Researchers developed a tiny antenna-named Cell Rover – that sends data from inside the body’s cells, ,without destroying or manipulating the cell, with microwave waves to the receiving systems.Deblina Sarkar, a researcher at the center of this research, says: This research is astonishing for scientific technology. This nanotechnology scientist at the Massachusetts Institute of Technology has provided unique details about her Cell Rover.
New engineering science allows scientists to produce tiny hardware the size of body cells to enter the cell and examine its details. These tiny devices need to receive commands and communicate with a controlling device, which increases the problems.Sarkar said: One of the biggest challenges we face is making an antenna so small that it fits inside a cell.
Among other problems of this work, we can mention the electromagnetic waves sent from inside this device, which will damage the cellular tissue if it malfunctions. For this antenna to work properly, it’s transmitted and received waves must be in the resonant frequency so that its wavelength is equal to the received or transmitted wavelength. Because of the mathematical relationship between speed, frequency, and wavelength, waves with shorter wavelengths have higher frequencies. Unfortunately, the antennas in the cell in this way must be small enough to be able to support these waves with a specific wavelength.
Just like other microwave waves, these types of waves also destroy cells. In research, Sarkar and her team are looking for ways to solve this problem. In an article published in Nature Communications, they consider a special design for this type of cellular antenna that works safely and acoustically. With this method, researchers can more easily and quickly with the antenna inside cells communicate, which ultimately leads to the diagnosis of problems inside the cell.
Sarkar and her team made the antenna from a type of magnetostrictive material that changes shape when exposed to a magnetic field. Researchers combine a certain amount of iron, nickel, boron, and molybdenum for this. When a special magnetic field is induced to the magnetostrictive antenna, the positive and negative poles of molecules will move with each change of the field and change the shape of the material. In this case, the antenna will oscillate. Like any type of magnetic material, the antenna generates its magnetic field to react to the external force. Each time the primary magnetic field changes, the antenna also responds, and this method is carried out as a two-way message from inside the cell.
The main difference between the conventional antenna and this new invention is the change of magnetic waves to acoustic waves. Jacob Robinson says: Antenna resonance is not based on visible wavelengths but based on sound waves. He is a neuroengineer at Rice University and participates in this research.
Just like larger classical antennas, the Cell Rover antenna reacts when it sees incoming waves equal to its resonant frequency, but these waves are sound waves that are slower than electromagnetic waves. Due to the relationship between the wavelength of a wave and its frequency, sound waves and electromagnetic waves have the same wavelength have different frequencies. The external magnetic field can send or receive messages to the Cell Rover without damaging the cellular system.
The researchers first tested the Cell Rover in air and water and found that the antenna’s frequency was 10,000 times smaller than an electromagnetic antenna. This causes the least amount of damage to the cell. After that, they tried to test the antenna in a living body. They put the Cell Rover inside the egg cell of an African frog to check the results of the calculations. After this test, the egg cell was not damaged and the antenna simply received and sent commands. The scientists also inserted a large number of these antennas into the cell for further testing and found that each of the devices worked correctly and independently.
Although the researchers had reduced the size of the Cell Rover as much as possible, it was still too large to fit inside a cell. The size of the manufactured Cell Rover is about 0.4 mm. After repeated checks, they realized that in practice, the size of the Cell Rover should be about 20 times smaller than the current size. In theory, antennas this small can also communicate effectively with the main broadcast waves.
Until now, the commands sent to the Cell Rover have been experimental, and in the next steps, the researchers will try to get specific information from the environment around the antenna. For example, they use a type of polymer coating to connect to the surrounding ions and proteins, when the antenna passes by these materials and the material sticks to the coating, the wavelength sent from the device changes, and the researchers noticed it.
Of course, Cell Rover will use for more complex commands in the future. We may be able to use these antennas to kill cancer cells or even charge other miniature robotic devices inside the body. It is also very effective to use them to receive intracellular biological information and even in the future, these can be equipped with a smart diagnosis system.
Scientists find new method for reverse aging process
In a new project, Harvard University researchers investigated an experimental method on mice that might be able to reverse the aging process.
Harvard Medical School (HMS) scientists have investigated the cause of aging and identified a possible way to reverse it. In experiments on mice, they showed that problems in epigenetics trigger the signs of aging and that a reboot can reverse them and perhaps extend life.
Our genome contains a complete map of the DNA found in every cell in our body. This is not the whole picture but an additional layer of information called the epigenome, which controls which genes are turned on and off in different cell types. It’s as if all the cells in our body work based on an operating manual, the genome, but the epigenome is like a list of contents that directs different cells to different chapters, which are genes. After all, lung cells need very further instructions from heart cells.
Reverse aging process
Environmental and lifestyle factors such as diet, exercise, and even childhood experiences can alter epigenetic expression. Epigenetic changes have been linked to the rate of biological aging, but whether they represent signs of aging or are themselves a symptom was not yet clear. Researchers in this project conducted experiments on mice to find out the answer. Using a system called ‘Induced Changes in the Epigenome’ (ICE), they sped up the natural process of DNA damage and repair in mice to see if this accelerated the signs of aging.
In mammalian cells, chromosomes undergo a million DNA breaks per minute, and epigenetic factors rapidly coordinate the repairs before returning to their original sites. The research group engineered mice that underwent DNA breakage at a rate three times faster than usual.
Over time, researchers discovered that epigenetic factors become increasingly disturbed and do not return home after repairing DNA breaks. This leads to epigenome scrambling. At six months, the mice showed physical signs of aging and appeared in significantly worse health than age-matched unedited mice.
Researchers say that this research has confirmed the role of the epigenome in aging. The next step was to test whether something could be done about the problem. Researchers tested a gene therapy combination of three genes named “Oct4”, “Sox2,” and “Klf4”. These genes are active in stem cells, and the researchers found in their previous study that they could be used to restore vision to mice with age-related glaucoma.
New experiments on reverse aging
In this case, the ICE mice experienced a dramatic reduction in biomarkers of aging. Their epigenome was ripped apart, restoring their tissues and organs to a youthful state. David Sinclair, the project’s lead researcher, said: “It’s like restarting a broken computer, and it sets off an epigenetic program that directs the cells to restore the epigenetic information they had when they were young.” This is a permanent reset.
Read more : How humans lose their body hairs
Researchers believe that this discovery is enormous. Many diseases caused by this natural process can be treated more effectively by tackling aging. Sinclair wrote in a tweet: “If the result is correct, it means that cancer, diabetes, and Alzheimer’s may have the same underlying cause.” In this way, the cause can be reversed to treat age-related diseases.
Although there is still much research to be done before such lofty goals can be realized, research is being done. A preprint paper, which has not yet been reviewed, applied the same gene therapy combination to aged mice, which are the equivalent of 77 years in humans. These mice lived 9% longer than untreated mice.
Via : New atlas
How humans lose their body hair
In their new research, a group of American scientists has investigated the reasons for body hair loss in mammals such as humans.
Body hair is a defining characteristic of mammals, but several mammals, such as whales, nudibranchs, and humans, have significantly less hair. Why we have significantly less hair than other mammals has long remained a mystery.
To find the genetic basis of hair loss, scientists at the University of Utah (UofU) and the University of Pittsburgh identified coding and non-coding sequences that evolve at different rates in hairless mammals compared to hairy mammals.
Humans body hair is about genetic
They found that humans seem to have the gene for a complete body hair covering. This research identifies several genes and genomic regions critical for hair growth. Also, this research shows that nature has used the same tactic at least nine times in different mammals. Ancestors of rhinos, nudibranchs, dolphins, and other hairless mammals used to swim and submerge to turn off a set of genes needed to lose hair and fur.
“We have taken a creative approach to use biodiversity to learn about our genetics,” said Dr. Nathan Clark, a human geneticist at the University of Utah who has conducted much of this research. This helps us identify regions of our genome that contribute to an important trait.
How humans lose their body hair
Scientists used an evolutionary rate-based method called RERconverge to perform a genome scan of 62 mammal species using 19,149 genes and 343,598 non-coding regions.
The analysis showed that many hairless mammals have mutations in many of the same genes. These genes encode keratin and extra elements that build the hair shaft and facilitate growth.
Also, this research showed that the genome’s regulatory regions seem equally important. Rather than encoding the structures that produce hair, these regions indirectly affect hair production. They control the amount of hair produced and when and where special genes are activated.
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Amanda Kowalczyk, one of the researchers of this project, said: There are many genes that we don’t know much about. We believe these genes can play a role in hair growth and maintenance.
As animals are under evolutionary pressure to lose hair, the genes that code for hair become less important, Clark said. This is why they increase the rate of genetic variation allowed by natural selection. Some genetic changes may lead to hair loss, and others may be collateral damage after hair growth stops.
He added: “When a screen identified known hair genes, it showed that this method was efficient.” Also, this research shows that the genes identified on the screen, which are not well defined, can be equally important for having hair. It is a way to determine the global genetic mechanisms that underlie different traits.
Creating eye tissue using stem cells
Scientists have discovered a way to create eye tissue using stem cells and 3D printing, which may lead to breakthroughs in the treatment of a wide range of degenerative eye diseases.
Scientists at the National Institute of Vision (NEI) have 3D printed a group of cells that can form the outer blood barrier of the retina. The outer retinal blood barrier is an eye tissue that supports the photoreceptor cells.
Creating eye tissue using stem cells
The method presented by this research group theoretically provides an unlimited source of patient-derived tissue to study retinal degenerative diseases such as macular degeneration (AMD) and use them to better understand how to treat these diseases.
Dr. Kapil Bharti, director of the stem cell and eye research at the National Institute of Vision, said: We know that macular degeneration begins in the outer blood barrier of the retina. Despite this, the mechanisms of initiation and progression of macular degeneration are still poorly understood due to the lack of physiologically relevant human models.
Nearly 20 million Americans suffer from some form of age-related macular degeneration. It is the leading cause of vision loss in Americans age 60 and older and the leading cause of irreversible blindness and vision loss worldwide.
Marc Ferrer, director of the 3D Tissue Bioprinting Laboratory at the National Institute of Vision, said: Our joint efforts have led to the presentation of retinal tissue models that are highly relevant to degenerative eye diseases. Such tissue models have many potential applications in therapeutic development.
Bharti and colleagues combined three types of immature choroidal cells into a hydrogel. These three types of cells are pericytes and endothelial cells, which are the main components of capillaries, and fibroblasts, which form the structure of tissues. They then printed the gel onto a biodegradable framework, and within days, the cells began to mature and transform into a dense capillary network.
On day 9, the scientists’ cultured retinal pigment epithelial cells on the other side of the biodegradable framework. Just one month later, the tissue reached full maturity. During subsequent experiments, the scientists found that the printed tissue resembled the outer blood barrier and retina of the real eye.
“By printing the cells, we facilitate the exchange of cellular signals that are essential for the normal anatomy of the blood-outer retinal barrier,” Bharti explained.
Via : NIH
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