23 条评论 发表在“Circulation 2009年4月28日”上

1. 1.Epidemiology
   流行病学
   Low-Density Lipoprotein Cholesterol Concentrations and Death Due to Intraparenchymal Hemorrhage: The Ibaraki Prefectural Health Study
   低密度脂蛋白浓度与脑实质出血引起的死亡之间的关系：Ibaraki Prefectural 健康研究
   Background-: Few studies have examined the association between low levels of low-density lipoprotein (LDL) cholesterol and risk of intraparenchymal hemorrhage.
   背景：几乎没有研究分析低密度脂蛋白胆固醇(LDL-c)降低与脑实质出血风险之间的关系。
   Methods and Results-: A total of 30 802 men and 60 417 women, 40 to 79 years of age with no history of stroke or coronary heart disease, completed a baseline risk factor survey in 1993 under the auspices of the Ibaraki Prefectural Health Study. Systematic mortality surveillance was performed through 2003, and 264 intraparenchymal hemorrhage deaths were identified. LDL cholesterol levels were calculated with the formula.
   方法和结果： 总计30802名男性和60417名女性入选，年龄40~79岁，无卒中和冠心病史，所有研究对象于1993年由Ibaraki Prefectural健康研究完成基线风险因素调查。通过对2003年全年总体死亡率的观察，确定264名脑实质出血死亡的患者，采用Friedewald公式计算LDL-c水平。
   Persons with LDL cholesterol >=140 mg/dL had half the sex- and age-adjusted risk of death due to intraparenchymal hemorrhage of those with LDL cholesterol <80 mg/dL.
   修正性别和年龄因素，LDL-c≥140mg/dl的人群脑实质出血死亡的风险是LDL-c<80 mg/dL人群的一半。
   After adjustment for cardiovascular risk factors, the multivariable hazard ratio compared with persons with LDL cholesterol <80 mg/dL was 0.65 (95% CI 0.44 to 0.96) for those with LDL cholesterol 80 to 99 mg/dL, 0.48 (0.32 to 0.71) for 100 to 119 mg/dL, 0.50 (0.33 to 0.75) for 120 to 139 mg/dL, and 0.45 (0.30 to 0.69) for >=140 mg/dL.
   修正冠心病危险因素的影响后，与LDL-c<80 mg/dL人群相比，LDL-c80 ~99 mg/dL人群的(出血)多因素风险比为0.65 (95%可信区间0.44，0.96) ，与LDL-c 100~119 mg/dL相比为0.48 (0.32，0.71)，与LDL-c120 ~139 mg/dL人群相比为0.50 (0.33， 0.75)，与LDL-c≥140mg/dl的人群相比为0.45 (0.30，0.69)。
   These inverse associations were not altered substantially after the exclusion of persons with hypertriglyceridemia, after analysis with a Cox proportional hazard model with time-dependent covariates, or in sensitivity analysis for the potential effect of competing risks.
   排除高甘油三酯血症患者、建立并分析时间相关变量的Cox比例风险回归模型以及对潜在的竞争性风险的敏感性分析均不会影响这种负相关。
   Conclusions-: Low LDL cholesterol levels are associated with elevated risk of death due to intraparenchymal hemorrhage
   结论：低密度脂蛋白胆固醇水平降低与脑实质出血死亡风险的升高之间存在相关关系。
   早上看的时候太匆忙了，出了点错误，谢谢战友指正。

2. 9.Vascular Medicine
   血管医学
   Risk Factors for Abdominal Aortic Aneurysms: A 7-Year Prospective Study: The Study,
   腹主动脉瘤的危险因素：一项历时7年的前瞻性研究- Tromso研究1994-2001
   Background-: Abdominal aortic aneurysm is an asymptomatic condition with a high mortality rate related to rupture.
   背景：腹主动脉瘤通常没有症状，一旦破裂死亡率极高。
   Methods and Results-: In a cohort of 2035 men and 2310 women in Tromso, Norway, who were 25 to 82 years old in 1994, the authors identified risk factors for incident abdominal aortic aneurysm over the next 7 years. The impact of smoking was studied in particular. Ultrasound examination was performed initially in 1994/1995 and repeated in 2001. There were 119 incident cases of abdominal aortic aneurysms (an incidence of 0.4% per year).
   方法和结果：1994年挪威Tromso，年龄25~82岁的2035名男性和2310名女性作为研究队列，随后7年的研究中作者对腹主动脉瘤的危险因素进行研究，重点研究吸烟的影响。1994/1995年完成首次超声检查，2001年进行第二次超声检查。共发现腹主动脉瘤119例(每年的发生率为0.4%)。
   Male sex and increasing age were strong risk factors. In addition, the following variables were significantly associated with increased abdominal aortic aneurysm incidence: Smoking (OR=13.72, 95% CI 6.12 to 30.78, comparing current smokers of >=20 cigarettes/d with never-smokers), hypertension (OR=1.54, 95% CI 1.03 to 2.30), hypercholesterolemia (OR=2.11, 95% CI 1.23 to 3.64, comparing subjects with serum total cholesterol >=7.55 mmol/L with those with total cholesterol <5.85 mmol/L), and low high-density lipoprotein cholesterol (OR=3.25, 95% CI 1.68 to 6.27, comparing subjects with high-density lipoprotein cholesterol <1.25 mmol/L with those with high-density lipoprotein >=1.83 mmol/L). In addition, use of statins was associated with increased risk of abdominal aortic aneurysm (OR=3.77, 95% CI 1.45 to 9.81), but this was probably a marker of high risk of cardiovascular diseases.
   男性和年龄是强危险因素。此外，以下因素与腹主动脉瘤发生几率增加显著相关：吸烟(吸烟>20支/天者与非吸烟者者相比，比值比OR值13.72, 95% 可信区间 6.12， 30.78)；高血压(OR=1.54, 95%可信区间1.03，2.30)；高胆固醇血症(血清总胆固醇≥7.55 mmol/L者与总胆固醇<5.85 mmol/L者相比，OR=2.11, 95%可信区间 1.23，3.64)；低HDL血症(HDL<1.25mmo/L者与HDL≥1.83 mmol/L者相比，OR=3.25, 95%可信区间1.68，6.27)。另外，服用他汀类xx也与腹主动脉瘤发生率增高相关(OR=3.77, 95%可信区间1.45，9.81)，这可能是心血管疾病高危的一个标志。
   Conclusions-: The results demonstrate strong associations between traditional atherosclerosis risk factors and the risk of incident abdominal aortic aneurysms
   结论：本研究证实传统的动脉粥样硬化危险因素与腹主动脉瘤发病风险密切相关。

5. Hypertension 高血压：
   Dietary Intake of Fruits and Vegetables Improves Microvascular Function in Hypertensive Subjects in a Dose-Dependent Manner
   高血压患者饮食摄入蔬果能以剂量依赖模式改善微血管功能
   Background— Observational evidence has consistently linked increased fruit and vegetable consumption with reduced cardiovascular morbidity; however, there is little direct trial evidence to support the concept that fruit and vegetable consumption improves vascular function. This study assessed the dose-dependent effects of a fruit and vegetable intervention on arterial health in subjects with hypertension.
   背景：观测性证据已经持续地将蔬果摄入增加与心血管疾病风险减少两者相关联，然而，能够支持蔬果摄入能改善血管功能这一理念的直接实验依据很少。本实验评估了蔬果摄入对高血压患者动脉健康状态所产生的剂量依赖效应。
   Methods and Results— After a 4-week run-in period during which fruit and vegetable intake was limited to 1 portion per day, participants were randomized to consume either 1, 3, or 6 portions daily for the next 8 weeks. Endothelium-dependent and -independent arterial vasodilator responses were assessed by venous occlusion plethysmography in the brachial circulation before and after intervention. Compliance was monitored with serial contemporaneous 4-day food records and by measuring concentrations of circulating dietary biomarkers.方法与结果：经过4周每天1份蔬果限制的进入期后，参加者随机分为三组，在接下来的8周中分别每天摄入1份、3份或6份蔬果。干预前后分别通过前臂静脉闭塞体积描记术来评估内皮依赖及非内皮依赖的动脉收缩反应。通过连续4天同期饮食记录和测量循环饮食标记物浓度来监控依从性。A total of 117 volunteers completed the 12-week study. Participants in the 1-, 3-, and 6-portions/d groups reported consuming on average 1.1, 3.2, and 5.6 portions of fruit and vegetables, respectively, and serum concentrations of lutein and β-cryptoxanthin increased across the groups in a dose-dependent manner.
   共有117名志愿者完成了12周的研究。三组参加者实际平均蔬果摄入量分别是1.1，3.2，5.6份；三组间叶黄素和β－隐黄质血清浓度的增加呈现剂量依赖关系。
   For each 1-portion increase in reported fruit and vegetable consumption, there was a 6.2% improvement in forearm blood flow responses to intra-arterial administration of the endothelium-dependent vasodilator acetylcholine (P=0.03). There was no association between increased fruit and vegetable consumption and vasodilator responses to sodium nitroprusside, an endothelium-independent vasodilator.
   每增加1份蔬果摄入，血管内给予内皮依赖的血管舒张因子――乙酰胆碱所引起前臂血流量变化可有6.2％的改善（P＝0.03）。蔬果摄入量增加与硝普纳（一种非内皮依赖的血管舒张因子）所引起的血管舒张反应无明显相关性。
   Conclusions— The present study illustrates that among hypertensive volunteers, increased fruit and vegetable consumption produces significant improvements in an established marker of endothelial function and cardiovascular prognosis.
   结论：本实验表明，在高血压志愿受试者中增加蔬果摄入，可xxxx现已明确的可反映内皮功能和心血管预后的标志物。

8. Influence of Systolic and Diastolic Blood Pressure on the Risk of Incident Atrial Fibrillation in Women
   收缩压和舒张压对女性房颤发病的影响
   Background— The influence of systolic and diastolic blood pressure (BP) on incident atrial fibrillation (AF) is not well studied among initially healthy, middle-aged women.
   背景：收缩压和舒张压（BP）对健康、中年女性房颤（AF）发病影响的研究还不够深入。
   Methods and Results— A total of 34 221 women participating in the Women’s Health Study were prospectively followed up for incident AF. The risk of AF across categories of systolic and diastolic BP was compared by use of Cox proportional-hazards models. During 12.4 years of follow-up, 644 incident AF events occurred. Using BP measurements at baseline, we discovered that the long-term risk of AF was significantly increased across categories of systolic and diastolic BP. Multivariable-adjusted hazard ratios for systolic BP categories (<120, 120 to 129, 130 to 139, 140 to 159, and 160 mm Hg) were 1.0, 1.00 (95% CI, 0.78 to 1.28), 1.28 (95% CI, 1.00 to 1.63), 1.56 (95% CI, 1.22 to 2.01), and 2.74 (95% CI, 1.77 to 4.22) (P for trend <0.0001). Adjusted hazard ratios across baseline diastolic BP categories (<65, 65 to 74, 75 to 84, 85 to 89, 90 to 94, and 95 mm Hg) were 1.0, 1.17 (95% CI, 0.81 to 1.69), 1.18 (95% CI, 0.84 to 1.65), 1.53 (95% CI, 1.05 to 2.23), 1.35 (95% CI, 0.82 to 2.22), and 2.15 (95% CI, 1.21 to 3.84) (P for trend=0.004). When BP changes over time were accounted for in updated models, multivariable-adjusted hazard ratios were 1.0, 1.14 (95% CI, 0.89 to 1.46), 1.37 (95% CI, 1.07 to 1.76), 1.71 (95% CI, 1.33 to 2.21), and 2.21 (95% CI, 1.45 to 3.36) (P for trend <0.0001) for systolic BP categories and 1.0, 1.12 (95% CI, 0.82 to 1.52), 1.13 (95% CI, 0.83 to 1.52), 1.30 (95% CI, 0.89 to 1.88), 1.50 (95% CI, 1.01 to 1.88), and 1.54 (95% CI, 0.75 to 3.14) (P for trend=0.026) for diastolic BP categories.
   方法和结果：我们对参加女性健康研究的34211名妇女进行随访以观察房颤的发病情况。通过Cox比例风险模型比较不同收缩压和舒张压水平的个体房颤的发病风险。经过12.4年的随访，共发生AF644例。使用基线的BP水平，我们发现AF的长期风险在不同水平的收缩压和舒张压显著升高。多变量校正后不同收缩压等级（<120, 120-129, 130-139, 140-159和160 mm Hg）的风险比依次为1.0, 1.00 (95% CI, 0.78-1.28), 1.28 (95% CI, 1.00-1.63), 1.56 (95% CI, 1.22-2.01)和2.74 (95% CI, 1.77-4.22) (趋势P值 <0.0001)。多变量校正后不同舒张压等级(<65, 65-74, 75-84, 85-89, 90-94和95 mm Hg)分别是1.0, 1.17 (95% CI, 0.81-1.69), 1.18 (95% CI, 0.84-1.65), 1.53 (95% CI, 1.05-2.23), 1.35 (95% CI, 0.82-2.22)和2.15 (95% CI, 1.21-3.84) (趋势P值=0.004)。模型中引入随时间变化的BP值时，多变量校正后不同收缩压等级的风险比依次为1.0, 1.14 (95% CI, 0.89-1.46), 1.37 (95% CI, 1.07-1.76), 1.71 (95% CI, 1.33-2.21)和2.21 (95% CI, 1.45-3.36) (趋势P值 <0.0001)，多变量校正后不同舒张压等级的风险比依次为1.0, 1.12 (95% CI, 0.82-1.52), 1.13 (95% CI, 0.83-1.52), 1.30 (95% CI, 0.89-1.88), 1.50 (95% CI, 1.01-1.88), and 1.54 (95% CI, 0.75-3.14) (趋势P值=0.026)。
   Conclusions— In this large cohort of initially healthy women, BP was strongly associated with incident AF, and systolic BP was a better predictor than diastolic BP. Systolic BP levels within the nonhypertensive range were independently associated with incident AF even after BP changes over time were taken into account.
   结论：在这个大规模的健康女性队列人群中，BP和AF发病之间存在很强的关联。收缩压比舒张压具有更好的预测能力。处于非高血压范围的收缩压水平也和AF的发病独立相关，在考虑血压随时间的变化后该关联依然存在。
   编译：
   收缩压和舒张压对女性房颤发病的影响
   背景：收缩压和舒张压（BP）对健康、中年女性房颤（AF）发病影响的研究还不够深入。
   方法和结果：我们对参加女性健康研究的34211名妇女进行随访以观察房颤的发病情况。通过Cox比例风险模型比较不同收缩压和舒张压水平的个体房颤的发病风险。经过12.4年的随访，共发生AF644例。使用基线的BP水平，我们发现AF的长期风险在不同水平的收缩压和舒张压显著升高。多变量校正后不同收缩压等级（<120, 120-129, 130-139, 140-159和160 mm Hg）的风险比依次为1.0, 1.00 (95% CI, 0.78-1.28), 1.28 (95% CI, 1.00-1.63), 1.56 (95% CI, 1.22-2.01)和2.74 (95% CI, 1.77-4.22) (趋势P值 <0.0001)。多变量校正后不同舒张压等级(<65, 65-74, 75-84, 85-89, 90-94和95 mm Hg)分别是1.0, 1.17 (95% CI, 0.81-1.69), 1.18 (95% CI, 0.84-1.65), 1.53 (95% CI, 1.05-2.23), 1.35 (95% CI, 0.82-2.22)和2.15 (95% CI, 1.21-3.84) (趋势P值=0.004)。模型中引入随时间变化的BP值时，多变量校正后不同收缩压等级的风险比依次为1.0, 1.14 (95% CI, 0.89-1.46), 1.37 (95% CI, 1.07-1.76), 1.71 (95% CI, 1.33-2.21)和2.21 (95% CI, 1.45-3.36) (趋势P值 <0.0001)，多变量校正后不同舒张压等级的风险比依次为1.0, 1.12 (95% CI, 0.82-1.52), 1.13 (95% CI, 0.83-1.52), 1.30 (95% CI, 0.89-1.88), 1.50 (95% CI, 1.01-1.88), and 1.54 (95% CI, 0.75-3.14) (趋势P值=0.026)。
   结论：在这个大规模的健康女性队列人群中，BP和AF发病之间存在很强的关联。收缩压比舒张压具有更好的预测能力。处于非高血压范围的收缩压水平也和AF的发病独立相关，在考虑血压随时间的变化后该关联依然存在。

9. {dy}篇翻译中，这一句我觉得：After adjustment for cardiovascular risk factors, the multivariable hazard ratio compared with persons with LDL cholesterol <80 mg/dL was 0.65 (95% CI 0.44 to 0.96) for those with LDL cholesterol 80 to 99 mg/dL, 0.48 (0.32 to 0.71) for 100 to 119 mg/dL, 0.50 (0.33 to 0.75) for 120 to 139 mg/dL, and 0.45 (0.30 to 0.69) for >=140 mg/dL. 应翻译为：
   修正冠心病危险因素的影响后，与LDL-c<80 mg/dL人群相比较，LDL-c80 ~99 mg/dL人群相比的多因素为0.65 (95%可信区间0.44，0.96) ，LDL-c 100~119 mg/dL风险比为0.48 (0.32，0.71)，LDL-c120 ~139 mg/dL风险比为0.50 (0.33， 0.75)，LDL-c≥140mg/dl的风险比为0.45 (0.30，0.69)。否则就得不出下面的结论了

10. Hypertension
    Vascular Smooth Muscle Cell–Selective Peroxisome Proliferator–Activated Receptor- Deletion Leads to Hypotension
    血管平滑肌细胞过氧化物酶体增殖物xx受体（PPAR）选择性缺失导致低血压。
    Background— Peroxisome proliferator–activated receptor- (PPAR ) agonists are commonly used to treat diabetes, although their PPAR -dependent effects transcend their role as insulin sensitizers. Thiazolidinediones lower blood pressure (BP) in diabetic patients, whereas results from conventional/tissue-specific PPAR experimental models suggest an important pleiotropic role for PPAR in BP control. Little evidence is available on the molecular mechanisms underlying the role of vascular smooth muscle cell–specific PPAR in basal vascular tone.
    背景――过氧化物酶体增殖物xx受体激动剂（PPAR）（胰岛素增敏剂）常用来xx糖尿病，实际上，其作用并非局限于此。噻唑啉二酮类xx还可降低糖尿病患者的血压，但来自常规/组织特异性PPAR实验模型结果表明，PPAR在血压控制中的作用效果不一。血管平滑肌细胞特异性PPAR参与了基础血管张力形成，但其分子机制尚未阐明。
    Methods and Results— We show that vascular smooth muscle cell–selective deletion of PPAR impairs vasoactivity with an overall reduction in BP. Aortic contraction in response to norepinephrine is reduced and vasorelaxation is enhanced in response to β-adrenergic receptor (β-AdR) agonists in vitro. Similarly, vascular smooth muscle cell–selective PPAR knockout mice display a biphasic response to norepinephrine in BP, reversible on administration of β-AdR blocker, and enhanced BP reduction on treatment with β-AdR agonists. Consistent with enhanced β2-AdR responsiveness, we found that the absence of PPAR in vascular smooth muscle cells increased β2-AdR expression, possibly leading to the hypotensive phenotype during the rest phase.
    方法和结果――结果表明，血管平滑肌细胞PPAR选择性缺失削弱了血管活性，导致机体血压下降。在体研究显示，主动脉对去甲肾上腺素的收缩反应减弱，而对β－肾上腺素能受体激动剂的舒张反应增强。选择性敲除小鼠血管平滑肌细胞PPAR基因，其血压对去甲肾上腺素呈双相反应：以β－肾上腺素能受体阻滞剂处理后，小鼠血压回升，以β－肾上腺素能受体激动剂处理后，小鼠血压明显下降。与β2－肾上腺素能受体功能增强的反应类似，血管平滑肌细胞PPAR缺失引起β2－肾上腺素能受体表达增加，可能引起静息相的低血压状态。
    Conclusion— These data uncovered the β2-AdR as a novel target of PPAR transcriptional repression in vascular smooth muscle cells and indicate that PPAR regulation of β2-adrenergic signaling is important in the modulation of BP.
    结论――本研究发现β2－肾上腺素能受体系血管平滑肌细胞PPAR转录抑制的新靶点，PPAR调节β2－肾上腺素能受体的信号转导在血压调节中具有重要作用。

12. Molecular Cardiology
    Neuropilin-1 Identifies Endothelial Precursors in Human and Murine Embryonic Stem Cells Before CD34 Expression
    神经纤毛蛋白－1可在人和鼠胚胎干细胞表达CD34前识别出前内皮细胞
    Background— In murine embryonic stem cells, the onset of vascular endothelial growth factor receptor 2 (VEGFR-2) expression identifies endothelial precursors. Undifferentiated human embryonic stem cells express VEGFR-2, and VEGFR-2 expression persists on differentiation. The objective of our study was to identify a single population of endothelial precursors with common identifying features from both human and murine embryonic stem cells.
    背景――血管内皮生长因子受体2 (VEGFR-2)在鼠胚胎干细胞中的表达可用于识别前内皮细胞。未分化人胚胎干细胞表达VEGFR-2，并在分化时持续表达。本研究旨在通过人和鼠胚胎干细胞表面共有细胞标志来识别前内皮细胞。
    Methods and Results— We report that expression of the VEGF coreceptor neuropilin-1 (NRP-1) coincides with expression of Brachyury and VEGFR-2 and identifies endothelial precursors in murine and human embryonic stem cells before CD31 or CD34 expression. When sorted and differentiated, VEGFR-2+NRP-1+ cells form endothelial-like colonies that express CD31 and CD34 7-fold more efficiently than NRP-1 cells. Finally, antagonism of both the VEGF and Semaphorin binding functions of NRP-1 impairs the differentiation of vascular precursors to endothelial cells.
    方法和结果――研究发现，血管内皮生长因子共同受体――神经纤毛蛋白－1(NRP-1)的表达与鼠短尾突变表型以及VEGFR-2表达一致，在鼠和人胚胎干细胞表达CD31 或 CD34前即可识别出前内皮细胞。随着细胞的分化，VEGFR-2和NRP-1阳性细胞形成内皮细胞样集落，其表达CD31和CD34是NRP－1细胞的7倍多。血管内皮生长因子和NRP－1的拮抗剂均可削弱前内皮细胞向内皮细胞的分化。
    Conclusions— The onset of NRP-1 expression identifies endothelial precursors in murine and human stem cells. The findings define the origin of a single population of endothelial precursors from human and murine stem cells to endothelial cells. Additionally, the function of both the VEGF and Semaphorin binding activities of NRP-1 has important roles in the differentiation of stem cells to endothelial cells, providing novel insights into the role of NRP-1 in a model of vasculogenesis.
    结论――NRP－1在鼠和人胚胎干细胞表达可识别前内皮细胞，而且，可在胚胎干细胞分化为内皮细胞过程的更早阶段确定前内皮细胞集落。此外，血管内皮生长因子以及NRP－1结合功能在干细胞分化为内皮细胞过程中起重要作用，从而为人们研究NRP－1在血管再生中的作用提供了新的视角。

15. 10.初译：
    Vascular Medicine
    血管医学
    Clinical Trial of Doxycycline for Matrix Metalloproteinase-9 Inhibition in Patients With an Abdominal AneurysmDoxycycline Selectively Depletes Aortic Wall Neutrophils and Cytotoxic T Cells
    临床试验示：在患有腹主动脉瘤的患者中，强力霉素不仅对基质金属蛋白酶-9有抑制作用，同时选择性耗竭主动脉壁中性粒细胞和细胞毒性T细胞
    Background— Doxycycline has been shown to effectively inhibit aneurysm formation in animal models of abdominal aortic aneurysm.
    背景：已证明多西环素：在腹主动脉瘤动物模型中，能够有效地抑制动脉瘤形成的。
    Although this effect is ascribed to matrix metalloproteinase-9 inhibition, such an effect is unclear in human studies.
    虽然这种影响作用是归因于对基质金属蛋白酶-9的抑制，但是在人类的研究中这种作用机制目前还不清楚。
    We reevaluated the effect of doxycycline on aortic wall protease content in a clinical trial and found that doxycycline selectively reduces neutrophil-derived proteases. We thus hypothesized that doxycycline acts through an effect on vascular inflammation
    在一项临床试验中，我们再次评估强力霉素对主动脉壁蛋白酶含量的影响，发现强力霉素能选择性降低中性粒细胞源性蛋白酶。因此，我们推测：强力霉素通过影响血管炎症起作用。
    Methods and Results— Sixty patients scheduled for elective open aneurysmal repair were randomly assigned to 2 weeks of low-, medium-, or high-dose doxycycline (50, 100, or 300 mg/d, respectively) or no medication (control group).
    方法和结果： 60例选择性开放性动脉瘤修复患者，随机分为低，中或高剂量强力霉素2周xx中（分别为：50 ， 100 ，或300毫克/天）或没有xx（对照组） 。
    Aortic wall samples were collected at the time of operation, and the effect of doxycycline treatment on vascular inflammation was evaluated.
    在手术操作时采集主动脉壁样本，并再次评估强力霉素xx血管炎症中的效果；
    Independently of its dose, doxycycline treatment resulted in a profound but selective suppression of aortic wall inflammation as reflected by a selective 72% reduction of the aortic wall neutrophils and a 95% reduction of the aortic wall cytotoxic T-cell content (median values; P<0.00003).
    单独剂量的强力霉素xx，即可产生了深远的影响作用，而且能选择性抑制血管壁炎症，其中选择性的降低主动脉壁中72 ％的中性粒细胞和血管壁中95 ％细胞毒性T细胞含量（中位数； P <0.00003 ） 。
    Evaluation of major inflammatory pathways suggested that doxycycline treatment specifically quenched AP-1 and C/EBP proinflammatory transcription pathways (P<0.0158, NS) and reduced vascular interleukin-6 (P<0.00115), interleukin-8 (P<0.00246, NS), interleukin-13 (P<0.0184, NS), and granulocyte colony-stimulating factor (P<0.031, NS) protein levels. Doxycycline was well tolerated; there were no adverse effects
    评估强力霉素xx血管炎症主要途径推荐为，特异性灭活AP – 1（xx蛋白-1）和C / EBP（转录因子CCAAT增强子结合蛋白）的促炎症转录途径（ P <0.0158 ，无显著性差异NS）和减少血管白细胞介素6 （ P < 0.00115 ） ，白细胞介素-8 （ P < 0.00246 ，无显著性差异（NS） ，白细胞介素13 （ P < 0.0184 ，无显著性差异(NS）和粒细胞集落刺激因子（ P < 0.031 ，无显著性差异(NS ）的蛋白水平。患者对强力霉素的耐受性良好；没有任何不良反应。
    Conclusions— A brief period of doxycycline treatment has a profound but selective effect on vascular inflammation and reduces aortic wall neutrophil and cytotoxic T-cell content.
    结论：短期的强力霉素xx具有深远的作用，并且在血管炎症反应中选择性减少主动脉壁中的中性粒细胞和细胞毒性T细胞的含量。
    Results of this study are relevant for pharmaceutical stabilization of the abdominal aneurysm and possibly for other inflammatory conditions that involve neutrophils and/or cytotoxic T cells.
    本次研究结果显示、：与腹主动脉瘤相关的xx学稳定作用，并可能对其他炎症（包括中性粒细胞和/或细胞毒性T细胞参与）的情况有效。

16. 10.编译：
    血管医学
    临床试验示：在患有腹主动脉瘤的患者中，强力霉素不仅对基质金属蛋白酶-9有抑制作用，同时选择性耗竭主动脉壁中性粒细胞和细胞毒性T细胞
    背景：已证明多西环素：在腹主动脉瘤动物模型中，能够有效地抑制动脉瘤形成的。虽然这种影响作用是归因于对基质金属蛋白酶-9的抑制，但是在人类的研究中这种作用机制目前还不清楚。在一项临床试验中，我们再次评估强力霉素对主动脉壁蛋白酶含量的影响，发现强力霉素能选择性降低中性粒细胞源性蛋白酶。因此，我们推测：强力霉素通过影响血管炎症起作用
    方法和结果： 60例选择性开放性动脉瘤修复患者，随机分为低，中或高剂量强力霉素2周xx中（分别为：50 ， 100 ，或300毫克/天）或没有xx（对照组） 。在手术操作时采集主动脉壁样本，并再次评估强力霉素xx血管炎症中的效果；单独剂量的强力霉素xx，即可产生了深远的影响作用，而且能选择性抑制血管壁炎症，其中选择性的降低主动脉壁中72 ％的中性粒细胞和血管壁中95 ％细胞毒性T细胞含量（中位数；P <0.00003 ） 。评估强力霉素xx血管炎症主要途径推荐为，特异性灭活AP – 1（xx蛋白-1）和C / EBP（转录因子CCAAT增强子结合蛋白）的促炎症转录途径（ P <0.0158 ，无显著性差异NS）和减少血管白细胞介素6 （ P < 0.00115 ） ，白细胞介素-8 （ P < 0.00246,无显著性差异NS） ，白细胞介素13 （ P < 0.0184 ，无显著性差异NS）和粒细胞集落刺激因子（ P < 0.031 ，无显著性差异NS ）的蛋白水平。患者对强力霉素的耐受性良好；没有任何不良反应。
    结论：短期的强力霉素xx具有深远的作用，并且在血管炎症反应中选择性减少主动脉壁中的中性粒细胞和细胞毒性T细胞的含量。本次研究结果显示、：与腹主动脉瘤相关的xx学稳定作用，并可能对其他炎症（包括中性粒细胞和/或细胞毒性T细胞参与）的情况有效。

18. 8.
    Preventive Cardiology
    Physician Alerts to Prevent Symptomatic Venous Thromboembolism in Hospitalized Patients
    住院病人预防静脉血栓栓塞症状的内科预警。
    Background— Venous thromboembolism (VTE) prophylaxis remains underused among hospitalized patients. We designed and carried out a large, multicenter, randomized controlled trial to test the hypothesis that an alert from a hospital staff member to the attending physician will reduce the rate of symptomatic VTE among high-risk patients not receiving prophylaxis.
    背景：住院病人需要持续地静脉血栓栓塞(VTE)预防。我们设立了一个大型多中心随机对照研究研究，来检验这样一个假说：来自以主治医生为主的医护人员的预警能减少未接受预防性xx的VTE高危人群症状的出现率。
    Methods and Results— We enrolled patients using a validated point score system to detect hospitalized patients at high risk for symptomatic VTE who were not receiving prophylaxis. We randomized 2493 patients (82% on Medical Services) from 25 study sites to the intervention group (n=1238), in which the responsible physician was alerted by another hospital staff member, or the control group (n=1255), in which no alert was issued. The primary end point was symptomatic, objectively confirmed VTE within 90 days. Patients whose physicians were alerted were more than twice as likely to receive VTE prophylaxis as control subjects (46.0% versus 20.6%; P<0.0001). The symptomatic VTE rate was lower in the intervention group (2.7% versus 3.4%; hazard ratio, 0.79; 95% CI, 0.50 to 1.25), but the difference did not achieve statistical significance. The rate of major bleeding at 30 days in the alert group was similar to that in the control group (2.1% versus 2.3%; P=0.68).
    方法和结果：我们登记了用有效的按点积分系统来检验未接受预防处理的VTE症状高危人群。我们从25个研究点的2493个病人（82%来自医疗机构）中随机抽取了介入组（n=1238），其中责任医师也受其他医院成员的警示，而对照组(n=1255)则没有接受预警。主要终点指标为90天的出现的症状，被客观证据证实的VTE。主治医师接受预警的病人接受VTE预防的可能性远远大于对照组的两倍(46.0%比 20.6%; P<0.0001).介入组的VTE症状出现率更小(2.7% 比 3.4%; 危害比, 0.79; 95% CI, 0.50 -1.25),但是该差异没有统计学意义。30天大出血发生率在警觉组和对照组相似(2.1% 比 2.3%; P=0.68).。
    Conclusions— A strategy of direct notification of the physician by a staff member increases prophylaxis use and leads to a reduction in the rate of symptomatic VTE in hospitalized patients. However, VTE prophylaxis continues to be underused even after physician notification, especially among Medical Service patients.
    结论：内科医生直接关注的政策能增加预防法应用，并能减少住院病人VTE症状的发生率。然而，即使内科医生通知的VTE预防也是使用不足的，特别是在医疗卫生机构病人中。

20. 6.分子心脏病学
    Mineralocorticoid Modulation of Cardiac Ryanodine Receptor Activity Is Associated With Downregulation of FK506-Binding Proteins
    盐皮质xx对心脏Ryanodine 受体活动的调节与降低FK506结合蛋白的表达有关
    Background— The mineralocorticoid pathway is involved in cardiac arrhythmias associated with heart failure through mechanisms that are incompletely understood. Defective regulation of the cardiac ryanodine receptor (RyR) is an important cause of the initiation of arrhythmias. Here, we examined whether the aldosterone pathway might modulate RyR function.
    研究背景— 盐皮质xx途径与心衰时的心律失常有关，其机制不甚明了。心脏ryanodine受体(RyR)的下调是心律失常的一个重要原因。在这里我们验证了醛固酮途径是否会调节RyR的功能。
    Methods and Results— Using the whole-cell patch clamp method, we observed an increase in the occurrence of delayed afterdepolarizations during action potential recordings in isolated adult rat ventricular myocytes exposed for 48 hours to aldosterone 100 nmol/L, in freshly isolated myocytes from transgenic mice with human mineralocorticoid receptor expression in the heart, and in wild-type littermates treated with aldosterone. Sarcoplasmic reticulum Ca2+ load and RyR expression were not altered; however, RyR activity, visualized in situ by confocal microscopy, was increased in all cells, as evidenced by an increased occurrence and redistribution to long-lasting and broader populations of spontaneous Ca2+ sparks. These changes were associated with downregulation of FK506-binding proteins (FKBP12 and 12.6), regulatory proteins of the RyR macromolecular complex.
    结果和方法—使用全细胞膜片钳的方法，我们在暴露于醛固酮100 nmol/L48小时的成年 大鼠心肌细胞、在新鲜分离的人盐皮质xx受体转基因鼠心肌细胞、在醛固酮饲养的野生鼠的同窝仔的心肌细胞中，均观察到了细胞动作电位时程中延迟后除极发生的增加。线粒体钙负荷及RyR的表达均没有改变，然而，我们用原位共聚焦显微镜在所有细胞中均观察到了长时间的自发性钙火花的发生和重新分配的增加，这也证明了RyR与活动的增加。这些变化与FK506结合蛋白这一RyR分子复合体的调节蛋白的下调有关。
    Conclusions— We suggest that in addition to modulation of Ca2+ influx, overstimulation of the cardiac mineralocorticoid pathway in the heart might be a major upstream factor for aberrant Ca2+ release during diastole, which contributes to cardiac arrhythmia in heart failure.
    研究结论—我们认为对心脏盐皮质xx的过度刺激不仅调节钙内流，而其也与心脏舒张时异常的钙释放有关，而这会引起心衰时的心律失常。
    请多多指教！

21. 全文链接及下载地址
    1，Low-Density Lipoprotein Cholesterol Concentrations and Death Due to Intraparenchymal Hemorrhage
    
    2，Influence of Systolic and Diastolic Blood Pressure on the Risk of Incident Atrial Fibrillation in Women
    
    3，Dietary Intake of Fruits and Vegetables Improves Microvascular Function in Hypertensive Subjects in a Dose-Dependent Manner
    
    4，Vascular Smooth Muscle Cell–Selective Peroxisome Proliferator–Activated Receptor- Deletion Leads to Hypotension
    
    5，Neuropilin-1 Identifies Endothelial Precursors in Human and Murine Embryonic Stem Cells Before CD34 Expression
    
    6，Mineralocorticoid Modulation of Cardiac Ryanodine Receptor Activity Is Associated With Downregulation of FK506-Binding Proteins
    
    7，Macrophage-Specific Expression of Mannose-Binding Lectin Controls Atherosclerosis in Low-Density Lipoprotein Receptor–Deficient Mice
    
    8，Physician Alerts to Prevent Symptomatic Venous Thromboembolism in Hospitalized Patients
    
    9，Risk Factors for Abdominal Aortic Aneurysms A 7-Year Prospective Study
    
    10，Clinical Trial of Doxycycline for Matrix Metalloproteinase-9 Inhibition in Patients With an Abdominal Aneurysm
    

22. Molecular Cardiology
    Macrophage-Specific Expression of Mannose-Binding Lectin Controls Atherosclerosis in Low-Density Lipoprotein Receptor–Deficient Mice
    巨噬细胞特异性表达的甘露糖结合凝集素调控低密度脂蛋白受体基因敲除小鼠动脉粥样硬化的进展。
    Background— With consideration of the central role of the innate immune system in atherogenesis and mannose-binding lectin (MBL) as an innate regulator of immunity, the role of MBL in experimental and human atherosclerosis was assessed.
    背景：考虑到固有免疫系统在动脉粥样硬化中起核心作用，而甘露糖结合凝集素(MBL)是一种固有免疫调节剂，因此我们研究了MBL在实验动物及人动脉粥样硬化中的作用。
    Methods and Results— With the use of immunohistochemistry and polymerase chain reaction, deposition and gene expression of MBL-A and -C were assessed in murine atherosclerosis from mice deficient for the low-density lipoprotein receptor (LDLR–/–) after 10 or 18 weeks of high-fat feeding. MBL was present and was produced in 10-week-old lesions, whereas deposition and gene expression were minimal after 18 weeks of high-fat feeding and absent in healthy vasculature. Interestingly, deposition of MBL-A and -C differed: MBL-A predominantly localized in upper medial layers, whereas MBL-C was found in and around intimal macrophages. To further study the role of local MBL production by monocytic cells in atherosclerosis, LDLR–/– mice with MBL-A and -C–/– monocytic cells were construed by bone marrow transplantation. Mice carrying MBL-A and -C double deficient macrophages had increased (30%) atherosclerotic lesions compared with wild-type controls (P=0.015) after 10 weeks of high-fat diet. Subsequently, analysis of MBL deposition and gene expression in advanced human atherosclerotic lesions revealed the presence of MBL protein in ruptured but not stable atherosclerotic lesions. Putatively in agreement with murine data, no MBL gene expression could be detected in advanced human atherosclerotic lesions.
    方法和结果：低密度脂蛋白受体基因敲除小鼠(LDLR–/–)予高脂饮食10或18周后建立小鼠动脉粥样硬化模型，用免疫组织化学和聚合酶链反应分别检测MBL-A和 –C在组织中蛋白沉积和基因表达。MBL在8周龄小鼠动脉粥样硬化损伤部位开始产生出现，高脂饮食18周后组织蛋白沉积和基因表达比较轻微，而在健康血管中没有相应表达。有趣的是，MBL-A和 –C的沉积部位是不同的，MBL-A主要位于血管中上层，而MBL –C主要在血管内膜巨噬细胞中表达。接着用骨髓移植的方法给LDLR–/–小鼠植入MBL-A 和 -C–/–单核细胞，以研究单核细胞局域性产生的MBL在动脉粥样硬化中的作用。高脂饮食10周后，相较于野生型对照组小鼠而言，MBL-A 和 –C双基因敲除小鼠动脉粥样硬化损伤部位有所增大(30%，P=0.015)。随后发现人进展期动脉粥样硬化损伤斑块中，破裂斑块中有MBL蛋白沉积和基因表达，而稳定性斑块中没有相应表现。由小鼠研究资料我们可以得出一致推论：在人进展期动脉粥样硬化损伤斑块中应该没有MBL基因表达。
    Conclusions— These results are the first to show that MBL is abundantly present and locally produced during early atherogenesis. Local MBL expression, by myeloid cells, is shown to critically control development of atherosclerotic lesions.
    结论：这些结果首次提示MBL在动脉粥样硬化早期局域性大量表达。髓系细胞表达的MBL在动脉粥样硬化损伤进展中起着临界控制的作用。