Pathways

Salicylic acid (also named rutranex or salonil) is a nonsteroidal anti-inflammatory drug. Salicylic acid is also an important active metabolite of aspirin (acetylsalicylic acid). It can be used to reduce pain and fever. Salicylic acid can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of Salicylic acid.

Salicylic acid is an acid used to treat acne, psoriasis, calluses, corns, keratosis pilaris, and warts. Salicylate's use in rheumatic diseases is due to it's analgesic and anti-inflammatory activity. It targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 convert arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase, or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme that is responsible for prostaglandin synthesis during inflammation. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Salicylic acid inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain. This drug is administered as a topical cream, ointment, shampoo, patch, lotion, or gel.

Salla disease, also called sialic acid storage disease, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of lysosomal storage caused by a defective SLC17A5 gene. SLC17A5 codes for the lysosomal transporter sialin which exports sialic acid from the lysosome into the cytoplasm. This disorder is characterized by a large accumulation of sialic acid in the urine. Symptoms of the disorder include seizures, intellectual disability, developmental delay, nystagmus, hypotonia, ataxia, spasticity, and athetosis. There are three forms of Salla disease: infantile free sialic acid storage disease (ISSD), Salla disease, and intermediate severe Salla disease. Since there is currently no cure for Salla disease, treatment involves managing the disorder's symptoms. Salla disease has been reported in approximately 150 people (mostly from Finland and Sweden) and ISSD has been reported in a few dozen infants.

Salla disease, also called sialic acid storage disease, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of lysosomal storage caused by a defective SLC17A5 gene. SLC17A5 codes for the lysosomal transporter sialin which exports sialic acid from the lysosome into the cytoplasm. This disorder is characterized by a large accumulation of sialic acid in the urine. Symptoms of the disorder include seizures, intellectual disability, developmental delay, nystagmus, hypotonia, ataxia, spasticity, and athetosis. There are three forms of Salla disease: infantile free sialic acid storage disease (ISSD), Salla disease, and intermediate severe Salla disease. Since there is currently no cure for Salla disease, treatment involves managing the disorder's symptoms. Salla disease has been reported in approximately 150 people (mostly from Finland and Sweden) and ISSD has been reported in a few dozen infants.

Salla disease, also called sialic acid storage disease, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of lysosomal storage caused by a defective SLC17A5 gene. SLC17A5 codes for the lysosomal transporter sialin which exports sialic acid from the lysosome into the cytoplasm. This disorder is characterized by a large accumulation of sialic acid in the urine. Symptoms of the disorder include seizures, intellectual disability, developmental delay, nystagmus, hypotonia, ataxia, spasticity, and athetosis. There are three forms of Salla disease: infantile free sialic acid storage disease (ISSD), Salla disease, and intermediate severe Salla disease. Since there is currently no cure for Salla disease, treatment involves managing the disorder's symptoms. Salla disease has been reported in approximately 150 people (mostly from Finland and Sweden) and ISSD has been reported in a few dozen infants.

Salla disease, also called sialic acid storage disease, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of lysosomal storage caused by a defective SLC17A5 gene. SLC17A5 codes for the lysosomal transporter sialin which exports sialic acid from the lysosome into the cytoplasm. This disorder is characterized by a large accumulation of sialic acid in the urine. Symptoms of the disorder include seizures, intellectual disability, developmental delay, nystagmus, hypotonia, ataxia, spasticity, and athetosis. There are three forms of Salla disease: infantile free sialic acid storage disease (ISSD), Salla disease, and intermediate severe Salla disease. Since there is currently no cure for Salla disease, treatment involves managing the disorder's symptoms. Salla disease has been reported in approximately 150 people (mostly from Finland and Sweden) and ISSD has been reported in a few dozen infants.

Salmeterol is a long acting beta-2 adrenergic receptor agonists used to treat asthma and COPD. Beta-2 agonists are G protein linked second messengers. It can be found under the brand names Advair, Airduo, Serevent, and Wixela. This drug is to be inhaled alongside corticosteroids to be most effective. It is useful for the prevention of exercise induced bronchospasm and airflow obstruction. Salmeterol can bind to both active and exo sites on the beta-2 adrenergic receptor; the saligenin moiety binds to the active site and the hydrophilic tail binds to leucine residues in the exo site almost irreversibly, leading to the long duration of action seen with Salmeterol. A single dose can last 12 hours. The result of taking this drug is relaxation of the bronchial smooth muscles causing bronchodilator and increased airflow. Once Salmeterol is administered and it binds to the beta-2 adrenergic receptor, the G protein signalling cascade begins. The alpha and beta/gamma subunits of the G protein separate and GDP is replaced with GTP on the alpha subunit. This alpha subunit then activates adenylyl cyclase which converts ATP to cAMP. cAMP then activates protein kinase A (PKA) which in turn phosphorylates targets and inhibits MLCK through decreased calcium levels causing muscle relaxation. PKA can phosphorylate certain Gq-coupled receptors as well as phospholipase C (PLC) and thereby inhibit G protein-coupled receptor (GPCR) -PLC-mediated phosphoinositide (PI) generation, and thus calcium flux. PKA phosphorylates the inositol 1,4,5-trisphosphate (IP3) receptor to reduce its affinity for IP3 and further limit calcium mobilization. PKA phosphorylates myosin light chain kinase (MLCK) and decreases its affinity to calcium calmodulin, thus reducing activity and myosin light chain (MLC) phosphorylation. PKA also phosphorylates KCa++ channels in ASM, increasing their open-state probability (and therefore K+ efflux) and promoting hyperpolarization. Since myosine light chain kinase is not activated, Serine/threonine-protein phosphatase continues to dephosphorylate myosin LC-P, and more cannot be synthesized so myosin remains unbound from actin causing muscle relaxation. This relaxation of the smooth muscles in the lungs causes the bronchial airways to relax which causes bronchodialation, making it easier to breathe. Some risks and side effects of Salmeterol include monotherapy, hypokalemia, hypoglycemia, seizures, headache, tremor, and fatigue. Salmeterol is administered via respiratory inhalation.