Model: nicher92/mpnet-base-v2-pharma-finetuned
Author: nicher92
Pipeline: sentence-similarity
Library: sentence-transformers
Tags: sentence-transformers, safetensors, mpnet, sentence-similarity, feature-extraction, dense, generated_from_trainer, dataset_size:2648974, loss:CachedGISTEmbedLoss, dataset:nicher92/mined_negatives_pharma_qa, arxiv:1908.10084, base_model:sentence-transformers/all-mpnet-base-v2, base_model:finetune:sentence-transformers/all-mpnet-base-v2, model-index, endpoints_compatible, region:us
Base models (finetune): id: sentence-transformers/all-mpnet-base-v2
Card metadata: tags: sentence-transformers, sentence-similarity, feature-extraction, dense, generated_from_trainer, dataset_size:2648974, loss:CachedGISTEmbedLoss
base_model: sentence-transformers/all-mpnet-base-v2
widget: source_sentence: What effect does montelukast have on eosinophils in the blood?
sentences: Prostaglandins and Leukotrienes
The eicosanoids are a group of substances derived from phospholipids. These substances are found in animals and plants where they display a wide variety of biological activities. In humans, they are available in all tissues of the body and are often formed de novo. The student should reflect on the pathogenesis and pharmacotherapy of many diseases – pain and inflammation, spontaneous abortion, asthma, peptic ulcer, thrombosis etc. Indeed knowledge of the eicosanoids has revolutionized the pharmacotherapy of pain and inflammation. The mechanisms of action of NSAIDs and glucocorticoids cannot be fully discussed without mention of their effects on eicosanoid biosynthesis. The term eicosanoids as used in this lecture refers to prostagladins, thromboxanes, leukotrienes and lipoxins all of which are derived from arachidonic acid (eicosatetraenoic acid). The term, prostanoids encompasses both prostaglandins and thromboxanes both of which have the same synthetic origin.
The precursor of the eicosanoids is arachidonic acid (5,8,11,14-eicosatetraenoic acid), a 20-carbon unsaturated fatty acid that is found in esterified form in phospholipids and glycerides of cell membranes. Phospholipids exist as: phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine, phosphatidylserine and diacylglycerol. Liberation of arachidonic acid (AA) from phospholipids may involve one or two steps. One-step process involves phospholipase A2 (PLA2) but the two-step process involves first phospholipase C (PLC) and diacylglycerol (DAG) lipase (or phospholipase D), and then finally PLA2. There are at least two forms of PLA2 – cytosolic and extracellular but the former is by far more important from the point of view of inflammation and is Ca2+-dependent. Certain factors which include antigen-antibody reactions, cell damage as well as thrombin in platelets, C5a in neutrophils and bradykinin in fibroblasts all trigger the release of AA. Arachidonic acid is metabolized through the cyclooxygenase pathway to form prostaglandins and thromboxanes or through the lipoxygenase pathways to form leukotrienes, the lipoxins and other compounds (Fig 2, page 6).
The Prostanoids These are formed by the action of cyclooxygenase [(COX) which may also be referred to as prostaglandin endoperoxide synthase] on AA. There are two forms of COX: COX-1 which is constitutive and is found in most cells. The action of COX-1 may involve normal homeostasis (e.g. actions on vascular responses as well as gastric cytoprotection). COX-2 is more pertinent to inflammation and is induced following an inflammatory stimulus. The enzyme converts AA to unstable PGG2 first and then PGH2 both of which are called cyclic endoperoxides. PGH2 is the immediate precursor of other prostanoids and the eventual product depends on the cell: TXA2 in platelets, PGE2 in macrophages, PGD2 in mast cells, PGI2 in vascular endothelium and the GIT. The term “prostaglandin” (PG) was coined from the observation by early workers that extracts of semen contracted the isolated uterus. While PGE was partitioned into ether, PGF was partitioned into phosphate (Fosfat in Swedish) buffer. PGA and PGB were artifacts stable in acidic and basic media respectively. Other PGs were named to fill the gaps. The subscript refers to the number of double bonds in the molecule. α – refers to the orientation of the hydroxy group above or below the plane of the ring. Action of COX on eicosatrienoic acid results in only a single bond as in PGE1.
Pharmacokinetics They are metabolized by several intracellular PG-specific enzymes which are very abundant in the lungs and then slowly by general fatty acid oxidizing enzymes at β-, ω-, 15-hydroxyl positions to the corresponding ketones. The products are excreted in the urine. The t½ of most PGs in circulation is less than 1 minute. PGI2 (t½ = 5 mins) is metabolized to 6-ketoPGF1α.
Pharmacological Actions The receptors for the prostanoids have been named one each f, Hyperglycemia and Diabetes Mellitus Patients should be advised of the potential risk of hyperglycemia-related adverse reactions. Patients should be monitored regularly for worsening of glucose control. Patients who have diabetes should follow their doctor's instructions about how often to check their blood sugar while taking olanzapine orally disintegrating tablets [see Warnings and Precautions ( 5.5, Montelukast causes inhibition of airway cysteinyl leukotriene receptors as demonstrated by the ability to inhibit bronchoconstriction due to inhaled LTD 4 4 The effect of montelukast sodium on eosinophils in the peripheral blood was examined in clinical trials. In patients with asthma aged 2 years and older who received montelukast sodium, a decrease in mean peripheral blood eosinophil counts ranging from 9% to 15% was noted, compared with placebo, over the double-blind treatment periods. In patients with seasonal allergic rhinitis aged 15 years and older who received montelukast sodium, a mean increase of 0.2% in peripheral blood eosinophil counts was noted, compared with a mean increase of 12.5% in placebo-treated patients, over the double-blind treatment periods; this reflects a mean difference of 12.3% in favor of montelukast sodium. The relationship between these observations and the clinical benefits of montelukast noted in the clinical trials is not known [see Clinical Studies (14), source_sentence: How does ramipril compare to other blood pressure medications?
sentences: 14.1 Hypertension Ramipril has been compared with other ACE inhibitors, beta-blockers, and thiazide diuretics as monotherapy for hypertension. It was approximately as effective as other ACE inhibitors and as atenolol. Administration of ramipril to patients with mild to moderate hypertension results in a reduction of both supine and standing blood pressure to about the same extent with no compensatory tachycardia. Symptomatic postural hypotension is infrequent, although it can occur in patients who are salt- and/or volume-depleted [see WARNINGS AND PRECAUTIONS ( 5.5 Use of ramipril in combination with thiazide diuretics gives a blood pressure lowering effect greater than that seen with either agent alone. In single-dose studies, doses of 5 mg to 20 mg of ramipril lowered blood pressure within 1 to 2 hours, with peak reductions achieved 3 to 6 hours after dosing. The antihypertensive effect of a single dose persisted for 24 hours. In longer term (4 to 12 weeks) controlled studies, once-daily doses of 2.5 mg to 10 mg were similar in their effect, lowering supine or standing systolic and diastolic blood pressures 24 hours after dosing by about 6/4 mmHg more than placebo. In comparisons of peak vs. trough effect, the trough effect represented about 50 to 60% of the peak response. In a titration study comparing divided (bid) vs. qd treatment, the divided regimen was superior, indicating that for some patients, the antihypertensive effect with once-daily dosing is not adequately maintained. In most trials, the antihypertensive effect of ramipril increased during the first several weeks of repeated measurements. The antihypertensive effect of ramipril has been shown to continue during long-term therapy for at least 2 years. Abrupt withdrawal of ramipril has not resulted in a rapid increase in blood pressure. Ramipril has been compared with other ACE inhibitors, beta-blockers, and thiazide diuretics. Ramipril was approximately as effective as other ACE inhibitors and as atenolol. In both Caucasians and Blacks, hydrochlorothiazide (25 or 50 mg) was significantly more effective than ramipril. Ramipril was less effective in blacks than in Caucasians. The effectiveness of ramipril was not influenced by age, sex, or weight. In a baseline controlled study of 10 patients with mild essential hypertension, blood pressure reduction was accompanied by a 15% increase in renal blood flow. In healthy volunteers, glomerular filtration rate was unchanged. 14.3 Heart Failure Post-Myocardial Infarction Ramipril was studied in the AIRE trial. This was a multinational (mainly European) 161-center, 2006-patient, double-blind, randomized, parallel-group study comparing ramipril to placebo in stable patients, 2 to 9 days after an acute myocardial infarction, who had shown clinical signs of congestive heart failure at any time after the myocardial infarction. Patients in severe (NYHA class IV) heart failure, patients with unstable angina, patients with heart failure of congenital or valvular etiology, and patients with contraindications to ACE inhibitors were all excluded. The majority of patients had received thrombolytic therapy at the time of the index infarction, and the average time between infarction and initiation of treatment was 5 days. Patients randomized to ramipril treatment were given an initial dose of 2.5 mg twice daily. If the initial regimen caused undue hypotension, the dose was reduced to 1.25 mg, but in either event doses were titrated upward (as tolerated) to a target regimen (achieved in 77% of patients randomized to ramipril) of 5 mg twice daily. Patients were then followed for an average of 15 months, with the range of follow-up between 6 and 46 months. The use of ramipril was associated with a 27% reduction (p=0.002) in the risk of death from any cause; about 90% of the deaths that occurred were cardiovascular, mainly sudden death. The risks of progression to severe heart failure and of congestive heart failure-related hospitalization were also reduced, by 23% (p=0.017) and 26% (p=0.011), respectively. The benefits of ramipril therapy were seen in both genders, and they were not affected by the exact timing of the initiation of therapy, but older patients may have had a greater benefit than those under 65. The benefits were seen in patients on (and not on) various concomitant medications. At the time of randomization these included aspirin (about 80% of patients), diuretics (about 60%), organic nitrates (about 55%), beta-blockers (about 20%), calcium channel blockers (about 15%), and digoxin (about 12%)., Ramipril capsules are indicated for the treatment of hypertension. It may be used alone or in combination with thiazide diuretics. In using ramipril capsules, consideration should be given to the fact that another angiotensin converting enzyme inhibitor, captopril, has caused agranulocytosis, particularly in patients with renal impairment or collagen-vascular disease. Available data are insufficient to show that ramipril capsules do not have a similar risk. (See WARNINGS. In considering use of ramipril capsules, it should be noted that in controlled trials ACE inhibitors have an effect on blood pressure that is less in black patients than in non-blacks. In addition, ACE inhibitors (for which adequate data are available) cause a higher rate of angioedema in black than in non-black patients. (See WARNINGS, Angioedema., Disease-modifying treatments (DMTs), which are the foundation of multiple sclerosis (MS) care, reduce clinical exacerbations (relapses) and slow disease progression; however, improving quality of life (QOL) is an unmet need for many individuals with MS. DMTs, including interferon-beta, glatiramer acetate, natalizumab, mitoxantrone, and fingolimod, reduce the rate and severity of relapses, the accumulation of brain and spinal cord lesions as shown on magnetic resonance imaging (MRI), and disability progression. Many studies link diminished QOL with specific MS symptoms (fatigue, impaired mobility, spasticity, etc). Even in patients already receiving DMTs, symptoms and QOL may improve with additional agents that treat specific symptoms, thereby improving patient function and ability to perform activities of daily living (ADLs). Patients have reported that mobility impairment is one of the worst aspects of MS. Almost half of patients treated with DMTs reported no improvement in mobility. However, blocking the voltage-dependent potassium channels on the surface of demyelinated nerve fibers may improve signal conduction. Dalfampridine, a potassium channel blocker, received Food and Drug Administration (FDA) approval for all forms of MS specifically to improve walking, which was demonstrated by increased walking speed. By improving walking in some patients with MS, the effects of dalfampridine may complement those of DMTs and address the stated priorities of many patients.
(Am J Manag Care. 2011;17:S146-S153)
MS Treatment and QOL
Improving quality of life (QOL) is an unmet need for many individuals with multiple sclerosis (MS). Disease-modifying treatments (DMTs), which are the foundation of MS care,1 reduce clinical exacerbations (relapses) and slow disease progression.2 QOL improvement, although assumed with fewer relapses, has not always been well documented.
Treatment individualization can include additional agents that treat specific symptoms, improving patient function and ability to perform activities of daily living (ADLs).3 Because many symptom-specific treatments are available, MS treatment should address QOL at every stage of disease progression.
Actions and Safety of DMTs
DMTs reduce the rate and severity of relapses, the accumulation of brain and spinal cord lesions as shown on magnetic resonance imaging (MRI), and disability progression as measured by Expanded Disability Status Scale (EDSS).2 Controlled clinical trials demonstrated relapse rate reductions of 28% to 68%.2 However, relatively few DMT trials documented QOL improvement with QOL metrics. The National Multiple Sclerosis Society (NMSS) stated that DMTs “can be looked upon as an investment in the future,” rather than treatment that makes patients feel better now.2 Thus, clinicians may appreciate the effects of DMTs while some patients on DMT therapy continue to suffer treatable symptoms, poor QOL, and sometimes, adverse effects (AEs).
Interferon-beta (IFNB) is a cytokine primarily secreted by fibroblasts as part of immune response4; recombinant DNA technology produces therapeutic IFNB agents.5 In MS, the IFNB mechanism seems to involve immunomodulatory effects mediated through interactions with specific cell-surface receptors.4 Whereas IFNB-1b is injected subcutaneously every other day, IFNB-1a is available in forms for intramuscular (weekly) and subcutaneous (3 times/week) injection.2 Four IFNB agents have received Food and Drug Administration (FDA) approval for relapsing forms of MS: interferon beta-1b (Betaseron) in 1993, interferon beta-1a (Avonex) in 1996, interferon beta-1a (Rebif) in 2002, and interferon beta-1b (Extavia) in 2009.2 Numerous randomized multicenter trials have demonstrated reduced rate and severity of relapses, delayed EDSS progression, and fewer MRI lesions with IFNB.4,5,6 Some patients develop neutralizing antibodies, potentially lessening efficacy over time.2,5
The evidence for IFNB using QOL metrics is mixed. An early IFNB study incor, source_sentence: Should I use ZYPREXA cautiously if I have a history of seizures?
sentences: The intravenous testing dose of ENLON in children weighing up to 75 lbs is 0.1 mL (1 mg); above this weight, the dose is
											0.2 mL (2 mg). If there is no response after 45 seconds, it may be titrated up to 0.5 mL (5 mg) in children under 75 lbs, given in increments of 0.1 mL (1 mg) every 30 to 45
											seconds and up to 1 mL (10 mg) in heavier children. In infants, the recommended dose is 0.05 mL (0.5 mg). Because of technical difficulty with intravenous injection in children,
											the intramuscular route may be used. In children weighing up to 75 lbs, 0.2 mL (2 mg) is injected intramuscularly. In children weighing more than 75 lbs, 0.5 mL (5 mg) is
											injected intramuscularly. All signs which would appear with the intravenous test appears with the intramuscular test except that there is a delay of two to ten minutes before a
											reaction is noted., TREXIMET should be used with caution in patients with a history of epilepsy or conditions associated with a lowered seizure threshold. There have been reports of seizure following administration of sumatriptan., During premarketing testing, seizures occurred in 0.9% (22/2500) of olanzapine-treated patients. There were confounding factors that may have contributed to the occurrence of seizures in many of these cases. Olanzapine should be used cautiously in patients with a history of seizures or with conditions that potentially lower the seizure threshold, e.g., Alzheimer's dementia. Olanzapine is not approved for the treatment of patients with Alzheimer's disease. Conditions that lower the seizure threshold may be more prevalent in a population of 65 years or older., source_sentence: How much erythromycin is in each pledget?
sentences: Theophylline There have been published reports suggesting that when oral erythromycin is given concurrently with theophylline there is a decrease in erythromycin serum concentrations of approximately 35%. The mechanism by which this interaction occurs is unknown. The decrease in erythromycin concentrations due to co-administration of theophylline could result in subtherapeutic concentrations of erythromycin. Hypotension, bradyarrhythmias, and lactic acidosis have been observed in patients receiving concurrent verapamil, belonging to the calcium channel blockers drug class. Concomitant administration of erythromycin and digoxin has been reported to result in elevated digoxin serum levels. There have been reports of increased anticoagulant effects when erythromycin and oral anticoagulants were used concomitantly. Increased anticoagulation effects due to interactions of erythromycin with oral anticoagulants may be more pronounced in the elderly. Erythromycin is a substrate and inhibitor of the 3A isoform subfamily of the cytochrome p450 enzyme system (CYP3A). Coadministration of erythromycin and a drug primarily metabolized by CYP3A may be associated with elevations in drug concentrations that could increase or prolong both the therapeutic and adverse effects of the concomitant drug. Dosage adjustments may be considered, and when possible, serum concentrations of drugs primarily metabolized by CYP3A should be monitored closely in patients concurrently receiving erythromycin. The following are examples of some clinically significant CYP3A based drug interactions. Interactions with other drugs metabolized by the CYP3A isoform are also possible. The following CYP3A based drug interactions have been observed with erythromycin products in post-marketing experience: Ergotamine/dihydroergotamine Post-marketing reports indicate that co-administration of erythromycin with ergotamine or dihydroergotamine has been associated with acute ergot toxicity characterized by vasospasm and ischemia of the extremities and other tissues including the central nervous system. Concomitant administration of erythromycin with ergotamine or dihydroergotamine is contraindicated (see CONTRAINDICATIONS Triazolobenzodiazepines (such as triazolam and alprazolam) and related benzodiazepines Erythromycin has been reported to decrease the clearance of triazolam and midazolam, and thus, may increase the pharmacologic effect of these benzodiazepines. HMG-CoA Reductase Inhibitors Erythromycin has been reported to increase concentrations of HMG-CoA reductase inhibitors (e.g., lovastatin and simvastatin). Rare reports of rhabdomyolysis have been reported in patients taking these drugs concomitantly. Sildenafil (Viagra) Erythromycin has been reported to increase the systemic exposure (AUC) of sildenafil. Reduction of sildenafil dosage should be considered. (See Viagra package insert.) There have been spontaneous or published reports of CYP3A based interactions of erythromycin with cyclosporine, carbamazepine, tacrolimus, alfentanil, disopyramide, rifabutin, quinidine, methyl-prednisolone, cilostazol, vinblastine, and bromocriptine. Concomitant administration of erythromycin with cisapride, pimozide, astemizole, or terfenadine is contraindicated. (See CONTRAINDICATIONS. In addition, there have been reports of interactions of erythromycin with drugs not thought to be metabolized by CYP3A, including hexobarbital, phenytoin, and valproate. Erythromycin has been reported to significantly alter the metabolism of the nonsedating antihistamines terfenadine and astemizole when taken concomitantly. Rare cases of serious cardiovascular adverse events, including electrocardiographic QT/QTc interval prolongation, cardiac arrest, torsades de pointes, and other ventricular arrhythmias have been observed. (See CONTRAINDICATIONS. There have been post-marketing reports of drug interactions when erythromycin was co-administered with cisapride, resulting in QT prolongation, cardiac arrhythmias, ventricular tachycardia, ventricular fibrillation, and torsades de pointes, most likely due to the inhibition of hepatic metabolism of cisapride by erythromycin. Fatalities have been reported. (See CONTRAINDICATIONS. Colchicine Colchicine is a substrate for both CYP3A4 and the efflux transporter P-glycoprotein (P-gp). Erythromycin is considered a moderate inhibitor of CYP3A4. A significant increase in colchicine plasma concentration is anticipated when co-administered with moderate CYP3A4 inhibitors such as erythromycin. If co-administration of colchicine and erythromycin is necessary, the starting dose of colchicine may need to be reduced, and the maximum colchicine dose should be lowered. Patients should be monitored for clinical symptoms of colchicine toxicity (see WARNINGS)., Patients receiving furosemide should be advised that they may experience symptoms from excessive fluid and/or electrolyte losses. The postural hypotension that sometimes occurs can usually be managed by getting up slowly. Potassium supplements and/or dietary measures may be needed to control or avoid hypokalemia. Patients with diabetes mellitus should be told that furosemide may increase blood glucose levels and thereby affect urine glucose tests. The skin of some patients may be more sensitive to the effects of sunlight while taking furosemide. Hypertensive patients should avoid medications that may increase blood pressure, including over-the-counter products for appetite suppression and cold symptoms., Each pledget is filled to contain 1 mL of Erythromycin Topical Solution USP 2%. Each mL of Erythromycin Topical Solution USP 2% contains 20 mg of erythromycin. Each pledget is supplied in an individual foil packet in boxes of 60. NDC 0168-0215-01. Store at 20°- 25°C (68°- 77°F)[See USP Controlled Room Temperature]. E. FOUGERA & CO. a division of Altana Inc. IF221501 Remove this portion before dispensing ERYTHROMYCIN PLEDGETS, USP, source_sentence: What does COAGADEX do to plasma levels of Factor X?
sentences: Substances increasing the plasma concentrations of COCs: see Warnings and Precautions ( 5.2, The recommended starting dose of valsartan tablets is 40 mg twice daily. Uptitrate to 80 mg and 160 mg twice daily or to the highest dose tolerated by the patient. Consider reducing the dose of concomitant diuretics. The maximum daily dose administered in clinical trials is 320 mg in divided doses., The administration of COAGADEX increases plasma levels of Factor X and can temporarily correct the coagulation defect in these patients, as reflected by decrease in the aPTT and PT.
datasets: nicher92/mined_negatives_pharma_qa
pipeline_tag: sentence-similarity
library_name: sentence-transformers
metrics: cosine_accuracy@1, cosine_accuracy@3, cosine_accuracy@5, cosine_accuracy@10, cosine_precision@1, cosine_precision@3, cosine_precision@5, cosine_precision@10, cosine_recall@1, cosine_recall@3, cosine_recall@5, cosine_recall@10, cosine_ndcg@10, cosine_mrr@10, cosine_map@100
model-index: name: SentenceTransformer based on sentence-transformers/all-mpnet-base-v2
results: task: type: information-retrieval
name: Information Retrieval
dataset: name: ir eval
type: ir-eval
metrics: type: cosine_accuracy@1
value: 0.5473816614565028
name: Cosine Accuracy@1
verified: no, type: cosine_accuracy@3
value: 0.7909768594735577
name: Cosine Accuracy@3
verified: no, type: cosine_accuracy@5
value: 0.8653558017794714
name: Cosine Accuracy@5
verified: no, type: cosine_accuracy@10
value: 0.9238637835038198
name: Cosine Accuracy@10
verified: no, type: cosine_precision@1
value: 0.5473816614565028
name: Cosine Precision@1
verified: no, type: cosine_precision@3
value: 0.2636589531578525
name: Cosine Precision@3
verified: no, type: cosine_precision@5
value: 0.1730711603558943
name: Cosine Precision@5
verified: no, type: cosine_precision@10
value: 0.09238637835038199
name: Cosine Precision@10
verified: no, type: cosine_recall@1
value: 0.5473816614565028
name: Cosine Recall@1
verified: no, type: cosine_recall@3
value: 0.7909768594735577
name: Cosine Recall@3
verified: no, type: cosine_recall@5
value: 0.8653558017794714
name: Cosine Recall@5
verified: no, type: cosine_recall@10
value: 0.9238637835038198
name: Cosine Recall@10
verified: no, type: cosine_ndcg@10
value: 0.7408592244566691
name: Cosine Ndcg@10
verified: no, type: cosine_mrr@10
value: 0.6814683692113697
name: Cosine Mrr@10
verified: no, type: cosine_map@100
value: 0.6844679271586943
name: Cosine Map@100
verified: no
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Created: 2025-11-25 10:18:04