Silver hair and health

Watch what you affirm.

Some say things like you are a pain in the neck when they are mad at some one. Then often times end up with a stiff neck or some discomfort in their neck .grey-hair585_204681a

Science now has found another link between the graying of one’s hair and stress. Now “genotoxic stress,” or stress from the toxic effects of chemicals or energy in our environment can damage DNA, like ultraviolet light. The researchers found that this cellular stress diminishes the supply of melanocyte stem cells (MSC) – cells in hair follicles that are responsible for making the pigment-producing cells that give hair its color.not necessarily age related and the stresses in one’s life.

melanin storage in melanocyte
melanin storage in melanocyte

Integrated medicine has known about this connection for year and routinely treat and help poeple destress. Applied kinesiology and homeopathy hves perfected the art of relieving the stress from physical, memory, emotional, and situational stres.
Melanocyte stem cells are so-called “adult stem cells.” They are not mature hair cells and they can continuously divide and supply our hair with the pigment producing cells it needs to have color. When a melanocyte stem cell matures into a pigment producing cell, or melanocyte, it is called differentiation.

For more information on ways to decreases stress in your life.

Resources

Excerpts courtesy of news.yahoo.com/s/livescience/rootsofgrayhairfoundincellularstress
Excerpts courtesy of livescience.com/health/080115-stress

Image 1. courtesy of  cdn-write.demandstudios.com/

Image 2. courtesy of    scf-online.com/issue22/images22/IllustrationMelanin22

Odor to make humans disappear- mosquitoes confusants

19-1The image at the right is an
electron micrograph of the head of a female Anopheles gambiae mosquito, showing the parts of olfactory appendages (antennae, maxillary palps and proboscis)

Dr. Leslie Vosshall and two colleagues at Rockefeller University published a series of experiments that seemed to settle the 50-year-old question of how the insect repellent DEET kept mosquitoes at bay (Science, 319:1838-42, 2008).

Vosshal explained their findings “It doesn’t smell bad to insects. It masks or inhibits their ability to smell you.”
The Bill & Melinda Gates Foundation funded the research to understand how and why DEET works. This is critical to creating the next generation of chemicals, which may head off insect-borne diseases such as malaria and dengue fever.
Related Articles
Laurence Zwiebel of Vanderbilt University (also a Gates’ grantee) and  Ulrich Bernier of the US Department of Agriculture are not sure the findings just didn’t make sense, given everything they knew about this system

In Vosshall experiment,  the response of the mosquito’s olfactory neurons to two separate, attractive odors in human breath. Then, she combined each odorant with DEET in a single odor cartridge and noticed a smaller neural response. Vosshall believes DEET was blocking the mosquito’s olfactory co-receptor.
Another teams experiment another interpretation

Using gas chromatography, Leal confirmed his suspicions this year. When he repeated Vosshall’s experiment using separate odor cartridges that blended DEET and each attractive odor only at their tips, the mosquito’s neural response was no longer diminished. Then, Leal identified a DEET-sensitive odor receptor neuron and showed that mosquitoes avoid passing through a “curtain” of DEET vapors.
Leal’s paper surprised Vosshall, but is unconvinced by Leal’s results, and has been trying to reproduce the effect in her own lab. “Competition in science is good,” she says, “It can be difficult when it’s a small field, and this is a very small field.”

Genomic studies in 2005 have since shown that this co-receptor is found in insects ranging from mosquitoes to moths,  making humans invisible to insects. Using tissue cultures, she uses targeted drug discovery to screen 91,520 compounds from a chemical library, short-listing about 150 that she believes have the potential to be insect “confusants.”

Even Vosshall’s skeptics admit the confusant strategy is fundamentally sound. Zwiebel says his unpublished molecular work confirms the existence of confusants, but when it comes to DEET, he and Vosshall aren’t willing to budge. “We have agreed to disagree on the DEET story,” he says.

Resources

Smells funny? – Brendan Borrell  The Scientist.com Volume 23 | Issue 1 | Page 19.

http://www.the-scientist.com/2009/01/1/19/1/

Mosquitoes smell and avoid the insect repellent DEET – Leal and Zainulabeuddin Syed,  PNAS 105:13598-603, 2008 September 2008.


Image courtesy
of LJ Zwiebel, colorization by Dominic Doyle / Vanderbilt University

Dysport cousin to Botox – possible birth defects

Health alert over the “use of anti-wrinkle treatments like Botox, after an Australian baby was born with serious birth defects.

The mother was given facial cosmetic injections of the drug Dysport in the first weeks of her pregnancy in 2005. Her baby was born deaf and blind.

A report by the manufacturer a year later admits a possible link with the drug’s use, News Ltd reported.”

Dysport is made from clostridium botulinum type A  a haemeglobulin and has,  far as the Australian Therapeutic Goods Administration is concerned, no warnings and no  specific indications are given for its use.

Haemeglobulin means it effects the blood and seems to cross the blood brain barrier in mom and fetus. The drugs effects on early stage  fetal development can possibly be due to the neurological stress causing the wrong chemical messages to be sent to the developing fetal systems.

From the Dysport commercial

Yes, “Dysport is a simple, effective, non-surgical treatment that works by relaxing facial muscles on the forehead, thereby reducing and smoothing away frown-lines and wrinkles this is true.”
Any drug that effects neurology and physiology of the body can cause troubles for the developing fetus in the womb.
Dysport has been used to treat

  • neurological and ophthalmic conditions.
  • frown lines
  • axillary hyperhidrosis (excessive sweating under the armpits).
  • nervous tics and muscle spasms of the face and neck.
  • neuro-muscular conditions
  • botulinum toxin Type A to be approved in New Zealand
  • spasticity in adults of many types
botoxneed270.jpg

Getty Images

ADVERSE REACTIONS TO DYSPORT46 REPORTED

  • Possible birth defects to the botulinum type A toxin used in Botox and Dysport
  • temporary facial paralysis
  • fatigue
  • dizziness
  • hallucinations
  • trouble swallowing
  • anxiety.

Dysport that have been reported to the Therapeutic Goods Administration since July 1, 1994.
Is temporary beauty worth losing your health or your baby’s chance at a normal life?

Dysport is manufactured in Britain by Ipsen Limited.

Resources

Brain Tumors-New Genetic Pathways

Comprehensive Study of Brain Tumors

New Genetic Mutations, Core Pathway

“The Cancer Genome Atlas (TCGA) Research Network, a collaborative effort funded by the National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI) of the National Institutes of Health (NIH), reported the first results of its large-scale, comprehensive study of the most common form of brain cancer, glioblastoma (GBM). “Sept. 4, 2008, in the advance online edition of the journal Nature, the TCGA team describes the discovery of new genetic mutations and other types of DNA alterations with potential implications for the diagnosis and treatment of GBM.

Among the TCGA findings are the identification of many gene mutations involved in GBM, including three previously unrecognized mutations that occur with significant frequency; and the delineation of core pathways disrupted in this type of brain cancer. Among the most exciting results is an unexpected observation that points to a potential mechanism of resistance to a common chemotherapy drug used for brain cancer.

“… The more we learn about the molecular basis of glioblastoma, the more swiftly we can develop better ways of helping patients,” said NIH Director Elias A. Zerhouni, M.D.

Like most cancers, GBM arises from changes that accumulate in cells’ DNA over the course of a person’s life – changes that may eventually lead to the cells’ uncontrolled growth. However, until recently, scientists have understood little about the precise nature of these DNA changes and their impact on key biological pathways that are important to the development of new interventions.

TCGA researchers sequenced 601 genes in GBM samples and matched control tissue, uncovering three significant genetic mutations not previously reported to be common in GBM. The affected genes were: NF1, a gene previously identified as the cause of neurofibromatosis 1, a rare, inherited disorder characterized by uncontrolled tissue growth along nerves; ERBB2, a gene that is well-known for its involvement in breast cancer; and PIK3R1, a gene that influences activity of an enzyme called PI3 kinase that is deregulated in many cancers. PI3 kinase already is a major target for therapeutic development. The discovery of frequent mutations in the PIK3R1 gene means that GBM patients’ responses to PI3 kinase inhibitors may be dictated by whether or not their tumors have mutated versions of the gene.

The TCGA team combined sequencing data with other types of genome characterization information… to generate an unprecedented overview that delineated core biological pathways potentially involved in GBM. The three pathways, each of which was found to be disrupted in more than three-quarters of GBM tumors, were: the CDK/cyclin/CDK inhibitor/RB pathway, which is involved in the regulation of cell division; the p53 pathway, which is involved in response to DNA damage and cell death; and the RTK/RAS/PI3K pathway, which is involved in the regulation of growth factor signals.

The three pathways were interconnected and coordinately deregulated in most of the GBM tumors analyzed. Therefore, combination therapies directed against all three pathways may offer an effective strategy, the TCGA researchers state.

As in the Human Genome Project, TCGA data are being made rapidly available to the research community through a database, http://cancergenome.nih.gov/dataportal. The database provides access to public datasets, and with required review and approval, allows researchers access to more in-depth data.

Additional information about NHGRI can be found at its Web site,” http://www.genome.gov.