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At least 955 records · Page 53Linked to original sources

PubMed2000

Physiological changes in pigs exposed to a blast wave from a detonating high-explosive charge.

The aim of this project was to study respiration, circulation, and brain activity in pigs during and after a blast wave exposure. Ten anesthetized pigs were used. Seven were exposed to blast and three were controls. Physiological parameters of respiration and circulation as well as cortical activity were followed from 30 minutes before until 120 minutes after the real or simulated blast. There were no significant changes in heart rhythm, cardiac output, arterial oxygen or carbon dioxide tension, blood pH, or mixed venous saturation during the experiment. The blast exposure caused intestinal injuries but no lung damage. A transient flattening of the electroencephalogram was seen immediately after the blast in four experimental animals, in contrast to the unchanged baseline electroencephalogram of the control animals. This momentary depression of cortical activity accompanied by short-lasting apnea indicates a blast wave-induced effect on the brainstem or higher controlling center.

Animals↗

PubMedDate not supplied

[Ascertainment of the cause and tempo of death in forensic medical practice].

In order to develop a method of ascertaining a cause of death and of evaluating its tempo the authors undertook a histological study and a study of a dehydration degree in 76 cases of death due to the below reasons: mechanical trauma, mechanical asphyxia, burn shock, and carbon monoxide intoxication. Acute emphysema of lungs, lack of edemas in lungs and brain, desquamation of pulmonary macrophages, hyperemia of renal capillaries, primary urine in some glomerules, prevalence of ischemic changes with karyopyknosis in medulla and hypohydration of brain were typical of fast death. Prevalence of dystelectasis in lungs, emptying of pulmonary capillaries, evident edema of lungs and brain, desquamation of pulmonary macrophages, lack of primary urine in glomerular capsules, acute circulatory disorders of renal hemodynamics with sweating of fibrin and erythrocyte glomerules into cavities, necrotic nephrosis, pigment cylinders in renal tubules, thrombi in vessels, prevalence of chromatolysis, karyolysis and cytolysis in medulla, pronounced glial reaction as well as pronounced edema of brain and its hyperhydration were typical of slow death.

Blood Volume↗

PubMedDate not supplied

[Post-mortem decay of rat skeletal muscle polysomes].

Post-mortem changes of cytoplasmic RNP particles from rat skeletal muscles are studied using sucrose density gradient. The polysome destruction is found to beign within 1-2 hours after the animal death. However, a part of polysomes turned to be stable at least within 48-60 hours after the death. These polysomes incorporated 14C-leucine into acid insoluble fraction in cell-free system and were decomposited by RNase treatment (10 mkg/ml). The data suggest that within 24-48 hours of the after-death destruction the decay begins to free monoribosomes while there are still active polysomes in muscles.

Animals↗

PubMed1983

Segmental demyelination and remyelination in lumbar spinal roots of patients dying with diabetes mellitus.

Morphometric evaluations of histopathological changes in postmortem materials from three patients with diabetes mellitus with neuropathy, nephropathy, and retinopathy were made on the sural nerve, lumbar spinal roots, lumbar dorsal root ganglion (2 cases), and fasciculus gracilis. In all three patients there was a marked decrease in densities of both the large and the small myelinated fibers in the sural nerves. In the lumbar spinal roots, segmental demyelination and remyelination with or without decrease in the number of myelinated fibers per root was the main finding in both dorsal and ventral roots, being more common in the dorsal roots. At the third cervical segment of the fasciculus gracilis, the myelinated fiber density was slightly decreased in one patient and moderately decreased in the other two. The number of cell bodies of the fifth dorsal root ganglion was within normal limits in the two patients where this was examined, although the median diameters approximated the lower limit found in controls. The potential presence of segmental demyelination and remyelination in dorsal and ventral spinal roots should be considered especially when assessing electromyographic changes and nerve conduction in diabetic patients.

Adult↗

PubMed2005

Abnormal Sp1 transcription factor expression in Alzheimer disease and tauopathies.

Sp1 transcription factor expression was examined by immunohistochemistry, immunofluorescence and confocal microscopy in Alzheimer disease (AD), Pick disease (PiD), progressive supranuclear palsy (PSP), Parkinson disease (PD) and Dementia with Lewy bodies (DLB). Sp1 partly co-localizes with hyper-phosphorylated tau deposits in neurofibrillary tangles, dystrophic neurites of senile plaques and neuropil threads in AD, and in neurons, astrocytes and oligodendrocytes bearing hyper-phosphorylated tau in PiD and PSP. Sp1 is not found in alpha-synuclein inclusions in PD and DLB. These modifications are not associated with changes in the total expression levels of Sp1, as revealed with gel electrophoresis and Western blotting of brain homogenates. Furthermore, no co-immunoprecipitation of Sp1 and phospho-tau was observed in AD and PiD cases. Since Sp1 binding sites are present in the promoters of several genes involved in amyloid and tau, and Sp1 is regulated by oxidative stress, the present findings suggest that Sp1 deposition in hyper-phosphorylated tau deposits may have functional consequences in the pathology of AD and other tauopathies.

Alzheimer Disease↗

PubMed1989

Loss of muscarinic cholinergic receptors from the temporal cortex of alcohol abusers.

It is currently controversial whether all the brain damage in alcohol abusers in the result of thiamine deficiency (Wernicke-Korsakoff's disease) or whether, in addition, alcohol abuse may affect the brain by other mechanisms as well. The purpose of this study was to determine if alcohol abuse affects muscarinic cholinergic and benzodiazepine receptors in histologically normal brains obtained at autopsy in a general hospital population. Patients were excluded from this study if they had clinical brain diseases (including Wernicke's disease), died in coma, or had liver disease, significant brain atrophy, or dementia severe enough to require institutionalization. We found that muscarinic cholinergic synaptic receptor density determined with [3H] quinuclidinly benzilate was decreased by 40% in homogenates of the tempeoral cortex of 26 alcohol abusers compared with 26 matched nonalcoholic controls. The affinities of the muscarinic receptors were not significantly different between the two groups. In contrast, receptor densities and affinities of benzodiazepine receptors determined with [3H]flunitrazepam were not significantly different in the two groups. Age and death-autopsy time interval had no significant effects on either wet tissue protein concentrations, yields of protein after centrifugation, or receptor binding. The contributions of age and time interval were each less than 2% of the total variance of protein concentrations and receptor binding. When patients were excluded or included who had received cholinergic, anticholinergic, or benzodiazepine medications before death, no significant effects on the final results were observed. Pneumonia, known to be associated with acute hypoxia, and chronic obstructive pulmonary disease, known to be associated with chronic hypoxia, where approximately equally distributed between the two groups and had no significant effects on the results reported here. The loss of muscarinic and the sparing of benzodiazepine receptors occurs in the temporal cortex of histologically normal brains in the absence of significant atrophy and of gross dementia. This means that these changes are early in the development of an alcohol encephalopathy. We have previously reported a decrease in both muscarinic and benzodiazepine receptor binding in the frontal cortex and a decreasing muscarinic but not benzodiazepine receptors in the temporal cortex of alcohol abusers. Taken together, these findings suggest that alcohol neurotoxicity does not simply result in a random loss of neurons and or their associated synapses with their receptors. Instead, different types of receptors, depending upon their location in different brain regions, are specifically affected or spared. This suggests the involvement of region- and receptor-specific mechanisms in chronic alcohol toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗

PubMed1998

Dating human skeletal remains: investigating the viability of measuring the equilibrium between 210Po and 210Pb as a means of estimating the post-mortem interval.

Estimating the post-mortem interval in skeletal remains is a notoriously difficult task; forensic pathologists often rely heavily upon experience in recognising morphological appearances. Previous techniques have involved measuring physical or chemical changes within the hydroxyapatite matrix, radiocarbon dating and 90Sr dating, though no individual test has been advocated. Within this paper it is proposed that measuring the equilibrium between two naturally occurring radio-isotopes, 210Po and 210Pb, and comparison with post-mortem examination samples would produce a new method of dating human skeletal remains. Possible limitations exist, notably the effect of diagenesis, time limitations and relative cost, though this technique could provide a relatively accurate means of determining the post-mortem interval. It is therefore proposed that a large study be undertaken to provide a calibration scale against which bones uncovered can be dated.

Bone and Bones↗

PubMedDate not supplied

[Methodology of post-mortem research. Apropos of setting-up a data bank for studying the biology of depression].

Investigation of post mortem neurobiochemical changes is an important field in biological psychiatry which allows analyses of the analogies between peripherical markers and the central neurochemical processes they represent. Our study discusses the pathological neuroanatomy (collection and conservation of the anatomical specimens) and clinical criteria (selection of an evaluation and diagnostic scale, analysis of results of retrospective clinical interviews: "the psychological autopsy"). We also discuss the many methodological issues which arise in interpretations of these correlations. We wish to encourage others to apply a standardized methodology to these scientific studies of post mortem neurochemical parameters and retrospective clinical diagnosis.

Adult↗

PubMed1990

Post-mortem visualization of peroxisomes in rat and in human liver.

This paper describes spontaneous post-mortem changes of peroxisomal staining in normal liver and kidney of rats and in human autopsy liver. At room temperature, regional staining loss is observed at 18 h after death in rat kidney, at 24 h in human liver and at 48 h in rat liver. Preservation at 4 degrees C delays this phenomenon. In human liver, the peroxisomal volume density is decreased at both temperatures at 48 h. After freezing of fresh tissue in dry ice, peroxisomal staining is decreased homogeneously. Under the electron microscope, peroxisomal alterations suggest a loss of catalase activity. These changes do not necessarily preclude the study of peroxisomal features since, even after 48 h at room temperature, peroxisomes are still well stained in the less affected regions. Catalase and three beta-oxidation enzymes, namely acyl-CoA oxidase, bifunctional protein (with enoyl-CoA hydratase and 3-hydroxyacyl-CoA dehydrogenase) and 3-oxoacyl-CoA thiolase, could be visualized immunocytochemically in human autopsy livers up to 48 h after death. However, the study of certain peroxisomal features such a catalase activity and peroxisomal distribution, may be hampered as the post-mortem period is prolonged.

Animals↗

PubMed1979

Post-mortem changes in skeletal muscle connectin.

Changes in connectin and elasticity of skeletal muscle were determined during post-mortem ageing. The amount of connectin decreased with increasing time of post-mortem storage whereas the rate of the decrease depended on the source of muscles. The loss in elasticity of muscle coincided well with the decrease in connectin contents. Electron microscopically, a network structure between the Z discs vanished when the amount of connectin fell to zero. We have concluded that the continuous net structure of connectin is responsible for about 30% of the total elasticity of living skeletal muscle and its degradtaion is responsible for post-mortem tenderization of meat.

Animals↗

PubMed1982

Monooxygenase activities of human liver, lung, and kidney microsomes - a study of 42 post mortem cases.

The cytochrome P-450-dependent monooxygenase system was examined in microsomal fractions prepared from 42 post mortem human livers and 9 lungs and kidneys. Electron microscopy studies indicated that the human liver samples were relatively free of mitochondrial and plasma membrane contamination, but samples of kidney and lung were less pure. The microsomal fractions from all organs were judged to be relatively free of haemoglobin and methaemoglobin. The specific enzyme activities for several drug substrates for the monooxygenase, NADPH-cytochrome c reductase activity and the content of the microsomal cytochromes were measured. The values of the biochemical parameters studied were found to be quite variable and the values for the human liver were appreciably lower than those obtained with liver microsomes from laboratory rodents. The enzyme activities of the human kidney and lung microsomal fractions were 1-10% of those seen for human liver samples, except for NADPH-cytochrome c(P-450) reductase activity. In order to evaluate any post mortem changes in human liver, correlations between drug metabolism activities and either cytochrome P-450 or NADPH-cytochrome c (P-450) reductase content were examined. Strong correlations (r greater than 0.91) were seen only between aminopyrine or ethylmorphine demethylase activity and cytochrome P-450 content in samples obtained within 4 hours of death. Longer post mortem times gave poorer correlation between activity and cytochrome content. These studies document several conditions required in order to obtain human microsomal fractions representative of the activities in fresh, viable tissue.

Adult↗

PubMed1996

Aspirin does not prevent the attenuation of myocardial stunning by the ACE inhibitor ramiprilat.

The attenuation of myocardial stunning by the ACE inhibitor ramiprilat is prevented by cyclooxygenase inhibition with indomethacin. In the clinical setting of ischemia/reperfusion however, the cyclooxygenase inhibitor aspirin is widely used to prevent platelet aggregation. The present study therefore investigated whether aspirin in dosages sufficient to inhibit platelet aggregation interferes with the attenuation of myocardial stunning by ramiprilat. Fifteen dogs received either 1 mg/(kg.day) (group I, n = 7) or 10 mg/(kg.day) (group II, n = 8) aspirin orally for 1 week. Both dosages of aspirin inhibited ADP-induced platelet aggregation. The dogs were then anesthetized thoracotomized and subjected to 15 min LCx-occlusion and 4 h reperfusion. Before LCx-occlusion, groups I and II received ramiprilat (20 micrograms/kg, i.v.). Systemic hemodynamics, posterior myocardial blood flow (PMBF, colored microspheres) and wall thickening (PWT, sonomicrometry) of these groups were measured and data compared to placebo-controls (group III, n = 11) and dogs receiving only ramiprilat before LCx-occlusion (group IV, n = 11). Four dogs received 10 mg/(kg.day) aspirin without ramiprilat (group V). Mean aortic pressure was kept constant by an intra-aortic balloon, and heart rate did not change. PMBF was not different between the five groups. Under control conditions and during myocardial ischemia PWT was also not different. At 4 h reperfusion PWT was still depressed in group III (-5 +/- 20% of control) and group V (-23 +/- 6%) whereas PWT recovered to the same extent in groups I (46 +/- 23%), II (50 +/- 15%) and IV (58 +/- 18%) (all P < 0.05 v groups III and V). The attenuation of myocardial stunning by the ACE inhibitor ramiprilat is not prevented by aspirin in dosages which are nevertheless sufficient to inhibit platelet aggregation.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1988

[The significance of collagen in determining the age of a wound].

The aim of the present study was to find out whether the quantitative and/or qualitative analysis of collagen can be useful in the determination of the age of healing skin wounds in various body regions of patients of different ages and sex. The quantitative measurement of total wound collagen revealed no clear time-dependent changes. Immunohistochemical staining for collagen types I and III demonstrated the presence of type III as early as 2 days after injury. Procollagen type I was found in wounds beginning from 4 days on, while type I collagen was not present before 6 days after the injury. Immunohistochemical analysis of specific basement membrane proteins, collagen type IV and laminin, showed a reconstruction of the epithelial basement membrane beginning from on day 5, while a completely rebuilt basement membrane was found in most cases after more than 14 days, depending on the dimension of the wound and its treatment.

Adolescent↗

PubMed1997

[Changes in the sodium, potassium and lithium ion concentration in human epidermis in relation to death].

The concentrations of Na+, K+, Li+ have been assayed in the epidermis samples from 58 cadavers and 20 healthy individuals. The samples have been taken from the heels, and assayed with 2 flame photometers (Corning 480), using standard solutions supplied by the manufacturer. A concentration of Na+ and K+ in men exceeded the levels of these ions in women by two-fold. A level of Li+ is the same in both sexes and amounts to 2.8 mEq/kg. The Na+:K+ ratio in the epidermis of women and men is about 4:1. In the samples collected from cadavers, the difference in Na+ and K+ levels has been lower but Li+ level has been higher, amounting to 4.3 mEq/kg.

Adult↗

PubMed2005

MRI evidence for multiple sclerosis as a diffuse disease of the central nervous system.

The classical view of MS as a chronic inflammatory demyelinating disease leading to the formation of focal central nervous system (CNS) white matter (WM) lesions has been recently challenged by pathological studies and by the extensive application of modern MRI-based techniques. There is now overwhelming evidence supporting the following statements: MS causes widespread tissue damage in the normal-appearing white matter (NAWM) of the brain and spinal cord, whose extent and severity is more strictly associated to the clinical manifestations of the disease than the extent of focal pathology. Discrete, macroscopic lesions are just the tip of the iceberg of MS pathology. Grey matter (GM) damage is a consistent feature of all MS phenotypes, which is progressive from the start of the relapsing-remitting phase of the disease. As is the case for WM, GM damage is also a mixture of focal lesions and diffuse pathology. High-field strength MR scanners are improving our ability to image focal GM lesions and modern MR-based techniques are enabling us to quantify in vivo the extent and severity of GM pathology, which have been shown to correlate only moderately with the amount of WM changes. At least part of GM pathology in MS is not secondary to retrograde degeneration of fibers traversing WM lesions. The neurodegenerative component of the disease is not a late phenomenon and it is not completely driven by inflammatory demyelination. In fact, neurodegeneration occurs very early in the course of MS and the correlation between MRI measures of inflammation and neurodegeneration is weak in all disease phases. The interplay of inflammation and neurodegeneration is a complex and still poorly understood phenomenon. At least part of MS-related neurodegeneration is not directly driven by Wallerian degeneration. Functional cortical changes can be seen in virtually all MS patients and are likely to play a central role in the ability of the MS brain to respond to tissue injury and, hence, limit the functional consequences of structural damage. MS disability is not just the result of tissue destruction but rather a balance between tissue destruction, tissue repair and adaptive cortical reorganization. All of this calls for the concept of MS as a focal, inflammatory demyelinating, WM disease to be reexamined and to start viewing MS as a diffuse CNS disease with an important neurodegenerative component. This is central for identifying novel and effective treatment strategies.

Central Nervous System Diseases↗

PubMed1985

Stability of immunocytochemical reactivity of neuronal substances following delayed fixation.

The rates of deterioration of immunocytochemical staining for 4 peptide and 2 neuronal antigens were studied on human, guinea pig and rat colon and urinary bladder. It was found that if the fixation started within 10 h after surgery or death, little change was seen in the pattern and intensity of the immunostains. When fixation was further delayed, the immunostaining gradually deteriorated in quality and decreased in quantity until, when fixation was delayed for 60-72 h, most of the original immunostaining was absent. The deterioration rates of the neuronal antigens in the urinary bladder were slower than in the colon and all antigens were preserved for longer at 4 degrees C than at 20 degrees C. The deterioration curves produced from the present findings provide a standard for comparison with the immunostaining results obtained on tissues where fixation is delayed.

Animals↗

PubMed2002

[Propranolol protects the myocardium and prevents arterial hypotension in an experimental organ donation model].

OBJECTIVE: To analyze the role that sympathetic nervous system hyperactivity immediately following brain death plays in the cardiovascular dysfunction of an organ donor. MATERIAL AND METHOD: Fifteen New Zealand white rabbits were placed in three groups: a control group, a brain-death group without propranolol and a brain-death group with propranolol. Brain death was caused by severe intracranial hypertension; in the third group propranolol was first perfused intravenously. We recorded hemodynamic (heart rate, number of extrasystoles, central venous pressure, systemic and pulmonary arterial pressure), biochemical (adrenaline, noradrenaline, dopamine and troponin T) and histologic data. RESULTS: Catecholamine levels rose significantly in both experimental groups after brain death, which coincided with clinical signs of sympathetic hyperactivity in the group not receiving propranolol but not in the group receiving the beta-blocker. The myocardium of animals not receiving the beta-blocker showed myocytolysis, edema, subendocardial bleeding and leukocyte infiltration. Such changes were practically absent in the animals that received beta-blockers. In the beta-blocker group, serum troponin, and index of myocytolysis, rose significantly less than in the non-premedicated group. Blood pressure in all the brain-dead animals was significantly lower than in the control group, but was more severe in animals that had not received propranolol. CONCLUSIONS: Sympathetic nervous system hyperactivity after brain death affects the histology and functioning of the myocardium in this experimental organ donor model. Pretreatment with propranolol prevents damage.

Adrenergic beta-Antagonists↗

PubMed1989

[The differential diagnosis of sudden infant death or child abuse--a case of fatal hyperthermia].

During summer-like outdoor temperature, a seven-month old female infant was put into a sleeping bag, wrapped up with a blanket and tied up by her mother and a friend of hers because of unrest and continuous screaming. Prior to that, between 0.30 a.m. and 0.45 a.m., occurred the rectal measurement of temperature: 37.5 degrees C. The infant died one to two hours later. At 10.00 a.m., about 8 hours after death, in the criminal investigations of the police measurements of temperature were made: rectal 38.1 degrees C; in the pharyngeal cavity 29.5 degrees C; surrounding temperature 22.2 degrees C. In the forensic autopsy, symptoms of maltreatment were noticed: hematoma of the skin at buttock and legs, no essential change of organs. The histological investigation showed an interstitial pulmonary oedema, an acute catarrhal tracheobronchitis and hyperaemic inner organs. Concerning the complete investigation results, an acute cardiac insufficiency and circulatory failure due to hyperthermy after wrapping up and immobilisation of the child were assumed to be the cause of death. In consequence of the avowal of the maltreater they were accused of murder and convicted for bodily injury with death. The difficulties of the differential diagnosis SIDS by hyperthermy and mortal hyperthermy due to maltreatment will be discussed. The necessity of a close cooperation between police and forensic physicians is emphasized as prerequisite to clarify such events.

Body Temperature↗