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Biomedical subjects

J Meyer

Publications and source records attributed to J Meyer.

At least 199 records · Page 11Linked to original sources
PubMed1999

Increased platelet sensitivity toward platelet inhibitors during physical exercise in patients with coronary artery disease.

Generalized atherosclerosis and coronary artery disease (CAD) are associated with endothelial dysfunction and during acute myocardial ischemia platelet activation has been reported. Activated platelets exert activated fibrinogen receptors (GP IIb/IIIa) and express CD 62p being regarded as reliable marker for platelet activation. Patients with angiographically proven CAD performed a bicycle exercise test until the onset of angina or ST-segment depression. We studied the ischemia-induced alterations in fibrinogen binding to activated platelet GP IIb/IIIa receptors and CD 62p expression. Therefore, the basal fibrinogen binding to GP IIb/IIIa and CD 62p expression and the thrombin-concentration for half-maximal platelet activation before and after exercise testing were determined. Additionally, inhibition of thrombin-induced platelet activation by increasing concentrations of the prostacyclin-analog iloprost and the NO-donor SIN-1 was examined. In patients with CAD, a significantly reduced basal activation and a highly significant reduction in sensitivity towards thrombin was measured. The thrombin-induced expression of GP IIb/IIIa and CD 62p was significantly diminished in patients with CAD after physical exercise and their platelets were significantly more sensitive towards the inhibitory effects of iloprost and SIN-1. These data demonstrate a significant reduction in platelet activation in response to physical exercise in patients with CAD and advanced atherosclerosis. Despite exercise induced myocardial ischemia as evidenced by angina and ECG-changes, the platelets are not generally activated, as it could be expected. Thus, patients with myocardial ischemia experienced a reduced platelet activity and enhanced sensitivity towards prostacyclin (PGI2) and nitric oxide, probably due to an augmented release of endogenous platelet inhibitory mediators.

Blood Platelets↗
PubMed1999

Comparison of primary angioplasty with conservative therapy in patients with acute myocardial infarction and contraindications for thrombolytic therapy. Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) Study Group.

The benefit of primary angioplasty in patients with acute myocardial infarction (AMI) and contraindications for thrombolysis compared to a conservative regimen is still unclear. Out of 5,869 patients with AMI registered by the MITRA trial, 337 (5.7%) patients had at least one strong contraindication for thrombolytic therapy. Out of these 337 patients 46 (13.6%) were treated with primary angioplasty and 276 (86.4%) were treated conservatively. Patients treated conservatively were older (70 years vs. 60 years; P=0.001), had a higher rate of a history with chronic heart failure (14.8% vs. 4.4%; P=0.053), a higher heart rate at admission (86 beats/min vs. 74 beats/min; P=0.001), and a higher prevalence of diabetes mellitus (27.1% vs. 12.8%; P=0.056). Patients treated with primary angioplasty received more often aspirin (91.3% vs. 74.6%; P=0.012), beta-blockers (60.9% vs. 46.1%; P = 0.062), angiotensin converting enzyme (ACE) inhibitors (71.7% vs. 44%; P=0.001), and the so-called optimal adjunctive medication (54.4% vs. 32.3%; P=0.004). Hospital mortality was significantly lower in patients who received primary angioplasty (univariate: 2.2% vs. 24.7%; P=0.001; multivariate: OR=0.46; P=0.0230). In patients with AMI and contraindications for thrombolytic therapy, primary angioplasty was associated with a significantly lower mortality compared to conservative treatment. Therefore, hospitals without the facilities to perform primary angioplasty should try to refer such patients to centers with the facilities for such a service, if this is possible in an acceptable time.

Aged↗
PubMed1999

A new thrombectomy catheter device (AngioJet) for the disruption of thrombi: An in vitro study.

In this study we examined a new thrombectomy catheter device. Different kinds of in vitro generated thrombi and cadaver thrombi were disrupted in test tubes. The mean disruption rate (and disruption time for 1 g of thrombus) was 225 +/- 65 mg/sec (5 +/- 2 sec) for whole-blood, 117 +/- 60 mg/sec (12 +/- 9 sec) for fibrin, 41 +/- 18 mg/sec (30 +/- 18 sec) for mixed, 70 +/- 42 mg/sec (17 +/- 5 sec) for unorganized, 45 +/- 8 mg/sec (22 +/- 4 sec) for partly, and 5 +/- 1 mg/sec (216 +/- 29 sec) for completely organized cadaver thrombi (P < 0.05). More than 99% of fragmented particles of whole-blood thrombi were 0-12 microm in diameter. The particle size of fibrin, mixed, and cadaver thrombi was similar, with 25%-40% of particles between 0-12 microm, 55%-71% >12-24 microm, and 2%-7% >24 microm. The device may be effectively used in the therapy of massive pulmonary embolism or acute peripheral and coronary artery syndromes when medical thrombolysis is contraindicated and organization of thrombus is absent. Further studies need to be performed to investigate the potential effects of particle microembolization. Cathet. Cardiovasc. Intervent. 47:381-389, 1999.

Cadaver↗
PubMed1999

[Venous paradoxical air embolism].

Paradoxical air embolism may occur with any venous air embolism. Air may either enter the systemic circulation through a patent foramen ovale or through transpulmonary passage of air. While small venous air emboli are mostly well tolerated, even the smallest paradoxical air emboli can have fatal consequences in the systemic circulation. Therapy and prophylaxis of paradoxical air embolism equal those of venous air embolism. This is especially true, since paradoxical air embolism may not become obvious under general anesthesia. More specific therapeutic regiments, such as hyperbaric oxygenation and the infusion of perfluorocarbons, are still in an experimental stage.

Embolism, Air↗
PubMed1999

[Diagnosis of an intramyocardial hematoma via MRI after a traumatic myocardial infarct].

Traumatic cardiac lesions occur in about 30% of all traumatized patients, in most cases they are due to traffic accidents. We report a patient who suffered from a traumatic anterior wall infarction following a ski accident. Consecutively, an extended intramyocardial hemorrhage occurred. A left ventricular pseudoaneurysm was considered first by echocardiography. Using MRI, an intramyocaridal hemorrhage could be diagnosed because of a thin myocardial border surrounding the hematoma. Consecutively, the patient underwent CABG surgery as well as a resection of the intramyocardial hematoma. This diagnosis could be manifested surgically and histologically.

Aged↗
PubMed1999

[Left ventricular remodeling after aortic valve replacement].

The aim of the study was the assessment of left ventricular (LV) systolic function and left ventricular mass following aortic valve replacement (AVR) due to aortic valve stenosis as well as the influence of regression of LV hypertrophy in patients with normal and impaired LV systolic function prior to surgery. 74 patients with severe aortic valve stenosis (29 female, 45 male, mean age 66 +/- 18 years) were divided into 2 groups according to LV ejection fraction (EF): Group 1 with EF > 50% (n = 40); Group 2 with EF < or = 50% (n = 34). Furthermore, patients were differentiated into a group A without (n = 53) and a group B with aortic regurgitation (< or = II degrees, n = 21). All patients were examined by transthoracic echocardiography before and 1 month after surgery. There was a significant decrease of LV enddiastolic and endsystolic volume indices following AVR in group 2 and group B. Patients with preoperatively lower EF (group 2) showed an increase in LV ejection fraction from 39 +/- 10% before AVR to 47 +/- 11% after AVR (p < 0.001), whereas patients with preoperative normal EF (group 1) showed a significant decrease in EF (from 62 +/- 8% to 57 +/- 10%, p < 0.05). Also patients with combined aortic valve disease before AVR had an increase of EF after surgery (from 45 +/- 14% to 56 +/- 14%, p < 0.03). There were significant decreases of interventricular septum thickness and LV posterior wall thickness in group 1 and group A, whereas a significant decrease of LV enddiastolic diameter index was noted only in group B. Improvement of the NYHA functional class could be demonstrated in group 2 from 2.8 +/- 0.7 before to 2.2 +/- 0.6 after AVR, as well as in group B from 2.9 +/- 0.7 before to 1.9 +/- 0.7 after surgery. In conclusion, patients with impaired LV function or combined aortic valve disease showed a significant improvement of left ventricular systolic function after AVR, while patients with normal LV function presented a slight decrease of EF. There was a significant regression of left ventricular muscle mass in all groups independent of the left ventricular functional status.

Adult↗
PubMed1999

[Quantitative detection of changes in the thoracic aorta in patients with chronic aortic dissection using transesophageal echocardiography].

The aim of this serial 3 year follow-up study in 42 clinically stable patients with chronic aortic dissection was to assess quantitatively morphologic changes of the descending thoracic aorta (AD) using transesophageal echocardiography (TEE). Communicating dissections (ca) were present in 16/19 patients with operated type I and in 11/23 patients with type III AD whereas 12/23 type III AD according to De Bakey were non-communicating (nc). Diametral enlargement of the disc. thoracic aorta was 4 mm (mean value) at 1 year in all patients, 5.9 mm in type I ca, 7.2 mm in type III ca but only 3.1 mm in type III nc at 3 years. The ratio between true lumen and false lumen (FL) changed in ca AD from 1:2 to 1:3 over the period of 3 years but remained constant at 1:1 in ncAD. Progressive thrombosis of the false lumen (FL) occurred in 76% of patients but complete thrombosis of the FL occurred in only 6% of type I ca, 18% type III ca but in 84% of type III nc patients. Our results confirm observations that non-communicating dissections seem to have a more favorable outcome and less aneurysmal dilatation compared to ca dissection.

Adult↗
PubMed1999

[Intraoperative flow measurement of coronary bypass grafts using the ultrasound transit time flowmeter].

The aim of the study was to compare the mean and maximum flow and the flow pattern of coronary vein grafts (SVG) supplying target vessels of the inferior and lateral wall with internal mammary (IMA) grafts to the left anterior descending artery (LAD). In 21 patients 25 bypass grafts (13/25 SVG, 12/25 IMA) were investigated. Using the transit time ultrasound method, flow was measured every 5 ms and the flow data of 60 s were acquired. The flow pattern showed significant differences between both graft types during their cycle. IMA grafts showed only one peak occurring after 22.1+/-12.3% and the second after 63.4+/-15.5% of their cycle. The mean flow was not different in both graft types (IMA: 45.3+/-27.0 ml/min and SVG: 41.8+/-26.7 ml/min, p = n. s.) as it was the case for the maximum flow (IMS: 98. 4+/-45.2 ml/min and SVG: 75.7+/-55.4 ml/min, p = n. s.). In conclusion, there is a different flow pattern for both graft types concerning the number and the occurrence of flow-peaks in the bypass cycle. The mean and peak flow showed no significant difference.

Adult↗
PubMed1999

[Release of troponin T following PTCA in patients with unstable and stable angina pectoris].

It is still uncertain to what extent PTCA contributes to a rise of the myocardial ischemic marker troponin T. The purpose of this study was to determine the release of troponin T in patients with unstable and stable angina pectoris pre- and post-PTCA. Serial troponin T measurements were performed in 66 patients with unstable angina (group A) and 55 patients with stable angina pectoris (group B) pre-PTCA and 4, 8 and 24 hours post-PTCA. In group A, 39 (59%) patients with unstable angina pectoris showed pathologic troponin T concentrations (troponin T > or = 0.1 ng/ml); in 27 (41%) patients already pre-PTCA the troponin T was elevated beyond the normal values. Medians of troponin T rose from initially 0.045 ng/ml pre-PTCA to a maximum of 0.21 ng/ml 8 hours post PTCA. In group B medians of troponin T were at all times within normal limits; there was no rise in the observation interval. Using the Chi-square test there were statistically significant differences between group A and B regarding the troponin T values pre- and post-PTCA. In group A medians of total creatine kinase ranging between 24 U/L and 30 U/L were to all times within normal limits. Also in group B medians of total creatine kinase were always within normal limits. Statistically significant differences between the two groups could not be shown. Our study could show a difference in the periinterventional course of the ischemic marker troponin T in patients with unstable and stable angina pectoris. The data indicate a PTCA induced reversible ischemia of the cardiac muscle cell with additional release of the cytoplasmatic bound part of troponin T in patients with unstable angina pectoris. Troponin T also appears to be a more sensitive marker of very short myocardial ischemia than creatine kinase.

Adult↗
PubMed1999

Galactose induction in yeast involves association of Gal80p with Gal1p or Gal3p.

Gal1p carries out two functions in the galactose pathway of yeast. It activates Gal4p by interacting with Gal80p--a function that can also served by Gal3p--and it catalyzes the formation of galactose-1-phosphate. Recently, we and others have presented biochemical evidence for complex formation between Gal1p and Gal80p. Here, we extend these data and present genetic evidence for an interaction between Gal1p and Gal80p in vivo, using a two-hybrid assay. Interaction between Gal1p and Gal80p depends on the presence of galactose, but not on the catalytic activity of Gal1p. A new class of Kluyveromyces lactis mutants was isolated, designated Klgal1-m, which have lost the derepressing activity but retain galactokinase activity, indicating that the two Gal1p activities are functionally independent. The KlGal1-m proteins are defective in their ability to interact with Gal80p in a two-hybrid assay. The locations of gall-m mutations identify putative interaction sites in Gal1p and Gal80p. A dominant mutation, KlGAL1-d, leads to a high level of constitutive expression of genes of the galactose pathway. The behavior of chimeric proteins consisting of Gal3p and KlGal1p sequences indicates that both the N-terminal and C-terminal halves of KlGal1p are involved in specific interaction with KlGal80p.

Alleles↗
PubMed1999

Mosaicism for a serotonin transporter gene promoter-associated deletion: decreased recombination in depression.

Transcriptional activity of the human serotonin transporter gene (5HTT) is modulated by complex interaction of multiple genomic and cellular factors. Variability of a polymorphic repetitive element (5HTTLPR) is associated with anxiety, depression, and aggression-related traits and may influence the risk to develop affective spectrum disorders. 5HTTLPR variants display a unique DNA secondary structure that has the potential to regulate the transcriptional activity of the associated 5HTT promoter. The structure of the 5HTTLPR is also likely to precipitate a 381-bp somatic deletion in the 5HTT's promoter region [del(17)(q11.2)] that is observed in 20-60% of genomic DNA isolated from mononuclear blood cells and postmortem brain. The localization of the deletion breakpoints adjacent to identical putative signal sequences (CAGCC) suggests a V(D)J recombinase-like rearrangement event. In comparison with healthy controls, del(17)(q11.2)/wildtype sequence ratios showed a decrease of the deleted variant in recurrent unipolar depression. Our results also suggest that mosaicism of del(17)(q11.2) is likely to be regulated by tissue-specific as well as 5HTTLPR-dependent mechanisms. The findings confirm that the pericentric region of human chromosome 17 is highly unstable and furnishs additional evidence for intricate complexity of 5HTT regulation under physiological condition and in disease.

Adult↗
PubMed1999

The [2Fe-2S] protein I (Shetna protein I) from Azotobacter vinelandii is homologous to the [2Fe-2S] ferredoxin from Clostridium pasteurianum.

The [2Fe-2S] protein from Azotobacter vinelandii that was previously known as iron-sulfur protein I, or Shethna protein I, has been shown to be encoded by a gene belonging to the major nif gene cluster. Overexpression of this gene in Escherichia coli yielded a dimeric protein of which each subunit comprises 106 residues and contains one [2Fe-2S] cluster. The sequence of this protein is very similar to that of the [2Fe-2S] ferredoxin from Clostridium pasteurianum (2FeCpFd), and the four cysteine ligands of the [2Fe-2S] cluster occur in the same positions. The A. vinelandii protein differs from the C. pasteurianum one by the absence of the N-terminal methionine, the presence of a five-residue C-terminal extension, and a lesser number of acidic and polar residues. The UV-visible absorption and EPR spectra, as well as the redox potentials of the two proteins, are nearly identical. These data show that the A. vinelandii FeS protein I, which is therefore proposed to be designated 2FeAvFdI, is the counterpart of the [2Fe-2S] ferredoxin from C. pasteurianum. The occurrence of the 2FeAvFdI-encoding gene in the nif gene cluster, together with the previous demonstration of a specific interaction between the 2FeCpFd and the nitrogenase MoFe protein, suggest that both proteins might be involved in nitrogen fixation, with possibly similar roles.

Amino Acid Sequence↗
PubMed1999

Thrombolysis with saruplase versus streptokinase in acute myocardial infarction: five-year results of the PRIMI trial.

BACKGROUND: Short-term safety and efficacy of thrombolysis with saruplase in acute myocardial infarction have been shown in several trials. To assess long-term outcome of patients treated with saruplase or streptokinase for myocardial infarction, a 5-year follow-up of patients included in the Pro-Urokinase in Myocardial Infarction Trial was performed. METHODS AND RESULTS: Follow-up data are available from 8 centers on 255 (92.4%) of 276 included patients. The 5-year mortality rate was comparable with 20.8% of patients in the saruplase group and 16.9% in the streptokinase group (odds ratio 1.29, 95% confidence interval 0.69 to 2.42). In both groups, a considerable number of fatal cardiovascular events occurred more than 1 year after study inclusion. Rates of percutaneous transluminal coronary angioplasty and coronary artery bypass grafting were comparable in both groups. Reinfarction within 5 years occurred in 19.0% of patients in the saruplase group and tended to be less frequent at 10.8% after streptokinase treatment (odds ratio 1.94, 95% confidence interval 0.98 to 3.84). In both groups, the majority of reinfarctions took place more than 3 months after study inclusion. The 5-year stroke rate was 3.6% and 7.2% in the saruplase and streptokinase groups, respectively (odds ratio 0.49, 95% confidence interval 0.16 to 1.47). Subjective symptoms of heart failure and angina pectoris were comparable in both groups. CONCLUSIONS: Our data are consistent with a similar long-term outcome for patients treated with saruplase or streptokinase. Despite the low-risk profile of the patient cohort, there were considerable adverse event rates over a 5-year period.

Aged↗
PubMed1999

Rhinovirus identification by BglI digestion of picornavirus RT-PCR amplicons.

Rhinoviruses are the main cause of the common cold and precipitate the majority of asthma exacerbations. RT-PCR followed by internal probe hybridisation or Southern blotting, or nested PCRs are currently the most sensitive methods for their identification. However, none of the published techniques can differentiate satisfactorily rhinoviruses from other picornaviruses. Examination of the restriction maps of sequenced rhinoviruses, revealed a highly conserved BglI restriction site (GCCnnnnnGGC), located exactly in the middle of the 380-bp amplicon generated with the OL26-OL27 primer pair, which has been used extensively in the past to identify picornaviruses. Such a site was either not present, or positioned differently in other picornaviruses of known sequence. It was, therefore, considered that digestion of rhinovirus amplicons with this enzyme would result in two equal length fragments, generating a single 190-bp band in gel electrophoresis. In contrast, either one undigested 380-bp band or a double-band pattern would appear in amplicons from other picornaviruses. To test this hypothesis, Bgl digestions of OL26-OL27 amplicons from cultured and wild-type rhinoviruses, whose identity was confirmed by acid lability, as well as from echo, polio and coxsackie viruses were carried out. All rhinovirus samples were digested successfully generating single bands. Among the other picornaviruses, only 6.6% presented a single band pattern, while the rest were as predicted from the model. With a sensitivity of 100% and a specificity over 90%, the method described, which is rapid and remarkably easy to perform, can be used to distinguish rhinoviruses from other picornaviruses to a considerable extent.

Deoxyribonucleases, Type II Site-Specific↗
PubMed1999

The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events.

OBJECTIVES: The impact of infection-associated antiphospholipid antibodies (APA) on endothelial cell activation, blood coagulation and fibrinolysis was evaluated in patients with infective endocarditis with and without major embolic events. BACKGROUND: An embolic event is a common and severe complication of infective endocarditis. Despite the fact that APAs are known to be associated with infectious diseases, their pathogenic role in infective endocarditis has not been clearly defined. METHODS: The relationship among the occurrence of major embolic events, echocardiographic vegetation size, endothelial cell activation, thrombin generation, fibrinolysis and APA was examined in 91 patients with definite infective endocarditis, including 26 patients with embolic events and 65 control subjects without embolic events. RESULTS: Overall, 14.3% of patients exhibited elevated APA levels. Embolic events occurred more frequently in patients with elevated levels of APA than in patients without (61.5% vs. 23.1%; p = 0.008). Patients with elevated levels of APA showed higher levels of prothrombin-fragment F1 +2 (p = 0.005), plasminogen-activator inhibitor 1 (p = 0.0002), von Willebrand factor (p = 0.002) and lower levels of activated protein C (p = 0.001) than patients with normal levels of APA. Thrombin generation and endothelial cell activation were both positively correlated with levels of APA. The occurrence of elevated APA levels was frequently associated with structural valve abnormalities (p = 0.01) and vegetations >1.3 cm (p = 0.002). CONCLUSIONS: Infection-associated elevated APA levels in patients with infective endocarditis are related to endothelial cell activation, thrombin generation and impairment of fibrinolysis. This may contribute to the increased risk for major embolic events in these patients.

Adult↗
PubMed1999

Use of infrared spectroscopy to assess secondary structure of human growth hormone within biodegradable microspheres.

The purpose of this study was to test the utility of infrared (IR) spectroscopy to determine protein secondary structure in biodegradable microspheres. Encapsulation of proteins within biodegradable polymers, [e.g. poly(lactic-co-glycolic acid) (PLGA)] for controlled drug release has recently been the subject of intense research effort. The ability to assess protein integrity after microsphere production is necessary to successfully produce microspheres that release native proteins. We used IR spectroscopy, a noninvasive method-as opposed to conventional organic solvent extraction or in vitro release at elevated temperature-to assess the secondary structure of recombinant human growth hormone (rhGH) within dry and rehydrated microspheres. PLGA microspheres containing rhGH with different excipients were prepared by a conventional double-emulsion method. The protein IR spectra indicated that the encapsulation process could perturb the structure of rhGH and that excipients could inhibit this damage to varying degrees. A strong positive correlation was found between intensity of the dominant alpha-helical band in the spectra of rhGH in rehydrated microspheres and the percent monomer released from microspheres during incubation in buffer. We also studied microspheres prepared with zinc-precipitated rhGH. The addition of Zn2+ during microsphere processing partially inhibited protein unfolding and fostered complete refolding of rhGH upon rehydration. In conclusion, IR spectroscopy can serve as a valuable tool to assess protein structure within both dried and rehydrated microspheres.

Delayed-Action Preparations↗