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Sudden Hair Loss While On Thyroid Medication

admin — Thu, 13 Jun 2013 15:40:25 +0000

Abnormal thyroid levels can be the cause of hair loss. Most people see an improvement in their hair loss while on Synthroid, a medication that treats hypothyroidism. However some people notice sudden hair loss while on synthroid and this may be puzzling. Why is that?

Over the past many years I have seen over 10,000 patients. I have seen many patients with hypothyroidism on thyroid medication. It has been my experience and experience of my colleagues that people are very sensitive to the change in levels of thyroid hormones. Meaning that increasing or decreasing the medication suddenly may cause sudden hair loss, also known as telogen effluvium. I have actually seen this multiple times when people are trying to correct their level too fast increasing the dose too fast or decreasing it too fast. Hormone levels are supposed to be almost nearly constant levels. Quick sudden changes in these levels may lead to shock loss of hair.

Recommendation suggestion;

If you take Synthroid for hypothyroidism is important that you slowly increase the dose until you reach normal levels. It is important that if you would like to decrease the dose, to do it gradually as well. Skipping doses or missing doses can lead to sudden fluctuations in thyroid level, which may cause sudden hair loss. I strongly recommend taking the medication everyday at the at the same time. I also recommend routinely check your thyroid levels to make sure it’s not too high or too low.

HELP! eyebrow hair loss!

admin — Wed, 12 Jun 2013 20:37:22 +0000

so it’s been going on for months…
at first i just started losing eye brow hairs, i would find them on my face or keyboard. over time (months) the amount of eyebrow hairs lost increased. i started to lose lots of them at once. then i noticed that when i got out of the shower the area around my eyebrows had dead skin.

female/ 20.
there is no redness.
they rarely itch.
no i dont overpluck my eyebrows.
my thyroids have been checked multiple times,
i recently had a lot of blood work done and everything came back fine.
i dont touch/ mess with my eyebrows.

i did notice that my skin has been more oily than normal,
but im not sure what that would have to do with it.

ive been to many doctors, most dont take me seriously but its getting to the point where i dont know if i can go to school much longer. eyebrows are important to me, ive always had great ones and i used to model and now they look jacked up. it sounds stupid but once your eyebrow hairs start falling out you’ll understand.

also…
the eyebrow hairloss started on the inner part of my eyebrow (the part near the middle of your face) its slowly worked its way out.

thanks to anyone that replies, feed back is appreciated.
if you’ve had similar problems or have any questions let me know!

Using Laser To Remove Tattoos

admin — Fri, 24 May 2013 18:44:21 +0000

Mistakes are often easily forgiven or forgotten, whereas a tattoo acts as a constant reminder. People sometimes change their mind; some don’t like the tattoo they initially loved anymore, while others are unhappy because their old tattoo shifted or the ink has blurred. For whatever reason, now it is possible to reverse the undesired effect and start with a clean slate!

Laser tattoo removal treatments

Compared to earlier days, Tattoo removal has advanced significantly. Thanks to advances in laser technology, the safety and effectiveness of removing tattoos has improved in recent years. Today’s modern laser procedures are capable of removing multicolor tattoos with minimal scarring in often fewer sessions. The laser treatment consists of very accurate, intense light pulses breaking down the pigments deep in the skin, which are then naturally absorbed through the body’s lymphatic system, resulting in the tattoo fading away gradually.
Are laser treatments easy?

Tattoo removal depends on various factors, such as color and location of the tattoo. Although black pigment is the easiest to remove, red and dark blue pigments also respond well. In the past, green, orange, light blue, and white pigments have been difficult to remove but today’s technology is able to dissolve these colors with time. Tattoos on areas where the skin is thicker, like the abdomen for example, require fewer sessions compared with areas where the skin is thinner like the ankle.

Depending on the size and color of a tattoo, the amount of sessions required can vary immensely, with the average number of treatments required consisting of between 6 and 15 sessions. In order to keep discomfort at a minimum, the therapist will apply a local anesthesia to the tattoo before treatment commences. Some people describe the sensation of the treatment as a rubber band being snapped against their skin.

Each session generally takes only a few minutes with a 6 to 12 week break between appointments in order to allow the treated area to heal sufficiently. Following treatment, some people may experience redness and minimal swelling of the affected area, both of which will subside shortly after the treatment.

Perelman School of Medicine Experts Identify Inhibitor Causing Male Pattern Baldness and Target for Hair Loss Treatments

admin — Fri, 24 May 2013 18:35:42 +0000

PHILADELPHIA — Researchers from the Perelman School of Medicine at the University of Pennsylvania have identified an abnormal amount of a lipid called Prostaglandin D2 in the bald scalp of men with male pattern baldness, a discovery that may lead directly to new treatments for the most common cause of hair loss in men. In both human and animal models, researchers found that a prostaglandin known as PGD2 and its derivative, 15-dPGJ2, inhibit hair growth. The PGD2-related inhibition occurred through a receptor called GPR44, which is a promising therapeutic target for androgenetic alopecia in both men and women with hair loss and thinning. The study is published in Science Translational Medicine.

Male pattern baldness strikes 8 of 10 men under 70 years old, and causes hair follicles to shrink and produce microscopic hairs, which grow for a shorter duration of time than normal follicles.

Researchers took an unbiased approach when scanning for potential biological causes of baldness, looking in scalp tissue from balding and non-bald spots from men with male pattern baldness and then corroborating findings in mouse models. They found that levels of PGD2 were elevated in bald scalp tissue at levels 3 times greater than what was found in comparative haired scalp of men with androgenetic alopecia. When PGD2 was added to cultured hair follicles, PGD2-treated hair was significantly shortened, while PGD2′s derivative, 15-dPGJ2, completely inhibited hair growth.

“Although a different prostaglandin was known to increase hair growth, our findings were unexpected, as prostaglandins haven’t been thought about in relation to hair loss, yet it made sense that there was an inhibitor of hair growth, based on our earlier work looking at hair follicle stem cells,” said George Cotsarelis, MD, chair and professor of Dermatology, and senior author on the studies. In a Penn study published in the Journal of Clinical Investigation last year, underlying hair follicle stem cells were found intact, suggesting that the scalp was lacking an activator or something was inhibiting hair follicle growth.

Prostaglandins are well characterized for their role in many bodily functions — controlling cell growth, constricting and dilating smooth muscle tissue — and a different prostaglandin (F2alpha) is known to increase hair growth. Researchers found that as PGD2 inhibits hair growth, other prostaglandins work in opposition, enhancing and regulating the speed of hair growth.

While these studies looked at AGA in men, the researchers noted that prostaglandins may represent a common pathway shared by both men and women with AGA. Future studies, potentially testing topical treatments that may target GPR44, can determine whether targeting prostaglandins will benefit woman with AGA as well.

The research team consisted of Dr. Cotsarelis, lead author Luis Garza, MD, PhD, (former post-doctoral fellow at Penn, now at Johns Hopkins University School of Medicine) and Yaping Liu (now at Merck & company), Zaixin Yang, Brinda Alagesan, Scott Norberg, Tailun Zhao, Hanz Blatt, from Penn’s Dermatology department; Garrett FitzGerald and John Lawson from Penn’s Department of Pharmacology and the Institute for Translational Medicine and Therapeutics; David Stanton and Lee Carrasco from Penn’s Department of Oral and Maxillofacial Surgery and colleagues at Gillette, and University of Texas M.D. Anderson Cancer Center.

The study was funded by grants from the National Institutes of Health (R01-AR46837, P30-AR057217, 5R01AR055309 and K08AR055666, 5-P30-AR-057217-02), the Pennsylvania Department of Health, the Edwin and Fannie Gray Hall Center for Human Appearance at Penn Medicine, American Skin Association, Dermatology Foundation and L’Oreal. Drs. Cotsarelis and Garza are co-inventors on a patent owned by the University of Pennsylvania describing the PGD2 pathway as a target for inhibiting hair loss.

Penn Medicine is one of the world’s leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation’s first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.

The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according to U.S. News & World Report’s survey of research-oriented medical schools. The School is consistently among the nation’s top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.

The University of Pennsylvania Health System’s patient care facilities include: The Hospital of the University of Pennsylvania — recognized as one of the nation’s top “Honor Roll” hospitals by U.S. News & World Report; Penn Presbyterian Medical Center; and Pennsylvania Hospital — the nation’s first hospital, founded in 1751. Penn Medicine also includes additional patient care facilities and services throughout the Philadelphia region.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2012, Penn Medicine provided $827 million to benefit our community.

source: http://www.uphs.upenn.edu/news/News_Releases/2012/03/hair/

Timing of cancer radiation therapy may minimize hair loss, researchers say

admin — Thu, 23 May 2013 17:40:06 +0000

Discovery of circadian clock in mice hair reveals period of time when damage from radiotherapy can be quickly repaired, keeping hair intact

May 20, 2013

LA JOLLA, CA—Discovering that mouse hair has a circadian clock – a 24-hour cycle of growth followed by restorative repair – researchers suspect that hair loss in humans from toxic cancer radiotherapy and chemotherapy might be minimized if these treatments are given late in the day.

The study, which appears in the early online edition of the Proceedings of the National Academy of Sciences (PNAS), found that mice lost 85 percent of their hair if they received radiation therapy in the morning, compared to a 17 percent loss when treatment occurred in the evening.

The researchers, from Salk Institute for Biological Studies, the University of Southern California (USC) and the University of California, Irvine (UCI), worked out the precise timing of the hair circadian clock, and also uncovered the biology behind the clockwork – the molecules that tells hair when to grow and when to repair damage. They then tested the clock using radiotherapy.

“These findings are particularly exciting because they present a significant step towards developing new radiation therapy protocols that include minimizing negative side effects on normal tissues, such as hair or bone marrow, while maintaining the desired effects on cancer cells,” says Maksim Plikus, assistant professor of developmental and cell biology at UCI and the study’s first author. “We will now apply our findings to design novel circadian rhythm-based approaches to cancer therapy.”

Salk researchers Satchin Panda and Amandine Chaix.

Images: Courtesy of the Salk Institute for Biological Studies

The scientists can’t say their findings will directly translate to human cancer therapy because they haven’t yet studied that possibility. But they say it is becoming increasingly clear that body organs and tissues have their own circadian clocks that, when understood, could be used to time drug therapy for maximum benefit.

“There are clocks everywhere in the body – clocks that have their own unique rhythm that, we found, have little to do with the central clock in our brains,” says the study’s co-lead investigator,Satchidananda Panda, an associate professor in Salk’s Regulatory Biology Laboratory and an expert on circadian rhythm.

“This suggests that delivering a drug to an organ while it is largely inactive is not a good idea. You could do more damage to the organ than when it is awake, repairing and restoring itself,” says Panda. “If you know when an organ is mending itself, you might be able to deliver more potent doses of a drug or therapy. That might offer a better outcome while minimizing side effects.”

Panda uses genetic, genomics and biochemical approaches to identify genes under circadian regulation in different organs and to understand the mechanism of such regulation. Plikus at UCI and Cheng-Ming Chuong, professor of pathology at the Keck School of Medicine of USC and the study’s co-lead investigator, are experts on hair regeneration.

These researchers and their colleagues teamed together to find and then take apart the mouse hair circadian clock. It was a long and difficult study, Chuong says.

“Hair is a very complicated organ, featuring different types of cells going through different stages in the life cycle in a very tiny space,” Chuong says. “We found that hair in mice grows fast in the morning and slows down at night, engaging a very powerful clock.”

Every time hair cells divide, they pick up DNA damage that needs to be repaired. The scientists discovered that mice hair cells repair that damage primarily in the evening. This process is akin to using a kitchen dishwasher, Panda says. “Most of us run the dishwasher after we have accumulated a lot of dirty dishes – we don’t run it every time a dish is dirty. The same is true for cells. They clean up – repair their DNA – at one time each day,” Panda says.

Radiotherapy damages DNA in cells that divide rapidly, which is why it is used against growing cancer cells. That means that DNA damage to hair cells from radiotherapy delivered in the morning is not repaired until the evening, leading to hair loss. Damage from radiotherapy at night, however, is minimized because hair cells, already in the process of repairing DNA, can quickly heal.

“While we don’t yet know if human hair follows that same clock we found in mice hair, it is true that facial hair in men grows during the day, resulting in the proverbial 5 o’clock shadow. There is no 5 a.m. shadow if you shave at night,” Panda says.

The researchers found that cancer cells do not have circadian clocks, because they are dividing all the time. “That means cancer therapy does not have to be timed to be more effective,” Panda adds. “The timing has to do with minimizing collateral damage from normal cells affected by these treatments.”

Scientists know for certain that other organs, such as the liver, use a circadian clock, and they suspect that all human tissue is similarly regulated, although the clocks may be timed differently.

“There are many clinical implications for this cacophony of internal clocks, beyond the timing of drug therapy,” Panda says. “For example, some researchers suspect that obesity and diabetes occurs when an organ or organs – perhaps the liver or stomach or pancreas – should be sleeping, but is awoken by food that needs to be processed.

“These local clocks do a lot more things than the central clock in the brain, which primarily regulates sleeping,” he says. “This field of research is exciting and may, someday, contribute to human health.”

Other contributing authors are Christopher Vollmers and Amandine Chaix from Salk, Damon de la Cruz from USC, and Raul Ramos from UCI.

The study was supported by grants from the National Institutes of Health (AR 42177, AR47364, DK091618, P30 CA014195), The Leona M. and Harry B. Helmsley Charitable Trust, the Dana Foundation, the Glenn Foundation for Medical Research and the Edward Mallinckrodt Jr. Foundation. The authors declare no conflicts of interest.

About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world’s preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer’s, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.

Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.

Alopecia Areata Associated With Autoimmune Comorbidity

admin — Thu, 23 May 2013 17:23:49 +0000

Many individuals with alopecia areata (AA) have comorbid conditions, according to a retrospective cross-sectional study. The authors compared the prevalence of comorbid conditions in patients with AA with the prevalence of comorbid conditions in patients in the Psoriasis and Psoriatic Arthritis Follow-up Study. The association between AA and comorbid conditions was consistent with findings from previous studies.

Kathie P. Huang, MD, from the Clinical Research Program, Department of Dermatology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, and colleagues report their results in an article published online May 22 in JAMA Dermatology.

“Our descriptive study aimed to characterize the comorbid conditions associated with AA in the Boston patient population seen at the Partners institutions during an 11-year period. The [Automated Retrieval Console] program, which harnessed properties of artificial intelligence and systematic natural language processing, allowed us to select a group of 2115 patients with AA. These patients were initially screened on the basis of their [International Classification of Diseases, Ninth Revision] codes, and their diagnosis was confirmed by using our innovative program, which created a model based on manual review of records,” the authors explain.

The study had the advantage of including a large, heterogeneous population. Patients with AA had a significantly increased incidence of atopy (38.2%), contact dermatitis (35.9%), gastroesophageal reflux disease (17.3%), and vitiligo (2.8%). The authors suggest that the connection between atopic disease and AA may be driven by changes in the integrity of the epidermal barrier resulting from filaggrin mutations.

“We found a high prevalence of autoimmune diseases in our AA cohort compared with previous studies,” the authors write. Specifically, they found that 35.0% of patients with AA were positive for thyroid peroxidase antibodies, an autoimmune marker.

“We found high psychiatric comorbidity among our patients with AA at 25.5%; this category included depression and anxiety, consistent with findings of previous studies that surveyed the most common psychiatric disorders in adult patients with AA,” they note. They also found an association between AA and hyperlipidemia and hypertension.

“The first practice gap is the need to understand whether this increase is real or just linked to advances in diagnostic methods or differences in the study population and methods,” writes Anatonella Tosti, MD, from the Department of Dermatology & Cutaneous Surgery, Miller School of Medicine, University of Miami, Florida, in an accompanying comment. “The second practice gap is the need for dermatologists to include in their review of systems for AA questions about autoimmune disorders, mood or depression, and bowel symptoms…. The third and most important practice gap for physicians is establishing the costs and benefits of ordering extensive laboratory and diagnostic tests to screen patients with AA for possible associated autoimmune diseases.”

One coauthor reported serving as a consultant for Abbott, the Centers for Disease Control and Prevention, Novartis, and Janssen, and receiving a grant from Amgen for an unrelated project. The questionnaire used was licensed to Pfizer and Merck for clinical trials. The other authors and Dr. Tosti have disclosed no relevant financial relationships.

JAMA Dermatol. Published online May 22, 2013. Article abstract, Comment extract

Fruit Flies Reveal Clues to Wound Healing in Humans

admin — Wed, 22 May 2013 20:29:47 +0000

In research presented at the Genetics Society of America’s ongoing annual Drosophila Conference in Washington, D.C.,
scientists describe how identification of fruit fly genes responsible for wound repair may lead to discoveries for healing
human skin wounds.
Washington, D.C. – April 5, 2013— A person’s skin and a fruit fly’s exoskeleton, called a “cuticle” may not look
alike, but both coverings protect against injury, infection, and dehydration. The top layers of mammalian skin
and insect cuticle are mesh-works of macromolecules, the mammal version consisting mostly of keratin
proteins and the fly version predominantly of the carbohydrate chitin. Yet the requirement of an outer
boundary for protection is so ancient that the outermost cells of both organisms respond to some of the same
signals. And because of these signaling similarities, the fruit fly Drosophila melanogasterserves as a model for
wound healing.
A presentation today at the Genetics Society of America’s 54th Annual Drosophila Research Conference in
Washington D.C. April 3-7 describes a new way to study wound healing in flies that suggests new targets for
wound-healing drugs. About 177 million people a year suffer from a wound, an opening that breaks the skin
and usually damages the tissue underneath, which may be surgical, traumatic as a burn or laceration, or may
be a chronic condition, as with people who have diabetes or those with immune system diseases.
Michelle T. Juarez, PhD, an assistant medical professor at the Sophie Davis School of Biomedical Education at
the City College of New York, presentsthe doctoral research on wound healing of Rachel A. Patterson, from
the University of California, San Diego (UCSD). William McGinnis, PhD, distinguished professor of the section of
cell and developmental biology at UCSD, completes the research team. He has been investigating the
“biological armor” of the fly for many years.
A desire to understand more about wound healing in people inspired the trio, particularly Ms. Patterson. “My
fiancé is a firefighter and a member of the U.S. military. Maybe one day our work will influence his medical
treatment if he sustains burns or injury wounds,” she said.
The fly is an excellent model to dissect skin repair at a cell and molecular level. “Many of the key molecules
and proteins involved in Drosophila wound healing are involved in mammalian wound healing. The genetics of
Drosophila is not as complicated as mammalian genetics, so it’s easier to attribute specific biological functions
to individual genes,” explained Ms. Patterson.During healing, molecular signals bind to receptors on the cells
that line a wound, influencing the cell division, growth, and migration that restores the barrier.

To study the biological function of wound healing, the researchers needed to develop a “clean puncture
wounding” protocol to damage the epidermis of fly embryos without allowing bacteria to infect the breach,
which would complicate the study. Researchers study fly embryos rather than adult flies because it’s easier
and the embryos offer a wider range of genetic mutationsthan adult flies. The first step was to collect fly eggs,
which contain developing embryos, and bleach them to remove the shells. Next they impaled the embryos
with microneedles, like using a toothpick to spear an olive.
Key to the technique was injecting trypsin, a member of a family of enzymes called serine proteases, which
control cell-to-cell signaling. Trypsin activates genes involved in wound healing throughout the embryo, and it
also amplifies the response in the affected cells, revealing new players in the choreography of healing. “We
took advantage of trypsin as a powerful wounding tool to pinpoint which genes are ‘turned on’ versus which
genes are ‘turned off’ after wounding,” Ms. Patterson said.
Researchers then looked at which genes were turned on and off at 30, 60, and 120 minutes post-stabbing that
illuminate events as the borders of a small, clean wound close. The researchers were surprised to discover
that an immune response begins as soon asthe cuticle has been breached, with signals that prepare the
embryo should bacteria or fungi enter soon after the injury.
Using microarray technology to assess gene action,the researchers surveyed 84 genes that are turned on and
78 genes that are turned off as the fly embryo responds to wounding.
At all three time periods, the embryo’s innate immune response kicked in, releasing the same types of
antimicrobial peptides (short proteins) that an adult fly uses to fight infection. At 120 minutes, genes whose
protein products repair the cuticle with new chitin, the meshwork composing the fly exoskeleton, respond.
(The human version of thisstep, which may occur over several days, actually produces new cells because the
cuts are larger.) Finally the fly embryo activates genes that color the cuticle.

The genes that aren’t accessed as an embryo’s wound heals are also telling. The fly cells atthe wound site
ignore genes involved in replicating DNA, maintaining chromosome structure, and cell growth and division.
Overall, tracking the expression of the 162 genes revealed that the embryo temporarily halts development to
repair the wound and keep infection at bay. Their findings made perfect sense; the organism concentrates its
activities on addressing the immediate problem, healing the wound.
Like many biological processes, wound healing is fine-tuned. “A balance of gene activation and inhibition is
required for efficient healing,” said Dr. Juarez. Otherwise, a problem such as an ulcer, a chronic non-healing
wound, or a thickening of the fly’s cuticle can persist, she added.

The experiments revealed activities of eight genes that hadn’t been suspected to participate in wound healing.
These genes are expressed at very low levels or not at all in most cells, but are called into action when an
injury breaks the cuticle.
Having identified these eight new genes that are activated in cells near puncture wounds in flies, researchers
can now explore if genes in humans play comparable roles. “I think one amazing application of our studies
may be to build a better bandage – containing compounds to promote wound healing,” said Dr. Juarez.
“Perhaps our results can be translated to existing human therapies by incorporating specific, regulated serine
proteases and antimicrobial peptides at the sites of diabetic ulcers or skin grafts for more efficient wound
healing,” Ms. Patterson said.
Ms. Patterson also suggeststhat this fly research may lead to broader discoveries regarding human skin
diseases. Further examination of the roles of serine proteases in wound healing may inform treatment for
chronic skin diseases, including psoriasis, severe dry skin, and eczema where levels of these enzymes are
known to be abnormal.
Session Title: Immunity and Pathogenesis
Program: #43 — Date and Time: Friday, April 5, 2013; 9:30-9:45 a.m.
Location: Marriott Wardman Park, Marriott Ballroom Salon 3, Lobby Level
Intersection of Drosophila innate immunity and epidermal wound response in the serine proteolytic
pathway. Michelle T. Juarez, Rachel A. Patterson, William McGinnis.University of California, San Diego, La
Jolla, CA.
FOR MEMBERS OF THE MEDIA: The 53rd Annual Drosophila Research Conference is open to print, online and
broadcast news media and freelance science, medical and health writers on a verifiable assignment from an
established news source. If you would like to attend all or part of the Conference, complimentary meeting
registration is available to members of the media who provide appropriate press credentials and
identification. Please contact: Phyllis Edelman, GSA Communications and Public Relations Manager,
pedelman@genetics-gsa.org, or phone: 301-351-0896.

Male pattern baldness and its association with coronary heart disease

admin — Wed, 22 May 2013 20:24:10 +0000

Abstract
Objective To confirm the association between male pattern baldness and coronary heart disease (CHD).

Design Meta-analysis of observational studies.

Data sources Medline and the Cochrane Library were searched for articles published up to November 2012 using keywords that included both ‘baldness’ and ‘coronary heart disease’ and the reference lists of those studies identified were also searched.

Study selection Observational studies were identified that reported risk estimates for CHD related to baldness. Two observers independently assessed eligibility, extracted data and assessed the possibility of bias.

Data synthesis The adjusted relative risk (RR) and 95% CI were estimated using the DerSimonian-Laird random-effect model.

Results 850 possible studies, 3 cohort studies and 3 case–control studies were selected (36 990 participants). In the cohort studies, the adjusted RR of men with severe baldness for CHD was 1.32 (95% CI 1.08 to 1.63, p=0.008, I2=25%) compared to those without baldness. Analysis of younger men (<55 or ≤60 years) showed a similar association of CHD with severe baldness (RR 1.44, 95% CI 1.11 to 1.86, p=0.006, I2=0%). In three studies employing the modified Hamilton scale, vertex baldness was associated with CHD and the relation depended on the severity of baldness (severe vertex: RR 1.48 (1.04 to 2.11, p=0.03); moderate vertex: RR 1.36 (1.16 to 1.58, p<0.001); mild vertex: RR 1.18 (1.04 to 1.35, p<0.001)). However, frontal baldness was not associated with CHD (RR 1.11 (0.92 to 1.32, p=0.28)).

Conclusions Vertex baldness, but not frontal baldness, is associated with an increased risk of CHD. The association with CHD depends on the severity of vertex baldness and also exists among younger men. Thus, vertex baldness might be more closely related to atherosclerosis than frontal baldness, but the association between male pattern baldness and CHD deserves further investigation.

source: http://www.bmjopen.bmj.com/content/3/4/e002537

UCLA scientists develop new therapeutics that could accelerate wound healing

admin — Wed, 22 May 2013 20:02:25 +0000

In “before” and “after” photos from advertisements for wound-healing ointments, bandages and antibiotic creams, we see an injury transformed from an inflamed red gash to smooth and flawless skin.

What we don’t appreciate is the vital role that our own natural biomolecules play in the healing process, including their contribution to the growth of new cells and the development of new blood vessels that provide nutrients to those cells.

Now, UCLA researchers led by Heather Maynard, a professor of chemistry and biochemistry and a member of UCLA’s California NanoSystems Institute, are working to take advantage of our body’s ability to heal itself by developing new bio-mimicking therapeutics that could be used to treat skin wounds.

Among the key players involved in natural wound-healing is a signaling molecule known as basic fibroblast growth factor, or bFGF, which is secreted by our cells to trigger processes that are involved in healing, as well as embryonic development, tissue regeneration, bone regeneration, the development and maintenance of the nervous system, and stem cell renewal.

bFGF has been widely investigated as a tool doctors could potentially use to promote or accelerate these processes, but its instability outside the body has been a significant hurdle to its widespread use, Maynard said.

Now, Maynard and her team have discovered how to stabilize bFGF based on the principle of mimicry. Relying on the growth factor’s ability to bind heparin — a naturally occurring complex sugar found on the surface of our cells — the team synthesized a polymer that mimics the structure of heparin. When attached to bFGF, the new polymer makes the protein stable to the many stresses that normally inactivate it, rendering it a more suitable candidate for medical applications.

The research is published Feb. 17 in the online edition of the journal Nature Chemistry and will appear in an upcoming print edition of the journal.

UCLA co-authors of the research include graduate students Thi Nguyen and Caitlin Decker, former postdocs Dr. Sung-Hye Kim and Dr. Darice Wong, and Joseph Loo, professor of chemistry and biochemistry.

The research was federally funded by the National Institutes of Health and the National Science Foundation.

Our ability to heal from wounds is essential to our survival. When those natural healing processes are compromised, serious wounds can lead to infection and other health problems. People with diabetes, for example, can have wounds that heal very slowly. The resulting chronic wounds are debilitating and can lead to loss of limbs or even death. Yet, despite the need for wound dressings that can stimulate the body to heal wounds, very few are curative.

“This very important clinical need is the motivation behind our research,” Maynard said.

The importance of fibroblast growth factor was recognized in 1973, when biologist Hugo Armelin discovered that this previously unknown chemical, extracted from the pituitary gland, successfully caused cells to divide. Since then, researchers have applied fibroblast growth factor to wounds such as foot ulcers resulting from diabetes, but the treatments have not been very effective. What scientists now recognize, Maynard said, is that these growth factors typically lose their activity quickly in storage.

Knowing that other key biomolecules have been stabilized before with the help of polymers, Maynard and her team developed a strategy to maintain bFGF activity by taking advantage of its known structure and binding capabilities. Their new polymer, p(SS-co-PEGMA), mimics heparin’s natural ability to stabilize the growth factor.

After showing that p(SS-co-PEGMA) was non-toxic to human cells important in wound healing, they used it to conjugate bFGF and demonstrated that they could keep the growth factor active outside of the body for extended periods of time, even after it is exposed to heat, cold, enzymes that would normally break it down, and acidic conditions like those found in the wound injury setting. Moreover, they showed that this bound bFGF functions just like normal bFGF to trigger the same signaling pathways involved in the healing process.

The advance is an important step in the use of growth factors for therapy. The ability to stabilize bFGF means that it can be potentially stored, shipped and made available for use by doctors and patients when needed any time and anywhere, Maynard said.

The group is testing their new material with dermatologists Dr. Lloyd Miller, an associate professor of dermatology at Johns Hopkins University, and Dr. Jenny Kim, an associate professor of clinical medicine and dermatology at the David Geffen School of Medicine at UCLA, a member of the CNSI, and chief of dermatology for the Veterans Affairs Greater Los Angeles Healthcare System. The group is also researching ways to stabilize other proteins involved in wound healing and ways to make bFGF more active.

“This stable bFGF–polymer conjugate may also be useful in diseases other than wound healing — for example, vocal chord repair, cardiac repair and bone regeneration,” Maynard said. “More generally, we think that this idea of making polymers that mimic natural stabilizers is useful in a wide range of fields.”

The California NanoSystems Institute is an integrated research facility located at UCLA and UC Santa Barbara. Its mission is to foster interdisciplinary collaborations in nanoscience and nanotechnology; to train a new generation of scientists, educators and technology leaders; to generate partnerships with industry; and to contribute to the economic development and the social well-being of California, the United States and the world. The CNSI was established in 2000 with $100 million from the state of California. The total amount of research funding in nanoscience and nanotechnology awarded to CNSI members has risen to over $900 million. UCLA CNSI members are drawn from UCLA’s College of Letters and Science, the David Geffen School of Medicine, the School of Dentistry, the School of Public Health and the Henry Samueli School of Engineering and Applied Science. They are engaged in measuring, modifying and manipulating atoms and molecules — the building blocks of our world. Their work is carried out in an integrated laboratory environment. This dynamic research setting has enhanced understanding of phenomena at the nanoscale and promises to produce important discoveries in health, energy, the environment and information technology.　

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Calcium Is The Initial Trigger In Our Immune Response To Healing

admin — Wed, 22 May 2013 19:44:47 +0000

For the first time scientists studying the cellular processes underlying the body’s response to healing have revealed how a flash of calcium is the very first step in repairing damaged tissue. The findings, published in Current Biology, could lead to new therapies that speed up the healing process following injury or surgery.
Until recently, very little was known about how damaged tissue activates and attracts the first white blood cells to the wound — the first stage in the healing process. However, researchers from the University of Bristol’s Schools of Biochemistry and Physiology and Pharmacology in collaboration with a team from the University of Bath, have shown that the very first trigger in this process is a flash of calcium which spreads like a wave back from the wound edge through gap junctions that connect all the cells.

This flash of calcium signal goes on to activate an enzyme known as DUOX that synthesises hydrogen peroxide, which, in turn, attracts the first white blood cells to the wound. This white blood cell invasion, which is initiated during our inflammatory responses, is needed to kill off invading microbes and stop the onset of septicaemia following tissue damage.

The findings indicate that the wound-induced calcium flash represents the earliest identified signal following wounding and might therefore orchestrate the rapid recruitment of immune cells.

To assess the impact of a reduced calcium flash upon the inflammatory response the team used Drosophila (fruit fly) embryos because they are translucent which makes it easy to image the inflammatory response and because of their simple genetics. The team found that blocking the calcium flash inhibited H2O2 release at the wound site leading to a reduction in the number of immune cells migrating to the wound.

Paul Martin, Professor of Cell Biology and an expert in wound healing at the University, said: “White blood cells are a little like ‘Jeckyll and Hyde’ in that they help us heal but are also the reason behind why we scar so we really need to know how they are regulated at wounds in order to learn how to control their behaviours for future therapeutic intervention.”

Will Razzell, the lead PhD researcher on this study, added: “We are more than ever understanding the pathways that lead to immune cell attraction to wounds. As calcium represents the immediate inflammatory signal, we now have a good foundation to investigate this complicated process further.”

Source: http://www.bristol.ac.uk/news/2013/9145.html