Effect of Out-Group Exposure on the Mirror Neuron System

Mirror neurons appear to play an important role in the experience of empathy, and may be critical for understanding the social signals of others in an interactive context between distinctly identified groups. Research has shown that mirror neuron activation is greater when observing in-group members (others that one most identifies with based on a certain factor or number of factors) as opposed to out-group members, which may implicate the mirror neuron system (MNS) in the neural aspect of social bias. However, no research had been conducted on the effect on the MNS of practice in interpreting and internalizing social signals of others through consistent exposure. We used electroencephalography to assess mirror neuron activity (via Mu-wave suppression) towards individuals of white and black ethnicity before and after a period of MNS exposure towards the participants’ ethnic out-group (black). We found that on average participants had significantly more Mu-wave suppression towards white individuals than black before exposure, and no significant difference in Mu-wave suppression between ethnicities after exposure. This indicates that the MNS is plastic and increasingly responsive towards individuals of proximate groups with which there is consistent social interaction, to the point where there may be little difference in ability to identify with in-group versus out-group members. This attribute of the MNS may be involved in the formation of social identity and intergroup biases, as well as the potential to either dissociate or empathize with others based on distinctive factors

Effect of Oxytocin Administration on Mirror Neuron Activation

This is the first study attempting to conclusively link oxytocin to MNS activity, in which we hypothesize the hormone plays a critical role, in healthy individuals and in an intergroup context

Preferential tau aggregation in von Economo neurons and fork cells in frontotemporal lobar degeneration with specific MAPT variants.

Tau aggregation is a hallmark feature in a subset of patients with frontotemporal dementia (FTD). Early and selective loss of von Economo neurons (VENs) and fork cells within the frontoinsular (FI) and anterior cingulate cortices (ACC) is observed in patients with sporadic behavioral variant FTD (bvFTD) due to frontotemporal lobar degeneration (FTLD), including FTLD with tau inclusions (FTLD-tau). Recently, we further showed that these specialized neurons show preferential aggregation of TDP-43 in FTLD-TDP. Whether VENs and fork cells are prone to tau accumulation in FTLD-tau remains unclear, and no previous studies of these neurons have focused on patients with pathogenic variants in the gene encoding microtubule-associated protein tau (FTLD-tau/MAPT). Here, we examined regional profiles of tau aggregation and neurodegeneration in 40 brain regions in 8 patients with FTLD-tau/MAPT and 7 with Pick's disease (PiD), a sporadic form of FTLD-tau that often presents with bvFTD. We further qualitatively assessed the cellular patterns of frontoinsular tau aggregation in FTLD-tau/MAPT using antibodies specific for tau hyperphosphorylation, acetylation, or conformational change. ACC and mid-insula were among the regions most affected by neurodegeneration and tau aggregation in FTLD-tau/MAPT and PiD. In these two forms of FTLD-tau, severity of regional neurodegeneration and tau protein aggregation were highly correlated across regions. In FTLD-tau/MAPT, VENs and fork cells showed disproportionate tau protein aggregation in patients with V337 M, A152T, and IVS10 + 16 variants, but not in patients with the P301L variant. As seen in FTLD-TDP, our data suggest that VENs and fork cells represent preferentially vulnerable neuron types in most, but not all of the MAPT variants we studied

A qualitative investigation into the determinants of perceived stress by intern clinical/counselling psychologists in consultation with a non-fatal suicidal client.

Thesis (M.A.)-University of KwaZulu-Natal, Durban, 2007.Aim: This study aims to investigate the experience of stress and the factors that impact on the intern psychologist in relation to first consultation with a non-fatal suicidal client. Intra and interpersonal factors, as well as institutional/environmental factors that influence/impact on intern clinical/counselling psychologist level of stress when assessing and managing a non-fatal suicidal client were identified. Methodology: The research methodology chosen for this study is based on the aim of the study, which is to investigate the experience of stress perceived by intern clinical/counselling psychologists in relation to consultation with a non-fatal suicidal client. A qualitative methodological approach will be used in this study as it allows for greater in-depth investigation and understanding of the experiences of intern clinical/counselling psychologists towards suicidal clients than would be generated by quantitative research methods. Five intern clinical/counseling psychologists were used in this qualitative study. They were interviewed using a semi-structured in- depth interview. The data was transcribed and analysed using thematic analysis. Findings: A variety of stressors were identified by the interns, but the majority described common variables. The main sources of stress for the interns was first contact with suicidal clients and lack of practical training and experience. The working environment, which included work load, administrative work and academic and competency based requirements, was also deemed stressful. In terms of personal stress, interns reported family and friends to be a source of stress at times. Personality also contributed to the interns levels of stress. Socio-cultural factors which impacted on the interns experience of stress in relation to consultation with non-fatal suicidal clients included, language difficulties and cultural differences. Recommendations: The internship was generally described as stressful. Recommendations included more practical experience and training prior to the commencement of the internship. This will equip interns with the skills and abilities necessary in successfully assessing and managing high risk clients. Organisational and professional factors can also be modified and include support as well as an understanding of the policies and procedures of the institution in which the internship is being done

Dynamic Interpretation of Hedgehog Signaling in the Drosophila Wing Disc

Morphogens are classically defined as molecules that control patterning by acting at a distance to regulate gene expression in a concentration-dependent manner. In the Drosophila wing imaginal disc, secreted Hedgehog (Hh) forms an extracellular gradient that organizes patterning along the anterior–posterior axis and specifies at least three different domains of gene expression. Although the prevailing view is that Hh functions in the Drosophila wing disc as a classical morphogen, a direct correspondence between the borders of these patterns and Hh concentration thresholds has not been demonstrated. Here, we provide evidence that the interpretation of Hh signaling depends on the history of exposure to Hh and propose that a single concentration threshold is sufficient to support multiple outputs. Using mathematical modeling, we predict that at steady state, only two domains can be defined in response to Hh, suggesting that the boundaries of two or more gene expression patterns cannot be specified by a static Hh gradient. Computer simulations suggest that a spatial “overshoot” of the Hh gradient occurs, i.e., a transient state in which the Hh profile is expanded compared to the Hh steady-state gradient. Through a temporal examination of Hh target gene expression, we observe that the patterns initially expand anteriorly and then refine, providing in vivo evidence for the overshoot. The Hh gene network architecture suggests this overshoot results from the Hh-dependent up-regulation of the receptor, Patched (Ptc). In fact, when the network structure was altered such that the ptc gene is no longer up-regulated in response to Hh-signaling activation, we found that the patterns of gene expression, which have distinct borders in wild-type discs, now overlap. Our results support a model in which Hh gradient dynamics, resulting from Ptc up-regulation, play an instructional role in the establishment of patterns of gene expression

Central and Peripheral α-Synuclein in Parkinson Disease Detected by Seed Amplification Assay

Objectives Detection of α‐synuclein aggregates by seed amplification is a promising Parkinson disease biomarker assay. Understanding intraindividual relationships of α‐synuclein measures could inform optimal biomarker development. The objectives were to test accuracy of α‐synuclein seed amplification assay in central (cerebrospinal fluid) and peripheral (submandibular gland) sources, compare to total α‐synuclein measures, and investigate within‐subject relationships. Methods The Systemic Synuclein Sampling Study aimed to characterize α‐synuclein in multiple tissues and biofluids within Parkinson disease subjects (n = 59) and compared to healthy controls (n = 21). Motor and non‐motor measures and dopamine transporter scans were obtained. Four measures of α‐synuclein were compared: seed amplification assay in cerebrospinal fluid and formalin‐fixed paraffin‐embedded submandibular gland, total α‐synuclein quantified in biofluids using enzyme‐linked immunoassay, and aggregated α‐synuclein in submandibular gland detected by immunohistochemistry. Accuracy of seed amplification assay for Parkinson disease diagnosis was examined and within‐subject α‐synuclein measures were compared. Results Sensitivity and specificity of α‐synuclein seed amplification assay for Parkinson disease diagnosis was 92.6% and 90.5% in cerebrospinal fluid, and 73.2% and 78.6% in submandibular gland, respectively. 25/38 (65.8%) Parkinson disease participants were positive for both cerebrospinal fluid and submandibular gland seed amplification assay. Comparing accuracy for Parkinson disease diagnosis of different α‐synuclein measures, cerebrospinal fluid seed amplification assay was the highest (Youden Index = 83.1%). 98.3% of all Parkinson disease cases had ≥1 measure of α‐synuclein positive. Interpretation α‐synuclein seed amplification assay (cerebrospinal fluid\u3esubmandibular gland) had higher sensitivity and specificity compared to total α‐synuclein measures, and within‐subject relationships of central and peripheral α‐synuclein measures emerged

Gli3 controls the onset of cortical neurogenesis by regulating the radial glial cell cycle through <i>Cdk6</i> expression

The cerebral cortex contains an enormous number of neurons, allowing it to perform highly complex neural tasks. Understanding how these neurons develop at the correct time and place and in accurate numbers constitutes a major challenge. Here, we demonstrate a novel role for Gli3, a key regulator of cortical development, in cortical neurogenesis. We show that the onset of neuron formation is delayed in Gli3 conditional mouse mutants. Gene expression profiling and cell cycle measurements indicate that shortening of the G1 and S phases in radial glial cells precedes this delay. Reduced G1 length correlates with an upregulation of the cyclin-dependent kinase gene Cdk6, which is directly regulated by Gli3. Moreover, pharmacological interference with Cdk6 function rescues the delayed neurogenesis in Gli3 mutant embryos. Overall, our data indicate that Gli3 controls the onset of cortical neurogenesis by determining the levels of Cdk6 expression, thereby regulating neuronal output and cortical size

TLS, 24 Nov 1967

This was a yearly Christmas letter sent from Wilma. She talks about the happenings of the year as well as the current needs of the School. She said they need library books, dishwasher for the cafeteria, clothes for the poorer students, recreational equipment, heat for the dormitories, and so on

Evaluating suspected CWD feral pig brain samples using RT-QuIC and protocol for the purification and quality control of recombinant monomeric proteins for RT-QuIC assay

Proteinopathy is a broad term used to describe any disease or condition that arises as a result of aberrant protein behavior. Most often it is used when discussing any of a wide range of neurodegenerative diseases that tend to result from an abnormal misfolding and subsequent aggregation of a normal cellular protein. The pathology of each of these diseases is largely dependent upon the nature of the protein aggregate that is responsible for or resulting from the disease. When viewed individually each disease seems only vaguely similar to others, but when a step back is taken to consider the broader aspects of the disease it begins to show similarities with other diseases, some of which are better studied and understood. The advances in other proteinopathies can then be experimentally applied to a specific disease of interest and the results compared to gain better understand the mechanisms underlying its pathogenesis and progression. Two examples of such proteinopathies are transmissible spongiform encephalopathies (TSE) and Parkinson’s disease (PD). TSEs are a subset of prion misfolding diseases, specifically identified as being transmissible to other individuals in a manner resembling viral, bacterial, or toxic exposure, that have been studied in animals for decades. While rare in humans, prion protein misfolding does occur in a handful of different forms. PD on the other hand is fairly common in older individuals, affecting approximately one million people in the United States and an estimated 10 million people worldwide. Both conditions share such notable traits as characteristic protein aggregates, being neurodegenerative, eventually fatally so, and having a link to the enteric nervous system. Techniques applied to the study of TSEs have been successfully applied to the study of PD, and inverse has occurred as well, leading to leap frog effect of advancement for both diseases. In this thesis, topics of two proteinopathies are covered. A literature review of chronic wasting disease (CWD) history, study, and further interests leads the paper. This is followed by a chapter on analysis of feral pig brainstem by RT-QuIC to determine the presence or absence of aggregated prion protein. The next chapter is dedicated to describing a protocol for the efficient and reliable production of recombinant human α-synuclein monomeric protein for use in research. Each of these techniques has been applied to the study of multiple diseases, but the refinement of each technique for application to the disease or species of interest is essential to achieving the best results.</p

EARLY NINETEENTH CENTURY BRITISH AUTHOR-PUBLISHER RELATIONS: A STUDY OF MURRAY\u27S, LONGMAN\u27S, BLACKWOOD\u27S, AND TAYLOR AND HESSEY\u27S RELATIONS WITH SELECTED AUTHORS.

Abstract not availabl