Complete Genome Sequences of Kinneretia sp. Strain XES5, Shinella sp. Strain XGS7, and Vogesella sp. Strain XCS3, Isolated from Xenopus laevis Skin.

Here, we report the genome sequences of three bacterial isolates, Kinneretia sp. strain XES5, Shinella sp. strain XGS7, and Vogesella sp. strain XCS3, which were cultured from skin of adult female laboratory-bred Xenopus laevis.

Abnormal high density lipoproteins from patients with liver disease regulate cholesterol metabolism in cultured human skin fibroblasts.

Apolipoprotein B (apoB) of plasma low density lipoproteins (LDL) binds to high affinity receptors on many cell types. A minor subclass of high density lipoproteins (HDL), termed HDL1, which contains apoE but lacks apoB, binds to the same receptor. Bound lipoproteins are engulfed, degraded, and regulate intracellular cholesterol metabolism and receptor activity. The HDL of many patients with liver disease is rich in apoE. We tested the hypothesis that such patient HDL would reduce LDL binding and would themselves regulate cellular cholesterol metabolism. Normal HDL had little effect on binding, uptake, and degradation of 125I-labeled LDL by cultured human skin fibroblasts. Patient HDL (d 1.063-1.21 g/ml) inhibited these processes, and in 15 of the 25 samples studied there was more than 50% inhibition at 125I-labeled LDL and HDL protein concentrations of 10 micrograms/ml and 25 micrograms/ml, respectively. There was a significant negative correlation between the percentage of 125I-labeled LDL bound and the apoE content of the competing HDL (r = -0.54, P less than 0.01). Patient 125I-labeled HDL was also taken up and degraded by the fibroblasts, apparently through the LDL-receptor pathway, stimulated cellular cholesterol esterification, increased cell cholesteryl ester content, and suppressed cholesterol synthesis and receptor activity. We conclude that LDL catabolism by the receptor-mediated pathway may be impaired in liver disease and that patient HDL may deliver cholesterol to cells.

The effect of television-mediated aggression and real-life aggression on the behavior of Lebanese children.

This study investigated the effect of television-mediated aggression and real-life aggression on the behavior of Lebanese children. The sample consisted of 48 boys and 48 girls of Lebanese origin who were students in an elementary school in Beirut, Lebanon. After controlling for pre-experimental aggression, the subjects were randomly assigned to one of the following treatment conditions: human-film aggression, cartoon-film aggression, neutral film, or real-life (act of war) aggression. The results indicated that boys as a group were more aggressive than girls and exhibited more imitative aggression after viewing both violent film and real-life violence. Girls were not more violent after viewing filmed aggression but were affected by the real-life violence. Comparisons of Bandura's work within the Lebanese culture are made.

A screw-connected fixed partial denture.

This technique provides one solution to the problem of using tilted abutment teeth for a fixed partial denture. It provides good retention without excessive tooth destruction and without excessive contour in the completed restoration.

Decreased erythrocyte membrane fluidity and altered lipid composition in human liver disease.

Abnormal plasma lipoproteins in patients with liver disease are associated with characteristic changes in erythrocyte membrane lipid composition. The membranes are enriched in cholesterol and phosphatidylcholine and both the cholesterol/phospholipid and phosphatidylcholine/sphingomyelin molar ratios are increased. Phospholipid fatty acid composition is also abnormal; the proportions of arachidonic acid and stearic acid are decreased and that of palmitic acid raised. In this study we have examined the effects of these membrane lipid abnormalities on membrane fluidity. Erythrocyte membrane fluidity was assessed in 30 patients with a variety of liver diseases and in 25 normal subjects using the hydrophobic, fluorescent probe 1,6-diphenylhexa-1,3,5-triene and the values were related to their lipid composition. Membrane fluidity was significantly decreased in the patient erythrocytes (lipid order parameter, S(v)[37 degrees C] = 0.713 +/- 0.018, mean +/- S.D. compared to 0.686 +/- 0.008 in the normal subjects, P < 0.001) and correlated significantly with the cholesterol/phospholipid ratio (r = 0.88, P < 0.001). The fluidity of lipid extracts from the membranes of patient erythrocytes was also decreased, suggesting that decreased membrane fluidity was mainly a consequence of altered lipid composition rather than protein abnormalities. Incubation of patient erythrocytes for 20 hr with normal, heated plasma removed the excess cholesterol without affecting the phosphatidylcholine/sphingomyelin ratio or phospholipid fatty acid composition; following incubation the fluidity of these membranes was similar to that of normal membranes. We conclude that in liver disease changes in the composition of the phospholipid bilayer matrix in the erythrocyte membrane have little influence on its fluidity; the reduced fluidity is predominantly a result of increases in cholesterol relative to phospholipid.-Owen, J. S., K. R. Bruckdorfer, R. C. Day, and N. McIntyre. Decreased erythrocyte membrane fluidity and altered lipid composition in human liver disease.

Platelet lipid composition and platelet aggregation in human liver disease.

Abnormal plasma lipoproteins in patients with liver disease are associated with an increase in erythrocyte cholesterol concentration and a raised erythrocyte cholesterol/phospholipid molar ratio. We hypothesized that their platelets would also have an increased cholesterol/phospholipid ratio and that this might affect aggregation in vitro. Platelet aggregates by adrenaline and ADP was measured in 34 patients with a variety of liver diseases and in 20 normal subjects and the values were related to platelet lipid composition. The platelet cholesterol/phospholipid ratio was 13% higher in the patients and correlated closely with erythrocyte cholesterol/phospholipid ratio. Platelet aggregation was reduced in most of the patients and inversely correlated with the cholesterol/phospholipid ratio. Cross-incubation and hemostasis studies indicated that there were no inhibitory factors present in the plasma; the defect was in the platelets. In contrast, other workers have shown that cholesterol-rich platelets, either from patients with Type IIa hyperlipoproteinemia or prepared in vitro, aggregate more readily than normal platelets. However, the phospholipid and fatty acid compositions of our patient platelets were also abnormal: the lecithin/sphingomyelin ratio was increased and was inversely correlated with aggregation; the proportion of arachidonic acid was decreased and positively correlated with the aggregation. In our patients with liver diseases the effects of the altered phospholipid and fatty acid composition presumably overrode those of the increased cholesterol content so that instead of enhanced aggregation, only reduced or normal aggregation was seen. We conclude that the reduced platelet aggregation seen in liver disease may reflect a decrease in arachidonic acid availability for prostaglandin and/or thromboxane production.

Lecithin-cholesterol acyltransferase and the lipoprotein abnormalities of parenchymal liver disease.

1. Detailed studies have been made of the plasma lipoprotein abnormalities in parenchymal liver disease to test the hypothesis that the abnormalities would correlate with plasma lecithin-cholesterol acyltransferase (LCAT) activity. 2. When LCAT was high, very-low-density-lipoproteins (VLDL) were normal in composition and had a normal pre-beta electrophoretic mobility. When LCAT was low, VLDL concentrations were greatly reduced. 3. With high LCAT low-density lipoproteins (LDL) were normal. The LDL particles found with low LCAT activity were of normal size but of abnormal composition, being triglyceride rich and cholesteryl ester poor. Regardless of LCAT activity LDL were present in normal amounts. 4. High-density lipoproteins (HDL) were normal in composition and electron-microscopic appearance when LCAT activity was high. When LCAT activity was low HDL were abnormal in composition and 'stacked discs' were seen on electron microscopy. 5. These results suggest that low LCAT activity may be the cause of at least some of the lipoprotein changes of parenchymal liver disease.

Systematic reinforcement: academic performance of underachieving students.

The effect of contingent tangible and social reinforcement on academic performance was investigated in an experimental classroom of 25 selected underachieving students. Measures were taken of both teacher and child behavior during a baseline and two experimental treatment periods. During Treatment I, a point system with tangible backup reinforcers was combined with contingent social reinforcers dispensed by the teaching staff to assess the effects on three measures of academic performance (i.e., per cent of time at work, work output per minute, and accuracy). During Treatment II, the contingencies for the tangible reinforcers were terminated while social reinforcement was continued to see if the positive effects of Treatment I on academic performance would persist. The results show that with combined tangible and social reinforcers, students' work time, rate of output per hour, and accuracy in all activities substantially increased. After termination of the tangible reinforcers, the students maintained their high rates of output per hour and accuracy for the remaining period of the study while the total amount of time at work returned to the baseline level.