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post-traumatic stress disorder/phosphatase
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Страница 1 от 52 полученные результаты
Post-traumatic dynamic change of carboxyterminal propeptide of type I procollagen, alkaline phosphatase and its isoenzymes as predictors for enhanced osteogenesis in patients with severe head injury.
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Patients suffering from severe head injury and fractures of long bones or large joints often show enhanced osteogenesis, with hypertrophic callus formation and/or heterotopic ossifications. The advantage of this phenomenon is early consolidation of the fractures. An extreme disadvantage is extensive
Post-traumatic variations in phosphatase and respiratory enzyme activities of the periosteum of aging rats.
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Association between posttraumatic stress disorder following myocardial infarction and liver enzyme levels: a prospective study.
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BACKGROUND
Research in rodents demonstrated that psychological stress increases circulating levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase reflecting liver injury. Moreover, chronic posttraumatic stress disorder and transaminases predicted coronary heart
[Alteration of apoptosis and Akt/mTOR signal pathway in hippocampal neurons of rat with post-traumatic stress].
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OBJECTIVE
To observe the changes of apoptosis and protein kinase B/the mammalian target of Rapamycin (Akt/mTOR) signal pathway in hippocampal neurons of rat with post-straumatic stress disorder (PTSD), and to investigate the mechanism of PTSD.
METHODS
Sixty male adult SD rats were divided into
Traumatic Brain Injury Causes a Tacrolimus-Sensitive Increase in Non-Convulsive Seizures in a Rat Model of Post-Traumatic Epilepsy.
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Epilepsy is a significant but potentially preventable complication of traumatic brain injury (TBI). Previous research in animal models of acquired epilepsy has implicated the calcium-sensitive phosphatase, calcineurin. In addition, our lab recently found that calcineurin activity in the rat
Involvement of calcineurin/NFATc4 pathway in a single-prolonged stress-based rat model of post-traumatic stress disorder.
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Post-traumatic stress disorder (PTSD) is a mental disease associated with the exposure of traumatic stress, and results in the structural and functional changes of hippocampus. Calcineurin (CaN), a calcium/calmodulin-regulated protein phosphatase ubiquitously expressed in brain, has a very important
Post-traumatic acalculous cholecystitis on a neurosurgical service.
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Post-traumatic acalculous cholecystitis is a potentially lethal complication that may develop in patients during hospitalization for trauma. Three case reports illustrate that obscuration of many early diagnostic symptoms and signs may make this complication particularly treacherous in the
Role of Striatal-Enriched Tyrosine Phosphatase in Neuronal Function.
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Striatal-enriched protein tyrosine phosphatase (STEP) is a CNS-enriched protein implicated in multiple neurologic and neuropsychiatric disorders. STEP regulates key signaling proteins required for synaptic strengthening as well as NMDA and AMPA receptor trafficking. Both high and low levels of STEP
Latexin expression correlated with mineralization of articular cartilage during progression of post-traumatic osteoarthritis in a rat model.
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As latexin has been linked with chondrocyte hypertrophic differentiation it is possible that this protein may also be involved in the mineralization of cartilage in OA. Therefore, we correlated latexin expression with the mineralization marker, alkaline phosphatase and determined the mineral
Deletion of Dual Specificity Phosphatase 1 Does Not Predispose Mice to Increased Spontaneous Osteoarthritis.
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BACKGROUND
Osteoarthritis (OA) is a degenerative joint disease with poorly understood etiology and pathobiology. Mitogen activated protein kinases (MAPKs) including ERK and p38 play important roles in the mediation of downstream pathways involved in cartilage degenerative processes. Dual specificity
The striatal-enriched protein tyrosine phosphatase gates long-term potentiation and fear memory in the lateral amygdala.
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BACKGROUND
Formation of long-term memories is critically dependent on extracellular-regulated kinase (ERK) signaling. Activation of the ERK pathway by the sequential recruitment of mitogen-activated protein kinases is well understood. In contrast, the proteins that inactivate this pathway are not as
Nuclear protein phosphatase-1: an epigenetic regulator of fear memory and amygdala long-term potentiation.
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Complex brain diseases and neurological disorders in human generally result from the disturbance of multiple genes and signaling pathways. These disturbances may derive from mutations, deletions, translocations or rearrangements of specific gene(s). However, over the past years, it has become clear
Inhibition of SDF-1α/CXCR4 Signalling in Subchondral Bone Attenuates Post-Traumatic Osteoarthritis.
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Previous studies showed that SDF-1α is a catabolic factor that can infiltrate cartilage, decrease proteoglycan content, and increase MMP-13 activity. Inhibiting the SDF-1α/CXCR4 signalling pathway can attenuate the pathogenesis of osteoarthritis (OA). Recent studies have also shown that SDF-1α
Sodium selenate retards epileptogenesis in acquired epilepsy models reversing changes in protein phosphatase 2A and hyperphosphorylated tau.
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There are no treatments in clinical practice known to mitigate the neurobiological processes that convert a healthy brain into an epileptic one, a phenomenon known as epileptogenesis. Downregulation of protein phosphatase 2A, a protein that causes the hyperphosphorylation of tau, is implicated in
Angiographic embolization as the definitive treatment of post-traumatic hemobilia.
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Hemobilia should be considered in all cases of blunt or penetrating trauma to the liver, no matter how trivial it may appear, whenever right upper quadrant pain and a persistently elevated alkaline phosphatase level give evidence of an otherwise unexplained biliary obstructin or hepatic mass lesion.
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