The Science of Solidarity

By: Alexandria Addesso

To many Charles Darwin is the utmost authority when it comes to the study of evolution. Many people took his findings about the importance of competition and how it plays a role in evolution and ran with it. Even as far as applying it to society and thus creating social Darwinism. Anarcho-scientist Peter Kropotkin was inspired by the publication of On the Origin of Species to go and do his own observations of a multitude of species and seemed to come to the opposite conclusion of such Darwinism backers. He argued against claims that competition alone led to evolution or ‘survival of the fittest’, and insisted that mutual aid is a major factor of evolution. The following is an introductory excerpt from Kropotkin’s book Mutual Aid: A Factor of Evolution.

Two aspects of animal life impressed me most during the journeys which I made in my youth in Eastern Siberia and Northern Manchuria. One of them was the extreme severity of the struggle for existence which most species of animals have to carry on against an inclement Nature; the enormous destruction of life which periodically results from natural agencies; and the consequent paucity of life over the vast territory which fell under my observation. And the other was, that even in those few spots where animal life teemed in abundance, I failed to find – although I was eagerly looking for it – that bitter struggle for the means of existence, among animals belonging to the same species, which was considered by most Darwinists (though not always by Darwin himself) as the dominant characteristic of struggle for life, and the main factor of evolution.



Kropotkin chronicled his findings while observing a wide variety of insects, birds, sea-life, and different mammals including humans. When it came to who was fittest to survive and further their species, it was most often those who cooperated via forms of mutual aid and solidarity.

As soon as we study animals – not in laboratories and museums only, but in the forest and the prairie, in the steppe and the mountains – we at once perceive that though there is an immense amount of warfare and extermination going on amidst various species, and especially amidst various classes of animals, there is, at the same time, as much, or perhaps even more, of mutual support, mutual aid, and mutual defense amidst animals belonging to the same species or, at least, to the same society. Sociability is as much a law of nature as mutual struggle. Of course it would be extremely difficult to estimate, however roughly, the relative numerical importance of both these series of facts. But if we resort to an indirect test, and ask Nature: "Who are the fittest: those who are continually at war with each other, or those who support one another?" we at once see that those animals which acquire habits of mutual aid are undoubtedly the fittest. They have more chances to survive, and they attain, in their respective classes, the highest development of intelligence and bodily organization. If the numberless facts which can be brought forward to support this view are taken into account, we may safely say that mutual aid is as much a law of animal life as mutual struggle, but that, as a factor of evolution, it most probably has a far greater importance, inasmuch as it favours the development of such habits and characters as insure the maintenance and further development of the species, together with the greatest amount of welfare and enjoyment of life for the individual, with the least waste of energy.



Solidarity scientifically leads to the continuation of life. Through the solidarity of family units, as wells even sometimes larger communities, children are able to be raised and protected. Solidarity is also pivotal for any revolution, social movement, or major change to occur. The slogan “workers of the world unite,” first mentioned in the Communist Manifesto in 1848, called for solidarity among all proletariat (the lower/working class) regardless to nation or ethnicity. These were truly powerful words of unity for those across a particular class line against their oppressors that belonged to the bourgeoisie (the middle/capitalist class).

A major group that unified lower class people across ethnic and gender lines on U.S. soil in the aftermath of the Democratic Convention protests of 1968 was the original Rainbow Coalition. It was formed by the Illinois Chapter of The Black Panthers in Chicago and also included the Young Patriots (a group of white youth who had migrated from Appalachia to Chicago), the Young Lords (a group of Puerto Rican nationalist youth), disenfranchised jewish youth and members of the women’s movement. The Rainbow Coalition epitomized solidarity and intersectionality within the class struggle. Because of its diversity, the Rainbow Coalition was able to bring about treaties among violent rivaling gangs as well as fight against police brutality that did nothing but add to the wave of violence. With unity comes power, and this was highly threatening to both local and national government.



“It seems to me that a lot of the real intense government repression didn’t happen until the Black Panthers started building coalitions,” said Bobby Lee a Black Panthers member who helped organize the Rainbow Coalition along with Deputy Chairman of the Illinois Chapter Fred Hampton, in an interview with Chicago Area. “Once the party departed from the ‘hate whitey’ trip and got serious about building real politics, we were a threat—plain and simple. The FBI were always watching us. But the Rainbow Coalition was their worst nightmare.”

For major changes to occur, for the preservation of life, and to strive towards survival and thus evolution, solidarity is a major factor.

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Scientists use parasite's internal clock to attack sleeping sickness

Trypanosoma brucei is a parasite that causes the deadly sleeping sickness. Scientists have determined the parasite has its own biological clock that makes it more vulnerable to medications in the afternoon.

The parasite that causes deadly sleeping sickness has its own biological clock that makes it more vulnerable to medications during the afternoon, according to international research that may help improve treatments for one of Africa's most lethal diseases.

The finding from the Peter O'Donnell Jr. Brain Institute could be especially beneficial for patients whose bodies can't handle side effects of toxic treatments used to eradicate the parasite. By knowing the optimal time to administer these medications - which can be fatal - doctors hope to reduce the duration and dosage of the treatment and save more lives.

"This research has opened a door," said Dr. Filipa Rijo-Ferreira, first author of the study from the O'Donnell Brain Institute at UT Southwestern Medical Center. "If the same therapeutic effect can be obtained with a lower dose, then it may be possible to reduce the mortality associated with the treatment."

Establishing that parasites have their own internal clock is a key step in finding new ways to treat a variety of parasitic conditions, from sleeping sickness to malaria. While many of these diseases are often not deadly, sleeping sickness has been among the most lethal.

The condition - known formally as African trypanosomiasis - is transmitted through the bite of the Tsetse fly and threatens tens of millions of people in sub-Saharan African countries. After entering the body, the parasite causes such symptoms as inverted sleeping cycles, fever, muscle weakness, and itching. It eventually invades the central nervous system and, depending on its type, can kill its host in anywhere from a few months to several years.

Control efforts have significantly reduced the number of cases over the last decade. However, an unknown number of people still die annually from sleeping sickness as scientists continue seeking a vaccine and alternative treatments to the arsenic-based medications that are occasionally fatal to patients.
Dr. Joseph S. Takahashi, who oversaw the collaborative study published in Nature

Microbiology with Dr. Luisa Figueiredo at the University of Lisbon in Portugal, said the finding will likely apply to all types of parasites and perhaps lead to improved treatment for their associated conditions.



"There have been many observations of the presence of daily patterns in parasites, but until now we didn't know if this was the result of an intrinsic molecular clock. In the future, we may consider biological rhythms when defining therapies to treat sleeping sickness and potentially other infections," said Dr. Takahashi, Chairman of Neuroscience at UT Southwestern, holder of the Loyd B. Sands Distinguished Chair in Neuroscience, and Investigator with the Howard Hughes Medical Institute.

Researchers from UT Southwestern and the Institute of Molecular Medicine at the University of Lisbon in Portugal made their finding after isolating the parasite - known as Trypanosoma brucei - in the lab and obtaining a type of genetic fingerprint to gauge its daily cycles independent of a host. They found the parasite has daily metabolic cycles that make it more vulnerable to treatments in the afternoon.

Scientists now hope to learn what drives the parasite's internal clock so they can target specific genes and disrupt its circadian rhythms. Much like humans struggle to cope when their sleep cycle is interrupted, scientists expect the parasite would become weaker if its cycle is disturbed.

"We know that in other organisms if we mutate their clock they are less adapted to the world," said Dr. Rijo-Ferreira, an HHMI Associate. "We're trying to jetlag these parasites, trying to make them less fit."

5 parasite diseases to watch for in the U.S.

While deadly sleeping sickness is primarily transmitted in rural regions of Africa, millions of people in the U.S. are exposed to other forms of parasitic diseases. Here are five such diseases the U.S. Centers for Disease Control and Prevention lists as public-health priorities.

Chagas: This disease is most commonly acquired through contact with the feces of an infected kissing bug, a blood-sucking insect. There may be swelling where the parasite enters the body, and in rare cases the disease results in life-threatening inflammation of the heart or brain. If untreated, infection is lifelong. CDC estimates about 300,000 people in the U.S. have the condition.

Toxoplasmosis: This condition is a leading cause of death related to food-borne illness in the U.S. More than 30 million Americans carry the parasite, though few show symptoms because their immune systems protect against the illness. People can become infected by eating undercooked, contaminated meat, and women who are infected during pregnancy sometimes pass the parasite to their unborn children. This transfer can result in a miscarriage, a stillborn child, eye disease, or unusual head size.



Toxocariasis: Caused by two species of roundworm and is typically spread through the feces of dogs and cats. Most infected people don't show symptoms, though in some cases the parasite can travel through parts of the body such as the liver, lungs, or central nervous system. The larvae can also travel to the eye and cause blindness. Each year about 70 people, mostly children, are blinded by the condition.

Cysticercosis: Spread through ingesting larval cysts of a tapeworm, causing infections in the muscles, brain, or other tissue. People become infected when they drink water or eat food contaminated with tapeworm eggs, or if they put contaminated fingers in their mouths. Cysts in the brain or spinal cord commonly cause seizures or headaches. The condition may also cause life-threatening brain swelling or strokes. CDC estimates that at least 1,000 people are hospitalized each year with the more severe brain-related form of the disease.

Trichomoniasis The parasite that causes trichomoniasis is transferred from human to human during sex. About 3.7 million people in the U.S. have the condition, though most do not know they have it. Symptoms may include itching, burning, redness or soreness in the infected areas. The parasite can be eradicated through medications. Without treatment, the infection can last for months or years.

Source: Nature Microbiology - Provided by: UT Southwestern Medical Center

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Viruses Created to Selectively Attack Tumor Cells

The image shows tumor cells infected by the virus, which expresses a fluorescent protein. Over the days (in the image fifth day), the virus multiplies, generating new virus that infect more cancer cells

It is an innovative approach that takes advantage of the different expression profiles of certain proteins between tumor and healthy cells that make the virus to only infect the first ones.

Scientists at the IDIBAPS Biomedical Research Institute and at the Institute for Research in Biomedicine (IRB Barcelona) lead a study in which they have designed a new strategy to get genetically modified viruses to selectively attack tumor cells without affecting healthy tissues. The study, published today by the journal Nature Communications, is part of Eneko Villanueva's work for his PhD and it is co-lead by Cristina Fillat, head of the Gene Therapy and Cancer Group at IDIBAPS, and Raúl Méndez, ICREA researcher at IRB Barcelona.

Conventional cancer treatment may cause undesirable side effects as a result of poor selectivity. To avoid them it is important that new therapies can efficiently remove cancer cells and preserve the healthy ones. One of the new approaches in cancer therapy is based on the development of oncolytic viruses, ie, viruses modified to only infect tumor cells. In recent years several studies have been focused on the development of viruses created by genetic engineering to maximize their anticancer effect but, as their potency increases, so does the associated toxicity. Limiting this effect on healthy cells is now the key for the application of this promising therapy.



An innovative and specific approach
In the study published in the journal Nature Communications, researchers from IDIBAPS and IRB Barcelona have developed an innovative approach to provide adenovirus with high specificity against tumor cells. "We have taken advantage of the different expression of a type of protein, CPEBs, in normal and tumor tissues," explains Raúl Méndez from IRB Barcelona.

CPEB is a family of four RNA binding proteins (the molecules that carry information from genes to synthesize proteins) that control the expression of hundreds of genes and maintain the functionality and the ability to repair tissues under normal conditions. When CPEBs become imbalanced, they change the expression of these genes in cells and contribute to the development of pathological processes such as cancer. "We have focused on the double imbalance of two of these proteins in healthy tissues and tumors: on the one hand we have CPEB4, which in previous studies we have shown that it is highly expressed in cancer cells and necessary for tumor growth; and, on the other hand, CPEB1, expressed in normal tissue and lost in cancer cells. We have taken advantage of this imbalance to make a virus that only attacks cells with high levels of CPEB4 and low CPEB1, that means that it only affects tumor cells, ignoring the healthy tissues," says Méndez.



"In this study we have worked with adenoviruses, a family of viruses that can cause infections of the respiratory tract, the urinary tract, conjunctivitis or gastroenteritis but which have features that make them very attractive to be used in the therapy against tumors," explains Cristina Fillat. To do this, it is necessary to modify the genome of these viruses. In the study researchers have inserted sequences that recognize CPEB proteins in key regions for the control of viral proteins. Their activity was checked in in vitro models of pancreatic cancer and control of tumor growth was observed in mouse models.

The onco-selective viruses created in this study were very sophisticated, being activated by CPEB4 but repressed by CPEB1. Thus, researchers achieved attenuated viral activity in normal cells, while in tumor cells the virus potency was maintained or even increased. "When the modified viruses entered into tumor cells they replicated their genome and, when going out, they destroyed the cell and released more particles of the virus with the potential to infect more cancer cells," says Fillat. She adds that, "this new approach is very interesting since it is a therapy selectively amplified in the tumor."



Since CPEB4 is overexpressed in several tumors, this oncoselective strategy may be valid for other solid tumors. Researchers are now trying to combine this treatment with therapies that are already being used in clinical practice, or that are in a very advanced stage of development, to find synergies that make them more effective.
Source: Materials provided by the Institute for Research in Biomedicine (IRB Barcelona)

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Do human Pheromones Actually Exist?

Can human pheromones really influence our attraction to others? A new study says two putative pheromones cannot.

You may have seen the ads: Just spray a bit of human pheromone on your skin, and you’re guaranteed to land a date. Scientists have long debated whether humans secrete chemicals that alter the behavior of other people. A new study throws more cold water on the idea, finding that two pheromones that proponents have long contended affect human attraction to each other have no such impact on the opposite sex—and indeed experts are divided about whether human pheromones even exist.

A pheromone, a hormone secreted or excreted, is a chemical factor that triggers a social response in members of the same species. Pheromones are chemicals capable of acting outside the body of the secreting individual to impact the behavior of the receiving individuals.

The study, published today in Royal Society Open Science, asked heterosexual participants to rate opposite-sex faces on attractiveness while being exposed to two steroids that are putative human pheromones. One is androstadienone (AND), found in male sweat and semen, whereas the second, estratetraenol (EST), is in women’s urine. Researchers also asked participants to judge gender-ambiguous, or “neutral,” faces, created by merging images of men and women together. The authors reasoned that if the steroids were pheromones, female volunteers given AND would see gender-neutral faces as male, and male volunteers given EST would see gender-neutral faces as female. They also theorized that the steroids corresponding to the opposite sex would lead the volunteers to rate opposite sex faces as more attractive.



That didn’t happen. The researchers found no effects of the steroids on any behaviors and concluded that the label of “putative human pheromone” for AND and EST should be dropped.
“I’ve convinced myself that ‘AND’ and ‘EST’ are not worth pursuing,” says the study’s lead author, Leigh Simmons, an evolutionary biologist at the University of Western Australia in Crawley.

Simmons belongs to a camp of researchers that believes human pheromones likely exist, but none has yet been identified. He sees ‘AND’ and ‘EST’ as an unfortunate distraction, pushed forward in part by science’s “file drawer problem,” which relegates negative results to the laboratory filing cabinet.

A push to publish more negative findings has led to studies like these emerging to question long-held views, says Tristram Wyatt, a pheromone researcher at the University of Oxford in the United Kingdom who was not involved with the work. “It’s an Emperor’s New Clothes kind of moment.”

Yet Wen Zhou, a behavioral psychologist at the Chinese Academy of Sciences in Beijing, contends that ‘AND’ and ‘EST’ may well be human pheromones. “My major concern with the experiments in this study is that they were not rigorously designed and conducted,” she wrote in an email to Science. Zhou, who in 2014 published a study finding that ‘AND’ and ‘EST’ do indeed influence whether participants judge walking dot figures with “genderless gaits” to be men or women, doubts the faces used were truly “gender neutral.” She’s also concerned that tape used to affix steroid-soaked cotton balls to participants’ faces may have covered up the chemicals.



Martha McClintock, a behavioral neuroscientist at the University of Chicago in Illinois who is widely credited with (and sometimes criticized for) elevating ‘AND’ and ‘EST’ to pheromone fame, along with the heavily contested idea that women living together will sync their menstrual cycles, says the findings only really negate an overly simplified view of ‘AND’ and ‘EST’ having an almost mystical ability to attract partners. She still thinks the compounds can affect behavior—just in a much more nuanced way than most people think. Her most recent research, for example, has examined how inhaling ‘AND’, perhaps from another person’s sweat, might influence someone’s emotions. “There’s no doubt that this compound, even in tiny amounts, affects how the brain functions,” she says.

Wyatt, who is convinced the new work is solid, hopes that investigators will now re-evaluate how they search for human pheromones. Studies focused on sex and attraction, are exploring a complicated realm, he says, as human sexual behavior is not well understood. Instead, he argues, scientists should examine babies, who have not developed confounding associations with smells, but seem to respond to pheromonelike substances from any mother’s areola gland secretions, which cause them to stick out their tongue and suckle.
Source: Lindzi Wessel

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Biologists propose to sequence the DNA of all life on Earth

Can biologists sequence the genomes of all the plants and the animals in the world, including this greater bird of paradise in Indonesia?

When it comes to genome sequencing, visionaries like to throw around big numbers: There’s the UK Biobank, for example, which promises to decipher the genomes of 500,000 individuals, or Iceland’s effort to study the genomes of its entire human population. Yesterday, at a meeting here organized by the Smithsonian Initiative on Biodiversity Genomics and the Shenzhen, China–based sequencing powerhouse BGI, a small group of researchers upped the ante even more, announcing their intent
to, eventually, sequence “all life on Earth.”

Their plan, which does not yet have funding dedicated to it specifically but could cost at least several billions of dollars, has been dubbed the Earth Bio Genome Project (EBP). Harris Lewin, an evolutionary geneticist at the University of California, Davis, who is part of the group that came up with this vision 2 years ago, says the EBP would take a first step toward its audacious goal by focusing on eukaryotes—the group of organisms that includes all plants, animals, and single-celled organisms such as amoebas.



That strategy, and the EBP’s overall concept, found a receptive audience at BioGenomics2017, a gathering this week of conservationists, evolutionary biologists, systematisms, and other biologists interested in applying genomics to their work. “This is a grand idea,” says Oliver Ryder, a conservation biologist at the San Diego Zoo Institute for Conservation Research in California. “If we really want to understand how life evolved, genome biology is going to be part of that.”

Ryder and others drew parallels between the EBP and the Human Genome Project, which began as an ambitious, controversial, and, at the time, technically impossible proposal more than 30 years ago. That earlier effort eventually led not only to the sequencing of the first human genome, but also to entirely new DNA technologies that are at the center of many medical frontiers and the basis for a $20 billion industry. “People have learned from the human genome experience that [sequencing] is a tremendous advance in biology,” Lewin says.

Many details about the EBP are still being worked out. But as currently proposed, the first step would be to sequence in great detail the DNA of a member of each eukaryotic family (about 9000 in all) to create reference genomes on par or better than the reference human genome. Next would come sequencing to a lesser degree a species from each of the 150,000 to 200,000 genera. Finally, EBP participants would get rough genomes of the 1.5 million remaining known eukaryotic species. These lower resolution genomes could be improved as needed by comparing them with the family references or by doing more sequencing, says EBP co-organizer Gene Robinson, a behavioral genomics researcher and director of the Carl R. Woese Institute for Genomic Biology at the University of Illinois in Urbana.



The entire eukaryotic effort would likely cost about the same as it did to sequence that first human genome, estimate Lewin, Robinson, and EBP co-organizer John Kress, an evolutionary biologist at the Smithsonian National Museum of Natural History here. It took about $2.7 billion to read and order the 3 billion bases composing the human genome, about $4.8 billion in today’s dollars.

With a comparable amount of support, the EBP’s eukaryotic work might be done in a decade, its organizers suggest. Such optimism arises from ever-decreasing DNA sequencing costs—one meeting presenter from Complete Genomics, based in Mountain View, California, says his company plans to be able to roughly sequence whole eukaryotic genomes for about $100 within a year—and improvements in sequencing technology that make possible higher quality genomes, at reasonable prices. “It became apparent to me that at a certain point, it would be possible to sequence all life on Earth,” Lewin says. Although some may find the multibillion-dollar price tag hard to justify for researchers not studying humans, the fundamentals of matter, or the mysteries of the universe, the EBP has a head start, thanks to the work of several research communities pursuing their own ambitious sequencing projects.

These include the Genome 10K Project, which seeks to sequence 10,000 vertebrate genomes, one from each genus; i5K, an effort to decipher 5000 arthropods; and B10K, which expects to generate genomes for all 10,500 bird species. The EBP would help coordinate, compile, and perhaps fund these efforts. “The [EBP] concept is a community of communities,” Lewin says. There are also sequencing commitments from giants in the genomics field, such as China’s BGI, and the Wellcome Trust Sanger Institute in the United Kingdom. But at a planning meeting this week, it became clear that significant challenges await the EBP, even beyond funding. Although researchers from Brazil, China, and the United Kingdom said their nations are eager to participate in some way, the 20 people in attendance emphasized the need for the effort to be more international, with developing countries, particularly those with high biodiversity, helping shape the project’s final form.



They proposed that the EBP could help develop sequencing and other technological experts and capabilities in those regions. The Global Genome Biodiversity Network, which is compiling lists and images of specimens at museums and other biorepositories around the world, could supply much of the DNA needed, but even broader participation is important, says Thomas Gilbert, an evolutionary biologist at the Natural History Museum of Denmark in Copenhagen.

The planning group also stressed the need to develop standards to ensure high-quality genome sequences and to preserve associated information for each organism sequenced such as where it was collected and what it looked like. Getting DNA samples from the wild may ultimately be the biggest challenge—and the biggest cost, several people noted. Not all museum specimens yield DNA preserved well enough for high-quality genomes. Even recently collected and frozen plant and animal specimens are not always handled correctly for preserving their DNA, says Guojie Zhang, an evolutionary biologist at BGI and the University of Copenhagen. And the lack of standards could undermine the project’s ultimate utility, notes Erich Jarvis, a neurobiologist at The Rockefeller University in New York City: “We could spend money on an effort for all species on the planet, but we could generate a lot of crap.”



But Lewin is optimistic that won’t happen. After he outlined the EBP in the closing talk at BioGenomics2017, he was surrounded by researchers eager to know what they could do to help. “It’s good to try to bring together the tribes,” says Jose Lopez, a biologist from Nova Southeastern University in Fort Lauderdale, Florida, whose “tribe” has mounted “GIGA,” a project to sequence 7000 marine invertebrates. “It’s a big endeavor. We need lots of expertise and lots of people who can contribute.”

Source: Elizabeth Pennisi

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Dwarf planet Ceres Hosts Home-grown Organic Material

Ceres is doing some home-brewing in the asteroid belt. Organic material has been found on the dwarf planet located between Mars and Jupiter – and it was produced in-house.

Using the Dawn space probe, which has been orbiting Ceres since early 2015, planetary scientists found pockets of carbon-based organic compounds on the surface of the space rock.

The identity of the tar-like minerals can’t be pinned down precisely, but their mineral fingerprints match the make-up of kerite or asphaltite. The constituents and concentrations of these organic materials suggest that it’s unlikely they came to Ceres from another planetary body.

First, they wouldn’t have survived the heat of an impact on the surface of Ceres. And if they had hitched a ride on another stellar object, they would be widely dispersed, rather than concentrated in pockets. That means they must have come from Ceres itself.



“Anything else, you would expect it to be more widespread,” says Michael Küppers at the European Space Agency.

Chris Russell at the University of California, Los Angeles, leads NASA’s Dawn science team and says this finding, along with recent discoveries of water ice and bright spots of mineral deposits on Ceres, points to a more complex picture of the dwarf planet than we once assumed.

“It’s not just an accumulation of rock, but in fact, it’s been doing things,” he says. What it’s doing on the inside is not entirely clear yet, but the organic material on the surface indicates that there are processes within Ceres regulated by heat and water.

All this might sound like the building blocks for life. But Russell is hesitant to go that far.

“This is a different type of material,” he says. “It’s prebiotic, which means that it’s something you would expect to make before you had biology. It’s sort of on the road to biology.”



Russell says that finding organic materials on Ceres makes it more likely that other asteroids may also harbour similar molecular building blocks.
Küppers agrees, adding that this changes our outlook on potential spots where we may look for life in the solar system.

“A couple of decades ago, when talking about life in the solar system, we were focused on Mars. And now, we are more and more looking at other locations, like Saturn’s moon Titan and the subsurfaces of places like [Jupiter’s moon] Europa,” he says. “And now, also Ceres in the asteroid belt.”
Journal reference: Science

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Sweat Sensors

By: Alexandria Addesso

Science and technology seems to steadily progress and the health field is one of the main industries that is reaping the benefits of the new innovations. As our health statuses and test results seem to be at our fingertips, people become more and more health conscious. Researchers at The University of Texas at Dallas have recently designed a biosensor that is capable of checking glucose levels of the person who wears it.

"We've been developing various thin, soft and flexible skin-mounted devices as a next-generation platform for wearable technologies for a few years now," said Dr. John Rogers, the senior author of the study as well as a materials scientist and director of Northwestern University's Center for Bio-Integrated Electronics in Evanston, Illinois. "Now, we've developed such a device to capture and analyze sweat."



The sensor sticks to the skin and is around the size of a quarter, which is a drastic upgrade in comparison to the handheld glucose reading devices that are currently being used. Such devices needed to pluck the user’s finger to draw a small amount of blood in order to read glucose levels, a task most people suffering with diabetes found daunting.

"Fitness trackers that monitor heart rate and step count are very popular, but wearable, non-invasive biosensors would be extremely beneficial for managing diseases," said Dr. Shalini Prasad, a professor of bioengineering at the Erik Jonsson School of Engineering and Computer Science.

"We used known properties of textiles and weaves in our design," said Prasad. "What was innovative was the way we incorporated and positioned the electrodes onto this textile in such a way that allows a very small volume of sweat to spread effectively through the surface."



Sweat and blood are not the only bodily secretions that have been tested to see if they can get glucose readings. Google Laboratories is currently working on a contact lense that can read glucose levels from tears. While none of these new sensors have hit the market or even yet been licensed, there is no doubt that they will soon make invasive blood collecting glucose readers obsolete.

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The Time Reality: How its Rules Your Body—and Your Social Life

Time is inescapable, even if you try to ignore it, as author Alan Burdick did, by not wearing a watch.

We can’t smell it, we can’t taste it, we can’t hear it or touch it, but time is with us every second of our lives. And for thousands of years, philosophers and psychologists, from St. Augustine to William James, have pondered its meaning and how we perceive it. For his book Why Time Flies: A Mostly Scientific Investigation, Alan Burdick, who refused to wear a watch for much of his life, set off on a journey in search of time, which took him from a research station in the Arctic to the office of Coordinated Universal Time in Paris.

Speaking from his home in Hastings-on-Hudson, New York, Burdick explains how having twins changed his ideas about time, why as far back as the Romans people have complained about being slaves to time, and how new discoveries in neuroscience show that our bodies are filled with clocks.

It’s ironic that, for many years, the author of a book about time refused to wear a watch. Why was that? And how did your perception of time change after you finally relented?

I started this book some time ago, when I was rather a different person. I really was of the mind that if I could take the time off of me physically, that I somehow made it go away. Part of it was that I am prone to think about mortality. Having a watch on me felt like being a grown up! It meant plugging into, and being subject to, all the things that time requires, like being on time, and it made me feel like my day was chopped up into little bits and my watch was going to parse them out to me, like pellets to a rat.



I used to think that this was a modern outlook but I came across a great quote from a Roman poet, complaining about the sundial and how awful it is that it chops our days up into hours.
A lot of other things changed, too. In my case, I had a family—two fraternal twin boys, ten years old—and that forced me to be on time and get more things done than I used to be able to. I had to come to peace with it in that regard. Also, the more I learned about my subject, the more I came to appreciate the extent to which time and timing is embedded in every aspect of our social lives. You and I are going to have a conversation on such-and-such date at such-and-such time and, in order to do that, the time on your watch in the U.K. has to exactly match my time in the U.S. That’s all made possible by this incredible process that goes into making universal coordinated time, which involves atomic clocks and this global coordinated.



One of the most original ideas in your book is that “time is contagious” and even leads us to feel empathy for one another. Unpack that idea for us.

Yes, it’s super weird! We can come at it from a bunch of different ways. One is that research has found that when people are in conversation in person, there are all these things we do without even noticing. If we’re having lunch, you and I will unconsciously pick up our forks more or less at the same time. There’s a great study about two people playing the game Whack-A-Mole. Even though they were competing against each other, their movements fell into synch, even at the expense of losing points. They would unconsciously work toward this synchrony. The more affiliated and friendly you are with that other person, the more you are in synch.



If I watch a video of two people talking, I will be able to tell, unconsciously, how friendly they are, based on the extent to which their movements fall into synch with each other. The difference between a fake and real smile is a matter of milliseconds. It’s incredibly important to know the difference, right? And, in order to tell the difference, you need, as a viewer, to have a really sensitive timing mechanism that can parse one from the other. We have these clocks in us, which are operating all the time. It’s a very open question where exactly in the brain they are and how they work. But it’s clear that they’re there and utterly essential to making our social interactions go smoothly.

The cool thing about hummingbirds is that their timing mechanism is super sophisticated. In one experiment, they flew around outdoors to different flowers, which recharge their nectar at different rates. The hummingbirds want to get to the flower when it has maximum nectar, before its competitor does. So it’s got to do this elaborate optimization and algorithm to figure out how to get there often enough to get what it wants, without getting there too soon and wasting time, or getting there too late and being beaten to it.

Scientists have known about circadian rhythms for a couple of hundred years in plants. But in the last 20 years, the genetic mechanism has become clear in humans. The idea is that each of our cells can essentially tell the time; they have a 24-hour clock, which enables the cell to organize all the things it needs to do, just like you and I. We need to meet at a certain time, or talk at a certain time. Within yourself, your organelles and proteins and genes have stuff to do. It has to happen in a certain order, and that requires a clock. In humans it’s a little over 24 hours long, pretty close to, but not exactly, the length of a day.



All your cells have this clock. Your stomach and liver, all your organs, have a clock. In order to keep those clocks in synch, mammals and we humans have a master clock in our brains that sends out a neuro-chemical signal on a regular basis. Like the conductor of an orchestra, it keeps all of these clocks in time so your body knows that when you eat, 30 minutes later, your liver’s going to jump into action, then your adrenal glands and kidneys are going to do their thing, and your fat cells are going to absorb energy on a certain schedule.

There’s been a lot of research showing that, for night shift workers, truck drivers and other people who work on schedules that don’t match the circadian rhythm, their metabolism is thrown off. Some cancers may even be associated with night shift work or circadian imbalances. Your body is expecting to metabolize food at certain times of the day but if you are living at a different time of day, you’re eating food when your fat cells want to be sleeping.

Michel Siffre is a French cave explorer. In the 1960s, at the height of the space race, scientists were thinking about whether humans could live for a long time in isolation in deep space. Siffre had this idea: What if I go live in this cave for a period of weeks, and monitor my own heart rate and sleep cycle? What does living in isolation away from the sun do to the body? It was clear that humans have circadian cycles and that our body temperatures go up and down on a reliable 24-hour cycle. But Siffre was the first to show that the circadian
cycle in humans is not exactly 24 hours long.

He went on to repeat a similar experiment in a cave in Texas. He was down there for about 6 months, all by himself. He could talk to people up on the surface every once in a while by message. But he had no idea what time it was. He all but went nuts from loneliness and sensory deprivation, because his sleep cycle went totally out of whack. There were times when he would sleep for 40 hours straight then be awake for a couple of days in a row, without knowing it. When he finally came out, he thought that he had been called out a month too soon because his count of the days was so far off.

Two very good but very separate questions! Time speeds up when we’re having fun for reasons that are going to sound circular and even tautological: i.e. when you’re having fun you aren’t looking at the clock or paying attention to the time. By contrast, when you’re bored and have nothing else to do, you’re thinking about the time.

Why does time seem to speed up as we get old? It’s one of the great paradoxes. The funny thing is, in surveys, whether they’re 20, 40, 60 or 80, 85 percent of people in every range say time is speeding up. All indications seem to be that it’s not so much that the time goes by faster, though. My sense of it is that, as you get older, you become more aware of how little time you have, so the time you have feels more precious.



The neatest experience I had was spending two weeks at a biological research station on the north slope of Alaska, just above the Arctic Circle. We were in constant daylight and I’d never experienced anything like that before. It was amazing and unnerving. Like everyone, I am accustomed to thinking of sleep as this demarcation between one day and the next. But when the sun is always up, I might sleep for 8 hours and it would seem like a nap. Two weeks was really one long day. It was deeply disorienting but that’s what I went there to experience.
I had hoped I would meet people who were studying circadian rhythms but none of them were. They were all studying different aspects of ecology and climate change on a much longer time scale than I had gone there to find. It did make me face the profound reality of the kind of long term change that we are now causing on the planet.

The thing that fascinated me most is the idea of time as a social glue, a language, which is
fundamental to all of our social interactions. We can’t interact and have social lives without it. What we do as a social species is share time. That’s almost the definition of being a social species. Once I understood that, it suddenly felt more important to wear a watch.

Even if I’m lying in bed at night with no clock or watch, I have clocks in every cell. All of those clocks together make a master clock. It’s not like I can get away from time. I might delude myself briefly into thinking so, but I can’t. We are filled with clocks.
By Simon Worrall

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First stable semisynthetic organism created

Professor Floyd Romesberg (right) and Graduate Student Yorke Zhang led the new study at The Scripps Research Institute, along with Brian Lamb (not pictured).Credit: The Scripps Research Institute (Photo by Madeline McCurry-Schmidt.)

Scientists have announced the development of the first stable semisynthetic organism.

Life's genetic code has only ever contained four natural bases. These bases pair up to form two "base pairs" -- the rungs of the DNA ladder -- and they have simply been rearranged to create bacteria and butterflies, penguins and people. Four bases make up all life as we know it.

Until now Scientists at The Scripps Research Institute (TSRI) have announced the development of the first stable semisynthetic organism. Building on their 2014 study in which they synthesized a DNA base pair, the researchers created a new bacterium that uses the four natural bases (called A, T, C and G), which every living organism possesses, but that also holds as a pair two synthetic bases called X and Y in its
genetic code.

TSRI Professor Floyd Romesberg and his colleagues have now shown that their single-celled organism can hold on indefinitely to the synthetic base pair as it divides. Their research was published January 23, 2017, online ahead of print in the journal Proceedings of the National Academy of Sciences.



"We've made this semisynthetic organism more life-like," said Romesberg, senior author of the new study.

While applications for this kind of organism are still far in the future, the
researchers say the work could be used to create new functions for single-celled organisms that play important roles in drug discovery and much more.

Building a Unique Organism
When Romesberg and his colleagues announced the development of X and Y in 2014, they also showed that modified E. coli bacteria could hold this synthetic base pair in their genetic code. What these E. coli couldn't do, however, was keep the base pair in their code indefinitely as they divided. The X and Y base pair was dropped over time, limiting the ways the organism could use the additional information possessed in their DNA.

"Your genome isn't just stable for a day," said Romesberg. "Your genome has to be stable for the scale of your lifetime. If the semisynthetic organism is going to really be an organism, it has to be able to stably maintain that information."
Romesberg compared this flawed organism to an infant. It had some learning to do before it was ready for real life.



In stepped TSRI Graduate Student Yorke Zhang and Brian Lamb, an American Cancer Society postdoctoral fellow in the Romesberg lab at the time of the study. Together, they helped develop the means for the single-celled organism to retain the artificial base pair.

First, Zhang and Lamb, co-first authors of the study, optimized a tool called a nucleotide transporter, which brings the materials necessary for the unnatural base pair to be copied across the cell membrane. "The transporter was used in the 2014 study, but it made the semisynthetic organism very sick," Zhang explained. The researchers discovered a modification to the transporter that alleviated this problem, making it much easier for the organism to grow and divide while holding on to X and Y.

Next, the researchers optimized their previous version of Y. The new Y was a chemically different molecule that could be better recognized by the enzymes that synthesize DNA molecules during DNA replication. This made it easier for cells to copy the synthetic base pair.

A New Use for CRISPR-Cas9
Finally, the researchers set up a "spell check" system for the organism using CRISPR-Cas9, an increasingly popular tool in human genome editing experiments. But instead of editing a genome, the researchers took advantage of CRISPR-Cas9's original role in bacteria.

The genetic tools in CRISPR-Cas9 (a DNA segment and an enzyme) originated in bacteria as a kind of immune response. When a bacterium encounters a threat, like a virus, it takes fragments of the invader genome and pastes them into its own genome -- a bit like posting a "wanted" poster on the off chance it sees the invader again. Later, it can use those pasted genes to direct an enzyme to attack if the invader returns.

Knowing this, the researchers designed their organism to see a genetic sequence without X and Y as a foreign invader. A cell that dropped X and Y would be marked for destruction, leaving the scientists with an organism that could hold on to the new bases. It was like the organism was immune to unnatural base pair loss.



"We were able to address the problem at a fundamental level," said Lamb, who now serves as a research scientist at Vertex Pharmaceuticals.

Their semisynthetic organism was thus able to keep X and Y in its genome after dividing 60 times, leading the researchers to believe it can hold on to the base pair indefinitely.

"We can now get the light of life to stay on," said Romesberg. "That suggests that all of life's processes can be subject to manipulation."

A Foundation for Future Research
Romesberg emphasized that this work is only in single cells and is not meant to be used in more complex organisms. He added that the actual applications for this semisynthetic organism are "zero" at this point. So far, scientists can only get the organism to store genetic information.

Next, the researchers plan to study how their new genetic code can be transcribed into RNA, the molecule in cells needed to translate DNA into proteins. "This study lays the foundation for what we want to do going forward," said Zhang.
Story Source: Scripps Research Institute

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Are we closer than ever to a timeline for human evolution?

Dating when our ancestors split from Neanderthals and other relatives has long been a puzzle, but DNA advances are making our evolutionaNeanderthalsy journey clearer

Anthropologists and geneticists had a problem. And the farther back in time they looked, the bigger the problem became.

For the past several years, there have been two main genetic methods to date evolutionary divergences - when our ancestors split from Neanderthals, chimpanzees, and other relatives. The problem was, the results of these methods differed by nearly two-fold.

By one estimate, modern humans split from Neanderthals roughly 300,000 years ago. By the other, the split was closer to 600,000 years ago. Likewise, modern humans and chimps may have diverged around 6.5 or 13 million years ago.

Puzzled by this wild disagreement, researchers with diverse expertise have been studying it from different angles. Their combined discoveries, recently reviewed, here, have shed light on how genetic differences accumulate over time and have advanced methods of genetic dating.



And if you’re in suspense, yes, they’ve also pinned down important events in our evolutionary timeline. Everyone alive today seems to share ancestors with each other just over 200,000 years ago and with Neanderthals between 765,000-550,000 years ago.

Dating with the molecular clock
Go back in time and you’ll find a population of Homo sapiens who were the ancestors of everyone living today. Go back farther and our lineage meets up with Neanderthals, then chimps, and eventually all primates, mammals, and life.
In order to date these evolutionary splits, geneticists have relied on the molecular clock - the idea that genetic mutations accumulate at a steady rate over time. Specifically this, concerns mutations that become neutral substitutions, or lasting changes to letters of the genetic code that do not affect an organism’s chances of surviving and reproducing.



If such mutations arise clocklike, then calculating the time since two organisms shared common ancestors should be as easy as dividing the number of genetic differences between them by the mutation rate - the same way that dividing distance by speed gives you travel time.

But you need to know the rate.
For decades, anthropologists used fossil calibration to generate the so-called phylogenetic rate (a phylogeny is a tree showing evolutionary relationships). They took the geologic age of fossils from evolutionary branch points and calculated how fast mutations must have arisen along the resulting lineages.

For example, the earliest fossils on the human branch after our split with chimps are identified by the fact that they seem to have walked on two legs; bipedalism is
the first obvious difference that distinguishes our evolutionary lineage of hominins from that of chimps. These fossils are 7-6 million years old, and therefore the chimp-human split should be around that age. Dividing the number of genetic differences between living chimps and humans by 6.5 million years provides a mutation rate.

Determined this way, the mutation rate is 0.000000001 (or 1x10-9) mutations per DNA base pair per year. Applied to genomes with 6 billion base pairs, that means over millions of years of chimp and human evolution, and there have been on average six changes to letters of the genetic code per year.

Why archaeology needs to come out of the cave and into the digital age
This rate can be used to date evolutionary events that are not evident from fossils, such as the spread of modern humans out of Africa.



But genetic dating got messy in 2010, when improvements to DNA sequencing allowed researchers to determine the number of genetic differences between parents and their children. Known as pedigree analysis, this provides a more direct measurement of the current mutation rate within one generation, rather than an average over millions of years.

Pedigree analysis counts 60-some mutations every generation; that converts to a rate approximately half the phylogenetic estimate—meaning evolutionary events would be twice as old.

The erratic molecular clock
Resolving this disagreement propelled researchers to reassess and revise their starting assumptions: How accurately were they counting the small number of differences between genomes of parents and children? Were fossils assigned to the correct branches of the evolutionary tree? And above all, how constant is the molecular clock?

It turns out that among primates, the molecular clock varies significantly by species, sex, and mutation type. A recent study found that New World monkeys (i.e. monkeys of the Americas like marmosets and squirrel monkeys) have substitution rates about 64% higher than apes (including humans). Within apes, rates are about 7% higher in gorillas and 2% higher in chimpanzees, compared to humans.



But even among humans, mutation rates differ, particularly between the sexes with age. As fathers get older, they gain about one additional mutation per year in the DNA they can pass on to children. Mothers, on the other hand, accumulate considerably fewer mutations with each passing year.

These species and sex differences make sense when you consider how mutations form. Most heritable mutations occur from mistakes when DNA copies itself in the germline, or cells leading to eggs and sperm. The number of times germline DNA has to copy itself depends on developmental and reproductive variables including age at puberty, age at reproduction, and the process of sperm production.
These traits vary across primates today and certainly varied over primate evolution.

For instance, average generation times are six years for New World monkeys, 19 years for gorillas, 25 years for chimps, and 29 years for humans.

And those extra mutations as fathers get older? Sperm are produced continuously after puberty, so sperm made later in life are the result of more rounds of DNA replication and opportunities for replication errors. In contrast, a mother’s stock of eggs is formed by birth. The small increase with maternal age could be due to mutations from DNA damage, rather than replication errors.

Ways forward for dating backwards
It’s now clear that one mutation rate cannot determine the dates for all divergences relevant to human evolution. However, researchers can secure the timeline for important evolutionary events by combining new methods of genetic dating with fossils and geologic ages.

Innovative computational methods have incorporated reproductive variables into calculations. By taking into account ages of reproduction in both sexes, age of male puberty, and sperm production rates, researchers have estimated split times that accord with the fossil record.



Another new approach has analyzed mutations that are mainly independent of DNA replication. It seems that certain classes of mutations, related to DNA damage, do behave more clocklike.

And some researchers have focused on ancient DNA. Comparing human fossils from the past 50,000 years to humans today, suggests a mutation rate that agrees with pedigree analysis.

At least one evolutionary split was pinned down in 2016, after ancient DNA was extracted from 430,000 year-old hominin fossils from ‘Sima de los Huesos’, Spain. The Sima hominins looked like early members of the Neanderthal lineage based on morphological similarities. This hypothesis fit the timing of the split between Neanderthals and modern humans based on pedigree analysis (765,000-550,000 years ago), but did not work with the phylogenetic estimate (383,000-275,000 years ago).
Where do the Sima hominins belong on our family tree? Were they ancestors of both Neanderthals and modern humans, just Neanderthals, or neither?

DNA answered this definitively. The Sima hominins belong to the Neanderthal branch after it split with modern humans. Moreover, the result provides a firm time point in our family tree, suggesting that the pedigree rate works for this period of human evolution.

Neanderthals and modern humans likely diverged between 765,000-550,000 years ago. Other evolutionary splits may soon be clarified as well, thanks to advances brought about by the mutation rate debates. Someday soon, when you see a chimp, you may be able to salute your great, great… great grandparent, with the correct number of “greats.”
Source: Biology News

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Scientists engineer animals with ancient genes to test causes of evolution

A transgenic fruit fly engineered to carry the alcohol dehydrogenase gene as it existed about 4 million years ago. Thousands of these 'ancestralized' flies were bred and studied for their ability to metabolize alcohol and to survive on an.

Scientists at the University of Chicago have created the first genetically modified animals containing reconstructed ancient genes, which they used to test the evolutionary effects of genetic changes that happened in the deep past on the animals' biology and fitness.

The research, published early online in Nature Ecology & Evolution on Jan. 13, is a major step forward for efforts to study the genetic basis of adaptation and evolution. The specific findings, involving the fruit fly's ability to break down alcohol in rotting fruit, overturn a widely-held hypothesis about the molecular causes of one of evolutionary biology's classic cases of adaptation.



"One of the major goals of modern evolutionary biology is to identify the genes that caused species to adapt to new environments, but it's been hard to do that directly, because we've had no way to test the effects of ancient genes on animal biology," said Mo Siddiq, a graduate student in the Department of Ecology and Evolution at the University of Chicago, one of the study's lead scientists.

"We realized we could overcome this problem by combining two recently developed methods—statistical reconstruction of ancient gene sequences and engineering of transgenic animals," he said.

Until recently, most studies of molecular adaptation have analyzed gene sequences to identify "signatures of selection"—patterns suggesting that a gene changed so quickly during its evolution that selection is likely to have been the cause. The evidence from this approach is only circumstantial, however, because genes can evolve quickly for many reasons, such as chance, fluctuations in population size, or selection for functions unrelated to the environmental conditions to which the organism is thought to have adapted.

Siddiq and his advisor, Joe Thornton, PhD, professor of ecology and evolution and human genetics at the University of Chicago, wanted to directly test the effects of a gene's evolution on adaptation. Thornton has pioneered methods for reconstructing ancestral genes—statistically determining their sequences from large databases of present-day sequences, then synthesizing them and experimentally studying their molecular properties in the laboratory. This strategy has yielded major insights into the mechanisms by which biochemical functions evolve.

Thornton and Siddiq reasoned that by combining ancestral gene reconstruction with techniques for engineering transgenic animals, they could study how genetic changes that occurred in the deep past affected whole organisms-their development, physiology, and even their fitness.



"This strategy of engineering 'ancestralized animals' could be applied to many evolutionary questions," Thornton said. "For the first test case, we chose a classic example of adaptation-how fruit flies evolved the ability to survive the high alcohol concentrations found in rotting fruit. We found that the accepted wisdom about the molecular causes of the flies' evolution is simply wrong."

The fruit fly Drosophila melanogaster is one of the most studied organisms in genetics and evolution. In the wild, D. melanogaster lives in alcohol-rich rotting fruit, tolerating far higher alcohol concentrations than its closest relatives, which live on other food sources. Twenty-five years ago at the University of Chicago, biologists Martin Kreitman and John McDonald invented a new statistical method for finding signatures of selection, which remains to this day one of the most widely used methods in molecular evolution. They demonstrated it on the alcohol dehydrogenase (Adh) gene—the gene for the enzyme that breaks down alcohol inside cells—from this group of flies. Adh had a strong signature of selection, and it was already known that D. melanogaster flies break down alcohol faster than their relatives. So, the idea that the Adh enzyme was the cause of the fruit fly's adaptation to ethanol became the first accepted case of a specific gene that mediated adaptive evolution of a species.

Siddiq and Thornton realized that this hypothesis could be tested directly using the new technologies. Siddiq first inferred the sequences of ancient Adh genes from just before and just after D. melanogaster evolved its ethanol tolerance, some two to four million years ago. He synthesized these genes biochemically, expressed them, and used biochemical methods to measure their ability to break down alcohol in a test tube.



The results were surprising: the genetic changes that occurred during the evolution of D. melanogaster had no detectable effect on the protein's function.
Working with collaborators David Loehlin at the University of Wisconsin and Kristi

Montooth at the University of Nebraska, Siddiq then created and characterized transgenic flies containing the reconstructed ancestral forms of Adh. They bred thousands of these "ancestralized" flies, tested how quickly they could break down alcohol, and how well the larvae and adult flies survived when raised on food with high alcohol content. Surprisingly, the transgenic flies carrying the more recent Adh were no better at metabolizing alcohol than flies carrying the more ancient form of Adh. Even more strikingly, they were no better able to grow or survive on increasing alcohol concentrations. Thus, none of the predictions of the classic version of the story were fulfilled. There is no doubt that D. melanogaster did adapt to high-alcohol food sources during its evolution, but not because of changes in the Adh enzyme.

"The Adh story was accepted because the ecology, physiology, and the statistical signature of selection all pointed in the same direction. But three lines of circumstantial evidence don't make an airtight case," Thornton said. "That's why we wanted to test the hypothesis directly, now that we finally have the means to do so."

Siddiq and Thornton hope that the strategy of making ancestralized transgenic will become the gold standard in the field to decisively determine the historical changes in genes to their changes on organisms' biology and fitness.

For his part, Kreitman, who is still a professor of ecology and evolution at UChicago, has been supportive of the new research, helping advise Siddiq on the project and sharing his vast knowledge about molecular evolution and Drosophila genetics.



"From the beginning, Marty was excited about our experiments, and he was just as supportive when our results overturned well-known conclusions based on his past work," Siddiq said. "I think that's extremely inspiring."

Source: University of Chicago, Medical Center

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The Mesentery: A 'new' organ you didn't know you had

The Mesentery, which connects the intestine to the abdomen, has been classified as a single organ. The organ's continuity can be seen only when it's exposed in a certain way.

In case you've ever wondered what connects your intestine to your abdomen, there's a word -- and now, a single organ -- for that: the Mesentery. But don't worry; you haven't grown a new organ. It's always been there, performing important functions that affect systems throughout the body, from cardiovascular to immunological.

Leonardo da Vinci depicted it as one contiguous organ, and it remained that way for centuries until 1885, when Sir Frederick Treves' findings presented the mesentery as fragmented amongst the small intestine, transverse colon and sigmoid colon.

J. Calvin Coffey, foundation chair of surgery at the University of Limerick, is reclassifying this part of the digestive system as a contiguous organ. In a new study, Coffey has established the anatomy and structure of the mesentery, using images and compiling research to show that the organ's continuity can be seen only when it's exposed in a certain way.



The current findings resonate with those of Carl Toldt, who accurately described the presence of the mesentery in 1878. But his research was largely overlooked. At the time, Treves' findings supported the statements of Henry Gray, who mentioned multiple mesenteries in the 1858 first edition of his book "Gray's Anatomy," the go-to medical textbook for students around the world.

Coffey's research has already prompted the latest edition of "Gray's Anatomy" to refer to the mesentery as a continuous organ.

What does it do?
Linking your gut to the rest of your body is an important task, and the mesentery performs it well.
Among its functions, it carries blood and lymphatic fluid between the intestine and the rest of the body. It also maintains the position of the intestine so that it's connected with the abdominal wall without being in direct contact.

That connection is key. "Without a mesentery to keep the intestine connected, the intestine would have to attach directly to the body wall," Coffey said. "It is unlikely that it would be able to contract and relax along its entire length if it were directly in contact. It maintains the intestine in a particular conformation, 'hitched up,' so that when you stand up or walk about, it doesn't collapse into the pelvis and not function."


How the mesentery functions in your body. (A) Peritoneum, mesentery, fascia and intestine. (B) Mesentery, fascia and intestine. (C) Mesentery and intestine. (D) Mesentery.

Although researchers know that the mesentery plays an important role in the intestinal, vascular, endocrine, cardiovascular and immunological systems, more research is needed to determine the extent of those roles.

But they do have evidence that the mesentery takes environmental signals from the intestine and orchestrates the body's response, Coffey said. One example is how bacteria are sampled in the lymph glands in the mesentery. In response, the glands then coordinate immune responses.

Why has it been misunderstood?
To look at the shape of the membrane, which Coffey calls remarkable, it's easy to see why the mesentery has been depicted differently. It has a spiral formation in the abdomen and is packaged along a spinal trajectory, starting in the upper abdomen and ending in the pelvis.

"In between, it fans out, like a Chinese fan, to span the length of the intestine from the upper small intestine to the end of the large bowel," Coffey said.
The latest anatomy and structure clarifications aid not only doctors, but medical students as well.

"For students, it greatly simplifies the matter of the mesentery," Coffey said. "This was traditionally regarded as a complex field. The current anatomic model is elegant and simple and will help students understand this structure. It will also provide them with a new perspective from which to view other organs in the abdomen. For example, we now know that the mesentery and intestine intersect along the entire length of the small and large intestine, whereas previously, this was though to occur in some regions only."



Improving surgery and treatment
More research will allow for better definition of the gut membrane's function, what happens when it functions abnormally and diseases that affect it. This also allows for mesenteric science to become its own field of medical study, like neurology.

Coffey hopes that creating a better understanding of the mesentery can help with diagnosing issues and less invasive ways of assessing them. Currently, its remote location in the body means the mesentery can be accessed only radiologically or surgically. This research lays the foundation for investigating possible prescriptions and how less-invasive endoscopic procedures during a colon-scopy could map the mesentery.

Adopting a universal classification like this in the medical world has benefits that extend to standardizing surgical procedures, such as moving or cutting into the intestine. The mesentery extends from the duodenum, or first part of the small intestine immediately beyond the stomach, all the way to the rectum, the final section of the large intestine.

Because of this, it can factor into diseases such as Crohn's, colorectal cancer, inflammatory bowel disease or cardiovascular disease and major health concerns like diabetes, obesity and metabolic syndrome. The more doctors know about the exact function of the mesentery, the more measures they can take to investigate the part it plays.

"For doctors, it provides us with an opportunity to refresh our approach to many diseases such as inflammatory bowel disease and others," Coffey said. "This could help in identifying the mechanisms underlying these conditions and help us in unraveling their cause and how they develop."
Source: Ashley Strickland, CNN

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Breakthrough in the fight against Decease including Cancer

A treatment billed as a potential breakthrough in the fight against disease, including cancer, could back-fire and make the disease fitter and more damaging, new research has found.

Ground-breaking research has found that introducing 'friendlier' less-potent strain into a population of disease-causing microbes can lead to increased disease severity.

The surprise findings by a team of scientists at the University of Exeter has led to call for urgent research into the implications of using 'fire to fight fire' to combat disease. The research shows that far from being a 'silver bullet' to weaken disease, the practice of introducing pacifist microbes into a host could make the aggressive pathogen stronger, which could hamper disease management.

Until now, introducing friendlier cousins which do not cause severe disease, into a population of pathogens has been shown to reduce disease severity and damage to the infected host. It has been suggested that this approach could be an effective way of treating cancer, and research so far has proved effective and promising. For example, scientists have already produced encouraging results in the fight against Clostridium difficile infections that are so common in our hospitals.


This photograph depicts Clostridium difficile colonies after 48hrs growth on a blood agar plate; Magnified 4.8X. C. difficile, an anaerobic gram-positive rod, is the most frequently identified cause of antibiotic-associated diarrhea (AAD).

But the University of Exeter scientists tested this strategy using a plant pathogen, and found the therapy could go dramatically wrong, with devastating consequences for the host plant.

A team lead by Professors Ivana Gudelj, a mathematical biologist and Nick Talbot, a plant disease specialist, investigated the devastating rice blast disease. They introduced a mixed population of the fungus that causes this disease into rice, where the mixture included an aggressive strain and a pacifist mutant. They expected that the overall disease severity would decrease because of the presence of the pacifist strain. However, they found the opposite. The rice plants succumbed to much more severe disease.

The Exeter University research, published in eLife, shows that the therapy can in some circumstances have the opposite effect and that the way the pathogen will behave can be unpredictable, leading to more severe disease. The research highlights the need for these new strategies to be carefully tested before they are used therapeutically.

The scientists used cooperation theory and mathematical modelling, to identify the reason for their surprising result. They found that in some circumstances pacifists "helped" aggressive microbes to be more efficient in utilizing resources obtained from the host.



Professor Ivana Gudelj, who led the research, said: "Our study shows that a promising disease management strategy may not always be effective and indeed may has damaging unforeseen consequences. Importantly, our work also provides a foundation for the analysis of when, and why, this can happen. We find that the mechanisms driving our unexpected findings when treating rice blast infection are pertinent for many diseases involving bacterial and fungal pathogens"

Developing new ways of treating infectious disease has become more pressing with the development of resistance to antibiotics.

One strategy being explored to treat infections that resist current drugs involves neutralizing the disease-causing agent. This strategy involves extracting the agent from the patient so that scientists can remove components of the microbe's DNA in order to neutralize the disease.

This new harmless agent is then grown in the lab and re-introduced to the disease site with the expectation that it will out-compete its more harmful cousin by stealing resources, the disease needs to proliferate. Such research has proved effective in several lab tests.



The University of Exeter scientists tested this method in rice blast infections, but they found more severe disease symptoms.

Professor Nick Talbot, Professor of Molecular Genetics and expert in plant diseases, said: "The strategy of introducing less aggressive microbes to fight more aggressive ones may prove effective to control some crop disease, but our study shows that they are not a silver bullet and caution needs to be exercised. We need to understand how microbes interact with each other in natural settings, before we can try to alter their ability to cause disease in this way. Our study also shows why mathematicians and biologists need to work together more often, because we would not have understood this phenomenon at all without the mathematical analysis carried out."

Richard Lindsay, a PhD student who worked on the research team, added: "Our findings are of central importance in understanding how microbial infections evolve, but also have wider significance for the treatment of cancer and the therapeutic control of disease in humans, animals and plants."
Source: Discovery Magazine

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Biologists unlock 51.7-million-year-old genetic secret to landmark Darwin theory

Scientists have identified the cluster of genes responsible for reproductive traits in the Primula flower, first noted as important by Charles Darwin more than 150 years ago. Darwin hypothesized that some plant species with two distinct forms of flower, where male and female reproductive organs were of differing lengths, had evolved that way to promote out-crossing by insect pollinators.

His ground-breaking insight into the significance of the two forms of flower known as 'pins' and 'thrums' coined the term 'heterostyly', and subsequent studies contributed to the foundation of modern genetic theory.

And now scientists at the University of East Anglia, working at the John Innes Centre, have identified exactly which part of these species' genetic code made them that way, through an event that occurred more than 51 million years ago.
Prof Philip Gilmartin from UEA's School of Biological Sciences said: "To identify the genes which control the biology noted by Darwin is an exciting moment. Many studies have been done over the past decades to explore the genetic basis of this phenomenon but now we have pinpointed the supergene directly responsible, the S locus."



Supergenes are clusters of closely-associated genes which are always inherited together as a unit and allow complex biology to be controlled. Researchers worked with the Earlham Institute to map the plant's genes and sequence the Primula genome to find the specific gene cluster responsible for creating the differing flower morphs.

Prof Gilmartin said: "Not only did we identify the supergene but we found it is specific to just one of the flower forms, the thrum. This insight has profound implications for our understanding of a key evolutionary innovation of flowering plants.
"Understanding of the genetics which underpin flower development and reproduction of a species broadens our knowledge about the entire system of pollination, which underpins biodiversity and food security.

"With challenges such as climate change and its effects on plants, crops and their insect pollinators, it's even more important to understand pollination mechanisms and how species can and will react.
In their hunt for the genes controlling heterostyly, researchers also managed to date the original mutation, to 51.7 million years ago.

Having found the S locus, they realized the gene was a close relative to another, identified six years ago as responsible for controlling the identity of petals on a Primula flower. At some point this gene duplicated, inserted itself in the S locus, and mutated to control the position of the anther in the flower. Finding this duplicated gene allowed the team to date how long ago the mutation occurred for the first time.



Prof Gilmartin has been researching the origins of heterostyly for a large part of his career. He said: "This study answers some of the crucial questions that have been asked since Darwin's time, and for me since I bought my first packet of Primula seeds twenty years ago."

The study 'Genetic architecture and evolution of the S locus supergene in Primula vulgaris' is published in the journal Nature Plants, on Friday 2 December 2016.

Sources: ‘How 16th Century observations paved the way for Darwin's landmark study’
More information: Jinhong Li et al. Genetic architecture and evolution of the S locus supergene in Primula vulgaris, Nature Plants (2016). DOI: 10.1038/nplants.2016.188
Journal reference: Nature Plants
Provided by: University of East Angli

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Autism and human evolutionary success

A subtle change occurred in our evolutionary history 100,000 years ago which allowed people who thought and behaved differently – such as individuals with autism - to be integrated into society, academics from the University of York have concluded.

The change happened with the emergence of collaborative morality - an investment in the well-being of everyone in the group - and meant people who displayed autistic traits would not only have been accepted but possibly respected for their unique skills.

It is likely our ancestors would have had autism, with genetics suggesting the condition has a long evolutionary history.

But rather than being left behind, or at best tolerated, the research team conclude that many would have played an important role in their social group because of their unique skills and talents.



“We are arguing that diversity, variation between people, was probably more significant in human evolutionary success than the characteristics of one person, “said Penny Spikins, senior lecturer in the archaeology of human origins, at the University of York.

“It was diversity between people which led to human success and it is particularly important as it gives you different specialised roles.
“We are arguing that it is the rise of collaborative morality that led to the possibility for widening the diversity of the human personality.”

Many people with autism have exceptional memory skills, heightened perception in realms of vision, taste and smell and enhanced understanding of natural systems such as animal behaviour.

The incorporation of some of these skills into a community would play a vital role in the development of specialists, the authors of the report, which is published in Time and Mind, suggest.

A previous ethnographic study in 2005 of an elderly reindeer herder from Siberia revealed a detailed memory of the parentage, medical history and character of each one of his 2,600 animals.

His vital knowledge would have made a significant contribution to their management and survival.

The grandfather was more comfortable in the company of the reindeer than of humans, but was much respected and had a wife and son and grandchildren.

Finding tangible evidence of autism in archaeological records has always been challenging for academics.



Dr. Spikins said “The archaeological record doesn’t give us a skeletal record for autism, but what it does do is give us a record for other people who have various differences and how they have been integrated.”

Other clues can be found in cave art and other artefacts.
“There has been a long-standing debate about identifying traits of autism in Upper Palaeolithic cave art.

“We can’t say some of it was drawn by someone with autism, but there are traits that are identifiable to someone who has autism. It was also roughly at that time that we see collaborative morality emerging.”
Source: Materials provided by University of York.

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The Alzheimer

A new nasal Spray Vaccine promises to protect Against the terrible disease

Researchers are working on a nasally-delivered vaccine that promises to protect against both Alzheimer’s and Stroke, repairing vascular damage in the brain

One in eight Americans will fall prey to Alzheimer's disease at some point in their life, current statistics say. Because Alzheimer's is associated with vascular damage in the brain, many of them will succumb through a painful and potentially fatal stroke.

But researchers led by Dr. Dan Frenkel of Tel Aviv University's Department of Neurobiology at the George S. Wise Faculty of Life Sciences are working on a nasally-delivered 2-in-1 vaccine that promises to protect against both Alzheimer's and stroke. The new vaccine repairs vascular damage in the brain by rounding up "troops" from the body's own immune system.



And in addition to its prophylactic effect, it can work even when Alzheimer's symptoms are already present. The research on this new technology was recently accepted for publication in the journal Neurobiology of Aging.

A natural way to fight Alzheimer's
"Using part of a drug that was previously tested as an influenza drug, we've managed to successfully induce an immune response against amyloid proteins in the blood vessels," says Dr. Frenkel, who collaborated on this project with Prof. Howard L. Weiner of Brigham and Women's Hospital, Harvard Medical School. "In early pre-clinical studies, we've found it can prevent both brain tissue damage and restore cognitive impairment," he adds.

Modifying a vaccine technology owned by Glaxo Smith Kline, a multinational drug company, Tel Aviv University's new therapeutic approach activates a natural mechanism in our bodies that fights against vascular damage in the brain.



The vaccine, Dr. Frenkel explains, activates macrophages — large proteins in the body that swallow foreign antigens. When the vaccine activates large numbers of these macrophages, they clear away the damaging build-up of waxy amyloid proteins in our brain's vascular system.

Animal models showed that once these proteins are cleared from the brain, further damage can be prevented, and existing damage due to a previous stroke can be repaired.

A new road to an Alzheimer's cure?
Could the breakthrough lead to both a vaccine and a long-sought cure for Alzheimer's disease? "It appears that this could be the case," says Dr. Frenkel, who worked on the study with his doctoral student Veronica Lifshitz and master degree students Ronen Weiss and Tali Benromano. "We've found a way to use the immune response stimulated by this drug to prevent hemorrhagic strokes which lead to permanent brain damage," he says.

In the animal models in mice, Dr. Frenkel's team worked with MRI specialist Prof. Yaniv Assaf and his Ph.D. student Tamar Blumenfeld-Katzir of Tel Aviv University's Department of Neurobiology and then with "object recognition" experiments, testing their cognitive functioning both before and after administration of the vaccine. MRI screenings confirmed that, after the vaccine was administered, further vascular damage was prevented, and the object recognition experiments indicated that those animals treated with the new vaccine returned to normal behavior.



Dr. Frenkel believes that this approach, when applied to a human test population, will be able to prevent the downward health spiral of Alzheimer's and dementia. The vaccine could be given to people who are at risk, those who show very early symptoms of these diseases, and those who have already suffered strokes to repair any vascular damage.
So far the vaccine has shown no signs of toxicity in animal models. Dr. Frenkel is hopeful that this new approach could lead to a cure, or at least an effective treatment, for the vascular dementia found in 80% of all people with Alzheimer's.
Source : Tel Aviv University

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New Glowing technique is been used in Brain surgery

The fluorescent dye technique, originally developed to treat lung cancer, illuminated brain tumors in real-time during surgery, helping physicians distinguish between healthy and cancerous tissue an experimental cancer imaging tool that makes tumors glow brightly during surgery has shown promise again in a new Penn Medicine clinical study, this time in patients with brain cancer. The fluorescent dye technique, originally developed by surgeons at the Penn Center for Precision Surgery to treat lung cancer, illuminated brain tumors in real-time during surgery, helping physicians distinguish between healthy and cancerous tissue. Each year, over 15,000 people in the United States undergo surgeries to remove brain tumors.

Findings from the pilot study, led by first author John Y.K. Lee, MD, MSCE, an associate professor of Neurosurgery in the Perelman School of Medicine at the University of Pennsylvania, and co-director of the Center for Precision Surgery, were reported in this week in Neurosurgery.

A big challenge with brain surgery is ensuring the entire tumor is removed. It is difficult to identify the margins of the tumor with current approaches. Cancer tissue not visible to the naked eye or felt by fingers is often missed during tumor removal, leading to recurrence in some patients -- about 20 to 50 percent.



Penn's approach, which relies on an injectable dye that accumulates in cancerous tissues more so than normal tissues, may help change that. "Fluorescent contrast agents take visualization to a whole new level," Lee said. "It has the potential for real-time imaging, identification of disease, and most importantly, precise detection of the tumor's margins. With this, we know better where to cut."

The study also includes co-author, Sunil Singhal, MD, an associate professor of Surgery, and co-director the Center for Precision Surgery at Penn's Abramson Cancer Center, who first started work on this approach in his lab nearly 10 years ago.
The technique uses near-infrared, or NIR, imaging and the contrasting agent indocyanine green (ICG), which fluoresce a bright green under NIR light. ICG was developed during World War II as a dye in photography and, in 1958 it was approved by the U.S. Food and Drug Administration (FDA) for use in medicine, primarily in liver diagnostics and later in cardiology.

However, for this study, researchers used a modified version of ICG at a higher concentration delivered intravenously about 24 hours before surgery to ensure margins were included. This is the first time, to the author knowledge, that this delayed imaging of ICG has been used to visualize brain tumors. Patients enrolled in the clinical study were between the ages of 20 and 81 with a diagnosis of a solitary brain tumor and a presumed glioma based on imaging or prior surgery or biopsy.

Twelve of the 15 tumors demonstrated strong intraoperative fluorescence. The lack of glow in the three remaining tumors could potentially be due to their disease grade and timing of the injection, the authors suggested. Eight of the 15 patients demonstrated a visible glow through the dura, a thick membrane on the meninges of the brain, was opened, demonstrating the technology's ability to see deeply within the brain before the tumor is exposed. Once opened, all tumors were picked up by NIR imaging. The researchers also studied the surgical margins using neuropathology and magnetic resonance imaging, (MRI) to assess the accuracy and precision of NIR fluorescence in identifying tumor tissue.



Of the 71 specimens collected from MRI-enhanced tumors and their surgical margins, 61 (85.9 percent) fluoresced and 51 of these (71.8 percent) were classified as glioma tissue of the 12 MRI-enhancing gliomas, four patients had biopsy specimens that were both non-fluorescent and negative for tumor, which matched the gross total resection seen on their MRI. In contrast, 8 patients had residual fluorescent signal in the resection cavity. Only 3 of these patients showed gross total resection on MRI. This suggests a benefit of true-negative NIR signal after resection, the authors said
Over the past three plus years, Singhal, Lee, and their colleagues have performed more than 300 surgeries with the imaging tool in patients with various types of cancer, including lung, brain, bladder and breast. "This technique, if approved by the FDA, may offer great promise to physicians and patients," Singhal said. "It's a strategy that could allow greater precision across many different cancer types, help with early detection, and hopefully better treatment success."

Source: Materials provide by Perelman School of Medicine at the University of Pennsylvania.

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