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Biomedical subjects

O Burghuber

Publications and source records attributed to O Burghuber.

10 recordsLinked to original sources
PubMed1989

Clinical biochemistry of neuron specific enolase.

The soluble brain protein 14-3-2 first described by Moore and McGregor in 1965 is now known to be a cell specific isoenzyme of the glycolytic enzyme enolase (EC 4.2.1.11), designated neuron specific enolase (NSE). It is not only a marker for all types of neurons, but also for all neuroendocrine or paraneuronal cells. The appearance of NSE is a late event in neural differentiation, thus making NSE a useful index of neural maturation. The demonstration that tumors of the nervous system and of neuroendocrine origin contain NSE has promoted the study of NSE as a possible tumor marker. Immunocytochemistry has been used to identify NSE in cytologic preparations from several types of tumors, offering useful indications for differential diagnosis. NSE levels in serum from tumor patients are not useful in the diagnosis of early stage disease. However, serum NSE levels have been shown to be helpful in the identification of advanced small cell lung cancer, neuroblastoma and several other neoplasms. The main use of serum NSE is the monitoring of chemotherapy and the detection of a relapse in these cases.

Biomarkers, Tumor↗
PubMed1984

Lung edema due to hydrogen peroxide is independent of cyclooxygenase products.

Active oxygen species can cause lung injury. Although a direct action on endothelial cells is proposed, the possibility exists that they might cause injury via mediators. We considered that active oxygen species would stimulate the generation of cyclooxygenase metabolites, which then alter pulmonary vasoreactivity and cause edema. We chemically produced hydrogen peroxide by adding glucose oxidase to a plasma- and cell-free, but beta-D-glucose-containing, solution, which perfused isolated rat lungs. Addition of glucose oxidase to the perfusate caused a marked decrease in pulmonary vasoreactivity, accompanied by an increase in the concentrations of prostacyclin, thromboxane A2, and prostaglandin F2 alpha. Pretreatment with catalase, a specific scavenger of hydrogen peroxide, preserved pulmonary vasoreactivity, inhibited the increase of the concentration of the measured prostaglandins, and prevented edema formation. Indomethacin effectively blocked lung prostaglandin production but neither prevented the decrease in vasoreactivity nor inhibited edema formation. From these data we conclude that hydrogen peroxide impaired pulmonary vasoreactivity and subsequently caused edema. Despite the fact that hydrogen peroxide stimulated lung prostaglandin production, cyclooxygenase-derived products neither caused the decrease in vasoreactivity nor the development of edema.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Right ventricular performance in chronic air flow obstruction.

Right ventricular pump performances were assessed in 14 patients with chronic obstructive pulmonary disease by means of radionuclide angiocardiography using krypton-81m as a tracer. Right ventricular ejection fraction (RVEF) was significantly lower in the patients than in normal volunteers. Additionally there was a striking difference in RVEF between patients with normal pulmonary artery pressure (PAP) and those with pathologically elevated PAP. A linear negative correlation between RVEF and mean PAP could be demonstrated. From this data we suggest that radionuclide angiocardiography using krypton-81m allows non invasive assessment of right heart afterload and thus indirectly PAP.

Adult↗
PubMed1981

Decreased prostacyclin sensitivity of human platelets after jogging and squash.

8 healthy male volunteers performed jogging (as an example of an aerobic metabolic condition) and squash (as an example of an intermittently anaerobic metabolic condition). The platelets sensitivity to prostacyclin (PGI2) decreased after jogging. After squash, a statistically significant (p 0,001) decrease in the sensitivity of the platelets could be seen. Our findings suggest that an early alteration of platelet sensitivity might play a key role in maintaining the hemostatic balance and could be of greater importance than the vascular wall PGI2-synthesis, as the sensitivity changes immediately, whereas the PGI2-formation change is a long-term process.

Adult↗
PubMed1979

[Aplastic anemia following indomethacin therapy].

A 78 year old woman developed non-fatal pure red cell aplasia after taking Indomethacin for a long period. We gave the patient red cell transfusions and treated her with Methylprednisolon. Approximately 3 months after discontinuation of Indomethacin the patient felt well and blood picture was normal.

Aged↗
PubMed1979

[Thrombocyte function and systemic effect of prostaglandin I2 inhalation].

After inhalation of prostaglandin I2 minimal effects on lung function and the cardiovascular system could be observed in healthy volunteers. Platelet function, however, decreased significantly. In the future the application of the prostaglandin I2 may be a new approach in the treatment of thromboembolic disorders in man.

Adult↗
PubMed1977

[Effects of experimental hypovolaemic shock on platelets in the pig (author's transl)].

The effects of standardized blood loss on the platelets, as well as on coagulation, fibrinolysis and complement parameters were studied in the pig. A simultaneous fall in arterial and venous platelet counts was demonstrated during the initial phase of blood loss, with a concomitat rise in pulmonary vascular resistance. After exsanguination to the extent of about 40% of the blood volume, the arterial platelet counts increased significantly, whilst the pulmonary vascular resistance, which was negatively correlated with the arterial platelet counts throughout the experiment, fell. Venous platelet counts, on the other hand, remained low during this experimental period and were correlated with cardiac output, but not with pulmonary vascular resistance.

Animals↗