Reproductive mode and fine-scale population genetic structure of grape phylloxera (Daktulosphaira vitifoliae) in a viticultural area in California.

BACKGROUND: Grape phylloxera (Daktulosphaira vitifoliae) is one of the world's most important viticultural pests. However, the reproductive mode, genetic structure and host adaptation of phylloxera in various viticultural environments remains unclear. We examined reproductive mode and genetic structure of phylloxera by analyzing microsatellite makers across the samples from four vineyard-sites in California. RESULT: The phylloxera populations in California are believed to have predominantly parthenogenetic reproduction. Therefore, genetic diversity of phylloxera is expected to be limited. However, this study showed relatively high levels of diversity in Napa and Yolo county populations with a large number of unique genotypes, average number of alleles (2.1 to 2.9) and observed heterozygosities (0.330 to 0.388) per vineyard-sites. Reproduction diversity index (G: N-unique genotypes versus number of samples) ranged from 0.500 to 0.656 among vineyard-sites. Both significant and non-significant Psex (probability of sexual reproduction) were observed among different repeated genotypes within each vineyard. Moreover, high variation of FIS was observed among different loci in each vineyard-site. Genetic structure analysis (UPGMA) and various measures of population differentiations (FST, PCA, and gene flow estimates) consistently separated AXR#1 (Vitis vinifera x V. rupestris-widely planted in California during the 1960s and 1970s) associated populations from the populations associated with other different rootstocks. CONCLUSION: Genetic diversity, G: N ratio, Psex and FIS consistently suggested the occurrence of both parthenogenetic and sexual reproduction in California populations. This study clearly identified two major groups of phylloxera obtained from various rootstocks, with one group exclusively associated with only AXR#1 rootstock, defined as "biotype B", and another group associated with vinifera-based rootstocks, known as "biotype A".

Impact of mild or moderate chronic kidney disease on the frequency of restenosis: results from the PRESTO trial.

OBJECTIVES: The goal of this study was to determine if restenosis is increased in mild and moderate chronic kidney disease (CKD) patients after percutaneous coronary intervention (PCI). BACKGROUND: Mortality is increased in CKD after PCI. Restenosis may contribute to increased late mortality. METHODS: We analyzed 11,187 patients with a creatinine <1.8 mg/dl from the Prevention of REStenosis with Tranilast and its Outcomes (PRESTO) trial, grouped by estimated creatinine clearance (CrCl) (<60, 60 to 89, >89 ml/min). The Cox proportional hazards models investigated the association between CrCl group and death, myocardial infarction, and target vessel revascularization (TVR). Generalized estimating equation regression models determined the association between CrCl group and lesion-specific restenosis. RESULTS: At 30 days, there was no difference in myocardial infarction, death, or TVR between the CrCl groups. At nine months, mortality was higher in the lowest CrCl group (2.2%, 1.2%, 0.8%; p < 0.001), which was no longer significant after adjusting for confounding variables. Myocardial infarction and TVR were not different between the groups. In patients undergoing protocol follow-up angiography, restenosis (>/=50%) was not increased with CKD (32%, 32%, 37%; p = 0.02). CONCLUSIONS: Mortality nine months after PCI is mildly increased in mild or moderate CKD patients. However, restenosis is not and does not account for the increased mortality.

Randomized, double-blind, placebo-controlled, international trial of the oral IIb/IIIa antagonist lotrafiban in coronary and cerebrovascular disease.

BACKGROUND: This is the primary report of the large-scale evaluation of lotrafiban, an orally administered IIb/IIIa receptor antagonist, a unique trial with respect to the platelet antagonist, protocol design, and inclusion of cerebrovascular disease in a significant proportion of patients. METHODS AND RESULTS: Patients with vascular disease were randomized to lotrafiban 30 or 50 mg BID on the basis of age and predicted creatinine clearance or placebo in addition to aspirin at a dose ranging from 75 to 325 mg/d at the discretion of the physician-investigator. Follow-up was for up to 2 years. The primary end point was the composite of all-cause mortality, myocardial infarction, stroke, recurrent ischemia requiring hospitalization, and urgent revascularization. Of 9190 patients enrolled from 23 countries and 690 hospitals, 41% had cerebrovascular disease at the time of entry, and 59% had coronary artery disease. Death occurred in 2.3% of placebo-assigned patients and 3.0% of lotrafiban-group patients (hazard ratio 1.33, 95% CI 1.03 to 1.72, P=0.026), and the cause of excess death was vascular related. There was no significant difference in the primary end point (17.5% compared with 16.4%, respectively; hazard ratio 0.94, 95% CI 0.85 to 1.03, P=0.19). Serious bleeding was more frequent in the lotrafiban group (8.0% compared with 2.8%; P<0.001). Serious bleeding was more common among patients who received higher doses of aspirin (>162 mg/d), with or without lotrafiban. CONCLUSIONS: Lotrafiban, an orally administered platelet glycoprotein IIb/IIIa blocker, induced a 33% increase in death rate, which was vascular in origin and not affected by the type of atherosclerotic involvement at entry to the trial. Although the dose of aspirin was not randomly assigned, the finding of increased bleeding with doses >162 mg/d is noteworthy.

Results of Prevention of REStenosis with Tranilast and its Outcomes (PRESTO) trial.

BACKGROUND: Restenosis after percutaneous coronary intervention (PCI) is a major problem affecting 15% to 30% of patients after stent placement. No oral agent has shown a beneficial effect on restenosis or on associated major adverse cardiovascular events. In limited trials, the oral agent tranilast has been shown to decrease the frequency of angiographic restenosis after PCI. METHODS AND RESULTS: In this double-blind, randomized, placebo-controlled trial of tranilast (300 and 450 mg BID for 1 or 3 months), 11 484 patients were enrolled. Enrollment and drug were initiated within 4 hours after successful PCI of at least 1 vessel. The primary end point was the first occurrence of death, myocardial infarction, or ischemia-driven target vessel revascularization within 9 months and was 15.8% in the placebo group and 15.5% to 16.1% in the tranilast groups (P=0.77 to 0.81). Myocardial infarction was the only component of major adverse cardiovascular events to show some evidence of a reduction with tranilast (450 mg BID for 3 months): 1.1% versus 1.8% with placebo (P=0.061 for intent-to-treat population). The primary reason for not completing treatment was > or =1 hepatic laboratory test abnormality (11.4% versus 0.2% with placebo, P<0.01). In the angiographic substudy composed of 2018 patients, minimal lumen diameter (MLD) was measured by quantitative coronary angiography. At follow-up, MLD was 1.76+/-0.77 mm in the placebo group, which was not different from MLD in the tranilast groups (1.72 to 1.78+/-0.76 to 80 mm, P=0.49 to 0.89). In a subset of these patients (n=1107), intravascular ultrasound was performed at follow-up. Plaque volume was not different between the placebo and tranilast groups (39.3 versus 37.5 to 46.1 mm(3), respectively; P=0.16 to 0.72). CONCLUSIONS: Tranilast does not improve the quantitative measures of restenosis (angiographic and intravascular ultrasound) or its clinical sequelae.