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Additionally, lack of sleep causes increased anxiety-like behaviors and impairs the brain's ability to block out unimportant stimuli when performing tasks requiring attention. Disruptions in important brain circuits and the downregulation of proteins necessary for cognitive stability are the causes of these behavioral abnormalities. [30]
Phenol sulfur transferase deficiency, in short PST deficiency, is the lack or the reduced activity of the functional enzyme phenol sulfur transferase, which is crucial in the detoxification of mainly phenolic compounds by catalysing the sulfate conjugation of the hydroxyl groups in the toxic phenolic compounds to result in more hydrophilic forms for more efficient excretion.
Sleep deprivation can sometimes be self-imposed due to a lack of desire to sleep or the habitual use of stimulant drugs. Revenge Bedtime Procrastination is a need to stay up late after a busy day to feel like the day is longer, leading to sleep deprivation from staying up and wanting to make the day "seem/feel" longer.
Ketone bodies are produced mainly in the mitochondria of liver cells, and synthesis can occur in response to an unavailability of blood glucose, such as during fasting. [4] Other cells, e.g. human astrocytes, are capable of carrying out ketogenesis, but they are not as effective at doing so. [6] Ketogenesis occurs constantly in a healthy ...
Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine.Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury.
Cell damage (also known as cell injury) is a variety of changes of stress that a cell suffers due to external as well as internal environmental changes. Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors. Cell damage can be reversible or irreversible.
Viloxazine is indicated to treat attention deficit hyperactivity disorder (ADHD) in children age 6 to 12 years, adolescents age 13 to 17 years, and adults. [1]Analyses of clinical trial data suggest that viloxazine produces moderate reductions in symptoms; it is about as effective as atomoxetine and methylphenidate but with fewer side effects.
Due to the blood–brain barrier, it would be fairly difficult for the body to constantly replace microglia. Therefore, instead of constantly being replaced with myeloid progenitor cells , the microglia maintain their status quo while in their quiescent state, and then, when they are activated, they rapidly proliferate in order to keep their ...