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Life cycles and annual production of the chironomidCladopelma virescens are studied at two different depths in the sublittoral (5m) and the profundal (12m) zones of the karstic Lake Banyoles (NE Spain). Two generations were completed by this chironomid in the two sampling stations studied. Production was estimated with two different methods: increment-summation (IS) and size-frequency (SF). In the IS method the smoothed survivorship curves were estimated because of the absence of the smaller instars in the samples. The mean annual production varied from 44 to 70 mg m–2y–1 in the deeper station and from 215 to 270 mg m–2y–1 in the shallower, depending on whether the size-frequency or increment summation method was used. Annual P/B varied between 5.07 and 5.67, and 6.14 and 4.11 respectively. Due to the many assumptions to be made with the IS method, we suggest the SF method in this case, because the values given by the two methods are of the same order of magnitude. 相似文献
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Enhanced Connexin-43 and α-Sarcomeric Actin Expression in Cultured Heart Myocytes Exposed to Triiodo-l-thyronine 总被引:2,自引:0,他引:2
Tribulova N Shneyvays V Mamedova LK Moshel S Zinman T Shainberg A Manoach M Weismann P Kostin S 《Journal of molecular histology》2004,35(5):463-470
This study examined whether triiodo-L-thyronine (T3) affects the expression of the major intercellular channel protein, connexin-43, and contractile protein alpha-sarcomeric actin. Cultured cardiomyocytes from newborn rats were treated on day three in culture with 10 or 100 nM T3 and examined 48 and 72 h thereafter. Treated and untreated cells were examined by immunofluorescence and electron microscopy. Expression levels of Cx43 and sarcomeric alpha-actin were monitored by Western blot analysis. Immunofluorescence labeling showed cell membrane location of Cx43 in punctuate gap junctions, whereby fluorescence signal area was significantly higher in cultured cardiomyocytes exposed to T3. This correlated with electron microscopical findings showing increased numbers and size of gap junction profiles, as well as with a significant dose-dependent increase of Cx43 expression detected by Western blot. Immunofluorescence of sarcomeric a-actin was enhanced and its expression increased dose- and time-dependently in T3-treated cultured heart myocytes. However, exposure to the higher dosage (100 nM) of T3 caused mild disintegration of sarcomeric a-actin in some myocytes, suggesting an over-dosage. The results indicate that T3 up-regulates Cx43 and accelerates gap junction formation in cultured neonatal cardiomyocytes. They suggest that thyroid status cannot only modulate the mechanical function of cardiomyocytes but also cell-to-cell communication essential for myocardial electrical and metabolic synchronizations. 相似文献
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The classification of a newly identified protein as a member of a superfamily is important for focusing experiments on its most likely functions. Such classification, often performed by hand, has now been fully automated. This sophisticated new approach takes into account not only alignment scores but also a number of other computable attributes, such as functional sites deduced from sequence conservation patterns. 相似文献
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Ziegelhöffer-Mihalovicová B Ziegelhöffer A Ravingerová T Kolár F Jacob W Tribulová N 《Molecular and cellular biochemistry》2002,236(1-2):37-44
Mitochondrial contact sites (MiCS) are dynamic structures involved in high capacity transport of energy from mitochondria into the cytosole. Previous studies revealed that in normal conditions the actual number of MiCS is in correlation with the energy requirements of the heart, particularly with those for its contractile work. Although the detailed mechanisms of signalling between the processes of energy utilisation and MiCS formation in the heart are not yet elucidated, it is known that intracellular Ca2+ transients are intimately involved in this crosstalk. The present study is devoted to investigation of Ca2+-linked MiCS formation in healthy adult hearts and in hearts with modified Ca2+-handling such as in developing, in juvenile and diabetic myocardium. Experiments were performed on hearts of healthy rats on the 22nd embryonal day, 1st, 4th, 7th and 14th postnatal days as well as on adult hearts. Diabetic hearts were investigated on the 8th day after streptozotocin injection (45 mg.kg–1
i.v.) to adult rats. Intracellular Ca2+ movements were affected by modulation of Ca2+ concentration in perfusion solution (1.6 or 2.2 mmol.l–1) in isolated, Langendorff-perfused hearts, by calcium paradox (CaP) or by replacing of Ca2+ by Cd2+ ions. Elevation of extracellular Ca2+ was reflected by 30.1, 10.4 and 24.1% increase in intracellular free Ca2+ concentration in healthy adult, diabetic and 14-day old hearts respectively. In developing hearts the amount of MiCS was culminating on the 4th postnatal day. In adult hearts, elevated calcium in the perfusion solution, CaP as well as diabetes led to a significant increase in the amounts of MiCS formed (58.1, 77.2 and 86.5% respectively; p < 0.05). Diabetic and 14-day old hearts naturally exhibited amounts of MiCS comparable to those obtained by Ca2+-stimulation of MiCS formation in adult healthy hearts. In contrast to healthy controls, perfusion of diabetic and 14-day old hearts with elevated Ca2+ as well as induction of CaP exerted little influence on MiCS formation (4.4 and 8.2% for elevated Ca2+; 2.9 and 10.7% for CaP; p > 0.05). A replacement of Ca2+ by Cd2+ ions lowered the amount of MiCS in healthy adult and diabetic hearts (61 and 52.2%; p < 0.05). In conclusion, during development, the formation of MiCS may be influenced by both, permanent stimulation by Ca2+-signalling and the availability of mCPK. In healthy adult hearts the amount of MiCS is modulated by intracellular Ca2+ transients in response to changes in extracellular Ca2+ concentration. In diabetic hearts the modulation of MiCS formation is naturally attenuated, apparently as a consequence of persisting alterations in Ca2+-handling. 相似文献
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Joan Segura Manuel Alejandro Marín-López Pamela F. Jones Baldo Oliva Narcis Fernandez-Fuentes 《PloS one》2015,10(3)
The experimental determination of the structure of protein complexes cannot keep pace with the generation of interactomic data, hence resulting in an ever-expanding gap. As the structural details of protein complexes are central to a full understanding of the function and dynamics of the cell machinery, alternative strategies are needed to circumvent the bottleneck in structure determination. Computational protein docking is a valid and valuable approach to model the structure of protein complexes. In this work, we describe a novel computational strategy to predict the structure of protein complexes based on data-driven docking: VORFFIP-driven dock (V-D2OCK). This new approach makes use of our newly described method to predict functional sites in protein structures, VORFFIP, to define the region to be sampled during docking and structural clustering to reduce the number of models to be examined by users. V-D2OCK has been benchmarked using a validated and diverse set of protein complexes and compared to a state-of-art docking method. The speed and accuracy compared to contemporary tools justifies the potential use of VD2OCK for high-throughput, genome-wide, protein docking. Finally, we have developed a web interface that allows users to browser and visualize V-D2OCK predictions from the convenience of their web-browsers. 相似文献
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Houman Ashrafian Louise Docherty Vincenzo Leo Christopher Towlson Monica Neilan Violetta Steeples Craig A. Lygate Tertius Hough Stuart Townsend Debbie Williams Sara Wells Dominic Norris Sarah Glyn-Jones John Land Ivana Barbaric Zuzanne Lalanne Paul Denny Dorota Szumska Shoumo Bhattacharya Julian L. Griffin Iain Hargreaves Narcis Fernandez-Fuentes Michael Cheeseman Hugh Watkins T. Neil Dear 《PLoS genetics》2010,6(6)
Mutations in a number of genes have been linked to inherited dilated cardiomyopathy (DCM). However, such mutations account for only a small proportion of the clinical cases emphasising the need for alternative discovery approaches to uncovering novel pathogenic mutations in hitherto unidentified pathways. Accordingly, as part of a large-scale N-ethyl-N-nitrosourea mutagenesis screen, we identified a mouse mutant, Python, which develops DCM. We demonstrate that the Python phenotype is attributable to a dominant fully penetrant mutation in the dynamin-1-like (Dnm1l) gene, which has been shown to be critical for mitochondrial fission. The C452F mutation is in a highly conserved region of the M domain of Dnm1l that alters protein interactions in a yeast two-hybrid system, suggesting that the mutation might alter intramolecular interactions within the Dnm1l monomer. Heterozygous Python fibroblasts exhibit abnormal mitochondria and peroxisomes. Homozygosity for the mutation results in the death of embryos midway though gestation. Heterozygous Python hearts show reduced levels of mitochondria enzyme complexes and suffer from cardiac ATP depletion. The resulting energy deficiency may contribute to cardiomyopathy. This is the first demonstration that a defect in a gene involved in mitochondrial remodelling can result in cardiomyopathy, showing that the function of this gene is needed for the maintenance of normal cellular function in a relatively tissue-specific manner. This disease model attests to the importance of mitochondrial remodelling in the heart; similar defects might underlie human heart muscle disease. 相似文献
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