Biomedical subjects

A Schulz

Publications and source records attributed to A Schulz.

274 records · Page 16Linked to original sources

PubMedDate not supplied

Selective effect of tumor necrosis factor on transformed versus nontransformed cells: nonselective signal recognition but differential target cell response.

TNF treatment causes oxidative down-modulation of endogenous survival factors in transformed as well as nontransformed fibroblasts. Endogenous survival factors are negative regulators of a constitutively expressed apoptosis machinery and have been defined in several cellular systems. As transformed cells harbour lower concentrations of endogenous survival factors than nontransformed parental cells, TNF-dependent down-modulation of endogenous survival factors in transformed cells is sufficient to release the apoptosis machinery from negative control and to cause cell death. In contrast, in nontransformed cells, due to their higher initial concentration of endogenous survival factors, down-modulation by TNF is not complete and therefore apoptosis is still prevented. Our data showed that perception of TNF signalling is not different between transformed and nontransformed cells, but that their differential response is due to quantitative differences in their regulatory setup. Furthermore, our data explained why application of low concentrations of cycloheximide can sensitize cells for apoptosis induction by TNF-alpha.

Animals↗

PubMedDate not supplied

Synergistic action between tumor necrosis factor-alpha and transforming growth factor type-beta: consequences for natural antitumor mechanisms.

TNF-alpha and TGF-beta are central signal molecules for natural antitumor mechanisms. Our data demonstrated that both factors act synergistically during apoptosis induction in transformed cells. This interaction of the two factors may have biological consequences for the efficiency of natural antitumor systems: 1) Transformed cells pretreated with TNF-alpha could be eliminated more efficiently by neighbouring nontransformed cells during intercellular induction of apoptosis; 2) TGF-beta pretreatment of transformed cells night sensitize them for apoptosis induction by macrophages. These findings allow three major conclusions: 1) Endogenous survival factors seem to be central regulatory elements for different apoptosis-inducing systems: 2) Macrophages and intercellular induction of apoptosis should be able to act in a synergistic way during the control of oncogenesis; 3) Resistance against one of the two mechanisms might cause resistance against the other as well.

Animals↗

PubMedDate not supplied

[Disabling senile osteoporosis].

Fractures of the proximal femur are the most dangerous complications of type-II-osteoporosis with a high rate of disability and mortality. In contrast to type-I-osteoporosis, men are affected rather frequently (ratio 1:3). We report on a 79-year old man who was completely in need of care after bilateral fractures of the humerus after having survived a previous pertrochanteric fracture of the left femur. Diagnostic procedures revealed that in this case an intestinal malabsorption has to be taken into consideration as a pathogenetic factor of this severe osteopathy. Bone biopsy confirmed a combination of osteoporosis and osteomalacia. Partial gastrectomy, which had been performed 10 years before, was obviously the reason for malabsorption having caused furthermore pernicious anemia, severe malnutrition and exsiccosis.

Aged↗

PubMedDate not supplied

Cell cycle control and initiation of DNA replication in Saccharomyces cerevisiae.

The cell cycle of budding yeast is controlled by a single cyclin-dependent protein kinase (Cdc28/Cdk1) which successively associates with the stage-specific activators Cln1-3 (G1 phase), Clb5,6 (S phase), Clb3,4 (S/G2 phase) and Clb1,2 (mitosis). The temporal pattern of these Cdk1/cyclin activities imposes a strict order of DNA replication events during the cycle: formation of a pre-replication complex at late M phase, initiation of replication at the G1/s transition, support of replication during S phase, and the prevention of re-replication at G2. A key component involved in S phase initiation is the Cdc6 protein, a transiently expressed DNA-independent ATP/GTPase interacting at late mitosis with an origin-recognizing complex.

Cell Cycle↗