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In a study recently published in Nature Communications, scientists from The Novo Nordisk Foundation Center for Biosustainability (DTU) and Yale University have investigated how bacteria that are commonly found in sugarcane ethanol fermentation affect the industrial process. By closely studying the interactions between yeast and bacteria, it is suggested that the industry could improve both its total yield and the cost of the fermentation processes by paying more attention to the diversity of the microbial communities and choosing between good and bad bacteria.
The scientists dissected yeast-bacteria interactions in sugarcane ethanol fermentation by reconstituting every possible combination of the microbial community structure, covering approximately 80% of the biodiversity found in industrial processes, and especially one bacterium deserves extra attention: Lactobacillus amylovorus. But how come exactly this one doesn’t fall into the category of “the bad guys”? The main reason is that it produces a lot of the molecule acetaldehyde, which is used to feed yeast and thus helps it to grow. You could say that Lactobacillus amylovorus is more generous by nature and shares the meal, whereas many other bacteria involved in these processes prefer simply to steal the food.
“It works almost in the same way as a probiotic that shields the bad bacteria from entering into the system. And when this bacterium grows, it will grow in a way that is almost symbiotic with the yeast which is very beneficial for the industrial process,” says Felipe Lino, former PhD Student at The Novo Nordisk Foundation Center for Biosustainability and Global R & D Manager at Anheuser-Busch InBev.
Significant improvement of yield
Thus, companies could take advantage of selecting not only for an ideal yeast strain for production, as they started doing already in the 90’s, but to select for the best-suited bacteria as well, since it is completely impossible to get rid of bacteria that are hanging around no matter what. An effort that could turn out to pay dividends already in a short-term perspective.
By using this probiotic in a sugarcane ethanol fermentation, it is estimated that the fermentation yield could increase by three percent. While three percent can sound like a rather low number this is definitely not the case. According to Brazil’s Biofuels Annual 2019, Brazil’s total ethanol production in 2019 was 34.5 billion liters with domestic demand for 34 billion liters making the country the home to the largest fleet of cars that use ethanol derived from sugarcane as an alternative fuel to fossil fuel-based petroleum.
These numbers indicate that optimised fermentation processes hold great potential. One way to start ensuring more efficient industrial production of ethanol would be to apply more targeted approaches and shift away from a “one-size fits all” strategy where sulfuric acid treatment is used without further consideration to lower the pH and kill the bacteria to keep the population under a certain threshold. This would be beneficial both economically and environmentally, says Morten Sommer, Professor and Group Leader at The Novo Nordisk Foundation Center for Biosustainability.
“Instead of using a broad range of antibiotics, one should go for a more specific solution where you keep the good bacteria inside the fermenter. This is definitely a paradigm shift because you are not per definition fighting against all bacteria, since some of the bacteria are actually good and improve your final output significantly while also having a positive effect on production costs and the environmental footprint.”

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Materials provided by Technical University of Denmark. Original written by Anders Østerby Mønsted, Bernadette Maria Grant. Note: Content may be edited for style and length.

Newly published research has revealed a close link between proteins associated with Alzheimer’s disease and age-related sight loss. The findings could open the way to new treatments for patients with deteriorating vision and through this study, the scientists believe they could reduce the need for using animals in future research into blinding conditions.
Amyloid beta (AB) proteins are the primary driver of Alzheimer’s disease but also begin to collect in the retina as people get older. Donor eyes from patients who suffered from age-related macular degeneration (AMD), the most common cause of blindness amongst adults in the UK, have been shown to contain high levels of AB in their retinas.
This new study, published in the journal Cells, builds on previous research which shows that AB collects around a cell layer called the retinal pigment epithelium (RPE), to establish what damage these toxic proteins cause RPE cells.
The research team exposed RPE cells of normal mouse eyes and in culture to AB. The mouse model enabled the team to look at the effect the protein has in living eye tissue, using non-invasive imaging techniques that are used in ophthalmology clinics. Their findings showed that the mouse eyes developed retinal pathology that was strikingly similar to AMD in humans.
Dr Arjuna Ratnayaka, a Lecturer in Vision Sciences at the University of Southampton, who led the study said, “This was an important study which also showed that mouse numbers used for experiments of this kind can be significantly reduced in the future. We were able to develop a robust model to study AMD-like retinal pathology driven by AB without using transgenic animals, which are often used by researchers the field. Transgenic or genetically engineered mice can take up to a year and typically longer, before AB causes pathology in the retina, which we can achieve within two weeks. This reduces the need to develop more transgenic models and improves animal welfare.”
The investigators also used the cell models, which further reduced the use of mice in these experiments, to show that the toxic AB proteins entered RPE cells and rapidly collected in lysosomes, the waste disposal system for the cells. Whilst the cells performed their usual function of increasing enzymes within lysosomes to breakdown this unwanted cargo, the study found that around 85% of AB still remained within lysosomes, meaning that over time the toxic molecules would continue to accumulate inside RPE cells.
Furthermore, the researchers discovered that once lysosomes had been invaded by AB, around 20 percent fewer lysosomes were available to breakdown photoreceptor outer segments, a role they routinely perform as part of the daily visual cycle.
Dr Ratnayaka added, “This is a further indication of how cells in the eye can deteriorate over time because of these toxic molecules collecting inside RPE cells. This could be a new pathway that no-one has explored before. Our discoveries have also strengthened the link between diseases of the eye and the brain. The eye is part of the brain and we have shown how AB which is known to drive major neurological conditions such as Alzheimer’s disease can also causes significant damage to cells in retina.”
The researchers hope that one of the next steps could be for anti-amyloid beta drugs, previously trialled in Alzheimer’s patients, to be re-purposed and trialled as a possible treatment for age-related macular degeneration. As the regulators in the USA and the European Union have already given approval for many of these drugs, this is an area that could be explored relatively quickly.
The study may also help wider efforts to largely by-pass the use of animal experimentation where possible, so some aspects of testing new clinical treatments can transition directly from cell models to patients.
This research was funded by the National Centre for the Replacement Refinement & Reduction of animals in research (NC3Rs). Dr Katie Bates, Head of Research Funding at the NC3Rs said:
“This is an impactful study that demonstrates the scientific, practical and 3Rs benefits to studying AMD-like retinal pathology in vitro.”

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Materials provided by University of Southampton. Note: Content may be edited for style and length.

Psychedelic healing may sound like a fad from the Woodstock era, but it’s a field of study that’s gaining traction in the medical community as an effective treatment option for a growing number of mental health conditions.
While the study of psychedelics as medicine is inching toward the mainstream, it still remains somewhat controversial. Psychedelics have struggled to shake a “counterculture” perception that was born in the 1960s, a view that had stymied scientific study of them for more than 50 years.
But that perception is slowly changing.
Mounting research suggests that controlled treatment with psychedelics like psilocybin mushrooms, LSD, and MDMA — better known as ecstasy — may be effective options for people suffering from PTSD, anxiety disorders, and depression. The U.S. Food & Drug Administration recently granted “breakthrough therapy” status to study the medical benefits of psychedelics. And two years ago this month, the FDA approved a psychedelic drug — esketamine — to treat depression.
An increasing number of states and municipalities are also grappling with calls to decriminalize psychedelic drugs, a move that UNLV neuroscientist Dustin Hines says could further the recent renaissance in psychedelic science.
“The resurgence in interest in psychedelic medicine is likely related to multiple factors, including decreasing societal stigma regarding drugs like hallucinogens and cannabis, increasing awareness of the potential therapeutic compounds found naturally occurring in plants and fungi, and the growing mental health crisis our nation faces,” says Hines. “Because of the intersection between the great need for innovation and wider social acceptance, researchers have started to explore psychedelics as novel treatments for depressive disorders, including work with compounds that have been used for millennia.”
In the Hines lab at UNLV, husband and wife researchers Dustin and Rochelle Hines are uncovering how psychedelics affect brain activity. Their work, published recently in Nature: Scientific Reports, shows a strong connection in rodent models between brain activity and behaviors resulting from psychedelic treatment, a step forward in the quest to better understand their potential therapeutic effects.

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Materials provided by University of Nevada, Las Vegas. Original written by Tony Allen. Note: Content may be edited for style and length.

Photosynthetic organisms harvest light from the sun to produce the energy they need to survive. A new paper published by University of Chicago researchers reveals their secret: exploiting quantum mechanics.
“Before this study, the scientific community saw quantum signatures generated in biological systems and asked the question, were these results just a consequence of biology being built from molecules, or did they have a purpose?” said Greg Engel, Professor of Chemistry and senior author on the study. “This is the first time we are seeing biology actively exploiting quantum effects.”
The scientists studied a type of microorganism called green sulfur bacteria. These bacteria need light to survive, but even small amounts of oxygen can damage their delicate photosynthetic equipment. So they must develop ways to minimize the damage when the bacterium does encounter oxygen.
To study this process, researchers tracked the movement of energy through a photosynthetic protein under different conditions — with oxygen around, and without.
They found that the bacterium uses a quantum mechanical effect called vibronic mixing to move energy between two different pathways, depending on whether or not there’s oxygen around. Vibronic mixing involves vibrational and electronic characteristics in molecules coupling to one another. In essence, the vibrations mix so completely with the electronic states that their identities become inseparable. This bacterium uses this phenomenon to guide energy where it needs it to go.
If there’s no oxygen around and the bacterium is safe, the bacterium uses vibronic mixing by matching the energy difference between two electronic states in an assembly of molecules and proteins called the FMO complex, with the energy of the vibration of a bacteriochlorophyll molecule. This encourages the energy to flow through the “normal” pathway toward the photosynthetic reaction center, which is packed full of chlorophyll.
But if there is oxygen around, the organism has evolved to steer the energy through a less direct path where it can be quenched. (Quenching energy is similar to putting a palm on a vibrating guitar string to dissipate energy.) This way, the bacterium loses some energy but saves the entire system.
To achieve this effect, a pair of cysteine residues in the photosynthetic complex acts as a trigger: They each react with the oxygen in the environment by losing a proton, which disrupts the vibronic mixing. This means that energy now preferentially moves through the alternative pathway, where it can be safely quenched. This principle is a bit like blocking two lanes on a superhighway and diverting some traffic to local roads where there are many more exits.
“What’s interesting about this result is that we are seeing the protein turn the vibronic coupling on and off in response to environmental changes in the cell,” said Jake Higgins, a graduate student in the Department of Chemistry and the lead author of the paper. “The protein uses the quantum effect to protect the organism from oxidative damage.”
These findings bring about an exciting new revelation about biology; using an explicitly quantum mechanism to protect the system shows an important adaptation and that quantum effects can be important to survival.
This phenomenon is likely not limited to green sulfur bacteria, the scientists said. As Higgins explained, “The simplicity of the mechanism suggests that it might be found in other photosynthetic organisms across the evolutionary landscape. If more organisms are able to dynamically modulate quantum mechanical couplings in their molecules to produce larger changes in physiology, there could be a whole new set of effects selected for by nature that we don’t yet know about.”
Air Force Office of Scientific Research (AFOSR), NSF, DOE Office of Science, Department of Defense (DoD), Arnold and Mabel Beckman Foundation.

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Materials provided by University of Chicago Medical Center. Original written by Sheila Evans. Note: Content may be edited for style and length.

New contact lens technology to help diagnose and monitor medical conditions may soon be ready for clinical trials.
A team of researchers from Purdue University worked with biomedical, mechanical and chemical engineers, along with clinicians, to develop the novel technology. The team enabled commercial soft contact lenses to be a bioinstrumentation tool for unobtrusive monitoring of clinically important information associated with underlying ocular health conditions.
The team’s work is published in Nature Communications. The Purdue Research Foundation Office of Technology Commercialization helped secure a patent for the technology and it is available for licensing.
“This technology will be greatly beneficial to the painless diagnosis or early detection of many ocular diseases including glaucoma” said Chi Hwan Lee, the Leslie A. Geddes assistant professor of biomedical engineering and assistant professor of mechanical engineering at Purdue who is leading the development team. “Since the first conceptual invention by Leonardo da Vinci, there has been a great desire to utilize contact lenses for eye-wearable biomedical platforms.”
Sensors or other electronics previously couldn’t be used for commercial soft contact lenses because the fabrication technology required a rigid, planar surface incompatible with the soft, curved shape of a contact lens.
The team has paved a unique way that enables the seamless integration of ultrathin, stretchable biosensors with commercial soft contact lenses via wet adhesive bonding. The biosensors embedded on the soft contact lenses record electrophysiological retinal activity from the corneal surface of human eyes, without the need of topical anesthesia that has been required in current clinical settings for pain management and safety.
“This technology will allow doctors and scientists to better understand spontaneous retinal activity with significantly improved accuracy, reliability, and user comfort,” said Pete Kollbaum, the Director of the Borish Center for Ophthalmic Research and an associate professor of optometry at Indiana University who is leading clinical trials.

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Materials provided by Purdue University. Original written by Chris Adam. Note: Content may be edited for style and length.

AdvertisementContinue reading the main storySupported byContinue reading the main storyPhys EdGetting to the Bottom of the Runner’s HighFor years we’ve been crediting endorphins, but it’s really about the endocannabinoids.Credit…Kevin Hagen for The New York TimesMarch 10, 2021, 5:00 a.m. ETWe can stop crediting endorphins, the natural opioid painkillers produced by our bodies, for the floaty euphoria we often feel during aerobic exercise, according to a nifty new study of men, women and treadmills. In the study, runners developed a gentle intoxication, known as a runner’s high, even if researchers had blocked their bodies’ ability to respond to endorphins, suggesting that those substances could not be behind the buzz. Instead, the study suggests, a different set of biochemicals resembling internally homegrown versions of cannabis, better known as marijuana, are likely to be responsible.The findings expand our understanding of how running affects our bodies and minds, and also raise interesting questions about why we might need to be slightly stoned in order to want to keep running.In surveys and studies of experienced distance runners, most report developing a mellow runner’s high at least sometimes. The experience typically is characterized by loose-limbed blissfulness and a shedding of anxiety and unease after half an hour or so of striding. In the 1980s, exercise scientists started attributing this buzz to endorphins, after noticing that blood levels of the natural painkillers rise in people’s bloodstreams when they run.More recently, though, other scientists grew skeptical. Endorphins cannot cross the blood-brain barrier, because of their molecular structure. So, even if runners’ blood contains extra endorphins, they will not reach the brain and alter mental states. It also is unlikely that the brain itself produces more endorphins during exercise, according to animal studies.Endocannabinoids are a likelier intoxicant, these scientists believed. Similar in chemical structure to cannabis, the cannabinoids made by our bodies surge in number during pleasant activities, such as orgasms, and also when we run, studies show. They can cross the blood-brain barrier, too, making them viable candidates to cause any runner’s high.A few past experiments had strengthened that possibility. In one notable 2012 study, researchers coaxed dogs, people and ferrets to run on treadmills, while measuring their blood levels of endocannabinoids. Dogs and humans are cursorial, meaning possessed of bones and muscles well adapted to distance running. Ferrets are not; they slink and sprint but rarely cover loping miles, and they did not produce extra cannabinoids while treadmill running. The dogs and people did, though, indicating that they most likely were experiencing a runner’s high and it could be traced to their internal cannabinoids.That study did not rule out a role for endorphins, however, as Dr. Johannes Fuss realized. The director of the Human Behavior Laboratory at the University Medical Center Hamburg-Eppendorf in Germany, he and his colleagues had long been interested in how various activities affect the inner workings of the brain, and after reading the ferret study and others, thought they might look more closely into the runner’s high.They began with mice, which are eager runners. For a 2015 study, they chemically blocked the uptake of endorphins in the animals’ brains and let them run, then did the same with the uptake of endocannabinoids. When their endocannabinoid system was turned off, the animals ended their runs just as anxious and twitchy as they had been at the start, suggesting that they had felt no runner’s high. But when their endorphins were blocked, their behavior after running was calmer, relatively more blissed-out. They seemed to have developed that familiar, mild buzz, even though their endorphin systems had been inactivated.Mice emphatically are not people, though. So, for the new study, which was published in February in Psychoneuroendocrinology, Dr. Fuss and his colleagues set out to replicate the experiment, to the extent possible, in humans. Recruiting 63 experienced runners, male and female, they invited them to the lab, tested their fitness and current emotional states, drew blood and randomly assigned half to receive naloxone, a drug that blocks the uptake of opioids, and the rest, a placebo. (The drug they had used to block endocannabinoids in mice is not legal in people, so they could not repeat that portion of the experiment.)The volunteers then ran for 45 minutes and, on a separate day, walked for the same amount of time. After each session, the scientists drew blood and repeated the psychological tests. They also asked the volunteers whether they thought they had experienced a runner’s high.Most said yes, they had felt buzzed during the run, but not the walk, with no differences between the naloxone and placebo groups. All showed increases, too, in their blood levels of endocannabinoids after running and equivalent changes in their emotional states. Their euphoria after running was greater and their anxiety less, even if their endorphin system had been inactivated.Taken as a whole, these findings are a blow to endorphins’ image. “In combination with our research in mice,” Dr. Fuss says, “these new data rule out a major role for endorphins” in the runner’s high.The study does not explain, though, why a runner’s high exists at all. There was no walker’s high among the volunteers. But Dr. Fuss suspects the answer lies in our evolutionary past. “When the open savannas stretched and forests retreated,” he says, “it became necessary for humans to hunt wild animals by long-distance running. Under such circumstances, it is beneficial to be euphoric during running,” a sensation that persists among many runners today, but with no thanks due, it would seem, to endorphins.AdvertisementContinue reading the main story

AdvertisementContinue reading the main storySupported byContinue reading the main storyPhys EdGetting to the Bottom of the Runner’s HighFor years we’ve been crediting endorphins, but it’s really about the endocannabinoids.Credit…Kevin Hagen for The New York TimesMarch 10, 2021, 5:00 a.m. ETWe can stop crediting endorphins, the natural opioid painkillers produced by our bodies, for the floaty euphoria we often feel during aerobic exercise, according to a nifty new study of men, women and treadmills. In the study, runners developed a gentle intoxication, known as a runner’s high, even if researchers had blocked their bodies’ ability to respond to endorphins, suggesting that those substances could not be behind the buzz. Instead, the study suggests, a different set of biochemicals resembling internally homegrown versions of cannabis, better known as marijuana, are likely to be responsible.The findings expand our understanding of how running affects our bodies and minds, and also raise interesting questions about why we might need to be slightly stoned in order to want to keep running.In surveys and studies of experienced distance runners, most report developing a mellow runner’s high at least sometimes. The experience typically is characterized by loose-limbed blissfulness and a shedding of anxiety and unease after half an hour or so of striding. In the 1980s, exercise scientists started attributing this buzz to endorphins, after noticing that blood levels of the natural painkillers rise in people’s bloodstreams when they run.More recently, though, other scientists grew skeptical. Endorphins cannot cross the blood-brain barrier, because of their molecular structure. So, even if runners’ blood contains extra endorphins, they will not reach the brain and alter mental states. It also is unlikely that the brain itself produces more endorphins during exercise, according to animal studies.Endocannabinoids are a likelier intoxicant, these scientists believed. Similar in chemical structure to cannabis, the cannabinoids made by our bodies surge in number during pleasant activities, such as orgasms, and also when we run, studies show. They can cross the blood-brain barrier, too, making them viable candidates to cause any runner’s high.A few past experiments had strengthened that possibility. In one notable 2012 study, researchers coaxed dogs, people and ferrets to run on treadmills, while measuring their blood levels of endocannabinoids. Dogs and humans are cursorial, meaning possessed of bones and muscles well adapted to distance running. Ferrets are not; they slink and sprint but rarely cover loping miles, and they did not produce extra cannabinoids while treadmill running. The dogs and people did, though, indicating that they most likely were experiencing a runner’s high and it could be traced to their internal cannabinoids.That study did not rule out a role for endorphins, however, as Dr. Johannes Fuss realized. The director of the Human Behavior Laboratory at the University Medical Center Hamburg-Eppendorf in Germany, he and his colleagues had long been interested in how various activities affect the inner workings of the brain, and after reading the ferret study and others, thought they might look more closely into the runner’s high.They began with mice, which are eager runners. For a 2015 study, they chemically blocked the uptake of endorphins in the animals’ brains and let them run, then did the same with the uptake of endocannabinoids. When their endocannabinoid system was turned off, the animals ended their runs just as anxious and twitchy as they had been at the start, suggesting that they had felt no runner’s high. But when their endorphins were blocked, their behavior after running was calmer, relatively more blissed-out. They seemed to have developed that familiar, mild buzz, even though their endorphin systems had been inactivated.Mice emphatically are not people, though. So, for the new study, which was published in February in Psychoneuroendocrinology, Dr. Fuss and his colleagues set out to replicate the experiment, to the extent possible, in humans. Recruiting 63 experienced runners, male and female, they invited them to the lab, tested their fitness and current emotional states, drew blood and randomly assigned half to receive naloxone, a drug that blocks the uptake of opioids, and the rest, a placebo. (The drug they had used to block endocannabinoids in mice is not legal in people, so they could not repeat that portion of the experiment.)The volunteers then ran for 45 minutes and, on a separate day, walked for the same amount of time. After each session, the scientists drew blood and repeated the psychological tests. They also asked the volunteers whether they thought they had experienced a runner’s high.Most said yes, they had felt buzzed during the run, but not the walk, with no differences between the naloxone and placebo groups. All showed increases, too, in their blood levels of endocannabinoids after running and equivalent changes in their emotional states. Their euphoria after running was greater and their anxiety less, even if their endorphin system had been inactivated.Taken as a whole, these findings are a blow to endorphins’ image. “In combination with our research in mice,” Dr. Fuss says, “these new data rule out a major role for endorphins” in the runner’s high.The study does not explain, though, why a runner’s high exists at all. There was no walker’s high among the volunteers. But Dr. Fuss suspects the answer lies in our evolutionary past. “When the open savannas stretched and forests retreated,” he says, “it became necessary for humans to hunt wild animals by long-distance running. Under such circumstances, it is beneficial to be euphoric during running,” a sensation that persists among many runners today, but with no thanks due, it would seem, to endorphins.AdvertisementContinue reading the main story