After the blood collection process, in vitro hemolysis can still occur in a sample due to external factors, such as prolonged storage, incorrect storage conditions and excessive physical forces by dropping or vigorously mixing the tube. From mechanical blood processing during surgery
In some surgical procedures (especially some heart operations) where substantial blood loss is expected, machinery is used for intraoperative blood salvage. A centrifuge process takes blood from the patient, washes the red blood cells with normal saline, and returns them to the patients blood circulation. Hemolysis may occur if the centrifuge rotates too quickly (generally greater than 500 rpm)—essentially this is hemolysis occurring outside of the body. Increased hemolysis occurs with massive amounts of sudden blood loss, because the process of returning a patients cells must be done at a correspondingly higher speed to prevent hypotension, pH imbalance, and a number of other hemodynamic and blood level factors. Modeling of fluid flows to predict the likelihood of red cell membrane rupture in response to stress is an active area of research. From bacteria culture
Visualizing the physical appearance of hemolysis in cultured blood samples may be used as a tool to determine the species of various Gram-positive bacteria infections (e.g., Streptococcus). Nomenclature
Hemolysis is sometimes called hematolysis, erythrolysis, or erythrocytolysis. The words hemolysis () and hematolysis () both use combining forms conveying the idea of "lysis of blood" (hemo- or hemato- + -lysis). The words erythrolysis () and erythrocytolysis () both use combining forms conveying the idea of "lysis of erythrocytes" (erythro- ± cyto- + -lysis).
In Alzheimers disease, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neurons transport system. Pathogenic tau can also cause neuronal death through transposable element dysregulation. Disease mechanism
Exactly how disturbances of production and aggregation of the beta-amyloid peptide give rise to the pathology of Alzheimers disease is not known. The amyloid hypothesis traditionally points to the accumulation of beta-amyloid peptides as the central event triggering neuron degeneration. Accumulation of aggregated amyloid fibrils, which are believed to be the toxic form of the protein responsible for disrupting the cells calcium ion homeostasis, induces programmed cell death (apoptosis). It is also known that Aβ selectively builds up in the mitochondria in the cells of Alzheimers-affected brains, and it also inhibits certain enzyme functions and the utilisation of glucose by neurons.Various inflammatory processes and cytokines may also have a role in the pathology of Alzheimers disease. Inflammation is a general marker of tissue damage in any disease, and may be either secondary to tissue damage in Alzheimers disease or a marker of an immunological response. There is increasing evidence of a strong interaction between the neurons and the immunological mechanisms in the brain. Obesity and systemic inflammation may interfere with immunological processes which promote disease progression.Alterations in the distribution of different neurotrophic factors and in the expression of their receptors such as the brain-derived neurotrophic factor (BDNF) have been described in Alzheimers disease.