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PubMed1999

Rat and human membrane dipeptidase: tissue distribution and developmental changes.

Distribution and developmental changes in membrane dipeptidase activity were examined in rat and human tissues. The activity to hydrolyze glycyl-D-alanine in rat and human tissues was completely or almost completely inhibited by 5 mM cilastatin, suggesting that the activity was due to membrane dipeptidase and that the contribution of leucine aminopeptidase to the activity was minor. In 8-week-old rats, the activity was high in lung, kidney, pancreas and testis, and in each pooled sample of ileal mucosa, duodenal mucosa, jejunal mucosa and adrenal mucosa. A low activity was found in spleen, liver, serum and heart. The activity in lung, kidney, adrenal and intestinal mucosa increased up to the age of 5 or 8 weeks, while that in pancreas, testis and spleen reached a maximal level at around 3 weeks and declined thereafter. The distribution profile of the enzyme in postmortem tissues of adult humans was similar to that in rat, except for an extremely low activity in lung. The enzyme was also found in serum and urine from healthy volunteers. In urine, the activity was significantly correlated to the creatinine content. No clear dependence of the activity on gender or age was observed in urine and serum.

Age Factors↗

PubMed2002

Time-dependent immunohistochemical detection of proinflammatory cytokines (IL-1beta, IL-6, TNF-alpha) in human skin wounds.

UNLABELLED: The proinflammatory cytokines interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) hold important functions in the early and late courses of inflammation, trauma and wound healing. In the present study, human skin wounds due to sharp force (n = 105) were collected during surgery and autopsy. The wound age mainly varied from several minutes to 5 h, some specimens aged up to 6 weeks. Control specimens from uninjured skin were available in each case. After preparation of cryostat sections, immunohistochemistry was performed according to the APAAP technique, using monoclonal and polyclonal antibodies. The results were evaluated semiquantitatively. All markers were weakly expressed in normal human skin constitutively. However, the staining pattern changed significantly in vital wounds concerning epidermal layers, subepidermal cells, vessels and sweat glands. IL-1beta and IL-6 showed enhanced expression after 15 and 20 min at the earliest (increase of epidermal reactivity). After 30-60 and 60-90 min, respectively, marked expression was observed with these markers. Similar alterations were detectable with TNF-alpha after 15 and 60-90 min. The reactivity of all three markers persisted over several hours, then decreased to basal levels again and sometimes reappeared after days and in granulation tissue. Leukocytes reacting with IL-1beta and IL-6 appeared after approximately 2 h. CONCLUSION: proinflammatory cytokines can serve as a useful tool for the estimation of vitality and wound age, in particular in the early post-traumatic interval prior to leukocyte reaction. Autolysis did not play a role in the samples investigated (postmortem interval up to 8 days). Problems could sometimes rise from constitutive expression. Therefore, it is recommended to examine control samples from the same individual and to compare the reactivity with wound specimens.

Adolescent↗

PubMed1990

Opposite alterations in cerebrospinal fluid uridine after severe cerebral ischemia or intrathecal blood injection.

1. Rats which survived hypoglycemia by insulin, hypoxia by 10% O2, or ischemia by carotid ligation and hypotension to 40 mm Hg, evidenced no changes in cerebrospinal fluid (CSF) uridine. Animals which died soon after the above interventions or as a result of KCl-induced cardiac arrest had elevated CSF uridine concentrations. 2. Injection of whole blood or the soluble contents of lysed blood cells into the lateral ventricle of rats reduced CSF uridine to less than one-half normal at 24 hrs but values returned to normal 3 days later. Changes in hypoxanthine resembled those of uridine, but were less dramatic, whereas xanthine concentrations were largely unaltered. Intraventricular injection of plasma or saline did not alter CSF uridine. 3. It seems most likely that low CSF uridine concentrations previously reported in head injury patients may be secondary to the effects of blood cell contents in the cerebrospinal fluid, rather than responses to altered metabolism in neurons or glia cells.

Animals↗

PubMed2006

Time of death dependent criteria in vitreous humor: accuracy of estimating the time since death.

Since more than 40 years reports on the rise of potassium concentration [K(+)] in vitreous humor have been published with different statements concerning the accuracy of death time estimation. In the last years several statistical approaches for a more accurate estimation of the time since death have been reported. While in most investigations the PMI has been used as the independent and [K(+)] as the dependent variable in linear regression analysis between PMI and [K(+)], recently it has been suggested to use [K(+)] as the independent variable for regression analysis. Changing the variables would lead to a higher accuracy of death time estimation. This has also been recommended for regression analysis between hypoxanthine concentration [Hx] and time since death. This hypothesis has been checked on independent cases with potassium and hypoxanthine in vitreous humor. Linear regression with [K(+)] or [Hx] as independent variable has revealed a slightly more accurate death time estimation compared to a linear regression with PMI as independent variable. Thus, e.g. the accuracy could have been improved from +/-25.96 to +/- 23.27h by using [K(+)] as independent variable. Another statistical approach has re-evaluated six large studies on the rise of vitreous [K(+)] using a local regression analysis (Loess procedure). Based on this re-evaluation an accuracy of death time estimation has been recommended (95% limits of confidence of +/-1h in the early PMI and +/-10h, 110h postmortem) which has surpassed even optimistic results of earlier investigations. This recommended accuracy of death time estimation has been checked on a random sample of 492 cases. Only 153 cases have been within the predicted postmortem interval, 339 lay outside with a systematic overestimation of the time since death.

Chromatography, High Pressure Liquid↗

PubMed1997

Acceleration of post-mortem changes in Tsaiya duck (Anas platyrhynchos) breast muscle by lactic acid marination.

1. The effect of lactic acid marination at 5 degrees C on post mortem changes in breast muscle pectoralis major of spent layer Tsaiya duck was studied. 2. Myofibrils were prepared from 0.1 M and 0.2 M lactic acid marinated muscle and control (non-marinated samples) sampled at 0, 1, 3, 7 and 14 d post mortem. 3. Changes in myofibril fragmentation index (MFI), myofibrillar proteins and Z-line structure were examined. 4. Marination of duck breast muscle in lactic acid at 5 degrees C enhanced fragmentation of myofibrils and degradation of myofibrillar proteins and Z-line structure as compared to control samples. 5. In summary, lactic acid marination at 5 degrees C can accelerate the post mortem degradation of myofibrils in Tsaiya duck breast muscle.

Actinin↗

PubMed2005

Somatostatin receptor type 2 undergoes plastic changes in the human epileptic dentate gyrus.

Temporal lobe epilepsy (TLE) is characterized by hippocampal sclerosis together with profound losses and phenotypic changes of different classes of interneurons, including those expressing somatostatin (SRIF). To understand the functional significance of the plasticity of SRIF transmission in TLE, unraveling the status of SRIF receptors is, however, a prerequisite. To address this issue, we characterized expression and distribution of the major SRIF receptor, the sst2 subtype, in hippocampal tissue resected in patients with TLE using complementary neuroanatomic approaches. In patients with hippocampal sclerosis, the number of cells expressing sst2 receptor mRNA as well as sst2 receptor-binding sites and immunoreactivity decreased significantly in the CA1-3, reflecting neuronal loss. By contrast, in the dentate gyrus, sst2 receptor mRNA expression was strongly increased in the granule cell layer, and sst2 receptor-binding sites and immunoreactivity was preserved in the inner but decreased significantly in the outer molecular layer. In this latter region, pronounced changes in SRIF terminal fields were observed. Decreased receptor density in the distal dendrites of granule cells is likely to reflect downregulation of sst2 receptors in response to physiopathologic release of SRIF. Because sst2 receptors have anticonvulsant and antiepileptogenic properties, this phenomenon may contribute to the etiology of TLE seizures.

Adolescent↗

PubMed1990

Post mortem kinetics of secobarbital.

Post-mortem changes in barbiturate concentrations were evidenced using a rat-secobarbital model. The method used for the extraction and HPLC assay of barbiturates is suitable for all biologic fluids and post-mortem tissues. Kinetic data obtained is of excellent quality. Various modelization constants were defined. This experimental work emphasizes the difficulty of post-mortem toxicology, as concentrations found at the time of autopsy may be different from concentrations at the time of death, in blood as well as in tissues.

Animals↗

PubMed1992

Calcium-induced fragmentation of skeletal muscle nebulin filaments.

When chicken breast muscle myofibrils were treated with a solution containing 0.1 mM CaCl2 and 30 micrograms of leupeptin/ml, nebulin filaments were fragmented into 200-, 180-, 40-, 33-, and 23-kDa subfragments. All the subfragments except the 180-kDa one were released from the myofibrils. The fragmentation of nebulin filaments seems to be induced by the binding of large amounts of calcium ions. Similar changes took place in nebulin filaments in post-mortem skeletal muscle. It has been proposed that nebulin co-exists with thin (actin) filaments and participates in stabilizing their organization [Wang, K. & Wright, J. (1988) J. Cell Biol. 107, 2199-2212]. Thus, the above result suggests that Ca-induced fragmentation of nebulin filaments destabilizes the organization of thin filaments and is a key factor in meat tenderization during post-rigor aging.

Animals↗

PubMed1999

Reduction in choline acetyltransferase immunoreactivity but not muscarinic-m2 receptor immunoreactivity in the brainstem of SIDS infants.

The cholinergic neurotransmitter system is vital for several brainstem functions including cardiorespiratory control and central chemosensitivity. This study has examined aspects of the cholinergic neurotransmitter system in the brainstem of sudden infant death syndrome (SIDS) and control infants. The cellular localisation and the optical density of the immunoreactivity of the cholinergic enzyme choline acetyltransferase (CHAT-IR) and the muscarinic acetylcholine receptor m2 (m2-IR) in the medulla was described in 14 SIDS and 9 control cases. There was a reduction in the number of CHAT-IR neurons in the hypoglossal nucleus (control: 71.2+/-8.3% vs SIDS: 46.1+/-5.3%) and the dorsal motor nucleus of the vagus (DMV) (control: 77.2+/-5.0% vs SIDS: 52.5+/-7.4%) and reduced optical density of CHAT-IR in the hypoglossal nucleus (control: 0.20+/-0.01 vs SIDS; 0.14+/-0.02) in SIDS infants. In contrast there were no changes in the optical density of m2-IR in the hypoglossal nucleus, the DMV, or the arcuate nucleus. Hypoplasia of the arcuate nucleus was observed in one SIDS infant. These results suggest that there is a specific defect in some cholinergic motor neurons in the medulla of SIDS infants. This could lead to abnormal control of cardiovascular and respiratory function and airway patency and may be one of the contributing factors in the etiology of SIDS.

Brain Stem↗

PubMed2007

Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: correlation with Parkinson's disease.

A real-time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67-kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA-specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes-3-phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, beta-peptide 2-like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging.

Adult↗

PubMed1981

The post-mortem vacuoles of Schlemm's canal.

A two-part study was conducted in which post-mortem changes were investigated in the baboon outflow system. It was found that the meshwork cells closest to the chamber angle were particularly susceptible to post-mortem advance. Post-mortem vacuoles developed in the endothelium of Schlemm's canal and by light microscopy these structures could be mistaken for giant vacuoles. On the other hand it was shown by electron microscopy that the giant vacuoles which have been implicated in the transendothelial transfer of aqueous humour and post-mortem vacuoles were distinct and separate entities.

Animals↗

PubMed1989

Post-mortem stability of membrane-associated sialidase activity in brain.

The post-mortem changes in membrane-associated sialidase (N-acetylneuraminosyl glycohydrolase, EC 3.2.1.18) were examined in rat brain obtained and stored in a manner which paralleled neuropathological handling of human brains. When whole brains were held at 4 degrees C in covered containers for varying periods of time (0.67 h), sialidase activity toward endogenous membrane substrate was elevated. This elevated activity was maximal at 8 h of storage and decreased thereafter. The apparent decrease in enzyme activation from 8 to 67 h of storage was not due to a reduction of activity, but was the result of depletion of endogenous membrane substrate, since activity toward exogenous ganglioside remained elevated. The changes were due to whole brain storage at 4 degrees C, and not a result of being stored at -80 degrees C. The post-mortem activation of sialidase was not due to the expression of a new form of the enzyme, since it displayed characteristics similar to those reported previously: (a) membrane gangliosides being the preferred native substrate, and (b) ganglioside GM1 and lactosylceramide being the major hydrolytic products. The results underscore the importance of post-mortem storage conditions when analyzing complex carbohydrates of brain.

Animals↗

PubMed2001

[Experimental study of restiffening of the rigor mortis].

OBJECTIVE: To observe changes of the length of sarcomere of rat when restiffening. METHODS: We measured the length of sarcomere of quadriceps in 40 rats in different condition by scanning electron microscope. RESULTS: The length of sarcomere of rigor mortis without destroy is obviously shorter than that of restiffening. CONCLUSION: The length of sarcomere is negatively correlative to the intensity of rigor mortis. Measuring the length of sarcomere can determine the intensity of rigor mortis and provide evidence for estimation of time since death.

Animals↗

PubMed1987

Pitfalls in membrane binding sites studies in post-mortem human brain.

A number of neurotransmitter receptor sites have been characterized biochemically in post-mortem human brain from normal subjects and in several neurological and psychiatric diseases. Such studies are valid, however, only when appropriate pre-mortem and post-mortem conditions are controlled. The effects of age, pre-mortem agonic conditions, drug therapy and post-mortem delay on the characteristics of five binding sites (alpha-1, alpha-2 and beta adrenergic receptors, 5HT-2 serotoninergic receptors, imipramine binding sites) were studied. Age related changes in receptor number were found. Pre-mortem anoxia and hypovolemia had no influence on receptor characteristics. The drugs administered before death, in particular neuroleptics, were found to affect binding to some receptors in post-mortem tissue. A post-mortem delay up to 24 hours after death had no effect on binding sites. Experimental strategies (single point values or saturation curves) were also compared.

Adult↗

PubMed1990

Quantifying synaptic number and structure: effects of stain and post-mortem delay.

Current research indicates the importance of synaptic number and structure in plastic processes such as development, learning and memory, and aging. As such, the examination of these neural features has become an important factor in research on human conditions such as mental retardation, aging and Alzheimer's disease. Synaptic research in human tissue typically involves delayed post-mortem fixation, therefore the current research was designed to examine the effect of post-mortem delay on synaptic number and structure in tissue stained with either routine osmium lead citrate/uranyl acetate (osmium) or ethanol phosphotungstic acid (EPTA). Results indicate that synaptic density shows either a gradual decline (EPTA) or an initial marked drop followed by a plateau (osmium) up to 10-15 h post-mortem depending on the stain used. The number of synaptic vesicles per synapse also undergoes a gradual decline. Measures of synaptic structure were more stable, with the primary change being an initial increase in the cross-sectional length of the synapse. Maximal height of the pre- and postsynaptic dense elements were not affected by post-mortem delay. The EPTA stain gave the best estimates of synaptic parameters with short post-mortem delays. These results indicate that different synaptic measures (and stains) show different responses to post-mortem fixation delay, and that experimental or statistical methods must be used to control for post-mortem effects.

Animals↗

PubMed1995

Changes in N-acetyl-aspartate content during focal and global brain ischemia of the rat.

N-Acetyl-aspartate (NAA) is almost exclusively localized in neurons in the mature brain and might be used as a neuronal marker. It has been reported that the NAA content in human brain is decreased in neurodegenerative diseases and in stroke. Since the NAA content can be determined by nuclear magnetic resonance techniques, it has potential as a diagnostic and prognostic marker. The objective of this study was to examine the change of NAA content and related substances following cerebral ischemia and compare the results to the damage of the tissue. We used rats to study the changes of NAA, N-acetyl-aspartyl-glutamate (NAAG), glutamate, and aspartate contents over a time course of 24 h in brain regions affected by either permanent middle cerebral artery occlusion (focal ischemia) or decapitation (global ischemia). The decreases of NAA and NAAG contents following global brain ischemia were linear over time but significant only after 4 and 2 h, respectively. After 24 h, the levels of NAA and NAAG were 24 and 44% of control values, respectively. The concentration of glutamate did not change, whereas the aspartate content increased at a rate comparable with the rate of decrease of NAA content. This is consistent with NAA being preferentially degraded by the enzyme amidohydrolase II in global ischemia. In focal ischemia, there was a rapid decline of NAA within the first 8 h of ischemia followed by a slower rate of reduction. The reductions of NAA and NAAG contents in focal ischemia were significant after 4 and 24 h, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

[Value of bacteriologic studies within the scope of forensic autopsies].

The various questions regarding bacteriological investigations within the scope of forensic autopsies are discussed in the light of our own cases and with regard to the relevant literature: estimate of the age of the corpse on the basis of decomposition changes caused by bacteria; determination of so-called bacteriograms from the point of view of criminalistics; supplementary investigations of the cause of death. Iatrogenic infections (e.g., gangrene) are gone into in more detail, as is so-called infantile botulism within the scope of the "sudden infant death syndrome". Finally, it is pointed out that when doing forensic autopsies, thought should also be given to illnesses that have only been known for a few years, examples being legionnaires' disease and the toxic shock syndrome ("tampon sickness").

Adult↗

PubMedDate not supplied

Senile dementia and Alzheimer's disease: lack of changes of the cortical content of quinolinic acid.

The content of Quinolinic Acid (QUIN) was fragmentographically measured in the frontal, parietal and temporal cortex obtained at autopsy from patients affected by Alzheimer's disease-senile dementia Alzheimer type (AD/SDAT) or matched controls. The density of large cholinergic neurons in the nucleus basalis magnocellularis and the density of plaques in the hippocampal formation, parietal and frontal cortex of these patients was also evaluated in order to obtain a quantitative estimation of the Alzheimer type changes. In the three cortical areas studied, the content of QUIN was similar in AD/SDAT patients and age matched controls. The AD/SDAT patients had an important reduction of the number of large cholinergic neurons in the nucleus basalis magnocellularis and a much higher density of plaques in cortex and in hippocampus than age matched controls. The data reported here do not support the possibility than an accumulation of QUIN plays a role in the neuronal degeneration occurring in the cortex of patients affected by AD/SDAT.

Aged↗