Girija Goyal

TL;DR: Use of the mechanical actuation functionalities of microfluidic organ-on-a-chip (organ chip) cell culture technology revealed a previously unknown sensitivity of lung cancer cell growth, invasion, and TKI therapeutic responses to physical cues associated with breathing motions, which appear to be mediated by changes in signaling through epidermal growth factor receptor (EGFR) and MET protein kinase.

TL;DR: In this paper, a microfluidic bronchial-airway-on-a-chip line was used to model the human airway epithelium and pulmonary endothelium to model viral infection, strain-dependent virulence, cytokine production and the recruitment of circulating immune cells.

TL;DR: It is found that IAP antagonists can augment human and mouse T cell responses to physiologically relevant stimuli and suggest that targeting IAPs using small molecule antagonists may be a strategy for developing novel immunomodulating therapies against cancer.

TL;DR: Human organ-on-a-chip (Organ Chip) microfluidic culture devices lined by a highly differentiated, primary, human lung airway epithelium cultured under an air-liquid interface and fed by continuous medium flow can be used to model virus entry, replication, strain-dependent virulence, host cytokine production, and recruitment of circulating immune cells in response to infection by influenza.

TL;DR: Evidence is presented that Rv1818c-induced apoptotic signaling is likely regulated in part by the Smac-dependent activation of caspases in T cells, anddepleting cellular pools of the mitochondrial protein Smac/DIABLO substantially reduces apoptosis consistent with mitochondrial involvement in this death pathway.