A correlation with type of sulfonamide resistance gene in Escherichia coli and synergy between trimethoprim and sulfamethoxazole.

Plasmids carrying type I or II sulfonamide-resistance (Sur) genes were evaluated for their effect on synergy between trimethoprim (Tmp) and sulfamethoxyzole (Smx) in E. coli. Strain J53 containing each of three plasmids (R1, pSa, and R388) with the type I Sur gene displayed a synergistic response to Tmp/Smx; strain LE392 containing a plasmid (RSF1010) with the type II Sur gene displayed no synergy. The difference in synergy between type I and type II Sur genes might be explained by the difference in amount of resistant enzyme produced.     

Tumor osteolysis in osteopetrotic mice

Details of the cellular and biochemical mechanisms involved in focal destruction of bone at sites of tumor osteolysis are unknown. It has been shown that tumors from sarcoma (2472) cell lines induce focal osteolysis in mice by stimulating formation and activation of osteoclasts. In this report, the influence of 2472 tumors on the skeletons of osteoclast-deficient animals (op/op) was studied. After op/op femora had been inoculated with 2472 cells, tumors developed and focal osteolysis occurred. There were more osteoclasts per histologic section in sham-injected femora (19 ± 5) than in tumor-bearing femora (412 ± 129) (p < 0.05). The size of the osteoclasts also increased from 304 ± 81 μm² in sham-injected limbs to 407 ± 62 μm² in tumor-bearing limbs (p < 0.001). Conditioned media from 2472 op/op tumor explants contained macrophage colony-stimulating factor. A deficiency of osteoclasts in op/op mice is the result of the absence of this factor; therefore, these data introduce the possibility that macrophage colony-stimulating factor derived from 2472 tumor may be responsible for directing osteoclast-mediated osteolysis at sites of the tumor.     

A comparison study of dynamic visual acuity between athletes and nonathletes

A comparison study of dynamic visual acuity (DVA) was conducted using samples of nonathletic college students and college baseball players. The experimental population consisted of 17 male baseball players ranging in age from 19-24 years. The control population was made up of 25 male graduate students ranging in age from 23-29 years. Subjects reported the direction of a 20/25 "Landolt C" target exhibiting uniform angular motion produced by a projection system. Angular target velocities between 10 deg/sec and 110 deg/sec with an exposure time of 400 ms were used. The results showed a statistically significant difference between the two groups' DVA. The mean DVA for the baseball players was 82.35 deg/sec and 69.90 deg/sec for the control group.     

The depressing effect of tetracaine and ryanodine on the slow outward current correlated with that of contraction in voltage-clamped frog muscle fibres

The effects of tetracaine (10–50 M) and ryanodine (0.1–10 M) were tested on the slow outward K⁺ current (I _so) and the mechanical tension of isolated frog muscle fibres in a voltage-clamp device (double mannitol-gap) connected to a mechanoelectric transducer. In the concentration range tested, both drugs induced a simultaneous inhibition of tension and current. In all cases the effect on tension was twice that on current. The tetracaine-induced current and tension blocks were fully reversible and dose-dependent. In contrast the ryanodine effects on current and tension were not reversible and did not exhibit a dose dependence except for the delay before the onset of the response, which was shortened when the concentration was raised. Linear regression analysis of the time-dependent and dose-dependent effects of both drugs indicated a strong correlation between the decreases in tension and current. It is concluded that the slow outward current is partly under the control of the Ca²⁺ release from sarcoplasmic reticulum during contraction.     

Interactions of rutaecarpine alkaloids with specific binding sites for 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver

Rutaecarpine alkaloids have the capacity to inhibit specific2,3,7,8-[1,6-³H]tetrachlorodibenzo-p-dioxin (TCDD) binding inrat liver cytosol, as analysed by electrofocusing in polyacrylamidegel. The IC₅₀ value for binding of 7,8-dehydrorutaecarpine wasestimated to 7 nM indicating a high-affinity interaction, whereasrutaecarpine appeared less active (IC₅₀ 110 nM). These findingsare of interest in view of the fact that analogues to thesecompounds may be formed following UV-irradiation of tryptophanand that such photo-products have been suggested to constitute(the) endogenous ligand(s) for the TCDD receptor. As furthersupport of this notion, the rutaecarpine alkaloids investigatedcould be fitted into a rectangle of 6.8x13.7 A, a characteristiccommon for most high affinity ligands of the TCDD receptor hithertostudied. In view of their structural similarity to dehydrorutaecarpineand the agreement of their mol. wt with that of the photoproductwith the highest affinity for the TCDD receptor, we suggestdeaza-analogues of dehydrorutaecarpine to represent possiblecandidates for the endogenous TCDD receptor ligand.     

Functional analysis of the cag pathogenicity island in Helicobacter pylori isolates from patients with gastritis, peptic ulcer, and gastric cancer

Helicobacter pylori is the causative agent of a variety of gastric diseases, but the clinical relevance of bacterial virulence factors is still controversial. Virulent strains carrying the cag pathogenicity island (cagPAI) are thought to be key players in disease development. Here, we have compared cagPAI-dependent in vitro responses in H. pylori isolates obtained from 75 patients with gastritis, peptic ulcer, and gastric cancer (n = 25 in each group). AGS gastric epithelial cells were infected with each strain and assayed for (i) CagA expression, (ii) translocation and tyrosine phosphorylation of CagA, (iii) c-Src inactivation, (iv) cortactin dephosphorylation, (v) induction of actin cytoskeletal rearrangements associated with cell elongation, (vi) induction of cellular motility, and (vii) secretion of interleukin-8. Interestingly, we found high but similar prevalences of all of these cagPAI-dependent host cell responses (ranging from 56 to 80%) among the various groups of patients. This study revealed CagA proteins with unique features, CagA subspecies of various sizes, and new functional properties for the phenotypic outcomes. We further showed that induction of AGS cell motility and elongation are two independent processes. Our data corroborate epidemiological studies, which indicate a significant association of cagPAI presence and functionality with histopathological findings in gastritis, peptic ulcer, and gastric cancer patients, thus emphasizing the importance of the cagPAI for the pathogenicity of H. pylori. Nevertheless, we found no significant association of the specific H. pylori-induced responses with any particular patient group. This may indicate that the determination of disease development is highly complex and involves multiple bacterial and/or host factors.