Imaging features and differential diagnoses of non-neoplastic diffuse mediastinal diseases.

Acute or chronic non-neoplastic diffuse mediastinal diseases have multiple causes, degrees of severity, and a wide range of management. Some situations require emergency care while others do not need specific treatment. Although the diagnosis may be suspected on chest X-ray, it is mainly based on CT. A delayed recognition is not uncommonly observed. Some findings may prompt the radiologist to look for specific associated injuries or lesions.This pictorial review will successively describe the various non-neoplastic causes of diffuse mediastinal diseases with their typical findings and major differentials.First, pneumomediastinum that can be provoked by extra- or intra-thoracic triggers requires the knowledge of patient's history or recent occurrences. Absence of any usual etiological factor should raise suspicion of cocaine inhalation in young individuals.Next, acute mediastinitis may be related to post-operative complications, esophageal perforation, or contiguous spread of odontogenic or retropharyngeal infections. The former diagnosis is not an easy task in the early stage, owing to the similarities of imaging findings with those of normal post-operative appearance during the first 2-3 weeks.Finally, fibrosing mediastinitis that is linked to an excessive fibrotic reaction in the mediastinum with variable compromise of mediastinal structures, in particular vascular and airway ones. Differential diagnosis includes tumoral and inflammatory infiltrations of the mediastinum

Plantar fascia ultrasound images characterization and classification using support vector machine

The examination of plantar fascia (PF) ultrasound (US) images is subjective and based on the visual perceptions and manual biometric measurements carried out by medical experts. US images feature extraction, characterization and classification have been widely introduced for improving the accuracy of medical assessment, reducing its subjective nature and the time required by medical experts for PF pathology diagnosis. In this paper, we develop an automated supervised classification approach using the Support Vector Machine (Linear and Kernel) to distinguishes between symptomatic and asymptomatic PF cases. Such an approach will facilitate the characterization and the classification of the PF area for the identification of patients with inferior heel pain at risk of plantar fasciitis. Six feature sets were extracted from the segmented PF region. Additionally, features normalization, features ranking and selection analysis using an unsupervised infinity selection method were introduced for the characterization and the classification of symptomatic and asymptomatic PF subjects. The performance of the classifiers was assessed using confusion matrix attributes and some derived performance measures including recall, specificity, balanced accuracy, precision, F-score and Matthew’s correlation coefficient. Using the best selected features sets, Linear SVM and Kernel SVM achieved an F-Score of 97.06 and 98.05 respectively

Identification of an enhancer that increases miR-200b~200a~429 gene expression in breast cancer cells

The miR-200b~200a~429 gene cluster is a key regulator of EMT and cancer metastasis, however the transcription-based mechanisms controlling its expression during this process are not well understood. We have analyzed the miR-200b~200a~429 locus for epigenetic modifications in breast epithelial and mesenchymal cell lines using chromatin immunoprecipitation assays and DNA methylation analysis. We discovered a novel enhancer located approximately 5.1kb upstream of the miR-200b~200a~429 transcriptional start site. This region was associated with the active enhancer chromatin signature comprising H3K4me1, H3K27ac, RNA polymerase II and CpG dinucleotide hypomethylation. Luciferase reporter assays revealed the upstream enhancer stimulated the transcription of the miR-200b~200a~429 minimal promoter region approximately 27-fold in breast epithelial cells. Furthermore, we found that a region of the enhancer was transcribed, producing a short, GC-rich, mainly nuclear, non-polyadenylated RNA transcript designated miR-200b eRNA. Over-expression of miR-200b eRNA had little effect on miR-200b~200a~429 promoter activity and its production did not correlate with miR-200b~200a~429 gene expression. While additional investigations of miR-200b eRNA function will be necessary, it is possible that miR-200b eRNA may be involved in the regulation of miR-200b~200a~429 gene expression and silencing. Taken together, these findings reveal the presence of a novel enhancer, which contributes to miR-200b~200a~429 transcriptional regulation in epithelial cells.Joanne L. Attema, Andrew G. Bert, Yat-Yuen Lim, Natasha Kolesnikoff, David M. Lawrence, Katherine A. Pillman, Eric Smith, Paul A. Drew, Yeesim Khew-Goodall, Frances Shannon, Gregory J. Goodal

Age-related sensitivity to lung oxidative stress during ozone exposure

As immature and aged rats could be more sensitive to ozone (O3)-linked lung oxidative stress we have attempted to shed more light on age-related susceptibility to O3 with focusing our interest on lung mitochondrial respiration, reactive oxygen species (ROS) production and lung pro/antioxidant status. For this purpose, we exposed to fresh air or O3 (500 ppb 12 h per day, for 7 days) 3 week- (immature), 6 month- (adult) and 20 month-old rats (aged). We determined, in lung, H2O2 release by mitochondria, activities of major antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT)], heat shock protein (HSP72) content and 8-oxodG and dG-HNE nDNA contents, as DNA oxidative damage markers. In adult rats we did not observe alteration of pro/antioxidant status. In contrast to adults, immature rats exposed to O3 higher nDNA 8-oxodG content and HSP72 and without antioxidant enzymes modification. Aged rats displayed mild uncoupled lung mitochondria, increased SOD and GPx activities, and higher 8-oxodG content after O3 exposure. Thus, in contrast to adults, immature and aged rats displayed lung oxidative stress after O3 exposure. Higher sensitivity of immature to O3 was partly related to ventilatory parameters and to the absence of antioxidant enzyme response. In aged rats, the increase in cytosolic SOD and GPx activities during O3 exposure was not sufficient to prevent the impairment in mitochondrial function and accumulation in lung 8- oxodG. Finally, we showed that mitochondria seem not to be a major source of ROS under O3 exposur