A twinning bare bones particle swarm optimization algorithm.

A twinning bare bones particle swarm optimization(TBBPSO) algorithm is proposed in this paper. The TBBPSO is combined by two operators, the twins grouping operator (TGO) and the merger operator (MO). The TGO aims at the reorganization of the particle swarm. Two particles will form as a twin and influence each other in subsequent iterations. In a twin, one particle is designed to do the global search while the other one is designed to do the local search. The MO aims at merging the twins and enhancing the search ability of the main group. Two operators work together to enhance the local minimum escaping ability of proposed methods. In addition, no parameter adjustment is needed in TBBPSO, which means TBBPSO can solve different types of optimization problems without previous information or parameter adjustment. In the benchmark functions test, the CEC2014 benchmark functions are used. Experimental results prove that proposed methods can present high precision results for various types of optimization problems.

Paeoniflorin attenuates oxidized low-density lipoprotein-induced apoptosis and adhesion molecule expression by autophagy enhancement in human umbilical vein endothelial cells.

Oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction is recognized as a driving force in the development of atherosclerosis (AS). Paeoniflorin (Pae), a typical traditional herbal medicine, possesses anti-inflammatory, antioxidative, antihyperglycaemic, and antiapoptotic properties. Our study aimed to investigate the effects of Pae on ox-LDL-induced injury of the human umbilical vein endothelial cells (HUVECs) and to explore its molecular mechanism. We found that ox-LDL stimulation inhibited cell viability, activated autophagy, and induced apoptosis and adhesion molecule expression in HUVECs. Pae rescued ox-LDL-induced viability reduction and enhanced the ox-LDL-induced autophagy activation in HUVECs. Pae inhibited ox-LDL-induced apoptosis and adhesion molecule expression by autophagy enhancement in HUVECs. In addition, inhibition of SIRT1 by EX-527 abolished the promoting effect of Pae on autophagy and restored the inhibitory effect of Pae on apoptosis and adhesion molecule expression in the presence of ox-LDL. In conclusion, Pae attenuated ox-LDL-induced apoptosis and adhesion molecule expression by autophagy enhancement via upregulation of SIRT1 in HUVECs, shedding light on the mechanism underlying the protective effect of Pae on ox-LDL-induced injury of HUVECs.

Osthole alleviates oxidized low-density lipoprotein-induced vascular endothelial injury through suppression of transforming growth factor-ß1/Smad pathway.

Osthole, a naturally-derived coumarin, has been shown to exhibit pharmacological activities including anti-inflammatory, anti-oxidative and cardiovascular protective effects. However, the effect of osthole on oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury and its underlying mechanism remain unknown. We found that osthole did not affect viability of human umbilical vein endothelial cells (HUVECs) but alleviated ox-LDL-induced cytotoxicity in HUVECs. Osthole repressed ox-LDL-induced release of tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, and IL-6 in HUVECs. Osthole reversed ox-LDL-induced elevation of reactive oxygen species (ROS) production and malondialdehyde (MDA) level, and reduction of superoxide dismutase (SOD) activity in HUVECs. Meanwhile, osthole attenuated ox-LDL-induced increase of mRNA expression and secretion of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in HUVECs. Osthole increased nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) phosphorylation in ox-LDL-treated HUVECs. Furthermore, osthole inhibited ox-LDL-induced activation of the transforming growth factor-ß1 (TGF-ß1)/Smad pathway and activation of TGF-ß1/Smad pathway by TGF-ß1 attenuated the protective effects of osthole on HUVECs injury. These results suggested that osthole attenuated ox-LDL-induced HUVECs injury by inhibiting the TGF-ß1/Smad pathway, suggesting that osthole might be a promising therapeutic agent for the treatment of atherosclerosis.

Platycodin D inhibits oxidative stress and apoptosis in H9c2 cardiomyocytes following hypoxia/reoxygenation injury.

Myocardial ischemia/reperfusion (I/R) injury is a complex pathophysiological process related to the occurrence of myocardial infarction (MI). Oxidative stress is known to play a crucial role in the pathogenesis of I/R injury. Platycodin D (PD) is an active natural saponin that possesses strong anti-oxidant activity. The aim of the present study was to investigate the effect of PD on myocardial I/R injury. An in vitro hypoxia/reoxygenation (H/R) model was established in cardiomyocyte H9c2 cells. The results showed that PD improved the cell viability in H/R-stimulated H9c2 cells. The H/R-induced increase in the production of reactive oxygen species (ROS) and malondialdehyde (MDA), and decrease in the activities of superoxide dismutase (SOD) and catalase (CAT) were reversed by PD pretreatment. The histone-associated DNA fragment was increased by H/R stimulation, while decreased after PD treatment. Besides, PD pretreatment reduced the expressions of Bax and cleaved caspase-3, while induced Bcl-2 expression in H/R-induced H9c2 cells. Furthermore, PD was found to induce the activation of Akt/Nrf2/HO-1 pathway. The inhibitor of Akt, LY294002, attenuated the effects of PD on H/R-induced H9c2 cells. These findings indicated that PD exerted its protective effect via inducing the activation of Akt/Nrf2/HO-1 pathway. Our work provided new insights into the potential therapeutic role of PD in myocardial I/R injury.

Circumferential-scanning endoscopic optical coherence tomography probe based on a circular array of six 2-axis MEMS mirrors.

We present a novel circumferential-scan endoscopic optical coherence tomography (OCT) probe by using a circular array of six electrothermal microelectromechanical (MEMS) mirrors and six C-lenses. The MEMS mirrors have a 0.5 mm × 0.5 mm mirror plate and a chip size of 1.5 mm × 1.3 mm. Each MEMS mirror can scan up to 45° at a voltage of less than 12 V. Six of those mirrors have been successfully packaged to a probe head; full circumferential scans have been demonstrated. Furthermore, each scan unit is composed of a MEMS mirror and a C-lens and the six scan units can be designed with different focal lengths to adapt for lesions with uneven surfaces. Configured with a swept source OCT system, this MEMS array-based circumferential scanning probe has been applied to image a swine's small intestine wrapped on a 20 mm-diameter glass tube. The OCT imaging result shows that this new MEMS endoscopic OCT has promising applications in large tubular organs.

Kaempferol alleviates ox-LDL-induced apoptosis by up-regulation of autophagy via inhibiting PI3K/Akt/mTOR pathway in human endothelial cells.

Oxidized low-density lipoprotein (ox-LDL) has been reported to induce apoptosis of endothelial cells (ECs) and contribute to the progression of atherosclerosis. Kaempferol has been shown to possess antiatherosclerotic effect. The aim of the present study was to evaluate the effect of kaempferol on ox-LDL-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and its possible molecular basis. The results showed that kaempferol alleviated ox-LDL-induced apoptosis. Kaempferol increased the ratio of LC3-II/I and beclin-1 level in ox-LDL-induced HUVECs. Moreover, the expression of p-Akt and p-mTOR was down-regulated after treatment with kaempferol in ox-LDL-treated HUVECs, which is similar to the effect of PI3K inhibitor (LY294002) or mTOR inhibitor [rapamycin (RAP)]. Besides, autophagy induced by kaempferol was enhanced by LY294002 or RAP, while kaempferol-induced autophagy was attenuated with insulin treatment, the activator of PI3K/Akt/mTOR pathway. Furthermore, insulin also abated the effect of kaempferol on cell viability and apoptosis in ox-LDL-induced HUVECs. The results indicated that kaempferol alleviated ox-LDL-induced cell apoptosis by up-regulation of autophagy via inhibiting PI3K/Akt/mTOR pathway in human ECs.