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Rose is the world’s most important ornamental plant, with economic, cultural and symbolic value. Roses are cultivated worldwide and sold as garden roses, cut flowers and potted plants. Roses are outbred and can have various ploidy levels. Our objectives were to develop a high-quality reference genome sequence for the genus Rosa by sequencing a doubled haploid, combining long and short reads, and anchoring to a high-density genetic map, and to study the genome structure and genetic basis of major ornamental traits. We produced a doubled haploid rose line (‘HapOB’) from Rosa chinensis ‘Old Blush’ and generated a rose genome assembly anchored to seven pseudo-chromosomes (512 Mb with N50 of 3.4 Mb and 564 contigs). The length of 512 Mb represents 90.1–96.1% of the estimated haploid genome size of rose. Of the assembly, 95% is contained in only 196 contigs. The anchoring was validated using high-density diploid and tetraploid genetic maps. We delineated hallmark chromosomal features, including the pericentromeric regions, through annotation of transposable element families and positioned centromeric repeats using fluorescent in situ hybridization. The rose genome displays extensive synteny with the Fragaria vesca genome, and we delineated only two major rearrangements. Genetic diversity was analysed using resequencing data of seven diploid and one tetraploid Rosa species selected from various sections of the genus. Combining genetic and genomic approaches, we identified potential genetic regulators of key ornamental traits, including prickle density and the number of flower petals. A rose APETALA2/TOE homologue is proposed to be the major regulator of petal number in rose. This reference sequence is an important resource for studying polyploidization, meiosis and developmental processes, as we demonstrated for flower and prickle development. It will also accelerate breeding through the development of molecular markers linked to traits, the identification of the genes underlying them and the exploitation of synteny across Rosaceae.

[EN] Phenylpropanoid volatiles are responsible for the key tomato fruit (Solanum lycopersicum) aroma attribute termed "smoky." Release of these volatiles from their glycosylated precursors, rather than their biosynthesis, is the major determinant of smoky aroma in cultivated tomato. Using a combinatorial omics approach, we identified the NON-SMOKY GLYCOSYLTRANSFERASE1 (NSGT1) gene. Expression of NSGT1 is induced during fruit ripening, and the encoded enzyme converts the cleavable diglycosides of the smoky-related phenylpropanoid volatiles into noncleavable triglycosides, thereby preventing their deglycosylation and release from tomato fruit upon tissue disruption. In an nsgt1/nsgt1 background, further glycosylation of phenylpropanoid volatile diglycosides does not occur, thereby enabling their cleavage and the release of corresponding volatiles. Using reverse genetics approaches, the NSGT1-mediated glycosylation was shown to be the molecular mechanism underlying the major quantitative trait locus for smoky aroma. Sensory trials with transgenic fruits, in which the inactive nsgt1 was complemented with the functional NSGT1, showed a significant and perceivable reduction in smoky aroma. NSGT1 may be used in a precision breeding strategy toward development of tomato fruits with distinct flavor phenotypes., We thank Syngenta Seeds, Seminis, Enza Zaden, Rijk Zwaan, Vilmorin, and de Ruiter Seeds for providing seeds of the 94 tomato cultivars. We acknowledge financial support from the Center for BioSystems Genomics, provided under the auspices of the Netherlands Genomics Initiative. R.C.H.d.V. and R.D.H. thank the Netherlands Metabolomics Centre for additional funding. We also thank the Metabolomics lab for assistance in volatile determination and Rafael Martinez at the Instituto de Biologia Molecular y Celular de Plantas for excellent plant management. We thank Gerco Angenent for discussions on the research and Ruud de Maagd for critical reading of the article. We also thank Fien Meijer-Dekens and A.W. van Heusden for excellent greenhouse management and plant cultivation. Finally, we thank Harry Jonker and Bert Schipper for preparation and analyses of the samples for LC-QTOF-MS.

Nonbacterial thrombotic endocarditis is the most prevalent endocarditis at autopsy. It is a clinically important cause of arterial embolisation. Often it is observed in association with malignancy (mainly gastrointestinal adenocarcinomata), severe infections and other fulminant acute disease processes. A deranged or damaged valvular surface and clotting disorders are important pathogenic factors. The valvular vegetations are pathologically characterized by a bland, fibrin-platelet thrombus; they usually affect the mitral and aortic valve. Neurologic events are the most common clinical manifestations, but any organ may be involved by emboli. The association of venous and arterial thromboses and pulmonary thromboembolism underscores the pathogenetic role of hypercoagulability in the development of nonbacterial thrombotic endocarditis. The clinician must be a vigilant observer in order to make the antemortem diagnosis. If possible, the underlying process should be treated; anticoagulation therapy with heparin sometimes is helpful.

BACKGROUND: Systemic administration of angiopeptin has been shown to inhibit myointimal thickening after arterial injury in several animal species. METHODS AND RESULTS: To explore to what extent high and long-lasting local concentrations of angiopeptin influence the healing process after vascular injury, tantalum balloon-expandable stents were first coated with a polymer loaded with angiopeptin 250 µg. Implantation of these stents in porcine coronary arteries resulted in tissue concentrations of 10.7 pg/ml wet weight in the stented arterial segment 24 hours after stent implantation, gradually declining to 2.0 pg/ml wet weight at day 8. Finally, 20 pigs were randomly treated with either an angiopeptin-loaded or a blank-coated stent. At baseline, the angiographic parameters were similar between both groups but, after 6 weeks, the minimal luminal diameter of the stented arterial segment was larger in the angiopeptin-treated pigs when compared to controls (2.20 +/- 0.57 mm vs 1.57 +/- 0.68 mm, p0.01) This angiographic finding was confirmed by post-mortem morphometry where the respective lumen area values were 1.00 +/- 0.54 mm2 and 0.43 +/- 0.28 mm2 (p0.01). CONCLUSION: Polymer coated stents can be loaded with angiopeptin, which after implantation in porcine right coronary arteries result in high local tissue concentrations gradually declining over more than 8 days. These high local concentrations inhibit myointimal proliferation induced by poly(organo)phosphazene coated overstretched stents.

AIM The administration of thrombolytic therapy after an acute myocardial infarction can reduce the size of the infarct and improve left ventricular function. We used pulsed Doppler to assess left ventricular diastolic function after an acute myocardial infarction in patients treated with recombinant tissue plasminogen activator (rTPA). PATIENTS AND METHODS We studied 104 patients after an acute myocardial infarction, 48 treated with a placebo and 56 with rTPA. They were compared with 36 age-matched controls. The Doppler parameters measured included the early peak in diastolic flow velocity, the peak during atrial contraction, the atrial: early ratio, mean deceleration, deceleration time, and half-filling fraction. Doppler parameters for large and small infarct sizes were compared. RESULTS The Doppler parameters did not differ between treatment groups. Compared with the normal controls, significant differences were observed in both treatment groups for the early peak (placebo P < 0.05; rTPA P < 0.001), the atrial: early ratio (placebo P < 0.05; rTPA P < 0.01), and the half-filling fraction (P < 0.001 for both). In patients with large infarcts, the atrial peak was depressed (P = 0.008). Multivariate analysis showed that end-diastolic pressure, age, end-systolic volume, and regional wall motion parameters were major predictors of Doppler parameters.

Using global constraints and dynamic programming, a new model-based segmentation algorithm was developed to determine myocardial borders and basal plane. The segmented image is transformed to a countrate polar map and the infarct size (I.S.) is determined by comparison with a reference polar map. In order to evaluate our method the algorithm was applied to heart phantoms, to software simulations and to animal studies. In the last experiments, Tc-99m Sestamibi was used as a perfusion agent. The total myocardial volume and infarct size of a Jasczack phantom were overestimated, especially when I.S. was expressed in absolute rather than relative values. It was proven by software simulations of cardiac Spect studies that those errors were mainly due to finite resolution effects causing a clear overestimation of myocardial thickness. Implementation of a constant thickness in the algorithm resulted in a much better correlation with actual values. In a dog experiment the size of total myocardial volume of the area at risk during occlusion and of the final infarct size after thrombolysis was correlated with the histologic values obtained by planimetry after TTC staining. In 8 studies, an excellent correlation between the histologic area at risk versus the estimated perfusion defects was obtained (r = 0.97). The automatic delineation of myocardial borders and valve plane was excellent even when perfusion defects were present. Manual intervention was only necessary in certain slices where a clear overlap between liver and myocardium was present in the dog studies. Segmental polar maps expressing count rate and volume information provided a visual and quantitative tool to evaluate the influence of thrombolysis in acute ligation experiments. It is concluded that the new algorithm is ready to be used in a clinical environment for the quantitative evaluation of perfusion defects after acute myocardial infarction and for the follow-up of the therapeutic strategy.

Ninety-three patients, who underwent DC shock ablation were reviewed over a mean follow-up period of 54 months (range 3 to 84 months). These patients (46 male and 47 female, mean age: 58 years) had failed an average of 3 drugs, and the duration of symptoms was more than 2 years. Paroxysmal atrial fibrillation or flutter was treated in 75 patients (80.6%); the remainder had supraventricular tachycardia or reciprocating tachycardia using an accessory pathway. One shock of 200 J was effective in producing third degree AV block in 40 patients (43%), while 2 or more shocks were used in another 53 patients (57%). Chronic complete heart block (CHB) was obtained in 85 patients (91%), modification of conduction was seen in 2 patients (2.1%), and failure to achieve an improvement in 6 patients (6.4). All the patients of the last group had received more than 4 shocks (200 to 400 J). However no significant difference between the amplitude of atrial and His electrograms could be shown between the CHB patients and those in whom conduction persisted. Over a mean follow-up of 54 months, 66 patients (72%) with successful ablation during the first 48 hours after the procedure remained in CHB. In 18 patients AV conduction resumed but they were all asymptomatic: 10 patients (10.8%) without antiarrhythmic therapy and 8 patients (8.6%) with medication. In conclusion, ablation of the AV junction is effective in more than 82% of patients. Most of the time long-term success can be predicted within 48 hours. However, due to the invasive character of DC shocks, this technique has been supplanted by the less aggressive radiofrequency method.

Since its introduction in 1984, percutaneous transvenous mitral balloon valvuloplasty (PTMV) has emerged as an effective technique in the treatment of selected patients with severe mitral stenosis. The most important factors determining the haemodynamic and clinical outcome after PTMV are the anatomic and pathological features of the mitral valve apparatus. In patients with pliable, non-calcified valves, immediate success rates of well over 90% are achieved. Short-term follow-up studies of such patients after PTMV demonstrate a low rate of valve restenosis, with the vast majority of patients remaining much improved clinically. Less favourable immediate and short-term results are observed in patients who have non-pliable, calcified valves. Major acute complications of PTMV include thromboembolic events and the production of severe mitral regurgitation. It appears that, as a result of increased operator experience, better patient selection and refinements in the technique of PTMV, the rates of these acute complications are now very low. Follow-up studies will be needed to assess the long-term efficacy of the procedure. The first publications on this field are encouraging.

To assess left ventricular diastolic filling in valvular aortic stenosis, pulsed Doppler echocardiography was used prospectively in 35 patients with severe aortic stenosis (valve area less than 1 cm2) and in 38 age-matched normal subjects. Twenty-seven patients had a normal left ventricular systolic function at rest (ejection fraction greater than 0.50) and a normal or only slightly increased mean pulmonary capillary wedge pressure (mean 11 +/- 4 mm Hg). Eight patients had a poor left ventricular systolic function (ejection fraction: 0.28 +/- 0.10) and an elevated mean pulmonary capillary wedge pressure (mean: 36 +/- 9 mm Hg). The Doppler derived filling parameters were correlated with hemodynamic data, left ventricular wall thickness derived from M-mode echocardiograms, heart rate and atrio-ventricular (A-V) conduction delay using stepwise multiple correlation. The data of this study suggest that left ventricular filling is significantly impaired in patients with severe aortic stenosis and left ventricular hypertrophy with an increase in late diastolic (A-wave) velocity, an increase in the A/E ratio, a decrease in the first one-half filling fraction and a prolongation of early diastolic deceleration time. These changes in filling hemodynamics are associated with alterations in mean pulmonary capillary wedge pressure, left ventricular wall thickness, heart rate and A-V conduction delay. When heart failure develops as a result of impaired left ventricular systolic function, an increase in left atrial filling pressure is associated with a shift of left ventricular filling towards early diastole with a 'normalisation' of the transmitral flow velocity curve. In extreme cases, a progression towards a 'restrictive' filling pattern is found with a marked shortening of the left ventricular early diastolic deceleration time. In the presence of high filling pressures, increased left atrial driving pressure (derived from the mean pulmonary capillary wedge pressure) is associated with changes in the left ventricular filling pattern irrespective of the presence and the degree of myocardial hypertrophy.