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.
We talk about "hard wiring" the brain but our central nervous system is a work in progress. From the first neuron through childhood and adolescence, the neuronal network grows in complexity and size but also prunes out unneeded connections using molecules like the recently characterized enzyme, fidgetin, which makes strategic cuts in the microtubule scaffolding that holds up the cell's cytoskeleton and supports these connections. The ability of nerves to grow and prune diminishes as we mature until our adult neurons have mostly lost the power to reshape themselves.
A whimsically named fly gene, Sunday Driver, a.k.a. syd, and its mammalian analog, JIP3, seem to be in the driver's seat when it comes to parking the multiple nuclei of a skeletal muscle cell in their correct places, say researchers at the Sloan Kettering Institute (SKI). Getting that wrong and having mispositioned nuclei is a classic diagnostic sign of human congenital myopathies, a string of inherited muscle diseases such as Emery-Dreifuss muscular dystrophy (EDMD).
Glioblastoma multiforme (GBM) is the most common and the most deadly adult primary brain tumor, with an average survival of just 14 months following diagnosis. Even with aggressive treatment by surgery, radiation, and chemotherapy, most therapeutic approaches targeting the glioma cells in GBM fail. Faced with this bleak picture, Johanna Joyce and colleagues at Memorial Sloan Kettering Cancer Center (MSKCC) in New York City looked for an alternative strategy and turned to non-tumor cells that are part of the glioma microenvironment, the cancer's cellular neighbors. In particular, they zeroed in on tumor-associated macrophages and microglia (TAMs). The results were startling.
As we have learned more about the biology of cancer, it has become obvious that, aside from changes to the cancer genome, there are many other factors that determine tumor outcomes. Epigenetics, influences from the microenvironment, exosomes, and interplay with the immune system are now all recognized major players in cancer progression. Fresh evidence from Alain Silk, Melissa Wong, and colleagues at Oregon Health & Science University (OHSU) in Portland implicates a century-old observation—fusion of cancer cells with macrophages—as a new potentiator of cancer progression.
E-cigarettes have put nicotine back in the news and into the hands of a growing number of American smokers who now "vape," that is, inhale a steam of nicotine, polyethylene glucose (PEG), and flavoring generated by cigarette-shaped, battery-powered vaporizers.
Cell division is the great domestic drama of a cell's life. In sickness and in health, cell division by mitosis is the complicated yet critical process by which a mother cell divides into two daughter cells. But first the mother cell has to pack up her cellular household contents, disassembling and dividing up everything for her soon-to-be-formed daughters. How cells manage division has been exhaustively studied for well over a century and yet basic mysteries remain.
Dramatic stories in cell biology often have sequels—"Duel of the Alzheimer's Proteins, Part XV"—and indeed this work is a nail-biting sequel to George Bloom's hypothesis that interaction between amyloid-beta peptides and the protein tau drives adult neurons into the forbidden pathway of "cell cycle re-entry" (CCR). The long-term result is Alzheimer's disease (AD). Bloom and colleagues at the University of Virginia (UVA) now say that they have found the critical balance point between tau and a master cellular regulator that amyloid-beta oligomers disrupt.
Fever, ache, and the other miseries of influenza viral infection afflict 5−20 percent of the U.S. population each year. The "flu" is usually not life-threatening to the majority of its victims, but as the Spanish flu pandemic of 1918 showed, flu viruses can evolve into lethal agents and spread worldwide. The ability of flu viruses to change continually through mutation and genetic swaps is the reason that the Centers for Disease Control (CDC) reformulates the flu vaccine each year, hoping to block the types and subtypes of influenza viruses that they believe are most likely to be in circulation.