Objective To investigate the electrophysiological characteristics of chronic alcoholic myopathy. Methods Muscle fiber conduction velocity, peripheral nerve conduction velocity, and induced potentials in 26 patients with chronic alcoholic myopathy, 13 patients with chronic alcoholic peripheral neuropathy, 21 patients with chronic alcoholic neuromuscular damage, and 20 normal subjects were detected by electromyography and single fiber electromyography. Results Electromyography revealed myogenic changes in 9 cases in the myopathy group, neurogenic changes in 7 cases in the peripheral neuropathy group, and both kind of changes in 4 cases in the neuromuscular damage group. Compared with the normal subjects, neuromuscular jitter and fiber density increased in all patients ( P 0.05). Slowed sensory nerve conduction velocity was found in 28 patients (82.35%) with peripheral neuropathy or neuromuscular damage. Conclusion Electromyography and determination of nerve conduction velocity can be used to differentiate the alcoholic myopathy from peripheral neuropathy. The abnormal muscle fiber conduction velocity can be helpful for the confirmation of myopathy.

The last two decades have witnessed a paradigm shift from cytotoxic drugs to targeted therapy in medical oncology and pharmaceutical innovation. Inspired by breakthroughs in molecular and cellular biology, a number of novel synthesized chemical compounds and recombinant antibodies have been developed to selectively target oncogenic signaling pathways in a broad array of tumor types. Although targeted therapeutic agents show impressive clinical efficacy and minimized adverse effects compared with traditional treatments, the challenging drug-resistant issue has also emerged to limit their benefits to cancer patients. In this regard, we aim to improve targeted therapy by presenting a systematic framework regarding the drug resistance mechanisms and alternative approaches to re-sensitize cancer cells/tissues therapeutically.
Antineoplastic Agents ; Drug Resistance, Neoplasm ; Humans ; Neoplasms ; Signal Transduction