Background and purpose Radiomics can quantify tumor phenotype characteristics non-invasively by applying advanced imaging feature algorithms. In this study we assessed if pre-treatment radiomics data are able to predict pathological response after neoadjuvant chemoradiation in patients with locally advanced non-small cell lung cancer (NSCLC). Materials and Methods 127 NSCLC patients were included in this study. Fifteen radiomic features selected based on stability and variance were evaluated for its power to predict pathological response. Predictive power was evaluated using area under the curve (AUC). Conventional imaging features (tumor volume and diameter) were used for comparison. Results Seven features were predictive for pathologic gross residual disease (AUC > 0.6, p-value < 0.05), and one for pathologic complete response (AUC = 0.63, p-value = 0.01). No conventional imaging features were predictive (range AUC = 0.51–0.59, p-value > 0.05). Tumors that did not respond well to neoadjuvant chemoradiation were more likely to present rounder shape (spherical disproportionality, AUC = 0.63, p-value = 0.009) and heterogeneous texture (LoG 5 mm 3D - GLCM entropy, AUC = 0.61, p-value = 0.03). Conclusion We identified predictive radiomic features for pathological response, although no conventional features were significantly predictive. This study demonstrates that radiomics can provide valuable clinical information, and performed better than conventional imaging features.

Neuroinflammation is a response against harmful effects of diverse stimuli and participates in the pathogenesis of brain and spinal cord injury (SCI). The innate immune response plays a role in neuroinflammation following central nervous system (CNS) injury via activation of multi-protein complexes termed inflammasomes that regulate the activation of caspase-1 and the processing of the pro-inflammatory cytokines IL-1β and IL-18. We report here that the expression of components of the nucleotide-binding-and-oligomerization domain (NOD)-like receptor protein-1 (NLRP-1) inflammasome, apoptosis speck-like protein containing a caspase recruitment domain (ASC) and caspase-1 are significantly elevated in spinal cord motor neurons and cortical neurons after CNS trauma. Moreover, NLRP1 inflammasome proteins are present in exosomes derived from cerebrospinal fluid (CSF) of SCI and traumatic brain-injured patients following trauma. To investigate whether exosomes could be used to therapeutically block inflammasome activation in the CNS, exosomes were isolated from embryonic cortical neuronal cultures and loaded with short-interfering RNA (siRNA) against ASC and administered to spinal cord-injured animals. Neuronal-derived exosomes crossed the injured blood-spinal cord barrier, and delivered their cargo in vivo, resulting in knock down of ASC protein levels by approximately 76% when compared to SCI rats treated with scrambled siRNA. Surprisingly, siRNA silencing of ASC also led to a significant decrease in caspase-1 activation and processing of IL-1β after SCI. These findings indicate that exosome-mediated siRNA delivery may be a strong candidate to block inflammasome activation following CNS injury.