Electron-Hole Asymmetric Chiral Breakdown of Reentrant Quantum Hall States.

Reentrant integer quantum Hall (RIQH) states are believed to be correlated electron solid phases, although their microscopic description remains unclear. As bias current increases, longitudinal and Hall resistivities measured for these states exhibit multiple sharp breakdown transitions, a signature unique to RIQH states. A comparison of RIQH breakdown characteristics at multiple voltage probes indicates that these signatures can be ascribed to a phase boundary between broken-down and unbroken regions, spreading chirally from source and drain contacts as a function of bias current and passing voltage probes one by one. The chiral sense of the spreading is not set by the chirality of the edge state itself, instead depending on electron- or holelike character of the RIQH state.

Modulation of polymorphonuclear leukocytes function by incubation with human serum from oxidant-challenged individuals.

Polymorphonuclear leukocytes (PMN) from healthy donors were tested for stimulated release of superoxide anions after being incubated with serum of welders and of a group of unexposed individuals. These two groups were further subdivided either according to age or to smoking habits. The experiments showed that stimulated superoxide production from PMN was inhibited (P < 0.05) by serum from young smokers as compared to that of young nonsmokers, both from the unexposed group. Incubation of PMN with serum from elderly nonsmoking individuals decreased superoxide production as compared to incubation with serum from young nonsmoking individuals, both from the unexposed group. A decrease in superoxide production by incubation with serum of welders as compared to that of unexposed individuals was significant only when the comparison was carried out between the young, non-smoking subgroups. These findings suggest that age, smoking, and exposure to oxidants induce appearance in serum of factors that affect the PMN function

Determination of urinary hippuric acid in toluene abuse.

BACKGROUND: Volatile substance abuse is practiced mainly by adolescents and young adults. Its effects are central nervous system excitation followed by central nervous system depression, at times accompanied by seizures. It may cause sudden death as a result of ventricular arrhythmias, reflex vagal inhibition, respiratory depression, and anoxia. Chronic toxicity may involve the nervous system, heart, kidney, and liver. Toluene-based adhesives are among the most commonly inhaled substances. CASE REPORT: A 14-year-old female presented with confusion, hallucinations, and intermittent laughing and crying after having inhaled contact glue several times daily in the course of 5 days. Her condition improved within 3 h. Urinary hippuric acid was 93.9 g/g creatinine indicating heavy toluene exposure (biological exposure index, BEI, is 1.6 g/g creatinine). CONCLUSION: In this patient, urinary hippuric acid was a biomarker for her toluene abuse.

Adhesion molecules of blood polymorphonuclear leukocytes and alveolar macrophages in rats: modulation by exposure to ozone.

1. Exposure to elevated levels of ozone results in an infiltration of polymorphonuclear leukocytes (PMNs) into the lungs. The purpose of this study was to investigate whether the ozone-induced inflammatory process is preceded by a change in the expression of adhesion molecules (integrins and selectins) in peripheral blood PMNs and alveolar macrophages in rats. 2. Female Sprague Dawley rats were exposed to air or ozone (1 p.p.m., 2 h). Bronchoalveolar lavage (BAL) was carried out and blood was collected via intracardiac puncture at 0 or 18 h after the exposure. There were no PMN in the BAL fluid at time 0 after the 2 h exposure to ozone. The expression of cell adhesion molecules from the integrin family (represented by CD18) on alveolar macrophages (AM) was lowered. The expression of cell adhesion molecules from the selectin family (represented by CD62L) on blood PMN was not affected by exposure to ozone, while the expression of integrins (CD11b) on blood PMN was lowered. 3. This effect was confirmed by experiments in which plasma of ozone-exposed animals was incubated with PMN from peripheral blood obtained from non-exposed animals. In these experiments, the expression of CD11b on PMNs of non-exposed animals was lower after incubation with plasma from ozone-exposed animals. 4. Our experiments suggest the presence of factor(s) in blood, which cause a decrease in the expression of CD11b on PMNs.

Paraquat-induced formation of leukotriene B4 in rat lungs: modulation by N-acetylcysteine.

The present work is focused on the formation of the inflammatory mediator leukotriene B4 (LTB4) in the lungs of paraquat (PQ)-intoxicated rats. The levels of LTB4 and the number of neutrophils in lung lavages of PQ-intoxicated rats, measured 12 h after 30 mg/kg PQ, increased significantly compared with those of control animals; administration of 50 mg/kg IP N-acetylcysteine (NAC), 8 h after PQ, inhibited this effect. The release of LTB4 from alveolar macrophages (AM) or alveolar epithelial type II cells from healthy animals incubated with PQ and/or NAC did not offer' an explanation for the effect of these chemicals on LTB4 in the bronchoalveolar lavage fluid (BALF). The PQ-enhanced, NAC-inhibited release of arachidonic acid (AA) by alveolar epithelial type II cells did, however, explain our in vivo results, when one assumes that the AM synthesize their 5-lipoxygenase products from alveolar epithelial cell-derived AA, an hypothesis demonstrated already by other researchers.

N-acetylcysteine increases the glutathione content and protects rat alveolar type II cells against paraquat-induced cytotoxicity.

A protective effect of N-acetylcysteine in oxidative lung damage was reported by a number of workers; however, the mechanism underlying this effect was not thoroughly elucidated. The present research investigates the protection by N-acetylcysteine against paraquat-induced cytotoxicity to alveolar type II cells, which are known to be specific targets of paraquat toxicity in vivo. We found that addition of 1 mM N-acetylcysteine to alveolar type II cells incubated with 1 mM paraquat reduced the cytotoxic index from 17.4 +/- 1.3% to 9.3 +/- 1.5%. This effect could not be explained by the interference of N-acetylcysteine with the active uptake of paraquat by type II cells. Incubation of these cells with N-acetylcysteine enhances their glutathione content, thus reducing the paraquat- induced depletion of glutathione in these cells. These results suggest that N-acetylcysteine exerts its protective effect by acting as a precursor for glutathione in alveolar type II cells.