MILLIPLEX^®人脓毒症磁珠板1-免疫应答多重测定

Luminex is a registered trademark of Luminex Corp

MILLIPLEX is a registered trademark of Merck KGaA, Darmstadt, Germany

xMAP is a registered trademark of Luminex Corp

MILLIPLEX^® Qualified assays undergo rigorous assay development, verification, and Quality Control testing to achieve optimal performance. Simultaneously analyze up to 6 analytes in human serum, plasma, and cell culture supernatants.Analytes included: MIF, PAI-1 (Total), sFas, sFasL, sICAM-1, sVCAM-1Assay Characteristics: Refer to kit protocol for assay cross-reactivity, sensitivity, precision, and accuracy.

For research use only. Not for use in diagnostic procedures.Label License/Sticker for Assay Product:By opening the packaging containing this Assay Product (which contains fluorescently labeled microsphere beads authorized by Luminex Corporation) or using this Assay Product in any manner, you are consenting and agreeing to be bound by the End User Terms and Conditions and the End User License Agreement available at http://support.diasorin.com/end-user-terms-and-conditions/. If you do not agree to all of the terms and conditions, you must promptly return this Assay Product for a full refund prior to using it in any manner.

Vascular and Apoptotic Research Panel: Luminex^® xMAP^® platform simultaneously quantitates 6 critical sepsis biomarkers (sFAS/TNFRSF6, sFasL, sICAM-1, MIF, PAI-1 total, sVCAM-1) targeting vascular dysfunction and apoptotic pathways in sepsis research.Versatile Sample Compatibility: Designed for human serum, plasma, tissue culture supernatants, and homogenates using 1:10 dilution for serum/plasma samples, accommodating diverse sepsis research applications and sample types.Endothelial Dysfunction Research: Investigate vascular adhesion molecules (sICAM-1, sVCAM-1), coagulation dysregulation (PAI-1), inflammatory mediators (MIF), and apoptotic signaling (sFas, sFasL) critical to sepsis-induced organ dysfunction.Specialized Research Applications: Target biomarkers specifically involved in endothelial activation, thrombotic complications, and programmed cell death pathways that characterize severe sepsis and progression to MODS in research studies.

Sepsis or SIRS (systemic inflammatory response syndrome) results from infection, whether bacterial, viral, fungal, or parasitic. The pathogenesis of sepsis is very complex. Both an innate and acquired immune response to infection interrupts homeostasis with a shift of cytokine expression that increases immunosuppression. In addition, migration of the leukocytes in the inflamed tissues secretes a tissue factor leading to the formation of thrombin, also triggering the release of chemokines and adhesion molecules through endothelial cells. Severe sepsis occurs when hypotension or hypoperfusion to one or more organs leads to organ dysfunction, which, in turn, can cause septic shock, multiple organ dysfunction syndrome (MODS) and death.