Positioning the six‐month review in the recovery process post‐stroke: The ideology of personal responsibility

Stroke is the UK's fourth highest cause of death and an estimated 300,000 people in England are living with related disability. This paper explores the six‐month review (6MR), a policy initiative that aimed to ameliorate unmet need. A multiple case study approach underpinned by critical realism was used to elicit the views of patients, carers, providers and commissioners across three sites using interviews, observations and documentation. Forty‐six patients (age range 28–91 years), 30 carers and 28 professionals were interviewed between December 2015 and October 2016. Twenty‐nine reviews were observed. Data was analysed thematically across sites. 6MRs carried out by stroke nurse specialists (SNSs) were found to be more medically orientated than those completed by a Stroke Association (SA) co‐ordinator who focused on social issues. Reviewers regarded reviews primarily as an opportunity to address unmet need and signpost to further services. Patients responded in three different ways: proactive and engaged, reflected an active orientation to recovery and self‐management; proactive and self‐managing on their own terms, encompassed patients who were striving for independence but took their own approach sometimes at odds with that of clinicians; and passive orientation, whereby patients did not engage in rehabilitation or self‐management. Patients identified different priorities to those of reviewers, particularly those with other long‐term conditions and this appeared to contribute to the dissatisfaction that some expressed. In conclusion, there was little evidence that the 6MR played a key role in recovery. Locally defined outcomes for the 6MR reflecting national policy were not substantiated by the findings. Our findings suggest that the 6MR should review therapy goals and facilitate patient‐led goals. Reviewers should be allowed the freedom to individualise the process rather than adhering to a rigid framework dictated by national policy and local protocols.     

原发性肾小球肾炎患者肾小管间质中整合素连接激酶的表达及意义

目的:检测不同间质纤维化程度的原发性肾小球肾炎患者肾组织中整合素连接激酶(ILK)的表达,观察ILK与肾间质纤维化程度之间的关系,探讨ILK在肾间质纤维化中可能的作用.方法:选取原发性肾小球肾炎患者肾活检标本88例,根据肾间质纤维化程度分为四组,采用免疫组化方法,检测各组标本ILK的表达,并将ILK的表达与间质纤维化程度和患者血尿β2微球蛋白水平进行相关分析.结果:ILK主要表达于病变肾小管上皮细胞,并且随间质病变的加重,表达量增加,范围增大.肾小管间质中ILK表达量与肾间质纤维化病变程度和患者血尿β2微球蛋白均呈正相关关系.结论:ILK可能参与了肾间质纤维化的形成.     

认真实施“一法一例” 抓好母婴保健工作

沈阳市人大、市政府高度重视《中华人民共和国母婴保健法》和《辽宁省母婴保健条例》的贯彻实施，认真抓好宣传工作，建立起一支高素质的执法队伍，加强监督执法的力度，清理整顿了母婴保健技术服务市场，使该市的妇幼卫生工作向法制化管理迈出了一大步     

姜黄素抑制人肝癌细胞BEL-7402中VEGF和HIF-1α表达通过PI3K／AKT／FRAP信号传导通路

目的探讨MAPK和PI3K信号传导通路在姜黄素调节VEGF和HIF-1α表达中的作用。方法分别加入LY29400225μmol／L、50μmol／L，U012610μmol／L、20μmol／L，rapamycin 5ng／ml、10ng／ml处理人肝癌细胞BEL-7402，30min后加入姜黄素10μmol／L，对照组单独加入0、10μmol／L姜黄素，缺氧环境中培养6h后，行RT—PCR和Western Blot检测VEGF蛋白、mRNA和HIF-1α蛋白表达；分别加入不同浓度的的姜黄素以及LY294002 25 μmol／L处理人肝癌细胞BEL-7402，缺氧环境中培养6h后，行Western Blot检测磷酸化AKT和总AKT蛋白表达。结果姜黄素10μmol／L＋LY29400225μmol／L组、姜黄素10μmol／L＋LY294002 50 μmol／L组、姜黄素10μmol／L＋rapamycin 5 ng／ml组、姜黄素10μmol／L＋rapamycin 10 ng／na组HIF-1α蛋白、VEGF蛋白、mRNA表达分别与姜黄素10μmol／L组相比降低，差异有统计学意义（P〈0．01）；而姜黄素10μmol／L＋U012610μmol／L组、姜黄素10μmol／L＋U0126 20 μmol／L组HIF—1α蛋白、VEGF蛋白、mRNA表达分别与姜黄素10μmol／L组相比差异无统计学意义（P〉0.05）；不同浓度的姜黄素、LY294002 25 μmol／L处理的人肝癌细胞BEL-7402缺氧6h后磷酸化AKT蛋白表达逐渐降低，LY294002 25 μmol／L可以基本阻断磷酸化AKT蛋白的表达，而对总AKT蛋白表达无明显变化。结论姜黄素对人肝癌细胞BEL-7402中HIF-1α蛋白和VEGF的表达通过P13K／AKT／FRAP信号传导通路。     

叶酸缺乏对小鼠脑组织PS1基因表达和Aβ沉积的影响

目的探讨叶酸缺乏对APP/PS1双转基因阿尔茨海默病(Alzheimer’s disease,AD)模型小鼠脑组织中早老素1(Presenilin1)基因表达和β-淀粉样蛋白(amyloid-β,Aβ)沉积的影响。方法将6月龄APP/PS1双转基因AD模型小鼠24只,随机分为AD叶酸缺乏组(AD+FA-D)和AD叶酸对照组(AD+FA-N),每组12只,12只正常同月龄C57小鼠作为阴性对照组(WT+FA-N)。AD+FA-D组给予叶酸缺乏饲料,AD+FA-N组和WT+FA-N组给予正常饲料。免疫组织化学技术检测脑组织β-淀粉样蛋白沉积;实时定量PCR(RT-PCR)和荧光原位杂交(FISH)检测脑组织中PS1m RNA表达;免疫印迹(Western blot)和免疫组织化学法检测脑组织中PS1蛋白表达。结果 WT+FA-N组脑组织Aβ沉积低于AD+FA-N组(P0.05);AD+FA-D组高于AD+FA-N组(P0.05);WT+FA-N组PS1 m RNA和蛋白表达均低于AD+FA-N组(P0.05);AD+FA-D组均高于AD+FA-N组(P0.05)。结论叶酸缺乏可以增加APP/PS1双转基因AD模型小鼠脑组织中PS1 m RNA和蛋白表达并促进β-淀粉样蛋白沉积。     

Facteurs de croissance intestinaux

The rate of cell proliferation is under the control of humoral factors, luminal nutrition and intestinal growth factors which maintain mucosal homeostasis by highly complex mechanisms. Among endocrine effectors, growth hormone (GH) has been noted to exert a trophic effect on the small intestine and stimulates the bowel morphologic and proliferative adaptation after resection. These effects may be mediated by IGF-I. The nutrients (lipids > proteins > polysacharids) and polyamines are the main effectors in the control of mucosal proliferation.A number of intestinal growth factors whose expression may be regulated by luminal or hormonal effectors may play an important role in the control of intestinal growth. Milk EGF (Epidermal Growth Factor) has a trophic effect in the suckling rat. In the adult only systemic EGF stimulates intestinal growth after resection, infection or treatment with methotrexate. TGFα (Transforming Growth Factor alpha), a ligand that binds to the same receptor as EGF, exerts the same trophic responses. TGFα may be the more physiologically ligand of the EGF receptor in the adult. In addition TGFα may be implicated in the progression of colonic tumours. IGF-I and IGF-II (Insulin-like Growth Factor), polypeptides structurally homologous to proinsulin, have mitogenic, morphogenic and metabolic properties. The members of the FGF (Fibroblast Growth Factor) family have only a moderate effect on the growth of intestinal epithelial cells and a main role in the repair of damaged tissue. TGFβ (Transforming Growth Factor) is an inhibitor of intestinal epithelial cell growth in the G1 phase of the cell cycle. TGFβ may be the physiological regulator of apoptosis in the colonic epithelium and the loss of this function may favour tumour progression. TGFβ also induces the production of constituents of the extracellular matrix and promotes the healing of wounded tissue.     

CD4＋CD25＋FOXP3＋调节性 T细胞在牛奶蛋白过敏发生及耐受中的作用

目的：探讨CD4＋CD25＋FOXP3＋调节性T细胞在牛奶蛋白过敏患儿发病及耐受过程中的作用。方法选取2013年1月至2015年1月东南大学医学院附属江阴市人民医院儿科明确诊断牛奶蛋白过敏的患儿20例,健康对照组20例,牛奶蛋白过敏患儿予深度水解或完全水解蛋白配方粉喂养6个月,6个月后行食物激发试验,过敏耐受者15例,耐受失败者3例。治疗前后测定外周血CD4＋CD25＋FOXP3＋调节性T细胞的水平,分析比较牛奶蛋白过敏患儿治疗前、治疗后及与对照组之间CD4＋CD25＋FOXP3＋调节性T细胞的差异,并比较治疗后过敏耐受患儿和耐受失败患儿CD4＋CD25＋FOXP3＋调节性T细胞的差异。结果牛奶蛋白过敏患儿CD4＋CD25＋FOXP3＋调节性T细胞水平明显低于对照组患儿（3．73±0．42％ vs 6．90±0．35％,t＝2．22,P＜0．05）;治疗后CD4＋CD25＋FOXP3＋调节性T细胞水平较治疗前明显升高（5．18±0．81％ vs 3．73±0．42％,t＝2．10, P＜0．05）;治疗后牛奶蛋白耐受患儿CD4＋CD25＋FOXP3＋调节性T细胞水平明显高于耐受失败患儿（5．36±0．76％ vs 4．28±0．36％,t＝2．31,P＜0．05）。结论 CD4＋CD25＋FOXP3＋调节性T细胞有助于减少牛奶蛋白过敏的发生,并帮助诱导免疫耐受。     

孤独症鼠模型脑组织CaMKⅡ和ERK表达的相关研究

目的 探讨钙调蛋白激酶Ⅱ(CaMK Ⅱ)和细胞外信号调节激酶(ERK)在孤独症谱系障碍发病中的作用。方法 孕12.5 d Sprague-Dawley孕鼠腹腔注射丙戊酸钠600 mg/kg建立子代孤独症谱系障碍模型大鼠,对照组注射同等剂量生理盐水。利用HE染色、免疫组化和图像分析技术观察比较出生后1、7、14 d和28 d两组大鼠脑部CaMK Ⅱ、ERK表达情况。结果 HE染色:出生后1 d、7 d模型组神经元数量较少,出生14 d后剧增,出生后28 d仍高于对照组。免疫组化:出生后1~14 d两组CaMKⅡ、ERK表达均显著升高(P<0.001),出生28 d后表达趋于稳定(P>0.05);与对照组相比,模型组各日龄大鼠CaMK Ⅱ、ERK表达水平均增高(P<0.001);CaMK Ⅱ、ERK于出生后1 d、7 d表达显著升高(P<0.001),出生后14 d表达量最多(P<0.001),出生28 d后趋于稳定(P>0.05)。结论 孤独症谱系障碍模型大鼠大脑皮层CaMK Ⅱ、ERK的表达增加,尤其是在出生后早期。     

Reductive Amination for LC–MS Signal Enhancement and Confirmation of the Presence of Caribbean Ciguatoxin-1 in Fish

Ciguatera poisoning is a global health concern caused by the consumption of seafood containing ciguatoxins (CTXs). Detection of CTXs poses significant analytical challenges due to their low abundance even in highly toxic fish, the diverse and in-part unclarified structures of many CTX congeners, and the lack of reference standards. Selective detection of CTXs requires methods such as liquid chromatography coupled to tandem mass spectrometry (LC–MS/MS) or high-resolution MS (LC–HRMS). While HRMS data can provide greatly improved resolution, it is typically less sensitive than targeted LC–MS/MS and does not reliably comply with the FDA guidance level of 0.1 µg/kg CTXs in fish tissue that was established for Caribbean CTX-1 (C-CTX-1). In this study, we provide a new chemical derivatization approach employing a fast and simple one-pot derivatization with Girard’s reagent T (GRT) that tags the C-56-ketone intermediate of the two equilibrating C-56 epimers of C-CTX-1 with a quaternary ammonium moiety. This derivatization improved the LC–MS/MS and LC–HRMS responses to C-CTX-1 by approximately 40- and 17-fold on average, respectively. These improvements in sensitivity to the GRT-derivative of C-CTX-1 are attributable to: the improved ionization efficiency caused by insertion of a quaternary ammonium ion; the absence of adduct-ions and water-loss peaks for the GRT derivative in the mass spectrometer, and; the prevention of on-column epimerization (at C-56 of C-CTX-1) by GRT derivatization, leading to much better chromatographic peak shapes. This C-CTX-1–GRT derivatization strategy mitigates many of the shortcomings of current LC–MS analyses for C-CTX-1 by improving instrument sensitivity, while at the same time adding selectivity due to the reactivity of GRT with ketones and aldehydes.     

丁苯酞联合TLR4抗体鼓室给药小鼠梅尼埃病模型的实验研究

目的研究丁苯酞联合TLR4抗体通过调控Hsp70通道蛋白表达对内淋巴积水(Endolymphatic hydrops,ELH)小鼠模型的诊疗价值。方法选取50只BALB/c雌性小鼠,并随机分为对照组(A组)、模型组(B组)、和实验组(C组)。对照组不予任何处理;模型组予内淋巴积水造模;实验组在模型组基础上2天后:A组予以鼓室注射TLR4抗体50μg+丁苯酞25mg/kg灌胃干预;B组予以鼓室注射TLR4抗体100μg+丁苯酞100mg/kg灌胃干预;C组予以鼓室注射TLR4抗体200μg+丁苯酞100mg/kg灌胃干预。连续干预4周。随后观察小鼠行为学改变,耳蜗切片Hsp70表达,测试耳蜗电图SP/AP值。检测MD小鼠在丁苯酞联合TLR4抗体干预前后血清Hsp70水平及TNF-α、IL-6炎性细胞因子表达。结果与对照组比较,模型组小鼠诱发出明显外周前庭症状,符合MD(Ménière’s Disease)动物造模改变;与模型组比较,实验组3个亚组经4w鼓室注射TLR4抗体50、100、200μg+丁苯酞25、100、100mg/kg灌胃干预后,小鼠前庭反应都明显减轻,模型组与实验组耳蜗电...