Sony Cyber-Shot W120 in various colors.

Sony has recently unveiled eight new cameras in its 2008 Cyber-Shot series. The cameras, which include entry level models and more advanced designs, will begin shipping this spring.
One of the unique characteristics of several of the cameras is the new face detection technology. The 8-megapixel Cyber-Shot DSC-H10, for example, can pick out up to eight faces per shot, and strive to make all the faces in focus, according to Physorg.com.
A new feature of the face detection technology is the addition of a child/adult priority mode. When set to child priority, the camera gives priority to focusing children«s faces, while in adult priority mode, it locates and focuses adults« faces.
Sony also has improved the smile shutter feature, which enables the camera to detect multiple smiles, and delay the shot until everyone is smiling. The smile shutter feature can be set to prioritize children or adults, and the new models with the feature will wait to snap a picture when a child in the frame smiles - even if it«s just for a second.
But if you still can«t get everyone to smile at once, that problem can be fixed with some improved editing technology. In playback mode, users can add smiles to people using the camera«s face detection and retouch menu.
Some of the cameras will also include an intelligent scene recognition feature that analyzes the shooting environment and applies the optimal scene mode for the shot. The intelligent scene mode can also improve image quality in low-light or backlit settings by taking a quick second shot after the shutter has been pressed.
Sony will incorporate new image-finding technologies into its cameras and software as well. Some of the cameras will be able to identify images captured with the smile shutter feature, and group those images under “smile“ for easier identification.
The cameras range in price from $150 to $400, and will be demonstrated at Photo Marketing Association (PMA) 2008, which begins January 31 in Las Vegas.

Some cells in the adult pancreas can, in times of extreme stress, produce new insulin-secreting cells, researchers have found.
The findings, based on work performed in mice, open up a new approach to replacing insulin-secreting cells in patients with diabetes.
They also address a raging controversy within the diabetes research community over whether such cells even exist, according to Nature.com.
“It’s a big discovery,“ says Emmanuel Baetge, chief scientific officer of Novocell, a stem cell company based in San Diego, California who was not involved with the work. “I think this will heat up the whole field.“
The blood and heart are known to be supplied with new cells by adult stem cells capable of generating a fresh stock. If such regenerative stem cells existed in the pancreas, they could perhaps be harnessed to restock the supply of pancreatic cells, which in turn produce insulin. This could form the basis of treatment for patients with type 1 diabetes who have fewer cells.
At least, that was the hope. Researchers tried and failed repeatedly to find such cells in the pancreas. “Most people, including me, concluded that the pancreas was very different,“ says Douglas Melton, a Harvard University stem-cell researcher in Cambridge, Massachusetts.
Without regenerative stem cells, there seemed to be only two ways to generate new cells in diabetics: encourage whatever few cells the patient still has to divide; or program embryonic stem cells to produce the needed cell type and inject those into the patient.
Unfortunately, cells are difficult to isolate and grow very slowly in culture, making it difficult to boost their numbers. Embryonic stem cells are easier to grow, but difficult to program. “There, the challenge is how to tell them what to do,“ says Melton. Researchers from Baetge’s group have come close: embryonic stem cells have been coaxed into forming cells1, but these cells were only marginally sensitive to glucose so wouldn’t be able to regulate insulin production in diabetics.

Researchers at The City College of New York (CCNY) and Rice University have developed a low-cost, environmentally friendly technique for embedding antimicrobial silver nanoparticles into vegetable oil-based paints.
The method, to be reported in the March issue (online January 20) of Nature Materials, could give homes and workplaces a new defense against germs by applying a fresh coat of paint, ScienceDaily said.
Silver’s antibacterial properties have been known for thousands of years, and silver nanoparticles offer superior antibacterial activity while being non-toxic. However, coatings containing antimicrobial agents have failed commercially in the past due to their complex, multi-step preparation methods and high cost of production.
The CCNY/Rice team developed a “green chemistry“ approach to synthesize metal nanoparticles in common household paints in situ without using hazardous reagents and solvents. “We extensively worked on poly-unsaturated hydrocarbon chain containing polymers/oils to devise a novel approach to nanoparticle formation“ said Dr. George John, Professor of Chemistry at CCNY and lead author of the article.
Polyunsaturated hydrocarbons undergo auto-oxidation-induced cross-linking, which is similar to lipid peroxidation, the process by which fatty acids are oxidized in biological systems. During this process a variety of chemically active species called ’free radicals’ are generated. These were used by the group as a tool to prepare metal nano-particles in situ in the oil medium.
“The simplicity of the process and economics should allow us to commercialize these paints as a versatile coating material for health and environmental applications“ says Dr. Pulickel M. Ajayan, Professor of Mechanical Engineering and Materials Science at Houston-based Rice University, and co-author.

Jeanne Louise Calment (February 21, 1875 Ð August 4, 1997) was a French woman who reached the longest confirmed lifespan in history at 122 years and 164 days.

A genetically engineered organism that lives 10 times longer than normal has been created by scientists in California. It is the greatest extension of longevity yet achieved by researchers investigating the scientific nature of ageing.
If this work could ever be translated into humans, it would mean that we might one day see people living for 800 years. Valter Longo is one of the small but influential group of specialists in this area who believes that an 800-year life isn’t just possible, it is inevitable. It was his work at the University of Southern California that led to the creation of a strain of yeast fungus that can live for 10 weeks or more, instead of dying at its usual maximum age of just one week, Independent.co.uk reported.
By deleting two genes within the yeast’s genome and putting it on a calorie-restricted diet, Longo was able to extend tenfold the lifespan of the same common yeast cells used by bakers and brewers.
There is, of course, a huge difference between yeast cells and people, but that hasn’t stopped Longo and his colleagues suggesting that the work is directly relevant to human ageing and longevity. There is a general view in this field that there is a maximum human lifespan of not more than about 125 years. Jeanne Calment, the oldest documented person, died at the age of 122 years and 164 days.
The attitude of most mainstream gerontologists towards the idea that people may one day live for many centuries--or even 1,000 years, as one scientific maverick has suggested--is best summed up by Robin Holliday, a distinguished British gerontologist, in his recent book Aging: The Paradox of Life. “How is it possible to make these claims?“ Holliday asks.
“The first requirement is to ignore the huge literature on ageing research... The second is to ignore the enormous amount of information that has been obtained by the study of human age-associated disease; in other words, to ignore the many well-documented textbooks on human pathology. The third is to propose that in the future, stem-cell technology, and other technologies, will allow vulnerable parts of the body to be replaced and/or repaired. The new ’bionic’ man will therefore escape from ageing,“ Holliday says.
An immense hinterland of biomedicine suggests that death at a maximum age of about 125 is inevitable, he says.
But that is precisely what Valter Longo is suggesting with his work on the yeast that can live longer than 10 weeks.
By knocking out two genes, known as RAS2 and SCH9, which promote ageing in yeast and cancer in humans, and putting the microbes on a diet low in calories, Longo achieved the sort of life extension that should in theory be impossible.
Calorie restriction is now a well-established route to extending the lives of many organisms, from yeast and nematode worms to fruit flies and mice.
Biologists believe that restricting calories causes many animals to flip into a state normally reserved for near starvation. Instead of spending their precious energy reserves on reproduction, they shut down everything but their basic body maintenance, in preparation for better times ahead when breeding would stand a better chance of success.
This idea fits in with the more general view that animals tend to follow one of two life strategies--either one of high fecundity and short lifespan, or one of long lifespan and low reproductive capacity.
Why do we age at all? Why don’t we live for ever?
One of the most convincing answers to this is known as the disposable soma theory. In short, the idea is that genes can extend an organism’s lifespan, but only as a trade-off between the costs and benefits of doing so. It is possible to keep on mending the machinery of the body as it suffers daily wear and tear, but there comes a point when it is no longer worthwhile and the costs become too expensive, much like the point when fixing an increasingly decrepit car gets too much.
At this point the body, or ’soma’, becomes disposable. By then, though, from the gene’s point of view, it won’t matter--as long as it has managed to ’escape’ this broken-down body and replicated itself inside the younger, fitter bodies of the next generation.
Longo says that the disposable soma theory, invented by Professor Tom Kirkwood of Newcastle University in the late 1970s, is one of the strongest ideas around to explain the nature of ageing.

Two enzymes, contribute individually to the ripening-related breakdown of the cell walls.

Using tomatoes as a research plant, scientists at the University of California, Davis, have discovered that two plant enzymes that occur in the plant’s cell walls cooperate with each other to make ripe fruit more susceptible to a disease-causing fungus.
“Identifying the role that these cell-wall enzymes play in making the harvested fruit more vulnerable to disease is important for designing strategies for limiting fruit losses to disease during storage, handling and distribution,“ said Ann Powell, a plant scientist who led the research team on this project, ScienceDaily wrote.
One of the hallmarks of plant cells is their tough exterior cell wall. As the fruit ripens, the cell walls break down, and the fruit becomes softer and more flavorful. At the same time, the fruit also becomes more susceptible to diseases caused by fungi and bacteria.
Researchers have known for some time that two enzymes, known as polygalacturonase and expansin, contribute individually to the ripening-related breakdown of the cell walls. (Enzymes are proteins that trigger and control chemical reactions.) The UC Davis research team wondered if these two cell wall enzymes might also be responsible for the increased disease-susceptibility of ripening fruit. These diseases are responsible for substantial losses of high-quality harvested fruit during storage, shipping, marketing and consumer handling.
To test this notion, they selected two genetically modified tomato plant varieties. One of the varieties had been altered so that it did not produce polygalacturonase, and the other did not produce expansin. Powell had crossed these two varieties, resulting in a variety that produced neither of these enzymes.
The researchers, including plant biology graduate student Dario Cantu and postdoctoral fellow Ariel Vicente, inoculated tomatoes from each of the genetically modified varieties, as well as the variety resulting from the cross, with Botrytis cinerea, a common fungus that causes rotting on many fruits and vegetables. Tomatoes from a control group, whose enzyme production had not been altered, were also inoculated with the fungus.
The research team found that tomatoes from the plants that were genetically modified to suppress production of only one of the cell-wall enzymes were not any less susceptible to the fungus. However, when both of the enzymes were lacking in the crossed variety, the cell walls of the fruit did not readily break down, and the fruit was dramatically less susceptible to infection by the Botrytis cinerea fungus.