Cyclic stretch upregulates SDF-1α/CXCR4 axis in human saphenous vein smooth muscle cells

Cyclic stretch (CS) mediates different cellular functions in vascular smooth muscle cells and involves in neointimal hyperplasia and subsequent atherosclerosis of vein grafts. Here, we investigated whether CS can modulate stromal cell-derived factor-1α (SDF-1α)/CXCR4 axis in human saphenous vein smooth muscle cells. We found CS induced the upregulation of SDF-1α and CXCR4 in human saphenous vein smooth muscle cells in vitro, which was dependent on PI3K/Akt/mTOR pathway. Furthermore, CS augmented human saphenous vein smooth muscle migration and focal adhesion kinase (FAK) activation by PI3K/Akt/mTOR pathway. Interestingly, the upregulation of SDF-1α/CXCR4 axis was instrumental in CS-induced saphenous vein smooth muscle cell migration and FAK activation, as showed by AMD3100, an inhibitor of SDF-1α/CXCR4 axis, partially but significantly blocked the CS-induced cellular effects. Thus, those data suggested SDF-1α/CXCR4 axis involves in CS-mediated cellular functions in human saphenous vein smooth muscle cells.     

Detection and Characterization of a Protein Isoaspartyl Methyltransferase Which Becomes Trapped in the Extracellular Space During Blood Vessel Injury

Injury to rat blood vessels in vivo was found to release intracellular pools of protein D-aspartyl/L-isoaspartyl carboxyl methyltransferase (PIMT) into the extracellular milieu, where it becomes trapped. This trapped cohort of PIMT is able to utilize radiolabeled S-adenosyl-L-methionine (AdoMet) introduced into the circulation to methylate blood vessel proteins containing altered aspartyl residues. As further shown in this study, methylated substrates are detected only at the specific site of injury. In vitro studies more fully characterized this endogenous PIMT activity in thoracic aorta and inferior vena cava. Methylation kinetics, immunoblotting, and the lability of methylated substrates at mild alkaline pH were used to demonstrate that both types of blood vessel contain an endogeneous protein D-aspartyl/L-isoaspartyl carboxyl methyltransferase (PIMT). At least 50% of the PIMT activity is resistant to nonionic detergent extraction, suggesting that the enzyme activity becomes trapped within or behind the extracellular matrix (ECM). Quantities of lactate dehydrogenase (LDH), another soluble enzyme of presumed intracellular origin, were found to be similarly trapped in the extracellular space of blood vessels.     

Relationship between ablation index and myocardial biomarkers after radiofrequency catheter ablation for atrial fibrillation

BackgroundFurther in-vivo evidence is needed to support the usefulness of ablation index (AI) in guiding atrial fibrillation (AF) ablation. We aimed at evaluating the relationship between AI and other lesion indicators and the release of myocardial-specific biomarkers following radiofrequency AF ablation.MethodsForty-six patients underwent a first-time radiofrequency AF ablation and were prospectively enrolled in this study. Pulmonary vein isolation was performed by six experienced electrophysiologists with a point-by-point approach, guided by strict Visitag criteria and consistent AI target values. Myocardial-specific biomarkers troponin T and creatine kinase myocardial band were measured after 6 (TnT6 and CKMB6) and 20 h (TnT20 and CKMB20) following sheath removal. Ablation duration, impedance drop (ID), force-time integral (FTI) and AI were registered automatically and analyzed offline.ResultsTnT release was 985 ± 495 ng/L and 1038 ± 461 ng/L (p = ns) while CKMB release was 7.3 ± 2.7 μg/L and 6.5 ± 2.1 μg/L (p < 0.001) at 6 and 20 h respectively. Ablation duration, ID, FTI and AI were all significantly correlated with the release of myocardial-specific biomarkers both at 6 and 20 h. Ablation index showed the highest degree of correlation with TnT6, TnT20, CKMB6 and CKMB20 (Pearson's R 0.69, 0.69, 0.61, 0.64 respectively, p < 0.001). Multiple regression analysis demonstrated that AI had the strongest association with TnT6, TnT20, CKMB6 and CKMB20 (β 0.43, β 0.71, β 0.44 and β 0.43 respectively).ConclusionAblation index appears as the strongest lesion indicator as measured by the release of myocardial-specific biomarkers following radiofrequency catheter ablation for AF.     

Differential inhibition of noradrenaline release mediated by inhibitory A1-adenosine receptors in the mesenteric vein and artery from normotensive and hypertensive rats

Mesenteric arteries and veins are densely innervated by sympathetic nerves and are crucial in the regulation of peripheral resistance and capacitance, respectively, thus, in the control of blood pressure. Presynaptic adenosine receptors are involved in vascular tonus regulation, by modulating noradrenaline release from vascular postganglionic sympathetic nerve endings. Some studies also suggest that adenosine receptors (AR) may have a role in hypertension. We aim at investigating the role of presynaptic adenosine receptors in mesenteric vessels and establish a relationship between their effects (in mesenteric vessels) and hypertension, using the spontaneously hypertensive rats (SHR) as a model of hypertension. Adenosine receptor-mediated modulation of noradrenaline release was investigated through the effects of selective agonists and antagonists on electrically-evoked [³H]-noradrenaline overflow. CPA (A₁AR selective agonist: 1–100 nM) inhibited tritium overflow, but the inhibition was lower in SHR mesenteric vessels. IB-MECA (A₃AR selective agonist: 1–100 nM) also inhibited tritium overflow but only in WKY mesenteric veins. CGS 21680 (A_2AAR selective agonist: up to 100 nM) failed to facilitate noradrenaline release in mesenteric veins, from both strains, but induced a similar facilitation in the mesenteric arteries. NECA (non-selective AR agonist: 1, 3 and 10 μM), in the presence of A₁ (DPCPX, 20 nM) and A₃ (MRS 1523, 1 μM) AR selective antagonists, failed to change tritium overflow. In summary, the modulatory effects mediated by presynaptic adenosine receptors were characterized, for the first time, in mesenteric vessels: a major inhibition exerted by the A₁ subtype in both vessels; a slight inhibition mediated by A₃ receptors in mesenteric vein; a facilitation mediated by A_2A receptors only in mesenteric artery (from both strains). The less efficient prejunctional adenosine receptor mediated inhibitory effects can contribute to an increase of noradrenaline in the synaptic cleft (both in arteries and veins), which might conduce to increased vascular reactivity.     

The dominant Basilicum Leaf mutation of sunflower controls leaf development multifariously and modifies the photosynthetic traits

Despite the remarkable morphological diversity in the leaf shape, usually higher plants maintain a flat lamina to ensure the desirable surface-to-volume ratio. The control of expansion of a flattened lateral organ is only partially known and the characterization of leaf mutants can be a useful strategy to add new information, as demonstrated in dicots with recessive mutants of model species. In sunflower, the dominant mutant Basilicum Leaf (BL) is characterized by prominent downward leaf curling. The central end of the present work is the detailed study of the BL phenotype to characterize the effects of this mutation, at organ and cellular levels, on both morphological and physiological traits. The geometry of mature leaves is obviously altered in BL plants because the lamina surfaces are downward curled and display a different length/width ratio with respect to wild type. The area of BL leaves is higher than that of wild type while the BL leaf perimeter is reduced. In BL leaves, the perimeter to the square root of area ratio is also abnormally low compared to the value of a flat sunflower lamina. These results suggest that the dominant mutation induces a deep change of the ratio between lamina and marginal growth. In addition, the epidermis and mesophyll of BL leaves comprised higher size pavement and palisade cells compared to those of wild type, indicating that the BL gene also control cell shape changes in the formation of the leaf lamina. Other leaf traits such as photosynthetic pigment content, pattern of minor vein architecture, margin type and stomatal density are affected by the mutation. In BL plants, the longitudinal axis of both cotyledons and ray flower corollas shows an unusual curvature while the diameter of shoot and inflorescence meristems is reduced. In mutant leaves, the gas exchange performance is influenced by low stomata conductance while the CO₂ assimilation rate is also depressed by a depleted Rubisco activity. Together, these data demonstrate the pleiotropic nature of the BL mutation, which affects a number of morphological aspects of flattened lateral organs as well as physiological parameters in sunflower.     

半永久性颈内静脉留置导管在血液透析中的临床价值

目的:研究半永久性颈内静脉留置导管在血液透析中的临床价值。方法:选取2013年10月到2014年10月我院收治的半永久性颈内静脉留置导管患者42例(研究组),另选取同期人造血管内瘘患者42例(对照组),分析两组患者的临床资料。结果:研究组导管留置时间(23.2±0.8)月显著长于对照组的(12.8±0.8)个月,两组比较差异具有统计学意义(P0.05);研究组导管功能不良和感染显著少于对照组,两组比较差异具有统计学意义(P0.05)。研究组无显著不良反应发生,对照组有2例止血困难,6例血栓形成。结论:半永久性颈内静脉留置导管具有方便、不良反应少的优点,可应用于需要血液透析的患者。     

Vascular elasticity measurement of the great saphenous vein based on optical coherence elastography

Vascular elasticity is important in physiological and clinical problems. The mechanical properties of the great saphenous vein (GSV) deserve attention. This research aims to measure the radial elasticity of ex vivo GSV using the optical coherence elasticity (OCE). The finite element model of the phantom is established, the displacement field is calculated, the radial mechanical characteristics of the simulation body are obtained. Furthermore, we performed OCE on seven isolated GSVs. The strain field is obtained by combining the relationship between strain and displacement to obtain the radial elastic modulus of GSVs. In the phantom experiment, the strain of the experimental region of interest is mainly between 0.1 and 0.4, while the simulation result is between 0.06 and 0.40. The radial elastic modulus of GSVs ranged from 3.83 kPa to 7.74 kPa. This study verifies the feasibility of the OCE method for measuring the radial elastic modulus of blood vessels.