Spectroscopic parameters for silacyclopropynylidene, SiC2_2, from extensive astronomical observations toward CW Leo (IRC +10216) with the Herschel satellite

A molecular line survey has been carried out toward the carbon-rich asymptotic giant branch star CW Leo employing the HIFI instrument on board of the Herschel satellite. Numerous features from 480 GHz to beyond 1100 GHz could be assigned unambiguously to the fairly floppy SiC$_2$ molecule. However, predictions from laboratory data exhibited large deviations from the observed frequencies even after some lower frequency data from this survey were incorporated into a fit. Therefore, we present a combined fit of all available laboratory data together with data from radio-astronomical observations.Comment: 7 pages, 1 figure, J. Mol. Spectrosc., appeared; CDMS links corrected (version 2; current version: 3; may be updated later this year

Exotoxin A eEF2 complex structure indicates ADP ribosylation by ribosome mimicry

The bacteria causing diphtheria, whooping cough, cholera and other diseases secrete mono ADP ribosylating toxins that modify intracellular proteins. Here, we describe four structures of a catalytically active complex between a fragment of Pseudomonas aeruginosa exotoxin A ETA and its protein substrate, translation elongation factor 2 eEF2 . The target residue in eEF2, diphthamide a modified histidine , spans across a cleft and faces the two phosphates and a ribose of the non hydrolysable NAD analogue, amp; 946;TAD. This suggests that the diphthamide is involved in triggering NAD cleavage and interacting with the proposed oxacarbenium intermediate during the nucleophilic substitution reaction, explaining the requirement of diphthamide for ADP ribosylation. Diphtheria toxin may recognize eEF2 in a manner similar to ETA. Notably, the toxin bound amp; 946;TAD phosphates mimic the phosphate backbone of two nucleotides in a conformational switch of 18S rRNA, thereby achieving universal recognition of eEF2 by ET

Energy content of stools in normal healthy controls and patients with cystic fibrosis

Stool energy losses and the sources of energy within the stool were determined in 20 healthy controls and 20 patients with cystic fibrosis while on their habitual pancreatic enzyme replacement treatment. Stool energy losses were equivalent to 3.5% of gross energy intake in healthy children (range 1.3-5.8%). Despite a comparable gross energy intake, stool energy losses were three times greater in patients with cystic fibrosis than controls averaging 10.6% of gross energy intake (range 4.9-19.7%). Stool lipid could account for only 29% and 41% of the energy within the stool in controls and patients with cystic fibrosis respectively and was poorly related to stool energy. Approximately 30% of the energy within the stool could be attributable to colonic bacteria in both the healthy children and patients with cystic fibrosis. These results suggest that stool energy losses in healthy children are relatively modest but that even when patients with cystic fibrosis are symptomatically well controlled on pancreatic enzyme replacement, raised stool energy losses may continue to contribute towards an energy deficit sufficient to limit growth in cystic fibrosis. As the energy content per gram wet weight remains relatively constant (8 kJ/g), stool energy losses may be estimated from simple measurements of stool wet weight