305 research outputs found
Coming Out to Doctors, Coming Out to ‘‘Everyone’’: Understanding the Average Sequence of Transgender Identity Disclosures Using Social Media Data
Purpose: Gender transition is a complex life change, and transgender identity disclosures are pivotal moments that delineate the gender transition process. The purpose of this study was to quantify the average sequence in which transgender people disclose their transgender identity to different people in their lives, such as medical professionals, family members, and online networks, and to understand the emotional implications of these disclosures.
Methods: We used mixed methods to identify 362 transgender identity disclosure social media posts within 41,066 total posts from 240 Tumblr transition blogs (online spaces in which transgender people document gender transitions). We manually assigned each disclosure post an audience category, and then calculated the average sequence in which people in this sample disclosed their transgender identity to different audiences.
Results: Health professionals, such as physicians and therapists, were on average some of the very first people to whom transgender Tumblr bloggers disclosed their transgender identity. Such disclosures were often anxiety provoking and emotionally difficult, whether intentional or involuntary. Next, they often disclosed to friends, followed by close family (e.g., parents and siblings) and then extended family (e.g., grandparents). Mass disclosures to large portions of a person's network, such as on one's Facebook profile, usually came late in the disclosure process.
Conclusion: Gender transition is a staged process that includes a series of disclosures to different audiences that follows an average sequence. Because health care providers (e.g., physicians and therapists) who work with transgender patients are often some of the very first people to whom transgender people in our sample disclosed, providers must practice extra sensitivity when responding to such disclosures.National Science Foundation Graduate Research Fellowships Program Grant No. DGE-1321846University of California, Irvine, James Harvey Scholar AwardPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/155363/1/trgh.2019.0045.pdfDescription of trgh.2019.0045.pdf : Main articl
The Influence of Signaling Conspecific and Heterospecific Neighbors on Eavesdropper Pressure
The study of tradeoffs between the attraction of mates and the attraction of eavesdropping predators and parasites has generally focused on a single species of prey, signaling in isolation. In nature, however, animals often signal from mixed-species aggregations, where interactions with heterospecific group members may be an important mechanism modulating tradeoffs between sexual and natural selection, and thus driving signal evolution. Although studies have shown that conspecific signalers can influence eavesdropper pressure on mating signals, the effects of signaling heterospecifics on eavesdropper pressure, and on the balance between natural and sexual selection, are likely to be different. Here, we review the role of neighboring signalers in mediating changes in eavesdropper pressure, and present a simple model that explores how selection imposed by eavesdropping enemies varies as a function of a signaling aggregation\u27s species composition, the attractiveness of aggregation members to eavesdroppers, and the eavesdroppers\u27 preferences for different member types. This approach can be used to model mixed-species signaling aggregations, as well as same-species aggregations, including those with non-signaling individuals, such as satellites or females. We discuss the implications of our model for the evolution of signal structure, signaling behavior, mixed-species aggregations, and community dynamics
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Some physical studies on ribonuclease-S and its component parts, S-protein and S-peptide
Striated Rootlet and Nonfilamentous Forms of Rootletin Maintain Ciliary Function
SummaryPrimary cilia are microtubule-based sensory organelles whose structures and functions must be actively maintained throughout animal lifespan to support signal transduction pathways essential for development and physiological processes such as vision and olfaction [1]. Remarkably, few cellular components aside from the intraflagellar transport (IFT) machinery are implicated in ciliary maintenance [2]. Rootletin, an evolutionarily conserved protein found as prominent striated rootlets or a nonfilamentous form, both of which are associated with cilium-anchoring basal bodies, represents a likely candidate given its well-known role in preventing ciliary photoreceptor degeneration in a mouse model [3, 4]. Whether rootletin is universally required for maintaining ciliary integrity, and if so, by what mechanism, remains unresolved. Here, we demonstrate that the gene disrupted in the previously isolated C. elegans chemosensory mutant che-10 encodes a rootletin ortholog that localizes proximally and distally to basal bodies of cilia harboring or lacking conspicuous rootlets. In vivo analyses reveal that CHE-10/rootletin maintains ciliary integrity partly by modulating the assembly, motility, and flux of IFT particles, which are critical for axoneme length control. Surprisingly, CHE-10/rootletin is also essential for stabilizing ciliary transition zones and basal bodies, roles not ascribed to IFT. Unifying these findings, we provide evidence that the underlying molecular defects in the che-10 mutant stem from disrupted organization/function of the periciliary membrane, affecting the efficient delivery of basal body-associated and ciliary components and resulting in cilium degeneration. Together, our cloning and functional analyses of C. elegans che-10 provide the first mechanistic insights into how filamentous and nonfilamentous forms of rootletin play essential roles in maintaining ciliary function in metazoans
A multi-mRNA host-response molecular blood test for the diagnosis and prognosis of acute infections and sepsis: Proceedings from a clinical advisory panel
Current diagnostics are insufficient for diagnosis and prognosis of acute infections and sepsis. Clinical decisions including prescription and timing of antibiotics, ordering of additional diagnostics and level-of-care decisions rely on understanding etiology and implications of a clinical presentation. Host mRNA signatures can differentiate infectious from noninfectious etiologies, bacterial from viral infections, and predict 30-day mortality. The 29-host-mRNA blood-based InSe
Reduced Efficacy of Anti-A\u3cem\u3eβ\u3c/em\u3e Immunotherapy in a Mouse Model of Amyloid Deposition and Vascular Cognitive Impairment Comorbidity
Vascular cognitive impairment and dementia (VCID) is the second most common form of dementia behind Alzheimer\u27s disease (AD). It is estimated that 40% of AD patients also have some form of VCID. One promising therapeutic for AD is anti-Aβ immunotherapy, which uses antibodies against Aβ to clear it from the brain. While successful in clearing Aβ and improving cognition in mice, anti-Aβ immunotherapy failed to reach primary cognitive outcomes in several different clinical trials. We hypothesized that one potential reason the anti-Aβ immunotherapy clinical trials were unsuccessful was due to this high percentage of VCID comorbidity in the AD population. We used our unique model of VCID-amyloid comorbidity to test this hypothesis. We placed 9-month-old wild-type and APP/PS1 mice on either a control diet or a diet that induces hyperhomocysteinemia (HHcy). After being placed on the diet for 3 months, the mice then received intraperotineal injections of either IgG2a control or 3D6 for another 3 months. While we found that treatment of our comorbidity model with 3D6 resulted in decreased total Aβ levels, there was no cognitive benefit of the anti-Aβ immunotherapy in our AD/VCID mice. Further, microhemorrhages were increased by 3D6 in the APP/PS1/control but further increased in an additive fashion when 3D6 was administered to the APP/PS1/HHcy mice. This suggests that the use of anti-Aβ immunotherapy in patients with both AD and VCID would be ineffective on cognitive outcomes
Apparent Loss of Vibrio vulnificus from North Carolina Oysters Coincides with a Drought-Induced Increase in Salinity
ABSTRACT Despite years of successful isolation of Vibrio vulnificus from estuarine waters, beginning in 2007, it was extremely difficult to culture V. vulnificus from either North Carolina estuarine water or oyster samples. After employing culture-based methods as well as PCR and quantitative PCR for the detection of V. vulnificus , always with negative results, we concluded that this pathogen had become nearly undetectable in the North Carolina estuarine ecosystem. We ensured that the techniques were sound by seeding North Carolina oysters with V. vulnificus and performing the same tests as those previously conducted on unadulterated oysters. V. vulnificus was readily detected in the seeded oysters using both classes of methods. Furthermore, oysters were obtained from the Gulf of Mexico, and V. vulnificus was easily isolated, confirming that the methodology was sound but that the oysters and waters of North Carolina were lacking the V. vulnificus population studied for decades. Strikingly, the apparent loss of detectable V. vulnificus coincided with the most severe drought in the history of North Carolina. The drought continued until the end of 2009, with an elevated water column salinity being observed throughout this period and with V. vulnificus being nearly nonexistent. When salinities returned to normal after the drought abated in 2010, we were again able to routinely isolate V. vulnificus from the water column, although we were still unable to culture it from oysters. We suggest that the oysters were colonized with a more salt-tolerant bacterium during the drought, which displaced V. vulnificus and may be preventing recolonization
Measurement of Biodiversity (MoB): A method to separate the scale-dependent effects of species abundance distribution, density, and aggregation on diversity change
Little consensus has emerged regarding how proximate and ultimate drivers such as productivity, disturbance and temperature may affect species richness and other aspects of biodiversity. Part of the confusion is that most studies examine species richness at a single spatial scale and ignore how the underlying components of species richness can vary with spatial scale. We provide an approach for the measurement of biodiversity that decomposes changes in species rarefaction curves into proximate components attributed to: (a) the species abundance distribution, (b) density of individuals and (c) the spatial arrangement of individuals. We decompose species richness by comparing spatial and nonspatial sample- and individual-based species rarefaction curves that differentially capture the influence of these components to estimate the relative importance of each in driving patterns of species richness change. We tested the validity of our method on simulated data, and we demonstrate it on empirical data on plant species richness in invaded and uninvaded woodlands. We integrated these methods into a new r package (mobr). The metrics that mobr provides will allow ecologists to move beyond comparisons of species richness in response to ecological drivers at a single spatial scale toward a dissection of the proximate components that determine species richness across scales
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