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Biomedical subjects

M Binder

Publications and source records attributed to M Binder.

At least 127 records · Page 7Linked to original sources
PubMed1997

Double-blind trial of botulinum A toxin for the treatment of focal hyperhidrosis of the palms.

We performed a randomized double-blind study within-group comparison in 11 patients to study the effect of subcutaneous injections of botulinum A toxin in focal hyperhidrosis of the palms. A total dose of 120 mU (mouse units) of botulinum A toxin (Dysport) was injected into six different sites on one palm, whereas the other was injected with sterile saline. Objective quantification of sweat production was performed using digitized ninhydrin-stained sheets. Three weeks after treatment, the mean reduction of sweat production in the botulinum A toxin-treated palms was 26% (P < 0.001), after 8 weeks 26% (P = 0.002) and after 13 weeks 31% (P < 0.001). Subjective assessment of sweat production by the patients using a visual analogue scale showed a 38% improvement in the botulinum A toxin-treated palms at 3 weeks (P = 0.002), 40% at 8 weeks (P = 0.002) and 38% at 13 weeks (P = 0.002). Neither the objective measurement nor the subjective rating showed a statistically significant reduction of sweating in the placebo-treated palms. Three patients reported reversible minor weakness of powerful handgrip after injection at the toxin-treated site, lasting between 2 and 5 weeks.

Adult↗
PubMed1997

Arg506 to Gln mutation in the factor V gene causes poor fibrinolytic response in children after venous occlusion.

To determine to what extent the Arg506 to Gln mutation in the factor V gene influences the fibrinolytic response after 20 min venous occlusion (VO) we investigated a population of APC resistant children (n = 60) and a group of age-matched healthy controls (n = 25). After 20 min VO, symptomatic (n = 30) carriers of the common factor V mutation showed significantly reduced t-PA activities compared with asymptomatic (n = 30) carriers (p <0.0001) and healthy controls (p <0.0001). In contrast, PAI 1 activity was significantly (p <0.0001) higher before and after VO in children with the factor V mutation compared with healthy children. No difference was found between symptomatic and asymptomatic probands. A significantly lower PAI 1 antigen decrease along with a lower t-PA antigen release was found in the APC resistant children compared with the controls. No significant difference was seen between individuals with and without previous vascular insults. As the lack of t-PA activity after VO in symptomatic carriers is the most conspicuous result, we suggest that the factor V gene mutation itself might induce the fibrinolytic impairment by increasing the thrombin levels and thus increasing the recently described thrombin-activable fibrinolysis inhibitor (TAFI).

Arginine↗
PubMed1996

The CBFbeta subunit is essential for CBFalpha2 (AML1) function in vivo.

The CBFbeta subunit is the non-DNA-binding subunit of the heterodimeric core-binding factor (CBF). CBFbeta associates with DNA-binding CBFalpha subunits and increases their affinity for DNA. Genes encoding the CBFbeta subunit (CBFB) and one of the CBFalpha subunits (CBFA2, otherwise known as AML1) are the most frequent targets of chromosomal translocations in acute leukemias in humans. We and others previously demonstrated that homozygous disruption of the mouse Cbfa2 (AML1) gene results in embryonic lethality at midgestation due to hemorrhaging in the central nervous system and blocks fetal liver hematopoiesis. Here we demonstrate that homozygous mutation of the Cbfb gene results in the same phenotype. Our results demonstrate that the CBFbeta subunit is required for CBFalpha2 function in vivo.

Alleles↗
PubMed1996

Creatine kinase-mb fraction and cardiac troponin T to diagnose acute myocardial infarction after cardiopulmonary resuscitation.

OBJECTIVES: This study sought to evaluate the diagnostic value of the biochemical markers creatine kinase (CK), creatine kinase-MB fraction (CK-MB) and cardiac troponin T (cTNT) to diagnose acute myocardial infarction (AMI) after cardiopulmonary resuscitation (CPR). BACKGROUND: Elevations of CK and CK-MB after CPR are a frequent finding and might be associated with ischemic myocardial injury, as well as physical trauma to the chest. METHODS: Patients who had cardiac arrest and primary successful resuscitation were included in the study. The diagnosis of AMI was confirmed or ruled out by means of typical electrocardiographic findings, thallium-201 myocardial scintigraphy or autopsy, if death occurred during the hospital period, in 39 primary survivors of sudden cardiac death. In 24 patients (62%) the diagnosis of AMI was established. Serum cTNT, CK and CK-MB were measured, and the CK-MB/CK ratio was calculated on admission and after 12 h. RESULTS: On admission all markers of myocardial injury proved to be weak methods for the diagnosis of AMI. After 12 h cTNT as well as CK-MB exhibited a similar diagnostic performance; CK and the CK-MB/CK ratio proved to be worthless. Sensitivity and specificity for a cTNT cutoff value of 0.6 ng/ml, 12 h after cardiac arrest, were 96% and 80%, respectively. For a CK-MB cutoff value of 26 U/liter, sensitivity was 96% and specificity was 73%. CONCLUSIONS: Cardiac TNT and CK-MB are valuable tools in detecting AMI as the cause of sudden cardiac death. However, there is a considerable lack of sensitivity and specificity. Cardiac injury is probably caused not only by AMI, but also by myocardial damage related to CPR efforts.

Animals↗
PubMed1996

103Pd brachytherapy and external beam irradiation for clinically localized, high-risk prostatic carcinoma.

PURPOSE: To summarize biochemical failure rates and morbidity of external beam irradiation (EBRT) combined with palladium (103Pd) boost for clinically localized high-risk prostate carcinoma. METHODS AND MATERIALS: Seventy-three consecutive patients with stage T2a-T3 prostatic carcinoma were treated from 1991 through 1994. Each patient had at least one of the following risk factors for extracapsular disease extension: Stage T2b or greater (71 patients), Gleason score 7-10 (40 patients), prostate specific antigen (PSA) > 15 (32 patients), or elevated prostatic acid phosphatase (PAP) (17 patients). Patients received 41 Gy EBRT to a limited pelvic field, followed 4 weeks later by a 103Pd boost (prescription dose: 80 Gy). Biochemical failure was defined as a PSA greater than 1.0 ng/ml (normal < 4.0 ng/ml). Patients whose PSA was still decreasing at the last follow-up were censored at that time. Patients whose PSA plateaued at a value greater than 1.0 were scored as failures at the time the PSA first plateaued. RESULTS: The overall, actuarial freedom from biochemical failure at 3 years after treatment was 79%. In Cox proportional hazard multivariate analysis, the strongest predictor of failure was elevated acid phosphatase (p = 0.04), followed by PSA (p = 0.17), Stage (p = 0.23), and Gleason score (p = 0.6). Treatment-related morbidity was usually limited to temporary, RTOG Grade 1-2 urinary symptoms. One patient, who had both a transurethral incision of the prostate (TUIP) and a transurethral resection of the prostate (TURP), developed low-volume urinary incontinence. The actuarial potency rate at 3 years after implantation was 77% for 46 patients who were sexually potent prior to implant. CONCLUSION: Biochemical freedom from failure rates following combined EBRT and 103Pd brachytherapy for clinically localized, high-risk prostate cancer compare favorably with that reported after conventional dose EBRT alone. Morbidity has been acceptable.

Aged↗
PubMed1996

Pip2p: a transcriptional regulator of peroxisome proliferation in the yeast Saccharomyces cerevisiae.

In Saccharomyces cerevisiae, peroxisomes are the exclusive site for the degradation of fatty acids. Upon growth with the fatty acid oleic acid as sole carbon source, not only are the enzymes of beta-oxidation and catalase A induced, but also the peroxisomal compartment as a whole increases in volume and the number of organelles per cell rises. We previously identified a cis-acting DNA sequence [oleate response element (ORE)] involved in induction of genes encoding peroxisomal proteins. The aim of our investigation was to test whether a single mechanism acting via the ORE coordinates the events necessary for the proliferation of an entire organelle. Here we report the cloning and characterization of the oleate-specific transcriptional activator protein Pip2p (pip: peroxisome induction pathway). Pip2p contains a typical Zn(2)-Cys(6) cluster domain and binds to OREs. A pip2 deletion strain is impaired in growth on oleate as sole carbon source and the induction of beta-oxidation enzymes is abolished. Moreover, only a few, small peroxisomes per cell can be detected. These results indicate that fatty acids activate Pip2p, which in turn activates the transcription of genes encoding beta-oxidation components and acts as the crucial activator of peroxisomes.

Amino Acid Sequence↗
PubMed1996

Disruption of the Cbfa2 gene causes necrosis and hemorrhaging in the central nervous system and blocks definitive hematopoiesis.

The CBFA2 (AML1) gene encodes a DNA-binding subunit of the heterodimeric core-binding factor. The CBFA2 gene is disrupted by the (8;21), (3;21), and (12;21) chromosomal translocations associated with leukemias and myelodysplasias in humans. Mice lacking a CBF alpha 2 protein capable of binding DNA die between embryonic days 11.5 and 12.5 due to hemorrhaging in the central nervous system (CNS), at the nerve/CNS interfaces of cranial and spinal nerves, and in somitic/intersomitic regions along the presumptive spinal cord. Hemorrhaging is preceded by symmetric, bilateral necrosis in these regions. Definitive erythropoiesis and myelopoiesis do not occur in Cbfa2-deficient embryos, and disruption of one copy of the Cbfa2 gene significantly reduces the number of progenitors for erythroid and myeloid cells.

Animals↗
PubMed1996

Creatine kinase and creatine kinase-MB release after nontraumatic cardiac arrest.

The aim of the study was to describe the course of serum creatine kinase (CK) and its MB fraction (CK-MB) in patients surviving cardiac arrest, and to identify factors influencing CK and CK-MB release. The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation, collected within a period of 33 months, were evaluated retrospectively and compared with laboratory blood investigations collected prospectively (on admission and after 6, 12, and 24 hours) in 107 adult patients surviving a witnessed cardiac arrest for 24 hours. CK and CK-MB were elevated in >75% of the patients within 24 hours. Release of CK and CK-MB was mainly associated with electrocardiographic evidence of acute myocardial infarction (AMI) cumulative energy administered during defibrillation, and duration of chest trauma by compression. The CK-MB/CK ratio was elevated in 32% of the patients. Of patients with electrocardiographic evidence of AMI, only 49% had an elevated CK-MB/CK ratio. In conclusion, the elevation in serum CK and CK-MB fraction in patients after nontraumatic cardiac arrest is a frequent finding, and is associated with ischemic myocardial injury, as well as physical trauma to the chest. This should be considered when interpreting the course of CK and CK-MB fraction for the diagnosis of AMI.

Adult↗
PubMed1996

Impaired hemorheology in patients with postmastectomy lymphedema.

Lymphedema of the arm is one of the most disabling and serious complications of breast cancer. Apart from tumor infiltration or fibrosis of lymphatic pathways, little is known about factors favoring the development of lymphedema. In the present study, we investigated the impact of rheologic parameters, e.g. red cell aggregation (EA) and plasma viscosity (PV), and of capillary morphology and capillary flow in patients with breast cancer with (n = 18) and without (n = 18) lymphedema. Patients with lymphedema showed a significant increase of red cell aggregation (p < 0.001) that indicates a systemic component of lymphedema and might offer a possibility of prevention and therapy of this condition. A hitherto unclassified protein factor favoring red cell aggregation and lymphedema might be postulated.

Aged↗
PubMed1996

Immunogold labeling of yeast cells: an efficient tool for the study of protein targeting and morphological alterations due to overexpression and inactivation of genes.

Immunogold labeling on Lowicryl HM20 resin sections is a valuable complement to biochemical methods as well as methods of molecular biology in the study of basic mechanisms in the yeast system. This contribution presents an overview of the state of the art. Emphasis is put on the explanation of caveats and pitfalls rather than on detailed bench protocols. In the Applications section the morphological aspect of genetic manipulation is accentuated and links to human pathology are indicated. The morphological consequences of genetic manipulations may gain importance in view of the efforts made to establish gene therapies. In particular, the contribution of immunoelectron microscopy to the elucidation of peroxisomal targeting signals and to the detection and identification of morphological alteration due to overexpressed, mutated or deleted genes in the context of peroxisome biogenesis is described.

Animals↗
PubMed1996

Hemodynamic effects of active compression-decompression after prolonged CPR.

BACKGROUND: This study was designed to test the effects of active compression-decompression (ACD) versus standard (STD) cardiopulmonary resuscitation (CPR) on hemodynamics after prolonged cardiac arrest (CA). METHODS AND RESULTS: After nontraumatic prehospital CA, 21 patients were resuscitated in a prospective nonblinded setting sequentially with STD and ACD CPR at the emergency department, if it had not been possible to achieve restoration of spontaneous circulation (ROSC) before admission. The compression rate was 80/min with a 50% duty cycle, and 1 mg epinephrine was given every 5th min. Invasive arterial, central venous pressure and end tidal CO2 (ETCO2) were monitored. Comparing coronary perfusion pressure (CoPP) and ETCO2, no significant differences between STD and ACD CPR were found. In 3 cases ROSC could be achieved for a short time. CONCLUSIONS: In our study, a comparison of STD and ACD CPR revealed no significant differences in coronary perfusion pressures and ETCO2. We conclude that after prolonged CA, ACD CPR does not provide an apparent hemodynamic advantage over STD CPR.

Aged↗
PubMed1996

Usefulness of a new rapid bedside troponin T assay in patients with chest pain.

We evaluated the usefulness of a rapid, qualitative, bedside immunoassay for cardiac-specific troponin T in patients with chest pain. A concordant result between quantitative troponin T and qualitative troponin T assay was observed in 183 (96%) tests. The sensitivity of the rapid troponin T assay for detecting acute myocardial infarction increased significantly according to the number of hours elapsed after onset of chest pain from 17% for patients presenting within 4 h to 71% for patients presenting in the time interval of greater than 8 h from onset of chest pain (P < 0.001). Specificity ranged from 83 to 93% in the three time intervals evaluated. A concordant result between CK-MB-measurement and rapid troponin T assay was observed in 159 (83%) tests. In 14/191 tests a positive rapid troponin T and a negative CK-MB assay was observed. In 9/14 (64%) cases this result was true positive for the rapid troponin T assay and in 5/14 (36%) cases false negative. As sensitivity and specificity of the rapid troponin T assay are comparable with CK-MB measurements, rapid troponin T assay is a simple and useful laboratory tool for the bedside triage in patients with chest pain.

Adult↗
PubMed1996

Assessment of myocardial injury by serum tumour necrosis factor alpha measurements in acute myocardial infarction.

Clinical and experimental data have shown that after acute myocardial infarction there is a significant release of tumour necrosis factor alpha. Therefore, an attempt was made to correlate changes in serum tumour necrosis factor alpha concentrations with indices of infarct extent in patients with acute myocardial infarction. In 50 patients with acute myocardial infarction, blood samples for evaluation of tumour necrosis factor alpha and alpha-hydroxybutyrate-dehydrogenase were collected every 6 h until 120 h after admission. Infarct extent was estimated by clinical parameters such as the occurrence of heart failure and rhythm disturbances, by enzymatic methods such as cumulative release of alpha-hydroxybutyrate-dehydrogenase and imaging techniques, by late resting single photon emission tomography--201 thallium scintigraphy--using an extent score and by echocardiography using a wall motion index. The maximum change in serum tumour necrosis factor alpha after infarction (delta TNF) was calculated by subtracting tumour necrosis factor alpha concentration on admission from peak tumour necrosis factor alpha concentration. The average peak tumour necrosis factor alpha level was observed 84 h after admission (median: 12 pg.ml-1). Between the 72nd and the 96th h no significant changes in tumour necrosis factor alpha values were observed. Analysis of the data showed that larger delta (TNF) values were found to be associated significantly with signs of heart failure (P = 0.003), the presence of rhythm disturbances (P = 0.001), increased enzymatic infarct extent indicated by cumulative release of alpha-hydroxybutyrate-dehydrogenase (r = 0.74; P < 0.001), large myocardial perfusion defects measured with 201 thallium scintigraphy (r = 0.80; P < 0.001), and a considerable number of left ventricular wall motion abnormalities (r = 0.57; P < 0.001). In conclusion, delta (TNF) is a reliable method of assessing damage severity in the myocardium after acute myocardial infarction. As only two blood samples are necessary within 84 h, the method may be one of the more convenient for the assessment of infarct size in clinical practice.

Adult↗
PubMed1996

Accuracy and reliability of noninvasive continuous finger blood pressure measurement in critically ill patients.

OBJECTIVE: To evaluate the accuracy and reliability of noninvasive continuous finger blood pressure measurement in critically ill patients. DESIGN: Prospective data collection. SETTING: Emergency department in a 2,000-bed hospital. PATIENTS: Thirty-nine patients admitted to the emergency department requiring invasive arterial blood pressure monitoring were enrolled to the study protocol. INTERVENTIONS: Continuous noninvasive blood pressure measurement was performed on the middle phalanx of the second and third finger, using a test instrument which provides continuous arterial waveform display with the use of a finger cuff. Invasive mean arterial blood pressure measurement was done by cannulation of the radial artery and direct transduction of the systemic arterial pressure waveform. MEASUREMENTS AND MAIN RESULTS: Three thousand one hundred eighteen pairs of simultaneous finger cuff and intra-arterial blood pressure measurements were collected in 1-min intervals from 39 patients over a total of 51.8 hrs. The overall discrepancy between both measurements was 0.10 mm Hg. The standard deviation of the differences was +/- 5.02 mm Hg. The mean bias in patients treated with catecholamines was 0.01 mm Hg and was not different from the bias observed in patients without catecholamines (mean bias: 0.23 mm Hg; p > .22). Whereas 95% of all comparisons between finger cuff and intra-arterial measurement had a discrepancy < or = +/- 10 mm Hg, 4.7% had a discrepancy between +/- 10.1 to 15 mm Hg and 0.3% exhibited a discrepancy > +/- 15 mm Hg. In 29 (74%) patients, the duration of errors > 10 mm Hg was < or = 1 min. In seven (18%) patients, the duration of errors > 10 mm Hg was between 2 to 3 mins and in three (8%) patients, the errors lasted for > 3 mins. CONCLUSIONS: Our data provide a guide to the accuracy and reliability of noninvasive finger blood pressure measurements in critically ill patients. Although most test instrument measurements were reliable, in 8% of all patients large discrepancies (> 10 mm Hg) between both measurements with a duration of > 3 mins were noted. Concerning the considerable risk for arterial cannulation, our preliminary data demonstrate that the test instrument (PORTAPRES, TNO Biomedical Instrumentation Research Unit; The Netherlands) is an advance in noninvasive monitoring of critically ill patients and may be useful in most emergency clinical settings.

Adult↗