Type 2 diabetes mellitus augments Parkinson’s disease risk or the other way around: Facts,challenges and future possibilities

About 10% of the adult population is living with type 2 diabetes mellitus (T2DM) and 1% of the population over 60 years of age is suffering from Parkinson’s disease (PD). A school of thought firmly believes that T2DM, an age-related disease, augments PD risk. Such relationship is reflected from the severity of PD symptoms in drug naive subjects possessing T2DM. Onset of Parkinsonian feature in case controls possessing T2DM corroborates the role of hyperglycemia in PD. A few cohort, meta-analysis and animal studies have shown an increased PD risk owing to insulin resistance. High fat diet and role of insulin signaling in the regulation of sugar metabolism, oxidative stress, α-synuclein aggregation and accumulation, inflammatory response and mitochondrial function in PD models and sporadic PD further connect the two. Although little is reported about the implication of PD in hyperglycemia and T2DM, a few studies have also contradicted. Ameliorative effect of anti-diabetic drugs on Parkinsonian symptoms and vague outcome of anti-PD medications in T2DM patients also suggest a link. The article reviews the literature supporting augmented risk of one by the other, analysis of proof of the concept, facts, challenges, future possibilities and standpoint on the subject.     

Evaluation of anaphylactoid constituents in vitro and in vivo

Natural medicine injections have been widely used in clinics, while adverse reaction reports also have increased rapidly in recent years. To examine the anaphylactoid constituents of natural medicine injections, RBL-2H3 cell degranulation and human serum complement activation models were used to screen the anaphylactoid constituents, and the BN rat model was used to explore the anaphylactoid mechanism of these constituents. The result of an in vitro study showed that the individual compounds of natural medicine injections (chlorogenic acid, hyodeoxycholic acid, cholalic acid, ginkgolic acid, phillyrin, schisandrin B, schisandrin A, puerarin, and tanshinone IIA) and polysaccharide could not induce RBL-2H3 to release histamine and β-hexosaminidase, while proteins Tween-80 and tannic acid were the main anaphylactoid constituents in the natural medicine injections. The in vivo study also indicated that > 10 kDa molecules (proteins) activated classical complement pathways through direct stimulation to cause an anaphylactoid reaction. Tween-80 activated direct stimulation and coagulation pathways through classical and alternative pathways; tannic acid induced anaphylactoid reaction through co-activation of the kallikrein-kinin system, coagulation, integrated, classical and alternative complement pathways. This is the first study to evaluate the anaphylactoid constituents systematically through in vitro and in vivo study. And tannic acid, > 10 kDa molecules (proteins), and injection additives such as Tween-80 are the main anaphylactoid constituents of natural medicine injections.     

乙肝后肝硬化证候的尿代谢组学研究

目的:运用代谢组学方法,探讨慢性乙型病毒性肝炎(乙肝)后肝硬化患者证候间尿代谢物的差异及其代谢模式。方法:采用GC/MS的尿液衍生化方法,分析乙肝后肝硬化患者不同证候内源性小分子代谢物,并进行单维和多维统计分析,通过与标准品的对照确认差异性代谢物。结果:在健康者与乙肝后肝硬化患者、不同中医证候的患者间,均获得了差异性尿代谢物,这些代谢物与能量代谢和氨基酸代谢等通路密切相关。其中在湿热内蕴证与肝肾阴虚证之间存在支链氨基酸的差异。结论:乙肝后肝硬化患者不同证候间存在着尿代谢物的差异,证候间可能具有不同的代谢模式。     

绿原酸及其肠道代谢产物对中枢神经系统疾病的作用和机制研究进展

绿原酸具有抗菌、抗病毒、清除自由基和兴奋中枢神经系统等多种生物活性。然而绿原酸仅有约1/3直接吸收入体内,其生物活性更多地是依靠其肠道代谢产物发挥效应得以实现。因此,研究绿原酸对中枢神经系统疾病的作用,有必要结合其肠道代谢产物的相关活性。该文结合近年来关于绿原酸的肠道代谢研究结果,综述了绿原酸及肠道代谢产物对于中枢神经系统疾病的潜在作用和作用机制,为进一步提高其应用价值提供依据。     

Transposon-based screens for cancer gene discovery in mouse models

Significant emphasis has recently been placed on the characterization of the human cancer genome. This effort has been assisted by the development of new DNA sequencing technologies that allow the genomes of individual tumors to be analyzed in much greater detail. However, the genetic complexity of human cancer has complicated the identification of driver mutations among the more abundant passenger mutations found in tumors. Recently, the Sleeping Beauty (SB) transposon system has been engineered to model cancer in mice. SB-induced tumors are produced by transposon insertional mutagenesis, thus the tagged mutations facilitate the identification of novel cancer genes. This review provides a brief summary of the SB system and its use in modeling cancer in mice.