Clinicopathologic significance of LAIR-1 expression in hepatocellular carcinoma

Aim

Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is an immune inhibitory receptor which is expressed within most types of hematopoietic cells and negatively regulates immune responses. Recently, we found LAIR-1 expression to be present within tumors of nonhematopoietic lineages. However, the roles of LAIR-1 in hepatocellular carcinoma (HCC) have yet to be examined. The purpose of this study was to investigate the expression of LAIR-1 in HCC tissue and assess its clinical significance at this site.

髋臼螺钉对非骨水泥全髋置换术中假体稳定性的影响

目的探讨髋臼螺钉在非骨水泥全髋置换术中对髋臼假体稳定性的影响。 方法回顾性分析2009年8月至2015年8月在深圳市龙岗区人民医院骨科行非骨水泥全髋置换术114例(117髋)病例资料，患者根据术中是否植入髋臼螺钉分成两组，其中A组无螺钉组59髋，B组螺钉固定组58髋。分别在术后3个月、12个月、24个月和末次随访时对病人进行随访，评估并比较影像学的改变及Harris评分。A组57髋B组56髋获得完整随访资料，平均随访(5.7±1.6)年。以Kaplan-Meier法分析两组假体生存率。 结果A组平均手术时间(t＝2.213, P<0.05)、术中出血量均小于B组(t＝2.342, P<0.05)；随访末期，A、B组术后平均Harris评分为(95.0±2.1)分及(93.0±5.5)分(P>0.05)；A、B组术后3个月、12个月、24个月分别有4髋(7.0%)、3髋(5.3%)、1髋(1.8%)和1髋(1.8%)、2髋(3.6%)及2髋(3.6%)出现髋臼周围透亮线；A组1髋术后4年出现骨溶解，B组2髋出现骨溶解。以影像学证明假体松动作为失败标准，计算两组假体平均随访(5.7±1.6)年生存率分别为97%和95%，两者差异无统计学意义(P >0.05)。 结论髋臼骨质条件良好时是否使用髋臼螺钉固定对臼杯的稳定性无明显影响，全髋关节置换术中植入髋臼螺钉不是必需的。     

急诊绿色通道在创伤性膈疝中的应用体会

目的阐述急诊绿色通道在创伤性膈疝中的应用体会。 方法回顾性分析2017年5月至2018年5月，江苏省人民医院收治的25例创伤性膈疝患者的临床资料，均采用急诊创伤绿色通道进行抢救。记录患者手术情况、治疗结果及术后并发症情况。 结果25例患者到达医院立即启动创伤通，所有创伤通道人员到位时间（5±5.5）min，到达医院至手术时间（60.7±6.2）min。23例入院后行急诊手术，另外2例均于入院后第2天手术。并发症发生率为8.70%，死亡率为8.00%，治疗成功率为92.0%。 结论急诊创伤绿色通道的设立可大大缩短受伤至手术时间，以最迅速的方式使创伤性膈疝患者得到及时救治，提倡更多的医院建立"急诊创伤绿色通道"，使更多的患者在最短的时间内接受有效的治疗。     

IL‐17A synergistically enhances TLR3‐mediated IL‐36γ production by keratinocytes: A potential role in injury‐amplified psoriatic inflammation

Skin injury can trigger formation of new lesions in psoriasis (Koebner phenomenon). The mechanisms through which injury exacerbates psoriasis are unclear. During wound repair, epidermal keratinocytes are activated and produce abundant IL‐36γ, further promoting the skin inflammation. IL‐17A is the cornerstone cytokine in the pathogenesis of psoriasis. We sought to investigate the effects of IL‐17A on injury‐induced keratinocyte activation and IL‐36γ production. Here, we demonstrated that dsRNA released from necrotic keratinocytes induced the expression of IL‐36γ. Silencing of TLR3 by siRNA decreased the IL‐36γ induction by necrotic keratinocyte supernatant. Co‐stimulation with dsRNA and IL‐17A synergistically increased the expression of IL‐36γ and other proinflammatory mediators (CCL20, CXCL8, DEFB4 and LCN2) in keratinocytes. The synergistic effects were not dependent on TLR3 upregulation, TNF receptor signalling and mRNA stabilization. Co‐stimulation with dsRNA and IL‐17A resulted in an accumulation of IκBζ. The synergistic upregulation of IL‐36γ and proinflammatory mediators were inhibited by IκBζ siRNA. Co‐stimulation with IL‐17A and poly(I:C) markedly activated the p38 MAPK and NF‐κB pathway, compared with poly(I:C). Blockade of p38 MAPK and NF‐κB suppressed dsRNA/IL‐17A–mediated IκBζ and IL‐36γ induction. These findings demonstrated that IL‐17A synergistically enhanced the dsRNA‐mediated IL‐36γ production through a p38 MAPK‐, NF‐κB–, and IκBζ‐dependent mechanism.