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Biomedical subjects

W Reiter

Publications and source records attributed to W Reiter.

At least 19 recordsLinked to original sources
PubMed1996

Clinical significance of the tumour markers CA 125 II and CA 72-4 in ovarian carcinoma.

In a retrospective study we compared the usefulness of the tumour marker CA 72-4 with the established marker CA 125 II (both EIA on Cobas-Core, Hoffmann LaRoche, Basel Switzerland) at the time of primary diagnosis of ovarian carcinoma (n = 123) in order to discriminate between ovarian carcinomas of different histological type. We compared their diagnostic value, behaviour in follow-up care and evaluated possible combinations. Fixing specificity at 95% vs. benign gynaecological diseases (n = 37) as the clinically relevant reference group, we found cut-off values of 160 U/mL for CA 125 II and 3.0 U/mL for CA 72-4. On the basis of this specificity, we found comparable sensitivity for CA 125 II and CA 72-4 for all kinds of ovarian carcinoma at the time of primary diagnosis. With regard to histology, we found best sensitivity for CA 125 II in serous ovarian cancer and for CA 72-4 in mucinous ovarian cancer. Additional sensitivities were found in ovarian carcinoma in general but little in serous ones. No additive sensitivity was found in mucinous ovarian carcinomas with CA 72-4 as leading marker. In follow-up care, CA 72-4 was the leading marker in II cases and CA 125 II in 16, while in one case both markers were negative. In 6 cases the change of values reflecting clinical follow-up-care was within the so-called reference range. According to our results, at the time of primary diagnosis because of lack of histological findings the combined determination of CA 125 II and CA 72-4 can be recommended. In follow-up care and control of efficacy of therapy the preoperative positive or leading marker is generally sufficient. The determination of both markers in follow-up care is indicated only if they both are negative at primary diagnosis and until one of them becomes clearly positive.

Adenocarcinoma, Mucinous↗
PubMed1995

Parameters of haemostasis during acute venous thrombosis.

Underlying disorders of the coagulation system such as inhibitor deficiencies or decreased fibrinolysis are common in patients suffering from venous thrombosis. They may lead to the necessity of a lifelong prophylaxis. Prompt diagnosis is obviously to the patients benefit. We investigated 22 patients suffering from venous thromboses for the inhibitors antithrombin III (ATIII), protein C, and protein S during the first 8 to 12 days after admission to hospital and in addition after withdrawal from anticoagulant treatment after several months. At the day of admission ATIII and protein C levels were comparable to those several months later, but after 2 days they shifted downward or upward, respectively. Protein S did not shift during the period of hospitalisation, but was initially slightly lower than several months later. For inhibitors the day of admission to hospital is most suitable to take the samples. About 50% of the patients still had elevated activation markers (prothrombin fragments F1+2, thrombin-antithrombin complex TAT, and D-dimers) after several months.

Acute Disease↗
PubMed1994

Long-term therapy with the new glucocorticosteroid deflazacort in rheumatoid arthritis. Double-blind controlled randomized 12-months study against prednisone.

The long-term anti-inflammatory and immunosuppressive properties and the safety of deflazacort (Calcort, CAS 14484-47-0) were assessed investigating the effect on clinical symptoms and safety parameters in patients with rheumatoid arthritis compared to prednisone as standard therapy in a randomized double-blind controlled clinical trial. Monitoring was performed according to GCP-guidelines closely in order to have a maximum of the patients entered completed at the end of the 12-month therapy with high data quality. 76 patients, meeting the criteria for classical or definite rheumatoid arthritis and requiring corticosteroid therapy, were randomly allocated to a 12-months treatment with either deflazacort (6 mg/tablet) or the corticoid standard prednisone (5 mg/tablet). Steady state dosage between 1/2 and 3 tablets per day was individually adjusted according to the severity of the clinical symptoms. Due to the close monitoring of the trial in the 6 study centres, 25 patients completed 12 months of deflazacort and 28 patients 12 months of prednisone treatment, being controlled 7 times during the trial. Five efficacy parameters were assessed at each visit: Ritchie Index, duration of morning stiffness, grip strength, effective dosage of study medication and global assessment of disease status. Following safety and tolerance parameters were controlled during the trial: vital signs, weight, Cushing's symptoms and adverse events at each visit; 32 laboratory parameters at 6 visits; ECG at 3 visits; and the global tolerance was assessed at the end of the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Guidelines for hemophilia care.

The patient with hemophilia has a multitude of medical and psychosocial concerns. The HIV epidemic has drastically exacerbated his needs. Physicians must continue to educate themselves to keep apace of the rapidly changing treatments for hemophilia and for HIV detection and treatment. These recommendations highlight changes that have taken place in the past several months and are up-to-date as of July 1990. It is likely that they will change, however, as more information becomes known about current factor products and better care for HIV infections.

AIDS Serodiagnosis↗
PubMed1990

Reninlike enzymes in human vasculature.

The present study was designed to identify angiotensin I (Ang I)-forming angiotensinogenases in human extrarenal vasculature and to examine the theory of Jiménez Días on their stimulation in essential hypertension. Vascular sections obtained intraoperatively from 14 normotensive and 16 hypertensive patients undergoing corrective surgery, 68 umbilical cord blood vessels from parturient women, tissue samples from nine explanted hearts, and serum from anephric and healthy individuals were investigated. Ang I-forming angiotensinogenase activities were determined enzyme-kinetically by using Ang I radioimmunoassay and purified sheep or human angiotensinogens. Three nonrenin Ang I-forming angiotensinogenases (pH optima of 4.0, 5.1, and 6.1) were identified in extrarenal vasculature, in cardiac tissues, and in plasma. Highest specific activities of nonrenin Ang I-forming angiotensinogenase (in nanograms Ang I per gram times hour; mean +/- SD) were found in cardiac tissue (2,821 +/- 497, n = 9), followed by carotid artery intima (1,448 +/- 982, n = 10), arteries (1,307 +/- 736, n = 18), and umbilical cord arteries (135 +/- 55, n = 35). Extrarenal arterial Ang I-forming angiotensinogenases were linearly correlated with those of local angiotensin converting enzyme and plasma renin activity. In essential hypertension, extrarenal arterial Ang I-forming angiotensinogenases were scattered, but not generally stimulated. The data obtained indicate the existence of nonrenin Ang I-forming angiotensinogenases in human extrarenal vasculature, in kidney, and in plasma. The postulate of stimulation of extrarenal arterial Ang I-forming angiotensinogenases in essential hypertension cannot be supported. Similar to the classification of plasma renin activity, a classification of Ang I-forming angiotensinogenase activity is proposed, consisting of patients with essential hypertension divided into subgroups exhibiting high, normal, or low vascular Ang I-forming angiotensinogenase activities.

Angiotensin I↗
PubMed1990

Angiotensin I-forming angiotensinogenases in extrarenal vasculature and in the kidney.

The intention of this study was to characterize angiotensin I-forming angiotensinogenases (AIFAs) in rat extrarenal arterial walls and to clarify whether these enzymes are also present in the kidney. A further aim was to identify AIFAs in human vasculature and to establish whether they are affected in essential hypertension. Sprague-Dawley rats and vascular sections of patients undergoing corrective surgery were studied. Enzyme kinetic assays were performed using angiotensin I radioimmunoassay and purified natural angiotensinogens. Fast protein liquid chromatography was employed for biochemical characterization. A series of AIFAs with various isoelectric points, molecular weights and pH optima was detected in rat extrarenal vascular and, with differing distributions of enzyme activities, in renal tissues. In extrarenal arteries the main form of renal renin was present with a relatively low activity only. AIFAs were also demonstrable in human extrarenal vasculature and behaved like plasma renin in essential hypertension. The results indicate the existence of an intrinsic human vascular RAS in extrarenal (and renal) arteries. Extrarenal arterial AIFAs are not generally stimulated in essential hypertensives, as previously postulated.

Angiotensin I↗
PubMed1987

Suppression of renin-angiotensin system in the heart of spontaneously hypertensive rats.

Renin-like enzyme and angiotensin converting enzyme (ACE) were identified and their specific activities measured in cardiac tissues of spontaneously hypertensive rats (SHR) and their Wistar-Kyoto (WKY) normotensive controls. In addition, the enzyme activities were determined following administration of hypotensive drugs. The pH optima of cardiac renin-like enzymes were identical with those in vascular walls, the specific activity being higher in the heart. Cardiac ACE revealed similarities with the venous wall enzyme. The highest specific cardiac renin-like activity was found in the septum and that of ACE in atria/auricles. Both enzyme values were lower in the hearts of SHR than in those of normotensive controls. Following nifedipine treatment, specific renin-like activities increased in all cardiac structures studied (P less than 0.01); with nitrendipine and muzolimine less pronounced elevations were obtained. Administration of these three hypotensive drugs resulted in a stimulation of ACE in all the cardiac structures except in atria/auricles, where their activities were lowered.

Animals↗
PubMed1987

Effect of hypotensive agents on the renin-angiotensin system in vascular walls of spontaneously hypertensive rats.

Previous investigations have shown that the renin-angiotensin system (RAS) is activated in vascular walls of spontaneously hypertensive rats (SHR). The present study was undertaken to determine whether antihypertensive drugs attenuate this activation. Two calcium channel blockers, nifedipine and nitrendipine, and the diuretic muzolimine were applied to SHR for 2-4 weeks, and angiotensin (ANG) I-forming angiotensinogenase (AIFA) and ANG I converting enzyme (ACE) activities were determined. The values for both enzymes were elevated in arterial tissues of SHR (P less than 0.01), whereas in venous walls AIFA activity was decreased (P less than 0.01). All hypotensive drugs reduced arterial ACE activities in SHR (nifedipine and muzolimine: P less than 0.01; nitrendipine: P less than 0.05). Angiotensin I-forming angiotensinogenase activity was increased following treatment with nifedipine (P less than 0.01) but reduced by nitrendipine (P less than 0.05); with muzolimine, no significant alterations were observed. The results obtained indicate that in SHR, stimulation of vascular wall ACE is abolished following treatment with hypotensive agents, and the effect is independent of their mode of action. It is assumed that the activation of vascular ACE is not caused by, but rather a reaction to, elevated blood pressure.

Animals↗
PubMed1986

[Medical findings on the trochlear nerve].

The exit-zone, the intracisternal course, the course in the sidewall of the cavernous sinus and inside the orbit were measured at 91 head-halves. Included are measurements of the length of the area nervosa, its nerve fibers and its distance to the total extracerebral length of the IVth nerve is estimated. The results are discussed with earlier investigations and some clinical approaches and neurophysiological methods are given.

Adult↗
PubMed1982

Intracellular adriamycin levels and cytotoxicity in adriamycin-sensitive and adriamycin-resistant P388 mouse leukemia cells.

Adriamycin (ADR) (NSC-123127) uptake and retention in ADR-sensitive P388 leukemia (P388/S) and ADR-resistant P388 leukemia (p388/R) cells were compared by fluorometry and laser flow cytometry (FCM) and were correlated with cytotoxic effects. Drug levels in P388/R cells treated in vitro with ADR (1-10 micrograms/ml) were twofold to fourfold lower than were levels in similarly treated P388/S cells FCM analysis of P388/S and P388/R cells exposed in vitro to ADR showed qualitative and quantitative differences in ADR fluorescence profiles of drug-treated cells (1-5 micrograms/ml) but not of the isolated nuclei (0.5- 10 micrograms/ml). Drug-induced perturbations in cell cycle traverse and chromosome aberrations were seen in P388/S but not in P388/R cells treated with 0.5-5 micrograms ADR/ml in vitro or 4-8 mg ADR/kg in vivo. The role of FCM in rapidly comparing and quantitating cellular ADR fluorescence profiles of ADR-sensitive and ADR-resistant tumors was demonstrated.

Animals↗