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1.  Deficient Adolescent Social Behavior Following Early-Life Inflammation is Ameliorated by Augmentation of Anandamide Signaling 
Brain, behavior, and immunity  2016;58:237-247.
Early-life inflammation has been shown to exert profound effects on brain development and behavior, including altered emotional behavior, stress responsivity and neurochemical/neuropeptide receptor expression and function. The current study extends this research by examining the impact of inflammation, triggered with the bacterial compound lipopolysaccharide (LPS) on postnatal day (P) 14, on social behavior during adolescence. We investigate the role that the endocannabinoid (eCB) system plays in sociability after early-life LPS. To test this, multiple cohorts of Sprague Dawley rats were injected with LPS on P14. In adolescence, rats were subjected to behavioral testing in a reciprocal social interaction paradigm as well as the open field. We quantified eCB levels in the amygdala of P14 and adolescent animals (anandamide and 2-arachidonoylglycerol) as well as adolescent amygdaloid cannabinoid receptor 1 (CB1) binding site density and the hydrolytic activity of the enzyme fatty acid amide hydrolase (FAAH), which metabolizes the eCB anandamide. Additionally, we examined the impact of FAAH inhibition on alterations in social behavior. Our results indicate that P14 LPS decreases adolescent social behavior (play and social non-play) in males and females at P40. This behavioral alteration is accompanied by decreased CB1 binding, increased anandamide levels and increased FAAH activity. Systemic administration of the FAAH inhibitor PF-04457845 (1mg/kg) prior to the social interaction task normalizes LPS-induced alterations in social behavior, while not affecting social behavior in the control group. Infusion of 10ng PF-04457845 into the basolateral amygdala normalized social behavior in LPS injected females. These data suggest that alterations in eCB signaling following postnatal inflammation contribute to impairments in social behavior during adolescence and that FAAH could be a novel target for disorders involving social deficits such as social anxiety disorders or autism.
doi:10.1016/j.bbi.2016.07.152
PMCID: PMC5461973  PMID: 27453335
Early-life inflammation; social behavior; endocannabinoid; LPS; FAAH; amygdala; anxiety; autism
2.  Well-posed continuum equations for granular flow with compressibility and μ(I)-rheology 
Continuum modelling of granular flow has been plagued with the issue of ill-posed dynamic equations for a long time. Equations for incompressible, two-dimensional flow based on the Coulomb friction law are ill-posed regardless of the deformation, whereas the rate-dependent μ(I)-rheology is ill-posed when the non-dimensional inertial number I is too high or too low. Here, incorporating ideas from critical-state soil mechanics, we derive conditions for well-posedness of partial differential equations that combine compressibility with I-dependent rheology. When the I-dependence comes from a specific friction coefficient μ(I), our results show that, with compressibility, the equations are well-posed for all deformation rates provided that μ(I) satisfies certain minimal, physically natural, inequalities.
doi:10.1098/rspa.2016.0846
PMCID: PMC5454347
granular flow; continuum modelling; rheology
3.  Sustained Glucocorticoid Exposure Recruits Cortico-limbic CRH Signaling to Modulate Endocannabinoid Function 
Psychoneuroendocrinology  2016;66:151-158.
Sustained exposure to stress or corticosteroids is known to cause changes in brain endocannabinoid (eCB) signaling, such that tissue contents of the eCBs N-arachidonylethanolamine (AEA) are generally reduced while 2-arachidonoylglycerol (2-AG) levels increase. These changes in eCB signaling are to be important for many of the aspects of chronic stress, such as anxiety, reward sensitivity and stress adaptation, yet the mechanisms mediating these changes are not fully understood. We have recently found that the stress-related neuropeptide corticotropin-releasing hormone (CRH), acting through the CRH type 1 receptor (CRHR1), can reduce AEA content by increasing its hydrolysis by the enzyme fatty acid amide hydrolase (FAAH) as well as increase 2-AG contents. As extra-hypothalamic CRH is upregulated by chronic corticosteroid or stress exposure, we hypothesized that increased CRH signaling through CRHR1 contributes to the effects of chronic corticosteroid exposure on the eCB system within the amygdala and prefrontal cortex. Male rats were exposed to 7 days of systemic corticosterone capsules, with or without concurrent exposure to a CRHR1 antagonist and examined eCB content. Consistent with previous studies in the amygdala, sustained corticosterone exposure increases CRH mRNA in the prefrontal cortex. As was shown previously, FAAH activity was increased and AEA contents reduced within the amygdala and prefrontal cortex following chronic corticosterone exposure. Chronic corticosterone exposure also elevated 2-AG content in the prefrontal cortex but not the amygdala. These corticosteroid-driven changes were all blocked by systemic CRHR1 antagonism. Consistent with these data indicating sustained increases in CRH signaling can mediate the effects of chronic elevations in corticosteroids, CRH overexpressing mice also exhibited increased FAAH-mediated AEA hydrolysis in the amygdala and prefrontal cortex compared to wild type. CRH overexpression increased 2-AG content in the amygdala, but not the prefrontal cortex. These data indicate that chronic elevations in CRH signaling, as is seen following exposure to chronic elevations in corticosterone or stress, drive persistent changes in eCB function. As reductions in AEA signaling mediate the effects of CRH and chronic stress on anxiety, these data provide a mechanism linking these processes together.
doi:10.1016/j.psyneuen.2016.01.004
PMCID: PMC4788523  PMID: 26821211
2-arachidonoylglycerol(2-AG); glucocorticoid; fatty acid amide hydrolase(FAAH); restraint; corticotropin-releasing; hormone receptor 1 (CRHR1); HPA axis
4.  A comparison of adult body size between captive and wild vervet monkeys (Chlorocebus aethiops sabaeus) on the island of St. Kitts 
Primates; journal of primatology  2016;57(2):211-220.
Weight and 34 morphological measures were obtained from 103 vervet monkeys living either in the wild or in captive colonies derived from the wild populations on the island of St. Kitts in the Eastern Caribbean. All measures were taken during the same week, eliminating bias that might result from changing seasonal environmental conditions. Vervets on St. Kitts are all descended from a small number of individuals brought to the island approximately 400 years ago from West Africa, thus also eliminating bias that might result from subspecific size differences. We conducted a principal components analysis (PCA) and compared individual traits between captive and wild adult animals. Morphological measures such as body length, arm and leg length did not differ significantly between animals living in the wild and animals in captivity. Weight and measures indicating condition- including BMI, chest girth, thigh girth, and upper arm girth were all higher for animals living in captivity. More consistent available food is probably the cause of differences in measures reflecting condition.
doi:10.1007/s10329-015-0509-8
PMCID: PMC4811751  PMID: 26801341
vervet monkey; adult body size; captive; wild
5.  Meta‐analysis of individual‐patient data from EVAR‐1, DREAM, OVER and ACE trials comparing outcomes of endovascular or open repair for abdominal aortic aneurysm over 5 years 
Powell, J. T. | Sweeting, M. J. | Ulug, P. | Blankensteijn, J. D. | Lederle, F. A. | Becquemin, J.‐P. | Greenhalgh, R. M. | Greenhalgh, R. M. | Beard, J. D. | Buxton, M. J. | Brown, L. C. | Harris, P. L. | Powell, J. T. | Rose, J. D. G. | Russell, I. T. | Sculpher, M. J. | Thompson, S. G. | Lilford, R.J. | Bell, P. R. F. | Greenhalgh, R. M. | Whitaker, S.C. | Poole‐Wilson, the late P.A. | Ruckley, C. V. | Campbell, W. B. | Dean, M. R. E. | Ruttley, M. S. T. | Coles, E. C. | Powell, J. T. | Halliday, A. | Gibbs, S. J. | Brown, L. C. | Epstein, D. | Sculpher, M. J. | Thompson, S. G. | Hannon, R. J. | Johnston, L. | Bradbury, A. W. | Henderson, M. J. | Parvin, S. D. | Shepherd, D. F. C. | Greenhalgh, R. M. | Mitchell, A. W. | Edwards, P. R. | Abbott, G. T. | Higman, D. J. | Vohra, A. | Ashley, S. | Robottom, C. | Wyatt, M. G. | Rose, J. D. G. | Byrne, D. | Edwards, R. | Leiberman, D. P. | McCarter, D. H. | Taylor, P. R. | Reidy, J. F. | Wilkinson, A. R. | Ettles, D. F. | Clason, A. E. | Leen, G. L. S. | Wilson, N. V. | Downes, M. | Walker, S. R. | Lavelle, J. M. | Gough, M. J. | McPherson, S. | Scott, D. J. A. | Kessell, D. O. | Naylor, R. | Sayers, R. | Fishwick, N. G. | Harris, P. L. | Gould, D. A. | Walker, M. G. | Chalmers, N. C. | Garnham, A. | Collins, M. A. | Beard, J. D. | Gaines, P. A. | Ashour, M. Y. | Uberoi, R. | Braithwaite, B. | Whitaker, S. C. | Davies, J. N. | Travis, S. | Hamilton, G. | Platts, A. | Shandall, A. | Sullivan, B. A. | Sobeh, M. | Matson, M. | Fox, A. D. | Orme, R. | Yusef, W. | Doyle, T. | Horrocks, M. | Hardman, J. | Blair, P. H. B. | Ellis, P. K. | Morris, G. | Odurny, A. | Vohra, R. | Duddy, M. | Thompson, M. | Loosemore, T. M. L. | Belli, A. M. | Morgan, R. | Adiseshiah, M. | Brookes, J. A. S. | McCollum, C. N. | Ashleigh, R. | Aukett, M. | Baker, S. | Barbe, E. | Batson, N. | Bell, J. | Blundell, J. | Boardley, D. | Boyes, S. | Brown, O. | Bryce, J. | Carmichael, M. | Chance, T. | Coleman, J. | Cosgrove, C. | Curran, G. | Dennison, T. | Devine, C. | Dewhirst, N. | Errington, B. | Farrell, H. | Fisher, C. | Fulford, P. | Gough, M. | Graham, C. | Hooper, R. | Horne, G. | Horrocks, L. | Hughes, B. | Hutchings, T. | Ireland, M. | Judge, C. | Kelly, L. | Kemp, J. | Kite, A. | Kivela, M. | Lapworth, M. | Lee, C. | Linekar, L. | Mahmood, A. | March, L. | Martin, J. | Matharu, N. | McGuigen, K. | Morris‐Vincent, P. | Murray, S. | Murtagh, A. | Owen, G. | Ramoutar, V. | Rippin, C. | Rowley, J. | Sinclair, J. | Spencer, S. | Taylor, V. | Tomlinson, C. | Ward, S. | Wealleans, V. | West, J. | White, K. | Williams, J. | Wilson, L. | Grobbee, D. E. | Blankensteijn, J. D. | Bak, A. A. A. | Buth, J. | Pattynama, P. M. | Verhoeven, E. L. G. | van Voorthuisen, A. E. | Blankensteijn, J. D. | Balm, R. | Buth, J. | Cuypers, P. W. M. | Grobbee, D. E. | Prinssen, M. | van Sambeek, M. R. H. M. | Verhoeven, E. L. G. | Baas, A. F. | Hunink, M. G. | van Engelshoven, J. M. | Jacobs, M. J. H. M. | de Mol, B. A. J. M. | van Bockel, J. H. | Balm, R. | Reekers, J. | Tielbeek, X. | Verhoeven, E. L. G. | Wisselink, W. | Boekema, N. | Heuveling, L. M. | Sikking, I. | Prinssen, M. | Balm, R. | Blankensteijn, J. D. | Buth, J. | Cuypers, P. W. M. | van Sambeek, M. R. H. M. | Verhoeven, E. L. G. | de Bruin, J. L. | Baas, A. F. | Blankensteijn, J. D. | Prinssen, M. | Buth, J. | Tielbeek, A.V. | Blankensteijn, J. D. | Balm, R. | Reekers, J. A. | van Sambeek, M. R. H. M. | Pattynama, P. | Verhoeven, E. L. G. | Prins, T. | van der Ham, A. C. | van der Velden, J. J. I. M. | van Sterkenburg, S. M. M. | ten Haken, G. B. | Bruijninckx, C. M. A. | van Overhagen, H. | Tutein Nolthenius, R. P. | Hendriksz, T. R. | Teijink, J. A. W. | Odink, H. F. | de Smet, A. A. E. A. | Vroegindeweij, D. | van Loenhout, R. M. M. | Rutten, M. J. | Hamming, J. F. | Lampmann, L. E. H. | Bender, M. H. M. | Pasmans, H. | Vahl, A. C. | de Vries, C. | Mackaay, A. J. C. | van Dortmont, L. M. C. | van der Vliet, A. J. | Schultze Kool, L. J. | Boomsma, J. H. B. | van Dop, H. R. | de Mol van Otterloo, J. C. A. | de Rooij, T. P. W. | Smits, T. M. | Yilmaz, E. N. | Wisselink, W. | van den Berg, F. G. | Visser, M. J. T. | van der Linden, E. | Schurink, G. W. H. | de Haan, M. | Smeets, H. J. | Stabel, P. | van Elst, F. | Poniewierski, J. | Vermassen, F. E. G. | Lederle, F. A. | Freischlag, J. A. | Kohler, T. R. | Latts, E. | Matsumura, J. | Padberg, F. T. | Kyriakides, T. C. | Swanson, K. M. | Guarino, P. | Peduzzi, P. | Antonelli, M. | Cushing, C. | Davis, E. | Durant, L. | Joyner, S. | Kossack, the late A. | Kyriakides, T. C. | LeGwin, Mary | McBride, V. | O'Connor, T. | Poulton, J. | Stratton, the late S. | Zellner, S. | Snodgrass, A. J. | Thornton, J. | Swanson, K. M. | Haakenson, C. M. | Stroupe, K.T. | Jonk, Y. | Hallett, J. W. | Hertzer, N. | Towne, J. | Katz, D. A. | Karrison, T. | Matts, J. P. | Marottoli, R. | Kasl, S. | Mehta, R. | Feldman, R. | Farrell, W. | Allore, H. | Perry, E. | Niederman, J. | Randall, F. | Zeman, M. | Beckwith, the late D. | O'Leary, T. J. | Huang, G. D. | Latts, E. | Bader, M. | Ketteler, E. R. | Kingsley, D. D. | Marek, J. M. | Massen, R. J. | Matteson, B. D. | Pitcher, J. D. | Langsfeld, M. | Corson, J. D. | Goff, J. M. | Kasirajan, K. | Paap, C. | Robertson, D. C. | Salam, A. | Veeraswamy, R. | Milner, R. | Kasirajan, K. | Guidot, J. | Lal, B. K. | Busuttil, S. J. | Lilly, M. P. | Braganza, M. | Ellis, K. | Patterson, M. A. | Jordan, W. D. | Whitley, D. | Taylor, S. | Passman, M. | Kerns, D. | Inman, C. | Poirier, J. | Ebaugh, J. | Raffetto, J. | Chew, D. | Lathi, S. | Owens, C. | Hickson, K. | Dosluoglu, H. H. | Eschberger, K. | Kibbe, M. R. | Baraniewski, H. M. | Matsumura, J. | Endo, M. | Busman, A. | Meadows, W. | Evans, M. | Giglia, J. S. | El Sayed, H. | Reed, A. B. | Ruf, M. | Ross, S. | Jean‐Claude, J. M. | Pinault, G. | Kang, P. | White, N. | Eiseman, M. | Jones, the late R. | Timaran, C. H. | Modrall, J. G. | Welborn, M. B. | Lopez, J. | Nguyen, T. | Chacko, J. K. Y. | Granke, K. | Vouyouka, A. G. | Olgren, E. | Chand, P. | Allende, B. | Ranella, M. | Yales, C. | Whitehill, T. A. | Krupski, the late W. C. | Nehler, M. R. | Johnson, S. P. | Jones, D. N. | Strecker, P. | Bhola, M. A. | Shortell, C. K. | Gray, J. L. | Lawson, J. H. | McCann, R. | Sebastian, M.W. | Kistler Tetterton, J. | Blackwell, C. | Prinzo, P. A. | Lee, N. | Padberg, F. T. | Cerveira, J. J. | Lal, B. K. | Zickler, R. W. | Hauck, K. A. | Berceli, S. A. | Lee, W. A. | Ozaki, C. K. | Nelson, P. R. | Irwin, A. S. | Baum, R. | Aulivola, B. | Rodriguez, H. | Littooy, F. N. | Greisler, H. | O'Sullivan, M. T. | Kougias, P. | Lin, P. H. | Bush, R. L. | Guinn, G. | Bechara, C. | Cagiannos, C. | Pisimisis, G. | Barshes, N. | Pillack, S. | Guillory, B. | Cikrit, D. | Lalka, S. G. | Lemmon, G. | Nachreiner, R. | Rusomaroff, M. | O'Brien, E. | Cullen, J. J. | Hoballah, J. | Sharp, W. J. | McCandless, J. L. | Beach, V. | Minion, D. | Schwarcz, T. H. | Kimbrough, J. | Ashe, L. | Rockich, A. | Warner‐Carpenter, J. | Moursi, M. | Eidt, J. F. | Brock, S. | Bianchi, C. | Bishop, V. | Gordon, I. L. | Fujitani, R. | Kubaska, S. M. | Behdad, M. | Azadegan, R. | Ma Agas, C. | Zalecki, K. | Hoch, J. R. | Carr, S. C. | Acher, C. | Schwarze, M. | Tefera, G. | Mell, M. | Dunlap, B. | Rieder, J. | Stuart, J. M. | Weiman, D. S. | Abul‐Khoudoud, O. | Garrett, H. E. | Walsh, S. M. | Wilson, K. L. | Seabrook, G. R. | Cambria, R. A. | Brown, K. R. | Lewis, B. D. | Framberg, S. | Kallio, C. | Barke, R. A. | Santilli, S. M. | d'Audiffret, A. C. | Oberle, N. | Proebstle, C. | Johnson, L. L. | Jacobowitz, G. R. | Cayne, N. | Rockman, C. | Adelman, M. | Gagne, P. | Nalbandian, M. | Caropolo, L. J. | Pipinos, I. I. | Johanning, J. | Lynch, T. | DeSpiegelaere, H. | Purviance, G. | Zhou, W. | Dalman, R. | Lee, J. T. | Safadi, B. | Coogan, S. M. | Wren, S. M. | Bahmani, D. D. | Maples, D. | Thunen, S. | Golden, M. A. | Mitchell, M. E. | Fairman, R. | Reinhardt, S. | Wilson, M. A. | Tzeng, E. | Muluk, S. | Peterson, N. M. | Foster, M. | Edwards, J. | Moneta, G. L. | Landry, G. | Taylor, L. | Yeager, R. | Cannady, E. | Treiman, G. | Hatton‐Ward, S. | Salabsky, the late B. | Kansal, N. | Owens, E. | Estes, M. | Forbes, B. A. | Sobotta, C. | Rapp, J. H. | Reilly, L. M. | Perez, S. L. | Yan, K. | Sarkar, R. | Dwyer, S. S. | Perez, S. | Chong, K. | Kohler, T. R. | Hatsukami, T. S. | Glickerman, D. G. | Sobel, M. | Burdick, T. S. | Pedersen, K. | Cleary, P. | Back, M. | Bandyk, D. | Johnson, B. | Shames, M. | Reinhard, R. L. | Thomas, S. C. | Hunter, G. C. | Leon, L. R. | Westerband, A. | Guerra, R. J. | Riveros, M. | Mills, J. L. | Hughes, J. D. | Escalante, A. M. | Psalms, S. B. | Day, N. N. | Macsata, R. | Sidawy, A. | Weiswasser, J. | Arora, S. | Jasper, B. J. | Dardik, A. | Gahtan, V. | Muhs, B. E. | Sumpio, B. E. | Gusberg, R. J. | Spector, M. | Pollak, J. | Aruny, J. | Kelly, E. L. | Wong, J. | Vasilas, P. | Joncas, C. | Gelabert, H. A. | DeVirgillio, C. | Rigberg, D. A. | Cole, L. | Becquemin, J.‐P. | Marzelle, J. | Becquemin, J.‐P. | Sapoval, M. | Becquemin, J.‐P. | Favre, J.‐P. | Watelet, J. | Lermusiaux, P. | Sapoval, M. | Lepage, E. | Hemery, F. | Dolbeau, G. | Hawajry, N. | Cunin, P. | Harris, P. | Stockx, L. | Chatellier, G. | Mialhe, C. | Fiessinger, J.‐N. | Pagny, L. | Kobeiter, H. | Boissier, C. | Lacroix, P. | Ledru, F. | Pinot, J.‐J. | Deux, J.‐F. | Tzvetkov, B. | Duvaldestin, P. | Watelet, J. | Jourdain, C. | David, V. | Enouf, D. | Ady, N. | Krimi, A. | Boudjema, N. | Jousset, Y. | Enon, B. | Blin, V. | Picquet, J. | L'Hoste, P. | Thouveny, F. | Borie, H. | Kowarski, S. | Pernes, J.‐M. | Auguste, M. | Becquemin, J.‐P. | Desgranges, P. | Allaire, E. | Marzelle, J. | Kobeiter, H. | Meaulle, P.‐Y. | Chaix, D. | Juliae, P. | Fabiani, J. N. | Chevalier, P. | Combes, M. | Seguin, A. | Belhomme, D. | Sapoval, M. | Baque, J. | Pellerin, O. | Favre, J. P. | Barral, X. | Veyret, C. | Watelet, J. | Peillon, C. | Plissonier, D. | Thomas, P. | Clavier, E. | Lermusiaux, P. | Martinez, R. | Bleuet, F. | C, Dupreix | Verhoye, J. P. | Langanay, T. | Heautot, J. F. | Koussa, M. | Haulon, S. | Halna, P. | Destrieux, L. | Lions, C. | Wiloteaux, S. | Beregi, J. P. | Bergeron, P. | Pinot, J.‐J. | Patra, P. | Costargent, A. | Chaillou, P. | D'Alicourt, A. | Goueffic, Y. | Cheysson, E. | Parrot, A. | Garance, P. | Demon, A. | Tyazi, A. | Pillet, J.‐C. | Lescalie, F. | Tilly, G. | Steinmetz, E. | Favier, C. | Brenot, R. | Krause, D. | Cercueil, J. P. | Vahdat, O. | Sauer, M. | Soula, P. | Querian, A. | Garcia, O. | Levade, M. | Colombier, D. | Cardon, J.‐M. | Joyeux, A. | Borrelly, P. | Dogas, G. | Magnan, P.‐É. | Branchereau, A. | Bartoli, J.‐M. | Hassen‐Khodja, R. | Batt, M. | Planchard, P.‐F. | Bouillanne, P.‐J. | Haudebourg, P. | Bayne, J. | Gouny, P. | Badra, A. | Braesco, J. | Nonent, M. | Lucas, A. | Cardon, A. | Kerdiles, Y. | Rolland, Y. | Kassab, M. | Brillu, C. | Goubault, F. | Tailboux, L. | Darrieux, H. | Briand, O. | Maillard, J.‐C. | Varty, K. | Cousins, C.
The British Journal of Surgery  2017;104(3):166-178.
Abstract
Background
The erosion of the early mortality advantage of elective endovascular aneurysm repair (EVAR) compared with open repair of abdominal aortic aneurysm remains without a satisfactory explanation.
Methods
An individual‐patient data meta‐analysis of four multicentre randomized trials of EVAR versus open repair was conducted to a prespecified analysis plan, reporting on mortality, aneurysm‐related mortality and reintervention.
Results
The analysis included 2783 patients, with 14 245 person‐years of follow‐up (median 5·5 years). Early (0–6 months after randomization) mortality was lower in the EVAR groups (46 of 1393 versus 73 of 1390 deaths; pooled hazard ratio 0·61, 95 per cent c.i. 0·42 to 0·89; P = 0·010), primarily because 30‐day operative mortality was lower in the EVAR groups (16 deaths versus 40 for open repair; pooled odds ratio 0·40, 95 per cent c.i. 0·22 to 0·74). Later (within 3 years) the survival curves converged, remaining converged to 8 years. Beyond 3 years, aneurysm‐related mortality was significantly higher in the EVAR groups (19 deaths versus 3 for open repair; pooled hazard ratio 5·16, 1·49 to 17·89; P = 0·010). Patients with moderate renal dysfunction or previous coronary artery disease had no early survival advantage under EVAR. Those with peripheral artery disease had lower mortality under open repair (39 deaths versus 62 for EVAR; P = 0·022) in the period from 6 months to 4 years after randomization.
Conclusion
The early survival advantage in the EVAR group, and its subsequent erosion, were confirmed. Over 5 years, patients of marginal fitness had no early survival advantage from EVAR compared with open repair. Aneurysm‐related mortality and patients with low ankle : brachial pressure index contributed to the erosion of the early survival advantage for the EVAR group. Trial registration numbers: EVAR‐1, ISRCTN55703451; DREAM (Dutch Randomized Endovascular Aneurysm Management), NCT00421330; ACE (Anévrysme de l'aorte abdominale, Chirurgie versus Endoprothèse), NCT00224718; OVER (Open Versus Endovascular Repair Trial for Abdominal Aortic Aneurysms), NCT00094575.
Survival comparable
doi:10.1002/bjs.10430
PMCID: PMC5299468  PMID: 28160528
6.  An initial investigation of associations between dopamine-linked genetic variation and smoking motives in African Americans 
Nicotine dependence (ND) is a heterogeneous phenotype with complex genetic influences that may vary across ethnicities. The use of intermediate phenotypes may clarify genetic influences and reveal specific etiological pathways. Prior work in European Americans has found that the four Primary Dependence Motives (PDM) subscales (Automaticity, Craving, Loss of Control, and Tolerance) of the Wisconsin Inventory of Smoking Motives represent core features of nicotine dependence and are promising intermediate phenotypes for understanding genetic pathways to ND. However, no studies have examined PDM as an intermediate phenotype in African American smokers, an ethnic population that displays unique patterns of smoking and genetic variation. In the current study, 268 African American daily smokers completed a phenotypic assessment and provided a sample of DNA. Associations among haplotypes in the NCAM1-TTC12-ANKK1-DRD2 gene cluster, a dopamine-related gene region associated with ND, PDM intermediate phenotypes, and ND were examined. Dopamine-related genetic variation in the DBH and COMT genes was also considered on an exploratory basis. Mediational analysis was used to test the indirect pathway from genetic variation to smoking motives to nicotine dependence. NCAM1-TTC12-ANKK1-DRD2 region variation was significantly associated with the Automaticity subscale and, further, Automaticity significantly mediated associations among NCAM1-TTC12-ANKK1-DRD2 cluster variants and ND. DBH was also significantly associated with Automaticity, Craving, and Tolerance; Automaticity and Tolerance also served as mediators of the DBH-ND relationship. These results suggest that PDM, Automaticity in particular, may be a viable intermediate phenotype for understanding dopamine-related genetic influences on ND in African American smokers. Findings support a model in which putatively dopaminergic variants exert influence on ND through an effect on patterns of automatic routinized smoking.
doi:10.1016/j.pbb.2015.09.018
PMCID: PMC4635661  PMID: 26410615
nicotine; intermediate phenotype; dopamine; haplotype; SNP; motives; African American
7.  Cellular Taxonomy of the Mouse Striatum as Revealed by Single-Cell RNA-Seq 
Cell reports  2016;16(4):1126-1137.
The striatum contributes to many cognitive processes and disorders, but its cell types are incompletely characterized. We show that microfluidic and FACS-based single-cell RNA sequencing of mouse striatum provides a well-resolved classification of striatal cell type diversity. Transcriptome analysis revealed 10 differentiated distinct cell types, including neurons, astrocytes, oligodendrocytes, ependymal, immune, and vascular cells, and enabled the discovery of numerous marker genes. Furthermore, we identified two discrete subtypes of medium spiny neurons (MSN) which have specific markers and which overexpress genes linked to cognitive disorders and addiction. We also describe continuous cellular identities, which increase heterogeneity within discrete cell types. Finally, we identified cell type specific transcription and splicing factors that shape cellular identities by regulating splicing and expression patterns. Our findings suggest that functional diversity within a complex tissue arises from a small number of discrete cell types, which can exist in a continuous spectrum of functional states.
Graphical abstract
doi:10.1016/j.celrep.2016.06.059
PMCID: PMC5004635  PMID: 27425622
8.  Multi-Wavelength Photoacoustic Visualization of High Intensity Focused Ultrasound Lesions 
Ultrasonic imaging  2015;38(1):96-112.
High intensity focused ultrasound (HIFU) thermal therapies are limited by deficiencies in existing image-guidance techniques. Previous studies using single-wavelength photoacoustic (PA) imaging have demonstrated that HIFU lesions generate contrast with respect to native tissues but have not sufficiently assessed lesion extent. The purpose of this study is to demonstrate feasibility of characterization of in vitro HIFU ablation lesion dimensions using 3D multi-wavelength PA imaging. Fresh porcine cardiac and liver tissue samples were embedded in agar phantoms and ablated using a 2.5 MHz small-animal HIFU system. Both 2D and 3D multi-wavelength photoacoustic-ultrasonic (PAUS) scans were performed in the near-infrared (NIR) range to characterize the change in the absorption spectrum of tissues following ablation and were compared to stained gross pathology to assess treatment margins and lesion extent. Comprehensive 2D multi-wavelength PA imaging yielded a spectrum in ablated tissue that did not display the characteristic local maximum in the optical absorption spectrum of deoxy-hemoglobin (Hb) near 760 nm. Two-dimensional tissue characterization map (TCM) images reconstructed from 3D TCM volumes reliably characterized lesion area and showed >70% area agreement with stained gross pathology. In addition, tissue samples were heated via water bath and concurrently interrogated with 2D PAUS imaging. PA signal exhibited an initial amplitude increase across all wavelengths, corresponding to an initial temperature increase, before then exhibiting a spectral change. This study suggests that multi-wavelength PA imaging has potential to obtain accurate characterization of HIFU lesion extent and may be better suited to guide HIFU ablation therapies during clinical treatments than single-wavelength methods.
doi:10.1177/0161734615593747
PMCID: PMC4961072  PMID: 26149314
photoacoustic; HIFU; multi-wavelength; ablation; cardiac; liver; tissue characterization
9.  Cloud-based Electronic Health Records for Real-time, Region-specific Influenza Surveillance 
Scientific Reports  2016;6:25732.
Accurate real-time monitoring systems of influenza outbreaks help public health officials make informed decisions that may help save lives. We show that information extracted from cloud-based electronic health records databases, in combination with machine learning techniques and historical epidemiological information, have the potential to accurately and reliably provide near real-time regional estimates of flu outbreaks in the United States.
doi:10.1038/srep25732
PMCID: PMC4863169  PMID: 27165494
10.  NCAM1-TTC12-ANKK1-DRD2 variants and smoking motives as intermediate phenotypes for nicotine dependence 
Psychopharmacology  2014;232(7):1177-1186.
Rationale
Nicotine dependence (ND) is a heterogeneous phenotype with complex genetic influences. The use of intermediate ND phenotypes may clarify genetic influences and reveal specific etiological pathways. Prior work has found that the four Primary Dependence Motives (PDM) subscales (Automaticity, Craving, Loss of Control, and Tolerance) of the Wisconsin Inventory of Smoking Motives (WISDM) represent heavy, pervasive smoking, which is a core feature of nicotine dependence, making these motives strong candidates as intermediate phenotypes.
Objective
This study examines the WISDM PDM as a novel intermediate phenotype of nicotine dependence.
Methods
The study used data from 734 European Americans who smoked at least 5 cigs/day [M=16.2 (SD=9.5) cigs/day], completed a phenotypic assessment, and provided a sample of DNA. Based on prior evidence of the role of genetic variation in the NCAM1-TTC12-ANKK1-DRD2 region on chromosome 11q23 in smoking behavior, associations among 12 region loci with nicotine dependence and PDM phenotypes were examined using haplotype and individual loci approaches. In addition, mediational analysis tested the indirect pathway from genetic variation to smoking motives to nicotine dependence.
Results
NCAM1-TTC12-ANKK1-DRD2 region loci and haplotypes were significantly associated with the motive of Automaticity and, further, Automaticity significantly mediated associations among NCAM1-TTC12-ANKK1-DRD2 cluster variants and nicotine dependence.
Conclusions
These results suggest that motives related to automaticity are a viable intermediate phenotype for understanding genetic contributions to nicotine dependence. Further, NCAM1-TTC12-ANKK1-DRD2 variants may increase the likelihood that a person will become dependent via a highly automatic smoking ritual that can be elicited with little awareness.
doi:10.1007/s00213-014-3748-2
PMCID: PMC4361268  PMID: 25273375
haplotype; SNP; dopamine; nicotine; endophenotype
11.  Functional proteomics identifies miRNAs to target a p27/Myc/phospho-Rb signature in breast and ovarian cancer 
Oncogene  2015;35(6):691-701.
The myc oncogene is overexpressed in almost half of all breast and ovarian cancers, but attempts at therapeutic interventions against myc have proven to be challenging. Myc regulates multiple biological processes, including the cell cycle, and as such is associated with cell proliferation and tumor progression. We identified a protein signature of high myc, low p27 and high phospho-Rb significantly correlated with poor patient survival in breast and ovarian cancers. Screening of a miRNA library by functional proteomics in multiple cell lines and integration of data from patient tumors revealed a panel of five microRNAs (miRNAs) (miR-124, miR-365, miR-34b*, miR-18a and miR-506) as potential tumor suppressors capable of reversing the p27/myc/phospho-Rb protein signature. Mechanistic studies revealed an RNA-activation function of miR-124 resulting in direct induction of p27 protein levels by binding to and inducing transcription on the p27 promoter region leading to a subsequent G1 arrest. Additionally, in vivo studies utilizing a xenograft model demonstrated that nanoparticle-mediated delivery of miR-124 could reduce tumor growth and sensitize cells to etoposide, suggesting a clinical application of miRNAs as therapeutics to target the functional effect of myc on tumor growth.
doi:10.1038/onc.2014.469
PMCID: PMC4522411  PMID: 25639871
12.  A parallel-arm phase I trial of the humanised anti-IGF-1R antibody dalotuzumab in combination with the AKT inhibitor MK-2206, the mTOR inhibitor ridaforolimus, or the NOTCH inhibitor MK-0752, in patients with advanced solid tumours 
British Journal of Cancer  2014;111(10):1932-1944.
Background:
Two strategies to interrogate the insulin growth factor 1 receptor (IGF-1R) pathway were investigated: vertical inhibition with dalotuzumab and MK-2206 or ridaforolimus to potentiate PI3K pathway targeting and horizontal cross-talk inhibition with dalotuzumab and MK-0752 to exert effects against cellular proliferation, angiogenesis, and stem cell propagation.
Methods:
A phase I, multi-cohort dose escalation study was conducted in patients with advanced solid tumours. Patients received dalotuzumab (10 mg kg–1) and escalating doses of MK-2206 (90–200 mg) or escalating doses of dalotuzumab (7.5–10 mg kg–1) and MK-0752 (1800 mg) weekly. Upon maximum tolerated dose determination, patients with low-RAS signature, high-IGF1 expression ovarian cancer were randomised to dalotuzumab/MK-2206 versus dalotuzumab/ridaforolimus, whereas patients with high IGF1/low IGF2 expression colorectal cancer received dalotuzumab/MK-0752.
Results:
A total of 47 patients were enrolled: 29 in part A (18 in the dalotuzumab/MK-2206 arm and 11 in the dalotuzumab/MK-0752 arm) and 18 in part B (6 in each arm). Dose-limiting toxicities (DLTs) for dalotuzumab/MK-2206 included grade 4 neutropenia and grade 3 serum sickness-like reaction, maculopapular rash, and gastrointestinal inflammation. For dalotuzumab/MK-0752, DLTs included grade 3 dehydration, rash, and diarrhoea. Seven patients remained on study for >4 cycles.
Conclusions:
Dalotuzumab/MK-2206 and dalotuzumab/MK-0752 combinations were tolerable. Further developments of prospectively validated predictive biomarkers to aid in patient selection for anti-IGF-1R therapies are needed.
doi:10.1038/bjc.2014.497
PMCID: PMC4229637  PMID: 25290091
dalotuzumab; MK-2206; ridaforolimus; MK-0752; ovarian cancer; colorectal cancer
13.  Corticotropin-Releasing Hormone Drives Anandamide Hydrolysis in the Amygdala to Promote Anxiety 
The Journal of Neuroscience  2015;35(9):3879-3892.
Corticotropin-releasing hormone (CRH) is a central integrator in the brain of endocrine and behavioral stress responses, whereas activation of the endocannabinoid CB1 receptor suppresses these responses. Although these systems regulate overlapping functions, few studies have investigated whether these systems interact. Here we demonstrate a novel mechanism of CRH-induced anxiety that relies on modulation of endocannabinoids. Specifically, we found that CRH, through activation of the CRH receptor type 1 (CRHR1), evokes a rapid induction of the enzyme fatty acid amide hydrolase (FAAH), which causes a reduction in the endocannabinoid anandamide (AEA), within the amygdala. Similarly, the ability of acute stress to modulate amygdala FAAH and AEA in both rats and mice is also mediated through CRHR1 activation. This interaction occurs specifically in amygdala pyramidal neurons and represents a novel mechanism of endocannabinoid–CRH interactions in regulating amygdala output. Functionally, we found that CRH signaling in the amygdala promotes an anxious phenotype that is prevented by FAAH inhibition. Together, this work suggests that rapid reductions in amygdala AEA signaling following stress may prime the amygdala and facilitate the generation of downstream stress-linked behaviors. Given that endocannabinoid signaling is thought to exert “tonic” regulation on stress and anxiety responses, these data suggest that CRH signaling coordinates a disruption of tonic AEA activity to promote a state of anxiety, which in turn may represent an endogenous mechanism by which stress enhances anxiety. These data suggest that FAAH inhibitors may represent a novel class of anxiolytics that specifically target stress-induced anxiety.
doi:10.1523/JNEUROSCI.2737-14.2015
PMCID: PMC4348185  PMID: 25740517
anxious behavior; basolateral amygdala; endocannabinoid signaling; HPA axis; stress
14.  Long-Term Safety and Efficacy of Factor IX Gene Therapy in Hemophilia B 
The New England journal of medicine  2014;371(21):1994-2004.
BACKGROUND
In patients with severe hemophilia B, gene therapy that is mediated by a novel self-complementary adeno-associated virus serotype 8 (AAV8) vector has been shown to raise factor IX levels for periods of up to 16 months. We wanted to determine the durability of transgene expression, the vector dose–response relationship, and the level of persistent or late toxicity.
METHODS
We evaluated the stability of transgene expression and long-term safety in 10 patients with severe hemophilia B: 6 patients who had been enrolled in an initial phase 1 dose-escalation trial, with 2 patients each receiving a low, intermediate, or high dose, and 4 additional patients who received the high dose (2×1012 vector genomes per kilogram of body weight). The patients subsequently underwent extensive clinical and laboratory monitoring.
RESULTS
A single intravenous infusion of vector in all 10 patients with severe hemophilia B resulted in a dose-dependent increase in circulating factor IX to a level that was 1 to 6% of the normal value over a median period of 3.2 years, with observation ongoing. In the high-dose group, a consistent increase in the factor IX level to a mean (±SD) of 5.1±1.7% was observed in all 6 patients, which resulted in a reduction of more than 90% in both bleeding episodes and the use of prophylactic factor IX concentrate. A transient increase in the mean alanine aminotransferase level to 86 IU per liter (range, 36 to 202) occurred between week 7 and week 10 in 4 of the 6 patients in the high-dose group but resolved over a median of 5 days (range, 2 to 35) after prednisolone treatment.
CONCLUSIONS
In 10 patients with severe hemophilia B, the infusion of a single dose of AAV8 vector resulted in long-term therapeutic factor IX expression associated with clinical improvement. With a follow-up period of up to 3 years, no late toxic effects from the therapy were reported. (Funded by the National Heart, Lung, and Blood Institute and others; ClinicalTrials.gov number, NCT00979238.)
doi:10.1056/NEJMoa1407309
PMCID: PMC4278802  PMID: 25409372
15.  Jet energy measurement and its systematic uncertainty in proton–proton collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s}=7$$\end{document}s=7 TeV with the ATLAS detector 
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The jet energy scale (JES) and its systematic uncertainty are determined for jets measured with the ATLAS detector using proton–proton collision data with a centre-of-mass energy of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s}=7$$\end{document}s=7 TeV corresponding to an integrated luminosity of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$4.7$$\end{document}4.7\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\,\,\text{ fb }^{-1}$$\end{document}fb-1. Jets are reconstructed from energy deposits forming topological clusters of calorimeter cells using the anti-\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$k_{t}$$\end{document}kt algorithm with distance parameters \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$R=0.4$$\end{document}R=0.4 or \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$R=0.6$$\end{document}R=0.6, and are calibrated using MC simulations. A residual JES correction is applied to account for differences between data and MC simulations. This correction and its systematic uncertainty are estimated using a combination of in situ techniques exploiting the transverse momentum balance between a jet and a reference object such as a photon or a \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Z$$\end{document}Z boson, for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${20} \le p_{\mathrm {T}}^\mathrm {jet}<{1000}\, ~\mathrm{GeV }$$\end{document}20≤pTjet<1000GeV and pseudorapidities \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$|\eta |<{4.5}$$\end{document}|η|<4.5. The effect of multiple proton–proton interactions is corrected for, and an uncertainty is evaluated using in situ techniques. The smallest JES uncertainty of less than 1 % is found in the central calorimeter region (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$|\eta |<{1.2}$$\end{document}|η|<1.2) for jets with \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${55} \le p_{\mathrm {T}}^\mathrm {jet}<{500}\, ~\mathrm{GeV }$$\end{document}55≤pTjet<500GeV. For central jets at lower \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p_{\mathrm {T}}$$\end{document}pT, the uncertainty is about 3 %. A consistent JES estimate is found using measurements of the calorimeter response of single hadrons in proton–proton collisions and test-beam data, which also provide the estimate for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p_{\mathrm {T}}^\mathrm {jet}> 1$$\end{document}pTjet>1 TeV. The calibration of forward jets is derived from dijet \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p_{\mathrm {T}}$$\end{document}pT balance measurements. The resulting uncertainty reaches its largest value of 6 % for low-\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p_{\mathrm {T}}$$\end{document}pT jets at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$|\eta |=4.5$$\end{document}|η|=4.5. Additional JES uncertainties due to specific event topologies, such as close-by jets or selections of event samples with an enhanced content of jets originating from light quarks or gluons, are also discussed. The magnitude of these uncertainties depends on the event sample used in a given physics analysis, but typically amounts to 0.5–3 %.
doi:10.1140/epjc/s10052-014-3190-y
PMCID: PMC4684939  PMID: 26709345
16.  Fatal Scopulariopsis Infection in a Lung Transplant Recipient: Lessons of Organ Procurement 
Seventeen days after double lung transplantation, a 56-year-old patient with idiopathic pulmonary fibrosis developed respiratory distress. Imaging revealed bilateral pulmonary infiltrates with pleural effusions and physical examination demonstrated sternal instability. Broad-spectrum antibacterial and antifungal therapy was initiated and bilateral thoracotomy tubes were placed. Both right and left pleural cultures grew a mold subsequently identified as Scopulariopsis brumptii. The patient underwent pleural irrigation and sternal debridement three times but pleural and wound cultures continued to grow S. brumptii. Despite treatment with five antifungal agents, the patient succumbed to his illness sixty-seven days after transplantation. Autopsy confirmed the presence of markedly invasive fungal disease and pleural rind formation. The patient’s organ donor had received bilateral thoracostomy tubes during resuscitation in a wilderness location. There were no visible pleural abnormalities at the time of transplantation. However, the patient’s clinical course and the location of the infection, in addition to the lack of similar infection in other organ recipients, strongly suggest that Scopulariopsis was introduced into the pleural space during pre-hospital placement of thoracostomy tubes. This case of lethal infection transmitted through transplantation highlights the unique risk of using organs from donors who are resuscitated in an outdoor location.
doi:10.1111/ajt.12940
PMCID: PMC4263480  PMID: 25376207
lung transplantation; donor-derived infection; procurement; Scopulariopsis
17.  Therapeutic Polyclonal human CD8+ Fox3+ TNFR2+ PD-L1+ Regulatory Cells Induced ex-vivo 
Clinical immunology (Orlando, Fla.)  2013;149(3):450-463.
We report that polyclonal CD8regs generated in one week ex-vivo with anti-CD3/28 beads and cytokines rapidly developed suppressive activity in vitro sustained by TGF-β. In immunodeficient mice, these CD8regs demonstrated a markedly protective, IL-10 dependent activity against a xeno-GVHD. They expressed IL-2Rα/β, Foxp3, TNFR2, and the negative co-stimulatory receptors CTLA-4, PD-1, PD-L1 and Tim-3. Suppressive activity in vitro correlated better with TNFR2 and PD-L1 than Foxp3. Blocking studies suggested that TNF enhanced PD-L1 expression and the suppressive activity of the CD8regs generated. Unlike other polyclonal CD4 and CD8 Tregs, these CD8regs preferentially targeted allogeneic T cells, but they lacked cytotoxic activity against them even after sensitization. Unlike CD4regs, these CD8regs could produce IL-2 and proliferate while inhibiting target cells. If these CD8regs can persist in foreign hosts without impairing immune surveillance, they could serve as a practical remission-inducing product for the treatment of autoimmune diseases, graft-versus-host disease, and allograft rejection.
doi:10.1016/j.clim.2013.08.007
PMCID: PMC3941976  PMID: 24211847
18.  Muon reconstruction efficiency and momentum resolution of the ATLAS experiment in proton–proton collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s}=7$$\end{document}s=7 TeV in 2010 
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This paper presents a study of the performance of the muon reconstruction in the analysis of proton–proton collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s}=7$$\end{document}s=7 TeV at the LHC, recorded by the ATLAS detector in 2010. This performance is described in terms of reconstruction and isolation efficiencies and momentum resolutions for different classes of reconstructed muons. The results are obtained from an analysis of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$J/\psi $$\end{document}J/ψ meson and \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Z$$\end{document}Z boson decays to dimuons, reconstructed from a data sample corresponding to an integrated luminosity of 40 pb\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$^{-1}$$\end{document}-1. The measured performance is compared to Monte Carlo predictions and deviations from the predicted performance are discussed.
doi:10.1140/epjc/s10052-014-3034-9
PMCID: PMC4371051  PMID: 25814911
19.  Cost-effectiveness of silicone and alginate impressions for complete dentures 
Journal of Dentistry  2014;42(8):902-907.
Objective
The aim of this study was to assess the cost effectiveness of silicone and alginate impressions for complete dentures.
Methods
Cost effectiveness analyses were undertaken alongside a UK single centre, double blind, controlled, crossover clinical trial. Taking the perspective of the healthcare sector, effectiveness is measured using the EuroQol (EQ-5D-3L) which provides a single index value for health status that may be combined with time to produce quality adjusted life years (QALYs); and Oral Health Impact Profile (OHIP-EDENT). Incremental cost effectiveness ratios are presented representing the additional cost per one unit gained.
Results
Mean cost was higher in the silicone impression group (£388.57 vs. £363.18). Negligible between-group differences were observed in QALY gains; the silicone group had greater mean OHIP-EDENT gains. The additional cost using silicone was £3.41 per change of one point in the OHIP-EDENT.
Conclusions
The silicone group was more costly, driven by the cost of materials. Changes in the EQ-5D and QALY gains over time and between arms were not statistically significant. Change in OHIP-EDENT score showed greater improvement in the silicone group and the difference between arms was statistically significant. Given negligible QALY gains and low level of resource use, results must be treated with caution. It is difficult to make robust claims about the comparative cost-effectiveness.
Clinical significance
Silicone impressions for complete dentures improve patients’ quality of life (OHIP-EDENT score). The extra cost of silicone impressions is £30 per patient. Dentists, patients and health care funders need to consider the clinical and financial value of silicone impressions. Different patients, different dentists, different health funders will have individual perceptions and judgements.
ISRCTN01528038.
NIHR-RfPB grant PB-PG-0408-16300.


This article forms part of a project for which the author (TPH) won the Senior Clinical Unilever Hatton Award of the International Assocation for Dental Research, Capetown, South Africa, June 2014.
doi:10.1016/j.jdent.2014.03.001
PMCID: PMC4119300  PMID: 24995472
Prosthodontics; Quality-of life; Impression materials; Cost effectiveness; Cost; Resource
20.  A Randomised Controlled Trial of complete denture impression materials 
Journal of Dentistry  2014;42(8):895-901.
Objectives
There is continuing demand for non-implant prosthodontic treatment and yet there is a paucity of high quality Randomised Controlled Trial (RCT) evidence for best practice. The aim of this research was to provide evidence for best practice in prosthodontic impressions by comparing two impression materials in a double-blind, randomised, crossover, controlled, clinical trial.
Methods
Eighty-five patients were recruited, using published eligibility criteria, to the trial at Leeds Dental Institute, UK. Each patient received two sets of dentures; made using either alginate or silicone impressions. Randomisations determined the order of assessment and order of impressions. The primary outcome was patient blinded preference for unadjusted dentures. Secondary outcomes were patient preference for the adjusted dentures, rating of comfort, stability and chewing efficiency, experience of each impression, and an OHIP-EDENT questionnaire.
Results
Seventy-eight (91.8%) patients completed the primary assessment. 53(67.9%) patients preferred dentures made from silicone impressions while 14(17.9%) preferred alginate impressions. 4(5.1%) patients found both dentures equally satisfactory and 7 (9.0%) found both equally unsatisfactory. There was a 50% difference in preference rates (in favour of silicone) (95%CI 32.7–67.3%, p < 0.0001).
Conclusion
There is significant evidence that dentures made from silicone impressions were preferred by patients.
Clinical significance
Given the strength of the clinical findings within this paper, dentists should consider choosing silicone rather than alginate as their material of choice for secondary impressions for complete dentures.
Trial Registration: ISRCTN 01528038.


This article forms part of a project for which the author (TPH) won the Senior Clinical Unilever Hatton Award of the International Assocation for Dental Research, Capetown, South Africa, June 2014.
doi:10.1016/j.jdent.2014.02.005
PMCID: PMC4119301  PMID: 24995473
Prosthodontics; Quality-of life; Patient outcomes; Impression materials; Edentulous; Removable prosthodontics
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A measurement is presented of the \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\phi \times \mathcal {BR}(\phi \rightarrow K^{+}K^{-})$$\end{document}ϕ×BR(ϕ→K+K-) production cross section at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s}$$\end{document}s = 7 TeV using \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$pp$$\end{document}pp collision data corresponding to an integrated luminosity of 383 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mathrm {\upmu b^{-1}}$$\end{document}μb-1, collected with the ATLAS experiment at the LHC. Selection of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\phi $$\end{document}ϕ(1020) mesons is based on the identification of charged kaons by their energy loss in the pixel detector. The differential cross section is measured as a function of the transverse momentum, \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p_{\mathrm {T,\phi }}$$\end{document}pT,ϕ, and rapidity, \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$y_{\phi }$$\end{document}yϕ, of the \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\phi $$\end{document}ϕ(1020) meson in the fiducial region 500 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$$$\end{document}pT,K> 230 MeV and kaon momentum \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p_{K}<$$\end{document}pK< 800 MeV. The integrated \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\phi (1020)$$\end{document}ϕ(1020)-meson production cross section in this fiducial range is measured to be \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sigma _{\phi } \times \mathcal {BR}(\phi \rightarrow K^{+}K^{-}) $$\end{document}σϕ×BR(ϕ→K+K-) = 570 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\pm $$\end{document}± 8 (stat) \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\pm $$\end{document}± 66 (syst) \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\pm $$\end{document}± 20 (lumi) \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\mathrm {\upmu b}$$\end{document}μb.
doi:10.1140/epjc/s10052-014-2895-2
PMCID: PMC4371126  PMID: 25814898
22.  DYNAMIC PLASTICITY: THE ROLE OF GLUCOCORTICOIDS, BRAIN-DERIVED NEUROTROPHIC FACTOR AND OTHER TROPHIC FACTORS 
Neuroscience  2012;239:214-227.
Brain-derived neurotrophic factor (BDNF) is a secreted protein that has been linked to numerous aspects of plasticity in the central nervous system (CNS). Stress-induced remodeling of the hippocampus, prefrontal cortex and amygdala is coincident with changes in the levels of BDNF, which has been shown to act as a trophic factor facilitating the survival of existing and newly born neurons. Initially, hippocampal atrophy after chronic stress was associated with reduced BDNF, leading to the hypothesis that stress-related learning deficits resulted from suppressed hippocampal neurogenesis. However, recent evidence suggests that BDNF also plays a rapid and essential role in regulating synaptic plasticity, providing another mechanism through which BDNF can modulate learning and memory after a stressful event. Numerous reports have shown BDNF levels are highly dynamic in response to stress, and not only vary across brain regions but also fluctuate rapidly, both immediately after a stressor and over the course of a chronic stress paradigm. Yet, BDNF alone is not sufficient to effect many of the changes observed after stress. Glucocorticoids and other molecules have been shown to act in conjunction with BDNF to facilitate both the morphological and molecular changes that occur, particularly changes in spine density and gene expression. This review briefly summarizes the evidence supporting BDNF’s role as a trophic factor modulating neuronal survival, and will primarily focus on the interactions between BDNF and other systems within the brain to facilitate synaptic plasticity. This growing body of evidence suggests a more nuanced role for BDNF in stress-related learning and memory, where it acts primarily as a facilitator of plasticity and is dependent upon the coactivation of glucocorticoids and other factors as the determinants of the final cellular response.
doi:10.1016/j.neuroscience.2012.08.034
PMCID: PMC3743657  PMID: 22922121
hippocampus; amygdala; glucocorticoids; BDNF; stress
23.  Measurement of jet shapes in top-quark pair events at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s} = 7 \ \mbox{TeV}$\end{document} using the ATLAS detector 
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