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JW Arntzen 《Frontiers in zoology》2006,3(1):1-11
Background
The two sympatric species of Tunisian desert ants, Cataglyphis bicolor and C. mauritanica, do not exhibit any differences in their foraging ecology, e.g. in food preferences and in their spatial and temporal activity patterns. Here we show that instead the two species markedly differ in their life histories.Results
We analysed mtDNA of specimens that were collected along a 250-km transect. C. bicolor exhibited a genetically unstructured population (with the genetic and geographic distances among colonies not being correlated). On the contrary the populations of the polygynous C. mauritanica were clearly structured, i.e. exhibited a strong correlation between genetic and geographic distances. This difference is in accordance with large queen dispersal distances due to far-reaching mating flights in C. bicolor and small queen dispersal distances due to colony foundation by budding in C. mauritanica. Furthermore, wherever we found populations of both species to coexist within the same habitat, the habitat was used agriculturally. Mapping nest positions over periods of several years showed that plowing dramatically decreased the nest densities of either species.Conclusion
We conclude that owing to its greater queen dispersal potential C. bicolor might be more successful in quickly re-colonizing disturbed areas, while the slowly dispersing C. mauritanica could later out-compete C. bicolor by adopting its effective nest-budding strategy. According to this scenario the observed sympatry of the two species might be an intermediate stage in which faster colonization by one species and more powerful exploitation of space by the other species have somehow balanced each other out. In conclusion, C. bicolor and C. mauritanica represent an example where environmental disturbances in combination with different life histories might beget sympatry in congeneric species with overlapping niches. 相似文献43.
Tervaert DG 《The Biochemical journal》1925,19(2):300-303
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Bart F. J. Heijnen Jelly Nelissen Helma van Essen Gregorio E. Fazzi Jan W. Cohen Tervaert Carine J. Peutz-Kootstra John J. Mullins Casper G. Schalkwijk Ben J. A. Janssen Harry AJ. Struijker-Boudier 《PloS one》2013,8(2)
Transient activation of the renin-angiotensin system (RAS) induces irreversible renal damage causing sustained elevation in blood pressure (BP) in Cyp1a1-Ren2 transgenic rats. In our current study we hypothesized that activation of the AT1-receptor (AT1R) leads to a T-cell response causing irreversible impairment of renal function and hypertension. Cyp1a1-Ren2 rats harbor a construct for activation of the RAS by indole-3-carbinol (I3C). Rats were fed a I3C diet between 4–8 weeks of age to induce hypertension. Next, I3C was withdrawn and rats were followed-up for another 12 weeks. Additional groups received losartan (20 mg/kg/day) or hydralazine (100 mg/kg/day) treatment between 4–8 weeks. Rats were placed for 24h in metabolic cages before determining BP at week 8, 12 and 20. At these ages, subsets of animals were sacrificed and the presence of kidney T-cell subpopulations was investigated by immunohistochemistry and molecular marker analysis. The development of sustained hypertension was completely prevented by losartan, whereas hydralazine only caused a partial decrease in BP. Markers of renal damage: KIM-1 and osteopontin were highly expressed in urine and kidney samples of I3C-treated rats, even until 20 weeks of age. Additionally, renal expression of regulatory-T cells (Tregs) was highly increased in I3C-treated rats, whereas the expression of T-helper 1 (Th1) cells demonstrated a strong decrease. Losartan prevented these effects completely, whereas hydralazine was unable to affect these changes. In young Cyp1a1-Ren2 rats AT1R activation leads to induction of an immune response, causing a shift from Th1-cells to Tregs, contributing to the development of irreversible renal damage and hypertension. 相似文献
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Sourabh Chand Julia U. Holle Marc Hilhorst Matthew J. Simmonds Stuart Smith Lavanya Kamesh Peter Hewins Amy Jayne McKnight Alexander P. Maxwell Jan Willem Cohen Tervaert Stefan Wieczorek Lorraine Harper Richard Borrows 《PloS one》2013,8(7)
Objective
Immunosuppression is cornerstone treatment of antineutrophil cytoplasmic antibody associated vasculitis (AAV) but is later complicated by infection, cancer, cardiovascular and chronic kidney disease. Caveolin-1 is an essential structural protein for small cell membrane invaginations known as caveolae. Its functional role has been associated with these complications. For the first time, caveolin-1 (CAV1) gene variation is studied in AAV.Methods
CAV1 single nucleotide polymorphism rs4730751 was analysed in genomic DNA from 187 white patients with AAV from Birmingham, United Kingdom. The primary outcome measure was the composite endpoint of time to all-cause mortality or renal replacement therapy. Secondary endpoints included time to all-cause mortality, death from sepsis or vascular disease, cancer and renal replacement therapy. Validation of results was sought from 589 white AAV patients, from two European cohorts.Results
The primary outcome occurred in 41.7% of Birmingham patients. In a multivariate model, non-CC genotype variation at the studied single nucleotide polymorphism was associated with increased risk from: the primary outcome measure [HR 1.86; 95% CI: 1.14-3.04; p=0.013], all-cause mortality [HR:1.83; 95% CI: 1.02-3.27; p=0.042], death from infection [HR:3.71; 95% CI: 1.28-10.77; p=0.016], death from vascular disease [HR:3.13; 95% CI: 1.07-9.10; p=0.037], and cancer [HR:5.55; 95% CI: 1.59-19.31; p=0.007]. In the validation cohort, the primary outcome rate was far lower (10.4%); no association between genotype and the studied endpoints was evident.Conclusions
The presence of a CC genotype in Birmingham is associated with protection from adverse outcomes of immunosuppression treated AAV. Lack of replication in the European cohort may have resulted from low clinical event rates. These findings are worthy of further study in larger cohorts. 相似文献47.
Autophagy regulates cellular homeostasis through degradation of aged or damaged subcellular organelles and components. Interestingly, autophagy-deficient beta cells, for example Atg7-mutant mice, exhibited hypoinsulinemia and hyperglycemia. Also, autophagy response is diminished in heart of diabetic mice. These results implied that autophagy and diabetes are closely connected and affect each other. Although protein O-GlcNAcylation is up-regulated in hyperglycemia and diabetes, and O-GlcNAcylated proteins play an important role in metabolism and nutrient sensing, little is known whether autophagy affects O-GlcNAc modification and vice versa. In this study, we suppressed the action of mTOR by treatment of mTOR catalytic inhibitors (PP242 and Torin1) to induce autophagic flux. Results showed a decrease in global O-GlcNAcylation, which is due to decreased OGT protein and increased OGA protein. Interestingly, knockdown of ATG genes or blocking of lysosomal degradation enhanced protein stability of OGT. In addition, when proteasomal inhibitor was treated together with mTOR inhibitor, protein level of OGT almost recovered to control level. These data suggest that mTOR inhibition is a more efficient way to reduce protein level of OGT rather than that of CHX treatment. We also showed that not only proteasomal degradation regulated OGT stability but autophagic degradation also affected OGT stability in part. We concluded that mTOR signaling regulates protein O-GlcNAc modification through adjustment of OGT stability. 相似文献
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MT Butcher JW Hermanson NG Ducharme LM Mitchell LV Soderholm JE Bertram 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2009,152(1):100-114
The forelimb digital flexors of the horse display remarkable diversity in muscle architecture despite each muscle-tendon unit having a similar mechanical advantage across the fetlock joint. We focus on two distinct muscles of the digital flexor system: short compartment deep digital flexor (DDF(sc)) and the superficial digital flexor (SDF). The objectives were to investigate force-length behavior and work performance of these two muscles in vivo during locomotion, and to determine how muscle architecture contributes to in vivo function in this system. We directly recorded muscle force (via tendon strain gauges) and muscle fascicle length (via sonomicrometry crystals) as horses walked (1.7 m s(-1)), trotted (4.1 m s(-1)) and cantered (7.0 m s(-1)) on a motorized treadmill. Over the range of gaits and speeds, DDF(sc) fascicles shortened while producing relatively low force, generating modest positive net work. In contrast, SDF fascicles initially shortened, then lengthened while producing high force, resulting in substantial negative net work. These findings suggest the long fibered, unipennate DDF(sc) supplements mechanical work during running, whereas the short fibered, multipennate SDF is specialized for economical high force and enhanced elastic energy storage. Apparent in vivo functions match well with the distinct architectural features of each muscle. 相似文献
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This report describes a lysozyme expressed at high levels in the stomach of
the hoatzin, the only known foregut-fermenting bird. Evolutionary
comparison places it among the calcium-binding lysozymes rather than among
the conventional types. Conventional lysozymes were recruited as digestive
enzymes twice in the evolution of mammalian foregut fermenters, and these
independently recruited lysozymes share convergent structural changes
attributed to selective pressures in the stomach. Biochemical convergence
and parallel amino acid replacements are observed in the hoatzin stomach
lysozyme even though it has a different genetic origin from the mammalian
examples and has undergone more than 300 million years of independent
evolution.
相似文献