Subterranean infestation by Holotrichia parallela larvae is associated with changes in the peanut (Arachis hypogaea L.) rhizosphere microbiome.

Rhizosphere microorganisms contribute to the health and development of crops and these beneficial microbes are recruited to the root-zone when plants experience biotic/abiotic stress. The subterranean pests Holotrichia parallela cause severe crop loss in peanut (Arachis hypogaea L.) fields. Hypothesizing that infestation by H. parallela larva may influence the composition of rhizosphere microbial communities, deep sequencing of V3 and V4 hypervariable regions of 16S rRNA gene was used to characterize the rhizosphere bacteria of infested and uninfested peanuts. A total of 2,673,656 reads were generated and an average of 2558 OTUs were obtained for each sample. Comparisons of rhizosphere bacterial community structure of peanuts with those infested by H. parallela larva revealed that the relative abundance of Proteobacteria and Bacteroidetes increased, while that of Actinobacteria decreased in the rhizosphere with infestation. A significant shift in bacterial communities was observed within 24 h after infestation by principal coordinate analysis. For the 332 genera identified in 24 h treatment, infestation of white grubs led to the significant changes of abundance of 67 genera. An increase in the Pseudomonas genus of infested-samples for 24 h was verified by real-time qPCR. Our results indicate H. parallela larvae infestation can quickly leads to the change of peanut rhizosphere microbiome and enrichment of specific bacterial species. But the effects were not persistent. This study provides the insight into the function of rhizosphere microbiome in the interaction between subterranean pests and crops.

No effect of Bt Cry1Ie toxin on bacterial diversity in the midgut of the Chinese honey bees, Apis cerana cerana (Hymenoptera, Apidae).

Cry1Ie protein derived from Bacillus thuringiensis (Bt) has been proposed as a promising candidate for the development of a new Bt-maize variety to control maize pests in China. We studied the response of the midgut bacterial community of Apis cerana cerana to Cry1Ie toxin under laboratory conditions. Newly emerged bees were fed one of the following treatments for 15 and 30 days: three concentrations of Cry1Ie toxin (20 ng/mL, 200 ng/mL, and 20 µg/mL) in sugar syrup, pure sugar syrup as a negative control and 48 ng/mL imidacloprid as a positive control. The relative abundance of 16S rRNA genes was measured by Quantitative Polymerase Chain Reaction and no apparent differences were found among treatments for any of these counts at any time point. Furthermore, the midgut bacterial structure and compositions were determined using high-throughput sequencing targeting the V3-V4 regions of the 16S rDNA. All core honey bee intestinal bacterial genera such as Lactobacillus, Bifidobacterium, Snodgrassella, and Gilliamella were detected, and no significant changes were found in the species diversity and richness for any bacterial taxa among treatments at different time points. These results suggest that Cry1Ie toxin may not affect gut bacterial communities of Chinese honey bees.

Bt Cry1Ie Toxin Does Not Impact the Survival and Pollen Consumption of Chinese Honey Bees, Apis cerana cerana (Hymenoptera, Apidae).

The cry1Ie gene may be a good candidate for the development of Bt maize because over-expression of Cry1Ie is highly toxic to Lepidopteran pests such as Heliothis armigera Hübner and Ostrinia furnacalis Guenée. The Bt cry1Ie gene also has no cross resistance with other insecticidal proteins such as Cry1Ab, Cry1Ac, Cry1Ah, or Cry1F. Chinese honey bees (Apis cerana cerana) are potentially exposed to insect-resistant genetically modified (IRGM) crops expressing Cry1Ie toxin via the collection of IRGM crop pollen. In this study, we tested whether Chinese honey bee workers are negatively affected by sugar syrup containing 20, 200, or 20,000 ng/ml Cry1Ie toxin and 48 ng/ml imidacloprid under controlled laboratory conditions. Our results demonstrated that the Cry1Ie toxin does not adversely impact survival and pollen consumption of Chinese honey bees. However, imidacloprid decreases Chinese honey bee survival and the total pollen consumption on the 5th, 6th, and 18th d of exposure. The described bioassay is suitable to assess the effects of GM expressed toxins against honey bee.

Bt Toxin Cry1Ie Causes No Negative Effects on Survival, Pollen Consumption, or Olfactory Learning in Worker Honey Bees (Hymenoptera: Apidae).

The honey bee ( Apis mellifera L.) is a key nontarget insect in environmental risk assessments of insect-resistant genetically modified crops. In controlled laboratory conditions, we evaluated the potential effects of Cry1Ie toxin on survival, pollen consumption, and olfactory learning of young adult honey bees. We exposed worker bees to syrup containing 20, 200, or 20,000 ng/ml Cry1Ie toxin, and also exposed some bees to 48 ng/ml imidacloprid as a positive control for exposure to a sublethal concentration of a toxic product. Results suggested that Cry1Ie toxin carries no risk to survival, pollen consumption, or learning capabilities of young adult honey bees. However, during oral exposure to the imidacloprid treatments, honey bee learning behavior was affected and bees consumed significantly less pollen than the control and Cry1Ie groups.

The effects of Bt Cry1Ie toxin on bacterial diversity in the midgut of Apis mellifera ligustica (Hymenoptera: Apidae).

The honey bee has been regarded as a key species in the environmental risk assessment of biotech crops. Here, the potential adverse effects of Cry1Ie toxin on the midgut bacteria of the worker bees (Apis mellifera ligustica) were investigated under laboratory conditions. Newly emerged bees were fed with different concentrations of Cry1Ie toxin syrups (20 ng/mL, 200 ng/mL, and 20 µg/mL), pure sugar syrup, and 48 ppb of imidacloprid syrups, then sampled after 15 and 30 d. We characterized the dominant midgut bacteria and compared the composition and structure of the midgut bacterial community in all samples using the Illumina MiSeq platform targeting the V3-V4 regions of 16S rDNA. No significant differences in the diversity of the midgut bacteria were observed between the five treatments. This work was the first to show the effects of Cry1Ie toxin on honey bees, and our study provided a theoretical basis for the biosafety assessment of transgenic Cry1Ie maize.

Anatomic properties of coronary arteries are correlated to the corrected thrombolysis in myocardial infarction frame count in the coronary slow flow phenomenon.

BACKGROUND: Coronary slow flow phenomenon (CSFP) is an important, angiographic clinical entity, but its etiology remains unclear. The purpose of this study was to explore the potential role of local coronary anatomic properties in the genesis of CSFP. METHODS: One hundred and thirty-one consecutive patients with CSFP and 131 patients with angiographically normal coronary flow were prospectively enrolled after documenting coronary flow by corrected thrombolysis in myocardial infarction frame count (CTFC). Local anatomic parameters including the tortuosity index (TI), the ostial-to-middle diameter ratio, the ostial-to-middle cross-sectional area ratio, and the number of distal branches (NDB) of arteries at end-systole were compared between patients with CSFP and controls. RESULTS: For each major coronary artery, CSFP patients had higher TI and NBD compared with controls (all P<0.05). The diameter ratio and cross-sectional area ratio of the three major coronary arteries were higher in the CSFP group (P=0.004 and 0.020, respectively). The TI (r=0.476, P<0.001) and NDB (r=0.186, P=0.004) were significantly correlated with CTFC. However, the higher TI (ß=0.424, P<0.001) was the only independent correlate to CTFC. Multivariate logistic analysis revealed that TI (adjusted odds ratio 1.17, 95% confidence interval 1.11-1.23, P<0.001) and NDB (adjusted odds ratio 2.20, 95% confidence interval 1.50-3.21, P<0.001) were independent predictors of CSFP. CONCLUSION: The presence of CSFP was associated with higher tortuosity and more distal branches in coronary arteries, indicating that the anatomic properties of coronary arteries could also play a role in the pathogenesis of CSFP.

[Effect of statin therapy on mortality in patients with non-ischemic dilated cardiomyopathy].

OBJECTIVE: To explore the effect of early statin therapy (atorvastatin and simvastatin) on mortality in patients with non-ischemic dilated cardiomyopathy. METHODS: A retrospective study was conducted at a single center. A total of 315 patients with non-ischemic dilated cardiomyopathy, admitted into our hospital from January 2002 to December 2008, were enrolled. The association of statin therapy at the initial hospitalization with all-cause mortality was evaluated. The median follow-up period was 45.1 months. RESULTS: By the single-factor analysis, we found that the follow-up mortality was 17.2% in statin group and it was significantly lower than 37.4% of non-statin users (P = 0.003); in patients with worsening cardiac function NYHA III - IV, the mortality of statin group was 17.2% while a much higher mortality of 47.4% was found in non-statin users (P = 0.003); in patients with NYHA I - II, no significant difference was found in mortality between two groups. By the multi-factor analysis adjusting for age, gender, history of hypertension, diabetes mellitus, current cigarette smoking, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, left ventricular ejection fraction, NYHA functional class, use of angiotensin-converting enzyme inhibitor, ß blocker, aldosterone, other diuretics, digoxin and calcium channel blocker, we found the relative risk (RR) of death in statin use was 0.352 (95%CI 0.135 - 0.920, P = 0.033). In patients with NYHA III - IV, the relative death risk of statin therapy was 0.250 (95%CI 0.081 - 0.778, P = 0.017). CONCLUSIONS: Early treatment of atorvastatin or simvastatin is closely correlated with the reduction of mortality in non-ischemic dilated cardiomyopathy patients, especially in those with severe heart failure. And the correlation is independent of the lipid-lowering effects of statins, ACEI and ß-blocker therapy.

Coronary slow flow phenomenon: a local or systemic disease?

Coronary slow flow phenomenon (CSFP) is an important, angiographic entity characterized by delayed progression of the contrast medium injected into the coronary tree. Since definition of this phenomenon in 1972, there has not been any clear-cut etiology. Original data often focused on histological or pathological changes in coronary artery itself. It was confirmed that small vessel structural defect as well as an underlying residual microvascular resistance abnormality coexists in the coronary microcirculation. Early atherosclerosis was also detected in epicardial coronary arteries by intravascular ultrasound (IVUS). Taken together, it can be suggested that a combination of morphological and functional abnormalities in small vessels and epicardial coronary arteries contributes to the pathogenesis of CSFP. CSFP may be defined as a local disease confined to coronary arteries. However, another feature of CSFP is its frequent occurrence in association with more widespread vascular abnormalities. Reduced endothelial function is implicated in CSFP as measured by flow-mediated dilatation (FMD) of the brachial artery, suggesting that endothelial dysfunction appears to be a generalized process affecting both coronary and peripheral vasculature. In addition, several studies have now demonstrated that carotid intima-media thickness (IMT) is significantly increased in patients with CSFP and there was a significant correlation between coronary intima-media thickness and carotid IMT. Therefore, we hypothesize that CSFP is not an isolated finding but may be part of a systemic vascular disturbance. CSFP is not an infrequently detected finding typically observed in patients presenting with an acute coronary syndrome, usually unstable angina. The subsequent clinical course is characterized by high frequency of relapsing chest pain resulting in considerable impairment in quality of life. Accordingly, further experimental investigations and clinical studies are warranted to shed light into the pathogenesis as well as therapeutics of CSFP.

Can transthoracic Doppler echocardiography be used to detect coronary slow flow phenomenon?

BACKGROUND: Coronary slow flow phenomenon (CSFP) is an important, angiographic clinical entity but is lacking non-invasive detecting techniques. This study aimed to elucidate the value of transthoracic Doppler echocardiography (TTDE) in the diagnosis and monitoring of coronary slow flow in left anterior descending (LAD) coronary artery. METHODS: We consecutively enrolled 27 patients with CSFP in LAD detected by coronary arteriography from August 2009 to April 2010. Thirty-eight patients with angiographically normal coronary flow served as control. Corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC) was used to document coronary flow velocities. All subjects underwent TTDE within 24 hours after coronary angiography. LAD flow was detected and the coronary diastolic peak velocities (DPV) and diastolic mean velocities (DMV) were calculated. RESULTS: Sixty of 65 (92.3%) subjects successfully underwent TTDE. Baseline clinical characteristics were similar between the two groups. Coronary DPV and DMV of LAD were significantly lower in the CSFP group than in the control group ((0.228 ± 0.029) m/s vs. (0.302 ± 0.065) m/s, P = 0.000; (0.176 ± 0.028) m/s vs. (0.226 ± 0.052) m/s, P = 0.000, respectively). There was a high inverse correlation between CTFC and coronary DPV and DMV (r = -0.727, P = 0.000; r = -0.671, P = 0.000, respectively). Receiver operating characteristic (ROC) curve showed that the area under the curve (AUC) was less than one half for coronary DPV (AUC = 0.104) and DMV (AUC = 0.204), respectively. CONCLUSIONS: In patients with CSFP, there is a high inverse correlation between CTFC and coronary diastolic flow velocities in the LAD coronary artery, as measured by TTDE. The value of TTDE in the monitoring and evaluation of coronary flow in patients with CSFP deserves further investigation.