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This study examines the intergenerational consequences of court-imposed monetary sanctions for parents and children. Research on punishment and families has generally focused on imprisonment, yet monetary sanctions are far more commonly imposed. We extend research on intergenerational financial exchanges to conceptualize payment of monetary sanctions as stigmatized transfers, analyzing 70 semi-structured interviews with debtholders in Minnesota. Adult children reported perceiving anger and financial strain from family members who provide assistance. Those with minor children expressed hopelessness, stress, and financial strain, as they prioritized basic needs over meeting their outstanding financial obligations. We conclude by discussing the implications of these intergenerational impacts for research, law, and policy. [ABSTRACT FROM AUTHOR]

Despite both scholarly and popular claims that citizen journalism (CJ) represents a growing democratizing force in the journalistic field, recent scholarship in the area has noted the decline of the organizational population of CJ. In this paper, we investigate how individual characteristics of sites and the dynamics of larger organizational population affect a CJ site’s risk of experiencing a mortality. Drawing on the largest sample to date of US-based English-language CJ sites, this study examines the risk of site mortality through an event history framework. Findings indicate that the strongest predictor of a site’s mortality is the age of the site, consistent with organizational population theory’s ‘liability of newness.’ We also find that for-profit and community-based sites have lower rates of site mortality, indicating that adopting legitimate conventions of journalism may serve as a protective buffer to site death. The results offer mixed evidence on whether CJ has become more professionalized via attrition. [ABSTRACT FROM AUTHOR]

While previous research has considered patterns of homogeneity and heterogeneity in the journalistic field, existing literature has largely ignored the factors that contribute to the growth and contraction of the field. Using citizen journalism (CJ) as a case study, we examine how four forces – organizational population dynamics, technological innovations, exogenous political events, and endogenous disruptions elsewhere in the field – shaped the growth of CJ over time and, consequently, the journalistic field. Using a snowball sampling method, we collected a “near-population” of U.S.-based, English-language CJ sites (n = 1829) to measure yearly density and rates of foundings and mortalities. The population of CJ sites increased through most of the period, foundings declined after a spike in 2005, and mortalities rose dramatically after 2010. The results provide evidence that organizational population and technological change affected the size of the population of CJ sites, while political upheaval and disruptions within professional journalism held less sway. [ABSTRACT FROM AUTHOR]

Thymic stromal lymphopoietin (TSLP) is an epithelial-derived cytokine that has been implicated in the initiation of allergic responses. CD4 T cells and dendritic cells are able to respond to TSLP in vitro; however, there has not been a careful dissection of the spatiotemporal response to TSLP by CD4 T cells in vivo during an allergic response. Previous work has suggested a requirement for TSLP in amplifying Th2 responses during allergen challenge by direct action on CD4 T cells; however, these studies did not determine whether there is an effect of TSLP on CD4 T cells during allergen sensitization. In this study we demonstrate an indirect role for TSLP on CD4 T cells during sensitization and challenge phases of an allergic response. This indirect effect of TSLP on CD4 T cells is due in part to the presence of TSLP exclusively in the allergen-sensitized and -challenged skin, rather than the draining lymph nodes. [ABSTRACT FROM AUTHOR]

Psoriasis is an immune-mediated chronic inflammatory skin disease, characterized by epidermal hyperplasia and infiltration of leukocytes into the dermis and epidermis. IL-23 is expressed in psoriatic skin, and IL-23 injected into the skin of mice produces IL-22-dependent dermal inflammation and acanthosis. The chemokine receptor CCR2 has been implicated in the pathogenesis of several inflammatory diseases, including psoriasis. CCR2-positive cells and the CCR2 ligand, CCL2 are abundant in psoriatic lesions. To examine the requirement of CCR2 in the development of IL-23-induced cutaneous inflammation, we injected the ears of wild-type (WT) and CCR2-deficient (CCR2−/−) mice with IL-23. CCR2−/− mice had increased ear swelling and epidermal thickening, which was correlated with increased cutaneous IL-4 levels and increased numbers of eosinophils within the skin. In addition, TSLP, a cytokine known to promote and amplify T helper cell type 2 (Th2) immune responses, was also increased within the inflamed skin of CCR2−/− mice. Our data suggest that increased levels of TSLP in CCR2−/− mice may contribute to the propensity of these mice to develop increased Th2-type immune responses. [ABSTRACT FROM AUTHOR]

The evolutionary survival of Mycobacterium tuberculosis, the cause of human tuberculosis, depends on its ability to invade the host, replicate, and transmit infection. At its initial peripheral infection site in the distal lung airways, M. tuberculosis infects macrophages, which transport it to deeper tissues. How mycobacteria survive in these broadly microbicidal cells is an important question. Here we show in mice and zebrafish that M. tuberculosis, and its close pathogenic relative Mycobacterium marinum, preferentially recruit and infect permissive macrophages while evading microbicidal ones. This immune evasion is accomplished by using cell-surface-associated phthiocerol dimycoceroserate (PDIM) lipids to mask underlying pathogen-associated molecular patterns (PAMPs). In the absence of PDIM, these PAMPs signal a Toll-like receptor (TLR)-dependent recruitment of macrophages that produce microbicidal reactive nitrogen species. Concordantly, the related phenolic glycolipids (PGLs) promote the recruitment of permissive macrophages through a host chemokine receptor 2 (CCR2)-mediated pathway. Thus, we have identified coordinated roles for PDIM, known to be essential for mycobacterial virulence, and PGL, which (along with CCR2) is known to be associated with human tuberculosis. Our findings also suggest an explanation for the longstanding observation that M. tuberculosis initiates infection in the relatively sterile environment of the lower respiratory tract, rather than in the upper respiratory tract, where resident microflora and inhaled environmental microbes may continually recruit microbicidal macrophages through TLR-dependent signalling. [ABSTRACT FROM AUTHOR]

Dendritic cells (DCs) are critical in immune responses, linking innate and adaptive immunity. We found here that DC-specific deletion of the transcription factor STAT5 was not critical for development but was required for T helper type 2 (TH2), but not TH1, allergic responses in both the skin and lungs. Loss of STAT5 in DCs led to the inability to respond to thymic stromal lymphopoietin (TSLP). STAT5 was required for TSLP-dependent DC activation, including upregulation of the expression of costimulatory molecules and chemokine production. Furthermore, TH2 responses in mice with DC-specific loss of STAT5 resembled those seen in mice deficient in the receptor for TSLP. Our results show that the TSLP-STAT5 axis in DCs is a critical component for the promotion of type 2 immunity at barrier surfaces. [ABSTRACT FROM AUTHOR]

The regulation of host-pathogen interactions during Mycobacterium tuberculosis (Mtb) infection remains unresolved. MicroRNAs (miRNAs) are important regulators of the immune system, and so we used a systems biology approach to construct an miRNA regulatory network activated in macrophages during Mtb infection. Our network comprises 77 putative miRNAs that are associated with temporal gene expression signatures in macrophages early after Mtb infection. In this study, we demonstrate a dual role for one of these regulators, miR-155. On the one hand, miR-155 maintains the survival of Mtbinfected macrophages, thereby providing a niche favoring bacterial replication; on the other hand, miR-155 promotes the survival and function of Mtb-specific T cells, enabling an effective adaptive immune response. MiR-155-induced cell survival is mediated through the SH2 domain-containing inositol 5-phosphatase 1 (SHIP1)/protein kinase B (Akt) pathway. Thus, dual regulation of the same cell survival pathway in innate and adaptive immune cells leads to vastly different outcomes with respect to bacterial containment. [ABSTRACT FROM AUTHOR]

High levels of transcription in Saccharomyces cerevisiae are associated with increased genetic instability, which has been linked to DNA damage. Here, we describe a pGAL-CAN1 forward mutation assay for studying transcription-associated mutagenesis (TAM) in yeast. In a wild-type background with no alterations in DNA repair capacity, ≈50% of forward mutations that arise in the CANI gene under high-transcription conditions are deletions of 2- 5 bp. furthermore, the deletions characteristic of TAM localize to discrete hotspots that coincide with 2-4 copies of a tandem repeat. Although the signature deletions of TAM are not affected by the loss of error-free or error-prone lesion bypass pathways, they are completely eliminated by deletion of the TOP1 gene, which encodes the yeast type IB topoisomerase. Hotspots can be transposed into the context of a frameshift reversion assay, which is sensitive enough to detect Topi-dependent deletions even in the absence of high transcription. We suggest that the accumulation of Topi cleavage complexes is related to the level of transcription and that their removal leads to the signature deletions. Given the high degree of conservation between DNA metabolic processes, the links established here among transcription, Topi, and mutagenesis are likely to extend beyond the yeast system. [ABSTRACT FROM AUTHOR]