NSAIDS have antipyretic activity and can be used to treat fever.   Fever is caused by elevated levels of prostaglandin E2 , which alters the firing rate of neurons within the hypothalamus that control thermoregulation.   Antipyretics work by inhibiting the enzyme COX, which causes the general inhibition of prostanoid biosynthesis ( PGE2 ) within the hypothalamus .   PGE2 signals to the hypothalamus to increase the body's thermal set point.   Ibuprofen has been shown more effective as an antipyretic than paracetamol (acetaminophen).   Arachidonic acid is the precursor substrate for cyclooxygenase leading to the production of prostaglandins F, D & E.
In the past several years, some newer medications have come on the market; these are commonly referred to as COX-2 inhibitors . Remember, all NSAIDs work against cyclooxygenase (COX). Traditional NSAIDs (. Ibuprofen, Motrin, Aleve) work against both COX-1 and COX-2. COX-1 and COX-2 are both types of cyclooxygenase enzymes that function in your body. The new medications (. Celebrex) work primarily against COX-2, and allow COX-1 to function normally. Because COX-1 is more important in producing the protective lining in your gut (gastric mucosa), these newer NSAIDs are believed to have less of a risk of causing stomach ulcers.
Family history is a risk factor for asthma, with many different genes being implicated.  If one identical twin is affected, the probability of the other having the disease is approximately 25%.  By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1 , IL10 , CTLA-4 , SPINK5 , LTC4S , IL4R and ADAM33 , among others.  Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested.  In 2006 over 100 genes were associated with asthma in one genetic association study alone;  more continue to be found.