Ferrofluids, with their mesmeric display of shape-shifting spikes, are a favorite exhibit in science shows. These eye-catching examples of magnetic fields in action could become even more dramatic through computational work that captures their motion.
A KAUST research team has now developed a computer model of ferrofluid motion that could be used to design even grander ferrofluid displays. The work is a stepping stone to using simulation to inform the use of ferrofluids in broad range of practical applications, such as medicine, acoustics, radar-absorbing materials and nanoelectronics.
Ferrofluids were developed by NASA in the 1960s as a way to pump fuels in low gravity. They comprise nanoscale magnetic particles of iron-laden compounds suspended in a liquid. In the absence of a magnetic field, ferrofluids possess a perfectly smooth surface. But when a magnet is brought close to the ferrofluid, the particles rapidly align with the magnetic field, forming the characteristic spiky appearance. If a magnetic object is placed in the ferrofluid, the spikes will even climb the object before cascading back down.
The Democratic Republic of Congo has confirmed the first case of Ebola in the eastern city of Goma, a major transport hub.
The World Health Organization (WHO) said the case could be a “game-changer” given the city’s population of more than two million.
But the WHO expressed confidence in plans to deal with the diagnosis.
Our Ending Age-Related Diseases conference in New York is over for this year and has been a huge success. We had the opportunity to interview one of the speakers, Dr. Mar í a Blasco, during the conference, and we asked her more about her work with telomeres, telomerase therapy, and aging.
Telomere loss is a proposed reason we age
Telomere attrition—the wearing out of your chromosomes’ protective caps with age—is widely thought to be one of the major drivers of aging. With each division, telomeres shorten a little bit, and after 50–70 divisions, they become critically short. Once this threshold (the Hayflick limit) is hit, cells undergo replicative senescence, and their division comes to a grinding halt.
The disability burden for people with multiple sclerosis (MS) can vary significantly depending on whether they have a relapsing/remitting form of the disease, where they experience periods of clinical remission, or a progressive form, where they have continued neurological deterioration without clinical remission. Effective therapies exist for managing relapsing/remitting MS, but treatment for progressive MS has proved more challenging. Now, a new paper published in the journal Brain from researchers at the Advanced Science Research Center (ASRC) at The Graduate Center, CUNY and Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai has identified potential mechanisms that may inform the development of therapies that effectively manage progressive MS.
Previous research had suggested that dysfunction of neuronal mitochondria—the energy-producing subcellular organelles—occurs in the brains of MS patients with progressive clinical disability. However, the molecular mechanisms underlying this process remained elusive.
“Because the brain is bathed by the cerebrospinal fluid (CSF), we asked whether treating cultured neurons with the CSF from MS patients with a relapsing/remitting or a progressive disease course would possibly elicit different effects on neuronal mitochondrial function,” said the study’s primary investigator Patrizia Casaccia, Einstein Professor of Biology at The Graduate Center and founding director of the Neuroscience Initiative at the ASRC. “We detected dramatic differences in the shape of the neuronal mitochondria and their ability to produce energy. Only exposure to the CSF from progressive MS patients caused neuronal mitochondria to fuse and elongate while rendering them unable to produce energy. We therefore searched for potential mechanisms of CSF-induced neurodegeneration with the intent to define therapeutic strategies.”
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This atlas of human CoRSIVs,” they write, “provides a resource for future population-based investigations into how interindividual epigenetic variation modulates risk of disease,” and may well transform understanding of the causes of illness in the human body.
A project 370 times larger than the Human Genome Project bears first fruit. Stephen Fleischfresser reports.
Any major breakthrough in extending human life would drastically alter population projections. The social effects, while obviously huge, would depend on whether the years of senility were prolonged, too; whether women’s age at menopause would increase; and how families would be structured if many generations were alive at the same time. Expensive treatments to extend human lives could also have implications for inequality; as in many other areas of technology, the wealthy would be most able to afford such services.
Almost everyone would welcome an extension of their healthy lifespan, and some scientists are looking at increasingly extreme ways to achieve that. But any major breakthrough in this area could have unwanted and far-reaching demographic, social, and economic implications.
CAMBRIDGE – Humans have long sought the elixir of youth, so it is not surprising that even non-scientists closely follow the latest research into aging. But is what most people consider simply a fact of life actually a “disease” that can be cured? Or is there some insurmountable limit to the lifespan of human bodies?
The modern biographical story of Stanislaw Burzynski, MD, PhD who discovered an innovative patent-protected cancer therapy currently enrolled in FDA clinical trials. This story sheds light on the current regulatory and industry roadblocks preventing these life-saving medications from reaching the market as of 2016.
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From “Burzynski: The Cancer Cure Cover-Up”
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