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Milk thistle, Silybum marianum (L.) Gaertn. (Asteraceae), is an economically important medicinal plant utilized for silymarin production. Moreover, the species has been positively evaluated for vegetable oil and biomass production. Despite these positive characteristics, milk thistle is still marked by traits that are typical of undomesticated species (most importantly natural fruit dispersal at maturity) and requires further genetic improvement for its complete exploitation. This manuscript summarizes all the information collected through time about a collection of nine milk thistle wild and mutant lines and it discusses the possible further utilization of these genotypes. The accessions are characterized by interesting traits related to: fruit silymarin composition (S. marianum chemotype A and B), fruit fatty acid composition (high oleic and high stearic acid lines), fruit condensed tannins content, vegetative biomass composition (modification of xylans or lignin content), vegetative biomass structure (dwarf and tall lines), modifications of leaf variegation (hypervareigated line) and different types of fruit shatter resistance at maturity. All the lines underwent subsequent generations of selfing and are stable for all the described traits. The accessions will be made available at the Genebank of the Leibniz Institute of Plant Genetics and Crop Plant Research (IPK, Gatersleben) and may prove to be a useful genetic material for the improvement of qualitative fruit traits (silymarin quality, fatty acid composition) and for the further development of shatter-resistant S. marianum genotypes towards the complete domestication of this promising species.

The Giant Cell Arteritis is considered one of the most prevalent autoimmune vasculitis syndromes, which affects arteries of medium and large caliber, being the most feared complication, anterior ischemic optic neuropathy that can evolve to an irreversible loss of vision. The symptoms are caused by local ischemia due to endovascular damage accompanied by systemic damage mediated by cytokines. In recent years, doppler ultrasound, Magnetic Resonance Imaging (MRI) and PET scans have become important in the search for tools that can confirm or exclude the diagnosis of GCA. However, the Temporal Artery Biopsy (BAT) continues to be the gold standard test for the diagnosis of this disease.

Reactive oxygen species (ROS) and endothelin-1 (ET-1) contribute to vascular pathophysiology in obesity. In this context, whether ET-1 modulates hydroxyl radical (•OH) formation and the function of ROS/•OH in obesity is not known. In the present study, formation and function of ROS, including •OH, were investigated in the aorta of lean and leptin-deficient obese ob/ob mice. Hydroxyl radical formation was detected ex vivo using terephthalic acid in intact aortic rings and the involvement of ROS in ET-1-mediated vasoreactivity was analyzed using the antioxidant EPC-K1, a combination of α-tocopherol and ascorbic acid. Generation of either •OH, •O2−, and H2O2was strongly inhibited by EPC-K1 (all P < 0.05). In obese mice, basal vascular •OH formation and ROS activity were reduced by 3-fold and 5-fold, respectively ( P < 0.05 vs. lean). ET-1 markedly enhanced •OH formation in lean (6-fold, P < 0.05 vs. untreated) but not in obese mice. Obesity increased ET-1-induced contractions ( P < 0.05 vs. lean), and ROS scavenging further enhanced the response ( P < 0.05 vs. untreated). Exogenous ROS, including •OH caused stronger vasodilation in obese animals ( P < 0.05 vs. lean), whereas endothelium-dependent relaxation was similar between lean and obese animals. In conclusion, we present a sensitive method allowing ex vivo measurement of vascular •OH generation and provide evidence that ET-1 regulates vascular •OH formation. The data indicate that in obesity, vascular formation of ROS, including •OH is lower, whereas the sensitivity to ROS is increased, suggesting a novel and important role of ROS, including •OH in the regulation of vascular tone in disease status associated with increased body weight.

This study investigated whether intrarenal endothelin-1(ET-1) contributes to sodium excretion in aged rats. Metabolic function studies were performed in male Wistar rats (3 and 24 months) treated with placebo or the orally active ET(A) receptor antagonist darusentan (20 mg/kg/d) for 4 weeks. Mean arterial pressure was measured using an intra-arterial catheter. Electrolytes, aldosterone levels, renin activity, and angiotensin converting enzyme activity were determined in plasma, and mRNA expression of epithelial sodium channel (ENaC) and Na(+), K(+)-ATPase subunits was measured in the renal cortex and medulla. Aging was associated with a marked decrease in urinary excretion of sodium, chloride, and potassium (all P < 0.001) as well as renin activity (P < 0.05), but had no significant effect on gene expression of ENaC or Na(+), K(+)-ATPase subunits. In aged rats, darusentan treatment increased ion excretion (P < 0.05), reduced cortical gene expression of alphaENaC and alpha(1)-Na(+), K(+)-ATPase (both P < 0.05), and increased plasma aldosterone levels (P < 0.01). These data demonstrate a decrease of sodium and potassium excretion in aged rats, changes that are partly sensitive to ETA receptor blockade. Treatment with darusentan also reduced cortical expression of alphaENaC and alpha(1)-Na(+), K(+)-ATPase and increased plasma aldosterone levels independently of blood pressure, electrolytes, renin activity, or angiotensin converting enzyme activity. These findings may provide new pathogenetic links between aging and sodium sensitivity.