[Tumors of the oral cavity arising in the salivary glands].
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Humans↗
Biomedical subjects
L Holczinger
Publications and source records attributed to L Holczinger.
The reaction of unsaturated fats with the acid hematein test.
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Chemical Phenomena↗
A multifactorial system controlling myeloid cell differentiation and division.
It has been demonstrated that mature granulocytes contain two stimulatory and three inhibitory factors of cell proliferation. Consequently, beyond the negative feedback inhibitor (chalone), myeloid cells are controlled presumably by other negative (inhibitory) and positive (stimulatory) mechanisms, in addition.
Animals↗
Modulative effect of endogenous granuloid inhibitors on cell proliferation.
The particle-free crude extract of differentiated granulocytes (GCE) and the GI-1, GI-2, GI-3 proliferation inhibitory fractions (M.W. larger than or equal to 70,000 approximately 11,500 and less than or equal to 4000) were studied for the effects they exert on cultured cells. As shown by the curve, in bone marrow suspension cultures, in the dose range of 0.01-10.0 microng/ml, GCE maximally inhibits 3H-TdR incorporation into the DNA for 5.5 hours. In agar-gel cultures, 1.0-5.0 microng/ml of GCE reduces both the number (by 50.6-54.8%) and the size of the colonies formed. The manifestation of the inhibitory effect of GI-1, GI-2 and GI-3 fractions requires 2.5-3.5 hours. The inhibitors designated GI-2 and GI-2 are target-cell specific but they do not reduce 3H-TdR incorporation either in thymocyte suspension or HeLa monolayer cultures. On the other hand GI-1 inhibis the proliferation in HeLa cultures, as well. These endogenous inhibitors exert their optimum effect, even in a partially purified state at 2-4 orders or magnitude lower concentrations than does 1,2/5,6-dianhydrogalactitol (DAD), a cell-aspecific inhibitor used for comparison in the same system.
Alkylating Agents↗
Changes in the rates of lipogenesis and hepatic triglyceride secretion in mice bearing Ehrlich ascites carcinoma.
The growth of Ehrlich ascites tumors (EAT) in mice induces hypertriglyceridemia and depletion of lipid stores. H-Riop: Swiss mice in early and late stages of tumor growth were examined to investigate whether an increase in liver synthesis of fatty acids (FA) and/or an increase in the liver triglyceride (TG) secretion rates (TGSR) would contribute to endogenous cancer-induced hypertriglyceridemia. Using 3H2O as tracer, FA synthesis decreased in the liver of tumorous animals. Hepatic TGSR also decreased during the development of hypertriglyceridemia. On the basis of these results, hypertriglyceridemia is probably not due to hyperproduction of lipids by the liver. In the late stage of tumor growth a considerable drop of FA synthesis also ensued in the adipose tissues, which probably participated in the loss of carcass lipids. At the early stage of tumor growth FA synthesis in the EAT cells was substantial in relation to the low lipid content of these cells, but in the late period FA synthesis slowed down, indicating that the triglyceride-rich "older" tumor cells obtained a large part of their lipids performed by the host.
Animals↗