648 research outputs found
Ten Years HIV Free: An Interview with “The Berlin Patient,” Timothy Ray Brown
No full textIt was just about 10 years ago that Timothy Ray Brown was cured of HIV infection by receiving bone marrow stem cell transplantations from an HLA matched donor who also was homozygous for the CCR5 delta 32 mutation that renders immune cells resistant to infection by most HIV viruses. During an October 2017 visit to Cleveland to help launch a number of clinical trials targeting the Cure, Timothy sat down with Pathogens and Immunity editor Michael Lederman and community activist Earl Pike to talk about his experiences
Ten Years HIV Free: An Interview with “The Berlin Patient,” Timothy Ray Brown
No full textIt was just about 10 years ago that Timothy Ray Brown was cured of HIV infection by receiving bone marrow stem cell transplantations from an HLA matched donor who also was homozygous for the CCR5 delta 32 mutation that renders immune cells resistant to infection by most HIV viruses. During an October 2017 visit to Cleveland to help launch a number of clinical trials targeting the Cure, Timothy sat down with Pathogens and Immunity editor Michael Lederman and community activist Earl Pike to talk about his experiences.</jats:p
HIV Pathogenesis: Abstracts from the March 2017 Cleveland Immunopathogenesis Consortium Meeting
No full textThe Cleveland Immunopathogenesis Consortium (CLIC) was launched in March 2004 by a small group of investigators (Ron Bosch, Jason Brenchley, Steven Deeks, Danny Douek, Zvi Grossman, Robert Kalayjian, Clifford Harding, Michael Lederman, Leonid Margolis, Miguel Quinones, Benigno Rodriguez, Rafick Sekaly, Scott Sieg, and Guido Silvestri) who were increasingly persuaded that immune activation was an important driver of HIV pathogenesis. We met around a chalk board and scribbled our models of pathogenesis, designed some experiments then went back home to do them. We met again soon to review our new and unpublished findings that refined and shaped these models. The data presentations were short, informal and heavy on discussion. The model worked well, the consortium was productive and the meetings catalyzed numerous collaborations and scores of high impact papers. The CLIC (less formally, the Bad Boys of Cleveland [1]) has been meeting regularly since then. Consortium membership has expanded to include other investigators (some are listed in the presentations below). Whether the goal is to prevent the morbid complications of HIV infection, to understand the determinants of HIV persistence or the factors that protect from acquisition of infection, a more clear understanding of HIV immunopathogenesis is central. Here in this issue of Pathogens and Immunity is a brief summary of the most recent CLIC//BBC meeting held in Cleveland in March 2017.</jats:p
HIV Pathogenesis: Abstracts from the March 2017 Cleveland Immunopathogenesis Consortium Meeting
No full textThe Cleveland Immunopathogenesis Consortium (CLIC) was launched in March 2004 by a small group of investigators (Ron Bosch, Jason Brenchley, Steven Deeks, Danny Douek, Zvi Grossman, Robert Kalayjian, Clifford Harding, Michael Lederman, Leonid Margolis, Miguel Quinones, Benigno Rodriguez, Rafick Sekaly, Scott Sieg, and Guido Silvestri) who were increasingly persuaded that immune activation was an important driver of HIV pathogenesis. We met around a chalk board and scribbled our models of pathogenesis, designed some experiments then went back home to do them. We met again soon to review our new and unpublished findings that refined and shaped these models. The data presentations were short, informal and heavy on discussion. The model worked well, the consortium was productive and the meetings catalyzed numerous collaborations and scores of high impact papers. The CLIC (less formally, the Bad Boys of Cleveland [1]) has been meeting regularly since then. Consortium membership has expanded to include other investigators (some are listed in the presentations below). Whether the goal is to prevent the morbid complications of HIV infection, to understand the determinants of HIV persistence or the factors that protect from acquisition of infection, a more clear understanding of HIV immunopathogenesis is central. Here in this issue of Pathogens and Immunity is a brief summary of the most recent CLIC//BBC meeting held in Cleveland in March 2017
sj-docx-1-pss-10.1177_09567976211073135 – Supplemental material for Lack of Belonging Predicts Depressive Symptomatology in College Students
No full textSupplemental material, sj-docx-1-pss-10.1177_09567976211073135 for Lack of Belonging Predicts Depressive Symptomatology in College Students by Janine M. Dutcher, James Lederman, Megha Jain, Stephen Price, Agam Kumar, Daniella K. Villalba, Michael J. Tumminia, Afsaneh Doryab, Kasey G. Creswell, Eve Riskin, Yasaman Sefdigar, Woosuk Seo, Jennifer Mankoff, Sheldon Cohen, Anind Dey and J. David Creswell in Psychological Science</p
Trade structure and growth
No full textLederman and Maloney examine the empirical relationships between trade structure and economic growth, particularly the influence of natural resource abundance, export concentration, and intra-industry trade. They test the robustness of these relationships across proxies, control variables, and estimation techniques. The authors find trade variables to be important determinants of growth, especially natural resource abundance and export concentration. In contrast with much of the recent literature, natural resource abundance appears to have a positive effect on growth, whereas export concentration hampers growth, even after controlling for physical and human capital accumulation, among other factors.Economic Conditions and Volatility,Environmental Economics&Policies,Health Monitoring&Evaluation,Economic Theory&Research,Public Health Promotion,Economic Theory&Research,Achieving Shared Growth,Environmental Economics&Policies,Economic Growth,Inequality
The business of product innovation : international empirical evidence
No full textIt is so widely recognized that innovation is a key driver of economic growth that it is cliché to say so. This article studies product innovation by firms with data from 68 countries, covering more than 25,000 firms in eight manufacturing sectors. The author assesses the predictions of inter-disciplinary research on innovation by firms. The econometric evidence suggests that globalization and local knowledge increase the likelihood that firms will introduce new products. By contrast, domestic regulatory impediments to competition are not robustly correlated with product innovation.E-Business,Innovation,Microfinance,Education for Development (superceded),Statistical&Mathematical Sciences
NAFTA, Trade, and Development
No full textThe post-Keynesian tradition contains two different models of long-run growth in open economies -- the model of export-led cumulative causation (ELCC) originally conceived by Nicholas Kaldor and the model of balance-of-payments-constrained growth (BPCG) developed by A.P. Thirlwall. These models diverge significantly in their core underlying assumptions. For example, they disagree about whether long-term gains in relative price competitiveness are possible and whether import demand constrains long-run growth. The two modeling approaches also yield conflicting policy implications. For example, some ELCC models imply that a domestic demand stimulus can boost long-run growth by sparking a virtuous circle of cumulative causation (including an endogenous increase in productivity growth), while most BPCG models imply that only policies that raise the income elasticity of export demand or lower the income elasticity of import demand can permit faster growth in the long run. The fact that both models have found econometric support suggests that each contains empirically supported elements, but the tests that have been conducted to date have not had sufficient power to distinguish between them. This paper will present both models in a common analytical framework to compare their theoretical differences and policy implications. The paper will argue that a generalized BPCG model that allows for financial flows and relative price effects can incorporate the cumulative causation feedbacks from the ELCC approach while also imposing the balance of payments equilibrium condition that is missing from the latter. The paper will also explore under what conditions different versions of the models apply.
An Assessment of How Urban Crime and Victimization Affects Life Satisfaction
No full textWe assess the effect of the homicide rate, individual´s perception of security in their neighborhood of residence, and of the effect of their having been victimized, on life satisfaction. We find a negative effect of the homicide rate on life satisfaction for the subsample of individuals living in their current houses for at least 10 years or more, who had moved to that place at some point in the past. We also find a positive and robust effect of the perception of security in the households´neighborhood for the whole sample, and for different subsamples considered. Having been victim of an offense is also robustly negatively related to life satisfaction, in particular in the cases where the offense was robbery.Quality of Life, Life Satisfaction, Crime. Classification JEL: I32, K40, K42.
IL-7 induces expression and activation of integrin alpha 4 beta 7 promoting naive T-cell homing to the intestinal mucosa
No full textInterleukin-7 (IL-7) is a nonredundant cytokine that plays a critical role in T-cell homeostasis and promotes immunologic reconstitution in lymphopenic hosts. Here, we show that IL-7, at doses that reflect suprahomeostatic concentrations achieved in lymphopenic hosts, is a potent and selective inducer of the guthoming integrin α4β7 in human T cells, as documented both ex vivo and in vivo in patients enrolled in a clinical trial of IL-7 treatment. Induction of α4β7 by IL-7 occurs primarily in naive T cells and is associated with functional activation of the integrin, as indicated by increased binding activity for the specific α4β7 ligand, MAdCAM-1. The physiologic relevance of these findings was validated by the preferential homing of IL-7-treated naive human T cells to the intestinal compartment in humanized NOD/SCID/IL-2 receptor-γnull (NSG) mice. We also show that IL-7 triggers a peculiar activation program in naive T cells, characterized by the acquisition of memory-like phenotypic features and proliferation uncoupled from expression of classic T-cell activation markers. These findings provide a mechanism for the transient in vivo depletion of circulating T cells after IL-7 administration and suggest that intestinal homing and memory-like conversion of naive T cells are critical steps in the IL-7-driven immunologic reconstitution of lymphopenic hosts
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