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PubMed2004

Heat shock protein 12A shows reduced expression in the prefrontal cortex of subjects with schizophrenia.

BACKGROUND: Deoxyribonucleic acid microarray analyses of dorsolateral prefrontal cortex (DLPFC) area 9 from 10 matched pairs of schizophrenic and control subjects revealed a consistent and significant decrease (p = .001; mean log2 signal difference = -.58) in transcript expression for a gene clone KIAA0417. This database entry has been recently annotated as two highly homologous members of a heat-shock protein family (HSPA12A and HSPA12B). METHODS: We followed up our initial results by in situ hybridization in subjects with schizophrenia, major depression, and a chronic haloperidol-treated nonhuman primate model. Furthermore, we investigated the distribution of HSPA12A and HSPA12B transcripts across the human and nonhuman primate brain. RESULTS: We found that HSPA12A (but not HSPA12B) is highly expressed in the human brain and shows a neuron- and region-specific transcript distribution, with strongest expression in the frontal and occipital cortical regions. HSPA12A messenger ribonucleic acid was significantly reduced (p < .01; mean log2 optical density difference = -.84) across subjects with schizophrenia but not in the DLPFC of subjects with major depression or in monkeys chronically treated with haloperidol. CONCLUSIONS: The data are consistent with metabolic alterations in schizophrenia, reflected in selective changes in the expression of certain genes encoding proteins involved in cellular metabolism or metabolic responsiveness.

Adult↗

PubMed1997

Serotonergic, noradrenergic, and dopaminergic measures in suicide brains.

Concentrations of the three main monoamines (5-HT, NA, and DA), their metabolites (5-HIAA, DOPAC, and HVA), and the serotonin precursor 5-hydroxy-L-tryptophan were simultaneously measured in frontal cortex, gyrus cinguli, and hypothalamus from 23 controls and 18 suicide victims. Overall suicides did not show significant differences with respect to the control group in any of the measured compounds. Significant increases in noradrenaline and dopamine concentrations were noted in the carbon monoxide poisoning suicides, together with a significant increased hypothalamic dopamine in the drug overdose suicides. It is suggested that the suicidal behavior is not related to substantial changes in cortical and hypothalamic monoaminergic function; however, the reported results could be secondary to the rapid effect of hypoxia and of the acute self-administration of certain drugs in specific metabolic pathways.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1981

[14C]acetylcholine synthesis and [14C]carbon dioxide production from [U-14C]glucose by tissue prisms from human neocortex.

1. [14C]Acetylcholine synthesis and 14CO2 production from [U-14C]glucose has been measured in tissue prism preparations from human neocortex. 2. Electron micrographs of prisms from human and rat neocortex show that both contain intact synaptic endings with evenly-distributed vesicles and normal-appearing mitochondria, but only poorly preserved cell body structure. 3. Synthesis of [14C]acetylcholine in prisms from rat neocortex is similar to estimates for turnover in vivo. Synthesis in prisms from human neocortex is 18% of that in rat tissue and 64% of that in tissue from baboon neocortex for incubations performed in 31 mM-K+. 4. Investigations of prisms prepared from rat brains stored at 37 degrees C after death revealed that synthesis of [14C]acetylcholine in the presence of 31 mM-K+ was greatly decreased within 30 min of post-mortem incubation, whereas synthesis at 5 mM-K+ and production of 14CO2 at both K+ concentrations were only significantly affected after longer periods. Changes were similar in neocortex and striatum. Thus human autopsy material is unlikely to be suitable for use with this system. 5. Investigations using animal models suggest that [14C]acetylcholine synthesis and 14CO2 production are not affected by surgical or anaesthetic procedures. 6. Neither [14C]acetylcholine synthesis nor 14CO2 production in human prisms was significantly changed with age between 15 and 68 years. 7. Samples from patients with the dementing condition Alzheimer's disease showed a significant decrease in [14C]acetylcholine synthesis to 47% of normal samples and a significant increase of 39% in production of 14CO2.

Acetylcholine↗

PubMed1994

Pulmonary micromorphology in fatal strangulations.

Pulmonary histopathology was studied in a group of 106 fatal strangulations including cases of hanging (n = 55; typical, n = 20; atypical, n = 35), ligature strangulation (n = 12), throttling (n = 15), combinations of throttling and ligature strangulation (n = 7) and other compressing force against neck (n = 17). The control group (n = 10) consisted of cases of sudden cardiovascular death. The following results were obtained: intra-alveolar edema of different degree and strong hyperemia could be regularly observed in nearly all cases, especially in fatal hanging (apart from the control cases, in this group the highest mean lung weights were observed). Further frequent histological patterns were perivascular and intra-alveolar hemorrhages, local dystelectasis and focal emphysema. Alterations of the lung vessel contents could be detected in a varying extent: fat embolism (n = 7), mainly of minor degree, embolism of bone marrow tissue (n = 5) and intravascular cell accumulations (n = 22). Embolism of fat and bone marrow tissue was nearly always restricted to cases with accompanying blunt force or resuscitation measures. Whereas only 4 out of 55 cases of hanging revealed intravascular cell accumulations (including different types of leukocytes and immature bone marrow cells), 18 out of 51 cases with the other forms of strangulation exhibited this phenomenon. These accumulations mainly occurred in a discrete and widely scattered manner, appeared in 3 out of 10 control cases (resuscitation measures) as well, and were limited to cases with either protracted courses or accompanying blunt violence. The following conclusions are drawn: the regularly observed general changes of lung microstructure (e.g. edema, hyperemia) are undoubtedly non-specific for strangulation; the alterations of blood vessel contents may serve as a general vitality marker, if resuscitation measures are excluded, but not as an evidence of strangulating force. In cases without signs of blunt force they point to protracted agony courses (shock equivalents).

Adult↗

PubMedDate not supplied

Investigations into the analysis of the rate of decay of the compound action potentials recorded from the rat sciatic nerve after death: significance for the prediction of the post-mortem period.

There have been a number of papers that have reported the investigations of electrical stimulation of muscle groups in order to determine the post-mortem period. To the authors knowledge, no techniques have been described that analyse the compound action potentials (CAP) of various nerve fibre groups after death. This paper reports the monitoring of both the amplitude and latency changes of the CAP recorded from a stimulated rat sciatic nerve after death. Initial results suggest that the method my be useful in determining the early post-mortem period within 1 or 2 h after death. It may also be of use in measuring nerve conduction delay in various pathological conditions that can affect the neural network; for example diabetes.

Action Potentials↗

PubMed1977

Chemical composition of the aqueous humor of bovine eyes dependent on predetermined time upon removal.

The content of several carbohydrates [glucose (alpha and beta), inositol, fructose, galactose] and aminoacids in the aqueous of bovine lenses was measured in dependence on time after globe puncture, using the method of gas liquid chromatography (carbohydrates) and ion exchange chromatography (amino acids). The contents of the investigated compounds show distinct postmortal changes. Aqueous humor which had been obtained immediately after enucleation of the bovine eyes and kept at 37 degrees C for different periods of time (1-8 h) showed for the carbohydrates investigated a decrease in fructose concentration, whereas almost all amino acid concentrations were increased, with the exception of leucine, tyrosine, and arginine, which were decreased.

Age Factors↗

PubMed1990

Decapitation-induced changes in inositol phosphates in rat brain.

Decapitation resulted in a time-dependent production of inositol phosphates in rat brain. This production was analyzed by measuring both the radioactivity and the concentrations of inositol phosphates generated from [3H]inositol-labeled phospholipids. Both measurements produced the same time-dependent changes, including a rapid decrease in inositol 1,4,5-trisphosphate within 1.5 min, a 6-fold increase in inositol 1,4-bisphosphate to a maximum at 1.5 min, a 5-fold rise in inositol 4-monophosphate to a maximum at 2.5 min, and little change in inositol 1-monophosphate. The temporal changes in the mass and radioactivity of these compounds, together with the decrease in labeling of phosphatidylinositol 4,5-bisphosphates, support the idea that the inositol phosphates originate from the hydrolysis of phosphatidylinositol 4,5-bisphosphates and not from either the direct hydrolysis of phosphatidylinositol 4-phosphates or phosphatidylinositols.

Animals↗

PubMed1977

[Peculiar bone injuries by grinding in a corpse with a long immersion period (author's transl)].

Injuries frequently occur after immersion of corpses in water. Depending on the type of water different sorts of injuries, caused by drifting and being dragged, can lead to more or less severe abrasions of the soft parts of the body predominantly skin abrasions. This case is unique among hover 3000 corpses in water found in the last 4 decades in the Elbe. The corpse was found with very severe and extensive bone injuries; in fact the bones were ground down (among other injuries was a large opening in the skull). The origin is discussed: it is assumed that the corpse changed its position only minimally in the half-year period after immersion and did not drift with the stream, but on the contrary had stuck fast on or under a pontoon and was rubbed and ground against a pole or something similar. The special conditions of the Elbe River appear to have played an important role in this process.

Autopsy↗

PubMed1998

The influence of post-mortem conditions on contractile and relaxant responsiveness of guinea-pig isolated tracheal smooth muscle.

Responsiveness to various contractile and relaxant agonists was assessed in tracheal preparations from guinea-pigs that had been incubated in situ at 4-37 degrees C for 0-168 h post-mortem. The potencies of histamine and acetylcholine were increased up to 168 h at 4 degrees C post-mortem and up to 24 h post-mortem at 22 degrees C. Histamine potency also increased with increasing post-mortem time at 37 degrees C. After 48 h at 22 degrees C and 8 h at 37 degrees C, responses to all spasmogens were abolished. Increases in histamine and acetylcholine potencies were similarly observed in tracheal tissue that had been removed at death and then incubated at 4 degrees C in oxygenated Krebs-bicarbonate solution for 0-168 h. The increased potency of these drugs may be explained by epithelial damage and/or loss of an epithelium-derived inhibitory factor (EpDIF). Both basal and spasmogen-stimulated increases in intracellular phosphoinositides fell with increasing time and ambient temperature post-mortem, despite the fact that contraction in response to these agonists could still be evoked. This suggests the selective failure of this signal transduction pathway and the maintenance of responsiveness via other mechanisms. The potencies and maximum effects of relaxant agonists remained unaltered in tracheal tissue with increasing time post-mortem, suggesting little change in the function of the appropriate receptor-signal transduction processes. This study has therefore demonstrated that at 4 degrees C. contractile and relaxant responses were preserved for up to 168 h post-mortem, although the modulatory influence of the epithelium on histamine and acetylcholine responses was rapidly lost.

Acetylcholine↗

PubMed2005

[The research progression of S100beta as a neurochemistry maker].

S100beta is one kind of the calcium binding proteins. As growth factor of neuraxon, it is excreted by neuroglial cell, and distributing in nerve tissue extensively. Although S100beta has very important values neurophysiological, it also has neurotoxicity with excreting overmuch. Concentration of S100beta changes regularity in serum after the brain injury. In addition, it has a close relations with the degree of brain damage, which can be regarded as the neural new marker of biochemistry after brain damage. The advances of S100beta protein, in the research on neurophysiological values and its application for nerve tissue injury, disease were reviewed.

Alzheimer Disease↗

PubMed1988

Post-mortem structural analyses of schizophrenic brain: study designs and the interpretation of data.

This paper discusses various factors that must be considered in designing histological studies of schizophrenic brain. An examination of the literature prior to 1952 reveals that much of the controversy arising during the first half of this century can be understood within the context of methodological flaws that included the use of inappropriate controls, the lack of systematic diagnosis of schizophrenia, an absence of blind quantitation and finally, a failure to control for the effects of several potential confounding variables. In addition to these latter concerns, the design of post-mortem structural analyses of schizophrenic brain must also consider what brain areas are reasonable to examine, what morphometric parameters should be evaluated to test a hypothesis in question and whether any differences noted represent primary, secondary or perhaps even epiphenomenal changes in the brain. The life cycle of schizophrenic patients should be considered in these designs so that factors intrinsic to the disorder, such as a genetic trait marker or the effects of perinatal insult, can be distinguished from changes that may arise later, perhaps in relation to the acquisition of the defect state. The basic principles of neurobiology and clinical psychiatry should be applied in developing a design and in interpreting data that emerges. Taking all of these issues into account, complex strategies will be required in order to obtain reliable, valid and clinically relevant information that can contribute to our understanding of the pathophysiology of schizophrenia.

Age Factors↗

PubMed1997

Ageing has a differential effect on nitric oxide synthase-containing and catecholaminergic amacrine cells in the human and rat retina.

In this study, we assessed the effects of normal ageing on the number, distribution, and somal area of nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-positive (NADPHd+) and tyrosine hydroxylase-immunoreactive (TH-IR) amacrine cells in human and rat retina. By using a double-labelling immunohistochemical technique, we have shown that these two enzymes are located in separate amacrine cell populations in the human retina. In normal human retinas from organ donors, we have shown that there was no change in the number, somal area, or retinal distribution of NADPHd+ neurons over an age range of 19-89 years. In contrast, there was a significant decrease (P < 0.05) of 52% in the total number of TH-IR neurons in the group aged 65-89 years compared with the group aged 19-64 years. CA1 and CA2 TH-IR neurons were reduced by 44% and 55%, respectively. In young (3 months) and old (2 years) rats, the number of NADPHd+ neurons did not decrease with ageing, but the number of TH-IR neurons was significantly reduced by 21% (P < 0.05). In a companion study on monkey retina, we have shown that a postmortem delay of 12.5 hours between death and fixation results in a decrease of 33% in the number of both NADPHd+ and TH-IR neurons in the retina compared with the number in retinas fixed immediately after death. The findings of this study on the two subsets of amacrine cells, therefore, are likely to demonstrate the consequences of ageing in the retina and might contribute to visual impairment in the elderly.

Adult↗

PubMed2005

Mitochondrial abnormalities in Alzheimer brain: mechanistic implications.

Reductions in cerebral metabolism sufficient to impair cognition in normal individuals also occur in Alzheimer's disease (AD). The degree of clinical disability in AD correlates closely to the magnitude of the reduction in brain metabolism. Therefore, we tested whether impairments in tricarboxylic acid (TCA) cycle enzymes of mitochondria correlate with disability. Brains were from patients with autopsy-confirmed AD and clinical dementia ratings (CDRs) before death. Significant (p < 0.01) decreases occurred in the activities of the pyruvate dehydrogenase complex (-41%), isocitrate dehydrogenase (-27%), and the alpha-ketoglutarate dehydrogenase complex (-57%). Activities of succinate dehydrogenase (complex II) (+44%) and malate dehydrogenase (+54%) were increased (p < 0.01). Activities of the other four TCA cycle enzymes were unchanged. All of the changes in TCA cycle activities correlated with the clinical state (p < 0.01), suggesting a coordinated mitochondrial alteration. The highest correlation was with pyruvate dehydrogenase complex (r = 0.77, r2= 0.59). Measures to improve TCA cycle metabolism might benefit AD patients.

Aged↗

PubMed2005

Changes in hippocampal GABABR1 subunit expression in Alzheimer's patients: association with Braak staging.

Alterations in the gamma-aminobutyric acid (GABA) neurotransmitter and receptor systems may contribute to vulnerability of hippocampal pyramidal neurons in Alzheimer's disease (AD). The present study examined the immunohistochemical localization and distribution of GABA(B) receptor R1 protein (GBR1) in the hippocampus of 16 aged subjects with a range of neurofibrillary tangle (NFT) pathology as defined by Braak staging (I-VI). GBR1 immunoreactivity (IR) was localized to the soma and processes of hippocampal pyramidal cells and some non-pyramidal interneurons. In control subjects (Braak I/II), the intensity of neuronal GBR1 immunostaining differed among hippocampal fields, being most prominent in the CA4 and CA3/2 fields, moderate in the CA1 field, and very light in the dentate gyrus. AD cases with moderate NFT pathology (Braak III/IV) were characterized by increased GBR1-IR, particularly in the CA4 and CA3/2 fields. In the CA1 field of the majority of AD cases, the numbers of GBR1-IR neurons were significantly reduced, despite the presence of Nissl-labeled neurons in this region. These data indicate that GBR1 expression changes with the progression of NFT in AD hippocampus. At the onset of hippocampal pathology, increased or stable expression of GBR1 could contribute to neuronal resistance to the disease process. Advanced hippocampal pathology appears to be associated with decreased neuronal GBR1 staining in the CA1 region, which precedes neuronal cell death. Thus, changes in hippocampal GBR1 may reflect alterations in the balance between excitatory and inhibitory neurotransmitter systems, which likely contributes to dysfunction of hippocampal circuitry in AD.

Adenosine Triphosphatases↗

PubMed1999

Neuron-specific enolase as an effective immunohistochemical marker for injured axons after fatal brain injury.

Recently, it has been reported that a diagnosis of diffuse axonal injury in cases with a short survival period can be made with the use of immunolabelling for beta-amyloid precursor protein (APP). We examined whether immunostaining for neuron-specific enolase (NSE) can also be a useful marker for the detection of axonal injury in its early stages. Sections of the corpus callosum from 19 cases of head injury and from 9 cases of no head injury were immunostained for NSE and stained by the standard Holmes' silver method. For comparison, serial sections from several cases were immunostained for APP. Immunostaining for NSE as well as for APP, labelled injured axons in head injury cases with as early as 1.5 h survival where Holmes' staining failed to detect any changes of axons. Since NSE and APP labelled only injured axons but not normal axons, the results were readily interpretable. These findings indicate that NSE should be an effective marker for the detection of axonal injury in its early stages.

Adolescent↗

PubMedDate not supplied

A scanning electron microscopy study of post mortem autolytic changes in the human and rat cochleas.

The use of SEM as an adjunct to TEM and electrophysiological examination of the cochlea is now well established. It has provided a relatively simple method of assessing the effect of noise, ototoxic drugs, electrical stimulation, etc. on the surface features of the organ of corti. A controlled experiment was undertaken to document the surface autolytic changes in rat cochleas by fixation at intervals up to eight hours post mortem. These were compared with human material fixed between 40 minutes and eight hours post mortem. The results complement previous light and transmission electron microscopy studies, gives insight into the optimal and acceptable fixation times for the two species and act as a guide for the interpretation of human material.

Adult↗

PubMedDate not supplied

[An analysis of the errors in determining the time of death by cadaveric changes during the performance of the initial inquiry activities].

Analysis of 265 forensic medical expert conclusions on murdered subjects' corpses permitted us to quantitatively and qualitatively evaluate the errors made by forensic medics examining the corpse at the site where it was found. In 23.4% of cases these errors were due to improper methodology of thanatometric investigations and were made by forensic medics of different length of service and qualification. Approaches to improving the diagnosis of time of death during the initial investigation are outlined.

Autopsy↗

PubMed1997

Retrospective study on skin reddenings and petechiae in the eyelids and the conjunctivae in forensic physical examinations.

Skin reddening with or without additional changes such as pinpoint intracutaneous hemorrhages and/or minute superficial scratches was observed in 165 out of 739 physical examinations (reddening with additional changes: n = 81; reddening only: n = 84). The most common site where reddening was observed was the neck region (reddening with additional changes: n = 30; reddening only: n = 34). In over 85% of the cases, the postinfliction interval (Pi) was < or = 1 day, and there were 12 and 10 cases with 1 < Pi < or = 3 days, respectively. Among these 22 cases, there were 5 cases with 2 < Pi < or = 3 days, (reddening with additional changes: n = 4; reddening only: n = 1). The maximum Pis were almost 3 days, and 2 days and 13 h, respectively. These results demonstrate that reddening of the skin with and that without additional changes (in particular petechiae) were detectable up to approximately 3 and 2 days after the event, respectively. Furthermore, in 17 out of 64 cases with reddening in the neck, petechial hemorrhages were seen in the eyelids and/or conjunctivae (reddening with additional changes: n = 10; reddening only: n = 7). The maximum Pi in which petechial hemorrhages were detectable in the eyelids and/or the palpebral conjunctivae was 1 day and 21 h. The present study indicates that physical examinations within 2 or 3 days after the event seem to be more suitable to find skin reddening and/or petechiae in the eye lids and/or the conjunctivae.

Autopsy↗