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O Haferkamp

Publications and source records attributed to O Haferkamp.

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

Relationships between lymphocyte cholesterol homeostasis and LDL-cholesterol.

The homeostasis of cholesterol was studied in lymphocytes freshly isolated from the blood and cultured with or without low-density lipoprotein (LDL). The content of cholesterol decreased in the lymphocytes cultured without LDL, whereas LDL substituted for cellular cholesterol losses, in spite of almost suppressed LDL-receptor and lymphocyte cholesterol synthesis. Free cholesterol was taken up from LDL mainly via cholesterol exchange and, in contrast to esterified cellular cholesterol, rapidly excreted into the medium. In vitro stimulation of lymphocyte cholesterol synthesis was correlated to the ratio of esterified to free LDL-cholesterol in the blood from which the lymphocytes had been isolated. This result probably reflects the different rates of influx and efflux of esterified or free cholesterol between plasma lipoproteins and lymphocytes. These effects should be taken into account if LDL-cholesterol is determined in plasma for the evaluation of an individual's atherosclerotic risk.

Cells, Cultured↗
PubMed1987

The effect of antibiotics on the intracellular survival of bacteria in human phagocytic cells.

[14C]-labeled josamycin (Wilprafen) readily enters several types of human phagocytic cells-polymorphonuclear leucocytes (PMNLs), adherent monocytes and alveolar macrophages - and is accumulated by these cells to a concentration about 20 times that in the extracellular medium. Similar studies using [14C]-benzyl penicillin revealed that the beta-lactam antibiotic penetrated these cells very poorly. Low concentrations of josamycin and the various phagocytes acted synergistically to inhibit the intracellular proliferation of L. pneumophila or H. influenzae. In contrast, penicillin G was not effective against legionellae ingested by PMNLs, monocytes or alveolar macrophages, even at high concentrations. The uptake of the antibiotics apparently correlates well with its efficacy against the intracellular survival of bacterial pathogens in human phagocytic cells.

Erythrocytes↗
PubMed1985

Morphogenesis and possible precursor lesions of invasive carcinoma of the papilla of Vater: epithelial dysplasia and adenoma.

Surgical specimens from 58 invasive carcinomas of the papilla of Vater were studied histomorphologically. Tubular or villous adenomas, adenomatous residues, and microadenomas were found in the vicinity of the carcinomas in 91.4 per cent of the cases; moderate or severe epithelial dysplasia in adenomatous structures or in surface and ductal epithelium was present in 81 per cent of the cases. The results of the present histomorphologic study support the hypothesis that invasive carcinomas arise from pre-existing mucosal lesions, such as adenoma or dysplasia.

Adenoma↗
PubMed1984

Echo 9 virus-induced order-disorder transition of chemotactic response of human polymorphonuclear leucocytes: phenomenology and molecular biology.

By means of functional, morphological, and biophysical methods the in vitro interaction of Echo virus, type 9, strain A. Barty with human polymorphonuclear leucocytes (PMNs) was investigated and analyzed by statistical methods. Control cells and virus-treated PMNs (15 min, 37 degrees C; PMN: virus (pfu)-ratio ranging from 1:1 to 1:50) were exposed to a chemotactic gradient (N-formylmethionyl-leucylphenylalanine = f-Met-Leu-Phe, 10(-8) M/mm) in a Zigmond chamber. Whereas the track velocity of the moving PMNs was not affected by the virus, the degree of orientation of virus-treated PMNs declined in a way dependent on the viral dose and on the time of PMN:virus interaction, resulting in a shift from chemotactic to chemokinetic response. This virus-induced order-disorder transition of chemotactic response can be described by a logarithmic law in analogy to the Weber-Fechner law. Parallel to the functional disturbances, virus-induced changes of cell shape, which could be confirmed by additional light and electron microscopy techniques, were also detected using statistical analysis of cytological data (median cell size, anisotropy of cell shape) by means of two-dimensional histograms. To investigate f-Met-Leu-Phe- or/and Echo 9 virus-induced PMN-cell membrane changes, the monomer-excimer technique with pyrenedecanoic acid as fluorescent probe was applied, which gives information about structural changes of the cell membrane. Addition of the chemotactic peptide (10(-8) M) to control PMNs resulted in a higher rate of excimer formation obviously due to the formation of new functional (receptor) units (= activated cell membrane). Echo 9 virus exhibited an opposite effect. Quantitative analysis of these results revealed that the f-Met-Leu-Phe-induced cell membrane changes were extinguished by the addition of 2 pfu Echo 9 virus. So far, we have additional indicators of a virus-induced order-disorder transition of chemotactic response of human PMNs on a molecular biological level.

Biophysical Phenomena↗
PubMed1984

F-Met-Leu-Phe and echo 9 virus interaction with human granulocytes. Changes of cell membrane structure.

Biophysical and biochemical methods were applied for investigation of cell membrane properties of human polymorphonuclear leukocytes (PMNs) exposed to the chemotactic peptide N-formylmethionyl-leucylphenylalanine (f-Met-Leu-Phe) and echovirus type 9, strain A, Barty. Steady-state fluorescence depolarization with diphenylhexatriene demonstrated no gross changes of the total membrane fluidity under the different experimental conditions. However, by means of the monomer-excimer technique with pyrenedecanoic acid (PDA), significant changes of the local membrane structure were detected for both agents. As demonstrated by a higher excimer ratio, the membrane area available for the PDA molecules was restricted by f-Met-Leu-Phe. This effect was dependent on the dose and on the time of interaction of the chemotactic peptide. These experimental findings were explained by the formation of functional receptor units ("activated membrane"). Echo 9 virus exhibited the opposite effect, characterized by a higher ratio of monomers, which also depended on the viral dose and the time of virus-PMN interaction. These virus-induced findings were explained by the dissolution of functional receptor units. Consecutive exposure of the PMNs to f-Met-Leu-Phe and echovirus, or vice versa, demonstrated a virus-predominant effect on the membrane structures.

Cell Membrane↗
PubMed1983

Somatostatinoma syndrome. Clinical, morphological and metabolic features and therapeutic aspects.

A case of somatostatinoma syndrome in a 30-year-old woman is presented. Basal levels of growth hormone and of pancreatic and gastric hormones were reduced and the response of growth hormone, insulin and C-peptide to stimuli such as arginine, glucose, glibenclamide and calcium was virtually abolished. Similarly, gastric acid secretion, pancreatic exocrine function and intestinal absorption were significantly reduced. On the other hand, basal and stimulated levels of adrenocorticotropic hormone (ACTH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and thyroid-stimulating hormone (TSH) were within the normal range. Plasma somatostatin-like immunoreactivity was increased to 600-2,000 pg/ml (normal: 88-140 pg/ml). Immunocytochemical studies demonstrated the presence of somatostatin immunoreactive material in the primary tumour in the head of the pancreas and in the liver metastases. In spite of two courses of chemotherapy with streptozotocin and 5-fluorouracil the patient died due to liver failure 5 months after the first admission to hospital.

Adenoma, Islet Cell↗
PubMed1983

Age dependence of paralysis induced by echovirus type 9 in infant mice.

Newborn mice of different strains (including NMRI) infected with 2-5 x 10(6) pfu of echovirus type 9 strain A. Barty developed progressive flaccid paralysis five days after inoculation, followed by death. Suckling mice injected with the same infective dose two, four, or six days after birth disclosed at most transient paresis and survived. Infectivity titrations revealed in all groups a similar rate of virus multiplication exceeding 10(8) 50% tissue culture infective doses per mouse four days after virus inoculation. Histologically, polymyositis resulting in muscle fiber necrosis was seen. The percentage of damaged muscle tissue declined with increasing age of the experimental groups. It is concluded that in order for paralysis to occur, at least 50% of skeletal muscle tissue must be destroyed by virus-induced lesions before the sixth day of life. Electron microscopy demonstrated additional age-dependent, virus-mediated disturbances of postnatal muscle growth. Reparative events in destroyed muscle fibers seemed to be unaffected in all age groups.

Age Factors↗
PubMed1983

Effects of prostanoid precursors and indomethacin on chick embryonic cartilage growth in organ culture.

Using the Fell technique of organ culture of 8-day chick embryo femoral and tibial rudiments, the effects of indomethacin, dihomo-gamma-linolenic acid and arachidonic acid on limb rudiment linear growth and differentiation were investigated. Indomethacin (50 and 100 mumol/l) elicited a statistically significant decrease in rudiment linear growth without affecting differentiation or cell structure. Dihomo-gamma-linolenic acid and arachidonic acid, both at 100 mumol/l, exerted no effect on limb rudiment linear growth or differentiation. From previous work, it has been shown that PGA1 and PGB1 caused a marked inhibition of linear growth, PGA1 being cytotoxic. The failure of the prostaglandin (PG) precursors to reproduce these effects suggests that PGA or PGB biosynthesis in embryonic chondrocytes plays no significant role in cartilage growth regulatory mechanisms. Moreover, the growth inhibitory effect of the PG cyclooxygenase inhibitor, indomethacin, suggests that a product of arachidonic acid metabolism via the cyclooxygenase pathway may promote cartilage growth.

8,11,14-Eicosatrienoic Acid↗
PubMed1983

[Radiochemical and immunohistochemical determination of surface binding of low density lipoproteins on lymphocytes].

Human peripheral blood lymphocytes bind and take up low density lipoprotein (LDL) by receptor-mediated endocytosis. The binding of LDL was determined by incubation with 125-I-LDL and an immunohistochemical assay. By both techniques a diminished rate of binding was found when cells were freshly isolated from the blood, but increased five- to ten-fold when lymphocytes were incubated in lipoprotein-deficient medium for 72 hours. In addition, it was shown immunohistochemically that only few cells showed an LDL-dependent fluorescent labelling: approximately 5 to 10 per cent of the freshly isolated lymphocytes and 40 to 50 per cent of the cells incubated for 72 hours under lipoprotein-free conditions. The present data indicate that not only the high affinity LDL-receptor described by Goldstein and Braun may be involved in the uptake of cholesterol by lymphocytes, but also other binding-sites, which may have immunological function in some lymphocyte subpopulations.

Endocytosis↗
PubMed1983

[Changes in the membrane fluidity of human neutrophilic granulocytes under the effect of a chemoattractant (FMLP) and of echo virus, type 9, A. Barty strain].

Preincubation of human polymorphonuclear leucocytes (PMNs) with different concentrations of Echo virus, type 9, strain A. Barty results in viral dose- and time-dependent inhibition of chemotactic cellular response to chemoattractant (N-formylmethionylleucylphenylalanine = FMLP). In the present experiments, by means of biophysical methods using excimer forming lipids (pyrendecanoic acid) the influence of FMLP and Echo 9 virus on membrane fluidity of PMNs was investigated. It is shown that the increase of membrane fluidity elicited by FMLP is reduced by the virus in a dose dependent manner. These results indicate virus-induced disturbance of molecular architecture and failure of natural signal processing of PMN-membranes. This biophysical method, therefore, can be used as a functional histochemical method to demonstrate functional defects in membranes of living cells.

Chemotaxis, Leukocyte↗
PubMed1982

Critical analysis of granulocyte function in 154 patients wtih different diseases.

Several granulocyte functions were analyzed in vitro in 154 patients with chronic or recurrent infections, as well as in a variety of disorders known or suspected to affect host resistance. Only a few specific abnormalities were diagnostic and occurred in congenital, hereditary disorders. Opposed to these permanent changes are those which were probably acquired or transient and are often multifactorial in origin. In the majority of these patients, an inconstant and nonspecific pattern emerged which is not helpful in the diagnosis of underlying disease. In selected patients, however, and as research procedures, these and related tests should be helpful in elucidating the basic functions of granulocytes and may implicate therapeutical approaches.

Adolescent↗
PubMed1982

Lipid storage in cultured articular chondrocytes due to prostanoid precursors and a prostanoid synthesis inhibitor.

Lapine articular chondrocytes were subcultured in the presence or absence of the prostanoid precursors, arachidonic acid or dihomo-gamma-linolenic acid, and the cyclooxygenase inhibitor indomethacin. Lipid storage was studied microscopically using the Sudan black staining method. Control chondrocyte cultures showed a weakly positive staining reaction until confluence was reached, at which point the intra-cytoplasmic lipid content decreased. Both arachidonic acid and dihomo-gamma-linolenic acid at 100 mumol/l caused a marked increase in lipid storage which continued even after confluence was achieved. 1 mumol/l concentrations were indistinguishable from controls, whereas 10 mumol/l concentrations elicited a slight increase in lipid storage compared with controls. The prostaglandin cyclooxygenase inhibitor indomethacin did not affect chondrocyte lipid storage. However, administration of a prostanoid precursor in the presence of indomethacin caused a massive increase in intra-cytoplasmic storage of lipid, eventually leading to cell death. A possible explanation is that indomethacin may alter chondrocyte lipid metabolism in the presence of substrate molecules by rechanneling lipid synthesis away from the prostaglandin pathway to other lipid synthetic pathways.

8,11,14-Eicosatrienoic Acid↗
PubMed1982

Disseminated mycobacterial histiocytosis due to M. Fortuitum associated with helper T-lymphocyte immune deficiency.

Mycobacterial histiocytosis is a rare disease usually associated with haematological or immunological disorders. We report a fatal case caused by M. fortuitum infection showing the typical disseminated histiocytosis. Immunological investigations revealed impaired cellular immunity demonstrated by negative skin tests with different "recall-antigens", and in vitro an isolated defect of helper T-lymphocytes in the peripheral blood which in combination with hypergammaglobulinemia suggests a "lymphocyte and distribution syndrome".

Adult↗
PubMed1982

Alterations in articular chondrocyte growth and proteoglycan synthesis due to prostanoid precursors.

The effects of the prostaglandin precursors, dihomo-gamma-linolenic acid and arachidonic acid, on chondrocyte proliferation, proteoglycan synthesis and morphological structure were studied using lapine articular chondrocytes in vitro. Neither substance exerted a cytotoxic effect on chondrocytes. Dihomo-gamma-linolenic acid caused a dose-dependent inhibition of chondrocyte proliferation (8% and 35% reduction at 10 and 100 mumol/l respectively) (P less than 0.01), whereas arachidonic acid failed to cause any significant alteration: 10 mumol/l of dihomo-gamma-linolenic acid stimulated proteoglycan synthesis by 14% (P less than 0.01), whilst 100 mumol/l elicited a reduction of 14% (P less than 0.01); 100 mumol/l of arachidonic acid also caused a statistically significant inhibition (31%) (P less than 0.001) of 35SO4 incorporation into proteoglycans. The inhibitory effects on proteoglycan synthesis may be mediated by intracellularly synthesized prostaglandins, which are known to exert this effect. This may also help explain the susceptibility of articular cartilage to damage with increasing age, as arachidonic acid is found in increasing concentrations in the superficial layers of articular cartilage.

8,11,14-Eicosatrienoic Acid↗
PubMed1982

The effects of nickel ions on articular chondrocyte growth in monolayer culture.

Monolayer cultures of lapine articular chondrocytes were used to study the effects of nickel ions (Ni++) on chondrocyte proliferative capacity, proteoglycan synthesis and cellular morphology. Nickel depressed chondrocyte proliferation at the highest concentration tested (100 mumol/l; P less than 0.01) and also exerted a dose-dependent inhibition of proteoglycan synthesis (50 and 100 mumol/l; P less than 0.01). Despite both these effects, no evidence of chondrocyte damage was detectable at the light-microscopical level. The possible significance of the nickel-induced reduction of articular chondrocyte proteoglycan synthesis for the functional integrity of the residual cartilage following hemiarthroplasty operations is discussed.

Animals↗