Stories about: Immune Disease Institute

“Good” cholesterol could be even better for you than you thought

When you get on a long flight, there's always a risk of developing a deep vein thrombosis (DVT): a blood clot in your legs. But "good" cholesterol may be able to help stop DVTs from happening. (randomduck/Flickr)

Most of us are familiar with “good” and “bad” cholesterol. Low-density lipoprotein (LDL) is “bad” because it keeps cholesterol in the body, while the “goodness” of high-density lipoprotein (HDL) stems from its ability to scoop up old, used cholesterol and escort it to the liver for disposal. Because high levels of HDL in the blood are associated with lower risk of cardiovascular disease (a link that has recently come under question), it has received much attention from researchers.

And anyone who travels a great deal has probably heard about deep vein thrombosis or DVT, often cited as a good reason to get up and stretch your legs on a long flight. Restriction of normal blood flow—whether from being bedridden, paralyzed or sitting for hours on airplanes—is a major cause of blood clots in the legs. Though these clots can be painful in and of themselves, if they break free and travel to the lungs they can cause a potentially fatal pulmonary embolism. In fact, DVTs afflict nearly a million Americans each year and claim a quarter of a million lives.

Now a team from the lab of Denisa Wagner, PhD, of Boston Children’s Hospital’s Program in Cellular and Molecular Medicine and the Immune Disease Institute (PCMM/IDI), directed by Alexander Brill, MD, PhD, has found a connection between “good” cholesterol and DVT that may change the way these dangerous clots are treated—and perhaps prevented.

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The shape of things in the genome, and how chromosomes break

While a cell's chromosomes (red, in a dividing cell) may look like they sit in a tangled jumble, they are actually organized in precise 3D fashion, which in turn influences what happens when chromosomes break. (Lothar Schmermelleh/Wikimedia Commons)

We’ve known for decades that our chromosomes can break and reshuffle, especially in cancer cells. We also see this process, called translocation, in naïve B cells when they start to produce antibodies for the first time: the cell breaks, shuffles and recombines genes to decide which threat it will defend against.

But knowing these things happen doesn’t mean that we’ve understood the rules for how and why they happen. By combining two powerful methods of genomic mapping, a research team led by Frederick Alt, director of the Program in Cellular and Molecular (PCMM) Medicine at Children’s Hospital Boston and the Immune Disease Institute (IDI), has brought some of those rules into clearer focus. It turns out that the genome’s three-dimensional organization – where each of the genome’s thousands of genes lie spatially within the cell’s nucleus – holds great influence over where broken chromosome ends rejoin.

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