BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: mice (Page 1 of 2)

Attention all Concert Attendees: Hearing Loss Is Potentially Reversible

Organ of cortiThe most common cause of hearing loss is the damage and loss of cells that grow the hairs inside the inner ear.  These cells are aptly named cochlear hair cells.  Repetitive exposure to loud environments, such as construction zones, concerts, or military bases can damage these cells, which, until recently, were thought to be irreplaceable.  Normally, these cells enter the G0 phase after initial development ends when the organism is mature, which makes them similar to the brain cells we learned about in class.  When a cell is in the G0 phase, it is frozen in the cell cycle, so the cell does not proceed through mitosis.  This means that once the organism is done growing, there is no replacement of the damaged cells, as no cells are dividing.  

In the animal kingdom, however, these cells are known to regenerate.  Birds and fish have a mechanism which relies on a gene called ERBB2.  The artificial expression of this gene in mammals has also been proven to trigger cell growth in a trial led by Jingyuan Zhang, PhD.  They found that activating the ERBB2 gene triggered a cascading series of cellular responses which made the active cochlear hair cells multiply as well as trigger stem cells to become cochlear hair cells. 

The research found that the activation of the ERBB2 gene caused stem-cell like development through the expression of a few proteins.  The most important protein to this process, SPP1, signals the CD44 receptor, which exists on cochlear hair cells.  The theory is that because these receptors are triggered, they somehow promote mitosis in the cells.  The promotion of mitosis, the process of cell division in the cell cycle, would mean that these cells could be reproduced and the damaged cells could be replaced by new cells. 

When this process was tested in adult mice, this cascade happened as previously shown in growing mice, meaning that the possibility of the development of new cochlear hair cells is possible in mature mammals, it just needs to be stimulated correctly.  

The next step in the research is to determine whether or not these new cochlear hair cells are functioning mechanically. I don’t know about you, but I would maybe not stop wearing my earmuffs to use a jackhammer if I were you.  

Has anthrax, a microbe globally known not to be messed with, become a medicine?

Researchers from the Harvard Medical School have recently shown a potential medical breakthrough with an animal pain study. They have discovered how the bacteria Bacillus Anthracis can silence the feeling of pain in a mouse experiment while not destroying the nerve cell to do it.

Bacillus anthracis Gram

 

Anthrax has been viewed as a deadly bacteria ever since its discovery, causing skin lesions, fatal lung infections, and many other problems in both humans and animals. Anthrax secretes a couple of toxins after it infects the animal and these toxins can be deadly. The specific anthrax toxin used in the pain experiment has the ability to alter the signaling between pain-sensing neurons and relieve pain in the mice. As they continued their research they combined the anthrax toxin with other molecular cargo and discovered that this treatment can be used to create pinpoint precision pain treatments. Opiods are used now to treat pain in patients but they can be very dangerous and addictive. The toxin would act on pain receptors to possibly be a more effective and more safe painkiller than opioids.  ““There’s still a great clinical need for developing non-opioid pain therapies that are not addictive but that are effective in silencing pain,” said study first author Nicole Yang, HMS research fellow in immunology in the Chiu Lab. “Our experiments show that one strategy, at least experimentally, could be to specifically target pain neurons using this bacterial toxin””(Science Daily). This wouldn’t be the first time a toxin has been used to treat pain since Botox is used today to treat some pain and is approved by the FDA to treat migraines.

This all started in a lab, with researchers trying to figure out how many pain-sensing neurons there were compared to other neurons in the body. They discovered that pain neurons had anthrax receptors, just like the receptors that we worked on in class. The anthrax receptor uses endocytosis to bring the anthrax toxin into the cell. Research led to the dorsal root ganglia, a link of neurocensors in the spine. They relay pain signals to the spinal cord that then combine with two proteins that are created by anthrax itself. Experiments revealed that this occurs when one of the bacterial proteins, protective antigen (PA), binds to the nerve cell receptors and forms a pore that serves as a gateway for two bacterial proteins, edema factor (EF) and lethal factor (LF), to be brought into the nerve cell. The research further demonstrated PA and EF together, known together as edema toxin, alter the signaling inside nerve cells in an attempt to silence pain.

When the toxin was injected into the spine of mice, it produced incredible pain-blocking effects. It prevented the animals from feeling high temperature and mechanical stimulations. Throughout all this, the animals heart rate, body temperature, and full motor control was not affected, indicating that the use of the anthrax toxins may be safe to use in humans in clinical studies. This lab breakthrough shows how much we still have to discover about a bacteria that has been on the earth for thousands of years. Although many bacteria and viruses haunt us now, as we progress and have more discoveries like this, who knows what the world will look like when I’m 50!

How Mice and Mental Health Led to This COVID-19 Treatment Breakthrough

Ever since the initial outbreak of COVID-19, scientists have worked tirelessly to innovate and find the antidote to the virus which has infected millions and tragically killed hundreds of thousands. Such unprecedented times have led researchers to reconsider everything they already know and take intellectual risks.

One innovator whose experimental hypothesis may save many is Angela Reiersen, a child psychiatrist from Washington University School of Medicine in St. Louis. When she fell ill with COVID-19 in March 2020, Reiersen thought back to a study she had read about the effects of the lack of the sigma-1 receptor in mice and how the lack of this receptor protein led to massive inflammation and overproduction of cytokines. Cytokines are a part of the inflammatory response that occurs when pathogens sneak past the barrier defenses of the innate immune system and permeate cells. Upon entry of a pathogen, mast cells secrete histamines and macrophages secrete these cytokines. These cytokines attract neutrophils which then digest and kill the pathogens and other cell debris. Although cytokines are crucial to a functioning immune system, overproduction of cytokines can be extremely dangerous as it can lead to septic shock, in which the immune system becomes extremely overactive. This has become the cause of death for many COVID-19 patients.

As a psychiatrist, Reiersen worked regularly with SSRIS, or selective serotonin uptake inhibitors, in the treatment of conditions like depression and obsessive compulsive disorder. SSRIs help the human brain by increasing the level of serotonin available between nerve cells, but they also activate the S1R in the Endoplasmic Reticulum. Reiersen wondered, if the lack of the S1R causes fatal levels of inflammation, can we prevent extreme inflammation from COVID-19 through the use of SSRIs?

There have been multiple studies performed to test this line of reasoning, both including and independent of Reiersen. The most notable study was performed as part of TOGETHER, an international organization seeking to test possible unorthodox treatments for COVID-19. The trial was a collaboration between researchers from McMaster University of Canada and Cardresearch, a research clinic located in Brazil. The team in Brazil located 1,497 unvaccinated adults who were deemed “high risk” for COVID complications in their first week of showing symptoms of COVID. Conducted at 11 different research sites in Brazil from January to August, the study provided participants with a 10 days supply of either 100 milligrams of fluvoxamine, an SSRI, or a placebo pill. The researchers monitored the participants for 28 days after, as well.

In the end, 15.7% of participants who were given a placebo pill ended up having major complications from COVID-19, compared to 10.1% of participants who were given fluvoxamine. The gap may seem slight, but this is because not all patients took their full dosage due to gastrointestinal complaints. However, out of patients who completed their course of medication, 66% were safe from any complications and the mortality rate was cut by 91%!

Thanks to the research of Reiersen and many others, fluvoxamine is now considered a solid treatment plan for COVID-19 infections, especially in high risk individuals. As COVID-19 continues to infect millions around the world, who knows what new scientific breakthroughs will be made?

Regeneration of Lost Limbs in Axolotls

Many salamanders have the special ability to regenerate a lost limb, but adult mammals cannot. The axolotl is a Mexican salamander that is an endangered species in the wild. However, it is unlike most salamanders.

Metamorphosis frog Meyers

Normally, amphibians, like salamanders and frogs, go through the process of metamorphosis which begins with an egg that hatches into a larvae with gills to live underwater. As they gradually reach the adult stage, salamanders and frogs begin to lose and gain certain traits that allow them to adapt from an aquatic environment to a terrestrial habitat.

Axolotl

Axolotls are adorable creatures that are a special species of salamanders. Instead of going to the process of metamorphosis, they go through the process of paedomorphosis in which they retain their aquatic juvenile state for the rest of their life cycle.

Most salamanders have regenerative abilities but none to the extent of the axolotl. Axolotls can regenerate almost any body part, including the brain, heart, lungs, spinal cord, skin, tail and more. This possibly has to do with their juvenile state. Mammalian embryos and juveniles have the ability to regenerate to some extent, such as the heart tissue and fingertips. However, once mammals reach the adult stage, regeneration just simply isn’t the solution anymore. Mammals being to form a scar at the location of injury.

A team of scientists led by James Godwin, Ph.D., of the Mount Desert Island Biological Laboratory in Bar Harbor, Maine, approached the mystery of molecular regeneration by studying the axolotl, a highly regenerative salamander, versus an adult mouse, a mammal that has limited regenerative ability. In this research, Godwin compared immune cells called macrophages in the axolotl to the macrophages in the mouse to identify the factor that contributed to regeneration. It turns out that the macrophages are crucial to the process of regeneration. When the macrophages were depleted in the axolotl, it formed a scar like mammals do instead of regenerating. Macrophage signalling was similar in both axolotls and mammals when exposed to pathogens such as bacteria, funguses, and viruses. However, when the axolotl was exposed to these pathogens, the signalling promoted new tissue growth while in the mouse, it promoted scarring. Continual research of macrophage signalling in axolotls might one day be able to pull us closer to human regeneration.

In the future, when we need to surgically remove parts of our organs, axolotl regeneration might come in quite handy to regrow our important organs!

This research article relates back to AP Biology because macrophages work together with the its lysosomes to break down foreign pathogens. These macrophages will engulf these invading pathogens into intracellular membrane vesicles through the process of phagocytosis. Once entrapped in the vesicles, the pathogens will be killed with acid.

The Impact of Newfound Generalized Taste Buds in Mice

Background Information on Taste buds

According to this article about how taste buds work, taste buds are composed of cells that are structural, and cells that are chemical receptors. The surfaces of the receptor cells have proteins that bind with the chemicals that cause our perception of taste. As you all (should) know, the tongue does not actually have different sections for each flavor but instead, it has many different types of receptors that are stimulated by certain chemicals in food. The different reactions of receptors, which recognize bitter, sweet, sour, and umami flavors, are determined by specific genes in the DNA (It’s important to take note that the production of certain proteins and certain sequences of the DNA will even affect something as “simple” as taste). The receptor for salt, aka the epithelial sodium channel, functions differently from these receptors. It is basically a membrane that allows ions of sodium to permeate into specific cells.

 

The Mouse Research

An article (source article) from sciencenews.org reveals the findings of a research project that resulted in the discovery of generalized taste buds in mice that have the ability to taste four of the five flavors that these cells can recognize. These flavors include bitter, sweet, sour, and umami. The traditional belief in taste bud functionality is that taste buds only sense one or two specific flavors. Although mice possess both types of taste buds, the new research shows that clearly, the process is not as simple as just sensing specific tastes. Another article from sciencenews.org explains an experiment that demonstrates how taste is not just dependent on the taste buds themselves, but the brain plays a significant role in taste reception. In this experiment, certain receptors in the brains of mice were stimulated while the mice were drinking normal water. This caused the mice to react as if they were tasting sweet or bitter substances. The results of this experiment show that taste buds work with the brain to stimulate the perception of flavor.

Going back to the first article, mice need a specific protein that allows the generalized taste bud to send signals to the brain. Through research, it was discovered that the taste buds with broader ranges did not function in the absence of this specific protein. This goes to show the many functions and the vast significance of proteins in organisms. Additionally, some of the taste buds that only sense specific flavors were not functioning as well. Due to this, researchers believe that these two different types of taste buds depend upon each other to send signals to the brain.

 

So What?

At this point, you may be wondering why certain functions of the taste buds of mice matter. In case you didn’t know, the taste buds of mice function similarly to those of humans. This means that further research on the taste buds of mice may contribute to human interests as well. For example, one’s sense of taste can be lost through certain treatments (ex: chemotherapy) and aging. This may potentially lead to loss of appetite, causing malnourishment and other issues. With more research, these conditions could be treated through artificial taste bud receptors and even more by understanding the relationship between taste buds and the brain. Personally, I believe that this research is good support for those who are struggling with the loss of appetite, as well as a gateway to even more possibilities. I’d like to know more about your thoughts on this research. Is it worth the time and effort to learn more about this topic? Do you think that there are more possibilities than just treating loss of appetite? What else could this research be useful for?

CRISPR used to Control Genetic Inheritance in Mice!

Scientists around the world have been using CRISPR/Cas9 in a variety of plant and animal species to edit genetic information. Although this has been tested recently on insects, it is currently moving towards testing mammals. It happens to be more difficult with mammals due to the longevity between generations. However, It’s been done!!

UC San Diego researchers have developed a new active genetic technology in mice. Graduate student Hannah Grunwald, Assistant Researcher Valentino Gantz and colleagues led by Assistant Professor Kimberly Cooper, layed the groundwork for further advances based on this technology, including biomedical research on human disease.Image result for mice

“To demonstrate feasibility in mice, the researchers engineered an active genetic “CopyCat” DNA element into the Tyrosinase gene that controls fur color. When the CopyCat element disrupts both copies of the gene in a mouse, fur that would have been black is instead white, an obvious readout of the success of their approach. The CopyCat element also was designed so that it cannot spread through a population on its own, in contrast with CRISPR/Cas9 “gene drive” systems in insects that were built on a similar underlying molecular mechanism.”

The project duration was two years, and the researchers used many ways to “determine that the CopyCat element could be copied from one chromosome to the other to repair a break in the DNA targeted by CRISPR”. Some gene that was originally existent on only one of the two chromosomes was copied to the other chromosome. They were able to convert one genotype from heterozygous to homozygous, and they were able to tell in that there were  as many as 86 percent of offspring that inherited the CopyCat element from the female parent instead of the usual 50 percent.

The test was successful for the female mice’s production of eggs, but not for the males production of sperm. The researchers predict this is a possibility to a difference in the timing of male and female meiosis.

As this test was only the beginning, researchers such as those at UC San Diego hope to soon move on to research on human disease. They say that “Future animal models may be possible of complex human genetic diseases, like arthritis and cancer, which are not currently possible.”, and with their hard work, their research can lead to miracles.

Successful Progeria Treatment in Mice Also Bodes Well For Humans

A successful CRISPR-Cas9 treatment of Progeria in mice may be the beginning of anti-aging in humans.

When Juan Carlos Izpisua Belmonte set out to study “the molecular drivers of aging,” he could not have picked a more appropriate disorder than Progeria. Progeria is an accelerated aging disorder “caused by a mutation in the LMNA gene.” In both mice and humans, progeria induces many symptoms of aging, such as “DNA damage, cardiac dysfunction and dramatically shortened life span,” early in life. Molecularly, Progeria “shifts the production of lamin A,” a protein, ” to progerin,” a toxic form of lamin A that builds up with age.

 

 

In order to “to diminish the toxicity from the mutation of the LMNA gene that leads to accumulation of progerin inside the cell,” the Belmonte-led group used CRISPR-Cas9 to disrupt both lamin A and progerin. To do so, RNA first guides Cas9 to a spot on the DNA. Then, it makes a cut that “renders lamin A and progerin nonfunctional.”

As a result, the treated mice enjoyed a 25% longer life span and were stronger and more active. The successful treatment bodes well not only for mice, but for humans. In the future, “efforts will focus on making the therapy more effective” and compatible for humans.

 

 

A Much-So-Symmetrical Embryo

Developmental biology has taken a step further in understanding the connection made between the placenta and fetus by testing a hypothesis that involved slowing down the growth of one limb on an animal. Scientist Alberto Roselló-Díez used laboratory raised mice to test out his hypothesis by genetically manipulating the cells of a fetus in a petri dish. He then inserted the genetically modified cells into the mouse’s back left leg. A deeper look at Díez’s work explains that he uses a “p21” suppressor which is also known as an “antiproliferative”. In doing so, Roselló-Díez is suppressing chondrocyte cells (found in cartilage) from forming, thus preventing the mouses bones from lengthening.

In response to the cellular suppression, the nature of the fetus’s growth as a whole slows down to the growth rate of the left hind leg;  putting me in the mind of the phrase- “no man left behind”. This is described to be a “compensatory mechanism”, in which the entire fetus makes up for the compromised development of the mouse to keep it’s symmetry.

You might be wondering- “how does the placenta play into this?” Apparently, the cells of the placenta systemically communicate to the tissues of the other limbs, and warn them to “SLOW DOWN!” Therefore the fetus of the mouse relies on biological signals from the mother’s placenta.

Picture by Maneesha S. Inamdar

All in all, minimizing the growth rate of limbs is intriguing because it leaves me wondering the extent of the experimental purpose. Will it be that in the future we will use the p21 suppressor on human fetuses? Will this study lead to a breakthrough for unanswered cosmetic and orthopedic phonomena? These questions are yet to be undertaken by developmental biologists and maybe even doctors.

Preferential Gene Expression: Not As Random As We Thought

Our conventional knowledge of genetics dictates that the activation of genes in our DNA is random. It is equally likely that our body will express our mother’s alleles as it is that our body will express our father’s. In the case that one parent donates a defective copy, it will be silenced; the other parent’s healthy set of DNA takes precedence and becomes activated.

However, a new study indicates that gene expression and activation is not as random as we thought. In certain regions of the body, our genes demonstrate preferential expression.

A team of scientists at the University of Utah found that almost 85 percent of genes in juvenile mice brains displayed preferential treatment. The mice brains activated one parent’s set of DNA over the other’s. This phenomenon was observed in other areas of the body, as well as in primates.

Although the preferential expression came to a close within ten days, it could provide explanations for vulnerability to brain diseases such as schizophrenia, ADD, and Huntington’s. The temporary preferential treatment to one parent’s copy of DNA could trigger a host of problems specific to that cell site that lead to such disorders, if the parent had given a defective copy of genes.

The study has the potential to alter our basic understandings of genetics, and how we are more prone to certain specialized diseases.

Image: (Public Domain, https://pixabay.com/en/dna-biology-medicine-gene-163466/)

“Selfish” DNA Defies Mendel’s Laws

R2D2 may be a heroic Star Wars character but in living animals it is a piece of DNA which violates laws of both genetic inheritance and Darwinian evolution. It has swept through mouse populations by mimicking helpful mutations when in fact it damages fertility. These new findings, described in this article by ScienceNews,  propose that even genes that are dangerous to an organism’s evolutionary chances can trick their way to the top. This is a warning for scientists looking for signs that natural selections has picked certain genes because they offer an evolutionary benefit. What looks like survival of the fittest may actually be a “cheater” prospering.

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Image Link

Geneticist John Didion and colleagues examined DNA samples from wild mice from Europe and North America to determine how widespread R2d2 has become. The proportion of mice with the selfish gene more than tripled in one laboratory population from 18 percent to 62 percent within 13 generations. In another breeding population, R2d2 shot from being in 50 percent of the lab mice to 85 percent in 10 generations. By 15 generations, the selfish element reached “fixation” — all the mice in the population carried it. The rate of spread was much faster than researchers predicted—it was projected it would take 184 generations for the selfish DNA to spread to all of the mice.

R2d2 is a “selfish element,” a piece of DNA that causes itself to be inherited preferentially. It is a stretch of DNA on mouse chromosome 2 that contains multiple copies of the Cwc22 gene. When seven or more copies of that gene build up on the chromosome, R2d2 gets “selfish.” In female mice, it pushes aside the chromosome that doesn’t contain the selfish version of the gene and is preferentially placed into eggs. This violates Gregor Mendel’s laws of inheritance in which each gene or chromosome is supposed to have a fifty-fifty chance of being passed on to the next generation. But there is a cost to R2d2’s selfishness: Female mice that carry one copy of the selfish element have small litter sizes compared with mice that don’t carry the greedy DNA. The loss of fertility should cause natural selection to sift out out R2d2. But the selfish element’s greed is greater than the power of natural selection to combat it, as the lab experiments show.

But based on further lab experiments, researchers may have found that even this successful cheat can get caught. These other results revealed a relatively low proportion of wild mice carrying R2d2. Evolutionary geneticist, Matthew Dean says this could mean that some mice have developed ways to suppress the gene’s selfishness. There is still much more research to conduct on this topic.

Original Source

Additional Reading:

https://www.sciencedaily.com/releases/2016/02/160224133715.htm

 http://www.futurity.org/r2d2-gene-natural-selection-1110832/

Long Term Effects of Bad Diet Linked to Epigenome

Epigenetics has become an increasingly popular topic of scientific study. It is universally understood that DNA carries genes, however the expression of those genes are at the whim of the epigenome. The long-term control of the epigenome over the expression of certain genes is not yet fully understood. Scientist Erik van Kampen of the Leiden Academic Centre for Drug Research at Leiden University in The Netherlands studies epigenetics. He was interested in the mystery of how the epigenome is influenced by diet. He explored the idea of how the effects of a poor diet continue to persist even after a better diet is adopted.

In his study, he used mice that naturally had a high susceptibility to getting high blood cholesterol and atherosclerosis. He fed these mice either a high fat, high-cholesterol diet or a normal diet. After time had passed, bone marrow was isolated from both the unhealthy and healthy diet mice. This bone marrow was transplanted into mice that had their bone marrow destroyed. The new mice with borrowed bone marrow were given a healthy, normal diet for several months. After this time had passed, the mice were measured for development of atherosclerosis in the heart. In addition to this, the mice were measured for the number and status of immune cells throughout the body and epigenetic markings on the DNA in the bone marrow.

The results of this study were staggering. Mr. Kampen found that DNA methylation (which inactivates the expression of genes) in the bone marrow was different in both types of mice. The transplants received from the unhealthy diet mice were seen as having a decreased immune system and increased atherosclerosis in comparison to the ones who had healthy donors. This study proves at least somewhat of a correlation between diet and long-term effects on the body and the expression of genes.

The original article can be found at this address: http://www.sciencedaily.com/releases/2014/11/141103102359.htm

Human Brain Gene Implant Greatly Effects Mice

A study conducted at MIT tested the effect of human Foxp2 gene on mice and observed their ability to navigate through a maze. Foxp2 is found in both mice and humans, but the human form of the gene is related to  learning and language but it has been hypothesized by neuroscientist Ann Graybiel of MIT’s McGovern Institute for Brain Research that perhaps the human gene is related to sub-conscious actions based on environmental cues.

The maze lead to a pile of food, and throughout the maze the scientists placed visual and sensory cues that lead to the end of the maze and to the food. At the end of the study, the results showed that the genetically modified mice would complete the maze 3 days faster than the wild, control mice when visual and sensory cues were both involved.

The significance of the study is the potential connection between specialized learning and the Foxp2 gene. Although the difference between learning how to run a maze and leaning how to speak is massive, tests like this one are the beginnings to analyzing the true significance of Foxp2.

Mice

Using Hair To Fix Nerves

Keratin

Scientists at Wake Forest University have discovered that the hair protein Keratin has been shown to speed up the regeneration of nerves in mice. When nerve function is lost, the best option is to use a nerve graft from another part of the body, however this is an issue because it creates another wound site for the patient, which may not be tolerable due to ones condition. In an attempt to create another means of regenerating nerves, Dr. Mark Van Dyke and his team of researchers began to test the Keratin protein (which is found in hair follicles).

To test Keratin for its regenerative properties, Dr. Van Dyke used human hair collected from a barber shop and removed the Keratin from it. They then purified it and created a gel out of it to fill nerve guidance conduits. In order to study how effective the protein was, they studied the Schwann cells. Schwann cells are important in this experiment because they create signals that begin nerve cell regeneration. The results of this experiment showed their hypothesis to be correct, the use of Keratin greatly increased the activity of the Schwann cells. After this proved to be true, the scientists used a keratin-filled tube to try to repair a large nerve gap in mice (about 4 millimeters). The animals treated with Keratin were compared to animals treated with a nerve graft, and animals treated with a placebo. after 6 weeks, the entire keratin group showed visible regeneration, versus the placebo group who had about 50% show signs of regeneration. In addition, the speed of repair for the keratin group was much faster the other groups. 

The results of all of his tests proved his hypothesis of the uses for keratin. “The results suggest that a conduit filler derived from hair keratins can promote an outcome comparable to a grafted nerve,” said Van Dyke.

Article: http://www.sciencedaily.com/releases/2008/01/080110102341.htm

 

The Ability to Control Genes with Your Thoughts

A research group led by Martin Fussenegger, a professor of Biotechnology and Bioengineering at the Swiss Federal Institute of Technology, has developed a method by which brainwaves control the creation of proteins from genes. The technology wirelessly transfers brainwaves to a network of genes that allows the human’s thoughts to control the protein synthesis of the genes. The system uses a uses an electroencephalogram (EEG) headset, which records and transmits a human’s brainwaves and sets it to the implant in the gene culture.

A successful experiment of the system included humans controlling gene implants in mice. When activated by brainwaves, the gene implant culture would light up by an installed LED light. The researches used the human protein SEAP as the protein that would be generated in the culture and diffused into the blood stream of the mice. The humans were categorized by their states of mind: “bio-feedback, meditation and concentration”. The concentrating group caused an average release of SEAP. The meditation group released high concentrations of the protein. Finally, the bio-feedback group produced varying degrees of SEAP, as they were able to visually control the production of the protein as they could view the LED light turning on and off during the production process. The LED light emits infrared light, which is neither harmful to human nor mice cells. The system proved successful in its ability to translate brainwaves into gene control and protein production and its potential for harmless integration into the living tissue of humans.

The research group hopes that in the future a thought-controlled implant could help prevent neurological diseases by recognizing certain brainwaves at an early stage of the disease and translating the brainwaves into the production of proteins and other molecules that would work to counteract the disease.

Lights of ideas

Chemical Changes Triggering Allergic Reactions

A research team at Oxford University recently conducted a study to determine what conditions are more likely to trigger an allergic reaction to nuts in mice. The team used roasted peanuts and raw (regular) peanuts, purifying the proteins from both and then introducing the 2 types of peanut proteins multiple ways.

The response was shocking: the mice who were exposed to dry roasted peanut proteins had many more immune responses than the mice exposed to raw peanut proteins. This “immune response” closely resembles a human allergic reaction.

8483070167_1a90af12df_zThe actual act of roasting peanuts seems like it wouldn’t change much other than taste, but the science of the act shows that with heat, the proteins are chemically modified. The common concept of enzyme performance being altered by changing the temperature or pH applied in this experience. Peanuts contain the enzyme Cyp11a1,  a recurring link in allergic reactions. When heat was applied to the protein of a peanut, the enzyme’s shape changed and therefore the active site was altered and the enzyme was unable to perform its function. Therefore, an allergic reaction to the heat-modified (roasted) nuts was more easily triggered.

Being someone who suffers from a nut allergy (I know, I’m missing out on Nutella), I found this article very interesting because I’ve experienced certain situation with inconsistent reaction triggers, and I’m curious as to what they might be. I also found the geographical link regarding the allergy outstanding – the Western population of nut allergies is reportedly much higher than that of the Eastern population, but in the article, the distinction is made that as Westerners, we tend to eat our peanuts roasted/dry-roasted, whereas the Eastern population is likely to eat their food raw.

Photo by: Daniella Segura ; Some Rights Reserved https://creativecommons.org/licenses/by/2.0/

Source: http://www.sciencedaily.com/releases/2014/09/140921223617.htm

Cuts, Scrapes, and Hair Loss a Thing of the Past!

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Can adults repair their tissues as easily as children can? A study currently conducted at Boston Children’s hospital is attempting to find the answer to this question. Researchers have found that by activating a gene called Lin28a, they were able to “regrow hair and repair cartilage, bone, skin and other soft tissues in a mouse model.”  The scientists found that Lin28a works by enhancing metabolism in mitochondria—which, as we learned in class, are the “powerhouses” of the cells. This in turn helps generate the energy needed to stimulate and grow new tissues.
This discovery is a very exciting one for the field of medicine. The study’s senior investigator George Daley said, “[Previous] efforts to improve wound healing and tissue repair have mostly failed, but altering metabolism provides a new strategy which we hope will prove successful.” Scientists were even able to bypass Lin28a and directly activate the mitochondrial metabolism with a small compound and still enhance healing. Researcher Shyh-Chang says of this, “Since Lin28 itself is difficult to introduce into cells, the fact that we were able to activate mitochondrial metabolism pharmacologically gives us hope.” Since it is difficult for scientist to actually introduce Lin28a into a cell, it might be easier to simply synthetically create a substitute and introduce that. Either way, I think this is a very promising discovery! What other uses can you think of for this discovery?

 

Source:

http://www.sciencedaily.com/releases/2013/11/131107123144.htm

We All Owe Mice a “thank you”

Recently in our AP Biology class, we read about advances in stem cell research. Important developments began with experiments involving mice. The scientists were able to generate induced pluripotent stem cells from mouse fibroblasts and were later able to generate iPS cells from human fibroblasts . The research as been extremely helpful and scientists were able to learn a lot through the mice cells. It turns out mice are useful for many other avenues of medical research.

Mice have become a critical tool in the quest for new drugs and medical treatments because their genes are remarkably similar to a person’s”. Mice affected with various human ailments, such as “obesity, diabetes, cancer and countless other conditions are being used to study both the illnesses themselves and potential treatments”.

photo from WikimediaCommons

 

 

 

 

 

 

 

 

The latest “mouse sacrifice” for society involves cigarette smoke. We know that cigarette smoke heavily damages the lungs but scientists and doctors have long wondered what it does to the brain. There is an established, but “murky”, relationship between cigarette smoking and Alzheimer’s. A recent study with mice inhaling cigarette smoke significantly strengthened the suggested relationship.

Scientists led by Claudio Soto of the University of Texas Medical School at Houston exposed mice to cigarette smoke for four months. These exposed mice all showed signs of Alzheimer’s. Additionally, mice were bred with Alzheimer’s and then later exposed to cigarette smoke. These mice exhibited significantly worsened Alzheimer’s symptoms.

This sort of research proves extremely beneficial to humans and will most likely continue to become even more popular. Already, there are as many as 25 million mice used for medical research each year.

It seems as though we will have many mice to thank in the future.

 

Main Article:

http://www.sciencenews.org/view/generic/id/348321/description/News_in_Brief_Smoking_damages_mouse_brains

Additional Articles:

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The Black Mamba an Ally?

As the fangs pierce the skin, passing through the epidermis and into the dermis, you  may notice a feeble prick. Then, you will experience a numbness, similar to the one you get with pins and needles, and it will begin spread throughout your appendages. Within minutes your central nervous system will begin to shut down, leaving you without any hope of survival.  Within a half hour, your body will be overcome by convulsions, paralysis, and eventually you will meet your end by suffocation.

The Black Mamba, due to an assortment of different elements, including its aggressive behavior and its lethal venom, is possibly the deadliest species of snake on the planet. Untreated bites have a mortality rate of 100%. That, to me, is pretty convincing evidence.Recently, scientists have discovered “pain-relieving” compounds, known as peptides, within the venomous cocktail of the Black Mamba. The researchwas led by Sylvie Diochot, of the Institute of Molecular and Cellular Pharmacology at Nice University. She and her team, purified the peptides from the snake’s venom and profiled the compounds’ structure. These peptides are called mambalgins. The researchers were able to test the mambalgins on different strains of mice. The team of researchers concluded that the mambalgins work by blocking, or inhibiting, the ASICs, a set of neurological ion channels associated with pain signaling, in either the central or peripheral neurons. They also discovered that the mambalgins are not toxic, and can have the same, strong effect as morphine. Even better, mambalgins cause a significantly less amount of tolerance than morphine, and generate no risk of respiratory distress and other side effects that are prevalent with “pain-relieving” drugs.The discovery of these mambalgins may prove to be an enormous medical breakthrough. Due to the venom of perhaps the world’s most deadly snake, the insufferable pain of many human beings may be be abolished indefinitely.

 

 

Mouse Stem Cells Become “Grandparents”

Copyright: Anne Burgess

Recently, researchers at Kyoto University in Japan were able to induce stem cells of rats to become viable eggs, which were then implanted in surrogate mothers. The resultant offspring were fertile, anatomically intact rats that were bred for additional generations, their ancestor being only a cell in a petri dish. This discovery has excited scientists the world over because it marks the first step towards making eggs for infertile humans or gays and lesbians.

 

The scientists at Kyoto began by taking female embryonic cells and “induced pluripotent stem cells”, and then inducing them to become an early form of eggs. Induced pluripotent stem cells (iPSCs) are adult cells that have been reprogrammed to express certain genes that make them effectively embryonic cells. There is some debate as to whether iPSCs differ from embryonic stem cells taken from harvested embryos, but in this instance they acted identically to the conventional stem cells.

 

The immature eggs, called “primordial germ-like cells” or PGCLCs, were then surrounded by “female gonadal somatic cells” (cells usually found in an ovary) to create a reconstituted ovary. These constructed ovaries were implanted into surrogate mothers, where the PGCLCs matured into “germinal vesicle-stage oocytes” or early embryos formed during the primary oocyte stage of oogenesis (egg formation), which occurs before birth. The mice that had been implanted with these constructed ovaries eventually gave birth to fertile offspring, which were followed by a few additional generations.

 

Though scientists have called this discovery a major step forward in reproductive biology, the lead scientist on the Kyoto team, Dr. Hayashi, cautioned: “it is impossible to immediately adapt this system to human stem cells” for a number of reasons scientific and moral. Creating egg cells from stem cells in humans could allow menopausal women to conceive, which brings its own set of moral quandaries as well. Ronald Green, a bioethicist at Dartmouth University, commented on NPR that one had to consider “the commercial possibilities of people selling to infertile people babies produced from George Clooney or Jennifer Aniston.” Evidently, the possibility that egg manufacture might one day be possible has sparked heated debate, but one must remember that it may only be speculation.

Forever Young

Photo Credit: Flickr user flatworldsedge

How would you feel if you discovered that your doctors may have found a real fountain of youth?  Well thanks to researchers at the University of Pittsburgh that could someday be a reality.

Dr. Laura Niedernhofer and her fellow researchers have discovered a way to slow down aging, for mice at least.  To conduct their experiment the researchers bred a line of mice with progeria, a disease found in chickens that rapidly increases the aging process.  Normally once a mouse contracts this disease they have only a few days left to live.  After the addition of stem cells as well as some progenitor cells (a similar type of cell) the mice survived up to 66 days.

Now don’t worry its not only some rare poultry disease that this study shows help for.  Mice with mild cases of progeria showed geriatric symptoms similar to those that older humans show, weak leg muscles, walking hunched over and trembling and saw a dramatic improvement.  In fact 75% of the symptoms the mice were experiencing were relieved with only two injections of the stem cell mix given over a period of a few weeks.  Imagine if 75% of an aging human’s symptoms could find relief!

These mice also appear to be showing evidence that the new stem cells didn’t replace their aging stem cells but rejuvenated them as they saw improvement in the brain’s of these mice although the stem cell mix was injected into each mouse’s stomach.  It’s too soon to tell if this stem cell therapy will be able to help humans, but if it did we may have found a real fountain of youth.

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