No abstract

Acute lung injury (ALI) is a respiratory disorder characterized by acute respiratory failure. circRNA mus musculus (mmu)-circ_0001679 was reported overexpressed in septic mouse models of ALI. Here the function of circ_0001679 in sepsis-induced ALI was investigated. In vitro models and animal models with ALI were, respectively, established in mouse lung epithelial (MLE)-12 cells and C57BL/6 mice. Pulmonary specimens were harvested for examination of the pathological changes. The pulmonary permeability was examined by wet-dry weight (W/D) ratio and lung permeability index. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in the bronchoalveolar lavage fluid (BALF), the lung tissues, and the supernatant of MLE-12 cells were measured by enzyme linked immunosorbent assay . Apoptosis was determined by flow cytometry. Bioinformatics analysis and luciferase reporter assay were used to assess the interactions between genes. We found that circ_0001679 was overexpressed in lipopolysaccharide (LPS)-stimulated MLE-12 cells. circ_0001679 knockdown suppressed apoptosis and proinflammatory cytokine production induced by LPS. Moreover, circ_0001679 bound to mmu-miR-338-3p and miR-338-3p targeted dual-specificity phosphatases 16 (DUSP16). DUSP16 overexpression reversed the effect of circ_0001679 knockdown in LPS-stimulated MLE-12 cells. Furthermore, circ_0001679 knockdown attenuated lung pathological changes, reduced pulmonary microvascular permeability, and suppressed inflammation in ALI mice. Overall, circ_0001679 knockdown inhibits sepsis-induced ALI progression through the miR-338-3p/DUSP16 axis.

No abstract

Identifying individuals with incipient Alzheimer’s disease (AD) are critical for early and targeted intervention before the dementia develops as AD progresses. Recently, emerging data have suggested that spatial navigation and neuroimaging could be utilized to identify individuals with prodromal AD. Compared to episodic memory, spatial navigation has fewer cultural and educational discrepancies and could serve as a promising marker for diagnosis and outcome measures in multicenter longitudinal studies with large cohorts. Furthermore, neuroimaging studies have contributed to our understanding of the structural and functional neural basis underlying spatial navigation and provided sensitive and non-invasive neuroimaging markers. The current review summarizes neuroimaging associations with spatial navigation impairment in the AD continuum, their potential pathophysiological mechanisms, and nonpharmacological interventions for spatial navigation impairments. We highlight the promising role of spatial navigation in the early identification of the preclinical and prodromal patients with potential risk of developing AD dementia. Multicenter large-scale longitudinal studies on patients across the AD continuum coupled with a standardized routine assessment of spatial navigation abilities in clinical settings are needed. This review may have implications for clinical practice and future research directions.