PURPOSE : To evaluate clinical and three dimensional (3D) dosimetric parameters associated with esophageal injury after radiotherapy for non-small cell lung cancer (NSCLC). MATERIALS AND METHODS : The records of 254 patients treated for NSCLC between 1992 and 2001 were reviewed. A variety of metrics describing the esophageal dose were extracted. Chemotherapy was given in 143 patients (56%). The RTOG toxicity criteria for grading of esophageal injury were used. The median follow-up time of all patients was 43 months with the range of 0.5~120 months. Logistic regression, contingency table analyses and Fisher's exact tests were used for statistical analysis. RESULTS : Acute toxicity occurred in 78% patients (199/254); grade 1,138; grade 2, 38; grade 3, 22 and grade 4, 1. For acute toxicity> or =Grade 2, BID-RT, age, nodal stage> or =N2, and most dosimetric parameters were predictive. Late toxicity occurred in 17 (7%) of 238 patients; grade 1, 5; grade 2, 4; grade 3, 5 and grade 4, 3. The median and maximum time to onset of late toxicity was 5 and 40 months after radiotherapy, respectively. Late toxicity occurred in 2%, 3%, 17%, 26%, and 100% of patients with acute grade 0, 1, 2, 3 and 4 toxicity, respectively. For late toxicity, the severity of acute toxicity was most predictive. CONCLUSION : A variety of dosimetric parameters are predictive for acute and late esophageal injury. A strong correlation between the dosimetric parameters prevented a comparison between the predictive abilities of these metrics. The presence of acute injury was the most predictive factor for the development of late injury. This suggests that late injury may be "consequential" and that aggressive treatment of acute effects may reduce the risk of late injury. Additional studies to better define predictors of RT-induced esophageal injury are needed
Carcinoma, Non-Small-Cell Lung ; Drug Therapy ; Follow-Up Studies ; Humans ; Logistic Models ; Radiotherapy

In the original publication the bands in Fig. 1J and Fig. 2B were not visible. The correct versions of Fig. 1J and Fig. 2B are provided in this correction.

Axonal transport of mitochondria is critical for neuronal survival and function. Automatically quantifying and analyzing mitochondrial movement in a large quantity remain challenging. Here, we report an efficient method for imaging and quantifying axonal mitochondrial transport using microfluidic-chamber-cultured neurons together with a newly developed analysis package named "MitoQuant". This tool-kit consists of an automated program for tracking mitochondrial movement inside live neuronal axons and a transient-velocity analysis program for analyzing dynamic movement patterns of mitochondria. Using this method, we examined axonal mitochondrial movement both in cultured mammalian neurons and in motor neuron axons of Drosophila in vivo. In 3 different paradigms (temperature changes, drug treatment and genetic manipulation) that affect mitochondria, we have shown that this new method is highly efficient and sensitive for detecting changes in mitochondrial movement. The method significantly enhanced our ability to quantitatively analyze axonal mitochondrial movement and allowed us to detect dynamic changes in axonal mitochondrial transport that were not detected by traditional kymographic analyses.
Animals ; Axonal Transport ; physiology ; Cerebral Cortex ; cytology ; metabolism ; Drosophila melanogaster ; cytology ; metabolism ; Embryo, Mammalian ; Gene Expression ; Lab-On-A-Chip Devices ; Microscopy, Confocal ; Mitochondria ; metabolism ; ultrastructure ; Motor Neurons ; metabolism ; ultrastructure ; Movement ; Mutation ; Primary Cell Culture ; RNA-Binding Protein FUS ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Software