Compulsory Heterosexuality and Lesbian Invisibility in Nursing.

Lesbian nurses have historically been silenced, but diversity initiatives within professional health programs suggest a need to initiate scholarly discussions that explore heteronormativity as increasing the risk of harm for nonheterosexual nurses as compared to their heterosexual counterparts. Nurses can reflect on relative privilege within the profession to better understand the ways in which normative health practices perpetuate adverse health outcomes among vulnerable patient populations. Nurses from diverse backgrounds, such as this lesbian author, offer insight into how the nursing profession might illuminate relational aspects of privilege.

Queer Phenomenology, the Disruption of Heteronormativity, and Structurally Responsive Care.

Lesbian, gay, bisexual, transgender, and queer (LGBTQ) health disparities persist and reflect larger structural inequities that negatively impact the health of historically marginalized communities. By way of using queer phenomenology, the author analyzes a personal experience that was harmful to her as a lesbian patient who required emergency medical attention. Also a registered nurse, the author draws on her lived experiences to reveal heteronormativity as a prevalent, but largely unacknowledged, source of structural harms for LGBTQ patients.

Correction to: Vulnerability, Harm, and Compromised Ethics Revealed by the Experiences of Queer Birthing Women in Rural Healthcare.

The following Acknowledgments were omitted in the original publication.

Vulnerability, Harm, and Compromised Ethics Revealed by the Experiences of Queer Birthing Women in Rural Healthcare.

Phenomenological interviews with queer women in rural Nova Scotia reveal significant forms of trauma experienced during labour and birth. Situating the accounts of participants within both phenomenological and intersectional analyses reveals harms enabled by structurally embedded heteronormative and homophobic healthcare practices and policies. Our account illustrates the breadth and depth of harm experienced and outlines how these violate core ethical principles and values in healthcare.

Accessing new understandings of trauma-informed care with queer birthing women in a rural context.

Aims And Objectives: Participant narratives from a feminist and queer phenomenological study aim to broaden current understandings of trauma. Examining structural marginalisation within perinatal care relationships provides insights into the impact of dominant models of care on queer birthing women. More specifically, validation of queer experience as a key finding from the study offers trauma-informed strategies that reconstruct formerly disempowering perinatal relationships.

Hyperactivated Wnt signaling induces synthetic lethal interaction with Rb inactivation by elevating TORC1 activities.

Inactivation of the Rb tumor suppressor can lead to increased cell proliferation or cell death depending on specific cellular context. Therefore, identification of the interacting pathways that modulate the effect of Rb loss will provide novel insights into the roles of Rb in cancer development and promote new therapeutic strategies. Here, we identify a novel synthetic lethal interaction between Rb inactivation and deregulated Wg/Wnt signaling through unbiased genetic screens.

Proteins in the nutrient-sensing and DNA damage checkpoint pathways cooperate to restrain mitotic progression following DNA damage.

Checkpoint pathways regulate genomic integrity in part by blocking anaphase until all chromosomes have been completely replicated, repaired, and correctly aligned on the spindle. In Saccharomyces cerevisiae, DNA damage and mono-oriented or unattached kinetochores trigger checkpoint pathways that bifurcate to regulate both the metaphase to anaphase transition and mitotic exit. The sensor-associated kinase, Mec1, phosphorylates two downstream kinases, Chk1 and Rad53.

Ginsenoside Rh2 induces apoptosis and paraptosis-like cell death in colorectal cancer cells through activation of p53.

Ginsenosides are the main bioactive components in American ginseng, a commonly used herb. In this study, we showed that the ginsenoside Rh2 exhibited significantly more potent cell death activity than the ginsenoside Rg3 in HCT116 and SW480 colorectal cancer cells. Cell death induced by Rh2 is mediated in part by the caspase-dependent apoptosis and in part by the caspase-independent paraptosis, a type of cell death that is characterized by the accumulation of cytoplasmic vacuoles.

Targeting Rb mutant cancers by inactivating TSC2.

Retinoblastoma (Rb), a tumor suppressor gene, is inactivated in many types of cancer. However little is known about how the loss of Rb function can be targeted in cancer therapies. We have identified that inactivation of TSC2 in Rb mutant cancer cells will induce a synergistic cell death.

A role for Saccharomyces cerevisiae Chk1p in the response to replication blocks.

Replication blocks and DNA damage incurred during S phase activate the S-phase and intra-S-phase checkpoint responses, respectively, regulated by the Atrp and Chk1p checkpoint kinases in metazoans. In Saccharomyces cerevisiae, these checkpoints are regulated by the Atrp homologue Mec1p and the kinase Rad53p. A conserved role of these checkpoints is to block mitotic progression until DNA replication and repair are completed.

Stopped for repairs: a new role for nutrient sensing pathways?

In order to prevent division of damaged chromosomes, cells activate a checkpoint to inhibit mitotic progression in order to repair the damaged DNA. Upon detection of DNA damage two downstream checkpoint kinases, Chk1 and Rad53, are activated by the sensor kinase, Mec1, to block the metaphase to anaphase transition and mitotic exit, respectively. Recent data from studies with budding yeast suggested that the DNA damage checkpoint also enlists the cAMP dependent protein kinase (PKA) pathway, which is an integral part of the nutrient sensing mechanism in budding yeast, to inhibit mitosis in response to DNA damage.

The DNA damage checkpoint and PKA pathways converge on APC substrates and Cdc20 to regulate mitotic progression.

The conserved checkpoint kinases Chk1 and Rad53-Dun1 block the metaphase to anaphase transition by the phosphorylation and stabilization of securin, and block the mitotic exit network regulated by the Bfa1-Bub2 complex. However, both chk1 and rad53 mutants are able to exit from mitosis and initiate a new cell cycle, suggesting that both pathways have supporting functions in restraining anaphase and in blocking the inactivation of mitotic cyclin-Cdk1 complexes. Here we find that the cyclic-AMP-dependent protein kinase (PKA) pathway supports Chk1 in the regulation of mitosis by targeting the mitotic inducer Cdc20.