Anthropologies of Unemployment: New Perspectives on Work and Its Absence

[Excerpt] Anthropologies of Unemployment offers accessible, theoretically innovative, and ethnographically rich examinations of unemployment in rural and urban regions across North and South America, Europe, Africa, and Asia. The diversity of case studies demonstrates that unemployment is a pressing global phenomenon that sheds light on the uneven consequences of free-market ideologies and policies. Economic, social, and cultural marginalization is common in the lives of the unemployed, but their experience and interpretation are shaped by local and national cultural particularities. In exploring those differences, the contributors to this volume employ recent theoretical innovations and engage with some of the more salient topics in contemporary anthropology, such as globalization, migration, youth cultures, bureaucracy, class, gender, and race. Taken together, the chapters reveal that there is something new about unemployment today. It is not a temporary occurrence, but a chronic condition. In adjusting to persistent, longstanding unemployment, people and groups create new understandings of unemployment as well as of work and employment; they improvise new forms of sociality, morality, and personhood. Ethnographic studies such as those found in Anthropologies of Unemployment are crucial if we are to understand the broader forms, meanings, and significance of pervasive economic insecurity and discover the emergence of new social and cultural possibilities

Marine Proteins and Peptides

Marine proteins and peptides have great potential application in developing pharmaceuticals, nutraceuticals, and cosmeceuticals. Proteins and peptides from marine sources are considered to be safe and inexpensive. Protein- and peptide-based drugs have been increasing in recent days to cure various diseases by serving multiple roles, such as antioxidants, anticancer drugs, antimicrobials, and anticoagulants. There are different marine sources (macroalgae, fish, shellfish, and bivalves), which possibly contain specific protein and peptides

Biomarker discovery and redundancy reduction towards classification using a multi-factorial MALDI-TOF MS T2DM mouse model dataset

Diabetes like many diseases and biological processes is not mono-causal. On the one hand multifactorial studies with complex experimental design are required for its comprehensive analysis. On the other hand, the data from these studies often include a substantial amount of redundancy such as proteins that are typically represented by a multitude of peptides. Coping simultaneously with both complexities (experimental and technological) makes data analysis a challenge for Bioinformatics

Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions

Monopoly Capital and Capitalist Inefficiency

This paper examines the arguments and assertions of Baran’s and Sweezy’s Monopoly Capital: An Essay on the American Economic and Social Order (1966) by assessing the degree of economic efficiency or inefficiency in how surplus value and economic surplus were created by 16 major capitalist economies during the 2000s using data envelopment analysis (DEA). After assigning a score to the degree of economic efficiency/inefficiency for each country, one can then assess which factors influence the degree of efficiency/inefficiency. This paper finds empirical support for many of the arguments put forth by the authors, Baran and Sweezy, as well as others regarding the inefficiency of the use of some forms of economic activity to help absorb economic surplus and to create surplus value

The Top One Percent and Exploitation Measures

With the Occupy Movement that recently took place on Wall Street and in other parts of the globe, a lot of attention has recently been given to growing income inequality. The 2008 United States financial crisis, the Great Recession, and the subsequent weak recovery have brought about a more serious focus on income inequality and the widening income gap between the top one percent and other groups. These events have brought about some social unrest and instability in American society perhaps not seen since the Great Depression. How much has the top 1 percent of households gained in terms of income versus the other 99 percent in the United States over the last 30 years or so? Mainstream economists and other social scientists point to various causes which have been mentioned in many scholarly and popular writings. All of these mainstream factors affecting inequality have been found to be statistically significant in one scholarly study or another. This research paper explores other major concepts to explain income inequality rather than to dispute the findings of other existing research efforts. The empirical findings of this paper support radical arguments that income accumulation of those at the top is not connected to the productivity of capital investment, but rather instead is connected to the declining incomes and exploitation of the rest of the US population despite the rising output per worker of the US workforce over the last 30 to 40 years

Newly uncovered physics of MHD instabilities using 2-D electron cyclotron emission imaging system in toroidal plasmas

Validation of physics models using the newly uncovered physics with a 2-D electron cyclotron emission imaging (ECEi) system for magnetic fusion plasmas has either enhanced the confidence or substantially improved the modeling capability. The discarded "full reconnection model" in sawtooth instability is vindicated and established that symmetry and magnetic shear of the 1/1 kink mode are critical parameters in sawtooth instability. For the 2/1 instability, it is demonstrated that the 2-D data can determine critical physics parameters with a high confidence and the measured anisotropic distribution of the turbulence and its flow in presence of the 2/1 island is validated by the modelled potential and gyro-kinetic calculation. The validation process of the measured reversed-shear Alfveneigenmode (RSAE) structures has improved deficiencies of prior models. The 2-D images of internal structure of the ELMs and turbulence induced by the resonant magnetic perturbation (RMP) have provided an opportunity to establish firm physics basis of the ELM instability and role of RMPs. The importance of symmetry in determining the reconnection time scale and role of magnetic shear of the 1/1 kink mode in sawtooth instability may be relevant to the underlying physics of the violent kink instability of the filament ropes in a solar flare

Monopoly Capital and Capitalist Inefficiency

This paper examines the arguments and assertions of Baran’s and Sweezy’s Monopoly Capital: An Essay on the American Economic and Social Order (1966) by assessing the degree of economic efficiency or inefficiency in how surplus value and economic surplus were created by 16 major capitalist economies during the 2000s using data envelopment analysis (DEA). After assigning a score to the degree of economic efficiency/inefficiency for each country, one can then assess which factors influence the degree of efficiency/inefficiency. This paper finds empirical support for many of the arguments put forth by the authors, Baran and Sweezy, as well as others regarding the inefficiency of the use of some forms of economic activity to help absorb economic surplus and to create surplus value

The E3 ubiquitin ligase TRIM25 regulates adipocyte differentiation via proteasomemediated degradation of PPAR gamma

Peroxisome proliferator-activated receptor gamma (PPAR??) is a ligand-dependent transcription factor that regulates adipocyte differentiation and glucose homeostasis. The transcriptional activity of PPAR?? is regulated not only by ligands but also by post-translational modifications (PTMs). In this study, we demonstrate that a novel E3 ligase of PPAR??, tripartite motif-containing 25 (TRIM25), directly induced the ubiquitination of PPAR??, leading to its proteasome-dependent degradation. During adipocyte differentiation, both TRIM25 mRNA and protein expression significantly decreased and negatively correlated with the expression of PPAR??. The stable expression of TRIM25 reduced PPAR?? protein levels and suppressed adipocyte differentiation in 3T3-L1 cells. In contrast, the specific knockdown of TRIM25 increased PPAR?? protein levels and stimulated adipocyte differentiation. Furthermore, TRIM25-knockout mouse embryonic fibroblasts (MEFs) exhibited an increased adipocyte differentiation capability compared with wild-type MEFs. Taken together, these data indicate that TRIM25 is a novel E3 ubiquitin ligase of PPAR?? and that TRIM25 is a novel target for PPAR??-associated metabolic diseases

RNAseq Analyses Identify Tumor Necrosis Factor-Mediated Inflammation as a Major Abnormality in ALS Spinal Cord

ALS is a rapidly progressive, devastating neurodegenerative illness of adults that produces disabling weakness and spasticity arising from death of lower and upper motor neurons. No meaningful therapies exist to slow ALS progression, and molecular insights into pathogenesis and progression are sorely needed. In that context, we used high-depth, next generation RNA sequencing (RNAseq, Illumina) to define gene network abnormalities in RNA samples depleted of rRNA and isolated from cervical spinal cord sections of 7 ALS and 8 CTL samples. We aligned \u3e50 million 2X150 bp paired-end sequences/sample to the hg19 human genome and applied three different algorithms (Cuffdiff2, DEseq2, EdgeR) for identification of differentially expressed genes (DEG’s). Ingenuity Pathways Analysis (IPA) and Weighted Gene Co-expression Network Analysis (WGCNA) identified inflammatory processes as significantly elevated in our ALS samples, with tumor necrosis factor (TNF) found to be a major pathway regulator (IPA) and TNFα-induced protein 2 (TNFAIP2) as a major network “hub” gene (WGCNA). Using the oPOSSUM algorithm, we analyzed transcription factors (TF) controlling expression of the nine DEG/hub genes in the ALS samples and identified TF’s involved in inflammation (NFkB, REL, NFkB1) and macrophage function (NR1H2::RXRA heterodimer). Transient expression in human iPSC-derived motor neurons of TNFAIP2 (also a DEG identified by all three algorithms) reduced cell viability and induced caspase 3/7 activation. Using high-density RNAseq, multiple algorithms for DEG identification, and an unsupervised gene co-expression network approach, we identified significant elevation of inflammatory processes in ALS spinal cord with TNF as a major regulatory molecule. Overexpression of the DEG TNFAIP2 in human motor neurons, the population most vulnerable to die in ALS, increased cell death and caspase 3/7 activation. We propose that therapies targeted to reduce inflammatory TNFα signaling may be helpful in ALS patients