Mitochondrial DNA variation analysis suggests extreme low genetic diversity in Guizhou snub-nosed monkeys （Rhinopithecus brelichi）

Guizhou snub-nosed monkey (Rhinopithecus brelichi) is a unique, endangered primate in China, mainly distributed in Fanjing Mountain National Natural Reserve, Guizhou Province, in an area of 275 km2. Recently, habitat loss and fragmentation have caused population isolation. To assess genetic diversity within this species and its population structure, we sequenced 400 bp of the hypervariable I segment from the mitochondrial DNA control region for 128 individuals. Only one haplotype was identified from these individuals. Compared with other primate species, R. brelichi can be regarded as a species with very low genetic diversity, which further adds to the conservation concern.     

Response of the northwestern Pacific upper water δ~(13)C to the last deglacial ventilation of the deep Southern Ocean

The deglacial δ~13C minimum events that originated from the ventilation of the deep Southern Ocean around Antarctica, have been recorded in a range of marine sediments from the southern to tropical oceans in late Pleistocene. However, the broad δ~13C minimum event was also reported as far as to the northern middle latitudes, in northwestern Pacific marginal sea areas, during the last deglaciation. In the northwestern Pacific, forcing from the northern high latitudes is strongly expressed, while the records of in- fluence from the southern high latitudes are few. The Kuroshio Source Region (KSR) forms a boundary between the northwestern Pacific and the southern, tropical Pacific. So, high-resolution planktonic foraminiferal records in core MD06-3054 from the KSR are well positioned to identify signals from the southern hemisphere in the northwestern Pacific. Planktonic foraminiferal tests from the upper 1030 cm of the core were subject to AMS14C, carbon and oxygen isotopic measurements. A negative excursion was found to occur from about 20.0-6.0 ka BP in δ~13C records of both surface (Globigerinoides ruber) and subsurface (Pulleni- atina obliquiloculata) dwellers, but the overall trends of the two curves have reversed since 26.5 ka BP. Moreover, the δ~13C rec- ord of G. ruber (the surface dweller) shows a robust link to the record of atmospheric CO2, and its changes precede the records of P. obliquiloculata (the subsurface dweller). According to the hydrologic conditions, the broad δ~13C minimum event recorded in the KSR is also a response to the increasing ventilation of the deep Southern Ocean around Antarctica during the last deglaciation. The inconsistency between the records of the surface and subsurface dwellers was possibly caused by the ways that the low δ~13C signal was transmitted. Subsurface water primarily received the low δ~13C signal from the Antarctic Intermediate Water (AAIW), whereas the surface water was probably mainly impacted by atmospheric CO2 in the KSR. The records from the KSR confirm the deduction that the broad δ~13C minimum event in the Okinawa Trough was due to the impact of tropical Pacific surface water dur- ing the last deglaciation, and suggest that signals from the southern high latitudes also can be delivered to the northern middle latitudes.     

Tert-butylhydroquinone-decorated graphene nanosheets and their enhanced capacitive behaviors

In the present work,tert-butylhydroquinone(TBHQ) was used to decorate graphene nanosheets to obtain a novel and environmentally friendly electrode material for supercapacitors.The fast redox reactions between hydroquinone and quinone generate pseudocapacitance.Graphene layers which have adsorbed TBHQ interact with each other to construct a three-dimensional network.Through this network,electrolyte ions can easily access the surface of graphene to generate electric double-layer capacitance.Electrochemical measurements have shown that using TBHQ as a redox modifier of graphene can obtain a maximum value of 302 F g-1 and provide a 51% enhancement in specific capacitance.Furthermore,excellent rate capability and cycling ability are achieved using the TBHQ-decorated graphene nanosheet electrode.     

伽罗瓦的代数方程思想

目的 探讨在代数方程根式可解性理论的发展中,伽罗瓦(Evariste Galois,1811-1832)的代数方程理论思想发展过程.方法 采用历史考察与数理分析法.结果 伽罗瓦是通过引进"伽罗瓦群"、"正规子群"、"置换群"等概念开始建立他的理论,并且找出了根式扩张塔和可解群之间的对应关系,利用这种对应关系最终解决了代数方程根式可解性理论这一难题.结论 伽罗瓦继承了拉格朗日(J.L.Lagrange,1736-1813)问题转化的思想,并且把这一思想进行发展,使得人们对方程根式解问题的研究进入到对"结构"观念的研究,导致了抽象代数学科的诞生;伽罗瓦的研究思路是通过继承和发展前人的思想成果得出来的.     

谈公路规划设计过程中如何做好环境保护

经济建设要符合持续、健康、快速发展的原则,而公路定线和施工建设稍有不慎就有可能导致沿线山体裸露、植被受损、水土流失、生态环境恶化现象的发生。文章以公路规划设计阶段为研究对象,就公路规划设计阶段如何做好生态环境的保护进行了分析。     

谈公路规划设计过程中如何做好环境保护

经济建设要符合持续、健康、快速发展的原则,而公路定线和施工建设稍有不慎就有可能导致沿线山体裸露、植被受损、水土流失、生态环境恶化现象的发生.文章以公路规划设计阶段为研究对象,就公路规划设计阶段如何做好生态环境的保护进行了分析.     

Natural polymorphisms in C. elegans HECW-1 E3 ligase affect pathogen avoidance behaviour

Heritable variation in behavioural traits generally has a complex genetic basis, and thus naturally occurring polymorphisms that influence behaviour have been defined only in rare instances. The isolation of wild strains of Caenorhabditis elegans has facilitated the study of natural genetic variation in this species and provided insights into its diverse microbial ecology. C. elegans responds to bacterial infection with conserved innate immune responses and, although lacking the immunological memory of vertebrate adaptive immunity, shows an aversive learning response to pathogenic bacteria. Here, we report the molecular characterization of naturally occurring coding polymorphisms in a C. elegans gene encoding a conserved HECT domain-containing E3 ubiquitin ligase, HECW-1. We show that two distinct polymorphisms in neighbouring residues of HECW-1 each affect C. elegans behavioural avoidance of a lawn of Pseudomonas aeruginosa. Neuron-specific rescue and ablation experiments and genetic interaction analysis indicate that HECW-1 functions in a pair of sensory neurons to inhibit P. aeruginosa lawn avoidance behaviour through inhibition of the neuropeptide receptor NPR-1 (ref. 10), which we have previously shown promotes P. aeruginosa lawn avoidance behaviour. Our data establish a molecular basis for natural variation in a C. elegans behaviour that may undergo adaptive changes in response to microbial pathogens.     

Structural insight into brassinosteroid perception by BRI1

Brassinosteroids are essential phytohormones that have crucial roles in plant growth and development. Perception of brassinosteroids requires an active complex of BRASSINOSTEROID-INSENSITIVE 1 (BRI1) and BRI1-ASSOCIATED KINASE 1 (BAK1). Recognized by the extracellular leucine-rich repeat (LRR) domain of BRI1, brassinosteroids induce a phosphorylation-mediated cascade to regulate gene expression. Here we present the crystal structures of BRI1(LRR) in free and brassinolide-bound forms. BRI1(LRR) exists as a monomer in crystals and solution independent of brassinolide. It comprises a helical solenoid structure that accommodates a separate insertion domain at its concave surface. Sandwiched between them, brassinolide binds to a hydrophobicity-dominating surface groove on BRI1(LRR). Brassinolide recognition by BRI1(LRR) is through an induced-fit mechanism involving stabilization of two interdomain loops that creates a pronounced non-polar surface groove for the hormone binding. Together, our results define the molecular mechanisms by which BRI1 recognizes brassinosteroids and provide insight into brassinosteroid-induced BRI1 activation.     

FAS and NF-κB signalling modulate dependence of lung cancers on mutant EGFR

Human lung adenocarcinomas with activating mutations in EGFR (epidermal growth factor receptor) often respond to treatment with EGFR tyrosine kinase inhibitors (TKIs), but the magnitude of tumour regression is variable and transient. This heterogeneity in treatment response could result from genetic modifiers that regulate the degree to which tumour cells are dependent on mutant EGFR. Through a pooled RNA interference screen, we show that knockdown of FAS and several components of the NF-κB pathway specifically enhanced cell death induced by the EGFR TKI erlotinib in EGFR-mutant lung cancer cells. Activation of NF-κB through overexpression of c-FLIP or IKK (also known as CFLAR and IKBKB, respectively), or silencing of IκB (also known as NFKBIA), rescued EGFR-mutant lung cancer cells from EGFR TKI treatment. Genetic or pharmacologic inhibition of NF-κB enhanced erlotinib-induced apoptosis in erlotinib-sensitive and erlotinib-resistant EGFR-mutant lung cancer models. Increased expression of the NF-κB inhibitor IκB predicted for improved response and survival in EGFR-mutant lung cancer patients treated with EGFR TKI. These data identify NF-κB as a potential companion drug target, together with EGFR, in EGFR-mutant lung cancers and provide insight into the mechanisms by which tumour cells escape from oncogene dependence.