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Biomedical subjects

B Müller

Publications and source records attributed to B Müller.

At least 415 records · Page 23Linked to original sources
PubMed1987

[Scanning electron microscopy of microbes and their mechanism of attachment to human small intestinal mucosa].

In connection with the electron-microscopy of bioptic material from the upper small intestine of children with intestinal diseases and diarrhea (10 months to 8 years) we found some cases of fungus infection (26%) besides many cases of bacterial attachment to the intestinal epithelium (72%). On the intestinal wall normal yeasts, pseudomycelium and common mycelium are visible. Partly the epithelium was entirely covered with mycelium. In some cases the hyphae invaded in the intestinal wall. The epithelium and the villi are not or only slightly altered. This gives the reason to believe that the fungi participate in inducing diarrhea. After medicamentous treatment with nystatine-preparations in some cases the health state of these children was improved.

Bacteria↗
PubMed1987

The accessibility of DNA to dimethylsulfate in complexes with recA protein.

recA protein coats DNA co-operatively to form filaments approximately 100 A thick, which in the presence of ATP, and more stably so in the presence of the non-hydrolyzable analog ATP gamma S, have a helical appearance with a deep cleft in the protein coat. This protein helix follows the DNA helix, to which it imparts a new helicity of 18.5 bp per turn of 97 A pitch. Here we test the accessibility of the DNA in the complex to modification by dimethylsulfate, and find that the complexed DNA is approximately 2-fold more reactive on the major groove side than it was in B-DNA (methylation of guanine N7), while it is protected approximately 2-fold on the minor groove side (methylation of adenine N3), suggesting that the protein coats the DNA along the minor groove. Furthermore, N3 of cytosine, a residue involved in base pairing, is found exposed in complexes with single strands as it is in naked single-stranded DNA, while it remains inaccessible in complexes with double strands, suggesting that the latter is not melted at this stage of the strand exchange reaction.

Alkylating Agents↗
PubMed1987

Covalent conjugates of monoclonal antibody and cobra venom factor mediate specific cytotoxicity via alternative pathway of human complement activation.

Because of lack of unspecific toxicity autologous serum is the optimal source of complement for in vitro cell depletion in human bone marrow transplantation. Covalent binding of cobra venom factor to an antibody leads to a specific complement activating conjugate with cytolytic potential independent of the capacity of the antibody to fix complement itself. Therefore this conjugation allows the use of various sera, including human as the source of complement. The kinetics of cobra venom factor-initiated cytolysis is compatible with in vitro treatment of bone marrow prior to transplantation.

Antibodies, Monoclonal↗
PubMed1987

Action of the stable prostacyclin analogue iloprost on microvascular tone and -permeability in the hamster cheek pouch.

In order to further elucidate the mechanisms involved in therapeutic effects of prostacyclin and Iloprost in peripheral ischemic disease, the actions on microvascular tone, capillary density, and increases in venular permeability induced by inflammatory mediators and by ischemia were investigated in the cheek pouch of anaesthetized Syrian hamsters using intravital videomicroscopy and--for quantification of vascular permeability--venular leakage of fluorescein-labelled dextran (FITC-D; Mw 70,000). Iloprost at the nonhypotensive, platelet aggregation-inhibiting dose of 0.5 microgram/kg/min i.v. significantly increased the diameters of arterioles and venules and the density of perfused capillaries and antagonized vasoconstriction and decrease of perfused capillary density as induced by Leukotriene D4 (LTD4; 10(-7) M). Iloprost significantly antagonized venular leakage of FITC-D induced by histamine (10(-5) M), serotonin (10(-5) M), bradykinin (10(-6) M) and reperfusion after 30 min ischemia. Topical application of Iloprost (10(-8) M), intraarterial infusion of Prostaglandin E1 (PGE1; 2.0 micrograms/kg/min), and topical Forskolin (10(-5) M) also attenuated histamine-induced venular FITC-D leakage, while topical PGE1 (10(-7) M) and i.v. infusion of Nifedipine (30 micrograms/kg + 10 micrograms/kg/min) were not effective. It is concluded, that microvascular effects of Iloprost by improvement of tissue perfusion and functional antagonism of mediator-induced tissue edema and vasospasm could contribute to therapeutic effectiveness in ischemic diseases.

Alprostadil↗
PubMed1987

Neurotensin induces hyperplasia of the pancreas and growth of the gastric antrum in rats.

We investigated whether chronic subcutaneous infusion of neurotensin during 14 days would affect pancreatic and gastric growth of rats. In another experiment, neurotensin (836 pmol/kg) was injected intraperitoneally three times a day for three days in 12 rats. Thereafter, pancreatic DNA and in vitro incorporation of 3H-thymidine into pancreatic DNA was determined. Long term infusion of 282 pmol/kg neurotensin induced an increase of pancreatic weight, DNA, and pancreatic polypeptide, whereas pancreatic protein, RNA, amylase and lipase contents were not increased. In relation to DNA, even these parameters were significantly depressed. Insulin remained unchanged. Neurotensin, therefore, caused hyperplasia of the pancreas. Intraperitoneal injection of neurotensin induced an increase of pancreatic DNA content and stimulated 3H-thymidine incorporation into DNA, whereas caerulein only augmented 3H-thymidine incorporation. Moreover, long term neurotensin infusion led to a rise in protein concentration and an increase in the thickness of the gastric antrum; antral DNA concentration was insignificantly stimulated. Neurotensin, therefore, can act as a trophic factor on pancreas and gastric antrum of the rat.

Animals↗
PubMed1987

Ambroxol increases the choline but not fatty acid incorporation into lung phospholipids in experimental lung disorders.

Ambroxol, a drug capable of elevating the phospholipid content in healthy rabbit lungs, was tested on two models of experimental lung injury, lung changes in sepsis induced by a peritonitis and in bromcarbamide intoxication. The phospholipid content of the lungs and the synthesis of the individual phospholipids phosphatidylcholine (PC) and sphingomyeline were measured in vitro by incubation of lung slices with labeled phospholipid precursors. Influenced by the drug, the phospholipid content increases to 132% in the peritonitis experiments and to 111% in the bromcarbamide experiments. The peritonitis experiments show the increase in phospholipid synthesis to result from an enhanced choline incorporation into PC up to 192% and into sphingomyeline up to 630%. The values for the bromcarbamide experiments are 411% for PC and 485% for sphingomyeline, respectively. There was no statistically significant difference in the incorporation of fatty acids in the treated and untreated animals. We conclude that ambroxol possibly stimulates the phospholipid synthesis in injured lungs by stimulating the choline phosphatcytidyltransferase, but not the incorporation of fatty acids into PC in those lungs. These findings may be important to the surfactant system of the lung consisting mainly of PC.

Ambroxol↗
PubMed1987

Microvascular effects of iloprost in the hamster cheek pouch.

In the hamster cheek pouch, microvascular effects of iloprost at a nonhypotensive dose include vasodilatation at the level of arterioles and venules without changes in microvascular permeability, increased number of perfused capillaries/cm2, prevention of microvascular spasm and capillary ischemia as caused by LTD4, and inhibition of histamine- and 5-HT-induced venular leakage of FITC-dextrane. As regards the effects on basal vessel tone, capillary density, and prevention of LTD4 effects, PGE1 had similar effects as also shown by others in the human cutaneous microcirculation. However, PGE1 did not prevent the microvascular leakage caused by histamine. The Ca2+-antagonist nifedipine, apart from arteriolar vasodilatation, neither increased venular diameter and capillary perfusion nor prevented the effects of LTD4 and histamine. The microvascular actions of iloprost by improvement of tissue perfusion and prevention of mediator-induced tissue edema and vasospasm could contribute to the beneficial effects observed in ischemic diseases.

Alprostadil↗
PubMed1987

[Indications for appendectomy. A retrospective analysis].

This retrospective study was conducted into 1.506 patients who had been admitted to the author's hospital for suspicion of acute appendicitis, between 1971 and 1979. Indications for appendectomy were handled with generosity, and primary laparotomy was applied to 44.2 per cent of all cases. Perforated appendicitis was of low incidence, accounting for only three per cent, while no acute inflammatory lesions were recordable at all from 36 per cent of removed appendices. Follow-up checks were made on all patients who had not been operated on, in the first place, not later than five years from first diagnosis. Only 15 per cent of these patients had to be eventually appendectomised. For them distribution of histological diagnoses was similar to that of patients with surgery as primary approach. Recurrence of pain was reported by one third of patients without surgery. However, only 14.9 per cent of them saw a doctor on their problem, and only 3.7 per cent had to be rehospitalised. Primary wait-and-see attitude caused no further increase in the incidence of perforated appendicitis.

Adolescent↗