Associations of the uric acid related genetic variants in SLC2A9 and ABCG2 loci with coronary heart disease risk

Background

Multiple studies investigated the associations between serum uric acid and coronary heart disease (CHD) risk. However, further investigations still remain to be carried out to determine whether there exists a causal relationship between them. We aim to explore the associations between genetic variants in uric acid related loci of SLC2A9 and ABCG2 and CHD risk in a Chinese population.

Results

A case–control study including 1,146 CHD cases and 1,146 controls was conducted. Association analysis between two uric acid related variants (SNP rs11722228 in SLC2A9 and rs4148152 in ABCG2) and CHD risk was performed by logistic regression model. Adjusted odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Compared with subjects with A allele of rs4148152, those with G allele had a decreased CHD risk and the association remained significant in a multivariate model. However, it altered to null when BMI was added into the model. No significant association was observed between rs11722228 and CHD risk. The distribution of CHD risk factors was not significantly different among different genotypes of both SNPs. Among subjects who did not consume alcohol, the G allele of rs4148152 showed a moderate protective effect. However, no significant interactions were observed between SNP by CHD risk factors on CHD risk.

Conclusions

There might be no association between the two uric acid related SNPs with CHD risk. Further studies were warranted to validate these results.

Electronic supplementary material

The online version of this article (doi:10.1186/s12863-015-0162-7) contains supplementary material, which is available to authorized users.     

Separation and purification of a keratinase as pesticide against root-knot nematodes

A new alkaline keratinase, which could kill Meloidogyne incognita (a root-knot nematode) was separated and purified from Bacillus sp. 50-3 in this study. The solid ammonium sulfate was selected to precipitate the enzyme and its proper adding mass was also determined. After solid ammonium sulfate precipitation and liquid chromatography on DEAE-Sephadex-A50 column, there was 17.7-fold purification with a yield of 46.5%, as determined by azokeratin as substrate. The purification effect was determined through SDS-PAGE and the molecular weight of the enzyme was found to be 27,423 Da by the MALDI-TOF-MS. When the second-stage juveniles of Meloidogyne incognita were exposed to 50 μg/ml of keratinase solution, 98.5% of Meloidogyne incognita mortality rates were obtained compared to control after 24 h. Its simple purification step and high yield from the cheap medium affords this keratinase great biotechnological potential, especially in controlling root-knot nematodes such as Meloidogyne incognita. To the best of our knowledge, this study is the first report that uses keratinase as a pesticide.     

Indication of intracellular physiological pH changes by L-cysteine-coated CdTe quantum dots with an acute alteration in emission color

A novel quantum dots (QDs) based biosensor was developed to monitor physiological pH changes in both fixed and living cells by means of pH-dependent emission color of the QDs. In our system, the nominally single-sized colloidal solution samples of the L-cysteine-capped CdTe QDs with intrinsically broadened size distributions were prepared by employing aqueous synthesis technique. The quench of fluorescence intensities of the QDs with a 16 nm red shift of the emission maximum and a color change from green to yellow was observed with a slight pH decrease (from 7.0 to 6.8) in the system. This pH-dependent emission could be attributed to the efficient exciton energy transfer from smaller QDs to larger ones, which was controlled by electrostatic-tuned aggregation/disaggregation (low/high pH values) processes of the QDs. In addition to high stability, the emission shift of the QDs was reversible for at least one cycle under optimal conditions. Our pH biosensor may find potential application for monitoring the intracellular pH changes in both physiological and pathological conditions.     

Uridine adenosine tetraphosphate induces contraction of airway smooth muscle

Contraction of airway smooth muscle (ASM) plays an important role in the regulation of air flow and is potentially involved in the pathophysiology of certain respiratory diseases. Extracellular nucleotides regulate ASM contraction via purinergic receptors, but the signaling mechanisms involved are not fully understood. Uridine adenosine tetraphosphate (Up(4)A) contains both pyrimidine and purine moieties, which are known to potentially activate P2X and P2Y receptors. Both P2X and P2Y receptors have been identified in the lung, including airway epithelial cells and ASM. We report here a study of purinergic signaling in the respiratory system, with a focus on the effect of Up(4)A on ASM contraction. Up(4)A induced contraction of rat isolated trachea and extrapulmonary bronchi as well as human intrapulmonary bronchioles. Up(4)A-induced contraction was blocked by di-inosine pentaphosphate, a P2X antagonist, but not by suramin, a nonselective P2 antagonist. Up(4)A-induced contraction was also attenuated by α,β-methylene-ATP-mediated P2X receptor desensitization. Several P2X receptors were detected at the mRNA level: P2X1, P2X4, P2X6, and P2X7, and to a lesser extent P2X3. Furthermore, the Up(4)A response was inhibited by removal of extracellular Ca(2+) and by the presence of the L-type Ca(2+) channel blocker, nifedipine, or the Rho-associated kinase inhibitor, H1152. We conclude that Up(4)A stimulates ASM contraction, and the underlying signaling mechanism appears to involve P2X (most likely P2X1) receptors, extracellular Ca(2+) entry via L-type Ca(2+) channels, and Ca(2+) sensitization through the RhoA/Rho-associated kinase pathway. This study will add to our understanding of the pathophysiological roles of extracellular nucleotides in the lung.     

An insight into planarian regeneration

BackgroundPlanarian has attracted increasing attentions in the regeneration field for its usefulness as an important biological model organism attributing to its strong regeneration ability. Both the complexity of multiple regulatory networks and their coordinate functions contribute to the maintenance of normal cellular homeostasis and the process of regeneration in planarian. The polarity, size, location and number of regeneration tissues are regulated by diverse mechanisms. In this review we summarize the recent advances about the importance genetic and molecular mechanisms for regeneration control on various tissues in planarian.MethodsA comprehensive literature search of original articles published in recent years was performed in regards to the molecular mechanism of each cell types during the planarian regeneration, including neoblast, nerve system, eye spot, excretory system and epidermal.ResultsAvailable molecular mechanisms gave us an overview of regeneration process in every tissue. The sense of injuries and initiation of regeneration is regulated by diverse genes like follistatin and ERK signaling. The Neoblasts differentiate into tissue progenitors under the regulation of genes such as egfr‐3. The regeneration polarity is controlled by Wnt pathway, BMP pathway and bioelectric signals. The neoblast within the blastema differentiate into desired cell types and regenerate the missing tissues. Those tissue specific genes regulate the tissue progenitor cells to differentiate into desired cell types to complete the regeneration process.ConclusionAll tissue types in planarian participate in the regeneration process regulated by distinct molecular factors and cellular signaling pathways. The neoblasts play vital roles in tissue regeneration and morphology maintenance. These studies provide new insights into the molecular mechanisms for regulating planarian regeneration.

Genetic and molecular mechanisms for regeneration control on various tissues in planarian.     

Liquid–liquid phase separation of amyloid-β oligomers modulates amyloid fibrils formation

Soluble amyloid-β oligomers (AβOs) are proposed to instigate and mediate the pathology of Alzheimer’s disease, but the mechanisms involved are not clear. In this study, we reported that AβOs can undergo liquid–liquid phase separation (LLPS) to form liquid-like droplets in vitro. We determined that AβOs exhibited an α-helix conformation in a membrane-mimicking environment of SDS. Importantly, SDS is capable of reconfiguring the assembly of different AβOs to induce their LLPS. Moreover, we found that the droplet formation of AβOs was promoted by strong hydrated anions and weak hydrated cations, suggesting that hydrophobic interactions play a key role in mediating phase separation of AβOs. Finally, we observed that LLPS of AβOs can further promote Aβ to form amyloid fibrils, which can be modulated by (−)-epigallocatechin gallate. Our study highlights amyloid oligomers as an important entity involved in protein liquid-to-solid phase transition and reveals the regulatory role of LLPS underlying amyloid protein aggregation, which may be relevant to the pathological process of Alzheimer’s disease.     

暴露生态学视角下绿地暴露健康效益研究进展

城市绿地与居民健康福祉密切相关,绿地暴露所带来的多重健康效益已经成为耦合城市生态与健康科学的前沿热点议题。尽管绿地健康效应的综述研究并不鲜见,但是目前仍缺乏基于统一理论框架视角下对绿地暴露健康效益的系统综述。近期提出的暴露生态学作为一个耦合"自然生态系统-生态暴露-健康效应"框架体系,能够全面剖析、归纳已有绿地暴露健康效应研究,并指引未来相关领域研究发展。因此,研究在暴露生态学研究视域下,在主体-现实,客体-现实,主体-虚拟,客体-虚拟界面下进行了研究进展的综述分析,并指出了研究截面(尺度)单一、阈值研究与虚拟(及多感官)研究不足等问题。最后提出了未来研究展望:(1)构建跨时空、多尺度的绿地暴露测度模型,并量化绿地健康之间的因果效应;(2)构建阈值模型,分析健康促进的绿地暴露主体阈值与客体阈值;(3)探索绿地特征、暴露方式和剂量、多感体验对健康的影响。研究成果可以进一步加深对相关领域前沿与不足的认识,也可以进一步促进暴露生态学理论体系的丰富和完善。     

唐古特白刺种源试验

唐古特白刺（Nitrariatangutorum）为蒺藜科白刺属灌木,是干旱、半干旱荒漠地区优良的固沙树种之一,也是重要开发利用的经济植物。我们从青海德令哈、吐鲁番、玉门和民勤等地引进4个不同地理的唐古特白刺种源,在民勤沙生植物园进行对比试验。研究结果表明,种源间的株高、地径、冠幅等生长量存在显著差异,生长表现均以来自民勤地区的种源最好,吐鲁番和玉门的较好,青海的次之。同时,这些不同地区的种源都具有抗旱、抗寒、抗风固沙和经济价值较高等优良特性。