Tag Archives: Life Science

The Life of the Queen Bee

A common mistake amongst non apiarists is the assumed fact that the queen directly controls the hive. Effectively, however, her duty is as an egg making machine. She can lay bout two thousand eggs a day in the spring. This amounts to more than her own weight in eggs each day. Surrounded continuously by workers, she needs for nothing. They give her food and take her waste away. They will also collect a pheromone which they then distribute to stop workers from starting queen cells.
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This very close up [follow link] of a queen bee shows one of its greatest – and smallest – enemies. The bee mite is an external parasite that attacks honey bees. It attaches itself to the bee’s body and sucks out its hemolymph. This is the blood analogue that is used by bees as they have an open circulatory system. Unfortunately the mite is more than just a pain in the neck. It can spread a host of viruses, including “Deformed Wing Virus” and the arrival of mites in a colony can often spell its demise. Scientists believe that the mite may contribute to the Colony Collapse Disorder (otherwise known as CCD) that is spreading throughout the United States.

Waste from Gut Bacteria Helps Host Control Weight

A single molecule in the intestinal wall, activated by the waste products from gut bacteria, plays a large role in controlling whether the host animals are lean or fatty, a research team, including scientists from UT Southwestern Medical Center, has found in a mouse study.

When activated, the molecule slows the movement of food through the intestine, allowing the animal to absorb more nutrients and thus gain weight. Without this signal, the animals weigh less.

The study shows that the host can use bacterial byproducts not only as a source of nutrients, but also as chemical signals to regulate body functions. It also points the way to a potential method of controlling weight, the researchers said.

“It’s quite possible that blocking this receptor molecule in the intestine might fight a certain kind of obesity by blocking absorption of energy from the gut,” said Dr. Masashi Yanagisawa, professor of molecular genetics at UT Southwestern and a senior co-author of the study, Proceedings of the National Academy of Sciences, open access: Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41.

Humans, like other animals, have a large and varied population of beneficial bacteria that live in the intestines. The bacteria break up large molecules that the host cannot digest. The host in turn absorbs many of the resulting small molecules for energy and nutrients.

In the Big Fat Lie I mentioned some related ideas:

It also makes perfect sense that our bodies evolved to store energy for worse times (and some of us have bodies better at doing that). Now we are in a new environment where (at least for many people alive today) finding enough calories is not going to be a problem so it would be nice if we could tell our bodies to get less efficient at storing fat

This research seems to be looking for a similar way to attack the obesity epidemic: reduce the efficiency of our bodies converting potential energy in the food we eat to energy we use or store. If we can make that part of the solution that will be nice. So far the reduction in our activity and increase in food intake have not been getting good results. And efforts to increase (from our current low levels) activity and reduce food intake have not been very effective.
Continue reading →

$400 Million More for Harvard and MIT

$400 million endowment for the Broad Institute of Harvard and MIT

“Today the Broad Institute is the world’s leading genomics and biomedical institute, and we’re now making a $600 million bet that the Broad will be the place where the greatest scientific discoveries take place,” Eli Broad said at today’s ceremony.
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In its short history, the Broad Institute’s accomplishments include cataloging and identifying genetic risk factors for diseases such as type 2 diabetes and autism; discovering new therapeutic targets for cancer, malaria, and other diseases; and applying genomic tools to better understand and treat human pathogens like tuberculosis.
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The Broads’ gift is the largest to support biomedical research at a university anywhere in the world. The Broads initially invested $100 million in 2003 as a way to test the institute’s new approach to biomedical research. By 2005, the Broad Institute had already made significant accomplishments and progress, and the Broads invested a second $100 million. Their endowment of $400 million today will allow the Broad Institute to transition to a permanent, non-profit 501(c)(3) organization with both Harvard and MIT still at the heart of it, continuing to help govern the institute.

Many countries would love to create a world class center of biomedical research. And several are trying. Boston sure seems to be staking a claim that it will be one of those centers of excellence. The economic benefits of that to Boston will be huge.

Ancient Ants

Blind “Ant From Mars” Found in Amazon

An ant so unlike all other living ants that it was given an extraterrestrial name has been discovered in the Amazon rain forest, biologists announced today. The tiny new species is the only known surviving member of an ant lineage that separated from the main family more than a hundred million years ago, DNA analysis revealed.

The pale, eyeless ant appears to be adapted to living underground, possibly surfacing at night to forage. Its long mandibles suggest that the 0.08-inch-long (2-millimeter-long) animal is a predator, most likely of soft-bodied creatures such as termite larvae.

Christian Rabeling, a graduate student at the University of Texas in Austin, found a single specimen of the new species, thought to be a worker ant, in tropical soils near Manaus, Brazil. Rabeling’s team named the new creature Martialis heureka—”Martialis” means “of Mars
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The new species’ genes suggest that it broke away from the main ant family before the origin of all other living ant groups, which include 20 subfamilies that together contain more than 12,000 species.

Autism and the MMR vaccine

Science Tuesday: Back into the hornets nest is a thoughtful follow-up post on the decision of a scientist to vaccinate his child.

Autism isn’t like tuberculosis, there’s not a bacteria that causes the disease. In fact,most researchers believe that “autism” is not a discrete disorder, rather “autism is a clinically defined pervasive developmental disorder with phenotypically diverse neuropsychiatric symptoms and characteristics. These manifest as a spectrum of social and communicative deficits, stereotypical patterns and disturbances of behaviour.”Â¹
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If a particular trait’s heritability is 100% then the trait is due entirely to genetic variation, if the heritability is 0% then the trait is due entirely to environmental variation. By some estimates, heritability of autism spectrum disorders exceeds 90%
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repeated studies have found that autism diagnoses continue to rise even after the removal of thimerosal from the vaccine.
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Finally, when thinking about the environmental influences on autism, it’s important to explore the role of the environment on genetics. Many of the types of genetic changes that have been identified as causative in autism are indicative of some sort of DNA damage – DNA damage that may result from exposure to an environmental toxin. Many scientists, and I count myself in their number, feel that the recent autism ‘epidemic’ is due primarily to improved screening and diagnosis. In other words, prior to the 1980’s, many people suffering from autism were diagnosed as “slow” or misdiagnosed with another type of mental retardation. Unfortunately, there is no way to quantify this hypothesis.

This is one of the examples of what is so good about blogs. Great content that probably would not be available but through a blog.

Life After the Chernobyl Nuclear Accident

Silent Spring by Lauren Monaghan, Cosmos

Ever since, a 30 km ‘exclusion zone’ has existed around the contaminated site, accessible to those with special clearance only. It’s quite easy, then, to conjure an apocalyptic vision of the area; to imagine an eerily deserted wasteland, utterly devoid of life.

But the truth is quite the opposite. The exclusion zone is teeming with wildlife of all shapes and sizes, flourishing unhindered by human interference and seemingly unfazed by the ever-present radiation. Most remarkable, however, is not the life buzzing around the site, but what’s blooming inside the perilous depths of the reactor.

Sitting at the centre of the exclusion zone, the damaged reactor unit is encased in a steel and cement sarcophagus. It’s a deathly tomb that plays host to about 200 tonnes of melted radioactive fuel, and is swarming with radioactive dust.

But it’s also the abode of some very hardy fungi which researchers believe aren’t just tolerating the severe radiation, but actually harnessing its energy to thrive.

“Our findings suggest that [the fungi] can capture the energy from radiation and transform it into other forms of energy that can be used for growth,” said microbiologist Arturo Casadevall from the Albert Einstein College of Medicine at Yeshiva University in New York, USA.
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Taken together, the researchers think their results do indeed hint that fungi can live off ionising radiation, harnessing its energy through melanin to somehow generate a new form of biologically usable growing power.

If they’re right, then this is powerful stuff, said fungal biologist Dee Carter from the University of Sydney. The results will challenge fundamental assumptions we have about the very nature of fungi, she said.

It also raises the possibility that fungi might be using melanin to secretly harvest visible and ultraviolet light for growth, adds Casadevall. If confirmed, this will further complicate our understanding of these sneaky organisms and their role in ecosystems.

Pretty amazing stuff. It really is great all that nature gives us to study and learn about using science.

Why ‘Licking Your Wounds’ Works

Why ‘Licking Your Wounds’ Actually Works

scientists found that histatin, a small protein in saliva previously only believed to kill bacteria was responsible for the healing.

To come to this conclusion, the researchers used epithelial cells that line the inner cheek, and cultured in dishes until the surfaces were completely covered with cells. Then they made an artificial wound in the cell layer in each dish, by scratching a small piece of the cells away.

In one dish, cells were bathed in an isotonic fluid without any additions. In the other dish, cells were bathed in human saliva. After 16 hours the scientists noticed that the saliva treated “wound” was almost completely closed. In the dish with the untreated “wound,” a substantial part of the “wound” was still open. This proved that human saliva contains a factor which accelerates wound closure of oral cells.

Because saliva is a complex liquid with many components, the next step was to identify which component was responsible for wound healing. Using various techniques the researchers split the saliva into its individual components, tested each in their wound model, and finally determined that histatin was responsible.

DNA Passed to Descendants Changed by Your Life

How your behaviour can change your children’s DNA

Until recently that would also have been the opinion of most scientists. Genes, it was thought, were highly resilient. Even if people did wreck their own DNA through bad diet, smoking and getting fat, that damage was unlikely to be passed to future generations.

Now, however, those assumptions are being re-examined. At the heart of this revolution is a simple but controversial idea: that DNA can be modified or imprinted with the experiences of your parents and grandparents.

According to this new science, known as epigenetics, your ancestors’ diet, smoking habits, exposure to pollutants and levels of obesity could be affecting you today. In turn, your lifestyle could affect your children and grandchildren.
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If we drink heavily, take drugs, get fat or wait too long to reproduce, then epigenetics might start tying up some of the wrong genes and loosening the bonds on others. Sometimes those changes will affect sperm and egg cells.

It seems to me this area is still far from having conclusive proof. But it is another great example of scientists seeking to improve our knowledge of how things work.

How Humans Evolved Allergies

Ancient antibody molecule offers clues to how humans evolved allergies

The chicken molecule, an antibody called IgY, looks remarkably similar to the human antibody IgE. IgE is known to be involved in allergic reactions and humans also have a counterpart antibody called IgG that helps to destroy invading viruses and bacteria. Scientists know that both IgE and IgG were present in mammals around 160 million years ago because the corresponding genes are found in the recently published platypus genome. However, in chickens there is no equivalent to IgG and so IgY performs both functions.

Lead researcher, Dr. Rosy Calvert said: “Although these antibodies all started from a common ancestor, for some reason humans have ended up with two rather specialised antibodies, whereas chickens only have one that has a much more general function.
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Professor Brian Sutton, head of the laboratory where the work was done said: “It might be that there was a nasty bug or parasite around at the time that meant that humans needed a really dramatic immune response and so there was pressure to evolve a tight binding antibody like IgE. The problem is that now we’ve ended up with an antibody that can tend to be a little over enthusiastic and causes us problems with apparently innocuous substances like pollen and peanuts, which can cause life-threatening allergic conditions.”

Bacteria Evolutionary Shift Seen in the Lab

Bacteria make major evolutionary shift in the lab

A major evolutionary innovation has unfurled right in front of researchers’ eyes. It’s the first time evolution has been caught in the act of making such a rare and complex new trait. And because the species in question is a bacterium, scientists have been able to replay history to show how this evolutionary novelty grew from the accumulation of unpredictable, chance events.
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sometime around the 31,500th generation, something dramatic happened in just one of the populations – the bacteria suddenly acquired the ability to metabolise citrate, a second nutrient in their culture medium that E. coli normally cannot use. Indeed, the inability to use citrate is one of the traits by which bacteriologists distinguish E. coli from other species.
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The replays showed that even when he looked at trillions of cells, only the original population re-evolved Cit+ – and only when he started the replay from generation 20,000 or greater. Something, he concluded, must have happened around generation 20,000 that laid the groundwork for Cit+ to later evolve.

Lenski and his colleagues are now working to identify just what that earlier change was, and how it made the Cit+ mutation possible more than 10,000 generations later.