Continuously varying skin potentials elicited by sinusoidally varying electric shock potentials

An investigation was carried out to determine whether a form of quasi-linear systems analysis can be applied to electrodormal responses to yield new insights into the nature of the response mechanisms and their interrelationships. The response investigated was the electrodermal response (galvanic skin potential, GSP) as elicited by an electric shock stimulus applied to the skin. The response subsequent to this stimulation was examined and its characteristics measured. A series of experimental runs on three Ss was accomplished, using sinusoidal modulation envelopes of frequencies. Results showed that it was possible to drive the GSP and to achieve relatively high coherence between the driving frequency and the response itself. The analysis was limited to Fourier analysis of the response in order to determine the relative energies at the driving frequency and at successive harmonics of that driving frequency, and correlational analysis in order to determine the degree of linear relationship between the driving frequency and the driven response

Integrative Genomics Identifies the Molecular Basis of Resistance to Azacitidine Therapy in Myelodysplastic Syndromes

© 2017 The Author(s) Myelodysplastic syndromes and chronic myelomonocytic leukemia are blood disorders characterized by ineffective hematopoiesis and progressive marrow failure that can transform into acute leukemia. The DNA methyltransferase inhibitor 5-azacytidine (AZA) is the most effective pharmacological option, but only ∼50% of patients respond. A response only manifests after many months of treatment and is transient. The reasons underlying AZA resistance are unknown, and few alternatives exist for non-responders. Here, we show that AZA responders have more hematopoietic progenitor cells (HPCs) in the cell cycle. Non-responder HPC quiescence is mediated by integrin α5 (ITGA5) signaling and their hematopoietic potential improved by combining AZA with an ITGA5 inhibitor. AZA response is associated with the induction of an inflammatory response in HPCs in vivo. By molecular bar coding and tracking individual clones, we found that, although AZA alters the sub-clonal contribution to different lineages, founder clones are not eliminated and continue to drive hematopoiesis even in complete responders