In the Interest of the State: Production Politics in the Nineteenth Century Prison

This is the published version. Copyright 1990 University of California Press.During the nineteenth century, the jails, penitentiaries, and reformatories of America were "industrialized" under both public and private production regimes. Society-centered revisionist writing in both sociology and history has failed to explain adequately the appearance, consequence, and ultimate dismantling of these regimes. In this paper I offer an alternative, state-centered analysis which locates the political state within its interdependent relationship with the economic and normative spheres of society. My view underscores the role of state managers and agents as historical subjects whose actions have consequences for the structuring of the state apparatus

Technology, Control, and the Social Organization of Work at a British Hardware Firm, 1791-1891

This is the published version. Copyright 1987 University of Chicago Press.This paper examines the social relations of production at a British metal-trades firm throughout the 19th century. The case study reveals the existence of two distinct political apparatuses, or regimes, identified in provious literature, that govern production relations. The first regime, between 1791 and 1867, is described as patriarchal because production is organized around adult, male, internal subcontactors and their families. In the second period, roughly 1868-91, the regime is characterized as paternalistic since it attempts to align the interests of capital and worker through family, work, and community life. The analysis uncovers social and economic forces that undermined the system of internal subcontracting and patriarchy and fostered paternalism. Emerging paternalism shaped the struggles over the introduction of new technologies that formed the basis for the real subordination of labor to capital

The Culture of Surveillance Revisited: Total Information Awareness and the New Privacy Landscape

Three things: 1) I expect, as we have already seen in fact, a shift in the scope and quality of social monitoring we can likely expect in the post 9/11 period. I would suggest that the attacks of September 11 have provided an extraordinary opportunity for the state to extend its "governability (Foucault 1991) of the popula tion through a new set of surveillance and control mechanisms; 2) I would argue that the only way that the state is going to implement this kind of large scale, integrated, digitized system of surveillance of the populace is through the cooperation of both corporate capital and, by extension, the populace itself; and 3) I would like to call attention to how a new digital surveillance system will work to constitute our virtual identities as both consumers and citizens

Toward a Structural Perspective on Gender Bias in the Juvenile Court

This is the published version. Copyright 1984 University of California Press.A number of hypotheses about the effect of gender on the likelihood of incarceration in the juvenile court are tested. A purposive sample of 3911 delinquent (nonstatus) offending youths from 19 juristictions throughout the United States is analyzed employing the log-linear technique to control for the legal variables of severity of offense and prior record. The results indicate that females were less likely to be incarcerated than were males throughout the jurisdictions sampled. These and other findings lend support for a structural theory of gender bias in the juvenile court

CDK4/6 inhibitor-mediated cell overgrowth triggers osmotic and replication stress to promote senescence

Summary. Abnormal increases in cell size are associated with senescence and cell cycle exit. The mechanisms by which overgrowth primes cells to withdraw from the cell cycle remain unknown. We address this question using CDK4/6 inhibitors, which arrest cells in G0/G1 and are licensed to treat advanced HR+/HER2− breast cancer. We demonstrate that CDK4/6-inhibited cells overgrow during G0/G1, causing p38/p53/p21-dependent cell cycle withdrawal. Cell cycle withdrawal is triggered by biphasic p21 induction. The first p21 wave is caused by osmotic stress, leading to p38- and size-dependent accumulation of p21. CDK4/6 inhibitor washout results in some cells entering S-phase. Overgrown cells experience replication stress, resulting in a second p21 wave that promotes cell cycle withdrawal from G2 or the subsequent G1. We propose that the levels of p21 integrate signals from overgrowth-triggered stresses to determine cell fate. This model explains how hypertrophy can drive senescence and why CDK4/6 inhibitors have long-lasting effects in patients

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

Phenotypic Characterization of EIF2AK4 Mutation Carriers in a Large Cohort of Patients Diagnosed Clinically With Pulmonary Arterial Hypertension.

BACKGROUND: Pulmonary arterial hypertension (PAH) is a rare disease with an emerging genetic basis. Heterozygous mutations in the gene encoding the bone morphogenetic protein receptor type 2 (BMPR2) are the commonest genetic cause of PAH, whereas biallelic mutations in the eukaryotic translation initiation factor 2 alpha kinase 4 gene (EIF2AK4) are described in pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis. Here, we determine the frequency of these mutations and define the genotype-phenotype characteristics in a large cohort of patients diagnosed clinically with PAH. METHODS: Whole-genome sequencing was performed on DNA from patients with idiopathic and heritable PAH and with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis recruited to the National Institute of Health Research BioResource-Rare Diseases study. Heterozygous variants in BMPR2 and biallelic EIF2AK4 variants with a minor allele frequency of <1:10 000 in control data sets and predicted to be deleterious (by combined annotation-dependent depletion, PolyPhen-2, and sorting intolerant from tolerant predictions) were identified as potentially causal. Phenotype data from the time of diagnosis were also captured. RESULTS: Eight hundred sixty-four patients with idiopathic or heritable PAH and 16 with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis were recruited. Mutations in BMPR2 were identified in 130 patients (14.8%). Biallelic mutations in EIF2AK4 were identified in 5 patients with a clinical diagnosis of pulmonary veno-occlusive disease/pulmonary capillary hemangiomatosis. Furthermore, 9 patients with a clinical diagnosis of PAH carried biallelic EIF2AK4 mutations. These patients had a reduced transfer coefficient for carbon monoxide (Kco; 33% [interquartile range, 30%-35%] predicted) and younger age at diagnosis (29 years; interquartile range, 23-38 years) and more interlobular septal thickening and mediastinal lymphadenopathy on computed tomography of the chest compared with patients with PAH without EIF2AK4 mutations. However, radiological assessment alone could not accurately identify biallelic EIF2AK4 mutation carriers. Patients with PAH with biallelic EIF2AK4 mutations had a shorter survival. CONCLUSIONS: Biallelic EIF2AK4 mutations are found in patients classified clinically as having idiopathic and heritable PAH. These patients cannot be identified reliably by computed tomography, but a low Kco and a young age at diagnosis suggests the underlying molecular diagnosis. Genetic testing can identify these misclassified patients, allowing appropriate management and early referral for lung transplantation

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