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At least 199 records · Page 11Linked to original sources
PubMed2006

Creatine monohydrate and glucose supplementation to slow- and fast-growing chickens changes the postmortem pH in pectoralis major.

The energy status of the chicken at slaughter has a large impact on the development of pH postmortem and thus on color and water-holding capacity (WHC). Supplementation of creatine monohydrate and glucose (CMH+GLU) may increase the creatine content in the muscles before slaughter, thereby delaying the formation of lactic acid and postponing the pH decline. The objective of this study was to examine the impact of supplementing CMH+GLU in the drinking water within the last 48 h before slaughter on the pH decline, meat color, and WHC in the pectoralis major from 2 strains of Ross chickens. Forty Ross 308 (fast-growing) female chickens and 40 Ross 1972 (slow-growing) female chickens had free access to drinking water either supplemented with CMH (15 g/ L) and glucose (50 g/L) within the last 48 h before slaughter or without supplementation. All chickens were slaughtered at 42 or 43 d of age irrespective of weight. Temperature and pH were measured at 1 and 30 min and at 1, 3, 8, and 24 h postmortem. Also, WHC measured as drip loss and color were determined postmortem. The CMH+GLU supplementation decreased pH (P < 0.05) at all time points between 1 min and 8 h postmortem in both strains, whereas at 24 h postmortem only pH in Ross 308 chickens were decreased significantly upon supplementation. Lightness was significantly increased in the meat from Ross 308 but not from Ross 1972 chickens upon supplementation. This interaction was significant (P < 0.05). The redness of the meat was decreased upon supplementation (P < 0.05), although only significantly in Ross 1972. The pH was lower for Ross 1972 chickens at the early time points (P < 0.01) and also a higher drip loss (P < 0.05), lightness (P < 0.01), and redness (P < 0.001) were observed. Thus, there seems to be no beneficial effect of CMH+GLU supplementation on chicken meat quality on the basis of results from this experiment.

Animals↗
PubMed1995

Postmortem acetaminophen pharmacokinetics: an experimental study of site and time-dependent concentration changes.

Postmortem blood drug concentrations are obtained routinely for assessment of the cause of mortality. However, the relationship of postmortem drug concentration to blood concentrations at the time of death remains poorly characterized. Using Ketamine sedation, 10 New Zealand white rabbits were sacrificed 20 minutes after oral gavage with liquid acetaminophen 160 mg/kg as a model drug. Blood samples were obtained from peripheral (femoral vein) and central sites (heart & inferior cava) over time and compared with heart blood concentrations obtained at the time of sacrifice. The mean +/- SE antemortem acetaminophen concentration was 63.1 +/- 14.6 mcg/ml. Postmortem central blood concentrations were as follows: T = 3 h: 200.8 +/- 129.2 micrograms/mL, T = 6 h: 100.8 +/- 39.6 micrograms/mL and T = 12 h: 480.8 +/- 128.8 micrograms/mL. Postmortem peripheral site results were: T = 3 h: 50.2 +/- 21.4 micrograms/mL, T = 6 h: 100.8 +/- 18.1 and T = 12 h: 117.7 +/- 37.2 micrograms/mL. Overall, blood acetaminophen concentrations increased significantly over time for central sampling sites. Drug concentration increases seen in the central sampling sites were several times higher than that seen in peripheral blood. Blood samples taken from peripheral sites did not alter significantly. The results of this controlled study were consistent with previous autopsy case series and case reports suggesting that postmortem drug concentrations do not reflect premortem values. Variables affecting postmortem drug concentrations include both postmortem sampling time and anatomic blood collection site.

Acetaminophen↗
PubMed1980

Postmortem biochemical changes in canine blood.

Antemortem and postmortem blood samples from 60 dogs were evaluated for sodium, chloride, potassium, urea nitrogen, glucose, creatinine, calcium, phosphorus, total protein, albumin, and carbon dioxide levels. Temperatures were 4, 20 and 37 degrees C. Postmortem intervals were 3, 6, 12, and 48 h. Blood urea nitrogen, calcium, and protein values remained stable after death, indicating diagnostic significance. Potassium, creatinine, and phosphorus levels increased with time and sodium, chloride, and total carbon dioxide levels decreased with time; therefore, determining these chemical values could be beneficial in estimating time of death. Glucose values were of limited value.

Animals↗
PubMed1990

1H-NMR studies of postmortem biochemical changes in rat skeletal muscle.

1H-nuclear magnetic resonance (NMR) has been applied to the study of postmortem biochemical changes in perchloric acid extracts of rat skeletal muscle. Several metabolites have been detected and the dependence upon the postmortem time has been considered. The simultaneous quantitative determination of metabolites showing up at very low and very high fields has been suggested to yield a satisfactory delineation of the thanatochronology.

Animals↗
PubMed1980

Postmortem biochemical changes in canine cerebrospinal fluid.

Time and temperature effects on postmortem cerebrospinal fluid samples from 60 adult mongrel dogs were studied. After death the dogs were held at 4, 20, or 37 degrees C for intervals of 3, 6, 12, 24, or 48 h. Antemortem and postmortem cerebrospinal fluid was evaluated for sodium, chloride, potassium, urea nitrogen, glucose, creatinine, calcium, phosphorus, and carbon dioxide. Sodium and urea nitrogen values remained stable. Chloride may be of forensic science value. Low levels of postmortem calcium might indicate antemortem hypocalcemia; high levels of postmortem glucose may indicate antemortem hyperglycemia. Calcium and creatinine levels increased slightly but continually after death; carbon dioxide values dropped.

Animals↗
PubMed1980

Postmortem biochemical changes in canine vitreous humor.

Time and temperature effects on postmortem vitreous humor from 60 adult mongrel dogs were studied. After death the dogs were held at 4, 20, or 37 degrees C for intervals of 3, 6, 12, 24, or 48 h. Antemortem and postmortem vitreous was analyzed for sodium, chloride, potassium, urea nitrogen, glucose, and creatinine. Potassium levels rose with increases in temperature and time. Sodium, chloride, and urea nitrogen values were stable at 4 degrees C for 48 h; they were less stable at higher temperatures. Glucose dropped to less than half within 3 h at all temperatures. Creatinine values were inconsistent. In that postmortem glucose and sodium levels remained below antemortem levels, diagnosis of hyperglycemia and hypernatremia should be possible. Consequently, a diagnosis of hypoglycemia could not be supported; the diagnosis of hyponatremia could be made in the early postmortem period.

Animals↗
PubMed2001

Postmortem microscopic changes observed at the human head hair proximal end.

Only two types of human hair roots (proximal ends) derived from decomposing scalps are reported in the literature. The most common representation of the putrid root includes a postmortem dark root band in published photomicrographs. In this study, 22 cases were reviewed in which there was reliable time of death documentation from medical investigator reports. A review of these cases finds that the most common putrid hair proximal end change does not contain the postmortem root band. Four primary types of hair proximal end postmortem change were identified. This study finds no correlation of time of death with scalp hair proximal end decomposition. In addition two examples are presented that suggest that hair roots do not decompose after fresh removal from the scalp and exposure to the outside elements.

Adult↗
PubMed2001

Comparison of morphological changes in white blood cells after death and in vitro storage of blood for the estimation of postmortem interval.

Estimation of the time of death is one of the most important problems for forensic medicine and law. Physical and chemical postmortem changes are evaluated together while estimating the time of death. In this study, in vitro storage and postmortem changes of white blood cells were aimed to be compared within the given postmortem interval, and a follow-up study was carried out. Blood smears which were obtained from 10 non-refrigerated cadavers (experimental group) and from 40 hospital patients (control group) have been evaluated to observe and compare changes during the in vitro storage and postmortem degenerative morphological changes that white blood cells undergo throughout the given postmortem intervals. The samples were examined by using a light microscope, and blood cells were differentiated by staining blood films with May-Grunwald stain, followed by Giemsa stain. Identifiable degenerated eosinophils and monocytes were first examined at 6h of death and the in vitro storage, and they were unidentifiable beyond 72 h of storage. Identifiable degeneration of neutrophils were first examined at 6h of death and storage while unidentifiable beyond 96 h of storage. Identifiable degeneration of lymphocytes were first examined at 24h of death, and they were still identifiable beyond 120 h. Cellular changes of leukocytes can be useful in the 6-120 h for estimating the time of in vitro storage, and the findings match during the first 21 h for both experimental and control groups. Finally, this follow-up study and the comparison will also be carried out for a longer postmortem interval, and other specific hypothesis that relate cellular changes in tissues other than blood with time since death are various points that needs to be studied.

Adult↗
PubMedDate not supplied

Neurochemical changes following postmortem ischemia in the rat retina.

Glutamate and gamma-aminobutyric acid (GABA) are the dominant amino acids in the retina and brain. The manufacturing and degradation pathways of both of these amino acids are intricately linked with the tricarboxylic acid cycle leading to rapid redistribution of these amino acids after metabolic insult. Postmortem ischemia in mammalian retina predominantly results in a loss of glutamate and GABA from neurons and accumulation of these amino acids within Müller cells. This accumulation of glutamate and GABA in Müller cells may occur as a result of increased release of these neurotransmitters from neurons, and decreased degradation. Quantification of the semisaturation value (half-maximal response) for glutamate and GABA Müller cell loading during postmortem ischemia indicated a shorter semisaturation value for GABA than glutamate. Such changes are consistent with a single aerobically dependent GABA-degradation pathway, and the existence of multiple glutamate-degradation pathways. Comparison with the in vitro ischemic model showed similar qualitative characteristics, but a markedly increased semisaturation time for glutamate and GABA Müller cell loading (a factor of 5-10) in the postmortem ischemia model. We interpret these differences to indicate that the in vitro condition provides a more immediate and/or severe ischemic insult. In the postmortem ischemia model, the delayed glial cell loading implies the availability of internal stores of both glucose and/or oxygen. Increased glial and neuronal immunoreactivity for the amino acids involved in transamination reactions, aspartate, alanine, leucine, and ornithine was observed, indicating a potential shift in the equilibrium of transamination reactions associated with glutamate production. These findings provide evidence that, in the rat retina, there are multiple pathways subserving glutamate production/degradation that include a multitude of transamination reactions. Further evidence is therefore provided to support a role for all four amino acids in glutamate metabolism within a variety of retinal neurons and glia.

Alanine↗