Search PubMed⌕ Search

Biomedical subjects

E Morgenstern

Publications and source records attributed to E Morgenstern.

At least 55 records · Page 3Linked to original sources
PubMed1985

Gray platelet syndrome: selective alpha-granule deficiency and thrombocytopenia due to increased platelet turnover.

Clinical and laboratory studies of two siblings, both suffering from gray platelet syndrome (GPS) are described. The patients had a mild bleeding disorder, their platelets were blue-gray in panoptic stains, and alpha-granules were markedly reduced, as shown by electron microscopy. The platelet content of platelet factor 4 and that of beta-thromboglobulin were significantly reduced (3%-7% of normal). Platelet count was decreased (33-150 X 10(9)/1) and small platelets were increased in platelet volume distribution. Bleeding time was prolonged on most occasions. Bone marrow aspiration was performed in one patient and revealed increased reticulin fibers, however, megakaryocyte count was normal. The mean platelet survival was 4.8 days using 111indium-labelled platelets. In this patient, platelet-associated IgG was within the normal range. Prednisone therapy failed to increase platelet count. Dental surgery was performed under cover of desmopressin and no bleeding complication occurred; however, no improvement of bleeding time was observed. The patient delivered a healthy male infant without hemorrhaging while under concurrent platelet transfusion therapy.

Adult↗
PubMed1985

Fibrinogen distribution on surfaces and in organelles of ADP stimulated human blood platelets.

The fibrinogen distribution in platelet organelles after ADP-stimulation was investigated with anti-human fibrinogen using protein A-gold applied to serial sections. Fibrinogen was detected in the so-called alpha-granules of platelets and also in granule protrusions which were observed after ADP-stimulation. The ends of these protrusions were formed as coated membranes and the tips were often in apposition to the surface connected membranes or the plasmalemma. At such places fusion events and hence signs of an exocytosis could be demonstrated by means of cryofixation and cryosubstitution. Examination of serial sections revealed fibrinogen on all these granule profiles. Surface connected membranes, free surfaces and the characteristic structure of the contact zones of aggregated platelets were also labelled by gold particles but less than anticipated. On the platelet surfaces and surface connected membranes fibrinogen was rarely demonstrable with ferritin-labelled anti-human fibrinogen on washed or thrombin-stimulated, almost fibrinogen free platelets. After addition of human fibrinogen to the thrombin stimulated and disaggregated platelets a part of the platelets aggregated spontaneously and formed characteristic contact zones. Anti-human fibrinogen was observed on the free surfaces, in filamentous bridges between the contact spaces and in a tubular surface connected membrane system with involvement of coated membranes at the central ends of these structures. The results indicate the following: all alpha-granules contain fibrinogen; after ADP-stimulation secretion takes place with involvement of coated membranes; during aggregation fibrinogen binds to platelet surfaces and forms contact spaces; fibrinogen is taken up by the surface connected system with involvement of coated membranes.

Adenosine Diphosphate↗
PubMed1985

[Analgesic effect, tolerance development and dependence potential of D-phenylalanine].

In comparison to well-established non-narcotic analgetics, the amino acid D-phenylalanine produces similar, dose-dependent analgesic effects in animal experiments, but acts significantly longer. Neither a tolerance of mice to D-Phe after administration for 10 d nor a development of drug dependence in rats following treatment for 6 weeks could be regarded.

Acetates↗
PubMed1984

Platelets and fibrin strands during clot retraction.

The ultrastructure of platelet fibrin contacts (PFC) and the course of the strands was investigated in serial sections of retracted clots with the help of specimen tilting. We found after retraction in a test tube as well as under isometric conditions in the resonance thrombograph, after HARTERT, an uniform type of PFC. The side to side contact between platelet surface and fibrin strands displayed a 15 nm wide space which was bridged of 10 - 30 nm by filamentary structure. In each case the direction of the fibrin strands changed on contact with the platelet surface (bend). These bends recurred if the adhering strands ran over a longer distance on the platelet surface. The bends can be explained by non-directional movement of the platelets or of their pseudopodia. Microfilaments (actomyosin) which run straight in pseudopodia and often also twisted in the platelet body support this assumption. The described mechanism - contact of the thrombin activated platelets with fibrin strands and simultaneous nondirectional movement of the platelets which bind further sections of the adhering strands to their surface - would provide a more satisfactory explanation for the retraction of the clot to 1/10 of its original volume.

Blood Platelets↗
PubMed1984

The platelet contacts during aggregation.

APD-stimulated and aggregated platelets show dense structures (DS) on their free surfaces and filament bridges within 40-50 nm wide spaces of contacts between aggregating platelets (bridge contacts). Within the bridge contacts tight contacts are observed. Adjacent to tight contacts plasmalemmal openings into a canalicular system are seen. Pits and the central ends of these membranes are coated as seen in serial sections. Cationized ferritin (CF) added before stimulation binds to the whole negatively charged surface. Closer packed CF particles were observed on the DS and in the contacts on the central part of the bridges. CF did not introduce qualitative changes to the formation of typical platelet contacts, in particular of the tight contacts. Surface bound CF was found in the adjacent plasmalemmal invaginations and in the canalicular endomembranes. This result suggests an endocytosis mechanism which cleans the platelets of surface material during formation of tight contacts in aggregates.

Adenosine Diphosphate↗
PubMed1984

Ultrastructural studies on the binding sites of fibrinogen on platelet surface during aggregation.

Activated human blood platelets show characteristic globular structures on their surface. Aggregated platelets in blood plasma form contact zones with 40-50 nm spaces between the plasmalemmata. These spaces are bridged by filamentous structures (5,000 per microns 2). To investigate whether the globules or bridges observed are caused by fibrinogen, platelets were washed and treated first with thrombin (1 U thrombin/ml) in order to remove fibrinogen from platelet storage organelles and then with plasmin (0.5-2 U/ml) in order to dissolve remnants of fibrinogen from the platelet surface. Platelets treated in this way were resuspended in tyrode-albumin buffer solution (containing hirudin and prostaglandin E1). No storage organelles were revealed but the platelets reconstituted their discoid shape and the marginal bundle of microtubules. By representing the platelet glycocalix with alcian blue it was observed that the previously homogeneous surface coat was interdispersed with holes of 60-70 nm in diameter, approx. 900 per microns 2. Fibrinogen (8 mg/ml) was then added and the suspension was stirred for 3 minutes at 37 degrees C. The platelets again aggregated and formed contact zones in blood plasma as described above. In spaces of 40 to 50 nm width filamentous bridges similar in size, structure and number to those between aggregated platelets in blood plasma were observed. In both cases the bridges appeared to adhere with small rods into the plasmalemma. Bridges and rods can be easily stained with protein stabilizing agents. In contrast, glycocalix treated with alcian blue are weakly stained. The findings strongly indicate that fibrinogen is the mediator of this type of platelet contact in aggregates. The fibrinogen binding sites are situated to the plasmalemmal outer leaf let and not on the peripheral glycocalix.

Adenosine Diphosphate↗
PubMed1983

[Synthesis and analgesic effect of 2-aryliminomethylquinolines].

2-Aryliminomethylquinolines were synthesized by the condensation of quinoline-2-carbaldehyde with the corresponding anilines. The compounds were evaluated for analgesic activity using the acetic acid writhing test. Some of them showed significant inhibition of the writhing syndrome. The most potent compound 3b was approximately as active as aminophenazone in the writhing and the hot-plate method.

Analgesics↗
PubMed1982

Coated membranes in blood platelets.

The simultaneous addition of alcian blue and tannic acid to human blood platelets during glutaraldehyde fixation leads to an excellent representation of coated membranes (CM). Coated membrane segments can be found (1) in plasmalemma, in vesicle system and lysosomal granules, or (2) as coated pits or coated vesicles. They possess the same morphological properties as in other animal cells. An increased number of coated membranes is observed in platelets which have been stimulated with ADP. The role played by coated membranes remains unsolved in contrast to the role of other endomembranes in platelets for instance the vesicle system.

Blood Platelets↗
PubMed1980

Substance P: does it produce analgesia or hyperalgesia?

In the hot plate test, substance P given intravenously at doses of 5 x 10-5 and 5 x 10-4 gram per kilogram caused analgesia, while lower doses caused hyperalgesia. The influence of substance P on nociception depended on the individual mouse's sensitivity to pain (control response latency). Analgesia was produced by substance P administered to mice with high sensitivity to thermic stimulation, whereas hyperalgesia occurred in mice whose control latencies were longer than normal. This result is interpreted as an indication that substance P is capable of normalizing responsiveness to pain and could be classified as a regulatory peptide.

Acetates↗
PubMed1980

Substance P--new aspect to its modulatory function.

The paper deals with a modulatory function of Substance P (SP) (Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-MetNH2) with bearing on nociperception, behaviour, and norepinephrine uptake. The effect of SP on both nociperception and behaviour was found to depend on the original condition of the individuals. The individual response time of mice to thermic stimuli becomes standardized by Substance P in the hot-plate test. Disorders in acquisition of avoidance reactions caused by noiseborne stress were found to be fully normalized by SP, like certain vegetative parameters, such as blood pressure, heart rate, and respiratory rate. SP was found to inhibit or stimulate norepinephrine uptake of hypothalamus preparations depending on the experimental conditions. It is recommended to name peptides of the above type of action as "regulatory peptides" (regulides).

Acoustic Stimulation↗