174 research outputs found

    The City is the Factory: New Solidarities and Spatial Strategies in an Urban Age

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    [Excerpt] Urban public spaces, from the streets and squares of Buenos Aires to Zuccotti Park in New York City, have become the emblematic sites of contentious politics in the twenty-first century. As the contributors to The City Is the Factory argue, this resurgent politics of the square is itself part of a broader shift in the primary locations and targets of popular protest from the workplace to the city. This shift is due to an array of intersecting developments: the concentration of people, profit, and social inequality in growing urban areas; the attacks on and precarity faced by unions and workers\u27 movements; and the sense of possibility and actual leverage afforded by local politics and the tactical use of urban space. Thus, the city —from the town square to the banlieu—is becoming like the factory of old: a site of production and profit-making as well as new forms of solidarity, resistance, and social reimagining.We see examples of the city as factory in new place-based political alliances, as workers and the unemployed find common cause with right to the city struggles. Demands for jobs with justice are linked with demands for the urban commons—from affordable housing to a healthy environment, from immigrant rights to urban citizenship and the right to streets free from both violence and racially biased policing. The case studies and essays in The City Is the Factory provide descriptions and analysis of the form, substance, limits, and possibilities of these timely struggles

    A Problem of Taxonomy

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    page 85-8

    A pilot randomized controlled trial comparing the efficacy of problem-solving therapy to enhanced treatment as usual for reducing high blood pressure

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    High blood pressure is a highly prevalent and modifiable risk factor for cardiovascular disease that has substantially contributed to disability, morbidity, mortality, health disparities and economic burden in the United States. Although relatively easy to diagnosis and inexpensive to treat, controlling high blood pressure, thereby reducing its sequelae, remains difficult, particularly for Black individuals, due to a host of psychosocial, biological, and environmental factors. There is a need to identify an efficacious stress-reduction intervention for lowering uncontrolled high blood pressure that can be effectively translated into practice. In the current pilot study, the preliminary efficacy and feasibility of Problem-Solving Therapy (PST), compared to telephone-delivered enhanced treatment as usual (ETAU), were evaluated on measures of blood pressure, social problem solving ability, medication adherence, perceived stress, depression, and health-related quality of life (HRQOL) at baseline, posttreatment, and three-month follow up. Recruitment from outpatient medical clinics yielded a sample of 14 participants, predominantly Black and female, with uncontrolled high blood pressure, who were randomly assigned to PST or ETAU. Mean differences between conditions from baseline to posttreatment assessments were examined using a series of intent-to-treat (N = 12) t-tests and repeated measures ANOVAs, none of which were statistically significant. Inspection of effect sizes and clinical significance indicated a trend toward efficacy of PST to improve medication adherence [F(1, 10) = 2.54, p = 0.14, ηp2 = 0.20] and physical HRQOL [F(1,10) = 2.54, p = 0.14, ηp2 = 0.20], as well as slightly more frequent clinically meaningful changes in systolic blood pressure, mental HRQOL, and depression for those who received PST. In terms of feasibility, about 13% of 108 recruited patients were enrolled, the rate of attrition was below 20% for treatment initiators, retention of treatment initiators was 100% for PST (nPST = 6) and 83.3% (nETAU = 5) for ETAU at posttreatment, and about 80% of participants rated the treatments as credible and effective. Three-month follow up assessments were too few to conduct meaningful analyses. Although a trend toward efficacy of PST was indicated, challenges in recruitment limited sample size, and, therefore, the aforementioned preliminary results must be interpreted with caution.Ph.D., Psychology -- Drexel University, 201

    Valproate induces the unfolded protein response by increasing ceramide levels

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    Bipolar disorder (BD), which is characterized by depression and mania, affects 1–2% of the world population. Current treatments are effective in only 40–60% of cases and cause severe side effects. Valproate (VPA) is one of the most widely used drugs for the treatment of BD, but the therapeutic mechanism of action of this drug is not understood. This knowledge gap has hampered the development of effective treatments. To identify candidate pathways affected by VPA, we performed a genome- wide expression analysis in yeast cells grown in the presence or absence of the drug. VPA caused up-regulation of FEN1 and SUR4, encoding fatty acid elongases that catalyze the synthesis of very long chain fatty acids (C24 to C26) required for ceramide synthesis. Interestingly, fen1Δ and sur4Δ mutants exhibited VPA sensitivity. In agreement with increased fatty acid elongase gene expression, VPA increased levels of phytoceramide, especially those containing C24–C26 fatty acids. Consistent with an increase in ceramide, VPA decreased the expression of amino acid transporters, increased the expression of ER chaperones, and activated the unfolded protein response element (UPRE), suggesting that VPA induces the UPR pathway. These effects were rescued by supplementation of inositol and similarly observed in inositol-starved ino1Δ cells. Starvation of ino1Δ cells increased expression of FEN1 and SUR4, increased ceramide levels, decreased expression of nutrient transporters, and induced the UPR. These findings suggest that VPA-mediated inositol depletion induces the UPR by increasing the de novo synthesis of ceramide

    Perilipin regulates the thermogenic actions of norepinephrine in brown adipose tissue

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    In response to cold, norepinephrine (NE)-induced triacylglycerol hydrolysis (lipolysis) in adipocytes of brown adipose tissue (BAT) provides fatty acid substrates to mitochondria for heat generation (adaptive thermogenesis). NE-induced lipolysis is mediated by protein kinase A (PKA)-dependent phosphorylation of perilipin, a lipid droplet-associated protein that is the major regulator of lipolysis. We investigated the role of perilipin PKA phosphorylation in BAT NE-stimulated thermogenesis using a novel mouse model in which a mutant form of perilipin, lacking all six PKA phosphorylation sites, is expressed in adipocytes of perilipin knockout (Peri KO) mice. Here, we show that despite a normal mitochondrial respiratory capacity, NE-induced lipolysis is abrogated in the interscapular brown adipose tissue (IBAT) of these mice. This lipolytic constraint is accompanied by a dramatic blunting (∌70%) of the in vivo thermal response to NE. Thus, in the presence of perilipin, PKA-mediated perilipin phosphorylation is essential for NE-dependent lipolysis and full adaptive thermogenesis in BAT. In IBAT of Peri KO mice, increased basal lipolysis attributable to the absence of perilipin is sufficient to support a rapid NE-stimulated temperature increase (∌3.0°C) comparable to that in wild-type mice. This observation suggests that one or more NE-dependent mechanism downstream of perilipin phosphorylation is required to initiate and/or sustain the IBAT thermal response

    A new negative control gene for amino acid biosynthesis in Saccharomyces cerevisiae

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    Enzyme levels in multiple amino acid biosynthetic pathways in yeast are coregulated. This control is effected largely at the transcriptional level by a number. of regulatory genes. We report the isolation and characterization of a new negative regulatory gene, GCD4 , for this general control system. GCD4 mutations are recessive and define a single Mendelian gene on chromosome 111. A gcd4 mutation results in resistance to different amino acid analogs and elevated, but fully inducible, mRNA levels of genes under general control. Epistasis analysis indicates that GCD4 acts more directly than the positive regulators GCN1, GCN2, GCN3 and GCN5 , but less directly than GCN4 , on the transcription of the amino acid biosynthetic genes. These data imply that GCD4 is a negative regulator of the positive effector, GCN4 . Although GCD4 occupies the same position relative to the GCN genes as other GCD genes, it produces a unique phenotype. These results illustrate the diversity of function of negative regulators in general control.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46958/1/294_2004_Article_BF00447382.pd

    Witness: The Modern Writer as Witness

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    Editor\u27s Note [Excerpt] The United States, as a society, is on the brink of profound and positive change. Demographically and culturally, things are improving, and the reason is obvious to people who study history: Conflict pushes us to be better, to strive for principled goals. Consider the inspired eco-advocacy of Greta Thunberg. Or the swearing in of most diverse class of lawmakers in history into the 116th Congress. Or billionaire Robert F. Smith’s pledge to pay off every Morehouse College (in Atlanta, Georgia) student’s debt. Indeed, there are many good people helping and great moments happening in spite of a bleak 24-hour news cycle designed to ruin happiness and to limit our understanding of our human potential. We at Witness see this yearning for transformation in the works we selected. The doorway must be crossed, and the voices and characters we featured in our Winter 2019 issue stand at the vestibule, ready for the light to warm them, primed to fight for that necessary illumination.https://digitalscholarship.unlv.edu/witness/1000/thumbnail.jp

    Mapping the cis-regulatory architecture of the human retina reveals noncoding genetic variation in disease

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    The interplay of transcription factors and cis-regulatory elements (CREs) orchestrates the dynamic and diverse genetic programs that assemble the human central nervous system (CNS) during development and maintain its function throughout life. Genetic variation within CREs plays a central role in phenotypic variation in complex traits including the risk of developing disease. We took advantage of the retina, a well-characterized region of the CNS known to be affected by pathogenic variants in CREs, to establish a roadmap for characterizing regulatory variation in the human CNS. This comprehensive analysis of tissue-specific regulatory elements, transcription factor binding, and gene expression programs in three regions of the human visual system (retina, macula, and retinal pigment epithelium/choroid) reveals features of regulatory element evolution that shape tissue-specific gene expression programs and defines regulatory elements with the potential to contribute to Mendelian and complex disorders of human vision
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