The accessory cell function of murine Peyer's patches

The cellular composition and certain functional characteristics of murine Peyer's patches (PP) were examined and compared with other lymphoid tissues. The composition of PP resembled most closely that of the spleen with the exception of a significant decrease in the number of adherent and phagocytic cells. Very few cells with dendritic morphology could be identified in Peyer's patches. Whole PP (and the nonadherent population) were capable of presenting antigen ovalbumin, human gammaglobulin, and purified protein derivative in a T proliferative assay to sensitized lymph node cells and to an antigen-specific T-cell clone. The antigen-presenting cell in both the spleen and PP was concentrated in the low-density population which floated on 1.080 bovine plasma albumin. However, equal numbers of whole and PP floaters were deficient in their capacity to present antigen compared with similar populations from spleen. Moreover, in PP the antigen-presenting cell appeared in the nonadherent rather than the adherent population as found with other lymphoid tissues. Similar results were obtained with (B6A)F1, CBA, A.TFR-1 and B10.S (12R) mice, suggesting that the inability of adherent cells from PP to present antigen effectively was not genetically determined. Whole and nonadherent PP contained cells capable of stimulating an allogeneic MLR, although again they were generally inferior to those of the spleen when comparable numbers of cells were employed. The adherent population of PP did not elicit an MLR. However, whole PP contained accessory cells needed for mitogen-induced proliferation since passage over nylon-wool columns resulted in a nonadherent fraction which did not respond to concanavalin A or phytohemagglutinin and the addition of adherent peritoneal exudate cells restored the lectin response. The differences noted in the accessory cell function in PP and other lymphoid tissues suggest the possibility that quantitative or qualitative differences in the function of these cells may explain some of the previously observed characteristics of PP, such as the inability to detect a primary antibody response in this tissue. The possibility that the development of gut-associated suppressor cells and their migration to peripheral tissues may be involved in the systemic tolerance that follows oral immunization and that these may be related to numerical and/or functional differences in macrophages or accessory cells is discussed.     

Increase in ovulation rate after treatment of ewes with bovine follicular fluid in the luteal phase of the oestrous cycle

Administration of charcoal-treated bovine follicular fluid to Damline ewes twice daily (i.v.) from Days 1 to 11 of the luteal phase (Day 0 = oestrus) resulted in a delay in the onset of oestrous behaviour and a significant increase in ovulation rate following cloprostenol-induced luteolysis on Day 12. During follicular fluid treatment plasma levels of FSH in samples withdrawn just before injection of follicular fluid at 09:00 h (i.e. 16 h after previous injection of follicular fluid) were initially suppressed, but by Day 8 of treatment had returned to those of controls. However, the injection of follicular fluid at 09:00 h on Day 8 still caused a significant suppression of FSH as measured during a 6-h sampling period. Basal LH levels were higher throughout treatment due to a significant increase in amplitude and frequency of pulsatile secretion. After cloprostenol-induced luteal regression at the end of treatment on Day 12, plasma levels of FSH increased 4-fold over those of controls and remained higher until the preovulatory LH surge. While LH concentrations were initially higher relative to those of controls, there was no significant difference in the amount of LH released immediately before or during the preovulatory surge. These results suggest that the increase in ovulation rate observed during treatment with bovine follicular fluid is associated with the change in the pattern of gonadotrophin secretion in the luteal and follicular phases of the cycle.     

The role of specific DNA base damages in the X-ray-induced inactivation of bacteriophage PM2

Two types of X-ray-induced base damages, alkali-labile sites and thymine ring saturation products, were quantitated in PM2 DNA irradiated in the phage capsid under oxic and anoxic conditions. The extent of formation of these base damages was compared with the number of single- and double-strand breaks and lethal hits produced under the same conditions. The individual inactivation efficiencies of alkali-labile sites and thymine ring saturation products were determined by selectively inducing each of these damages in isolated PM2 DNA by chemical means in vitro and determining the rate of biological inactivation of the treated DNA by transfection. For each lethal X-ray hit induced in oxic conditions there were 1.06 alkali-labile sites, 0.40 thymine ring saturation products, 2.09 singe-strand breaks and 0.11 double-strand breaks in the PM2 genome. In anoxic conditions, the respective number of lesions was 1.00, 0.19, 1.73 and 0.09. The individual inactivation efficiencies of thymine ring saturation products and alkali-labile sites were found to be essentially equal, 7-8 lesions per lethal event in the PM2 genome. Alkali-labile sites and thymine ring saturation products together accounted for 15-20% of the biological inactivation of X-irradiated bacteriophage PM2. The presence or absence of oxygen during irradiation did not affect the contribution to inactivation made by alkali-labile sites, but the contribution by thymine ring saturation products to inactivation was about 2-fold higher in oxic compared with anoxic conditions. With the 4 lesions measured, we have accounted for some 28-34% of the lethal events in X-irradiated PM2 phage, most of the remaining events being caused by as yet unidentified base damages.     

Responses of an African tall-grass (Hyparrhenia filipendula stapf.) to defoliation and limitations of water and nitrogen

Summary Hyparrhenia filipendula stapf., a tall (1–1.5 m) perennial grass common in dry-subhumid African savannas, was collected from Serengeti National Park in Tanzania, propagated vegetatively, and grown in controlled environments simulating conditions in nature. Plants were subjected to a factorial experiment with combinations of watering frequency, nitrogen supply, clipping height (10 and 15 cm) and clipping frequency (7 and 14 d). Biomass yield and allocation to various tissue types, morphometric traits, and growth processes were measured.Watering frequency affected leaf elongation rate while nitrogen affected tiller number. Clipped yield was strongly correlated with leaf elongation rate but not tiller number, therefore it was primarily controlled by the activities of intercalary rather than apical meristems. There was a negative exponential relationship between tillering and clipped yield per tiller. Plants that received both high nitrogen and high water closely followed a-3/2 power law in this tradeoff. The fraction of total net photosynthate allocated to roots was not significantly related to any environmental treatment. Root and crown growths were not affected by defoliation treatment; leaf blade and stem growths were inhibited; and sheaths were inhibited only under low water.Despite a tall stature, H. filipendula tolerated herbivory by increased photosynthetic rate (Wallace et al. 1984), through continued production of young tissues by intercalary meristems balanced against tiller number, and by a statistically constant proportional allocation to roots. Clipped yield increased only when both nitrogen and water were abundant, and then, proportional clipped yield did not surpass an upper asymptotic limit.     

Intestinal epithelial cells and musculature contain different muscarinic binding sites

Muscarinic receptors on epithelial cells mediate intestinal secretion, while those in intestinal smooth muscle mediate motility. Experiments were carried out to determine whether the muscarinic receptors mediating each of these two functions in intestinal tissue might be associated with differences in the way agonist and antagonist drugs interact with the receptors. The inhibition constant (Kj) values for atropine, pirenzepine, and oxotremorine competition of specifically bound (3H)QNB were determined using membrane preparations from the muscular coat and from epithelial cells of rat jejunum, ileum, and colon. The Kj values of atropine were similar (1.2-10 nM) when comparing muscle layers and epithelial cells from any intestinal region. In contrast, the Kj values for pirenzepine were significantly higher in membranes from the musculature (400-1,200 nM) than in any of the epithelial cell membranes (20-100 nM). Kj values for pirenzepine in gut muscle were similar to those in heart (300 nM), whereas the Kj values in the cerebral cortex (39 nM) and the epithelial cell membranes closely approximated one another. The Kj values for oxotremorine competition of QNB binding in all intestinal muscular tissues (29-48 nM) and in heart (16 nM) were less than those of the intestinal epithelial cells (100-1,300 nM) or cerebral cortex (71 nM). Thus, pirenzepine and oxotremorine binding studies show that the nature of interactions between these agents and muscarinic sites is different when comparing epithelial cells and musculature of the gut.     

Genetic determinants of resistance to ectromelia (mousepox) virus-induced mortality.

Resistance to ectromelia (mousepox) virus-induced mortality was examined in crosses between susceptible DBA/2J, A/J, and BALB/cByJ mice and resistant C57BL/6J and AKR/J mice. Depending on the cross, resistance to mousepox virus was shown to be determined by one or more independently assorting autosomal loci with dominant alleles for resistance in AKR/J and C57BL/6J mice and recessive alleles in A/J, BALB/cByJ, and DBA/2J mice. A sexual dimorphism in resistance to disease was also observed.     

Heparin-binding growth factor type one and platelet-derived growth factor are required for the optimal expression of cell surface low density lipoprotein receptor binding activity in human adult arterial smooth muscle cells

Summary Purified heparin-binding growth factor-1 (HBGF-1) stimulated low density lipoprotein binding, internalization, and degradation in isolated human adult arterial smooth muscle cells. Exposure of quiescent cells to HBGF-1 in serum-free, defined medium increased both low density lipoprotein (LDL) receptor activity and de novo cholesterol biosynthesis. Both events preceded the onset of DNA synthesis by 6 to 9 h. HBGF-1 acted additively with platelet-derived growth factor (PDGF) to maximally stimulate cell surface LDL receptor binding activity and DNA synthesis in the smooth muscle cells. The presence of LDL was required for maximal mitogenic activity of HBGF-1 and PDGF. In the presence of LDL, growth factor-stimulated, proliferating human smooth muscle cells accumulated cholesterol ester and triglycerides. The results suggest that HBGF-1, PDGF, and LDL act together to promote the maximal proliferation of smooth muscle cells in culture. Chronic exposure to the three growth promoters may contribute to the smooth muscle cell hyperplasia and lipid accumulation observed in atherosclerotic lesions. This work was supported by the National Cancer Institute grants CA 37589 and HD 03275, National Council for Tobacco Research grant 1718, and a grant from RJR Nabisco, Inc.     

The acid phosphatases of Thermoascus crustaceus, a thermophilic fungus

Thermoascus crustaceus, a filamentous, thermophilic ascomycete with pathogenic potential was cultured on Sabouraud's liquid medium at temperatures from 27 to 47 degrees C for periods up to 7 days. Growth rate and yield were optimal at 37 degrees C. Morphological changes were confined to the cell walls, the thickness being greatest at 47 degrees C, which were also more resistant to mechanical disruption. Significant amounts of acid phosphatase (EC 3.1.3.2) activity occurred in the spent media of all cultures but were greatest at 37 degrees C. The proportions of acid phosphatase activity which were operationally defined as soluble or bound were also documented; the optimum pH for acid phosphatase activity in all fractions was 5.0. Extracts were subjected to polyacrylamide gel electrophoresis under non-denaturing conditions and the gels were stained for acid phosphatase activity. This revealed four electrophoretically distinct acid phosphatases which had different susceptibilities to inhibition by fluoride, phosphate, or tartrate. Effects of growth temperature, or phosphate supplement in the culture medium, on the acid phosphatase isoenzyme pattern were judged to be minor. Cytochemistry at the electron microscope level indicated acid phosphatase activity on the surface, in the periplasmic space, and in the cytoplasm, but no trends with regard to growth conditions. A substantial temperature range can be tolerated by this species but it is concluded that neither the general shape of the cells nor the acid phosphatase isoenzyme pattern changes substantially; this contrasts with previously documented differences for this class of enzyme in dimorphic Sporotrix schenckii.     

Role of plasma membrane redox activities in elongation growth in plants

Comparing isolated plasma membrane vesicles and excised hypocotyl segments from etiolated seedlings of soybean [ Glycine max (L.) Merr. cv. Williams], certain antiproliferative agents that inhibited growth inhibited plasma membrane redox activities. Additionally, auxins that stimulated growth stimulated plasma membrane redox activities. Hormone stimulation was restricted to NADH oxidase (determined from disappearance of NADH) and was given both by isolated plasma membranes and by a soluhilizedenzyme preparation. Comparing IAA, the native auxin regulator, and 2,4-D, a synthetic regulator, stimulation was observed, hut the dose-response curves were different. Yet, the dose-response relationships of both stimulation of auxin growth and stimulation of NADH oxidase were parallel. Inhibition of auxin-induced growth by antiproliferative drugs was more complex. Some, like actinomycin D, preferentially inhibited NADH oxidase (EC 1.6.99.2) but inhibited NADH-ferricya-nide oxido-reductase (EC 1.6.99.3) as well. Others, like adriamycin, inhibited primarily the NADH-ferricyanide oxido-reductase. Therefore, growth control by auxin appeared to involve NADH oxidase as a rate-limiting terminal oxidase to link electron flow from NADH to oxygen. This observation may provide a fundamental difference from animal cells. With the latter, impermeant electron acceptors such as diferric transferrin or ferricyanide fulfill such a role. In plants, these impermeant electron acceptors were without effect on growth or were growth inhibitory.