Oilseed rape (Brassica napus) as a resource for farmland insect pollinators: quantifying floral traits in conventional varieties and breeding systems

This is the final version of the article. Available from the publisher via the DOI in this record.Oilseed rape (OSR; Brassica napus L.) is a major crop in temperate regions and provides an important source ofnutrition to many of the yield-enhancing insect flower visitors that consume floral nectar. The manipulation ofmechanisms that control various crop plant traits for the benefit of pollinators has been suggested in the bid toincrease food security, but little is known about inherent floral trait expression in contemporary OSR varieties orthe breeding systems used in OSR breeding programmes. We studied a range of floral traits in glasshouse-grown, certified conventional varieties of winter OSR to test for variation among and within breeding systems.We measured 24-h nectar secretion rate, amount, concentration and ratio of nectar sugars per flower, and sizesand number of flowers produced per plant from 24 varieties of OSR representing open-pollinated (OP), genicmale sterility (GMS) hybrid and cytoplasmic male sterility (CMS) hybrid breeding systems. Sugar concentrationwas consistent among and within the breeding systems; however, GMS hybrids produced more nectar and moresugar per flower than CMS hybrid or OP varieties. With the exception of ratio of fructose/glucose in OP vari-eties, we found that nectar traits were consistent within all the breeding systems. When scaled, GMS hybridsproduced 1.73 times more nectar resource per plant than OP varieties. Nectar production and amount of nectarsugar in OSR plants were independent of number and size of flowers. Our data show that floral traits of glass-house-grown OSR differed among breeding systems, suggesting that manipulation and enhancement of nectarrewards for insect flower visitors, including pollinators, could be included in future OSR breeding programmes.This work was fundedby the BBSRC, including support from an Insect Pollinators Ini-tiative grant awarded to GAW (BB/I000968/1) that was jointlyfunded by the BBSRC, NERC, the Wellcome Trust, Defra, andthe Scottish Government. Support was also received from HighWycombe Beekeepers’ Association. Rothamsted Researchreceives strategic funding from the Biotechnology and BiologicalSciences Research Council (BBSRC) of the UK

The Risk of Amenorrhea Is Related to Chemotherapy-Induced Leucopenia in Breast Cancer Patients Receiving Epirubicin and Taxane Based Chemotherapy

BACKGROUND: Chemotherapy-induced amenorrhea (CIA) is common in young breast cancer patients. The incidence of CIA associated with regimens involving epirubicin and taxane was not well known. Furthermore, previous studies suggested leucopenia and amenorrhea may reflect inter-individual variations in pharmacokinetics. The purpose of this study was to investigate the association between leucopenia after first cycle of chemotherapy and CIA in young breast cancer patients receiving epirubicin and taxane based chemotherapy. Furthermore, the incidence of CIA was also assessed. METHODOLOGY AND PRINCIPAL FINDINGS: Between October 2008 and March 2010, 186 consecutive premenopausal patients, treated with epirubicin and taxane based chemotherapy, were recruited. Information about CIA was collected by telephone and out-patient clinic. Of these 186 patients, data from 165 patients were included and analyzed. Of all 165 patients, CIA occurred in 72 patients (43.64%). In multivariate analysis, age older than 40 y (OR: 16.10, 95% CI: 6.34-40.88, P<0.001) and previous childbearing (OR: 3.17, 95% CI: 1.06-9.47, P = 0.038) were significantly associated with probability of CIA. Compared to patients treated without taxane, patients treated with taxane-contained regimens did not have a significantly higher rate of CIA (P>0.05). The rate of CIA in leucopenia group (52.56%) was significantly higher than that in normal leukocyte group (34.62%) (P = 0.024). In patients treated with a FEC regimen (cyclophosphamide, epirubicin and 5-fluorouracil), the rate of CIA in leucopenia group (59.57%) was significantly higher than that in normal leukocyte group (36.84%) (P = 0.037). CONCLUSIONS: Age at diagnosis and previous childbearing were both found to significantly increase the risk of CIA, whereas additional taxane was not associated with increased rate of CIA. Importantly, leucopenia after first cycle of chemotherapy was associated with increased risk of CIA, which suggested that leucopenia may be an early predictor of chemotherapy-induced infertility

Leadership and capacity building in international chiropractic research: introducing the chiropractic academy for research leadership (CARL).

In an evidence-based health care environment, healthcare professions require a sustainable research culture to remain relevant. At present however, there is not a mature research culture across the chiropractic profession largely due to deficiencies in research capacity and leadership, which may be caused by a lack of chiropractic teaching programs in major universities. As a response to this challenge the Chiropractic Academy for Research Leadership, CARL, was created with the aim of develop a global network of successful early-career chiropractic researchers under the mentorship of three successful senior academics from Australia, Canada, and Denmark. The program centres upon an annual week-long program residential that rotates continental locations over the first three-year cycle and between residentials the CARL fellows work on self-initiated research and leadership initiatives. Through a competivite application process, the first cohort was selected and consists of 13 early career researchers from five professions in seven countries who represent diverse areas of interests of high relevance for chiropractic. The first residential was held in Odense, Denmark, with the second being planned in April 2018 in Edmonton, Canada, and the final residential to be held in Sydney, Australia in 2019

Anticancer prodrugs of butyric acid and formaldehyde protect against doxorubicin-induced cardiotoxicity

Formaldehyde has been previously shown to play a dominant role in promoting synergy between doxorubicin (Dox) and formaldehyde-releasing butyric acid (BA) prodrugs in killing cancer cells. In this work, we report that these prodrugs also protect neonatal rat cardiomyocytes and adult mice against toxicity elicited by Dox. In cardiomyocytes treated with Dox, the formaldehyde releasing prodrugs butyroyloxymethyl diethylphosphate (AN-7) and butyroyloxymethyl butyrate (AN-1), but not the corresponding acetaldehyde-releasing butyroyloxydiethyl phosphate (AN-88) or butyroyloxyethyl butyrate (AN-11), reduced lactate dehydrogenase leakage, prevented loss of mitochondrial membrane potential (ΔΨm) and attenuated upregulation of the proapoptotic gene Bax. In Dox-treated mice, AN-7 but not AN-88 attenuated weight-loss and mortality, and increase in serum lactate dehydrogenase. These findings show that BA prodrugs that release formaldehyde and augment Dox anticancer activity also protect against Dox cardiotoxicity. Based on these observations, clinical applications of these prodrugs for patients treated with Dox warrant further investigation

Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.

Ischaemia-reperfusion injury occurs when the blood supply to an organ is disrupted and then restored, and underlies many disorders, notably heart attack and stroke. While reperfusion of ischaemic tissue is essential for survival, it also initiates oxidative damage, cell death and aberrant immune responses through the generation of mitochondrial reactive oxygen species (ROS). Although mitochondrial ROS production in ischaemia reperfusion is established, it has generally been considered a nonspecific response to reperfusion. Here we develop a comparative in vivo metabolomic analysis, and unexpectedly identify widely conserved metabolic pathways responsible for mitochondrial ROS production during ischaemia reperfusion. We show that selective accumulation of the citric acid cycle intermediate succinate is a universal metabolic signature of ischaemia in a range of tissues and is responsible for mitochondrial ROS production during reperfusion. Ischaemic succinate accumulation arises from reversal of succinate dehydrogenase, which in turn is driven by fumarate overflow from purine nucleotide breakdown and partial reversal of the malate/aspartate shuttle. After reperfusion, the accumulated succinate is rapidly re-oxidized by succinate dehydrogenase, driving extensive ROS generation by reverse electron transport at mitochondrial complex I. Decreasing ischaemic succinate accumulation by pharmacological inhibition is sufficient to ameliorate in vivo ischaemia-reperfusion injury in murine models of heart attack and stroke. Thus, we have identified a conserved metabolic response of tissues to ischaemia and reperfusion that unifies many hitherto unconnected aspects of ischaemia-reperfusion injury. Furthermore, these findings reveal a new pathway for metabolic control of ROS production in vivo, while demonstrating that inhibition of ischaemic succinate accumulation and its oxidation after subsequent reperfusion is a potential therapeutic target to decrease ischaemia-reperfusion injury in a range of pathologies