Electronics are often bought with one thing in mind—how long are they going to last? A new class of electronics might be on its way to reversing this paradigm. New on the technology block are ‘transient electronics’ that dissolve in water, and importantly, body fluids.
From Use-and-throw to Use-and-Disappear
Researchers at the University of Illinois, Tufts University and Northwestern University have pioneered biocompatible electronics that are both robust and high performance, and also capable of dissolving and thus free of the problems of waste disposal that accompany conventional electronic goods.
The applications of this class of devices could be wide-ranging and important. Starting with medical implants that perform a biological function for a specified duration of time or record biological parameters before being resorbed into the body’s system, and moving to environmental monitors that dissolve and reduce environmental impact, these ‘transient electronics’ have great potential.
How Do They Dissolve?
The key to this invention is the use of ultra-thin silicon sheets which are so thin they easily dissolve. Used together with soluble conductors employing primarily magnesium and magnesium oxide, they offer the raw materials for a wide range of applications. Wireless power coils, radio transmitters and antennae, solar cells and temperature sensors are some devices that have already been constructed.
The engineers have also come up with a way to control the time after which these devices dissolve, by wrapping them in a layer of silk. It is the structure of the silk that determines the rate of dissolution. The timescales for dissolution can range from as small as a few minutes to days, weeks, months or potentially, years, all depending on the silk packaging.
Every summer, when I return home for my vacations, I am hesitant about eating food at roadside stalls because, you know, who knows how unhygienic the food there is? In a role reversal that I still find amusingly ironic, my mother would accuse me of being wimpy and shove a plateful of food into my hands. Her logic—if we are over-protective of our immune systems, they will ‘forget’ how to respond when hit by a major infection. Blood them in battle, she said.
I’m still going to hold off from the delicious and teeming-with-microbes sugarcane juice on Indian roads, but as it turned out my mother was on the right track. A variant of her statement does apply in the case of allergies in what has been proposed as the ‘Hygiene Hypothesis’. Did you know that the incidence of autoimmune diseases (allergies being a prime example of these) is much higher in industrialized countries? Exposure to infectious agents in childhood primes your immune system for a more effective immune response as you grow up. Conversely, an extremely sanitized environment (often seen in industrialized countries) during childhood can make your immune system weak, unprepared to face infections and respond to harmless molecules that then become allergens.
How, and why does this happen? The answer lies in an ‘evolutionary mismatch’. Our bodies evolved in an environment which is very different from the one we live in now.
Let’s travel back in time for a little bit. In the first stage of human history, members of our species were hunter-gatherers. Our immune systems were constantly being exposed to a host of microbial organisms and worms. Around 12,000 years ago, we started settling down and took to agriculture. We continued being exposed to microbes, and in fact the sedentary lifestyle led us to being exposed to them for longer periods and increased human-human transmission. And then came the Industrial Revolution, bringing with it sanitation, vaccines and the beginning of the world as we know it. Many of the organisms that our ancestors encountered on a daily basis are now depleted from our present-day environment.
‘The Old Friends’ Hypothesis’
We have grown up in the industrial age, but our immune system has evolved over centuries in the first and second stages of human history. Microbes and worms were so omnipresent that our immune systems learned to tolerate their presence in the body if they were harmless. Reacting to an infection is costly for the body, as we know from the all-pervading weakness we experience after a fever. A wiser route for the immune system was to just let the microbe exist, and simultaneously, the worms evolved to release certain molecules that would down-regulate certain components of the human inflammatory system. In the current environment, our bodies do not contain the micro-organisms that regulated our immune system. Our immune systems thus rise to inflammatory baits in a heartbeat.
It’s still a hypothesis, but there’s plenty of evidence that supports it. Guts of children with allergies have been found to have fewer numbers of a bacterial species called lactobacillus. Another study in Argentina showed that people with fewer worms called helminths have fewer incidences of multiple sclerosis (MS).
Our bodies are thus not adapted to the environments we live in, leading to this kind of a mismatch. In context of public health, it is not feasible to think of returning to the environments of our ancestors, nor is it feasible to think of infecting allergic patients with 50 hookworms that would downregulate the immune response. However, learning more about the symbiotic mechanisms between our ‘old friends’ and our immune systems could help design more effective therapies towards autoimmune disorders.
The next time you make a face at the cilantro (coriander in certain parts of the world) on your plate, you can blame your genes. A genetic component for the intense dislike of cilantro has been found.
Before you get outraged by the thought of studies performed on culinary preferences, responses to cilantro has been thought of as interesting for quite a while. There are polarizing reactions to it, with some people comparing its taste to soap. On the other hand, it continues to be used generously in South Asian and Latin American cuisines. This even prompted the New York Times to publish an article called ‘Cilantro Haters, It’s Not Your Fault’.
The distinct flavor of cilantro is because it contains a class of molecules called aldehydes. It was thus hypothesized that differences in proteins that can detect these molecules—called receptors—could be responsible for the strong variation in response to the herb. Now, researchers at the sequencing company 23andMe have used genome sequences of 14000 Europeans to hunt out a genetic cause.
This research was part of a larger group of projects under 23andMe, which could be called crowdsourcing. In this process, the company sequences people’s genomes and provides genetic analysis. Clients willing to participate in 23andMe’s research are then asked to fill up a questionnaire about various traits that might be genetic, for instance, whether they think cilantro has a ‘soapy’ taste (another example could be eye color). The company then uses this data for their analysis. In this experiment, they found that one varying position in the genome—called a single nucleotide polymorphism (SNP)—was found to be associated with the way people think cilantro tastes. To put it another way, people who detest cilantro were much more likely to have one version of this SNP as opposed to people who like it, who are more likely to have another version.
Having found this SNP, they realized that it lies within a cluster of 8 olfactory receptor genes, genes involved in the perception of smells. This could thus be a strong candidate gene responsible for the divisive response to cilantro.
However, this SNP only explains a very low percentage of the variance in the trait. What does this mean? Ideally, we would expect to be able to predict a person’s response to cilantro based on the SNP she has. However, that is not the case, only 1.5% of the variance in the trait can be explained. This could be because there are multiple genes that act together in determining cilantro response (and they have only managed to capture one of them), or that only a small amount of cilantro response is actually genetic. Thus, in the latter case, even a significant SNP cannot significantly affect cilantro detection. This study was only performed on a European population, studies capturing a greater diversity could yield further answers.
We all know we acquire grey hair, declining senses and feel our body changing as we age, but how do our cells—those microscopic components that make up our body—change as we grow old? Biologists have known the answer for most cells in our bodies. As cells age, their DNA gets accumulatively damaged over time, and this DNA damage leads to a ‘senescence pathway’ via a DNA damage response (DDR). This DDR permanently arrests any further division of the cell and leads to changes in the expression of many genes (including many inflammatory genes) and also leads to dysfunction of the cell’s respiratory machine, the mitochondria. It doesn’t stop here. The DDR induces the damaged cell to release a host of toxic ‘reactive oxidative species’, which then affect the entire tissue.
However, this sequence of events has only been observed in cells that have the ability to divide—a category that includes most cells in the body, but leaves out the cells of the brain, the neurons. Researchers at Newcastle university have recently studied brain cells of mice to study how they age, and they have found the same senescence pathway active in the aging brain. To study this, they isolated cells from various brain regions of mice and looked for the presence of ‘molecular markers’—in this case, molecules that would indicate that a certain pathway or gene was activated. For instance, Interleukin-6 was a protein molecule that was used as a molecular marker for the inflammation found in aging cells. Using many such markers, they found that the exact senescence pathway previously found in dividing cells was also active in neurons.
Until now, it was assumed that aging pathways in the brain would be different, but this research shows that this is not the case. Using this information about aging neurons gives us an avenue to better understand the mechanisms of age-related mental disorders such as cognitive decline.
If the results from a recent psychological experiment are to be believed, the saying ‘’Face Your Fears’ might just have to be changed to ‘Blurt Your Fears’. Researchers at the University California, Los Angeles, have found that saying your fears before facing them actually reduces the fear itself.
Fooling Yourself into Being Less Scared
Similar to other actions that intentionally regulate emotions, such as distraction, it has been increasingly believed that giving an emotion a label, either in verbal or in written form, can help downregulate it. This downregulation is not merely at a superficial level. Brain regions that are involved in emotional processing are actually found to be less active when an emotion is labelled as opposed to when it is not.
Is Labeling One’s Fear Better than Distracting Oneself or Rationalizing Away the Fear?
Scientists decided to apply this in a real-world context, by testing how different groups of people could change their fear of spiders (arachnidophobia). Participants were divided into four groups—each of which had to face a tarantula. The first group, called the ‘’affect labeling’ group, had to state their fear before they went closer to the spider. The second group, called the ‘reappraisal’ group, had to vocalize something neutral (and definitely not negative) about the spider and their emotions towards it, something that would prime them to think less negatively about how they approached the spider (for example, “Looking at the spider is not dangerous for me”). The third group was the ‘distraction’ group in which participants had to describe furniture in their room. Participants in a fourth ‘control’ group did not vocalize anything. Participants from all groups were again exposed to the spider a week following this test.
Our Bodies Show Different Responses From Our Minds
The skin conductance response test (SCR) was used as one indicator of emotional arousal while approaching the spider, so as to reduce subjectivity. It was found the the degree of this arousal (representing fear) decreased much more in participants of the ‘labeling’ group as opposed to all other groups, i.e., participants who had stated their fear of the spider showed the greatest reduction in this fear response a week later. Interestingly, none of the participants said they felt less scared when they were asked to self-report their fear, it was just that their bodies responded less…fearfully.
The authors propose that this result is similar to those achieved by being in a state of mindfulness, which is also associated with reduced activity in the regions of the brain involved in emotional response.
Thus, speaking out your fears might just be all you need to face them more easily. You can read the published article on this experiment here.
‘Anosmia’ is the inability to smell, which is more harmful than it sounds, primarily because it could lead to a tendency to eat less, often leading to starvation and weight loss in mice. Anosmia can be caused by a number of factors, one of which is ciliopathy—when there are problems with the tiny protuberances on sensory cells called cilia. Among other cells, these cilia are found on the neurons that function in odor perception, and serve as ‘antennae’.
Scientists at the University of Michigan have treated mice that had genetic defects in a protein IFT88, which causing them to have no cilia across the body. They injected a common virus into these mice carrying DNA with the normal version of this gene. As the virus inserted itself into the genomes of these mice, they started producing cilia and their feeding patterns were found to change considerably. Moreover, the mice showed a 60% increase in body weight. “By restoring the protein back into the olfactory neurons, we could give the cell the ability to regrow and extend cilia off the dendrite knob, which is what the olfactory neuron needs to detect odorants,” says postdoctoral fellow and first author Jeremy McIntyre, Ph.D.
This is only a starting point for ciliary disorders, primarily because a mutation in IFT88 in humans is fatal, and does not cause the same defects as in mice. Thus, though this research has some way to go before it could be extended to humans, it shows promise in treating olfactory diseases that are genetic and due to malfunctioning cilia. Moreover, cilia perform important functions in diseases that aren’t just related to smell perception. Polycystic kidney disease and a disease called retinitis pigmentosa in the eye also result from a problem with the cilia.
Have you ever wondered why you are decent at Mathematics? Well, it isn’t just because of wonderful Mrs. Gunderson who taught you in high school. It’s because certain parts of your brains have more ‘wires’, or neurons, connecting them.
Division of Labor—Recognizing Quantities and Computing Are Done by Two Different Halves
There is a region of the brain called the parietal cortex that performs the role of numerical cognition. Additionally the left and the right halves of this cortex perform different parts of this activity. While the right parietal cortex primarily processes quantities, i.e. this half confers an intuitive sense of the magnitudes of numbers and their relationships, the left half performs numerical operations. What has remained unknown is how these two halves work together while we perform arithmetic that requires the functions of both halves.
Researchers at the University of Texas and the University of Michigan used functional MRI to image the brains of 27 adults and found that the neural connectivity between the left and the right parietal cortex increased in each of these individuals when they were given mathematical problems to solve. Individual participants who were faster at performing the arithmetic tasks (subtraction in this case) were found to have greater connectivity between the two halves, whereas no such correlation was found between speed of computing and activity within each half. This implies that the speed at which we compute depends to some extent on how fast numerical quantities and operations transmit between the two halves of the cortex.
Before some of us rush to place the blame for our mathematics grades on our genes, it should be noted that the brain is remarkably plastic. The more we work on something, the better the brain becomes at it. The neural structure of our brains might be a result of extensive mathematics practice rather than inherited. This study therefore reflects the mechanism, and not the cause of arithmetic ability. Thus, you might just have to thank Mrs. Gunderson for your enhanced neuronal structure after all.
One evolutionary quandary that has plagued biologists is the existence of a menopause in women—the time after which a woman loses her ability to reproduce. Why would females of a species stop reproducing? What is the evolutionary advantage to this? Wouldn’t it be better for a woman if she could keep producing offspring and thus propagating her genes for as long as possible? In fact, menopause is relatively uncommon in animals, though it has not been widely studied.
Grandmothering Effect and Other Hypothesis
One hypothesis that has been proposed to explain this is the aging effect. As women age, they are more likely to develop mutations that they pass on to their children. Stopping their ability to reproduce could help protect the species from defective mutations. Another hypothesis is the ’Grandmother effect’. If older women use their resources to help bring up existing off-spring instead of creating new ones, the additional resources given to a child increases its fitness.
A research team has used data from a pre-industrial Finnish population to test these hypotheses. Since the 17th century, the Lutheran church has collected a register of all births, deaths and marriages in Finland. The researchers had access to three generations of 5 Finnish populations.
Mothers-in-Law Compete with Daughters-in-law, But Not With Their Daughters
Their most interesting result was that when a mother-in-law and a daughter-in-law had children within two years of each other, their off-springs had significantly smaller lifespan by up to 66%. This suggests that competition between in-laws have led to menopause evolving as an adaptation. On the other hand, when a mother-daughter pair had children within two years of each other, no reduction in children’s ages were seen.
A woman shares no genes with her daughter-in-law, and her grandchild only shares 1/4th of her DNA as opposed to her child (which has ½ of her DNA). Thus, there is no co-operation between the two during child-rearing leading to reduced fitness of all the off-spring. It is interesting to note the contrast when mother-daughter pairs bear children simultaneously and show no competition. The authors suggest that in-laws fought over resources for their children instead of co-operating as mothers and daughters might do.
Modeling this data, the authors of this research have proposed a combination of factors that lead to the evolution of menopause. The first is the grandmother effect, and the second is the avoidance of reproductive conflict between mothers-in-law and daughters-in-law.
Sleep is a state of being characterized by a lack of consciousness. But are we capable to perceiving sensory stimuli while we are asleep, or we totally oblivious to the world around us? It is known that humans can strengthen previously acquired memories during sleep, but it is not known if we can actually take in new information.
If a Skunk Passes By While We Sleep, Would Our Brain Know It?
Researchers at the University of Israel decided to test the assimilation and acquisition of new non-verbal information during sleep. It is known that we respond to unpleasant smells by producing shorter sniffs, and to pleasant smells by longer, deeper sniffs. The research team used this information to create a unique test. While participants were asleep, they paired odors with musical tones, i.e., an odor-tone pairing was created with the tone being separated by the odor by at least 1 second. To ensure that these were being detected by the participants, their sniffing behavior was studied, and it was ensured that their sniffs were shorter when unpleasant odors were being presented. They also ensured that participants did not wake up in response to these odors; participants who did wake up within 30 minutes of the experiment were excluded from the analysis.
Upon waking up, the same participants were presented to the tones alone, and it was found that the tones which were paired with unpleasant odors induced a shorter sniffing response in the participants. Moreover, they were unaware of the experiments that had been conducted while they were asleep. This shows that their brains could process at least two things—odor processing, and association of tones with odors while sleep. This shows that our senses are definitely at work while we sleep!
What, and How Much Can We Take In While Asleep?
These participants only learned a simple non-verbal response. More studies will have to be conducted to determine the extent to which we can learn during sleep. Head researcher Anat Ariz says, “There will be clear limits on what we can learn in sleep, but I speculate that they will be beyond what we have demonstrated.” Though it is unlikely that we can learn all our Algebra by listening to recordings while we are asleep, this research could have implications in treating addictive disorders, for example, by using conditioning that pairs addictive drugs with a negative connotation. As Arzi says, perhaps the best way to cure such disorders might be learning at a level of non-awareness.
A protein being termed ‘Ovulation-inducing Factor’ has been found in the seminal fluid of a variety of male mammals, which stimulates the female brain to produce eggs (the process of which is called ovulation).
The presence of such a protein was first discovered when female camels ovulated soon after injection with semen. This experiment was repeated with llamas and alpacas to see the same results. However, the species in which it was first discovered (rabbits and koalas, besides camels) are called ‘induced ovulators’, meaning that the females produce eggs only upon insemination by the male. In other mammals including horses, pigs and humans, ovulation is spontaneous—meaning that there is a biological cycle in the female which leads to a buildup of hormones leading to the release of the egg. It turned out that OIF was also present in the semen of these spontaneous ovulators. Did OIF actually change ovulation rhythms in them?
The conservation of this protein must have a biological significance, and one way to determine that was to characterize the protein OIF. Researchers isolated this protein from llamas and bulls and tried to identify it in order to determine how its mechanism of action in the female body. By comparing protein structures, they found that this protein is actually a Nerve Growth Factor (NGF), a protein commonly found in nerve cells of the body. To confirm this finding, they isolated NGF from mice and injected it into llamas, and found that ovulation was induced in the llamas.
NGF Acts as a Hormone on the Female Brain
The NGF protein can act on the hypothalamus of the female brain via a system of hormones. What this means is that a substance that is a part of the male body can interfere with the female’s reproductive cycle. Is this true in humans too? We don’t know, but it might mean that we can rely less on birth control methods relying on abstinence during some days of the menstrual cycle. We know that human semen contains NGF, and that NGF can act on female hormones, but the female reproductive cycle is one that is tightly controlled, and further studies will have to be performed to determine the extent to which OIF/NGF can influence ovulation in spontaneous ovulators. In cows, injection of OIF has shown to alter ovarian function and shortens the ovarian cycles of cows.
“The idea that a substance in mammalian semen has a direct effect on the female brain is a new one,” says Gregg Adams, who headed the research team. “This latest finding broadens our understanding of the mechanisms that regulate ovulation and raises some intriguing questions about fertility.” Perhaps a host of fertility-related issues could be traced back to deficiencies in NGF in male semen, or NGF receptors in females.