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With the discovery of Hygrobia hermanni, the family Hygrobiidae is reported for the first time from Turkey. An illustration of the habitus and line drawings of diagnostic characters are provided.  相似文献   
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MOTIVATION: Co-evolution is a powerful mechanism for understanding protein function. Prior work in this area has shown that co-evolving proteins are more likely to share the same function than those that do not because of functional constraints. Many of the efforts founded on this observation, however, are at the level of entire sequences, implicitly assuming that the complete protein sequence follows a single evolutionary trajectory. Since it is well known that a domain can exist in various contexts, this assumption is not valid for numerous multi-domain proteins. Motivated by these observations, we introduce a novel technique called Coevolutionary-Matrix that captures co-evolution between regions of two proteins. Instead of using existing domain information, the method exploits residue-level conservation to identify co-evolving regions that might correspond to domains. RESULTS: We show that the Coevolutionary-Matrix method can detect greater number of known functional associations for the Escherichia coli proteins when compared with earlier implementations of phylogenetic profiles. Furthermore, co-evolving regions of proteins detected by our method enable us to make hypotheses about their specific functions, many of which are supported by existing biochemical studies.  相似文献   
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With an ever-increasing amount of available data on protein-protein interaction (PPI) networks and research revealing that these networks evolve at a modular level, discovery of conserved patterns in these networks becomes an important problem. Although available data on protein-protein interactions is currently limited, recently developed algorithms have been shown to convey novel biological insights through employment of elegant mathematical models. The main challenge in aligning PPI networks is to define a graph theoretical measure of similarity between graph structures that captures underlying biological phenomena accurately. In this respect, modeling of conservation and divergence of interactions, as well as the interpretation of resulting alignments, are important design parameters. In this paper, we develop a framework for comprehensive alignment of PPI networks, which is inspired by duplication/divergence models that focus on understanding the evolution of protein interactions. We propose a mathematical model that extends the concepts of match, mismatch, and gap in sequence alignment to that of match, mismatch, and duplication in network alignment and evaluates similarity between graph structures through a scoring function that accounts for evolutionary events. By relying on evolutionary models, the proposed framework facilitates interpretation of resulting alignments in terms of not only conservation but also divergence of modularity in PPI networks. Furthermore, as in the case of sequence alignment, our model allows flexibility in adjusting parameters to quantify underlying evolutionary relationships. Based on the proposed model, we formulate PPI network alignment as an optimization problem and present fast algorithms to solve this problem. Detailed experimental results from an implementation of the proposed framework show that our algorithm is able to discover conserved interaction patterns very effectively, in terms of both accuracies and computational cost.  相似文献   
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Objectives:Whole-body vibration (WBV) is applied to the sole of the foot, whereas local mechanical vibration (LMV) is applied directly to the muscle or tendon. The time required for the mechanical stimulus to reach the muscle belly is longer for WBV. Therefore, the WBV-induced muscular reflex (WBV-IMR) latency may be longer than the tonic vibration reflex (TVR) latency. The aim of this study was to determine whether the difference between WBV-IMR and TVR latencies is due to the distance between the vibration application point and the target muscle.Methods:Eight volunteers participated in this study. The soleus reflex response was recorded during WBV, LMVs, and tendon tap. LMVs were applied to the Achilles tendon and sole of the foot. The latencies were calculated using the cumulative averaging technique.Results:The latency (33.4±2.8 ms) of the soleus reflex induced by the local foot vibration was similar to the soleus TVR latency (30.9±3.2 ms) and T-reflex (32.0±2.4 ms) but significantly shorter than the latency of the soleus WBV-IMR (42.3±3.4 ms) (F(3,21)=27.46, p=0.0001, partial η2=0.797).Conclusions:The present study points out that the neuronal circuitries of TVR and WBV-IMR are different.  相似文献   
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Fatty acid synthase (FAS) promotes energy storage through de novo lipogenesis and participates in signaling by the nuclear receptor PPARα in noncardiac tissues. To determine if de novo lipogenesis is relevant to cardiac physiology, we generated and characterized FAS knockout in the myocardium (FASKard) mice. FASKard mice develop normally, manifest normal resting heart function, and have normal cardiac PPARα signaling as well as fatty acid oxidation. However, they decompensate with stress. Most die within 1 h of transverse aortic constriction, probably due to arrhythmia. Voltage clamp measurements of FASKard cardiomyocytes show hyperactivation of L-type calcium channel current that could not be reversed with palmitate supplementation. Of the classic regulators of this current, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) but not protein kinase A signaling is activated in FASKard hearts, and knockdown of FAS in cultured cells activates CaMKII. In addition to being intolerant of the stress of acute pressure, FASKard hearts were also intolerant of the stress of aging, reflected as persistent CaMKII hyperactivation, progression to dilatation, and premature death by ~1 year of age. CaMKII signaling appears to be pathogenic in FASKard hearts because inhibition of its signaling in vivo rescues mice from early mortality after transverse aortic constriction. FAS was also increased in two mechanistically distinct mouse models of heart failure and in the hearts of humans with end stage cardiomyopathy. These data implicate a novel relationship between FAS and calcium signaling in the heart and suggest that FAS induction in stressed myocardium represents a compensatory response to protect cardiomyocytes from pathological calcium flux.  相似文献   
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