Punnett's Square

Scientists have discovered the structure of a receptor protein that plays a vital role in the growth of cancer and HIV infection. The receptor is nicknamed CXCR4. Scientists say that the finding of this receptor will help them understand how it works, and how they can stop its activity of infecting cells. Also, by knowing the structure of the receptor protein, researchers will now be able to block its binding site that can prevent signals from being received or given out from the cell.

Study researcher Raymond C.  Stevens, of the Scripps Research Institute Of California, and other scientists found the CXCR4′s molecules using an imaging technique called X-ray crystallography. The molecules were forming pairs that allow the receptor to receive signals from outside the cell. In order to read about the article click on the word “receptor protein”. I think that it is great that the protein structure of HIV cancer has been discovered. Now, this epidemic can be stopped and hopefully cured.

Gene test for heart disease may reduce need for angiogram

There is a new genetic test that has just been developed that can tell doctors whether the patient has heart disease or not. The test isn’t perfect yet, but it is thought that once the test has been perfected, it should be able to replace doctors having to do angiograms on patients. The test right now is just a simple blood test to show which patients doctors should be giving angiograms to.  The test is meant for non-emergency patients, meaning patients that don’t think they are currently having a heart attack, but maybe patients that have been experiencing a little bit of chest pain, enough to concern them to see a doctor. The reason for this is because the test results take three days to arrive.

The test is a good idea if they can perfect it to being more accurate. It would save patients the stress of going through an angiogram.  It would also save patients a lot of money. Angiograms cost around $30,000. This new genetic test cost just over $1000.

I believe this genetic test, if perfected, will be a good idea. It not only will save patients the time and money on an angiogram, but also, if detected early enough, it will give people the time to possibly prevent a heart attack. People will know that they have an extremely high risk for having heart disease and if the those that test positive choose too, they can take the necessary steps to leading a healthier life.

Phys Ed: Are Bad Knees in Our Genes?

Researchers associated with Cincinnati Children’s Hospital and Ohio State University have been attempting to determine the risk factors for A.C.L injuries. While performing their research, they began to find indications that led them to wonder if familial predisposition influences one’s risk for an A.C.L tear.   For example, when they examined a set of athletic twin girls with A.C.L tears, it appeared that both had characteristics that are considered major risk factors for the injury– “unusually loose, flexible knee joints,… angled at least one knee outward during landings and had narrower-than-average notches in the knee bone, where the A.C.L. attaches to the bone”. Not only this, but their own father also had torn his A.C.L., along with both his triplet brothers. This examination as well as others has helped to demonstrate that these attributes may indeed run in the family.

Because of findings such as these, research has been conducted to find the “genetics of weak knees”. There have been several studies done in the past year that have found several genes that seem to be related to A.C.L. tears. One experiment produced by researchers at the University of Cape Town in South Africa “found that the women who had torn their A.C.L.’s were significantly more likely to share a specific variation in one of their genes”. The gene is known to affect the elasticity of collagen and connective tissue in tendons and ligaments (like the A.C.L.). Another study by the same group of scientists also showed an irregularity on a different gene that also affects the structure of collagen.

These discoveries are now leading scientists to consider the future possibility of DNA screenings for athletes to assess their potential risk for certain injuries, such as the A.C.L. tear. While this may produce benefits for the athlete, it also raises a lot of questions, such as “What advice do you give a young woman athlete whose genetic test shows that her knee is extremely vulnerable?” particularly since no A.C.L. injury prevention program has been entirely successful.  Perhaps with more time and more research, a direct link between genetics and A.C.L. tears can be found and questions such as these may be answered.

What an A.C.L. tear looks like:

“Cancer-Linked Epigenetic Effects Of Smoking Revealed By Study.”

Recent studies done by the UK scientists show clear evidence that smoking causes epigenetic changes linked directly to cancer.

The results of these studies were presented in front of the 35th Congress of the European Society for Medical Oncology (ESMO), in Milan, Italy. These results show that smoking causes epigenetic changes such as methylation, “which alter gene expression, without causing changes to the actual DNA sequence.”

The scientists chose a group of 2,011 healthy young women from ages 15 to 19, who were smokers, for their research. In this particular study, the scientists were looking at a gene called p16, which is a tumor suppressor gene. When a methylation occurs to this gene, it’s function of tumor suppressing is inactivated.

Dr. Yuk Ting Ma, who presented the results, and her research team found that women who smoked were more than three times as likely to get p16 methylation.

“Our study showed that compared with never-smokers, women who first started to smoke during follow-up had an increased risk of acquiring methylation of p16,” Dr Ma said.

Dr. Ma and her research team are now trying to find evidence that shows women, who received p16 methylation due to the results of smoking, are at increased risk of developing cancer.

“Tug of War Pits Genes of Parents in the Fetus”

According to Mendelian genetics, offspring inherit half of each parent’s genome. There is growing evidence, however, which suggests an asymmetrical relationship between certain maternal and paternal genes. The genetic mechanism responsible for this is called imprinting, and it may explain “differences in a mother’s and father’s contributions to social behavior.” The idea behind imprinting is that either the mother’s or father’s copy of a specific gene is inactivated.

A prime example of this involves the insulin-like growth factor 2 gene, which helps a fetus grow. In the paternal genome this gene is active, but is not in the maternal genome. Harvard evolutionary biologist Dave Haig’s theory helps to explain this. His theory proposes a conflict of interests between the fetus and the mother. The fetus wants as much nutrition as possible, while the mother wants to distribute her resources evenly to all her future children. This particular gene is imprinted in humans, mice, and various other mammals. 1300 imprinted genes have been discovered in mice. It is estimated that 1% of the human genome is imprinted.

Another example of imprinted genes involves the sex chromosomes. Female offspring receive an X chromosome from both parents. One copy, in theory, is chosen at random to be switched off. There is a much greater chance that the paternal X will be switched off in the cortex. Imprinting may be responsible for some diseases. Since one copy of the gene is switched off, a mutation to the other could be extremely harmful.

The Article below contains a small overview into the hunt for the genetics behind Osteoporosis.

I found this to be fascinating  because  although they have not discovered a direct link to the gene or loci the scientists have made a good overview of where they think to begin the search. The disease its self reduces the bone mass and causes some defects in the bone tissues microarchitecture, and we also know from basic information that diet and exercise affect the severeness of the case but genetics seems to also be playing a role in your susceptibility to osteoporosis. Seeing that we now so much about the disease I feel that they are pushing along a good path as to where to begin the search for the gene and loci.

Article written and published by:Stuart H. Ralston^* and André G. Uitterlinden

This older article contains some more information leading to the culprit gene(s) and loci behind Osteoporosis.

http://www.csa.com/discoveryguides/archives/osteo.php

The article featured above is from 1997 explains the four main area that they look for the genetics behind the disease.

I found this information to be quite more  just because it listing actual Ideas and providing back up reasoning to there opinion. the COLIA1 Gene to go further which I found to be even more interesting because of its role playing in the regulatory region with low bone mass and that it was confirmed in three populations. so as they said then there must be a connection to follow further.

following further just a quick article on the COLIA1 gene to explain its role in bone mass density.

http://www.thebonejournal.com/article/S8756-3282(01)00639-1/abstract

“What makes a good blog post?”

This is a question that everyone asks when we begin this project.  The best thing to do is, of course, google the phrase, “what makes a good blog post“.  There are lots of hits.

For our purposes here are some hints:

1. Take the pressure off.  A good blog post is no more than a couple of paragraphs.  Certainly no more than 250 words.
2. Include links to the original article.
3. In fact, include lots of links.  Your article is probably not the only one, what about the others?
4. If your post is about the inheritance of mid-digital hairs in humans — then include  a picture/diagram/photo that describes the trait.
5. Make sure and include your opinion.  Do you agree? Disagree? If you find the article interesting, WHY??
6. Finally, try writing an initial draft (saving it, of course); then, go back and edit it before submitting.

Finally, have fun out there!!