Factors Impacting Transgender Patients’ Discomfort with Their Family Physicians: A Respondent-Driven Sampling Survey

Background

Representing approximately 0.5% of the population, transgender (trans) persons in Canada depend on family physicians for both general and transition-related care. However, physicians receive little to no training on this patient population, and trans patients are often profoundly uncomfortable and may avoid health care. This study examined factors associated with patient discomfort discussing trans health issues with a family physician in Ontario, Canada.

Methods

433 trans people age 16 and over were surveyed using respondent-driven sampling for the Trans PULSE Project; 356 had a family physician. Weighted logistic regression models were fit to produce prevalence risk ratios (PRRs) via average marginal predictions, for transmasculine (n = 184) and transfeminine (n = 172) trans persons.

Results

Among the 83.1% (95% CI = 77.4, 88.9) of trans Ontarians who had a family physician, approximately half reported discomfort discussing trans health issues. 37.2% of transmasculine and 38.1% of transfeminine persons reported at least one trans-specific negative experience. In unadjusted analysis, sociodemographics did not predict discomfort, but those who planned to medically transition sex, but had not begun, were more likely to report discomfort (transmasculine: PRR = 2.62 (95% CI = 1.44, 4.77); transfeminine: PRR = 1.85 (95% CI = 1.08, 3.15)). Adjusted for other factors, greater perceived physician knowledge about trans issues was associated with reduced likelihood of discomfort, and previous trans-specific negative experiences with a family physician with increased discomfort. Transfeminine persons who reported three or more types of negative experiences were 2.26 times as likely, and transmasculine persons 1.61 times as likely, to report discomfort. In adjusted analyses, sociodemographic associations differed by gender, with being previously married or having higher education associated with increased risk of discomfort among transfeminine persons, but decreased risk among transmasculine persons.

Conclusions

Within this transgender population, discomfort in discussing trans health issues with a family physician was common, presenting a barrier to accessing primary care despite having a regular family physician and “universal” health insurance.     

Molecular detection of intra-population structure in a threatened potoroid,Potorous tridactylus: conservation management and sampling implications

Fine-scale genetic structure was investigated in three regional populations of the long-nosed potoroo (Potorous tridactylus) a threatened endemic marsupial. Two populations were from the Australian mainland and one from an island. Populations were sub-sampled at two sites, 6–8 km apart, connected by suitable habitat for dispersal. Factors influencing fine-scale structure were investigated by genotyping 157 individuals at 10 microsatellite loci and sequencing a ~621 bp region of the mtDNA control region. Results indicated that P. tridactylus populations exhibit significant intra-population structure, with significant F _ST and Φ _ST values recorded between subpopulations. This structure appeared mediated by small neighbourhood size, female philopatry and limited dispersal over 6–8 km, predominantly by males. Results highlighted several important features of P. tridactylus populations that have implications for conservation. Firstly, the small neighbourhood size suggests any investigations of intra-population structure should be conducted on a finer scale (e.g. 25–50 m) than many current monitoring programs. Secondly, the island populations were genetically depauperate, which may reflect processes occurring in many isolated ‘mainland island’ populations. Thirdly, the lower gene flow identified between populations separated by anthropogenically modified habitat suggests P. tridactylus is sensitive to changes in habitat configuration.     

Comparative in vitro and experimental in vivo studies of the anti–epidermal growth factor receptor antibody nimotuzumab and its aglycosylated form produced in transgenic tobacco plants

A broad variety of foreign genes can be expressed in transgenic plants, which offer the opportunity for large‐scale production of pharmaceutical proteins, such as therapeutic antibodies. Nimotuzumab is a humanized anti–epidermal growth factor receptor (EGFR) recombinant IgG1 antibody approved in different countries for the treatment of head and neck squamous cell carcinoma, paediatric and adult glioma, and nasopharyngeal and oesophageal cancers. Because the antitumour mechanism of nimotuzumab is mainly attributed to its ability to interrupt the signal transduction cascade triggered by EGF/EGFR interaction, we have hypothesized that an aglycosylated form of this antibody, produced by mutating the N₂₉₇ position in the IgG₁ Fc region gene, would have similar biochemical and biological properties as the mammalian‐cell‐produced glycosylated counterpart. In this paper, we report the production and characterization of an aglycosylated form of nimotuzumab in transgenic tobacco plants. The comparison of the plantibody and nimotuzumab in terms of recognition of human EGFR, effect on tyrosine phosphorylation and proliferation in cells in response to EGF, competition with radiolabelled EGF for EGFR, affinity measurements of Fab fragments, pharmacokinetic and biodistribution behaviours in rats and antitumour effects in nude mice bearing human A431 tumours showed that both antibody forms have very similar in vitro and in vivo properties. Our results support the idea that the production of aglycosylated forms of some therapeutic antibodies in transgenic plants is a feasible approach when facing scaling strategies for anticancer immunoglobulins.     

Modulation ofTcf7l2 expression alters behavior in mice

The comorbidity of type 2 diabetes (T2D) with several psychiatric diseases is well established. While environmental factors may partially account for these co-occurrences, common genetic susceptibilities could also be implicated in the confluence of these diseases. In support of shared genetic burdens, TCF7L2, the strongest genetic determinant for T2D risk in the human population, has been recently implicated in schizophrenia (SCZ) risk, suggesting that this may be one of many loci that pleiotropically influence both diseases. To investigate whether Tcf7l2 is involved in behavioral phenotypes in addition to its roles in glucose metabolism, we conducted several behavioral tests in mice with null alleles of Tcf7l2 or overexpressing Tcf7l2. We identified a role for Tcf7l2 in anxiety-like behavior and a dose-dependent effect of Tcf7l2 alleles on fear learning. None of the mutant mice showed differences in prepulse inhibition (PPI), which is a well-established endophenotype for SCZ. These results show that Tcf7l2 alters behavior in mice. Importantly, these differences are observed prior to the onset of detectable glucose metabolism abnormalities. Whether these differences are related to human anxiety-disorders or schizophrenia remains to be determined. These animal models have the potential to elucidate the molecular basis of psychiatric comorbidities in diabetes and should therefore be studied further.     

The Sea Peoples, from cuneiform tablets to carbon dating

The 13(th) century BC witnessed the zenith of the Aegean and Eastern Mediterranean civilizations which declined at the end of the Bronze Age, ～3200 years ago. Weakening of this ancient flourishing Mediterranean world shifted the political and economic centres of gravity away from the Levant towards Classical Greece and Rome, and led, in the long term, to the emergence of the modern western civilizations. Textual evidence from cuneiform tablets and Egyptian reliefs from the New Kingdom relate that seafaring tribes, the Sea Peoples, were the final catalyst that put the fall of cities and states in motion. However, the lack of a stratified radiocarbon-based archaeology for the Sea People event has led to a floating historical chronology derived from a variety of sources spanning dispersed areas. Here, we report a stratified radiocarbon-based archaeology with anchor points in ancient epigraphic-literary sources, Hittite-Levantine-Egyptian kings and astronomical observations to precisely date the Sea People event. By confronting historical and science-based archaeology, we establish an absolute age range of 1192-1190 BC for terminal destructions and cultural collapse in the northern Levant. This radiocarbon-based archaeology has far-reaching implications for the wider Mediterranean, where an elaborate network of international relations and commercial activities are intertwined with the history of civilizations.     

Growth anomalies on the coral genera Acropora and Porites are strongly associated with host density and human population size across the Indo-Pacific

Growth anomalies (GAs) are common, tumor-like diseases that can cause significant morbidity and decreased fecundity in the major Indo-Pacific reef-building coral genera, Acropora and Porites. GAs are unusually tractable for testing hypotheses about drivers of coral disease because of their pan-Pacific distributions, relatively high occurrence, and unambiguous ease of identification. We modeled multiple disease-environment associations that may underlie the prevalence of Acropora growth anomalies (AGA) (n = 304 surveys) and Porites growth anomalies (PGA) (n = 602 surveys) from across the Indo-Pacific. Nine predictor variables were modeled, including coral host abundance, human population size, and sea surface temperature and ultra-violet radiation anomalies. Prevalence of both AGAs and PGAs were strongly host density-dependent. PGAs additionally showed strong positive associations with human population size. Although this association has been widely posited, this is one of the first broad-scale studies unambiguously linking a coral disease with human population size. These results emphasize that individual coral diseases can show relatively distinct patterns of association with environmental predictors, even in similar diseases (growth anomalies) found on different host genera (Acropora vs. Porites). As human densities and environmental degradation increase globally, the prevalence of coral diseases like PGAs could increase accordingly, halted only perhaps by declines in host density below thresholds required for disease establishment.     

Dispersal and species’ responses to climate change

Dispersal is fundamental in determining biodiversity responses to rapid climate change, but recently acquired ecological and evolutionary knowledge is seldom accounted for in either predictive methods or conservation planning. We emphasise the accumulating evidence for direct and indirect impacts of climate change on dispersal. Additionally, evolutionary theory predicts increases in dispersal at expanding range margins, and this has been observed in a number of species. This multitude of ecological and evolutionary processes is likely to lead to complex responses of dispersal to climate change. As a result, improvement of models of species’ range changes will require greater realism in the representation of dispersal. Placing dispersal at the heart of our thinking will facilitate development of conservation strategies that are resilient to climate change, including landscape management and assisted colonisation. Synthesis This article seeks synthesis across the fields of dispersal ecology and evolution, species distribution modelling and conservation biology. Increasing effort focuses on understanding how dispersal influences species' responses to climate change. Importantly, though perhaps not broadly widely‐recognised, species' dispersal characteristics are themselves likely to alter during rapid climate change. We compile evidence for direct and indirect influences that climate change may have on dispersal, some ecological and others evolutionary. We emphasise the need for predictive modelling to account for this dispersal realism and highlight the need for conservation to make better use of our existing knowledge related to dispersal.     

White doctors and nurses on racial inequality in health care in the USA: whiteness and colour-blind racial ideology

In this paper we report on an interdisciplinary project interviewing doctors and nurses about racial inequality in health care in the USA. We analysed data from interviews with twenty-two white doctors and nurses in which they were asked to offer explanations for racial inequality in health care. Results provide insight into how whiteness operates to provide white patients more often with appropriate health care and how colour-blind ideology can be adapted to accommodate naming white advantage and potential racial discrimination. However, even when naming mechanisms of white advantage in accessing resources, the white respondents avoided acknowledging how they are implicated in racial inequality in health care. We discuss the implications for understanding whiteness and colour-blind ideology.     

Phospholipase D Toxins of Brown Spider Venom Convert Lysophosphatidylcholine and Sphingomyelin to Cyclic Phosphates

Venoms of brown spiders in the genus Loxosceles contain phospholipase D enzyme toxins that can cause severe dermonecrosis and even death in humans. These toxins cleave the substrates sphingomyelin and lysophosphatidylcholine in mammalian tissues, releasing the choline head group. The other products of substrate cleavage have previously been reported to be monoester phospholipids, which would result from substrate hydrolysis. Using ³¹P NMR and mass spectrometry we demonstrate that recombinant toxins, as well as whole venoms from diverse Loxosceles species, exclusively catalyze transphosphatidylation rather than hydrolysis, forming cyclic phosphate products from both major substrates. Cyclic phosphates have vastly different biological properties from their monoester counterparts, and they may be relevant to the pathology of brown spider envenomation.