Login with your Social Account

Researchers identify the physical effects of stress and anxiety on cells

Researchers identify the physical effects of stress and anxiety on cells

As per new research, a combination of stress and anxiety might physically change the makeup of the mitochondrial cells. In our lifetime, we often deal with events that leave a lasting impression on our minds. Major incidents such as losing a loved one, war, divorce can lead to anxiety disorders along with panic attacks. Anxiety disorder is different from normal worrying since it is prolonged and does not reduce with time. It can be bad for our emotional and physical health since it interferes with the normal daily activities making them difficult to perform. 

According to the National Institute of Mental Health, anxiety disorders are impacted by a combination of our genes and the environment resulting in an overall stressful life. It has been observed that not all people facing traumatic events develop anxiety disorder raising the question of what makes some persons respond differently than others. 

To find the answer, scientists studied mice that had displayed symptoms of depression and anxiety such as staying alone after facing highly stressful situations. Changes in the genetic activity were then tracked along with the production of protein in the area of the brain which deals with stress and anxiety. These areas are the hippocampus, prefrontal cortex, nucleus accumbens, and amygdala. The research team used the “cross-species multi-omics” technique for analyzing the genes and proteins that are associated with mitochondrial cells. They found many changes in the mitochondria of the mice’s brain cells who were exposed to stress as compared to those who were not. After that blood samples of the patients who had panic disorder were tested and scientists detected similar mitochondrial changes in them.

The researchers mentioned in PLOS Genetics that the studies revealed a regular convergence of differentially expressed pathways related to mitochondria in blood samples of patients dealing with a panic disorder after a panic attack. This method of cellular energy metabolism might be a way in which animals deal with stress. 

Mitochondria, also known as the powerhouse of cells turn the food consumed into 90 percent of the chemical energy needed for the functioning of the body along with destroying the rogue cells. Dealing with a high amount of stress can affect how the mitochondria function leading to complicated health symptoms. 

Iiris Hovatta, University of Helsinki said that right now there is very little information on the effects of chronic stress on cellular energy metabolism. So these underlying mechanisms might be essential to the prevention of diseases related to stress. Genetic studies of the persons suffering from anxiety might lead to informed treatment which is currently limited to psychotherapy and medicines. 

Journal Reference: PLOS Genetics

Sixth death reported due to mysterious lung illness related to vaping

Sixth death reported due to mysterious lung illness related to vaping

Health officials in the state of Kansas confirmed the first death caused by a serious lung disease related to using e-cigarettes or vaping. This is the sixth death of this nature reported in the country. 

In a news release, health officials said that the resident was more than 50 years old with a history of health issues. The person was hospitalized with symptoms that progressed rapidly. Officials reported that they do not have complete information on the nature of the products which were used by the patient. 

The national investigation did not identify any specific e-cigarette products related to the cases. Several people reported using vaping products with liquids containing cannabinoid products such as THC. It is the main ingredient present in marijuana which causes the high. 

Officials in Minnesota and Los Angeles reported deaths in older persons previously. The Kansas death takes the tally for a middle-aged person to a minimum of four. 

The patient in Minnesota had a history of lung problems and was hospitalized with a serious lung injury. It was related to the use of illicit THC products. The patient was more than 65 years old and died after being hospitalized for a long period of time. 

The death of a middle-aged person was also reported in Oregon who died of respiratory illness due to the use of an e-cigarette that contained marijuana oil. The person had bought it at a legal dispensary and this was the first death related to a vaping product that was bought at a shop.

Deaths have also been reported in Indiana and Illinois however no information was provided about the type of products and their ages. It is now suspected that there is a minimum of 450 possible cases in 33 states where illnesses are caused due to the consumption of contaminants or counterfeit products in e-cigarettes. The possible culprits for the illnesses could be the adulterants in vaping products having THC. 

For these mysterious illnesses and severe symptoms in patients, health investigators are focusing on the contaminants rather than the standard vaping products that are being used for several years. US Food and Drug Administration found an oil that is derived from Vitamin E, vitamin E acetate in cannabis products collected from the patients who fell ill. This was also found in the samples from the patients who reported illness in New York recently. 

New York officials will be issuing subpoenas to three companies in the charge of selling “thickening agents” which contain high Vitamin E levels. Black market dealers have been using it to dilute the THC oil in illegal products. 

A new drug could revolutionize the treatment of neurological disorders

A new drug could revolutionize the treatment of neurological disorders

The international team of scientists from Gero Discovery LLC, the Institute of Biomedical Research of Salamanca, and Nanosyn, Inc. has found a potential drug that may prevent neuronal death through glucose metabolism modification in stressed neurons. The positive results obtained in mice are rather promising for future use in humans. The new drug can be advantageous in neurological conditions ranging from Amyotrophic lateral sclerosis, Alzheimer’s, and Huntington’s diseases to traumatic brain injury and ischemic stroke. The results have been published in the Scientific Reports Journal.

Brain injuries of different nature and neurological disorders are among the most important causes of death worldwide. According to WHO, stroke is the second most common cause of mortality, and more than a third of people who have survived a stroke will have a severe disability.

What is more, as the population ages, millions of more people are posed to develop Alzheimer’s or Parkinson’s diseases in the near future. However, there are no efficient drugs for major neurodegenerative diseases. It is thus critically important to understand the biology of these diseases and to identify new drugs capable of improving quality of life, survival, and,  in the best-case scenario, curing the disease completely.

Glycolysis is generally considered as the metabolic pathway essential for cell survival since it meets cell energy needs in case of intensive energy consumption. However, it is already known that in the brain tissue, the situation is quite different – different cell types show distinct glucose metabolism patterns.  In neurons, only a small portion of glucose is consumed via the glycolysis pathway. At the same time, astrocytes provide nutrients to neurons and utilize glycolysis to metabolize glucose. These differences are mostly due to the special protein called PFKFB3, which is normally absent in neurons and is active in astrocytes. In the case of certain neurological diseases, stroke being one of them, the amount of active PFKFB3 increases in neurons, which is highly stressful for these cells and leads to cell death.

An international team of researchers led by Peter Fedichev, a scientist and biotech entrepreneur from Gero Discovery, and professor Juan P. Bolaños from the University of Salamanca, suggested and further confirmed in the in vivo experiments that a small molecule, the inhibitor of PFKFB3, may prevent cell death in the case of ischemia injury. Inhibition of PFKFB3 improves motor coordination of mice after stroke and reduced brain infarct volume. Moreover, in the experiments using mouse cell cultures, it was shown that PFKFB3 inhibitor protects neurons from the amyloid-beta peptide, the main component of the amyloid plaques found in the brains of Alzheimer’s disease patients.

Professor Juan P. Bolaños: “Excitotoxicity is a hallmark of various neurological diseases, stroke being one of them. Our group has previously established a link between this pathological condition and high activity of PFKFB3 enzyme in neurons, which leads to severe oxidative stress and neuronal death“

“We are glad that our hypothesis that pharmacological inhibition of  PFKFB3 can be beneficial in an excitotoxicity-related condition, such as stroke was confirmed. I would like to note that In our work, we used a known molecule to demonstrate that PFKFB3 blockage has a therapeutic effect. But, we have also performed the same experiments with other proprietary small molecule designed in our company and showed that it had a similar effect. There is, of course, still much work to do. We are currently investigating the efficacy of our compounds in the models of orphan excitotoxicity-related neurological diseases. We have already obtained good safety results in mice and believe that we will be successful in our future investigations” said Olga Burmistrova, Director of preclinical development in Gero Discovery.

Gero Discovery team is planning to proceed with preclinical trials and to move into clinical trials soon. “These promising results bring hope to dozens of millions of patients suffering from life-threatening neurological diseases and provide tremendous business opportunities in many indications with unmet needs. We start communicating with potential investors and co-development partners and invite interested parties to collaborate on the further development of this breakthrough medicine through the preclinical and early clinical stage” mentioned Maksim Kholin, the Gero Discovery Co-Founder and Business Development Director.

Journal Reference: Scientific Reports Journal

MRI scans improve prostate cancer detection

MRI scans improve prostate cancer detection

The research, led by the National Institute for Health Research (NIHR) and Universities of Bristol, Ottawa, Exeter and Oxford, combined the results from seven studies covering 2,582 patients.

The researchers found that the use of pre-biopsy MRI combined with targeted prostate biopsy was better than a biopsy alone in detecting prostate cancers that are likely to need treatment, despite the differences between the seven individual studies. Using pre-biopsy MRI led to fewer biopsy cores being taken per procedure, which in turn reduced side effects, and may potentially lead to avoiding biopsies for some men.

Taken together, this new evidence supports the use of pre-biopsy MRI in diagnostic pathways for suspected prostate cancer.

Prostate biopsies can cause side effects, and do not always identify the severity of a cancer when it is present. MRI scans are increasingly being used before undertaking a prostate biopsy as part of the clinical pathway to diagnose prostate cancer, but their use isn’t yet widespread in many countries. In the UK, pre-biopsy MRI has recently been recommended by the National Institute for Health and Care Excellence (NICE).

The researchers looked at existing research in this area, focusing on men who had never had a prostate biopsy before.

Professor Richard Bryant, an Academic Consultant Urologist at the Nuffield Department of Surgical Sciences at Oxford University and one of the authors of the paper, said: ‘This research adds to the growing body of evidence that targeting biopsies through pre-biopsy MRI, in men being checked for possible prostate cancer, leads to a more accurate sampling of the prostate gland. It could also potentially lead to fewer biopsies and less chance of a misleading biopsy result, through better initial sampling.

‘Whilst there are obviously benefits for men to have a prostate biopsy if indicated, so that we can diagnose and then treat clinically significant prostate cancer, if we can reduce the potential side effects and increase the accuracy of the initial biopsy procedure, then that will be better for patients.’

Dr Martha Elwenspoek, Research Associate at the NIHR Collaboration for Leadership in Applied Health Research and Care West (NIHR CLAHRC West) and the University of Bristol, said: ‘Our findings suggest that using an MRI to guide prostate biopsies is superior to performing a biopsy alone. This is increasingly used in the UK but isn’t yet common practice in many other countries. However our work shows that this approach is better at detecting cancer that requires treatment, while also potentially avoiding some unnecessary biopsy procedures.

‘This chimes with the findings of another recent paper looking at this issue.’

The full publication, ‘Comparison of multiparametric magnet resonance imaging and targeted biopsy with systematic biopsy alone for the diagnosis of prostate cancer: a systematic review and meta-analysis‘, is available to read in the journal JAMA Network 

Materials provided by Oxford University

A new way to deliver drugs with pinpoint targeting

A new way to deliver drugs with pinpoint targeting

Most pharmaceuticals must either be ingested or injected into the body to do their work. Either way, it takes some time for them to reach their intended targets, and they also tend to spread out to other areas of the body. Now, researchers at MIT and elsewhere have developed a system to deliver medical treatments that can be released at precise times, minimally-invasively, and that ultimately could also deliver those drugs to specifically targeted areas such as a specific group of neurons in the brain.

The new approach is based on the use of tiny magnetic particles enclosed within a tiny hollow bubble of lipids (fatty molecules) filled with water, known as a liposome. The drug of choice is encapsulated within these bubbles, and can be released by applying a magnetic field to heat up the particles, allowing the drug to escape from the liposome and into the surrounding tissue.

The findings are reported today in the journal Nature Nanotechnology in a paper by MIT postdoc Siyuan Rao, Associate Professor Polina Anikeeva, and 14 others at MIT, Stanford University, Harvard University, and the Swiss Federal Institute of Technology in Zurich.

“We wanted a system that could deliver a drug with temporal precision, and could eventually target a particular location,” Anikeeva explains. “And if we don’t want it to be invasive, we need to find a non-invasive way to trigger the release.”

Magnetic fields, which can easily penetrate through the body — as demonstrated by detailed internal images produced by magnetic resonance imaging, or MRI — were a natural choice. The hard part was finding materials that could be triggered to heat up by using a very weak magnetic field (about one-hundredth the strength of that used for MRI), in order to prevent damage to the drug or surrounding tissues, Rao says.

Rao came up with the idea of taking magnetic nanoparticles, which had already been shown to be capable of being heated by placing them in a magnetic field, and packing them into these spheres called liposomes. These are like little bubbles of lipids, which naturally form a spherical double layer surrounding a water droplet.

When placed inside a high-frequency but low-strength magnetic field, the nanoparticles heat up, warming the lipids and making them undergo a transition from solid to liquid, which makes the layer more porous — just enough to let some of the drug molecules escape into the surrounding areas. When the magnetic field is switched off, the lipids re-solidify, preventing further releases. Over time, this process can be repeated, thus releasing doses of the enclosed drug at precisely controlled intervals.

The drug carriers were engineered to be stable inside the body at the normal body temperature of 37 degrees Celsius, but able to release their payload of drugs at a temperature of 42 degrees. “So we have a magnetic switch for drug delivery,” and that amount of heat is small enough “so that you don’t cause thermal damage to tissues,” says Anikeeva, who holds appointments in the departments of Materials Science and Engineering and the Brain and Cognitive Sciences.

In principle, this technique could also be used to guide the particles to specific, pinpoint locations in the body, using gradients of magnetic fields to push them along, but that aspect of the work is an ongoing project. For now, the researchers have been injecting the particles directly into the target locations, and using the magnetic fields to control the timing of drug releases. “The technology will allow us to address the spatial aspect,” Anikeeva says, but that has not yet been demonstrated.

This could enable very precise treatments for a wide variety of conditions, she says. “Many brain disorders are characterized by erroneous activity of certain cells. When neurons are too active or not active enough, that manifests as a disorder, such as Parkinson’s, or depression, or epilepsy.” If a medical team wanted to deliver a drug to a specific patch of neurons and at a particular time, such as when an onset of symptoms is detected, without subjecting the rest of the brain to that drug, this system “could give us a very precise way to treat those conditions,” she says.

Rao says that making these nanoparticle-activated liposomes is actually quite a simple process. “We can prepare the liposomes with the particles within minutes in the lab,” she says, and the process should be “very easy to scale up” for manufacturing. And the system is broadly applicable for drug delivery: “we can encapsulate any water-soluble drug,” and with some adaptations, other drugs as well, she says.

One key to developing this system was perfecting and calibrating a way of making liposomes of a highly uniform size and composition. This involves mixing a water base with the fatty acid lipid molecules and magnetic nanoparticles and homogenizing them under precisely controlled conditions. Anikeeva compares it to shaking a bottle of salad dressing to get the oil and vinegar mixed, but controlling the timing, direction and strength of the shaking to ensure a precise mixing.

Anikeeva says that while her team has focused on neurological disorders, as that is their specialty, the drug delivery system is actually quite general and could be applied to almost any part of the body, for example to deliver cancer drugs, or even to deliver painkillers directly to an affected area instead of delivering them systemically and affecting the whole body. “This could deliver it to where it’s needed, and not deliver it continuously,” but only as needed.

Because the magnetic particles themselves are similar to those already in widespread use as contrast agents for MRI scans, the regulatory approval process for their use may be simplified, as their biological compatibility has largely been proven.

The team included researchers in MIT’s departments of Materials Science and Engineering and Brain and Cognitive Sciences, as well as the McGovern Institute for Brain Research, the Simons Center for Social Brain, and the Research Laboratory of Electronics; the Harvard University Department of Chemistry and Chemical Biology and the John A. Paulsen School of Engineering and Applied Sciences; Stanford University; and the Swiss Federal Institute of Technology in Zurich. The work was supported by the Simons Postdoctoral Fellowship, the U.S. Defense Advanced Research Projects Agency, the Bose Research Grant, and the National Institutes of Health.

Materials provided by Massachusetts Institute of Technology

Study finds lack of racial diversity in cancer drug clinical trials

Study finds lack of racial diversity in cancer drug clinical trials

New research published this week in JAMA Oncology has found a lack of racial and ethnic diversity in clinical trials for cancer drugs.

The study—conducted by researchers from UBC, the University of Texas MD Anderson Cancer Center, the Fred Hutchinson Cancer Center in Seattle and Baylor University in Texas—raises concerns about the effectiveness of cancer drugs in some patients, especially since genetic differences may affect how well a patient responds to a drug.

The researchers found that fewer than eight per cent of cancer drug trials reported participation from the four major races in the United States — white, Asian, black and Hispanic — between 2008 and 2018. Black and Hispanic patients were particularly underrepresented at 22 per cent and 44 per cent, respectively, considering their populations’ incidence of cancer.

“Our findings show that the science might not be applicable to the population that’s going to receive the medications,” said the study’s lead author, Dr. Jonathan Loree, assistant professor in the department of medicine, division of medical oncology. “If patients are going to be receiving the drug, we need to know that it’s going to work for them with the same effectiveness that’s seen in the trial.”

Loree cited an example of a medication used to treat lung cancer that showed mediocre trial results in the global population, but exhibited incredible success with young women who had never smoked in a study in Asia due to a genetic mutation that’s common in this population.

The researchers found that both reporting about race in trials and enrolment rates had changed minimally over the decade.

For this study, Loree and colleagues reviewed all reported trials supporting U.S. Food and Drug Administration (FDA) oncology drug approvals granted between July 2008 and June 2018. They scrutinized 230 trials with a total of 112,293 participants. They calculated the U.S. population-based cancer estimates by race using National Cancer Institute and U.S. Census data.

Although the researchers used U.S. data, Loree said the findings are relevant in Canada, as well. Pharmaceutical companies typically apply for drug approvals through the FDA first, because it serves the largest market, and then submit to the European Medicines Agency and Health Canada. The trials considered in the approvals are usually the same.

“One thing particularly relevant to the Canadian context is that we weren’t able to analyze the participation of Native Americans in trials because there were only 13 patients reported out of a total of 112,000 participants,” Loree said. “That’s shocking and definitely shows an area where improvement is needed.”

The researchers are now looking at whether clinical trials represent the same gender ratio as the general population to ensure the drugs are effective in all people.

Materials provided by University of British Columbia

Golden gate bridge smog

Study finds air pollution to be as harmful as smoking cigarettes

Emphysema is a smoker’s disease but according to a study, it turns out that exposure to air pollution may create the same lung conditions which cause emphysema. A new study finds that long-term exposure to high levels of air pollution can be linked to a higher rate in the development of lung damage even for non-smokers. The study looked at the effects of breathing in different pollutants like ground-level ozone which is main content behind smog.

People with exposure to high levels of ground-level ozone developed changes in lungs which were similar to that of smokers. Joel Kaufman, physician and epidemiologist at the University of Washington said that an increase of 3 parts per billion of ground-level ozone is equivalent to smoking a pack of cigarettes daily for 29 years.

The study involved close to 7000 adults from six US cities with average annual exposure between 10 to 25 parts per billion of ground-level ozone. However this is not limited to cities, but people across the US are exposed to similar concentrations that keep on varying. Ground-level ozone is formed due to pollution released from cars and from smokestacks in the sunlight.

Kaufman was surprised to see the effects similar in magnitude to that of cigarette smoking. For correct evaluation, Each person had done 5 CT scans over a decade which gave a 3D picture of their lungs and can detect changes and developments over time. Emily Brigham, a pulmonologist and assistant professor of medicine at Johns Hopkins University says that when airways get narrowed and damaged, it becomes harder to breathe and the air gets trapped. The symptoms are not noticeable at an early stage but get worse over time with prolonged exposure and with irreversible effects. Chronic respiratory diseases is a leading cause of death in the U.S and close to 7 million deaths annually are linked to air pollution.

A significant proportion of the US population who has COPD is actually non-smokers, but this study answers the reason behind their lung disease. Clean Air Act has however led to declining pollution in the US but ground-level ozone or smog is harder to control and that increasing hot days means the conditions are more favorable for ozone formation, we are going to see increased effects due to global warming even in healthy populations. The past concerns dealt with short term exacerbation of symptoms during smog days for people with asthma or COPD. In the past, EPA had not accepted that COPD is caused by long-term, chronic air pollution but now the study has shown the evidence that the benefits of cleaning the air because the findings suggest that long-term exposure to air pollution is damaging to lung health.

Tissue model reveals role of blood-brain barrier in Alzheimer’s

Tissue model reveals role of blood-brain barrier in Alzheimer’s

Beta-amyloid plaques, the protein aggregates that form in the brains of Alzheimer’s patients, disrupt many brain functions and can kill neurons. They can also damage the blood-brain barrier — the normally tight border that prevents harmful molecules in the bloodstream from entering the brain.

MIT engineers have now developed a tissue model that mimics beta-amyloid’s effects on the blood-brain barrier, and used it to show that this damage can lead molecules such as thrombin, a clotting factor normally found in the bloodstream, to enter the brain and cause additional damage to Alzheimer’s neurons.

“We were able to show clearly in this model that the amyloid-beta secreted by Alzheimer’s disease cells can actually impair barrier function, and once that is impaired, factors are secreted into the brain tissue that can have adverse effects on neuron health,” says Roger Kamm, the Cecil and Ida Green Distinguished Professor of Mechanical and Biological Engineering at MIT.

The researchers also used the tissue model to show that a drug that restores the blood-brain barrier can slow down the cell death seen in Alzheimer’s neurons.

Kamm and Rudolph Tanzi, a professor of neurology at Harvard Medical School and Massachusetts General Hospital, are the senior authors of the study, which appears in the August 12 issue of the journal Advanced Science. MIT postdoc Yoojin Shin is the paper’s lead author.

Barrier breakdown

The blood vessel cells that make up the blood-brain barrier have many specialized proteins that help them to form tight junctions — cellular structures that act as a strong seal between cells.

Alzheimer’s patients often experience damage to brain blood vessels caused by beta-amyloid proteins, an effect known as cerebral amyloid angiopathy (CAA). It is believed that this damage allows harmful molecules to get into the brain more easily. Kamm decided to study this phenomenon, and its role in Alzheimer’s, by modeling brain and blood vessel tissue on a microfluidic chip.

“What we were trying to do from the start was generate a model that we could use to understand the interactions between Alzheimer’s disease neurons and the brain vasculature,” Kamm says. “Given the fact that there’s been so little success in developing therapeutics that are effective against Alzheimer’s, there has been increased attention paid to CAA over the last couple of years.”

His lab began working on this project several years ago, along with researchers at MGH who had engineered neurons to produce large amounts of beta-amyloid proteins, just like the brain cells of Alzheimer’s patients.

Led by Shin, the researchers devised a way to grow these cells in a microfluidic channel, where they produce and secrete beta-amyloid protein. On the same chip, in a parallel channel, the researchers grew brain endothelial cells, which are the cells that form the blood-brain barrier. An empty channel separated the two channels while each tissue type developed.

After 10 days of cell growth, the researchers added collagen to the central channel separating the two tissue types, which allowed molecules to diffuse from one channel to the other. They found that within three to six days, beta-amyloid proteins secreted by the neurons began to accumulate in the endothelial tissue, which led the cells to become leakier. These cells also showed a decline in proteins that form tight junctions, and an increase in enzymes that break down the extracellular matrix that normally surrounds and supports blood vessels.

As a result of this breakdown in the blood-brain barrier, thrombin was able to pass from blood flowing through the leaky vessels into the Alzheimer’s neurons. Excessive levels of thrombin can harm neurons and lead to cell death.

“We were able to demonstrate this bidirectional signaling between cell types and really solidify things that had been seen previously in animal experiments, but reproduce them in a model system that we can control with much more detail and better fidelity,” Kamm says.

Plugging the leaks

The researchers then decided to test two drugs that have previously been shown to solidify the blood-brain barrier in simpler models of endothelial tissue. Both of these drugs are FDA-approved to treat other conditions. The researchers found that one of these drugs, etodolac, worked very well, while the other, beclomethasone, had little effect on leakiness in their tissue model.

In tissue treated with etodolac, the blood-brain barrier became tighter, and neurons’ survival rates improved. The MIT and MGH team is now working with a drug discovery consortium to look for other drugs that might be able to restore the blood-brain barrier in Alzheimer’s patients.

“We’re starting to use this platform to screen for drugs that have come out of very simple single cell screens that we now need to validate in a more complex system,” Kamm says. “This approach could offer a new potential form of Alzheimer’s treatment, especially given the fact that so few treatments have been demonstrated to be effective.”

Materials provided by Massachusetts Institute of Technology

Pacemaker

Researchers develop implantable device which produces energy with the help of ultrasound

Scientists affiliated with different institutions in the Republic of Korea have created a type of implantable device which produces energy with the help of an external ultrasound source. It was then tested on animal tissue and scientists reported it in a paper which has been published in the Science journal.

Although pacemaker has saved many lives, it has several risks for the patient who have them implanted into the chests. They have to be replaced at periodic intervals of time which creates an additional risk of infection in the patients along with a degree of pain and irritation in the bodies. There might be bruising, bleeding or swelling at the generator site, which is more if the patient has been taking blood thinners.

Pacemaker-mediated tachycardia (PMT) is also another form of complication of artificial pacemakers. Because of these reasons, researchers have searched for techniques to produce power inside the body which will make the batteries unnecessary. As a new result, scientists have designed a generator which develops power when it is exposed to an ultrasound source.

The generator is a kind of triboelectric generator. These type of generators harvest energy from the triboelectric effect. In this effect, contact electrification occurs when two dissimilar materials touch and are then pulled away. An example of this effect is static electricity. The team used the generator which had two squares of material inside that were forced together in exposure to ultrasound. After the removal of the ultrasound signal, the objects got separated and a small electricity amount was generated which was captured in the generator. Along with this, the team added several other components to the device which allows interfacing with other devices. Scientists also had to make sure that it could withstand when implanted inside a living being.

For testing the generator, the team of researchers implanted it into pig tissue at different depths and then emitted ultrasound through the skin. They reported that at a depth of five millimeters, electricity was produced by the generator with a value of current up to 156 microamperes and a voltage of 2.4 volts. And at depths of one centimeter, the generator managed to develop 98 microamperes and 1.9 volts. Researchers identify the prospect that if they manage to run the different kinds of pacemakers and implantable devices with the generator then it would save the patients of the pain to replace it at periodic time intervals with the help of surgery.

Feedspot has one of the most comprehensive list of top 100 science blogs, websites and newsletters. ScienceHook has been featured in it recently at the 78 position. You can check it out here

human embryo

Japanese Government approves experiments to be conducted for human-animal embryos

Japan has approved the first human-animal embryo that could lead to new sources of organ transplant. Though there are still technical and ethical hurdles. Government of Japan is supporting a stem cell scientist Hiromitsu Nakauchi who leads teams at the University of Tokyo and Stanford University in California for creating animal embryos that contain human cells and transplant them into surrogate creatures as the restriction to practice was overturned this year.

Human cells are planned to be grown in mouse and rat embryos and then it could be transplanted into surrogate animals. Nakauchi said that he wants to produce animals with organs made from human cells which can be eventually transplanted into individuals. He also said that he is planning to grow a hybrid mouse for 14.5 days when the organs are mostly formed, almost to be termed and 15.5 days for the same experiment on rats. He is awaiting government approval for up to 70 days, for growing hybrid embryos in pigs. The study has been published in Nature journal.

Bioethicists are concerned that the human cells might stray beyond the development of the specific organ and travel to the animal’s brain and affect the cognition. He also added that these concerns were taken into consideration during experiments and that he made sure that cells go only to the pancreas and not the entire body.

Scientists are investigating a strategy to make an animal embryo that lacks a gene vital for the generation of a specific organ, like the pancreas and then infuse human induced pluripotent stem (iPS) into the animal fetus. iPS cells have been programmed to an embryonic-like state which can offer ascent to all cell types. As the animal starts to develop, it will make use of the human iPS cells to make an organ which it cannot make on its own.

At the American Association for the Advancement of Science meeting in Austin, Texas in 2018 scientists reported they had put human iPS cells into the sheep embryos and had been engineered not to produce a pancreas but even after growth for 28 days, it contained very less human cells and nothing resembling organs. Nakauchi thinks that is due to the genetic distance between humans and sheep.

Jun Wu who is a researcher at the University of Texas Southwestern Medical Center in Dallas said that it is not useful to bring human-animal hybrid embryos in evolutionarily distant species like pigs and sheep as human cells will be eliminated by the host early on. There is a need to understand the molecular basics and then develop strategies to overcome problems. The approval in Japan will be helpful in experimenting with iPS cells at different stages to find out the limit of growth of human cells in animal embryos.