Explore the vast range of titles available.

Thomas Piketty's Capital in the Twenty-First Century is the most widely discussed work of economics in recent history, selling millions of copies in dozens of languages. But are its analyses of inequality and economic growth on target? Where should researchers go from here in exploring the ideas Piketty pushed to the forefront of global conversation? A cast of economists and other social scientists tackle these questions in dialogue with Piketty, in what is sure to be a much-debated book in its own right. After Piketty opens with a discussion by Arthur Goldhammer, Piketty's translator into English, of the reasons for Capital's phenomenal success, followed by the published reviews of Nobel laureates Robert Solow and Paul Krugman. The rest of the book is devoted to newly commissioned essays that interrogate Piketty's arguments. Suresh Naidu and other contributors ask whether Piketty said enough about power, slavery, and the complex nature of capital. Laura Tyson and Michael Spence consider the impact of technology on inequality. Heather Boushey, Branko Milanovic, and others consider topics ranging from gender to trends in the global South. Emmanuel Saez lays out an agenda for future research on inequality, while a variety of essayists examine the book's implications for the social sciences more broadly. Piketty replies to these questions in a substantial concluding chapter. An indispensable interdisciplinary work, After Piketty does not shy away from the seemingly intractable problems that made Capital in the Twenty-First Century so compelling for so many.-- Provided by publisher

Two papers in this issue, by Bruns et al . and Zhao et al ., show that megakaryocytes constitute a niche for hematopoietic stem cells in the mouse bone marrow and produce factors that regulate hematopoietic stem cell quiescence and proliferation. Multiple bone marrow stromal cell types have been identified as hematopoietic stem cell (HSC)-regulating niche cells 1 , 2 , 3 , 4 , 5 , 6 , 7 . However, whether HSC progeny can serve directly as HSC niche cells has not previously been shown. Here we report a dichotomous role of megakaryocytes (MKs) in both maintaining HSC quiescence during homeostasis and promoting HSC regeneration after chemotherapeutic stress. We show that MKs are physically associated with HSCs in the bone marrow of mice and that MK ablation led to activation of quiescent HSCs and increased HSC proliferation. RNA sequencing (RNA-seq) analysis revealed that transforming growth factor β1 (encoded by Tgfb1 ) is expressed at higher levels in MKs as compared to other stromal niche cells. MK ablation led to reduced levels of biologically active TGF-β1 protein in the bone marrow and nuclear-localized phosphorylated SMAD2/3 (pSMAD2/3) in HSCs, suggesting that MKs maintain HSC quiescence through TGF-β–SMAD signaling 8 , 9 . Indeed, TGF-β1 injection into mice in which MKs had been ablated restored HSC quiescence, and conditional deletion of Tgfb1 in MKs increased HSC activation and proliferation. These data demonstrate that TGF-β1 is a dominant signal emanating from MKs that maintains HSC quiescence. However, under conditions of chemotherapeutic challenge, MK ablation resulted in a severe defect in HSC expansion. In response to stress, fibroblast growth factor 1 (FGF1) signaling from MKs transiently dominates over TGF-β inhibitory signaling to stimulate HSC expansion 10 , 11 . Overall, these observations demonstrate that MKs serve as HSC-derived niche cells to dynamically regulate HSC function.

\"Surviving the Gulag is the first-person account of a complex woman who survived five horrifying years in Russian prison camps: starved, beaten, and worked nearly to death. A story like Ilse Johansen's is rarely told--of a woman caught in the web of fascism and communism at the end of the Second World War and beginning of the Cold War. Her candid account of her time as a prisoner, written soon after her release, provides startling insight into the trials of a German female prisoner under Soviet rule. Readers of memoir and history, and students of feminism and war studies, will learn more about women's experience of the Soviet gulag through the eyes of Ilse Johansen.\"-- Provided by publisher.

The review article \"The Political Economy of Health: Revisiting Its Marxian Origins to Address 21st Century Health Inequalities\" by Harvey in the February issue of AJPH provides a brief history of the origins of the political economy perspective, with a focus on its application within public health. The article provides a practical \"refresher\" for public health thinkers and practitioners as to where to locate the essential causes of social epidemiological patterns in health and illness by foregrounding the perennial relevance of concepts within the Marxist tradition. Though concepts such as class cleavage, class struggle, and class exploitation can seem parochial or anachronistic, depending upon their presentation, Harvey reminds us of the key contributions to public health provided by Marx's teachings and their application via Engels, Virchow, and others. In turn, the author advocates a more common and widespread application of Marxian political economy within public health given the framework's peerless utility for \"explaining and addressing persistent health inequalities and emerging public health crises under global capitalism.

Bycatch mortality is a major factor contributing to shark population declines. Post-release mortality (PRM) is particularly difficult to quantify, limiting the accuracy of stock assessments. We paired blood-stress physiology with animal-borne accelerometers to quantify PRM rates of sharks caught in a commercial bottom longline fishery. Blood was sampled from the same individuals that were tagged, providing direct correlation between stress physiology and animal fate for sandbar ( Carcharhinus plumbeus , N = 130), blacktip ( C . limbatus , N = 105), tiger ( Galeocerdo cuvier , N = 52), spinner ( C . brevipinna , N = 14), and bull sharks ( C . leucas , N = 14). PRM rates ranged from 2% and 3% PRM in tiger and sandbar sharks to 42% and 71% PRM in blacktip and spinner sharks, respectively. Decision trees based on blood values predicted mortality with >67% accuracy in blacktip and spinner sharks, and >99% accuracy in sandbar sharks. Ninety percent of PRM occurred within 5 h after release and 59% within 2 h. Blood physiology indicated that PRM was primarily associated with acidosis and increases in plasma potassium levels. Total fishing mortality reached 62% for blacktip and 89% for spinner sharks, which may be under-estimates given that some soak times were shortened to focus on PRM. Our findings suggest that no-take regulations may be beneficial for sandbar, tiger, and bull sharks, but less effective for more susceptible species such as blacktip and spinner sharks.

The study by Oh et al. in the June issue of AJPH examines the impact of two distinct types of job-related training programs on employment outcomes and substance use patterns among disadvantaged youths.1 The primary takeaway from the study is that job training programs that focus on skills acquisition appear to be associated with better long-term employment outcomes, which, in turn, may contribute to modification of substance use behaviors. Although the finding is of interest in its own right, its implications take on special significance in view of current socioeconomic conditions wherein the growing presence of job insecurity and precarious work has been identified as a key driver of workrelated health inequalities. Still, although research aimed at discovering employment interventions that are effective in helping individuals develop stronger ties to the labor market is critical, I think a more fulsome understanding of the problem requires application of a sociological lens that brings into view structural determinants. Therefore, I think that studies like that of Oh et al. can deepen both their evidentiary value and their implications for public policy by shifting their focus to the fundamental causes of work-related health inequalities.Oh et al. identify their sample as \"youths with economic disadvantages\" based on participation in a government-sponsored employment training program. The authors state that program participation is a major indicator of preexisting employment barriers among a segment of the youth population typically in receipt of Temporary Assistance for Needy Families (TANF). Studies of the TANF population consistently show that this segment exhibits a significantly higher prevalence of serious health conditions, including substance use behaviors.2 Furthermore, the presence ofserious health conditions in economically disadvantaged populations has been identified as a substantial barrier to work participation. To date, the majority of studies that test the efficacy of various types of employment interventions among economically disadvantaged groups-including those that directly address healthrelated barriers-find that achieving secure long-term attachment to the labor market is the exception.

Type 1 IFNs get induced by viral nucleic acids and proteins acting on cellular signaling molecules such as Toll-like receptors and RNA helicases, which, in turn, release transcription factors into the nucleus. T cells that are exposed to their cognate peptide antigen presented in the context of MHC (pMHC) on APC-like dendritic cells (DCs) get costimulated through receptors such as CD28 and CD40 ligand and undergo a differentiation program associated with several cycles of division, the expression of the transcription factors t-bet and eomesodermin, followed by the acquisition of effector functions (Figure 1D).

To replicate, lentiviruses such as HIV must integrate DNA copies of their RNA genomes into host cell chromosomes. Lentiviral integration is favored in active transcription units, which allows efficient viral gene expression after integration, but the mechanisms directing integration targeting are incompletely understood. A cellular protein, PSIP1/LEDGF/p75, binds tightly to the lentiviral-encoded integrase protein (IN), and has been reported to be important for HIV infectivity and integration targeting. Here we report studies of lentiviral integration targeting in 1) human cells with intensified RNAi knockdowns of PSIP1/LEDGF/p75, and 2) murine cells with homozygous gene trap mutations in the PSIP1/LEDGF/p75 locus. Infections with vectors derived from equine infections anemia virus (EIAV) and HIV were compared. Integration acceptor sites were analyzed by DNA bar coding and pyrosequencing. In both PSIP1/LEDGF/p75-depleted cell lines, reductions were seen in lentiviral infectivity compared to controls. For the human cells, integration was reduced in transcription units in the knockdowns, and this reduction was greater than in our previous studies of human cells less completely depleted for PSIP1/LEDGF/p75. For the homozygous mutant mouse cells, similar reductions in integration in transcription units were seen, paralleling a previous study of a different mutant mouse line. Integration did not become random, however-integration in transcription units in both cell types was still favored, though to a reduced degree. New trends also appeared, including favored integration near CpG islands. In addition, we carried out a bioinformatic study of 15 HIV integration site data sets in different cell types, which showed that the frequency of integration in transcription units was correlated with the cell-type specific levels of PSIP1/LEDGF/p75 expression.

Persistent staffing shortages in health care driven by years of inadequate funding and deficiencies in human resources planning, which overlooked the impacts of population aging, have converged into a crisis in health care settings. An essential consequence of the widespread and growing staffing shortfalls in health care has been increased pressure on nurses to work longer hours. The present rapid review has two major objectives: (1) to systematically review and synthesize evidence considering the health and human consequences of excessive work hours, work-related fatigue and associated occupational health and safety hazards; and, (2) to identify policies and practices that demonstrate efficacy in managing or mitigating the adverse effects of occupational fatigue. Findings show that shifts lasting longer than 12 h elevate the risk of occupational fatigue, leading to several fatigue-based hazards. Despite governmental restrictions on long work hours and occupational fatigue in safety-critical industries such as transport, aviation, and nuclear sectors, health care remains largely unregulated in this regard. Ensuring safe and high-quality care over the long term requires implementing adequate regulatory supports for work hour limits for nurses. These measures not only improve workplace satisfaction but also enhance patient outcomes, ultimately fostering a healthier and more resilient health care system.

T follicular helper cells (Tfh) are crucial for the initiation and maintenance of germinal center (GC) reactions and high affinity, isotype-switched antibody responses. In this study, we demonstrate that direct TGF-β signaling to CD4 T cells is important for the formation of influenza-specific Tfh cells, GC reactions, and development of isotype-switched, flu-specific antibody responses. Early during infection, TGF-β signaling suppressed the expression of the high affinity IL-2 receptor α chain (CD25) on virus-specific CD4 T cells, which tempered IL-2 signaling and STAT5 and mammalian target of rapamycin (mTOR) activation in Tfh precursor CD4 T cells. Inhibition of mTOR allowed for the differentiation of Tfh cells in the absence of TGF-βR signaling, suggesting that TGF-β insulates Tfh progenitor cells from IL-2-delivered mTOR signals, thereby promoting Tfh differentiation during acute viral infection. These findings identify a new pathway critical for the generation of Tfh cells and humoral responses during respiratory viral infections. The influenza virus is thought to cause illness in up to 10% of adults and 30% of children each year worldwide. Most of these cases resolve on their own and don’t require treatment, but three to five million people are hospitalized and up to half a million people die each year. Unfortunately, the vaccines currently available to protect against influenza only target particular varieties or “strains” of the virus. The strains that circulate vary from year-to-year so it is necessary to develop new influenza vaccines every year. However, it is difficult to correctly predict which strains will circulate, so a more effective solution would be to develop a new vaccine that can help the body defend itself against many, or ideally any influenza strain. During a viral infection, a type of immune cell in the host can specialize into two different types of cells to help fight the virus: T helper 1 cells and CD4 T follicular helper cells. T helper 1 cells help to kill host cells that have become infected. CD4 T follicular helper cells promote the production of proteins called antibodies, which identify and neutralize the virus. Here, Marshall et al. studied how T helper 1 cells and CD4 T follicular helper cells form in mice suffering from a lung infection similar to influenza. It was already known that a protein called transforming growth factor beta (TGF-β) helps the immune response to mount an effective defense against an infection without causing too much harm to the host. Marshall et al. show that TGF-β increases the number of CD4 T follicular helper cells in the mice by suppressing the production of another protein—called IL-2—on the surface of CD4 T cells. Treating mice lacking the ability to detect TGF-β with a drug that blocks a protein controlled by IL-2 also allows more CD4 T follicular helper cells to be produced. Marshall et al.’s findings reveal that TGF-β is involved in controlling the balance of T helper 1 cells and CD4 T follicular helper cells produced during viral infections of the respiratory tract. Since TGF-β also has other roles in immune responses against viruses, it is now an attractive target for the development of a vaccine that may protect us against all strains of the influenza virus.