Cancer cells need food to survive and grow, and the food they rely upon most is glucose. This has led to attempts to kill cancer cells by blocking access to this energy-rich sugar. Surprisingly, glucose-starved tumors don’t die but continued to grow and become more aggressive.
In a study of colon cancer, researchers at the Sanford-Burnham Medical Research Institute have discovered the role of a specific protein that, when missing, allows tumors to use an alternative nutrient (glutamine). Using human tumor samples and a mouse model, the team determined the protein-deficient tumors are able to reprogram their metabolism and survive in conditions that would otherwise be lethal.
The research suggests that finding a way to add the protein back into tumors that lack it, could make them less suited for survival and more sensitive to current therapies.
The study appears in the journal Cell. News release at http://bit.ly/VqqcPZ
Chemical reaction thwarts self-repair in stroke-damaged brain
, a gaseous molecule produced in the brain, can damage neurons. When the brain produces too much nitric oxide, it contributes to the severity and progression of stroke and neurodegenerative diseases such as
Learning and memory are, in part, controlled by receptors in the brain linked to pores in the nerve cell membrane that regulate the flow of calcium and sodium in and out of the nerve cells. Over-activated receptors trigger the production of nitric oxide which attaches to other proteins, some of which are involved in cell survival and lifespan. When this is the case, nitric oxide can cause these brain cells to die prematurely—a hallmark of neurodegenerative disease.
Researchers at Sanford-Burnham Medical Research Institute explored nitric oxide’s relationship with proteins that help repair neuronal damage, using cultured neurons as well as a living mouse model of stroke. They found that nitric oxide reaction with a specific enzyme inhibits a protective cascade of molecular events, thus blocking the brain’s ability to self-repair.
Heat produced in winter months by everyday activities in metropolitan areas is significant enough to influence the jet stream and other major atmospheric systems, thousands of miles away.
Researchers at Scripps Institution of Oceanography, UC San Diego, studied energy consumption – from heating buildings to powering vehicles – that, in turn, releases waste heat. The result is a so-called “urban heat island” effect; an increase in the warmth of cities compared to unpopulated areas. Because many urban heat islands in the Northern Hemisphere lie directly under major atmospheric troughs and jet streams, the effect can widen the jet stream and strengthen atmospheric flows at mid-latitudes.
The authors contend that the urban heat effect accounts for the discrepancy between observed warming and winter warming simulated in the models used by the climate science community for analysis and prediction of climate. They suggest, therefore, that the influence of energy consumption be added as a variable, along with heat-trapping gases and aerosols, computer models of climate change.
The study appears in the journal Nature Climate Change. News release at http://bit.ly/112L8mM
Lynne Friedmann is a science writer based in Solana Beach.