Nigerian scam e-mails and the charms of capital

So-called '419' or 'advance-fee' e-mail frauds have proved remarkably successful. Global losses to these scams are believed to run to billions of dollars. Although it can be assumed that the promise of personal gain which these e-mails hold out is part of what motivates victims, there is more than greed at issue here. How is it that the seemingly incredible offers given in these unsolicited messages can find an audience willing to treat them as credible? The essay offers a speculative thesis in answer to this question. Firstly, it is argued, these scams are adept at exploiting common presuppositions in British and American culture regarding Africa and the relationships that are assumed to exist between their nations and those in the global south. Secondly, part of the appeal of these e-mails lies in the fact that they appear to reveal the processes by which wealth is created and distributed in the global economy. They thus speak to their readers’ attempts to map or conceptualise the otherwise inscrutable processes of that economy. In the conclusion the essay looks at the contradictions in the official state response to this phenomena

Functional principal component analysis as a new methodology for the analysis of the impact of two rehabilitation protocols in functional recovery after stroke

[EN] Background: This study addressed the problem of evaluating the effectiveness of two protocols of physiotherapy for functional recovery after stroke. In particular, the study explored the use of Functional Principal Component Analysis (FPCA), a multivariate data analysis in order to assess and clarify the process of regaining independence after stroke. Methods: A randomized double-blind controlled trial was performed. Thirteen subjects with residual hemiparesis after a single stroke episode were measured in both in- and outpatient settings at a district hospital. All subjects were able to walk before suffering the stroke and were hemodynamically stable within the first week after stroke. Control and target groups were treated with conventional physiotherapy for stroke, but specific techniques were added for treatment of the target group depending on patients' functional levels. Independence level was assessed with the Barthel Index (BI) throughout 7 evolution stages (hemodynamic stability, beginning of standing, beginning of physical therapy sessions in the physiotherapy ward and monthly assessment for 6 months after stroke). Results: FPCA was applied for data analysis. Statistically significant differences were found in the dynamics of the recovery process between the two physiotherapy protocols. The target group showed a trend of improvement six months after stroke that was not present in the control group. Conclusions: FPCA is a method which may be used to provide greater insight into the analysis of the rehabilitation process than that provided by conventional parametric methods. So, by using the whole curves as basic data parameters, subtle differences in the rehabilitation process can be found. FPCA represents a future aid for the fine analysis of similar physiotherapy techniques, when applied in subjects with a huge variability of functional recovery, as in the case of post-stroke patients.This contribution has been carried out with financial support from the European Commission within the Seventh Framework Programme under contract FP7-ICT-2009-247935: BETTER BNCI-dr. The authors wish to thank the Stroke Rehabilitation Team of Hospital Universitari i Politecnic La Fe (Valencia, Spain), specially Dr. M.R. Beseler, physiotherapist M. Matas and physiotherapist A. Estaun. We also gratefully acknowledge patients who have participated in this study with great enthusiasm.Sánchez-Sánchez, M.; Belda Lois, JM.; Mena Del Horno, S.; Viosca Herrero, E.; Gisbert-Morant, B.; Igual-Camacho, C.; Bermejo Bosch, I. (2014). Functional principal component analysis as a new methodology for the analysis of the impact of two rehabilitation protocols in functional recovery after stroke. Journal of NeuroEngineering and Rehabilitation. 11:1-9. https://doi.org/10.1186/1743-0003-11-134S191

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)

Determining crystal structures through crowdsourcing and coursework

We show here that computer game players can build high-quality crystal structures. Introduction of a new feature into the computer game Foldit allows players to build and real-space refine structures into electron density maps. To assess the usefulness of this feature, we held a crystallographic model-building competition between trained crystallographers, undergraduate students, Foldit players and automatic model-building algorithms. After removal of disordered residues, a team of Foldit players achieved the most accurate structure. Analysing the target protein of the competition, YPL067C, uncovered a new family of histidine triad proteins apparently involved in the prevention of amyloid toxicity. From this study, we conclude that crystallographers can utilize crowdsourcing to interpret electron density information and to produce structure solutions of the highest quality

Clinical effectiveness of grip strength in predicting ambulation of elderly inpatients

MR Beseler,1 C Rubio,1 E Duarte,1 D Herv&aacute;s,2 MC Guevara,1 M Giner-Pascual,1 E Viosca1 1Physical Medicine and Rehabilitation, La Fe Hospital, Valencia, Spain; 2Statistical Unit, La Fe Hospital, Valencia, Spain Background: Assessing the clinical effectiveness of measuring grip strength as a prognostic tool in recovering ambulation in bed-confined frail elderly patients. Methods: A prospective study was carried out with 50 elderly inpatients (mean age: 81.6 years old). Manual muscle test was used for checking strength of hip flexor muscles, hip abductor muscles and knee extensor muscles. Grip strength was assessed by hydraulic dynamometer. Walking ability was assessed by functional ambulation categories and Functional Classification of Sagunto Hospital Ambulation. Existence of cognitive impairment (Short Portable Mental Status of Pfeiffer) and comorbidity (abbreviated Charlson index) were considered to be confounding variables. Statistical analysis: Simple comparisons and mixed models of multiple ordinal regression. Results: The sample presented generalized weakness in scapular (mean 4.22) and pelvic (mean 3.82) muscle. Mean hand grip values were similar: 11.98 kg right hand; 11.70 kg left hand. The patients had lost walking ability. After treatment, there was a statistically significant for scapular waist strength (P=0.001), pelvic waist strength (P=0.005) and walking ability (P=0.001). A statistically significant relationship in the regression analysis was found between the grip (right and left hands) and walking ability post-treatment (P=0.009; odds ratio 1.14&nbsp;and P=0.0014 odds ratio 1.113 for each walking scale). The confounding variables showed no statistical significance in the results.Conclusion: Grip strength is associated with walking ability in hospitalized frail elderly. Grip strength assessment by hydraulic dynamometry is useful in patients with poor collaboration. Walking ability training in frail elderly inpatients is useful. Keywords: gait, elderly, hand grip, physical therap

A new methodology based on functional principal component analysis tostudy postural stability post-stroke

[EN] Background. A major goal in stroke rehabilitation is the establishment of more effective physical therapy techniques to recover postural stability. Functional Principal Component Analysis provides greater insight into recovery trends. However, when missing values exist, obtaining functional data presents some difficulties. The purpose of this study was to reveal an alternative technique for obtaining the Functional Principal Components without requiring the conversion to functional data beforehand and to investigate this methodology to determine the effect of specific physical therapy techniques in balance recovery trends in elderly subjects with hemiplegia post-stroke. Methods: A randomized controlled pilot trial was developed. Thirty inpatients post-stroke were included. Control and target groups were treated with the same conventional physical therapy protocol based on functional criteria, but specific techniques were added to the target group depending on the subjects' functional level. Postural stability during standing was quantified by posturography. The assessments were performed once a month from the moment the participants were able to stand up to six months post-stroke. Findings: The target group showed a significant improvement in postural control recovery trend six months after stroke that was not present in the control group. Some of the assessed parameters revealed significant differences between treatment groups (P < 0.05). Interpretation: The proposed methodology allows Functional Principal Component Analysis to be performed when data is scarce. Moreover, it allowed the dynamics of recovery of two different treatment groups to be determined, showing that the techniques added in the target group increased postural stability compared to the base protocol.Sánchez, M.; Belda Lois, JM.; Mena Del Horno, S.; Viosca Herrero, E.; Igual-Camachoa, C.; Gisbert-Moranta, B. (2018). A new methodology based on functional principal component analysis tostudy postural stability post-stroke. Clinical Biomechanics. 56:18-26. https://doi.org/10.1016/j.clinbiomech.2018.05.003S18265