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When the structure of DNA was elucidated in 1953, an unimaginable world of possibilities was opened. But we couldn’t even begin to dream about how we would go about using such powerful knowledge. Thirty years later, PCR — the process to replicate DNA in the lab — was developed, and innovation exploded. In 2001 — nearly twenty years ago — the first full human genome was sequenced and published.

The information we’ve uncovered through DNA is enabling us to explore and develop solutions for a variety of problems, from how to mimic human disease in animal models to finding new treatments and cures for devastating diseases such as cancer and Alzheimer’s.

Our ability to engineer biology is making DNA even more powerful. We are building upon the blueprint that was already there, strengthening it, giving it new and improved functions, and leveraging its characteristics to do useful things for us. Perfect examples include engineering the genomes of T cells to turn them into highly specific cancer fighters or modifying bacteria to produce useful products like insulin, food ingredients, or bioplastics. We are even beginning to use DNA to store information, perhaps one day replacing the physical hard drive.

Great Diet Information: #Longevity

Inflammation is also called the silent killer. It is silent because as your body struggles with inflammation, it also does all it can to maintain balance. This means that symptoms are sometimes hard to decipher and can even be hidden for some time.

Inflammation can be a good thing

A little bit of inflammation is a good thing, a lot can be extremely dangerous. When we are injured or sick, the immune system jump into gear and brings an army of white blood cells to the area of concern by increasing blood flow. For instance, when you get a cut or a scrape it generally becomes puffy, red and hot. This is inflammation – more white blood cells have arrived to handle the situation. Acute inflammation is how the body responds to foreign pathogens – it protects us from harm.

Researchers at the Buck Institute, including Dr. Judy Campisi, have published a new study that shows, for the first time, that senescent cells are associated with age-related blood clots [1].

As we get older, increasing numbers of our cells enter into a state known as cellular senescence. Senescent cells do not divide or support the tissues of which they are part; instead, they emit a range of potentially harmful chemical signals known as the senescence-associated secretory phenotype (SASP), which encourages nearby healthy cells to enter the same senescent state.

The presence of high levels of SASP reduces tissue repair, increases chronic inflammation, and can even raise the risk of cancer and other age-related diseases.

Well, it’s sound weird but in the upcoming future, your toilet will be your mini doctor. A company called Micron is developing a smart artificial intelligence-powered toilet that will reportedly be able to diagnose your state of health and risk of disease by analyzing your bodily waste.

The major goal of this technology is to analyze bowel movements and recognize the signs for health issues or ailments early on. This information will also use to understand early symptoms of certain diseases.

STOCKHOLM — A new trial of autologous mesenchymal stem cells in progressive multiple sclerosis (MS) has shown encouraging results, with significant benefits vs placebo in several measures of disability.

The double-blind placebo-controlled phase 2 study — described as “very pioneering” and “provocative” by outside commentators — was presented at the recent 35th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) 2019.

Both intravenous and intrathecal administration of the stem cells showed beneficial clinical effects compared with placebo in terms of Expanded Disability Status Scale (EDSS) changes and several other functional outcomes, but the intrathecal route appeared superior to intravenous administration, reported Dimitrios Karussis, Hadassah University Hospital, Jerusalem, Israel.

A quasi-particle that travels along the interface of a metal and dielectric material may be the solution to problems caused by shrinking electronic components, according to an international team of engineers.

“Microelectronic chips are ubiquitous today,” said Akhlesh Lakhtakia, Evan Pugh University Professor and Charles Godfrey Binder Professor of Engineering Science and Mechanics, Penn State. “Delay time for signal propagation in metal-wire interconnects, electrical loss in metals leading to temperature rise, and cross-talk between neighboring interconnects arising from miniaturization and densification limits the speed of these chips.”

These are in our smartphones, tablets, computers and and they are used in hospital equipment, defense installations and our transportation infrastructure.

A new study shows that scientists might be able to not only slow the process of aging but actually reverse it, Benjamin Button-style.

Volunteers in a California study were given a cocktail of three common drugs for one year— a growth hormone and two diabetes medications. Scientists had been testing the drugs in the hope of regenerating the thymus gland.

But upon further analysis, they found that participants had lost an average of 2.5 years on their “epigenetic clock,” measured by analyzing marks on a person’s genomes, according to the journal Nature. Participants’ immune systems also showed signs of rejuvenation.

Telomeres are the protective caps of our chromosomes and play a central role in the aging process. Shorter telomeres are associated with chronic diseases and high stress levels can contribute to their shortening. A new study now shows that if telomeres change in their length, that change is also reflected in our brain structure. This association was identified by a team of scientists including Lara Puhlmann and Pascal Vrtička from the Max Planck Institute for Cognitive Brain Sciences in Leipzig together with Elissa Epel from the University of California and Tania Singer from the Social Neuroscience Lab in Berlin as part of Singer’s ReSource Project.

Telomeres are protective caps at the ends of chromosomes that become shorter with each cell division. If they become so short that the genes they protect could be damaged, the cell stops dividing and renewing. Consequently, the cell is increasingly unable to perform its functions. This mechanism is one of the ways in which we age.

Telomere length is therefore regarded as a marker for the biological age of a person—in contrast to their chronological age. For two people of the same chronological age, the person with has an increased risk of developing age-related diseases such as Alzheimer’s or cancer, and even a shorter life expectancy.