This beautiful image of a banded garden spider caught my eye before I realized that this story was about one of my favorite subjects – biomimicry. In this case, researchers are trying to figure out the properties of the glue-like substance that spiders deposit along the rings of silk in their webs that give the web its stickiness.
This is one the many fascinating biomimicry projects in an emerging field of devoted to the study and imitation of nature’s remarkably efficient designs. Scientists around the world are trying to unlock the evolutionary secrets of nature to develop such practical applications as wound healing inspired by flies, vaccines without refrigeration inspired by the resurrection plant, and water-resistant glues inspired by the tenacious adhesive properties of mussels.
It’s well-known that silk is, by weight, stronger than steel. By finding out precisely what makes spider webs so sticky, professor Ali Dhinojwala of the University of Akron, hopes to create more efficient and environment-friendly materials based on natural material, particularly bandages and other “bio-adhesives” that must retain their stickiness when in contact with water. An expert in the surface properties of polymers, Dhinojwala has also helped design synthetic carbon nanotube-based (in other words, glue-less) adhesive tapes inspired by another critter known for its stickiness– geckos. This time he’s investigating the microscopic substance that orb-weaving spiders deposit along the round rings of silk they spin as part of their webs. Those droplets–three times thinner than the diameter of a single hair–capture the flies and other insects that spiders eat. Turns out those drops, composed of highly entangled polymers, are both viscous and elastic. For details and a cool video, click here.
photo credit: Allison Hazen
While leprosy has long been regarded as a rural disease, the reasons why have been little understood. But scientists now think the answer may have to do with the way cities serve as a factor in natural selection: The gene variant that protects against certain diseases like tuberculosis and leprosy—which have been around for thousands of years–is more prevalent in populations with long histories of urban living.
By analyzing DNA samples from 17 different human populations living across Europe, Asia and Africa, and then searching archaeological and historical literature to find the oldest records of the first city or urban settlement in these regions, scientists from University of London and Royal Holloway compared rates of genetic disease resistance with urban history. In a study recently published in the journal Evolution, they showed that past exposure to pathogens led to disease resistance spreading through populations, with our ancestors passing their resistance to their descendents.
“The results show that the protective variant is found in nearly everyone from the Middle East to India and in parts of Europe where cities have been around for thousands of years,” says Mark Thomas, a UCL professor of genetics, evolution and environment, in a press release from the school. “Population density seems to play an important role in shaping so many aspects of our species. It was a vital factor in our species maintaining the complex skills and culture that distinguish us from other primates. It drove many of the genetic differences we see today between different populations from around the world. And now, it seems, it also influenced how infectious diseases spread in the past and how we evolved to resist those diseases”.
His co-author of the study, Ian Barnes, professor of biological sciences at Royal Holloway, called the finding “an elegant example of evolution in action,” saying that “the method we have employed here makes novel use of historical and archaeological data, as a means to explain the distribution and frequency of a genetic variant, and to identify a source of natural selection … It flags up the importance of a very recent aspect of our evolution as a species, the development of cities as a selective force. It could also help to explain some of the differences we observe in disease resistance around the world.”