular assist device, extracorporeal membrane oxygenation, or vasoactive-inotropic score >25. RandomForestSRC was used to identify its predictors.
RESULTS: Postcardiotomy cardiogenic shock occurred in 27% (65/238). Pulmonary artery pulsatility index <3.5 and pulmonary capillary wedge pressure >19 mm Hg were the most important factors predictive of postcardiotomy cardiogenic shock in ischemic cardiomyopathy. Cardiac index <2.2 L·min-1 m-2 and pulmonary capillary wedge pressure >21 mm Hg were the most important predictive factors in nonischemic cardiomyopathy. Operative mortality was 1.7%. Ejection fraction at 12 months after surgery increased to 39% (confidence interval, 35-40%) in the ischemic group and 37% (confidence interval, 35-38%) in the nonischemic cardiomyopathy group.
CONCLUSIONS: Predictors of postcardiotomy cardiogenic shock were different in ischemic and nonischemic cardiomyopathy. Right heart dysfunction, indicated by low pulmonary artery pulsatility index, was the most important predictor in ischemic cardiomyopathy, whereas greater degree of cardiac decompensation was the most important in nonischemic cardiomyopathy. Therefore, preoperative right heart catheterization will help identify patients with low ejection fraction who are at greater risk of postcardiotomy cardiogenic shock.
Considering that interventions related to lifestyle, especially nutrition have been proposed as the first line of prevention and treatment of polycystic ovarian syndrome (PCOS), and regarding the proven relationship between PCOS and inflammation, the present study was designed to find out the possible association of Diet Inflammatory Index (DII) with the inflammatory markers like C-reactive protein (CRP) and Interleukin-6 (IL-6), and compare the obtained results in PCOS and non-PCOS women. This case-control study was conducted on 45 PCOS and 40 non-PCOS women. Food intake and DII were measured using a 147-item Food Frequency Questionnaire. All participants were tested for the serum levels of IL-6 and CRP. Finally, the obtained results were compared between the two groups of PCOS and non-PCOS women. Significant differences were observed between the two groups in terms of age, menstrual status and number of pregnancies (P < 0.05). Comparison of DII values showed no significant difference between the two groups of women (P = 0.68), but IL-6 was significantly higher in the PCOS group than in the control group (4.94 ± 1.97 vs. 3.48 ± 1.77, P < 0.001). Also in terms of CRP, no significant difference was observed between the two groups (P > 0.05). The difference of DII between the case and control groups were not significant and Pearson's correlation test did not show a significant correlation between DII and IL-6 (P˃0.05). This result can be due to the influence of several factors affecting the determination of DII such as education level, health status, physical activity level, age, and calorie intake. It seems that diet, especially consumption of more carbohydrates plays a role in causing chronic inflammation, as well as the occurrence and exacerbation of PCOS.
Patients receive olaparib PO BID on days 1-21 of each cycle. Cycles repeat every 21 days for up to 2 years in the absence of disease progression or unacceptable toxicity. Patients may also receive bevacizumab IV on day 1 of each cycle. Cycles of bevacizumab repeat every 21 days for up to 1 year in the absence of disease progression or unacceptable toxicity. Patients also undergo blood sample collection and CT and/or MRI throughout the study.
This study addressed the efficacy of a liposome-encapsulated nine amino acid peptide [peroxiredoxin 6 PLA2 inhibitory peptide-2 (PIP-2)] for the prevention or treatment of acute lung injury (ALI) +/- sepsis. PIP-2 inhibits the PLA2 activity of peroxiredoxin 6 (Prdx6), thereby preventing rac release and activation of NADPH oxidases (NOXes), types 1 and 2. Female Yorkshire pigs were infused intravenously with lipopolysaccharide (LPS) + liposomes (untreated) or LPS + PIP-2 encapsulated in liposomes (treated). Pigs were mechanically ventilated and continuously monitored; they were euthanized after 8 h or earlier if preestablished humane endpoints were reached. Control pigs (mechanical ventilation, no LPS) were essentially unchanged over the 8 h study. LPS administration resulted in systemic inflammation with manifestations of clinical sepsis-like syndrome, decreased lung compliance, and a marked decrease in the arterial Po2 with vascular instability leading to early euthanasia of 50% of untreated animals. PIP-2 treatment significantly reduced the requirement for supportive vasopressors and the manifestations of lung injury so that only 25% of animals required early euthanasia. Bronchoalveolar lavage fluid from PIP-2-treated versus untreated pigs showed markedly lower levels of total protein, cytokines (TNF-α, IL-6, IL-1β), and myeloperoxidase. Thus, the porcine LPS-induced sepsis-like model was associated with moderate to severe lung pathophysiology compatible with ALI, whereas treatment with PIP-2 markedly decreased lung injury, cardiovascular instability, and early euthanasia. These results indicate that inhibition of reactive oxygen species (ROS) production via NOX1/2 has a beneficial effect in treating pigs with LPS-induced ALI plus or minus a sepsis-like syndrome, suggesting a potential role for PIP-2 in the treatment of ALI and/or sepsis in humans.NEW & NOTEWORTHY Currently available treatments that can alter lung inflammation have failed to significantly alter mortality of acute lung injury (ALI). Peroxiredoxin 6 PLA2 inhibitory peptide-2 (PIP-2) targets the liberation of reactive O2 species (ROS) that is associated with adverse cell signaling events, thereby decreasing the tissue oxidative injury that occurs early in the ALI syndrome. We propose that treatment with PIP-2 may be effective in preventing progression of early disease into its later stages with irreversible lung damage and relatively high mortality.
The placebo supplement will have no polyphenol content and will consist of 100 mL of the following mixture: black cherry Koolaid, blue and red food coloring, sucrose and sorbitol. This placebo will match the sugar content of the chokeberry juice. Dose of 100 mL is consumed once daily for duration of 28-30 day supplementation period.
Docetaxel (75 mg/m2) will be administered intravenously every 3 weeks with 5 mg prednisone twice a day continuously and pre-medication with dexamethasone. Step-down to 60 mg/m\^2 is allowed as per the approved docetaxel label.
AML is a clonal myelopoietic stem cell disorder characterized by the accumulation of neoplastic cells in the bone marrow and in the peripheral circulation. The median age of AML patients is 68 years. Although intensive chemotherapy and allogeneic stem cell transplant (allo-HSCT) are standard approaches for newly diagnosed patients, they are associated with higher rates of treatment related complications and inferior outcomes in older patients. Venetoclax, a newly orally available and selective B cell lymphoma-2 (BCL2) inhibitor, Venetoclax in combination with hypomethylation agents or cytarabine has been approved by the Food and Drug Administration (FDA) for the treatment of patients with newly diagnosed AML unfit for intensive chemotherapy. However, the emergence of resistance to Venetoclax based combinations has become an important clinical dilemma. Resistance to Venetoclax can be acquired through the up regulation of anti-apoptotic proteins, such as myeloid cell leukaemia 1 (MCL1). Chidamide, a newly designed selective histone deacetylase inhibitor, Chidamide could down Bregulate MCL1 expression in Venetoclax resistant AML cells. Our experience showed that the Chidamide+VA could improve the condition of R/R AML patients who are resistant to VA. Cladribine is a purine analogue widely used in hematologic malignancies. It was demonstrated that addition of Cladribine to the VA regimen increases eradication of primary AML containing monocytic leukemia stem cell activity in both in vitro and in vivo preclinical models. Chidamide or Cladribine have synergistic anti-leukemia effects with VA through their unique mechanisms, which can eradicate leukemia stem cells and prevent the occurrence of drug resistance, thereby increasing response rate, prolonging patient survival, reducing recurrence, and improving prognosis without increasing treatment-related complications. Therefore, this prospective, multi-center, randomized, controlled Phase II study is to compare the therapeutic efficacy and side effect of VACl (Venetoclax,Azacitidine,Cladribine) alternating with VACh (Venetoclax,Azacitidine,Chidamide), VACl, VACh and VA in newly diagnosed adult AML patients ineligible for intensive therapy or declining.
Critically ill patients admitted to intensive care units (ICUs) experience a broad variety of life-threatening conditions. Irrespective of the initial cause of hospitalization, many experience systemic immune dysregulation. Dendritic cells (DCs) are the most potent antigen-presenting cells and play a pivotal role in regulating the immune response by linking the innate to the adaptive immune system. The aim of this study was to analyze whether DCs or their respective subsets are associated with 30-d mortality in an unselected patient cohort admitted to a medical ICU with a cardiovascular focus. A total of 231 patients were included in this single-center prospective observational study. Blood was drawn at admission and after 72 h. Subsequently, flow cytometry was utilized for the analysis of DCs and their respective subsets. In the total cohort, low percentages of DCs were significantly associated with sepsis, respiratory failure, and septic shock. In particular, a significantly lower percentage of circulating plasmacytoid DCs (pDCs) was found to be a strong and independent predictor of 30-d mortality after adjustment for demographic and clinical variables with an hazard ratio of 4.2 (95% confidence interval: 1.3-13.3, P = 0.015). Additionally, low percentages of pDCs were correlated with additional markers of inflammation and organ dysfunction. In conclusion, we observed low percentages of DCs in patients admitted to an ICU experiencing sepsis, respiratory failure, and cardiogenic shock, suggesting their depletion as a contributing mechanism for the development of immune paralysis. In our cohort, pDCs were identified as the most robust subset to predict 30-d mortality.
Mycophenolate mofetil is an antimetabolite immunosuppressant. It is the 2-morpholinoethyl ester of mycophenolic acid (MPA), an immunosuppressive agent; inosine monophosphate dehydrogenase (IMPDH) inhibitor.

The chemical name for mycophenolate mofetil (MMF) is 2-morpholinoethyl (E)-6-(1,3-dihydro-4-hydroxy-6-methoxy-7-methyl-3-oxo-5-isobenzofuranyl)-4-methyl-4-hexenoate. It has a molecular formula of C23H31NO7, a molecular weight of 433.50, and the following structural formula:

Mycophenolate mofetil is a white to off-white crystalline powder. It is slightly soluble in water (43 mcg/mL at pH 7.4); the solubility increases in acidic medium (4.27 mg/mL at pH 3.6). It is freely soluble in acetone, soluble in methanol, and sparingly soluble in ethanol. The apparent partition coefficient in 1-octanol/water (pH 7.4) buffer solution is 238. The pKa values for mycophenolate mofetil are 5.6 for the morpholino group and 8.5 for the phenolic group.

Inactive Ingredients:

Tablets - Mycophenolate mofetil tablets are available for oral administration as tablets containing 500 mg of mycophenolate mofetil. In addition, each tablet contains the following inactive ingredients: croscarmellose sodium, magnesium stearate, microcrystalline cellulose, povidone, talc, hypromellose, hydroxypropyl cellulose, polyethylene glycol, titanium dioxide, iron oxide black and iron oxide red.

Capsules - Mycophenolate mofetil capsules, USP are available for oral administration as capsules containing 250 mg of mycophenolate mofetil. In addition, each capsule contains the following inactive ingredients: croscarmellose sodium, FD&C blue #2, gelatin, magnesium stearate, povidone (K-90), pregelatinized starch and titanium dioxide. The capsule is printed with edible black ink. The black ink is comprised of butyl alcohol, black iron oxide, dehydrated alcohol, isopropyl alcohol, potassium hydroxide, propylene glycol, purified water, shellac and strong ammonia solution.
The invention provides an anticancer drug, which takes the Chinese yew essential oil as the raw material. The anticancer drug can be made into oral suspensions, capsules, or emulsions, and then is absorbed by intestine and stomach to cure cancer. The anticancer drug can also be made into foaming agents, emulsions, or suspensions, and then is directly sprayed or coated on the lesion parts. The principle of external application of the drug is that Chinese yew essential oil has a strong penetration effect, so the Chinese yew essential oil can be absorbed by skins or mucous membranes and directly acts on the lesion parts. External drug application is mainly used for curing various cancers on female breasts and genital system, such as breast cancer, lymph cancer, cervical carcinoma, uterus cancer, and the like. The anticancer drug prepared from Chinese yew essential oil is divided into two types: the oral type and the external type, the oral type can be divided into following dosage forms: suspension, capsule, emulsion, or the like; and the external type can be divided into following dosage forms: foaming agent, emulsion, and suspension.
This is an open label study. The study will consist of 2 treatment group: coated Nifedipine suppository containing 12 mg of Nifedipine applied twice daily (group 1) and coated Nifedipine suppository containing 12 mg of Nifedipine applied once daily (group 2). Approximately 30 subjects will participate into this 8-week study. A screening visit will be used to determine subject suitability for inclusion in the trial. Within one week of the screening visit, subjects who meet all inclusion criteria and none of the exclusion criteria will receive Coated Nifedipine 12 mg Suppository X2 a day (BID) (24 mg/day total) OR Coated Nifedipine 12 mg Suppository X1 a day (OD) (12 mg/day total) for a period of 8 weeks. During this period, 4 study visits (at 0, 2, 5, and 8 weeks) will take place. Study medication will be administered BID (in the morning and in the evening) or OD (only in the morning). In addition to receiving study medication, subjects will be maintained on a standard treatment for Anal Fissure: sitz baths, high fiber diet.
Patients over 18 years of age with a diagnosis of non-small cell lung cancer and being received cytotoxic chemotherapy or tyrosine kinase inhibitors (epidermal growth cell receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibitors) from August 2017 to September 2018. Each patient switching to PD-1 inhibitor will be matched to three reference standard chemotherapy users.