One hundred sixty-four isolates of Xanthomonas campestris pv. campestris and other X. campestris pathovars known to infect cruciferous hosts (X. campestris pvs. aberrans, raphani, armoraciae, and incanae) were inoculated onto a differential series of Brassica spp. to determine both pathogenicity to brassicas and race. Of these, 144 isolates were identified as X. campestris pv. campestris and grouped into six races, with races 1 (62%) and 4 (32%) being predominant. Other races were rare. The remaining 20 isolates from brassicas and other cruciferous hosts were either nonpathogenic or very weakly pathogenic on the differential series and could not be race-typed. Five of these isolates, from the ornamental crucifers wallflower (Cheiranthus cheiri), stock (Matthiola incana) and candytuft (Iberis sp.), showed clear evidence of pathovar-like specificity to the hosts of origin. A gene-for-gene model based on the interaction of four avirulence genes in X. campestris pv. campestris races and four matching resistance genes in the differential hosts is proposed. Knowledge of the race structure and worldwide distribution of races is fundamental to the search for sources of resistance and for the establishment of successful resistance breeding programs.

The aim of this study was to investigate selective processing biases towards smoking-related stimuli in relation to acute abstinence and smoking history. Differences in the processing of smoking-related and control cues in current smokers, ex-smokers and never-smokers on the modified Stroop task were investigated, with smokers randomized to either abstain or smoke normally for a period of 24 h. The results indicated no significant effect of deprivation (abstinent versus non-abstinent smokers), or of smoking history (ex- versus never-smokers) on colour-naming times for smoking-related versus control words. However, there was a significant effect of smoking status (current versus non-smokers) on colour-naming times for smoking words compared to control words (i.e. slower colour-naming of smoking-related words in smokers). This effect approached significance when stimuli were presented in a masked exposure condition. Among smokers, colour-naming interference was associated with the personality trait of Sensitivity to Reward. These results indicate a processing bias for smoking-related cues in current smokers. However, this bias does not appear to be a permanent feature of nicotine addiction, given the lack of difference between ex-smokers and never-smokers.

Two hundred and seventy-six accessions of mainly Brassica spp. were screened for resistance to Xanthomonas campestris pv. campestris races. In Brassica oleracea (C genome), the majority of accessions were susceptible to all races, but 43% showed resistance to one or more of the rare races (2, 3, 5, and 6) and a single accession showed partial resistance to races 1, 3, 5, and 6. Further searches for resistance to races 1 and 4, currently the most important races worldwide, and race 6, the race with the widest host range, were made in accessions representing the A and B genomes. Strong resistance to race 4 was frequent in B. rapa (A genome) and B. napus (AC genome), indicating an A genome origin. Resistance to races 1 and 4 was present in a high proportion of B. nigra (B genome) and B. carinata (BC genome) accessions, indicating a B genome origin. B. juncea (AB genome) was the most resistant species, showing either strong resistance to races 1 and 4 or quantitative resistance to all races. Potentially race-nonspecific resistance was also found, but at a lower frequency, in B. rapa, B. nigra, and B. carinata. The combination of race-specific and race-nonspecific resistance could provide durable control of black rot of crucifers.

Abstract-NO is known to induce expression of heme oxygenase-1, an antioxidant enzyme in blood vessels. We tested whether NO might modulate the endothelial NADPH oxidase function via heme oxygenase-1. In human microvascular endothelial cells, the NO donor DETA-NONOate (0.1 to 1 mmol/L) strongly induced expression of heme oxygenase-1 but not Cu/Zn superoxide dismutase. This was associated with a reduction of the superoxide-generating capacity of NADPH oxidase, an effect that depended on de novo gene transcription and heme oxygenase-1 activity. Activation of NADPH oxidase by tumor necrosis factor (TNF) ␣ increased generation of reactive oxygen species. DETA-NONOate alone had little effect on TNF-stimulated reactive oxygen species, but it enhanced the TNF response when: (1) heme oxygenase-1 expression was blocked with specific small-interfering RNA; (2) heme oxygenase-1 activity was blocked by zinc-protoporphyrin; or (3) NADPH oxidase activity was blocked by diphenyleneiodonium. Moreover, the heme oxygenase-1 end product bilirubin directly inhibited fully functional NADPH oxidase and seemed to interrupt the assembly and activation of the oxidase. In conclusion, NO may modulate superoxide production by NADPH oxidase in human vascular endothelial cells, at least partly by inducing heme oxygenase-1. Our results indicate that suppression of NADPH oxidase-dependent reactive oxygen species formation may represent a novel mechanism underlying the cardiovascular protective actions of heme oxygenase-1 and bilirubin. Key Words: bilirubin Ⅲ endothelium Ⅲ heme oxygenase-1 Ⅲ NADPH oxidase Ⅲ nitric oxide Ⅲ oxidant stress N itric oxide is crucial for maintaining normal vascular function, and inactivation of NO by excessive production of reactive oxygen species (ROS) is implicated in several cardiovascular diseases. 1,2 There is increasing evidence that NADPH oxidase expressed in endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) is a major source of superoxide. 3 Five isoforms of the Nox subunit of NADPH oxidase have been identified (named Nox1 to Nox5), of which Nox1, Nox2, and Nox4 are found in vascular tissues. 4 -6 Increased NADPH oxidase activation is associated with conditions such as endothelial dysfunction, intimal hyperplasia, atherosclerosis, and hypertension 7 and has been linked to impairment of endothelial NO function in patients with coronary artery disease. 8 Recently, we found that treatment of human microvascular ECs (HMECs) with NO donors inhibited the superoxidegenerating capacity of NADPH oxidase, which may involve S-nitrosylation of the p47phox subunit. 9 In addition, previous studies have revealed that exposure of ECs to exogenous NO induces Nrf2-dependent expression of heme oxygenase-1 (HO-1), 10 the rate-limiting enzyme in heme degradation. Several lines of evidence have indicated that induction of HO-1 has remarkable antioxidant effects, because: (1) bilirubin is a free radical scavenger and has chain-breaking antioxidant activity which may prevent lipid peroxidation 11 ;(2) HO-1 expression ...