Purpose: To summarize and analyze the current evidence about surgical, oncological, and functional outcomes between laparoscopic partial nephrectomy (LPN) and open partial nephrectomy (OPN).Materials and Methods: Through a systematical search of multiple scientific databases in March 2020, we performed a systematic review and cumulative meta-analysis. Meanwhile, we assessed the quality of the relevant evidence according to the framework in the Cochrane Handbook for Systematic Reviews of Interventions.Results: A total of 26 studies with 8095 patients were included. There was no statistical difference between the LPN and OPN in the terms of operation time (p=0.13), intraoperative complications (p=0.94), recurrence (p=0.56), cancer-specific survival (p=0.72), disease-free survival (p=0.72), and variations of estimated glomerular filtration rate (p=0.31). The LPN group had significantly less estimated blood loss (P<0.00001), lower blood transfusion (p=0.04), shorter length of hospital stay (p<0.00001), lower total (p=0.03) and postoperative complications (p=0.02), higher positive surgical margin (p=0.005), higher overall survival (p<0.00001), and less increased serum creatinine (p=0.002). The subgroup analysis showed that no clinically meaningful differences were found for T1a tumors in terms of operation time (p=0.11) and positive surgical margin (p=0.23). In addition, the subgroup analysis also suggested that less estimated blood loss (p<0.0001) and shorter length of hospital stay (p<0.00001) were associated with the LPN group for T1a tumors.Conclusions: This meta-analysis revealed that the LPN is a feasible and safe alternative to the OPN with comparable surgical, oncologic, and functional outcomes. However, the results should be applied prudently in the clinic because of the low quality of evidence. Further quality studies are needed to evaluate the effectiveness LPN and its postoperative quality of life compared with OPN.

Background Zika virus (ZIKV) infection and ZIKV epidemic have been continuously spreading silently throughout the world and its associated microcephaly and other serious congenital neurological complications poses a significant global threat to public health. Type I interferon response to ZIKV infection in host cells suppresses viral replication by inducing the expression of interferon-stimulated genes (ISGs). Methods The study aims to demonstrate the anti-ZIKV mechanism of PARP11. PARP11 knock out and overexpressing A549 cell lines were constructed to evaluate the anti-ZIKV function of PARP11. PARP11−/−, PARP12−/− and PARP11−/−PARP12−/− HEK293T cell lines were constructed to explain the synergistic effect of PARP11 and PARP12 on NS1 and NS3 protein degradation. Western blotting, immunofluorescence and immunoprecipitation assay were performed to illustrate the interaction between PARP11 and PARP12. Results Both mRNA and protein levels of PARP11 were induced in WT but not IFNAR1−/− cells in response to IFNα or IFNβ stimulation and ZIKV infection. ZIKV replication was suppressed in cells expressed PARP11 but was enhanced in PARP11−/− cells. PARP11 suppressed ZIKV independently on itself PARP enzyme activity. PARP11 interacted with PARP12 and promoted PARP12-mediated ZIKV NS1 and NS3 protein degradation. Conclusion We identified ADP-ribosyltransferase PARP11 as an anti-ZIKV ISG and found that it cooperated with PARP12 to enhance ZIKV NS1 and NS3 protein degradation. Our findings have broadened the understanding of the anti-viral function of ADP-ribosyltransferase family members, and provided potential therapeutic targets against viral ZIKV infection.

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Highlights d HDAC3 deficiency impairs the antiviral immunity of macrophages in vivo and in vitro d HDAC3 interacts with FOXK1 and co-localizes at the promoters of STAT1 and STAT2 d HDAC3 and FOXK1 positively regulate the expression of STAT1/2 and downstream ISGs d HDAC3 is required for preventing FOXK1 from lysosomal degradation