[Endothelial cell proliferation in vitro induced by sera of patients with progressive systemic sclerosis and systemic lupus erythematosus]. / Endothelzellproliferation in vitro durch Seren von Patienten mit progressiver Systemsklerose (PSS) und systemischem Lupus erythematodes (SLE).

Endothelial cells from human umbilical cord veins proliferate in vitro up to 35-fold over control values when incubated for prolonged periods of time (up to 144 hrs) in the presence of sera from patients with SLE or PSS. The proliferation inducing capacity of patients' sera was high during remission and low during relapses. Similarly, induction of endothelial cell proliferation increased significantly following plasma separation; however, this effect did only last for a few hours. The in vitro stimulation of endothelial cells observed may be correlated to histological findings of hyperplasia and neoproliferation of vascular intima cells in SLE and PSS.

[Pfeifer-Weber-Christian panniculitis (PWCP). Description of a case and review of the literature]. / Pfeifer-Weber-Christian-Panniculitis (PWCP). Beschreibung eines Falles und Literaturübersicht.

We report on a case of Pfeifer-Weber-Christian panniculitis (PWCP) in a 40 year old woman. PWCP is a rare inflammatory disorder of the subcutaneous fatty tissue. It is characterized by painful relapsing, subcutaneous nodules occurring preferentially at the upper arm, thigh and trunk regions. The disease is often accompanied by recurrent temperatures and constitutional symptoms. The clinical course of our patient had already lasted for four years when we saw her for the first time. Besides local panniculitis of the arms and the trunk she suffered from recurrent temperatures. Antibiotics and/or antiinflammatory therapy failed to control the disease. Laboratory tests and chest X-ray did not reveal noteworthy pathological results. PWCP was proven histologically and distinguished from other soft tissue disorders. The findings are discussed in the context of previous reports. The etiopathology of PWCP remains unclear and a specific therapy still awaits introduction.

Temperature dependence of leukemic cell destruction by alkyl-lysophospholipids (NSC 324368).

Alkyl-analogs (ALP) of 2-lysophosphatidylcholine induce a progressive destruction of neoplastic cells by interfering with the continuous turnover of membrane phospholipids. Using leukemic blast cells from patients with acute forms of leukemia the effect of temperature was evaluated. It was found that temperature strongly influences the cytotoxic activity of ALP. High temperatures potentiate whereas a slight decrease in temperature reduces leukemic cell destruction by ALP. At temperatures below 30 degrees C even high doses of ALP will not destroy these tumor cells. Furthermore, cell destruction initiated at 37 degrees C can be abolished by lowering the incubation temperature to 25 degrees C. These biological data have been confirmed by biochemical studies, showing a temperature dependence of ALP adsorption not accompanied by a corresponding increase of alkyl-cleavage enzyme activity. The rate of membrane phospholipid turnover seems to be essential for temperature dependent ALP induced cell destruction.

Studies on various parameters influencing leukemic cell destruction by alkyl-lysophospholipids.

Critical parameters of alkyl-lysophospholipid (ALP) induced destruction of freshly isolated human leukemic cells have been evaluated. The destructive activity of ALP is shown to be competitively inhibited by metabolizable lysophospholipids added to the cultures. It has also been found that destruction depends on the amount of serum present. Temperature and Ph strongly influence the cytotoxic activity of ALP. A slight decrease in temperature causes a reduction in cell death, whereas a temperature increase results in a marked potentiation. At low pH ALP cytotoxicity is inhibited. Incubation of cells with combinations of ALP and other cytotoxic drugs revealed a striking cytotoxic synergism with vinca-alkaloids, whereas corticosteroids retarded ALP induced cell destruction.