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Biomedical subjects

G Bode

Publications and source records attributed to G Bode.

At least 19 recordsLinked to original sources
PubMed1992

[Polymorphism in Helicobacter pylori--a key function in recurrence of infection?].

Despite the fact that Helicobacter (H.) pylori is ubiquitous throughout the world, little is known at present about the source of infection and mode of transmission. Person-to-person transmission may be of importance. The fact that Helicobacter pylori can revert to a coccoid form stimulated speculation about its role in transmission and as a possible cause of reinfection in duodenal ulcer disease. Various antibacterial agents (bismuth subcitrate 32 mg/l bismuth subsalicylate 64 mg/l, amoxicillin 0.05 mg/l, ampicillin 2 mg/l, erythromycin 4 mg/l, glycochenodeoxycholic acid 423 mg/l, ursodeoxycholic acid 540 mg/l) inhibit the growth of H. pylori and stimulate the formation of coccoid structures. Ultrastructural and biochemical results show that the coccoid form meets the necessary criteria for survival. Thus, to be successful, treatment must aim not only at eliminating the vegetative form, but also at preventing the development of the coccoid form.

Anti-Bacterial Agents↗
PubMed1992

Influence of colloidal bismuth subcitrate on enzyme secretion from isolated rat pancreatic acinar cells.

Bismuth salts are currently used as monotherapy or in combination with antibiotics for the treatment of Helicobacter pylori-associated peptic ulcer disease. Besides encouraging clinical results with colloidal bismuth subcitrate (CBS), there is an ongoing fear of organ toxicity with the use of bismuth salts. To study potential toxic effects of CBS under short-term exposure, we tested the influence of CBS on amylase secretion from isolated rat pancreatic acinar cells under basal conditions and following carbachol (CCh) and ceruletide (CRT) stimulation. Basal secretion was reduced by 8.9 +/- 9.6% (n = 10) (mean +/- SEM) (P < 0.05), 5.2 +/- 9.2% (P < 0.05), 9.4 +/- 6.4% (P < 0.01), and 6.2 +/- 12.2% (P < 0.05) with 0.001, 0.01, 0.1, and 1 micrograms/ml CBS, respectively. With 10 micrograms/ml and 100 micrograms/ml CBS, basal amylase secretion was increased in a dose-dependent manner, by 13.7 +/- 11.7% (P < 0.05) and 24.5 +/- 12.8% (P < 0.01). CCh (10(-5) M)- and CRT (3 x 10(-10) M)-stimulated secretory responses were not altered significantly by any of the CBS doses used. In concentrations above 1 microgram/ml, CBS increased pancreatic amylase secretion. Amylase secretion in response to secretagogues was not affected by CBS. These findings are unlikely to be associated with a toxic effect of CBS on exocrine pancreatic acinar cell function.

Amylases↗
PubMed1992

Stimulation of bone marrow by administration of excessive doses of recombinant human erythropoietin.

Recombinant human erythropoietin (rhEPO) was administered intravenously to Beagle dogs in daily doses of 100, 500 and 3000 units/kg/day for 3 months. The high dose was more than 200-fold the therapeutic human maintenance dose. Such excessive rhEPO doses elicited extreme erythropoiesis. There was a dose-dependent stimulation of bone marrow fibroblasts, leading to bone marrow fibrosis in some of the high dose animals. The extent of myelofibrosis was intra- and interindividually different in various bones. Sternebrae proved to be practical for morphometric studies. The point-counting method was used for measurement. The portion of fatty tissue, sinusoids and fibrous tissue in the medullary space as well as the number of blood vessels and megakaryocytes were calculated. Such experimental conditions are not of relevance in human patients whose rhEPO therapy is interrupted as soon as their PCV reaches 35 vol%. Experimentally induced myelofibrosis should therefore not be considered as a risk in patients receiving therapeutic doses of rhEPO.

Adipose Tissue↗
PubMed1992

Effect of recombinant human erythropoietin on the growth of human tumor cell lines in vitro. Micro-titertec-tetrazolium assay.

Cells derived from 9 human tumors were tested in vitro using 5 doses ranging from 1 to 5000 units of recombinant human erythropoietin (rhEpo) per ml to assess a proliferation response to this hormone. The following tumors were used: 2 melanomas, 1 hepatoma, 3 renal cell carcinomas, 1 adenocarcinoma of the lung, and 2 mammary carcinomas (with and without sex steroid hormone receptors). Compared to untreated cells, none of the cell lines exposed to rhEpo revealed differences in proliferation extending beyond the limits of methodological fluctuation. rhEpo thus does not have any effect on the growth of human tumors in vitro under the experimental conditions applied.

Cell Division↗
PubMed1991

In vitro inhibition of Helicobacter pylori urease: biochemical and ultrastructural analysis.

Inhibition of H. pylori urease was studied by means of electron-microscopy and electrophoretic methods using different urease inhibitors, such as acetohydroxamic-acid (AHA), L-ascorbic acid (AsA), copper ions, a combination of L-ascorbic acid with copper ions and UV light. AHA in two different concentrations and AsA at a concentration of 0.1 mg ml-1 showed incomplete inhibition of H. pylori urease activity in our electrophoretic experiments. Only membrane-bound activity was inhibited with AHA but not the activity localized within the cytoplasma as demonstrated by electron-microscopy. AsA at a concentration of 0.5 mg ml-1 and the combination of copper ions (1 microgram ml-1) with AsA completely inhibited the urease activity as demonstrated by electron-microscopy and electrophoretic experiments. Cu2+ ions in high concentrations (100 micrograms ml-1) and UV light exposure for more than 4 h induced a complete disintegration of H. pylori. Electrophoresis showed no active protein after UV light exposure of 2 h. Different urease inhibitors tested in this study showed dose-dependent inhibitory effects on H. pylori urease in vitro.

Ascorbic Acid↗
PubMed1991

Fine structure of active and healed duodenal ulcer.

In order to characterize the fine structure of active and healed duodenal ulcers, we examined tissue specimens of patients with active duodenal ulcer disease (n = 30) before and after treatment with either antacids (n = 16) or H2-receptor antagonists (n = 14), by light microscopy and various electron microscopic techniques, e.g., scanning and transmission electron microscopy. The characteristic histological feature of both the active and healed duodenal ulcer was the appearance of periodic acid-Schiff (PAS)-positive epithelial cells at the edge of the ulcers. Electron microscopy revealed that these cells were similar to a special type of mucus-secreting cell in the antrum (surface mucous cell). Their mucus granules contained mainly neutral glycoproteins. Helicobacter pylori were found attached to these cells in tissue specimens from 12 of 30 patients (40%). The mucous structure destroyed during the ulcerative phase regained its normal net-like structure after treatment. The ultrastructural healing process of duodenal ulcer was characterized by the presence of gastric metaplasia, by stunted microvilli of the duodenal epithelium (p less than 0.001 vs. control group), and an increased number of lysosome-like bodies (p less than 0.001 vs. control group) of the epithelial cells. These results were independent of the type of treatment, and showed that the repair mechanisms were incomplete after a 4-wk period of treatment.

Adult↗
PubMed1989

Automatic image analysis as a valuable aid for the objective assessment of the enlargement of hepatocytes in toxicological studies.

Evaluation of histopathological slides is a subjective science; objectivity is needed, especially with minimal alterations. Quantitation using measurement procedures is of special value in toxicological studies. The present study tests a method in which the hepatocytic nuclei were measured per area of liver tissue, excluding the sinusoidal space. Different grades of hepatocellular enlargement were induced by different dose levels of a test compound (combination of two diuretics). The method demonstrates the well-established dose dependence of liver cell enlargement and permits differentiation between slight drug-induced enlargement and the normal variation in cell size. Special reference is made to avoid measurement artefacts.

Animals↗
PubMed1989

Gastric metaplasia and Campylobacter pylori in duodenal ulcer disease: an ultrastructural analysis.

An ultrastructural analysis was carried out on duodenal mucosa specimens, obtained during duodenoscopy from the edge of ulcers and distal duodenal cap mucosa in 42 patients with active duodenal ulcer disease, and in 12 controls. In 18 of 42 patients (43 p. 100), Campylobacter pylori was found in duodenal mucosa but not in controls (chi 2 = 5.91, p less than 0.05). In all 42 cases, gastric-type surface mucus cells were seen at the edge of the ulcer crater, and in 38 of the patients (90 p. 100) these metaplastic cells were also seen in the distal duodenal cap. C. pylori was always localized within the mucus layer, frequently in the intercellular spaces and, in 4 of 18 cases (22 p. 100), within the cytoplasm. C. pylori was detected exclusively in the proximity of gastric type metaplastic surface mucus cells with apparent fusion of membranes. It is suggested that the metaplastic surface mucus cell in the duodenal epithelium of patients with active duodenal ulcer disease is the target cell for colonization by C. pylori.

Adult↗
PubMed1988

[Bismuth subsalicylate treatment in chronic Campylobacter pylori-associated erosive gastritis].

In a prospective open study 21 patients with upper abdominal complaints and chronic active gastritis as well as endoscopically proven erosions were treated with bismuth subsalicylate (4 X 30 ml/day, corresponding to 4 X 314 mg Bi3+) for three weeks. In 20 patients (95%) Campylobacter pylori (CP) was found in at least two of three examinations (culture, CLO quick-test, special histology). After the treatment 17 of 21 patients (81%) were CP negative, and the clinical symptoms had gradually disappeared. The histologically demonstrated degree of activity had regressed significantly after the three-week treatment; in 90% of patients the inflammatory process had completely abated. These results demonstrate that bismuth subsalicylate is highly effective in the acute treatment of CP-associated chronic erosive gastritis.

Adult↗
PubMed1988

Chronic erosive gastritis--a therapeutic approach with bismuth.

37 patients with epigastric pain and chronic erosive gastritis underwent an open controlled therapeutic trial with bismuthsubsalicylate (BS). Group A (21 patients) was treated with BS, liquid, 4 X 314 mg for three weeks, group B (16 patients) with BS tablets, 3 X 300 mg for two weeks. A significant reduction of symptoms (p less than 0.001) and endoscopically assessed chronic erosions (p less than 0.001) was achieved in both groups. Campylobacter pylori was detected in 89% of the patients before treatment, but was absent in 78% of the patients after treatment. The histological grading of antral mucosa showed a significant reduction (p less than 0.001) of polymorphonuclear cell (PML) infiltration after two and three weeks treatment respectively. While in group A PML cells had disappeared from gastric mucosa in all but two patients, in group B 50% of the patients had some degree of PML cell infiltration left in the antral mucosa. This study confirms the beneficial effect of BS in the treatment of C. pylori associated active chronic gastritis and reemphasizes the pathogenetic role of C. pylori in this disease.

Adult↗
PubMed1988

Pathogenetic implications of ultrastructural findings in Campylobacter pylori related gastroduodenal disease.

There is now substantial evidence that Campylobacter pylori (Cp) is able to colonize the gastroduodenal mucosa and is responsible for active chronic gastritis, its role in duodenitis, gastric ulceration and duodenal ulceration is still under debate. Cp has a lot of characteristics which are prerequisites for a pathogen: the typical S-shape, the corkscrew-like movement and the powerful urease and protease enzymes. These features allow a rapid movement through the mucous layer to permit access to the apical membranes of the surface mucous cells. There they adhere directly to the membranes and induce several ultrastructural alterations: degeneration of microvilli, depletion of mucous granules and an increase in sialic-acid rich glycoproteins in the apical part of the cytoplasma. Cp weakens the tight-junction complex and is found between the cells and sometimes intracellularly. Cp is phagocytized by invading polymorphonuclear leukocytes and causes an intense inflammatory response. These observations clearly demonstrate pathological alterations which in the cellular level induced by Cp with the result of a disrupted mucosal barrier of the stomach and the duodenum.

Bacterial Adhesion↗
PubMed1987

[Campylobacter pylori--is there a connection with peptic ulcer?].

In 67 patients, mucosal biopsies were taken in gastroduodenoscopy and culture set up to demonstrate Campylobacter pylori. Campylobacter pylori was cultured from 91% of the patients with peptic ulcer, in 76% of patients with gastritis and in 28% of patients without histological detection of gastritis. Electron microscopic investigations of duodenal mucosa showed that this bacterium attaches to the metaplastic cells of the antral type. This cell type is regularly encountered in the duodenal mucosa in healing duodenal ulcer. The ultrastructural features permit a clear distinction between Campylobacter pylori and other Campylobacter species. Campylobacter pylori may possibly have a pathogenic effect on the mucosa owing to its penetration into the interstitial spaces between the cells and into the interior of the cells.

Adult↗
PubMed1987

Invasion of campylobacter-like organisms in the duodenal mucosa in patients with active duodenal ulcer.

The ultrastructure of campylobacter-like organisms found within duodenal biopsy specimens from 7 of 24 patients (28%) with active duodenal ulcer is described. Their curved shape and variable size are similar to what has previously been reported in descriptions of light microscopies. The organisms were found at the edge of active duodenal ulcers exclusively near neutral-mucous producing antral cells, to which they can adhere. The presence of these bacteria within cells and in the intercellular fluid implies that they can penetrate through the cell membrane or through tight intercellular junctions. The occurrence of these bacteria as well as numerous polymorphonuclear leukocytes in the afflicted regions suggests that the bacteria originally described by Warren and Marshall are indeed pathogenic and that their influence on ulcer healing should be included in designing treatment protocols.

Campylobacter↗
PubMed1987

[Differential diagnosis of accident and resuscitation traumas].

The purpose of this paper is to define the criteria for the differential diagnosis of trauma following resuscitation and road accidents. To this end, 311 cases of thoracic and epigastric trauma were selected from the 2893 medico-legal autopsies carried out between 1979 and 1982 at the Institute of Forensic Medicine of the University of Heidelberg. Cardiopulmonary resuscitation had to be considered as the cause of trauma in 140 of these, but 45 of this group were excluded from further evaluation as they had been the victims of blunt trauma and no clear-cut distinction was possible between trauma resulting from an accident and trauma resulting from resuscitation. Thus, we were left with 95 cases of internal injury that presented as emergencies and in whom death followed resuscitation, as a group for comparison with 171 road accident victims who had not received cardiopulmonary resuscitation. Rib fractures, predominantly on the left side, were established in half the cases resuscitated, sternal fractures also being found in one-third of these victims. Bleeding at various sites, including hemato-thorax, was rare, with an incidence of 15%, thus making it highly unlikely that serious traumas caused by resuscitation were a major factor in the cause of death. This paper encompasses an extensive discussion on serious injuries, such as aortic and gastric ruptures, in this connection.

Abdominal Injuries↗