(J Thorac Cardiovasc

Surg 2011;142:278-84)”
“There i

(J Thorac Cardiovasc

Surg 2011;142:278-84)”
“There is ample empirical evidence for an asymmetry in the way that adults use positive versus negative information to make sense of their world; specifically, across an array of psychological situations and tasks, adults display a negativity bias, or the propensity to attend to, learn from, and use negative information far more than positive information. This bias is argued to serve critical evolutionarily adaptive functions, but its developmental presence PF-4708671 mw and ontogenetic emergence have never been seriously considered. The authors argue for the existence of the negativity bias in early development and that it is evident especially in research on infant social referencing but also in other developmental domains. They discuss ontogenetic mechanisms underlying the emergence of this bias and explore not only its evolutionary but also its developmental functions and consequences. Throughout, the authors suggest ways to further examine LDK378 the negativity bias in infants and older children, and they

make testable predictions that would help clarify the nature of the negativity bias during early development.”
“Techniques for the single-step amplification of whole genomes have been developed into powerful Sitaxentan tools for phylogenetic analyses, epidemiological studies and studies on genome organization. Recently, the bacteriophage phi29 DNA polymerase has been used for the efficient amplification of circular DNA viral genomes without the need of specific primers by a rolling-circle amplification (RCA) mechanism. Various protocols have been applied for detection of novel viruses, for differentiation between circular and linear forms of viral genomes and for generation of infectious genomic clones directly from specimens. Here, we summarize the broad application of the RCA technique to DNA viruses infecting humans, animals and plants.”


cardiomyopathy and hypertrophic cardiomyopathy arise from mutations in many genes. TTN, the gene encoding the sarcomere protein titin, has been insufficiently analyzed for cardiomyopathy mutations because of its enormous size.


We analyzed TTN in 312 subjects with dilated cardiomyopathy, 231 subjects with hypertrophic cardiomyopathy, and 249 controls by using next-generation or dideoxy sequencing. We evaluated deleterious variants for cosegregation in families and assessed clinical characteristics.


We identified 72 unique mutations (25 nonsense, 23 frameshift, 23 splicing, and 1 large tandem insertion) that altered full-length titin.

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