脆弱类杆菌脂多糖对正常人外周血单个核细胞分泌白细胞介素的影响

目的　通过研究脆弱类杆菌脂多糖 (LPS)对正常人外周血单个核细胞 (PBMC)分泌白细胞介素 2 (IL 2 )和白细胞介 4素 (IL 4 )的影响 ,探讨脆弱类杆菌感染的机制。　方法　采用脆弱类杆菌临床分离菌和标准菌株 (NCTC9343)提取的LPS ,以不同浓度作用于PBMC ,2 4h后收集培养细胞上清 ,运用ELISA法检测其IL 2和IL 4的含量变化。　结果　脆弱类杆菌LPS对正常人PBMC分泌IL 2有显著抑制作用 ,并呈明显的浓度依赖关系 (r=0 .80 2 4 ,P <0 .0 1)。脆弱类杆菌LPS对正常人PB MC分泌IL 4有显著刺激作用 (P <0 .0 5 ) ,但无浓度依赖关系。脆弱类杆菌临床分离菌与标准菌株LPS对正常人PBMC分泌IL 2和IL 4具有相同效应 ,两组之间无明显差异 (r =0 .10 95 ,P >0 .0 5 )。　结论　脆弱类杆菌LPS对正常人PBMC分泌IL 2有抑制作用 ,而对IL 4的分泌有刺激作用     

王会仍教授自拟“王氏止咳方”治疗慢性咳嗽的临床疗效观察

目的:观察"王氏止咳方"治疗慢性咳嗽的临床效果。方法:在呼吸内科门诊选择124例诊断为慢性咳嗽的患者,随机分为对照组和观察组,每组62例。对照组用西药常规治疗,观察组口服"王氏止咳方"加减治疗,观察两组的临床疗效。结果:经治疗后对照组总有效率为70.97%,观察组总有效率为91.94%,观察组总有效率明显优于对照组(P0.05)。结论:"王氏止咳方"加减治疗慢性咳嗽疗效明显,且无不良反应,值得临床推广应用。     

CK-MB活性测定方法的影响及其与疾病临床关系分析

目的：探讨临床患者CK-MB测定采用免疫抑制法出现假性增高的影响因素以及分析增高与疾病谱的关系。方法选用自2010年12月-2012年2月来该院就诊2100例患者作为研究对象,运用免疫抑制法和速率法分别测定磷酸激酶同工酶(CK-MB)和磷酸激酶(CK)活性。计算其比值(CK-MB/CK)与疾病谱的关系和分析CK-MB活性出现假性升高的影响因素。结果在2100例标本中测定出153例为CK-MB/CK超过30%患者,占总人数的7.28%,其中49例临床诊断为心肌梗死,104例临床诊断为非心肌梗死,占总人数4.95%。非心肌梗死患者中发生率最高的为恶性肿瘤31例(29.8%),其次是心血管病患者,CK-MB/CK增高程度与性别、年龄存在直线相关性(r=-0.307,-0.329、P=0.002,0.001<0.05)。结论 CK-MB/CK增高超过30%现象在恶性肿瘤等非心肌梗死疾病中存在率极高,并且存在导致CK-MB活性假性增高现象,故临床采用免疫抑制法检测应重视假性增高对疾病检测的影响。     

肿瘤转移抑制蛋白在肝癌中的表达及其意义

目的 探讨肿瘤转移抑制蛋白1(metastasis suppressor 1,MTSS1)在肝癌组织,肝硬化组织,正常肝组织中的表达及其意义.方法采用免疫组织化学检测MTSS1在肝癌组织,肝硬化组织,正常肝组织中的表达,并用单因素分析表达与临床病理因素的关系.用Spearman等级相关分析MTSSl表达水平与肝癌患者TNM分期的关系.对肝癌患者进行5年生存随访,采用Kaplan-Meier生存曲线分析.结果 肝癌组织MTSS1表达水平与正常肝组织比较,差异有统计学意义(U=168.000,P＜0.05);肝癌组织比肝硬化组织高,二者比较差异有统计学意义(U=106.000,P＜0.05);MTSS1表达水平与肝癌患者的TNM分期、有无血管侵袭和肿瘤包膜有关(分别U=259.000,258.500,202.000,均P＜0.05),与肝癌患者的年龄、性别、肿瘤大小、AFP水平、乙肝表面抗原无关(P＞0.05).MTSS1表达水平与临床TNM分级间呈负相关,即临床TNM分级越早期所对应的MTSS1表达水平越高(rs=-0.383,P＜0.05).MTSS1阳性表达患者5年生存率明显低于MTSS1阴性及弱阳性表达患者,差异有统计学意义(分别34.1%,52.3%,x2=6.386,P＜0.05).结论 MTSS1高表达可能在早期肝癌进展中发挥重要作用,预示预后不良.

Abstract：

Objective To explore the expression and significance of MTSS1 ( metastasis suppressor 1) in hepatocellular carcinoma.Methods MTSS1 expression was detected by immunohistochemistry in hepatocellular carcinoma, liver cirrhosis and normal liver tissues.Single-factor analysis was used to study the relationship with clinicopathological factor.Correlations between MTSS1 expression and TNM stage were analyzed with Spearman rank correlation analysis.Postoperative 5-year survival was evaluated using Kaplan-Meier survival curve analysis.Results The expression of MTSS1 in hepatocellular carcinoma was higher than normal liver tissue ( U = 168.000, P ＜ 0.05), and liver cirrhotic tissue ( U = 106.000, P ＜ 0.05); MTSS1 expression was correlated with TNM stage of hepatocellular carcinoma patients, lymph vascular invasion and tumor capsule ( separately U = 259.000, 258.500, 202.000, all P ＜ 0.05).MTSS1 expression in hepatocellular carcinoma was not correlated with patients age, gender, tumor size, AFP level, and hepatitis B surface antigen.MTSS1 expression and TNM stage of liver cancer patients was negatively correlated ( rs = - 0.383 , P ＜ 0.05 ).Postoperative 5-year survival of hepatocellular carcinoma patients with MTSS1 positive expression was significantly poorer than patients with negative and weakly positive expression (respectively 34.1% and 52.3% , x2 =6.386, P ＜ 0.05).Conclusions MTSS1 high expression may play an important role in the early hepatocellular carcinoma progression, indicating a poor prognosis.     

Clinical Outcomes Associated With Chronic Antimicrobial Suppression Therapy in Patients With Continuous‐Flow Left Ventricular Assist Devices

This retrospective cohort study evaluates the effect of chronic antimicrobial suppression (CAS) therapy on clinical outcomes in patients with continuous‐flow left ventricular assist devices (CF‐LVADs) and a history of device‐related infection. Patients with CF‐LVAD implantation between January 2008 and August 2011 who received systemic CAS after index antibiotic treatment of a device‐related infection were included. Chronic suppression was defined as continuation of antibiotics for longer than 6 weeks after the index infection. Standard International Society for Heart and Lung Transplantation definitions were used. The primary outcome is failure of CAS, defined as a clinical deterioration resulting in the need for transition from oral to intravenous (IV) therapy or a need to change to a different IV antibiotic, elevation to status 1A on the transplant list as a result of ongoing infection, or device/driveline exchange. Of 140 patients screened, 16 patients were included (69% male, 63% African American, median age 52 years). The driveline was the most common site of infection (69%). Organisms isolated included Gram‐positive cocci (n = 7), Gram‐negative bacilli (n = 10), and Candida (n = 1). Oral trimethoprim/sulfamethoxazole treatment was most commonly used for suppression (37.5%). Failure of CAS occurred in 5/16 (31%) patients after a mean time of 175 days on therapy (range 10–598). The majority of failures (60%) required device exchanges. Side effects of nausea, vomiting, or diarrhea were reported in three patients; all required changes in oral suppression regimen. Clostridium difficile infection was noted in two patients. These results, which must be confirmed by a larger analysis, suggest that one‐third of CF‐LVAD patients may develop recurrent infections while on CAS therapy.     

miR-21靶向E2F1对三阴性乳腺癌细胞恶性生物学活性及裸鼠肿瘤抑制率的影响

目的 探究miR-21靶向E2F1对三阴性乳腺癌细胞恶性生物学活性及裸鼠肿瘤抑制率的影响。方法将MDA-MB-231细胞分为5组,即MDA-MB-231组、miR-21 inhibitor组、miR-NC inhibitor组、siRNA-E2F1组和siRNA-NC组。检测细胞中miR-21表达（RT-PCR法）;分别检测细胞增殖（MTT法）、侵袭（Transwell法）、迁移（划痕实验）和凋亡能力（流式细胞仪）;检测细胞中E2F1蛋白表达;检测miR-21与E2F1的靶向关系（双荧光素酶实验报告）。结果MDA-MB-231细胞中miR-21表达明显高于MCF10A细胞（P<0.05）;miR-21 inhibitor组细胞细胞中miR-21表达明显低于MDA-MB-231组（P<0.05）。与MDA-MB-231组相比,miR-21 inhibitor组细胞吸光度值、侵袭能力、迁移能力和细胞中E2F1蛋白表达均明显降低,细胞凋亡能力明显升高（P<0.05）;MDA-MB-231组细胞吸光度值、侵袭、迁移、凋亡能力和细胞中E2F1蛋白表达与miR-NC inhibitor组相比差异无统计学意义（P>0.05）。预测软件显示E2F1的3′UTR端与miR-21有碱基互补结合点位。通过向MDA-MB-231细胞中转染野生型E2F1（E2F1-WT）时,miR-21组荧光素酶活性明显低于miR-NC组（P<0.05）;miR-21组和miR-NC组突变体荧光素酶活性相比差异无统计学意义（P>0.05）。与siRNA-NC组相比,siRNA-E2F1组细胞增殖、侵袭、迁移和细胞中E2F1蛋白表达均明显降低,细胞凋亡能力明显增加（P<0.05）。与miR-NC inhibitor组裸鼠移植肿瘤第8天时相比,miR-21 inhibitor组裸鼠肿瘤体积明显降低,肿瘤抑制率为45.3%（P<0.05）。结论低表达miR-21可抑制三阴性乳腺癌细胞增殖、侵袭,促进凋亡,且抑制裸鼠移植瘤体积,其作用机制可能与抑制E2F1表达有关。     

Using UNFOLD to remove artifacts in parallel imaging and in partial-Fourier imaging.

In dynamic MRI, it is often difficult to achieve the acquisition speed required to resolve or freeze the temporal variations of the imaged object. Several MRI methods aim at speeding up the image acquisition process. Through assumptions and/or prior knowledge, these dynamic MRI methods allow part of the needed data to be calculated instead of acquired. For example, partial-Fourier imaging assumes that phase varies smoothly within the object, and parallel imaging (e.g., simultaneous acquisition of spatial harmonics (SMASH) and sensitivity encoding (SENSE)) uses prior knowledge about receiver-coil sensitivity. While these methods accelerate acquisition, they can introduce artifacts or amplify noise in doing so. The present work aims at accelerating image acquisition significantly, while introducing almost no artifacts or noise amplification. It is shown here that new, extra information is gained if dynamic MRI methods are modified so that the sampling function changes in specific ways from time-frame to time-frame. In other words, the set of k-space locations that are acquired (instead of calculated) changes with time. The present temporal strategy, based on the UNaliasing by Fourier-encoding the Overlaps in the temporaL Dimension (UNFOLD) method, can be incorporated into common dynamic MRI methods. Results with partial-Fourier, SMASH, and SENSE imaging are presented here, where UNFOLD's contribution is to very significantly reduce the artifact and/or amplified noise content. Used in this way, UNFOLD contributes indirectly, rather than directly to the improvement in image acquisition speed, as it allows companion methods to operate properly at greater acceleration settings than would otherwise be feasible.     

Proliferation of DU145 prostate cancer cells is inhibited by suppressing insulin-like growth factor binding protein-2

BACKGROUND: Insulin-like growth factor binding protein-2 (IGFBP-2) is expressed by all human prostate cancer cell lines and dramatically increases in the serum of prostate cancer patients. However, the role of IGFBP-2 in prostatic tumorigenesis is not known. The aim of the present study was to investigate the effects of IGFBP-2 on the proliferation of DU145 human prostate cancer cells in culture. METHODS: Using cell proliferation assays, we examined the effects of exogenously administered and endogenously modulated levels of IGFBP-2 on the proliferation of DU145 cells. RESULT: Cell growth was stimulated by exogenously administered IGFBP-2, but significantly retarded (P < 0.05) by its neutralizing antibody. Overexpression of IGFBP-2 by transfection also stimulated cell growth, which was significantly (P < 0.05) inhibited in transfectants expressing antisense mRNA to IGFBP-2. Furthermore, the proliferation of IGFBP-2 overexpressing cells was significantly dampened by exogenously administered IGFBP-2 antibody. CONCLUSIONS: IGFBP-2 is an autocrine growth factor for DU145 human prostate cancer cells and cell proliferation can be significantly retarded by neutralizing or inhibiting its synthesis. These findings provide a strong rationale for targeting IGFBP-2 in the testing of novel strategies to treat prostate cancer.     

Use of superparamagnetic contrast media to suppress signal from flowing spins: Preliminary experience

The authors describe their preliminary experience with the use of superparamagnetic magnetic resonance (MR) imaging contrast media for suppression of signal from flowing blood. The goal of this work was to determine if a superparamagnetic contrast agent could successfully eliminate blood signal during cardiac-gated MR imaging, thereby eliminating or reducing flow artifacts associated with the complex and variable hemodynamics within the heart chambers. Imaging and data analysis were performed in 17 dogs subjected to experimental myocardial infarction as part of a parallel project. Six doses (0.2, 1, 2, 3.5, 4, 5, and 10 mg/kg) of AMI-25, an experimental contrast agent, were used in the study. Spin-echo imaging was performed immediately before and every 5 minutes (for an average of 25 minutes) after bolus injection of the contrast agent. Variations in the image signal-to-noise ratio relative to a baseline (before injection of contrast agent) image were assessed as a function of dose and time. Preliminary results suggest that a considerable reduction in blood flow artifacts and, hence, increases in image signal-tonoise ratio can be achieved at doses greater than or equal to 3.5 mg/kg, for approximately 20 minutes after injection. Doses equal to or less than 2 mg/kg and images obtained more than 20 minutes after injection (regardless of dose) did not reliably show hemodynamic artifact suppression.     

Reward association facilitates distractor suppression in human visual search

Although valuable objects are attractive in nature, people often encounter situations where they would prefer to avoid such distraction while focusing on the task goal. Contrary to the typical effect of attentional capture by a reward‐associated item, we provide evidence for a facilitation effect derived from the active suppression of a high reward‐associated stimulus when cuing its identity as distractor before the display of search arrays. Selection of the target is shown to be significantly faster when the distractors were in high reward‐associated colour than those in low reward‐associated or non‐rewarded colours. This behavioural reward effect was associated with two neural signatures before the onset of the search display: the increased frontal theta oscillation and the strengthened top‐down modulation from frontal to anterior temporal regions. The former suggests an enhanced working memory representation for the reward‐associated stimulus and the increased need for cognitive control to override Pavlovian bias, whereas the latter indicates that the boost of inhibitory control is realized through a frontal top‐down mechanism. These results suggest a mechanism in which the enhanced working memory representation of a reward‐associated feature is integrated with task demands to modify attentional priority during active distractor suppression and benefit behavioural performance.