Carrot yellow leaf virus is associated with carrot internal necrosis.

Internal necrosis of carrot has been observed in UK carrots for at least 10 years, and has been anecdotally linked to virus infection. In the 2009 growing season some growers had up to 10% of yield with these symptoms. Traditional diagnostic methods are targeted towards specific pathogens. By using a metagenomic approach with high throughput sequencing technology, other, as yet unidentified causes of root necrosis were investigated. Additionally a statistical analysis has shown which viruses are most closely associated with disease symptoms. Carrot samples were collected from a crop exhibiting root necrosis (102 Affected: 99 Unaffected) and tested for the presence of the established carrot viruses: Carrot red leaf virus (CtRLV), Carrot mottle virus (CMoV), Carrot red leaf associated viral RNA (CtRLVaRNA) and Parsnip yellow fleck virus (PYFV). The presence of these viruses was not associated with symptomatic carrot roots either as single viruses or in combinations. A sub-sample of carrots of mixed symptom status was subjected to MiSeq sequencing. The results from these tests suggested Carrot yellow leaf virus (CYLV) was associated with symptomatic roots. Additionally a novel Torradovirus, a novel Closterovirus and two novel Betaflexiviradae related plant viruses were detected. A specific diagnostic test was designed for CYLV. Of the 102 affected carrots, 98% were positive for CYLV compared to 22% of the unaffected carrots. From these data we conclude that although we have yet to practically demonstrate a causal link, CYLV appears to be strongly associated with the presence of necrosis of carrots.

Infusion of Mg in humans acutely reduces serum insulin levels: a pilot study.

BACKGROUND: Infusion of Mg for therapeutic purposes is still a matter for debate. Dosages vary considerably, yet subclinical effects on normal physiology are largely ignored. In human and animal models, interactions between Mg and insulin exist, thus we have investigated the effect of infusing Mg on serum insulin, ionised Mg (Mg(2+)) and Ca (Ca(2+)) and plasma glucose in human volunteers. METHODS: Six male volunteers were infused with magnesium sulphate (MgSO(4)) dissolved in normal saline, using a high-dose "loading" bolus, followed by a lower-level "maintenance" period. FINDINGS: Serum Mg(2+) rose rapidly throughout the bolus infusion, declined during the maintenance phase, but remained higher than pre-infusion levels throughout the experimental period; serum Ca(2+) rose when serum Mg(2+) was highest. Infusion of MgSO(4) had no effect on heart rate or blood pressure, but caused a rapid, pronounced drop in circulating fasting insulin (p<0.0005), which slowly recovered to basal values during the course of the maintenance infusion. A slight, transient rise in plasma glucose (p<0.05) concomitant with the decline in serum insulin was also observed. INTERPRETATION: It is possible that the effect of Mg(2+) on insulin may have been due to antagonism of Ca(2+) entry in pancreatic beta-cells, the insulin decline causing a subsequent rise in circulating glucose levels. We suggest that these effects of MgSO(4) infusions should be considered where the aim is to achieve high doses of blood Mg(2+) levels by clinical intervention.

Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.

AIM: Exposure to road traffic and air pollution may be a trigger of acute myocardial infarction, but the individual pollutants responsible for this effect have not been established. We assess the role of combustion-derived-nanoparticles in mediating the adverse cardiovascular effects of air pollution. METHODS AND RESULTS: To determine the in vivo effects of inhalation of diesel exhaust components, 16 healthy volunteers were exposed to (i) dilute diesel exhaust, (ii) pure carbon nanoparticulate, (iii) filtered diesel exhaust, or (iv) filtered air, in a randomized double blind cross-over study. Following each exposure, forearm blood flow was measured during intra-brachial bradykinin, acetylcholine, sodium nitroprusside, and verapamil infusions. Compared with filtered air, inhalation of diesel exhaust increased systolic blood pressure (145 ± 4 vs. 133 ± 3 mmHg, P< 0.05) and attenuated vasodilatation to bradykinin (P= 0.005), acetylcholine (P= 0.008), and sodium nitroprusside (P< 0.001). Exposure to pure carbon nanoparticulate or filtered exhaust had no effect on endothelium-dependent or -independent vasodilatation. To determine the direct vascular effects of nanoparticulate, isolated rat aortic rings (n= 6-9 per group) were assessed in vitro by wire myography and exposed to diesel exhaust particulate, pure carbon nanoparticulate and vehicle. Compared with vehicle, diesel exhaust particulate (but not pure carbon nanoparticulate) attenuated both acetylcholine (P< 0.001) and sodium-nitroprusside (P= 0.019)-induced vasorelaxation. These effects were partially attributable to both soluble and insoluble components of the particulate. CONCLUSION: Combustion-derived nanoparticulate appears to predominately mediate the adverse vascular effects of diesel exhaust inhalation. This provides a rationale for testing environmental health interventions targeted at reducing traffic-derived particulate emissions.

The role of ACE inhibitor therapy in treating cardiovascular disease.

The first angiotensin-converting enzyme (ACE) inhibitors were introduced in 1981. They are used in the management of a variety of cardiovascular disorders and their role in hypertension, heart failure, managing asymptomatic and symptomatic left-ventricular dysfunction, post-myocardial infarction, stroke prevention, and diabetes is now well established. This is recognised in the National Service Framework for Coronary Heart Disease (Department of Health, 2000) and the guidelines from the British Hypertension Society (Ramsay et al, 1999). Nurses have a responsibility as part of the multidisciplinary team to have knowledge of various aspects of these drugs.