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Biomedical subjects

G Paulsen

Publications and source records attributed to G Paulsen.

At least 37 records · Page 2Linked to original sources
PubMed1987

Determination of the HLA-DR profile of an HLA class II negative carcinoma cell line by restriction fragment length polymorphism (RFLP) analysis.

The human colonic adenocarcinoma cell line HT-29 does not normally express HLA class II molecules. By restriction fragment length polymorphism (RFLP) analysis of DNA with a DR beta-probe, we analysed the genomic DR beta polymorphism of this cell-line, and compared it with the RFLP patterns seen in DNA from a reference panel of different DR homozygous and heterozygous cells. The HT-29 cell-line expressed DR beta fragments similar to the sum of the fragments expressed by DR4 and DR7 homozygous cells. The DR4 and DR7 haplotypes of HT-29 was further confirmed by comparing the RFLP patterns of four DR4/7 heterozygotes with that of HT-29. Furthermore, the HT-29 cell line expressed a Hind III 9.3 kb fragment previously found to be strongly associated to DRw53. Following treatment with gamma-interferon, the HT-29 cells could be induced to express class II molecules. Serological typing revealed the presence of the DR4, DR7 and DRw53 antigenic determinants.

Adenocarcinoma↗
PubMed1987

The mumps-specific T cell response in healthy individuals and insulin-dependent diabetics: preferential restriction by DR4-associated elements.

An increased frequency of mumps-specific T lymphocytes restricted by DR4-associated elements has previously been described in DR4 heterozygotes. Here we report that the preferential restriction elements may be present on DR4 molecules expressing either Dw4 or Dw14. No particular genomic DQ-beta-polymorphism was associated with the preferential restriction elements.

Diabetes Mellitus, Type 1↗
PubMed1987

Aspirin-induced gastric injury in the rat: histologic changes and sucralfate cytoprotection.

The effect of pretreatment with intragastric sucralfate on aspirin acid-induced gastric mucosal lesions in the rat was studied. The finding by others that sucralfate is cytoprotective and that this cytoprotective effect probably is mediated, at least in part, by stimulation of endogenous prostaglandin synthesis was confirmed. In addition, a time course study revealed that the maximum cytoprotective effect was present 1 min after sucralfate administration and persisted for at least 6 hr. Microscopic evaluation of histologic sections revealed that sucralfate significantly decreased aspirin-induced deep mucosal erosions (those extending into the parietal cell area) but not superficial mucosal damage. Superficial mucosal damage (surface cell injury and erosions involving the mucous neck cell area) could not be detected grossly. The lesions seen grossly were deeper erosions involving the parietal cell area of the mucosa.

Animals↗
PubMed1986

Hemorrhagic shock and acid gastric injury in the rat. Comparison of gross and histologic findings.

The purpose of this study was to compare the gross and histologic changes in the corpus and antrum in the rat hemorrhagic shock plus acid model of gastric injury, and to determine the effect of transfusion of shed blood or albumin on gastric lesion formation. The data indicate that (a) despite the gross appearance of more severe damage in the corpus, histologic damage was more severe in the antrum; (b) covering mucus and cell debris partly explain the difficulty in recognizing antral lesions grossly; (c) the severity of histologic injury was similar in transfused and nontransfused rats; and (d) transfusion of shed blood rendered corpus lesions more recognizable grossly but did not affect the severity of histologic injury. The latter findings raise questions about the pathogenetic importance of reperfusion in gastric ischemic injury and the validity of using gross lesions as an index of gastric injury.

Albumins↗
PubMed1985

Identification, at the genomic level, of an HLA-DR restriction element for cloned antigen-specific T4 cells.

Two T4 cell clones (TLC) specific for antigenic epitopes on Chlamydia trachomatis were studied. Using a panel of allogeneic antigen-presenting cells (APC), both TLC were found to be restricted by HLA class II elements closely associated with, but not identical to the DRw5S specificity, as determined by highly selected alloantisera, a monoclonal antibody (mAb), 109d6, and confirmed on the DNA level by determination of restriction fragment length polymorphisms (RFLP) with a DR beta probe. Furthermore, HLA-DR-specific mAb, including 109d6, but not other HLA class II- or class I-specific antibodies inhibited the two TLC, strongly suggesting that the restriction element is expressed by a DR molecule. Using digestion with Hind III restriction enzyme and a DR beta probe, we found a complete concordance between the appearance of a 9.3 kilobase band and the ability of allogeneic APC to restimulate the T cell clones. Thus, the restriction element for these T cell clones appear to be expressed by DR molecules, but can, at present, only be detected at the genomic level.

Antibodies, Monoclonal↗
PubMed1985

Salicylic acid blocks indomethacin-induced cyclooxygenase inhibition and lesion formation in rat gastric mucosa.

Salicylic acid has been shown to decrease gastric mucosal lesions induced by indomethacin in the rat. In vitro, it has also been shown to counteract the inhibitory effect of indomethacin and aspirin on the cyclooxygenase enzyme system in seminal vesicle microsomes and in platelets and vascular tissue. The hypothesis that the mechanism of salicylic acid "protection" against indomethacin-induced gastric lesions involves interference with indomethacin-induced mucosal cyclooxygenase inhibition was tested. Male, fasted rats were treated with intragastric salicylic acid in doses of 50, 100, 200, 300, or 400 mg/kg concomitantly with a sc injection of 20 mg/kg of indomethacin. Gastric mucosal lesions and mucosal cyclooxygenase activity (as measured by ex vivo prostaglandin F2 alpha synthesis) were examined 3 hr later. Intragastric salicylic acid, 200-400 mg/kg, significantly reduced indomethacin-induced lesion formation, while counteracting significantly indomethacin inhibition of prostaglandin synthesis. Salicylic acid alone did not significantly change cyclooxygenase activity. It is concluded that topical salicylic acid can decrease indomethacin-induced gastric mucosal lesion in the rat, in part, by counteracting the inhibitory effect of indomethacin at the cyclooxygenase level.

Animals↗
PubMed1985

Prostaglandin cytoprotection: role of microcirculatory changes.

Both the fluorescent in vivo microscopic study and the hydrogen-gas-clearance study revealed complete absence of blood flow in the areas of gross ethanol damage. PG pretreatment prevented this cessation of flow. However, the hydrogen-gas-clearance study demonstrated that PG administered in a cytoprotective dose did not increase blood flow. It maintained blood flow by some other mechanism. The final in vivo microscopic studies demonstrated a marked leak of albumin from microvessels and slowing and then cessation of flow very shortly after topical ethanol application. This suggests that an increase in blood viscosity due to plasma leak may be the mechanism of the ethanol-induced flow stasis. PG prevented this leak. PG cytoprotection, by preventing this permeability change, maintains mucosal blood flow and may thus protect the mucosa against the deeper and more severe ethanol injury.

16,16-Dimethylprostaglandin E2↗
PubMed1985

[Psychodiagnostic studies in dialysis patients of a center and a limited care facility].

In order to find out how far center hemodialysis (ZD) and limited-care hemodialysis (LCD) influence adjustment and being of the afflicted persons, 21 ZD-patients and 19 LCD-patients were examined psychodiagnostically with the following tests: Rosenzweig Picture-Frustration Study, Taylor's Manifest Anxiety Scale (adapted to German conditions), and Freiburger Persönlichkeits-Inventar. By means of statistical analysis it could be shown that the hemodialysis patients do not present themselves to their fellow-men in accordance with their real thinking and feeling. This behaviour brings on the peril of deviating attitudes which can affect their vigour. The LDC-patients gave much more indications of autonomous self-responsibility than the ZD-patients did. Psychotherapeutic efforts primarily should counteract regressive tendencies.

Adaptation, Psychological↗
PubMed1984

Effect of sodium selenite on the ciliary activity, adenosine triphosphate, and protein synthesis in mouse trachea organ cultures.

Trachea from albino mice were cut transversely into nearly identical rings and incubated in medium 199 with Hanks salts and HEPES buffer at 37 degrees C. Sodium selenite at 0.5-5 mM depressed the ciliary activity. With 1 and 5 mM sodium selenite, a 50% reduction in the activity index was observed after approximately 5 and 1.5 h, respectively. The ATP content in trachea rings was reduced with 0.05-5 mM sodium selenite, and increasing concentrations gave decreasing amount of ATP after incubation for 4 and 21 h. The rate of protein synthesis as determined by incorporation of radioactive leucine was reduced with 0.5 and 2 mM sodium selenite. The synthesis was reduced quickly by 2 mM sodium selenite, which gave a 30% reduction after incubation for 1 h. It seems that the ATP levels may be used as the most sensitive indication of sodium selenite toxicity in mouse trachea.

Adenosine Triphosphate↗
PubMed1984

Histologic and microcirculatory changes in alcohol-induced gastric lesions in the rat: effect of prostaglandin cytoprotection.

The effect of 16,16-dimethyl prostaglandin E2 (dmPGE2) on histologic and microcirculatory changes in alcohol-induced gastric mucosal injury was studied. A histologic study confirmed that dmPGE2 does not protect the surface mucous cells against ethanol injury but does protect against the deeper necrotic lesion. Both the gross injury and the necrotic lesion were as severe after 1 min of ethanol exposure as after 60 min. A study of benzidine-stained sections and hematoxylin and eosin-stained sections revealed marked engorgement of microvessels and hemorrhage in the superficial mucosa after ethanol injury. Pretreatment with dmPGE2 prevented these. An in vivo fluorescent microscopy study revealed that there was total stasis of blood flow in the injured area. After the intravascular injection of a fluorescein-albumin conjugate, the conjugate filled microvessels in grossly normal areas of mucosa but not in grossly injured areas. Pretreatment with dmPGE2 prevented this microcirculatory change. This alcohol-induced stasis of flow in injured areas may be of pathogenetic significance and prostaglandin protection might involve prevention of this microcirculatory change.

16,16-Dimethylprostaglandin E2↗
PubMed1983

Prostaglandin cytoprotection. Prostaglandin does not protect against aspirin- or alcohol-induced red blood cell hemolysis.

The hypothesis that prostaglandin cytoprotection involves cell membrane stabilization was tested in vitro using rat erythrocytes. Low concentrations of sodium acetylsalicylate, 0.02, 0.2, 2.0, and 20 mM, inhibited hypotonic hemolysis of red blood cell suspensions. While 35, 140, and 280 mM sodium acetylsalicylate had no hemolytic effect, 560 mM caused marked hemolysis. The prostaglandin E2 analog, 16,16-dimethyl prostaglandin E2, 0.4 X 10(-3), 10(-4), and 10(-5) M concentrations, did not alter this hemolysis. Fourteen percent ethanol caused red cell hemolysis, and this was unaffected by the prostaglandin. The findings do not support the hypothesis.

Animals↗
PubMed1983

Age-related changes in the gastric submucosal arterioles and gastric acid secretion.

The purpose of this study was to determine whether alterations in the reactivity of gastric submucosal arterioles to norepinephrine and changes in acid secretion occur in the same time period in the rat. Experiments were performed on animals 6 weeks and 10, 18, and 25 months of age. Arteriolar diameter was measured by an image splitting in vivo microscopy technique before and after superfusion of the gastric submucosa with graded doses of norepinephrine. Acid secretion was measured in the pylorus-ligated rat. The percentage of arteriolar media stained with periodic acid-Schiff reagent (an age-related change) was determined for each age group. A dose-dependent response to norepinephrine was observed in 6-week and 10-, 18-, and 25-month age groups. Only in the 25-month-old rats were arterioles significantly more responsive to norepinephrine. Acid secretion at 10, 18, and 25 months was significantly less (about one-quarter) than that observed in the 6-week-old animals. Periodic acid-Schiff positive material deposited in the arteriolar media was significantly greater in the 18- and 25-month-old rats than in younger animals. We conclude that by 10 months of age in the rat, acid secretion is markedly reduced. The reactivity of the gastric submucosal arterioles is significantly increased at 25 months, but in the 18-month-old animal, when increased periodic acid-Schiff deposits are clearly evident, the reactivity to norepinephrine is not different from the 6-week-old rat.

Aging↗
PubMed1983

Gastrointestinal and in vitro release of copper, cadmium, indium, mercury and zinc from conventional and copper-rich amalgams.

Particles of a conventional lathe-cut, a spherical non-gamma 2 and a copper amalgam have been gastrointestinally administered to rats for the purpose of evaluation of the dissolution resistance. The animals were sacrificed after 20 hrs. The contents of copper, cadmium, indium, mercury and zinc in kidney, liver, lung or blood were measured using nuclear tracer techniques. From a copper amalgam an extreme release of copper was demonstrated. This study stimulates the clinical condition of elemental release from swallowed amalgam particles after amalgam insertion or after removal of old amalgam fillings. Specimens of the same types of amalgams were also exposed to artificial saliva for a period of 10 days. The amounts of copper and mercury released were measured with flame and flameless atomic absorption spectrophotometry respectively. The levels of copper and mercury released from the copper amalgam were approximately 50 times those of the two other amalgam types studied.

Animals↗
PubMed1982

Effect of increased gastric mucosal histamine on alcohol-induced gastric damage in rats.

The aim of this study was to determine whether the cytoprotective effect of prostaglandin might be mediated, at least in part, by inhibition of intramucosal histamine release. Intragastric instillation of increasing concentrations of ethanol in 150 mM HCl resulted in increasing lesion scores and increasing histamine release into the gastric content. Pretreatment with 16,16-dimethyl prostaglandin E2 significantly reduced both lesion scores and gastric histamine output. The intragastric instillation of histamine with tracer [14C]histamine either with or after 50% ethanol resulted in significant gastric tissue uptake of histamine and increased acid secretion. However this had no effect on lesion score, protein output or the protective effect of prostaglandin pretreatment. We conclude that the cytoprotective effect of 16,16-dimethyl prostaglandin E2 in the rat is independent of intramucosal histamine release.

Animals↗
PubMed1981

Manganese-nickel interaction in a tracheal ring model system.

The effects of NiCl2 and MnCl2 on the ciliary activity in mouse trachea were observed in an organ culture system. Following exposure for 2 hours to NiCl2 (0.5 or 2.0 mM) in Medium 199 40 respectively 0% of the ciliary activity remained. By simultaneous exposure to increasing concentrations of MnCl2 the toxic effect of NiCl2 was reduced and the ciliary activity following 2 hours incubation in the presence of 0.5 or 2.0 mM NiCl2 was 81 and 62%. At these nickel-concentrations optimal protection was obtained by about half the molar concentration of MnCl2. Preincubation in medium supplemented with NiCl2 followed by incubation in medium with MnCl2 added gave better protection than that obtained by changing to Medium 199 alone. Preincubation in 0.25 mM MnCl2 did not reduce nickel toxicity.

Animals↗
PubMed1980

Pulmonary deposition following inhalation of chromium-cobalt grinding dust in rats and distribution in other tissues.

Twenty rats were exposed to dust particles of chromium-cobalt alloy abrasives produced in dental material handling. The exposure was carried out in chambers for periods up to 107 days at concentrations of particulate matter of about 10-50 mg/m3. The content of chromium and cobalt in autopsy specimens of lung, liver, kidney and trachea was measured with nuclear techniques. The alloy particles were found to be markedly accumulated in lung tissue. Increased levels of chromium and cobalt were also observed in the trachea. In addition, a moderate increase of cobalt in liver and kidney was demonstrated. The lungs of six exposed rats were examined microscopically. The main part of the dust particles was observed within macrophages. Only a minor fraction of particles were seen in the bronchial lumen close to the epithelial surface. The majority of dust-filled macrophages were located in groups within the bronchial wall or in the interstitium close to the terminal broncheoli. No fibrosis, dysplasia or tumor formation occurred. No acute adverse effects in the lungs were observed.

Air Pollutants↗
PubMed1979

Effect of parental aspirin on the gastric mucosal barrier in the rat.

The purpose of the present study was to determine in the rat whether parenteral aspirin, like topical aspirin, injures the gastric mucosa by diffusely disrupting the gastric mucosal barrier to hydrogen ion back-diffusion. Back-diffusion studies, including the ion fluxes and lumenal potential difference, were performed in control situations and either 0.5 or 4 h after the intraperitoneal administration of sodium acetylsalicylate. Gastric mucosal lesions were scored. After 0.5h, lesions developed but the barrier was intact. However, after 4 h, lesion formation was more severe and changes characteristic of diffuse barrier disruption, fall in potential difference and increased loss of hydrogen ion occurred. Since lesions occurred before evidence of diffuse barrier disruption could be detected, we conclude that in the present model diffuse barrier disruption is a consequence rather than a cause of lesions.

Animals↗