face_with_colon_three circa 2016.
Tough ‘water bears’ defy intense radiation by apparently wrapping their genetic material in a bizarre protein that can also protect human cells.
When our neurons—the principle cells of the brain—die, so do we.
Most neurons are created during embryonic development and have no “backup” after birth. Researchers have generally believed that their survival is determined nearly extrinsically, or by outside forces, such as the tissues and cells that neurons supply with nerve cells.
A research team led by Sika Zheng, a biomedical scientist at the University of California, Riverside, has challenged this notion and reports the continuous survival of neurons is also intrinsically programmed during development.
The thalamus is a “Grand Central Station” for sensory information coming to our brains. Almost every sight, sound, taste and touch we perceive travels to our brain’s cortex via the thalamus. It is theorized that the thalamus plays a major role in consciousness itself. Not only does sensory information pass through the thalamus, it is also processed and transformed by the thalamus so our cortex can better understand and interpret these signals from the world around us.
One powerful type of transformation comes from interactions between excitatory neurons that carry data to the neocortex and inhibitory neurons of the thalamic reticular nucleus, or TRN, that regulate flow of that data. Although the TRN has long been recognized as important, much less has been known about what kinds of cells are in the TRN, how they are organized and how they function.
Now a paper published in the journal Nature addresses those questions. Researchers led by corresponding author Scott Cruikshank, Ph.D., and co-authors Rosa I. Martinez-Garcia, Ph.D., Bettina Voelcker, Ph.D., and Barry Connors, Ph.D., show that the somatosensory part of the TRN is divided into two functionally distinct sub-circuits. Each has its own types of genetically defined neurons that are topographically segregated, are physiologically distinct and connect reciprocally with independent thalamocortical nuclei via dynamically divergent synapses.
Scientists have discovered extinct strains of smallpox in the teeth of Viking skeletons — proving for the first time that the killer disease plagued humanity for at least 1400 years.
Smallpox spread from person to person via infectious droplets, killed around a third of sufferers and left another third permanently scarred or blind. Around 300 million people died from it in the 20th century alone before it was officially eradicated in 1980 through a global vaccination effort — the first human disease to be wiped out.
Now an international team of scientists have sequenced the genomes of newly discovered strains of the virus after it was extracted from the teeth of Viking skeletons from sites across northern Europe. The findings have been published in Science today (July 23, 2020).
Amazing.
The human DNA is a biological internet and superior in many aspects to the artificial one. Russian scientific research directly or indirectly explains phenomena such as clairvoyance, intuition, spontaneous and remote acts of healing, self healing, affirmation techniques, unusual light/auras around people (namely spiritual masters), mind’s influence on weather patterns and much more. In addition, there is evidence for a whole new type of medicine in which DNA can be influenced and reprogrammed by words and frequencies WITHOUT cutting out and replacing single genes.
Only 10% of our DNA is being used for building proteins. It is this subset of DNA that is of interest to western researchers and is being examined and categorized. The other 90% are considered “junk DNA.” The Russian researchers, however, convinced that nature was not dumb, joined linguists and geneticists in a venture to explore those 90% of “junk DNA.” Their results, findings and conclusions are simply revolutionary!
Continue reading “Scientists prove DNA can be reprogrammed by Words and Frequencies” »
Summary: APOEe4, a gene associated with Alzheimer’s disease risk, doesn’t appear to directly affect memory performance or brain activity in older adults without cognitive impairment. However, the gene does seem to influence brain regions and systems that older at-risk adults activate to support successful memory recall.
Source: McGill University
Researchers at McGill University and the Douglas Mental Health University Institute, in collaboration with the StoP-AD Center, have published a new paper in the Journal of Alzheimer’s Disease, examining how a known genetic risk factor for late-onset Alzheimer’s disease (AD) influences memory and brain function in cognitively intact older adults with a family history of AD.
Want to learn how we age and whether we can slow or even reverse aging? David Sinclair, PhD, professor of genetics at Harvard Medical School, says in his book “Lifespan” that aging is a disease, and that disease is treatable. Tune in to Homeroom with Sal on Tuesday at noon PT to get your questions answered by a leading expert on aging and age-associated diseases.
For more information visit: keeplearning.khanacademy.org
Continue reading “Homeroom with Sal & David Sinclair, PhD — Tuesday, July 14” »
Aging/longevity link!
Molecular biologists and bioengineers at the University of California San Diego have unraveled key mechanisms behind the mysteries of aging. They isolated two distinct paths that cells travel during aging and engineered a new way to genetically program these processes to extend lifespan.
The research is described July 17 in the journal Science.
Continue reading “Researchers discover 2 paths of aging and new insights on promoting healthspan” »
New insights into an elusive process that protects developing sperm cells from damage in growing embryos, sheds light on how genetic information passes down, uninterrupted, through generations.
The study identified a protein, known as SPOCD1, which plays a key role in protecting the early-stage precursors to sperm, known as germ cells, from damage in a developing embryo.
During their development, germ cells undergo a reprogramming process that leaves them vulnerable to rogue genes, known as jumping genes, which can damage their DNA and lead to infertility.
It might seem as though humans have little in common with the lowly yeast cell. Humans have hair, skin, muscles, and bones, among other attributes. Yeast have, well, none of those things.
But besides their obvious differences, yeast and humans, and much of life for that matter, have a great deal in common, especially at the cellular level. One of these commonalities is the enzyme our cells use to make RNA copies of sections of our DNA. The enzyme slides along a strand of DNA that has been unpacked from the chromosome in which it resides, to “read” the genetic code, and then assembles an RNA strand that contains the same code. This copying process, known as transcription, is what happens at a molecular level when a gene is activated in an organism. The enzyme responsible for it, RNA polymerase, is found in all eukaryotic cells (cells with a nucleus) and it is essentially the same in all of them, whether the cells are from a redwood, an earthworm, a caribou, or a mushroom.
That fact has presented a mystery for scientists, though: Although the DNA in a yeast cell is different in many ways from the DNA in a human cell, the same enzyme is able to work with both. Now, a team of Caltech researchers has discovered one way this happens.
