Tag Archives: cells

Curing Cancer: a Giant Problem with a Nano- Solution

What if scientists could treat cancer without the extreme side effects of chemotherapy? Could scientists create a tiny way to cure a giant health crisis? Nanoparticle drug delivery systems could be the answer to our prayers.

Image of nanoparticles (small red circles) in a rat brain that has a tumor (green string-like material)
Nano-particles (red) in rat brain with tumor (green). Image taken from Washington Post.

Almost everyone knows a friend or family member who has had cancer and suffered through chemotherapy to recover. Currently, chemotherapy for treating cancer causes extreme side effects. For years, scientists have been researching methods to mitigate the adverse effects of treating cancers with the hope of one day creating a cure.

Delivering therapeutic drugs via nanoparticles (NP) are currently used in some FDA approved cancer treatments. Nanoparticles are extremely small–on the scale of the cells in our body. This is even smaller than a strand of hair on your head. Their size makes them ideal candidates for transporting drugs to tumors without damaging healthy tissue . In theory, NPs could hold drugs inside them, travel through our blood (ignoring healthy cells) and deposit the drugs right into the tumor.  However, there is a lot of research and improvements to be made before NPs can live up to their full potential. One of the largest unknowns in the study of NPs is their mechanical properties and how these properties interact with the body.

How does our body automatically know how to function without us telling it? Our body has biological sensors which govern our bodily functions in response to the world around us. For example, to prevent unwanted particles that may enter our bloodstream from getting to our brain or lungs, we have filters (like the spleen) that prevent them from passing through. Blood cells are soft, so they can squeeze through biological filters that dirt or stiffer blood cells could not pass through. To reach cancer cells, NPs must pass through these filters.

Stiffness is a mechanical property that measures how much an object moves when it is pushed on. Greater stiffness corresponds to larger applied forces.  For example, a piece of wood is stiff but a pillow is soft because it is easier to dent a pillow than to dent wood. To deliver NPs to the tumor through blood, the NPs have to get through the biological filters as they flow through the blood.

Image of blood cells squeezing through cell walls. Imagine a trying to push a pillow through a narrow opening. The blood cells (pillow) deform to pass through.
Blood cells squeeze through spleen walls, which acts as a filter for foreign objects in the bloodstream. Image taken from Zhang, et. al.

To allow passage through these filters, the NP’s mechanical properties must mimic blood. Scientists have performed tests on NPs with various stiffnesses and found that the soft NPs (like blood) were more likely to be allowed through the biological filters, whereas the stiffer (harder) NPs were blocked. If the NPs are blocked, they cannot travel through the blood streams to reach the tumor and are thus ineffective in treating the diseased cells.

The NPs (represented by the red circles) travel further into the tumor (blue and irregular shaped) than the stiff NPs do, allowing for more effective drug delivery. Image adapted from Hui, et. al.

Furthermore, soft NPs have been shown to penetrate deeper into tumor cells. The soft NPs can deform, allowing them to maneuver through the gaps between tumor cells (intercellular spaces). The deeper the NPs travel into the tumor, the more effective the drug treatment will be in attacking cancerous cells.

Nanoparticles hold the potential to revolutionize cancer treatment and prevention. By optimizing the mechanical properties of NPs, they could automatically release drugs in the presence of the tumors in response to their biological environment without delivering drugs to other cells. Further development of nanoparticle drug delivery methods may one day lead to a cure that will save loved ones’ lives. 

COVID-19 Vaccines: Helping You Combat One Spike Protein at a Time

COVID-19 vaccinations reduce the risk of infection and have the potential to ensure life returns to normal. Everywhere you turn someone is talking about which vaccine they have received: Pfizer, Moderna, Janssen, AstraZeneca… But what is the difference? How do the different types of COVID-19 vaccinations protect us? And does it matter which vaccine you receive?

COVID-19 vaccine comparison chart illustrating Pfizer and Moderna are RNA vaccines and Janssen and AstraZeneca are viral vector vaccines.
COVID-19 Vaccine Comparison. Photo by BBC News on Wikimedia Commons.

To start off, it is important to understand how coronavirus enters our cells: spike protein. Spike proteins are visually the spikes protruding from the spherical coronavirus and what bind to our cells to transmit the RNA virus (a code for COVID-19), enveloped inside the coronavirus, to our cell’s cytoplasm (the area inside a cell excluding the nucleus). The spike proteins fuse to our cell membrane (the outside of the cell) and are the target for researchers and vaccine developers.

Image of SARS-CoV-2 with red spike protein protruding from the spherical coronavirus.
SARS-CoV-2 (red spike proteins). Photo by Alissa Eckert, MS; Dan Higgins, MAM on Wikimedia Commons.

There are various types of vaccines that stop the spike proteins from fusing to our cell membrane, however, the two main types of vaccines used in the United States are mRNA vaccines and viral vector vaccines. Pfizer and Moderna are mRNA vaccines, while Janssen and AstraZeneca are viral vector vaccines. Both types of vaccines have the same goal: create antibodies to bind to spike proteins to block the spikes from attaching to and infecting healthy cells.  

The Pfizer and Moderna vaccines use messenger RNA technology to deliver genetic code to our cells to instruct how to make the SARS-CoV-2 spike protein. mRNA is very fragile thus it is encapsulated in something called lipid nanoparticles (LNPs) in order to reach the cell. LNPs increase translatability and stability to ensure mRNA’s delivery to the cell. When the mRNA vaccine is delivered to our cell it breaks free of the LNPs. 

Diagram of mRNA with LNPs.
mRNA and LNPs. Photo by Andreas M. Reichmuth, Matthias A. Oberli, Ana Jaklenec, Robert Langer, and Daniel Blankschtein, “mRNA vaccine delivery using lipid nanoparticles,” NCBI, PMID: 27075952.

After the mRNA is released from the LNPs, the cell begins making spike proteins. The spike proteins then trigger an immune response to begin producing antibodies. Ultimately, the antibodies latch onto the coronavirus’s spikes making the virus unable to latch onto other cells.

The Janssen and AstraZeneca vaccines incorporate viral vector vaccine technology. The viral vector is a genetic code that creates an instruction manual for human cells to produce the SARS-CoV-2 spike protein transported into the body by a harmless virus called an adenovirus. The adenovirus acts as the delivery system for this important DNA code and helps the body to trigger an immune response. 

The vector vaccine attaches onto proteins on the cell’s surface and the adenovirus is pulled into the cell. The main difference between the mRNA vaccine and the viral vector vaccine is that the DNA in the adenovirus of the viral vector vaccine must travel into the cell’s nucleus in order to be transcribed whereas the mRNA vaccine remains in the cytoplasm throughout the process. From there viral vector vaccine acts very similar to mRNA vaccines—once the DNA is transcribed into mRNA, the mRNA leaves the nucleus and the cell begins assembling spike proteins.

Further research is being completed to determine exactly how COVID-19 vaccines enter the cell. However, endocytosis is thought to be the answer based on previous vaccine knowledge. Endocytosis is a cellular process in which something is brought into the cell by engulfing it in a vesicle (small fluid bubble). In mRNA vaccines, the LNPs take advantage of the natural process of endocytosis. The LNPs are engulfed in a bubble, triggering a reaction that allows the nanoparticle to enter the cell and eventually release the mRNA.

Image depicting endocytosis in COVID-19 vaccines.
Endocytosis in COVID-19 vaccines. Photo by Oleg O. Glebov, “Understanding SARS‐CoV‐2 endocytosis for COVID‐19 drug repurposing,” NCBI, PMID: 32428379.

Overall, both the mRNA and viral vector vaccinations are great options each with their own unique design to produce antibodies and stop coronavirus from latching onto our cells.

Doses of the Pfizer COVID-19 vaccine.
Doses of the COVID-19 vaccine are seen at Walter Reed National Military Medical Center, Bethesda, Md., Dec. 14, 2020. Photo by Lisa Ferdinando on Wikimedia Commons.

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 Scientificanimations.com

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. https://doi.org/10.3390/plants9050587

Sampath, Bhuvaneshwari. “Molecular Magic behind the ‘Touch Me Not’ Plant.” Science India, scienceindia.in/home/view_article/58.

Song, K., Yeom, E. & Lee, S. Real-time imaging of pulvinus bending in Mimosa pudicaSci Rep 4, 6466 (2014). https://doi.org/10.1038/srep06466

Featured image:

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

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). https://doi.org/10.1038/nature11499.

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

This Toner Might Be More Expensive: 3-D Printing Artificial Organs

For most people in the United States who need an organ transplant, they will need to wait an average of three to five years on a list before they can get a lifesaving surgery. On average, 20 people die daily waiting on this list. There is a possibility of being able to bypass the wait time by manufacturing the required organs with 3D printing. This manufacturing technique was first used in the medical field for prosthetics and surgery practice models, with a goal to create fully functioning organs for those in need. Instead of using plastic or printer ink, the 3D printer uses cells to create biological constructions. 

A biological 3D printer making a small model of a human heart
Biological 3D Printing Market Update Photo

Traditional methods of artificial tissue and organ creation involve the use of stem cells, which are cells that do not have a designated purpose yet, to create a scaffold or frame for the organ. If cells for a desired organ are placed on the appropriate scaffold, they could multiply and grow into an artificial organ over time. If 3D printing is implemented using the same scaffold procedure, cells could be placed more precisely; the cell diameter can be better controlled, and the speed of the process can be controlled digitally. All of these aspects allow for better replication of the complex networks and structures found within biological tissues. A major advantage of the 3D printed organs are the customizations and variability that can be implemented with the method. Implants can be made to different sizes to suit each unique individual. If the original cells used for 3D printer material are from the intended recipient, the compatibility of the implant or artificial organ is nearly guaranteed. The risk of organ rejection is always present in the time following a transplant operation. 

A man who received 3D printed skull implants following deformation from a bicycle crash.
Xilloc Medical Before and After Photo

The 3D printing process is near perfect for certain medical uses, such as prosthetics, and dental implants, but more work needs to be done with the printing of tissues and organs. Small simple organs with thin walls can be done but printing larger organs such as hearts and kidneys requires integration of the vascular network, which cannot be done at this time. As printers become more precise and able to use a higher variety of cells, the creation of these vascular networks becomes more and more plausible. 

Scientists are currently investigating a new way to print these complex organs by combining organic material with mechanical chips. These chips are able to replicate certain biological stimuli, including fluid flow and chemical gradients, in order to achieve some degree of organ function within a much simpler biological structure. Using these chips will allow for better mass production of a variety of tissues and organs. This particular technology is being used to create tissues that will be used for testing pharmaceutical drugs. There is an opportunity for these tissues to be expanded to use in the human body, but the majority of companies using this technology are still in the startup phase. 

            While the use of 3D printing to create complex artificial organs is not completely viable today, the technology is improving rapidly. Within a few years, the waiting times and problems with organ transplants could be a thing of the past.  

What Makes and Breaks the World’s Tallest Trees

Trees have the potential to be the largest organisms on Earth. The world’s tallest tree, dubbed Hyperion, is 380 ft tall and weighs over 1,600,000 lbs. Compared this to the world’s largest animal, a particularly massive blue whale which was 100 ft long and weighed 380,000 lbs, the simply massive size of this tree should be obvious. And unlike a whale, a tree is much less likely collapse and crush itself under its own weight. Trees need to be tall, even if doing so consumes a lot of resources, in order to compete for sunlight. So what lets trees get this big, and what limits their height?

A diagram showing a space shuttle, which when prepared to launch is less than half the height of Hyperion, General Sherman, a wider but slightly shorter tree of a different family sequoia, a blue whale that is much shorter than either tree, and the statue of liberty, whose torch barely comes close to the shorter of the two trees
Comparison diagram of the World’s largest trees – Sequoia Tree Comparison Chart, Sequoias

There are two primary rules that govern tree sizes. The first is mechanics, the way the trunk of the tree is built and how it responds to weight. The wood of the biggest trees has a very high strength to weight ratio, which enables a tree to carry its own massive weight without collapsing. The layout and structure of this wood is analyzed at length in the journal by M. Ramage, but in summary, tall trees have internal cells called tracheids. These tiny circular tubes are 2-4 mm long and around 30 μm wide and provide support to the tree and allow water to flow throughout it, without adding as much weight. 

an image showing the tracheid cell structure of wood, many small cylinders stacked on top of each other.
A section of the annual ring of a conifer- M. Ramage’s The wood from the trees: The use of timber in construction and Dr. Krzysztof Wicher.

The high strength to weight ratio of wood allows trees to support themselves at incredible heights. Using B. Blonder’s research about the scaling of trees, it can be shown that trees are so strong and yet comparatively light weight that a tree would not actually collapse under its own weight until it was almost 15 Empire State Buildings tall. Obviously no tree is this tall, meaning some other factors must limit their height, but the incredible strength of wood should now be clear!

A diagram showing the decreasing size of pine needle branch segments. They decrease dramatically as height increases.
Leaf samples taken from the same type of tree with the height they were taken from listed adjacently in meters, – G. Koch’s The limits of tree height

The second primary rule that governs tree size is hydraulics, and it restricts the height a tree can reach. Hydraulics defines a tree’s ability to move water from its roots to its upper leaves in order to perform photosynthesis. The taller a tree gets, the more difficult this process becomes until the tree becomes incapable of growing any taller. G. Koch’s article, The Limits to Tree Height, explores how this hydraulic system works and how it restricts the heights a tree can reach. Xylem, tiny internal pipes that run from the roots to the tops of the tree, and carry water in a long continuous column this whole length. The longer this column becomes, the more difficult it is to maintain and the greater suction pressure that occurs at the highest leaves. Koch studied how properties in leaves changed the higher up they could be found, determining that the efficiency of Photosynthesis decreased, the pressure at the end of the xylem increased, and the size of leaves decreased. At great heights, the status of leaves seemed remarkably similar to those of a tree undergoing a severe drought.


Koch determined that these changes with height would eventually hit a maximum limit which they could not exceed, a limit that was determined to occur between 122-130 meters. So while the efficient properties of wood allow trees to reach incredible heights, their restricted ability to move water limits just how tall they can grow.

Sources and Further Reading:

  • Ramage M., Burridge H., Busse-Wicher M., et al. The wood from trees: The use of timber in construction. Renewable and Sustainable Energy Reviews 68, 333-359 (2017)
  • Blonder B. The size of trees: exploring biological scaling (2010)
  • Koch, G., Sillett, S., Jennings, G. et al. The limits to tree height. Nature 428, 851–854 (2004)

Why your scar tissue isn’t an issue

What do knee scrapes, adolescent acne, and paper cuts have in common? They all have the potential to leave a nasty scar. For people who have undergone trauma that results in serious wounds, especially on the face, scar aging is a serious concern. What are scars, and why does scar tissue tend to look different than regular skin as aging occurs?

In 1861, Karl Langer began observing the nature of the skin’s tensile properties. He cut small, circular holes into cadavers, and looked to see where on these holes the skin pulled the most. From these experiments, he developed “Langer’s Lines,” which he asserted were lines of tension all around the human skin. Later, Borges noticed that Langer’s lines only applied to cadavers, and began to perform similar experiments on live people to see if he saw different results. He pinched the skin of live people, and then saw how the direction of pinching impacted the length of the wrinkle formed. From these experiments, he identified RSTL, or relaxed skin tension lines. More and more researchers after Langer and Borges investigated the “tension line” phenomena, and they all noticed the same thing: wounds cut across these lines always led to nastier, uglier scars than wounds parallel to the tension lines. Why would that happen?

Figure 1 outlines the differences of Langer's lines, Kraissl's lines, and Borges's RSTL on the human face.
Image courtesy of MedMedia

To answer this question, let’s first identify the cellular mechanisms at work during healing. According to David Leffell of the Yale School of Medicine, there are three key stages of scar formation. The first stage of scar formation is inflammation. This happens right after the wound is incurred. Blood flows to the site, and tissue called granulation tissue begins to form at the base of the wound. Next is proliferation, when that granulation tissue helps the surrounding fibroblast cells to duplicate as quickly as possible. Fibroblasts are very important; they are the cells that produce collagen, a key protein in tissue formation. During proliferation, more and more fibroblasts fill the site, and they begin rebuilding the collagen networks for new skin. The final stage of scar formation is maturation/remodeling, when fibroblast levels decrease slowly as fresh tissue is rebuilt.

This figure shows each stage of wound healing, as is outlined by the supporting paragraph.
Image courtesy of biodermis.com

Because scars are formed differently than regular skin, they also tend to age differently. Normal consequences of skin aging can be seen around us in older people every day. As you may notice in your parents and grandparents, older skin tends to be dry, rough, wrinkly, and sometimes discolored. While these changes can also occur within scar tissue, the biggest factor in scar tissue aging is the difference in the rate of skin cell renewal. Skin cell renewal occurs when new skin cells travel from the basal layer of the skin up to the epidermis. Scar tissue’s renewal rate is different than normal skin’s renewal rate. This is why adults recover from wounds more slowly than young people – there is a greater difference between their cell renewal rates. The age at which the scar was formed, and the quality of the care provided, are critical in evaluating how well the scar will age.

If you’re interested in learning more about how that cut on your hand might heal and age, watch this video from TED-Ed, or for more detailed reading, check out this article.

Can we 3D print our own skin?

Can you imagine a world where amputees receive replacement limbs which are able to detect temperature and pressure like an actual limb? How about a world where when you get a cut, you can 3D print some of your own skin to patch the wound?

To the average citizen, this might seem like something out of a science fiction movie. To researchers at the Graz University of Technology, the Wake Forest School of Medicine, and the Universidad Carlos III de Madrid, this is a reality that they are helping bring ever closer. Both of these scenarios are discussed in a recent article by Mark Crawford, who investigated the recent breakthroughs in 3D printing human skin and creating sense-sensitive artificial skin.

photograph of an arm reaching into the sky to feel the rain in the palm of their hand
photo by Alex Wong on Unsplash

At the Graz University of Technology, researchers are working on creating an artificial skin that can sense temperature, humidity, and pressure. Currently, artificial skins can measure one sense at best, but with the use of the nanoscale sensors that these researchers are developing, sensing all three at once could be possible. This is achieved through the materials that the nanosensors are created out of: a smart polymer core and a piezoelectric shell. The smart polymer core can detect humidity and temperature through expansion, and the piezoelectric shell detects pressure through an electric signal that is created when pressure is applied. With this technology, prosthetics could be made which could allow the wearer to retain some of their lost senses.

At the Wake Forest School of Medicine, researchers have created a handheld 3D printer which produces human skin. This device could be used to replace skin grafts, as it can apply layers of skin directly onto the wound. Through the use of bioink, this handheld printer can create different types of skin cells. After scanning the wound to see what layers of tissue have been disrupted, it can print the appropriate skin needed to correct the injury.

Photograph of the 3D skin printer created at the Universidad Carlos III de Madrid, which is still in its prototype phase.
modified from Crawford, ASME January 2019

At the Universidad Carlos III de Madrid, researchers are also 3D printing human skin using bioink. They are creating both allogenic and autologous skin to create the optimal skin, which is a combination of the patient’s own cells and cells created from a stock. Although they have managed to print functioning skin in its natural layered state, it is tricky to create the cells in such a way that they do not deteriorate.

It is also tricky to correctly deposit the product. To illustrate, more research needs to be done on the mechanical properties of artificial skin before it could be used on humans. The artificial skin must be able to stretch and react to tension in a similar manner to the real skin it will be connected to. Additionally, researchers must figure out how to safely send the signals the artificial skin is detecting to the brain.

Overall, both advancing artificial skins and 3D printing human skins could largely impact humanity. Even though we have yet to use these skins on people, they are already being used in industries, such as L’Oreal, to limit testing on humans and animals. Already, these skins are being used on robots, as seen in this video, to help prepare the skin for human transplant:


Interested in seeing more? Check out some more articles on the advancement of artificial skin from Caltech and Time.