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Background: Atrial fibrillation is a well-documented complication following cardiac surgery. It is associated with increased inpatient and long-term mortality. There have been few prior studies on perioperative atrial fibrillation following burn surgery in severely burned patients. The purpose of this study was to identify the incidence, predictors, and prognosis of perioperative atrial fibrillation after burn surgery in severely burned patients.Methods: Patients aged older than 18 years with 30% burned total body surface area (TBSA) were enrolled in this study. Patients who had a previous history of atrial fibrillation or atrial fibrillation on the preoperative electrocardiogram were excluded. We reviewed medical records retrospectively, and the data of 214 patients were studied.Results: A total of 214 critically ill burned patients and 1132 operations were available for analysis during the 5-year study period; 12 (1.1%) patients were diagnosed with newly developed atrial fibrillation after a burn operation, of whom 4 patients showed paroxysmal atrial fibrillation (all related to surgical stimulation) and none changed to persistent atrial fibrillation. The incidence of perioperative atrial fibrillation was associated with TBSA%, full-thickness TBSA%, and hypertension. Multiple logistic regression analysis indicated that TBSA% (OR=13.851, P < 0.001) and full-thickness TBSA% (OR=15.223, P = 0.018) were independent predictors for developing perioperative atrial fibrillation. All of our patients had at least one risk factor, with blood volume variation or burn sepsis occurring most commonly. Perioperative atrial fibrillation developed after a median of 0 days after burn surgery. Three patients died, and the causes of death were noncardiovascular events such as sepsis and multiple organ failure.Conclusion: Atrial fibrillation was a relatively rare complication among severely burned patients admitted to surgery and was associated with TBSA% and full thickness TBSA%. All of our patients exhibited at least one of the modifiable risk factors for atrial fibrillation, confirming the importance of optimization of electrolytes and fluid status and limitation of sympathetic activation. [ABSTRACT FROM AUTHOR]

Abstract: Icaritin is a native compound from Epimedium Genus, a traditional Chinese herbal medicine which is effective in treating asthma, autoimmune diseases and viral infections. In the present paper, the immunosuppressive effects of icaritin were found through in vitro and in vivo studies. Icaritin could dose-dependently inhibit murine CD4+ T cells proliferation stimulated with mitogens or specific antigen ovabumin (OVA). Icaritin at 0.25–25μM could down-regulate T cell activation marker CD25 expression and inhibit IL-2 production. It could also reduce the Th1 cytokine IFN-γ production significantly if the T cells were activated by ConA or anti-CD3; while the inhibition of IL-4 secretion was only seen on anti-CD3 activated T cells treated with low concentrations of icaritin. In vivo study showed that treatment of icaritin at 10mg/kg/day on mice could suppress the immune response with prolonged allograft skin survival. Further study demonstrated that it reduced the alloantigen-induced splenocytes proliferation and Th1/Th2 cytokines. It could also increase NF-AT luciferase activity in Jurkat-NF-AT-luc T cells. The above results suggested that icaritin might be used to treat Th1 dominated immune diseases by interfering T cells activation with mechanism different to CsA. [Copyright &y& Elsevier]

Abstract: To elucidate the effects of particle size and surface charge on cellular uptake and biodistribution of polymeric nanoparticles (NPs), rhodamine B (RhB) labeled carboxymethyl chitosan grafted NPs (RhB-CMCNP) and chitosan hydrochloride grafted NPs (RhB-CHNP) were developed as the model negatively and positively charged polymeric NPs, respectively. These NPs owned well defined particle sizes (150–500 nm) and Zeta potentials (−40 mV – +35 mV). FITC labeled protamine sulfate (FITC-PS) loaded RhB-CMCNP and camptothecin (CPT) loaded RhB-CHNP with high encapsulation efficiency were prepared. The fluorescence stability in plasma and towards I− was investigated, and the result indicated it was sufficient for qualitative and quantitative analysis. NPs with high surface charge and large particle size were phagocytized more efficiently by murine macrophage. Slight particle size and surface charge differences and different cell lines had significant implications in the cellular uptake of NPs, and various mechanisms were involved in the uptake process. In vivo biodistribution suggested that NPs with slight negative charges and particle size of 150 nm were tended to accumulate in tumor more efficiently. These results could serve as a guideline in the rational design of drug nanocarriers with maximized therapeutic efficacy and predictable in vivo properties, in which the control of particle size and surface charge was of significance. [Copyright &y& Elsevier]

Background & Aims: Hepatocyte-like cells can be derived from pluripotent stem cells such as embryonic stem (ES) cells, but ES cell-derived hepatic cells with extensive capacity to repopulate liver have not been identified. We aimed to identify and purify ES cell-derived hepatoblast-like progenitor cells and to explore their capacity for liver repopulation in mice after in vitro expansion. Methods: Unmanipulated mouse ES cells were cultured under defined conditions and allowed to undergo stepwise hepatic differentiation. The derived hepatic cells were examined by morphologic, fluorescence-activated cell sorting, gene expression, and clonal expansion analyses. The capacities of ES cell-derived hepatic progenitor cells to repopulate liver were investigated in mice that were deficient in fumarylacetoacetate hydrolase (Fah) (a model of liver injury). Results: Mouse ES cells were induced to differentiate into a population that contained hepatic progenitor cells; this population included cells that expressed epithelial cell adhesion molecule (EpCAM) but did not express c-Kit. Clonal hepatic progenitors that arose from single c-Kit−EpCAM+ cells could undergo long-term expansion and maintain hepatoblast-like characteristics. Enriched c-Kit−EpCAM+ cells and clonally expanded hepatic progenitor cells repopulated the livers of Fah-deficient mice without inducing tumorigenesis. Conclusions: ES cell-derived c-Kit−EpCAM+ cells contain a population of hepatoblast-like progenitor cells that can repopulate livers of mice. [ABSTRACT FROM AUTHOR]

A thin porous film inorganic-organic heterostructure photocathode has been successfully fabricated and applied in photoelectrochemical (PEC) water splitting. Our work optimized the best structure of CuBi 2 O 4 (CBO) base on FTO (fluorine doped tin oxide). Furthermore, it was passivated with polythiophene (PTh), a kind of conducting polymers of excellent environmental and thermal stability, to decrease the capture ability of surface state for photogenerated charge. Benefiting from the high light capture rate of porous structure of CBO and low electron-hole recombination rate of CBO/PTh heterojunctions, the as-fabricated FTO/CBO/PTh electrode delivers excellent PEC performance with a ultimate photocurrent density of 0.41 mA cm −2 at 0.3 V vs RHE (reversible hydrogen electrode) doubled to that of pure FTO/CBO electrode, which would be due to the significantly improved light absorption and rapid separation efficiency. [ABSTRACT FROM AUTHOR]

Objective GTS-21, a selective α7 nicotinic acetylcholine receptor agonist, has recently been established as a promising treatment for inflammation. However, the detailed molecular mechanism of GTS-21 in suppressing pro-inflammatory cytokine production is only partially explored. The study aimed to analyze cytokine expression suppressed by GTS-21 with lipopolysaccharide (LPS)-induced inflammation in vitro and to gain insights into the role of Akt/NF-κB signaling pathway in this process. Materials and methods Cell Counting Kit-8 (CCK-8) assay was performed to detect drug cytotoxicity. RAW 264.7 cells were stimulated with LPS and treated with GTS-21. Interleukin (IL)-1β, IL-6, or tumor necrosis factor (TNF)-α production was detected using enzyme-linked immunosorbent assay. Western blot was used to assess the expression patterns of signal transduction protein. Nuclear translocation of nuclear factor (NF)-κB was analyzed by confocal fluorescence microscopy. In addition, α7 nicotinic acetylcholine receptors (α7 nAChR) were detected on RAW264.7, and the α7 nAChR-specific antagonist was adopted to verify whether the effect of GTS-21 was mediated by α7 nAChR. Results The CCK-8 assay showed that GTS-21 did not significantly affect cell proliferation. The production of IL-1β, IL-6, and TNF-α decreased after being treated with GTS-21 in LPS-stimulated RAW 264.7 cells. GTS-21 also suppressed LPS-induced phosphorylation of NF-κBp65, IKKα/β, IκBα, and Akt, as well as NF-κB p65 nuclear translocation. Moreover, α7 nAChR was expressed on the surfaces of RAW264.7 cells, and the α7 nAChR-specific antagonist almost completely prohibited the inhibitory effect of GTS-21 on NF-κB activation. Conclusion These findings indicate that GTS-21 suppresses LPS-induced inflammation by inhibiting the Akt/NF-κB signal pathway through α7 nAChR. GTS-21 has a potential application in inflammatory disease therapy. [ABSTRACT FROM AUTHOR]

Abstract: The abnormal proliferation and polarization of Th17/Th1 subsets are believed to contribute to the progression of multiple sclerosis. We demonstrated that neural stem cells (NSCs) could inhibit CD4+T cells from mice of experimental autoimmune encephalomyelitis to proliferate and polarize into Th17 but promote their apoptosis and to generate regulatory T cells in response to myelin antigen via releasing prostaglandin E2 by activated Th1-derived IFN-γ. The study indicated that NSCs play a negatively regulatory role in T cell responses and provided novel evidence for the therapeutic mechanisms underlying the usage of NSCs to treat autoimmune diseases of central nervous system. [Copyright &y& Elsevier]

Peripheral nerve injury (PNI) is encountered relatively commonly in the clinic and often results in long-term functional deficits. Research to develop methods to improve regeneration following nerve injury is ongoing. Numerous studies have shown that adipose-derived stem cells (ADSCs) promote the regeneration of peripheral nerve injury; however, the mechanism is unclear. Autophagy, a highly conserved intracellular process responsible for maintaining cellular homeostasis, and Schwann cells (SCs), play important roles in regeneration after PNI. In the present study, we explored the effect and mechanism of exosomes produced by adipose-derived stem cells (ADSC-Exos) on autophagy of SCs in PNI, as well as their effect on the regeneration of the nerve myelin sheath. The levels of autophagy and the expression of karyopherin subunit alpha 2 (Kpna2) in SCs increased markedly after the sciatic nerve was injured in SCs (SNI-SCs). The enhanced autophagy and the upregulated Kpna2 in SNI-SCs were inhibited after treatment with ADSC-Exos in vivo and in vitro. The effect of ADSC-Exos on inhibiting SC autophagy was blocked by overexpression of Kpna2 in SNI-SCs. Using quantitative real-time reverse transcription PCR, ADSC-Exos were demonstrated to contain a large amount of miRNA-26b, which was predicted to regulate Kpna2 on the TargetScan website. The effect of ADSC-Exos on inhibiting SCs autophagy was blocked after the silencing of miRNA-26b. Moreover, ADSC-Exos promoted the regeneration of the myelin sheath by inhibiting SC autophagy in rat SNI models. In conclusion, our results indicated that ADSC-Exos promote the regeneration of the myelin sheath by moderately reducing autophagy of injured SCs via miRNA-26b downregulation of Kpna2. [ABSTRACT FROM AUTHOR]