The Planning, Implementation, and Evaluation of California's Inaugural Food Waste Prevention Week.

Preventing food waste can divert food from landfills to feed people, combat climate change, preserve natural resources, and save money. In February 2017, the Nutrition Policy Institute and the Public Health Alliance of Southern California initiated a multisector collaboration among California state agencies to raise awareness about food waste. After development and distribution of a Communications Guide, Food Waste Prevention Week was launched successfully in March 2018, with official support from California's Governor, Secretary of Agriculture, Superintendent of Public Instruction, and other leaders. The multiagency shared messaging campaign was estimated to reach millions, based on unique page views via social and traditional media. In a follow-up survey, partners expressed satisfaction with Food Waste Prevention Week and interest in participating in future efforts. Organizing leaders across multiple sectors to raise awareness about food waste is possible; such efforts can contribute to driving behavioral and structural changes to reduce food waste.

California Healthy Places Index: Frames Matter.

INTRODUCTION: We describe the California Healthy Places Index (HPI) and its performance relative to other indexes for measuring community well-being at the census-tract level. The HPI arose from a need identified by health departments and community organizations for an index rooted in the social determinants of health for place-based policy making and program targeting. The index was geographically granular, validated against life expectancy at birth, and linked to policy actions. MATERIALS AND METHODS: Guided by literature, public health experts, and a positive asset frame, we developed a composite index of community well-being for California from publicly available census-tract data on place-based factors linked to health. The 25 HPI indicators spanned 8 domains; weights were derived from their empirical association with tract-level life expectancy using weighted quantile sums methods. RESULTS: The HPI's domains were aligned with the social determinants of health and policy action areas of economic resources, education, housing, transportation, clean environment, neighborhood conditions, social resources, and health care access. The overall HPI score was the sum of weighted domain scores, of which economy and education were highly influential (50% of total weights). The HPI was strongly associated with life expectancy at birth (r = 0.58). Compared with the HPI, a pollution-oriented index did not capture one-third of the most disadvantaged quartile of census tracts (representing 3 million Californians). Overlap of the HPI's most disadvantaged quartile of census tracts was greater for indexes of economic deprivation. We visualized the HPI percentile ranking as a web-based mapping tool that presented the HPI at multiple geographies and that linked indicators to an action-oriented policy guide. PRACTICE IMPLICATIONS: The framing of indexes and specifications such as domain weighting have substantial consequences for prioritizing disadvantaged populations. The HPI provides a model for tools and new methods that help prioritize investments and identify multisectoral opportunities for policy action.

T follicular helper-like cells contribute to skin fibrosis.

Systemic sclerosis (SSc) is a debilitating inflammatory and fibrotic disease that affects the skin and internal organs. Although the pathophysiology of SSc remains poorly characterized, mononuclear cells, mainly macrophages and T cells, have been implicated in inflammation and fibrosis. Inducible costimulator (ICOS), which is expressed on a subset of memory T helper (TH) and T follicular helper (TFH) cells, has been shown to be increased in SSc and associated with disease pathology. However, the identity of the relevant ICOS+ T cells and their contribution to inflammation and fibrosis in SSc are still unknown. We show that CD4+ ICOS-expressing T cells with a TFH-like phenotype infiltrate the skin of patients with SSc and are correlated with dermal fibrosis and clinical disease status. ICOS+ TFH-like cells were found to be increased in the skin of graft-versus-host disease (GVHD)-SSc mice and contributed to dermal fibrosis via an interleukin-21- and matrix metalloproteinase 12-dependent mechanism. Administration of an anti-ICOS antibody to GVHD-SSc mice prevented the expansion of ICOS+ TFH-like cells and inhibited inflammation and dermal fibrosis. Interleukin-21 neutralization in GVHD-SSc mice blocked disease pathogenesis by reducing skin fibrosis. These results identify ICOS+ TFH-like profibrotic cells as key drivers of fibrosis in a GVHD-SSc model and suggest that inhibition of these cells could offer therapeutic benefit for SSc.

Type I IFNs Regulate Inflammation, Vasculopathy, and Fibrosis in Chronic Cutaneous Graft-versus-Host Disease.

Type I IFNs play a critical role in the immune response to viral infection and may also drive autoimmunity through modulation of monocyte maturation and promotion of autoreactive lymphocyte survival. Recent demonstrations of type I IFN gene signatures in autoimmune diseases, including scleroderma, led us to investigate the pathological role of IFNs in a preclinical model of sclerodermatous graft-versus-host disease. Using a neutralizing Ab against the type I IFN receptor IFNAR1, we observed a marked reduction in dermal inflammation, vasculopathy, and fibrosis compared with that seen in the presence of intact IFNAR1 signaling. The ameliorative effects of IFNAR1 blockade were restricted to the skin and were highly associated with inhibition of chronic vascular injury responses and not due to the inhibition of the T or B cell alloresponse. Inhibition of IFNAR1 normalized the overexpression of IFN-inducible genes in graft-versus-host disease skin and markedly reduced dermal IFN-α levels. Depletion of plasmacytoid dendritic cells, a major cellular source of type I IFNs, did not reduce the severity of fibrosis or type I IFN gene signature in the skin. Taken together, these studies demonstrate an important role for type I IFN in skin fibrosis, and they provide a rationale for IFNAR1 inhibition in scleroderma.

Resolution of Skin Fibrosis by Neutralization of the Antifibrinolytic Function of Plasminogen Activator Inhibitor 1.

OBJECTIVE: Systemic sclerosis (SSc) is a fibrotic disease characterized by an obliterative vasculopathy with thrombosis and impairment of the coagulation-fibrinolysis balance. Plasminogen activator inhibitor 1 (PAI-1) is the major inhibitor of profibrinolytic plasminogen activators (PAs). This study was undertaken to evaluate the contribution of PAI-1 to SSc pathology in the skin. METHODS: PAI-1 was evaluated in skin from patients with diffuse SSc (dSSc) and those with limited SSc (lSSc) by immunohistochemistry. The contribution of PAI-1 to SSc pathology was tested in vivo in murine graft-versus-host disease (GVHD) and bleomycin models of progressive skin fibrosis and in vitro in dermal human microvascular endothelial cells (HMVECs) using a monoclonal antibody that selectively prevents the binding of PAI-1 to PA. RESULTS: Skin from patients with dSSc and those with lSSc showed increased PAI-1 levels in the epidermis and microvessel endothelium. PAI-1 neutralization in the GVHD model led to a dramatic, dose-dependent improvement in clinical skin score, concomitant with vasculopathy resolution, including a reduction in fibrinolysis regulators and vascular injury markers, as well as reduced inflammation. Resolution of vasculopathy and inflammation was associated with resolution of skin fibrosis, as assessed by reduction in collagen content and expression of key profibrotic mediators, including transforming growth factor ß1 and tissue inhibitor of metalloproteinases 1. Similar to the GVHD model, PAI-1 neutralization reduced dermal inflammation and fibrosis in the bleomycin model. PAI-1 neutralization stimulated plasmin-mediated metalloproteinase 1 activation in dermal HMVECs. CONCLUSION: Our findings indicate that neutralization of the antifibrinolytic function of PAI-1 resolves skin fibrosis by limiting the extent of initial vascular injury and connective tissue inflammation. These data suggest that PAI-1 represents an important checkpoint in disease pathology in human SSc.

Monetary matched incentives to encourage the purchase of fresh fruits and vegetables at farmers markets in underserved communities.

INTRODUCTION: Farmers market programs may increase access to more healthful foods and reduce the high prevalence of obesity in low-income communities. The objective of this study was to examine outcomes of the Fresh Fund farmers market program serving low-income neighborhoods in San Diego, California. METHODS: Through its Farmers Market Fresh Fund Incentive Program, the County of San Diego Health and Human Services Agency offered monetary incentives to government nutrition assistance recipients to purchase fresh produce at 5 farmers markets. Participants enrolled at participating markets from June 1, 2010, through December 31, 2011; they completed baseline and follow-up surveys of daily consumption and weekly spending on fruits and vegetables. We examined enrollment, participation, participant health perceptions, and vendor revenue. RESULTS: During the study period, 7,298 eligible participants enrolled in Fresh Fund; most (82%) had previously never been to a farmers market. Among 252 participants with matched surveys at baseline and 12-month follow-up, the proportion who reported their diet to be "healthy" or "very healthy" increased from 4% to 63% (P < .001); nearly all (93%) stated that Fresh Fund was "important" or "very important" in their decision to shop at the farmers market. Vendors reported that 48% of all market revenue they received was received through the Fresh Fund program. At 2 markets, revenue from June 1, 2011, through January 31, 2012, increased by 74% and 68% compared with revenue from June 1, 2010, through January 31, 2011. CONCLUSION: Participants in the Fresh Fund program self-reported increases in daily consumption and weekly spending on fruits and vegetables, and vendors at participating farmers markets also increased their revenue.

Macrophage impairment underlies airway occlusion in primary respiratory syncytial virus bronchiolitis.

Although respiratory syncytial virus (RSV) infection is the most important cause of bronchiolitis in infants, the pathogenesis of RSV disease is poorly described. We studied histopathologic changes in a panel of lung tissue specimens obtained from infants with fatal cases of primary RSV infection. In these tissues, airway occlusion with accumulations of infected, apoptotic cellular debris and serum protein was consistently observed. Similar observations were found after RSV infection in New Zealand black (NZB) mice, which have constitutive deficiencies in macrophage function, but not in BALB/c mice. A deficiency in the number of alveolar macrophages in NZB mice appears to be central to enhanced disease, because depletion of alveolar macrophages in BALB/c mice before RSV exposure resulted in airway occlusion. In mice with insufficient numbers of macrophages, RSV infection yielded an increased viral load and enhanced expression of type I interferon-associated genes at the height of disease. Together, our data suggest that innate, rather than adaptive, immune responses are critical determinants of the severity of RSV bronchiolitis.

Blocking inducible co-stimulator in the absence of CD28 impairs Th1 and CD25+ regulatory T cells in murine colitis.

Several autoimmune disease models depend on an imbalance in the activation of aggressor T(h)1 and CD4(+)CD25(+) regulatory T (T(reg)) cells. Here we compare the requirement for signals through the co-stimulatory molecules CD28 and inducible co-stimulator (ICOS) in chronic murine colitis, a model for inflammatory bowel disease. We used a colitis model in which disease-causing CD45RB(hi) T cells alone or in combination with CD4(+)CD25(+) T cells from either CD28-deficient or wild-type donors were transferred into T cell-deficient animals, half of which were treated with ICOS-blocking reagents. Blocking ICOS on the surface of CD28-deficient T(h)1 cells abrogated development of colitis, whereas blocking CD28 or ICOS alone had little to no effect on disease induction. In contrast to T(h)1 cells, regulatory T cell functioning depended mostly on CD28 signaling with only a minor contribution for ICOS. We conclude that CD28 and ICOS collaborate to development of murine colitis by aggressor T(h)1 cells, and that CD28 is required for T(reg) cells, which should caution against the use of CD28-blocking reagents in inflammatory bowel disease.

Essential role for the C5a receptor in regulating the effector phase of synovial infiltration and joint destruction in experimental arthritis.

A characteristic feature of rheumatoid arthritis is the abundance of inflammatory cells in the diseased joint. Two major components of this infiltrate are neutrophils in the synovial fluid and macrophages in the synovial tissue. These cells produce cytokines including tumor necrosis factor alpha and other proinflammatory mediators that likely drive the disease through its effector phases. To investigate what mechanisms underlie the recruitment of these cells into the synovial fluid and tissue, we performed expression analyses of chemoattractant receptors in a related family that includes the anaphylatoxin receptors and the formyl-MetLeuPhe receptor. We then examined the effect of targeted disruption of two abundantly expressed chemoattractant receptors, the receptors for C3a and C5a, on arthritogenesis in a mouse model of disease. We report that genetic ablation of C5a receptor expression completely protects mice from arthritis.

Behavioral health issue brief: mental health and substance abuse parity: year end report-2002.

Parity benefits for mental health continue to be on the agenda of many state legislatures. A broad spectrum of opinions surround what mental health parity could and should be. There are strong proponents that advocate for nothing less than full parity for mental health and substance abuse treatment; equally strong are the groups that oppose parity because they believe it will lead to a health care cost increase and, therefore, an increase in the number of uninsured. Both sides continue to make progress as the victories and the defeats unfold on the floors of state legislatures.

Behavioral health issue brief: minimum mandated benefits and mandated offerings for mental health and substance abuse: year end report-2002.

Benefit mandates require that some service be provided. Mental health and substance abuse treatment mandates are two of the many types of benefit mandates in state law. The debate over mandated benefit legislation typically centers around consumer protection versus cost. Proponents contend that mandates are necessary to ensure adequate health care for consumers. However, opponents generally argue that mandates drive up premiums, which contributes to the growing number of uninsured.