Commencing on day 100 ± 10 of lactation, 10 Italian Friesian cows averaging 32·6 kg milk per day were injected biweekly with recombinant bovine somatotropin (BST), while 10 other cows averaging 33-4 kg milk per day were injected with a placebo. Cows were offered ad libitum a total mixed diet throughout the lactation. The experiment lasted 16 weeks; milk samples were taken before and 16, 62 and 91 days after the commencement of BST injection. The objective was to determine the impact of biweekly injections of BST on the synthesis and proportion of milk fatty acids, particularly on cis and trans isomers and on fatty acids with an odd number of carbon atoms (C15 and C17). A decrease in the proportion of shortchain (C4 to C14) fatty acids (P < 0·001) and an increase in the proportion of long-chain (C16 to C20) fatty acids (P < 0·001) were observed in the first period of the treatment. With regard to cis and trans isomers, a considerable increase of the cis isomers (P < 0·001), particularly C18.1cis9 (oleic acid) was observed, while differences in trans isomers were not statistically significant. Concentrations of C15 (pentadecanoic acid) were not affected but heptadecanoic acid (C17) concentration showed a considerable increase (P < 0·01) but only in the sample taken after 16 days.

Hereditary hemorrhagic telangiectasia (HTT) is an autosomal dominant disease, most frequently caused by a mutation in either ENG or ACVRL1, which can be associated with pulmonary arterial hypertension (PAH). In this report, we describe a new unpublished ACVRL1 mutation segregating in three members of the same family, showing three different types of pulmonary hypertension (PH) in the absence of BMPR2 mutations. The first patient has a form of heritable PAH (HPAH) in the absence of hepatic arteriovenous malformations (AVMs); the second one has a severe form of portopulmonary hypertension (PoPAH) associated with multiple hepatic AVMs; the third one has hepatopulmonary syndrome (HPS) with numerous hepatic arteriovenous fistulas and a form of post-capillary PH due to high cardiac output. In summary, a single mutation in the ACVRL1 gene can be associated, in the same family, with an extreme phenotypic variability regarding not only the clinical presentation of HHT but also the type of PH in the absence of BMPR2 mutations. More studies are needed to evaluate if this variability can be explained by the presence of additional variants in other genes relevant for the pathogenesis of HHT.

A restrictive left-ventricular filling pattern at Doppler echocardiography is the most important prognostic indicator in chronic heart failure patients. Plasma levels of BNP and hsTnI do not provide additional relevant information to identify patients at higher risk of cardiovascular outcomes.