sentence-transformers How to use nicher92/mpnet-base-v2-pharma-finetuned with sentence-transformers:
from sentence_transformers import SentenceTransformer
model = SentenceTransformer("nicher92/mpnet-base-v2-pharma-finetuned")
sentences = [
"What effect does montelukast have on eosinophils in the blood?",
"Prostaglandins and Leukotrienes\nThe 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.\nThe 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).\nThe 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.\nPharmacokinetics 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.\nPharmacological 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)"
]
embeddings = model.encode(sentences)
similarities = model.similarity(embeddings, embeddings)
print(similarities.shape)
# [4, 4] 
