Objective To explore rationale and clinical application of simplified modified radical thyroideetomy for differentiated thyroid carcinoma.Methods From Jan.2007 to Jun.2010,349 cases of differentiated thyroid carcinoma received simplified operative procedure based on standard modified radical thyroidectomy.The simplified procedure took a low small collar incision(about 10-12 cm).In separating upper and lower skin flaps,subcutaneous tissues covering posterior triangle of neck and posterior edge of sternoeleidomastoid muscle were spared to protect sensory nerves.Subtotal thyroidectomy Was performed to resect the affected lobe,isthmus,and the majority of opposite lobe without considering the size of primary tumor or whether metastasis to the neck lymph nodes happened.Soft tissues of the mainly metastatic areas(Ⅱ a、Ⅲ、Ⅳ、Ⅴb)were cleared.The accessory nerve was not exposed routinely to avoid stimulation.Lymph nodes metastasis in different areas was recorded respectively.Complications in different operative modes were compared.Results Compared with standard modified radical thyroidectomy,the simplified mode had shorter scar-and no limit of neck mobility.Because of muscles and nerves pemervation,movement dysfunction and abnormal sensation of neck and shoulder decreased obviously.The operation duration was shortened.Cervical lymph node status Was evaluated,which provided basis for prognosis judgment and comprehensive treatment.Conclusions The simplified modified radical procedure has the benefit of decreased trauma while maintains the similar recurrence rate compared to modified radical thyroidectomy.It improvs the life quality of patients.This procedure fits the principle of functional radical neck dissection better.

Huntington's disease (HD) is a deadly neurodegenerative disease with abnormal expansion of CAG repeats in the huntingtin gene. Mutant Huntingtin protein (mHTT) forms abnormal aggregates and intranuclear inclusions in specific neurons, resulting in cell death. Here, we tested the ability of a natural heat-shock protein 90 inhibitor, Gedunin, to degrade transfected mHTT in Neuro-2a cells and endogenous mHTT aggregates and intranuclear inclusions in both fibroblasts from HD patients and neurons derived from induced pluripotent stem cells from patients. Our data showed that Gedunin treatment degraded transfected mHTT in Neuro-2a cells, endogenous mHTT aggregates and intranuclear inclusions in fibroblasts from HD patients, and in neurons derived from induced pluripotent stem cells from patients in a dose- and time-dependent manner, and its activity depended on the proteasomal pathway rather than the autophagy route. These findings also showed that although Gedunin degraded abnormal mHTT aggregates and intranuclear inclusions in cells from HD patient, it did not affect normal cells, thus providing a new perspective for using Gedunin to treat HD.