Twenty-one eyes of 13 patients with juvenile glaucoma confirmed by ocular tension, vision, eye ground and gonioscope underwent trabeculectomy combined with amniotic membrane transplantation. The posttransplant intraocular pressure significantly decreased compared to pretreatment (P

Objective To investigate new methods of osteonecrosis of femoral head (ONFH) with retrospective analysis of the clinical cases with technique of rotary cutting pressure-relief,impacted graft,and tantalum rod supporting treatment of early-stage femoral head necrosis.Methods From June 2010 to June 2014,32 cases (38 hips,23 males and 9 females) with ONFH were treated with technique of rotary cutting pressure-relief,impacted graft,and tantalum rod supporting,with the mean age of 24 ～ 52 (36.2 ± 3.8) years old.According to the Association Research Circulation Osseous (ARCO) classification,there were 11 hips on Ⅱ A stage,12 hips Ⅱ B,8 hips Ⅱ c,7 hips Ⅲ A.The averaged Harris score of all cases was 65 ～ 81 (72.5 ± 5.8) points.All cases were cured with minimally invasive technique,rotary cutter pressure-relief in femoral head,thoroughly remove sequestrum and implant allogeneic bone.Postoperative patients laid in bed for 1 month,after 1 month hold crutch gradually began to functional training.Postoperative 1 month,X ray film was reviewed every 3 months.According to the clinical symptoms,imaging findings,Harris scoring system was graded to evaluate the effectiveness.Results All the cases were followed up for average of 12 ～32 (20.2 ± 2.6) months,31 hips Kept hips succeed,hips pain; lame line symptoms were reduced or disappeared; x-ray showed femoral head necrosis area formed new bone,Harris scoring was upgraded to 75 ～ 95 (87.7 ± 6.4) points ; and seven hips failed with operation of total hip arthroplasty.The overall good rate was promoted from 26.3％ to 84.2％.Conclusions The technique treating for early-stagefemoral head necrosis with minimally invasive,rotary cutting pressure-relief,impacted graft,and tantalum rod supporting had a good short-term effects.

Object To define the optimal proportion of four ingredients in Danxintong (DXT). Methods Uniform design method combined with pharmacodynamics (Rat acute myocardial ischemia model was used in this study) was used. Results The optimal proportion and components of DXT (Composed of Rhizoma Chuanxiong, Rhizoma Cyperi, Borneolum Syntheticum, and paeonol) were 5∶ 1.7∶ 1.4∶ 4.4; DXT 138 mg/kg could obviously inhibit acute myocardial ischemia of rats induced by iso prenaline (Iso) and pituiturin (Pit). DXT has antimyocardial ischemia effects in preliminary experimental studies. Conclusion Uniform design method is an effective method to define the optimal proportion of ingredients in DXT;

Objective To investigate changes in coagulation function and inflammation levels during sepsis.Methods A rat model of sepsis was established using the multiple infection sepsis model(MIM)based on cecal ligation and puncture.Forty-eight male Sprague-Dawley rats were assigned randomly to the following groups:control group,sham group,4 h sepsis group,8 h sepsis group,12 h sepsis group,and 16 h sepsis group(n=8 per group).Inflammatory markers and coagulation-related indicators were measured by enzyme-linked immunosorbent assay and coagulation analysis.Results(1)Lipopolysaccharide(LPS)and interleukin-6(IL-6)levels were significantly higher in the model rats at all time points compared with the sham group(P＜0.001).LPS and IL-6 levels increased gradually with disease progression,with no further changes in LPS after 12 hours.(2)Prothrombin time(PT)was significantly prolonged in the middle and late stages of the sepsis model,starting from 8,compared with the sham group(P＜0.01).(3)Partially activated prothrombin time(APTT)time was significantly prolonged in the 8,12,and 16 h groups compared with the sham group(P＜0.05,P＜0.01).APTT gradually lengthened from 8 h,but approached control levels thereafter.(4)Fibrinogen(Fbg)content was significantly higher in all sepsis groups,except for the 8 h group,compared with the sham group(P＜0.01).(5)Fibrin degradation products(FDP)differed significantly between the control and sham groups(P＜0.01),but not between the sham and sepsis groups.(6)Antithrombin-Ⅲ(AT-Ⅲ)levels decreased significantly throughout each stage of sepsis progression compared with the sham group(P＜0.01),and AT-Ⅲ showed a downward trend with the course of disease,with significant differences among the 4,8,and 16 h groups.Conclusions The MIM rat model can reflect the development of inflammatory and blood coagulation disorders and their relationship during the course of sepsis,and may thus provide a good foundation for further research into the disease course of sepsis.

Inflammation-driven endothelial dysfunction is the major initiating factor in atherosclerosis, while the underlying mechanism remains elusive. Here, we report that the non-canonical stimulator of interferon genes (STING)-PKR-like ER kinase (PERK) pathway was significantly activated in both human and mice atherosclerotic arteries. Typically, STING activation leads to the activation of interferon regulatory factor 3 (IRF3) and nuclear factor-kappa B (NF-κB)/p65, thereby facilitating IFN signals and inflammation. In contrast, our study reveals the activated non-canonical STING-PERK pathway increases scaffold protein bromodomain protein 4 (BRD4) expression, which encourages the formation of super-enhancers on the proximal promoter regions of the proinflammatory cytokines, thereby enabling the transactivation of these cytokines by integrating activated IRF3 and NF-κB via a condensation process. Endothelium-specific STING and BRD4 deficiency significantly decreased the plaque area and inflammation. Mechanistically, this pathway is triggered by leaked mitochondrial DNA (mtDNA) via mitochondrial permeability transition pore (mPTP), formed by voltage-dependent anion channel 1 (VDAC1) oligomer interaction with oxidized mtDNA upon cholesterol oxidation stimulation. Especially, compared to macrophages, endothelial STING activation plays a more pronounced role in atherosclerosis. We propose a non-canonical STING-PERK pathway-dependent epigenetic paradigm in atherosclerosis that integrates IRF3, NF-κB and BRD4 in inflammatory responses, which provides emerging therapeutic modalities for vascular endothelial dysfunction.