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T Arendt

Publications and source records attributed to T Arendt.

At least 91 records · Page 5Linked to original sources
PubMed1997

Analysis of selenium in bovine liver by gas chromatography with mass-selective, electron-capture and nitrogen-phosphorus detection.

The concentration of selenium (Se) in liver was determined by gas chromatography (GC) with mass-selective (GC-MS), electron capture (GC-ECD) and nitrogen-phosphorus (GC-NPD) detection. Liver samples were digested in a mixture containing HNO3 and Mg(NO3). SeVI was converted to SeIV. SeIV was derivatized with 4-nitrophenylenediamine and then extracted in toluene. A 1-microliter volume of the toluene extract was analyzed by the GC-MS, GC-ECD or GC-NPD methods. The detection limits of the GC-ECD, the GC-NPD and the GC-MS methods were 25, 50 and 800 pg, respectively. The GC-NPD method was more selective for the derivatized Se than the GC-ECD method. The GC-MS method had the advantage of using the 76Se isotope as the internal standard. Se concentrations in liver samples determined by the three methods were comparable.

Animals↗
PubMed1997

Plastic neuronal remodeling is impaired in patients with Alzheimer's disease carrying apolipoprotein epsilon 4 allele.

A relationship between the apolipoprotein E (apoE) genotype and the risk to develop Alzheimer's disease has been established recently. Apolipoprotein synthesis is implicated in developmental processes and in neuronal repair of the adult nervous system. In the present study, we investigated the influence of the apolipoprotein polymorphism on the severity of neuronal degeneration and the extent of plastic dendritic remodeling in Alzheimer's disease. Changes in length and arborization of dendrites of Golgi-impregnated neurons in the basal nucleus of Meynert, locus coeruleus, raphe magnus nucleus, medial amygdaloid nucleus, pedunculopontine tegmental nucleus, and substantia nigra were analyzed after three-dimensional reconstruction. Patients with either one or two apoE epsilon 4 alleles not only showed a more severe degeneration in all areas investigated than in patients lacking the apoE 4 allele but also revealed significantly less plastic dendritic changes. ApoE epsilon 4 allele copy number, furthermore, had a significant effect on the pattern of dendritic arborization. Moreover, the relationship between the intensity of dendritic growth and both the extent of neuronal degeneration and the stage of the disease seen in patients lacking the apoE epsilon 4 allele was very weak in the presence of one epsilon 4 allele and completely lost in patients homozygous for the epsilon 4 allele. The results provide direct evidence that neuronal reorganization is affected severely in patients with Alzheimer's disease carrying the apoE epsilon 4 allele. This impairment of neuronal repair might lead to a more rapid functional decompensation, thereby contributing to an earlier onset and more rapid progression of the disease.

Aged↗
PubMed1997

Cerulein-induced acute pancreatitis in rats--does bacterial translocation occur via a transperitoneal pathway?

Bacterial infectious complications are the most common cause of morbidity and mortality associated with acute pancreatitis. Most pathogens are common gastrointestinal flora, indicating that the gut is the source of pancreatitis-related infections. However, the route whereby the microorganisms reach distant organs remains speculative. We tested the hypothesis that spread of bacteria occurs via a transperitoneal pathway. Acute interstitial pancreatitis (AIP) was induced in antibiotic (gentamicin, bacithracin, neomycin)-decontaminated rats by intravenous infusion of cerulein. Effects of pancreatic necrosis (PN) were studied in rats that received additional injections into the peritoneal cavity of pancreatic tissue obtained from donor rats. The rats were inoculated with Escherichia coli (O2:KN:H18) resistant to the antibiotics used for decontamination either orally (10(12) microorganisms; experiment I) or intraperitoneally (10(8) microorganisms; experiment II). Moreover, the rat peritoneal cavity wash was inoculated with 10(8) E. coli in vitro (experiment III). In rats with AIP and PN, recovery of the bacteria from liver, spleen, pancreas, lung, and blood following oral inoculation demonstrated that acute pancreatitis promotes bacterial translocation from the gut. The absence of E. coli in these organs following intraperitoneal inoculation showed that the bacteria do not spread from the peritoneal cavity. Rats with PN cleared E. coli from the peritoneal cavity in a shorter period than rats with AIP and controls (5 vs. 7 and 8 days; p < 0.05). The multiplication rate of E. coli in peritoneal cavity wash was lower in rats with PN than in rats with AIP and controls (p < 0.01). We conclude that (1) translocation of E. coli from the gut during cerulein-induced acute pancreatitis occurs via nonperitoneal pathways, (2) the peritoneal cavity acts as a trap for the bacteria rather than a source of bacterial seeding, and (3) PN impairs survival of E. coli in the peritoneal cavity via inhibition of the bacterial multiplication in this model.

Acute Disease↗
PubMed1997

Santorini's duct--risk factor for acute pancreatitis or protective morphologic variant? Experiments in rabbits.

BACKGROUND AND AIMS: Gallstone pancreatitis is assumed to result from stone passage through the choledochoduodenal junction. Stone impactions may either result in the obstruction of the pancreatic duct or occur below the confluence of the biliary tract and the pancreatic duct and, thus, may favour bile reflux into the pancreatic duct. We studied effects of a patent Santorini's duct upon secretory flow and pancreas morphology under both conditions. METHODS: A catheter in the distal rabbit pancreatic duct created a second outlet for pancreatic juice and, thus, mimicked a patent Santorini's duct. A second catheter was introduced into the proximal pancreatic duct and into the common bile duct. This catheter mimicked a common channel behind a papillary obstruction. Clamping of this catheter mimicked a stone obstruction of the pancreatic duct. A catheter in the cystic duct allowed for the infection of bile with 10(7) Escherichia coli bacteria/ml. The flow direction of bile and pancreatic juice was directly observed. Pancreatic histology was analysed after 24 h. RESULTS: Pancreatic duct obstruction produced an oedema of the gland. Creation of a patent Santorini's duct prevented development of the histological changes caused by pancreatic duct obstruction. In rabbits in which a common channel obstruction was mimicked, Santorini's duct produced flow of bile along the pancreatic duct system. Flow of sterile bile along the duct did not cause pancreatic inflammatory lesions. Bile that was infected with E. coli bacteria produced an acute interstitial-oedematous pancreatitis. CONCLUSIONS: (1) A patient Santorini's duct protects the gland from the effects of main pancreatic duct obstruction; (2) Santorini's duct promotes biliary pancreatic reflux during obstruction of the common channel and subsequent development of pancreatitis caused by infected choledochal secretions; (3) Santorini's duct may thus be both a protective morphological variant and a risk factor for pancreatitis dependent upon the site of stone impaction within the choledochoduodenal junction.

Acute Disease↗
PubMed1997

Cardiac tamponade--a rare complication in acute pancreatitis.

A patient with recurrent acute pancreatitis developed pericardial effusion and cardiac tamponade. His systolic blood pressure fell to 70 mmHg and sinus tachycardia (150/min) developed. The central venous pressure rose from 3 cm H2O to 27 cm H2O. A chest radiograph showed an enlargement of the cardiac shadow. Pericardial paracentesis was performed and 300 ml fluid was aspirated. This produced rapid clinical improvement. The literature related to this uncommon complication is reviewed and possible pathogenetic mechanisms are discussed.

Acute Disease↗
PubMed1997

Differential changes in the expression of AMPA receptors genes in rat brain after chronic exposure to ethanol: an in situ hybridization study.

Chronic treatment with ethanol of adult rat was used as an experimental paradigm to investigate changes in the expression of glutamate receptor genes under the condition of a slowly progressing neurodegeneration that is associated with a plastic neuronal growth response. Effects of chronic oral ethanol exposure (20% v/v, 28 weeks) on the expression of the AMPA receptor mRNA subtypes GluR-A, GluR-B and GluR-C (flip variants) were analysed in the rat hippocampus by in situ hybridization and subsequent quantitative autoradiography. In both controls and ethanol treated animals strong hybridization signals could be detected over pyramidal neurones and dentate gyrus cells. GluR-C mRNA was elevated by 15% to 30%, while expression of the AMPA receptor transcripts GluR-A and GluR-B were not significantly altered after ethanol treatment. The present findings demonstrate that chronic ethanol exposure affects gene expression of AMPA receptor subtypes differentially. Differential influences of distinct AMPA-receptor subtypes on neuronal survival and plastic neuronal response under conditions of chronic neuronal degeneration might, therefore, be suggested.

Alcoholism↗
PubMed1997

A case of Behçet's syndrome presenting with Dieulafoy's ulcer.

Behçet's syndrome represents a multisystemic disease with vasculitic changes. We here describe a patient with Dieulafoy's ulcer and oral, genital and bronchial mucosal lesions who met the criteria of incomplete Behçet's syndrome. The rare observation of Behçet's syndrome presenting with Dieulafoy's ulcer in our patient raises the question as to whether this type of ulcer, usually caused by a developmental malformation of a submucosal gastric artery, may occasionally be due also to submucosal aneurysms that result from a vascular inflammation.

Aged↗
PubMed1996

Expression of the cyclin-dependent kinase inhibitor p16 in Alzheimer's disease.

Recent evidence indicates that an impairment of neuronal adaptive and reparative processes might be a key feature of the pathomechanism of Alzheimer's disease. Aberrations in the reparative neuronal response are likely to result from alterations of intracellular signal transduction cascades. As a consequence of abnormal intracellular signalling, the activation of those molecular events might be triggered in neurones which, in dividing cells, would lead to cellular transformation. In the present study, changes in the expression of the cyclin-dependent kinase inhibitor p16, a regulator of the orderly progression through the cell cycle, were investigated by immunocytochemical methods in the temporal cortex of patients with Alzheimer's disease. Both neurofibrillary tangles and neuritic components of plaques showed strong p16 immunoreactivity. These findings support the hypothesis that an aborted attempt of terminally differentiated neurones to re-enter the cell cycle might be a critical event in the pathology of Alzheimer's disease.

Aged↗
PubMed1996

NGF level in the rat sciatic nerve is decreased after long-term consumption of ethanol.

Long-term effects of ethanol consumption on endogenous nerve growth factor (NGF) level were investigated in NGF-producing target organs and tissues of the peripheral nervous system. Rats were treated with ethanol (20% v/v) for 9 months, detoxified for an additional 2 weeks and kept without ethanol for an additional month prior to sacrifice. NGF level in the NGF-producing target tissues such as iris and submandibular gland and in the trigeminal ganglion and superior cervical ganglion, where NGF-responsive perikarya are located, did not differ significantly from corresponding controls. In contrast, NGF level in the sciatic nerve was significantly reduced by 54%. This indicates that long-term ethanol consumption affects retrograde axonal transport of the neurotrophic factor NGF, suggesting that NGF deficiency may be part of the pathophysiology of peripheral neuropathy due to chronic alcoholism.

Alcoholism↗
PubMed1996

Distribution of isoforms of the microtubule-associated protein tau in grey and white matter areas of human brain: a two-dimensional gelelectrophoretic analysis.

The microtubule-associated protein tau in human brain consists of six molecular isoforms derived from a single gene by alternative mRNA-splicing and further modified by posttranslational processing. In the present study, the distribution of tau isoforms in grey and white matter of human temporal cortex was investigated by two-dimensional gelelectrophoresis. More than 80 isoforms were detected. The pattern of isoforms obtained after treatment with alkaline phosphatase was still more complex than those of recombinant tau, indicating that posttranslational modifications other than phosphorylation contribute to the molecular heterogeneity of tau. The tau isoform D according to Goedert containing four tubulin-binding regions shown to promote tubulin polymerisation most efficiently was present in higher amounts in white as compared to grey matter. The pattern of isoform distribution was not significantly altered in Alzheimer's disease. It is concluded that molecular isoforms that differ in their tubulin-binding characteristics are differentially distributed in subcellular neuronal compartments and/or neuronal types.

Alzheimer Disease↗
PubMed1996

Chylous cardiac tamponade in acute pancreatitis.

A 47-year-old woman with acute necrotizing pancreatitis developed sudden cardiorespiratory arrest and needed resuscitation. A pericardial effusion was found, and 350 ml of a white nontransparent milky fluid was aspirated that contained 1020 mg triglycerides/100 ml. The diagnosis of chylous cardiac tamponade was made. Absence of amylase in the chylous effusion militates against the popular hypothesis that lymphatic transport of exocrine digestive enzymes from the inflamed pancreas produces the frequent intrathoracic serosal effusions in acute pancreatitis. The data of our patient rather suggest that these effusions result from the leakage of pancreatic inflammatory exudates through the diaphragm which, apparently, may even result in the loss of pericardial and adjacent thoracic lymph vessel integrity. Although pericardial tamponade is a rare complication, it should be considered if otherwise unexplained circulatory deterioration occurs in a patient with acute pancreatitis.

Acute Disease↗
PubMed1996

Changes of activity and isozyme pattern of phosphofructokinase in the brains of patients with Alzheimer's disease.

A severe reduction of the in vivo cerebral glucose consumption rate is generally found in patients with Alzheimer's disease. In postmortem studies changes in the activities of key regulatory glycolytic enzymes, including 6-phosphofructokinase (PFK), have been reported in Alzheimer's disease brains, but the results obtained so far are inconsistent and controversial. We reevaluated the activity of PFK in brain tissue from clinically and neuropathologically confirmed cases of Alzheimer's disease using optimized tissue disintegration and assay methods and determined the PFK isozyme pattern. PFK activity in brains from patients with Alzheimer's disease was significantly increased in frontal and temporal cortex and unchanged in the other brain areas studied when compared with control brains. All three PFK isozymes were detected in each of the brain areas studied. In brains of Alzheimer's disease patients the level of the C-type PFK was slightly reduced at the expense of the M- and L-type subunits. The data presented do not support the results of other groups, which reported up to a 90% reduction of PFK activity in Alzheimer's disease. In contrast, the data presented clearly rule out the suggestion that changes of PFK activity might be one of the causes for the reduced glucose consumption in Alzheimer's disease brains.

Aged↗
PubMed1996

Does high pancreatic duct pressure compromise the duct mucosal barrier function to pancreatic exocrine proteins?

The effect of duct pressure on the barrier function of the pancreatic duct mucosa to both activated and nonactivated pancreatic exocrine enzymes was studied in a feline model. The cat main pancreatic duct was perfused from the tail to the head of the gland with rat pancreatic juice at high duct pressure (40 cm H2O). In a first experiment, nonactivated pancreatic juice was perfused. Analysis of the juice for loss of fluid volume (measurement by weight) and for loss of individual proteins (two-dimensional isoelectric focusing/sodium dodecyl sulphate gel electrophoresis, reversed phase-high performance liquid chromatography) after duct passage showed that pancreatic secretions were completely recovered from the duct lumen. In another experiment, applying the same pressure, the duct was perfused with activated pancreatic juice. Morphologic analysis showed a preservation of the pancreatic duct mucosal integrity immediately after duct perfusion and absence of pancreatic inflammatory lesions 24 h after duct passage. We conclude that the pancreatic duct mucosa is impermeable to the leakage of pancreatic exocrine proteins from the duct lumen at duct pressure < or = 40 cm H2O. Flow of activated pancreatic juice along the pancreatic duct at duct pressure < or = 40 cm H2O does not cause acute pancreatitis. These data do not support the hypothesis that leakage of pancreatic juice from the duct lumen caused by high intraductal pressure due to duct obstruction initiates acute pancreatitis.

Animals↗
PubMed1995

Induction of p21ras in Alzheimer pathology.

Changes in the expression of the small G-protein p21ras, a critical regulator of cell proliferation and differentiation, were investigated by immunohistochemical methods in the temporal cortex of patients with Alzheimer's disease. In both normal brain and in Alzheimer's disease, the H-ras, K-ras and N-ras gene products were equally detected in almost all neurones and occasionally also in glial cells. In Alzheimer's disease an increased expression of p21ras was observed within neuritic plaques as well as in neurones and glial cells closely associated with plaques. Neurones containing tangle-bearing material also showed a high level of expression. It is suggested that activation of p21ras dependent signalling pathways are involved in the processes of neurodegeneration and/or aberrant repair in Alzheimer's disease.

Aged↗
PubMed1995

Dendritic reorganisation in the basal forebrain under degenerative conditions and its defects in Alzheimer's disease. I. Dendritic organisation of the normal human basal forebrain.

In the present study, the dendritic organisation of neurones in the normal human basal forebrain was analysed as a prerequisite for the evaluation of pathological changes occurring in Alzheimer's disease and related conditions (see other Arendt et al. papers in this issue). Neurones in the basal nucleus of Meynert (NbM), the nucleus of the vertical limb of the diagonal band, and the medial septal nucleus were examined after Golgi impregnation. Cells were classified according to the dendritic branching pattern and soma shape as either reticular neurones or multipolar giant neurones. The reticular type of neurones constitutes more than 90% of neurones in the BnM. Cholinergic neurones also belong to this cell type. Reticular neurones were further subdivided into four subtypes. Morphological features and arrangement of reticular basal forebrain neurones were identical to those described for "reticular formation cells" or "isodendritic" neurones. Dendritic trees of reticular neurones show a spatial orientation perpendicular to passing fibres as well as a high degree of overlap, both of which are hallmarks of "open nuclei." The qualitative classification of Golgi-impregnated basal forebrain neurones was substantiated by a computer-based three-dimensional analysis. Topologic and metric parameters of the dendritic tree were calculated for each type of neurone to characterise the degree of dendritic branching, the shape and orientation of the dendritic arborisation, the spatial extension of the dendritic tree, and soma size. The classification criteria were evaluated according to their power of discrimination between different cell types by means of a discriminant analysis. The quantitative approach applied in the present study not only provides an objective measure for the description and comparison of the structure of various types of neurones but also makes it possible to elucidate fine structural changes that might occur under pathologic conditions and that are not evident during qualitative studies alone.

Adult↗
PubMed1995

Dendritic reorganisation in the basal forebrain under degenerative conditions and its defects in Alzheimer's disease. II. Ageing, Korsakoff's disease, Parkinson's disease, and Alzheimer's disease.

Changes in the dendritic arborisation of Golgi-impregnated basal forebrain neurones with respect to size, shape, orientation, and topology of branching were quantitatively investigated in ageing, Alzheimer's disease (AD), Korsakoff's disease (KD), and Parkinson's disease (PD). A reorganisation of the whole dendritic tree characterized by an increase in both the total dendritic length and the degree of dendritic arborisation as well as by changes in the shape of the dendritic field was found during ageing, in KD, PD, and AD. Dendritic growth under these conditions was related to the extent of cell loss in basal forebrain nuclei. There appeared to be major differences, however, with respect to the overall pattern of dendritic reorganisation between AD on one side and ageing, KD, and PD on the other side. In both ageing and KD, dendritic growth was largely restricted to the terminal dendritic segments, resulting in an increase of the size of the dendritic field (pattern of "extensive growth") In AD, however, dendritic growth mainly resulted in an increase of the dendritic density within the dendritic field without being accompanied by an increase in the size of the volume occupied by the dendritic tree (pattern of "intensive growth"). In AD, aberrant growth processes were frequently observed in the perisomatic area or on distal dendritic segments of basal forebrain neurones of the reticular type. Neurones with aberrant growth profiles were typically located in the direct vicinity of deposits of beta/A4 amyloid. Perisomatic growth profiles were covered by the low-affinity receptor of nerve growth factor p75NGFR. Aberrant growth processes were not present in ageing, KD, and PD. On the basis of the present study, it is concluded that under certain degenerative conditions, reticular basal forebrain neurones undergo a compensatory reorganisation of their dendritic arborisation, a process that has become defective in AD, thereby converting a physiological signal into a cascade of events contributing to the pathology of the disease.

Adult↗
PubMed1995

Dendritic reorganisation in the basal forebrain under degenerative conditions and its defects in Alzheimer's disease. III. The basal forebrain compared with other subcortical areas.

The distribution of the reticular neuronal type in the human brain and its involvement in both degeneration and dendritic reorganisation under the conditions of ageing, Korsakoff's disease (KD), Alzheimer's disease (AD), and Parkinson's disease (PD) was comparatively investigated after Golgi impregnation. Reticular neurones are distributed throughout different areas along the brain axis. The cholinergic basal forebrain nuclei, i.e., the basal nucleus of Meynert, the nucleus of the diagonal band, and the medial septal nucleus form the most rostral part of this network of "open nuclei," which is collectively referred to as the "reticular core." Reticular neurones of the following areas were quantitatively investigated by a computer-based three-dimensional analysis: caudate nucleus, globus pallidus, medial septal nucleus, nucleus of the vertical limb of the diagonal band, basal nucleus, medial amygdaloid nucleus, reticular thalamic nucleus, lateral hypothalamic area, subthalamic nucleus, substantia nigra, locus coeruleus, pedunculopontine tegmental nucleus, and raphe magnus nucleus. There are three major findings. First, neurones that were found to be susceptible to degeneration in AD were largely part of the same neuronal populations prone to degeneration during ageing, in KD and PD. Thus, areas could be classified according to their overall degree of vulnerability under the present degenerative conditions as being highly vulnerable (basal forebrain nuclei, caudate nucleus, locus coeruleus), moderately vulnerable (medial amygdaloid nucleus, raphe magnus nucleus, lateral hypothalamic area, substantia nigra, pedunculopontine tegmental nucleus), or marginally vulnerable (globus pallidus, subthalamic nucleus, reticular thalamic nucleus). Second, neuronal populations that are particularly vulnerable to degenerative changes show a high degree of structural plasticity. Third, the degree of this dendritic plasticity is inversely related to the complexity of dendritic arborisation of the neurone. It is concluded that the sparsely ramified reticular type of neurone forms a pool of pluripotent neurones that have retained their plastic capacity throughout life, which makes them vulnerable to a variety of perturbations.

Adult↗