Purpose To investigate the role and related mechanisms of miR-106a in sepsis-induced AKI. Methods Serum from sepsis and healthy patients was collected, sepsis mouse model was established by cecal ligation and puncture (CLP). TCMK-1 cells were treated with lipopolysaccharide (LPS) and transfected with THBS2-small interfering RNA (siTHBS2), miR-106a inhibitor, miR-106a mimics and their negative controls (NCs). The expression of miR-106a, thrombospondin 2 (THBS2), Bax, cleaved caspase-3 and Bcl-2, cell viability, relative caspase-3 activity and TNF-α, IL-1β, IL-6 content were respectively detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Cell Counting Kit-8 (CCK-8) and enzyme linked immunosorbent assay (ELISA). The relationship between miR-106a and THBS2 was confirmed by dual luciferase reporter assay. Results MiR-106a was up-regulated in serum of sepsis patients, CLP-induced mice models and LPS-induced TCMK-1 cells. LPS reduced cell viability and Bcl-2 expression, and increased caspase-3 activity, Bax expression, the content of TNF-α, IL-1β, IL-6. THBS2 was a target of miR-106a. The decreases of caspase-3 activity, TNF-α, IL-1β, IL-6, Bax expression and the increases of cell viability, Bcl-2 expression caused by miR-106a knockdown were reversed when THBS2 silencing in LPS-stimulated TCMK-1 cells. Conclusion MiR-106a aggravated LPS-induced inflammation and apoptosis of TCMK-1 cells via regulating THBS2 expression.

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Spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disease caused by a heterozygous CAG repeat expansion in the ataxin 3 gene ( ATXN3). However, patients with homozygous SCA3 carrying expanded CAG repeats in both alleles of ATXN3 are extremely rare. Herein, we present a case of a 50-year-old female who had homozygous SCA3 with expansion of 62/62 repeats. Segregation analysis of the patient’s family showed both a contraction pattern of CAG repeat length and stable transmission. The present case demonstrated an earlier onset and more severe clinical phenotype than that seen in heterozygous individuals, suggesting that the gene dosage enhances disease severity.

Objective Acute Exacerbation Chronic Obstructive Pulmonary Disease (AECOPD) is associated with an acute worsening of respiratory symptoms that have effects on lung function, quality of life and health economic burden. In addition, the development of pulmonary infections is a common complication of Chronic Obstructive Pulmonary Disease (COPD). In the pathophysiology of AECOPD, interleukin (IL)-6 is a pleiotropic cytokine that can be produced by inflammatory and primary lung epithelial cells in response to a variety of different stimuli. We aim to investigate the correlation between serum cytokine levels and AECOPD with pulmonary infection. Methods 37 AECOPD patients diagnosed with pulmonary infection and 33 patients diagnosed with AECOPD only were selected. All COPD patients were diagnosed according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria. Serum samples for C-reactive protein (CRP) and cytokines were obtained from the patients immediately after admission. Serum concentrations of cytokines were measured using a fluorescent bead immunoassay on a flow cytometer. Logistic regression was used to identify risk factors for AECOPD co-infection of the lungs. Results Serum characterization of our cohort showed patients with AECOPD and pulmonary infection had higher levels of IL-6 and IL-10 compared with the AECOPD group, and IL-6 was independently associated with AECOPD with pulmonary infection. ROC curve analysis showed that IL-6 was a useful predictor of the incidence of pulmonary infection in AECOPD patients. Conclusions Our findings highlight the role of IL-6 in the pathogenesis of AECOPD with pulmonary infection.