IMO, it would be a lot clearer than the table. JPD can create the new graphs, like the ones used at Australian federal election, ?
Biomarkers can be broadly defined as qualitative or quantitative measurements that convey information on the physiopathological state of a subject at a certain time point or disease state. Biomarkers can indicate health, pathology, or response to treatment, including unwanted side effects.
When used as outcomes in clinical trials, biomarkers act as surrogates or substitutes for clinically meaningful endpoints.
In addition, genetic biomarkers can be used to quantify the risk of developing a certain disease.
In the specific case of traumatic brain injury, surrogate blood biomarkers of imaging can improve the standard of care and reduce the costs of diagnosis. In addition, a prognostic role for biomarkers has been Ronaldson promotional material company case study in the case of post-traumatic epilepsy.
Given the extensive literature on clinical biomarkers, we will focus herein on biomarkers which are present in peripheral body fluids such as saliva and blood.
They can indicate health, pathology, or response to treatment, including unwanted side effects. They can act as surrogate endpoints in clinical trials or can, rarely, substitute for clinically meaningful endpoints. For traumatic brain injury TBIbrain-derived protein biomarkers are commonly used as discussed below.
TBIs are heterogeneous and can occur in a variety of ways. TBI can be classified by the mechanism of injury eg, motor vehicle accidents, falls, and assaultsthrough clinical severity as graded by the Glasgow Coma Scale GCSor by the characterization of structural damage for review, see the study by Maas et al 2 and Buonora et al 3.
The heterogeneity of the disease makes it difficult to accurately assess the level of trauma and predict the clinical outcome for individual patients. These considerations have made establishing a universal and comprehensive TBI assessment protocol a challenging hurdle in the field of health care.
As discussed below, the understanding of this moving target is confounded by the fact that many biomarkers have complex kinetics relating to release from brain cells, transfer across the blood—brain barrier BBBand clearance from the peripheral blood.
These kinetic behaviors are at best indirectly related to the pathology of TBI. Several clinical-grade imaging modalities currently exist ranging from traditional computed tomography CT and MRI scans to more novel imaging techniques, such as susceptibility-weighted imaging, diffusion-weighted imaging, and diffusion tensor imaging.
All have been utilized in the context of TBI identification and clinical management. In addition, imaging modalities, such as functional MRI, positron emission tomography, single-photon emission computed tomography, and magnetic resonance spectroscopy, provide insight into metabolic abnormalities, which may have resulted from TBI, providing yet another level of information that could aid in diagnosis and treatment.
In these patients, symptoms of bleeding may not be present at the time of emergency room visit and are manifest only after appropriate imaging.
SDH and EDH may change the course of clinical management, as these events mandate admission to an intensive care unit and often require neurosurgical intervention.
Subacute and chronic SDHs are relatively common in patients with mTBI, especially in the geriatric population and when anticoagulation is present for pre-existing conditions.
It is important to accurately diagnose SDH, as an expanding mass lesion may necessitate surgery. Moreover, SDH is often associated with breakdown of the BBB, disproportionate tissue inflammation, and cerebral edema, which may cause progressive neurological deterioration. These are some of the most common rationales to use surrogate biomarkers because their appearance in blood and other fluids is facilitated or caused by BBB disruption.
EDHs are caused by acceleration—deceleration injuries and can be commonly ascribed to the rupture of a meningeal artery. The timely diagnosis of EDH is also of critical importance, as expanding hematomas may become life threatening, and progressive neurological deterioration, often after a lucid interval, require neurosurgical intervention.
Again, this underscores the need for surrogate biomarkers when CT scans are unavailable or during transport from a remote location. Bleeding into the subarachnoid space after mTBI may also occur, but is less likely to require surgical intervention.
Thus, it is critically important that acute intracranial pathology and bleeding are accurately diagnosed with a noninvasive biomarker-based test. As underscored in the introductory paragraphs, TBI additionally evolves with time, and the injury develops into two distinct phases, a primary injury phase and secondary injury phase.
Notably, the relationship between the primary phase and the secondary phase is weak and inconsistent. This is followed by a systemic and neuroinflammatory response or secondary phase, which is mediated by peripheral immune cells and the activation of immunocompetent neural cells.
Molecular mediators such as cytokines, growth factors, and adhesion molecules are released, causing the activation of a complex network of pathways. The secondary injury phase can evolve over a period of hours to days and months following the primary injury.
Some of these pathways are restorative in nature, while others contribute to metabolic dysregulation and hypoxic events secondary to brain swelling and edema.Herbert timberdesignmag.com Caruso. Herbert Bayer embodied the modernist desire to reduce designs to as few elements as possible and repeatedly experimented with typography to reduce the alphabet to a single case.
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