Financial Elder Abuse: New York State Prevalence, Interventions, & Future Directions

Millions of older adults living in the United States are victims of elder abuse and financial exploitation is the most common form of abuse. Additionally, the adult population age 65 and older is projected to more than double by 2060 (Colby & Ortman, 2015) which will increase the likelihood of elder abuse. New York State has a substantial older adult population, was the focus of largest and most comprehensive elder abuse prevalence study, and utilizes multiple forms of financial abuse interventions including the widely supported use of multidisciplinary teams. Thus, the purpose of this thesis is to describe the prevalence and current interventions pertaining to the issue of financial elder abuse in New York State.SUNY BrockportSocial WorkSenior Honors These

SNC Employee / Parent / Townie Dishes on 50 Years of Campus Life

Todd Danen \u2777 tells SNC parents about his life with SNC in Spring 219

Financial Elder Abuse: New York State Prevalence, Interventions, & Future Directions

Millions of older adults living in the United States are victims of elder abuse and financial exploitation is the most common form of abuse. Additionally, the adult population age 65 and older is projected to more than double by 2060 (Colby & Ortman, 2015) which will increase the likelihood of elder abuse. New York State has a substantial older adult population, was the focus of largest and most comprehensive elder abuse prevalence study, and utilizes multiple forms of financial abuse interventions including the widely supported use of multidisciplinary teams. Thus, the purpose of this thesis is to describe the prevalence and current interventions pertaining to the issue of financial elder abuse in New York State

Neutrophil-Mediated Experimental Metastasis Is Enhanced by VEGFR Inhibition in a Zebrafish Xenograft Model

Inhibition of VEGF signalling effectively suppresses localized tumour growth but accelerates tumour invasiveness and micrometastasis by unknown mechanisms. To study the dynamic and reciprocal interactions between tumour cells and their microenvironment during these processes, we established a xenograft model by injecting tumour cells into the blood circulation of transparent zebrafish embryos. This reproducibly results in rapid simultaneous formation of a localized tumour and experimental micrometastasis, allowing time-resolved imaging of both processes at single-cell resolution within 1 week. The tumour vasculature was initiated de novo by remodelling of primitive endothelial cells into a functional network. Roles of myeloid cells in critical tumourigenesis steps such as vascularization and invasion were revealed by genetic and pharmaceutical approaches. We discovered that the physiological migration of neutrophils controlled tumour invasion by conditioning the collagen matrix and forming the metastatic niche, as detected by two-photon confocal microscopy and second harmonic generation. Administration of VEGFR inhibitors blocked tumour vascularization and a localized tumour growth but enhanced migration of neutrophils, which in turn promoted tumour invasion and formation of micrometastasis. This demonstrates the in vivo cooperation between VEGF signalling and myeloid cells in metastasis and provides a new mechanism underlying the recent findings that VEGFR targeting can promote tumour invasiveness

Coronin-1C and RCC2 guide mesenchymal migration by trafficking Rac1 and controlling GEF exposure

Sustained forward migration through a fibrillar extracellular matrix requires localization of protrusive signals. Contact with fibronectin at the tip of a cell protrusion activates Rac1, and for linear migration it is necessary to dampen Rac1 activity in off-axial positions and redistribute Rac1 from non-protrusive membrane to the leading edge. Here, we identify interactions between coronin-1C (Coro1C), RCC2 and Rac1 that focus active Rac1 to a single protrusion. Coro1C mediates release of inactive Rac1 from non-protrusive membrane and is necessary for Rac1 redistribution to a protrusive tip and fibronectin-dependent Rac1 activation. The second component, RCC2, attenuates Rac1 activation outside the protrusive tip by binding to the Rac1 switch regions and competitively inhibiting GEF action, thus preventing off-axial protrusion. Depletion of Coro1C or RCC2 by RNA interference causes loss of cell polarity that results in shunting migration in 1D or 3D culture systems. Furthermore, morpholinos against Coro1C or RCC2, or mutation of any of the binding sites in the Rac1-RCC2-Coro1C complex delays the arrival of neural crest derivatives at the correct location in developing zebrafish, demonstrating the crucial role in migration guidance in vivo

Economic potential of human motion for electricity production in gymnasiums

With the continuous rise of energy demand at a global scale and, the significant environmental impacts that the current energy sector causes, political decision-makers feel the need to increasingly invest in renewable energy sources, such as solar and wind energy, and find new ways to produce electricity with minimal environmental impact. The use of human movement to produce energy has already been a study subject, but with very few applications in the current market. This is mainly due to the relation between the investment costs and the electric output that current generators are able to produce. A scarcity of studies about the economic potential of these technologies is noted, which contributes to the weak interest of potential investors in their implementation. In this work an attempt is made to synthesize the results related to the analysis of the economic aspects associated to the technologies that use human motion, which already have real-life applications and have been extensively studied. Simultaneously the concept is developed, and a prototype is constructed of a system capable of using linear human movement, of which the performance is evaluated. As such, it becomes possible to compare the electric output of the rotational system, based on existing literature, with the output of the linear system based on the results acquired during the preliminary tests of a developed prototype. These values are used to calculate the reduction of greenhouse gas emissions that these systems enable. The experiments with the prototype were developed in a gymnasium, because these establishments concentrate a considerable amount of daily human motion. Currently, that movement is wasted in the machine’s resistance. Meanwhile, the economic analysis and potential GHG savings of these systems are studied in four different gymnasiums with varying characteristics. It was determined that the use of rotational human motion to produce electric energy has a considerable economic potential in the current market, which is supported by the fact that a few establishments have already incorporated equipment that permit their exploitation. However, linear human movement is incapable of reaching an acceptable return period in almost all scenarios. Only large-scale gymnasium, such as Be-Fit Setúbal, possess the capacity to adopt this technology and reach a return period with economic viabilit

Coronin-1C Protein and Caveolin Protein Provide Constitutive and Inducible Mechanisms of Rac1 Protein Trafficking

Sustained directional fibroblast migration requires both polarized activation of the protrusive signal, Rac1, and redistribution of inactive Rac1 from the rear of the cell so that it can be redistributed or degraded. In this work, we determine how alternative endocytic mechanisms dictate the fate of Rac1 in response to the extracellular matrix environment. We discover that both coronin-1C and caveolin retrieve Rac1 from similar locations at the rear and sides of the cell. We find that coronin-1C-mediated extraction, which is responsible for Rac1 recycling, is a constitutive process that maintains Rac1 protein levels within the cell. In the absence of coronin-1C, the effect of caveolin-mediated endocytosis, which targets Rac1 for proteasomal degradation, becomes apparent. Unlike constitutive coronin-1C-mediated trafficking, caveolin-mediated Rac1 endocytosis is induced by engagement of the fibronectin receptor syndecan-4. Such an inducible endocytic/degradation mechanism would predict that, in the presence of fibronectin, caveolin defines regions of the cell that are resistant to Rac1 activation but, in the absence of fibronectin leaves more of the membrane susceptible to Rac1 activation and protrusion. Indeed, we demonstrate that fibronectin-stimulated activation of Rac1 is accelerated in the absence of caveolin and that, when caveolin is knocked down, polarization of active Rac1 is lost in FRET experiments and culminates in shunting migration in a fibrous fibronectin matrix. Although the concept of polarized Rac1 activity in response to chemoattractants has always been apparent, our understanding of the balance between recycling and degradation explains how polarity can be maintained when the chemotactic gradient has faded

Tumor-induced remote ECM network orientation steers angiogenesis

Tumor angiogenesis promotes tumor growth and metastasis. Here, we use automated sequential microprinting of tumor and endothelial cells in extracellular matrix (ECM) scaffolds to study its mechanical aspects. Quantitative reflection microscopy shows that tumor spheroids induce radial orientation of the surrounding collagen fiber network up to a distance of five times their radius. Across a panel of ~20 different human tumor cell lines, remote collagen orientation is correlated with local tumor cell migration behavior. Tumor induced collagen orientation requires contractility but is remarkably resistant to depletion of collagen-binding integrins. Microvascular endothelial cells undergo directional migration towards tumor spheroids once they are within the tumor-oriented collagen fiber network. Laser ablation experiments indicate that an intact physical connection of the oriented network with the tumor spheroid is required for mechanical sensing by the endothelial cells. Together our findings indicate that, in conjunction with described activities of soluble angiogenic factors, remote physical manipulation of the ECM network by the tumor can help to steer angiogenesis

Ignoring matrix boundaries when the LKB1 master kinase is gone.

Gradients of soluble attractants as well as extracellular matrix (ECM) proteins serve as cues for directional cell movement. Such "chemotaxis" and "haptotaxis" steers migration of cells during embryonic development, wound healing, and immune responses. In this issue, Chan et al. (2014. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201404067) show that the tumor suppressor LKB1 controls haptotaxis through the microtubule affinity-regulating kinase (MARK) family, one of the many substrates of the LKB1 master kinase. In the absence of this pathway, melanoma cells migrate irrespective of ECM gradients, which may explain the increased metastatic spread observed in LKB1-deficient tumors.Toxicolog