Objective To study the value of reverse CT scan in eliminating the respiratory motion artifacts in the thoracic CT of the patients with chronic obstructive pulmonary diseases(COPD).Methods Fourty patients with COPD were randomly selected and underwent chest CT examinations with the technique of GR-Helical including directive and reverse CT scans.The images were blindly evaluated by three experienced doctors.Results In 40 cases,the respiratory motion artifacts were present in 17 cases,among them,70.59%(12/17) artifacts was in lower lung field,and 64.7%(11/17) artifacts occurred in the people over 60 years of age.The rate of artifact was 35% at directive scan,while it was reduced to 7.5% at reverse scan,the image quality was improved at 27.5%.There was statistical significance in eliminating respiratory motion artifacts between two scanning method (P＜0.05).Conclusion Reverse CT scanning can effectively eliminating or reducing the respiratory motion artifacts in lower lung field,it is the best choice of scanning mode in elderly patients with COPD.

Neurogenesis decline in hippocampal dentate gyrus (DG) participates in stress-induced depressive-like behaviors, but the underlying mechanism remains poorly understood. Here, we observed low-expression of NOD-like receptor family pyrin domain containing 6 (NLRP6) in hippocampus of stress-stimulated mice, being consistent with high corticosterone level. NLRP6 was found to be abundantly expressed in neural stem cells (NSCs) of DG. Both Nlrp6 knockout (Nlrp6^-/-) and NSC-conditional Nlrp6 knockout (Nlrp6CKO) mice were susceptible to stress, being more likely to develop depressive-like behaviors. Interestingly, NLRP6 was required for NSC proliferation in sustaining hippocampal neurogenesis and reinforcing stress resilience during growing up. Nlrp6 deficiency promoted esophageal cancer-related gene 4 (ECRG4) expression and caused mitochondrial dysfunction. Corticosterone as a stress factor significantly down-regulated NLRP6 expression, damaged mitochondrial function and suppressed cell proliferation in NSCs, which were blocked by Nlrp6 overexpression. ECRG4 knockdown reversed corticosterone-induced NSC mitochondrial function and cell proliferation disorders. Pioglitazone, a well-known clinical drug, up-regulated NLRP6 expression to inhibit ECRG4 expression in its protection against corticosterone-induced NSC mitochondrial dysfunction and proliferation restriction. In conclusion, this study demonstrates that NLRP6 is essential to maintain mitochondrial homeostasis and proliferation in NSCs, and identifies NLRP6 as a promising therapeutic target for hippocampal neurogenesis decline linked to depression.