For people who are transgender, transsexual, or transitioned (trans), access to primary, emergency, and transition-related health care is often problematic. Results from Phase I of the Trans PULSE Project, a community-based research project in Ontario, Canada, are presented. Based on qualitative data from focus groups with 85 trans community members, a theoretical framework describing how erasure functions to impact experiences interacting with the health care system was developed. Two key sites of erasure were identified: informational erasure and institutional erasure. How these processes work in a mutually reinforcing manner to erase trans individuals and communities and produce a system in which a trans patient or client is seen as an anomaly is shown. Thus, the impetus often falls on trans individuals to attempt to remedy systematic deficiencies. The concept of cisnormativity is introduced to aid in explaining the pervasiveness of trans erasure. Strategies for change are identified.

No abstract

No abstract

BackgroundAcross Europe, Canada, and the United States, 22–43 % of transgender (trans) people report a history of suicide attempts. We aimed to identify intervenable factors (related to social inclusion, transphobia, or sex/gender transition) associated with reduced risk of past-year suicide ideation or attempt, and to quantify the potential population health impact.MethodsThe Trans PULSE respondent-driven sampling (RDS) survey collected data from trans people age 16+ in Ontario, Canada, including 380 who reported on suicide outcomes. Descriptive statistics and multivariable logistic regression models were weighted using RDS II methods. Counterfactual risk ratios and population attributable risks were estimated using model-standardized risks.ResultsAmong trans Ontarians, 35.1 % (95 % CI: 27.6, 42.5) seriously considered, and 11.2 % (95 % CI: 6.0, 16.4) attempted, suicide in the past year. Social support, reduced transphobia, and having any personal identification documents changed to an appropriate sex designation were associated with large relative and absolute reductions in suicide risk, as was completing a medical transition through hormones and/or surgeries (when needed). Parental support for gender identity was associated with reduced ideation. Lower self-reported transphobia (10th versus 90th percentile) was associated with a 66 % reduction in ideation (RR = 0.34, 95 % CI: 0.17, 0.67), and an additional 76 % reduction in attempts among those with ideation (RR = 0.24; 95 % CI: 0.07, 0.82). This corresponds to potential prevention of 160 ideations per 1000 trans persons, and 200 attempts per 1,000 with ideation, based on a hypothetical reduction of transphobia from current levels to the 10th percentile.ConclusionsLarge effect sizes were observed for this controlled analysis of intervenable factors, suggesting that interventions to increase social inclusion and access to medical transition, and to reduce transphobia, have the potential to contribute to substantial reductions in the extremely high prevalences of suicide ideation and attempts within trans populations. Such interventions at the population level may require policy change.

Activity-dependent changes in neuronal excitability and synaptic strength are thought to underlie memory encoding. In hippocampal CA1 neurons, small conductance Ca 2ϩ -activated K ϩ (SK) channels contribute to the afterhyperpolarization, affecting neuronal excitability. In the present study, we examined the effect of apamin-sensitive SK channels on the induction of hippocampal synaptic plasticity in response to a range of stimulation frequencies. In addition, the role of apamin-sensitive SK channels on hippocampal-dependent memory encoding and retention was also tested. The results show that blocking SK channels with apamin increased the excitability of hippocampal neurons and facilitated the induction of synaptic plasticity by shifting the modification threshold to lower frequencies. This facilitation was NMDA receptor (NMDAR) dependent and appeared to be postsynaptic. Mice treated with apamin demonstrated accelerated hippocampal-dependent spatial and nonspatial memory encoding. They required fewer trials to learn the location of a hidden platform in the Morris water maze and less time to encode object memory in an object-recognition task compared with saline-treated mice. Apamin did not influence long-term retention of spatial or nonspatial memory. These data support a role for SK channels in the modulation of hippocampal synaptic plasticity and hippocampal-dependent memory encoding.