Four New Species of Subsection from China.

Four new species of subsection from northern and southwestern China under coniferous and deciduous trees are proposed as , , , and . Illustrations and descriptions of , , , and the above four new species are provided based on evidence of morphological characters and phylogenetic analyses of the internal transcribed spacer (ITS), as well as the multi-locus of mtSSU, nLSU, , and -α. The relationships between these new species and allied taxa are discussed.

Acid-Sensing Ion Channel 1/Calpain1 Activation Impedes Macrophage ATP-Binding Cassette Protein A1-Mediated Cholesterol Efflux Induced by Extracellular Acidification.

Background: Extracellular acidification is a common feature of atherosclerotic lesions, and such an acidic microenvironment impedes ATP-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux and promotes atherogenesis. However, the underlying mechanism is still unclear. Acid-sensing ion channel 1 (ASIC1) is a critical H receptor, which is responsible for the perception and transduction of extracellular acidification signals.

Three new Russula species in sect. Ingratae (Russulales, Basidiomycota) from southern China.

Three new species of Russulasection Ingratae, found in Guizhou and Jiangsu Provinces, southern China, are proposed: , and . Photographs, line drawings and detailed morphological descriptions for these species are provided with comparisons against closely-related taxa. Phylogenetic analysis of the internal transcribed spacer (ITS) region supported the recognition of these specimens as new species.

The crosstalk: exosomes and lipid metabolism.

Exosomes have been considered as novel and potent vehicles of intercellular communication, instead of "cell dust". Exosomes are consistent with anucleate cells, and organelles with lipid bilayer consisting of the proteins and abundant lipid, enhancing their "rigidity" and "flexibility". Neighboring cells or distant cells are capable of exchanging genetic or metabolic information via exosomes binding to recipient cell and releasing bioactive molecules, such as lipids, proteins, and nucleic acids.

Direct Interaction of Daxx and Androgen Receptor Is Required for Their Regulatory Activity in Cholesterol Biosynthesis.

Introduction: Homeostasis of cholesterol is crucial for cellular function, and dysregulated cholesterol biosynthesis is a metabolic event that can lead to hepatic and cardiovascular abnormalities.

Objective: The aim of this study was to investigate the effects and mechanisms of domain-associated protein (Daxx) and androgen receptor (AR) on intracellular cholesterol synthesis.

Methods: HepG2 cells were transfected with pCDNA3.

Autophagy in chronic stress induced atherosclerosis.

Atherosclerosis, a complex multifactorial disease, is the leading cause of acute cardiovascular events. Substantial evidence confirms that chronic stress plays a pivot role in the occurrence and development of atherosclerosis, but the specific mechanism remains unclear. Autophagy serves as a safeguard mechanism for sustaining cellular homeostasis via eliminating unnecessary or/and harmful components, and damaged organelles in response to various stress.

Acid-sensing ion channels: Linking extracellular acidification with atherosclerosis.

Extracellular acidification in atherosclerosis-prone regions of arterial walls is considered pro-atherosclerotic by exerting detrimental effect on macrophages, endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). Acid-sensing ion channels (ASICs), a family of extracellular H (proton)-gated cation channels, are present extensively in the nervous system and other tissues, implying physiologic as well as pathophysiologic importance. Aberrant activation of ASICs is thought to be associated in EC dysfunction, macrophage phenotypic switch, and VSMC migration and proliferation.

Autophagy: a killer or guardian of vascular smooth muscle cells.

Vascular smooth muscle cells (VSMCs) is one of the main intracellular components of the blood vessel wall. The abnormalities of VSMCs participate in the development of cardiovascular diseases such as atherosclerosis, hypertension, and restenosis, especially the formation and stability of atherosclerotic plaques. Autophagy is involved in the regulation of proliferation, migration and phenotype switching of VSMCs, which in turn affects the pathological process of atherosclerosis.

Astragaloside VI Promotes Neural Stem Cell Proliferation and Enhances Neurological Function Recovery in Transient Cerebral Ischemic Injury via Activating EGFR/MAPK Signaling Cascades.

Radix Astragali (AR) is a commonly used medicinal herb for post-stroke disability in Traditional Chinese Medicine but its active compounds for promoting neurogenic effects are largely unknown. In the present study, we tested the hypothesis that Astragaloside VI could be a promising active compound from AR for adult neurogenesis and brain repair via targeting epidermal growth factor (EGF)-mediated MAPK signaling pathway in post-stroke treatment. By using cultured neural stem cells (NSCs) and experimental stroke rat model, we investigated the effects of Astragaloside VI on inducing NSCs proliferation and self-renewal in vitro, and enhancing neurogenesis for the recovery of the neurological functions in post-ischemic brains in vivo.

Ablation of endothelial prolyl hydroxylase domain protein-2 promotes renal vascular remodelling and fibrosis in mice.

Accumulating evidence demonstrates that hypoxia-inducible factor (HIF-α) hydroxylase system has a critical role in vascular remodelling. Using an endothelial-specific prolyl hydroxylase domain protein-2 (PHD2) knockout (PHD2 KO) mouse model, this study investigates the regulatory role of endothelial HIF-α hydroxylase system in the development of renal fibrosis. Knockout of PHD2 in EC up-regulated the expression of HIF-1α and HIF-2α, resulting in a significant decline of renal function as evidenced by elevated levels of serum creatinine.

Oxidized low-density lipoprotein induced mouse hippocampal HT-22 cell damage via promoting the shift from autophagy to apoptosis.

Aims: Although oxidized low-density lipoprotein (ox-LDL) in the brain induces neuronal death, the mechanism underlying the damage effects remains largely unknown. Given that the ultimate outcome of a cell is depended on the balance between autophagy and apoptosis, this study was performed to explore whether ox-LDL induced HT-22 neuronal cell damage via autophagy impairment and apoptosis enhancement.

Methods: Flow cytometry and transmission electron microscopy (TEM) were used to evaluate changes in cell apoptosis and autophagy, respectively.

Notch3 deficiency impairs coronary microvascular maturation and reduces cardiac recovery after myocardial ischemia.

Rationale: Vascular maturation plays an important role in wound repair post-myocardial infarction (MI). The Notch3 is critical for pericyte recruitment and vascular maturation during embryonic development.

Objective: This study is to test whether Notch3 deficiency impairs vascular maturation and blunts cardiac functional recovery post-MI.

Loss of prolyl hydroxylase domain protein 2 in vascular endothelium increases pericyte coverage and promotes pulmonary arterial remodeling.

Pulmonary arterial hypertension (PAH) is a leading cause of heart failure. Although pulmonary endothelial dysfunction plays a crucial role in the progression of the PAH, the underlying mechanisms are poorly understood. The HIF-α hydroxylase system is a key player in the regulation of vascular remodeling.

Ezetimibe-mediated protection of vascular smooth muscle cells from cholesterol accumulation through the regulation of lipid metabolism-related gene expression.

Background: Ezetimibe is a potent inhibitor of Niemann-Pick type C1-Like 1 and has been approved for the treatment of hypercholesterolemia. Our preliminary study showed that ezetimibe promotes cholesterol efflux from vascular smooth muscle cells (VSMCs). Our aim was to investigate the cellular mechanisms underlying the ezetimibe actions.

Inhibition of smooth muscle cell proliferation by ezetimibe via the cyclin D1-MAPK pathway.

Proliferation of vascular smooth muscle cells (VSMCs) contributes to the development of atherosclerosis. Ezetimibe is a new lipid lowering agent that inhibits cholesterol absorption. In the present study we attempted to investigate whether ezetimibe has any effect on VSMC proliferation and the potential mechanisms involved.

[Effect of left ventricular ejection fraction on clinical long-term follow-up outcomes in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention].

Objective: To evaluate the effect of left ventricular ejection fraction (LVEF) on clinical outcomes in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Methods: A total of 158 patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention between January 2005 to December 2007 were enrolled. They were divided into three groups: LVEF≤40% (n=14), LVEF 41%-55% (n=46) and LVEF>55% group (n=98).