[Clinical-biological approaches to the spectrophotometric detection of oxyhemoglobin and bilirubin in CSF in the management of aneurysmal subarachnoid hemorrhage].

The diagnosis of subarachnoid hemorrhage (SAH) is extremely important for appropriate management. Cerebral computed tomography (CT), used as the first-line investigation to detect bleeding, has excellent sensitivity if performed promptly, but its sensitivity falls sharply with the time elapsed since the onset of SAH. Oxyhemoglobin and bilirubin, the breakdown products of heme, are detectable in cerebrospinal fluid (CSF) by spectrophotometric absorption, which defines the search for xanthochromia pigment in CSF.

Exploring strategies to rapidly identify false positives in high-sensitivity cardiac troponin I assay: A prospective study.

Background: Cardiac troponin is the pivotal biomarker of myocardial injury, playing a central role in the diagnosis of acute coronary syndrome and various clinical situations. Nevertheless, challenges arise when patients exhibit elevated cardiac troponin levels in the absence of evident cardiac origin, as evidenced by extensive cardiac exploration, which suggests the presence of an interfering factor. Despite the high performance of high-sensitive cardiac troponin immunoassays, these tests remain susceptible to interferences that may lead to false-positives.

ROR2/PCP a New Pathway Controlling Endothelial Cell Polarity Under Flow Conditions.

Background: Endothelial cells (ECs) are sensitive to physical forces created by blood flow, especially to laminar shear stress. Among the cell responses to laminar flow, EC polarization against the flow direction emerges as a key event, particularly during the development and remodeling of the vascular network. EC adopt an elongated planar cell shape with an asymmetrical distribution of intracellular organelles along the axis of blood flow.

Increased Capillary Permeability in Heart Induces Diastolic Dysfunction Independently of Inflammation, Fibrosis, or Cardiomyocyte Dysfunction.

Background: While endothelial dysfunction is suggested to contribute to heart failure with preserved ejection fraction pathophysiology, understanding the importance of the endothelium alone, in the pathogenesis of diastolic abnormalities has not yet been fully elucidated. Here, we investigated the consequences of specific endothelial dysfunction on cardiac function, independently of any comorbidity or risk factor (diabetes or obesity) and their potential effect on cardiomyocyte.

Methods: The ubiquitine ligase , expressed in endothelial cells (ECs), was shown to destabilize tight junction.