Effect of bacterial seed treatment on number of galls and egg masses of <i>M. incognita</i> after propagation on tomato plants.

a<p>Tukey-Kramer grouping for least squares means (α = 0.05): Means followed by the same letter are not significantly different (n = 12).</p

Comparison of the effects by direct and by plant-mediated antagonism on root penetration by juveniles.

<p><i>M. incognita</i> juveniles (J2) and bacterial strains were inoculated spatially separated in opposite pots of one split-root system (white bars), or co-inoculated with J2 in one pot of another split root system (gray bars). Controls were inoculated with J2 and the not antagonistic strain <i>E. coli</i> JM109, or only with nematodes. J2 penetrated into tomato roots were counted 10 days after inoculation (A). Numbers of galls (B), egg masses (C), eggs per root (D), and eggs per egg mass (E) were determined 50 days after J2 inoculation. Error bars represent standard deviations. Different letters indicate significant differences at <i>P≤0.05</i> according to Tukey's test (n = 10).</p

Effect of bacterial culture supernatants on plant growth of tomato infected with <i>M. incognita.</i>

<p>^* Significantly different (<i>P</i>≤0.05, Dunnett adjustment, n = 10) to both control treatments (JM109 culture supernatant and sterile culture medium).</p

<i>M. incognita</i> reproduction affected by bacterial antagonists through induced systemic resistance of tomato.

<p>Juveniles and bacteria were inoculated in opposite pots of split root systems. Controls were inoculated with the not antagonistic strain <i>E. coli</i> JM109, or left uninoculated. A: Experimental setup of the split root system. B: Mean numbers of galls (white bars) and egg masses (gray bars) counted 50 days after nematode inoculation; error bars represent standard deviations, different letters indicate significant differences at <i>P≤0.05</i> according to Tukey's test (n = 10).</p

Bacterial isolates used in this study.

a<p>GB: G. Berg, University of Technology, Graz, Austria; KS: K. Smalla, Julius Kühn-Institut, Braun­schweig, Germany: RS: R. Sikora, Bonn University, Germany; P: Promega, Mannheim, Germany.</p

Effect of bacterial culture supernatants on reproduction of <i>M. incognita</i> on tomato plants.

a<p>Tukey-Kramer grouping for least squares means: Means followed by the same letter within each column are not significantly different (α = 0.05, n = 10).</p

Effect of bacterial antagonists on repellence of <i>M. incognita</i> juveniles.

<p>Juveniles were attracted by tomato roots and moved from a tube connecting two pots either to the side inoculated with an antagonistic strain or to the opposite side. Controls were inoculated on one side with the not antagonistic strain <i>E. coli</i> JM109, or left uninoculated. Juveniles penetrated into the roots were counted on both sides. Error bars represent standard deviations. Different letters indicate significant differences at <i>P≤0.05</i> according to Tukey's test (n = 10).</p

Outpatient parenteral antimicrobial therapy (OPAT) for aortic vascular graft infection; a five-year retrospective evaluation

Objectives: An estimated 1% of endovascular aneurysm repair (EVAR) devices become infected, carrying a high mortality rate. Surgical explantation is recommended and prognosis is guarded. This retrospective cohort analysis focuses on the role of outpatient parenteral antimicrobial therapy (OPAT) in the management of aortic vascular graft infections following EVAR. Methods: Patients who received OPAT for aortic graft infections (AGI) following EVAR from 2014 to 2018 inclusive were identified using the OPAT database. Clinical, microbiological and radiological data were collected. Survivors were followed up for a median of 36 months (range 25-60) after first presentation with infection. Outcomes were assessed. Results: Eleven cases with 20 OPAT episodes were identified: 10/11 male, median age 76 (IQR 71-81). Median time to presentation was 7 months (range 0-81 months) after EVAR. OPAT lead to a 55% reduction in length of hospital stay. One patient had graft explantation; four others had temporising measures. Eight of 11 were alive a median of 36 months after presentation with infection, having had a median of 2 re-treatments on OPAT (range 1-3). Seven of the eight survivors were on continuous suppressive oral antimicrobials; three were also intermittently on intravenous antibiotics for flares of infection. Patient/ infection outcomes were cure (1/11), improved (7/11), failure (3/11). Conclusion: AGI following EVAR usually presents in the first year after graft deployment. OPAT has an important peri-operative role in patients suitable for curative surgery. OPAT followed by oral suppressive antimicrobial therapy can be a feasible long-term treatment for non-curative management of AGI. Survival in our cohort was longer than expected, and OPAT was feasible despite the complexity of these infections. OPAT can avoid multiple and lengthy hospital admissions and maximise time at home and quality of life in this cohort with life-limiting infection.</p

Data_Sheet_1_Valproic Acid Induces Endothelial-to-Mesenchymal Transition-Like Phenotypic Switching.PDF

<p>Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, is a widely used anticonvulsant drug that is currently undergoing clinical evaluation for anticancer therapy due to its anti-angiogenic potential. Endothelial cells (ECs) can transition into mesenchymal cells and this form of EC plasticity is called endothelial-to-mesenchymal transition (EndMT), which is widely implicated in several pathologies including cancer and organ fibrosis. However, the effect of VPA on EC plasticity and EndMT remains completely unknown. We report herein that VPA-treatment significantly inhibits tube formation, migration, nitric oxide production, proliferation and migration in ECs. A microscopic evaluation revealed, and qPCR, immunofluorescence and immunoblotting data confirmed EndMT-like phenotypic switching as well as an increased expression of pro-fibrotic genes in VPA-treated ECs. Furthermore, our data confirmed important and regulatory role played by TGFβ-signaling in VPA-induced EndMT. Our qPCR array data performed for 84 endothelial genes further supported our findings and demonstrated 28 significantly and differentially regulated genes mainly implicated in angiogenesis, endothelial function, EndMT and fibrosis. We, for the first time report that VPA-treatment associated EndMT contributes to the VPA-associated loss of endothelial function. Our data also suggest that VPA based therapeutics may exacerbate endothelial dysfunction and EndMT-related phenotype in patients undergoing anticonvulsant or anticancer therapy, warranting further investigation.</p

Table_1_Valproic Acid Induces Endothelial-to-Mesenchymal Transition-Like Phenotypic Switching.PDF

<p>Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, is a widely used anticonvulsant drug that is currently undergoing clinical evaluation for anticancer therapy due to its anti-angiogenic potential. Endothelial cells (ECs) can transition into mesenchymal cells and this form of EC plasticity is called endothelial-to-mesenchymal transition (EndMT), which is widely implicated in several pathologies including cancer and organ fibrosis. However, the effect of VPA on EC plasticity and EndMT remains completely unknown. We report herein that VPA-treatment significantly inhibits tube formation, migration, nitric oxide production, proliferation and migration in ECs. A microscopic evaluation revealed, and qPCR, immunofluorescence and immunoblotting data confirmed EndMT-like phenotypic switching as well as an increased expression of pro-fibrotic genes in VPA-treated ECs. Furthermore, our data confirmed important and regulatory role played by TGFβ-signaling in VPA-induced EndMT. Our qPCR array data performed for 84 endothelial genes further supported our findings and demonstrated 28 significantly and differentially regulated genes mainly implicated in angiogenesis, endothelial function, EndMT and fibrosis. We, for the first time report that VPA-treatment associated EndMT contributes to the VPA-associated loss of endothelial function. Our data also suggest that VPA based therapeutics may exacerbate endothelial dysfunction and EndMT-related phenotype in patients undergoing anticonvulsant or anticancer therapy, warranting further investigation.</p