Plasma levels of selected proteins of coagulation, fibrinolysis and complement from patients with septic shock have been investigated. All values were corrected on the basis of a plasma protein content of 5.5%. Considerable decreases were found in the plasma levels of the contact factors activity. The antigen content in the case of HMW-kininogen remained in the normal range, whereas in the case of prekallikrein it dropped to about 30% of norm. Considering the proteins of the unspecific defense and the complement system, primarily HRG, alpha 2-macroglobulin and C4 showed remarkable decreases. From the changes of the plasma levels of the considered proteins one can conclude that in septic shock primarily the contact phase of coagulation and the alternative pathway of complement are involved. The consumption of F XIII points to a thrombin generation during shock. The marked reduction of the C4-component could be due to an isolated proteolysis of this component, since the classical pathway of complement activation seems not to be involved in the shock events. Serial controls of the plasma levels of the proteins under investigation showed in some patients considerable individual deviations from the general trend. A considerable increase of the F XIII A level appears to be a prognostically favorable result, whereas constantly low values of F XIII and fibronectin without a tendency to normalization or a constant decrease of these proteins often is connected with a fatal outcome.
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Cardiovasc Diabetol
January 2025
Department of Cardiology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Nanjing, 210009, Jiangsu, China.
Background: Atherosclerotic dyslipidemia is associated with an increased risk of type 2 diabetes (T2D). Although previous studies have demonstrated an association between the atherogenic index of plasma (AIP) and insulin resistance, there remains a scarcity of large cohort studies investigating the association between AIP and the long-term risk of T2D in the general population. This study aims to investigate the potential association between AIP and the long-term risk of T2D in individuals with normal fasting plasma glucose levels.
View Article and Find Full Text PDFBMC Nephrol
January 2025
Department of Nephrology, Jinshan Hospital Affiliated to Fudan University, Shanghai, China.
Background: To explore the prevalence of hyperuricemia and its associated factors in uremic patients undergoing maintenance hemodialysis (MHD).
Methods: Two hundred two uremic patients undergoing MHD for ≥ 3 months, in Jinshan Hospital, Fudan University, were enrolled. Pre-dialysis blood samples were tested during March 1st, 2023 to April 30th, 2023.
Leukemia
January 2025
Department of Pathology, Duke University School of Medicine, Durham, NC, 27710, USA.
Multiple myeloma (MM) remains an incurable hematological malignancy that necessitates the identification of novel therapeutic strategies. Here, we report that intracellular levels of very long chain fatty acids (VLCFAs) control the cytotoxicity of MM chemotherapeutic agents. Inhibition of VLCFA biosynthesis reduced cell death in MM cells caused by the proteasome inhibitor, bortezomib.
View Article and Find Full Text PDFSci Rep
January 2025
Population Health Sciences, University of Bristol, Bristol, UK.
Multiple myeloma (MM) is an incurable blood cancer with unclear aetiology. Proteomics is a valuable tool in exploring mechanisms of disease. We investigated the causal relationship between circulating proteins and MM risk, using two of the largest cohorts with proteomics data to-date.
View Article and Find Full Text PDFClin Investig Arterioscler
January 2025
Unitat de Recerca de Lípids i Arteriosclerosi, Universitat Rovira i Virgili, 43201 Reus, Spain; Institut d'Investigació Sanitària Pere Virgili (IISPV), 43007 Reus, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 28029 Madrid, Spain. Electronic address:
Introduction: Rheumatoid arthritis (RA) is an autoimmune and inflammatory disorder that leads to cartilage and bone deterioration. This inflammatory activity causes extra-articular manifestations, including the acceleration of the atherosclerotic process. However, the exact causes of this accelerated process are under investigation.
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