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Biomedical subjects

H Burkhardt

Publications and source records attributed to H Burkhardt.

At least 109 records · Page 6Linked to original sources

Influence of different culture conditions on BLV expression in permanently infected FLK cell lines.

The permanently BLV-infected FLK cell line 44/2 and FLK sublines were tested for the stability of their BLV and antigen synthesis by three virus markers, p24, gp51, and activity of reverse transcriptase. The extent of BLV production in the FLK line correlated directly with the surface for cell growth in roller and stationary cultures. The synthesis and secretion of non-virus-associated gp51 is especially stimulated in the roller culture, and is largely independent of the quality of the culture medium. The roller culture allows considerable economy of the medium, at the same time retaining its full biological activity. As much as 2 mg of gp51 per litre of culture supernatant was obtained by this procedure. Appropriate markers for estimation of BLV production are p24 and gp51. For this purpose, the activity of reverse transcriptase on its own was not sufficient. The BLV yield differed by one order of magnitude among the 18 cloned FLK sublines. Three sublines have been identified, which showed a comparatively high virus production, under conditions of stationary cultures. The amount or activity of viral markers could not be correlated with the number of BLV proviruses.

Animals↗

[Therapy of heart failure with combined furosemide retard/triamterene].

20 patients with an average age of 73.3 years suffering from left cardiac insufficiency in stage II to III of the NYHA, who could not be recompensated alone by means of digitalisation, received additionally the diuretic combination furosemide-retard (30 mg)/triamterene (50 mg) for 2 to 3 weeks. Subjective side effects were not observed. The laboratory parameters did not show any substantial changes. A short increase of uric acid and serum creatinine in the older patients returned to normal spontaneously. A decreased potassium level returned to normal; a hyperkaliemia was not observed. The repeated administration of the combination did not lead to any accumulation; only a balanced concentration at a low level appeared. The urine elimination, the decrease in body weight, the regression of the lung congestion and the size of the heart were statistically significant.

Aged↗

[Long-term drug therapy in inflammatory rheumatic diseases using chronic polyarthritis as an example. 2. Basic principles of long-term drug therapy: choice of optimal therapeutic agents].

The article reviews the principles of the long-term drug therapy of rheumatoid arthritis. A nomogram is presented which allows selection of adequate antiphlogistic and long-term drugs according to activity and progression of the disease. Steroids, non-steroidal antiphlogistics, gold, D-penicillamine and azathioprine are described in the order of their application during treatment of a severe polyarticular flare-up. Some of the drug regimens are relevant also to diseases other than rheumatoid arthritis, but drug therapy reflects only a single aspect in the treatment of these diseases and has to be applied together with non-pharmacologic methods (surgery, physical therapy, functional therapy, psychology etc.).

Antimalarials↗

[Proteolytic occurrences in the metabolism of cartilage and their modification by antirheumatics].

Rheumatic diseases are characterized by the progressive loss of articular cartilage. According to a well established hypothesis proteolytic enzymes take part in these events. The initial attack in an normal cartilage can be exerted by proteoglycanases originating from either chondrocytes or cells from outside the cartilage like neutrophilic granulocytes or macrophages. In rheumatoid arthritis these latter cells are found in immediate vicinity to cartilage and it is assumed that they release their enzymes directly into the cartilage. Lysosomal elastase from neutrophilic granulocytes is a key enzyme made responsible for the degradation of cartilage, since it is able to soften up this tissue and thereby to deprive it of its normal mechanical properties. Therefore the pharmacological inactivation of elastase bears a therapeutic potential for rheumatic joint disease. The ultimate value of enzyme inhibitory antirheumatic drugs needs, however, further investigation since also enzyme independent variables play an important role in maintaining normal function of cartilage.

Anti-Inflammatory Agents↗

Lysosomal elastase: effect on mechanical and biochemical properties of normal cartilage, inhibition by polysulfonated glycosaminoglycan, and binding to chondrocytes.

Rheumatic joint destruction usually starts with the destabilisation of cartilage. Lysosomal elastase is a candidate effector of this process, since this enzyme is found at the site of cartilage erosion by rheumatoid synovial tissue. In order to prove this hypothesis we assessed the mechanical stability of cartilage during treatment by this enzyme in vitro. An indentation apparatus was used for this purpose and biochemical as well as microscopic techniques were used to supplement the results thus obtained. Our findings show that elastase irreversibly impairs the stability of cartilage by lysis of matrix proteoglycans without the help of additive enzymes. Collagen fragmentation played no significant role during elastase-induced destabilisation, while specific collagenase attacked the collagen network within the matrix only subsequent to the removal of proteoglycans. These findings suggest that elastase is a leading enzyme during proteolytic cartilage degradation. In addition polysulfonated glycosaminoglycan was found to reduce the mechanical effect of elastase on normal cartilage. It is therefore concluded that local inhibition of elastase promises therapeutic benefit during rheumatic cartilage degradation. Upon treatment of cartilage with elastase we observed this enzyme not only within the matrix under destruction but also bound to chondrocytes. These findings support the hypothesis that elastase plays a role on the matrix not only by direct degradation, but also by an indirect effect mediated through living chondrocytes.

Adolescent↗

[Coagulation factors in human born blisters (author's transl)].

Following clotting factor assays were performed on the fluid of burn blisters of 11 patients with severe burns: Fibrinogen levels, Factor II, V, X and XIII, thrombin time, fibrin split products, plasminogen, antithrombin III, IgA, IgM, IgG, ethanol gelation test and total proteins. The results showed, that a quantity of Factor II, X and XIII, antithrombin III, plasminogen and IgG had left the circulation. On the contrary we found only small concentrations of Factor V, fibrinogen, IgM and IgA in the fluid of burn blisters. This distribution suggested that the losses of plasma proteins into the burn blisters were correlated to their concentration and their molecular weight. The decrease of plasma coagulation proteins during the first days after severe burns was probably partly due to losses through the walls of the vessels, because of the increased capillary permeability.

Antithrombins↗

The influence of fluocortolone treatment on the collagen content in guinea pig skin.

Specific pathogen free guinea pigs were treated with varying dosis of fluocortolone for 15 days. The treated animals showed the same per cent weight gain as the controls. The total hydroxyproline content of the skin and the hydroxyproline content in different collagen fractions was the same in treated and untreated animals. Thus fluocortolone seems to have no specific effect on the synthesis or the breakdown of collagen in the guinea pig skin. Also the physical development of the animals, kept under defined conditions, failed to show a catabolic effect of of fluorcortolone.

Animals↗

[Factor XIII deficiency in burns].

In 34 patients with severe burn injuries platelets, fibrinogen, prothrombin time, partial thromboplastin time, thrombin time and factor XIII were measured daily. Half of the patients were administered 15 000 IE of heparin per 24 hours. In the first 4 days there was a rapid fall of factor XIII to a value of approximately 30%. Values remained very low during the whole observation period of up to 20 days. However, in patients treated with heparin, values tended to be 10--15% higher. After an initial decline on the tenth day, the platelets had risen to the lowest normal level. Platelets were identical in both groups. The causes for the changes in these haemostasis parameters, their significance, and possible consequences of therapy are discussed.

Blood Coagulation Tests↗

[Platelet dysfunction as a result of inhibition of ADP release (aspirin-like defect) in two identical twins(author's transl)].

An abnormal release of platelet adenosine diphosphate (ADP), as seen after intake of acetylsalicylic acid, was demonstrated to be the cause of a clotting disorder in two identical female twins. The signs of bleeding occurred at the age of 26 and consisted of an increased frequency of haematomas, hypermenorrhoea not explained on gynaecological grounds, and prolonged bleeding after minor injuries. Increased bleeding time, abnormal aggregation after stimulation with collagen and absence of the second aggregation phase after addition of ADP were the abnormal findings of this clearly hereditary form of platelet dysfunction. The platelets were slightly larger than normal ones and there were changes in ultrastructure.

Adenosine Diphosphate↗

[Doppler measurement of arterial pressure for assessing therapeutic measures after arterial occlusion (author's transl)].

Arterial pressure differences between arm and foot arteries can be easily measured by the Doppler method and in this way the gradient across an arterial occlusion of the lower limbs approximately quantified. An increase in gradient after induced ischemia is inversely proportional to its compensation. Pre- and postoperative measurements on 51 limbs demonstrated that functional results of arterial reconstruction can be thus assessed and their further course objectified.

Adult↗