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Biomedical subjects

M H Salaman

Publications and source records attributed to M H Salaman.

At least 19 recordsLinked to original sources
PubMed1976

Growth of a transplantable lymphoma and its modification in mice infected with the inducing virus.

The growth of a transplantable lymphoma was examined in normal mice and in mice previously infected with the lymphoma-inducing virus (ULV). Normal BALB/c mice respond to a footpad injection of X-irradiated lymphoma cells (ULMC) with popliteal lymph node (PLN) enlargement; mice previously infected with ULV do not. 106 viable ULMC injected into the footpads of ULV-infected mice grew progressively, and the animals died with disseminating malignant lymphoma. In contrast, this dose of cells injected into normal animals evoked strong host responses in the foot and draining lymph node, and no progressive growth of the lymphoma occurred. This increased susceptibility of the ULV-infected animals was also observed when ULMC were injected s.c. into the back or i.m. into the calf muscle, but not after s.c. injection of an unrelated 3-methylcholanthrene-induced sarcoma. Resistance to tumour growth after i.v. injection of ULMC is clearly ineffective, since 10 cells can grow and kill the animal, and in this case no increased susceptibility of ULV-infected animals was observed.

Animals↗
PubMed1965

Studies on the mechanism of action of Riley virus. I. Action of substances affecting the reticuloendothelial system on plasma enzyme levels in mice.

Plasma LDH levels were determined in normal and Riley virus-infected mice following treatment with various drugs known to alter the activity of the RES. The rise in plasma LDH level after Riley virus infection was considerably enhanced by previous treatment with thorotrast (to produce blockade of the RES), and decreased by previous treatment with stilboestrol (to stimulate the RES). A dose of 2000 r whole-body x-irradiation, lethal within 3 to 4 days, did not alter the phagocytic activity of the RES, and was without effect on plasma LDH activity in normal mice, or on the rise in plasma LDH level following infection with Riley virus. Blockade of the RES with cholesterol oleate, thorotrast, or zymosan, resulted in a 2- to 3-fold rise in plasma LDH level within a few hours. The level returned to normal by 1 to 3 days. Stimulation of the RES with stilboestrol resulted in a decrease in plasma LDH level by 1 to 2 days in both normal and infected mice, with a return to normal by about a week. Blockade of the RES in uninfected mice with thorotrast or cholesterol oleate, besides increasing the plasma LDH level caused a rise in plasma phosphoglucose isomerase level, but no significant alterations in plasma aldolase or alanine transaminase levels, studied up to 10 days. Riley virus causes a similar pattern of enzyme elevation. It is suggested that the increased levels of certain plasma enzymes in Riley virus-infected mice may be due to competitive inhibition by virus particles of plasma enzyme clearance by the RES.

Alanine Transaminase↗
PubMed1965

Studies on the mechanism of action of Riley virus. II. Action of substances affecting the reticuloendothelial sysem on the level of viraemia.

The level of viraemia was determined in serial blood samples obtained from 2 mice after the injection of Riley virus. The plasma virus titre rose rapidly to a peak value of 10(9) to 10(10)ID(50) per ml by 24 hours after infection, and then fell slowly to a level of 10(5) to 10(6)ID(50) per ml by the 10th day after infection, where it remained relatively stable. Neither blockade of the RES with thorotrast, zymosan, or carbon, nor stimulation of the RES with stilboestrol or zymosan, before the injection of Riley virus, produced any observable alteration in the level of viraemia attained 24 hours after infection. However 10 days or more after infection with Riley virus blockade of the RES with thorotrast caused a transitory rise, and stimulation of the RES with stilboestrol caused a slight but prolonged fall, in the level of viraemia. Zymosan injection at this period of infection caused an initial rise, followed by a fall, in the level of viraemia; these changes correlated with the initial period of blockade and the subsequent period of stimulation of the RES observed in carbon clearance studies. The clearance of injected Riley virus particles from the plasma over a period of 3 hours after injection was measured in previously uninfected mice and mice which had been infected with Riley virus for 3 weeks. The mice which had been infected 3 weeks before the test cleared rather more of the injected virus than the previously uninfected mice. It is concluded that although the activity of the RES affects, and may determine, the level of viraemia, the permanence of the viraemia in Riley virus-infected mice does not appear to be due to a failure of the RES to clear virus particles from the plasma.

Animals↗