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Biomedical subjects

P Müller

Publications and source records attributed to P Müller.

At least 235 records · Page 13Linked to original sources
PubMed1994

Angiotensin II receptor blockade with single doses of valsartan in healthy, normotensive subjects.

Valsartan (CGP 48933), a specific blocker of the angiotensin II (Ang II) receptor subtype 1 (AT1 receptor) was administered in single, oral doses of 40 mg and 80 mg to six healthy, normotensive male volunteers in a double-blind, placebo-controlled, randomized crossover trial. The aims of the study were a) to assess the extent, time course and dose-dependency of inhibition of the pressor effect of exogenous Ang II; and b) to attempt to correlate AT1 receptor blockade with the drug levels in plasma and with other markers of biological activity of the trial drug such as plasma renin activity (PRA). Using the Finapres device and i.v. bolus injections of exogenous Ang II, AT1 receptor blockade was assessed by measuring blood pressure (BP) and heart rate (HR) on a beat-by-beat basis. A dose-response curve for Ang II was obtained for each subject before and at 2, 4, 6, 8 and 24 h after administration of placebo and of the two doses of valsartan. PRA was measured with a conventional radioimmunoassay method. Data evaluation included a) descriptive analysis of the changes of the Ang II dose-response curves after valsartan, as compared to the curve on placebo; b) calculation of the pressor dose D30 of Ang II at each time-point, using linear regression; c) assessment of the effect of 4 micrograms Ang II on systolic BP and HR and the calculation of the percentage inhibition of these effects after valsartan; d) description of the relationship between drug levels in plasma and the measures of AT1 blockade, including pharmacokinetic-pharmacodynamic modeling with an Emax model for the percentage inhibition of systolic BP and HR.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

Effect of exercise supplementation during adenosine infusion on hyperemic blood flow and flow reserve.

Physical stress might modulate myocardial blood flow in near-maximally dilated coronary arteries by increasing coronary perfusion pressure, myocardial contractility, and heart rate. The net effect of these changes on hyperemic blood flows has not yet been defined in humans. To quantify the effect of physical exercise on pharmacologically induced hyperemia, myocardial blood flow was measured in 11 healthy volunteers. Measurements were performed with positron emission tomographic imaging with nitrogen-13 ammonia at rest, during intravenous (i.v.) adenosine administration (140 micrograms.kg-1.min-1 over 6 minutes), and during i.v. adenosine administration plus supine bicycle exercise with a maximal workload of 125 W. Myocardial blood flow was quantified by using a previously validated graphic analysis. Heart rate, systolic blood pressure, rate-pressure product, and mean aortic blood pressures were significantly higher during combined physical and pharmacologic stress than during pharmacologic stress alone. However, myocardial blood flow decreased from 2.6 +/- 0.4 to 2.2 +/- 0.4 ml.min-1.gm-1 with the addition of physical stress (p < 0.05). This decline was associated with a significant increase in coronary vascular resistance (35 +/- 6 vs 52 +/- 13 mm Hg.ml-1.gm.min; p < 0.05). Accordingly, myocardial flow reserve declined, from 5.0 +/- 0.9 to 4.3 +/- 1.0, with exercise supplementation (p < 0.05). Exercise in addition to pharmacologic stress increases coronary vascular resistance and thus significantly decreases hyperemic myocardial blood flow and flow reserve. This decrease results most likely from an increase in extravascular restrictive forces caused by higher ventricular pressures and contractility during physical stress.

Adenosine↗
PubMed1994

Short report: long-term management of peptic ulcer disease with ranitidine in Germany.

One hundred and twenty-five patients with duodenal ulcer disease were given continuous ranitidine therapy after initial acute healing. Cumulative remission rates indicated that 95% of patients were ulcer-free after 1 year, 89% at 2 years, 81% at 3 years, 70% at 4 years and 60% at 5 and 6 years. Nine patients had a second recurrence after healing of the first. No patient developed an ulcer complication. These results support the view that long-term continuous ranitidine therapy prevents ulcer recurrence and complications.

Duodenal Ulcer↗
PubMed1994

Human papillomavirus DNA in oral squamous cell carcinomas and normal mucosa.

Human papillomavirus (HPV) infections in oral carcinomas and normal oral mucosa were studied by consensus primer screening and typing for HPV types 6/11, 16 and 18 DNA. After polymerase chain reaction (PCR) the DNA species of interest were identified by Southern blot hybridization with digoxigenin-labeled oligonucleotide probes. Frozen tissue and scrapings were equally suitable for HPV testing and yielded high HPV detection rates in carcinomas. By comparison, HPV analysis of paraffin-embedded material was much less efficient. HPV were demonstrated in 61.5% (16/26) of oral squamous cell carcinomas, high risk HPV 16 and 18 being the preferential types. The frequency of HPV detection in non-neoplastic mucosa of tumor patients decreased clearly with increasing distance from the tumor (range 26.9-3.8%) suggesting focal HPV infections. In contrast, normal buccal mucosa of a group of healthy volunteers contained HPV DNA only in 1% (1/97).

Adolescent↗
PubMed1994

Nizatidine in therapy and prevention of non-steroidal anti-inflammatory drug-induced gastroduodenal ulcer in rheumatic patients.

Two hundred and sixty-nine patients with various rheumatic disorders who had been treated with non-steroidal anti-inflammatory drugs (NSAID) for at least 3 weeks were enrolled in this randomized double-blind multicentre trial. Entry criteria were the presence of an ulcer in the gastric and/or duodenal mucosa (> 3 mm and < 20 mm in diameter) and dyspeptic symptoms. The patients were treated with 150 mg nizatidine nocte (n = 86), 2 x 150 mg/d (n = 93) and 2 x 300 mg/d (n = 90) nizatidine. All patients continued to take their original NSAID medication. The three nizatidine groups were well matched with respect to important patient characteristics. After 8 weeks of treatment more than 90% of gastric and duodenal ulcers (DU) had healed under all three nizatidine dosages. There was a tendency to higher healing rates in the case of gastric ulcers after 4 weeks following the higher dose of nizatidine. Erosion, in the stomach and duodenum as well as oesophagitis, improved to a similar degree with all nizatidine doses. There were similar improvements in clinical symptoms such as epigastric pain, heartburn etc. Consumption of additional antacids were similar in all three groups. In the subsequent prevention trial, 237/221 patients were followed for 3/6 months. In addition to their continued antirheumatic medication 116/107 received nizatidine 150 mg nocte and 121/114 patients 2 x 150 mg nizatidine daily. The cumulative relapse rates within 6 months averaged 5.5% in the low and 1.8% in the high dose group (NS). The safety of nizatidine was assessed as good in both the therapeutic and the preventive trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1994

[p53 alterations and HPV status in oral squamous cell carcinomas].

Immunohistochemical examination of p53 protein accumulation, analysis of the p53 gene using amplification of the exons 5-8 followed by TGGE, and PCR based HPV typing were carried out on 40 oral squamous cell carcinomas. 28 of 40 oral carcinomas (70%) contained DNA of the oncogenic HPV types 16 and 18. A p53 accumulation was present in 20 of 37 tumors (54%). Mutations of the p53 gene were detected in 15 of 39 carcinomas (38%). 15 of 20 oral carcinomas with abnormal p53 expression and 11/15 tumors with mutations of the p53 gene were HPV positive. Our results demonstrate a frequent occurrence of p53 abnormalities in HPV positive oral squamous cell carcinomas. This pattern is divergent from HPV related genital carcinomas and could reflect differences in the etiology of squamous cell carcinomas of different sites.

Biopsy↗
PubMed1994

[Comparison of the protective effects of roxatidine and misoprostol on diclofenac gastroduodenal pathology. An endoscopic, controlled study of volunteers].

For prophylaxis of gastroduodenal lesions induced by non-steroidal antirheumatic drugs (NSAID) acid-lowering as well as mucosa protective substances are used. Direct comparison of both therapeutic regimens are lacking. In randomized parallel studies the gastroduodenal tolerability of 100 mg diclofenac daily in slow-release form was evaluated in the presence and absence of 150 mg roxatidine (CAS 78273-80-0) daily as well as in the presence of 75 mg bid roxatidine or 200 micrograms bid misoprostol (CAS 59122-46-2). The drugs were taken over a period of 14 days. Endoscopic controls were performed at entry, as well as after 14 days of treatment. A quantitative damaging score was used. Study A: Both treatment groups (n = 20) had at entry comparable mucosal damages: placebo/diclofenac: 0.9 +/- 0.1 (+/- SEM), roxatidine/diclofenac: 0.9 +/- 0.1; after 14 days of treatment the score increased in the diclofenac/placebo group to 7.6 +/- 1.9 and, in the corresponding diclofenac/roxatidine group, only to 2.1 +/- 0.9. The difference between the two treatment groups after 14 days was significant (p < 0.05). Study B: Both treatment groups (n = 24) had comparable mucosal damages at entry: diclofenac/roxatidine: 0.9 +/- 0.1, diclofenac/misoprostol: 0.8 +/- 0.1. Following 14 days treatment with 100 mg diclofenac daily the damaging score in both group rose to comparable levels: roxatidine group 2.1 +/- 0.7 and misoprostol group 2.0 +/- 0.4 (n.s.). The data suggest that for prophylaxis of NSAID-induced gastroduodenal lesions substances with different mechanism of action can be used. The findings underline the complex way by which NSAID can damage the mucosa of the upper gastrointestinal tract.

Adult↗
PubMed1994

Ranitidine in the treatment of non-ulcer dyspepsia. A placebo-controlled study in the Federal Republic of Germany.

The trial randomly assigned 652 patients with non-ulcer dyspepsia (NUD), defined as chronic or recurrent complaints of acid-related (heartburn, acid regurgitation, epigastric pain) and non-acid related (fullness/vomiting, nausea) symptoms and with no evidence of organic disease, to treatment for 4 weeks with 150 mg of ranitidine (Zantic, CAS 66357-59-3) twice a day, or placebo, according to a double-blind design. The presence and duration of all dyspeptic symptoms were recorded by interviews at the beginning and after 2 and 4 weeks of treatment as well as by diaries. The complete disappearance of all dyspeptic symptoms after 4 weeks in the placebo group was 36%; ranitidine treatment resulted in a significant improvement after 4 weeks (p < 0.05). The effect of ranitidine was slightly more pronounced in acid-related than in non-acid-related symptoms. We conclude that suppression of gastric acid secretion is of clinical value in NUD patients, especially in those suffering from epigastric pain, acid regurgitation and heartburn.

Adult↗
PubMed1994

[Factors affecting the results of in vitro fertilization. II. The effect of andrologic factors].

We studied 297 couples in our IVF and ET programme and male factor was present in 113 cases (38%). The parameters of standard spermiograms cannot predict the fertilization potential of the specimen in vitro. However, we could demonstrate that the number of the sperm cells after the swim-up procedure correlates very well with the fertilization rate in vitro and pregnancy rate (fertilization rate 63.6% vs. 27.7% in couples with less than 1 million spermcells/ml after swim-up, pregnancy rate 20.2% vs. 5.0%). In these cases the use of the more sophisticated laboratory methods is indicated.

Female↗
PubMed1994

[Factors affecting the results of in vitro fertilization--I. The effect of age].

Age is a major factor affecting the results of IVF and ET. We studied the results of 697 couples treated in our programme of in vitro fertilisation and embryotransfer. We demonstrated increasing numbers of cancelled cycles in older women--the cancellation rate was 17.7% in patients under thirty and 50% in women 38-40 years old. The cut-off line of effectivity is the age of 36-37 years. In women aged 38 and older we demonstrated a decrease of pregnancy rate per transfer from 25.5% to 14-16%. However, there was no higher pregnancy loss in older women in our series.

Adult↗
PubMed1994

Effects of ibuprofen lysinate and acetylsalicylic acid on gastric and duodenal mucosa. Randomized single-blind placebo-controlled endoscopic study in healthy volunteers.

Acetylsalicylic acid (ASA, CAS 50-78-2) and ibuprofen (IB) are commonly used over-the-counter drugs for short-term treatment of pain of different origin. Ibuprofen lysinate (IBL, CAS 57469-76-8) is a water soluble form of ibuprofen for rapid absorption. This single blind, randomized, controlled study compared the incidence and severity of irritation of gastric and duodenal mucosa in normal healthy subjects (n = 45) following administration of IBL (Dolormin) 800 mg/d, ASA 2000 mg/d or placebo for 3 consecutive days. Gastric and duodenal mucosal injury were assessed endoscopically using a severity scale of 0-4 for mucosal erosions and mucosal hemorrhages. Mean gastric hemorrhage and erosion scores for ASA and IBL were significantly higher than those for placebo. In addition, ASA was found to be significantly more irritating to gastric mucosa than IBL, in both the incidence and severity of gastric erosions. No duodenal hemorrhages were detected in this study. The incidence of duodenal erosions was significantly higher in the ASA group (64%) than in both the IBL (6%) and placebo groups (0%) which were not significantly different. Only one subject (in the placebo group) reported an adverse experience (mild headache) during the study. The data suggest that both active treatments are more injurious to the gastric mucosa than placebo when given for 3 days to normal healthy volunteers, but that IBL 800 mg/d is significantly less injurious to the gastric and duodenal mucosa than ASA 2000 mg/d.

Adult↗
PubMed1994

[Circadian aspects of acetylsalicylic acid induced injury and protective effect of ranitidine on the the upper gastrointestinal tract].

Circadian Aspects of Acetylsalicylic Acid Induced Injury and Protective Effect of Ranitidine on the Upper Gastrointestinal Tract. In a randomised parallel double-blind study the gastric and duodenal effects of 300 mg acetylsalicylic acid (ASA, CAS 50-78-2) daily in the presence and absence of 150 mg ranitidine (Zantic, CAS 66357-35-5) daily was evaluated in 32 healthy volunteers undergoing upper gastrointestinal endoscopy. Drugs were taken over a period of 7 days either at 8 a.m. (n = 16) or at 8 p.m. (n = 16). Endoscopic controls were performed at entry and repeated after 7 days of treatment. At entry both groups showed comparable mucosal damages: 8 a.m. group: ASA/placebo 0.8 +/- 0.1 (stomach) and 0.1 +/- 0.1 (duodenum): ASA/ranitidine 1.0 +/- 0.0 (stomach) and 0.07 +/- 0.06 (duodenum). 8 p.m. group: ASA/placebo 0.9 +/- 0.06 (stomach) and 0.1 +/- 0.09 (duodenum). ASA/ranitidine 0.8 +/- 0.08 (stomach) and 0.07 +/- 0.06 (duodenum). After 7 days of treatment the lesions score increased in the ASA/Placebo group in the 8 a.m. group to 9.1 +/- 1.1 (stomach) and 2.7 +/- 1.0 (duodenum), and in the 8 p.m. group to 10.9 +/- 1.1 (stomach) and to 3.9 +/- 0.9 duodenum). The corresponding values in the ASA/ranitidine group were 2.6 +/- 0.8 (stomach) and 0.2 +/- 0.08 (duodenum) (8 a.m.) and 4.8 +/- 0.8 (stomach) and 0.3 +/- 0.1 (duodenum) (8 p.m.). There was no statistical difference between the morning- and the evening dose of ASA. In addition, ranitidine protection was also time-independent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Transmembrane mobility and distribution of phospholipids in the membrane of mouse beta-thalassaemic red blood cells.

Using spin-labelled lipid analogues, the transmembrane mobility and distribution of phospholipids in normal and beta-thalassaemic murine red blood cells were investigated. The velocities of spin-labelled phosphatidylserine (PS*) and spin-labelled phosphatidylethanolamine (PE*) active transport into the inner leaflet were not significantly different between normal and pathological cells. The stationary distribution of PE* in thalassaemic erythrocytes (79.5 +/- 2.0% inside) differed from that of control cells (91.1 +/- 1.6% inside), while that of PS* was unaffected. In thalassaemic cells the passive diffusion of spin-labelled phosphatidylcholine (PC*) was accelerated 4-fold and its stationary distribution was shifted to 34.5 +/- 2.3% inside compared to 19.5 +/- 1.6% in control cells. Spin-labelled sphingomyelin (SM*), which showed no inward movement in normal cells, diffused partially towards the inner leaflet of thalassaemic erythrocyte membranes. These results indicate that modifications of the transverse lipid organisation in beta-thalassaemic red blood cells are due to changes in passive diffusion movements, and not to changes in aminophospholipid translocase activity.

Animals↗
PubMed1993

[A comparison of the gastroduodenal tolerance of ticlopidine and acetylsalicylic acid].

Changes in the gastroduodenal mucosa caused by 250 mg ticlopidine twice daily (group 1; n = 12) or 300 mg aspirin daily (group 2; n = 12) were compared in a randomized double-blind trial of 24 healthy men, aged 20 to 35 years. An oesophago-gastroduodenoscopy was performed before and after either drug had been taken for 7 days. Results were tabulated according to a uniform scoring system (normal mucosa, erythema, petechiae, erosions, ulcer, and blood in the lumen). Both groups had identical scores at the start of the trial (group 1: 0.9 +/- 0.1; group 2: 0.8 +/- 0.1). After the seven days, the score in group 2 had risen to 9.7 +/- 1.5 (median 9.0), while it had hardly changed in group 1 (1.7 +/- 0.5; median 1.0), a statistically significant difference (P < 0.05). The data indicate that ticlopidine is better tolerated by the gastroduodenal mucosa than low dosage aspirin.

Adult↗
PubMed1993

Mathematical modelling of lipid transbilayer movement in the human erythrocyte plasma membrane.

A model is presented to simulate transverse lipid movement in the human erythrocyte membrane. The model is based on a system of differential equations describing the time-dependence of phospholipid redistribution and the steady state distribution between the inner and outer membrane monolayer. It takes into account several mechanisms of translocation: (i) ATP-dependent transport via the aminophospholipid translocase; (ii) protein-mediated facilitated and (iii) carrier independent transbilayer diffusion. A reasonable modelling of the known lipid asymmetry could only be achieved by introducing mechanism (iii). We have called this pathway the compensatory flux, which is proportional to the gradient of phospholipids between both membrane leaflets. Using realistic model parameters, the model allows the calculation of the transbilayer motion and distribution of endogenous phospholipids of the human erythrocyte membrane for several biologically relevant conditions. Moreover, the model can also be applied to experiments usually performed to assess phospholipid redistribution in biological membranes. Thus, it is possible to simulate transbilayer motion of exogenously added phospholipid analogues in erythrocyte membranes. Those experiments have been carried out here in parallel using spin labeled lipid analogues. The general application of this model to other membrane systems is outlined.

Adenosine Triphosphate↗
PubMed1993

On the confounding effects of phosphor persistence in oscilloscopic displays.

Phosphor persistence has been a source of confounding in studies of temporal integration in vision. We examined the confounding by assessing the effects of the persistence of two commonly-used phosphors (P15 and P31) on performance of a temporal-integration task. In one experiment we eliminated the visibility of phosphor persistence by closing two mechanical shutters upon display termination. In a second experiment we estimated the duration of phosphor persistence by displaying the image behind closed shutters which opened upon display termination. No detectable persistence was every produced by P15 phosphor. By contrast, P31 phosphor produced persistence that lasted several hundred milliseconds even when a veiling light was projected on the screen. We ascribe the earlier instances of confounding to inadequate interpretation of the technical data on phosphor decay.

Humans↗