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Oligodendrocyte precursor cells in primary culture, which were isolated from the spinal cord 3 days after contusion injury. Improving the ability of such endogenous cells to promote recovery by increasing cAMP levels (see paper by Pearse et al., page 610 may be a new therapeutic target for the treatment of spinal cord injury. Image courtesy of Soonmoon Yoo and Jean Wrathall.
Obese people, who are already subject to adverse health effects, are additionally victimized by a social stigma predicated on the Hippocratic nostrum that weight can be controlled by 'deciding' to eat less and exercise more. This simplistic notion is at odds with substantial scientific evidence illuminating a precise and powerful biologic system that maintains body weight within a relatively narrow range. Voluntary efforts to reduce weight are resisted by potent compensatory biologic responses. This article will review some of this evidence, together with promising avenues of research. Further progress in understanding and treating obesity will come not from repetition of anachronistic preconceptions but rather from the rigorous scientific approach that has driven advances in so many other areas of medicine.
The question “When are research risks reasonable in relation to anticipated benefits?” is at the heart of disputes in the ethics of clinical research. Institutional review boards are often criticized for inconsistent decision-making, a problem that is compounded by a number of contemporary controversies, including the ethics of research involving placebo controls, developing countries, incapable adults and emergency rooms. If this pressing ethical question is to be addressed in a principled way, then a systematic approach to the ethics of risk in research is required. Component analysis provides such a systematic approach.
Two clinical studies have identified mutations affecting the EGF receptor in lung cancers from patients who respond robustly to gefitinib, a small-molecule inhibitor of the receptor tyrosine kinase. This work highlights the importance of conducting clinical trials with an eye to delivering molecule-targeted therapeutics to those patients most likely to benefit.
Cancer treatment is evolving from the empirical administration of chemotherapeutics to the precise deployment of molecularly targeted agents. This new paradigm depends on the ability to monitor therapy using molecular signatures of target inhibition in tumor tissue. Genetically engineered mice may prove useful for deriving such signatures, as shown for an analog of the anticancer drug rapamycin (pages 594–601).
Thyroid hormone regulates cellular energetics in multiple organs and sets the metabolic rate of the body. The hormone action takes days to weeks, working by altering gene transcription. Now its ability to also function over the short term is coming to light (pages 638–642).
The body carefully balances muscle atrophy and muscle hypertrophy in response to stimuli such as starvation or immobilization. Three new studies point to Akt1 phosphorylation of the transcription factor Foxo as a central regulator of this balance.
During oral tolerance cells communicate with each other to dampen the immune response, creating an agreeable environment for oral antigens. Even T cells directed against non-oral antigens are suppressed, generating a response known as the 'bystander effect'. Dendritic cells now emerge as mediators of this communication.
The FDA-approved drug suramin is best known for combating trypanosome infection. Now it takes on the liver, where it prevents apoptosis and fends off damage in mouse models of hepatitis (pages 602–609).