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Postmortem changes

Lee, C. and Hajra, A.K. Molecular species of diacylglycerols and phosphoglycerides and the postmortem changes in the molecular species of diacylglycerols in rat brain. /. Neurochem. 56 370-379,1991. [Pg.49]

Clinicians should be aware that significant postmortem changes in TCA plasma levels may occur, and interpretation must be done cautiously. Sudden death may only be coincidentally associated with a drug the patient was taking. Nevertheless, if a patient is found to have a toxic level postmortem and no anatomical cause of death at autopsy, the clinician may have a legal problem if TDM was not used at least once early in treatment to rationally adjust the dose. [Pg.140]

It is often necessary to add preservatives to specimens to protect against postmortem changes. For example, the addition of sodium fluoride to a tissue specimen can prevent the production of bacterial ethanol (which can potentially yield a false positive result for the presence of ingested ethanol). [Pg.401]

Clark, M. A., Worrell, M. B., and Pless, J. E. (1997). Postmortem changes in soft tissue, in Forensic Taphonomy The Postmortem Fate of Human Remains (W. D. Haglund and M. H. Sorg, Eds.). Boca Raton, FL CRC Press, 151-164. [Pg.46]

Micozzi, M. S. (1986). Experimental study of postmortem change under field conditions Effects of freezing, thawing and mechanical injury. /. Forensic Sci. 31, 953-961. [Pg.48]

Micozzi, M. S. (1991). Postmortem Change in Human and Animal Remains A Systematic Approach. Springfield, IL Charles C. Thomas. [Pg.48]

Postmortem changes at the hair root (proximal) end in 22 forensic hair samples derived from decomposed scalps included fibers with dark stained bands located toward the proximal end, defined as postmortem root banding, as well as unstained fibers with hard points or brush-like ends (Linch and Prahlow 2001). There remains little evidence as to how these different microscopic features originate, but postmortem root banding probably results from putrefaction and is not noted in older hair from archeological remains. [Pg.134]

DNLM 1. Forensic Anthropology—methods. 2. Soil—analysis. 3. Postmortem Changes. 4. Soil Microbiology. W 750 S6826 2008]... [Pg.360]

Poole, D. F. G. Tratman, E. K. (1978). Postmortem changes in human-teeth from late... [Pg.326]

Figure 21.1. Scheme summarising early postmortem changes in muscle and its influence on water binding. Reprodueed with permission from Toldra (2002). [Pg.504]

There is circumstantial evidence to support this suggestion, because the liver content of biotin is lower in infants who have died from cot death than in infants who have died from known causes. By parallel with the fatty liver and kidney syndrome, it has been suggested that a modest metabolic stress, such as a mild fever, causes a higher requirement for gluconeogenesis than can be met, resulting in acute hypoglycemia. There are rapid postmortem changes in... [Pg.339]

Berretta S, Munno DW, Benes EM. Amygdalar activation alters the hippocampal GABA system partial modelling for postmortem changes in schizophrenia. J. Comp. Neurol. 2001 431 129-138. [Pg.2291]

Inside the muscle fiber there is also a cytoskeleton — the protein structures assuring the integrity of muscle cells. Cytoskeletal proteins such as titin and nebulin are located in myofibrils and anchored in the Z line. Desmin is made up of costamers, which connect the myofibrils vinculin connects myofibrils and sarcolemma. Postmortem changes in cytoskeletal proteins probably play a role in the improvement of meat functional properties, especially its tenderness and water-holding capacity. [Pg.12]

Burstein and Hunter (1995) observed that THC stimulated the biosynthesis of anandamide in neuroblastoma cells employing either ethanolamine or arachidonic acid as the label. Anandamide bios5mthesis has also been shown to occur in primary cultures of rat brain neurons labelled with [H]-ethanolamine when stimulated with ionomycin, a Ca ionophore (Di Marzo et al. 1994). These authors proposed an alternate model for the biosynthesis of anandamide in which N-arachidonoyl phosphatidyl ethanolamine is cleaved by a phospholipase D activity to yield phosphatidic acid and ararchidonoylethanolamide. This model is based upon extensive studies undertaken by Schmid and collaborators (1990), who have shown that fatty acid ethanolamide formation results from the N-acylation of phosphatidyl ethanolamine by a transacylase to form N-acyl phosphatidylethanolamine. Possibly resulting from postmortem changes, this compound is subsequently hydrolyzed to the fatty acid ethanolamide and the corresponding phosphatide by a phosphodiesterase, phospholipase D. [Pg.67]


See other pages where Postmortem changes is mentioned: [Pg.209]    [Pg.942]    [Pg.107]    [Pg.130]    [Pg.23]    [Pg.27]    [Pg.942]    [Pg.49]    [Pg.203]    [Pg.216]    [Pg.221]    [Pg.553]    [Pg.503]    [Pg.503]    [Pg.339]    [Pg.196]    [Pg.34]    [Pg.2]    [Pg.145]    [Pg.156]    [Pg.181]    [Pg.83]   
See also in sourсe #XX -- [ Pg.32 , Pg.33 , Pg.66 , Pg.67 , Pg.83 , Pg.84 , Pg.219 , Pg.220 ]




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