Restoration of Old Forest Features in Coast Redwood Forests Using Early‐stage Variable‐density Thinning

To accelerate development of old forest features in coast redwood, two thinning treatments and an unthinned control were compared in three treatment areas in north coastal California. One thinning treatment was designed to restore old forest densities of 125 trees/ha and the other 250 trees/ha representing a one‐step and partial treatments to the desired stand density. Four years after treatment, numbers of trees had increased in the thinning treatments due to recruitment of new trees, but had decreased in the control due to self‐thinning. Residual trees increased in stem volume following thinning by 128% in low‐density thinning compared to 70% in the controls indicating thinning accelerated stand development. The thinning treatments also moved the species composition of these stands to a greater proportion of redwood. Considerable slash was produced by the thinning treatments but was decomposing rapidly. Black bears damaged approximately 15% of all trees and more than 38% of residual trees in the thinned treatments compared to less than 2% of all trees in the control. This damage included killing some trees and damaging other trees that survived. Decisions over restoration densities in these stands are complicated by prolonged stand development, and balancing risks and costs. In this case, the bears represent a stochastic factor that dramatically increases risk. Thinning appears to be an effective means of enhancing old forest development by accelerating tree growth, modifying species composition, and increasing stand‐level variability. Continued monitoring will be necessary to evaluate long‐term trends in density relative to effects of bear damage.     

Proposed follow up programme after curative resection for lower third oesophageal cancer

Cyclins are indispensable elements of the cell cycle and derangement of their function can lead to cancer formation. Recent studies have also revealed more mechanisms through which cyclins can express their oncogenic potential. This review focuses on the aberrant expression of G1/S cyclins and especially cyclin D and cyclin E; the pathways through which they lead to tumour formation and their involvement in different types of cancer. These elements indicate the mechanisms that could act as targets for cancer therapy.