the percentage retention of Ca45 about twofold, while having no significant effect on Sr90 retention.The last column of Table 1 shows the total calcium derived from the diet, which is deposited and retained during the course of the experiment. These figures are calculated from the measured Ca45 concentration in the bone and the known ratio of Ca45 to stable calcium in the diet. While rather close physiological control of dietary calcium utilization is evidenced at the two lower dietary levels, this control is no longer very effective at the 2-percent calcium level.Blood levels of Sr90 and Ca45 at different times of sacrifice were reasonably constant within a given dietary group. Between dietary groups, the blood levels of Sr90 and Ca45 varied in essentially the same manner as their concentrations in the femur. In general, for a given group of animals, the ratio of Sr90/Ca45 in the blood was not significantly different from the ratio of Sr90/Ca45 in the bone; this suggests, as others have pointed out (2), that the major discrimination between dietary calcium and strontium does not occur in the specific processes of deposition on the bone. Because total calcium analyses on blood were not obtained, and in view of the limited time period studied, closer intercomparison of the blood and bone data with a view toward elucidating discrimination mechanisms would not seem to be justified.Wasserman et al. have recently described an experiment in which Sr90 and Ca45 were chronically administered with diets varying in total calcium content from 0.5 to 2.0 percent (4). The skeletal deposition of both Sr90 and Ca45 in their experiment was inversely proportional to
By using cloned types 1 and 2 herpes simplex virus, obtained by selecting large and small plaques produced by material from human lesions, studies were performed to compare properties between preparations of each type. Regarding the rate of inactivation by ultraviolet light, no differences were found between the two antigenic types and none between the preparations obtained from either type. In contrast, type 1 preparations were found to be more readily inactivated at 45 C than type 2. Plaque size of cloned preparations changed by passage in cell culture. A broader range of plaque sizes was obtained, and average plaque size was larger. After 20 passages, preparations obtained from different types gave rise to one of three kinds of cytopathic effect. The cytopathic effect produced by type 1 preparations remained as before 20 passages and consisted of round cells in a compact central mass. For type 2, two kinds of cytopathic effect were seen in cloned preparations. This consisted of aggregates of round cells (seen in preparations before 20 passages) or of large, loose aggregates of round cells of various sizes. Results from neutralization studies using virus before and after 20 passages in cell culture versus antisera prepared against live or ultraviolet-inactivated virus showed no differences between cloned preparations obtained from a given type.
We studied the interactions between rabbit polymorphonuclear leukocytes (PMN) and the RE strain of herpes simplex virus type 1 (HSV-1) to determine better the role of inflammatory cells in herpetic stromal keratitis. PMN were found to be nonpermissive for HSV replication and were unable to bind virus in the absence of antibody. However, PMN did bind and internalize HSV-antibody complexes in vitro as was demonstrated visually by electron microscopic studies and quantitatively by measurement of activity associated with radiolabeled HSV-antibody complexes. Virus used for immune complex formation was labeled with either 125Iodine or 35S-methionine. In some experiments, anti-HSV IgG used for immune complex formation was labeled with 125Iodine before incubation with virus. Use of all three radiolabeling approaches resulted in the same general pattern of binding, indicating a requirement for both antibody and virus for interaction with PMN. The activity associated with PMN was increased by preincubation with complement. The results suggest an active role for PMN in controlling HSV infection through their ability to bind and ingest virus-antibody complexes.
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