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How are the stages of mitosis related to the creation of identical daughter cells? The primary function of the stages of mitosis is to make certain that each daughter cell is genetically identical to the mother cell. The mother cell's DNA is copied during interphase. During mitosis the chromosomes condense from long strands to highly coiled structures. The two copies of each DNA strand, called sister chromatids, are physically attached to one another. The chromosomes are moved to the center of the cell and split apart in a highly coordinated fashion. The condensation of the chromosomes, the physical connection of the sister chromatids, and the precise movement of the chromosomes are all important in making sure that each daughter cell has one copy of each chromosome and is genetically identical to the mother cell.

In a paper this week in Science, Vogelstein and Cristian Tomasetti, who joined the biostatistics department at Hopkins in 2013, put forth a mathematical formula to explain the genesis of cancer. Here's how it works: Take the number of cells in an organ, identify what percentage of them are long-lived stem cells, and determine how many times the stem cells divide. With every division, there's a risk of a cancer-causing mutation in a daughter cell. Thus, Tomasetti and Vogelstein reasoned, the tissues that host the greatest number of stem cell divisions are those most vulnerable to cancer. When Tomasetti crunched the numbers and compared them with actual cancer statistics, he concluded that this theory explained two-thirds of all cancers.

When a person dies from cancer, the culprit is usually not the original tumor but rather the cancerous cells that spread throughout the body and replicate in distant organs, a process called metastasis. Researchers have long known that metastasizing cancer cells slip their bonds and avoid immune detection by altering the sugars on their surfaces. They've even come up with a would-be drug to prevent such sugar alterations. But that compound interferes with needed sugars on normal cells, too, with lethal results in animals. Now, Dutch researchers report that they've packaged the drug in nanoparticles targeted exclusively to cancer cells, and they've shown that this combination prevents cancer cells from metastasizing in mice.  

In 1977, a University of Oxford statistician named Richard Peto pointed out a simple yet puzzling biological fact: We humans should have a lot more cancer than mice, but we don't. Dr. Peto's argument was beguilingly simple. Every time a cell divides, there's a small chance it will gain a mutation that speeds its growth. Cells that accumulate several of these mutations may become cancerous. The bigger an animal is, the more cells it has, and the longer an animal lives, the more times its cells divide. We humans undergo about 10,000 times as many cell divisions as mice - and thus should be far more likely to get cancer.

One of my favorite "proofs" of evolution is the recurrent laryngeal nerve (RLN)-the nerve that innervates the larynx from the brain, helping us speak and swallow. It takes a very circuitous course, looping from the brainstem down around the aorta and then back up to the larynx. Here's its course in humans:

CRISPR still has a long way to go before it can be used safely and effectively to repair-not just disrupt-genes in people. That is particularly true for most diseases, such as muscular dystrophy and cystic fibrosis, which require correcting genes in a living person because if the cells were first removed and repaired then put back, too few would survive. And the need to treat cells inside the body means gene editing faces many of the same delivery challenges as gene transfer-researchers must devise efficient ways to get a working CRISPR into specific tissues in a person, for example. CRISPR also poses its own safety risks. Most often mentioned is that the Cas9 enzyme that CRISPR uses to cleave DNA at a specific location could also make cuts where it's not intended to, potentially causing cancer.

This PowerPoint-driven case study presents three different stories, each of which explores an aspect of membranes. The first (The Exploding Fish) covers diffusion, specifically addressing the question of why animal cells explode in freshwater but fish do not, and differences between saltwater and freshwater fish. The second case (The Pleasurable Poison) is designed to show that alcohol can slip across membranes and also highlights some of the problems of ingesting this toxin. The third case (The Dangerous Diet) explores a weight-loss drug, DNP, and how it operates in mitochondrial membranes. The first of these case studies also includes a number of "clicker" questions. These cases were originally designed for a semester-long, introductory biology course for non-majors, and instructors can choose to use one or all of the cases to suit their course.

Bowhead whales (Balaena mysticetus), denizens of Arctic seas, are known to live more than 200 years, yet they show few signs of the age-related ailments that plague other animals, including humans. Even the bowhead's closest cetacean relative, the much smaller minke whale, lives only 50 years. That suggests the larger whales (which have more than 1000 times as many cells as humans) have evolved some special natural mechanisms that protect them against cancer and aging.

Adverse life experiences, particularly those in childhood, contribute to disease morbidity and mortality [1, 2, 3, 4, 5, 6, 7]. There is considerable interest in understanding the mechanisms through which they do so, as it remains unclear how illness becomes apparent decades after the presumed initiating event. Long-standing hypotheses include chronic activation of the hypothalamic-pituitary-adrenal axis [8, 9, 10] and alterations of neuroimmune function [11]. Molecular signatures of stressful life experiences and their relation to disease are therefore of special interest to clarify the causal relationship between signature, disease, and stress.