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Biomedical subjects

C Sommer

Publications and source records attributed to C Sommer.

At least 109 records · Page 6Linked to original sources
PubMed1997

Cultured dermal papilla cells of the rat vibrissa follicle. Proliferative activity, adhesion properties and reorganization of the extracellular matrix in vitro.

The dermal papilla of the mammalian hair follicle plays an important role in regulating and controlling the hair cycle. Distinct functional stages of dermal papilla cells (DPC) are involved in this process, thus suggesting that the dermal papilla is a highly specialized suborgan of the pilosebaceous unit. The aim of the present study was to investigate the functional properties of cultured DPC in various assays and to compare their functional properties with those of dermal fibroblasts (DFB). In monolayer cell cultures DPC showed an aggregative growth pattern, different to that of DFB, and lower proliferation rates, as compared to the controls. Adhesion assays performed using a 51[Cr]labeling method showed strong adhesion of both cell populations to collagen types I and IV, fibronectin and laminin, but DPC in vitro showed significantly higher adhesiveness to collagen type IV, a major component of the basement membrane of dermal papillae in vivo. The capacity of DPC to reorganize extracellular matrix components, as measured by gel contraction with three-dimensional collagen type I lattices, proved to be significantly lower than that of DFB and, moreover, DPC lysed the collagen lattices completely after 48 h in culture. The functional differences between DPC and DFB were paralleled by higher surface expression and synthesis levels of the beta 1, alpha 1, and alpha 5 chains of integrin adhesion receptors in DPC, as detected by fluorescence-activated cell-sorter analysis and radioimmunoprecipitation. These findings provide evidence that DPC are a highly specialized cell population, which clearly differs from another mesenchymal cell type, DFB. After their isolation and cultivation in vitro, DPC still preserve functional properties related to important steps of cell-matrix interaction involved in the hair cycle.

Animals↗
PubMed1997

Effect of global system for mobile communication microwave exposure on the genomic response of the rat brain.

The acute effect of global system for mobile communication (GSM) microwave exposure on the genomic response of the central nervous system was studied in rats by measuring changes in the messenger RNAs of hsp70, the transcription factor genes c-fos and c-jun and the glial structural gene GFAP using in situ hybridization histochemistry. Protein products of transcription factors, stress proteins and marker proteins of astroglial and microglial activation were assessed by immunocytochemistry. Cell proliferation was evaluated by bromodeoxyuridine incorporation. A special GSM radiofrequency test set, connected to a commercial cellular phone operating in the discontinuous transmission mode, was used to simulate GSM exposure. The study was conducted at time averaged and brain averaged specific absorption rates of 0.3 W/kg (GSM exposure), 1.5 W/kg (GSM exposure) and 7.5 W/kg (continuous wave exposure), respectively. Immediately after exposure, in situ hybridization revealed slight induction of hsp70 messenger RNA in the cerebellum and hippocampus after 7.5 W/kg exposure, but not at lower intensities. A slightly increased expression of c-fos messenger RNA was observed in the cerebellum, neocortex and piriform cortex of all groups subjected to immobilization, but no differences were found amongst different exposure conditions. C-jun and GFAP messenger RNAs did not increase in any of the experimental groups. 24 h after exposure, immunocytochemical analysis of FOS and JUN proteins (c-FOS, FOS B, c-JUN JUN B, JUN D), of HSP70 or of KROX-20 and -24 did not reveal any alterations. Seven days after exposure, neither increased cell proliferation nor altered expression of astroglial and microglial marker proteins were observed. In conclusion, acute high intensity microwave exposure of immobilized rats may induce some minor stress response but does not result in lasting adaptive or reactive changes of the brain.

Animals↗
PubMed1996

Characterization of genomic alterations associated with glioma progression by comparative genomic hybridization.

Genomic alterations associated with glioma progression were determined by comparative genomic hybridization (CGH) 30 tumors from 15 patients with primary gliomas of World Health Organization (WHO) grade II that on recurrence showed progression to malignant gliomas of WHO grades III or IV (five cases of astrocytoma grade II (A II) to grade III (AA III), five cases of A II to glioblastoma multiforme grade IV (GBM) and five cases of oligodendroglioma grade II (O II) to grade III (AO III)). All tumors were additionally screened for p53 mutations by single strand conformational polymorphism and heteroduplex analysis of exons 5-8, followed by direct sequencing. Mutations of p53 were found in the primary and recurrent tumors of all cases of A II progressing to GBM and three of five cases of A II recurring as AA III. Alterations identified by CGH in more than one primary A II included losses on Xp (3/10) and 5p (2/10), gains on 8q and 19p (2/10 each), and gain/amplification on 12p (2/10). Common progression associated changes found in AA III or GBM were losses on 4q, 9p, 10q, 11p, 13q (4/10 each) and gains on 1q, 6p, 20q (2/10 each). The most frequent amplification site was located on 12p13 (1/10 A II, 3/5 AA III, 1/5 GBM). Other amplified chromosomal regions were 13q32-q34 (1/10 AII, 2/5 GBM), 7q31-qter (1/5 AA III, 1/5 GBM), 12q22-qter and 18p (1/5 AA III). In contrast to the astrocytic gliomas, only one of five oligodendroglial cases showed a p53 mutation. Genetic abnormalities identified by CGH to occur more than once were restricted to four chromosomes (1, 4, 9 and 19). Our results provide a comprehensive overview of the genomic alterations associated with the progression of individual gliomas and substantiate the hypothesis that glioma progression is associated with a cumulative acquisition of multiple genetic changes.

Adult↗
PubMed1996

Vascular pathology in CCI neuropathy: a quantitative temporal study.

An experimental neuropathy in rats produced by tying loosely constrictive ligatures around one sciatic nerve evokes pain-related behavior that follows a reproducible time course. We have previously investigated the pathologic changes in the sciatic nerve in this model, and a striking feature was protrusion and proliferation of endoneurial endothelial cells. In the present study, we quantified these changes at time points from 1 day to 12 weeks after surgery. One day after surgery, vessels were distended, shown by an increase of the slope of a graph in which the vessel areas were plotted on the x axis and luminal areas on the y axis. From Day 7, the slope was reduced; i.e., vessel walls had thickened and lumina were smaller. By Day 14, narrowing of lumina was observed in the contralateral (control) nerve also. We suggest that endothelial cell proliferation, known to be induced by cytokines produced by macrophages, indicates increased activity and pathogenic significance of these cytokines in the CCI model.

Animals↗
PubMed1996

Digital image analysis and identification of eggs from bovine parasitic nematodes.

Computer-assisted microscopy and multivariate statistics were used to establish and evaluate a procedure for identification of bovine strongylid eggs. Ostertagia ostertagi, Cooperia oncophora, Haemonchus placei, Trichostrongylus axei, and Oesophagostomum radiatum eggs were obtained from faeces voided by monospecifically infected calves. Images of single eggs (400 x magnification) were recorded by a CCD camera fitted onto a microscope and digitized on a PC. After separation of eggs from the image background, the pixel (picture element) positions of the egg outline were analysed by algorithms to describe size and shape. A stepwise discriminant analysis was subsequently used to select and rank descriptive features of 4207 eggs according to discriminatory power. Classification criteria were developed by linear discrimination analysis on the basis of selected features, and the criteria evaluated by cross-validation. A maximum average percentage of correct classification of 85.8% resulted when nineteen features were employed in a linear classification criterion. The percentages correct classification for each species were: O. ostertagi 76.3%, C. oncophora 90.8%, O. radiatum 87.8%, H. placei 90.1%, and T. axei 83.8%. Classification based on the five most important features gave an overall correct classification of 81.5%. Images of "unknown' eggs could be identified automatically by the classification criteria after procedural steps performed by PC were linked in a batch program.

Animals↗
PubMed1996

Editing of GluR2 RNA in the gerbil hippocampus after global cerebral ischemia.

Postischemic delayed neuronal death (DND) in CA1 of the gerbil hippocampus is thought to be caused by an abnormal increase of Ca2+ influx into the cell, mediated by excessive activation of glutamate receptors. One subtype of glutamate receptors, the AMPA receptor, is not permeable to calcium ions as long as an edited form of its GluR2 subunit is present. It is possible that global ischemia interferes with the posttranscriptional editing of the GluR2 mRNA and thus leads to calcium influx via the AMPA receptor. In order to test this hypothesis, we examined the extent of GluR2 RNA editing in CA1 and CA3 microdissected from gerbil hippocampus after 5 min of global ischemia and various recirculation intervals. At each interval tested, quality and quantity of mRNA editing in the vulnerable CA1 region were the same as in CA3. Furthermore, postischemic mRNA editing in both hippocampal regions was indistinguishable from editing in untreated control animals. Our results clearly demonstrate that global ischemia does not cause impairment of GluR2 RNA editing, which is thus not responsible for the abnormal calcium permeability of the postischemic cell membrane.

Animals↗
PubMed1996

Influence of ankle ligaments on tibial rotation: an in vitro study.

The purpose of this study was to clarify the role of the ankle ligaments in controlling the tibial rotation for different foot positions. A 6 degrees of freedom device was constructed for in vitro simulation of this movement transfer during the support phase of gait. Tibia rotation angle was measured for different foot positions and vertical loads, while the ligament integrity was modified. Data were collected from eight legs of four different cadavers. The results showed that vertical loading is unimportant to influence tibial rotation, while the lateral ankle ligaments have significant influence, especially during eversion. It was concluded that chronic partial or total lateral ankle instability may contribute to knee and foot injuries through abnormal tibial rotation.

Aged↗
PubMed1996

Clinically distinct subgroups of glioblastoma multiforme studied by comparative genomic hybridization.

Studies investigating genetic alterations potentially constituting prognostic factors in glioblastoma multiforme (GBM) have centered mainly around amplification events. Comparative genomic hybridization (CGH) is a recent molecular cytogenetic technique that allows the detection of chromosomal imbalances and amplification sites in tumor DNA prepared from fresh or archival material. A group of 94 patients with GBM underwent surgery followed by a standard course of radiotherapy. Neuroradiologic monitoring with gadolinium-enhanced serial magnetic resonance imaging was applied to study the radiologically progression-free interval (RPFI) and tumor regrowth velocity. These parameters provided a clinical estimate of the postoperative tumor regrowth kinetics and yielded two clinically distinct groups. The most pronounced cases were selected from each group, i.e., those with the most favorable and unfavorable prognosis. Two subgroups with a statistically significant difference in RPFI (p < 0.001, Mann-Whitney U test) containing 10 patients each were formed: Subgroup A (slow tumor regrowth kinetics) and subgroup B (fast tumor regrowth kinetics). For a search of chromosomal alterations that might be correlated with tumor regrowth kinetics, we applied CGH to formalin-fixed, paraffin-embedded tumor tissue from these 20 patients. Except for autosomes 18 and 21, all chromosomes were involved at least once in copy-number aberrations. Events commonly associated with GBM, i.e., gains of chromosome 7, complete and partial losses of 9p, 10, and 22q, were not distributed differently between the two subgroups. The following differences were noticeable. Gains (including amplifications) of 12q14-q21 and of 19 were observed more often in subgroup A. Losses of 6q16-qter and parts of 13, and gains of 20, were more frequent in subgroup B. RPFI was significantly shorter for patients without amplification sites than for patients with gene amplification. RPFI did not differ significantly between patients with or without 7p12 amplification, where the epidermal growth factor receptor gene is localized. New amplification sites for GEM tumors were revealed at 11q13 and 11q22-q23. Loss of chromosome 10 was restricted to bands 10q25-q26 in one case. Although differences in the copy-number karyotypes of patients with slow and fast postoperative tumor-regrowth kinetics were noted, the present CGH study did not reveal any single alteration useful as a prognostic factor. In particular, these data do not support the assumption that patients suffering from GBM with amplification events would have a poorer prognosis than others.

Adult↗
PubMed1995

Developmental expression of GAP-43 and SNAP-25 in heterotopic rat cortical grafts.

In situ hybridization techniques were used to assess (i) whether the temporal developmental profiles of the nervous system specific growth associated phosphoprotein (GAP-43) and the 25-kDa synaptosomal-associated protein (SNAP-25) are maintained in heterotopic cortical transplants, and (ii) whether the hybridization intensity in morphologically differentiated heterotopic transplants is comparable to that in the cortex of host animals. Cortical primordia at embryonic day 14 were stereotactically grafted into the striatum of adult recipient rats. Grafts at days 4, 7, 14, 35 and 56 after transplantation demonstrated developmental changes with a progressive decline of GAP-43 and a continuous up-regulation of SNAP-25 expression. Our data provide evidence of distinct molecular alterations during the differentiation process of cortical grafts, which are strikingly similar to previous studies investigating the temporal profile and intensity of GAP-43 and SNAP-25 gene expression in normal developing cortex of the rat.

Animals↗
PubMed1995

HLA-DR expression in peripheral neuropathies: the role of Schwann cells, resident and hematogenous macrophages, and endoneurial fibroblasts.

The expression of HLA-DR and the macrophage marker CD 68 was studied in 44 sural nerve biopsies from patients with inflammatory and non-inflammatory neuropathies and controls using immunohistochemistry on non-osmicated semithin sections, a technique that has not been used before in such a biopsy study. Most HLA-DR-immunoreactive (ir) cells were fibroblasts, macrophages or perineural cells, some were perivascular and endothelial cells, and only few were Schwann cells. Counts of immunoreactive cells revealed (a) increased HLA-DR expression in severe as compared to less severe neuropathies and to controls, (b) no correlation between the numbers of HLA-DR-ir cells and CD 68-ir macrophages, and (c) no close correlation between diagnostic groups and the number of HLA-DR-ir cells, but higher numbers in inflammatory neuropathies. We conclude that endoneurial fibroblasts and macrophages as antigen-presenting cells may be mediators in various peripheral nerve diseases, not only in inflammatory disorders.

Adolescent↗
PubMed1995

Neurotransmitters in the spinal cord dorsal horn in a model of painful neuropathy and in nerve crush.

We tested the hypothesis that neurochemical changes in the spinal cord dorsal horn associated with neuropathic pain states differ from those seen in association with non-painful neuropathies. Immunohistochemistry was performed on spinal cord sections from rats with a chronic constriction injury (CCI), which develop hyperalgesia, and from animals with a nerve crush injury, which do not develop hyperalgesia or other signs of a painful syndrome. Immunohistochemistry was quantified by computer-assisted densitometry. Calcitonin gene-related peptide (CGRP) immunoreactivity and substance P (SP) immunoreactivity were decreased from 1 to 4 weeks after injury in CCI and from 2 to 6 weeks in crush. Gamma-aminobutyric acid immunoreactivity was unchanged in both conditions at all time points. Met-enkephalin (Met-enk) immunoreactivity was increased in CCI and unchanged in crush. Although SP and CGRP are involved in pain transmission, we conclude that their decrease in immunoreactivity is not specific for the CCI model, but rather a more general event in nerve de- and regeneration. The increase in immunoreactivity for the opioid peptide Met-ink, however, was only seen in the late phase of CCI, and may be specific for conditions associated with neuropathic pain and its resolution.

Animals↗
PubMed1995

Rare diseases mimicking acute vertebrobasilar artery thrombosis.

Acute ischaemia of the vertebrobasilar circulation leads to a variety of clinical manifestation and is mostly due to cardiogenic or artery-to-artery embolism. We describe four neurological emergency situations involving vertebrobasilar artery aclusion of other origins; basilar migraine, extrinsic compression by rheumatoid inflammatory tissue, generalized vasculitis in subacute rheumatic fever and basilar artery dissection. The differential diagnosis of acute vertebrobasilar artery occlusion may have an important impact on patient management.

Acute Disease↗
PubMed1995

Quantitative neuropathology of a focal nerve injury causing hyperalgesia.

The chronic constriction injury (CCI) model of neuropathy in the rat produces hyperalgesia and allodynia in the sciatic distribution of one hindlimb. We previously described the pathology of the affected nerves at the light microscopic and electron microscopic levels and in this report quantify the morphological changes of the nerves. This analysis gives new insights into the pathophysiology and pain-related mechanisms in this model of human neuropathy. We observed that total fascicular area increased up to fourfold due to an initial massive increase in edema and, later, endoneurial cells. Intact myelinated nerve fibers were reduced from 75% of fascicular area to 29.7% on day 1 and to a minimum of less than 0.5% on day 14 when edema had resolved. The few surviving myelinated fibers were in the small to medium size range. Fiber size histograms revealed an increase in fiber size early on, corresponding to fiber swelling, and the later loss of large as well as small myelinated fibers. Unmyelinated nerve fibers dropped from 19.36/1,000 microns 2 to 6.08/1,000 microns 2 on day 5, and increased from there on. Sprouts were first visible on light micrographs on day 7, occupying 6.8% of fascicular area, while regenerating fibers that were undergoing myelination reached 42.6% of fascicular area by day 42. Macrophage numbers were maximal on day 14 and were still increased on day 42. These data support the hypothesis that the pathogenesis of the extended hyperalgesia following chronic constrictive nerve injury is temporally linked with Wallerian-like degeneration and macrophage activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Selective c-JUN expression in CA1 neurons of the gerbil hippocampus during and after acquisition of an ischemia-tolerant state.

The selective delayed neuronal death of CA1 pyramidal cells after transient global ischemia in the gerbil brain can be prevented by preconditioning with a short sublethal period of ischemia 1-7 days prior to a subsequent, usually lethal ischemia of 5 min duration. Since changes of neuronal gene expression may play a crucial role in this tolerance induction, we investigated the postischemic expression profile of the fos, jun and Krox transcription factor families. We have previously reported that a single 5 min period of cerebral ischemia does not cause a de novo synthesis of immediate early gene (IEG) encoded proteins in CA1 neurons. In the present study, two experimental groups of Mongolian gerbils were investigated: one group was subjected to a single tolerance-inducing 2.5 min period of ischemia by bilateral occlusion of the common carotid artery. The second (combined ischemia) group was subjected to 2.5 min of ischemia, followed by 5 min of ischemia 4 days later. Post-ischemic expression of c-FOS, FOS B, c-JUN, JUN B, JUN D and KROX-24 was investigated by in situ hybridization and immunocytochemistry up to 48 h of recirculation. In contrast to a single 5 min period of ischemia, 2.5 min caused a postischemic expression of c-JUN protein, but no other IEGs, in CA1 neurons (peak at 6 h). Similarly, a selective but delayed c-JUN expression (peak at 18 h) was observed in animals subjected to combined ischemia. These results indicate that the induction of an endogenous neuroprotective state in CA1 neurons is associated with the activation of a genetic program which involves the expression of specific transcription factors.

Animals↗
PubMed1995

Degradation of 1,4-dichlorobenzene by Xanthobacter flavus 14p1.

Xanthobacter flavus 14p1 was isolated from sludge of the river Mulde by selective enrichment with 1,4-dichlorobenzene as the sole source of carbon and energy. The bacterium did not use other aromatic or chloroaromatic compounds as growth substrates. During growth on 1,4-dichlorobenzene, stoichiometric amounts of chloride ions were released. Degradation products of 1,4-dichlorobenzene were identified by gas chromatography-mass spectrometry analysis. 3,6-Dichloro-cis-1,2-dihydroxycyclohexa-3,5-diene and 3,6-dichlorocatechol were isolated from culture fluid. 2,5-Dichloromuconic acid and 2-chloromaleylacetic acid as well as the decarboxylation product 2-chloroacetoacrylic acid were identified after enzymatic conversion of 3,6-dichlorocatechol by cell extract. 1,4-Dichlorobenzene dioxygenase, dihydrodiol dehydrogenase, and catechol 1,2-dioxygenase activity were induced in cells grown on 1,4-dichlorobenzene. The results demonstrate that 1,4-dichlorobenzene degradation is initiated by dioxygenation and that ring opening proceeds via ortho cleavage.

Biodegradation, Environmental↗
PubMed1995

Influence of ligament transection on tibial and calcaneal rotation with loading and dorsi-plantarflexion.

The purpose of this study was to quantify the effect of sequential ligament transection (anterior talofibular, calcaneofibular, posterior talofibular, deltoid, and subtalar interosseous ligaments) on the rotational movement of the tibia and the calcaneus as associated with axial loading and dorsi-plantarflexing the foot. Eight cadaver foot-leg specimens were investigated using a unconstrained testing apparatus. As the ankle complex was axially loaded, almost the same internal rotation of the tibia and the same calcaneus eversion was found with and without the various degrees of lateral and medial ligament release; additional sectioning of the subtalar interosseous ligament tremendously increased the resulting tibial and calcaneal rotation. While tibial and calcaneal rotation from foot dorsi-plantarflexing did not alter significantly with transection of the lateral ligaments, almost no tibial and calcaneal rotation occurred after additional sectioning of the deltoid and subtalar interosseous ligament. These results indicate that, after release of the lateral ligaments, the foot becomes partially mechanically disconnected from the tibia by additional transection of the medial ligaments and even further disconnected after transection of the subtalar interosseous ligament.

Aged↗
PubMed1995

[From quality assurance to continuous quality improvement in the American health care system. Personal experiences gained through a 3-week educational stay].

We present our personal experience we got during a three week period in the United States studying different quality control programs in the American health care system. Quality Assurance, a control system leaning on inspections, is widespread in the American industry and the health care organizations. W.E. Deming, an economist, developed some decades ago a philosophy to lead any kind of organization more efficiently and successfully. This theory is called CQI, Continuous Quality Improvement. Following Deming's ideas, first the Japanese and then the American industry have made great improvements during the last two decades. Since 1987 American health care organizations are using more and more the tools of the CQI to improve their quality and reduce the rising costs. Visiting nearly twenty different hospitals or institutes, sponsored and organized by "Johnson&Johnson", we could convince ourselves, that the CQI has several advantages in comparison to the traditional quality control or assurance methods.

Cost Control↗