CHICAGO—The "Triple A-S" meeting is like no other scientific gathering in that it is not really for scientists but for journalists who follow science. Scientists do come to present talks or to serve on AAAS governing sections, but to understand the meeting's central purpose, think of AAAS as the world's largest annual science press conference.
For those who think scientific discoveries pop up overnight, consider Tom Rapoport's tale of the holiday carp and how it led him to study the translocation channel through which proteins, such as insulin, are secreted. Rapoport's latest discovery starts with a fish 30 years ago and ends, or at least continues, this month with a publication in Nature of the first x-ray structure of an open protein translocation channel.
John Pringle has been going to different sorts of meetings this last decade. He is still a regular at the ASCB Annual Meeting and at smaller yeast biology gatherings. Indeed he was in New Orleans for the ASCB Annual Meeting in December to receive the E.B. Wilson Medal, the ASCB's highest scientific honor, for his pioneering work on cell polarization and cytokinesis. But Pringle also goes, when he can, to the International Coral Reef Symposium, the Society for Microbial Ecology, and the International Symbiosis Society. He still has a small yeast group in his lab although his other interests have represented the majority since 2007. He is becoming known at these marine biology and ecology meetings, but Pringle says that he wishes there were more cell biologists there. John Pringle aims to correct that.
Biologists are passionate about papers. Here we ask an ASCB member to pick two journal articles that were important, either personally or scientifically, and to answer—briefly and informally—three questions: Why did you pick this paper? What's it about? What does it mean to you?
Making pluripotent stem cells, cells with the ability to turn into almost any cell type, is easier than ever, according to new papers published this week in Nature. Just add stress.
In the "big data" realms of genome sequencing, there are many surprises left to be untangled. A new bioinformatics paper published January 10 in Nature Chemical Biology unwinds one—a new class of RNA-catalysts.
Modeling membranes, nano-magnets to control cell activity, and a gain-of-function protein behind a severe progressive brainstem disorder were hot topics at the 2013 ASCB Annual Meeting in New Orleans, December 14-18. This year, ASCB continued the tradition of weaving two scientific threads—biophysics and medicine—through many of the 254 science presentations.
Mathieu Coppey imagines using tiny magnets to move cells within living organisms. Coppey, a researcher at the Institut Curie in Paris, isn't envisioning a modern day version of "magnet therapy" touted a century ago by quack medical practitioners. Instead Coppey is using nanoparticle-size magnets to manipulate processes in cells.
It may begin as a "simple" foot blister, but for patients with type 2 diabetes there is nothing simple about wounds that won't heal. That blister can evolve into a seriously infected wound that refuses to heal and, if gangrene develops, the patient's foot may have to be amputated. Such "simple" foot blisters and other diabetic ulcers or sores account for the vast majority of foot and leg amputations in the U.S. today. Paraplegics, quadriplegics, and anyone with severely limited mobility are also highly vulnerable to these chronic skin wounds as well as pressure ulcers and bedsores. Together, chronic wounds affect an estimated 6.5 million Americans at an annual cost of about $25 billion.
It seems an unlikely connection, and yet there is a significant link between Gaucher disease (GD), a purely genetic disease affecting lipid storage, and Parkinson's disease, a largely untreatable progressive degenerative movement disorder of the central nervous system that is often without a clear genetic cause. Those born with two recessive GD mutations, which cause a dangerous build-up of lipids, have a higher risk of developing Parkinson's disease than those with normal GD genes. More surprising is the higher risk for Parkinson's disease among carriers of GD mutation who have no overt GD symptoms, but still produce some level of the defective enzyme called glucocerebrosidase.