Radical radiotherapy in older patients with muscle invasive bladder cancer

Background

Muscle invasive bladder cancer (MIBC) is prevalent in the older patients, who are a vulnerable population with multiple co-morbidities and at increased risk of complications. Radical cystectomy is often not suitable, hence radical radiotherapy (RT) is an alternative option. We reviewed the outcomes of older patients treated with RT with or without concurrent chemotherapy (CRT) at our institution.

《邵氏医案》从血辨治痛经浅析

[目的]分析总结浙江近代著名临床医家邵兰荪治疗痛经的经验,以期为临床治疗提供借鉴。[方法]通过研读裘吉生编《邵氏医案》,筛选出其中治疗痛经的医案十余则,并结合邵氏在妇科方面的学术思想,进一步分析其辨证立法遣方特色,从而总结邵氏治疗痛经的临证经验。[结果]邵氏治疗痛经多从血辨治,且分虚实两端,其中属虚者血虚内热用益母胜金丹养血清热、活血止痛,血虚肝风治以养血柔肝、息风止痛;属实者水结血瘀用五苓散利水散瘀、行气止痛,气阻血滞治从行气活血、调经止痛。[结论]在治疗妇人痛经方面,邵氏辨治遣方确有独特经验,这些经验可为中医药治疗此类疾病拓宽诊治思路,有助于提高临床疗效。     

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。     

Association Between Serum C-Reactive Protein Concentration and Nutritional Status of Malignant Tumor Patients

Background: The level of the systemic inflammatory marker C-reactive protein (CRP) is elevated in many patients with malignant disease and may be related to nutritional status.

Objective: To analyze the association between serum CRP levels in patients with malignant tumors and their nutritional status.

Method: A total of 3,692 cases were analyzed and the serum CRP levels were determined using an immunometric assay. Nutritional status was assessed by using patient-generated subjective global assessment (PG-SGA). The biochemical evaluation of prealbumin (PA), albumin (ALB), cholesterol (CHOL), and triglycerides (TG) were assayed within 48?h admission to the hospital. The association between serum CRP concentration and the nutritional status, the stage of the tumor and other factors was analyzed by univariate and multivariate logistic regression analysis.

Result: Elevated serum CRP was observed in 47.6% (1,548/3,269) of patients compared with the reference value, and the median CRP concentration was 18.29?mg/l. Patient serum CRP concentrations in the malnourished group (PG-SGA B?+?C) were higher than in the well-nourished (PG-SGA A) patients (P?<?0.05). The serum CRP level was related to the patients' age, gender, tumor stage, and was affected by hepatitis, liver cirrhosis, diabetes, but it has no effect on hypertension. The CRP high patients had lower PA and ALB levels, lower Karnofsky performance status scores, and higher PG-SGA scores (P?<?0.05), and there was no relationship with CHOL and TG levels. Weight loss in the previous 1?mo was seen with CRP positive patients (P?<?0.05).

Conclusion: Almost 50% of malignant tumor patients had elevated serum CRP levels indicating a systemic inflammatory state. The nutritional status was worse in cancer patients with higher concentrations of serum CRP. The level of CRP was associated with the tumor stage, and, as stage is a prognostic factor, so can CRP be used as a prognostic maker in malignant tumors patients.     

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.