Apparent Mutagenic Effect of Induction of Lambda Prophage Inserted Between lysA and thyA

Induction of a heat-inducible abnormal lambda prophage inserted between lysA and thyA in Escherichia coli resulted in a number of auxotrophic mutants in the surviving cured-cell populations. These mutants could not be accounted for by deletions arising on formation of lambda hybrid particles carrying regions adjacent to the insertion site. The properties of these mutants, which were almost all spontaneously revertable, have been described and mapped by F′ episome complementation. Tentatively, it was suggested that induction of the lambda lysogen leads to a mutagenic state.     

Autoradiographic and immunofluorescent studies of cytological changes induced inBacillus cereus by chloramphenicol

Autoradiographic and fluorescent antibody techniques were used to study the formation of protrusions on the cell periphery ofBacillus cereus. The cells were grown in a synthetic medium containing chloramphenicol and H³-labelleddl-alanine, and examined at time intervals for cytological changes. One or more protrusions were detected on approximately 4% of the cell population. Active cell-wall synthesis was found to take place in these cells except at the periphery of the protrusions. On this basis it is suggested that the protrusions are not abnormal growing points but represent osmotically fragile zones where cell-wall synthesis has not taken place.The study was supported by a grant from the National Research Council of Canada.     

Role of thromboxane A2 in airway microvascular leakage induced by inhaled platelet-activating factor.

We studied the effects of OKY-046 (1, 10, and 30 mg/kg iv), a selective thromboxane synthase inhibitor, and of ICI 192605 (0.5 mg/kg), a selective thromboxane A2 receptor antagonist, on airflow obstruction and airway microvascular leakage induced by inhaled platelet-activating factor (PAF). Extravasated Evans blue dye content was measured as a reflection of airway microvascular leakage. In control animals, PAF caused a significantly higher increase in extravasation of dye and significantly less increase in lung resistance (RL) than histamine. OKY-046 significantly inhibited both changes in RL and airway microvascular leakage after PAF in a dose-dependent manner, whereas it inhibited histamine-induced airway microvascular leakage only at main bronchi, without any significant effect on RL. ICI 192605 significantly inhibited both RL and airway microvascular leakage induced by PAF, but not after histamine. After both PAF and histamine, changes in RL correlated significantly with the degree of microvascular leakage. Airway microvascular leakage and airflow obstruction after PAF, but not after histamine, may be dependent on thromboxane A2 generation.