Punnett's Square

An article in Science Daily describes a study at the University of Wisconsin-Madison. It is here where is has been shown that human stem cells can successfully implant themselves in the brain and then heal neurological deficits, says senior author Su-Chun Zhang, a professor of neuroscience and neurology. After the transplant, the mice scored significantly better on common tests of learning and memory in mice. To control for the damage in the brain in the experiment in the mice, the mice brain’s were manipulated and deliberated damaged in the part that is involved in learning and memory.

The transplanted cells were then placed in the hippocampus,at the other end of those memory circuits. After the transferred cells were implanted, in response to chemical directions from the brain, they started to specialize and connect to the appropriate cells in the hippocampus, which is extremely significant. For more on the hippocampus, check out this sight

Even though this being a possibility in humans is a longggg way off, it is still crazy to think that this one day might be a possibility. The potential implications for people with brain damage or dementia is exciting, if this is transferable to humans!

An article in science daily references a journal from Nature 2013.  This journal explores the part the gene Meis1 plays in regeneration of heart cells in mammals.

                Dr. Hesham Sadek observed that this gene is present in the heart cells after birth about when the heart tissue is finished dividing.  This is why a heart cannot repair itself after damage caused by things like heart attacks.  Through research with mice he discovered that if this gene is removed then the cells can continue to divide.   

                His research in mice verified that taking out the Meis1 gene, which is a transcription factor,  prolongs the time in which newborn mice heart cells divide.  When the Meis1 gene was taken out of adult mice the heart began regeneration processes which did not have any negative effects on cardiac function.  This new discovery could possible steer research away from the controversial issue of stem cells.

Scientists use lab rats for experiments for the different research they do. These said rats are called knock out rats, they are believed to carry
specific genes to trigger diseases. this used to be a long and timely process,but with the findings of Professor Wurst and Dr. Ralf Kühn and their team thisprocess is much shorter. They just modified the genes directly in the mouseeggs. The process now takes a little over four months. with this there will bemuch fewer test animals in the labs and they can save time.  They used TALEN enzymes to implant mutations associated with human dementia and in mouse germ cells.  Scientist think that having mmice in the labratory will help us cure hereditary diseases.  There should be a better way of finding cures.  Rather than killing an animal for human needs.  Using mice in a labratory is very cruel. Mice feel pain just like humans and they do not deserve to be treated so harshly.  The mice are grouped together in small cages that do not get cleaned often.  Once scientists are ready to perform experiments they animals are tortured.  Animals should not be suffering and than killed to help humans with cosmetics or disease preventions.  There is an article attached about mice playing a critical role in medical research.
Article: http://www.sciencedaily.com/releases/2013/04/130402124811.htm

Other article: http://www.nbcnews.com/id/11700807/ns/technology_and_science-science/t/mice-play-critical-role-medical-research/

Obesity is a clear and debilitating epidemic in our society today, not only nationally, but globally as well. Researchers throughout the world have been unrelentingly searching for the easiest, fastest, and safest way to combat this problem in humans. Recently, researchers at the University of Colorado School of Medicine believe they have found the “obesity gene”, Perilipin (Plin2), that when deleted, it prevents mice from becoming obese regardless of their dietary macronutrient intake.

“When fed a diet that induces obesity these mice don’t get fat. It may be possible to duplicate this in humans using existing technology that targets this specific gene,” Prof McManaman said.

This discovery is exceedingly significant in human obesity since we possess the same exact gene, Plin2, just as mice do. If this process can be replicated in humans, that is deleting the gene Plin2, then there shows great promise to fight the mostly eternal problem of obesity that plagues the globe today. The results of the research were published in the Journal of Lipid Research.

A team of reserchers from Imperial College, London have gotten closer to revealing how red blood cells are formed and also how the body regulates the amount of haemoglobin that is packaged inside red blood cells. The researchers used genomic analysis techniques to figure out the possible genetic regions linked to red blood cell formatiom.

Hundreds of millions of fresh red blood cells have to be formed by blood stem cells to replace the ones that die each day. Haemoglobin is what gives blood its red color and it is a protein that captures oxygen from the lungs for transport and delivery to tissues. If there is an insuficient production of red blood cells than anaemia can occur, which is a very common disorder.  ”This new genetic information is laying the foundations for future studies into the roots of anaemia by uncovering new biological pathways and mechanisms involved in controlling the size and number of red blood cells and the levels of haemoglobin.”-Medical News Today.

By using the genomes of 135,367 people the researchers were able to identify 75 genetic regions that directly influenced six different physical parameters of red blood cells. More than half of these genetic regions are new in people. By using computational biology they found more than 3,000 genes that are responsible for protein production that lie close to these 75 regions. They then choose 121 ‘candidate’ genes suspected to regulate a red blood cell trait and investigated their functions. The researchers used model systems from databases and also new data from fruit flies. They found that 29 out of the 121 genes were linked to red blood cell formation in mice. Also if these genes were turned off in mice than red blood cell production would be minimized. To gather even more information the researchers silenced the 121 genes in fruit flies. Eventhough fruitflies dont have red blood cells they still  share some of the gene functions leading to the formation of blood elements. Once the genes were silenced the data collected confirmed that sets of genes involved in controlling human red blood cell traits in people were also important for the formation of blood cells in fly. Dr Nicole Soranzo said, “This is exciting because it means that we can obtain extensive new insights into the genetics and biological pathway of human health by studying model organisms.” Eventhough the researcher’s study is not finished and the underlying mechanisms for most of the discovered genes are still unknown, their research could lead to better understanding of red blood cells and also better treatment for anaemia.

I think any new discovery about such an important part of our body is interesting. Before reading this i did not know that we were unaware of how red blood cells were produced and regulated. Hopefully this will open the doors to further discoveries and eventually we will completely understand how red blood cells are controlled in humans.

The discovery of a gene known as SRPK might become the most helpful discovery for people trying to become pregnant.  A correlation has been identified between the absence of this gene and infertility.  In order for development and fertilization to take place in the egg, chromosomes must gather together (referred to as huddling).  Studies that were performed with mice and fruit flies led to the huddling findings, which detail the formation of karyosomes (the clustered chromosomes).  

Further, two meiotic steps involving the kinase SRPK are now considered to be directly correlated to oocytes.  When there is a mutation or complete absence of the SRPK gene, meiotic chromosomes cannot group together and form a karyosome, which in turn restricts the assembly of spindle microtubules.  Without these spindles, oocytes cannot mature, thus leading to infertility or sterility.  There is still more research to be done on this whole process and the functions involving SRPK, but this is already a fantastic find that might leave hope for those who want to have a pregnancy, but currently cannot.

I am curious as to why SRPK might be absent some individuals.  That being the case, infertility would seem like an almost easy fix.  If scientists could figure out a way to either insert SRPK into the DNA or find another way to conjoin the spindle microtubules and form a karyosome, it seems the oocyte could mature.  With such complicated processes, however, I wonder if there are more causes for the absence of SRPK or other reasons as to why the chromosomes do not gather into the karyosome form.  With the simultaneous studies of both fruit flies and mice, hopefully a simple cure to infertility and sterility will be on its way sooner than hoped for!

Autism is defined as a developmental disorder that appears in the first 3 years of life, and affects the brain’s normal development of social and communication skills. “According to the U.S.-based Centers for Disease Control and Prevention, 1 in 88 children suffer from autism spectrum disorder, and the disorder is reported to occur in all racial, ethnic, and socioeconomic groups. Autism spectrum disorder’s are almost five times more common among boys (1 in 54) than among girls (1 in 252).” According to Science Daily, Autism can be rectified in adult mice with compounds restraining protein synthesis, or with gene-therapy focusing on neuroligins.

The study took place at McGill University and the University of Montreal. In the study they used a mouse replica where a key gene controlling initiation of protein synthesis was erased. In the mice, the study showed that the production of neuroligins was increased. They also came to the conclusion that neuroligins are very important for the configuration and regulation of connections known as synapses between neuronal cells in the brain and essential for the maintenance of the balance in the transmission of information from neuron to neuron. The researchers have linked together protein synthesis and autism spectrum disorder. They used mice in the study, which showed that abnormally high synthesis of a group of neuronal proteins called neuroligins results in symptoms similar to those diagnosed in ASD. They also figured out that autism-like behaviors could be cured in mice with the proper compounds which inhibited protein synthesis. They could also be cured by gene-therapy focusing on the neuroligins.

The researchers final finding was that dysregulated synthesis of neuroligins augments synaptic activity, resulting in an imbalance between excitation and inhibition in single brain cells, opening up exciting new avenues for research that may unlock the secrets of autism. This study can be used to answer all of the unanswered questions that autism disorders have left for us. Also this article really interested me because it is amazing how these finding can make such a huge impact on the world.

In a new study in Nature Medicine shows that the deletion of the clock gene in fat cells caused mice to become obese.  The clock gene is known as Arntl or Bmal1.  The recent findings shed light on the causes of obesity in humans.  The study was conducted by Georgios Paschos PhD, a research associate in the lab of Garret FitzGerald, MD, FRS director of the Institute for Translational Medicine and Therapeutics, Perelman School of Medicine, University of Pennsylvania.  The studies show that food consumption during what is considered the rest period for mice favored energy storage.  This caused the mice to become obese without consuming more calories.  This behavioral change in mice is similar to night-eating syndrome in humans, which is also associated with obesity.

Mice with a broken clock in their fat get fat as they eat when they should be sleeping. (Credit: Georgios Paschos PhD, Perelman School of Medicine, University of Pennsylvania)

When the clock was broken in fat cells, the hypothalamic rhythm was disrupted to favor food consumption at inappropriate times.  This means the mice would get the urge to eat in the daytime when they should be asleep.  The change in daily rhythm caused changes in metabolism.  The Penn team also found a handful of genes that were altered by the broken clock in the fat cells.  Those genes governed how unsaturated fatty acids, such as EPA and DHA were released into the blood stream.  The Penn team found that EPA and DHA levels were low at the time of inappropriate feeding.  Interestingly enough, Paschos states that the team supplemented EPA and DHA to the knockout mice, which “rescued the entire phenotype”.  The findings show that show-term changes have an immediate effect on the rhythm of eating.  These changes lead to an increase in body weight.  I really enjoyed this study.  I think it should be brought to the attention of others about the importance of not eating past a certain time.  I know there has been conflicting reports regarding nighttime eating and weight gain.  Some say it doesn’t matter when you eat, while we hear sayings like, “Eat breakfast like a king, lunch like a prince, and dinner like a pauper” all of the time.  This study seems like it supports the latter opinion.

According to Science Daily, researchers have genetically engineered tomatoes so they decrease plaque build up in mice. The mice that ate the engineered tomatoes had less inflammation and reduced atherosclerosis. The plants produced a peptide that mimics the action of good cholesterol when it is consumed.The peptide used was 6F. 6F is a small peptide that acts the same as the protein ApoA-1, the chief protein in high density lipoprotein. The tomatoes were not given to just any mice. They were given to mice that can’t remove the low density lipoprotein and are unable to produce inflammation.

The mice showed lower blood levels of inflammation, higher paraoxonase activity, an anti-oxidant enzyme associated with good cholesterol and related to a lower risk of heart disease, higher levels of good cholesterol, decreased lysophosphatidic acid, a tumor promoter that accelerates plaque build-up in arteries in animal models and less plaque. This is the first time that a plant was engineered to produce such effects without total isolation. The mice were not hurt during this study.

Researchers at UT Southwestern Medical Center have genetically altered mice in a way that their bodies will metabolize excess energy and have lower levels of obesity, despite a caloric surplus.  The mice were modified to produce a larger amount of MED13, a chemical that affects thyroid function.  Mice with the elevated levels were much leaner than their normal counterparts.  In contrast, another group of mice had the MED13 gene deleted.  These mice had a much higher level of bodyfat and stored a much greater amount of excess energy.  The results of this experiment were not exactly surprising since we already have the knowledge concerning how thyroid function affects energy storage and other factors such as insulin sensitivity that often lead to obesity.  The reason it is significant is that the researchers used genetic modification rather than drugs to manipulate metabolism.