A delightful book to get the whole picture of simulation applications in developmental biology and easily readable for those who would like to overlook the field in one quick sweep. If you would like to get a more detailed perspective, a great number of literature references provides this opportunity.

In the March 1982 issue of the Journal Dr Pheby, a community health doctor, was one of several writers to discuss medical confidentiality. Dr Pheby urged doctors to minimise subjective and judgmental comments in medical records and to make clear when their assessments were speculative. He also urged `vigorous reappraisal of the extent to which information about a patient needs to be circulated' to members of other disciplines, for instance, in child health practice. If doctors did not take such steps (...) themselves legal changes might well be imposed upon them, giving patients the right of access to their medical records and perhaps making breach of medical confidentiality a criminal offence. Mr Jacob, a lawyer, commenting on the papers by Dr Pheby and Mr Kenny, a health administrator, argued that increased legal intervention in medical ethics could quite possibly actually erode traditional medical ethical standards of confidentiality based on peer review and `the ethic of virtue'. (shrink)

IPCC SPECIAL REPORT ON CLIMATE CHANGE AND LAND (SRCCL) -/- Chapter 3: Climate Change and Land: An IPCC special report on climate change, desertification, land degradation, sustainable land management, food security, and greenhouse gas fluxes in terrestrial ecosystems.

Cyclin-dependent kinase 5 has been implicated in Alzheimer's disease pathogenesis. Here, we demonstrate that overexpression of p25, an activator of cdk5, led to increased levels of BACE1 mRNA and protein in vitro and in vivo. A p25/cdk5 responsive region containing multiple sites for signal transducer and activator of transcription was identified in the BACE1 promoter. STAT3 interacts with the BACE1 promoter, and p25-overexpressing mice had elevated levels of pSTAT3 and BACE1, whereas cdk5-deficient mice had reduced levels. Furthermore, mice with a (...) targeted mutation in the STAT3 cdk5 responsive site had lower levels of BACE1. Increased BACE levels in p25 overexpressing mice correlated with enhanced amyloidogenic processing that could be reversed by a cdk5 inhibitor. These data demonstrate a pathway by which p25/cdk5 increases the amyloidogenic processing of APP through STAT3-mediated transcriptional control of BACE1 that could have implications for AD pathogenesis. (shrink)