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 levels of IL-18,IL-10 and MMP-9 in coronary heart disease(CAD)patients with in-stent restenosis(ISR)after percutaneous coronary intervention (PCI)treatment,so as to discuss the influence of inflammatory fac-tors to ISR after PCI.Methods CAD patients with ISR after PCI were angiographically re-evaluated and formed the ISR group(n=68)and the non-ISR group(n=173)based on the presence or absence of ISR.109 subjects without angiographic evidence of CAD formed a reference control group(control group).The plasma IL-18,IL-10 and MMP-9 concentrations of subjects were measured. Results The concentrations of serum IL-18 and MMP-9 in ISR group and non-ISR group were significantly higher than control group,while IL-10 level was the opposite.Contrasted with non-ISR group,the concentrations of serum IL-18 and MMP-9 in ISR group were significantly higher,but IL-10 level was the opposite too.There were significantly statistical differences(P <0.05)Con-clusion There is significant correlation between ISR and serum levels of IL-18,IL-10 and MMP-9.The inflammation may have im-portant impact on the process of ISR.

Myocardial infarction promotes cardiac remodeling and myocardial fibrosis, thus leading to cardiac dysfunction or heart failure. Peiminine has been regarded as a traditional anti-fibrotic Chinese medicine in pulmonary fibrosis. However, the role of peiminine in myocardial infarction-induced myocardial injury and fibrosis remained elusive. Firstly, rat model of myocardial infarction was established using ligation of the left coronary artery, which were then intraperitoneally injected with 2 or 5 mg/kg peiminine once a day for 4 weeks. Echocardiography and haemodynamic evaluation results showed that peiminine treatment reduced left ventricular end-diastolic pressure, and enhanced maximum rate of increase/decrease of left ventricle pressure (± dP/dt max) and left ventricular systolic pressure, which ameliorate the cardiac function. Secondly, myocardial infarction-induced myocardial injury and infarct size were also attenuated by peiminine. Moreover, peiminine inhibited myocardial infarction-induced increase of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α production, as well as the myocardial cell apoptosis, in the rats. Thirdly, peiminine also decreased the myocardial fibrosis related protein expression including collagen I and collagen III. Lastly, peiminine reduced the expression of p38 and phosphorylation of extracellular signal-regulated kinase 1/2 in rat model of myocardial infarction. In conclusion, peiminine has a cardioprotective effect against myocardial infarction-induced myocardial injury and fibrosis, which can be attributed to the inactivation of mitogen-activated protein kinase pathway.

OBJECTIVETo explore the efficacy and safety of deferasirox in aplastic anemia (AA)patients with iron overload.

METHODSA single arm, multi- center, prospective, open- label study was conducted to evaluate absolute change in serum ferritin (SF)from baseline to 12 months of deferasirox administration, initially at a dose of 20 mg·kg(-1)·d(-1), and the safety in 64 AA patients with iron overload.

RESULTSAll patients started their deferasirox treatment with a daily dose of 20 mg · kg(-1) ·d(-1). The mean actual dose was (18.6±3.60) mg · kg(-1)·d(-1). The median SF decreased from 4 924 (2 718- 6 765)μg/L at baseline (n=64) to 3 036 (1 474- 5 551)μg/L at 12 months (n=23) with the percentage change from baseline as 38%. A median SF decrease of 651 (126-2 125)μg/L was observed at the end of study in 23 patients who completed 12 months' treatment, the median SF level decreased by 1 167(580-4 806)μg/L [5 271(3 420-8 278)μg/L at baseline; 3 036(1 474-5 551)μg/L after 12 months' treatment; the percentage change from baseline as 42% ] after 12 months of deferasirox treatment. The most common adverse events (AEs) were increased serum creatinine levels (40.98%), gastrointestinal discomfort (40.98%), elevated liver transaminase (ALT: 21.31%; AST: 13.11%)and proteinuria (24.59%). The increased serum creatinine levels were reversible and non-progressive. Of 38 patients with concomitant cyclosporine use, 12(31.8%)patients had two consecutive values >ULN, 10(26.3%)patients had two consecutive values >1.33 baseline values, but only 1(2.6%)patient's serum creatinine increased more than 1.33 baseline values and exceeded ULN. For both AST and ALT, no patients experienced two post- baseline values >5 ×ULN or >10 × ULN during the whole study. In AA patients with low baseline PLT count (less than 50 × 10(9)/L), there was no decrease for median PLT level during 12 months' treatment period.

CONCLUSIONSAA patients with iron overload could achieve satisfactory efficacy of iron chelation by deferasirox treatment. The drug was well tolerated with a clinically manageable safety profile and no major adverse events.

Anemia, Aplastic ; drug therapy ; Benzoates ; therapeutic use ; Blood Transfusion ; China ; Ferritins ; blood ; Humans ; Iron ; blood ; Iron Chelating Agents ; therapeutic use ; Iron Overload ; drug therapy ; Liver ; Prospective Studies ; Triazoles ; therapeutic use

In the original publication the bands in Fig. 1J and Fig. 2B were not visible. The correct versions of Fig. 1J and Fig. 2B are provided in this correction.