The lamina cribrosa (LC) is a complicated collagenous meshwork of trabeculae and laminar pores contain capillaries, nerves and neurogliocytes, which provides structural and nutrient support to the retinal ganglion cell axons as they exit the eye. The intraocular pressure causes direct damage or deformation and remodeling of LC, leads to axoplaxmic transport and blood supply disturbance. The preponderance of evidence suggests that LC is the principal site of glaucomatous damage. The development of optic coherence tomography (OCT) technology has improved the imaging quality of deep structures of the optic nerve head and makes it possible to detect LC. The quantitative research indexes of LC structure include LC depth, laminar curvature, laminar thickness, prelaminar tissue, laminar pore, laminar defect and hemodynamics. To improve the understanding of LC structure, explore the characteristics of LC and understand the biomechanical and hemodynamic pathogenesis of glaucoma, which would be contribute to the application of big data research in the diagnosis and treatment of glaucoma.

Objective To investigate the role of outer membrane protein in clinical isolated car-bapenem resistance Acinetobacter baumannii. Methods Carbapenem resistance and sensitive strains were collected from the same patient. After MIST and REP-PCR analysis, carbapenemases were detected by isoe-lectric focusing. Different expressed membrane proteins were identified by two-dimension electrophoresis and mass spectrometry analysis. We also used efflux pump inhibitor PAβN(Phe-Arg-β-naphthylamide) to con-firm the phenotype. Results Carbapenem resistance and sensitive strains were attributed to the same pat-tern. At positions of P17.6 and P19.0, two β-lactamases were expressed in two investigated strains, no cabapenemases were detected. Six differential expressed membrane proteins were identified, a 34 × 10~3 membrane protein that was confirmed by efflux pump inhibitor PAβN experiment (imiponem MIC decreased from far above 32 μg/ml to 8μ/ml) and OprD and CarO. Conclusion Up-regulation of exported protein accompanied with down-regulation of OprD and CarO other than carbaponemases are responsible for carbap-enem resistance in A. baumannii.

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.