Design, Implementation, and Evaluation of an Elder Financial Abuse Program

Financial exploitation of elders is the fastest growing crime in America, with telemarketing schemes being the prime methods used. The authors developed the Striking Back program, which includes a Leader\u27s Guide, videotape, practice scenarios, and handouts, to make elders aware of the problem and provide strategies for dealing with solicitors. Pre/post knowledge tests were used to determine if learning occurred as a result of the educational program, and a 6-week follow-up evaluation was conducted to determine whether elders had adopted key practices that deter telemarketers. This article presents the program design and implementation strategies as well as evaluation results

Geology of Caphouse Colliery, Wakefield, Yorkshire, UK

The National Coal Mining Museum in West Yorkshire affords a rare opportunity for the public to visit a former colliery (Caphouse) and experience at first hand the geology of a mine. The geology at the museum can be seen via the public tour, limited surface outcrop and an inclined ventilation drift, which provides the best geological exposure and information. The strata encountered at the site are c. 100 m thick and are of latest Langsettian (Pennsylvanian) age. The ventilation drift intersects several coal seams (Flockton Thick, Flockton Thin, Old Hards, Green Lane and New Hards) and their associated roof rocks and seatearths. In addition to exposures of bedrock, recent mineral precipitates of calcium carbonates, manganese carbonates and oxides, and iron oxyhydroxides can be observed along the drift, and there is a surface exposure of Flockton Thick Coal and overlying roof strata. The coals and interbedded strata were deposited in the Pennine Basin in a fluvio-lacustrine setting in an embayment distant from the open ocean with limited marine influence. A lacustrine origin for mudstone roof rocks of several of the seams is supported by the incidence of non-marine bivalves and fossilized fish remains whilst the upper part of the Flockton Thick Coal consists of subaqueously deposited cannel coal. The mudstones overlying the Flockton Thick containing abundant non-marine bivalves are of great lateral extent, indicating a basin-wide rise of base level following coal deposition that may be compared with a non-marine flooding surface

Early observed transient prostate-specific antigen elevations on a pilot study of external beam radiation therapy and fractionated MRI guided High Dose Rate brachytherapy boost

PURPOSE: To report early observation of transient PSA elevations on this pilot study of external beam radiation therapy and magnetic resonance imaging (MRI) guided high dose rate (HDR) brachytherapy boost. MATERIALS AND METHODS: Eleven patients with intermediate-risk and high-risk localized prostate cancer received MRI guided HDR brachytherapy (10.5 Gy each fraction) before and after a course of external beam radiotherapy (46 Gy). Two patients continued on hormones during follow-up and were censored for this analysis. Four patients discontinued hormone therapy after RT. Five patients did not receive hormones. PSA bounce is defined as a rise in PSA values with a subsequent fall below the nadir value or to below 20% of the maximum PSA level. Six previously published definitions of biochemical failure to distinguish true failure from were tested: definition 1, rise >0.2 ng/mL; definition 2, rise >0.4 ng/mL; definition 3, rise >35% of previous value; definition 4, ASTRO defined guidelines, definition 5 nadir + 2 ng/ml, and definition 6, nadir + 3 ng/ml. RESULTS: Median follow-up was 24 months (range 18–36 mo). During follow-up, the incidence of transient PSA elevation was: 55% for definition 1, 44% for definition 2, 55% for definition 3, 33% for definition 4, 11% for definition 5, and 11% for definition 6. CONCLUSION: We observed a substantial incidence of transient elevations in PSA following combined external beam radiation and HDR brachytherapy for prostate cancer. Such elevations seem to be self-limited and should not trigger initiation of salvage therapies. No definition of failure was completely predictive

Social capital and active membership in the Ghana National Health Insurance Scheme - a mixed method study

BACKGROUND: People’s decision to enroll in a health insurance scheme is determined by socio-cultural and socio-economic factors. On request of the National health Insurance Authority (NHIA) in Ghana, our study explores the influence of social relationships on people’s perceptions, behavior and decision making to enroll in the National Health Insurance Scheme. This social scheme, initiated in 2003, aims to realize accessible quality healthcare services for the entire population of Ghana. We look at relationships of trust and reciprocity between individuals in the communities (so called horizontal social capital) and between individuals and formal health institutions (called vertical social capital) in order to determine whether these two forms of social capital inhibit or facilitate enrolment of clients in the scheme. Results can support the NHIA in exploiting social capital to reach their objective and strengthen their policy and practice. METHOD: We conducted 20 individual- and seven key-informant interviews, 22 focus group discussions, two stakeholder meetings and a household survey, using a random sample of 1903 households from the catchment area of 64 primary healthcare facilities. The study took place in Greater Accra Region and Western Regions in Ghana between June 2011 and March 2012. RESULTS: While social developments and increased heterogeneity seem to reduce community solidarity in Ghana, social networks remain common in Ghana and are valued for their multiple benefits (i.e. reciprocal trust and support, information sharing, motivation, risk sharing). Trusting relations with healthcare and insurance providers are, according healthcare clients, based on providers’ clear communication, attitude, devotion, encouragement and reliability of services. Active membership of the NHIS is positive associated with community trust, trust in healthcare providers and trust in the NHIS (p-values are .009, .000 and .000 respectively). CONCLUSION: Social capital can motivate clients to enroll in health insurance. Fostering social capital through improving information provision to communities and engaging community groups in health care and NHIS services can facilitate peoples’ trust in these institutions and their active participation in the scheme

Brain size regulations by cbp haploinsufficiency evaluated by in-vivo MRI based volumetry

The Rubinstein-Taybi Syndrome (RSTS) is a congenital disease that affects brain development causing severe cognitive deficits. In most cases the disease is associated with dominant mutations in the gene encoding the CREB binding protein (CBP). In this work, we present the first quantitative analysis of brain abnormalities in a mouse model of RSTS using magnetic resonance imaging (MRI) and two novel self-developed automated algorithms for image volumetric analysis. Our results quantitatively confirm key syndromic features observed in RSTS patients, such as reductions in brain size (-16.31%, p < 0.05), white matter volume (-16.00%, p < 0.05), and corpus callosum (-12.40%, p < 0.05). Furthermore, they provide new insight into the developmental origin of the disease. By comparing brain tissues in a region by region basis between cbp(+/-) and cbp(+/+) littermates, we found that cbp haploinsufficiency is specifically associated with significant reductions in prosencephalic tissue, such us in the olfactory bulb and neocortex, whereas regions evolved from the embryonic rhombencephalon were spared. Despite the large volume reductions, the proportion between gray-, white-matter and cerebrospinal fluid were conserved, suggesting a role of CBP in brain size regulation. The commonalities with holoprosencephaly and arhinencephaly conditions suggest the inclusion of RSTS in the family of neuronal migration disorders.We are grateful to Begona Fernandez for her excellent technical assistance. We would like to thank S. Sawiak (Wolfson Imaging Centre, University of Cambridge, Cambridge, United Kingdom) for the mouse brain tissue probability maps and the SPMmouse plug-in, and to N. Kovacevic (Mouse Imaging Centre, Hospital for Sick Children, Toronto, Ontario, Canada) for the atlas of the mouse brain. Supported by grants from the Spanish MINECO to S.C. (BFU 2012-39958) and MINECO and FEDER to D.M. (TEC 2012-33778) and from MINECO (SAF2011-22855) and Generalitat Valenciana (Prometeo/2012/005) to A.B. The Instituto de Neurociencias is "Centre of Excellence Severo Ochoa".Ateca Cabarga, JC.; Cosa, A.; Pallares, V.; Lopez-Atalaya, JP.; Barco, A.; Canals, S.; Moratal Pérez, D. (2015). Brain size regulations by cbp haploinsufficiency evaluated by in-vivo MRI based volumetry. Scientific Reports. 5. https://doi.org/10.1038/srep16256S5Rubinstein, J. H. & Taybi, H. Broad thumbs and toes and facial abnormalities. A possible mental retardation syndrome. Am J Dis Child 105, 588–608 (1963).Van Belzen, M., Bartsch, O., Lacombe, D., Peters, D. J. & Hennekam, R. C. Rubinstein-Taybi syndrome (CREBBP, EP300). Eur J Hum Genet. 19, preceeding 118–120 (2011).Hennekam, R. C. Rubinstein-Taybi syndrome. Eur J Hum Genet. 14, 981–985 (2006).Wiley, S., Swayne, S., Rubinstein, J. H., Lanphear, N. E. & Stevens, C. A. Rubinstein-Taybi syndrome medical guidelines. Am J Med Genet A. 119A, 101–110 (2003).Michail, J., Matsoukas, J. & Theodorou, S. Pouce bot arqué en forte abduction-extension et autres symptomes concomitants. Rev Chir Orthop 43, 142–146 (1957).Barco A. The Rubinstein-Taybi syndrome: modeling mental impairment in the mouse. Genes Brain Behav 6, 32–39 (2007).Lopez-Atalaya, J. P., Valor, L. M. & Barco, A. Epigenetic factors in intellectual disability: the Rubinstein-Taybi syndrome as a paradigm of neurodevelopmental disorder with epigenetic origin. Prog Mol Biol Transl Sci. 128, 139–176 (2014).Petrij, F., Giles, R. H., Dauwerse, H. G., Saris, J. J., Hennekam, R. C. M., Masuno, M., Tommerup, N., Van Ommen, G. J. B., Goodman, R. H., Peters, D. J. M. & Breuning, M. H. Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP. Nature 376, 348–351 (1995).Zimmermann, N., Acosta, A. M., Kohlhase, J. & Bartsch, O. Confirmation of EP300 gene mutations as a rare cause of Rubinstein-Taybi syndrome. Eur J Hum Genet. 15, 837–842 (2007).Bartholdi, D. et al. Genetic heterogeneity in Rubinstein-Taybi syndrome: delineation of the phenotype of the first patients carrying mutations in EP300. J Med Genet. 44, 327–333 (2007).Roelfsema, J. H. et al. Genetic heterogeneity in Rubinstein-Taybi syndrome: mutations in both the CBP and EP300 genes cause disease. Am J Hum Genet. 76, 572–580 (2005).Tanaka, Y., Naruse, I., Maekawa, T., Masuya, H., Shiroishi, T. & Ishii, S. Abnormal skeletal patterning in embryos lacking a single Cbp allele: a partial similarity with Rubinstein-Taybi syndrome. Proc Natl Acad Sci USA 94, 10215–10220 (1997).López-Atalaya, J. P. et al. CBP is required for environmental enrichment-induced neurogenesis and cognitive enhancement. EMBO J 30, 4287–4298 (2011).Wang, J. et al. CBP histone acetyltransferase activity regulates embryonic neural differentiation in the normal and Rubinstein-Taybi syndrome brain. Dev Cell. 18, 114–125 (2010).Marzuillo, P. et al. Brain magnetic resonance in the routine management of Rubinstein-Taybi syndrome (RTS) can prevent life-threatening events and neurological deficits. Am J Med Genet A. 164A, 2129–2132 (2014).de Kort, E., Conneman, N. & Diderich, K. A case of Rubinstein-Taybi syndrome and congenital neuroblastoma. Am J Med Genet A. 164A, 1332–1333 (2014).Lee, J. S. et al. Clinical and mutational spectrum in Korean patients with Rubinstein-Taybi syndrome: the spectrum of brain MRI abnormalities. Brain Dev. 37, 402–408 (2015).Marzuillo, P. et al. Novel cAMP binding protein-BP (CREBBP) mutation in a girl with Rubinstein-Taybi syndrome, GH deficiency, Arnold Chiari malformation and pituitary hypoplasia. BMC Med Genet. 14, 28 (2013). 10.1186/1471-2350-14-28.Li, Z. et al. Phenotypic expansion of the interstitial 16p13.3 duplication: a case report and review of the literature. Gene. 531, 502–505 (2013).Demeer, B. et al. Duplication 16p13.3 and the CREBBP gene: confirmation of the phenotype. Eur J Med Genet. 56, 26–31 (2013).Kumar, S., Suthar, R., Panigrahi, I. & Marwaha, R. K. Rubinstein-Taybi syndrome: Clinical profile of 11 patients and review of literature. Indian J Hum Genet. 18, 161–166 (2012).Giussani, C. et al. The association of neural axis and craniovertebral junction anomalies with scoliosis in Rubinstein-Taybi syndrome. Childs Nerv Syst. 28, 2163–2168 (2012).Parsley, L., Bellus, G., Handler, M. & Tsai, A. C. Identical twin sisters with Rubinstein-Taybi syndrome associated with Chiari malformations and syrinx. Am J Med Genet A. 155A, 2766–2770 (2011).Thienpont, B. et al. Duplications of the critical Rubinstein-Taybi deletion region on chromosome 16p13.3 cause a novel recognisable syndrome. J Med Genet. 47, 155–161 (2010).Kim, S. H., Lim, B. C., Chae, J. H., Kim, K. J. & Hwang, Y. S. A case of Rubinstein-Taybi Syndrome with a CREB-binding protein gene mutation. Korean J Pediatr. 53, 718–721 (2010).Wójcik, C. et al. Rubinstein-Taybi syndrome associated with Chiari type I malformation caused by a large 16p13.3 microdeletion: a contiguous gene syndrome? Am J Med Genet A. 152A, 479–483 (2010).Wachter-Giner, T., Bieber, I., Warmuth-Metz, M., Bröcker, E. B. & Hamm, H. Multiple pilomatricomas and gliomatosis cerebri--a new association? Pediatr Dermatol. 26, 75–78 (2009).Verstegen, M. J., van den Munckhof, P., Troost, D. & Bouma, G. J. Multiple meningiomas in a patient with Rubinstein-Taybi syndrome. Case report. J Neurosurg. 102, 167–168 (2005).Agarwal, R., Aggarwal, R., Kabra, M. & Deorari, A. K. Dandy-Walker malformation in Rubinstein-Taybi syndrome: a rare association. Clin Dysmorphol. 11, 223–224 (2002).Ihara, K., Kuromaru, R., Takemoto, M. & Hara, T. Rubinstein-Taybi syndrome: a girl with a history of neuroblastoma and premature thelarche. Am J Med Genet. 83, 365–366 (1999).Sener, R. N. Rubinstein-Taybi syndrome: cranial MR imaging findings. Comput Med Imaging Graph 19, 417–418 (1995).Robinson, T. W., Stewart, D. L. & Hersh, J. H. Monozygotic twins concordant for Rubinstein-Taybi syndrome and implications for genetic counseling. Am J Med Genet. 45, 671–673 (1993).Guion-Almeida, M. L. & Richieri-Costa, A. Callosal agenesis, iris coloboma and megacolon in a Brazilian boy with Rubinstein-Taybi syndrome. Am J Med Genet. 43, 929–931 (1992).Albanese, A. et al. [Role of diagnostic imaging in Rubinstein-Taybi syndrome. personal experience with 8 cases]. Radiol Med. 81, 253–261 (1991).Rubinstein, J. H. Broad thumb-hallux (Rubinstein-Taybi) syndrome 1957-1988. Am J Med Genet Suppl. 6, 3–16 (1990).Hennekam, R. C., Stevens, C. A. & Van de Kamp, J. J. Etiology and recurrence risk in Rubinstein-Taybi syndrome. Am J Med Genet Suppl. 6, 56–64 (1990).Bonioli, E., Bellini, C. & Di Stefano, A. Unusual association: Dandy-Walker-like malformation in the Rubinstein-Taybi syndrome. Am J Med Genet. 33, 420–421 (1989).Beluffi, G., Pazzaglia, U. E., Fiori, P., Pricca, P. & Poznanski, A. K. [Oto-palato-digital syndrome. Clinico-radiological study]. Radiol Med. 74, 176–184 (1987).Cantani, A. & Gagliesi, D. Rubinstein-Taybi syndrome. Review of 732 cases and analysis of the typical traits. Eur Rev Med Pharmacol Sci. 2, 81–87 (1998).Viosca, J., Lopez-Atalaya, J. P., Olivares, R., Eckner, R. & Barco, A. Syndromic features and mild cognitive impairment in mice with genetic reduction on p300 activity: Differential contribution of p300 and CBP to Rubinstein-Taybi syndrome etiology. Neurobiol Dis. 37, 186–194 (2010).Martínez-Martínez, M. A., Pacheco-Torres, J., Borrell, V. & Canals, S. Phenotyping the central nervous system of the embryonic mouse by magnetic resonance microscopy. Neuroimage. 97, 95–106 (2014).Heikkinen, T. et al. Characterization of neurophysiological and behavioral changes, MRI brain volumetry and 1H MRS in zQ175 knock-in mouse model of Huntington’s disease. PLoS One. 7, e50717 (2012), 10.1371/journal.pone.0050717.Alarcón, J. M. et al. Chromatin acetylation, memory and LTP are impaired in CBP+/− mice: a model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration. Neuron. 42, 947–959 (2004).Smith, S. M. et al. Advances in functional and structural MR image analysis and implementation as FSL. Neuroimage 23 Supp 1, S208–19 (2004).Smith, S. M. Fast robust automated brain extraction. Hum Brain Mapp 17, 143–155 (2002).Ashburner, J. & Friston, K. J. Unified segmentation. Neuroimage 26, 839–851 (2005).Sawiak, S. J., Wood, N. I., Williams, G. B., Morton, A. J. & Carpenter, T. A. Voxel-based morphometry in the R6/2 transgenic mouse reveals differences between genotypes not seen with manual 2D morphometry. Neurobiol Dis 33, 20–27 (2009).Kovačević, N. et al. A three-dimensional MRI atlas of the mouse brain with estimates of the average and variability. Cereb Cortex 15, 639–645 (2005).Zacharoff, L. et al. Cortical metabolites as biomarkers in the R6/2 model of Huntington’s disease. J Cereb Blood Flow Metab. 32, 502–514 (2012).Petryk, A., Graf, D. & Marcucio, R. Holoprosencephaly: signaling interactions between the brain and the face, the environment and the genes and the phenotypic variability in animal models and humans. Wiley Interdiscip Rev Dev Biol. 4, 17–32 (2015).Solomon, B. D., Gropman, A. & Muenke, M. Holoprosencephaly Overview. In: GeneReviews (eds Pagon, R. A. et al.), Seattle (WA): University of Washington, Seattle; 1993-2014, 2000 Dec 27 [Updated 2013 Aug 29]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK1530/ [Date of access: September 4, 2015].Mazzone, D., Milana, A., Praticò, G. & Reitano, G. Rubinstein-Taybi syndrome associated with Dandy-Walker cyst. Case report in a newborn. J Perinat Med. 17, 381–384 (1989).Barson, A. J. Proceedings: Rubinstein-Taybi syndrome. Arch Dis Child. 49, 495 (1974).Tsui, D. et al. CBP regulates the differentiation of interneurons from ventral forebrain neural precursors during murine development. Dev Biol. 385, 230–241 (2014).Ross, M. E. & Walsh, C. A. Human brain malformations and their lessons for neuronal migration. Annu Rev Neurosci. 24, 1041–1070 (2001).Tanaka, T., Ling, B. C., Rubinstein, J. H. & Crone, K. R. Rubinstein-Taybi syndrome in children with tethered spinal cord. J Neurosurg. 105, 261–264 (2006).Dubourg, C. et al. Holoprosencephaly. Orphanet J Rare Dis. 2, 2–8 (2007)