the novel coronavirus: how an invisible invader halted the world

Last year the world changed. With modifications to daily life such as wearing masks and attending class online, a lot of what was common became uncommon. More severely, millions of deaths globally shook the world. All of this change and devastation can be attributed to a coronavirus variant that was shockingly good at two things… 1.) Stability outside of cells 2.) Breaching the lower respiratory tract. A few questions must be understood as to why this virus is so effective in its affinity towards destruction. First, How does COVID-19 penetrate a cell? How does COVID 19 replicate? Finally, why is COVID-19 able to survive outside of a cell so well?

Detailing of S spike Proteins on Coronavirus Molecule
Coronavirus Spike Illustration Provided by NIH

With regards to cellular penetration, Coronavirus has two main parts in order to enter a cell. The first part is the use of its spike-like proteins to bind to the outside of a cell, otherwise known as the cell’s surface receptors. This spiky outer layer of the coronavirus makes it easily bindable to a number of human cells. After an initial bind between the coronavirus and the cell’s surface receptors, the coronavirus is absorbed into the inside of the cell, analogous to the way an amoeba absorbs an organism. The second part of this process involves what is called protein priming. Before entering the cell, coronavirus primes the S protein through the host cell’s proteases. From there, the S protein allows for ACE-2 binding which can be thought of as the mode for physically transporting the coronavirus into the cell. The current variant of Coronavirus is exceptionally dangerous because its spike proteins are able to attach to cells in the lower respiratory tract, a very vulnerable system in many humans.

Scanning Electron Micrograph of Coronavirus infected tissue
Coronavirus Scanning Electron Micrograph From Patient

Once in the cell, coronavirus seeks to reproduce. In order to reproduce, Coronavirus seeks out ribosomes to make copies. The viral molecule carries the blueprint on how to convert RNA into more RNA via creating a polymerase. This polymerase reproduces the genetic RNA genome and ultimately forces the ribosomes to produce more Coronavirus molecules. Because there are millions of ribosomes in every human cell, it does not take long for this process to occur. One of the key modes of trying to treat people with extreme cases is medicine that targets this polymerase. The drug fakes out the polymerase into replicating genomic material that will not lead to greater virus production.

Coroanvirus armor and encasement illustrated.
Coronavirus armor and encasement illustration from

Finally, Coronavirus is exceptional at surviving outside of the cellular environment. It has been noted that in the right conditions (humid), coronavirus can survive on a given surface anywhere from a few hours to 9 days. On paper, the virus may only survive for a few hours while on glass, the virus can exist for 5 days. Why Coronavirus is able to survive on these surfaces relates back to its spike proteins. These proteins act as armor in protecting the genomic material inside the virus. If this armor is broken, the genome of the virus is spilled out as well the virus no longer having a physical form.

Understanding is the first step in disarming. By having a better understanding of how coronavirus binds and enters into cells, replicates, and survives in outside environments, better strategies to prevent the spread of this dangerous virus can be better developed.

The plant that hates to be touched

If you think you’re shy, you should meet the plant known to botanists as Mimosa pudica! Also known as a touch-me-not, shame plant, or humble plant, M. pudica reacts rapidly to external stimuli – such as being touched, changes in heat, or changes in light intensity. The reaction generally includes the folding in of the plant’s leaves and the stem bending downward. These movements make the touch-me-not one of the most curious plants on the planet.

A touch-me-not reacting to being touched! Source

So how does the M. pudica react so quickly? The answer lies in the pulvini and changes in turgor pressure. Pulvini are the thickened bases of leaf stalks and leaves that act as joints for the plant. Because of the pulvini, M. pudica is able to fold in any direction. This manifests itself as what we see as “drooping” of the stem and folding of the leaves.

Image pointing out the pulvini of a touch-me-not plant. The pulvini is the thickened base of a leaf stalk connecting it to the stem.
Pulvini of a touch-me-not. Source

Turgor pressure refers to the force exerted by a fluid in a cell onto the cell wall. In other words, the fluid – in this case, water – pushes the cell membrane up against the cell wall. When the turgor pressure is high, the plant is more rigid, as a healthy touch-me-not is before stimulus. When the turgor pressure decreases – caused by the external stimulus – the pulvini and leaves droop, resulting in the “shy” appearance of the plant.

The final piece of the puzzle of the shame plant is how and why external stimulus results in this rapid change of turgor pressure. This is caused by potassium and chlorine ions – K+ and Cl-, respectively. When the plant experiences external stimulus, the ions move out of the cell through the ion channel. Because of the resulting increased ion concentration outside of the cell – and the decreased concentration inside of the cell – water also moves out of the cell. Because turgor pressure relies on the force of the water against the cell wall, the pressure quickly decreases. This results in M. pudica drooping and folding its leaves.

The uniqueness of M. pudica comes from its ability to react quickly. This rapid reaction is a result of the water channels known as aquaporins. Aquaporins are selective channels that allow water molecules to move outside of the cell without allowing the movement of other ions/molecules. This allows the water molecules to move outside of the cell at a rapid pace – about 2 seconds.

Image showing water molecules moving through a cell membrane by way of an aquaporin.
Water molecules moving through a cell membrane by way of an aquaporin. Source

In summary, Mimosa pudica is a curious little plant with more to it than initially meets the eye. External stimulus results in the movement of ions from inside the plant cells to outside the plant cells. This change in ion concentration creates an imbalance, causing water to rapidly leave the cell through aquaporins. This decreases the turgor pressure, resulting in folding of leaves and the appearance of wilting through the use of the pulvini. Remember all of this next time you come across a touch-me-not; one little tap of its leaves will set off this entire chain reaction!

Sources and Further Reading:

Ahmad H, Sehgal S, Mishra A, Gupta R. Mimosa pudica L. (Laajvanti): An overview. Pharmacogn Rev. 2012;6(12):115-124. doi:10.4103/0973-7847.99945

Hagihara T, Toyota M. Mechanical Signaling in the Sensitive Plant Mimosa pudica L. Plants. 2020; 9(5):587.

Sampath, Bhuvaneshwari. “Molecular Magic behind the ‘Touch Me Not’ Plant.” Science India,

Song, K., Yeom, E. & Lee, S. Real-time imaging of pulvinus bending in Mimosa pudicaSci Rep 4, 6466 (2014).

Featured image:

Nash, Tainaya. “This Plant Moves When You Touch It, and the Video Is Wild.” House Beautiful, House Beautiful, 28 June 2019.

sticks and stones may break my bones but dirt will wash right off

There you are, sitting in the park eating your spaghetti picnic on your favorite picnic blanket when your pollen allergy acts up. You let out a sneeze powerful enough to compete with Aeolus’ bag of wind, but now your spaghetti is all over your favorite picnic blanket. You immediately go to rinse it off, but your fine Italian sauce has thoroughly soaked in. If only nature had a solution to keep a surface clean. Enter: the lotus leaf.

The lotus leaf is renowned for its ability to stay clean in murky environments. This characteristic of the plant is regularly attributed to its superhydrophobic surface features and chemistry. A superhydrophobic surface is a surface which can maintain a contact angle with water above 150o and is correlated with a low free surface energy—which really means water pools and rolls off rather than soaking into the surface.

Nearly perfectly spherical water droplet on an artificially prepared surface

Modified from Zorba et al. 2008

A key attribute of the superhydrophobic surface is a hierarchical micro- and nanostructure. The microstructure is composed of plant cells grown in little mounds known as a “papillae” with small channels for air flow in between called “stomata.” The nanostructure is composed of hair-like wax crystal towers (epicuticular wax) built on the peaks of the papillae topography. The elevated wax towers combined with the stomata trap air and reduce the contact area of the water with the surface. The epicuticular wax chemistry reduces the adhesion to the towers themselves by being naturally hydrophobic.

Graphic of water drop resting across uneven wax pillars on a lotus leaf

Modified from Zorba et al. 2008

The tips of the wax towers create the largest repelling forces which form larger contact angles, while shorter towers can actually produce adhesive forces that reduce the contact angle. If the air is displaced and filled with water, the contact angle will decrease due to the water-water adhesion which “pulls” the droplet to the surface. Similarly, if the surface is damaged, the wax can be removed and decrease the surface’s hydrophobicity. The wax is naturally soft material and prone to mechanical damage increasing water adhesion and reducing the self-cleaning abilities of the leaf.

The papillae topography is the key to the robustness of the lotus leaf hydrophobicity. The papillae create natural valleys and creases which—like the tops—are still densely packed with wax hairs. When the surface is impacted, only the top of the papillae are exposed to the mechanical force so the wax tubules in the valleys are left undeformed and maintain their hydrophobic characteristics.

Water beads on rain jacket

Photo by Chase Pellerin via Gear Patrol

Hydrophobic surfaces have many applications in everyday life, for example rain jackets and umbrellas perform their best when they are hydrophobic. Manufacturing processes rely on hydrophobic surfaces to reduce oxidation and stay clean in past-paced environments, and your favorite picnic blanket would be much less prone to spaghetti stains if it were hydrophobic. Nature has solutions to keeping surfaces clean; we just have to recognize them.

Oops I Did It Again: The Biomechanics Behind Repetitive Ankle Injuries

Ankle injuries – either sprains or fractures – are one of the most common sports traumas plaguing the US today. Sprains are overextensions or tears in ligaments.  Fractures, on the other hand, are broken bones.

Here, we will focus on sprains of which there are three grades. To help visualise a sprain, think of a Fruit By the Foot (the gummy fruit snack you may have eaten as a child). A Grade 1 sprain involves stretching like if you were to pull on either end of the fruit rope and small tears start to develop along the middle. A Grade 2 sprain develops when the tear is larger and originates from a side; a grade 3 sprain is a complete tear into two pieces.

A Little Background

The ankle joint, also known as the talocrural joint is a synovial hinge joint that mainly moves in dorsiflexion and plantarflexion 1. If you were sitting on the ground with both legs extended in front of you, dorsiflexion is the movement of your foot upwards toward your shin, and plantarflexion is the action associated with pointing your toes moving away from your body.

Video Explanation of Ankle Movements in Dorsiflexion and Plantarflexion

Sprains & Pains

The most common type of ligament injury are lateral ankle sprains or inversion sprains where the ankle joint over rotates in the outward direction, especially an inversion while in plantarflexion 2. Exercises that include running, jumping, and/or cutting put the athlete’s ankle at high risk for sprains. This is especially seen in soccer, football, basketball and volleyball players.

Depiction of ankle position with an inversion sprain. Light purple items are bones and have rectangular callouts, while red items are ligaments with circular call outs. Labeled items include: Tibia, Fibula, Talus, Cuboid, and Calcaneus bones as well as the ATFL, PTFL, and CFL (ligaments).
Figure 1 – Left Foot/Ankle in an over-rotation with main bones (in square callouts) and ligaments (in circle callouts) identified

Figure 1 above shows an ankle in the common and compromising position of an inversion sprain. The circled ATFL, PTFL, and CFL are ligaments in the joint, namely the Anterior Talo-Fibular ligament, the Posterior Talo-fibular ligament, and the Calcaneofibular ligament respectively. Additionally, the boxed call outs are bones in the foot.

Numbers show that close to 70% of patients that had experienced a lateral ankle sprain in the past repeated the same injury to their ankle1.

What is the medical explanation behind repeated ankle injuries?

One study by Doherty et al. followed emergency room visits for ankle injuries and found that 40% of patients with ankle sprains had to seek medical treatment for another ankle injury within the year. Yet, another statistic found that over half of people who experience ankle sprains don’t even go to a hospital.

Ankle sprains are sometimes deemed as a “walk-off injury“, or one that hurts momentarily but just needs a few minutes before resuming activity. However, many people suffer from prevalent and reoccurring ankle sprains. Officially dubbed Chronic Ankle Instability or Sprained Ankle Syndrome, this condition is characterised by a host of symptoms including pain, swelling, perceived and actual instability, balance issues, and joint weakness. Chronic Ankle Instability, or CAI more commonly, can also cause a decrease in physical activity, changes to walking or running form, onset arthritis, and problems with knees and hips due to overcompensation1.

The tried-and-true course of action to prevent CAI is efficient rehabilitation. A study showed that if the patient recovers fast enough, the body won’t change movement patterns.

Problem: Altered Movement Patterns

The changing of movement patterns in the ankle joint, or arthrokinematics1 is one of the main factors that contributes to CAI. The brain, like a protective mama bear, trains the body to operate (walk, run, jump) in a different manner to protect the strained ligaments. Over time, muscle memory kicks in and the compensation for ankle mobility becomes your new normal. This adoption of an incorrect form of walking, running, jumping, etc. can backfire and translate to repeated ankle injuries. This muscle memory has been identified as a neurosignature2 from Melzack’s neuromatrix of pain theory; however, this pain theory also describes how elimination of the pain, stress, or chronic symptoms associated with an ankle sprain can prevent reoccurrence – elimination, that is, through efficient rehab.

Solution: Efficient Rehabilitation

A quick recovery can be achieved through various muscle strengthening exercises from a licensed physical therapist or “ankle disk training,” which basically consists of a flat board mounted on a semi-circle. By standing on this unbalanced board, stability can be practiced as well as specific ligament targeting to build muscle. A more serious solution of ankle surgery showed a 90% success rate of mediating mechanical instability, but this is not a widely-practiced nor traditional treatment plan for CAI3. In fact, ankle taping and/or lace-up 3 bracing when exercising proved most helpful in preventing over rotations of the lateral ligaments.

the hairy feet of the gecko

Have you ever thought about what it would be like to walk on walls? If you’ve ever watched a Spiderman movie or watched a gecko maneuver around its habitat, you probably have. While geckos don’t fight crime, their climbing ability is as fantastic as that of any superhero. Geckos have one of the most unique climbing adaptations of any animal, and scientists are examining the source of this ability to see if human technology could one day achieve something similar.

Geckos are able to cling to almost any surface, no matter how smooth or rough it is. They are also able to detach quickly and easily from these surfaces as they climb. This climbing ability is due to tiny hairs, called setae, on the bottoms of their feet that can only be seen with a microscope. Each hair branches off into even smaller fibers called spatulae. Each gecko has about three million setae, and a billion spatulae! When the gecko places its foot on a surface, these hairs cling to the surface and form intermolecular bonds, called Van der Waals bonds, with the molecules of that surface. These bonds are strong enough to hold the gecko in place, but can be broken easily when the gecko lifts up its foot.

A close-up view of the bottom of a gecko foot, with the microscopic hairs visible.
Close-up of setae on gecko foot. Image by Science Photo Library

In addition to enabling the gecko to attach itself to surfaces, these hairs on the bottom of the gecko’s feet have the ability to clean themselves. If the gecko did not have some sort of ability to clean its feet, dust and dirt would get stuck on the gecko’s feet and break the connection between the feet and the surface. However, the hairs on the gecko’s feet are shaped so that it is difficult for water to stick to the feet. When the gecko gets water on its foot, the water rolls off of it and takes any particles of dirt with it.

Scientists have long been fascinated by the gecko’s ability to stick to surfaces, and many have been working on creating adhesives with fibers similar to the hairs on the bottom of the gecko’s feet. These adhesives are dry, like the gecko’s feet, and can be attached firmly and removed easily. The possibilities for application of adhesives like this are vast in number, and include everyday fasteners as well as use in electronics, robotics, and even outer space technology. One of the areas being explored by scientists is the use of these adhesives in the medical industry. The manufacture of gecko-hair fibers for bandages could mean farewell to the pain of removing a bandage, as well as the sticky residue left behind on your skin. This type of adhesive could even one day replace stitches after surgery.

Polymer fibrillar adhesive based on gecko foot Setae. Image by G.J. Shah, M. Sitti.

Most people probably don’t think about geckos very often apart from what they see in advertisements for car insurance. But for some scientists, these creatures hold the key to a world of possibilities. So next time you’re at the pet store, take a look in the lizard tanks and watch the geckos climb. Someday, thanks to those geckos, humans might be able to do the same thing.

Read more:

What Can Different Types of Facial Wrinkles Tell Us?

Few people enjoy having wrinkles. Some people spend a lot of time, money and efforts trying to reduce the wrinkles on their face, while others simply appreciate them as something naturally occurs with aging. Regardless, wrinkles are always associated with aging. However, if we look into what different types of wrinkles are and how they form, we will find that not all wrinkles are bad. Not all wrinkles are caused by aging, and not all wrinkles should be treated the same way. Here, we introduce different types of facial wrinkles categorized by plastic surgeon and their corresponding treatment.

A person smiling that shows some wrinkles on her face.
The wrinkles created by the motion of smiling are dynamic wrinkles. They will disappear once the smile stops. Credit: Masterfile.

In general, there are two main types of wrinkles, dynamic wrinkles and static wrinkles. Dynamic wrinkles are the type of wrinkles that only appear when you make expressions such as smiling, laughing, or frowning. These wrinkles disappear once your expressions stop. The facial muscles have enough elasticity to return to their original positions. These are temporary wrinkles that everyone may have, even little kids!

Static wrinkles, on the other hand, are wrinkles that form when your muscles cannot return to their original position due to gravity and loss of collagen and elastin. These wrinkles cannot disappear like the dynamic wrinkles. When the collagen fibers become thinner, the skin loses elasticity and gets more wrinkles, whose width and height grow with age. (Lemperle, 2001) Lemperle et al. from the University of California put these wrinkles into three categories.

Three hand-drawn figures that show textures of different wrinkles.
Figures that show the textural change of skin experiencing (a) superficial wrinkles, (b) mimetic wrinkles, (c) folds. Source: A Classification of Facial Wrinkles.

The first type is superficial wrinkles. These are the less severe wrinkles that only involve textural changes of the skin surface. These wrinkles lines are separate lines at first but will gradually group together. (Arumugam, 2015) Common causes are aging, excessive exposure to UV light, and gravity. Superficial wrinkles, according to Lemperle, can be reduced or removed by chemical peeling (applying chemical solution on the face to peel off the top layer and then grow it back), or laser resurfacing. (Lemperle, 2001)

A figure with 2 side-by-side photos that show the effect of laser resurfacing before and after the treatment. The wrinkles of the person's face reduces.
Before and after laser resurfacing. Credit: Tahoe Aesthetic Medicine.

The second type is mimetic wrinkles. These are more severe and visible dermal creasing. Major causes include aging and repeated dramatic facial expression. (Arumugam, 2015) Because the facial creasing is deeper, the reduction methods include more complicated procedures such as muscle resection (cut out a portion of muscle and inserted the shortened muscle at the same place), botulinum toxin (a neurotoxic protein), or skin filler injection. (Lemperle, 2001)

The picture shows a person's lower half of the face with dash line indicating where the nasolabial line is. A needle is pointing at the dash line mimicking the process of skin filler injection.
Skin filler injection to reduce the effects of nasolabial lines. Credit: Filling in Wrinkles Safely

The last type is folds, the part of the face where droopy skin overlaps. Folds and mimetic wrinkles usually occur together. To correct the overlapping skin, tightening procedures such as blepharoplasty (surgery that repairs droopy eyelids), face lift, or skin excision are needed. (Kligman, 1985)

Noticeably, researchers have discovered that wrinkles formation may be different by gender, race, etc. For example, women in general have finer and less apparent wrinkles than men because their skin is thinner and softer. (Wu, 1995) Asian skin connects more firmly to the tissues underneath because of its thicker dermis and higher collagen density. Therefore, the repetitive pulling of the skin surface affects wrinkles on Asians and Caucasians differently. (Ahn, 1999)

Wrinkles are nothing horrible. They are something that everyone has or will have in the future. There is nothing wrong with wanting to reduce the wrinkles on your face, either. Just remember that there are many types of wrinkles and each of them requires a bit of a different treatment. Spending some time finding the appropriate treatment will most likely save you more time, money, and effort in the future.


[1] Lemperle, Gottfried, et al. “A Classification of Facial Wrinkles.” Plastic and Reconstructive Surgery, vol. 108, no. 6, 2001, pp. 1751–1752., doi:10.1097/00006534-200111000-00050.

[2] Arumugam, P, et al. “Facial Forehead Wrinkles Detection using Colour based Skin Segmentation.” Advances in Natural and Applied Sciences, Aug. 2015, pp. 71–80., doi:10.22587/anas.

[3] Kligman, A.M., et al. “The Anatomy and Pathogenesis of Wrinkles.” British Journal of Dermatology, vol. 113, no. 1, 1985, pp. 37–42., doi:10.1111/j.1365-2133.1985.tb02042.x.

[4] Wu, Yin, et al. “A Dynamic Wrinkle Model in Facial Animation and Skin Ageing.” The Journal of Visualization and Computer Animation, vol. 6, no. 4, 1995, pp. 195–205., doi:10.1002/vis.4340060403.

[5] Ahn, Ki-Young, et al. “Botulinum Toxin A for the Treatment of Facial Hyperkinetic Wrinkle Lines in Koreans.” Plastic & Reconstructive Surgery, vol. 105, no. 2, 2000, pp. 778–784., doi:10.1097/00006534-200002000-00050.

It’s The Little Things That Make Trees Strong

Plants come in all shapes and sizes, from the smallest blades of grass to trees so big that the tops can’t even be seen from the ground. But all plants are made from the same basic cell structures and components. So why is it that I can easily pick a flower, but could spend hours chopping at a tree and hardly make a dent? Trees are so much stronger than almost every other plant that they have become a staple in the construction industry. The key to the success of the tree is small differences in the structure.

Microscopic view of growth ring structure – Smithsonian Environmental Research Center

Cell walls are made up of cellulose, pectin, and lignin. Cellulose, with a Young’s Modulus of 120-140 GPa, provides the most structure to the cell wall, and the cell walls of trees have high concentrations of cellulose, averaging 45%. The other components in-between the cellulose, also can greatly impact the stiffness of the cell wall. Along with the cellulose, the secondary wall of tree cells contain more lignin that pectin as a binding agent. Lignin is found in all plant cells, but the high concentrations found in tree cells are what set it apart from other plants. Lignin has a Young’s Modulus of 3 GPa, while pectin is a gelatinous component that provides little structure. A study conducted by Donaldson also showed the presence of lignin has increased the size of the microfibrils and cellulose matrix to make the cell wall less porous, further increasing stiffness. The high concentration of lignin in the cell wall is a defining characteristic of tree cells and greatly increases their stiffness and rigidity.

The arrangement of the lignin and cellulose in the cell wall also increases stiffness. As tree cells divide, different layers of the cell are formed. This process is described by Plomion et al. in their article on wood formation.

The layers of a cell wall, from Plomion et al, Wood Formation in Trees.

The first layer is the middle lamella, which is made up mostly of pectin, but lignin is added throughout the differentiation period to eventually increase stiffness. This layer is mostly used to adhere the cell together. The next layer is the primary wall, which can consist up to 70% lignin. The primary wall is very elastic, to allow the cell to continue to grow. In other plants, this layer can have a higher concentration of pectin. The lignin in this layer means the tree cell is less malleable, but also increases stiffness and strength. The final layer is the secondary wall, which is separated into three layers, S1, S2, and S3. Most plants only have only one secondary wall, so having three distinct layers increases the strength and stiffness of the tree. Each layer consists of cellulose microfibrils, which are arranged in parallel, but in a different orientation for each layer. As the cell grows, the secondary layer is packed with more lignin, increasing the stiffness of cell wall. The S2 layer is the thickest, and contains about 45% cellulose and 20% lignin. Again, the higher lignin content, instead of pectin, allows for more rigidity, strength, and stiffness in the layer that provides the most structure to the cell. All of the cellulose and lignin layers, closely packed together, create a very stiff cell wall unlike any other plant.

It’s the small changes to the structure of the cell wall, such as adding lignin and layers into the secondary wall, that make the difference in the structure between a flower cell and that of a tree.

Sources and Further Reading:

How Mice Could Help You Regenerate a Lost Limb

If you have ever experienced a nasty scrape or burn, you know the process of healing is not very fun. Human skin can take several weeks to regenerate after an injury and that often comes with a fair amount of pain. For a bigger injury that involves tissue damage, there is often little the human body can do to regenerate larger parts. However, thanks to a small rodent – the African spiny mouse – regenerative medicine for humans could be making huge advances in the near future.

The concept of regeneration is not something new in the animal world – we have seen creatures like salamanders regenerate lost tails and starfish regrow lost limbs. However, the African spiny mouse is the only mammal ever observed to be able to completely regenerate tissue such as skin, fur, hair follicles, sweat glands, and even cartilage. Being able to quickly shed skin caught in the mouths of large predators comes in handy for the mouse to be able to escape, but they must also be able to quickly heal those wounds.

African spiny mice in a research lab have spiny hair shown in (a) and (b). A skin wound was administered to a mouse in (c). Scabbing has occurred over the full injury as seen in (d) by Day 3. By Day 30, the original wound has healed and new hair follicles have been regenerated as seen in (e) and (f).
Figure 1. African spiny mice in a research lab have spiny hair shown in (a) and (b). A skin wound was administered to a mouse in (c). Scabbing has occurred over the full injury as seen in (d) by Day 3. By Day 30, the original wound has healed and new hair follicles have been regenerated as seen in (e) and (f). Source: Seifert, A., Kiama, S., Seifert, M. et al. Skin shedding and tissue regeneration in African spiny mice (Acomys). Nature 489, 561–565 (2012).

How exactly does this happen? Researchers have found that the skin of the spiny mice is much weaker than that of most other mammals – think 20 times weaker than the skin of your regular old house mouse. Upon being handled, the skin is quick to shed leaving gaping wounds across the backs of these mice. This is due to the density of hair follicles found in their skin – a greater proportion of follicles means there is much less connective tissue to hold the skin leading to very easy tears. The weakness of the skin is contrasted by the rapidity by which it heals – the wounds can shrink to two thirds of their original size in a single day!

To understand a little bit more about the biomechanics of this process, we must look at how exactly the skin heals. As it turns out, collagen, the structural protein found in tissues which is responsible for skin elasticity among other things, is partly responsible for this phenomenon. Whereas mammals like you and I heal injuries through the generation of dense layers of collagen fibers aligned in parallel layers, these mice produce collagen fibers in crisscross networks that resemble the original makeup of tissue. This leaves the healed skin completely scar-free.

In addition, researchers have noted that ear wounds in the mice heal in a way similar to salamander tail regeneration. When a mouse’s ear gets injured, a ball of cells forms at the site of the wound that resembles cells in the embryonic state. This cell clump, called a blastema, is what allows the lost tissue to regrow on the ear. Scientists hope to use this information to study regeneration of tissue in humans.

An experiment was performed on both an African spiny mouse (Acomys) and another genus of rodents comparable to a house mouse (Mus) by making 4mm punctures in each species' ears. The size of the puncture was then observed over the following days showing that Acomys completely healed the ear puncture after 56 days while the size of the ear puncture in Mus remained relatively the same size showing no regeneration.
Figure 2. An experiment was performed on both an African spiny mouse (Acomys) and another genus of rodents comparable to a house mouse (Mus) by making 4mm punctures in each species’ ears. The size of the puncture was then observed over the following days showing that Acomys completely healed the ear puncture after 56 days while the size of the ear puncture in Mus remained relatively the same size showing no regeneration. Source: Matias Santos D, Rita AM, Casanellas I, et al. Ear wound regeneration in the African spiny mouse Acomys cahirinus. Regeneration (Oxf). 2016;3(1):52-61. Published 2016 Mar 9. doi:10.1002/reg2.50.

While there is still more research to do on the healing mechanism of the spiny mice tissue, the research done on these little mammals provides an excellent foundation for regenerative medicine for humans – something that studying regeneration in other animal species has not been able to accomplish. Being able to regenerate a lost limb was something once found only in science-fiction but could be a real possibility in the future.

Read More:

Insights into the regeneration of skin from Acomys, the spiny mouse

Optimal skin regeneration after full thickness thermal burn injury in the spiny mouse, Acomys cahirinus

Unique behavior of dermal cells from regenerative mammal, the African Spiny Mouse, in response to substrate stiffness

African spiny mice can regrow lost skin

Advances In Prostheses: Restoring the Sense of touch to amputees

Whether or not you know someone who has lost a limb, we can all easily imagine the hardships that would follow such a tragedy. Thanks to scientific advancements, prosthetic limbs have become more and more available and functional over the past few decades. However, one of the greatest challenges—which has only recently been started to be addressed—still facing the industry is the question of how to restore tactility through prosthetic hands. Having the sense of touch in your hands is essential to everyday activities, such as putting on your clothes in the morning or drinking a glass of water; and, unfortunately, in the US alone there are over 100,000 persons registered who had an amputation of a complete arm, hand, or partial hand.

When it comes to tactility, there are three main pieces of information that need to be transferred to your somatosensory cortex, the part of your brain that receives and processes sensory information. Those three pieces of information are contact location, pressure, and timing (i.e., when the contact begins and ends). Most studies that have looked into transferring this information to a brain from a prosthesis have done so through a brain-machine interface using intracortical microsimulation (ICMS), which activates neurons though implanted microelectrodes within the somatosensory cortex. The brain-machine interface would work in the following way: First, the prosthesis would gather force data from mechanical stimuli to the prosthesis. Next, the prosthesis would send the data to a microelectrode array capable of ICMS via a computer processing unit. Finally, the microelectrode array would deliver electrical pulses to activate neurons within the somatosensory cortex, causing you to “feel” the mechanical stimuli.

Shows the location of the somatosensory cortex in the brain. The somatosensory cortex is a part of the forebrain in the parietal lobe, located near the top of the brain.
Location of Somatosensory Cortex

The contact location and pressure of the mechanical stimuli would be determined from the force data gathered by the prosthesis; and the contact timing would be determined by having the force data be sent as a constant feed-back loop to the somatosensory cortex—that way a change of force from zero to some arbitrary, non-zero value and from some arbitrary, non-zero value to zero would indicate the beginning and end of the contact timing, respectively.

Shows a diagram of a somatosensory prosthesis transmitting percept to monkey. The prosthesis receives mechanical stimulus and then sends force data to a console. The console then delivers pulses to the cortex via a machine and microelectrode array. Finally, the monkey responds to the stimulus.
Diagram of Somatosensory Prosthesis

In studies by Tabot et al., O’Doherty et al., and Berg et al.;  ICMS feedback has been shown to work with various species monkeys. Tabot’s and Bergs’s studies in particular are very promising, as both studies showed that the monkeys would respond in the same way when a mechanical stimulus was applied to either a prosthetic hand/finger or a native, biological hand/finger. Based on these works and others, there are now a few working prototypes of prosthetics arms and hands that can “feel” that have been given to the general population, such as the one that Marine veteran Claudia Mitchell has. Further work in this field of study will hopefully bring us to the point where all amputees are able to have a prosthetic limb that allows them to live out their daily lives just as easily as the rest of us. Additional readings on bioinspired prosthetic interfaces and prosthetic tactile feedback can be found here and here.

Top Gun Trauma: the Effects of Ejecting From a Fighter Jet on the Spine

The need for speed places fighter pilots in electrifying yet dangerous situations. When things go wrong during flight, pilots must consider ejecting, a terrifying choice. Ejection is a last resort due to the large compressive forces and the high wind speeds that can cause many different serious injuries, including spinal injuries. Approximately 20-30% of people who survive ejection endure spinal fractures. Understanding the dangers of flight that servicemembers face increases awareness of the military lifestyle within the civilian population and is critical in finding solutions to lessen the severity of injury.

During ejection, the rocket-propelled ejection seat thrusts the pilot upward out of the aircraft. The pilot experiences around 18 g-forces (18 times your bodyweight)! The acceleration from the thrust of the seat, peaking at 140 to 160 m/sec2, compresses the spine vertically, loading the thoracic and lumbar spinal regions seen below. 

Anatomy of the spine
Photo from Patel et al., Pediatric Practice: Sports Medicine, 2009

The large rate of loading causes spinal fractures that can be either unstable and require surgery due to the movement of vertebrae or stable and treated with a brace. Thoracolumbar (lower back) fractures can be modeled using a variety of methods. One study applied axial loads of 5.2 kN (1,169 lbs) on two different spines from cadavers with a peak acceleration of around 20 g to simulate ejection. The resulting fractures for both specimens were on the L1 vertebrae, and one fracture was stable while the other was unstable. Another study constructed a drop tower and subjected 23 lumbar spines (T12-L5) to axial forces between 2.1 (472 lbs) and 7.3 kN (1,641 lbs) and accelerations between 8 and 23 g. Data analysis produced injury probability curves, which showed a 95% chance of injury with an acceleration of 20 g. The larger loads and accelerations also correlated with lower-level injuries (L4 and L5 vertebrae). 

One study modeled ejection using the finite element method, which can mathematically model the spine’s response to forces, and imaging software to investigate the effect of posture on spine injury severity. 

Software model of thoracolumbar spines in normal and relaxed postures.
Modified from Du et al., Int. J. Numer. Meth. Biomed. Engng., 2014

Thoracolumbar spines in normal and relaxed postures shown in the image above were simulated with an acceleration peak of 15 g for 0.2 sec. The relaxed posture correlates with increased stress on the endplate (the region between a vertebrae and an intervertebral disc), as the relaxed posture increases anterior flexion (forward bending) of the spine that is then increased by compression. Sitting straight up could help decrease the chance of injury during ejection. 

Ejection is a harsh reality that some pilots face. But as dangerous as ejecting is, ejection seats have a 92% survival rate, and sustaining a spinal injury is worth keeping your life. One B-1 Bomber crew member who ejected over the Indian Ocean said, “I lost a full inch in height.” It’s the price service members pay to dominate the skies and fly faster than the speed of sound. 

For more information, check out this retrospective study of French forces and this analysis of accident reports from the Royal Air Force