Objective: To assess the technique, efficacy, security and side effects of percutaneous ethanol injection(PEI) in treating the cystic thyroid adenomas. Methods: Fifty seven patients(male 34, female 23) with unilateral and solitary benign cystic thyroid adenoma received PEI therapy under high resolution ultrasound guidance. The medial age of the patients was 47 years(ranging 29 62). The mean diameter in the largest section of the thyroid adenomas was (37.55?5.64) mm(17 59 mm). The thyroid lesions in 12 patients consisted of cystic lumen mixed with solid structure, and the rest 45 had entire cystic thyroid lesions. Ultrasound reexamination of thyroid lesions was done 3 months after the initial treatment. Significant curative effect was defined as an adenoma volume shrinkage rate larger than 50%. The efficacious result was defined as a volume shrinkage rate between 40% and 50% together with a further shrink over a 6 month duration follow up. Those patients with adenoma volume shrinkage rate less than 40% underwent a second PEI after 6 months. Results: Over a mean duration of 25.5 months follow up, 66.7% subjects with entirely cystic had significant curative outcome; 19.3% subjects had efficacious result; and 9.8% subjects needed a second PEI and their thyroid lesions contained more solid tissue. There were 5.3% subjects were transfered to open surgery due to colloid cyst fluid. Twenty one patients complained of intraoperative local transient pain; 15 patients had transient pyrexia in the 48 h after injection, and 3 patients were affected by post operative transient dysphonia. No serious bleeding were encountered, and no apparent change of serum T 3,T 4,TSH level was observed. Conclusion: Ultrasound guided PEI therapy is an effective, safe and simple procedure for the ablation of cystic thyroid adenoma. Careful selection of subjects according to their preoperative thyroid ultrasonographies can reduce the unsuccessful PEI. A selective volume of ethanol injection consistent with the adenoma size on sonograms and a thorough flush with ethanol can improve the efficacy of PEI.

Objective To investigate the role and neuroinflammatory mechanism of iron on dopamine ( DA) neurons in multiple primary midbrain cultures that mimic human substantia nigra pars compacta.Methods Ferrous chloride ( Fe2+ ) with the desired concentrations of 5,25 and 100 μmol/L was used to ( 1 ) treat primary midbrain neuron-microglia-astroglia cultures for 7 days and the numbers of DA neurons and total neurons were counted after tyrosine hydroxylase (TH) and neuron-specific neuclear protein neurons in 5,25 and 100 μmol/L Fe2 + -treated groups were 89%,70% and 55% of control group,and 25,100 μmol/L Fe2+ significantly decreased DA neuronal numbers compared with control group ( F = 12.047,P ＜0.01);DA neuronal bodies were shrunk and smaller,cytoplasmic stainings were reduced,neuronal dendrites were decreased;(2) The numbers of Neu-N ( + ) total neurons in 5,25 and 100 μmol/L Fe2+-treated groups were 100%,104% and 101% of control group and Fe2+ did not decrease DA neuronal numbers compared with control group (t =4.458,P ＞ 0.05 );5,25 and 100 μmol/L Fe2+-induced difference between total neurons and DA neurons were 11%,34% and 46%,and 25 and 100 (Amol/L Fe2+ produced significant difference(t =8.098,P ＜0.05;t = 11.218,P＜0.05);(3) In primary midbrain neuron-microglia-astroglia and neuron-astroglia cultures,the numbers of DA neurons in 25 μmol/L Fe+-treated group were 70% and 98% of control group,respectively.The difference between two groups was 28%,which was statistically significant (t =8.061,P＜0.05);The numbers of DA neurons in 100 μmol/L groups were 183%,190 % and 240% of control group,and 25 and 100 μmol/L Fe2 + significantly increased microglial numbers compared with control group ( F = 6.101,P ＜ 0.01 );dramatic changes of microglial morphology were indicated by the enlarged cell bodies and irregular shape.Conclusions Fe2 + provokes selective DA neuronal damage and microglia are the mediators of the neurotoxic effect,which may be due to microglial over-activation featured by the significant production of neurotoxic factors and morphological changes of microglia.This investigation cast a new light for PD therapy by inhibiting Fe2+ -induced neuroinflammation characterized by the microglial over-activation.