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S M Rankin

Publications and source records attributed to S M Rankin.

23 records · Page 2Linked to original sources

Macrophages possess both neutral and acidic protease activities toward low density lipoproteins.

Low density lipoproteins (LDL) have been strongly implicated in the pathogenesis of atherosclerosis. We have studied the proteolytic degradation of these lipoproteins by macrophages, which are a major cellular constituent of atherosclerotic lesions. Mouse peritoneal macrophages contained both an acidic and a less active but distinct neutral/alkaline protease activity toward human 125I-labelled LDL. The acidic activity had a pH optimum of 4.5 and the neutral/alkaline activity one of 8-8.5. The acidic activity started to plateau with increasing lipoprotein concentrations whereas the neutral activity was directly proportional to the lipoprotein concentration up to at least 150 micrograms of protein/ml. The acidic protease activity had a complex time course whereas the neutral activity was directly proportional to the time of incubation up to at least 48 h. Leupeptin (35 microM) and pepstatin (5 microM) inhibited the acidic activity by about 70% individually and almost entirely in combination, indicating that cathepsins B and D are important in the degradation of LDL by lysosomal cathepsins. In contrast, there was little, if any, inhibition of the neutral protease activity by leupeptin or pepstatin. The acidic protease activity was increased by both DL-dithiothreitol (5 mM) and disodium EDTA (1 mM) whereas the neutral protease activity was increased by dithiothreitol but inhibited partially by EDTA. The possible significance of macrophage neutral and acidic protease activities toward LDL in atherosclerosis needs to be assessed.

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Ultrastructure of corpora allata of known activity during the vitellogenic cycle in the cockroach Diploptera punctata.

Ultrastructure was correlated with rates of juvenile hormone synthesis in corpora allata from females of the viviparous cockroach Diploptera punctata at seven daily intervals during the first vitellogenic cycle. Synthetic activity of the glands was determined by in vitro radiochemical assay before the glands were fixed for electron microscopic analysis. The cycle in rates of juvenile hormone synthesis progressed from about 20 pmol h-1 per gland pair (oocytes 0.60 mm long) to a maximum mean rate of 140 pmol h-1 per pair (oocytes 1.40-1.47 mm long) and declined to about 20 pmol h-1 per pair at ovulation (oocytes about 1.65 mm long). Conspicuous ultrastructural changes occurred with changing synthetic rates. In glands with increasing rates of synthesis, mitochondria showed less electron-dense matrix, greater diameter and more irregular shape. Smooth endoplasmic reticulum changed from easily seen to obscure tubules, networks, and vesicles. Rough endoplasmic reticulum appeared in longer, more curved segments. Newly formed autophagic vacuoles appeared in all glands of highest activity rates. In glands with decreasing rates of synthesis, the mitochondrial matrix became denser, width smaller, and shapes less irregular. Smooth endoplasmic reticulum again appeared tubular and distinct. Golgi complexes were more conspicuous. Rough endoplasmic reticulum in whorls and large numbers of autophagic vacuoles continued to be present.

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Ovarian inhibition of juvenile hormone synthesis in the viviparous cockroach, Diploptera punctata.

The mature ovary can actively prevent increases in rates of juvenile hormone (JH) synthesis by corpora allata (CA). This was unequivocally shown in two ways. (1) By combining in a single host female one ovary known to be stimulatory and one known to be nonstimulatory. Since the combination of a stimulatory and nonstimulatory mature ovary resulted in rates of JH synthesis intermediate between those found following implantation of either of these ovaries alone, it is concluded that the nonstimulatory mature ovary is indeed inhibitory (a nonstimulatory immature ovary had no such inhibitory effect). (2) By implanting nearly mature ovarioles and female CA into males. The ovarioles prevented the increase in rates of JH synthesis by the implanted CA that occurs in the absence of implanted ovarioles. This ovarian-elicited difference in rates of JH synthesis by CA implanted into males was not accompanied by differences in hemolymph ecdysteroid titers. Also, following removal of nearly mature ovaries from normal females the rates of JH synthesis remained above those of control females for only 24 hr and then declined to rates of controls. This suggests that there is an additional factor regulating the decline in JH synthesis at the end of the gonadotrophic cycle.

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The changing effect of the ovary on rates of juvenile hormone synthesis in Diploptera punctata.

The ovary is necessary for the cycle of juvenile hormone (JH) synthesis by the corpora allata which normally accompanies oocyte development in mated adult Diploptera punctata (B. Stay and S. S. Tobe, Gen. Comp Endocrinol. 34, 276-286, 1978; B. Stay, S. S. Tobe, E. C. Mundall, and S. Rankin, Gen. Comp. Endocrinol. 52, 341-349, 1983). Implanting parts of the ovary into ovariectomized females showed that only the basal oocytes were capable of stimulating an increase in rates of JH synthesis (measured by an in vitro radiochemical assay) within 4 days of implantation; apical oocytes and the oviduct were ineffective. Ovariectomized 2-day-old, mated females were used to test the capacity of ovaries of various developmental stages to stimulate increases in rates of JH synthesis within 24 or 48 hr. Previtellogenic ovaries, with basal oocytes less than 0.8 mm long, and those near the end of vitellogenesis, with basal oocytes greater than 1.5 mm long, did not result in an increase in rates of JH synthesis above Ringer-injected controls. Vitellogenic ovaries within this size range did elicit an increase in rates of JH synthesis. Furthermore the degree of increase was dependent upon the size of the oocytes; the ovaries with largest oocytes showed the greatest capacity to increase rates of JH synthesis.

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