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Biomedical subjects

G Berger

Publications and source records attributed to G Berger.

At least 235 records · Page 13Linked to original sources
PubMed1980

A binding site on mast cells and basophils for the anti-allergic drug cromolyn.

Calcium permeability of basophil and mast cell membranes is stimulated on allergen binding to its specific membrane-bound IgE. This entry of Ca2+ ions into the cell triggers the degranulation and secretion process. Disodium cromoglycate (cromolyn DSCG), the disodium salt of 1,3-bis(-2-carboxychromon-5-yloxy)-2-hydroxypropane, inhibits the degranulation and release of anaphylactic mediators, and has found wide application in the treatment of allergic bronchial asthma. Accumulated evidence indicates that this inhibition takes place by blocking the calcium uptake. To localize its site of action, the drug has been covalently conjugated to fluorescent polyacrylamide and polyglutaraldehyde beads (0.7 and 0.2 microns in diameter, respectively). We show here that these drug-bead conjugates (DBC) do prevent the drug penetrating into the cell without reducing its ability to inhibit histamine release (Table 1). Furthermore, we show a specific Ca2+-dependent binding of the DBC to the membranes of rat peritoneal mast cells (RPMC) and basophils.

Animals↗
PubMed1980

Acute action of guanfacine on peripheral circulation in hypertensive patients: measurements of arterial flow of the calf and of the forefoot, of venous capacity of the calf, of the blood pressure and of the heart rate.

1. The acute action of an intravenous infusion (5 min) of guanfacine in doses of 0.01, 0.02 and 0.04 mg/kg on peripheral circulation was studied in five hypoertensive patients and compared with a placebo in a randomized study. The observations were combined for 2 h after drug administration. 2. Two phases of drug action were seen during and immediately after the administration of guanfacine; a dose-dependent decrease in blood flow mainly of the forefoot but also in the calf was combined with an increase in systolic and diastolic blood pressures and a decrease in heart rate. Peripheral resistance was increased in this phase. Later, an increase in blood flow to the foot combined with a tendency towards a decrease in blood pressure were observed. 3. These preliminary results show that this second phase of action of guanfacine is dependent on the dose given.

Adult↗
PubMed1980

[Comparative scanning electron microscopical investigation of the bond between bone and different alloplastic implant materials (author's transl)].

The traditional alloplastic implant materials and their applications are represented and are investigated in a comparative scanning electron microscopical study between bone and alloplastic. Provable are clear in "bio-vitroceramic Ap 40" compounds to the bone in the scanning electron microscopical photo-contrary to titanium, tantalum and teflon.

Animals↗
PubMed1980

[Experiences with oral N-acetyl-cysteine treatment in children suffering from cystic fibrosis (author's transl)].

A clinical test with the oral use of Fluimucil was performed by ourselves: Forty-two children, who had been in stable condition for 8--10 years under inhalation therapy with Mucosolvin, were treated for a period of 6 months with Fluimucil used orally. We compared the clinical, bronchoscopic and lung function finding s before and after the 6-month period. In the case of 7 children the oral treatment had to be discontinued and replaced by a resumption of inhalation therapy after 6 to 12 weeks on an account of an exacerbation of the lungstate. The bronchoscopic studies showed results worse in 44% of the cases, unchanged in 22%, and improved in 34%. For lung-function the figures were 31%, 51% and 18% respectively. We can conclude from our results that it is not possible to replace inhalation therapy by an oral treatment for all children with cystic fibrosis. We can, however, surmise that such a treatment will be possible for 50--60% of the children and this must be considered as a significant step forward in the care of these children.

Acetylcysteine↗