Why Getting Distracted Isn't a Bad Thing

Alexander Graham Bell was never a fan of multitasking. He felt that true creativity comes from a single-minded concentration on the issue under consideration and that any other thoughts would only take you further away from your goal.

 

Psychological research, until recently, seemed to agree with him, showing that we’re more efficient and accurate when we keep our minds firmly on track. However, a couple of eye-catching new studies have called this assumption into question, at least when it comes to the kind of creative tasks that were so close to Bell’s heart. When you’re trying to come up with new ideas, a sharp focus might actually backfire and a distraction of some sort could actually increase your chances of finding a novel solution to your problem.

  This is because our minds often become stuck in a rut, meaning that we spend far too much time concentrating on the first ideas we thought of, rather than coming up with some truly novel solutions. This phenomenon is known as cognitive fixation, and many psychologists now consider it to be the principle barrier to true creativity.

 

To find out whether multitasking can actually help people break out of a rut, a team of researchers used a common laboratory test of creativity. The participants in this study had to think of as many uses as possible for a common object, such as a kitchen bowl, within a fixed amount of time.

The participants then had to find alternative uses for a brick and a toothpick. The only difference was that some were asked to do so in blocks, listing all the uses for a brick first before listing all the uses of a toothpick, while others were asked to alternate between the two.

According to Bell’s opinion that immersed concentration is better for creativity, you’d expect that the first group would have performed better, but this wasn’t the case. While they might have believed that they were on a roll, the reality was that without the breaks afforded by the continual task switching, their progress was limited.

From the sheer number of ideas that they produced to the perceived novelty of their ideas, the multitaskers performed much better.
For more evidence, the team next looked at a test of convergent thinking, in which you’re given three words and you have to think of a common linking word. This test is meant to measure your ability to find the associations between apparently unconnected concepts, and unlike the previous task, you’re looking for a single answer that comes in a single flash of insight.

Once again, some of the participants were asked to consider two problems simultaneously, by switching their attention between the two, while others were asked to look at them in sequence. The end results were even more striking than the team’s first experiment, with 51% of the multi-taskers solving both problems compared to just 14% who looked at them sequentially.  

 

Perhaps the biggest benefits can be found in group brainstorms – something that we’ve all been involved in at one time or another – which often involve a lot of talking and not much innovation.

The problem is that besides facing the cognitive fixation of each individual member, the group as a whole becomes distracted by one person’s idea rather than considering the ideas of others. This means that teams working together often produce fewer ideas that individuals who are working independently. “There are a lot of findings showing that working as a group is not very efficient, and even a tiny improvement would have a big impact,” says another researcher.

By working with colleagues, the researcher has shown that forcing groups of students to multitask (by switching between two problems) can break those dynamics, leading to more creative solutions to questions about the ways to improve the campus, including potential ideas to increase the students’ physical activity or measures to increase access for disabled people. Importantly, the benefits seemed to grow over time, so the longer the brainstorming was, the more advantageous it was to switch between tasks.

It doesn’t need too much thinking to see how you might put these findings to immediate use. If you’re struggling to think of a title for your project or the name of a new product, you might have been tempted to devoting a fixed amount of time to thinking about it. However, this research would suggest that you’d be better off keeping a notepad next to your computer and jotting down new solutions while working on other tasks.

At its simplest, this research might just be another excuse to take a much-needed break. When you’re working on tasks that would benefit from creative thinking, take regular breaks to refresh your approach.

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A New Way to Fight Against Cavities

Most of us brush at least once a day, many do it after each meal, floss daily, but then still end with cavities ! One of the worst thing is to sit on the dental chair, with all the drilling, which gives you not just headache, but jaw pain due to opening your jaws wide for long. Above all the dentist charges are at times equal to a minor surgery ! Quite often dentists makes sure that they take the fees in advance, so you've to keep going to them as and when you're told ! You pay for the transport/ fuel and above waste couple of hours commuting, waiting and the pain to add to your woes. Now when you read about the new possible treatment to overcome all those dreadful days of visiting the dentist, you'll be amazed !

The best defense against cavities might not be your own attentiveness, much less those fillings, sealants, or fluoride treatments. In fact, what could work better is warm, moist, and a bit slimy. That's correct, mucus.

Mucus, along with tears and skin, makes up our first line of defense against disease. They all form a barrier against invading germs. And, as it turns out, according to a study published recently in the "Applied and Environmental Microbiology" journal, the crucial proteins found in mucus known as salivary mucins can protect our teeth from cavity causing bacteria known as Streptococcus mutans. Unlike toothpaste and mouthwash, which destroy bacteria, mucins prevent bacteria from attaching themselves onto your teeth and secreting acid that bores holes through the enamel. Now,the researchers who led the study are trying to engineer synthetic mucus that could be added to toothpaste or bubble gum. Sounds lovely doesn't it?

As disgusting as this sounds, synthetic mucus might go well beyond just preventing cavities. Studies have suggested that mucins might also be able to defend against respiratory infections, stomach ulcers, and even HIV. Since mucins do not actually kill bacteria (they merely prevent bacteria from causing damage), they are seen by some as a much better alternative to antibiotics, which may kill not only harmful bacteria, but helpful bacteria as well, allowing more dangerous strains to take their place. This means that synthetic mucin might offer a less intrusive alternative, used "not necessarily to resolve infections but to stabilize or prevent infections," says Katharina Ribbeck, an assistant professor in the department of biological engineering at MIT, who co-authored this study alongside Erica Shapiro Frenkel, a Ph.D student in her lab. 


We get cavities when bacteria such as S. mutans cling to our teeth, forming an intricate, mesh-like arrangement known as biofilm. The bacteria that make up this biofilm feed on the sugars found in the food we eat to produce acid that can then dissolve the tooth enamel. To investigate how much mucus might be needed to guard against this process, Ribbeck's group got down to the molecular level and homed in on a mucin known as MUC5B. This is the most commonly found mucin in the mouth.

 First, the researchers isolated MUC5B from saliva samples of some volunteers. Then, they grew S. mutans bacteria with sugar and a special broth in plates containing wells that were made from a plastic which imitates a tooth's enamel. Some of the wells also contained MUC5B. At the end of the experiment, Ribbeck and Frenkel counted the number of attached S. mutans bacteria at several points in time and found more of them floating in the growth broth than attached to the plastic in the wells containing MUC5B. This suggests that the mucin somehow prevents S. mutans from sticking to the surface of the tooth.

How, exactly? The researcher aren't sure, but, according to Ribbeck, it's possible that MUC5B encases S. mutans in a "3-D spiderweb" that traps the acid that they secrete. MUC5B might even form a bacteria-repellent coating over the tooth's surface, or even turn off S. mutans genes that are involved in attachment and biofilm formation. Ribbeck and Frenkel are still trying to find the most likely mechanism, though they suspect that mucins might maintain bacterial diversity in the mouth by not only keeping S. mutans alive, but by also neutralizing the toxins that different bacterial strains release to outdo each other.


Of course, scientists still need to confirm the protective role of mucins before investigating the mechanisms involved. William Bowen, a professor at the University of Rochester's School of Medicine and Dentistry, also points out that cavity-causing bacteria embed themselves in plaque - not directly to the surface of the tooth. And many other bacteria in the mouth cause cavities, not just S. mutans, which is not a "major acid producer."

 Still, having said that, Ribbeck and Frenkel have reported similar results with other surfaces, hinting at "a more general mechanism" of MUC5B. Translation? Benefits of synthetic mucus could extend far beyond human health, and could be used to prevent food spoilage, and the accumulation of bacteria on ship hulls and other surfaces, for example. "The applications are enormous," Ribbeck declared.

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Suppressing protein may stem Alzheimer's disease process

Scientists  have discovered a potential strategy for developing treatments to stem the disease process in Alzheimer's disease. It’s based on unclogging removal of toxic debris that accumulates in patients’ brains, by blocking activity of a little-known regulator protein called CD33.

Too much CD33 appears to promote late-onset Alzheimer's by preventing support cells from clearing out toxic plaques, key risk factors for the disease . Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.

Variation in the CD33 gene turned up as one of four prime suspects in the largest genome-wide dragnet of Alzheimer's affected families. The gene was known to make a protein that regulates the immune system, but its function in the brain remained elusive. To discover how it might contribute to Alzheimer's  the researchers brought to bear human genetics, biochemistry and human brain tissue, mouse and cell-based experiments.

They found over-expression of CD33 in support cells, called microglia, in post-mortem brains from patients who had late-onset Alzheimer's disease, the most common form of the illness. The more CD33 protein on the cell surface of microglia, the more beta-amyloid proteins and plaques — damaging debris — had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from Alzheimer's conspicuously showed reduced amounts of CD33 on the surface of microglia and less beta-amyloid.

Brain levels of beta-amyloid and plaques were also markedly reduced in mice engineered to under-express or lack CD33. Microglia cells in these animals were more efficient at clearing out the debris, which the researchers traced to levels of CD33 on the cell surface.

Evidence also suggested that CD33 works in league with another Alzheimer's risk gene in microglia to regulate inflammation in the brain.

The study results — and those of a recent rat study that replicated many features of the human illness — add support to the prevailing theory that accumulation of beta-amyloid plaques are hallmarks of Alzheimer's pathology. They come at a time of ferment in the field, spurred by other recent contradictory evidence  suggesting that these presumed culprits might instead play a protective role.

Since increased CD33 activity in microglia impaired beta-amyloid clearance in late onset Alzheimer’s, researchers are now searching for agents that can cross the blood-brain barrier and block it.

Activity of a regulator protein called CD33 (green) clogs removal of brain-damaging debris, beta-amyloid protein (red), by support cells, microglia. Left: Microglia of normal control mice (A”) show more CD33 and less beta-amyloid than mice in which CD33 expression is experimentally knocked-out (B”). Right: Little beta-amyloid can be seen in microglia of a mouse line in which CD33 is over-expressed (C”), compared to microglia of mice in which CD33 is experimentally inactivated (D”). Evidence from post-mortem human brains indicates that CD33 is similarly overactive in Alzheimer’s disease, suggesting that a treatment that impedes it might help treat or prevent the disease. Source:Rudolph Tanzi, Ph.D. , of Massachusetts General Hospital and Harvard University