快速测定厚朴中厚朴酚及其含量的方法

目的:通过建立系统的HPLC快速检测方法,分析厚朴中主要药用成分厚朴酚与和厚朴酚的含量,确定厚朴的药用价值及开发利用价值.方法:用HPLC法对张家界、隆回及恩施地区的厚朴植株的不同部位的药材中厚朴酚与和厚朴酚的含量进行了含量的分析.结果:结果快速、准确、重现性好、HPLC分析图谱理想.结论:本文所运用的HPLC分析条件能快速准确的鉴定厚朴酚及和厚朴酚的含量,确定厚朴药材的品质,并对混乱的药材市场有一定的监控作用.     

PEMFs对绝经后骨质疏松症的影响

目的:探讨低频率低强度脉冲电磁场(PEMFs)对绝经后骨质疏松症大鼠的影响.方法:选取3-5月龄雌性SD大鼠,随机分为五组,即阴性对照组(Sham),模型组(Model),阳性对照组(XLGB),脉冲磁场照射组(PEMFs)和给药十照射治疗组(X+P),除Sham实行假性手术外,其余四组经手术分别摘取两侧卵巢(OVX).OVX术后1月按照分组开始治疗,3个月后处死动物,测量大鼠骨转化生化指标(血清ALP,OC和尿DPD),股骨总BMD,BMC,股骨干骺端骨小梁微结构(BV/TV,Conn.D,SMI,Tb·N、Tb·Th、Th·Sp及Tb·Ar),骨生物力学性能(Stress)变化并计算,结果:XLGB、PEMFs、X+P组BMD、BMC、Th·"N、Tb·Th值显著增强,SMI,Th·Sp值显著减小(P<0.01);ALP值有所减小BV/TV,Conn.D值有所增加(P<0.05);Sham组Stress值有明显差异(P<0.01),PEMFs组有一定差异(P<0.05);提示经过磁场照射和(或)药物治疗后股骨生物力学显著增强,骨组织结构骨质疏松症状得到明显改善.结论:PEMFs对绝经后雌激素缺乏引起的OP大鼠有较好的治疗作用.     

Targeting CD24 for treatment of ovarian cancer by short hairpin RNA

Background aimsCD24 is markedly overexpressed in ovarian cancer and plays a critical role in ovarian cancer survival and metastasis, rendering it an interesting target for anti-tumor therapy. Using short hairpin RNA (shRNA) targeting CD24, we aimed to investigate the anti-tumor efficacy of CD24 knockdown in ovarian cancer cells in vitro and in vivo.MethodsCD24 shRNA vector (CD24–shRNA) and empty plasmid vector (EP) were transfected into ovarian cancer SKOV3 cells and the knockdown efficacy assessed by Western blot analysis. The effects of CD24 knockdown in SKOV3 cells in vitro, including cell viability and apoptosis, were determined using methyl thiazolyl blue tetrazolium bromide (MTT), flow cytometry and propidium iodide (PI) staining assays. The effects in vivo of CD24 knockdown on angiogenesis, cell proliferation and apoptosis were assessed using immunohistochemistry against CD31, proliferating cell nuclear antigen (PCNA) and terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) assays.ResultsTransfection of CD24–shRNA effectively down-regulated CD24 expression in vitro and in vivo. Administration of CD24–shRNA into nude mice bearing ovarian cancer significantly suppressed tumor volume growth.ConclusionsKnockdown of CD24 expression by CD24–shRNA significantly inhibited cell viability and induced apoptosis of SKOV3 cells in vitro. Administration with CD24–shRNA in vivo suppressed tumor volume increase by microvessel density (MVD) decrease, cell proliferation inhibition and apoptosis induction. All the data suggested that knockdown of CD24 by shRNA might be a potential therapeutic approach against human ovarian cancer.     

Review of forest landscape models: Types, methods, development and applications

Forest landscape models simulate forest change through time using spatially referenced data across a broad spatial scale (i.e. landscape scale) generally larger than a single forest stand. Spatial interactions between forest stands are a key component of such models. These models can incorporate other spatio-temporal processes such as natural disturbances (e.g. wildfires, hurricanes, outbreaks of native and exotic invasive pests and diseases) and human influences (e.g. harvesting and commercial thinning, planting, fire suppression). The models are increasingly used as tools for studying forest management, ecological assessment, restoration planning, and climate change. In this paper, we define forest landscape models and discuss development, components, and types of the models. We also review commonly used methods and approaches of modeling forest landscapes, their application, and their strengths and weaknesses. New developments in computer sciences, geographic information systems (GIS), remote sensing technologies, decision-support systems, and geo-spatial statistics have provided opportunities for developing a new generation of forest landscape models that are increasingly valuable for ecological research, restoration planning and resource management.     

Staphylococcus aureus α-Hemolysin Activates the NLRP3-Inflammasome in Human and Mouse Monocytic Cells

Community Acquired Methicillin Resistant Staphylococcus aureus (CA-MRSA) causes severe necrotizing infections of the skin, soft tissues, and lungs. Staphylococcal α-hemolysin is an essential virulence factor in mouse models of CA-MRSA necrotizing pneumonia. S. aureus α-hemolysin has long been known to induce inflammatory signaling and cell death in host organisms, however the mechanism underlying these signaling events were not well understood. Using highly purified recombinant α-hemolysin, we now demonstrate that α-hemolysin activates the Nucleotide-binding domain and leucine-rich repeat containing gene family, pyrin domain containing 3 protein (NLRP3)-inflammasome, a host inflammatory signaling complex involved in responses to pathogens and endogenous danger signals. Non-cytolytic mutant α-hemolysin molecules fail to elicit NLRP3-inflammasome signaling, demonstrating that the responses are not due to non-specific activation of this innate immune signaling system by bacterially derived proteins. In monocyte-derived cells from humans and mice, inflammasome assembly in response to α-hemolysin results in activation of the cysteine proteinase, caspase-1. We also show that inflammasome activation by α-hemolysin works in conjunction with signaling by other CA-MRSA-derived Pathogen Associated Molecular Patterns (PAMPs) to induce secretion of pro-inflammatory cytokines IL-1β and IL-18. Additionally, α-hemolysin induces cell death in these cells through an NLRP3-dependent program of cellular necrosis, resulting in the release of endogenous pro-inflammatory molecules, like the chromatin-associated protein, High-mobility group box 1 (HMGB1). These studies link the activity of a major S. aureus virulence factor to a specific host signaling pathway. The cellular events linked to inflammasome activity have clear relevance to the disease processes associated with CA-MRSA including tissue necrosis and inflammation.     

PGC-1α Is a Key Regulator of Glucose-Induced Proliferation and Migration in Vascular Smooth Muscle Cells

Background

Atherosclerosis is a complex pathological condition caused by a number of mechanisms including the accelerated proliferation of vascular smooth muscle cells (VSMCs). Diabetes is likely to be an important risk factor for atherosclerosis, as hyperglycemia induces vascular smooth muscle cell (VSMC) proliferation and migration and may thus contribute to the formation of atherosclerotic lesions. This study was performed to investigate whether PGC-1α, a PPARγ coactivator and metabolic master regulator, plays a role in regulating VSMC proliferation and migration induced by high glucose.

Methodology/Principal Findings

PGC-1α mRNA levels are decreased in blood vessel media of STZ-treated diabetic rats. In cultured rat VSMCs, high glucose dose-dependently inhibits PGC-1α mRNA expression. Overexpression of PGC-1α either by infection with adenovirus, or by stimulation with palmitic acid, significantly reduces high glucose-induced VSMC proliferation and migration. In contrast, suppression of PGC-1α by siRNA mimics the effects of glucose on VSMCs. Finally, mechanistic studies suggest that PGC-1α-mediated inhibition of VSMC proliferation and migration is regulated through preventing ERK1/2 phosphorylation.

Conclusions/Significance

These results indicate that PGC-1α is a key regulator of high glucose-induced proliferation and migration in VSMCs, and suggest that elevation of PGC-1α in VSMC could be a useful strategy in preventing the development of diabetic atherosclerosis.     

Microglia and Microglia-Like Cell Differentiated from DC Inhibit CD4 T Cell Proliferation

The central nervous system (CNS) is generally regarded as a site of immune privilege, whether the antigen presenting cells (APCs) are involved in the immune homeostasis of the CNS is largely unknown. Microglia and DCs are major APCs in physiological and pathological conditions, respectively. In this work, primary microglia and microglia-like cells obtained by co-culturing mature dendritic cells with CNS endothelial cells in vitro were functional evaluated. We found that microglia not only cannot prime CD4 T cells but also inhibit mature DCs (maDCs) initiated CD4 T cells proliferation. More importantly, endothelia from the CNS can differentiate maDCs into microglia-like cells (MLCs), which possess similar phenotype and immune inhibitory function as microglia. Soluble factors including NO lie behind the suppression of CD4 T cell proliferation induced by both microglia and MLCs. All the data indicate that under physiological conditions, microglia play important roles in maintaining immune homeostasis of the CNS, whereas in a pathological situation, the infiltrated DCs can be educated by the local microenvironment and differentiate into MLCs with inhibitory function.