Category Archives: Personalized medicine

Induce new hair follicles for baldness – a future personalized hair regeneration method


Columbia University Medical Center and University of Durham scientists collaborated to bring us a step closer to cure baldness (2013, October 21). Bald guys be patient. This step closer to a  cure in mice may reach humans.  Hair regeneration method is first to induce new human hair growth.  Many laboratories are working on curing baldness.  Growing hair follicle cells further in the laboratory are proving frustrating.  This laboratory circumvented that hurdle by using specific cells called dermal papillae cells and figuring out how the cells “speak” to each other and other cells around them to create a hair follicle. For the first time, researchers have been able to take human dermal papilla cells (those inside the base of human hair follicles) and use them to create new hairs. Dermal papillae cells are embedded in a rich, matrix at the base of the hair follicle and are essential for induction and maintenance of hair growth.

How new hair grows from a hair follicle

How new hair grows from a hair follicle

The study was published today in the online edition of the Proceedings of the National Academy of Sciences (PNAS) on October 21st, 2013, which you may click here to read. 
The significance of this study, briefly quoted below, is that it has the potential to grow new hair using a patient’s own cells – providing a personalized hair growth solution for baldness, says co-study leader Angela M. Christiano. Additionally, according to co-study leader Dr. Jahoda, this is an important step toward the goal of creating a replacement skin that contains hair follicles for use with, for example, burn patients

Significance

Growth of de novo hair follicles in adult skin occurs by a process known as hair neogenesis. One way of initiating neogenesis is to place dermal papillae isolated from the hair follicle in contact with an overlying epidermis where they reprogram the epidermis to adopt a follicular fate. This approach, however, has not been successful using cultured human dermal papilla cells in human skin because the cells lose their ability to induce hair growth after expansion in vitro. In this paper, we demonstrate that by manipulating cell culture conditions to establish three-dimensional papilla spheroids, we restore dermal papilla inductivity. We also use several systems biology approaches to gain a comprehensive understanding of the molecular mechanisms that underlie this regenerative process.

Similar baldness research in other laboratories
For years, scientists had thought that people suffering from hair loss had a depletion of hair follicles and follicle stem cells, which are necessary to grow hair. Dr. George Cotsarelis, a professor of dermatology at the University of Pennsylvania, published a study showing that bald people have the same number of follicle stem cells as those with hair. So if researchers could identify the signals that stimulate the stem cells into producing more hair follicle progenitor cells, then it would be possible to generate bigger hair follicles that could grow hair. Such studies have shown that men with male pattern baldness still have stem cells in follicle roots but these stem cells lose the ability to initiate hair regeneration.

University of Toronto scientists have discovered cells in hair follicles that seem to function like dermal stem cells and could have potential uses in many areas of medicine.

Whilst nobody currently offer stem cell therapy for hair loss, this research offers insight into how stem cell therapy can be used for a range of skin conditions, including scarring and skin cancer.

Freda Miller, Ph.D., professor of molecular and medical genetics at the University, reviewed her and her colleagues’ current and prior research at a recent International Society for Stem Cell Research meeting.

The research may someday offer stem cell therapy for hair loss.

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SynapDx Corporation lands 15.4 million for Big Autism clinical Study


Geneticists and venture capitalists alike believe that a Massachusetts-based company, SynapDx, can develop the earliest and most informative blood test for autism, and Autism Spectrum Disorders (ASD) using advanced technologies. They specialize in differential expression of certain genes in blood cells that may form the basis of an ASD biomarker. The best diagnostic tests in the near future will combine the knowledge of your genomes, which you inherited from your parents and will pass on to your children, with the technology of computer skills able to handle incredibly large data. A medical technology startup, SynapDx, is currently studying large databases of children who have been clinically diagnosed with autism to discover a shared genomic blueprint. Since all children do not have autism, there might be a particular genomic blueprint among the children that are diagnosed with autism. It is also working on a RNA based blood test to differentiate between patients referred for developmental concerns.  Interested in SynapDx’s clinical study for autism? To learn more click here.

Venture Capital
A group of venture capitalists led by Google Ventures have backed SynapDx autism blood test with 15.4 million, which will help fund the large-scale effort to research 660 children at the same time using advanced computer technology.  The children will be between the ages of 18 months and five years in North America and include children from the Lurie Center of Autism in Massachusetts.  The study will be led by Stan Lapidus, the company CEO. The potential to diagnose children at a very young age, as early as 19 months, is a breakthrough technology currently in clinical trials. Today, an autism diagnosis can be confirmed when a child is 4-5 years, when a child can no longer communicate effectively in society.  This is considered disastrously late.  This infusion of funding will enable the clinical trial to be expanded to 20 sites. The hope is that Google’s expertise with handling big data will aid in pinpointing the role of genome changes in early autism diagnosis.

Autism Diagnosis and Therapy
The earlier a child is diagnosed, the faster a parent may be advised to begin therapy and the use of communication aids. The ipad from Apple company has been a boon for children with ASD helping them to communicate more effectively. More such Apps are also being funded for development to simultaneously pair with therapy of autism.

The role of the gut microbiome has also been recognized as critical since all children with autism have very restrictive eating habits. Research into probiotics and prebiotics are playing a significant role in therapy of autism and ASD. Read “Related Articles” below.

Hopefully, researchers will be able to find a clue as to why parents with multiple sclerosis have children with autism, allergy, and ASD. Is there a genomic blueprint that predisposes a family when exposed to certain unknown triggers? When exposed as a child – ASD; when exposed as an adult – multiple sclerosis. Read “Related Articles” below for discussions on autism, role of aging parents, shank gene, coffee intake of father, G-proteins that try to prevent autism, gut microbiome and good/bad germs, role of Vit-D, and more.

Is Autism observed only in Developed Countries?
Although, this company may only provide a partial answer to the mysterious rise in the number of children developing autism, especially boys, it may give researchers a clue into why children from certain ethnicities develop autism when born in developed countries. Why is autism not observed in developing countries? To read a discussion click here for “Why is Autism observed in America and not in underdeveloped countries?”.  Autism does not discriminate by ethnicity.  It has been observed in Caucasians, Asians, Hispanics and blacks. When children of Somali descent are born in underdeveloped Somalia, they do not develop autism while they do in developed countries like Sweden and USA.  This has led to research on the role of Vitamin D from sunlight in autism, since Somalia is in Africa and has mostly sunny days, while Sweden and USA have far less sunny days, and more indoor activities of an advanced civilization with computer games and television. However, since all children in Sweden and USA have mostly similar indoor activities, why do only some of them have autism? The answer may lie in their genomic blueprint differences and/or exposure to a yet unknown environmental trigger.

Today, developing countries may show more cases of dyslexia or mild autism spectrum disorder. However, as these countries become more like Sweden or USA, will there be more cases of autism diagnosed there too? The answer might be yes, since the autism trigger suspects might be in a developed country lifestyle.  The answer might lie in the way we eat, live, clean, and prevent in an effort to be healthier.  Yet, in that very effort we may unwarily be introducing the triggers like pesticides or herbicides or toxic landfills and spills, that set up local children for autism by damaging the genome of the growing delicate foetus in the womb, depleting our gut of healthy germs that protect symbiotically, or by not understanding all the complex cellular interactions of some of our vaccine components and how they interact with a damaged genome (see below Related Articles).

Related Articles
Autism
The Gut Microbiota: your good germ friends to nurture to strengthen your immune system against “Allergy”
Worm Theory: to improve the immune system to fight asthma, multiple sclerosis and more
Autistic child or severely Allergic child with Multiple Sclerosis parent
G proteins: the connector proteins that try to prevent Autism Spectrum Disorder
Know your G proteins: relevant for Allergy, Autism, Aspergers and ASD
Four facts about allergy: parents, children, patients, genes and researchers
Autism in pristine Phu Quoc island of Vietnam – is the rise in numbers simple overdiagnosis?
A single shared component has been confirmed in allergy and autoimmune diseases
World’s largest collection of frozen Autism brains ruined in freezer malfunction
Are we less healthy than our parents and grandparents – both mentally and physically?
Are there any Gays and Lesbians who are autistic?
Why and how to add Calcium in the diet of a person with Autism Spectrum Disorder

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A single shared component has been confirmed in allergy and autoimmune diseases


Previous studies had shown that patients with a diverse range of autoimmune diseases often had minor changes in the BACH2 gene. Today’s cutting edge technology allowed scientists to glimpse some of the interactions this gene had with the entire genome to control immune function, says lead author Dr. R. Roychoudhuri. BACH2 plays a key role in the immune system. Although, the intracacy of the immune system remains elusive, it is understood that a healthy immune system knows how to recognize a foreign body and can attack it, to keep a person healthy while in an unhealthy immune system, the body’s own cells or friendly agents are mistaken as “foreign” and attacked resulting in allergy or autoimmune diseases like rheumatoid arthritis and asthma.

This non-profit kids health site lists in the chapter “Health Problems” the many allergy and autoimmune diseases a child may suffer from today. Perhaps, this discovery published in the respected journal Nature might some day help a child and the parent lead a healthier life (Click here to read Nature, June 2, 2013 article).

The Discovery

NIAMS researcher Kiyoshi Hirahara, M.D and colleagues discovered that the Bach2 gene played a key role in regulating the switch between inflammatory and regulatory cells in mice. The loss of the Bach2 gene in specific immune cells caused them to become inflammatory, even under what would be a protective situation. Says a team leader, Dr. Nicholas P. Restifo, “The gene shares its name with the famous composer Bach, since it orchestrates many components of the immune response, which, like the diverse instruments of an orchestra, must act in unison to achieve symphonic harmony”

Potential for Gene Therapy?
The studies were done in mice and will have to be replicated in human clinical trials, which as you know could take time. When the mice lacked the BACH2 gene the mice died within a few months of life.  If the BACH2 gene was introduced into the mice lacking this gene, it restored their immune health. Thus, gene therapy with BACH2, a gene common in patients with allergy and autoimmune disease, restored the immune health of lab mice.

A laboratory research mouse

A laboratory research mouse

Related Article

A multiple sclerosis parent with autistic child
Know your G protein – for autism, allergy, aspergers and ASD

G proteins – the connector proteins that try to prevent autism spectrum disorder
Do anorexics and autism spectrum disorder share any common characteristics?

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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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Did you know that your medicine might damage your nerves?


You take medicine to cure an illness. Did you know that your medicine might have a side reaction? Most people may not get serious side reactions and can tolerate their medicine and begin to feel better. Very few, however, may get a side reaction called peripheral neuropathy or numbness of fingers from nerve damage. In most cases, stopping the medicine will stop this damage.

If you want to read more about what to do if your fingers feel numb after taking a certain few prescribed drugs, then click on the title of the following excellent current scientific articles, which are not too unpleasant to read because they are so full of simple facts. However, always consult your doctor since the risks must be balanced with the positive aspects of taking this medicine.

Peripheral neuropathy

Many more agents are suspected of causing neuropathy than discussed. Despite the lengthy and fastidious drug approval process, rare and idiosyncratic causes of medication-induced neuropathy may only become evident after wide-usage. Medication-induced toxicity should be at least considered in new cases of neuropathy including apparent idiopathic forms. Also importantly, patients with existing neuropathy of known or presumed cause should have their current regimen and planned therapy considered for potential neurotoxicity. Some preventative agents against chemotherapy toxicity show promise, but none are yet approved for routine use against neurotoxic effects.

Platinum neurotoxicity

Current research has shown insight into the mechanisms of nerve damage caused by the platinum agents. After entering the DRG, the platinum agent forms an adduct with DNA. Apoptosis has been observed in DRG neurons following cisplatin treatment both in vitro and in vivo (31) and is correlated with increased platinum-DNA binding in these DRG neurons (31). Oxaliplatin and cisplatin differ in their severity of neurotoxicity to the DRG. Cisplatin produced about three times more platinum-DNA adducts in the DRG (32) than equimolar doses of oxaliplatin, consistent with clinical observations that cisplatin is associated with greater neurotoxicity.

A genome wide association study (which asks if your genes dictate a tendency towards nerve damage)

Purpose:Sensory peripheral neuropathy is a common and sometimes debilitating toxicity associated with paclitaxel therapy. This study aims to identify genetic risk factors for development of this toxicity. Experimental Design: A prospective pharmacogenetic analysis of primary breast cancer patients randomized to the paclitaxel arm of CALGB 40101 was used to identify genetic predictors of the onset and severity of sensory peripheral neuropathy.

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