排序方式: 共有85条查询结果,搜索用时 15 毫秒
61.
Blain S Quéguiner B Armand L Belviso S Bombled B Bopp L Bowie A Brunet C Brussaard C Carlotti F Christaki U Corbière A Durand I Ebersbach F Fuda JL Garcia N Gerringa L Griffiths B Guigue C Guillerm C Jacquet S Jeandel C Laan P Lefèvre D Lo Monaco C Malits A Mosseri J Obernosterer I Park YH Picheral M Pondaven P Remenyi T Sandroni V Sarthou G Savoye N Scouarnec L Souhaut M Thuiller D Timmermans K Trull T Uitz J van Beek P Veldhuis M Vincent D Viollier E Vong L Wagener T 《Nature》2007,446(7139):1070-1074
The availability of iron limits primary productivity and the associated uptake of carbon over large areas of the ocean. Iron thus plays an important role in the carbon cycle, and changes in its supply to the surface ocean may have had a significant effect on atmospheric carbon dioxide concentrations over glacial-interglacial cycles. To date, the role of iron in carbon cycling has largely been assessed using short-term iron-addition experiments. It is difficult, however, to reliably assess the magnitude of carbon export to the ocean interior using such methods, and the short observational periods preclude extrapolation of the results to longer timescales. Here we report observations of a phytoplankton bloom induced by natural iron fertilization--an approach that offers the opportunity to overcome some of the limitations of short-term experiments. We found that a large phytoplankton bloom over the Kerguelen plateau in the Southern Ocean was sustained by the supply of iron and major nutrients to surface waters from iron-rich deep water below. The efficiency of fertilization, defined as the ratio of the carbon export to the amount of iron supplied, was at least ten times higher than previous estimates from short-term blooms induced by iron-addition experiments. This result sheds new light on the effect of long-term fertilization by iron and macronutrients on carbon sequestration, suggesting that changes in iron supply from below--as invoked in some palaeoclimatic and future climate change scenarios--may have a more significant effect on atmospheric carbon dioxide concentrations than previously thought. 相似文献
62.
Church C Moir L McMurray F Girard C Banks GT Teboul L Wells S Brüning JC Nolan PM Ashcroft FM Cox RD 《Nature genetics》2010,42(12):1086-1092
Genome-wide association studies have identified SNPs within FTO, the human fat mass and obesity-associated gene, that are strongly associated with obesity. Individuals homozygous for the at-risk rs9939609 A allele weigh, on average, ~3 kg more than individuals with the low-risk T allele. Mice that lack FTO function and/or Fto expression display increased energy expenditure and a lean phenotype. We show here that ubiquitous overexpression of Fto leads to a dose-dependent increase in body and fat mass, irrespective of whether mice are fed a standard or a high-fat diet. Our results suggest that increased body mass results primarily from increased food intake. Mice with increased Fto expression on a high-fat diet develop glucose intolerance. This study provides the first direct evidence that increased Fto expression causes obesity in mice. 相似文献
63.
A Mal functional variant is associated with protection against invasive pneumococcal disease, bacteremia, malaria and tuberculosis 总被引:1,自引:0,他引:1
Khor CC Chapman SJ Vannberg FO Dunne A Murphy C Ling EY Frodsham AJ Walley AJ Kyrieleis O Khan A Aucan C Segal S Moore CE Knox K Campbell SJ Lienhardt C Scott A Aaby P Sow OY Grignani RT Sillah J Sirugo G Peshu N Williams TN Maitland K Davies RJ Kwiatkowski DP Day NP Yala D Crook DW Marsh K Berkley JA O'Neill LA Hill AV 《Nature genetics》2007,39(4):523-528
Toll-like receptors (TLRs) and members of their signaling pathway are important in the initiation of the innate immune response to a wide variety of pathogens. The adaptor protein Mal (also known as TIRAP), encoded by TIRAP (MIM 606252), mediates downstream signaling of TLR2 and TLR4 (refs. 4-6). We report a case-control study of 6,106 individuals from the UK, Vietnam and several African countries with invasive pneumococcal disease, bacteremia, malaria and tuberculosis. We genotyped 33 SNPs, including rs8177374, which encodes a leucine substitution at Ser180 of Mal. We found that heterozygous carriage of this variant associated independently with all four infectious diseases in the different study populations. Combining the study groups, we found substantial support for a protective effect of S180L heterozygosity against these infectious diseases (N = 6,106; overall P = 9.6 x 10(-8)). We found that the Mal S180L variant attenuated TLR2 signal transduction. 相似文献
64.
Intra- and intercellular RNA interference in Arabidopsis thaliana requires components of the microRNA and heterochromatic silencing pathways 总被引:2,自引:0,他引:2
In RNA interference (RNAi), double-stranded RNA (dsRNA) is processed into short interfering RNA (siRNA) to mediate sequence-specific gene knockdown. The genetics of plant RNAi is not understood, nor are the bases for its spreading between cells. Here, we unravel the requirements for biogenesis and action of siRNAs directing RNAi in Arabidopsis thaliana and show how alternative routes redundantly mediate this process under extreme dsRNA dosages. We found that SMD1 and SMD2, required for intercellular but not intracellular RNAi, are allelic to RDR2 and NRPD1a, respectively, previously implicated in siRNA-directed heterochromatin formation through the action of DCL3 and AGO4. However, neither DCL3 nor AGO4 is required for non-cell autonomous RNAi, uncovering a new pathway for RNAi spreading or detection in recipient cells. Finally, we show that the genetics of RNAi is distinct from that of antiviral silencing and propose that this experimental silencing pathway has a direct endogenous plant counterpart. 相似文献
65.
Christophe Schmit 《Annals of science》2013,70(4):493-530
This article intends to propose new hypotheses concerning the origin of the ‘Principe général’ of mechanics of Jean Le Rond D'Alembert expressed in its Traité de dynamique in 1743. The examination of the statics of Pierre Varignon and its inheritance suggests that D'Alembert retains, through a case of oblique collision on a hard surface, a method of decomposition and equilibrium of forces which is close to its principle. On the other hand, this principle requires a definition of the equilibrium widely spread in the 17th and 18th centuries, D'Alembert seeming then more to innovate from an epistemological point of view that on a technical one. Finally, the determination of rules of collision based at the same time on decompositions of movements at the level of the centre of mass and on appeal to a principle of relativity constitutes a know-how at the beginning of the 18th century which can be moved closer to methods developed by D'Alembert. These three aspects try then to replace the science of D'Alembert in a context by insisting on the essential role of the collisions of body and on that of the notion of equilibrium concerning the birth of its principle. 相似文献
66.
KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron 总被引:1,自引:0,他引:1
Louis-Dit-Picard H Barc J Trujillano D Miserey-Lenkei S Bouatia-Naji N Pylypenko O Beaurain G Bonnefond A Sand O Simian C Vidal-Petiot E Soukaseum C Mandet C Broux F Chabre O Delahousse M Esnault V Fiquet B Houillier P Bagnis CI Koenig J Konrad M Landais P Mourani C Niaudet P Probst V Thauvin C Unwin RJ Soroka SD Ehret G Ossowski S Caulfield M;International Consortium for Blood Pressure 《Nature genetics》2012,44(4):456-60, S1-3
Familial hyperkalemic hypertension (FHHt) is a Mendelian form of arterial hypertension that is partially explained by mutations in WNK1 and WNK4 that lead to increased activity of the Na(+)-Cl(-) cotransporter (NCC) in the distal nephron. Using combined linkage analysis and whole-exome sequencing in two families, we identified KLHL3 as a third gene responsible for FHHt. Direct sequencing of 43 other affected individuals revealed 11 additional missense mutations that were associated with heterogeneous phenotypes and diverse modes of inheritance. Polymorphisms at KLHL3 were not associated with blood pressure. The KLHL3 protein belongs to the BTB-BACK-kelch family of actin-binding proteins that recruit substrates for Cullin3-based ubiquitin ligase complexes. KLHL3 is coexpressed with NCC and downregulates NCC expression at the cell surface. Our study establishes a role for KLHL3 as a new member of the complex signaling pathway regulating ion homeostasis in the distal nephron and indirectly blood pressure. 相似文献
67.
Mesenchymal stem cells and neural crest stem cells from adult bone marrow: characterization of their surprising similarities and differences 总被引:1,自引:1,他引:0
68.
Yoshiura K Kinoshita A Ishida T Ninokata A Ishikawa T Kaname T Bannai M Tokunaga K Sonoda S Komaki R Ihara M Saenko VA Alipov GK Sekine I Komatsu K Takahashi H Nakashima M Sosonkina N Mapendano CK Ghadami M Nomura M Liang DS Miwa N Kim DK Garidkhuu A Natsume N Ohta T Tomita H Kaneko A Kikuchi M Russomando G Hirayama K Ishibashi M Takahashi A Saitou N Murray JC Saito S Nakamura Y Niikawa N 《Nature genetics》2006,38(3):324-330
Human earwax consists of wet and dry types. Dry earwax is frequent in East Asians, whereas wet earwax is common in other populations. Here we show that a SNP, 538G --> A (rs17822931), in the ABCC11 gene is responsible for determination of earwax type. The AA genotype corresponds to dry earwax, and GA and GG to wet type. A 27-bp deletion in ABCC11 exon 29 was also found in a few individuals of Asian ancestry. A functional assay demonstrated that cells with allele A show a lower excretory activity for cGMP than those with allele G. The allele A frequency shows a north-south and east-west downward geographical gradient; worldwide, it is highest in Chinese and Koreans, and a common dry-type haplotype is retained among various ethnic populations. These suggest that the allele A arose in northeast Asia and thereafter spread through the world. The 538G --> A SNP is the first example of DNA polymorphism determining a visible genetic trait. 相似文献
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70.
The cellular basis of depressive disorders is poorly understood. Recent studies in monkeys indicate that neurons in the lateral habenula (LHb), a nucleus that mediates communication between forebrain and midbrain structures, can increase their activity when an animal fails to receive an expected positive reward or receives a stimulus that predicts aversive conditions (that is, disappointment or anticipation of a negative outcome). LHb neurons project to, and modulate, dopamine-rich regions, such as the ventral tegmental area (VTA), that control reward-seeking behaviour and participate in depressive disorders. Here we show that in two learned helplessness models of depression, excitatory synapses onto LHb neurons projecting to the VTA are potentiated. Synaptic potentiation correlates with an animal's helplessness behaviour and is due to an enhanced presynaptic release probability. Depleting transmitter release by repeated electrical stimulation of LHb afferents, using a protocol that can be effective for patients who are depressed, markedly suppresses synaptic drive onto VTA-projecting LHb neurons in brain slices and can significantly reduce learned helplessness behaviour in rats. Our results indicate that increased presynaptic action onto LHb neurons contributes to the rodent learned helplessness model of depression. 相似文献