Researchers Discover a Way to Produce More Red Blood Cells

As a result of the shortage of blood supply in blood banks, scientists found a way to use stem cell techniques and genomic editing that cause red blood cells to grow rapidly. According to a new TIME article, Dr. Vijay Sankaran and his colleagues took blood stem cells and conducted genetic surgery to find a specific gene that is linked to lower red blood cell production. Then they were able to turn off this gene and allow more cells to be produced. "The process of surgically altering the gene in question and coaxing the stem cells to develop and produce blood cells, resulted in a tripling of the number of red blood cells compared to control stem cells that were simply allowed to grow in a lab dish."

This is a huge discovery in genetics and health because the process could be improved upon to create more blood cells for medical procedures that require transfusions. I know if scientists further this research and continue to perform genetic surgery to alter genes, there will be incredible advances within medical care in curing chronic conditions. If we could alter a gene to produce more cells, it could be possible to alter them to stop producing the cells. Imagine where that could lead us in cancer treatment and could even replace invasive chemotherapy. This is the beginning of major findings in the human genome and the power we have to manipulate it.

A Possible Cure for Sickle Cell Anemia

                Sickle Cell anemia is a blood disorder that affects 100,000 people in the United States alone. Sickle cell is an inherited genetic disease that results in an abnormal amount of hemoglobin causing blood cells to be  crescent shaped. While normal red blood cells live for about 120 days, sickle cells only live ten to twenty days max.

                 The current treatment for sickle cell anemia is blood and marrow transplants. However many complications arise with these procedures. Some patient's body's simply cannot handle the transplant procedure, while others begin to develop an immune response to the foreign blood.

                In response to the problems regarding sickle cell treatments, researchers at John Hopkins University  are looking for new ways to cure the disease. By extracting stem cells from sickle cell patient, researchers have successfully corrected the genetic mutation that cause sickle cell. Linzhao Cheng, one of the researchers explained how the process occurs.  The patient's own blood cells are extracted and then  reprogrammed to act as stem cells. By making these stem cells and reproducing them, the researchers can cut out the sickle cell defect and replace it with a healthy gene. The last step of the procedure is to create an environment in which the stem cells would grow into healthy red blood cells.

                This is an amazing breakthrough in science however it is extremely time consuming. Before this treatment is available to sickle cell patients everywhere, the side effects of the lab grown blood cells must be tested and a much more efficient way to create these cells must be determined. Although this research is still in its early stages, the discoveries that comes from this could help people avoid other blood diseases such as malaria.

Original Article: http://www.medicalnewstoday.com/releases/290673.php

Second Article: http://www.nhlbi.nih.gov/health/healthtopics/topics/sca/treatment

Viruses and Diversity

Viruses are known to range in severity, and an experiment in mice was conducted to find out more about them. More specifically, five genetically identical mice were infected with a virus that was much more virulent than when the same virus infected five genetically diverse mice one at a time. One reason for this is that the virus wasn't able to adapt to the different genetic makeups of the different mice, and therefore was less effective. However, this has only been able to be experimentally proven with mice, plants, and insects. Research in this field was done by biologists Jason Kubinak and Wayne Potts.

Since viruses tend to be less virulent in a more diverse population, researchers encourage the diversification of cattle to lessen the probability of disease spreading. Potts and Kubinak use their study to show that the "sex-against virulence hypothesis." This hypothesis states that sexual reproduction evolved in order to increase genetic diversity, which in turn decreased the chance of viral infection.Therefore, the group of mice that had the same genetic makeup showed what would happen if mice reproduced asexually, and this reiterates the importance of diversification as an effect of sexual reproduction. Sexual reproduction enables organisms to gain resistance to viruses and diseases that they may have be vulnerable to otherwise. In the experiment, the virus used is mouse leukemia combined with a virus that causes a drastic increase in the number of red blood cells. Together, the virus is called the "Friend virus complex." The red blood cell count is increased in the spleen, and the more there are, the more likely the spleen will be inflamed, endangering the mouse's life. With the help of this combination of viruses, a virus in the spleen is able to replicate itself.


To start, a healthy mouse was injected with infected spleen tissue from another mouse. The previously healthy mouse was tested for how well it was fitted to the virus (i.e. if it allowed the virus to replicate easily). This was done by weighing the spleen because an enlargement of the spleen yields a more harmful virus.

Although there has been no experimental proof of this in other vertebrates, plants and insects have shown that genetic similarity allows a virus to adapt to a host more efficiently, and thus become more detrimental. Being able to replicate itself faster is lethal to the organism, as well as the rest of the organisms with its identical genetic makeup.

Article: http://www.sciencedaily.com/releases/2014/11/141118072528.htm
Supporting Article: http://www2.estrellamountain.edu/faculty/farabee/BIOBK/biobookdiversity_1.html

New Discovery Revels Potential for Blood Cancer Treatment

Researchers working together from the Centre for Immunology and Infection at York University as well as the Department of Medicine at Stony Brook University have made a significant discovery that may lead to the development of new treatments for specific blood cancers. The therapeutic target discovered has potential to lead to improved therapies for a group of specific haematological cancers, myeloproliferative neoplasms (MPNs).

These cancers are characterized by increases in one or more blood cell types, specifically red blood cells. Red blood cells carry oxygen around the body as well as prevent bleeding and bruising from easily occurring. It is important for tight control of the number of red blood cells in circulation in the body; however, in the bulk of patients with MPN have a mutation in the JAK2 protein. The mutation in the protein causes the patients’ blood cells to propagate too quickly.

The research team discovered that the protein molecule Mpl is necessary for the occurrence of the mutation in the JAK2 protein. Specifically, the team identified that turning off half the gene in the Mpl receptor reduced the expression enough so that the mutation did not occur in the JAK2 protein; therefore, the disease does not develop.

Dr. Ian Hitchcock, of the Centre for Immunology and Infection at York University, stated, “This is potentially important medically because it means we can target Mpl. If you can disrupt its activity you have a completely novel treatment for the disease. We found that it is unnecessary to get rid of the receptor entirely, you just need to reduce its expression to have a significant effect on the development of MPN.”

This article was very interesting because of the potential the research team’s discovery has. Despite the significant improvements made in cancer research there still remains a lot to be discovered. This research has the potential to completely change how specific blood cancers are treated. I am curious to see the results of further research,  in particular clinical trials that compare the outcomes of subjects/patients using treatments based off of this discovery compared to subjects/patients who are treated using current treatments. 

Main Article: http://www.sciencedaily.com/releases/2014/11/141110124344.htm

Secondary Article: http://ghr.nlm.nih.gov/gene/JAK2

age of red blood cells and transfusion

http://www.buzzle.com/articles/red-blood-cells.html

Anaemia is common in critically ill patients: up to 90 per cent of patients will be anaemic by day three of their intensive care unit stay.

Red blood cells transfusion rates in critically ill patients are reported between 20 per cent and 40 per cent in ICU, with a mean of 2 to 5 RBC units transfused per patient. Such anaemia of critical illness has been associated with a poor prognosis even in the absence of ischemic heart disease. This association supports the value of RBC transfusion in critically ill patients. Nonetheless, although potentially life-saving for individual patients, RBC transfusion also has been associated with an increased risk of morbidity and/or mortality in critically ill, surgical, and trauma populations.

In this setting, studies have increasingly focused on the possible deleterious role played by RBC storage duration (so-called age of red cells). In particular, they have raised concerns that prolonged RBC storage may lead to harm once such “older” red cells are transfused into ICU patients.

To avoid wasting RBC units and improve the provision of blood stock, standard practice worldwide consists of transfusing the oldest compatible and available RBC unit. In addition, RBC can be stored up to 42 days, maximising their availability and the likelihood that red cells older than two weeks will be transfused into critically ill patients.

75 New Genetic Regions Suspected to Influence Red Blood Cell Formation

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.

Treating Sickle Cell Disease

New Scientist reported that switching off a certain gene could treat sickle cell disease.  The disease creates

[caption id="attachment_3761" align="alignleft" width="200" caption="Silenced gene. Turning off a gene called BCL11A in mice with sickle cell (right) disease helps them to produce red blood cells (left) with working hemoglobin molecules. Credit: Fotosearch"][/caption]

mutated blood cells which contain long sticky chains.  The mutated cells could clog small vessels, cutting off oxygen to organs.  The gene scientists are targeting is called BCL11A. The gene switches fetal haemoglobin to adult haemoglobin.  Studies have been conducted to turn off the BCL11A gene in mice.  By doing so this allows the mice to produce fetal blood cells with working hemoglobin molecules.  Harvard Medical School conducted an experiment to switch of the BCL11A gene in mice with sickle cell disease.  After doing so it was observed that the mice produced 20 times more fetal haemoglobins, the cells produced contained nearly zero sickle cells.  Organs in the mice were virtually completely healthy.  The article goes on to explain that the gene could be targeted in humans by redesigning the length of the patients RNA and injecting it into the blood stream.  The drug hydroxyurea could also be taken to produce fetal haemoglobin.  The problem with redesigning RNA is the expense.  On the other hand hydroxyurea has been known to reduce white blood cells.  Science Now reported identical results from the Harvard experiment.  Science Now explains that more complications would arise if the gene was targeted in humans rather than mice.  All in all more research has to be performed before targeting the BCL11A gene in human beings.  Perhaps within the next few years scientists will have a better method to targeting the gene and individuals with sickle cell disease will be cured.