Monthly Archives: May 2013

Pain killers may decrease the effect of anti-depressant drugs says nobel prize winner Dr Paul Greengard


Even a single advil or aspirin a week or month might interfere with the remission effect of an anti-depressant drug says Dr Paul Greengard, of Rockefeller University in 2011 as reported by science daily.com in “Anti-inflammatory drugs reduce effectiveness of SSRI anti-depressant drugs“.p_33931_thumb

Dr Paul Greengard was interviewed in “A conversation with Nobel Laureate Paul Greengard” by filmannex.com. His laboratory works on unraveling the signalling process of the brain, but in particular the serotonin receptor and the P11 interaction. They are working on a clinical study using mRNA of P11 as therapy.

On September 26, 2006, a  New York Times article interviews Dr. Paul Greengard about the work in his laboratory in the 1970s which led to the discovery of the anti-depressant Prozac. It also discusses the discovery of a new brain protein, P11, in his laboratory. It is the first brain protein whose levels correlate with a neurological disorder. This protein has been jokingly called the “lesbian gene” because when it is administered to two female mice constantly fighting with each other, it transforms them into two mice that love each other. Perhaps, a similar brain protein will be discovered and turn men at war into men who love each other.

He won a Nobel Prize in 2000 and donated his prize money to recognize the contribution of women scientists in the memory of his mother who died giving birth to him.  Dr Greengard says that since he won the potato sack race in his elementary school, the Nobel Prize in 200o gave him that much pleasure.

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Sperm and Egg Donation: Should the children know their origins before choosing a mate?


Yes, because there are a few donors who are increasingly selected and are quite popular. Which means that a child born from such a donor might very well be meeting a half-sibling often and not know it at all. Now, normally that would not be a major issue. How often do we realize that we do not enjoy the company of our relatives?  We cannot choose our relatives. This situation is truly magnified in a child born from a popular donor sperm. The mothers may very well be from the same town and the children may even be in the same classroom. Yet, the donor himself might have been flown in from a different state for a few hours. This way the donor is not morally or emotionally connected to the results of his donation. This impending tsunami of children born to same sex unions or infertile couples is waiting to happen in twenty years when they grow up and form their own unions. Many of the donor’s childrens’ parents are single men/women, gay or lesbian couples or infertile couples.

“Are you my sibling?” Will that be the first question after “hello”?

Hilarious situations can arise when if in a hypothetical high school classroom a dozen students discover they are half-siblings through a donor. Now imagine the number of happy reunions in which the same sex couples choose to have a donor. Add to this the following scenario: a check list of donors. Why? is that very important? See this chart of rising number of same sex unions. If each union uses a donor and more than one uses the same popular donor do you see what might happen? How do we help a teen be sure that good looking teen is not a sibling from the same anonymous donor? Should we legislate an anonymous number system for those donors who wish to remain anonymous?

How many eggs can a woman donate?
A woman can donate only so many eggs and yet a woman may choose to be a popular donor. Even her most enthusiastic attempts cannot match that of an inspired male sperm donor. Department of Health admits that donors are not well informed. A Columbia university student asks anonymously questions about donating eggs on reading an advertisement on a Columbia Health site, where “Go Ask Alice” addresses her fears and concerns. On this Huffington Post site a woman donor explains how she does not want to be a mother and yet, donating her eggs to a couple who want to have children made her feel less guilty.

How many sperms can a man donate
A man has the potential to donate an unlimited number of sperms. Fortunately, ethical sperm banks will allow the donator to have a maximum of ten children. The sperm donor goes through a stringent selection process as described in this Stanford University list for a sperm donor. Intelligent, virile young men are much in demand as sperm donors to father a child. Not surprisingly, such men are found in universities and so, many such sperm clinics are near universities.

More than a dozen siblings from a sperm donor?
A documentary film “Donor Unknown” documents the search for Donor 150 who is the anonymous donor of more than a dozen children in a small beach community, who discover each other on a web site set up for such descendants. There is an interesting article on Boston.com about this young father who sired more than 70 children through donating his sperm in college. His fiance was a little miffed on finding out about his offsprings on a reality TV show, during which he was introduced to two of his biological children.

A typical male sperm donor description

If you are at least 5’10”, between the ages of 18 and 35 years, have post-secondary education (college, vocational or technical) and are within normal limits of weight for your muscular build and height, you may be a potential candidate to become a donor. We need donors with all types of racial and ethnic backgrounds. We are not able to accept applicants who use tobacco products in any form, including smoking or ingesting marijuana. Use of these substances will be tested for throughout the donation process.

The quote above is from a real sperm bank that has a several locations. Yet, what if several women selected the same donor at the same location? Well, many children would be born in the same town not knowing they are siblings, unless they had a way to know that.

Donors donate for financial or emotional reasons or both. Legislators need to plan for this impending tsunami of children born to same sex unions or infertile couples who in twenty years will want to be certain they are not dating their sibling, from an anonymous donor.

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How do your genes control the lipid levels in your blood plasma?


How can two people lead the same unhealthy lifestyle and yet, one person remains healthy while the other develops fatty liver disease, and is waiting for a liver to become available for a transplant? The answer was discovered in a laboratory in Texas. Helen Hobbs MD is one of the leading bioscience visionaries with her novel lipid metabolism research to improve human health. She is Director at the McDermott center for Human Growth and Development which serves as the Center for Human Genetics at UT South Western.She has recieved Germany’s highly respected Heinrich Wieland prize for her research on lipids. This prestigious prize is given annually to an individual who has conducted outstanding research.

Her interests in fatty liver disease began when a pediatrician approached her. He had several Hispanic children who were quite obese and had developed fatty liver disease. Dr Helen Hobbs began to search for a genetic answer to explain this observation and you may click here to read the 2011 summary of her results published in the journal Science entitled, “Human fatty liver disease: old questions and new insights”. hobbs

Faced with the discovery that there is a gene that can predict which person may develop liver cirrhosis or liver cancer, what is the ethical way to handle the knowledge when a 3 year old in a family with this disease also has this gene. Which means this child will have to take extreme precautions. One of them is to prevent getting obese and remain super fit. How do you tell a 3 year old?

African Americans, interestingly, are the group least likely to develop fatty liver disease since this gene is less common than among Hispanics. Caucasians lie inbetween Hispanics and African Americans in their ability to develop fatty liver disease. You may click here to read the details in the 2008 scientific journal, Nature Genetics. For those of you interested in scientific jargon, the gene is PNPLA3. Chromosome number 22 is of specific interest. Some members of four generations of an obese family may carry this gene. Those who carry two copies of this type of gene will get a very sick fatty liver. Those who have only a single copy of this gene, will remain slightly healthier. This gene is inherited.

Fructose travels straight to the liver and is strongly associated with a rise in obesity. Corn syrup contributes fructose. Obesity is associated with fatty liver disease. Carbohydrates add to the problem.

Another ethical question: what is the role of society and community when they observe a person getting super obese? Does one tell them about the connection between this gene, obesity, role of fructose and carbohydrates leading to fatty liver disease?

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Could the cure for cancer be a simple master switch solution by a Massachusetts based company?


Yes, blocking of a few master genetic switches associated with “super enhancers” might be a simple cure for cancer, says Dr. Richard Young, of Whitehead research institute, MA, senior author in two papers in the prestigious, peer – reviewed paper, Cell, and founder of a start-up company, Syros Pharmaceuticals, with the goal to cure cancer. The company has raised 30 million dollars to support its goal to cure cancer by finding and switching off the master switches in each type of cancer. You may click here to read the Cell paper led by Dr. Jakob Loven, for “Selective inhibition of tumor oncogenes by disruption of super enhancers”, and here to read the Cell paper led by Dr. Warren A. Whyte, for “Master transcription factors and mediator establish super enhancers at key cell identity genes.  Both the papers have a single, master illustration explaining the main concept. It is must see to understand how simple the hypothesized solution is. images-1

Dr Young’s team says a normal cell regulation is remarkably less complex, with core genes controlled by only a few hundred super enhancers. With this hypothesis, cancer research focus is forever changed since April 2013, and gives remarkable insight to how a single fertilized egg from a father and mother can develop into a unique individual, with two-thirds of his/her diseases having a genetic determination. Loss of old super enhancers and assembling a cluster of new enhancers drives cell identity as a human grows develops.

For years cancer scientists have been reporting their discoveries of the mediators responsible for over expression of cancer genes. What makes Dr Young’s work more unique is that it suggests that a few master switches might control this gene at super enhancer regions. There are thousands of cancer gene transcription factors in the literature. One example is the study of pancreatic cancer, the fourth commenest cause of cancer related deaths in the western hemisphere. Several key genes have been shown to play a role in pancreatic cancer, including the oncogene K-RAS and several tumor suppresor genes including some from the TGFbeta signalling pathway. The researchers discovered that the Fibroblast growth factor receptor gene 4 (FGFR4) was overexpressed in almost two-thirds of pancreatic cancers. They found a research outside this gene called intron 1, was greatly extended in pancreatic cancer cells. Two sites binding transcripton factors and two sites binding mediators were identified, and additionally, the team discovered which mediator was essential for over expression of FGFR4 to cause pancreatic cancer. You may read about this pancreatic cancer work led by Dr. Helen C Hurst of London by clicking here. Might this deadly pancreatic cancer too be controlled by inhibiting one or more of the several hundred master switches?

Do you prefer a non scientific explanation of the above solution? A very simple explanation of the complex work done by Dr. Richard Young and his team of enthusiastic young scientists is given by Amy Maxmen in the respected weekly journal, Nature and you might read it by clicking here. She appropriately titles it “Super-powered switches may decide cell fate”. Different cells in the body have the same genes swithced on at different times. When such cells are switched on by a super enhancer complex due to unknown factors (as yet), then the cell becomes cancerous. You might say that cancer cells are “fueled” by “super enhancers”, and might suggest inhibiting such a fueling source to cure cancer and you might be correct to be hopeful, albeit with a heavy dose of patience. Last year it was discovered there are a million enhancers in the human genome. Dr Young speculates that some of these enhancers act together in large clusters and function as a unit. How are cancer cells able to employ such super enhancers to produce more of their harmful factors that lead to aggressive tumorsimages

Dr. Richard Young and his team of enthusiastic young scientists deserve to know if you support their goal. Do write to them if you do to encourage them. Scientists work long hours tied to a laboratory bench. Although they love their job to solve mighty goals, receiving your notes of encouragement will inspire them further. Do keep in mind that discovery through clinical trials with FDA approval to doctors office may take a decade or longer and might cost a billion dollars for each drug in research over that period. So 30 million dollars will not take them too far without your support and creative solutions to funding.
Email: Dr Richard A. Young and his team at young@wi.mit.edu
Snail mail: Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA

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