Clinicopathological and prognostic value of lncRNA PANDAR expression in solid tumors: Evidence from a systematic review and meta-analysis

PANDAR (promoter of CDKN1A antisense DNA damage activated RNA) has been shown to be aberrantly expressed in many types of cancer. Considering conflicting data, the current study was aimed to assess its potential role as a prognostic marker in malignant tumors. A comprehensive literature search of PubMed, Medline, and Web of Science was performed to identify all eligible studies describing the use of PANDAR as a prognostic factor for different types of cancer. Data related to overall survival (OS) and clinicopathologic features were collected and analyzed. The pooled hazard ratio (HR) and odds radio (OR) with a 95% confidence interval (CI) were used to estimate associations. Ten original studies containing 1,231 patients were included. The results showed that in patients with cancer, high PANDAR expression is correlated with lymph node metastasis (LNM; OR = 2.57; 95% CI, 1.76–3.81; p < 0.001), tumor stage (OR = 2.90; 95% CI, 1.25–6.75; p = 0.013), and tumor size (OR = 1.79; 95% CI, 1.11–2.91; p = 0.018). However, sensitivity analysis further demonstrated a significant association between high PANDAR expression and OS, both in multivariate and univariate analysis models (pooled HR 2.01; 95% CI, 1.17–3.44 and pooled HR 2.62; 95% CI, 1.98–3.47, respectively), after omitting one study. These results suggested that PANDAR expression might be indicative of advanced disease and poor prognosis in patients with cancer. Further studies are necessary to determine the value of this risk stratification biomarker in clinical management of patients with cancer.     

Evidence that PAR2-triggered prostaglandin E2 (PGE2) formation involves the ERK-cytosolic phospholipase A2-COX-1-microsomal PGE synthase-1 cascade in human lung epithelial cells

We investigated possible involvement of three isozymes of prostaglandin E synthase (PGES), microsomal PGES-1 (mPGES-1), mPGES-2 and cytosolic PGES (cPGES) in COX-2-dependent prostaglandin E(2) (PGE(2)) formation following proteinase-activated receptor-2 (PAR2) stimulation in human lung epithelial cells. PAR2 stimulation up-regulated mPGES-1 as well as COX-2, but not mPGES-2 or cPGES, leading to PGE(2) formation. The PAR2-triggered up-regulation of mPGES-1 was suppressed by inhibitors of COX-1, cytosolic phospholipase A(2) (cPLA(2)) and MEK, but not COX-2. Finally, a selective inhibitor of mPGES-1 strongly suppressed the PAR2-evoked PGE(2) formation. PAR2 thus appears to trigger specific up-regulation of mPGES-1 that is dependent on prostanoids formed via the MEK/ERK/cPLA(2)/COX-1 pathway, being critical for PGE(2) formation.     

CTRP3/cartducin is induced by transforming growth factor‐β1 and promotes vascular smooth muscle cell proliferation

CTRP3 (C1q and tumour necrosis factor‐related protein 3)/cartducin, a novel serum protein, is a member of the CTRP superfamily. Although the CTRP3/cartducin gene is markedly up‐regulated in rat carotid arteries after balloon injury, little is known about its biological roles in arterial remodelling and neointima formation in injured blood vessels. We have investigated the mechanisms underlying CTRP3/cartducin up‐regulation and the in vitro effects of CTRP3/cartducin on vascular smooth muscle cells. CTRP3/cartducin expression in cultured p53LMAC01 vascular smooth muscle cells was induced by TGF‐β1 (transforming growth factor‐β1), but not by bFGF (basic fibroblast growth factor) or PDGF‐BB (platelet‐derived growth factor‐BB). Exogenous CTRP3/cartducin promoted the proliferation of p53LMAC01 cells in a dose‐dependent manner via ERK1/2 (extracellular signal‐regulated kinase 1/2)‐ and MAPK (p38 mitogen‐activated protein kinase)‐signalling pathways. In contrast, CTRP3/cartducin exhibited no effect on the migration of p53LMAC01 cells. Taken together, the results of the present study demonstrate a novel biological role of CTRP3/cartducin in promoting vascular smooth muscle cell proliferation in blood vessel walls after injury.     

Life-Cycle Assessment of Biosolids Processing Options

Biosolids, also known as sewage sludge, are reusable organic materials separated from sewage during treatment. They can be managed in a variety of ways. Different options for biosolids handling in Sydney, Australia, are compared in this study using life-cycle assessment. Two key comparisons are made: of system scenarios (scenario 1 is local dewatering and lime amendment; scenario 2 is a centralized drying system) and of technologies (thermal drying versus lime amendment). The environmental issues addressed are energy consumption, global warming potential (GWP), and human toxicity potential (HTP).
Scenario 2 would consume 24% more energy than scenario 1. This is due to the additional electricity for pumping and particularly the petrochemical methane that supplements biogas in the drier. A centralized system using the same technologies as scenario 1 has approximately the same impacts. The GWP and HTP of the different scenarios do not differ significantly.
The assessment of technology choices shows significant differences. The ample supply of endogenous biogas at North Head sewage treatment plant for the drying option allows reductions, relative to the lime-amendment option, of 68% in energy consumption, 45% in GWP, and 23% in HTP.
Technology choices have more significant influence on the environmental profile of biosolids processing than does the choice of system configurations. Controlling variables for environmental improvement are the selection of biogas fuel, avoidance of coalsourced electrical energy, minimization of trucking distances, and raising the solids content of biosolids products.     

冷型小麦旗叶衰老和活性氧代谢特性研究

以典型的冷型小麦和暖型小麦为试验材料,研究了同一环境背景下不同温度型小麦开花后的旗叶衰老和活性氧代谢特性。结果表明,与暖型小麦相比,冷型小麦籽料灌浆期旗叶叶绿素和可溶性蛋白质含量下降缓慢、含量高,整个业粒形成和灌浆期ＭＤＡ积累速度慢、含量低,籽粒灌浆期防御活性氧伤害的关键性保护酶（ＳＯＤ、ＣＡＴ和ＰＯＤ）活性下隆幅度小,灌浆中后期活性水平高。由此认为,小麦旗叶衰老和活性氧代谢特性与其温度型的归属关     

pp60c-src在血管平滑肌细胞内丝裂原活化蛋白激酶激活中的作用

观察ｐｐ６０ｃ－ｓｒｃ在血管紧张素Ⅱ（ＡｎｇⅡ）诱导血管平滑肌细胞（ＶＳＭＣｓ）内丝裂原活化蛋白激酶（ＭＡＰＫ）激活中的作用,以了解ＡｎｇⅡ促ＶＳＭＣｓ增殖的信号转导过程。将合成的反义ｃ－ｓｒｃ寡脱氧核苷酸（ｏｌｉｇｏｄｅｏｘｙｎｕｃｌｅ－ｏｔｉｄｅｓ,ＯＤＮｓ）以脂质体包裹转染培养的大鼠ＶＳＭＣｓ,用Ｗｅｓｔｅｒｎ印迹测得细胞裂解液中ｐｐ６０ｃ－ｓｒｃ含量明显下降,免疫沉淀方法测得ｐｐ６０ｃ－ｓ     

酸碱调控污泥厌氧发酵实现乙酸累积及微生物种群变化

摘要：【目的】通过对污泥厌氧发酵pH调控,研究挥发性脂肪酸的累积、产酸微生物种群变化及产氢产乙酸菌群对乙酸产生的贡献。【方法】测定不同pH条件下污泥厌氧发酵过程中挥发性脂肪酸的累积;分别应用末端限制性片段长度多态性（T-RFLP）和荧光原位杂交技术（FISH）分析产酸系统中微生物种群结构的变化及产氢产乙酸菌的数量。【结果】 pH为10.0时,有机酸和乙酸的产率在发酵结束时分别达到652.6 mg COD/g-VS和322.4 mg COD/g-VS,显著高于其它pH条件。T-RFLP结果表明,pH值为12     

Synergistic effect of conjugated linolenic acid isomers against induced oxidative stress,inflammation and erythrocyte membrane disintegrity in rat model

Background

α-Eleostearic acid and punicic acid, two typical conjugated linolenic acid (CLnA) isomers present in bitter gourd and snake gourd oil respectively, exhibit contrasting cis-trans configuration which made them biologically important.

Methods

Rats were divided into six groups. Group 1 was control and group 2 was treated control. Rats in the groups 3 and 4 were treated with mixture of α-eleostearic acid and punicic acid (1:1) (0.5% and 1.0% respectively) while rats in the groups 5 and 6 were treated with 0.5% of α-eleostearic acid and 0.5% of punicic acid respectively along with sodium arsenite by oral gavage once per day.

Results

Results showed that increase in nitric oxide synthase (NOS) activity, inflammatory markers expression, platelet aggregation, lipid peroxidation, protein oxidation, DNA damage and altered expression of liver X receptor-α (LXR-α) after arsenite treatment were restored with the supplementation of oils containing CLnA isomers. Altered activities of different antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and ferric reducing ability of plasma (FRAP) also restored after oil supplementation. Altered morphology and fluidity of erythrocyte membrane studied by atomic force and scanning electron microscopy, after stress induction were significantly improved due to amelioration in cholesterol/phospholipid ratio and fatty acid profile of membrane. Oils treatment also improved morphology of liver and fatty acid composition of hepatic lipid.

Conclusions

Overall two isomers showed synergistic antioxidant and anti-inflammatory effect against induced perturbations and membrane disintegrity.

General significance

Synergistic antioxidant and anti-inflammatory role of these CLnA isomers were established by this study.