Hereditary Hemorrhagic Telangiectasia

HHT is a genetic disorder that causes abnormalities of blood vessels. Most of the blood vessels in the body of a person with HHT are normal. However, some of the vessels do have an abnormality. There are two types of blood vessels: arteries and veins. An artery does not usually connect directly a vein. Usually there are very small blood vessels called capillaries that connect artery to a vein. A person with HHT has a tendency to form blood vessels that lack the capillaries between an artery and vein. This means that arterial blood under high pressure flows directly into a vein without first having to squeeze through the very small capillaries. This place where an artery is connected directly to a vein tends to be a fragile site that can rupture and result in bleeding. When a blood vessel is abnormal this way, it is called telangiectasia. Telangiectases tend to occur at the surface of the body such as the skin and the mucous membrane that lines the nose. The telangiectases of HHT occur primarily in the nose, skin of the face, hands, and mouth and the lining of the stomach and intestines, lungs, liver and brain. We are still not sure why these abnormalities occur in these specific areas.

The study I picked had to deal with mutations of HHT found in Spanish families. They identified two different mutations, 22 ALK1 mutations and 15 ENG mutations, in independent Spanish families affiliated with HHT. They identified mutations in 37 unrelated families. An analysis of all the symptoms were recorded for each patient that was analyzed. They found there were more abnormalities in HHT1 patients than HHT2 patients. Twenty-two mutations in ALK1 and fifteen in ENG genes were identified. Many of them, almost half, represented new mutations in ALK1 and in ENG.

Overall, ALK1 mutations (HHT2) were predominant over ENG mutations (HHT1) in the Spanish population. This data goes along with another previous study that was based on Mediterranean countries such as France and Italy, but different to Northern Europe or North America. There was a significant increase of abnormal blood vessels associated with HHT1 over HHT2 in these families.

Christina Moreno

MicroRNAs involved in transformation of liver cancer stem cells

The existence of cancer stem cells in hepatocellular carcinoma (also known as HCC), which is a cancer of the liver, has been confirmed. This discovery was made possible by characterizing certain cells based on the information gathered from the Hoechst 33342 dye used to stain stem cells. This stain is easy to use on stem cells since it is easily “excited” by ultraviolet light. Recent discoveries in microRNA biology have revealed that these types of RNA's do indeed play an important role in the development of embryos and the formation of tumors. This type of RNA protein is“noncoding”and made up of 19 to 25 nucleotides in length. They regulate gene expression by inhibiting and transforming the layers of mRNAs through base-pairing. However, it is still unclear which microRNAs actually take part in the conversion of normal cells into tumor cells during the production of cancer in the liver.

Cancer stem cells have been identified in cells located in the blood and in solid tumors, including hepatocellular carcinoma (HCC). The isolation and characterization of cancer stem cells are usually based on the presence of stem cell markers. Although, in many tissues, certain markers of bodily stem cells are still unclear. There have been many attempts made to identify cancer stem cells in tumors, based on the results from the use of the Hoechst 33342 dye. The ability to isolate these cells by sorting them, makes it possible to improve both normal bodily stem cells and cancer stem cells without the use of stem cell markers.

Researchers used a gene knockout mouse model to show that microRNAs may be critical regulators of the development of organs in embryonic stem cells. However, data suggests that “dysregulation” of these microRNAs occurs in a many types of cancers, such as lung, colon, and liver. The effects of these specific RNAs in both cancer production and the differences of normal stem cells suggest that microRNA may be involved in the transformation of normal stem cells into cancer stem cells.

Hepatocellular carcinoma is one of the most malignant tumors in existence. However, when researchers divide certain population cells, the presence of liver cancer stem cells in many hepatocellular carcinomas cell lines can be verified using this technique. However, few experiments have focused on the characterization of population cells isolated from HCC cells. The researchers in this study saw that if normal stem cells and liver cancer stem cells could be enriched when the side population cells were isolated, then they could create an in vitro model to determine whether this type of liver cancer could develop through these types of bodily cells.

Biomarkers in Rare Disorders: The Experience with Spinal Muscular Atrophy

Spinal muscular atrophy also known as (SMA) is an autosomal recessive neuromuscular disorder caused by homozygous mutations of the SMN2 gene. Which means both parents must carry the gene mutation for it to be passed on to their children; however, rarely will either show symptoms. There is a 25% chance having a child that is affected. There are three forms of it, all depending on its severity. All patients with SMA will have at least one copies of the homologous gene (SMN2) which produces insufficient levels of the functional SMN protein. Currently there is no known cure for SMA is available. One possible therapeutic idea is based on attempts at increasing the amount of SMN protein produced by SMN2 genes. Recently, evidence has been provided that SMN2 mutation can be altered many different ways. The availability of participating patients to treat SMA has been an issue, but that doesn’t stop the search for a biomarker. This includes the availability of data on the history of the disease and other variables.

So far, different tools have been proposed as biomarkers in SMA. A biomarker can be simply explained as a molecule that is present or absent from a particular cellular type, which indicates whether a specific disease is there or not. The biomarkers that are used in SMA can be classifiable into two groups: instrumental and molecular. The molecular biomarker consists of the SMN gene products in dosages, either transcripts molecules or protein molecules. And the instrumental biomarkers are the Compound Motor Action Potential, the Motor Unit Number Estimation, and the Dual-energy X-ray absorptiometry. Unfortunately, neither of these biomarkers is even close to being available currently for this specific gene.

The authors stated that since the science community deiced to do clinical studies on SMA then the development of biomarkers must be created to further the understanding of this disease. Also since the topic was brought up none of the biomarkers that were used in this experiment meet the “gold standard” quality. These biomarkers just weren’t the most suitable and reliable measures for SMA. Even though some of the results came back positive for the substances that were being tested for, there are still several crucial issues which should be resolved before that biomarker is even considered being available for SMA research.

The biomarker technology is what is being used in this experiment. The SMN transcripts are the only potential molecular biomarker available. The SMN transcript measures the protein in peripheral blood. There are other possible variations of SMN transcripts/protein levels as evaluated in leukocytes may not reflect the real effect of pharmacological treatment in target tissues, like the spinal cord and, possibly, skeletal muscle. Other tissues are being considered as biomarkers, such as skin tissue or muscle biopsies. Muscle biopsies are simply muscle tissue, which has been removed for another use. Also preclinical studies and double-blind, placebo-controlled studies have been mentioned as approach for treatment. Preclinical studies on SMA positive animal models can provide information on some issues. And a double-blind, placebo- controlled studies are crucial to evaluate the effectiveness of specific biomarkers. Even though there has not been a lot of success with the search of a biomarker for SMA, the search doesn’t stop until that day.

-C. Freycinet

Kartagener Syndrome

Kartagener Syndrome is a recessive autosomal disease. This causes a defect of the cilia lining in the respiratory tract as well as the fallopian tubes in women. Patients with Kartagener Syndrome present chronic inflammation of the nasal passages usually causes by an upper respiratory infection. Another chronic inflammation is the ear passages and gives the middle ear an infection. Pneumonia and bronchiectasis which is widening on the air passages and causes them to become flappy and scarred. Diagnostic test can be done to prove the impaired cilia fuctions and genetic test. In severe cases the likely outcome can fatal if the bilateral lung transplant is delayed. In this case of a 66 year old women is chronic reoccuring upper respriatory infections, pneumonia and bronchiectasis, was also presented with acute respiratory failure. She was diagnosed with Kartagener syndrome based on genetic studies and clinical presentation. This lady passed away on a ventilator with refractory respiratory and multiorgan failure. This lady denied chest pains, nausea, vomiting, urinary symptoms and headaches. Once a physical exam was done, it showed this elderly lady was in moderate respiratory distressed. She also had two sister who died of chronic progressive lung disease.

Megan Rutherford

Bio-305-B

Genetic factors affecting bone marrow transplantation

Nine-year-old Laura Mosley has been battling leukemia for most of her short life. The chemotherapy she underwent destroyed her bone marrow’s ability to produce blood cells, so she had to have a bone marrow transplant. Blood-forming cells from another person were injected straight into her bloodstream. She responded well, and her blood cell counts steadily rose. Then a few months later, her body began to reject the marrow. Despite all the tests that had been done beforehand to make sure that the transplant would be successful, the donor’s cells apparently didn’t match her cells closely enough. Laura is now back on the waiting list. Her family members, friends, and even people in her community gotten tested to see if they might be a match for her, but so far, she has had no luck.

Finding someone with a matching tissue type is very difficult, much more so than finding someone with a matching blood type. Tissue type depends on a set of proteins called Human Leukocyte Antigens, or HLA. These antigens can be found on the surface of nearly every cell in the body, including blood cells. They serve as “self” markers, meaning that they allow the body’s immune cells to differentiate between the body’s own cells and foreign cells, like bacteria or viruses. If the free-floating immune cells ever encounter a cell without the right HLA markers, they recognize the cell as foreign and attack it. Thus, HLA is an indispensible component of the immune system. Unfortunately, it also complicates tissue transplants. If the donor HLA type is not similar enough to the recipient’s HLA type, the recipient’s immune cells will attack the blood cells that have formed from the donor’s marrow.

The oldest way to type potential donors’ tissue is serotyping, a technique based on antibody-antigen recognition. Antibodies are proteins produced by the body. These proteins are designed to bind specific antigens, almost like a lock (the antibody) and a key (the antigen). Once the antigen-antibody complex is formed, the antigen is marked for destruction. A person with a specific antigen on their cells will not produce the antibody that binds with it; otherwise the antibodies would attack the body’s own cells! So let’s say that we are looking for a donor with the antigen HLA-B21. We would take a sample of the potential donor’s serum, which is what you get when you take the cells and clotting factors out of the blood. Then we would add an antibody that is known to bind with antigen HLA-B21 to the serum. If we observed evidence of binding, like clumping of the sample or a color change, then we would know that HLA-A is present in the sample. If it is present in the sample, then it is present on all of potential donor’s cells.

Serotyping antibodies have become more and more refined over time, and are increasingly sensitive to slight differences between different types of antigen. But there are limitations to this technique. Serotyping does not preclude the possibility that the transplant will be rejected, as was the case with Laura. The differences between antigens are often so minute that they will bind with the same antibody. Thus, the donor and recipient antigens appear to be the same, when in fact they are “subtypes” of a particular antigen. The differences between the two subtypes may be enough to activate the recipient’s immune response.

Another higher-resolution technique based on DNA matching is now the preferred method for tissue typing. Three or more different loci (or regions) on the gene that codes for HLA are examined. A perfect match at these loci is ideal, though nearly impossible to find, unless the patient has an identical twin. Of course, most people do not have a twin, so they look for a match among their relatives. According to the National Marrow Donor Program, however, the chance that a patient will find a match this way is only 35 percent, so most patients rely on unrelated volunteers. Sadly, only four out of ten people looking for an unrelated donor actually get a transplant. Part of the reason that it’s so difficult to find a suitable match is that there are many different forms of the HLA gene. These forms, or alleles as they are called, arose when the DNA sequence that makes up the HLA gene mutated. These mutations may have occurred long ago or recently. Perhaps the gene is still mutating. Whatever the case, new alleles continue to be identified. It is these different alleles that account for the antigen subtypes. For instance, if a certain allele is found at loci A, then the individual has a particular subtype of HLA-A.

Of the 40 percent of patients who do get find an unrelated donor, practically none of them manage to find a perfect match. Some of these recipients survive; others do not survive or they require a second transplant. The question now is, how much mismatching can the body tolerate? The National Marrow Donor Program conducted a study in order to answer this question. Data was obtained from 3857 transplantations. It was found that mismatches at a single HLA-A, -B, -C, or –DRB1 locus (7/8) was associated with lower survival rate. Of the patients who had a single mismatch at these loci (7/8), 43% survived, compared with a 54% survival rate for perfect matches (8/8). Mismatching (7/8) at these loci is also associated with complications, like “treatment-related mortality” or and Graft-Versus-Host-Disease. Mismatched alleles at the HLA-DQ or –DP loci did not appear to have an effect on survival rate. There were no differences in the survival rates of patients whose donors had been selected using high-resolution DNA typing, or low-resolution serological typing. indicating that allele matching is just as valid a method of tissue typing as antigen matching, contrary to many researchers' opinions.

By AB

Researching the Lactase persistence genotypes and malaria susceptibility in Fulani of Mali

Over the past couple of centuries humans have been forced to evolve to endure with malaria and lactase persistence, being able to drink milk. These are two key factors that have shaped our genomes. Having a predisposed protection against malaria is extremely important, 1.5 million people died from malaria in 2009 alone. Having a resistance against malaria would be beneficial in certain parts of Africa such as in the holoendemic regions of tropical Africa.
Also, having lactase persistence has been beneficial in all cultures that have been able to maintain cattle to obtain milk. Being lactase non-persistence is a genetically normal trait, but genetic mutations have allowed adult humans to tolerate milk lactase. Multiple single polymers have been associated with lactase persistence in the enhancer region.
In the Western Africa these two environmental factors have come together in the traditionally nomadic Fulani people; they are trading people who raise goats and herd cattle. Being lactose tolerant is rare among people of African descent, but the Fulani are an exception. The Fulani have been known to be more resistant to malaria then other surrounding tribes in Western Africa.
Their hypothesis is that they suspect that the dietary habits of the Fulani have an impact on their partial malaria resistance. The Fulani consume vast quantities of milk and are known to drink more milk than other surviving tribes, such as the Dogon. The Dogon also use milk, but not in the quantities of the Fulani. To test this hypothesis the experimenters tested a 400 bp area with the known lactase persistence variants and the relation between malaria and lactase persistence genotypes between the 162 Fulani and 79 Dogon.
The study was carried in rural villages in the Sahelian area in Mali. This area is normally mesoendemic, an area with some transmission, for malaria and is caused by a protozoan that is transmitted to people by the bite of a female mosquito. They have seasonal cases due to the dry and wet seasons. Most of the cases are reported from June until December.
Blood smears of the participants, 162 Fulani and 79 Dogon, were collected and stained with 3% Giemsa and they were compared to the control. The participants had several factors recorded including age, body temperature, and spleen enlargement. Also, the hemoglobin levels and presence of Plasmodium genetic material was tested from blood samples by polymerase chain reaction also there genotypes were assesed. Once this was done the test groups were then compared for chronic malaria infections.
Each of the malaria variables were then grouped into two different categories so chi squared could be used to check for the actual probability of the events happening.
The results, in the correlation between malaria and lactase persistence, CC corresponds to lactase non-persistence, and both CT and TT to lactase persistence. Among the Fulani with the CC genotype 24 % of them had Malaria. This is compared to the 18% with the TT/CT genotype. When tested for P. falciparum, malaria causing bacteria, was positive in 60% of subjects with lactase non-persistence (CC) and in 51% of lactase persistence (CT/TT). The results show that P. falciparum, is more common in individuals that were lactose intolerant, but when chi squared is used the results that were obtained aren’t statistically relevant.
I think this was a good study to conduct because malaria is an extremely prevalent disease in the world. If this disease could be defeated by something as simple as drinking more milk being lactose-tolerant it is always worth a shot.
D. Tarver

Liver Studies in Dogs

The liver is an important organ in the body that helps regulate metabolism, detoxification, and many other functions necessary for survival. Age and diet influence liver function and as the body ages, liver function declines. Older dogs share many of the liver diseases that older humans have. An aged liver weighs less, and has a decline in blood flow, regeneration rate, and detoxification. In the paper that I am reviewing, liver tissue samples were collected from six senior and 6 young adult female beagles. All of these dogs were fed either a meat protein-based diet or a plant protein-based diet for a year. RNA was extracted from the liver tissue of each dog and was studied through canine microarrays to determine the expression of genes in the liver. Depending on the age of the dog, the diet altered nutrient digestibility, blood chemistry, gastrointestinal morphology, and microbial fermentation. The liver contains 13,778 genes and it was discovered that 234 of those genes were altered by age, and 137 genes were altered by diet. Alterations in the genes for an aged liver included cellular development, nutrient metabolism, and signal transduction. The gene expressions that were observed indicated that older dogs had an increased chance of liver disease and liver dysfunction, which have also been seen in older humans and mice. In the aged liver, inflammation, oxidative stress, and glycolysis genes were up-regulated while regeneration and cholesterol related genes were down-regulated. Diet affected gene expression more in the young adult dogs than in the older dogs. Young adults had thirty-three genes affected while older dogs had only three genes affected. Age and diet interactions appeared to be present because changes in the age related gene expression in the liver were more common in dogs fed the meat protein-based food (thirty-eight genes) than for dogs fed the plant protein-based food (twenty-one genes). These results provide insight into the molecular aspects of the liver and also predisposition to disease and irregularities in the liver. These results may help in a future study to determine if diet is a way to decrease age related liver dysfunction and disease.
I found this to be an interesting article because the liver is an organ that is necessary for all living beings to survive. The liver needs to be taken care of as much as possible and this article was researching how age and diet could affect the functionality of the liver. If we know what can damage the liver, then we can avoid foods and other things that could make the liver irreparable. Although age is not something that we can stop, we could help take care of our liver by watching what we ingest and what we do to our bodies that may affect liver function.

Erika

Are elite athletes genetically predisposed to lesser risk of disease?

Genetics plays an extremely important role in modern sports. Most elite athletes are genetically predispositioned to be bigger, faster, and stronger individuals, and therefore tend to be more successful athletically. Doctors F. Gomez-Gallego and J. R. Ruiz collaborated to study the genetic makeup of elite athletes further by examining if they are genetically predisposed to have lower risk of developing disease.

This article included a study of 100 male non-athletes (control subjects) and 100 male elite endurance athletes (test subjects). The elite athlete group consisted of 50 endurance runners, all of which had participated in at least one Olympiad, and 50 professional road cyclists, who had all participated in the Tour de France. Researches extracted DNA from either saliva or blood samples from all test subjects between 2004 and 2008. These samples were then analyzed for 33 disease risk-related mutations and polymorphisms. All genotyping was done using low-density DNA microarray based on allele-specific probes. From this information, the researchers created a total genotype score (0-100) by combining point values based on the number of unfavorable alleles (associated with susceptibility to diseases) that an individual possessed. This total genotype scoring procedure has been used in several other application studies.

After analyzing all 200 DNA samples and calculating their total genotype score, researches analyzed the data. They concluded that the total genotype scores for the control group were 23.8+/-1.0, and the scores for the athletes were 24.2+/-0.8. The slight difference in these scores was analyzed and considered to be statistically irrelevant. Based on the analyse done in this article, athletes are not genetically predisposed to lower disease risk.

Although elite athletes are not genetically predisposed to lower disease risk, they often have much lower rates of common diseases, such as cardiovascular disease. This is primarily due to the fact that their lifestyle promotes much healthier living than sedimentary individuals. In some sense, they may be considered genetically predisposed to lower disease risk. Although not directly related, elite athletes' genetic predisposition to being more athletic tends to push them towards a healthier lifestyle than those whose genes do not provide them with as much athletic ability.

The study was limited in several aspects, primarily the fact that it only examined 33 polymorphisms and mutations that could potentially affect disease risk. The study was also limited by the fact that the model used does not account for potential complex interactions between genetic variants. This happened because these interactions are mostly either not known, or not fully understood. Further research about how genetic variants interact with each other would need to be done in order to expand the credibility of this type of genetic testing even further.

-Josh Liptak

Epigenetic Contribution to Covariance Between Relatives

Epigenetic inheritance is a physical variation from generation to generation from influences other than DNA. Epigenetic inheritance occurs between asexual and sexually reproducing organisms, and directly affects the hereditary structures of populations, which can potentially lead to evolution. Research has pointed to considerable epigenetic inheritance from generation to generation. This research can be used to evaluate the risk for disease and responses to environmental stresses in a population. They introduced a model that takes both the probability of passing on ancestral phenotypes and stimulations from the environment. By doing this they are able to show changes between relatives. They were able to identify physical characteristics and populations where epigenetic inheritance had occurred.

To make this model they looked at heritable epigenetic variability, which is a physical characteristic that is brought upon by the environment or inherited by previous generations. The also looked at the reset coefficient which refers to the probability of a generation changing its epigenetic state, so that it can respond to its current environment with no memory of the past. The last thing they looked at was coefficient of epigenetic transmissibility, which is the probability of passing on the epigenetic changes to the next generation, without reset. These apply to both asexually and sexually reproducing organisms.

They looked at a continuous trait with genetic, epigenetic, and environmental variability. They simulated environmental exposure to organisms by way of heat shock or chemicals. After doing this two questions arose: “Can we distinguish between heritable epigenetic and genetic inheritance?” and “How can we estimate the epigenetic transmissibility?” To answer this they compared covariance between relatives. They measured the covariance between parents and offspring, between sibs, and between uncles and nephews. To examine asymmetric (parent is not identical to its offspring) and symmetrical (parent cell is also the offspring cell) they followed single cells over multiple generations. They found that during sexual reproduction, the reset mechanism is more noticeable than in asexual reproduction.

Transgenerational, ecological or developmentally induced physical characteristic changes have been mainly studied with maternal effects and are looked at as temporary effects. While cultural transmission was just studied as the complex system of cultural practices. Thus these studies have only started in recent years. Without detailed molecular studies, it is very difficult to detect epigenetic inheritance, since deviations from classical Mendelian ratios can be always explained by assuming interactions with modifier genes. In asexually reproducing, multicellular organisms, rapid and heritable physical characteristic switches are usually explained within the support of somatic mutations and somatic selection or various types of phase variations.

This research is interesting to see how our environment and lifestyles can change us and effect our future generations. It shows us that not all diseases and mutation are brought upon by genes, but rather by our environment and the environment or our past generations. We have an astounding effect on our bodies and if we are not careful and take care of it, we can bring drastic and dangerous effects to our future generations and ourselves.

~Kevin Reynolds

Cloning Plants are Beneficial (Jessica Foley)

As we may all know, if you cut a limb off of a plant, it can heal and grow back unlike humans. Therefore, you can easily clone a plant by cutting a piece of the stem or limb off, allow it to root, and place it in a soil medium. It is considered a clone because it has the same genetic make-up as the parent plant. However, scientists have discovered ways to clone a plant and make it beneficial. They found that by splicing (cutting pieces of new DNA and inserting it into an existing strand) specific genes into another plant can improve many different traits. In doing so, adding spliced genes into crop plants can make them disease-resistant, drought-tolerable, or even larger. Then all they have to do after they splice a specific gene into the plant is clone it. Now there are thousands of plants with the same disease-resistant gene that was spliced earlier into the original parent plant. It may seem like a lot of work, but most of the fruits and vegetables we eat today are genetically modified clones, unless the label reads "organic".
It is interesting to know that most of the fruits and vegetables we buy at a store are genetically modified, by splicing in a gene from another plant. This technique can help growers produce better and more reliable fruits and vegetables. However, I wonder how much it is costing the growers to splice in specific genes?

Which alleles influence human disease susceptibility for diabetes

Genetic studies are increasingly being used to identify specific alleles that affect human susceptibility to disease. This particular study focused on the alleles believed to be associated with type 1 diabetes. Type 1 diabetes occurs when the pancreas does not produce enough of the hormone insulin. This insulin is necessary to transport blood sugar into cells. Without the proper amount of insulin in the body, glucose builds up in the blood instead of going to the cells to be used for energy.

In the study in the article cells were used from the individual patients using the logic of genetic interaction screens. Small-molecule probes were used to look at how small molecules, like specific drugs, interacted and functioned in the presence or absence of the mutation. In order to find these interactions, the authors look for the small molecules that induce particular phenotypes, or observable characteristics, of the disease. The measurements found can focus on specific biological pathways to measure the cell function and/or capability. The effects of the small-molecule tests were measured using a luminescence assay for the content of cellular assay. This ATP assay is chosen because ATP concentrations in the pancreas indicate insulin secretion.

The research was conducted on a family with a history of the type 1 diabetes, looking at 10 members with the disease and 8 members without. The affected members were found to have a mutation called Q268X nonsense mutation. This change in DNA sequence causes damaged DNA binding to occur. In this impaired binding, the specific receptor associated with the function of the liver and the pancreas, called the HNF4α, shows low expression levels as well. Overall, the data that was found showed that disease allele interactions studied by small-molecule probes can be used to identify mutant pathways associated with the diseases, and also show the effects on the phenotypes of the diseases.

Diabetes is becoming more and more of a problem in society today. Any information that can be used to fight against the increasing number of those affected in the population is beneficial. I was interested in this article because my family has a history of diabetes, and wanted to know more information about various causes of the disease. What I took from this article was that specific genes are linked to increased insulin secretion, leading to various forms of diabetes. Targeting specific molecules that interact with the pathway to secrete insulin can allow for more specific drugs to be developed to aid in the balance of this insulin production. The information and processes used to examine the small-molecule probes is fascinating. This approach can not only be used for diabetes but also in to detect the presence of other mutant alleles associated with diseases, and taking patient-derived cells allows the scientist to really look at individual genetics and the interactions in complex human diseases. The information found in this type of research can also be used to develop new medications to assist with the symptoms and maybe even reverse the effects of the diseases people are facing today.
~Erin Hodges