Communicating Organizational and Transgender Intersectional Identities: an Ethnography of a Transgender Outreach Center

This dissertation examined the communicative construction of identity by members of a transgender outreach organization. It focused on how members&rsquo; communication created and modified organizational identities in relationship to participants&rsquo; individual identities. Through my three-year ethnography of and volunteering with the Transgender Resource Center of New Mexico (TGRC), I conducted 415 hours of participant observation, 64 hours of semi-structured interviews (n=36), document analysis, and over nine hours of creative focus groups (n=5) of one of the only transgender-centered organizations in the United States. I investigated how TGRC members negotiated the significance of relevant individual and organizational identities, their relationships, and their implications for transgender organizational outreach. I argued that TGRC&rsquo;s transgender-centered organizational outreach and their emic, ambiguous emphasis on their members&rsquo; intersectional identities revealed important complexities for organizational communication inquiry. My data analysis reviewed two salient identity intersections for many TGRC participants: (1) homeless and transgender identities and (2) indigenous and transgender identities, which both tied to other identity intersections. Next, I presented TGRC organizational identity ideals responding to participants&rsquo; transgender intersectional identities: (1) TGRC as family and (2) TGRC as support for all facets of transgender living. I then examined four communication constraints for sustaining those organizational identity ideals: (1) family tensions, (2) non-binary critiques, (3) Harm Reduction Program competition, and (4) Nonprofit Industrial Complex hegemony.My dissertation revealed theoretical and practical recommendations for studying the communicative construction of organizational identity for transgender intersectional outreach organizing. Specifically, we need increased understanding of how organizational members create organizational identities that account for complex, intersectional participant identities as they simultaneously organize around a strategic, focused identity category. This research offered a unique examination of the complexities of constructing organizational identities for an identity-based organization&mdash;collectives advancing outreach and justice for members &ldquo;sharing&rdquo; one or more social identities (e.g., race, disability, sexuality, etc.). I offer three future extensions for organizational identity research grounded in prior scholarship and in my ethnographic findings: (1) contrasting communication, (2) detypification, and (3) crystallized organizational identity using ambiguous intersectionality. I end by calling for future engaged transgender and intersectional organizational communication research.</p

Functional Imaging of Numerical Processing in Adults and 4-y-Old Children

Adult humans, infants, pre-school children, and non-human animals appear to share a system of approximate numerical processing for non-symbolic stimuli such as arrays of dots or sequences of tones. Behavioral studies of adult humans implicate a link between these non-symbolic numerical abilities and symbolic numerical processing (e.g., similar distance effects in accuracy and reaction-time for arrays of dots and Arabic numerals). However, neuroimaging studies have remained inconclusive on the neural basis of this link. The intraparietal sulcus (IPS) is known to respond selectively to symbolic numerical stimuli such as Arabic numerals. Recent studies, however, have arrived at conflicting conclusions regarding the role of the IPS in processing non-symbolic, numerosity arrays in adulthood, and very little is known about the brain basis of numerical processing early in development. Addressing the question of whether there is an early-developing neural basis for abstract numerical processing is essential for understanding the cognitive origins of our uniquely human capacity for math and science. Using functional magnetic resonance imaging (fMRI) at 4-Tesla and an event-related fMRI adaptation paradigm, we found that adults showed a greater IPS response to visual arrays that deviated from standard stimuli in their number of elements, than to stimuli that deviated in local element shape. These results support previous claims that there is a neurophysiological link between non-symbolic and symbolic numerical processing in adulthood. In parallel, we tested 4-y-old children with the same fMRI adaptation paradigm as adults to determine whether the neural locus of non-symbolic numerical activity in adults shows continuity in function over development. We found that the IPS responded to numerical deviants similarly in 4-y-old children and adults. To our knowledge, this is the first evidence that the neural locus of adult numerical cognition takes form early in development, prior to sophisticated symbolic numerical experience. More broadly, this is also, to our knowledge, the first cognitive fMRI study to test healthy children as young as 4 y, providing new insights into the neurophysiology of human cognitive development

Fine-mapping of the HNF1B multicancer locus identifies candidate variants that mediate endometrial cancer risk.

Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 × 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression

Missing Information, Unresponsive Authors, Experimental Flaws : The Impossibility of Assessing the Reproducibility of Previous Human Evaluations in NLP

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Structural brain anomalies in patients with FOXG1 syndrome and in Foxg1+/- mice

Objective FOXG1 syndrome is a rare neurodevelopmental disorder associated with heterozygous FOXG1 variants or chromosomal microaberrations in 14q12. The study aimed at assessing the scope of structural cerebral anomalies revealed by neuroimaging to delineate the genotype and neuroimaging phenotype associations. Methods We compiled 34 patients with a heterozygous (likely) pathogenic FOXG1 variant. Qualitative assessment of cerebral anomalies was performed by standardized re-analysis of all 34 MRI data sets. Statistical analysis of genetic, clinical and neuroimaging data were performed. We quantified clinical and neuroimaging phenotypes using severity scores. Telencephalic phenotypes of adult Foxg1+/- mice were examined using immunohistological stainings followed by quantitative evaluation of structural anomalies. Results Characteristic neuroimaging features included corpus callosum anomalies (82%), thickening of the fornix (74%), simplified gyral pattern (56%), enlargement of inner CSF spaces (44%), hypoplasia of basal ganglia (38%), and hypoplasia of frontal lobes (29%). We observed a marked, filiform thinning of the rostrum as recurrent highly typical pattern of corpus callosum anomaly in combination with distinct thickening of the fornix as a characteristic feature. Thickening of the fornices was not reported previously in FOXG1 syndrome. Simplified gyral pattern occurred significantly more frequently in patients with early truncating variants. Higher clinical severity scores were significantly associated with higher neuroimaging severity scores. Modeling of Foxg1 heterozygosity in mouse brain recapitulated the associated abnormal cerebral morphology phenotypes, including the striking enlargement of the fornix. Interpretation Combination of specific corpus callosum anomalies with simplified gyral pattern and hyperplasia of the fornices is highly characteristic for FOXG1 syndrome.Peer reviewe

Bypassing cellular EGF receptor dependence through epithelial-to-mesenchymal-like transitions

Over 90% of all cancers are carcinomas, malignancies derived from cells of epithelial origin. As carcinomas progress, these tumors may lose epithelial morphology and acquire mesenchymal characteristics which contribute to metastatic potential. An epithelial-to-mesenchymal transition (EMT) similar to the process critical for embryonic development is thought to be an important mechanism for promoting cancer invasion and metastasis. Epithelial-to-mesenchymal transitions have been induced in vitro by transient or unregulated activation of receptor tyrosine kinase signaling pathways, oncogene signaling and disruption of homotypic cell adhesion. These cellular models attempt to mimic the complexity of human carcinomas which respond to autocrine and paracrine signals from both the tumor and its microenvironment. Activation of the epidermal growth factor receptor (EGFR) has been implicated in the neoplastic transformation of solid tumors and overexpression of EGFR has been shown to correlate with poor survival. Notably, epithelial tumor cells have been shown to be significantly more sensitive to EGFR inhibitors than tumor cells which have undergone an EMT-like transition and acquired mesenchymal characteristics, including non-small cell lung (NSCLC), head and neck (HN), bladder, colorectal, pancreas and breast carcinomas. EGFR blockade has also been shown to inhibit cellular migration, suggesting a role for EGFR inhibitors in the control of metastasis. The interaction between EGFR and the multiple signaling nodes which regulate EMT suggest that the combination of an EGFR inhibitor and other molecular targeted agents may offer a novel approach to controlling metastasis

Missing Information, Unresponsive Authors, Experimental Flaws: The Impossibility of Assessing the Reproducibility of Previous Human Evaluations in NLP

We report our efforts in identifying a set of previous human evaluations in NLP that would be suitable for a coordinated study examining what makes human evaluations in NLP more/less reproducible. We present our results and findings, which include that just 13% of papers had (i) sufficiently low barriers to reproduction, and (ii) enough obtainable information, to be considered for reproduction, and that all but one of the experiments we selected for reproduction was discovered to have flaws that made the meaningfulness of conducting a reproduction questionable. As a result, we had to change our coordinated study design from a reproduce approach to a standardise-then-reproduce-twice approach. Our overall (negative) finding that the great majority of human evaluations in NLP is not repeatable and/or not reproducible and/or too flawed to justify reproduction, paints a dire picture, but presents an opportunity for a rethink about how to design and report human evaluations in NLP