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1.
J Genet Couns ; 2024 Jan 11.
Article in English | MEDLINE | ID: mdl-38213115

ABSTRACT

Medical assistance in dying (MAiD) is the Canadian equivalent of Physician aid-in-dying (PAD) in the United States. Through changes to the eligibility criteria for MAiD in 2021, Canada now has one of the most permissive assisted dying regimens in the world. This study describes Canadian genetic counselors' experiences, knowledge, and preparedness to discuss MAiD with their patients. Survey responses were collected from Canadian genetic counselors (n = 44) and were followed by semi-structured interviews with 14 survey participants. Survey data were analyzed using descriptive statistics, and interview transcripts were analyzed using phronetic iterative analysis and an interpretive description approach. Survey data revealed that genetic counselors have discussed MAiD with patients referred for cancer, neurologic, metabolic, connective tissue, and cardiac indications (n = 18, 40.9%). While most thought that it was important for genetic counselors to be knowledgeable of (n = 41, 93.2%) and prepared to discuss MAiD (n = 43, 97.7%), many were not familiar with the eligibility criteria (n = 27, 61.4%) and the process for accessing MAiD in Canada (n = 29, 65.9%). Interview participants described discussions about MAiD that were initiated by themselves or their patients. Most participants felt prepared to explore a patient's thoughts about MAiD when the patient initiated the discussion but did not feel well-prepared to share detailed information about MAiD. Participants were interested in education and professional guidance to assist them in preparing to discuss MAiD. Learning objectives were developed based on participants' suggestions to assist genetic counselors in their clinical work and self-directed research and to aid in the development of professional guidelines and educational materials for practicing genetic counselors and genetic counseling trainees. As genetic counselors continue engaging in discussions about MAiD, it is critical that these sensitive conversations are approached with increased knowledge and awareness of MAiD legislation, the ethical issues surrounding MAiD in Canada, and relevant patient resources.

2.
Sci Rep ; 11(1): 21657, 2021 11 04.
Article in English | MEDLINE | ID: mdl-34737324

ABSTRACT

Cell lines are widely used in research and for diagnostic tests and are often shared between laboratories. Lack of cell line authentication can result in the use of contaminated or misidentified cell lines, potentially affecting the results from research and diagnostic activities. Cell line authentication and contamination detection based on metagenomic high-throughput sequencing (HTS) was tested on DNA and RNA from 63 cell lines available at the Canadian Food Inspection Agency's National Centre for Foreign Animal Disease. Through sequence comparison of the cytochrome c oxidase subunit 1 (COX1) gene, the species identity of 53 cell lines was confirmed, and eight cell lines were found to show a greater pairwise nucleotide identity in the COX1 sequence of a different species within the same expected genus. Two cell lines, LFBK-αvß6 and SCP-HS, were determined to be composed of cells from a different species and genus. Mycoplasma contamination was not detected in any cell lines. However, several expected and unexpected viral sequences were detected, including part of the classical swine fever virus genome in the IB-RS-2 Clone D10 cell line. Metagenomics-based HTS is a useful laboratory QA tool for cell line authentication and contamination detection that should be conducted regularly.


Subject(s)
Cell Line Authentication/methods , Cell Line/classification , Cyclooxygenase 1/genetics , Animals , Genome/genetics , High-Throughput Nucleotide Sequencing/methods , Humans , Mycoplasma/genetics , Polymerase Chain Reaction/methods , Species Specificity
3.
Pharmacol Ther ; 225: 107840, 2021 09.
Article in English | MEDLINE | ID: mdl-33753132

ABSTRACT

Purinergic signaling encompasses the cycle of adenosine 5' triphosphate (ATP) release and its metabolism into nucleotide and nucleoside derivatives, the direct release of nucleosides, and subsequent receptor-triggered downstream intracellular pathways. Since the discovery of nerve terminal and glial ATP release into the neuropil, purinergic signaling has been implicated in the modulation of nervous system development, function, and disease. In this review, we detail our current understanding of the roles of the pannexin 1 (PANX1) ATP-release channel in neuronal development and plasticity, glial signaling, and neuron-glial-immune interactions. We additionally provide an overview of PANX1 structure, activation, and permeability to orientate readers and highlight recent research developments. We identify areas of convergence between PANX1 and purinergic receptor actions. Additional highlights include data on PANX1's participation in the pathophysiology of nervous system developmental, degenerative, and inflammatory disorders. Our aim in combining this knowledge is to facilitate the movement of our current understanding of PANX1 in the context of other nervous system purinergic signaling mechanisms one step closer to clinical translation.


Subject(s)
Adenosine Triphosphate , Connexins , Nerve Tissue Proteins , Signal Transduction , Adenosine Triphosphate/metabolism , Connexins/metabolism , Humans , Nerve Tissue Proteins/metabolism , Nervous System Diseases , Neurons
4.
eNeuro ; 7(4)2020.
Article in English | MEDLINE | ID: mdl-32737184

ABSTRACT

The integration of neurons into networks relies on the formation of dendritic spines. These specialized structures arise from dynamic filopodia-like dendritic protrusions. It was recently reported that cortical neurons lacking the channel protein pannexin 1 (PANX1) exhibited higher dendritic spine densities. Here, we expanded on those findings to investigate, at an earlier developmental time point (with more abundant dendritic protrusions), whether differences in the properties of dendritic protrusion dynamics could contribute to this previously discovered phenomenon. Using a fluorescent membrane tag (mCherry-CD9-10) to visualize dendritic protrusions in developing neurons [at 10 d in vitro (DIV10)], we confirmed that lack of PANX1 led to higher protrusion density, while transient transfection of Panx1 led to decreased protrusion density. To quantify the impact of PANX1 expression on protrusion formation, elimination, and motility, we used live cell imaging in DIV10 neurons (one frame every 5 s for 10 min). We discovered that at DIV10, loss of PANX1 stabilized protrusions. Notably, re-expression of PANX1 in Panx1 knock-out (KO) neurons resulted in a significant increase in protrusion motility and turnover. In summary, these new data revealed that PANX1 could regulate the development of dendritic spines, in part, by controlling dendritic protrusion dynamics.


Subject(s)
Dendritic Spines , Neural Stem Cells , Neurons , Pseudopodia
5.
Cell Calcium ; 90: 102253, 2020 09.
Article in English | MEDLINE | ID: mdl-32688074

ABSTRACT

A new study by Yang and colleagues has revealed that TNF-alpha regulates PANX1 levels through an NF-kB-dependent mechanism in human endothelial cells. PANX1 modulates Ca2+ influx contributing to IL-1beta production independent of purinergic signaling. These novel findings expand our understanding of TNF-alpha-mediated upregulation of IL-1beta with implications for responses to tissue injury and infection.


Subject(s)
Connexins/metabolism , Infections/metabolism , Infections/pathology , Inflammation/metabolism , Inflammation/pathology , Nerve Tissue Proteins/metabolism , Human Umbilical Vein Endothelial Cells/metabolism , Humans , Inflammasomes/metabolism , Models, Biological , Signal Transduction , Tumor Necrosis Factor-alpha/metabolism
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