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Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater ...
A charged device model (CDM) test is used to define the ESD a device can withstand when the device itself has an electrostatic charge and discharges due to metal contact. This discharge type is the most common type of ESD in electronic devices and causes most of the ESD damages in their manufacturing.
Chronic solvent-induced encephalopathy (CSE) is a condition induced by long-term exposure to organic solvents, often—but not always—in the workplace, that lead to a wide variety of persisting sensorimotor polyneuropathies and neurobehavioral deficits even after solvent exposure has been removed.
Brain ischemia has been linked to a variety of diseases or abnormalities. Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison to the average population.
In PRES secondary to other causes, the blood vessel damage has been attributed to other mechanisms. The "cytotoxic" theory suggests that it is direct cell damage by toxins (usually medications) that precipitates the edema. The "immunogenic" theory suggests a role for the immune system (specifically T cells).
Another factor in secondary injury is loss of cerebral autoregulation, the ability of the brain's blood vessels to regulate cerebral blood flow. [5] Other factors in secondary damage are breakdown of the blood–brain barrier, edema, ischemia and hypoxia. [15] Ischemia is one of the leading causes of secondary brain damage after head trauma. [9]
Aβ was found manipulating the level of nicotine in the brain along with the MAP kinase, another signaling receptor, to cause cell death. Another chemical in the brain that Aβ regulates is JNK; this chemical halts the extracellular signal-regulated kinases (ERK) pathway, which normally functions as memory control in the brain. As a result ...
Brain trauma or stroke can cause ischemia, in which blood flow is reduced to inadequate levels. Ischemia is followed by accumulation of glutamate and aspartate in the extracellular fluid , causing cell death, which is aggravated by lack of oxygen and glucose .