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Imagine being asked to copy a library of books. Doing it yourself would take forever. You’d probably call some friends and come up with a plan to divide and conquer.

That’s what a human cell does when faced with the task of replicating six billion letters of DNA each time it divides. Instead of reading each chromosome in one slow pass, DNA replication machinery dives in at many origin points. Some segments get copied earlier or later than others.

By combing through the DNA of more than 100,000 people, researchers at ӳý, Massachusetts General Hospital, and elsewhere have identified rare, protective genetic mutations that lower the levels of LDL cholesterol — the so-called “bad” cholesterol — in the blood. The researchers’ findings, which appear online November 12 in the reveal that these naturally occurring mutations also reduce a person’s risk of coronary heart disease by about 50 percent. Remarkably, the mutations disrupt a gene called Niemann-Pick C1-Like 1 (NPC1L1) — the molecular target of the FDA-approved drug ezetimibe, often used as a treatment for high LDL.

Scientists have created a molecular map that pinpoints genetic variants that play a role in 21 different autoimmune diseases, they report Oct. 27 in the journal Nature.

Researchers at Yale, the University of California-San Francisco (UCSF), and the ӳý of MIT and Harvard developed a sophisticated mathematical model and created maps of different cell types that together enabled them to identify which variants cause the immune response to go awry and cause specific diseases.

RNF43

A mutation that may be driving as many as 20 percent of endometrial and colorectal cancers has come to light this week, thanks to a study by researchers from the ӳý of MIT and Harvard and Dana-Farber Cancer Institute.

The researchers describe finding the connection between the gene RNF43 and these cancers earlier this week in .