Dispersal of a plasmid-borne chloramphenicol resistance gene in streptococcal and enterococcal plasmids

Plasmids coding for chloramphenicol resistance, five isolated from streptococci of groups A, B, and G, ten from enterococci (Enterococcus faecalis, Enterococcus faecium), and two from staphylococci, were tested for sequence homology with the chloramphenicol resistance gene of pIP501, a 30-kb plasmid originally isolated from a group B Streptococcus. The 6.3-kb HindIII fragment of pIP501, known to carry the chloramphenicol resistance gene, was cloned into pBR322. A 1.6-kb portion of the cloned fragment, which included most of the chloramphenicol resistance gene, was used as probe in DNA-DNA hybridization experiments. Sequence homology was detected between the probe and four of the streptococcal, seven of the enterococcal, and one of the staphylococcal plasmids. The absence of hybridization between this probe and one plasmid isolated from a group B Streptococcus, as well as three isolated from E. faecalis, indicated that there are at least two different plasmid-borne chloramphenicol resistance determinants in the streptococci and in the enterococci.     

Chondrocytes inhibit endothelial sprout formation in vitro: evidence for involvement of a transforming growth factor-beta.

Using a quantitative in vitro model of spontaneous endothelial sprout formation, we have attempted to define physiological inhibitors of angiogenesis from hyaline cartilage, a tissue whose antiangiogenic properties have been well described. The model consists of embedding bovine microvascular endothelial cell aggregates into fibrin or collagen gels, which results in the formation of radially growing sprouts. When chondrocytes derived from the permanent cartilagenous region of the chick embryo sternum are cocultured with the endothelial cell aggregates, sprout formation is markedly inhibited. Addition of anti-TGF-beta antibodies to the cocultures significantly reduced the inhibitory effect of chondrocytes on sprout formation. Chondrocyte-conditioned medium or exogenously added TGF-beta 1 have a similar albeit transient inhibitory effect. Depletion of TGF-beta from chondrocyte conditioned medium with anti-TGF-beta antibodies and solid-phase protein-A significantly decreases the inhibition of sprout formation. These results demonstrate that a chondrocyte-derived TGF-beta-like molecule inhibits capillary sprout formation in vitro and suggest that the antiangiogenic properties of cartilage may at least in part, be mediated by TGF-beta.     

Changes in nutrient intakes of conditioned men during a 5-day period of increased physical activity and other stresses

Nutrient intakes and selected blood and urinary constituents of 16 Navy servicemen were obtained before and during a period of 113 hours of physical activity, sleep deprivation, and psychological stress, to document the dietary adaptation of physically conditioned men to an extended period of hard physical work and other stresses. Food intakes were monitored by 1-day diet records prior to and by direct observation during the period. The factorial method was used to calculate energy expenditure. Carbohydrates provided 45 and 43% of the total energy intake before and during the experiment. Protein intakes and intakes of all the vitamins and minerals studied exceeded the Recommended Dietary Allowances, both before and during the period. Total energy intake averaged 18.7 MJ.d-1 before and 24.4 MJ.d-1 during the experiment. Body weight increased significantly by 2.7 +/- 0.4 kg (mean +/- s.e.) during the experiment (p less than 0.0001). There was a significant correlation (r = 0.74; p less than 0.001) between the change in body weight and urinary sodium from before to after the experiment suggesting that increased dietary sodium may have contributed to the weight gain. A significant increase in plasma volume (11.9 +/- 3.2%; p less than 0.0003) provided further support that the observed weight gain was due to sodium intake rather than a positive energy balance. In conclusion, conditioned men increased food consumption adequately to meet increased energy demands.     

The immunoelectronmicroscopic localization of human platelet factor 4 in tissue mast cells

Initial immunohistochemical localization of human platelet factor 4 (PF4) in tissue mast cells suggested that the protein was present in the mast cell granule. It was proposed that this could reflect binding of PF4 to heparin or heparan sulphate, known granule constituents. We report here the confirmation of granule localization by an immunoelectron microscopical method. The possible role of such binding is unknown, but the potential for cationic proteins of platelet origin interacting with vessel wall constituents is discussed.