Minimally Invasive versus Open Ureteral Reimplantation in Children: A Systematic Review and Meta-Analysis.

PURPOSE: We performed a systematic review and meta-analysis to compare the safety and efficacy of minimally invasive surgery (MIS) versus open ureteral reimplantation (OUR) in children. METHODS: Literature searches were conducted to identify studies that compared MIS (laparoscopic ureteral reimplantation or robot-assisted laparoscopic ureteral replantation) and OUR in children. Parameters such as operative time, blood loss, length of hospital stay, success rate, postoperative urinary tract infection (UTI), urinary retention, postoperative hematuria, wound infection, and overall postoperative complications were pooled and compared by meta-analysis. RESULTS: Among the 7,882 pediatric participants in the 14 studies, 852 received MIS, and 7,030 received OUR. When compared with the OUR, the MIS approach resulted in shorter hospital stays (I 2 = 99%, weighted mean difference [WMD] -2.82, 95% confidence interval [CI] -4.22 to -1.41; p < 0.001), less blood loss (I 2 = 100%, WMD -12.65, 95% CI -24.82 to -0.48; p = 0.04), and less wound infection (I 2 = 0%, odds ratio 0.23, 95% CI 0.06-0.78; p = 0.02). However, no significant difference was found in operative time and secondary outcomes such as postoperative UTI, urinary retention, postoperative hematuria, and overall postoperative complications. CONCLUSION: MIS is a safe, feasible, and effective surgical procedure in children when compared with OUR. Compared with OUR, MIS has a shorter hospital stay, less blood loss, and less wound infection. Furthermore, MIS is equivalent to OUR in terms of success rate and secondary outcomes such as postoperative UTI, urinary retention, postoperative hematuria, and overall postoperative complications. We conclude that MIS should be considered an acceptable option for pediatric ureteral reimplantation.

Hyperfibrinogenemia and hyponatremia as predictors of perforated appendicitis in children: A retrospective cohort study.

PURPOSE: The aim of this study was to investigate the predictive value of hyperfibrinogenemia and hyponatremia for perforated appendicitis in children. METHODS: A retrospective review of 521 pediatric patients (≤ 15 years) with acute appendicitis confirmed by histopathology from January 2017 to December 2020 was performed. Patients were divided in two groups, those with non-perforated (n = 379; 73%) and perforated appendicitis (n = 142; 27%). The serum values of sodium and fibrinogen were taken before surgery. We performed the receiver operating characteristic analysis for the two biochemical markers. The sensitivity, specificity, positive and negative predictive values for perforated appendicitis in the presence of hyponatremia and hyperfibrinogenemia were calculated. RESULTS: Hyperfibrinogenemia (≥ 4.0 g/L) was found in 58.45% of perforated appendicitis and 104 of 142 (73.34%) children with perforated appendicitis had hyponatremia (≤ 135 mmol/L). The perforated appendicitis group had a higher mean fibrinogen concentration (P = 0.001). There was a statistically significant difference in mean serum sodium levels between the perforated appendicitis and non-perforated appendicitis groups (P = 0.016). Receiver operating characteristic curve analysis for fibrinogen, sodium and combination of the both markers shown the combination had the largest area under the curve in identifying children with perforated acute appendicitis (0.858) (95% CI, 0.82-0.90) compared with fibrinogen (0.815) (95% CI, 0.77-0.86) and sodium 0.818 (95% CI, 0.78-0.86) alone. Furthermore, the combination of both markers had the best positive and negative predictive value for appendix perforation compared to fibrinogen and sodium. CONCLUSION: Hyponatremia and/or hyperfibrinogenemia are excellent markers for predicting perforated appendicitis in children. We propose that plasma sodium and/or fibrinogen concentrations be utilized as a supplementary to guide individual treatment decisions in children with appendicitis, such as surgery timing and nonoperative management options.

DDX1 from Cherry valley duck mediates signaling pathways and anti-NDRV activity.

Novel duck reovirus (NDRV) causes severe economic losses to the duck industry, which is characterized by hemorrhagic spots and necrotic foci of the livers and spleens. DEAD-box helicase 1 (DDX1) plays a critical role in the innate immune system against viral infection. However, the role of duck DDX1 (duDDX1) in anti-RNA virus infection, especially in the anti-NDRV infection, has yet to be elucidated. In the present study, the full-length cDNA of duDDX1 (2223 bp encode 740 amino acids) was firstly cloned from the spleen of healthy Cherry valley ducks, and the phylogenetic tree indicated that the duDDX1 has the closest relationship with Anas platyrhynchos in the bird branch. The duDDX1 mRNA was widely distributed in all tested tissues, especially in the duodenum, liver, and spleen. Overexpression of duDDX1 in primary duck embryo fibroblast (DEF) cells triggered the activation of transcription factors IRF-7 and NF-κB, as well as IFN-ß expression, and the expression of the Toll-like receptors (TLR2, TLR3, and TLR4) was significantly increased. Importantly, after overexpressing or knocking down duDDX1 and infecting NDRV in DEF cells, duDDX1 inhibits the replication of NDRV virus and also regulates the expression of pattern recognition receptors and cytokines. This indicates that duDDX1 may play an important role in the innate immune response of ducks to NDRV. Collectively, we first cloned DDX1 from ducks and analyzed its biological functions. Secondly, we proved that duck DDX1 participates in anti-NDRV infection, and innovated new ideas for the prevention and control of duck virus infection.

High-mobility group box 1 protein (HMGB1) from Cherry Valley duck mediates signaling pathways and antiviral activity.

High-mobility group box 1 protein (HMGB1) shows endogenous damage-associated molecular patterns (DAMPs) and is also an early warning protein that activates the body's innate immune system. Here, the full-length coding sequence of HMGB1 was cloned from the spleen of Cherry Valley duck and analyzed. We find that duck HMGB1(duHMGB1) is mostly located in the nucleus of duck embryo fibroblast (DEF) cells under normal conditions but released into the cytoplasm after lipopolysaccharide (LPS) stimulation. Knocking-down or overexpressing duHMGB1 had no effect on the baseline apoptosis rate of DEF cells. However, overexpression increased weakly apoptosis after LPS activation. In addition, overexpression strongly activated the IFN-I/IRF7 signaling pathway in DEF cells and significantly increased the transcriptional level of numerous pattern recognition receptors (PRRs), pro-inflammatory cytokines (IL-6, TNF-α), IFNs and antiviral molecules (OAS, PKR, Mx) starting from 48 h post-transfection. Overexpression of duHMGB1 strongly impacted duck virus replication, either by inhibiting it from the first stage of infection for novel duck reovirus (NDRV) and at late stage for duck Tembusu virus (DTMUV) or duck plague virus (DPV), or promoting replication at early stage for DTMUV and DPV infection. Importantly, data from duHMGB1 overexpression and knockdown experiments, time-dependent DEF cells transcriptional immune responses suggest that duHMGB1 and RIG-I receptor might cooperate to promote the expression of antiviral proteins after NDRV infection, as a potential mechanism of duHMGB1-mediated antiviral activity.