Science Magazine

As you age, the style of your skin changes. You start with a tight-fitting sports jacket, and you wind up with something closer to a pair of baggy pajamas. This transition is quite traumatic for many people, as our culture considers it deeply embarrassing for one’s body to betray any sign that it’s a day over 18. If given the choice to look wise and experienced or young and nubile, most of us would choose the baby face every time. Many factors work together to cause midlife wrinkles and the pruniness of old age. As the years tick by, the collagen and elastin fibers in your dermis— those components that make your skin flexible and resilient—begin to break down, loosening their hold on your skin. Unfortunately, there’s not much you can do to intervene. But if you must try, here are a few wrinkleavoiding strategies:

• Choose the right parents. Your genes have the greatest say in deciding how elastic your skin is, and how long it stays relatively smooth and unwrinkled. That’s why some people in their sixties look like they’re in their thirties, much to the chagrin of everyone around them. If you want a quick prediction of how your skin will fare over the next few decades, look at your parents. And if this leaves you too depressed to continue through the rest of this chapter, consider the possibility that you were adopted from a passing circus.

• Don’t use your face. Many of the deeper grooves in your face are usage lines that mark where your skin folds when you scowl, smile, frown, or look utterly confused. To reduce the rate at which these wrinkles form, stop expressing any of these emotions. Or just accept the fact that wrinkles add character to your face.

• Don’t smoke. Cigarette smoke damages skin, causing it to wrinkle prematurely. This probably happens because cigarette smoke reduces blood flow to your skin, starving it of important nutrients. And while quitting the habit may improve your lungs, it won’t repair skin that’s already sagging.

• Limit sun exposure. Ultraviolet light (both UVA and UVB) breaks down the collagen in your skin. This weathering process speeds up aging and increases wrinkles. To prevent sun damage, slap on some sunscreen and follow the good sun habits.

These techniques may slow the rate at which your skin becomes progressively more wrinkled, but what can you do to remove the wrinkles you already have?

There’s certainly no shortage of cosmetic products that promise ageconquering miracles. However, most skin creams do relatively little. On the practical side, they may moisturize your skin (as dry skin looks older) and shield it from sun damage (with sunscreen). The effect of other ingredients is less clear-cut. Although many anti-aging skin creams are packed with anti-inflammatory ingredients, their concentrations are low and there’s little independent research to suggest that they actually do anything. Similarly, vitamins, collagen, antioxidants, and other useful-sounding substances are unlikely ever to reach the lower-level dermis, which is where wrinkling takes place. Some creams contain ingredients that obscure fine wrinkles or scatter light, giving skin a “soft-focus” effect. Whatever the case, these creams can only hide aging rather than make lasting improvements. And lotion lovers beware: Some ingredients can actually aggravate sensitive skin or clog pores, exacerbating acne.

More drastically, cosmetic procedures like chemical peels, laser resurfacing, and microdermabrasion can improve wrinkles by removing excess dead skin in a strategic way. The effect is temporary, usually limited to fine lines rather than deep wrinkles, and may cause redness and peeling. For all but the most wrinkle-averse, it hardly seems worth the trouble. The truth is that if you live in your body for half a century, it will gradually develop the creases of use and abuse. The over-80 crowd will tell you that the relentless march of time leaves the human face with more grooves than a 45-rpm record (but first they’ll have to explain what a 45-rpm record is). The real decision you have to make is not how to fight wrinkles, but whether you want to accept them with dignity or become an increasingly desperate chaser of youth.

A variation of this wrinkle-avoiding technique is Botox injections, which paralyze the face muscles using a highly toxic nerve agent. (It’s the same substance that causes death by paralysis in improperly canned foods.) A Botoxed face temporarily loses some of its ability to move, and a face that can’t move has a hard time furrowing up a decent wrinkle. What you get is a sort of blander, wax museum version of your face. If you prefer being wrinkle-free to being able to move your forehead, Botox just might be your ticket.


Source of Information : Oreilly - Your Body Missing Manual (08-2009)

MICROSCOPES capable of revealing the astonishing beauty of an atom can hardly be called blunt instruments. But to date, these tools have either been too destructive or offered disappointing resolution. Now researchers at IBM have come up with a delicate method which has provided unparalleled details of the structure of a molecule.

The earliest pictures of individual atoms were captured in the 1970S by blasting a target typically a chunk of metal – with a beam of electrons, a technique known as transmission electron microscopy (TEM). Later iterations of this technique, such as the TEAM project at the Lawrence Berkeley National Laboratory in California, achieved resolutions of less than the radius of a hydrogen atom. But while this method works for atoms in a lattice or thin layer, the electron bombardment destroys more fragile individual molecules.

Other techniques use a tiny stylus-like scanning probe. This can be used to measure either the effect of quantum tunnelling of electrons between the probe and the surface of the target, called scanning tunnelling microscopy (STM), or the attractive force between atoms in the probe and the target, called atomic force microscopy (AFM). These methods are suitable for individual molecules but have not been able to approach the detail ofTEM.

Leo Gross and colleagues at IBM in Zurich, Switzerland, modified the AFM technique to make the most detailed image yet of pentacene, an organic molecule consisting of five benzene rings. Although the molecule is highly fragile, the researchers were able to capture the details of the hexagonal carbon rings and deduce the position of the surrounding hydrogen atoms (Science, DOl: 10.1126/science.1176210). The team first fixed a single carbon monoxide molecule to the end of the probe. This allowed them to invoke a quantum mechanical effect called the Pauli exclusion principle, which says that electrons in the same quantum state cannot approach each other too closely. As the electrons around the pentacene and carbon monoxide molecules are in the same state, a repulsive force operated between them. The image was created by bumping the probe over the atoms in the molecule – much in the way we might navigate around in a dark bedroom. The researchers measured the amount of repulsive force the probe encountered at each point, and used this to construct a "force map" of the molecule. The level of detail available depends on the size of the probe : the smaller the tip, the better the picture. The image is " astonishing", says Oscar Custance of Japan's National Institute for Materials Science. In 2007, his team used AFM to distinguish individual atoms on a silicon surface . "This is the highest resolution I have ever seen," he says of the IBM image. The IBM researchers believe their technique may open the door to super-powerful computers made from components built out of precisely positioned atoms and molecules. The work may also provide insights into the actions of catalysts in chemical reactions, potentially allowing researchers to understand what is happening at the atomic level, says Gross. Mac Gregor Campbell.

Source of Information : NewScientist(2009-09-05)

A spineless solution - A better way to find novel antibiotics

NEW antibiotics are always welcome. Natural selection means the existing
ones are in constant danger that pathogens will evolve resistance to them. But
winnowing the few chemicals that have antibiotic effects from the myriad that
might do, but don’t, is tedious. So a technique invented recently by Frederick
Ausubel of Harvard University and his colleagues, which should help to speed
things up, is welcome.

Dr Ausubel’s method, the details of which have just been published in ACS Chemical Biology, employs nematode worms of a species called C. elegans as its sacrificial victims. C. elegans is one of the most intensively studied animals on Earth (it was the first to have its genome read completely). It is a mere millimetre long, and can be mass produced to order, so it is ideal for this sort of work.

Dr Ausubel set out to make an automated system that could infect worms with bacteria, treat them with chemical compounds that might have antibiotic effects, and then record the results. The device he has built starts by laying the worms on a “lawn” of pathogenic bacteria for 15 hours and then mixing them with water to create a sort of worm soup. It then places the infected worms into individual enclosures, using a machine called a particle sorter that is able to drop a precise number of worms (in this case 15) into each of 384 tiny wells arrayed on a single plate. These wells have, in turn, each been preloaded with a different chemical that is being tested for possible antibiotic properties. Once in place, the worms are left alone for five days.

Until now, researchers engaging in this sort of work have had to monitor each wellful of worms by eye (assisted by a microscope) to determine whether the inmates were alive or dead. To avoid this time-consuming process, Dr Ausubel and his team exposed their worms to an orange stain once the five days were over. The stain in question enters dead cells easily, but cannot enter living ones. They were thus able to distinguish the quick from the dead by colour, rather than propensity to wriggle.

Moreover, using a stain in this way meant they could automate the process by attaching a camera to the microscope, taking photographs of all 384 wells, and feeding the images into a computer that had been programmed to measure the area of orange in a well and contrast that with the total area occupied by worms. When they compared this automated mechanism for identifying dead worms with manual methods that depended upon human eyes, they found it was every bit as effective.

So far Dr Ausubel and his colleagues have managed to test around 37,000 compounds using their new method, and they have found 28 that have antibiotic properties. Their most exciting discovery is that some of these substances work in completely different ways from existing antibiotics. That means entirely new types of resistance mechanism would have to evolve in order for bacteria to escape their effects.

Mass screening of this sort is not, itself, a new idea in the search for drugs, but extending it so that it can study effects on entire animals rather than just isolated cells should make it even more productive. And worms, unlike, say, white mice, have few sentimental supporters in the outside world.

Source of Information : The Economist 2009-09-05

It sounds like a cop-out, but the future of schooling may lie with video games SINCE the beginning of mass education, schools have relied on what is known in educational circles as “chalk and talk”. Chalk and blackboard may sometimes be replaced by felt-tip pens and a whiteboard, and electronics in the form of computers may sometimes be bolted on, but the idea of a pedagogue leading his pupils more or less willingly through a day based on periods of study of recognisable academic disciplines, such as mathematics, physics, history, geography and whatever the local language happens to be, has rarely been abandoned.

Abandoning it, though, is what Katie Salen hopes to do. Ms Salen is a games designer and a professor of design and technology at Parsons The New School for Design, in New York. She is also the moving spirit behind Quest to Learn, a new, taxpayer-funded school in that city which is about to open its doors to pupils who will never suffer the indignity of snoring through double French but will, rather, spend their entire days playing games.


Source of Information : The Economist 2009-09-05

Quest to Learn draws on many roots. One is the research of James Gee of the University of Wisconsin. In 2003 Dr Gee published a book called “What Video Games Have to Teach Us About Learning and Literacy”, in which he argued that playing such games helps people develop a sense of identity, grasp meaning, learn to follow commands and even pick role models. Another is the MacArthur Foundation’s digital media and learning initiative, which began in 2006 and which has acted as a test-bed for some of Ms Salen’s ideas about educational-games design. A third is the success of the Bank Street School for Children, an independent primary school in New York that practises what its parent, the nearby Bank Street College of Education, preaches in the way of interdisciplinary teaching methods and the encouragement of pupil collaboration.

Ms Salen is, in effect, seeking to mechanise Bank Street’s methods by transferring much of the pedagogic effort from the teachers themselves (who will now act in an advisory role) to a set of video games that she and her colleagues have devised. Instead of chalk and talk, children learn by doing—and do so in a way that tears up the usual subjectbased curriculum altogether.

Periods of maths, science, history and so on are no more. Quest to Learn’s school day will, rather, be divided into four 90-minute blocks devoted to the study of “domains”. Such domains include Codeworlds (a combination of mathematics and English), Being, Space and Place (English and social studies), The Way Things Work (maths and science) and Sports for the Mind (game design and digital literacy). Each domain concludes with a two-week examination called a “Boss Level”—a common phrase in video-game parlance.


Freeing the helots
In one of the units of Being, Space and Place, for example, pupils take on the role of an ancient Spartan who has to assess Athenian strengths and recommend a course of action. In doing so, they learn bits of history, geography and public policy. In a unit of The Way Things Work, they try to inhabit the minds of scientists devising a pathway for a beam of light to reach a target. This lesson touches on maths, optics—and, the organisers hope, creative thinking and teamwork. Another Way-Things-Work unit asks pupils to imagine they are pyramid-builders in ancient Egypt. This means learning about maths and engineering, and something about the country’s religion and geography.

Whether things will work the way Ms Salen hopes will, itself, take a few years to find out. The school plans to admit pupils at the age of 12 and keep them until they are 18, so the first batch will not leave until 2016. If it fails, traditionalists will no doubt scoff at the idea that teaching through playing games was ever seriously entertained. If it succeeds, though, it will provide a model that could make chalk and talk redundant. And it will have shown that in education, as in other fields of activity, it is not enough just to apply new technologies to existing processes—for maximum effect you have to apply them in new and imaginative ways.

They may simply be getting bad instructions—from you

GENES are acquired at conception and carried to the grave. But the same gene can be expressed differently in different people—or at different times during an individual’s life. The differences are the result of what are known as epigenetic marks, chemicals such as methyl groups that are sometimes attached to a gene to tell it to turn out more of a vital protein, or to stop making that protein altogether.

Many researchers believe epigenetic marks hold the key to understanding, and eventually preventing, a number of diseases—and one whose epigenetic origins they are particularly interested in is type 2, or lateonset, diabetes. Juleen Zierath and her colleagues at the Karolinska Institute in Stockholm, Sweden, are trying to find out how people develop insulin resistance, the underlying cause of type 2 diabetes.

Insulin is a hormone produced by the pancreas. When all is going well, it lets cells know when they need to mop up glucose from the blood, usually just after a person has eaten. If the hormone is absent or is produced in insufficient quantities because of damage to the pancreatic cells that secrete it, the result is classical (or type 1) diabetes. But people with insulin resistance—and thus the late-onset version of the disease—do produce insulin. Their problem is that their glucose-absorbing cells cannot heed its advice. The sugar stays in their bloodstreams, where it damages the vessels, leading to ailments such as heart disease, kidney failure and blindness.

As they report in Cell Metabolism, Dr Zierath and her team decided to look at one of the main consumers of glucose: muscle tissue. They took muscle biopsies from 17 healthy people, 17 people with type 2 diabetes and eight people with early signs of insulin resistance, so-called “pre-diabetics”. They then compared the patterns of the methyl groups attached to the genes of the healthy volunteers with those of the diabetic and pre-diabetic ones.

As it turned out, they found hundreds of genes in which the patterns differed systematically, so to whittle the problem down they concentrated on those involved in the function of the mitochondria. These are the components of a cell that extract energy from glucose and use it to manufacture a chemical called ATP, which is the universal fuel of biological processes. Having fewer or less effective mitochondria causes a drop in demand for glucose, and might thus cause a cell to become insulin resistant.

Even narrowing the question down like this, though, left 44 genes to look at. Of these, Dr Zierath and her team picked one called PGC-1 alpha for further study. This gene is involved in the development of mitochondria, and the extra epigenetic marks the researchers found on it in diabetics and pre-diabetics had the effect of instructing the cells the marked genes were located in to produce fewer and smaller mitochondria than is normal.

The next question was how those marks got there. It is well known that poor diet and lack of exercise make insulin resistance more likely, so one hypothesis is that these things change the epigenetic marks on genes such as PGC-1 alpha. To test that idea, the researchers bathed cells in glucose and fats (chosen as surrogates for bad diet and lack of exercise for obvious reasons) and also in inflammation-producing proteins called cytokines. These proteins, they knew, are produced abundantly in the obese. And obesity, the consequence of bad diet and lack of exercise, is another risk factor for type 2 diabetes. Lo and behold, doses of both fats and cytokines caused PGC-1 alpha to be methylated.

Next, Dr Zierath wanted to know if she could prevent that. So, this time, before bathing the healthy cells in fats or cytokines, the team added a chemical that blocks the activity of DNMT3B, an enzyme which they found methylates PGC-1 alpha. When that was done, no extra methyl groups appeared. These findings have two interesting implications. First, the fact the team was able to stop PGC-1 alpha being methylated suggests that a drug might be developed to do the same. Second, they show that bodily abuse can stretch all the way down to the genetic level. As Dr Zierath puts it, “we are not victims of our genes. If anything, our genes are victims of us.”

Source of Information : The Economist 2009-09-05

The answer to the age-old riddle is biologically obvious

In March 2006, on the occasion of the release of Chicken Little on DVD, Disney convened a panel to put an end to the long-standing riddle: Which came first, the chicken or the egg? The verdict was unanimous. “The first chicken must have differed from its parents by some genetic change [that] caused this bird to be the first ever to fulfill our criteria for truly being a chicken,” said John Brookfield, an evolutionary biologist at the University of Nottingham in England. “Thus the living organism inside the eggshell would have had the same DNA as the chicken that it would develop into, and thus would itself be a member of the species of chicken.” What we recognize as the DNA of a chicken exists first inside an egg. Egg came first. Yet despite the unified front of the three-person panel—David Papineau, a philosopher of science, and Charles Bourns, a chicken farmer, agreed in spirit with Brookfield’s analysis—the question is at best incomplete, at worst misleading. If we take “chicken” to mean a member of Gallus gallus domesticus (a subspecies of junglefowl that evolved in Southeast Asia and has been domesticated for perhaps 10,000 years), we could ask at what point the first member of this species appeared (and whether it was in bird or egg form). Yet speciation is not a process that happens in an instant or in an individual. It takes generations on generations of gradual change for a group of animals to cease interbreeding with another group; only then can we say that speciation has occurred. Viewed in this way, it does not make sense to talk about the first chicken or the first egg. There was only the first group of chickens—some of whom, presumably, were in egg form. And if one relaxes the species qualification, then the race is not even close. Invertebrates as simple as sponges rely on some form of egg for reproduction, which means that eggs probably predate the Cambrian explosion in biodiversity of 530 million years ago. Fish and amphibians lay gelatinous eggs; ancestors of reptiles and birds laid the first shelled eggs 340 million years ago, and that innovation, which allowed their eggs to survive and mature on dry land, enabled the rise of land vertebrates long before the first rooster crowed.

Source of Information : Scientific American September 2009

They long predate the smile

Paleontologists used to wonder whether the first teeth were on the inside or the outside of prehistoric bodies. Sharks are covered in thousands of tiny denticles–toothlike nubs of dentine and collagen that make sharkskin coarse to the touch. If the denticles of some very early vertebrate had migrated into the jaw, grown larger and gained new functions, the speculation went, they could have given rise to modern choppers. But over the past decade fossil and genetic evidence has confirmed that teeth are much older than even the ancient shark lineage—indeed, older than the jaw or the denticle. And they originated inside the body, though not in the mouth.

The first sets of teeth belonged to eel-like swimmers that lived some 525 million years ago and ranged from four to 40 centimeters long. Collectively they are known as conodonts for the ring of long, conical teeth in their pharynx. Some fish species still have a set of vestigial teeth in their throat, but pharyngeal teeth for the most part are believed to have migrated forward into the mouth, perhaps as the jaw was evolving. Supporting that idea, the programmed gene activity that builds teeth differs from the instructions that build a jaw, even though both types of structure grow in tandem. The marriage of tooth and jaw, however, likely gave rise to specialized tooth shapes. By the 10th day of a human embryo’s development, molecular signaling that initiates tooth formation is taking place between two basic embryonic tissue layers. At the same time, signals from the growing jaw imprint a shape onto the primordial tooth that cannot be changed. Even when the bud of a future molar, for instance, is transplanted into a different area of the jaw, the final tooth will become whatever its original location fated it to be. Unfortunately, dental researchers are finding it difficult to recapitulate half a billion years of evolution in the laboratory. Because burgeoning teeth depend on information from the budding embryonic jaw, work toward generating replacement teeth from dental stem cells focuses on growing them in the desired location in the recipient’s mouth–but scientists are not yet sure the adult jaw can provide the necessary signals to shape made-toorder teeth.

Source of Information : Scientific American September 2009

Cheap steel was key to allowing the routine design of parts that rolled against one another

If the utility of an invention were somehow derived from the genius of its inventor, it would be pardonable that so many sources trace the idea for the ball bearing to a 1497 drawing by Leonardo da Vinci. But good ideas, like useful evolutionary traits, tend to emerge more than once, in diverse times and places, and the idea of arranging for parts to roll against one another instead of sliding or slipping is very old indeed. The Egyptians already had the basic idea when they moved great blocks of stone on cylindrical rollers. Similar ideas occurred to the builders of Stonehenge as early as 1800 B.C. and to the craftsmen who constructed the cylindrical-shaped bearings on the wheel hubs of wagons around 100 B.C. (On these wagons the axle turned with the wheels, so the bearings enabled the axle to roll against the wagon chassis.)

The first design for a ball bearing that would support the axle of a carriage did not appear until 1794, in a patent filed by a Welsh ironmaster named Philip Vaughan. Ball bearings between the wheel and the axle enabled the axle to remain fixed to the carriage chassis. But cast iron ball bearings were brittle and tended to crack under stress. It took the invention of the Bessemer process for making inexpensive steel, plus the invention of the bicycle, to fix the ball bearing permanently in the minds of engineers everywhere. Jules-Pierre Suriray, a Parisian bicycle mechanic, patented his steel ball-bearing design in 1869, and in that same year a bicycle outfitted with Suriray’s ball bearings won an international cycling race. The demand for ball bearings—on automobiles, tanks or guidance systems—has pushed manufacturers ever closer to the ideal of shaping a perfect sphere. No turning wheel will survive for long on its axle without ball bearings machined to a tolerance of less than a thousandth, or even a 10-thousandth, of an inch. Many sources claim that the most perfect spheres occur in the bearings of computer hard drives, but in fact that honor goes to the ping pong–size spheres of fused quartz that serve as gyroscopic bearings for the satellite Gravity Probe B. Its gyroscopes are 30 million times more accurate than any other gyroscope ever built.


Source of Information : Scientific American September 2009