Are humans causing cancer in wild animals?

As humans, we know that some of our activities can cause cancer to develop in our bodies. Smoking, poor diets, pollution, chemicals used as additives in food and personal hygiene products, and even too much sun are some of the things that contribute to an increased risk of cancer.

But, are human activities also causing cancer in wild animals? Are we oncogenic -- a species that causes cancer in other species?

Researchers from Arizona State University's School of Life Sciences think so and are urgently calling for research into this topic. In a paper published online today in "Nature Ecology & Evolution," Mathieu Giraudeau and Tuul Sepp, both postdoctoral researchers in the lab of ASU life sciences professor Kevin McGraw, say that humans are changing the environment in a way that causes cancer in wild animal populations.

"We know that some viruses can cause cancer in humans by changing the environment that they live in -- in their case, human cells -- to make it more suitable for themselves," said Sepp. "Basically, we are doing the same thing. We are changing the environment to be more suitable for ourselves, while these changes are having a negative impact on many species on many different levels, including the probability of developing cancer."

In the paper, Giraudeau and Sepp and a team of international researchers, point out many pathways and previous scientific studies that show where human activities are already taking a toll on animals. These include chemical and physical pollution in our oceans and waterways, accidental release of radiation into the atmosphere from nuclear plants, and the accumulation of microplastics in both land- and water-based environments. In addition, exposure to pesticides and herbicides on farmlands, artificial light pollution, loss of genetic diversity and animals eating human food are known to cause health problems.

"Cancer in wild populations is a completely ignored topic and we wanted to stimulate research on this question," shared Giraudeau. "We recently published several theoretical papers on this topic, but this time, we wanted to highlight the fact that our species can strongly influence the prevalence of cancer in many other species of our planet.

"Cancer has been found in all species where scientists have looked for it and human activities are known to strongly influence cancer rate in humans. So, this human impact on wild environments might strongly influence the prevalence of cancer in wild populations with additional consequences on ecosystem functioning," he said.

Even something such as artificial light and light pollution, as well as food meant for humans, are negatively affecting wild animals.

Sepp said: "It is already known in human studies that obesity and nutrient deficiency can cause cancer, but these issues have been mostly overlooked in wild animals. At the same time, more and more wild species are in contact with anthropogenic food sources. In humans, it's also known that light at night can cause hormonal changes and lead to cancer. Wild animals living close to cities and roads face the same problem -- there is no darkness anymore. For example, in birds, their hormones -- the same that are linked to cancer in humans -- are affected by light at night. So, the next step would be to study if it also affects their probability of developing tumors."

While these scientists are urgently calling for studies on cancer and its causes in wild animal populations, they realize that this is no easy subject to study.

"The next step is definitely to go into the field and measure cancer rate in wild populations," said Giraudeau. "We are now trying to develop some biomarkers to be able to study this. I think it would be interesting to measure cancer prevalence in wild animals in human-impacted environments and also in more preserved areas for the same species."

If humans are the cause of cancer in wild animals, then many species may be more threatened than people realize. Yet Tuul said, there is reason to hold out hope.

"To me, the saddest thing is that we already know what to do. We should not destroy the habitats of wild animals, pollute the environment, and feed wild animals human food," shared Sepp. "The fact that everybody already knows what to do, but we are not doing it, makes it seem even more hopeless.

"But I see hope in education. Our kids are learning a lot more about conservation issues than our parents did. So, there is hope that the decision-makers of the future will be more mindful of the anthropogenic effects on the environment."

Scientists discover new way that HIV evades the immune system

Scientists have just discovered a new mechanism by which HIV evades the immune system, and which shows precisely how the virus avoids elimination. The new research shows that HIV targets and disables a pathway involving a number of biological molecules that are key in blocking viral activity and clearing infection.

HIV remains a major global health problem, with over 40 million people infected worldwide. And while people living with HIV have been treated with anti-retroviral therapy for over 30 years, this favoured therapeutic option merely prevents the progression of the disease to AIDS - it doesn't cure patients of HIV.

The discovery, which opens the door to a new era of HIV research focused on curing people living with the , has just been published in international journal, EBioMedicine, which is a collaborative online journal from Cell Press and the Lancet.

During any viral our immune system produces a powerful molecule (Interferon), which 'interferes' with the infection and the replication of viruses. Interferon activates an assembly line of molecules in our cells—via the Interferon signalling pathway - which causes the body to make antivirals that help to clear the infection.

However, when patients are being treated with anti-retroviral therapy, HIV is not fully cleared by our immune system. Therefore, the scientists from Trinity College Dublin behind the research investigated whether HIV was somehow blocking the Interferon signalling pathway and thus avoiding the immune response that is designed to cure viral infection. The findings confirmed their suspicions.

Assistant Professor in Immunology at Trinity, Nigel Stevenson, led the work. He said: "We discovered that HIV promotes the destruction of the anti-viral Interferon signalling pathway. Essentially, HIV uses the machinery in our own cells to do this, and the virus is thus able to reduce the production of many important anti-viral molecules. Without these anti-viral , our immune system can't clear ."

"Our new revelation sheds new light on how HIV avoids elimination, which, in turn, may explain why HIV is still not a curable disease. We feel this discovery could mark a paradigm shift in our understanding of how this virus evades our . It should open the door to a new era of HIV research aiming to cure and eradicate this deadly virus."

Coming soon: Male contraceptive pill inches closer

Researchers are one step closer to developing a male contraceptive pill, a medical conference has heard. Early trials show the pill to be both safe and effective.

The study, led by Professor Stephanie Page of the University of Washington, included 100 men aged between 18 and 50. The men were split into groups of between 17-20 and given three different doses of pills known as dimethandrolone undecanoate, or DMAU. Out of each group, five subjects were given a placebo while another 12-15 were given daily doses of DMAU for 28 days. Some 83 men completed the study.

READ MORE: ‘One size does not fit all’: Chinese condoms are too small for Zimbabweans, says health minister

The highest dose, 400mg of DMAU, showed “marked suppression” of testosterone levels as well as two other hormones required for the production of sperm. The results were compared to longer-term studies and appeared consistent with effective male contraception.

@RTUKnews Teach kids how to get pregnant, UK doctors say https://trib.al/Ml0P6ax
 

"DMAU is a major step forward in the development of a once-daily 'male pill,'" Page reportedly told the Endocrine Society’s 100th annual meeting in Chicago. "Many men say they would prefer a daily pill as a reversible contraceptive, rather than long-acting injections or topical gels, which are also in development."

Page also said that few participants in the study reported having symptoms consistent with testosterone deficiency, although all groups reported weight gain and decreases in healthy cholesterol. "These promising results are unprecedented in the development of a prototype male pill," Page said. "Longer term studies are currently underway to confirm that DMAU taken every day blocks sperm production."

@RT_com Condom-free male contraceptive successfully trialed on monkeys - next stop, human testing https://on.rt.com/82jm

Various male contraceptives have been trialed in the past. In February last year, a gel injection used to block the sperm-carrying tubes, known as vas deferens, was trialed on monkeys. The Vasalgel injection, made by the Parsemus Foundation, has gone forward for human trials.

Brain is less flexible than we thought when learning

Nobody really knows how the activity in your brain reorganizes as you learn new tasks, but new research reveals that the brain has various mechanisms and constraints by which it reorganizes its neural activity when learning over the course of a few hours. The new research finds that, when learning a new task, the brain is less flexible than previously thought.

The research, published today in Nature Neuroscience, examined the changes that take place in the brain when learning a new task. To truly see how neural activity changes during learning, we need to look bigger -- at populations of neurons, rather than one neuron at a time, which has been the standard approach to date.

The research team used a brain-computer interface (BCI), where subjects move a cursor on a computer screen by thought alone. As with learning to play a new sport, they found that subjects learned to control the cursor more accurately with practice. They then investigated how the activity in the brain changed during learning that enabled the improved performance. They found that, on a time scale of a few hours, the brain does not reconfigure its neural activity to maximize the speed and accuracy by which it moves the cursor.

"In this experimental paradigm, we're able to track all of the neurons that can lead to behavioral improvements and look at how they all change simultaneously," says Steve Chase, an associate professor of biomedical engineering at Carnegie Mellon and the Center for the Neural Basis of Cognition. "When we do that, what we see is a really constrained set of changes that happen, and it leads to this suboptimal improvement of performance. And so, that implies that there are limits that constrain how flexible your brain is, at least on these short time scales."

When we're learning a new task, we can't instantaneously learn it to proficiency, in part due to the way in which the neurons are wired up in the brain. Learning takes time, and there are mechanisms by which neurons can change the way they communicate with each other to enable learning -- some of which can be fast, and some of which can take longer. The team found that the brain operates under a more stringent set of constraints than originally thought, resulting in good learning on the short term, but nevertheless suboptimal performance in controlling the BCI cursor.

Imagine a tennis player whose friends have asked her to play squash. When she picks up the squash racket, it's lighter than the tennis racket she is used to, and it has a slightly different balance point. But since she's a good tennis player, this difference in rackets doesn't cause her to miss the ball completely. She adjusts quickly, but she hasn't immediately picked up the swing form of a squash player. To really become an expert, it will require a long period of training with the new equipment. However, her experienced squash-playing friends will quickly see that she is a tennis player, because until she's learned the proper technique, she'll be swinging the squash racket the same as she would a tennis racket.

"Just as it takes time to train a person to swing a squash racket like an expert, it takes time to train one's neurons to produce the ideal activity patterns," says Byron Yu, associate professor of biomedical engineering and electrical and computer engineering at Carnegie Mellon. "When faced with a new task, we're finding that the brain is constrained to take the neural activity patterns that it's capable of generating right now and use them as effectively as possible in this new task."

"When we learn, at first the brain tends to not produce new activity patterns, but to repurpose the activity patterns it already knows how to generate," says Aaron Batista, an associate professor in the Department of Bioengineering at the University of Pittsburgh. "Learning over the course of a few hours is suboptimal. When first learning something new, our brain doesn't seem to be able to change its activity in the best possible way to allow us to be proficient at new skills.."

Acquiring a skill is very difficult, and it takes a lot of time and a lot of practice. But when you're first starting to learn a new skill, your brain has to adjust quickly to the new task. The researchers found that the brain is constrained to take neural activity patterns it already knows and use them for the new task. By repurposing neuron patterns the brain is already capable of generating, the brain applies a "quick and dirty fix" to the new problem it's facing.

"None of us predicted this outcome," says Matthew Golub, a postdoctoral researcher in electrical and computer engineering at Carnegie Mellon. "Learning is far more limited on the scale of a few hours than any of us were expecting when we started this. We were all surprised that the brain wasn't able to choose the best strategy possible."

The research was done in collaboration with the Center for Neural Basis of Cognition, a cross-university research and educational program between Carnegie Mellon and the University of Pittsburgh that leverages each institution's strengths to investigate the cognitive and neural mechanisms that give rise to biological intelligence and behavior.

Air pollutants linked to abnormal fetal growth

The findings, published in the International Journal of Epidemiology, were based on data collected from more than 8,000 women in Lanzhou, China from 2010 to 2012.

The researchers said that, to their knowledge, it is the first study of its kind to be conducted in areas with very high .

"There is a lack of studies investigating the association between air and fetal overgrowth," said Yawei Zhang, M.D., associate professor at YSPH. "We analyzed data from Lanzhou Birth Cohort Study to investigate the hypothesis that exposure to high levels of PM10 during pregnancy increases the risk of abnormal fetal growth, including both undergrowth and overgrowth, to determine if and how expectant mothers could protect themselves from possible contributing pollutants."

In collaboration with researchers from the Gansu Provincial Maternity and Child Care Hospital, the Yale scientists collected the daily average concentration for PM10—a diverse class of air pollution with health implications—from the government monitoring stations in Lanzhou. Using ultrasound measures of four fetal growth parameters during pregnancy, the researchers examined the associations between PM10 exposure and risk of abnormal fetal growth.

The researchers consistently identified positive associations between higher levels of exposure to a mixture of pollutants from car fumes, industry emissions, or construction activities and fetal head circumference overgrowth, they said.

Pregnant women's home and work addresses were collected through in-person interviews, and researchers calculated daily PM10 concentrations by incorporating each participant's home and work addresses.

Zhang says the novel finding that high levels of PM10 are associated with risk of overgrowth should be confirmed by other studies in different populations, and that it is also important to identify the specific pollutants that are responsible for this association by investigating the components of PM10.

"Our results have important public health implications and call for future studies to explore the underlying mechanisms and postnatal consequences to the findings," says Zhang. "We are going to replicate the findings in another and will continue to identify individuals who are more susceptible to air pollution."

Women in the region may lower the risk of fetal overgrowth by choosing their inception time and reducing their outdoor activities during the days with high , said Zhang.

Pregnant women who came to the Gansu Provincial Maternity and Child Care Hospital for delivery in 2010-2012 and who were 18 years or older with gestation age of more than 20 weeks were eligible to participate in this study.

Is punishment as effective as we think?

Punishment might not be an effective means to get members of society to cooperate for the common good, according to a social dilemma experiment.

A game to study human behavior has shown punishment is an ineffective means for promoting cooperation among players. The result has implications for understanding how cooperation has evolved to have a formative role in human societies.

Human societies maintain their stability by forming cooperative partnerships. But, cooperation often comes at a cost. For example, a person taking time to raise the alarm in order to alert other members of a group to impending danger could be losing valuable time to save oneself. It is unclear why natural selection favors cooperativeness among individuals who are inherently selfish.

In theoretical studies, punishment is often seen as a means to coerce people into being more cooperative. To examine such theory, a team of international researchers led by Marko Jusup of Hokkaido University in Japan and Zhen Wang of Northwestern Polytechnical University in China has conducted a "social dilemma experiment." The team investigated if providing punishment as an option helps improve the overall level of cooperation in an unchanging network of individuals.

They used a version of the commonly employed "prisoner's dilemma" game. Two hundred and twenty-five students in China were organized into three trial groups and played 50 rounds each of the game.

In group one, every student played with two opponents which changed every round. The students could choose between "cooperate" or "defect," and points were given based on the combined choices made. If a student and the two opponents chose "defect," the student gained zero points. If they all chose "cooperate," the student gained four points. If only a student chose to defect while the other two chose to cooperate, the gain for the student was eight points.

The second group was similar to the first one in every aspect except that the people playing the game with each other remained the same for the duration of the 50 rounds, enabling them to learn each other's characteristics.

In the third group, players also remained the same. However, a new option, "punish," was introduced. Choosing punishment led to a small reduction in points for the punisher and a larger reduction of points for the punishees.

At the end of the game, overall points were counted and the students were given monetary compensation based on the number of points won.

The expectation is that, as individuals play more with the same opponents over several rounds, they see the benefit of cooperating in order to gain more points. Introducing punishment as an option is basically saying: if you don't cooperate with me, I'll punish you. In theory, it is expected that applying this option would lead to more cooperation.

The researchers found that players in the constantly changing groups cooperated much less (4%) than those in the static groups (38%), where they were able to establish which players were willing to cooperate and thus gain a larger average financial payoff for all involved.

Surprisingly, however, adding punishment as an option did not improve the level of cooperation (37%). The final financial payoffs in this trial group were also, on average, significantly less than those gained by players in the static group. Interestingly, less defection was seen in the punishment group when compared to the static group; some players replaced defection with punishment.

"While the implied message when punishing someone is 'I want you to be cooperative,' the immediate effect is more consistent with the message 'I want to hurt you,'" write the researchers in their study published in the journal Proceedings of the National Academy of Sciences.

Punishment seems to have an overall demoralizing effect, as individuals who get punished on multiple occasions may see a good chunk of their total payoff vanish in a short period of time, explain the researchers. This could lead players to lose interest in the game and play the remaining rounds with less of a rational strategy. The availability of punishment as an option also seems to reduce the incentive to choose cooperation over competition.

Why, then, is punishment so pervasive in human societies? "It could be that human brains are hardwired to derive pleasure from punishing competitors," says Jusup. "However, it is more likely that, in real life, a dominant side has the ability to punish without provoking retaliation," adds Wang.

Although the study provides valuable insights into how cooperation arises in human society, the team advises it would be unwise to extrapolate the implications of their study far beyond the experimental setting.

Could humans ever regenerate a heart? A new study suggests the answer is 'yes'

When Mark Martindale decided to trace the evolutionary origin of muscle cells, like the ones that form our hearts, he looked in an unlikely place: the genes of animals without hearts or muscles.

In a new study published in the journal Proceedings of the National Academy of Sciences, the University of Florida scientist and colleagues found genes known to form hearts cells in humans and other animals in the gut of a muscle-less and heartless sea anemone. But the sea anemone isn't just any sea creature. It has superpower-like abilities: Cut it into many pieces and each piece will regenerate into a new animal.

So why does the sea anemone regenerate while humans cannot? When analyzing the function of its "heart genes," study researchers discovered a difference in the way these genes interact with one another, which may help explain its ability to regenerate, said Martindale, a UF biology professor and director of the Whitney Lab for Marine Bioscience in St. Augustine.

The study's findings point to potential for tweaking communication between human genes and advancing our ability to treat heart conditions and stimulate regenerative healing, he said.

"Our study shows that if we learn more about the logic of how genes that give rise to heart cells talk to each other, muscle regeneration in humans might be possible," Martindale said.

These heart genes generate what engineers calls lockdown loops in vertebrates and flies, which means that once the genes are turned on, they tell each other to stay on in an animal's cells for its entire lifetime. In other words, animals with a lockdown on their genes cannot grow new heart parts or use those cells for other functions.

"This ensures that heart cells always stay heart cells and cannot become any other type of cell," Martindale said.

But in sea anemone embryos, the lockdown loops do not exist. This finding suggests a mechanism for why the gut cells expressing heart genes in sea anemones can turn into other kinds of cells, such as those needed to regenerate damaged body parts, Martindale said.

The study supports the idea that definitive muscle cells found in the majority of animals arose from a bifunctional gut tissue that had both absorptive and contractile properties. And while the gut tissue of a sea anemone might not look like a beating heart, it does undergo slow, rhythmic peristaltic waves of contraction, much like the human digestive system.

Study authors argue that the first animal muscle cells might have been very heart-like, Martindale said.

"The idea is these genes have been around a long time and preceded the twitchy muscles that cover our skeleton," Martindale said.

Continued research could one day allow scientists to coax muscles cells into regenerating different kinds of new cells, including more heart cells, Martindale said

Sleep loss affects your waistline

Sleep loss increases the risk of obesity through a combination of effects on energy metabolism. This research, presented at the European Congress of Endocrinology in Lisbon, will highlight how disrupted sleep patterns, a common feature of modern living, can predispose to weight gain, by affecting people’s appetite and responses to food and exercise.

In the 24/7 culture of the modern world, an increasing number of people report routine reduced quality of sleep and several studies have correlated sleep deprivation with weight gain. The underlying cause of increased obesity risk from sleep disruption is unclear but may relate to changes in appetite, metabolism, motivation, physical activity or a combination of factors.

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Dr Christian Benedict from Uppsala University, Sweden and his group have conducted a number of human studies to investigate how sleep loss may affect energy metabolism. These human studies have measured and imaged behavioural, physiological and biochemical responses to food following acute sleep deprivation. The behavioural data reveal that metabolically healthy, sleep-deprived human subjects prefer larger food portions, seek more calories, exhibit signs of increased food-related impulsivity, experience more pleasure from food, and expend less energy.

The group’s physiological studies indicate that sleep loss shifts the hormonal balance from hormones that promote fullness (satiety), such as GLP-1, to those that promote hunger, such as ghrelin. Sleep restriction also increased levels of endocannabinoids, which is known to have appetite-promoting effects. Further work from Dr Benedict’s team shows that acute sleep loss alters the balance of gut bacteria, which has been widely implicated as key for maintaining a healthy metabolism. The same study also found reduced sensitivity to insulin after sleep loss.

Dr Christian Benedict remarks, “Since perturbed sleep is such a common feature of modern life, these studies show it is no surprise that metabolic disorders, such as obesity are also on the rise.”

Although Dr Benedict’s work has shed light on how short periods of sleep loss can affect energy metabolism, longer-term studies are needed to validate these findings. The group are now investigating longer-term effects and also whether extending sleep in habitual short sleepers can restore these alterations in appetite and energy metabolism.

Dr Christian Benedict says, “My studies suggest that sleep loss favours weight gain in humans. It may also be concluded that improving sleep could be a promising lifestyle intervention to reduce the risk of future weight gain.”

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