Objective To evaluate the role of MSCT in diagnosing Cantrell syndrome.Methods Five patients with Cantrell syndrome were enrolled in this study retrospectively.All clinical data,especially imaging data were collected at enrolment.Maximum intensity projection(MIP),multi planar reconstruction(MPR)and volume rendering(VR)of the analysis method of MSCT were used to describe the characteristics of Cantrell syndrome.Results The age of 5 patients ranged from 2 days to 24 years,4(4/5)cases were Cantrell syndrome and 1(1/5)case was incomplete Cantrell syndrome,3(3/5)cases were confirmed by surgery.Five cases were all diagnosed as ectocardia,thoracocyllosis,pericardium defect and diaphragm defect with MSCT.Four had sternum dysplasia,abdominal wall defect, 3 had ventricular diverticulum,2 had umbilical hernia.Conclusion MSCT can be used in accurately diagnosing Cantrell syndrome in clinical work.

Objective:To study the effects of beta tricalcium phosphate(β-TCP)/collagen scaffold loaded with human bone morphogenetic protein 2 (hBMP2) plasmid on the osteogenesis ability of MC3T3-E1 cells.Methods:hBMP2 DNA plasmid-modified β-TCP/collagen scaffold and the naked plasmid(control) were constructed.MC3T3-E1 cells were respectively in vitro cultured onto the β-TCP/collagen scaffold with hBMP2(Z) and with control plasmid(Z0),on peace dish with the saffold and hBMP2(M) and with the control plasmid(M0).The surface morphology of the samples was observed by SEM.Osteogenesis of the cells was examined by alkaline phosphatase activity(ALP) test,real-time fluorescent quantitative PCR for the detection of Runx2,OCN,ALP and OPN mRNA expression.Data were statistically analyzed.Results:The composite sample surface of plasmid DNA containing hBMP2 modified β-TCP/collagen was porous;group Z and M showed highter ALP activity and higher mRNA expression of Runx2,OCN,ALP and OPN than group Z0 and M0;so did group Z than group M.Conclusion:Porous β-TCP/collagen scaffold loaded with BMP2 DNA is potential for osteoinduction.

Objective To evaluate the effect of hypothermic machine perfusion (HMP) on the expression levels of inflammatory cytokines in rat kidney. Methods Thirty male rats were randomly divided into the control (Control group), static cold storage group (SCS group) and HMP group, with 10 rats in each group. The velocity, intrarenal resistance and pH value of perfusion effluent were recorded during HMP. The expression levels of CXC chemokine ligand (CXCL)1, CXCL2, interferon (IFN)-β1, IFN-α4, CC chemokine ligand (CCL)2, CCL20, interleukin (IL)-17α, IL-17C and tumor necrosis factor (TNF)-α messenger RNA (mRNA) in renal tissues were evaluated by reverse transcription polymerase chain reaction (RT-PCR). Pathological changes of the kidney were observed by hematoxylin-eosin (HE) staining. Results During HMP, the velocity and intrarenal resistance remained stable, and the pH value of perfusion effluent was decreased slowly. RT-PCR showed that the relative expression levels of CXCL1, CXCL2, CCL2, CCL20, IL-17α, IL-17C and TNF-α mRNA in the SCS and HMP groups were higher compared with those in the Control group. Compared with the SCS group, the relative expression levels of CXCL1, CXCL2, CCL2, CCL20, IL-17α and TNF-α mRNA were up-regulated in the HMP group (all P<0.05). HE staining revealed that the morphology of renal cells was normal in the Control group, whereas evident epithelial necrosis, cytoplasmic vacuolation, brush border loss and epithelial shedding were observed in the SCS group. Compared with the SCS group, pathological changes in the HMP group were alleviated. Conclusions HMP may activate renal inflammation, and inhibiting the activation of inflammation during HMP is expected to further improve the effect of allograft preservation.

Macroautophagy (referred to as autophagy hereafter) is a major intracellular lysosomal degradation pathway that is responsible for the degradation of misfolded/damaged proteins and organelles. Previous studies showed that autophagy protects against acetaminophen (APAP)-induced injury (AILI) via selective removal of damaged mitochondria and APAP protein adducts. The lysosome is a critical organelle sitting at the end stage of autophagy for autophagic degradation via fusion with autophagosomes. In the present study, we showed that transcription factor EB (TFEB), a master transcription factor for lysosomal biogenesis, was impaired by APAP resulting in decreased lysosomal biogenesis in mouse livers. Genetic loss-of and gain-of function of hepatic TFEB exacerbated or protected against AILI, respectively. Mechanistically, overexpression of TFEB increased clearance of APAP protein adducts and mitochondria biogenesis as well as SQSTM1/p62-dependent non-canonical nuclear factor erythroid 2-related factor 2 (NRF2) activation to protect against AILI. We also performed an unbiased cell-based imaging high-throughput chemical screening on TFEB and identified a group of TFEB agonists. Among these agonists, salinomycin, an anticoccidial and antibacterial agent, activated TFEB and protected against AILI in mice. In conclusion, genetic and pharmacological activating TFEB may be a promising approach for protecting against AILI.