Structural and biochemical changes in stored platelets are influenced by collection and processing methods. During platelet concentrate storage, lesions can appear of which certain can be involved in adverse reaction after transfusion. The aim of this study was to investigate the lipidome in the supernatant of platelet concentrates (PCs) dependent on processing and storage conditions comparing apheresis (SDA)
versus
buffy coat (BC) platelet concentrate (PC) methods. We investigated various lipid mediator accumulation (Lysophospholipids and Eicosanoids), in either platelet concentrates (SDA-PCs and BC-PCs) stored from 0 to 5 days. All components were produced following French Blood Establishment protocols according to European (EDQM-GTS) Standards; lipids were measured with LS/MS spectrometry. Our data showed no difference between SDA-PC and BC-PC regarding lysophosphatidic acid; however, lysophosphatidylcholine levels were higher in BC-PC than in SDA-PC. Other eicosanoids were affected by either collection or storage conditions of PC. Along the storage, some lipid mediator levels are modulated in SDA-PC and BC-PC. It could be defined as standard platelet components ready for transfusion. To what extent differences, even minimal, matter in clinical outcome remains to be evaluated.
Blood transfusion is a life-saving procedure in which whole blood, or blood components are provided to a patient. Platelet concentrates (PC) may sometimes induce adverse reactions, that are occasionally severe. PC comprise active biomolecules such as cytokines and lipid mediators. Platelet storage lesions are structural and biochemical changes in PC and vary in collection and processing conditions. We investigated lipid mediators as bioactive molecules along storage conditions and in adverse reactions after transfusion. The PC left over were analysed after transfusion, classified with/out severe reaction. Our data presented a decrease of lysophosphatidylcholine species to produce lysophosphatidic acid species. This balance could lead and be correlated with complication symptoms, as other lipids. Lysophosphatidic acid increased with primarily platelet-inhibitor-lipids when single donor apheresis platelet upon storage. Anti-inflammatory and platelet-induced-inhibition lipids were weakly expressed in case of severe adverse reaction. Thus, a decrease in lysophosphatidylcholine and an increase in lysophosphatidic acid could be reliable predictors of serious adverse transfusion reactions transfusion. These data highlighted the importance of PC manufacturing and storage processing, not only to maximize clinical efficacy but also to minimize adverse reactions.
Discerning potential associations between plasma biomarkers and the evolution of suicidal ideation (SI) in mood disorders could advance our understanding of disease progression. We evaluated a cohort of 149 mood disorder patients, assessing 32 plasma soluble proteins implicated in neuroplasticity and inflammation at baseline and six-month follow-up. The primary outcome was the occurrence of suicidal ideation during the six-month follow-up. Secondary outcomes included the presence of suicidal ideation and depression severity at six-month follow-up. We employed Principal Component Analysis and Elastic Net regression for feature extraction and selection. Selected markers were then examined in covariate-adjusted regression models. Our results showed that high baseline levels of interferon-γ and a pro-inflammatory principal component score were linked to the occurrence of SI during follow-up. At the six-month point, SI presence was associated with elevated interferon-γ, interleukin-1β, and diminished serotonin levels, with the latter connection dissipating post-adjustment. High interferon-γ, and low orexin-A at baseline were associated with increased depression severity at follow-up, with specific associations between interferon-γ and anxious symptoms, and orexin-A and atypical depressive symptoms. These findings identify elevated interferon-γ, interleukin-1β, and reduced orexin-A as potential biomarkers associated with the occurrence of SI and severity of depression in mood disorders over six months. With further validation in larger cohorts, these insights could enable more personalized risk assessment and intervention strategies, representing a step forward in improving therapeutic outcomes.
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