基于自动勾画和快速蒙特卡罗计算的放射治疗全身器官剂量数据库平台的可行性研究

目的:探讨建立一种放射治疗全身器官剂量数据库平台的可行性。方法:使用基于深度学习的自动勾画软件DeepViewer?1例食管癌患者的全身CT上勾画全身器官，然后利用基于GPU加速的蒙特卡罗软件ARCHER计算相应的器官剂量分布，最后利用Lyman-Kutcher-Burman（LKB）模型评估放疗患者正常组织并发症概率（NTCP）。结果:针对该病例，成功建立基于DeepViewer?ARCHER和LKB模型的全身器官剂量数据库，发现距离靶区越近的器官剂量越大，其中心脏与靶区间距离最小，剂量为14.11 Gy，但因其模型参数特殊，通过LKB模型计算的NTCP为0.00%；左、右肺的剂量分别为3.19和1.16 Gy，但是NTCP值却很大，分别为2.13%和1.60%。对于距离靶区较远的头颈部器官（视交叉、视神经和眼）和腹部器官（直肠、膀胱和股骨头）剂量分别约为9和2 mGy，并且NTCP均近似为0.00%。结论:研究结果证明通过自动勾画软件DeepViewer?蒙特卡罗软件ARCHER和LKB模型建立全身器官剂量数据库的可行性。     

羊水粪染与羊膜腔感染的关系

【摘要】 目的 :探讨羊水粪染与羊膜腔感染的关系。方法 :选择未临产且胎膜完整的剖宫产产妇 5 6例 ,根据术中所见羊水性状分为羊水清亮组、羊水Ⅰ～II度粪染组和羊水III度粪染组。于剖宫产术中取羊水用双抗体夹心ELISA法测IL 6含量 ,取胎盘胎膜做病理检查以了解有无炎性细胞浸润 ,并记录新生儿Apgar评分 ,观察产妇术后有无产褥感染。结果 :3组羊水中IL 6含量差异无显著性 ,3组胎盘标本病理检查示炎性细胞浸润之差异亦无显著性 ,而羊水粪染组新生儿窒息发生率较清亮组明显增加 (P <0 .0 5 )。结论 :羊水粪染尤其是III度粪染是胎儿窘迫的标志 ,而与羊膜腔感染无明显相关性。     

Theophylline and status epilepticus in children

We studied the role of theophylline on outcome of status epilepticus (SE) in children. During a two-year-period, 16 of 114 episodes of SE occurred in children receiving theophylline. At the onset of SE, theophylline blood levels were elevated in 8 episodes, and were therapeutic or subtherapeutic in 8 episodes. In the 8 episodes of SE with elevated theophylline levels, one child died and three suffered permanent new neurologic deficits. In the 8 episodes of SE with normal or low theophylline levels, only one child had a transient deficit. The occurrence of death or disability in 4 of 8 episodes of SE with elevated theophylline was considerably higher than the 23% incidence of death or persistent CNS deficit in the overall series of 114 episodes of SE. We conclude that theophylline, at toxic levels, is a significant factor in increased morbidity. We suspect that the hypoxia from the respiratory disorder for which theophylline was used, and the reduced cerebral blood flow known to occur with theophylline led to a failure to compensate for the increased cerebral metabolic rate of SE, thus increasing the risk of a poor outcome.     

A study of 10 cases of velopharyngeal incompetence treated by flap pharyngoplasty

Velopharyngeal incompetence (VPI) is a condition of incomplete closure of V.P. port area, normally formed by velum and posterior pharyngeal watt. The condition primarily results in various types of speech defects, which form- the main complaint of the patient. We have studied 10 cases of VPI due to various causes and the speech improvement obtained by flap pharyngoplasty procedures. The results have been evaluated with a follow-up of six months. Highly encouraging results only indicate a more frequent need to undertake such surgery without any hesitation if the ENT surgeon is familiar with and has an adequate exposure to this simple and effective procedure.     

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征患者前列腺液中炎症因子差异表达的临床意义

Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.     

An oral selective M3 cholinergic receptor antagonist in COPD.

Cholinergic antagonists have been used since the early 1900s as bronchodilators for chronic obstructive pulmonary disease (COPD). The present study investigated whether an oral muscarinic M3-selective anticholinergic agent (OrM3) would provide an improved therapeutic advantage compared with an inhaled anticholinergic agent in patients with COPD. A 6-week, multicentre, randomised, placebo- and active-controlled, parallel-group study was performed at 56 sites in the USA. In total, 412 male and female patients (aged 35-86 yrs) with a clinical history consistent with COPD were randomised to receive OrM3 0.5, 2, 3 or 4 mg orally once daily, ipratropium bromide 36 mug by inhalation four times daily or placebo. OrM3 demonstrated a significant dose-related improvement in serial forced expiratory volume in one second and a trend for dose-related improvement in patient-reported symptoms compared with placebo. However, at a dose that provided efficacy less than that of ipratropium, the incidence of dose-related, mechanism-based side-effects for OrM3 exceeded those observed for ipratropium. In patients with chronic obstructive pulmonary disease, the oral M3-selective agent did not offer a therapeutic advantage over inhaled ipratropium. These results do not support the hypothesis that high selectivity for muscarinic M3 receptors over airway neuronal M2 receptors will represent a more effective therapy than current inhaled anticholinergics in obstructive airway disease.     

Prostaglandin E2 inhibition of keloid fibroblast migration, contraction, and transforming growth factor (TGF)-β1–induced collagen synthesis

Keloid formation has been linked to aberrant fibroblast activity, exacerbated by growth factors and inflammatory mediators. Prostaglandin E2 (PGE2), synthesized from arachidonic acid by cyclooxygenases (COX) and synthases (PGES), acts as both an inflammatory mediator and fibroblast modulator. Although PGE2 has known antifibrotic effects in the lower airway, its role in dermal fibrosis in general, and keloid formation in particular, remains unclear. This study focused on: (1) the effects of PGE2 on keloid fibroblast migration, contraction, and collagen synthesis and (2) endogenous PGE2 synthesis in response interleukin-1beta. PGE2 decreased keloid fibroblast migration and contraction via an EP2/EP4-cAMP mechanism that disrupted actin cytoskeletal dynamics and reversed transforming growth factor-beta1-induced collagen I and III synthesis. Impaired fibroblast PGE2 production has been linked to lower airway fibrosis and recently to keloid formation. Here, we showed that interleukin-1beta stimulation leads to nuclear factor-kappaB translocation to the nucleus, resulting in up-regulation of COX-2 and microsomal PGE2 synthase 1. Up-regulation of COX-2 in, and secretion of PGE2 by keloid fibroblasts are diminished compared with their normal fibroblast counterparts. We suggest that the antifibrotic effects of PGE2 during keloid formation are potentially diminished due to aberrant paracrine fibroblast signaling. Exogenous PGE2 may supplement decreased endogenous levels and inhibit keloid formation or progression.