Rosacea Support Group » research

UV Exposure leads to Oxidative Stress

David Pascoe — Wed, 21 Dec 2011 10:45:00 +0000

As researchers try to further describe exactly what is going on in rosacea, more tiny bits of information arise. Here, this abstract is telling us that;

Ferritin positive cells are much more prevalent in rosacea sufferers
Severe rosacea sufferers have significantly more ferritin positive cells
Blood peroxide levels are higher in rosacea sufferers
Total anti-oxidative levels are significantly lower in rosacea patients

The conclusion of the paper is that exposure to UV light results in ferritin positive cells that are fundamental to the resulting oxidative stress.

What is Oxidative Stress?

Oxidative stress has to do with the amount of reactive oxygen species present in our bodies. When there are too many, damage to cell components result.

In broad terms, antioxidants are helpful when the balance is wrong and too many ROS are present.

It is a complicated science; oxidative stress has been linked to many diseases and needs to carefully dissected to understand any real implications for a particular disease.

We do know that rosacea is the end result of an inflammatory pathway. We need to describe the entire system before we can say that we have rosacea licked.

The role of oxidative stress and iron in pathophysiology of rosacea

Lijec Vjesn. 2011 Jul-Aug;133(7-8):288-91.

[Article in Croatian], Tisma VS, Poljak-Blazi M., Poliklinicki odjel za kozne i spolne bolesti, KB Dubrava, Zagreb.

Rosacea is a common skin disease of unknown etiology.

The aim of the present paper is to explain the role of oxidative stress triggered by UV light and iron metabolism in the pathophysiology of rosacea.

It was recently described that the number of ferritin positive cells was significantly higher in skin samples of rosacea patients compared to controls of healthy skin samples.

The presence of ferritin was significantly higher in patients with the severe stage of disease. In addition, serum peroxide levels were significantly higher and serum total antioxidative potential levels were significantly lower in rosacea patients than in healthy controls.

These results support the role of oxidative stress and affected metabolism of iron in etiology of rosacea.

The higher presence of ferritin in skin cells of rosacea patients explains the exacerbation of symptoms by exposure to UV light, that releases ferritin free iron, which is fundamental in the generation of oxidative stress.

This paper appears to be a followup to a 2009 paper , Oxidative stress and ferritin expression in the skin of patients with rosacea, J Am Acad Dermatol. 2009 Feb;60(2):270-6.

Sanofi-Pasteur to make an Acne Vaccine

David Pascoe — Tue, 27 Sep 2011 10:45:00 +0000

A vaccine for acne ? Well it appears that one may actually become a reality. A recent article in the New Scientists explains how targeting a protein called CAMP can lead to a form of Propionibacterium acnes (the believed main culprit in acne) that can function but not produce the inflammation that leads to acne.

Great news.

Simply eradicating Propionibacterium acnes is not viable because it still has important functions to perform on the surface of the skin. By targeting the protein thought to be responsible for the inflammation, just that function can be controlled, leaving the bacteria to perform other functions that are still necessary.

The modified protein required was cultured in the asian vegetable known as daikon.

The article mentions that the proposed vaccine may be “delivered locally, using microneedles, within the skin of people with acne.” which sounds a bit scary don’t you think?

Hope for Rosacea?

Whilst there is little discussion suggesting the involvement of P. acnes in rosacea, the approach undertaken is still promising.

If researchers are able to isolate the inflammatory pathway that leads to rosacea symptoms, then being able to turn off only the slice that is misbehaving would be a major breakthrough.

I still hold hope that one day we might find a rosacea gene, leading to a promise of a rosacea vaccine. One can dream, right?

In development: a vaccine for acne

Pimples develop when oil-producing sebaceous glands in the skin become clogged. As the oxygen level within the pore falls, some of its otherwise benign bacterial inhabitants turn nasty and start killing skin cells to break into the blood. In response the immune system unleashes local inflammation, bringing in white blood cells and germ-killing chemicals to battle the bacteria – creating a pimple.

The chief culprit is the main bacterium in sebaceous glands, Propionibacterium acnes. Current acne treatments, such as benzoyl peroxide and antibiotics, aim to kill the bacterium. But acne can be chronic, and long-term use of antibiotics can lead to drug resistance in P. acnes, while other antibacterials damage the skin – partly by killing off its normal bacteria.

…

This showed that antibodies to P. acnes might reduce pimples. However, a stable community of normal skin bacteria is known to protects the skin from colonisation by nastier germs. A vaccine that encourages the body to indiscriminately attack P. acnes could cause worse trouble than acne.

So the team tried a different approach: targeting a protein called CAMP, which is used by various bacteria to kill host cells. The team found a CAMP gene in the DNA sequence of P. acnes, which coded for a protein that killed cells in sebaceous glands and triggered inflammation.

The team put the gene into young daikon radish plants, which duly made the protein. They then sprayed tiny amounts of the ground-up leaves into the noses of mice, which caused the mice to make antibodies to CAMP.

Placebos Get Better Over Time: The Weird World of Placebos

David Pascoe — Tue, 20 Sep 2011 10:45:00 +0000

More from the weird and wonderful world of clinical trials and the mysterious Placebo Effect.

We know that somehow even dummy pills can kick-start the body’s recovery engine. This latest article from WIRED tells us that drug developers are noticing that over time that the placebo effect is increasing.

Drugs that once clearly outperformed placebo are losing their edge. Also an increasing trend of new drugs in development are unexpectedly failing to outperform placebo.

How is this possible? Read on to find out.

Encouraging News

One good thing for consumers is that the FDA mandates all new drugs must outperform placebo in authorized blind trials. Thus drug companies must come to grips with the placebo effect (or perhaps better called placebo response as we read below) in order to be able to develop new drugs.

The encouraging bit of this is that we will discover and be able to prove our body’s in-built recovery and healing ability.

Placebos Are Getting More Effective. Drugmakers Are Desperate to Know Why.

By Steve Silberman 08.24.09

From 2001 to 2006, the percentage of new products cut from development after Phase II clinical trials, when drugs are first tested against placebo, rose by 20 percent. The failure rate in more extensive Phase III trials increased by 11 percent, mainly due to surprisingly poor showings against placebo.

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Half of all drugs that fail in late-stage trials drop out of the pipeline due to their inability to beat sugar pills.

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Last November, a new type of gene therapy for Parkinson’s disease, championed by the Michael J. Fox Foundation, was abruptly withdrawn from Phase II trials after unexpectedly tanking against placebo.

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Two comprehensive analyses of antidepressant trials have uncovered a dramatic increase in placebo response since the 1980s. One estimated that the so-called effect size (a measure of statistical significance) in placebo groups had nearly doubled over that time.

It’s not that the old meds are getting weaker, drug developers say. It’s as if the placebo effect is somehow getting stronger.

Why is This So ?

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Now, after 15 years of experimentation, he [Bendetti] has succeeded in mapping many of the biochemical reactions responsible for the placebo effect, uncovering a broad repertoire of self-healing responses. Placebo-activated opioids, for example, not only relieve pain; they also modulate heart rate and respiration. The neurotransmitter dopamine, when released by placebo treatment, helps improve motor function in Parkinson’s patients. Mechanisms like these can elevate mood, sharpen cognitive ability, alleviate digestive disorders, relieve insomnia, and limit the secretion of stress-related hormones like insulin and cortisol.

In one study, Benedetti found that Alzheimer’s patients with impaired cognitive function get less pain relief from analgesic drugs than normal volunteers do. Using advanced methods of EEG analysis, he discovered that the connections between the patients’ prefrontal lobes and their opioid systems had been damaged. Healthy volunteers feel the benefit of medication plus a placebo boost. Patients who are unable to formulate ideas about the future because of cortical deficits, however, feel only the effect of the drug itself. The experiment suggests that because Alzheimer’s patients don’t get the benefits of anticipating the treatment, they require higher doses of painkillers to experience normal levels of relief.

Benedetti often uses the phrase "placebo response" instead of placebo effect. By definition, inert pills have no effect, but under the right conditions they can act as a catalyst for what he calls the body’s "endogenous health care system." Like any other internal network, the placebo response has limits. It can ease the discomfort of chemotherapy, but it won’t stop the growth of tumors. It also works in reverse to produce the placebo’s evil twin, the nocebo effect. For example, men taking a commonly prescribed prostate drug who were informed that the medication may cause sexual dysfunction were twice as likely to become impotent.

Finding a Way Out

Big Pharma wants to know why more and more of their drugs are failing to beat placebo.

Under the auspices of the FNIH, Potter and his colleagues are acquiring decades of trial data—including blood and DNA samples—to determine which variables are responsible for the apparent rise in the placebo effect. Merck, Lilly, Pfizer, AstraZeneca, GlaxoSmithKline, Sanofi-Aventis, Johnson & Johnson, and other major firms are funding the study, and the process of scrubbing volunteers’ names and other personal information from the database is about to begin.

In typically secretive industry fashion, the existence of the project itself is being kept under wraps. FNIH staffers² are willing to talk about it only anonymously, concerned about offending the companies paying for it.

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In standard trials, the act of taking a pill or receiving an injection activates the placebo response. In open/hidden trials, drugs and placebos are given to some test subjects in the usual way and to others at random intervals through an IV line controlled by a concealed computer. Drugs that work only when the patient knows they’re being administered are placebos themselves

Ironically, Big Pharma’s attempt to dominate the central nervous system has ended up revealing how powerful the brain really is. The placebo response doesn’t care if the catalyst for healing is a triumph of pharmacology, a compassionate therapist, or a syringe of salt water. All it requires is a reasonable expectation of getting better. That’s potent medicine.

I’d recommend reading the whole article: Placebos Are Getting More Effective. Drugmakers Are Desperate to Know Why.

Why Should I Care?

All rosacea sufferers need to be aware of the powers of the placebo effect, as it needs to be included in all evaluations of new treatments.

If a new treatment can’t demonstrate that it is superior to placebo, well then we might be better of taking sugar pills (or just using the inactive vehiclie in a topical) and hoping for the best.

NRS Funds New Rosacea Studies for 2011

David Pascoe — Mon, 22 Aug 2011 10:45:00 +0000

In the Summer 2011 Rosacea Review, The National Rosacea Society announced that they are funding 3 studies in new areas of rosacea research.

This is great news; not only is the NRS continuing to fund 5 existing studies, it is funding the 3 new research areas.

1. PACAP and Rosacea

Dr. Ferda Cevikbas will be studying the role of PACAP, a neuropeptide in rosacea.

They plan to define the distribution of PACAP in skin samples from rosacea patients, determine whether PACAP induces inflammation and test whether cathelicidin — a known factor in rosacea’s pathophysiology — modulates the release of PACAP. The researchers also plan to test whether countering the effects of PACAP is beneficial and may thus be used as a rosacea therapy.

2. Cytokines in Ocular Rosacea

Dr. Edward Wladis, assistant professor of ophthalmology at Albany Medical College, was awarded $12,100 to identify specific cytokines — molecules that regulate the immune system — that are involved in ocular rosacea by studying eyelid tissue from individuals with and without the disorder. Dr. Wladis noted that while inflammation is normally a healthy part of the immune response, aberrations in the cytokines’ concentrations and functioning in rosacea may result in unhealthy and prolonged inflammation.

3. Th17 Cells and Inflammation

Dr. Richard Granstein, chairman of dermatology at Cornell University, and colleagues were awarded $25,000 to study the potential role of Th17 cells, a newly discovered class of cells that appear to be involved in a number of inflammatory and autoimmune disorders. Earlier study results strongly indicated that release of ATP — a neurotransmitter and carrier of chemical energy throughout the body — from nerves under stressful situations may initiate a sequence of events leading to or exacerbating inflammation in the skin. This study will investigate whether this inflammation results because Th17 cells are produced during this process in rosacea.

NRS Continues Leading Edge Research Funding

David Pascoe — Fri, 19 Aug 2011 10:45:00 +0000

The National Rosacea Society recently announced that they will be continuing to fund 5 existing rosacea research streams.

Confirming their faith in the on-going NRS sponsored research, the NRS has announced additional funding to the following researchers.

1. Dr. Richard Gallo – Cathelicidins

The NRS is also continuing to fund studies by Dr. Richard Gallo and colleagues at the University of California-San Diego on the potential role of cathelicidins in rosacea.

For more information see NRS Blog: cathelicidins show allergic basis for rosacea ?

2. Dr. Joseph Rothnagel – Kallikreins

Dr. Joseph Rothnagel and colleagues at the University of Queensland, Australia, received further funding to study kallikreins and rosacea.

We learnt in 2009 that Dr. Joseph Rothnagel, and Dr. Manuela Trabi, adjunct lecturer,Department of Molecular and Microbial Sciences, The University of Queensland, Australia, were awarded $18,000 for their study, "The role of tissue kallikreins in rosacea." They noted that these previous studies reported involvement of the enzyme hK5 and protein CAP18, and hypothesize that at least one other enzyme is also elevated in rosacea. They will study whether proteins known to be crucial for skin integrity are also digested at a higher than normal rate by these enzymes, allowing easier access for pathogens.

3. Dr. Thad Wilson – Nerve Activity

Dr. Thad Wilson and colleagues at Ohio University will study nerve activity in rosacea.

In 2010, Dr. Thad Wilson, associate professor of physiology and medicine; Dr. Kumika Toma, postdoctoral fellow; Dr. Michael Tomc, associate professor of otorhinolaryngology; and Dr. Dawn Sammons, assistant professor of dermatology, Ohio University, were awarded $25,000 for their study, "Role of skin sympathetic nerve activity in rosacea."

4. Dr. Aki Ikoma – Neurovascular Aspects

Dr. Aki Ikoma and colleagues at the University of California-San Francisco received their grant on the neurovascular system and rosacea.

5. Dr. Noreen Lacey – Sebocyte Cells

Dr. Noreen Lacey and colleagues at the University College in Ireland are studying the effect of antibiotics on sebocyte cells in rosacea.

Dr. Lacey is a coauthor of the article that has sparked interested in the role of demodex mite bacteria in rosacea inflammation.

Gallo to trial Aminocaproic Acid as Cathelicidin Inhibitor

David Pascoe — Thu, 21 Jul 2011 01:40:31 +0000

Just posted are some details of a new trial rising out of the work of Dr. Richard Gallo’s group at the University of California, San Diego. Gallo is well known for his work on the relationship between antimicrobial peptides such as cathelicidin, and rosacea.

The trial will compare topical 25% aminocaproic acid (ACA) mixed with Vanicream vs Vanicream on its own. The trial will measure how well Topical Aminocaproic Acid inhibits the activation of antimicrobial peptides in the skin.

Aminocaproic Acid (ACA) is an analogue of the amino acid Lysine and is marketed as the main active ingredient in Amicar. Amicar is used to treat acute bleeding during surgery.

As a related note, we know from other research from Dr. Gallo’s group that the active ingredient in Finacea, azelaic acid can decrease the expression of 2 substances thought to be important in rosacea – kallikrein 5 (KLK5) and cathelicidin.

It is encouraging to see research that leads to the experimentation of novel treatments for rosacea. It is only through formal well conducted trials that we can know for sure whether new treatments are truly effective.

NCT01398280 Effects of Aminocaproic Acid (ACA) on Rosacea-specific Inflammation

The purpose of this study is to determine the effect of topical aminocaproic acid on the immune system by assessing the levels of antimicrobial peptides in the skin of patients with rosacea. It is hypothesized that aminocaproic acid applied topically will alter the body’s immune system in patients with rosacea by inhibiting activation of antimicrobial peptides.

A Single Site Evaluation of the Effect of Topical Application of Aminocaproic Acid (ACA) to Inhibit Kallikrein 5 Serine Protease Activity and Production of LL-37 Cathelicidin Peptide, Biochemical Markers of Rosacea-specific Inflammation.

Primary Outcome Measures: To determine the effect of aminocaproic acid on the antimicrobial peptide cathelicidin in adult skin from patients with rosacea.

Secondary Outcome Measures: To determine the effect of topical aminocaproic acid on serine protrease activity of kallikrein 5 in adult skin from patients with rosacea.

Subjects will treat their facial skin twice daily for up to 12 weeks with 5-6 visits and 2 telephone visits. Investigator and subject will be blinded. Tape strip samples will be collected from facial skin at each visit to assess KLK activity and LL-37 expression.

Study Start Date: July 2011

Estimated Primary Completion Date: July 2012

Cosmetics and Makeup work fine applied after Metrogel

David Pascoe — Tue, 12 Jul 2011 10:45:00 +0000

This research comes up with the finding that using a foundation after applying Metrogel 1% won’t worsen rosacea symptoms. Most of the participants in the trial were happy with the appearance of foundation, when used in combination with Metrogel.

The authors tell us that there is little research into whether makeup both makes rosacea worse or whether those who suffer from rosacea can also successfully use makeup like foundation.

What Makeup Did they Apply?

We are told in the paper that no particular foundation was used, but that participants applied a foundation, powder and eye shadow. As a cleanser, Cetaphil Gentle Skin Cleanser was provided to each trialist.

Each participant was instructed to wash the face with the provided Cetaphil Gentle Skin Cleanser, rinse, and pat dry.

They then were told to apply metronidazole gel 1% once daily (morning) and wait 10 minutes for it to dry before applying their usual facial foundation (no particular foundation was used), powder, and eye shadow.

This regimen continued for 2 weeks. The first and last doses of metronidazole gel 1% and cosmetic applications were applied under the supervision of study staff at the study site during the baseline visit and the final visit at week 2

Foundation and other cosmetics, used for covering up rosacea symptoms can be a powerful weapon in the battle against rosacea. The boost in self esteem when one is able to cover over unsightly lumps and bumps and facial redness should not be underestimated.

Your Tips

Have you any makeup tips you would like to pass on ? Feel free to leave a comment below, thanks.

Abstract

The appearance of facial foundation cosmetics applied after metronidazole gel 1%, Cutis. 2011 May;87(5):251-9.

Draelos ZD, Colón LE, Preston N, Johnson LA, Gottschalk RW, Dermatology Consulting Services, High Point, North Carolina, USA.

The purpose of this study was to assess the cosmetic appearance of commonly marketed facial cosmetics when used after the application of metronidazole gel 1%.

An observational. open-label, single-site study was conducted with women (N=30) aged 20 to 75 years and diagnosed with moderate papulopustular rosacea (investigator global severity score of 3).

After cleansing the face with a gentle skin cleanser, participants applied metronidazole gel 1% once daily before applying their usual facial foundation.

Two surveys were conducted:

investigator assessment of cosmetic appearance; and

participant assessment of cosmetic appearance.

The investigator also evaluated erythema, disease severity, and tolerability at baseline and week 2. Adverse events were collected. The 28 per-protocol (PP) participants had a mean age (standard deviation [SD]) of 54.0 (10.3) years and a mean duration (SD) of rosacea of 15.4 (13.2) years. The median response score for both the investigator and participant assessments of cosmetic appearance was 10 (best) for each survey question.

Signs and symptoms of rosacea did not increase with use of metronidazole gel 1% and the participants’ selected cosmetic regimen. At baseline all 28 participants were classified as having moderate erythema. At week 2, 18 (64%) participants were classified as having moderate erythema and 10 (36%) mild. At baseline all 28 (100%) participants were classified as having moderate rosacea according to the investigator global severity score. At week 2, 10 (36%) participants were classified as mild and 18 (64%) moderate. In addition, few participants reported cutaneous irritation during the study. At week 2, 10 participants had dryness, 2 had itching, 8 had scaling, and 2 had stinging/burning.

According to surveys completed by the investigator and the participants themselves, most participants had a good cosmetic appearance with their facial foundation cosmetics that were applied after metronidazole gel 1%.

The use of various cosmetic regimens after application of metronidazole gel 1% did not cause rosacea symptoms to worsen and treatment was well-tolerated.

Why, Oh Why Did I Get Rosacea ?

David Pascoe — Thu, 21 Apr 2011 10:45:56 +0000

I hear you.

My skin was great. I have had beautiful skin all my life, but now wham! rosacea has reared its ugly head.

Well the NRS Blog has an answer to this plea. It is all about your risk profile. If you are over 30 with fair skin, have a relative with rosacea and are of Northern European Ancestry then the statistics suggest that you are at risk for having rosacea.

Sorry, but sometimes it is just down to sheer probability.

Risks Answer ‘Why Me?’

Tuesday, April 19, 2011

“Why me?” is a question many ask when they find themselves with the embarrassing effects of rosacea – which may include facial redness, visible blood vessels, bumps, pimples, eye irritation and other symptoms if left untreated. While rosacea can strike all segments of the population, surveys by the National Rosacea Society have revealed a profile of those most at risk for this conspicuous and chronic condition:

Other Reasons

Of course if you are outside the common risk profile, you could still have rosacea. Other common reasons include over use of steroids, exposure to the sun and elements, stress, tendency to flush and more.

There is Hope!

It might feel unfair, but now that you have a diagnosis of rosacea, you are already on the way to relief. Here are some articles that will get you started.

[update:] There is also a thread at the Rosacea Community Forum that you might find helpful: Why did I get rosacea NOW in my 40′s?

Green Jelly Beans Linked to Acne!

David Pascoe — Wed, 06 Apr 2011 10:45:45 +0000

OK so now I have gotten your attention.

Have read of this comic. Lets talk after you finish reading it.

xkcd: Significant

So what is all this about then ?

You mean what apart from highlighting how news articles cherry pick research findings and just confuse us to get a headline?

Often you see things like (p < 0.05) in a journal abstract. What does that mean? Well it is based on probability theory and relates to the confidence of one thing causing another.

What is a P-value?

The “P-value” is a measure of how likely something is to occur compared to just pure chance. For us who read medical abstracts, often we seem them used in statements like “Treatment X Significantly Reduced Symptom Y (p<0.05)”.

Here the value 0.05 means the probability that the result is related to pure chance is less than 5/100 or 5%.

This says that there was a strongly significant link between using Treatment X and seeing your Symptom Y reduced. The element of chance has been mostly eliminated as contributing to the result.

Once chance has been reduced to less than 5% researchers can say that there is strong significance in the results. This is the best result for a researcher looking for a new treatment; being able to use statistics to prove their treatment actually works.

The Punch Line

By the way, the punch line from the comic, visible if you hover over the graphic was “So, uh, we did the green study again and got no link. It was probably a “RESEARCH CONFLICTED ON GREEN JELLY BEAN/ACNE LINK; MORE STUDY RECOMMENDED!”

So there you go, our comic researcher just made a mistake

Want to ask a Question?

Statistics and probability theory can be quite complicated. Is there something you always wanted to ask about this topic? Leave it in the comments below and I’ll do my best to answer it.

Nailfold Capillaroscopy: If only Rosacea was that Easy to Diagnose

David Pascoe — Tue, 05 Apr 2011 10:45:47 +0000

I thought this abstract was interesting because of its failure. The authors proposed that a passive diagnostic test known as Nailfold Cappillaroscopy could be used to test for rosacea.

Nailfold Capillaroscopy is a procedure where a drop of oil is placed on the nailfold. This is the small fold of skin at the base of a fingernail. The stained area is then examined under magnification to look for abnormalities in the vasculature.

Measurements obtained from the procedure can be used to identify characteristics such as blood flow and capillary dimensions aiding in the diagnosis of conditions such as Raynaud’s and Sjogren Syndrome.

As we now know from this abstract, the capillary patterns of a rosacea sufferers don’t appear to be any different to someone who doesn’t have rosacea. Oh well, maybe one day there will be a simple quantitative diagnostic test for rosacea.

Nailfold capillaroscopy as a diagnostic and prognostic method in rosacea

An Bras Dermatol. 2011 Feb;86(1):87-90., Fonseca GP, Brenner FM, Muller CD, Wojcik AL., Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, PR, Brasil.

BACKGROUND: There is no appropriate and reliable method of evaluating and monitoring severity in rosacea.

OBJECTIVE: To determine the importance of nailfold capillaroscopy as a diagnostic and prognostic method for patients with rosacea.

METHODS: A cross-sectional study where eight patients with rosacea and 8 control subjects were submitted to nailfold capillaroscopy from May to July 2009. We collected clinical data related to gender, age, skin phototype, and rosacea stage according to Plewig and Kligman classification and the classification of the National Rosacea Society. Additionally, we evaluated the progression of the disease and treatment therapies previously used.

RESULTS: The majority of the patients evaluated (6 out of 8 patients) had rosacea subtype I (vascular) or erythematotelangiectatic rosacea. The mean duration of the disorder was 5.96 years, and 87.5% of the patients were under treatment with topical metronidazole. Nailfold cappilaroscopy showed that evidence of devascularization was absent in both groups.

CONCLUSION: Nailfold capillaroscopy presents a nonspecific pattern and does not seem to help in the diagnosis or prognosis of rosacea.

Rosacea Support Group » research

UV Exposure leads to Oxidative Stress

What is Oxidative Stress?

Related Articles

Sanofi-Pasteur to make an Acne Vaccine

Hope for Rosacea?

More Reading

Related Articles

Placebos Get Better Over Time: The Weird World of Placebos

Encouraging News

Why is This So ?

Finding a Way Out

Why Should I Care?

Related Articles

NRS Funds New Rosacea Studies for 2011

1. PACAP and Rosacea

2. Cytokines in Ocular Rosacea

3. Th17 Cells and Inflammation

Related Articles

NRS Continues Leading Edge Research Funding

1. Dr. Richard Gallo – Cathelicidins

2. Dr. Joseph Rothnagel – Kallikreins

3. Dr. Thad Wilson – Nerve Activity

4. Dr. Aki Ikoma – Neurovascular Aspects

5. Dr. Noreen Lacey – Sebocyte Cells

Related Articles

Gallo to trial Aminocaproic Acid as Cathelicidin Inhibitor

Related Articles

Cosmetics and Makeup work fine applied after Metrogel

What Makeup Did they Apply?

Your Tips

Abstract

Related Articles

Why, Oh Why Did I Get Rosacea ?

Other Reasons

There is Hope!

Green Jelly Beans Linked to Acne!

So what is all this about then ?

What is a P-value?

The Punch Line

Want to ask a Question?

Related Articles

Nailfold Capillaroscopy: If only Rosacea was that Easy to Diagnose

Related Articles