Currently in the United Kingdom, anyone donating gametes has the status of an open-identity donor. This means that, at the age of 18, persons conceived with gametes donated since April 1, 2005 have a right to access certain pieces of identifying information about their donor. However, in early 2015, the UK Parliament approved new regulations that make mitochondrial donors anonymous. Both mitochondrial donation and gamete donation are similar in the basic sense that they involve the contribution of gamete materials to create future persons. Given this similarity, this paper presumes that both types of donor should be treated the same and made open-identity under the law, unless there is a convincing argument for treating them differently. I argue that none of the existing arguments that have been made so far in favor of mitochondrial donor anonymity are convincing and mitochondrial donors should therefore be treated as open-identity donors under UK law.
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http://dx.doi.org/10.1093/jmp/jhx022 | DOI Listing |
Biomedicines
January 2025
Division of Hepatic Surgery and Liver Transplantation, Azienda Ospedaliera Universitaria Pisana, Via Paradisa 2, 56124 Pisa, Italy.
: The rising use of liver grafts from donation after circulatory death (DCD) has been enabled by advances in normothermic regional perfusion (NRP) and machine perfusion (MP) technologies. We aimed to identify predictive biomarkers in DCD grafts subjected to NRP, followed by randomization to either normothermic machine perfusion (NMP) or dual hypothermic oxygenated perfusion (D-HOPE). : Among 57 DCD donors, 32 liver grafts were transplanted, and recipients were monitored for one week post-transplant.
View Article and Find Full Text PDFJ Am Chem Soc
January 2025
Key Laboratory of Bioorganic Phosphorus Chemistry and Chemical Biology (Ministry of Education), Department of Chemistry, Tsinghua University, Beijing 100084, P. R. China.
Effective delivery and controlled release of metallo-prodrugs with sustained activation and rapid response feed the needs of precise medicine in metal chemotherapeutics. However, gold-based anticancer drugs often suffer from detoxification binding and extracellular transfer by sulfur-containing peptides. To address this challenge, we integrate a thiol-activated prodrug strategy of newly prepared hypercoordinated carbon-centered gold(I) clusters (HCGCs) with their photosensitization character to augment the mitochondrial release of Au(I) in tumors.
View Article and Find Full Text PDFJ Biol Inorg Chem
December 2024
Department of Chemistry and Biochemistry, University of Toledo, Toledo, OH, USA.
The outer mitochondrial membrane protein known as mitoNEET was discovered when it was labeled by a photoaffinity derivative of the anti-diabetes medication, pioglitazone. The biological role for mitoNEET and its specific mechanism for achieving this remains an active subject for research. There is accumulating evidence suggesting that mitoNEET could be a component of mitochondrial FeS cofactor biogenesis.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Cardiac Surgery, Boston Children's Hospital, 300 Longwood Ave, Boston, MA, 02115, USA.
Heart transplantation remains the ultimate treatment strategy for neonates and children with medically refractory end-stage heart failure and utilization of donors after circulatory death (DCD) can expand th donor pool. We have previously shown that mitochondrial transplantation preserves myocardial function and viability in neonatal swine DCD hearts to levels similar to that observed in donation after brain death (DBD). Herein, we sought to investigate the transcriptomic and proteomic pathways implicated in these phenotypic changes using ex situ perfused swine hearts.
View Article and Find Full Text PDFActa Neuropathol Commun
December 2024
Department of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Mitochondrial dysfunction and α-synuclein (αSyn) aggregation are key contributors to Parkinson's Disease (PD). While genetic and environmental risk factors, including mutations in mitochondrial-associated genes, are implicated in PD, the precise mechanisms linking mitochondrial defects to αSyn pathology remain incompletely understood, hindering the development of effective therapeutic interventions. Here, we identify the loss of branched chain ketoacid dehydrogenase kinase (BCKDK) as a mitochondrial risk factor that exacerbates αSyn pathology by disrupting Complex I function.
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