Hou X.,Capital Medical University |
Hou X.,Beijing Institute of Heart Lung and Blood Vessel Diseases |
Yang X.,Capital Medical University |
Yang X.,Beijing Institute of Heart Lung and Blood Vessel Diseases |
And 20 more authors.
Introduction: Differential hypoxia is a pivotal problem in patients with femoral veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) support. Despite recognition of differential hypoxia and attempts to deliver more oxygenated blood to the upper body, the mechanism of differential hypoxia as well as prevention strategies have not been well investigated. Methods: We used a sheep model of acute respiratory failure that was supported with femoral VA ECMO from the inferior vena cava to the femoral artery (IVC-FA), ECMO from the superior vena cava to the FA (SVC-FA), ECMO from the IVC to the carotid artery (IVC-CA) and ECMO with an additional return cannula to the internal jugular vein based on the femoral VA ECMO (FA-IJV). Angiography and blood gas analyses were performed. Results: With IVC-FA, blood oxygen saturation (SO2) of the IVC (83.6 ± 0.8%) was higher than that of the SVC (40.3 ± 1.0%). Oxygen-rich blood was drained back to the ECMO circuit and poorly oxygenated blood in the SVC entered the right atrium (RA). SVC-FA achieved oxygen-rich blood return from the IVC to the RA without shifting the arterial cannulation. Subsequently, SO2 of the SVC and the pulmonary artery increased (70.4 ± 1.0% and 73.4 ± 1.1%, respectively). Compared with IVC-FA, a lesser difference in venous oxygen return and attenuated differential hypoxia were observed with IVC-CA and FA-IJV. Conclusions: Differential venous oxygen return is a key factor in the etiology of differential hypoxia in VA ECMO. With knowledge of this mechanism, we can apply better cannula configurations in clinical practice. © 2015 Hou et al. Source
Liu H.,Capital Medical University |
Zhang H.,Capital Medical University |
Zhang H.,Peking University |
Wan G.,Capital Medical University |
And 5 more authors.
Journal of Viral Hepatitis
Summary Acute-on-chronic hepatitis B liver failure (ACHBLF) has a poor prognosis in patients with hepatitis B virus infection. The role of the neutrophil-lymphocyte ratio (NLR), which reflects the inflammatory status of the patient before treatment, has never been studied in this setting. To investigate the predictive value of NLR in patients with ACHBLF, a retrospective cohort with 216 patients and a prospective validation cohort with 73 patients were recruited. Multivariate analyses showed that total bilirubin (TBIL), NLR, age and model for end-stage liver disease (MELD) score had prognostic significance for survival. Both NLR (0.781) and MELD score (0.744) had higher ROC curves, which differed significantly from those for age (0.615) and TBIL (0.691), but not from each other (P = 0.94). NLR ≤2.36 predicted lower mortality (with 91.6% sensitivity and 86.0% negative predictive value), and NLR >6.12 was a warning sign for higher mortality risk (with 90.1% specificity and 80.3% positive predictive value). These results demonstrated that pretreatment NLR was associated with the prognosis of patients with ACHBLF, and elevated NLR predicted poor outcome within 8 weeks. We suggest that NLR cut-offs of ≤2.36 and >6.12 are powerful markers for predicting mortality in ACHBLF. © 2013 John Wiley & Sons Ltd. Source
Kong Y.,Capital Medical University |
Kong Y.,Beijing Key Laboratory of Emerging Infectious Diseases |
Wang H.,Peking University |
Wang S.,Peking University |
Tang N.,Peking University
FTY720 is a novel immunosuppressant that modulates sphingosine 1-phosphate (S1P) receptors for the treatment of several diseases. Several hallmarks of liver fibrosis are influenced by S1P, and the interference of S1P signaling by treatment with FTY720 results in beneficial effects in various animal models of fibrosis. However, whether these treatment strategies suppress liver fibrosis progression is incompletely understood. Here, we investigated the effects and mechanisms by which FTY720 improves liver fibrosis in the carbon tetrachloride (CCl4)-induced mouse model. FTY720 treatment significantly attenuated the expression of fibrotic markers in the injured liver of both wild-type and SCID-beige mice. The migration of bone marrow-derived mesenchymal stem cells (BMSCs) to circulation, and subsequently the injured liver, was suppressed by FTY720. Furthermore, in vitro, phosphorylated-FTY720 blocked the migration of BMSCs mediated by S1P. Thus, FTY720 is an effective therapy for liver fibrosis via the suppression of BMSC migration in the CCl4-induced mouse model. © 2014 Springer Science+Business Media. Source
Fan X.,Capital Medical University |
Fan X.,Beijing Key Laboratory of Emerging Infectious Diseases |
Chuan S.,Capital Medical University |
Chuan S.,Beijing Key Laboratory of Emerging Infectious Diseases |
And 2 more authors.
It was reported that O glycosylation is associated with hepatic stellate cell activation and regulates collagen expression. In this study, we aimed to investigate the effect of O glycosylation on the activation of human hepatic stellate cells. We found that the inhibitor of O glycosylation, benzyl-α-GalNAc (2 and 4 mM), could significantly inhibit cells proliferation in a dose-dependent manner. Moreover, benzyl-α-GalNAc decreased the expressions of α-smooth muscle actin, collagen I, and collagen III. The results indicate that O glycosylation is involved in the activation of hepatic stellate cells. © 2013 Springer Science+Business Media New York. Source
He Y.,Central South University |
Bei J.,Capital Medical University |
Bei J.,Beijing Key Laboratory of Emerging Infectious Diseases |
Zeng H.,Capital Medical University |
And 2 more authors.
Purpose: To explore the effects of adoptive transferring sepsis induced myeloid-derived suppressor cells (iMDSCs) in mice corneal, skin, and combined corneal-skin survival. Methods: Allogeneic full-thickness corneal transplantation, fully mismatched skin transplantation, and corneal-skin combined transplantation (donor C57BL/6 to recipient Balb/c mice) were performed. Sepsis-induced infectious-MDSCs (iMDSCs), were purified from bone marrow of cecal ligated and punctured (CLP) Balb/c mice. Recipient-derived iMDSCs were adoptively transferred into different recipient groups by retro-orbital injection after surgeries. Corneal and skin grafts were examined and photographed routinely for a period of 45 days. Histopathology was performed to evaluate corneal-graft inflammation. Bone marrow and/or corneal grafts in each group were harvested from executed recipients on postoperative days 15, 25, 35. Corneal cells and bone marrow cells were stained with CD11b-PE and Gr1-FITC, analyzed by FACS. Results: iMDSCs were able to significantly prolong allograft survival in both corneal and corneal-skin combined transplant groups. A substantial expansion of MDSCs was observed in recipients' bone marrow, particularly in combined groups at an early stage postoperatively, and accordingly the concentration of MDSCs in corneal grafts increased significantly in adoptive transferred groups. Conclusions: Sepsis-induced MDSCs may suggest a novel cellular therapeutic approach for preventing various types of allograft rejection. © 2015 Elsevier B.V.. Source