18 F-fluorodeoxyglucose positron emission tomography to evaluate recurrent gastric cancer: a systematic review and meta-analysis

Background and Aim: We aimed to explore the role of the diagnostic accuracy of ¹⁸F‐fluorodeoxyglucose positron emission tomography (¹⁸F‐FDG PET) in detecting recurrent gastric cancer through a systematic review and meta‐analysis. Methods: The MEDLINE, EMBASE, Cancerlit, and Cochrane Library database, from January 2001 to July 2011, were searched for studies evaluating the diagnostic performance of ¹⁸F‐FDG PET in detecting recurrent gastric cancer. We determined the sensitivities and specificities across studies, calculated positive and negative likelihood ratios (LR+ and LR?), and constructed summary receiver operating characteristic curves. We also compared the performance of ¹⁸F‐FDG PET with computed tomography (CT) by analyzing studies that had also used these diagnostic methods on the same patients. Results: Across nine studies (526 patients), the overall sensitivity of ¹⁸F‐FDG PET was 0.78 (95% confidence interval [CI]: 0.68–0.86), and the overall specificity was 0.82 (95% CI: 0.76–0.87). Overall, LR+ was 3.52 (95% CI: 2.68–4.63) and LR? was 0.32 (95% CI: 0.22–0.46). In studies in which both ¹⁸F‐FDG PET and other diagnostic tests were performed, the sensitivity and specificity of ¹⁸F‐FDG PET were 0.72 (95% CI: 0.62–0.80) and 0.84 (95% CI: 0.77–0.90), respectively; of contrast CT, they were 0.74 (95% CI: 0.64–0.83) and 0.85 (95% CI: 0.78–0.90), respectively; and of combined PET and CT, they were 0.75 (95% CI: 0.67–0.82) and 0.85 (95% CI 0.79–0.90), respectively. Study sensitivity was not correlated with the prevalence of recurrent gastric cancer. Conclusion: ¹⁸F‐FDG PET has good diagnostic performance in the overall evaluation of recurrent gastric cancer, but still has some limited performance compared with contrast CT. ¹⁸F‐FDG PET combined with CT might improve the diagnostic performance in detecting recurrent gastric cancer.     

A comparison of intracoronary with intravenous glycoprotein IIb/IIIa inhibitors during percutaneous coronary intervention in patients with acute coronary syndrome: a meta-analysis of randomized controlled trials

Background : It is still debatable whether intracoronary (IC) administration of glycoprotein IIb/IIIa inhibitors (GPIs) is superior to intravenous (IV) administration for patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). Methods: We performed a meta‐analysis of randomized controlled clinical trials. A literature search was conducted for relevant trials. Primary end‐points were short‐term (1–3 months) and mid‐/long‐term (6/12 months) major adverse cardiovascular events (MACEs) (mortality, reinfarction, target vessel revascularization [TVR]). Secondary end‐points were thrombolysis in myocardial infarction (TIMI) grade flow, TIMI myocardial perfusion grade (TMPG) flow, left ventricular ejection fraction (LVEF) within 2 weeks, and bleeding complication. Results: Twelve studies were included in the meta‐analysis. IC administration of GPIs did not decrease short‐term mortality (OR: 0.71, 95% CI: 0.41–1.23, P = 0.22) and reinfarction rate (OR: 0.76, 95% CI: 0.45–1.29, P = 0.31) compared with IV administration. There was a trend toward reduction of short‐term TVR rate in IC group compared with IV group but not reaching statistical significance (OR: 0.57, 95% CI: 0.31–1.04, P = 0.07). IC administration of GPIs significantly increased TIMI grade 3 flow (OR: 1.48, 95% CI: 1.06–2.06, P = 0.02) and TMPG grade 2–3 flow (OR: 2.63, 95% CI: 1.53–4.51, P = 0.0004) compared with IV administration. No significant difference was observed in long‐term MACEs rate, LVEF, and bleeding complication between the 2 groups. Conclusion: IC administration of GPIs in patients with ACS undergoing PCI can significantly increase target coronary flow and myocardial reperfusion without increasing the risk of bleeding complication, but cannot improve clinical outcome compared with IV administration. (J Interven Cardiol 2012;25:223–234)     

Common variants of the UMOD promoter associated with blood pressure in a community-based Chinese cohort

Hypertension is an important risk factor for chronic kidney disease. The kidney, in turn, has an important role in the regulation of blood pressure (BP). On the basis of a genome-wide association study, single-nucleotide polymorphisms in the uromodulin (UMOD) promoter region had been considered to influence both renal sodium reabsorption and BP. In this study, we asked whether common variants across the UMOD gene influence BP in a community-based Chinese cohort. We screened seven common variants across the UMOD locus in a community-based population from Beijing, including 1000 individuals with 48% males and an average age of 63.7±9.0 years. The urinary UMOD concentration was measured by enzyme-linked immunosorbent assay. We then analyzed the association of common variants of UMOD with BP. The UMOD promoter common variant rs13333226 G/A is associated with diastolic BP (DBP), and G allele carriers have higher DBP compared with A/A homozygotes (P=0.035). The variant rs6497476 C/T predicted the DBP level, with C homozygotes having a higher DBP compared with CT heterozygotes and T homozygotes (P=0.025). Urinary UMOD excretion was correlated with urinary sodium excretion (R=0.239, P=0.656*10(-13)). We determined that common variants of UMOD are associated with DBP level in a community-based Chinese cohort.     

Allicin Ameliorates Cardiac Hypertrophy and Fibrosis through Enhancing of Nrf2 Antioxidant Signaling Pathways

Aim

To evaluate the protective effects of allicin on Ang II-induced cardiac hypertrophy.

Methods

Sprague?CDawley male rats were randomized into 3 groups:1)sham group (saline)(n?=?12), 2) Ang II group(n?=?9), 3) allicin group (Ang II + allicin)(n?=?9). They received infusions of either saline or Ang II (250?ng/kg body weight per min) through mini-osmotic pumps implanted subcutaneously for 2?weeks and given a diet containing 180?mg/kg/day of allicin for 8 consecutive weeks. Hemodynamic, morphological, histological, and biochemical changes were evaluated at corresponding time points.

Results

Ang II infusion increased blood pressure, heart rate and heart weight to body weight ratio, and resulted in anatomical and functional changes, such as increased LV mass, posterior wall thickness and LV end-diastolic diameter, and decreased fractional shortening and EF compared with sham rats. Nrf2 and HO-1 in the hearts of rats in the Ang II group were moderately elevated at both mRNA and protein levels compared to sham group mice, but NQO1 and??-GCS were significantly lower. GPx activities, levels of GSH and T-AOC in the hearts of the rats in the Ang II group were also significantly lower, and the levels of TBARS, reactive oxygen species and protein carbonyl were significant increased. Allicin attenuated LV mass, posterior wall thickness and LV end-diastolic diameter (1.10?±?0.04 vs. 1.37?±?0.05, 2.26?±?0.08 vs. 2.96?±?0.12, 7.27?±?0.36 vs. 8.56?±?0.41, respectively; all P?<?0.05), and increased fractional shortening and EF (28.30?±?3.21 vs. 25.40?±?2.57, 60.27?±?5.63 vs. 51.30?±?4.78, respectively; both P?<?0.05) in the Ang II-induced hypertrophic rats compared to the untreated Ang II rats. Furthermore, allicin treatment attenuated the accumulation of interstitial collagen and collagen I/III (P?<?0.01 vs. the untreated Ang II group), decreased the levels of reactive oxygen species, protein carbonyl and TBARS and increased GPx activities. Moreover, allicin significantly increased mRNA expression and protein levels of Nrf2, NQO1, and ??-GCS ( P?<?0.01, P?<?0.05 vs. the untreated Ang II group).

Conclusion

Allicin could prevent the development of cardiac remodeling and the progression of cardiac hypertrophy to cardiac dysfunction caused by enhancing the Nrf2 antioxidant signaling pathways.     

细粒棘球绦虫EgA31重组蛋白的抗原表位分析预测

根据GenBank中细粒棘球绦虫EgA31序列(GenBank登录号为AF067807)设计引物,以细粒棘球绦虫mRNA为模板,RT-PCR扩增EgA31基因,将其克隆入pUCm-T载体,转化大肠埃希菌(E coli)DH5α,筛选阳性克隆,经BamH I、Sac I双酶切和PCR鉴定,获得阳性重组质粒pUCm-T/EgA31,并将测序正确的片段连接表达载体,成功构建重组质粒pET30a-EgA31。经序列分析和同源性比较,以及对其编码产物进行B细胞和T细胞表位分析,结果表明PCR扩增的特异条带为636 bp,与预期相符,与GenBank已知基因序列同源性为100%。编码产物B细胞和T细胞联合表位预测,氨基酸区域可能在32～79、79～95、105～124和141～154位。     

哈萨克族心力衰竭患者血浆生长分化因子15和B型利钠肽的临床意义

目的:研究血浆生长分化因子15(GDF-15)、B型利钠肽(BNP)对新疆哈萨克族(哈族)心力衰竭(HF)的意义及与其严重程度之间的关系。方法:选取新疆哈族HF患者90例(NYHAⅡ～IV级)及哈族NYHAⅠ级患者30例为研究对象,均采取空腹静脉血,测定血浆BNP及GDF-15水平,同时超声心动图测定各项心功能指标。结果:哈族HF组患者血浆GDF-15和BNP水平明显高于对照组[GDF-15(132.14±56.36)ng/L∶(34.08±10.80)ng/L;BNP(273.78±93.37)ng/ml∶(82.80±15.18)ng/ml,P<0.01],并随NYHA心功能分级的增加而升高,各组间差异均有统计学意义(均P<0.01)。哈族HF患者血浆GDF-15水平与血肌酐(Cr)、左心房前后径(LAD)、左心室舒张末期内径(LVEDd)、NYHA、BNP呈正相关(r=0.266、0.423、0.668、0.925、0.845,P<0.05);与左心室射血分数(LVEF)、左心室短轴缩短率(FS)呈显著负相关(r=-0.807、-0.733,P<0.01)。结论:哈族HF患者血浆GDF-15、BNP水平明显升高,与哈族HF程度密切相关,血浆GDF-15水平是判断哈族HF严重程度有价值的指标。     

起搏器电池耗竭的心电图表现及临床意义

目的探讨起搏器电池耗竭的心电图表现及其临床意义。方法对23例临床证实起搏器电池耗竭患者的临床资料及心电图进行回顾性分析。结果起搏频率减慢或起搏频率不均6例;起搏频率奔放1例;感知功能异常6例;起搏功能异常3例;感知及起搏功能均异常4例;起搏方式改变3例。结论起搏器电池耗竭可以有多种心电图表现,但必须结合临床,要除外起搏器系统的机械故障及起搏器参数设置不当引起类似的心电图改变,对于证实起搏器电池耗竭的患者要及时更换起搏器。     

Peg-IFNa-2a/RBV antiviral efficacy in cirrhotic hepatitis C patients after splenectomy or partial splenic embolization

To investigate the antiviral efficacy of combination therapy with peglyated-interferon alpha (peg-IFNa)-2a and ribavirin (RBV) in hepatitis C patients with liver cirrhosis after splenectomy or partial splenic embolization. Forty-nine hepatitis C patients with liver cirrhosis who were unable to use antiviral therapy because of hypersplenism were recruited for study and treated with splenectomy or partial splenic embolization. Three months later, a regimen of antiviral combination therapy was initiated with peg-IFNa-2a (once-weekly subcutaneous injection: 135 μg or 180 μg) and RBV (daily oral: 800 to 1200 mg), and was maintained for 48 weeks. The patients were followed up at treatment weeks 1, 2, 4, 6, 8, and 12. Thereafter, follow-up was conducted every four weeks. The patients were observed until 24 weeks after treatment discontinuation. Follow-up testing included liver function, blood chemistry, renal function, and HCV RNA level. Any adverse reactions were recorded. HLiver cirrhosis patients complicated by hypersplenism can be treated effectively with peg-IFNa-2a/RBV combination antiviral therapy after splenectomy or partial splenic embolization. The antiviral-induced sustained viral response rates was 65.00% in cirrhotic/hypersplenic hepatitis C patients receiving splenectomy and 58.62% in those receiving partial splenic embolization. Hypersplenism patients with hepatitis C-related cirrhosis achieved a good antiviral therapeutic effect with peg-IFNa-2a/RBV combination therapy following splenectomy or partial splenic embolization. This sequence of treatment may help to decrease incidences of chronic hepatitis C-induced liver failure and liver cancer in these patients.     

婴幼儿室间隔缺损合并重度肺动脉高压术后心排量与氧代谢的变化规律

目的:总结分析婴幼儿期室间隔缺损合并重度肺动脉高压心脏直视术后心排量与氧供、氧耗的变化规律及临床意义。方法:室间隔缺损合并重度肺动脉高压患儿25例,男性15例,女性10例。年龄0.5～2.75(1.25±0.68)岁,体质量5～13.7(8.68±2.49)kg,术前经皮血氧饱和度(SPO2)0.95～0.99(0.97±0.70),超声心动图检查平均肺动脉压力65～82(67.86±21.35)mmHg(1 mmHg=0.133 kPa)。合并心脏畸形包括:房间隔缺损9例,动脉导管未闭5例,主动脉弓缩窄3例。麻醉时经颈内静脉置入4F Swan-Ganz漂浮导管,经桡动脉置入动脉测压管。分别于手术结束即刻、术后4 h、8 h、12h、24 h、48 h及72 h,由桡动脉及漂浮导管抽取动脉和混合静脉血标本行血气分析。热稀释法测定心排量(CO),PHLIPS M:8007 A计算心排指数(CL)、氧供指数(DO2I)、氧耗指数(VO2I)、氧摄取率(O2ER)。结果:①术后DO2I与VO2I显著相关,术后即刻呈线性依赖;②术后8 h CI、DO2I、VO2I最低;O2ER最高。结论:婴幼儿期室间隔缺损合并重度肺动脉高压,术后即刻存在着病理性氧供依赖,术后8 h既存在氧供不足又有氧耗下降,应积极提高心排量改善组织氧分。     

Increased expression of chondroitin sulphate proteoglycans in rat hepatocellular carcinoma tissues

AIM: To investigate the expression of chondroitin sulphate proteoglycans (CSPGs) in rat liver tissues of hepatocellular carcinoma (HCC).METHODS: Thirty male Sprague Dawley rats were randomly divided into two groups: control group (n = 10) and HCC model group (n = 20). Rats in the HCC model groups were intragastrically administrated with 0.2% (w/v) N-diethylnitrosamine (DEN) every 5 d for 16 wk, whereas 0.9% (w/v) normal saline was administered to rats in the control group. After 16 wk from the initiation of experiment, all rats were killed and livers were collected and fixed in 4% (w/v) paraformaldehyde. All tissues were embedded in paraffin and sectioned. Histological staining (hematoxylin and eosin and Toluidine blue) was performed to demonstrate the onset of HCC and the content of sulphated glycosaminoglycan (sGAG). Immunohistochemical staining was performed to investigate the expression of chondroitin sulphate (CS)/dermatan sulphate (DS)-GAG, heparan sulphate (HS)-GAG, keratan sulphate (KS)-GAG in liver tissues. Furthermore, expression and distribution of CSPG family members, including aggrecan, versican, biglycan and decorin in liver tissues, were also immunohistochemically determined.RESULTS: After 16 wk administration of DEN, malignant nodules were observed on the surface of livers from the HCC model group, and their hepatic lobule structures appeared largely disrupted under microscope. Toluidine blue staining demonstrated that there was an significant increase in sGAG content in HCC tissues when compared with that in the normal liver tissues from the control group [0.37 ± 0.05 integrated optical density per stained area (IOD/area) and 0.21 ± 0.01 IOD/area, P < 0.05]. Immunohistochemical studies demonstrated that this increased sGAG in HCC tissues was induced by an elevated expression of CS/DS (0.28 ± 0.02 IOD/area and 0.18 ± 0.02 IOD/area, P < 0.05) and HS (0.30 ± 0.03 IOD/area and 0.17 ± 0.02 IOD/area, P < 0.01) but not KS GAGs in HCC tissues. Further studies thereby were performed to investigate the expression and distribution of several CSPG components in HCC tissues, including aggrecan, versican, biglycan and decorin. Interestingly, there was a distinct distribution pattern for these CSPG components between HCC tissues and the normal tissues. Positive staining of aggrecan, biglycan and decorin was localized in hepatic membrane and/or pericellular matrix in normal liver tissues; however, their expression was mainly observed in the cytoplasm, cell membranes in hepatoma cells and/or pericellular matrix within HCC tissues. Semi-quantitative analysis indicated that there was a higher level of expression of aggrecan (0.43 ± 0.01 and 0.35 ± 0.03, P < 0.05), biglycan (0.32 ± 0.01 and 0.25 ± 0.01, P < 0.001) and decorin (0.29 ± 0.01 and 0.26 ± 0.01, P < 0.05) in HCC tissues compared with that in the normal liver tissues. Very weak versican positive staining was observed in hepatocytes near central vein in normal liver tissues; however there was an intensive versican distribution in fibrosis septa between the hepatoma nodules. Semi-quantitative analysis indicated that the positive rate of versican in hepatoma tissues from the HCC model group was much higher than that in the control group (33.61% and 21.28%, P < 0.05). There was no positive staining in lumican and keratocan, two major KSPGs, in either normal or HCC liver tissues.CONCLUSION: CSPGs play important roles in the onset and progression of HCC, and may provide potential therapeutic targets and clinical biomarkers for this prevalent tumor in humans.