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Biomedical subjects

R Lemke

Publications and source records attributed to R Lemke.

At least 19 recordsLinked to original sources
PubMed1999

Interleukin-1beta, inducible nitric oxide synthase, and nuclear factor-kappaB are induced in morphologically distinct microglia after rat hippocampal lipopolysaccharide/interferon-gamma injection.

In a number of pathological states of the brain, the activation of the inducible nitric oxide synthase (iNOS) plays a major role. Interleukin (IL)-1beta is believed to be an essential factor in the induction of iNOS. However, little is known about the cascade of events culminating in iNOS expression in vivo. To identify the morphological as well as temporal relationship of lipopolysaccharide (LPS)/interferon-gamma (IFN-gamma) -induced microglial iNOS- and IL-1beta expression, a mixture of LPS and IFN-gamma was injected into the rat hippocampus. IL-1beta immunoreactivity was detected as early as 3 hr following surgery in ramified microglia in the lesioned hippocampus and in distal cortical layers adjacent to the pia mater. By 12 hr post-injection, IL-1beta immunoreactive, ramified microglia with swollen processes were widely distributed throughout hippocampal and neocortical areas, and staining was observed up to 48 hr after treatment. In contrast, iNOS immunostaining was seen in activated amoeboid microglia/macrophages in the ipsilateral hippocampus and around blood vessels but not earlier than 12 hr post-surgery. The temporal pattern of iNOS and IL-1beta expression corresponded to newly induced transcriptional activity as revealed by RT-PCR. Activation of NF-kappaB was restricted to brain regions in which IL-1beta was expressed and was detected both in microglia and astrocytes. A number of LPS/IFN-gamma-stimulated, IL-1beta-expressing microglia exhibited co-staining for activated NF-kappaB. The finding that IL-1beta precedes iNOS expression is consistant with a role of IL-1beta in the intercellular signaling events leading to microglial iNOS-induction. Co-localization of IL-1beta and NF-kappaB suggests an association between IL-1beta and NF-kappaB induction.

Animals↗
PubMed1999

Leukemia inhibitory factor expression is not induced in activated microglia and reactive astrocytes in response to rat basal forebrain cholinergic lesion.

In adult intact rat brain, leukemia inhibitory factor (LIF) mRNA has been found to be constitutively expressed in basal forebrain cholinergic neurons. To reveal a functional role of LIF in neurodegenerative events, the cellular expression pattern of LIF was determined by combining in situ hybridization and immunocytochemistry after specific and selective degeneration of basal forebrain cholinergic cells by a single intracerebroventricular application of the cholinergic immunotoxin 192IgG-saporin. Although basal forebrain cholinergic lesion resulted in a dramatic activation of micro- and astroglial cells at the lesion site, LIF mRNA expression was not detected in any of the lesion-induced activated glial cell types. As the cholinergic immunotoxin exerts its degenerative action by the ribosome-inactivating property of saporin, the lack of glial LIF induction might be due to the incapability of the dying cholinergic cell to form and release factors which induce LIF expression in activated glial cells.

Animals↗
PubMed1999

Iliac cancellous bone in drug addicts: a histomorphometric study.

Histomorphometry was used to determine structural bone changes in drug addicts. Iliac crest bone biopsies were obtained at autopsy from 28 subjects (21 male, 7 female, aged 18 to 45 years) who had a history of drug abuse and had died due to overdose of illicit drugs. For histomorphometry, undecalcified sections were investigated using the Merz grid. The following histomorphometric indices were measured and calculated: BV/TV, BS/BV, Tb.Th, Tb.N, Tb.Sp, OV/TV, OS/BS, Ob.S/BS, O.Th, ES/BS, Oc.S/BS, and N.Oc/T.A. In 28 controls (24 male, 4 female, aged 17 to 47 years) trabecular bone specimens were investigated in the same way. The parameters in drug addicts did not show any correlation to age, body weight, height or sex differences. Trabecular bone volume and trabecular thickness were slightly but not significantly increased (BV/TV: 23.37 +/- 5.77% (mean, SD), controls 22.23 +/- 5.08%, p = 0.434; Tb.Th: 172.67 +/- 36.83 mcm, controls 169.73 +/- 36.13 mcm, p = 0.764). Only the eroded surface was significantly different to the controls (ES/BS: 8.16 +/- 2.04%, controls 6.96 +/- 2.17%, p = 0.038). We conclude that the incidence of metabolic bone disease in drug addicts is low.

Adolescent↗
PubMed1999

Differential injury-dependent glial expression of interleukins-1 alpha, beta, and interleukin-6 in rat brain.

Interleukins (IL)-1 alpha, beta and IL-6 may play essential roles in early inflammatory processes in response to degenerating cholinergic cells observed in the basal forebrain of Alzheimer patients. To address this question in vivo, two distinct lesion paradigms were used. A specific and selective basal forebrain cholinergic cell loss was achieved by a single intracerebroventricular application of the cholinergic immunotoxin, 192IgG-saporin. Intrahippocampal injection of lipopolysaccharide and interferon-gamma was used to produce an exogenously-induced acute inflammation in the brain. In order to disclose the lesion-induced temporal cascade of the expression pattern of IL-1 alpha, IL-1 beta, and IL-6, and the cell types expressing IL-1 alpha, beta/IL-6 mRNA, Western analysis, RT-PCR, and double labeling immunocytochemistry were applied. In the intact brain, IL-6, IL-1 alpha and IL-1 beta demonstrated a constitutive expression in neurons. Following cholinergic lesion neither IL-1 beta nor IL-6 expression could be detected in any of the activated glial cell types, whereas IL-1 alpha was found to be expressed in astroglial cells only. In contrast, hippocampal administration of lipopolysaccharides/interferon-gamma resulted in expression of IL-1 alpha in microglial but not astroglial cells. These in vivo studies clearly demonstrate that the cellular expression of IL-1 alpha, IL-1 beta, and IL-6 in the brain is differentially regulated depending on the kind of injury producing the inflammatory response in the brain. The data suggest that each glial cell seems to be equally capable of expressing a number of various cytokines, but it depends on the kind of stimulus which temporal and cellular cascade of cytokine expression pattern is initiated under a particular pathological condition in the brain.

Animals↗
PubMed1998

Phrenic nerves and diaphragms in sudden infant death syndrome.

Disturbances of the respiratory system may be an important factor in the cascade of events leading to sudden infant death syndrome (SIDS). Even though the diaphragm is the major respiratory muscle in infants, little is known about alterations of this muscle and of the phrenic nerve in SIDS. In the present study, diaphragms and phrenic nerves of 24 SIDS infants and seven controls were analyzed. Morphometric analysis revealed only slightly larger cross sectional areas of phrenic nerve axons but no increase in myelin sheath thickness in SIDS cases. However, in one SIDS case, myelinated nerve fibre density was severely reduced. Using electron microscopy, several nerve fibres of SIDS infants showed focal accumulations of neurofilaments. Muscle fibre diameters in SIDS diaphragms were significantly larger compared to controls (P < 0.0001). However, in almost all SIDS and control cases, axons and myelin sheaths were artificially swollen, and acute segmental muscle fibre ruptures and contracture bands were found. These prominent nonspecific ultrastructural alterations should advise caution in the interpretation of morphometric data. Thus, in some cases exemplified by one case of the present series, decreased density of phrenic nerve myelinated axons might contribute to SIDS. Still, the present results indicate that development of phrenic nerves and diaphragms is not delayed in most SIDS infants.

Autopsy↗
PubMed1998

Interleukin-6 is not expressed in activated microglia and in reactive astrocytes in response to lesion of rat basal forebrain cholinergic system as demonstrated by combined in situ hybridization and immunocytochemistry.

Interleukin-6 may play an essential role in early inflammatory processes as response to degenerating cholinergic cells in the nucleus basalis of Meynert in patients suffering Alzheimer's disease. The cholinergic immunotoxin, 192IgG-saporin, was applied to produce selective and specific degenerations of basal forebrain cholinergic cells. To disclose the lesion-induced temporal cascade of the expression pattern of IL-6, and to reveal the cellular source for production and secretion of IL-6 in vivo after endogeneously induced basal forebrain cholinergic cell loss, both in situ hybridization and immunocytochemistry for IL-6 were performed. To identify the cell types expressing IL-6 mRNA, double labeling techniques were applied combining in situ hybridization technique with immunocytochemistry and lectin histochemistry for both micro- and astroglia and a number of neuronal markers including choline acetyltransferase, parvalbumin, and neurofilaments. In the intact brain, IL-6 is mainly localized in neurons, in particular in both cholinergic and GABAergic neurons of the basal forebrain. Although basal forebrain cholinergic lesion resulted in a dramatic increase in the number of micro- and astroglial cells at the lesion site, IL-6 expression could not be detected in any of the lesion-induced activated glial cell types. Moreover, cholinergic lesion led to a reduced number of IL-6-expressing cells in the basal forebrain, which is assumed to be due to the loss of cholinergic cells. The predominantly neuronal localization in rat brain suggests a role for IL-6 in activating micro- and astroglial cells in response to degenerating cholinergic neurons.

Animals↗
PubMed1997

Leukemia inhibitory factor (LIF) mRNA-expressing neuronal subpopulations in adult rat basal forebrain.

We have previously found leukemia inhibitory factor (LIF) mRNA in neurons of the adult rat brain. To identify which neuronal subpopulations are expressing LIF transcripts, non-radioactive in situ hybridization was combined with immunocytochemistry for various neuronal markers. Studying the rat basal forebrain and cerebral cortex, we find LIF mRNA is expressed in both cholinergic and GABAergic neurons. These data suggest a role for LIF in the function of these mature neurons.

Animals↗
PubMed1997

[Psychiatric involuntary commitment. Historical development and current status of legal principles].

An enforced treatment and institutionalization of psychiatric patients are implying a deep cut in the personal rights and freedom of these people. To prevent an abuse of psychiatry as a federal instrument of power and for the protection of all participants (patients and psychiatry personnel) a strict obeyance of federal rules and regulation required. Following to those aspects it is possible to minimate the uncertainty and retention of non-experienced doctors in psychiatry opposite the classical conflict concerning mental cruelty.

Commitment of Persons with Psychiatric Disorders↗
PubMed1996

Neuronal expression of leukemia inhibitory factor (LIF) in the rat brain.

Very little is known about the action of the leukemia inhibitory factor (LIF) in the central nervous system. To analyze LIF expression in adult rat brain, we used non-radioactive in situ hybridization with digoxigenin-labeled RNA probes, in combination with immunohistochemistry to identify the cell types expressing LIF mRNA. Hippocampal pyramidal cells, hilar interneurons and granule cells of the dentate gyrus display strong hybridization signals, while neurons of the cerebral cortex, cerebellum, cholinergic basal forebrain nuclei, and the striatum are labeled as well. The most prominent expression in cerebral cortex is in layers IV and VI. Glial fibrillary acidic protein-positive astrocytes did not display a detectable LIF hybridization signal suggesting that LIF mRNA is predominantly expressed in neurons in the normal, adult rat brain, although a presence in resting microglial cells cannot be excluded.

Animals↗
PubMed1996

Identification and characterization of the caiF gene encoding a potential transcriptional activator of carnitine metabolism in Escherichia coli.

Expression of the Escherichia coli caiTABCDE and fixABCX operons involved in carnitine metabolism is induced by both carnitine and anaerobiosis. When cloned into a multicopy plasmid, the 3' region adjacent to the caiTABCDE operon was found to increase levels of carnitine dehydratase activity synthesized from the chromosomal caiB gene. The nucleotide sequence was determined, and it was shown to contain an open reading frame of 393 bp named caiF which is transcribed in the direction opposite that of the cai operon. This open reading frame encodes a protein of 131 amino acids with a predicted molecular mass of 15,438 Da which does not have any significant homology with proteins available in data libraries. In vivo overexpression consistently led to the synthesis of a 16-kDa protein. The caiF gene was transcribed as a monocistronic mRNA under anaerobiosis independently of the presence of carnitine. Primer extension analysis located the start site of transcription to position 82 upstream of the caiF initiation codon. It was preceded by a cyclic AMP receptor protein motif centered at position -41.5. Overproduction of CaiF resulted in the stimulation of transcription of the divergent cai and fix operons in the presence of carnitine. This suggested that CaiF by interacting with carnitine plays the role of an activator, thereby mediating induction of carnitine metabolism. Moreover, CaiF could complement in trans the regulatory defect of laboratory strain MC4100 impaired in the carnitine pathway. Expression of a caiF-lacZ operon fusion was subject to FNR regulator-mediated anaerobic induction and cyclic AMP receptor protein activation. The histone-like protein H-NS and the NarL (plus nitrate) regulator acted as repressors. Because of the multiple controls to which the caiF gene is subjected, it appears to be a key element in the regulation of carnitine metabolism.

Acyltransferases↗
PubMed1995

[Case studies of sudden infant death cases (SIDS)].

Parents and attending physicians of 100 SIDS victims were interviewed applying a questionnaire especially designed for this purpose. Particular attention was focussed on the courses of pregnancy and birth, medical check-ups and the infants' unusual behaviour during the last days of their lives. As far as possible we compared our data with the results of the Rhenian Perinatal Survey 1990.

Cause of Death↗
PubMed1994

Vitiligo and other diseases: coexistence or true association? Hamburg study on 321 patients.

In the past, several authors described an association of vitiligo with autoimmune disorders and the presence of different tissue autoantibodies. A review of the literature showed large differences in the results. Therefore, 321 patients with vitiligo (male/female ratio 114/207) were examined to see whether the frequencies of associated diseases and phenomena (i.e. Koebner phenomenon, canities praecox, halo nevi, poliosis circumscripta), the number of pigmented lesions and the presence of autoantibodies are of significance in order to support (a) a subentity of childhood vitiligo and (b) whether there is a true predisposition or association of autoimmune or other diseases in this group of patients. The data confirm earlier results of a prevalence of thyroid disease and the presence of thyroid antibodies, whereas other diseases are a random event. 6.2% of the patients had congenital nevi compared with 2.8% in a normal healthy population. Based on the results of this study and the significant higher risk for development of melanomas in this patient group, an annual checkup is recommended.

Adolescent↗
PubMed1993

Postmortem serum selenium concentrations and their possible etiological role in sudden infant death (SID).

The importance of selenium (Se) deficiency in the pathogenesis of human diseases such as Keshan Disease has been extensively studied. It is possible that low Se-levels could cause immunosuppression and be an etiological factor in Sudden Infant Death (SID). We investigated 50 serum samples (40 SID and 10 non-SID victims) by atomic absorption spectrometry. The results show that there is no evidence of a serum selenium deficiency in SID-victims in the region of Aachen. A relationship between selenium concentration and the infant immune system still remains speculative and 21 samples even showed increased serum levels. It could be necessary to define a 'local' normal range by examining a greater number of healthy infants.

Female↗
PubMed1993

[Can psycho-education of chronic schizophrenic patients have a short-term effect on drug-related attitude and behavior?].

Within a controlled intervention study with schizophrenic outpatients we investigated the question of whether regular attendance at psychoeducational training for medication management has an influence on patients' illness-related behavior. The patients in the treatment group show better outcome of compliance and some treatment-related attitudes, though without statistical significance. Despite extensive information they are no more content with their knowledge of drugs than the control group, but more aware of problems, i.e. more cautious in medication co-determination.

Adult↗
PubMed1992

Production of catecholamines in the human epidermis.

Cell-free extracts from human full thickness skin (i.e., epidermis and dermis), suction blister roofs (i.e., epidermis) and from human keratinocytes express biopterin-dependent tyrosine hydroxylase a well as phenylethanolamine-N-methyl transferase, both representing key enzymes for the biosynthesis of epinephrine. These enzyme activities could not be detected in cell extracts from human melanocytes and human fibroblasts. Since keratinocytes in the human epidermis, and in cell cultures, express a high density of beta-2-adrenoceptors, and this signal transduction system regulates intracellular calcium homeostasis, it can be concluded that epinephrine production in the epidermis activates calcium transport via the beta-2-adrenoceptor system. Our results show for the first time that the human epidermis has the capacity to independently produce epinephrine.

Biopterins↗