Grounded Encounter Therapy: Its Characteristics and Process

Grounded Encounter Therapy (GET) is a sociodiagnostic and sociotherapeutic approach for clinicians applying sociological knowledge to problems that are lodged in a social context. It is a process of encounter which allows for the discovery of essential facts and explanations grounded in the social context of the client. It allows for a creative interplay between research, theory, education and practice to produce knowledge and courses of action. It helps clients discover, determine, understand and decide on a plan of action for problem solving and for growth. This article describes the basic philosophy and some of the techniques of GET

CLINICAL SOCIOLOGY: PROBLEMS AND PROSPECTS

The notion that sociology and sociologists can be "clinical" is beginning to take roots, even though the roots are not well established in the field of "mental health" and other fields having to do with therapy and change. Other clinical professionals do not question the argument that sociology has knowledge and information that can be applied to problems affecting the individual, group, organization, industry and the community. Neither is there any question regarding sociological methods and techniques for producing information and creating knowledge about group life. However, there are various questions being raised by established clinical professionals regarding the "clinical" and "therapeutic" potential and skills of sociologists and sociology. An examination of the clinical nature of psychiatry, clinical psychology, and psychiatric or clinical social work is presented in this paper, and four brief examples are used to demonstrate the clinical nature ofsociology

The Social Psychology of Driving Behavior: Communicative Aspects of Joint-Action

This paper identifies destiny-drivers, casual-cautious drivers, and socialoccasion drivers, as the primary participations in the driving environment, and argues that accidents occur when there is a breakdown in establishing joint-action" among and between these drivers. Leftlaners are also discussed within the context of the above designated drivers, and another potentially dangerous driver; the meditator, is introduced. The meditator is one who, for a variety of reasons, has some unresolved issue in contemplation. Other drivers emerging in the driving environment are dining-room, powder-room, library, and indicator drivers

A metagenomic assessment of winter and summer bacterioplankton from Antarctica Peninsula coastal surface waters

© The Author(s), 2012. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in The ISME Journal 6 (2012): 1901-1915, doi:10.1038/ismej.2012.31.Antarctic surface oceans are well-studied during summer when irradiance levels are high, sea ice is melting and primary productivity is at a maximum. Coincident with this timing, the bacterioplankton respond with significant increases in secondary productivity. Little is known about bacterioplankton in winter when darkness and sea-ice cover inhibit photoautotrophic primary production. We report here an environmental genomic and small subunit ribosomal RNA (SSU rRNA) analysis of winter and summer Antarctic Peninsula coastal seawater bacterioplankton. Intense inter-seasonal differences were reflected through shifts in community composition and functional capacities encoded in winter and summer environmental genomes with significantly higher phylogenetic and functional diversity in winter. In general, inferred metabolisms of summer bacterioplankton were characterized by chemoheterotrophy, photoheterotrophy and aerobic anoxygenic photosynthesis while the winter community included the capacity for bacterial and archaeal chemolithoautotrophy. Chemolithoautotrophic pathways were dominant in winter and were similar to those recently reported in global ‘dark ocean’ mesopelagic waters. If chemolithoautotrophy is widespread in the Southern Ocean in winter, this process may be a previously unaccounted carbon sink and may help account for the unexplained anomalies in surface inorganic nitrogen content.CSR was supported by an NSF Postdoctoral Fellowship in Biological Informatics (DBI-0532893). The research was supported by National Science Foundation awards: ANT 0632389 (to AEM and JJG), and ANT 0632278 and 0217282 (to HWD), all from the Antarctic Organisms and Ecosystems Program

Time-resolved angiography with stochastic trajectories for dynamic contrast-enhanced MRI in head and neck cancer: Are pharmacokinetic parameters affected?

Purpose To investigate the effects of different time-resolved angiography with stochastic trajectories (TWIST) k-space undersampling schemes on calculated pharmacokinetic dynamic contrast-enhanced (DCE) vascular parameters.Methods A digital perfusion phantom was employed to simulate effects of TWIST on characteristics of signal changes in DCE. Furthermore, DCE-MRI was acquired without undersampling in a group of patients with head and neck squamous cell carcinoma and used to simulate a range of TWIST schemes. Errors were calculated as differences between reference and TWIST-simulated DCE parameters. Parametrical error maps were used to display the averaged results from all tumors.Results For a relatively wide range of undersampling schemes, errors in pharmacokinetic parameters due to TWIST were under 10% for the volume transfer constant, Ktrans, and total extracellular extravascular space volume, Ve. TWIST induced errors in the total blood plasma volume, Vp, were the largest observed, and these were inversely dependent on the area of the fully sampled k-space. The magnitudes of errors were not correlated with Ktrans, Vp and weakly correlated with Ve.Conclusions The authors demonstrated methods to validate and optimize k-space view-sharing techniques for pharmacokinetic DCE studies using a range of clinically relevant spatial and temporal patient derived data. The authors found a range of undersampling patterns for which the TWIST sequence can be reliably used in pharmacokinetic DCE-MRI. The parameter maps created in the study can help to make a decision between temporal and spatial resolution demands and the quality of enhancement curve characterization

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

“A General Separation of Colored and White”: the WWII riots, military segregation, and racism(s) beyond the White/Nonwhite binary

This article uses archival research to explore important differences in the discursive and institutional positioning of Mexican American and African American men during World War II. Through the focal point of the riots which erupted in Los Angeles and other major cities in the summer of 1943, I examine the ways in which black and Mexican ‘rioters’ were imagined in official and popular discourses. Though both groups of youth were often constructed as deviant and subversive, there were also divergences in the ways in which their supposed racial difference was discursively configured. I also consider the experiences of each group in the WWII military, a subject that has received little attention in previous work on the riots. Though both groups were subject to discrimination and brutality on the home front, only African Americans were segregated in the military - a fact that profoundly influenced the 1943 riots. Examining the very different conditions under which these men served, as well as the distinct ways in which their presence within the military and on the home front was interpreted and given meaning by press, law enforcement and military officials helps to illuminate the uneven and complex workings of racism in America, disrupting the common conceptualization of a definitive white/nonwhite color line