Publications by authors named "Oehmichen Manfred"

We examined 10 histomorphological alterations of 222 cases of subdural hemorrhages following mechanical closed brain injury (MBI) to determine the posttraumatic interval (PTI). These morphological features included red blood cells (RBCs), polymorphonuclear leukocytes (PMNs), macrophages (Ms), RBC-containing Ms, hemosiderin-containing macrophages, hematoidin, fibroblasts, endothelial cells, collagenous fibers and membrane formation. The interval between the time of brain injury and death ranged from a few minutes to 33 years.

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It will be vital to the practical activity of every forensic and/or clinical pathologist to be able to answer three questions regarding the reconstruction of a lethal event: the type and cause of death, as well as the survival time. The authors offer an overview of the application of selected morphological techniques in general forensic neuropathology, techniques that provide answers to some of the main questions in forensic neurotraumatology. The methods are illustrated by individual cases of lethal gunshot injury to the head from low velocity handguns.

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Sudden infant death syndrome (SIDS) is characterized by a lack of any known morphological or functional organ changes that could explain the lethal process. In the present study we investigated the hypothesis of an association between hypoxic/ischemic injury and SIDS deaths. In a previous study, we could demonstrate by quantitative immunohistochemistry a distinct drop in microtubule-associated protein (MAP2) reactivity in neurons of adult, human brains secondary to acute hypoxic-ischemic injuries.

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It has been suggested that deletions of mitochondrial DNA (mtDNA) are important players with regard to the ageing process. Since the early 1990s, the 4977 bp deletion has been studied in various tissues, especially in postmitotic tissues with high energy demand. Unfortunately, some of these studies included less than 10 subjects, so the aim of our study was to quantify reliably the deletion amount in nine different regions of human brain, heart and skeletal muscle in a cohort of 92 individuals.

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The discussion surrounding shaken baby syndrome (SBS) arose from the lack of evidence implicating diffuse axonal injury (DAI) as a cause of death. It was assumed instead that injury to the cervical cord, medulla, and nerve roots played a causal role. The present pathomorphological study examines 18 selected infants (<1-year-old) whose deaths were highly suspicious for SBS, exhibiting the classical SBS triad of acute subdural hemorrhage (SDH), retinal bleeding, and encephalopathy.

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Autosomal STR typing alone seems to be no sufficient tool for resolving deficiency cases (e.g. cases of questioned paternity or half-sibships).

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Opposite to clinical laboratory findings in experimental drowning of animals (erythrocytic lysis, hyperkalemia, and final cardial fibrillation) are the observations in drowned humans (increase of pCO2, hypoxic encephalopathy), which leads to a different pathophysiological interpretation of the drowning process. This process, however, is recently discussed again, therefore an additional study seemed to be recommended. In a retrospective study, 31 cases of near-drowning (23 cases: fresh water; 8 cases: brackish water) clinical laboratory data were analysed.

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The pituitary adenylate cyclase-activating peptide (PACAP) is involved in many processes of the developing and mature central nervous system, such as proliferation, differentiation, apoptosis, neurotransmission, inflammation and neuroprotection. Alternative posttranslational processing of PACAP results in two biologically active, amidated 27- and 38-amino acid peptides termed PACAP27 and PACAP38. In the present study, we examined whether traumatic brain injury (TBI) affects cellular immunopositivity for PACAP27 and PACAP38.

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The primary mechanism for eliminating synaptically released glutamate is uptake by astrocytes. In the present study, we examined whether traumatic brain injury (TBI) affects the cellular expression of glutamate transporters EAAT1 and EAAT2. Morphometrical immunohistochemical analysis demonstrated a predominant expression of EAAT1 and EAAT2 in astrocytes of normal human neocortex (n = 10).

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Nowadays, kinship studies based only on STR analysis are a very common practice. Apart from regular paternity cases, there is a rising number of cases in which the type of sibship between two persons has to be determined. Very often the parents or further relatives are unavailable for testing, so that the probability e.

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Aging is a multifactorial process and a lot of theories have been put forward to explain the deterioration of organ function with advancing age. The free radical hypothesis developed by Harman is amongst the most prominent today and has been focused on mitochondrial aging in the last decades. Applying a long PCR approach we screened human skeletal muscle, heart, caudate nucleus and cerebellum of 50 individuals for large-scale deletions of mitochondrial DNA (mtDNA).

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The loss of neuronal immunoreactivity of the cytoskeletal microtubule-associated protein 2 (MAP2) is known to be a marker of--at least--transient functional failure of neurons following ischemia. Because there are no specific neuropathological findings in forensic types of acute hypoxia-ischemia, detection of this relevant cause of death is often complicated and a reliable ischemic biomarker would be of great importance. We therefore investigated the neuronal immunoreactivity of MAP2 in human cases of forensic significance.

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In a certain amount of paternity investigations, only DNA from child and alleged father is analyzed, thus increasing the possibility of false paternity inclusions. The aim of this study was to determine how many wrong paternity inclusions could be detected in a rather small geographical area comparing empirical results from 336 children and 348 men (13-15 STRs were investigated per person). This comparison between each child and all unrelated men (i.

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During the ageing process, an increase of mitochondrial DNA (mtDNA) deletions and other mutations have been reported. These structural alterations of mtDNA are assumed to cause a reduction in the respiratory chain activity and may contribute to the ageing process. Therefore, the question arises if the accumulation of deleted mtDNA is compensated in vivo by an increase of mtDNA synthesis via a feedback mechanism.

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During the last few years, the number of privately ordered paternity investigations has increased considerably. Probably due to financial reasons in more and more cases only the putative father and the child are investigated. Additionally, very often only one method, such as STR analysis, is employed.

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Diagenesis of macromolecules is a not yet fully understood process that can be important for anthropological and forensic research. Trying to elucidate the diagenesis of DNA and proteins we investigated the process of fragmentation of DNA and razemisation of aspartic acid in human bone material. We created an in vitro-model of accelerated aging by incubating bone samples in hot water.

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STR typing becomes more and more valuable for different approaches of science. It revolutionized determining of zygosity in twin research and it is very often the only possibility for discrimination in forensic trace analysis. In this study 55 twin pairs from Denmark were genetically investigated to determine their zygosity.

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Typing of DNA from ancient or otherwise highly degraded material, e.g. formalin fixed tissues, can be difficult, time consuming and costly.

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A review is given summarizing different methods that have been applied to the specific forensic neuropathological question of brain hypoxia/ischemia. On the microscopic level the authors applied routine stains and immunohistochemistry (MAP2, ALZ 50, GFAP, CD68, beta-APP) for characterization of the functional activity of neurons as well as of different cell types in various brain areas. Moreover, using molecular techniques for evaluation of the mitochondrial 4977-bp deletion in correlation to hypoxia and to age brain tissue and single cell analyses are described.

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Accumulation of alterations to the mitochondrial DNA (mtDNA) would be expected to significantly impair the bioenergetic function of mitochondria in the affected host cells. Many of these changes have been associated with several specific diseases and the process of aging. These mutations may be the result of mitochondrial oxidative stress, which is increased with age of individuals and specific degenerative diseases.

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Varicella or chicken-pox are one of the most frequent diseases in childhood. Severe or even lethal complications are rare (in about 0.03 per thousand ).

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An experimental design is presented that simulates an accelerated process of DNA degradation in human bone tissues and thus provides a possibility for a systematic investigation of factors hampering DNA extraction and amplification. Equal sized slices of human femoral bones were incubated in 90 degrees C water for 2 h up to 30 days. DNA was extracted and subjected to a human specific Duplex polymerase chain reaction (PCR) and also to a Multiplex short tandem repeat (STR) PCR.

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We examined 305 autopsied brains for histomorphological alterations to determine the time course of reactions in cortical hemorrhages following traumatic closed brain injury. Eighteen morphological criteria were considered: red blood cells (RBCs), polymorphonuclear leukocytes (PMNs), macrophages (Ms), RBC-containing Ms, hemosiderin, hematoidin, lipid-containing Ms, fibroblasts, endothelial cells, collagenous fibres, gemistocytic astrocytes, fibrillary gliosis, hemosiderin-containing astrocytes, neuronal damage, neuronophagy, axonal swelling (beta-amyloid precursor protein: beta-APP), axonal bulbs (van Gieson stain), and mineralisation of neurons. The interval between the time of brain injury and death ranged from 1 min to 58 years.

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The study was performed to distinguish fatal from non-fatal blood concentrations of morphine. For this purpose, blood levels of free morphine and total morphine (free morphine plus morphine conjugates) in 207 cases of heroin-related deaths were compared to those in 27 drivers surviving opiate intoxication. The majority of both survivors and non-survivors were found to show a concomitant use of depressants including alcohol or stimulants.

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