Fluridone: a combination germination stimulant and herbicide for problem fields?

BACKGROUND: Problem weeds in agriculture, such as Lolium rigidum Gaud., owe some of their success to their large and dormant seed banks, which permit germination throughout a crop-growing season. Dormant weed seed banks could be greatly depleted by application of a chemical that stimulates early-season germination and then kills the young seedlings. Fluridone, a phytoene desaturase-inhibiting herbicide that can also break seed dormancy, was assessed for its efficacy in this regard. RESULTS: The germination of fluridone-treated Lolium rigidum seeds was stimulated on soils with low organic matter, and almost 100% seedling mortality was observed, while the treatment was only moderately effective on a high-organic-matter potting mix. Seedlings from wheat, canola, common bean and chickpea seeds sown on fluridone-treated sandy loam were bleached and did not survive, but lupins and field peas grew normally. CONCLUSION: This proof-of-concept study with fluridone suggests that it may be possible to design safe and effective molecules that act as germination stimulants plus herbicides in a range of crop and soil types: a potentially novel way of utilising herbicides to stimulate seed bank germination and a valuable addition to an integrated weed management system.

Cogeneration of biodiesel and nontoxic rapeseed meal from rapeseed through in-situ alkaline transesterification.

In-situ alkaline transesterification of rapeseed oil with methanol for the production of biodiesel and nontoxic rapeseed meal was carried out. Water removal from milled rapeseed by methanol washing was more effective than vacuum drying. The conversion rate of rapeseed oil into FAME was 92%, FAME mass was 8.81 g, glucosinolates content in remaining rapeseed meal was 0.12% by methanol washing, while by vacuum drying the values were 46%, 4.44 g, 0.58%, respectively. In the presence of 0.10 mol/L NaOH in methanol, with methanol/oil molar ratio of 180:1 and a 3h reaction at 40 °C, a conversion rate of 98% was achieved, and the glucosinolates content was reduce to 0.07%, a value which below the GB/T 22514-2008 standard in China. Thus the rapeseed meal can be used as a source of protein in animal feed. The FAME prepared through in-situ alkaline transesterification met the ASTM specifications for biodiesel.

Cadmium accumulation in different pakchoi cultivars and screening for pollution-safe cultivars.

The selection and breeding of pollution-safe cultivars (PSCs) is a practicable and cost-effective approach to minimize the influx of heavy metal to the human food chain. In this study, both pot-culture and field experiments were conducted to identify and screen out cadmium pollution-safe cultivars (Cd-PSCs) from 50 pakchoi (Brassica rapa L. ssp. chinensis) cultivars for food safety. When treated with 1.0 or 2.5 mg/kg Cd, most of the pakchoi cultivars (>70%) showed greater or similar shoot biomass when compared with the control. This result indicates that pakchoi has a considerable tolerance to soil Cd stress. Cd concentrations in the shoot varied significantly (P<0.05) between cultivars: in two Cd treatments (1.0 and 2.5 mg/kg), the average values were 0.074 and 0.175 mg/kg fresh weight (FW), respectively. Cd concentrations in the shoots of 14 pakchoi cultivars were lower than 0.05 mg/kg FW. In pot-culture experiments, both enrichment factors (EFs) and translocation factors (TFs) of six pakchoi cultivars were lower than 1.0. The field studies further confirmed that the Hangzhouyoudonger, Aijiaoheiye 333, and Zaoshenghuajing cultivars are Cd-PSCs, and are therefore suitable for growth in low Cd-contaminated soils (≤1.2 mg/kg) without any risk to food safety.

Hipertensión pulmonar con el ejercicio en el síndrome del aceite tóxico / Pulmonary hypertension during exercise in toxic oil syndrome

Fundamento y objetivo: Los pacientes con síndrome del aceite tóxico son una población de riesgo de padecer hipertensión arterial pulmonar. La elevación anómala de la presión sistólica pulmonar (PSP) durante el ejercicio podría considerarse un marcador temprano de hipertensión pulmonar en poblaciones de riesgo. El objetivo del presente estudio ha sido analizar mediante ecocardiografía la respuesta de la PSP al ejercicio en pacientes con síndrome del aceite tóxico. Pacientes y método: Se estudió a 50 pacientes con síndrome del aceite tóxico y a 20 voluntarios sanos con ecocardiograma en reposo y en el máximo ejercicio (cicloergómetro semisupino) y se midió la PSP. En los pacientes se determinó la capacidad de difusión de monóxido de carbono. Resultados: No se observaron diferencias en el valor medio de la PSP en el ejercicio entre los pacientes y los voluntarios sanos. En un 8% de los primeros se observó un valor igual o superior a 80 mmHg, lo que se asoció a hipertensión pulmonar leve en reposo, disminución de la función ventricular derecha y trastornos de la difusión pulmonar. Un valor de corte de la PSP en reposo igual o superior a 27 mmHg tuvo una sensibilidad del 100% y una especificidad del 71% para predecir una PSP pico de 80 mmHg o superior. Conclusiones: Una minoría de pacientes con síndrome del aceite tóxico muestra hipertensión pulmonar grave con el ejercicio. Este tipo de respuesta anormal se asocia a otros marcadores de vasculopatía pulmonar. Futuros estudios han de esclarecer la relación entre estas anomalías y el riesgo de desarrollar ulteriormente hipertensión arterial pulmonar

Background and objective: Toxic oil syndrome is a risk factor for pulmonary arterial hypertension (PAH) and new cases of this entity are emerging after more than 20 years since the initial toxic oil epidemic. Abnormal elevation of pulmonary systolic pressure with exercise may be considered an early marker of PAH in populations at risk. We aimed to analyze the pulmonary systolic pressure with exercise echocardiography in toxic oil syndrome patients. Patients and method: 50 toxic oil syndrome patients (cases), and 20 healthy control subjects were submitted to rest and peak exercise echocardiography (semi supine cicloergometer) measuring pulmonary systolic pressure. In toxic oil syndrome patients, pulmonary carbon monoxide diffusion capacity was also analyzed. Results: Peak exercise pulmonary systolic pressure was statistically similar in cases and controls. Nevertheless, 8% of cases reached a pulmonary systolic pressure >= 80 mmHg and this fact was associated with mild pulmonary arterial hypertension, reduced right ventricular function and abnormal pulmonary diffusion capacity in the rest study. A rest pulmonary systolic pressure cut-off value >= 27 mmHg had a 100% sensitivity and 71% specificity to predict a peak exercise systolic pulmonary pressure >= 80 mmHg. Conclusions: A minority of toxic oil syndrome patients develop severe pulmonary arterial hypertension during exercise. This abnormal response is associated with other markers of pulmonary vasculopathy. Further studies are needed to elucidate the relation between these findings and the likelihood to develop pulmonary arterial hypertension in the future

Immunoglobulin and autoantibody responses in MRL/lpr mice treated with 'toxic oils'.

The toxic oil syndrome (TOS) occurred in Spain in 1981 as a result of ingestion of oil mixtures containing aniline-denatured rapeseed oil. The disease afflicted almost 20000 people, resulted in more than 400 deaths, and mimicked an autoimmune disease in all patients. Phenilamine-propanediol (PAP) has been implicated as a possible etiologic agent of TOS but absence of an acceptable animal model to evaluate the autoimmune potential of the 'case oil' has hindered identification of the actual etiologic agent(s). The purpose of this study was twofold; (1) to develop an animal model of human disease to investigate the immunological etiology and pathogenesis of TOS and (2) to determine if the 'case oil' responsible for TOS and/or two synthesized oils either induced or exacerbated the systemic autoimmune disease that occurs spontaneously in the MRL/lpr mouse. The oils tested were a denatured rapeseed oil collected from a family (case oil) who were affected by the TOS (CO756), a rapeseed oil denatured with 2% aniline and enriched with a mixture of diesters of PAP (RSD), and a rapeseed oil denatured with 2% aniline but contained no diesters of PAP (RSA). Female MRL/lpr mice, 7 weeks of age, received orally either an undiluted (neat) or a 1:10 diluted dose of each test oil, canola oil (oil control), water (nai;ve control), or 50-ppm mercury (positive control). Half of each group was sacrificed after 5 weeks of exposure and the remaining mice after 10 weeks of exposure. Serum IgG1, IgG2a, IgE isotypes and antinuclear (ANA), collagen type II, histone, single-stranded DNA (ssDNA), double-stranded DNA (dsDNA) and Sm autoantibody concentrations were determined after 5 and 10 weeks of exposure. The oils did not significantly affect the concentrations of the serum immunoglobulins, although a shift in the IgG1:IgG2a ratio towards IgG1 was noted from 12 to 17 weeks of age (5-10 weeks of treatment). The oils did however stimulate the systemic autoimmune response. The RSD neat treatment resulted in a nonsignificant but noted increase in autoantibodies to collagen (10 weeks), histone (10 weeks) and dsDNA (5 and 10 weeks). CO756 neat increased the serum levels of ANA (5 weeks), collagen (5 weeks) and dsDNA (5 and 10 weeks). The RSA 1:10 dilution increased ssDNA and dsDNA autoantibodies at 5 weeks. The results suggest that PAP is an active principle of these noted responses. These data, coupled with the toxicology and pathology data from this study (Toxicol. Path. 29 (2001) 630), revealed that the three oils incited induction of the lymphoproliferative syndrome and that the two oils containing PAP induced and enhanced the systemic autoimmune response that develops spontaneously at an early age in the MRL/lpr mouse. There was also a positive correlation noted between serum autoantibody concentrations and progression of the idiopathic autoimmune syndrome in the MRL/lpr mouse.

Riesgo y seguridad alimentarias: revisitando la colza / Food risks and safety: Revisiting rapeseed oil

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