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Biomedical subjects

H J Reimers

Publications and source records attributed to H J Reimers.

At least 19 recordsLinked to original sources
PubMed1996

[Physical complaints, stress and quality of life of oncologic patients. Effects and patient assessment in inpatient rehabilitation].

AIM: To what extent do cancer patients use an inpatient aftercare programme and how is its effect been estimated by them? How is the progress of "general physical complaints", "psychosocial stress" and "satisfaction with life" in some cases over a period of up to eight months? PATIENTS AND METHODS: To 201 patients with breast or intestinal cancer respectively, who were going to be or had already been admitted to an inpatient aftercare, standardised and unstandardized questionnaire were presented to be filled out at 4 or 5 different dates before and during the programme as well as 3 and 6 months later. RESULTS: Many patients tried to take part in the aftercare programme actively. Even 6 months later 95.6% estimated it as being "successful" and 70% said that there had been a lasting positive effect after the treatment. The "general physical complaints" and "psychosocial stress" grew significantly less during the inpatient aftercare programme and "satisfaction with life" improved. After the treatment these effects were declining again. CONCLUSIONS: The results indicate that many patients, who participate in an inpatient aftercare programme, profit by it directly. As the positive effects partially get lost during the following months, the patients should be prepared more intensely for the time after dismission with its higher level of strain and should get an especially attentive ambulant care at home.

Adaptation, Psychological↗
PubMed1992

Small cell undifferentiated carcinoma of the pancreas. Report of a patient with tumor marker studies.

BACKGROUND: Small cell undifferentiated carcinoma of the pancreas is a rare type of pancreatic neoplasm. METHODS: The authors report the clinical and pathologic aspects of a patient with this malignant lesion and an extensive serologic and immunohistochemical survey of potential ectopically produced hormones or tumor markers. RESULTS: Neuron-specific enolase (NSE) emerged as a tumor marker. CONCLUSIONS: NSE could be valuable in the diagnosis and management of other patients with this rare disease.

Biomarkers, Tumor↗
PubMed1988

Expression of tissue factor and factor VIIa/tissue factor inhibitor activity in endotoxin or phorbol ester stimulated U937 monocyte-like cells.

Previously, unstimulated cells of the human monocytic tumor cell line U937 have been shown to possess a negligible cell-surface tissue factor (TF) activity, and to secrete a small amount of factor VIIa/tissue factor (VIIa/TF) inhibitor activity. On stimulation with endotoxin or with phorbol myristate acetate (PMA), TF of these cells is known to be increased approximately fourfold. In this report, we demonstrate that VIIa/TF inhibitor is also increased on stimulation of U937 cells with endotoxin (approximately equal to threefold) or with PMA (approximately equal to 20-fold). Notably, the secretion of the inhibitor persisted after the cell surface TF had started to decline. Further, when serum-free media from PMA stimulated cells was electrophoresed on a sodium dodecyl sulfate (SDS) gel, we eluted two inhibitor activity peaks corresponding to Mr approximately equal to 47,000 and Mr approximately equal to 36,000. The molecular weights of these peaks are similar to those obtained earlier from human plasma for this inhibitor(s).

Endotoxins↗
PubMed1987

Impaired thromboxane synthesis in preactivated human blood platelets: agonist-specific, irreversible desensitization to thrombin.

The causes for reduced platelet thromboxane synthesis in patients with acquired platelet storage pool disease are incompletely understood. The present study was designed to define the nature of the defect(s) underlying diminished thromboxane synthesis in human platelets previously exposed to thrombin in vitro. Platelets pretreated with high concentrations of thrombin were unable to form measurable amounts of thromboxane in response to a second stimulation with thrombin. In contrast, thrombin-pretreated platelets formed additional thromboxane in response to arachidonate, collagen, or A23,187. Thrombin-pretreated platelets did not recover with respect to thrombin-inducible thromboxane synthesis when incubated for two hours in plasma either in the presence or absence of added arachidonic acid. These observations suggest that neither inactivation of cyclooxygenase nor depletion of endogenous arachidonic acid is responsible for the impaired thrombin-induced thromboxane synthesis in thrombin-prestimulated platelets. Impaired thrombin-induced thromboxane synthesis in these platelets may be due to agonist-specific, irreversible receptor uncoupling.

Arachidonic Acids↗
PubMed1987

Deaggregation of in vitro-degranulated human platelets: irreversibility of aggregation may be agonist-specific rather than related to secretion per se.

Based on studies with thrombin, it has been proposed that human platelets exposed to strong release-inducing agents undergo irreversible aggregation and cannot be deaggregated without the use of proteolytic enzymes. We tested the hypothesis that irreversible human platelet aggregation occurs as a result of thrombin-specific platelet alterations rather than induction of the release reaction per se. Washed human platelets were exposed to either thrombin (THR) or the aminophospholipid N-(7-Nitro-2,1,3-benzoxydiazol-4-yl) phosphatidylserine (NBD-PS) for 20 seconds. Both agents caused similarly extensive release of platelet dense- and alpha-granule contents. After neutralization of thrombin and NBD-PS, and addition of PGE1 and apyrase, the platelets were sedimented, resuspended and incubated at 37 degrees C with gentle agitation. Single, disc-shaped, degranulated platelets which were recovered in both systems were capable of aggregation in response to a second exposure to aggregating and release-inducing stimuli. Deaggregation was more rapid, more extensive, and more reproducible with NBD-PS- than with THR-degranulated platelets. Platelets exposed to thrombin for longer than 20 seconds showed a progressive loss of deaggregability which was not observed after prolonged incubation with NBD-PS. These findings do not support the concept that extensive secretion per se causes irreversible aggregation of human platelets. Instead it appears that formation of irreversible linkages between platelets involves the specific, time-dependent interaction of THR with platelets, released fibrinogen and possibly one or more other substances secreted from platelets.

4-Chloro-7-nitrobenzofurazan↗
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↗
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

Thrombin pretreatment of human platelets impairs thromboxane A2 synthesis from endogenous precursors in the presence of normal cyclooxygenase activity.

Exposure of horse platelets to thrombin has been reported to cause nearly complete inactivation of cyclooxygenase within 30 sec. This contrasts with the observation that human platelets, depleted of their granule constituents by stimulation with thrombin, still aggregate in response to arachidonic acid, a reaction presumably mediated by thromboxane A2 (TxA2) formation. Because of this conflicting evidence, TxA2 formation was measured by radioimmunoassay in washed human platelets depleted of their alpha- and dense-storage granule constituents by prior stimulation with thrombin. These platelets aggregated in response to adenosine diphosphate (ADP), collagen, arachidonic acid, and thrombin, and formed TxA2. However, collagen- and thrombin-induced TxA2 formation by these platelets was reduced in comparison to control platelets that had not been depleted of their storage granule constituents by prior thrombin stimulation. In contrast, arachidonic acid-induced TxA2 formation was not significantly different in thrombin-depleted and control platelets. These results demonstrate that thrombin can induce degranulation of platelets without concomitant inactivation of cyclooxygenase.

Arachidonic Acid↗
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

ADP-induced changes in [32P]phosphate labeling of phosphatidylinositol-4,5-bisphosphate in washed rabbit platelets made refractory by prior ADP stimulation.

Changes in 32P labeling of phosphatidylinositol-4,5-bisphosphate (PIP2) were examined during ADP-induced aggregation of washed rabbit platelets prelabeled with [32P]phosphate. ADP caused a significant decrease in the amount and 32P labeling of PIP2 at 10 and 60 sec. The decrease in labeling persisted at 2.5 min when the platelets were still aggregated, but disappeared by 10 min. Platelets refractory to ADP showed no further significant change in 32P in PIP2 when exposed to ADP; a decrease in PIP2 labeling could be induced, however, after platelets had recovered their disc shape and sensitivity to ADP. These data indicate that PIP2 may play a role in the response of platelets to ADP.

Adenosine Diphosphate↗
PubMed1980

[Platelets and coronary artery disease (CAD) (author's transl)].

During recent years, platelets have been increasingly implicate in the pathogenesis of coronary artery disease and its complications. This is based on new knowledge of platelet physiology as well as on clinical observations. Experimentally, it can be demonstrated that platelet vessel wall interaction is important in atherogenesis. In animal, platelet aggregates in the arterial circulation may cause ischemic myocardial lesions. In patients who died suddenly platelet thrombi can often be found in the microcirculation at autopsy. Compounds released during platelet aggregation may cause a spasm of the coronary arteries. Hyperactive platelets can be demonstrated in patients with CAD as well as in patients with the known risk factors of CAD. In some clinical trials, platelet function inhibitors reduced death from cardiac causes. Here we review the theoretical and experimental basis of the "platelet hypothesis" of CAD and its complications as well as the rationale for treating patients with CAD with "'antiplatelet" drugs.

Animals↗
PubMed1979

Disassembly of microtubules in the Lesch-Nyhan Syndrome? (Lesch-Nyhan syndrome and microtubules).

The Lesch-Nyhan syndrome is an unusual disease. It combines neurological disorders, behavioural disturbances, metabolic changes and haematological symptoms. The syndrome is caused by an X-chromosomal transmitted enzyme deficiency of the 'salvage pathway' in purine metabolism. The hitherto unexplained pathogenesis was the reason for investigations into metabolism and morphology of the blood cells of a patient suffering from the syndrome. Along with the defect in guanine nucleotide resynthesis there was a defect of microtubules in platelets and a sphaerocytosis in red cells, which could be the result of a disassembly of structural proteins. The development and maintenance of the highly heteromorphic structure of nerve cells and the neuronal function including axonal transport of cell organelles and transmitters is dependent on microtubules. Thus a disassembly of microtubules could be the mechanism in the pathogenesis of this complex syndrome.

Adenine Phosphoribosyltransferase↗