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Muscle wasting is a common and prominent feature of advanced cancer, including lung cancer. Evidence from animal experiments suggests that accelerated proteolysis via the ubiquitin--proteasome pathway is the primary cause of cancer-related cachexia. However, there are few data on the role of this pathway in determining muscle wasting in human cancer. The present study was designed to measure whether skeletal muscle gene expression of components of the ubiquitin-proteasome pathway and/or the lysosomal proteolytic pathway was increased in patients with early lung cancer. A total of 36 patients with lung cancer referred for curative resection and 10 control subjects had biopsies of latissimus dorsi muscle taken at operation. mRNA levels of four components of the ubiquitin-proteasome pathway, i.e. polyubiquitin, C2 alpha proteasome subunit, 14 kDa ubiquitin-carrier protein and ubiquitin-activating protein, and of two lysosomal proteolytic enzymes, i.e. cathepsin B and cathepsin D, were measured using quantitative Northern blotting. mRNA levels for cathepsin B, but not for components of the ubiquitin--proteasome pathway, were higher in patients with cancer compared with controls (P=0.01). Among lung cancer patients, cathepsin B mRNA levels correlated with fat-free mass index (r = -0.57, P=0.003) and tumour stage (r(s)=0.45, P=0.03), and were higher in smokers (P=0.04). Thus gene expression of the lysosomal protease cathepsin B is increased in the skeletal muscle of patients with early lung cancer, and the strong inverse relationship with fat-free mass suggests that cathepsin B may have a role in inducing muscle wasting in the early stages of lung cancer.

The charmless decays B±→K± π+ π- and B±→K± K+ K- are reconstructed using data, corresponding to an integrated luminosity of 1.0  fb(-1), collected by LHCb in 2011. The inclusive charge asymmetries of these modes are measured as ACP(B±→K± π+ π-)=0.032±0.008 (stat)±0.004 (syst)±0.007(J/ψK±) and ACP(B±→K± K+ K-)=-0.043±0.009 (stat)±0.003 (syst)±0.007(J/ψK±), where the third uncertainty is due to the CP asymmetry of the B±→J/ψK± reference mode. The significance of ACP(B±→K± K+ K-) exceeds three standard deviations and is the first evidence of an inclusive CP asymmetry in charmless three-body B decays. In addition to the inclusive CP asymmetries, larger asymmetries are observed in localized regions of phase space.

Amongst samples of the sweet potato chlorotic stunt crinivirus (SPCSV) obtained from crops of sweet potato in Uganda, two serotypes (S EA1 and S EA2 ) were distinguished using a panel of monoclonal antibodies (Mabs) to a Kenyan isolate of SPCSV. S EA1 serologically resembled the Kenyan isolate of SPCSV whereas S EA2 has not previously been reported. S EA1 was predominant in eastern Uganda whereas S EA2 was predominant in southern and western Uganda. S EA2 tended to occur in more severely diseased sweet potato plants than S EA1 . RNA was extracted from eight plants and replicate clones representing the heat shock protein 70 (HSP70) homologue and coat protein (CP) genes were generated by reverse transcription and PCR. Sequence analyses revealed substitutions at two nucleotide positions in the HSP70 homologue gene, although neither affected deduced amino-acid sequences. Nucleotide substitutions in the CP gene region, which led to 11 amino-acid substitutions, revealed two major groupings plus other minor variants.The EMBL accession numbers of the sequences reported in this paper are AJ010754 through to AJ01769 (coat protein sequences) and AJ010914 through to AJ010929 (partial HSP70 homologue gene sequences).