带蒂大网膜瓣在乳腺癌术后乳房再造中的应用研究

目的探讨带蒂大网膜瓣在乳腺癌术后乳房再造中的临床应用。方法2013 年 5 月—2017 年 10 月，对 205 例乳腺癌患者行改良根治术联合带蒂大网膜瓣移植再造乳房。患者均为女性；年龄 26～58 岁，平均 34.9 岁。左侧 127 例、右侧 78 例；肿瘤直径 2～5 cm，平均 2.9 cm。乳腺癌分期：Ⅰ期 120 例，Ⅱ期 85 例。病理诊断：浸润性导管癌 126 例，浸润性小叶癌 79 例。病程 10～92 d，平均 38.5 d。肿物切除后遗留缺损范围为 9 cm×6 cm～18 cm×12 cm。带蒂大网膜瓣切取范围为 18 cm×10 cm～22 cm×16 cm。结果根据术中观察的组织特点，将大网膜分为 4 种类型，稀薄型（42 例，20.5%）、中间型（133 例，64.9%）、肥厚型（24 例，11.7%）、缺如型（6 例，2.9%）。术后带蒂大网膜瓣均成活，切口Ⅰ期愈合。患者均获随访，随访时间 6～74 个月，平均 24.5 个月；其中 83 例随访达 5 年以上。再造乳房外形可、弹性好，无挛缩变形。供区仅遗留线性瘢痕，腹部功能无影响。随访期间无乳腺癌复发。结论带蒂大网膜瓣切取安全可靠、质地优良，是乳腺癌术后乳房再造的理想方法之一。     

乳房血供及乳房缩小术的研究进展

目的总结近年来乳房血供及乳房缩小术式的研究进展。方法广泛查阅近年来有关乳房神经分布、血供、乳房缩小术式的发展和术后哺乳功能等情况的国内外文献，并结合临床经验进行分析总结。结果随着对乳房腺体及乳头乳晕复合体的神经分布与血供的解剖研究，乳房缩小术已形成了多种手术方式，各有优缺点，适应证亦不同。通过辅助检查技术的应用，术后乳头、乳晕坏死等严重并发症发生率明显降低；通过对切口与蒂部位置的选择、保留蒂部腺体量的程度、辅助吸脂技术的应用和缝合技术方面的改进，减轻了术后切口瘢痕，更好地保留了乳头乳晕感觉，获得了更为满意的乳房形态。行乳房缩小术后部分分娩患者具有一定哺乳功能。结论乳房缩小术需根据患者特点采用个性化手术方式。在如何更好地保留乳头、乳晕感觉，获得良好而持久的乳房形态，生育期妇女术后哺乳功能保留等方面有待进一步研究。     

吲哚菁绿造影在乳房重建中的应用进展

目的对吲哚菁绿（indocyanine green，ICG）造影在乳房重建中的应用进展进行综述。方法查阅国内外有关 ICG 造影在乳房重建中应用的文献，总结 ICG 造影历史沿革、化学成分、使用原理、使用方法及注意事项。结果ICG 是一种适用于术中血管灌注造影成像的荧光物质。ICG 造影及 SPY 灌注评估系统已逐渐用于乳房重建术中，包括组织扩张器及假体植入乳房重建和自体组织乳房重建，其与术者主观评估、手持多普勒血流探测仪、组织血氧测量及荧光素钠造影相比，有着明显优势及更多用途。结论ICG 造影可较准确评估乳房重建术中皮瓣灌注情况，从而指导术中决策，降低术后皮瓣相关并发症发生，并具有一定经济学效益。     

GP73在肝癌患者外周血CD4+T淋巴细胞中的异常表达及其相关机制研究

目的 探讨肝癌患者外周血CD4+T淋巴细胞中高尔基体蛋白73(GP73)的异常表达及其对Th1/Th2/Th17亚型分化的影响.方法 选择该院2015年5月至2016年2月住院的肝癌患者50例为研究对象,50例健康志愿者作为对照.采集外周血并分离CD4+T淋巴细胞,采用实时荧光定量PCR检测CD4+T淋巴细胞中GP73表达水平;另将分选的20例健康者CD4+T淋巴细胞分别转染GP73小干扰RNA或过表达载体,实时荧光定量PCR及蛋白质印迹法(Western blot)检测CD4+T淋巴细胞中GP73及核因子κB(NF-κB)表达水平,ELISA检测上清液中白细胞介素4(IL-4)、γ干扰素(IFN-γ)、白细胞介素17(IL-17)的分泌水平.结果 肝癌患者外周血CD4+T淋巴细胞中GP73 mRNA的表达与健康者相比明显上调,差异有统计学意义(P<0.05).GP73过表达组NF-κB表达水平明显升高(P<0.05),GP73干扰组NF-κB表达水平明显降低(P<0.05).过表达GP73导致CD4+T淋巴细胞中IL-4、IL-17水平明显升高,IFN-γ水平明显降低(P<0.05);沉默GP73导致CD4+T淋巴细胞IL-4、IL-17水平明显降低,IFN-γ水平明显升高(P<0.05).结论 GP73在肝癌患者的外周血CD4+T淋巴细胞中过表达,而GP73很有可能通过激活N F-κB参与炎症反应,导致患者体内T h1/T h2/T 17失衡,促进肝癌的发生与发展.     

Expression of DeltaNp73 in hippocampus of APP/PS1 transgenic mice following GFP-BMSCs transplantation

Abstract

Objective: To study the effect of hippocampal bone marrow stromal cells (GFP-BMSCs) transplantation on spatial memory and DeltaNp73 expression in APP/PS1 transgenic mice.

Methods: Twelve APP/PS1 transgenic mice randomly received either 10 μl GFP-BMSCs suspension in medium (GFP-BMSCs transplantation group) or 10 μl complete medium (sham-operated group). Learning and memory function of mice in both groups were observed and tested in Morris water maze experiment at 2 weeks after surgery. Senile plaques and DeltaNp73 protein in hippocampuses were determined by immunohistochemistry and western blot at 3 weeks after surgery, respectively.

Results: APP/PS1 mice treated with BMSCs performed significantly better on the water maze test than those in sham-operated group (P<0·05). Immunohistochemistry showed that GFP-BMSCs distributed uniformly and the number of Alzheimer’s senile plaques reduced after transplantation. Western blot showed that quantified DeltaNp73 protein expression was significantly higher in BMSCs transplantation group when compared with sham-operated group (P<0·01).

Conclusions: Our results suggest that BMSCs transplatation could retard Alzheimer’s disease (AD) like pathology and upregulate DeltaNp73 expression in hippocampuses of APP/PS1 transgenic mice. GFP-BMSCs transplantation will be a potential treatment for AD.     

Do illness perceptions predict health outcomes in primary care patients? A 2-year follow-up study

OBJECTIVE: Little is known about whether illness perceptions affect health outcomes in primary care patients. The aim of this study was to examine if patients' illness perceptions were associated with their self-rated health in a 2-year follow-up period. METHODS: One thousand seven hundred eighty-five primary care patients presenting a new or recurrent health problem completed an adapted version of the illness perception questionnaire and the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36) at baseline and 3, 12, and 24 months' follow-up. Linear regressions were performed for (1) all patients, (2) patients without chronic disorders presenting physical disease, and (3) patients presenting medically unexplained symptoms (MUS). RESULTS: Negative illness perceptions were associated with poor physical and mental health at baseline. They most strongly predicted changes in health status at follow-up for the whole group of patients. Patients presenting with MUS had more negative illness perceptions and lower mental and physical components subscale of the SF-36 scores at all time points. CONCLUSIONS: Patients' perception of a new or recurrent health problem predicts self-reported physical and mental health up to 2 years after consulting the general practitioner and offers an obvious starting point for addressing nonbiomedical aspects of illness.     

Localization and pharmacological modulation of GABA-B receptors in the globus pallidus of parkinsonian monkeys

Changes in GABAergic transmission in the external and internal segments of the globus pallidus (GPe and GPi) contribute to the pathophysiology of the basal ganglia network in Parkinson's disease. Because GABA-B receptors are involved in the modulation of GABAergic transmission in GPe and GPi, it is possible that changes in the functions or localization of these receptors contribute to the changes in GABAergic transmission. To further examine this question, we investigated the anatomical localization of GABA-B receptors and the electrophysiologic effects of microinjections of GABA-B receptor ligands in GPe and GPi of MPTP-treated (parkinsonian) monkeys. We found that the pattern of cellular and ultrastructural localization of the GABA-BR1 subunit of the GABA-B receptor in GPe and GPi was not significantly altered in parkinsonian monkeys. However, the magnitude of reduction in firing rate of GPe and GPi neurons produced by microinjections of the GABA-B receptor agonist baclofen was larger in MPTP-treated animals than in normal monkeys. Injections of the GABA-B receptor antagonist CGP55845A were more effective in reducing the firing rate of GPi neurons in parkinsonian monkeys than in normal animals. In addition, the injections of baclofen in GPe and GPi, or of CGP55845A in GPi lead to a significant increase in the proportion of spikes in rebound bursts in parkinsonian animals, but not in normal monkeys. Thus, despite the lack of changes in the localization of GABA-BR1 subunits in the pallidum, GABA-B receptor-mediated effects are altered in the GPe and GPi of parkinsonian monkeys. These changes in GABA-B receptor function may contribute to bursting activities in the parkinsonian state.     

Lipidomic analysis reveals the significant increase in diacylglycerophosphocholines in umbilical cord blood from pregnant women with gestational hypercholesterolemia

Gestational hypercholesterolemia has been recognized as a risk factor of some pregnancy complications. We supposed that maternal hypercholesterolemia modified the lipid profile of the fetus. Thirty pregnant women with hypercholesterolemia and matched controls were recruited and cord blood was sampled. Lipidomic analysis was used to evaluate the lipid profile change between the two groups. The results showed that the content of diacylglycerophosphocholines (PC) was significantly high in cord blood from hypercholesterolemic pregnant women. PC (16:0/20:4) and PC (18:0/20:4) were selected as the most important lipid species in cord plasma and their contents were positively related to the total cholesterol and high-density lipoprotein cholesterol levels in cord blood. The contents of these two PCs were significantly higher in the hypercholesterolemic group than in the control group. These results suggested that gestational hypercholesterolemia might program the phospholipid metabolism in offspring.     

A mechanism of ubiquitin-independent proteasomal degradation of the tumor suppressors p53 and p73

Protein degradation is an essential and highly regulated process. The proteasomal degradation of the tumor suppressors p53 and p73 is regulated by both polyubiquitination and by an ubiquitin-independent process. Here, we show that this ubiquitin-independent process is mediated by the 20S proteasomes and is regulated by NQO1. NQO1 physically interacts with p53 and p73 in an NADH-dependent manner and protects them from 20S proteasomal degradation. Remarkably, the vast majority of NQO1 in cells is found in physical association with the 20S proteasomes, suggesting that NQO1 functions as a gatekeeper of the 20S proteasomes. We further show that this pathway plays a role in p53 accumulation in response to ionizing radiation. Our findings provide the first evidence for in vivo degradation of p53 and p73 by the 20S proteasomes and its regulation by NQO1 and NADH level.