Communicating Science Course 2012 Blogs

Deaf No More? Fixing the Pipes

By: Steven DeGroot

Recently, Akil and other scientists restored hearing to mice born with a genetic defect, which had rendered them completely deaf from birth. This improvement in hearing allowed the mice to distinguish a range of pure tones (discrete, single frequencies) at close to the same level as a normal mouse. While this may be great news for mice, what does it mean to us humans? Do we now have a treatment that restores hearing in humans? Well not quite, there are a few bugs to resolve before this treatment is ready for us. However, it is a large step in the correct direction.

Our ears pick up sound through a series of cells called “inner hair cells”, so named because they send up tiny hairs inside your inner ear. These hair cells work similar to a flushing toilet. When sound vibrates your ear, it exerts force on the hairs, as your hand would turn the handle on a toilet. This results in the movement of the plunger like structure on the surface of the cell and a flush of charged particles into the inner hair cells. This flush transmits the sound information down the bend and into our brains. The majority of hearing loss is due to damage to these inner hair cells. According to the scientists’ article in Neuron, their method is specific to inner hair cells; meaning they can now fix your toilet without risks of breaking your kitchen sink. Their method uses a form of virus, which inserts new genes into cells without changing the DNA already present. These genes also contain little pieces of DNA called regulatory elements, which are able to regulate the off or on state of the inserted gene. The new method that avoids extra damage to surrounding cells targets inner hair cells through these regulatory elements, which only allow the gene to turn on in inner hair cells. Avoiding extra damage is always important.

While selectivity is an important advancement, their technique still has a while to go before completion. For example, the current version of the technique only fixes the single genetic defect in a gene called VGLUT3. VGLUT3 is one of the genes responsible for maintaining the inner hair cell’s ability to connect to your brain. In our toilet analogy, VGLUT3 is like the plumbing’s final connection to the sewer. As you might expect, when VGLUT3 is not the problem this treatment will not be effective. This caveat is not as significant as it may first seem because with a little manipulation researchers could adapt the regulatory elements to other genes that could in turn fix or prevent other forms of hearing deficiencies. As long as there is a broken toilet, this method could potentially fix it. Unfortunately, for many of those already deaf or losing their hearing many of their inner hair cells die. This method cannot improve these patients’ hearing because genes of nonexistent cells are unchangeable. It is feasible that adaptations of this treatment could prevent future hearing loss in families prone to hearing loss.

There is one more bug in this treatment; the treatments’ effect is not permanent because it does not actually change the cells’ DNA. Mice under this treatment had their hearing restored for seven weeks to one and a half years in one of twenty cases. The nature of the treatment requires that the solution must arrive at the inner ear behind the delicate eardrum, making repetitive treatment risky and undesirable. If ways to increase the effective time of the treatment exist, this technique would become much more desirable. The authors tell us that the theoretical effective time of their treatment should be one year. They suggest that there are mechanisms in play that lower the effectiveness and further study could lead to prolonged effectiveness.

You might wonder why they do not make the treatment permanently modify the inner hair cell’s DNA. While, it is possible and relatively simple to change the treatment to permanently modify DNA by changing the method of delivery to deliver through a retrovirus, this could be dangerous. Retroviruses are a type of virus that randomly inserts its genes directly into the human genome. As you might expect, modifying the human genome in such a way could cause serious problems. Retroviruses used in the few human trials attempted caused a high incidence of cancer. This is why the method of the current study is so appealing. With further study and modifications, this method may become a viable treatment or preventative measure for hearing loss.

Scientific research is advancing steadily towards new treatment options, and it is likely the current study will help pave the way for a treatment capable of eliminating deafness in humans. This system capable of restoring the function of VGlut in mice is one step in the process of developing such a treatment.

Reference:
1. Akil, O. et al. Restoration of Hearing in the VGLUT3 Knockout Mouse Using Virally Mediated Gene Therapy. Neuron 75, 283–93 (2012).

 

Alcohol: a substitute for sex?

By: Shubham Dutta

My dad always said, “Alcohol is the cause to many life’s problems” and probably we all know why. It is no secret that alcohol consumption causes major health problems, including liver damage, anemia, cardiovascular disease and injuries sustained in automobile accidents. Alcohol has been prescribed as the most widely abused drug of all times and has destroyed the lives of millions. This is a bad news for drinkers, right? Wrong! While it has ill-effects on person’s behaviors, abilities, and emotions, a group of researchers have scientifically proven the “healing effect” of alcohol.

Scientists at the University of California, San Francisco have shown that when fruit fly (Drosophila) males are deprived of mating they choose to consume more alcohol than their happily-mated peers. Interestingly, they also discovered that sex and alcohol consumption stimulate the same neural pathways in their brains.

Drosophila, like other flies have elaborate courtship behavior. The males usually sing a courtship song using wing vibrations and caress the female in order to woo her; when she is impressed, they mate. But, when the female has already mated, however hard the male tries to be romantic with her, she will not succumb. Scientists exploited this obstinate conduct of females to study whether rejection alters drinking behavior in males.

Drosophila has been utilized to model human brain. Like humans, they have complex addiction-like behavior. “Alcohol is one of the most widely used and abused drugs in the world,” explains lead author Galit Shohat-Ophir. “The fruit fly Drosophila melanogaster is an ideal model organism to study how the social environment modulates behavior.” Researchers paired males with three kinds of females: a) unmated females which will willingly mate, b) mated females not willing to mate and, c) headless or decapitated females.

The males that were sexually satisfied drank significantly less amount of ethanol than their unsatisfied peers. The ones that were paired with decapitated females drank more ethanol than the satisfied males. This observation suggests that it’s not social rejection but rather abstinence from sex that triggered this yearning towards ethanol. It is also surprising to know that even when an unsatisfied male gets to spend some time with a willing female, his craving for ethanol decreased.

The question now arises: why sexually unsatisfied males preferred ethanol spiked food than satisfied males? In order to unravel the underlying mystery, scientist looked at fly brains. Brain cells or neurons talk and relay messages to each other using substances called neurotransmitters. Past scientific studies connected a neurotransmitter called neuropeptide F (NPF) is to ethanol related behavior in flies. The human counter part of NPF is neuropeptide Y (NPY) which again has been shown to be linked to ethanol.

Researchers demonstrated that sexual frustration lead to an immediate drop in the levels of NPF, while sex increased it. When they used genetics to artificially remove NPF in the satisfied flies, they drank as much as their “not-so-satisfied” friends. Likewise, when the researchers artificially increased NPF, flies stayed moderate. For the first time, it was demonstrated that NPF levels associate sexual activity to drinking. Clearly, NPF levels controlled the flies’ desire to drink, so the team further explored how NPF works in the fly’s brain.
When NPF was artificially increased in the absence of sex or ethanol, flies were happy. Consistent with this observation, constantly activating NPF led to less addiction to alcohol in flies thus confirming the hypothesis.

Humans, including all animals, have a neurological system which strengthens moral behavior. Using it, we all assign pleasure or optimistic feelings to certain things we do that are essential for species survival, including sex, eating, and social interaction. Certain drugs stimulate pleasure, leading to addiction. Research has shown that, like humans, flies find intoxication rewarding. This has led to the hypothesis that NPF may play a role in this system.

While this is a novel discovery in flies, the mammalian version of NPF, called the NPY, which is linked to alcohol addiction, has not been tested yet. This is due to lack of animal models. Scientists now believe that NPY may have a similar effect in humans. Trauma or unfavorable experiences often lead to depression and drug abuse. Activation of the NPY using drugs can reverse these detrimental effects and help humans recover from trauma. This will make our lives happier.

 

How Superbugs Evade Your Body’s Police Force

By: Nathaniel Erskine

Superbugs scare doctors. They are a set of bacteria that commonly infect patients during hospitals stay. These organisms possess resistance to most antibiotics, making treatment difficult. They have the disconcerting ability to acquire additional genes that may make them resistant to all medicines. Researchers study the molecules that superbugs produce, hoping to find new ways to treat sick patients should antibiotics be completely ineffective.

A team of researchers from universities in the Netherlands, Scotland and Iowa found a key mechanism by which the superbug Staphylococcus aureus (nicknamed Staph can evade the immune system and infect a patient. Staph possesses an arsenal of toxins and proteins, with unknown functions. Dr. Suzan Rooijakkers of the University Medical Center of Utrecht, led this group to discover how one of these bacterial weapons, a protein known as Staphopain A, neutralizes the body’s defenses.

We have special blood cells, known as neutrophils that quickly attack invading bacteria. Neutrophils behave as policemen that spread out and patrol the body. When bacteria invade, cells in the infected area release signals called cytokines, similar to the way in which a watchman radios the police for help upon spotting burglars. These cytokines bind to the neutrophils through a special protein known as a CXC receptor. The receptor behaves like the radio set in the police car. The cytokines “activate the radio,” causing the cellular policemen to move to the source of infection. Once the neutrophils arrive at the “crime scene,” they will kill the bacteria or keep it occupied long enough for the heavier artillery of the immune system to arrive.

Dr. Rooijakkers and her colleagues found that the Staph protein Staphopain A breaks the CXC receptor that neutrophils have for an important cytokine. This is akin to having someone clip the radio antenna on a police car. Without a functional CXC receptor, the neutrophils cannot “hear” the cry for backup and will carry on patrolling the body while the crime occurs. In other words, the Staphopain A provides Staph with stealth against the immune system.

Prior studies identified Staphopain A as a protease, or protein scissors that will snip protein chains. Dr. Rooijakkers and her associate had to first determine what those scissor cut. They bathed neutrophils in a solution of Staphopain A to allow the protein to clip away at the neutrophils. Afterwards, they covered the neutrophils with different antibodies that act as a kind of tag that tells the scientists what kinds of proteins reside on the surface of the neutrophil. They found that antibodies that bind only to the CXC receptor would not bind to the neutrophils treated with the Staphopain scissors. They thus confirmed that Staphopain A cleaves CXC receptor.

Next, the scientists had to prove that having Staphopain A cleave the CXC receptor on neutrophils would prevent the neutrophils from coming to the site of infection. To stimulate the conditions in a body, they divided a small bowl in half with a fine mesh. On one side of the mesh, the researchers added neutrophils, while on the other side they added the cytokines CXCL1 and CXCL7, the alert signals that normally attract neutrophils. Normally the neutrophils would migrate towards the cytokines and would pass through the meshwork. The scientists could use special light instruments to witness this migration of neutrophils. When treated with Staphopain A, the neutrophils were 50 to 70% less likely to cross the mesh towards cytokines. They therefore possessed strong evidence that Staph could use its molecular scissors to prevent the neutrophils from bothering it.

These experiments highlight one of the many clever ways that bacteria have devised to be able to protect themselves from our immune system. Over the coming years scientists hope to discover even more tricks that bacteria employ to override our defenses in order to infect our bodies with minimal disturbances.

The authors suggest that Staphopain A may become an important target for new drugs should Staph become resistant to all antibiotics. Chemists could develop a drug that prevents Staphopain A from destroying the neutrophil’s cytokine receptor. Instead of ignoring the pleas for help against the Staph, the neutrophils could respond and arrive to the site of infection and could help fight the Staph. The police could save the day and protect a patient’s life.

Reference
Laarman et al. Staphylococcus aureus Staphopain A inhibits CXCR2-dependent neutrophil activation and chemotaxis. EMBO; 2012, 1-12.

One Man’s Trash: The Unexpected Function of the same Amyloids Responsible for Alzheimer’s

By: Kingsley Essien

When scientists and physicians want to treat a disease, they focus on what’s causing the problem; they attack the root of the issue. This approach makes sense but it’s a lot easier to say than do especially when it isn’t crystal clear what the root of the issue is. This is the case when it comes to Alzheimer’s disease.

Alzheimer’s disease is a debilitating form of dementia that affects millions of people worldwide. [1] Currently there is no cure for the disease which progressively worsens robbing those affected of their long term memory, their ability to communicate, reason and essentially function. [1] The progression of the disease is different for each individual but unfortunately the outcome is always the same, death.

To date Alzheimer’s disease is an illness shrouded in mystery. Researchers and physicians alike are unsure of what causes the disease or the rapid deterioration of neurons characteristic of the disease. This makes managing the symptoms of disease and finding a cure difficult if not impossible.

After examining the brains of those afflicted with Alzheimer’s researchers and physicians noticed an abundance of amyloid plaques deposited in the spaces surrounding neurons. [1] These plaques are accumulations of small fiber like tangles called amyloid beta proteins. [1] Proteins are molecules that serve diverse functions throughout the body. They act as building blocks, processors and even messengers depending on the circumstances. Amyloid beta proteins can accumulate on top of each other, a snow ball effect if you will, and many believe that it is the accumulation of these small protein tangles that causes the progression of Alzheimer’s disease. [1] While it is unknown exactly how beta amyloid accumulation is responsible for disease progression, experts think that these amyloid deposits interfere with the normal functions of neurons and eventually cause their death. [1]

Previously experts believed that the amyloid plaques like those identified in Alzheimer’s patients served no function. They were regarded as little more than troublesome clutter. However a collaborative effort by a group of researchers has shown that amyloid fibers can transmit signals and this finding can reshape the way researchers and physicians approach treatment of the disease. [2]

The body is composed of a number of diverse microscopic entities called cells. These different types of cells come together to make different organs and tissues and work together to ensure that the body functions normally. When the body encounters stress, like injury or infection by a virus or bacteria, it may make the decision to kill certain cells in order to ensure that the remaining un-afflicted cells can grow and function properly. This is called programmed cell death and the body can accomplish this in a number of ways. One way the body can accomplish programmed cell death is through a process called necrosis. Necrosis is essentially a process where a cell receives and propagates signals that result in the rupture and death of the cell.

Cells send signals that initiate necrosis through a messenger complex composed of two proteins named RIP1 and RIP3. This complex, referred to as the necrosome, is formed when the RIP1 and RIP3 attach to each other inside a cell. After RIP1 and RIP3 attach to form the necrosome, the necrosome can signal the cell to undergo necrosis and die. [2] Recently work done by Jixi Li and a group of collaborating scientists in “The RIP1/RIP3 Necrosome Forms a Functional Amyloid Signaling Complex Required for Programmed Necrosis”, has shown that the necrosome signaling complex is an amyloid fiber similar to those seen in patients suffering from Alzheimer’s disease.

Researchers first noticed that RIP1 and RIP3 complexes isolated were much larger than expected. Proteins exist in a number of different 3D shapes, and are made of 21 different types of building blocks called amino acids. The shape that a protein folds into depends on the specific arrangement of the amino acids. The amino acid sequence of many proteins are known and stored on computer data bases. Li et al took the amino acid sequences for RIP1 and RIP3 and ran them through computer programs that use the arrangement of amino acids to predict the 3D shape of the protein. The result of the simulation suggested that RIP1 and RIP3 can form the same shape seen in amyloids thus encouraging Li et al to investigate whether or not the necrosome is an amyloid fiber.

Li and colleagues then performed a number of experiments that confirmed that the necrosome had amyloid characteristics. They used high powered microscopes to visualize the complex and saw that the necrosome appeared similar to amyloids. They also showed that the necrosome binds to dyes that have been previously shown to interact only with amyloids, further suggesting that the necrosome is amyloidal in nature.

The results from this study demonstrate that amyloid deposits can be more than just clutter. The necrosome while an amyloid fibril is a functional signaling complex that can signal the cell to undergo necrosis. Could this new information impact the way we look at treatments for Alzheimer’s disease? Could all amyloid fibrils have the ability to send signals? It is unknown how amyloid plaques contribute to disease progression but could the amyloid fibrils found in the brains of Alzheimer’s patients also send signals to cells or function in some other way? The answers to these questions remain to be seen but the fact that amyloid fibers have been shown to have a function could revolutionizes the way we approach Alzheimer’s research. Plaques seem to play a role in the progression of the disease and new knowledge about how they work or what they do, could be used to make the lives of thousands of suffers a little bit better.

References
1. Cummings, Jeffrey L., M.D. "Alzheimer's Disease." The New England Journal of Medicine 351 (2004): 56-67. Web.
2. The RIP1/RIP3 Necrosome Forms a Functional Amyloid Signaling Complex Required for Programmed Necrosis Jixi Li et al. Cell 3 August, 2012: 150, 443 – 662


Sonic Hedgehog: The Dr. Jekyll and Mr. Hyde of Pancreatic Cancer

By: Leticia Fridman

In 2009, popular film actor Patrick Swayze and NBA coach Chuck Daly both succumbed to pancreatic cancer, the fourth leading cause of cancer-related deaths in the United States. Currently, there is no effective treatment to prolong life for people who develop this devastating disease because of difficulties in diagnosis. Symptoms of pancreatic cancer are often ambiguous, and by the time of diagnosis, the cancer already spread, or metastasized, from the pancreas to the liver, creating another obstacle for treatment.

In recent years, researchers discovered that a protein called Sonic Hedgehog (Shh) and its less studied colleagues, Indian and Desert Hedgehogs, are implicated in the majority of pancreatic cancers. As one would image, Hedgehog proteins are named after their shape similarity to the 90s cartoon character; however, unlike the protagonist of the cartoon series, Hedgehog proteins act as antagonists in the context of cancer. The presence of hedgehog proteins floating around in mature cells of the pancreas marks early pre-cancer lesions called PanINs. Like the cartoon character however, Shh acts quickly, contributing to the rapid increase in cell proliferation and resistance to apoptosis, a process where the cell commits suicide that is vital for the destruction of tumor cells. It is also important to mention that Shh is not always Mr. Hyde, for example, in early development of the mouse embryo, Shh acts more like Dr. Jekyll, assuring proper development of the face and limbs. Mutations in the Shh protein in humans are usually lethal and cause severe facial and cranial developmental defects such as cyclopia, or the condition where only one eye forms in the center of the face.

Independent of either cancer or developmental contexts, the presence of Shh in the cell triggers a cascade of events to occur much like knocking down the first piece in a row of upright dominoes. The first domino is knocked down when Shh is present, which causes the next domino, a protein called Patched, to release another protein called Smoothened, the third domino of the series. The release of Smoothened allows the activation of survival and proliferation enhancing proteins downstream of Smoothened. Conversely, in the absence of Shh, the domino pieces continue to stand upright undisturbed. Patched holds on to Smoothened, prohibiting the cell from activating the synthesis of proteins that aid survival and proliferation.

Identifying small molecules that target the Smoothened protein and inhibit its function may be useful for pancreatic cancer therapy. A recent study by Singh et al, reports that a small molecule named GDC-0449 blocks Smoothened and induces apoptosis in a human pancreatic cancer cells. Higher dosages of GDC-0449 also blocked synthesis of proteins involved in survival and proliferation of cancer cells. Surprisingly, the study also uncovers that both genes Gli1 and Gli2, which are downstream of Smoothened in the Shh cascade, are crucial for blocking proliferation and inducing apoptosis following GDC-0449 treatment in cancer cells.

The study shows that blocking Smoothened may be an effective treatment for pancreatic cancer due to the shutting off of the Shh signaling pathway in human cancer cells. The observed increase in apoptosis induction following GDC-0449 administration is desirable so that out of control proliferation of cells does not occur. Uncontrolled proliferation of cells leads to tumor formation and rapid progression of the disease. Moreover, a decrease in cell survival, triggered by an increase in apoptosis can bring tumor formation to a screeching halt.

Tumor cells attempt to mimic Darwin’s survival of the fittest by out-competing other cells in the organism in order to increase in number and survive; however, this behavior leads to the demise of the organism as a whole and ultimately to the death of the tumor cells themselves, which is one of the biggest Shakespearean-style ironies occurring in nature. Unlike other cancers, patients diagnosed with pancreatic cancer usually have a few months left to live. Characterizing the effects of a new molecule that targets Smoothened and stops downstream effects of Shh signaling is an exciting and promising new road to therapy that gives patients a ray of hope.

Reference:
Singh BN, J Fu, RK Srivastava, and S Shankar. 2011. "Hedgehog signaling antagonist GDC-0449 (Vismodegib) inhibits pancreatic cancer stem cell characteristics: molecular mechanisms". PloS One. 6 (11).

 

Goodbye Insulin Injections, Hello Stem Cells

By: Ryan Genga

Stem cells are changing the face of medicine and becoming a cornerstone in biomedical research because of their ability to become any cell type of the body. This unique ability allows researchers to coax stem cells into becoming different cell types of interest on the bench-top. Stem cells open up the possibility of regenerative medicine, a field of research focused on the generation of new tissues and organs for transplant and potentially for the treatment of disease. Despite this potential, the ethical issues of isolating embryonic stem cells have led to scrutiny. To circumvent this scrutiny, groups have recently transformed adult cell types into induced pluripotent stem (iPS) cells, cells that have the ability to act like embryonic stem cells. Researchers use viruses to supply stem cell-specific factors to adult skin and blood cells to reprogram the cells into iPS cells. Following defined protocols, groups transform the reprogrammed iPS cells into various cell types of the body. Furthermore, iPS cells have the same genetic profile as their initial adult cells, potentially allowing for patient-specific organ generation which will reduce the risk of rejection after transplantation.

Type 1 diabetes (T1D) is a genetic disorder characterized by the body’s attack on its own beta cells, the insulin producing cells of the pancreas. Insulin regulates a person’s blood sugar and the destruction of beta cells results in the inability to produce enough insulin to properly regulate blood sugar levels in the body. Currently T1D patients receive insulin injections directly into the bloodstream as their main treatment option; however, insulin injection can be painful and dangerous if unmanaged. Recently, groups have coerced both embryonic stem cells and iPS cells into becoming beta cells by supplying these cells with necessary factors in a step-wise manner to induce development. They have shown that these iPS cell-derived beta cells actually respond to glucose, the main sugar we ingest while eating. In response to glucose, the iPS cell-derived beta cells release insulin. This response directly reflects the reaction of natural beta cells to insulin, which opens up the possibility of utilizing iPS cell-derived beta cells in regenerative medicine for the treatment of T1D. Groups can generate insulin producing beta cells in a dish and potentially use these cells for transplant and management of blood sugar levels in diabetic patients.

Dr. Alipio and colleagues demonstrate the reality of this possibility. This group successfully reprogrammed mouse skin cells into iPS cells and demonstrated that these iPS cells can become any of the various cell types of the body. Following a defined protocol, they generated beta-like cells that release insulin in response to glucose. The next step determined if these beta-like cells can effectively regulate blood sugar levels in animals. The group transplanted their beta-like cells into the livers of mice that have T1D or Type 2 diabetes (T2D). The cells incorporated into the liver and corrected blood sugar levels in the diabetic mice. Furthermore, the beta-like cells survived in the transplanted mice for weeks and managed blood sugar levels throughout the experiment time course. Four months after transplantation, most of the treated mice were healthy and had normal blood sugar levels due to the restoration of insulin production. Even though much more work remains, this study initially suggests iPS-derived beta-like cells can be generated and used as a treatment option for diabetes.

Will stem cells be the answer for organ regeneration and for the treatment of devastating genetic disorders that have affected the human population for centuries? Dr. Alipio and colleagues have shown that researchers continue to make headway, at least in diabetic mice, and the answer is pointing more towards “yes” everyday. Though not immediately applicable to humans, the promise of stem cell technology and regenerative medicine remains clear. iPS cells have opened the door to a better understanding into the onset and progression of poorly understood genetic disorders, like Type 1 diabetes. A better understanding will lead to the opportunity to use stem cell-derived tissues and organs for the treatment of these disorders. Stem cells, and their unique ability to become any other cell type in the body, will change the face of medicine. Researchers continue to take steps daily towards using stem cells for potential treatment options that may not only mitigate the symptoms of a disorder but may actually cure the disorder all together.

Reference
Alipio Z, et al. (2010) Reversal of hyperglycemia in diabetic mouse models using induced-pluripotent stem (iPS)-derived pancreatic beta-like cells. PNAS 107(30), 13426-13431.


Social Media: a new form of peer pressure or an understanding into human behavior?

By: Priya Ghosh

Technology has changed communication. The US postal system is struggling thanks to electronic mail, the English sentence has been reduced to tweets worth 140 characters and you get the latest world news on your Facebook homepage rather than the newspaper. While the social network has indeed made the world a smaller place, opponents of this new found mode of communication criticize the reductionist effects it has had on the quality of human relationships. People no longer talk to each other; instead they peer into their smartphones frantically checking the latest status updates, tweets and pins. The cyber community has greatly changed human behavior. Children pester their parents about the latest gadgets because their friends posted pictures of it on their Facebook wall. The question thus arises, has social media become a new form of peer pressure? Is it the voiceless bully that forces you to buy products, dress in a certain way and even plan life events based on what other people do? Recently scientists have tapped into this very influential nature of social media to understand human behavior. It has long been believed that smoking, obesity, depression is contagious and keeping healthier, happier company may actually help in treating aforementioned health problems. Using a highly sophisticated statistical program, scientists at the Stern School of Business at New York University studied how certain groups of people are more influential than others and how some people are more susceptible to influence than others. Studying a random pool of 1.3 million Facebook users Drs. Aral and Walker concluded the following; younger people are more susceptible to influence than elders, men influence women and women influence men more than their fellow female users. Single and engaged people are prime candidates to susceptibility in comparison to their more stable married counterparts. This alogorithm, known as Hazard Modeling has been previously used in fields of sociology, economics and marketing. What makes this study better is that the scientists accounted for bias influences. The pool of people was selected at random and the experiment was conducted over a large population adding to the validity of the outcomes. The researchers chose a product of analysis like the quality of a movie and asked a particular user to rate the movie. This rating was then sent to a randomly selected group of the user’s friends as an automated message. The content of the message was exactly the same and the user had no control over the friends to whom the message was sent to. This allowed for a completely unbiased study towards the reaction to the friends. To add to the rigidity of the study, the researchers analyzed the friends based on how they processed the ratings of the movie. They were studied based on whether they reacted solely to the automated message or whether they had any external influence such as advertisements. They also looked into how the group of friends adapted to the “peer influence” and whether they could propagate the influenced opinion about the movie to other people. Integrating the information collected from these controlled studies into statistical models and formulas, the general outcome was this; people who are generally powerful and influential are less susceptible to peer opinions and people who are more susceptible to “peer effect” are less likely to influence their peers. So why care about all these social interactions? Some of these findings may seem logical and intuitive, but there is great strength in the corroboration of idea with numerical data. Social behavior analysts have long debated over the hypotheses of “peer effects”. Is studying the persona of influential people more important than understanding the psychology of susceptible people? Or is it the other way around? Or should equal importance be paid to both sides of the behavior? The jury is still out. But studies like the one done at NYU shows with robust certainty that utilizing the extensive data set of the existing virtual social network can be valuable¬¬ in understanding the nature of “peer effects”. Information from such studies can allow us to take advantage of susceptible nature of humans and influence them towards a healthier happier life.

Original Paper:
Aral, et al. Identifying Influential and Susceptible Members of Social Networks. Science 20 July 2012: 337-341.

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