Oh Helen!

https://digitalcommons.library.umaine.edu/mmb-vp/2275/thumbnail.jp

Etniniai periodai

Publikuojamas L. H. Morgano veikalo „Senovės visuomenė“ skyriaus vertimas. Naujausieji ankstyvosios žmonių būklės tyrinėjimai leidžia manyti, kad žmonija pradėjo savo veiklą nuo pačios žemiausios raidos pakopos ir prasiskynė kelią iš laukinės būklės į civilizaciją, lėtai kaupdama patyrimą. Žmogus sukūrė dvi pagrindines valdymo formas: gimininę socialinę, kuri sudaro visuomenę, ir politinę, kuri sudaro valstybę. Pirmoji remiasi asmenimis ir giminyste, o antroji – teritorija ir nuosavybe. Pirmoji yra senovės visuomenės, antroji – šiuolaikinės, arba civilizuotos, visuomenės valdymo forma. Nagrinėjami namų institutai žmonijos raidoje. Teigiama, kad nuosavybės idėja formavosi lėtai, atsirado laukinės būklės periode. Autorius išskiria etninius periodus: 1) Žemutinė laukinės būklės pakopa; 2) vidurinė laukinės būklės pakopa; 3) aukštutinė laukinės būklės pakopa; 4) žemutinė barbarybės pakopa; 5) vidurinė barbarybės pakopa; 6) aukštutinė barbarybės pakopa; 7) civilizacijos pakopa. Šis skyrimas leidžia traktuoti kiekvieną atskirą visuomenę pagal jos santykinės pažangos būklę ir laikyti ją savarankiško tyrimo objektu

An Ethnohistorical Perspective on Cheyenne Demography

Administrative censuses of the Southern Cheyenne Indians from 1880,1891, and 1900 permit family reconstitution, identification of residence groups, and comparisons of fertility between monogamous and polygynous women, when the records are approached by ethnohistori cal methods. This approach includes an awareness of the aboriginal adoption practices, kinship system, and naming practices. It is argued that the biases and distortions of administrative records can be effectively corrected to add to our store of information on band and tribal societies.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Parental Substance Abuse As an Early Traumatic Event. Preliminary Findings on Neuropsychological and Personality Functioning in Young Drug Addicts Exposed to Drugs Early.

open5noParental substance use is a major risk factor for child development, heightening the risk of drug problems in adolescence and young adulthood, and exposing offspring to several types of traumatic events. First, prenatal drug exposure can be considered a form of trauma itself, with subtle but long-lasting sequelae at the neuro-behavioral level. Second, parents’ addiction often entails a childrearing environment characterized by poor parenting skills, disadvantaged contexts and adverse childhood experiences (ACEs), leading to dysfunctional outcomes. Young adults born from/raised by parents with drug problems and diagnosed with a Substance Used Disorder (SUD) themselves might display a particularly severe condition in terms of cognitive deficits and impaired personality function. This preliminary study aims to investigate the role of early exposure to drugs as a traumatic event, capable of affecting the psychological status of young drug addicts. In particular, it intends to examine the neuropsychological functioning and personality profile of young adults with severe SUDs who were exposed to drugs early in their family context. The research involved three groups, each consisting of 15 young adults (aged 18–24): a group of inpatients diagnosed with SUDs and exposed to drugs early, a comparison group of non-exposed inpatients and a group of non-exposed youth without SUDs. A neuropsychological battery (Esame Neuropsicologico Breve-2), an assessment procedure for personality disorders (Shedler-Westen Assessment Procedure-200) and the Symptom CheckList-90-Revised were administered. According to present preliminary results, young drug addicts exposed to drugs during their developmental age were characterized by elevated rates of neuropsychological impairments, especially at the expense of attentive and executive functions (EF); personality disorders were also common but did not differentiate them from non-exposed youth with SUDs. Alternative multi-focused prevention and intervention programs are needed for children of drug-misusing parents, addressing EF and adopting a trauma-focused approach.openParolin, Micol; Simonelli, Alessandra; Mapelli, Daniela; Sacco, M.; Cristofalo, P.Parolin, Micol; Simonelli, Alessandra; Mapelli, Daniela; Sacco, M.; Cristofalo, P

Social Class

Discussion of class structure in fifth-century Athens, historical constitution of theater audiences, and the changes in the comic representation of class antagonism from Aristophanes to Menander

What Do Unions Do for Economic Performance?

Twenty years have passed since Freeman and Medoff's What Do Unions Do? This essay assesses their analysis of how unions in the U.S. private sector affect economic performance - productivity, profitability, investment, and growth. Freeman and Medoff are clearly correct that union productivity effects vary substantially across workplaces. Their conclusion that union effects are on average positive and substantial cannot be sustained, subsequent evidence suggesting an average union productivity effect near zero. Their speculation that productivity effects are larger in more competitive environments appears to hold up, although more evidence is needed. Subsequent literature continues to find unions associated with lower profitability, as noted by Freeman and Medoff. Unions are found to tax returns stemming from market power, but industry concentration is not the source of such returns. Rather, unions capture firm quasi-rents arising from long-lived tangible and intangible capital and from firm-specific advantages. Lower profits and the union tax on asset returns leads to reduced investment and, subsequently, lower employment and productivity growth. There is little evidence that unionization leads to higher rates of business failure. Given the decline in U.S. private sector unionism, I explore avenues through which individual and collective voice might be enhanced, focusing on labor law and workplace governance defaults. Substantial enhancement of voice requires change in the nonunion sector and employer as well as worker initiatives. It is unclear whether labor unions would be revitalized or further marginalized by such an evolution

The Public Repository of Xenografts enables discovery and randomized phase II-like trials in mice

More than 90% of drugs with preclinical activity fail in human trials, largely due to insufficient efficacy. We hypothesized that adequately powered trials of patient-derived xenografts (PDX) in mice could efficiently define therapeutic activity across heterogeneous tumors. To address this hypothesis, we established a large, publicly available repository of well-characterized leukemia and lymphoma PDXs that undergo orthotopic engraftment, called the Public Repository of Xenografts (PRoXe). PRoXe includes all de-identified information relevant to the primary specimens and the PDXs derived from them. Using this repository, we demonstrate that large studies of acute leukemia PDXs that mimic human randomized clinical trials can characterize drug efficacy and generate transcriptional, functional, and proteomic biomarkers in both treatment-naive and relapsed/refractory disease

Microglial activation and chronic neurodegeneration

Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurode-generative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-α, nitric oxide, interleukin-1β, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson’s disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype