Electromyography, which should be accompanied by a nerve conduction velocity study (NCV), has the unique ability to detect nerve-root-level axon damage (damage to the tiny nerve fibers that makeup the nerve root) and will really finalize the diagnosis of disc-herniation-related radicular pain if found to be positive. This test also has the ability to differentiate between disc herniation-related sciatica and other causes of sciatica (., diabetes and herpes zoster), as well as differentiate between acute and chronic radicular pain.
Recently, a specific peptide inhibitor for ATGL was isolated from white blood cells, specifically mononuclear cells. This peptide was originally identifed as being involved in the regulation of the G 0 to G 1 transition of the cell cycle . This peptide was, therefore, called G0G1 switch protein 2 (G0S2). The protein is found in numerous tissues, with highest concentrations in adipose tissue and liver. In adipose tissue G0S2 expression is very low during fasting but increases after feeding. Conversely, fasting or PPARα-agonists increase hepatic G0S2 expression. The protein has been shown to localize to LDs, cytoplasm, ER, and mitochondria. These different subcellular localizations likely relate to multiple functions for G0S2 in regulating lipolysis, the cell cycle , and, possibly, apoptosis via its ability to interact with the mitochondrial antiapoptotic factor Bcl-2. With respect to ATGL regulation, the binding of the enzyme to LDs and subsequent is dependent on a physical interaction between the N-terminal region of G0S2 and the patatin domain of ATGL.