Disease relevance of Postmortem Changes

• It is possible that the differences in the proportion of muscle fibre types and in glycogen level in muscles influences the postmortem change in ATP and lactic acid, which would accelerate or retard rigor mortis of the muscles [1].
• NADPH diaphorase-containing nerve fibers and neurons in the myenteric plexus are resistant to postmortem changes: studies in Hirschsprung's disease and normal autopsy material [2].
• An experimental model of death from anaphylactic shock with compound 48/80 and postmortem changes in levels of histamine in blood [3].
• The present study demonstrated that MAP2 disruption is remarkable in the CA1-subiculum region of autopsied brains and that hypothermia reduces the postmortem change of MAP2, as observed in ischemic brain [4].
• We compared the effects of myocardial ischemia and postmortem changes on beta-adrenergic receptors and their coupling to adenylate cyclase activity [5].

Psychiatry related information on Postmortem Changes

• The Blessed Dementia Rating Scale (Part 1) correlates well with postmortem changes but is not an effective antemortem index of functional change since disparate behavioral domains are assessed [6].

High impact information on Postmortem Changes

• These data suggest that postmortem changes in various biochemical parameters of dopamine function are more rapid than has been generally appreciated [7].
• Since the viability of cells is considered to depend on the capacity of oxidative phosphorylation, it is highly likely that the delayed appearance of mitochondrial aspartate aminotransferase in blood indicates the postmortem changes of injured cells [8].
• Even when the data were adjusted for differences in tryptophan concentration, a putative biochemical index for agonal and postmortem changes of brain tissue, no new differences emerged in the concentrations of neuroactive amino acids between suicide victims and control subjects [9].
• Postmortem changes in human brain amines are discussed in relation to those occurring postmortem in the rat brain, in which phenylethylamine, p-tyramine, and tryptamine have been shown to increase to levels greater than those prevailing in vivo [10].
• Endogenous gamma-hydroxybutyrate in rat brain areas: postmortem changes and effects of drugs interfering with gamma-aminobutyric acid metabolism [11].

Chemical compound and disease context of Postmortem Changes

• Other kinetic parameters of dopamine-sensitive adenylate cyclase can also be measured independently of postmortem changes [12].
• Postmortem changes of normetanephrine determined by a mass-fragmentographic technique in different rat brain areas [13].
• Amygdalar activation alters the hippocampal GABA system: "partial" modelling for postmortem changes in schizophrenia [14].
• Postmortem changes in serum concentrations of triiodothyronine in rats [15].
• Postmortem changes of the hypoxanthine in vitreous humor in humans were investigated [16].

Biological context of Postmortem Changes

• Species differences in dopamine transporters: postmortem changes and glycosylation differences [17].
• Pharmacokinetics and postmortem changes of cimetidine in body tissues [18].

Anatomical context of Postmortem Changes

• There were no significant postmortem changes in kynurenic acid concentrations in cerebral cortex, hippocampus, and striatum at intervals ranging from 0 to 24 h [19].
• Adipose tissues with and without livor mortis from the thigh area of the same decedent were analyzed for cocaine [20].
• We examined the postmortem changes in the levels of ATP, glycogen and lactic acid in two masticatory muscles and three leg muscles of rats [1].
• Effects of ion channel blockers on rapid postmortem changes in extracellular dopamine and serotonin levels in the rat nucleus accumbens [21].
• A detailed, correlative, histologic evaluation of postmortem changes in the nasal mucosa of chronic cocaine users has shown characteristic mucosal and arteriolar changes as well as typical perivascular and subepithelial alterations compatible with chronic inflammation [22].

Gene context of Postmortem Changes

• G protein-coupled receptor kinases, beta-arrestin-2 and associated regulatory proteins in the human brain: postmortem changes, effect of age and subcellular distribution [23].
• There was no difference between groups in clinical signs, postmortem changes, CTL activity, cytokine message expression, or IFN-gamma production [24].
• Postmortem changes in the activities of tyrosine hydroxylase, dopa decarboxylase, and dopamine-beta-hydroxylase were examined in various areas of rat brain [25].
• Postmortem changes in cytochrome c oxidase activity in various organs of the rat and in human heart [26].
• The increased expression of IL-10 mRNA could be considered a vital reaction in skin specimens with postmortem change [27].

Analytical, diagnostic and therapeutic context of Postmortem Changes

• A study of non-isotopic in situ hybridization histochemistry on postmortem changes in vasopressin mRNA in rat brain [28].
• Postmortem changes of uric acid in various rat tissues: determination of uric acid by reversed-phase high-performance liquid chromatography with electrochemical detection [29].
• Rapid postmortem changes of rat striatum dopamine, serotonin, and their metabolites as monitored by brain microdialysis [30].
• Cervical dislocation-induced rapid postmortem changes were inhibited markedly by perfusion with CSF containing the CA2+ entry blocker verapamil [21].
• The purpose of this study was to characterize postmortem changes in cocaine and metabolite concentrations relative to premortem concentrations over time at two anatomic sites: peripheral blood and vitreous humor, in a controlled, large animal model [31].

References