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as symptom experience and influencing factors. Evidence-based guidelines are needed for symptom management, and for high quality of care for patients experiencing low PBT-related HRQoL.

The use of cranial re-irradiation is growing with improving overall survival and the advent of high-precision radiotherapy techniques. Still the value of re-irradiation needs careful evaluation regarding safety and efficacy. We analyzed dosimetric and clinical data of patients receiving cranial re-irradiation using EQD2 sum plans.

We retrospectively analyzed the data of 76 patients who received repeated cranial radiotherapy from 02/2013 to 09/2016. 34 patients suffered from recurrent primary brain tumors, 42 from brain metastases. Dosimetric analysis was performed accumulating EQD2 dose distributions based on rigid image registration. Clinical and radiological data was collected at follow-ups including toxicity, local control and overall survival.

In total 76 patients had at least 2 courses of intracranial radiotherapy. The median accumulated prescription EQD2 dose was 96.5Gy

for all radiation courses combined. The median D(0.1cc) of the brain for patients receiving more than 100Gy

was 114Gy

with a highest dose of 161.5Gy

. 74% of patients suffered from low grade (G1-G2) acute toxicity, only two high grade (>G3) toxicities were recorded.Median overall survival from the time of first re-irradiation was 57weeks (range 4-186weeks). The median time to local failure for patients with a primary brain tumor was not reached and 24weeks (range 1-77weeks) for patients with brain metastases.

Repeated radiotherapy appears both safe and efficient in patients with recurrent primary or secondary brain tumors with doses to the brain up to 120Gy

EQD2, doses below 100Gy

for brainstem and doses below 75Gy

EQD2 to chiasm and optic nerves.

Repeated radiotherapy appears both safe and efficient in patients with recurrent primary or secondary brain tumors with doses to the brain up to 120 Gy2 EQD2, doses below 100 Gy2 for brainstem and doses below 75 Gy2 EQD2 to chiasm and optic nerves.

Adjuvant radiotherapy of internal mammary nodes (IMN) improves survival in high-risk early breast cancer patients but inevitably leads to more dose to heart and lung. Target coverage is often compromised to meet heart/lung dose constraints. We estimate heart and lung dose when target coverage is not compromised in consecutive patients. These estimates are used to guide the choice of selection criteria for the randomised Danish Breast Cancer Group (DBCG) Proton Trial.

179 breast cancer patients already treated with loco-regional IMN radiotherapy from 18 European departments were included. If the clinically delivered treatment plan did not comply with defined target coverage requirements, the plan was modified retrospectively until sufficient coverage was reached. The choice of selection criteria was based on the estimated number of eligible patients for different heart and lung dose thresholds in combination with proton therapy capacity limitations and dose-response relationships for heart and lung.

Median mean heart dose was 3.0Gy (range, 1.1-8.2Gy) for left-sided and 1.4Gy (0.4-11.5Gy) for right-sided treatment plans. Median V17Gy/V20Gy (hypofractionated/normofractionated plans) for ipsilateral lung was 31% (9-57%). The DBCG Radiotherapy Committee chose mean heart dose≥4Gy and/or lung V17Gy/V20Gy≥37% as thresholds for inclusion in the randomised trial. Using these thresholds, we estimate that 22% of patients requiring loco-regional IMN radiotherapy will be eligible for the trial.

The patient selection criteria for the DBCG Proton Trial are mean heart dose≥4Gy and/or lung V17Gy/V20Gy≥37%.

The patient selection criteria for the DBCG Proton Trial are mean heart dose ≥ 4 Gy and/or lung V17Gy/V20Gy ≥ 37%.Jasmonic acid (JA) is regarded as an endogenous regulator which plays an important role in regulating plant growth, development and stress response. Using the seedlings of A. thaliana ecotype Col-0 (wild-type, WT), phospholipase Dδ (PLDδ) deficient mutant (pldδ), the G protein α subunit (GPA1) deficient mutant (gpa1-4), 9-Lipoxygenase (9-LOX) deficient mutants (lox1 and lox5) as materials, the effects of JA responding to osmotic stress and the functions of G protein and PLDδ in this response were investigated. The results showed that GPA1 involved in the regulation of JA to PLDδ under osmotic stress. Both GPA1 and PLDδ participated in the regulation of JA on the seed germination and osmotic tolerance. Exogenous MeJA reduced the EL and MDA in WT, but increased the EL and MDA in gpa1-4 and pldδ, indicating that GPA1 and PLDδ were involved in the protection of JA on the membrane. The genes expression levels, and the activities of PLDδ and LOX1 were significantly induced by osmotic stress. The LOX activity and JA content in pldδ seedings were lower obviously than those in WT, but were markedly increased and were higher than WT after applying phosphatidic acid (PA). These results demonstrated that JA responded to osmotic stress by regulating G protein and PLDδ in A. thaliana. PLDδ was located upstream of 9-LOX and involved in the JA biosynthesis.Virulence factor regulator (Vfr) is an indispensable transcription factor in the expression of virulence in the phytopathogenic bacteria Pseudomonassyringae. However, the function of Vfr is not known so far. The deletion of vfr resulted in the loss of surface swarming motility and reduced the virulence in P. syringae pv. tabaci (Pta) 6605. In order to identify the target genes of Vfr, we screened the sequences that bind to Vfr by chromatin immune precipitation (ChIP) and sequencing methods using the closely related bacterium P. syringae pv. syringae (Pss) B728a. For this purpose we first generated a strain that possesses the recombinant gene vfrFLAG in Pss B728a, and performed ChIP using an anti-FLAG antibody. Immunoprecipitated DNA was purified and sequenced with Illumina HiSeq. Entospletinib solubility dmso The VfrFLAG-specific peaks were further subjected to an electrophoresis mobility-shift assay, and the promoter regions of locus tag for Psyr_0578 , Psyr_1776, and Psyr_2237 were identified as putative target genes of Vfr. These genes encode plant pathogen-specific methyl-accepting chemotaxis proteins (Mcp).