A Strategic Vision for Telemedicine and Medical Informatics in Space Flight

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/63255/1/15305620050503924.pd

National Telemedicine Initiatives: Essential to Healthcare Reform

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78116/1/tmj.2009.9960.pd

Implementing Telemedicine in Medical Emergency Response: Concept of Operation for a Regional Telemedicine Hub

A regional telemedicine hub, providing linkage of a telemedicine command center with an extended network of clinical experts in the setting of a natural or intentional disaster, may facilitate future disaster response and improve patient outcomes. However, the health benefits derived from the use of telemedicine in disaster response have not been quantitatively analyzed. In this paper, we present a general model of the application of telemedicine to disaster response and evaluate a concept of operations for a regional telemedicine hub, which would create distributed surge capacity using regional telemedicine networks connecting available healthcare and telemedicine infrastructures to external expertise. Specifically, we investigate (1) the scope of potential use of telemedicine in disaster response; (2) the operational characteristics of a regional telemedicine hub using a new discrete-event simulation model of an earthquake scenario; and (3) the benefit that the affected population may gain from a coordinated regional telemedicine network

The Empirical Foundations of Telemedicine Interventions for Chronic Disease Management

The telemedicine intervention in chronic disease management promises to involve patients in their own care, provides continuous monitoring by their healthcare providers, identifies early symptoms, and responds promptly to exacerbations in their illnesses. This review set out to establish the evidence from the available literature on the impact of telemedicine for the management of three chronic diseases: congestive heart failure, stroke, and chronic obstructive pulmonary disease. By design, the review focuses on a limited set of representative chronic diseases because of their current and increasing importance relative to their prevalence, associated morbidity, mortality, and cost. Furthermore, these three diseases are amenable to timely interventions and secondary prevention through telemonitoring. The preponderance of evidence from studies using rigorous research methods points to beneficial results from telemonitoring in its various manifestations, albeit with a few exceptions. Generally, the benefits include reductions in use of service: hospital admissions/re-admissions, length of hospital stay, and emergency department visits typically declined. It is important that there often were reductions in mortality. Few studies reported neutral or mixed findings.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140284/1/tmj.2014.9981.pd

Altered differentiation in acute myeloid leukemias; Role of ERG and FUS-ERG fusion protein

The FUS-ERG chimeric oncogene has been associated with fatal acute myeloid leukemias (AML) carrying the non-random t(16;21) (p11;q22) chromosomal aberration. In these leukemias, the presence of the t(16;21) translocation product FUS-ERG is associated with a) an increase in blasts with a round or irregular nucleus, basophilic cytoplasm, vacuoles and, occasionally, with phagocytosis features; b) the presence of micromegakaryocytes; and c) impaired myeloid differentiation with dysplastic neutrophils. Reportedly, ectopic expression of FUS-ERG in murine myeloid precursor (L-G) and in human cord blood cells induces changes which, in part, might account for the phenotype observed in t(16;21) AML patients. However, the FUS-ERG-dependent mechanisms underlying multilineage hematopoietic differentiation defects are still unclear. To understand how FUS-ERG affects granulocytic differentiation, we independently generated 32Dcl3-derived myeloid progenitor cell lines expressing HA-tagged ERG, FUS, and FUS-ERG oncoprotein. In the presence of the growth factor, IL-3, all cell lines showed similar proliferation rate without acquiring cytokine-independent growth. However, FUS and FUS-ERG, but not ERG, expression decreased the susceptibility to apoptosis induced by cytokine-deprivation in a dose-dependent manner. Interestingly, viable FUS-ERG-expressing cells (30%) were observed after five days in IL-3-deprived culture, whereas no parental cells were viable after 24 hours. Conversely, FUS-ERG-expressing cells showed enhanced proliferation and delayed differentiation when cultured in the presence of G-CSF, a growth factor important in granulocytic differentiation. By contrast, marked apoptosis was observed in G-CSF-treated FUS- and ERG-expressing cells. To dissect the FUS-ERG-dependent molecular mechanisms underlying altered differentiation, we assessed protein levels of G-CSF receptor (G-CSFR) and of the two major regulators of myelopoiesis, PU.1 and C/EBPα. Surprisingly, G-CSFR and C/EBPα, but not PU.1, levels were markedly increased in FUS-ERG-expressing cells but not in FUS- or ERG-transduced lines. Moreover, by microarray analysis we found that FUS-ERG expression specifically induced a) downregulation of genes either required for granulocytic differentiation or inhibiting G-CSF-induced proliferation; b) downregulation of pro-apoptotic and growth-suppressor genes and upregulation of positive regulators of survival and proliferation; and c) upregulation of genes that either promote megakaryocytic differentiation or are markers of differentiation into other hematopoietic lineages. Thus, it appears that FUS-ERG, rather than FUS or ERG overexpression, enhances survival and induces proliferation of myeloid progenitors by negatively affecting their ability to respond to differentiation stimuli