Thresholds for adding degraded tropical forest to the conservation estate

Logged and disturbed forests are often viewed as degraded and depauperate environments compared with primary forest. However, they are dynamic ecosystems1 that provide refugia for large amounts of biodiversity2,3, so we cannot afford to underestimate their conservation value4. Here we present empirically defined thresholds for categorizing the conservation value of logged forests, using one of the most comprehensive assessments of taxon responses to habitat degradation in any tropical forest environment. We analysed the impact of logging intensity on the individual occurrence patterns of 1,681 taxa belonging to 86 taxonomic orders and 126 functional groups in Sabah, Malaysia. Our results demonstrate the existence of two conservation-relevant thresholds. First, lightly logged forests (68%) of their biomass removed, and these are likely to require more expensive measures to recover their biodiversity value. Overall, our data confirm that primary forests are irreplaceable5, but they also reinforce the message that logged forests retain considerable conservation value that should not be overlooked

Inhibition studies on the nuclear inclusion protein a protease of turnip mosaic potyvirus C5

The nuclear inclusion protein a (NIa) protease of turnip mosaic potyvirus is responsible for processing the viral precursor polyprotein into mature proteins. The NIa protease was found to be inhibited by several metal ions at micromolar concentrations, especially copper, zinc, and cadmium ions. This implies that the NIa protease may contain cysteine or histidine residues essential for the catalytic activity. Substitution of His-46 or Cys-151 to Tyr or Ser, respectively, abolished the catalytic activity almost completely, supporting the hypothesis that cysteine and histidine are involved in the catalysis. N??-p-tosyl-L-phenylalanine chloromethylketone (TPCK) and N??-p-tosyl-L-lysine chloromethylketone (TLCK) exhibited significant inhibitory effects on the catalytic activity of the NIa protease with IC50 values of 50 ??M and 200 ??M, respectively. This suggests chloromethylketone-conjugated peptides could work as potent inhibitors against NIa protease. Iodoacetamide, iodoacetate, and N-ethylmaleimide, which are known to modify cysteine or histidine, showed moderate inhibitory effects. The protease was inhibited negligibly by other serine or cysteine protease inhibitors such as leupeptin, antipain, aprotinin, phenylmethylsulfonyl fluoride, elastatinal, L-trans-epoxysuccinyl-leucylamido(4-guanidino)butane (E-64), and cystatin. These results suggest that although the active site of the NIa protease is structurally similar to that of the chymotrypsin-like serine protease, it has a unique active site specificity distinct from those of other serine proteases.open7

Second‐Line Therapy for Advanced NSCLC

Most patients with lung cancer have non-small cell lung cancer (NSCLC) subtype and have advanced disease at the time of diagnosis. Improvements in both first-line and subsequent therapies are allowing longer survival and enhanced quality of life for these patients. The median overall survival observed in many second-line trials is approximately 9 months, and many patients receive further therapy after second-line therapy. The cytotoxic agents pemetrexed and docetaxel and the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) erlotinib and gefitinib are standard second-line therapies. For patients with EGFR mutation, a TKI is the favored second-line therapy if not already used in first-line therapy. For patients without the EGFR mutation, TKIs are an option, but many oncologists favor cytotoxic therapy. The inhibitor of the EML4/ALK fusion protein, crizotinib, has recently become a standard second-line treatment for patients with the gene rearrangement and has promise for patients with the ROS1 rearrangement