Lifeboat Foundation

So what’s the catch?

For one, iPSCs can take months to make and the process is expensive. Furthermore, reverting cells back to a stem cell state wipes out their history, which is sometimes useful for studying disease progression.

In essence, iPSCs are the middlemen between one cell type and another. What if we could simply take out the middleman altogether?

Continue reading “Transdifferentiation Can Create An Endless Supply of Brain Cells—And Fast” »

Scientists at Hollings Cancer Center at the Medical University of South Carolina have found that human lung cancer cells resist dying by controlling parts of the aging process, in results published online May 10th in the Journal of Biological Chemistry. The discovery could help us better understand aging and eventually could lead to new treatments for cancer.

Cancer becomes more common as people get older, but scientists are still searching for answers about why this happens. At Hollings Cancer Center, research into the connections between aging and cancer is led by Besim Ogretmen, Ph.D., SmartState Endowed Chair in Lipidomics and Drug Discovery. Ogretmen’s team found that cancer cells have specific ways to resist dying the way normal cells do. They do so by protecting the tips of their chromosomes, which hold our DNA, from age-related damage.

Ogretmen studies how cancer cells are different than normal cells to understand how cancer grows and spreads in the body. His work is part of an $8.9 million program project grant to research how alterations of lipid metabolism affect cancer therapy. The grant is helping fund a clinical trial of an anticancer medicine to inhibit cellular signaling that helps cancer survive. The drug was found to be useful against cancer in the research reported in the group’s new paper.

In the longer term, our descendants may face even more existential decisions (provided the machines allow them to make them). How might they organise society in a world in which few people can do anything that is obviously economically productive? The world might become techno-feudal, with an owning elite hiring great numbers of cheap human servants not for their value, but for the pleasure of domination. People might instead share the abundance more equally, with all enjoying the civilised leisure that was once the province of the very few. Ours is the first civilisation to view work as the highest calling. Maybe that strange prejudice will need to be discarded.

How do you organise a society in which few people do anything economically productive?

Sorry, T-Rex — blame Nemesis.

Most if not all stars in the universe might also have a twin.

“I am extremely excited about the research involved in the current Scientific Reports article,” said Joseph I. Shapiro, M.D., senior author and dean of the Joan C. Edwards School of Medicine. “I believe that our team has not only implicated the NAKL discovered by our colleague, Dr. Zijian Xie, in the aging process but identified a novel therapeutic target as well as a specific pharmacological strategy to actually slow the aging process. Although it will be some time before we can test these concepts in human subjects, I am cautiously optimistic that clinical therapeutics will ultimately result.”

The team’s extensive year-long study first focused on aging mice who were given a western diet to stimulate oxidant stress to antagonize the NAKL. The western diet increased the functional and structural evidence for aging; however, the introduction of pNaKtide slowed these changes in the mice. The same results were then replicated when human dermal fibroblasts were exposed to different types of oxidant stress in vitro by stimulating the NAKL, increasing expression of senescence markers, and causing cell injury. With pNaKtide treatment, the researchers demonstrated that the negative attributes associated with aging were significantly dampened.

“Our data clearly suggest that the Na/K-ATPase oxidant amplification loop is intimately involved in the aging process and, if confirmed in human studies, might ultimately serve as a therapeutic target,” said first author Komal Sodhi, M.D., an associate professor of surgery and biomedical sciences at the Joan C. Edwards School of Medicine. “If the pNaKtide can be safely used in humans, it might be possible to study the applicability of that specific agent to the problem of clinical aging.”

Would you? www.disclose.tv

Google, Facebook, Twitter and Microsoft formed the Global Internet Forum to Counter Terrorism last year to prevent terrorists from exploiting their services.

• By Stuart Macdonald, The Conversation US on June 26, 2018

A remarkable new study has successfully used the CRISPR-Cas9 gene editing technique to edit a specific gene in mice engineered to have fragile X syndrome (FXS), a single-gene disorder often related to autism. The single gene edit in the live mice resulted in significant improvements in repetitive and obsessive behaviors, making this the first time gene editing has been used to effectively target behavioral symptoms related to autism spectrum disorder (ASD).

FXS is a genetic disorder associated with intellectual disability, seizures and exaggerated repetitive behavior. Previous studies have shown that the repetitive behaviors associated with FXS are related to a specific excitatory receptor in the brain that, when dysregulated, causes exaggerated signaling between cells.

The CRISPR technique homes in on the gene that controls that excitatory receptor, the metabotropic glutamate receptor 5 (mGluR5), and essentially disables it, dampening the excessive signaling the corresponds with repetitive behaviors. In mice treated with the new system, obsessive digging behavior was reduced by 30 percent and repetitive leaping actions dropped by 70 percent.

For the first time ever researchers have had a breakthrough in creating a cocktail of drugs that caused new neurons to grow in the brains of mice.

In my last article I gave a detailed account on the debate of neurogenesis. While some neuroscientists claim that neurogenesis takes place within the adult mammalian human brain other researchers contest that idea claiming that new neurons stop developing at a very young age. Whichever side of the debate you are on one thing remains certain, that there are neurological diseases that leave negative impacts on cognitive function. This has left researchers looking for various ways to treat Alzheimer’s, Parkinson’s, and other brain damage.

Continue reading “Experimental Drug Injection Causes the Brain to Grow New Neurons” »