Prevalence of red blood cell alloimmunization in multiply transfused patients

Introduction: To analyze the prevalence of alloantibodies in multiply transfused patients. Methods: This study was a retrospective, exploratory and descriptive study with a quantitative approach. The study sample comprised 185 patients transfused at a referral service in the city of Passo Fundo, Rio Grande do Sul, from January 2016 to February 2018. Results: Overall, the antibodies identified were as follows: anti-E in 47 patients (18%), anti-D and anti-K in 28 patients each (11%), anti-C in 21 patients (8.1%), and inconclusive antibody results in 23 patients (8.9%). Females were a majority (55.7%), mean age was 48.8 years and mean quantity of blood transfused was 7.2 bags. Cardiovascular disorders were the most common comorbidities, in 39 patients (21.2%), followed by oncological disorders, in 38 patients (18.4%). Conclusion: Alloimmunization is an important and frequent clinical condition that increases the risk of hemolytic reactions and is associated with significant patient morbidity and mortality

Selective Disruption of Mitochondrial Thiol Redox State in Cells and In Vivo.

Mitochondrial glutathione (GSH) and thioredoxin (Trx) systems function independently of the rest of the cell. While maintenance of mitochondrial thiol redox state is thought vital for cell survival, this was not testable due to the difficulty of manipulating the organelle's thiol systems independently of those in other cell compartments. To overcome this constraint we modified the glutathione S-transferase substrate and Trx reductase (TrxR) inhibitor, 1-chloro-2,4-dinitrobenzene (CDNB) by conjugation to the mitochondria-targeting triphenylphosphonium cation. The result, MitoCDNB, is taken up by mitochondria where it selectively depletes the mitochondrial GSH pool, catalyzed by glutathione S-transferases, and directly inhibits mitochondrial TrxR2 and peroxiredoxin 3, a peroxidase. Importantly, MitoCDNB inactivates mitochondrial thiol redox homeostasis in isolated cells and in vivo, without affecting that of the cytosol. Consequently, MitoCDNB enables assessment of the biomedical importance of mitochondrial thiol homeostasis in reactive oxygen species production, organelle dynamics, redox signaling, and cell death in cells and in vivo.We acknowledge the Biotechnology and Biological Sciences Research Council (BB/I012826/1), the Wellcome Trust (WT110158/Z/15/Z, 110159/Z/15/Z and RG88195), the University of Glasgow (JMG Studentship), and the Medical Research Council (MC_U105663142 and MC_ UU_00015/7)

Prevalence of red blood cell alloimmunization in multiply transfused patients

Introduction: To analyze the prevalence of alloantibodies in multiply transfused patients. Methods: This study was a retrospective, exploratory and descriptive study with a quantitative approach. The study sample comprised 185 patients transfused at a referral service in the city of Passo Fundo, Rio Grande do Sul, from January 2016 to February 2018. Results: Overall, the antibodies identified were as follows: anti-E in 47 patients (18%), anti-D and anti-K in 28 patients each (11%), anti-C in 21 patients (8.1%), and inconclusive antibody results in 23 patients (8.9%). Females were a majority (55.7%), mean age was 48.8 years and mean quantity of blood transfused was 7.2 bags. Cardiovascular disorders were the most common comorbidities, in 39 patients (21.2%), followed by oncological disorders, in 38 patients (18.4%). Conclusion: Alloimmunization is an important and frequent clinical condition that increases the risk of hemolytic reactions and is associated with significant patient morbidity and mortality

Selective Disruption of Mitochondrial Thiol Redox State in Cells and In Vivo.

Mitochondrial glutathione (GSH) and thioredoxin (Trx) systems function independently of the rest of the cell. While maintenance of mitochondrial thiol redox state is thought vital for cell survival, this was not testable due to the difficulty of manipulating the organelle's thiol systems independently of those in other cell compartments. To overcome this constraint we modified the glutathione S-transferase substrate and Trx reductase (TrxR) inhibitor, 1-chloro-2,4-dinitrobenzene (CDNB) by conjugation to the mitochondria-targeting triphenylphosphonium cation. The result, MitoCDNB, is taken up by mitochondria where it selectively depletes the mitochondrial GSH pool, catalyzed by glutathione S-transferases, and directly inhibits mitochondrial TrxR2 and peroxiredoxin 3, a peroxidase. Importantly, MitoCDNB inactivates mitochondrial thiol redox homeostasis in isolated cells and in vivo, without affecting that of the cytosol. Consequently, MitoCDNB enables assessment of the biomedical importance of mitochondrial thiol homeostasis in reactive oxygen species production, organelle dynamics, redox signaling, and cell death in cells and in vivo.We acknowledge the Biotechnology and Biological Sciences Research Council (BB/I012826/1), the Wellcome Trust (WT110158/Z/15/Z, 110159/Z/15/Z and RG88195), the University of Glasgow (JMG Studentship), and the Medical Research Council (MC_U105663142 and MC_ UU_00015/7)