Organizational Supports Of Rape Culture In Higher Education

Rape culture has roots in our gendered history of the United States which manifests itself on college campuses as well. Attending college has been found to be the riskiest time for women in terms of sexual assault, as up to 1 in 4 women may experience some type of sexual assault or attempt during their collegiate years. This study explored how one college campus, the University of Vermont (UVM), has organizational policies, procedures and values that are perceived to support rape culture on campus. Guided by critical feminist theory as its epistemological foundation, this qualitative study uses an applied thematic analysis to explore how organizational conditions at UVM help support a rape culture. Ten participants were recruited for the study via snowball sampling. Each participant was identified as current or former staff member, or student at UVM. Each was interviewed using semi-structured interviews. The interviews were analyzed using an applied thematic analysis. Six overarching themes were discovered in the data. Participants identified a series of student cultures like alcohol abuse and a hook-up culture that together support risk taking and contribute to rape culture. Respondents noted a variety of organizational pressures, both external and internal, to the University that were intertwined with their descriptions of rape culture. Pressures from outside the organization tended to be regulative in nature and included specific references to federal or state law, or court actions. Organizational pressures from inside the organization were also regulative in nature, but typically internal policies, procedures and practices were identified. For example, at UVM there are a variety of departments whose policies and procedures are specifically designed to address sexually based violence on campus. These include offices like the Police or the Center for Student Conduct. Interviewees spoke at length about how policies and procedures designed to increase safety and responsibility, can actually contribute to perceived support for rape cultures on campus. Examples include safeguards around alcohol consumption on campus, lengthy Title IX adjudication processes when assaults occur, public image protection, and institutional silencing of victims. Taken together these findings describe a variety of organizational conditions that work to support and perpetuate rape culture, at the same time concerted efforts are made to reduce the likelihood of harm and to promote safety on college campuses. Findings from this study can be used by UVM and other higher education organizations to address organizational structures, actions and policies that have contributed to rape culture

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

The presence of donor-type immunoglobulins in anaemic mice of the W-series transplanted with allogeneic foetal liver cells

W(v)W(v) mice have a genetically determined macrocytic anaemia. They may be cured by the injection of haemopoietic cells derived from foetal liver from haematologically normal mice, owing to the induction of bone marrow chimaerism. Using foetal liver cells from mice that produce immunoglobulins of a different allotype from the anaemic recipients, it is shown that, after a period of time, all cured mice produce immunoglobulins of both the donor and recipient allotypes