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[Comparison of postmortal changes in the ultrastructure of the masseter muscle and the longissimus dorsi muscle in pigs with PSE-meat].

Samples of the two muscles were taken from 8 Landrace fattened pigs, affected with pale, soft exudative meat, during stunning and 15, 30, 45 and 60 minutes after death; also 2, 3, 6, 12, 24 and 48 hours after slaughter, with storage at 20 degrees C for the first six hours and 2-5 degrees C subsequently. Considerable changes were found during the first hour after death, or even in samples taken during stunning, in longissimus dorsi samples. These consisted of destruction of mitochondria and sarcoplasmic reticulum, breakdown of cell membranes, liberation of clumps of fibre protein, disappearance of glycogen, rigor and destruction of capillaries. Such changes would account for the features of pale, soft exudative meat such as water loss, brief rigor, pale colour, deficiency of energy-rich phosphates. By contrast, in the masseter muscles of the same animal these changes did not occur until later, or were in port absent. In both muscle the breakdown of fibres took place by destruction of the "I" bands and the "Z" strips, and this process also commenced in longissimus dorsi before masseter.

Animals↗

[Changes in several lipid metabolism indices following death and resuscitation].

The lipolytic activity in the adipose tissue, unesterified fatty acids (UFA) in the blood and adipose tissue, as well as ketone bodies and beta-lipoproteins in the blood were determined in dogs during dying of acute blood loss and the restorative period after the revival of the organism. During agony the activation of lipolysis in the adipose tissue, a decrease of UFA and beta-lipoproteins and an increase of ketane bodies contents in the blood were detected. At the end of the third minute of clinical death there occurred a depression of lipolysis and an increase of UFA content in the adipose tissue. One hour after the revival of the organism the blood UFA content and beta-proteins decrease, but the ketone bodies content rises; simultaneously there occurs some reduction of lipolytic activity of the adipose tissue. At the late postreanimation period (in 1, 3, and 7 days) an activation of lipolysis in the adipose tissue and an increase of UFA, ketone bodies, and beta-lipoproteins content in the blood was noted. The adipose tissue UFA content was low during the postreanimation period. The given results have shown that the changes in the lipid metabolism could play some role in the pathogenesis of non-reversibility during dying and after the revival of the organism.

Adipose Tissue↗

The relevance of the detection of troponins to the forensic diagnosis of cardiac contusion.

The forensic diagnosis of cardiac contusion has hitherto been based mainly on anamnesis, concomitant thoracic injuries and the detection of macroscopic changes to the heart. Parallel histological and serological investigations of the heart-specific troponins have been conducted with varying results. This paper aims to show whether heart-specific troponins are suitable as a means of securing the diagnosis in proven cases of cardiac contusion and of determining which of the three heart-specific troponins cTnT, cTnI and cTnC are most significant in serology and histology for postmortem diagnosis. In the study, 25 cases of known cardiac contusion and 11 controls without vital myocardial trauma taken from autopsy material were prospectively investigated. Investigation of the venous serum revealed significant differences in the concentrations of the case and control groups for troponin T (mean value 5.5056 versus 0.4982; p=0.014), for troponin C (mean value 263.9280 versus 68.5640; p=0.001) and for troponin I (mean value 1404.0560 versus 36.1650; p=0.003). In histology there are also significantly different depletions between the groups investigated (cTnT: p=0.002; cTnC: p=0.003; cTnI: p<0.001) taking into account the autolysis time.

Case-Control Studies↗

[Pathomorphological study in craniocerebral injury].

Time course of the posttraumatic process in craniocerebral injuries is analyzed. Pathomorphological picture of changes in soft tissues of the head, meninx, and brain matter are described. Several periods are distinguished. Factors affecting the course of the posttraumatic process in the above-mentioned structures are discussed.

Brain↗

Changes in relative levels of specific brain mRNA species associated with schizophrenia and depression.

Total cellular polyadenylated RNA (poly(A)+ RNA, mRNA) was prepared after guanidinium thiocyanate extraction of frozen brain tissue from age-matched controls and patients suffering from schizophrenia and unipolar depression. These mRNA populations were analysed by in vitro translation followed by two-dimensional gel analysis. Data were obtained from fluorograms derived from 10 different schizophrenic patients, 10 different controls and 5 different depressive patients. The relative concentrations of mRNA species coding for 4 translation products (33 kDa, pI 5.8; 26 kDa, pI 5.8; 35 kDa, pI 7.1; 23 kDa, pI 6.1) were significantly reduced in schizophrenia compared to controls when determined by computerised image analysis of the fluorograms. In the case of depression, the relative concentrations of mRNA species coding for 6 translation products were significantly altered, 4 being increased (38 kDa, pI 6.2, 17 kDa, pI 5.7, 35 kDa, pI 7.1; 23 kDa, pI 6.1) and two decreased (34 kDa, pI 6.2; 33 kDa, pI 5.8). Three translation products were altered in both schizophrenia and depression, one (33 kDa, pI 5.8) being altered according to the same trend, a decrease relative to controls, but two (35 kDa, pI 7.1; 23 kDa, pI 6.1) being altered differently in schizophrenia (reduced) and depression (increased). The effects of post mortem delay, mode of death and drug treatment on mRNA composition were also examined and found not to affect the levels of these translation products significantly. The significance of these changes will be discussed in relation to their relevance of biological mechanisms in the psychoses.

Aged↗

A new staining method for constriction marks in skin.

A modified Poley's acid fuchsin-methyl green stain was used to demonstrate ligature marks in tissues taken at autopsy. This stain was compared in 30 cases with haematoxylin-eosin, Mallory's trichrome and Ogata's picro-indigocarmine stains. Using the modified Poley method, it was possible to demonstrate the compression mark in corpses even when post-mortem changes were advanced. The method was found useful in evaluating the cases when the force used was minimal or when the mark was atypical using the usual haematoxylin-eosin method.

False Positive Reactions↗

A high-performance liquid chromatography method for hypoxanthine determination in vitreous humour: application to estimation of post mortem interval.

We have developed a new technique to determine the concentration of hypoxanthine [Hx] in a reverse phase column using a modified high-performance liquid chromatography (HPLC) method that is faster and more reliable than those previously described. In this paper we present a formula for estimating the post mortem interval (PMI) based on this HPLC method by applying the inverse prediction method. The regression line obtained by changing the variables gives PMI = 0.183 [Hx] + 0.599 (PMI in hours, [Hx] in micromol/L, R2 = 0.531, P < 0.05).

Chromatography, High Pressure Liquid↗

[Ultrastructural changes in the nephron during ischemia and organ "survival"].

Ultrastructural analysis of the epithelium of the proximal and the distal portions of the kidney nephron of albino rats in "survival" of the organ in the cadaver and in experimental ischemia showed a different reaction of the cells to these actions. An intracellular edema and characteristic changes in the ultrastructure of the mitochondria appear in the tubular epithelium during the organ autolysis in the animal cadaver. Under conditions of experimental ischemia, against the background of intracellular edema, there develop marked changes in the lysosomal apparatus of the cells, swelling of the mitochondria and also a marked dilatation of the cysternae of the endoplasmic reticulum and of the Golgi complex.

Animals↗

Is the G72/G30 locus associated with schizophrenia? single nucleotide polymorphisms, haplotypes, and gene expression analysis.

BACKGROUND: The genes G72/G30 were recently implicated in schizophrenia in both Canadian and Russian populations. We hypothesized that 1) polymorphic changes in this gene region might be associated with schizophrenia in the Ashkenazi Jewish population and that 2) changes in G72/G30 gene expression might be expected in schizophrenic patients compared with control subjects. METHODS: Eleven single nucleotide polymorphisms (SNPs) encompassing the G72/G30 genes were typed in the genomic deoxyribonucleic acid (DNA) from 60 schizophrenic patients and 130 matched control subjects of Ashkenazi ethnic origin. Case-control comparisons were based on linkage disequilibrium (LD) and haplotype frequency estimations. Gene expression analysis of G72 and G30 was performed on 88 postmortem dorsolateral prefrontal cortex samples. RESULTS: Linkage disequilibrium analysis revealed two main SNP blocks. Haplotype analysis on block II, containing three SNPs external to the genes, demonstrated an association with schizophrenia. Gene expression analysis exhibited correlations between expression levels of the G72 and G30 genes, as well as a tendency toward overexpression of the G72 gene in schizophrenic brain samples of 44 schizophrenic patients compared with 44 control subjects. CONCLUSIONS: It is likely that the G72/G30 region is involved in susceptibility to schizophrenia in the Ashkenazi population. The elevation in expression of the G72 gene coincides with the glutamatergic theory of schizophrenia.

Adolescent↗

Biological markers in mental disorders: post-mortem studies.

Many neurotransmitters, related enzymes and receptors are stable post-mortem and can be measured in routine autopsy material. Comparison of brain tissue from control and disease cases can provide evidence of alterations in neurotransmitter systems in mental disorders. However, before attributing a difference in the neurochemical profile to the disease process itself, care has to be taken to exclude non-specific influences such as age, agonal state, drug therapy and post-mortem stability. Changes in a chemical marker can be used to assess the specificity of neuronal loss in degenerative disease but it may be impossible to distinguish such changes from alterations in turnover in surviving neurones. These problems are discussed with particular reference to post-mortem studies of schizophrenia and Alzheimer's disease.

Age Factors↗

Differential changes in apolipoprotein E in schizophrenia and bipolar I disorder.

BACKGROUND: This study extends an initial finding of increased levels of apoE in Brodmann's area (BA) 9 from subjects with schizophrenia to determine if apoE is altered in other brain regions and in brains from subjects with bipolar I disorder (BID). METHODS: ApoE was quantified apoE in BA 9, 10, 40, 46 and caudate putamen from control (n = 18), schizophrenic (n = 19) and BID (n = 8) subjects using Western blotting. RESULTS: In schizophrenia, there was increased apoE in BA9 (mean +/- SEM: schizophrenia 3.8 +/- .18 vs. control 3.2 +/- .19) and BA46 (schizophrenia 2.7 +/- .26 vs. control 1.6 +/- .20). In BID, increased levels of the apolipoprotein were detected in the caudate putamen (BID 3.3 +/- .44 vs. control 2.4 +/- .19) and BA9 (BID 4.0 +/- .27 vs. control 3.2 +/- .19) with a decrease in apoE being measured in BA10 (BID 1.6 +/- .16 vs. control 3.9 +/- .53). CONCLUSIONS: This study has shown disease specific, regionally discrete changes in levels of apoE in brain obtained post mortem from schizophrenic and BID subjects. Our data adds weight to the hypothesis that changes in the levels of apolipoproteins may be involved in the pathologies of schizophrenia and bipolar disorder.

Adult↗

Repeated antidepressant drug treatment, time of death and frequency of handling do not affect [3H]paroxetine binding in rat cortex.

[3H]Paroxetine binding to the serotonin transporter has been shown to be altered in brain tissue from schizophrenic subjects. Some schizophrenic subjects are treated with antidepressant drugs, some of which bind to the serotonin transporter and their time of death is variable. To determine if these confounding factors could affect [3H]paroxetine binding, [3H]paroxetine binding to cortical membrane from rats treated with the antidepressant drugs for 10 or 28 days and in non-treated rats that were killed at different times of the day was measured. Drug treatment, when compared to injection with 0.9% saline and time of death, did not affect [3H]paroxetine binding. Treatment with imipramine [10 days: mean +/- S.D.: 590 +/- 59 fmol/mg protein (P < 0.05); 28 days: 653 +/- 59 fmol/mg protein (P < 0.01)] or mianserin [10 days: 600 +/- 43 (P < 0.05)] caused a significant decrease in the density of [3H]paroxetine binding compared to that in fluoxetine-treated rats (10 days: 820 +/- 211 fmol/mg protein; 28 days: 764 +/- 100 fmol/mg protein). Thus, overall, these data do not suggest changes in [3H]paroxetine binding reported in the human brain tissue would be due to antidepressant drug treatment or time of death.

Animals↗

Changes in somatodendritic but not terminal dopamine regulation in aged rhesus monkeys.

For these studies, young (8-9 years), middle-aged (14-17 years) and aged (23-28 years) rhesus monkeys were used as a model of normal aging in humans to investigate changes in dopamine (DA)-containing neurons in senescence. Aged monkeys exhibited significant age-related motoric declines as compared to the young animals. In vivo microdialysis studies showed that basal levels of the DA metabolites, homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) were diminished by 44% and 79%, respectively, in the substantia nigra (SN) of aged monkeys. In addition, d-amphetamine-evoked overflow of DA in the SN was diminished by 30% in the middle-aged animals and 67% in the aged monkeys. Post-mortem measures of DA and DA metabolites showed significant decreases in DA (20%), DOPAC (47%) and HVA (22%) levels in the putamen and a 25% decline in HVA tissue levels in the SN of the aged monkeys as compared to the young animals. Unbiased stereological cell counting of tyrosine hydroxylase (TH)-immunoreactive neurons in the SN showed a small (15-20%) but significant age-related decline in TH-positive neurons. In addition, there was a small (15-20%) but significant decline in TH-positive fiber density and TH-positive cell size. In comparison to the massive loss of DA neurons responsible for the movement dysfunctions seen in Parkinson's disease, pronounced functional changes in DA release in the SN and putamen may significantly contribute to the motoric dysfunctions characterizing normal aging in rhesus monkeys.

Aging↗

Post-mortem dopamine dynamics assessed by voltammetry and microdialysis.

The effects of total brain ischemia (decapitation) on striatal extracellular levels of dopamine (DA) dihydroxyphenyl acetic acid (DOPAC) and ascorbic acid (AA) in chloral hydrate anesthetized rats were monitored at 1-min intervals by differential normal pulse voltammetry (DNPV) with numerical deconvolution of the catechol peak. Changes in pH were assessed by the shift of AA oxidation potential and incorporated into the computational procedure. The AA peak showed a sharp, short-lived (less than 15 min) postdecapitation rise, followed by a slower secondary increase. The DA signal increased 100-fold in the first 20 min followed by a slow decline. DOPAC levels fell 80% within 15 min after death. The post-mortem changes in extracellular DA and DOPAC were verified by a similar experiment using microdialysis. These observations probably reflect massive release and impaired uptake of DA combined with reduced monoamine oxidase activity. Changes in membrane permeability to DOPAC as a consequence of a post-mortem drop in pH may also contribute to the decline in extracellular DOPAC levels.

3,4-Dihydroxyphenylacetic Acid↗

Morphology and synaptic input of substance P receptor-immunoreactive interneurons in control and epileptic human hippocampus.

Substance P (SP) is known to be a peptide that facilitates epileptic activity of principal cells in the hippocampus. Paradoxically, in other models, it was found to be protective against seizures by activating substance P receptor (SPR)-expressing interneurons. Thus, these cells appear to play an important role in the generation and regulation of epileptic seizures. The number, distribution, morphological features and input characteristics of SPR-immunoreactive cells were analyzed in surgically removed hippocampi of 28 temporal lobe epileptic patients and eight control hippocampi in order to examine their changes in epileptic tissues. SPR is expressed in a subset of inhibitory cells in the control human hippocampus, they are multipolar interneurons with smooth dendrites, present in all hippocampal subfields. This cell population is considerably different from SPR-positive cells of the rat hippocampus. The CA1 (cornu Ammonis subfield 1) region was chosen for the detailed morphological analysis of the SPR-immunoreactive cells because of its extreme vulnerability in epilepsy. The presence of various neurochemical markers identifies functionally distinct interneuron types, such as those responsible for perisomatic, dendritic or interneuron-selective inhibition. We found considerable colocalization of SPR with calbindin but not with parvalbumin, calretinin, cholecystokinin and somatostatin, therefore we suppose that SPR-positive cells participate mainly in dendritic inhibition. In the non-sclerotic CA1 region they are mainly preserved, whereas their number is decreased in the sclerotic cases. In the epileptic samples their morphology is considerably altered, they possessed more dendritic branches, which often became beaded. Analyses of synaptic coverage revealed that the ratio of symmetric synaptic input of SPR-immunoreactive cells has increased in epileptic samples. Our results suggest that SPR-positive cells are preserved while principal cells are present in the CA1 region, but show reactive changes in epilepsy including intense branching and growth of their dendritic arborization.

Adult↗

Post-mortem changes in the rabbit retina. A study by light microscopy.

The course of post-mortem changes in rabbit retina has been followed. Short post-mortem periods are accompanied by degenerative changes limited mainly to the visual cells and retinal pigment epithelium. Long post-mortem periods are associated with degenerative changes throughout the retina. Retinal tissue maintained at room temperature was less affected than that kept at body temperature (37degreesC). Post-mortem changes are similar to those observed following periods of pressure induced ischaemia and it is thought that the mechanical effects of pressure on retinal tissue are minimal at the level of resolution afforded by light microscopy.

Animals↗

The effect of different storage methods on the mechanical properties of trabecular bone.

The effect of different storage methods on the elastic and viscoelastic properties of trabecular bone was examined using non-destructive compression tests to 0.45% specimen strain. There was a 10% decrease in stiffness during the first 24 h post mortem. Storage by freezing or in ethanol for 100 d did not change the stiffness, and neither did several thawing, testing and refreezing sequences. The viscoelastic properties were more sensitive to storage and showed significant although small changes during 100 d of storage. The effect of defatting the specimens was a 30% increase in stiffness and a 50% decrease in viscoelastic energy dissipation.

Adult↗

Effect of post-mortem delay on density of tachykinin receptors in rat peripheral tissues.

The effect of post-mortem delay on the affinity and density of tachykinin NK1 and NK2 receptors was examined in the rat submandibular gland and gastric fundus, respectively, using saturation binding studies with the radioligands [125I]Bolton-Hunter [Sar9, Met(O2)11]SP and [125I][Lys5, Tyr(I2)7, MeLeu9, Nle10]NKA(4-10). For NK1 receptors, no significant changes were seen in either Kd (control 375 +/- 35 pM, n = 5; 32 h post-mortem 390 +/- 59 pM, n = 5) or Bmax (control 96 +/- 16 fmol/mg protein, n = 5; 32 h post-mortem 62 +/- 10 fmol/mg protein, n = 5). For NK2 receptors, no alterations were seen up to 16 h post-mortem. However, significant (p < 0.001) changes were seen at 32 h post-mortem (n = 4), where values for Kd were increased (3.0 +/- 0.2 nM) and those for Bmax were reduced (42 +/- 5.9 fmol/mg protein), relative to control (Kd = 1.3 +/- 0.2 nM; Bmax = 208 +/- 30 fmol/mg protein, n = 5). These changes are probably related to observed histological deterioration. This study demonstrates the stability of tachykinin receptors in these peripheral tissues and indicates the suitability of post-mortem tissue as a valid control in future tachykinin receptor studies.

Animals↗