Our data explain why only certain elements of BCM have been amenable to modification and serve as a template for the design of new inhibitors.
Those traits are related to business growth, and our conceptual mediation model is supported by our data explaining in part how a biological construct like entrepreneurs' sex can relate to business growth, that is, our work documents that growth intentions reflect rational trade-offs among both financial and nonfinancial factors (Eddleston & Powell, 2008; Jennings & Brush, 2013).
Taken together, our data explain why the pBcl-2/ Bcl-2+Mcl-1) pBcl-2/ Bcl-2+Mcl-1he sensitivity to S1 tratioent.
Morbidity with cardiovascular disease (angina pectoris, MI, hypertension, hypercholesterolemia) did not in our data explain absence from screening in underweight or obese women.
Our data explain how different isomeric states, methyl groups and carbamate linkers can independently and decisively alter the speed of SPAAC, SPIEDAC and the newly defined SPINEDAC reactions.
Our polygenic score analysis indicates that the PGC-derived panel of SNPs conveying risk specifically for schizophrenia is also predictive of case control status in our data, explaining around 2% of the phenotypic variance.
Thus, our data explain part of the mechanisms by which β-cells maintain maturity: Combinatorial Insm1/Neurod1/Foxa2 binding identifies regulatory sequences that maintain the mature gene expression program in β-cells, and disruption of this network results in functional failure.
Collectively our data explain several of the SLP-65 controlled biological responses elucidated by genetic means and further support the role of SLP-65 as the key integrator of BCR-signaling.
Our data explains the failure of this and other previous studies [ 20, 53] to uncover the functional role of the NA hemadsorption site as neither study used polyvalent substrates.
Our data explain the recent epidemiological evidence for the increased incidence of acute kidney injury post-stroke and provide an important roadmap for the future analysis of the mechanisms and cellular repercussions of the stroke-induced bystander-like effects in distal somatic organs.
