Adhesion Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Adhesion and links to relevant pages within the course.
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| Specimen Collection (continued) A syringe is used to remove 6 - 15 ml of spinal fluid. Less fluid is removed in babies and small children. The CSF sample is divided among 3 - 4 tubes, with 2 - 4 ml in each tube.
Glass tubes should be avoided due to cell adhesion which may affect the cell counts or differential. The tubes are numbered in the order in which the CSF is obtained.
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| Review 1 Francois P. Vaudaux P. Foster TJ. Lew DP.:
Host-bacteria interactions in foreign body infections.
Infection Control & Hospital Epidemiology. 17:514-20, 1996Persistent staphylococcal infections are a major medical problem, especially when they occur on implanted materials or intravascular catheters.This review describes some of the recently discovered molecular mechanisms of Staphylococcus aureus attachment to host proteins coating biomedical implants.These interactions involve specific surface proteins, called bacterial adhesins, that recognize specific domains of host proteins deposited on indwelling devices, such as fibronectin, fibrinogen, or fibrin.Elucidation of molecular mechanisms of S. aureus adhesion to the different host proteins may lead to the development of specific inhibitors blocking attachment of S. aureus, which may decrease the risk of bacterial colonization of indwelling devices. | View Page |
| Review 2 Cunningham MW.:
Pathogenesis of group A streptococcal infections.
Clinical Microbiology Reviews. 13):470-511, 2000Group A streptococci are model extracellular gram-positive pathogens responsible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephritis. A resurgence of invasive streptococcal diseases and rheumatic fever has appeared in outbreaks over the past 10 years, with a predominant M1 serotype as well as others identified with the outbreaks.Emm (M protein) gene sequencing has changed serotyping, and new virulence genes and new virulence regulatory networks have been defined. The emm gene superfamily has expanded to include antiphagocytic molecules and immunoglobulin-binding proteins with common structural features.At least nine superantigens have been characterized, all of which may contribute to toxic streptococcal syndrome. An emerging theme is the dichotomy between skin and throat strains in their epidemiology and genetic makeup. Eleven adhesions have been reported, and surface plasmin-binding proteins have been defined.The strong resistance of the group A streptococcus to phagocytosis is related to factor H and fibrinogen binding by M protein and to disarming complement component C5a by the C5a peptidase. Molecular mimicry appears to play a role in autoimmune mechanisms involved in rheumatic fever, while nephritis strain-associated proteins may lead to immune-mediated acute glomerulonephritis. Vaccine strategies have focused on recombinant M protein and C5a peptidase vaccines, and mucosal vaccine delivery systems are under investigation. | View Page |
| Platelet adhesion involves the absorption of this factor between receptors on the exposed subendothelial tissue, and by receptors on the platelets themselves? | View Page |
| Which of the following is not true in terms of platelet characteristics? | View Page |
| All of the following activities are associated with platelets except | View Page |
| Primary Hemostasis – The Vascular System & Platelet Involvement As discussed earlier, a break in the vessel endothelium leads to exposure of collagen and the vessel's subendothelial surface. Ruptured endothelial cells leak ADP and Serotonin, which are the chemical triggers that induce platelet adhesion, the next step in the sequence of hemostatic events. Circulating platelets are drawn to the area by those liberated chemical signals, and begin to physically attach themselves to the rough, damaged surfaces of the breach. As platelets continue to arrive and bind to the exposed collagen and basement membrane, a rudimentary barrier begins to form, as the platelets themselves serve to fill in the breached vessel wall. Platelets possess an inherent “sticky” property which enables them to adhere to one another, and not just to the damaged vessel endothelium. The process by which platelets bind to one another is referred to as platelet aggregation, and is vital because it allows for a platelet plug to be formed. The platelet plug is the structure responsible for plugging the hole in the vessel wall. | View Page |
| Primary Hemostasis – Platelet Kinetics Kinetic Processes Specific to Platelets. Adhesion – When platelets adhere to exposed collagen, they take on a characteristic “spiny” shape. Their inherent stickiness, and the aforementioned spiny shape serve to compliment each other during this process. Von Willebrands Factor (vWF) is absorbed by surface receptors on both the platelet and exposed subendothelial tissue, thereby linking the platelets to the tissue. Release – This process occurs prior to aggregation. Platelets dump the contents of their granules (ADP, Serotonin, & Calcium), which aids the upcoming aggregation process by acting as a chemical signal. Aggregation – Platelets physically bind to each other, not just to the exposed subendothelial walls and collagen of the breached vessel. Platelet aggregation requires sufficient chemical signal stimulation. Stabilization (technically part of secondary hemostasis as fibrin is a product of secondary hemostasis)– This process strengthens the platelet plug with the addition of interwoven fibrin strands, ultimately producing a fibrin clot. The durable fibrin clot is the ultimate goal of hemostatic processes. | View Page |
| All of the following are activities associated with platelets except: | View Page |
| Coagulation Disorders - Inherited Von Willebrands Disease is a platelet disorder. This disorder is characterized by a functional defect in Von Willebrands factor (vWF) itself. This disease often clinically manifests with a concurrent deficiency of factor VIII, but will present with a normal platelet count. As far as genetics and inheritance, both men and women are affected equally. Von Willebrands factor is essential for platelet binding, therefore, a defect in vWF causes impaired platelet adhesion and aggregation. The treatment of Von Willebrands Disease involves the administration cryoprecipitate, as it is rich in vWF. | View Page |