465 research outputs found

    Multi‐scale heterogeneity in vegetation and soil carbon in exurban residential land of southeastern Michigan, USA

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    Exurban residential land (one housing unit per 0.2–16.2 ha) is growing in importance as a human‐dominated land use. Carbon storage in the soils and vegetation of exurban land is poorly known, as are the effects on C storage of choices made by developers and residents. We studied C storage in exurban yards in southeastern Michigan, USA, across a range of parcel sizes and different types of neighborhoods. We divided each residential parcel into ecological zones (EZ) characterized by vegetation, soil, and human behavior such as mowing, irrigation, and raking. We found a heterogeneous mixture of trees and shrubs, turfgrasses, mulched gardens, old‐field vegetation, and impervious surfaces. The most extensive zone type was turfgrass with sparse woody vegetation (mean 26% of parcel area), followed by dense woody vegetation (mean 21% of parcel area). Areas of turfgrass with sparse woody vegetation had trees in larger size classes (> 50 cm dbh) than did areas of dense woody vegetation. Using aerial photointerpretation, we scaled up C storage to neighborhoods. Varying C storage by neighborhood type resulted from differences in impervious area (8–26% of parcel area) and area of dense woody vegetation (11–28%). Averaged and multiplied across areas in differing neighborhood types, exurban residential land contained 5240 ± 865 g C/m2 in vegetation, highly sensitive to large trees, and 13 800 ± 1290 g C/m2 in soils (based on a combined sampling and modeling approach). These contents are greater than for agricultural land in the region, but lower than for mature forest stands. Compared with mature forests, exurban land contained more shrubs and less downed woody debris and it had similar tree size‐class distributions up to 40 cm dbh but far fewer trees in larger size classes. If the trees continue to grow, exurban residential land could sequester additional C for decades. Patterns and processes of C storage in exurban residential land were driven by land management practices that affect soil and vegetation, reflecting the choices of designers, developers, and residents. This study provides an example of human‐mediated C storage in a coupled human–natural system.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/122437/1/eap1313.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/122437/2/eap1313_am.pd

    “Can you see me?” videoconferencing and eating disorder risk during COVID-19: anxiety, impairment, and mediators

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    Objective: The use of videoconferencing has increased during the pandemic, creating prolonged exposure to self-image. This research aimed to investigate whether eating disorder (ED) risk was associated with videoconferencing performance for work or study and to explore whether the use of safety behaviors and self-focused attention mediated the relationship between ED risk and perceived control over performance anxiety, impaired engagement, or avoidance of videoconferencing for work or study. Method: In 2020, an online survey was distributed within Australia to those aged over 18 years via academic and social networks, measuring: use of videoconferencing for work/study, demographics, ED risk, safety behaviors for appearance concerns, self-focused attention, perceived control over performance anxiety, perceived engagement impairment, and avoidance of videoconferencing. A total of 640 participants (77.3% female, Mage = 26.2 years) returned complete data and were included in analyses. Results: 245 participants (38.7%) were considered at-risk for EDs (SCOFF > 2). Those at-risk reported significantly more safety behaviors, self-focused attention, impaired engagement, and avoidance, plus lower perceived control over performance anxiety than those not at-risk. Multiple mediation models found the effects of ED risk on control over performance anxiety, impaired engagement, and avoidance were partially mediated by safety behaviors and self-focused attention. Discussion: Our cross-sectional findings suggest videoconferencing for work/study-related purposes is associated with performance anxiety, impaired engagement, and avoidance among individuals at-risk for EDs. Poorer videoconferencing outcomes appear more strongly related to social anxiety variables than ED status. Clinicians and educators may need to provide extra support for those using videoconferencing. Public Significance: Because videoconferencing often involves seeing your own image (via self-view) we wondered whether the appearance concerns experienced by those with eating disorders (EDs) might interfere with the ability to focus on or to contribute to work/study videoconferencing meetings. We found that although those with EDs experience more impairments in their videoconferencing engagement/contribution, these were linked just as strongly to social anxiety as they were to appearance concerns

    Hematopoietic IKBKE limits the chronicity of inflammasome priming and metaflammation

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    Obesity increases the risk of developing life-threatening metabolic diseases including cardiovascular disease, fatty liver disease, diabetes, and cancer. Efforts to curb the global obesity epidemic and its impact have proven unsuccessful in part by a limited understanding of these chronic progressive diseases. It is clear that low-grade chronic inflammation, or metaflammation, underlies the pathogenesis of obesity-associated type 2 diabetes and atherosclerosis. However, the mechanisms that maintain chronicity and prevent inflammatory resolution are poorly understood. Here, we show that inhibitor of ÎşB kinase epsilon (IKBKE) is a novel regulator that limits chronic inflammation during metabolic disease and atherosclerosis. The pathogenic relevance of IKBKE was indicated by the colocalization with macrophages in human and murine tissues and in atherosclerotic plaques. Genetic ablation of IKBKE resulted in enhanced and prolonged priming of the NLRP3 inflammasome in cultured macrophages, in hypertrophic adipose tissue, and in livers of hypercholesterolemic mice. This altered profile associated with enhanced acute phase response, deregulated cholesterol metabolism, and steatoheptatitis. Restoring IKBKE only in hematopoietic cells was sufficient to reverse elevated inflammasome priming and these metabolic features. In advanced atherosclerotic plaques, loss of IKBKE and hematopoietic cell restoration altered plaque composition. These studies reveal a new role for hematopoietic IKBKE: to limit inflammasome priming and metaflammation

    The Threat of Capital Drain: A Rationale for Public Banks?

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    This paper yields a rationale for why subsidized public banks may be desirable from a regional perspective in a financially integrated economy. We present a model with credit rationing and heterogeneous regions in which public banks prevent a capital drain from poorer to richer regions by subsidizing local depositors, for example, through a public guarantee. Under some conditions, cooperative banks can perform the same function without any subsidization; however, they may be crowded out by public banks. We also discuss the impact of the political structure on the emergence of public banks in a political-economy setting and the role of interregional mobility

    Meta-analysis of genome-wide association studies for neuroticism, and the polygenic association with major depressive disorder

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    IMPORTANCE Neuroticism is a pervasive risk factor for psychiatric conditions. It genetically overlaps with major depressive disorder (MDD) and is therefore an important phenotype for psychiatric genetics. The Genetics of Personality Consortium has created a resource for genome-wide association analyses of personality traits in more than 63 000 participants (including MDD cases)

    Phenotypic screen for oxygen consumption rate identifies an anti-cancer naphthoquinone that induces mitochondrial oxidative stress.

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    A hallmark of cancer cells is their ability to reprogram nutrient metabolism. Thus, disruption to this phenotype is a potential avenue for anti-cancer therapy. Herein we used a phenotypic chemical library screening approach to identify molecules that disrupted nutrient metabolism (by increasing cellular oxygen consumption rate) and were toxic to cancer cells. From this screen we discovered a 1,4-Naphthoquinone (referred to as BH10) that is toxic to a broad range of cancer cell types. BH10 has improved cancer-selective toxicity compared to doxorubicin, 17-AAG, vitamin K3, and other known anti-cancer quinones. BH10 increases glucose oxidation via both mitochondrial and pentose phosphate pathways, decreases glycolysis, lowers GSH:GSSG and NAPDH/NAPD+ ratios exclusively in cancer cells, and induces necrosis. BH10 targets mitochondrial redox defence as evidenced by increased mitochondrial peroxiredoxin 3 oxidation and decreased mitochondrial aconitase activity, without changes in markers of cytosolic or nuclear damage. Over-expression of mitochondria-targeted catalase protects cells from BH10-mediated toxicity, while the thioredoxin reductase inhibitor auranofin synergistically enhances BH10-induced peroxiredoxin 3 oxidation and cytotoxicity. Overall, BH10 represents a 1,4-Naphthoquinone with an improved cancer-selective cytotoxicity profile via its mitochondrial specificity

    ATP Release from Vascular Endothelia Occurs Across Cx43 Hemichannels and Is Attenuated during Hypoxia

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    Background: Extracellular ATP is an important signaling molecule for vascular adaptation to limited oxygen availability (hypoxia). Here, we pursued the contribution of vascular endothelia to extracellular ATP release under hypoxic conditions. Methodology, Principal Findings: We gained first insight from studying ATP release from endothelia (HMEC-1) pre-exposed to hypoxia. Surprisingly, we found that ATP release was significantly attenuated following hypoxia exposure (2 % oxygen, 2263 % after 48 h). In contrast, intracellular ATP was unchanged. Similarly, lactate-dehydrogenase release into the supernatants was similar between normoxic or hypoxic endothelia, suggesting that differences in lytic ATP release between normoxia or hypoxia are minimal. Next, we used pharmacological strategies to study potential mechanisms for endothelialdependent ATP release (eg, verapamil, dipyridamole, 18-alpha-glycyrrhetinic acid, anandamide, connexin-mimetic peptides). These studies revealed that endothelial ATP release occurs – at least in part- through connexin 43 (Cx43) hemichannels. A real-time RT-PCR screen of endothelial connexin expression showed selective repression of Cx43 transcript and additional studies confirmed time-dependent Cx43 mRNA, total and surface protein repression during hypoxia. In addition, hypoxia resulted in Cx43-serine368 phosphorylation, which is known to switch Cx43 hemi-channels from an open to a closed state. Conclusions/Significance: Taken together, these studies implicate endothelial Cx43 in hypoxia-associated repression o
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