Events, concert and galleries to visit in Porto during your stay

The Skin Ageing & Challenges 2018 will be held in Porto in one week’s time.

We invite you participants to check wonderful city of Porto during your stay.

 
Urban Market Special 6th Anniversary

Target audience: General public
From: 23.02.2018
To: 25.02.2018


28. Basketball

Target audience: General public
From: 01.01.2018
To: 28.02.2018


C for heads / H para cabeças

Target audience: General public
From: 03.02.2018
To: 03.03.2018


Target audience: General public
From: 17.11.2017
To: 04.03.2018
To: 04.03.2018


Fantasporto

Target audience: General public
From: 20.02.2018


 

Nu Umbigo

Target audience: General public
From: 10.02.2018
To: 10.03.2018


José de Almada Negreiros: drawing in motion

Target audience: General public
From: 30.11.2017
To: 18.03.2018


To: 18.03.2018Alviceleste

Target audience: General public
From: 15.02.2018


PortoCartoon 2018

Target audience: General public
From: 06.01.2018
To: 31.03.2018

 

If you want to know more about Events in Porto, Please visit the official site here: http://www.visitporto.travel/Agenda/Paginas/default.aspx

 

Special Topic on Sniff-Camera: a gas-imaging system of dermal volatiles for skin condition and ageing analysis

Prof. Kohji Mitsubayashi, from the Department of Biomedical Devices and Instrumentation at Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, Japan will give a strategic presentation about the Gas-imaging system (SNIFF-CAM) of dermal volatiles for skin condition and aging analysis during Porto Skin Ageing & Challenges Congress 2018.

In his presentation, Prof. Mitsubayashi  will explain how his team was able to image the ethanol vapor contained in the transdermal vapor emitted from the palm, and confirmed the spreading of the ethanol emissions across the palm. The system presented can would be applied for detailed evaluation of the skin condition and measurement of skin aging odor.

To know more about this study, don’t hesitate to join the attendees of Porto Skin Challenges 2018 via www.skin-challenges.com

 

Researchers identify millions of new genes in the human microbiome

A new study of the human microbiome — the trillions of microbial organisms that live on and within our bodies — has uncovered millions of previously unknown genes from microbial communities in the human gut, skin, mouth, and vaginal microbiome, allowing for new insights into the role these microbes play in human health and disease.

The study, from researchers at the University of Maryland School of Medicine (UM SOM), Harvard T.H. Chan School of Public Health, the Broad Institute of MIT and Harvard, and the University of California San Diego, triples the amount of data previously analyzed in this project, and is the largest human microbiome study ever.

This work appears on September 20, 2017 in the journal Nature.

The results are a significant jump in the amount of information available to scientists. This publication provides new insight into the changes in our microbiome over time and could lead to a greater understanding of the genetic differences that are unique to an individual’s microbes.

“This new data really expands our appreciation for the fingerprint created by microorganisms that make up each human’s microbiome,” says Owen White, professor of epidemiology and public health and associate director at the Institute for Genome Sciences (IGS) at UM SOM. “These organisms play a crucial role in many key aspects of our health. The more we know about them and their role, the more likely it is that we will be able to manipulate them to improve our health.”

This study is part of the National Institutes of Health Human Microbiome Project, launched in 2008 to identify and characterize human microbes, explore microbes’ relationship to health and disease, and develop computational tools to analyze the microbes. The microbiome has been linked to various aspects of human health including the robustness of our immune system and our susceptibility to chronic illnesses such as Crohn’s disease and cancer.

This work is a continuation of work published in Nature in 2012. In the new study, the researchers analyzed an additional 1,635 new microbiome samples, for a total of 2,355 sampled from 265 people over time. The scientists used DNA sequence analysis tools to identify which organisms are present in various body sites, determine whether they change or stay relatively stable over time, and explore their function. This study also provides one of the largest profiles of non-bacterial members — viruses and fungi — of the microbiome. In addition, it unraveled some of the biochemical activity that allows microbes to play a role in human health.

Although the new study illuminates a great deal about the microbiome, an enormous amount remains unknown. Learning more about it will take time, said Anup Mahurkar, the executive director of software engineering & information technology at IGS. “These communities of organisms are tremendously complex. In one sense, this study is a great advancement for the research community,” he said. Mahurkar was responsible for the months of intensive computations required to process the data. However, he was also cautious, saying “On the other hand, it still just moves the needle. There will always be more we can learn.” Mahurkar is confident that the work will provide a large data resource for other scientists to use in their future research.

News source: www.eurekalert.org

Skin “Remembers” Wounds, Heals Faster the Second Time Around

 Image No 1
FIX-IT-CREW: Epithelial stem cells (green) migrate into a wound in mouse skin to repair the damaged tissue barrier. SAMANTHA LARSEN, ELAINE FUCHS LAB/ROCKEFELLAR UNIVERSITY


The skin barrier is the body’s first line of defence against environmental assaults, and is maintained by epithelial stem cells (EpSCs). Despite the vulnerability of EpSCs to inflammatory pressures, neither the primary response to inflammation nor its enduring consequences are well understood. Here we report a prolonged memory to acute inflammation that enables mouse EpSCs to hasten barrier restoration after subsequent tissue damage. This functional adaptation does not require skin-resident macrophages or T cells. Instead, EpSCs maintain chromosomal accessibility at key stress response genes that are activated by the primary stimulus. Upon a secondary challenge, genes governed by these domains are transcribed rapidly. Fuelling this memory is Aim2, which encodes an activator of the inflammasome. The absence of AIM2 or its downstream effectors, caspase-1 and interleukin-1β, erases the ability of EpSCs to recollect inflammation. Although EpSCs benefit from inflammatory tuning by heightening their responsiveness to subsequent stressors, this enhanced sensitivity probably increases their susceptibility to autoimmune and hyperproliferative disorders, including cancer.

News source: www.the-scientist.com
Authors: Shruti Naik, Samantha B. Larsen, Nicholas C. Gomez, Kirill Alaverdyan, Ataman Sendoel, Shaopeng Yuan, Lisa Polak, Anita Kulukian, Sophia Chai & Elaine Fuchs


Scientists make cells that enable the sense of touch

Human embryonic stem cell-derived neurons (green) showing nuclei in blue. Left: with retinoic acid added. Right: with retinoic acid and BMP4 added, creating proprioceptive sensory interneurons (pink). Credit: UCLA Broad Stem Cell Research Center/Stem Cell Reports

Researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have, for the first time, coaxed human stem cells to become sensory interneurons—the cells that give us our sense of touch. The new protocol could be a step toward stem cell-based therapies to restore sensation in paralyzed people who have lost feeling in parts of their body.

The study, which was led by Samantha Butler, a UCLA associate professor of neurobiology and member of the Broad Stem Cell Research Center, was published today in the journal Stem Cell Reports.

Sensory interneurons, a class of neurons in the spinal cord, are responsible for relaying information from throughout the body to the central nervous system, which enables the of touch. The lack of a sense of touch greatly affects people who are paralyzed. For example, they often cannot feel the touch of another person, and the inability to feel pain leaves them susceptible to burns from inadvertent contact with a hot surface.

“The field has for a long time focused on making people walk again,” said Butler, the study’s senior author. “‘Making people feel again doesn’t have quite the same ring. But to walk, you need to be able to feel and to sense your body in space; the two processes really go hand in glove.”

In a separate study, published in September by the journal eLife, Butler and her colleagues discovered how signals from a family of proteins called bone morphogenetic proteins, or BMPs, influence the development of sensory interneurons in chicken embryos. The Stem Cell Reports research applies those findings to human in the lab.

When the researchers added a specific called BMP4, as well as another signaling molecule called retinoic acid, to human , they got a mixture of two types of sensory interneurons. DI1 sensory interneurons give people proprioception—a sense of where their body is in space—and dI3 sensory interneurons enable them to feel a sense of pressure.

The researchers found the identical mixture of sensory interneurons developed when they added the same signaling molecules to induced , which are produced by reprogramming a patient’s own mature such as skin cells. This reprogramming method creates stem cells that can create any cell type while also maintaining the genetic code of the person they originated from. The ability to create sensory interneurons with a patient’s own reprogrammed cells holds significant potential for the creation of a cell-based treatment that restores the sense of touch without immune suppression.

Butler hopes to be able to create one type of interneuron at a time, which would make it easier to define the separate roles of each cell type and allow scientists to start the process of using these cells in clinical applications for who are paralyzed. However, her research group has not yet identified how to make stem cells yield entirely dI1 or entirely dI3 cells—perhaps because another signaling pathway is involved, she said.

The researchers also have yet to determine the specific recipe of growth factors that would coax stem cells to create other types of sensory interneurons.

The group is currently implanting the new dI1 and dI3 sensory interneurons into the spinal cords of mice to understand whether the cells integrate into the nervous system and become fully functional. This is a critical step toward defining the clinical potential of the cells.

“This is a long path,” Butler said. “We haven’t solved how to restore but we’ve made a major first step by working out some of these protocols to create sensory interneurons.”

News source: www.phys.org

More information: Sandeep Gupta et al. Deriving Dorsal Spinal Sensory Interneurons from Human Pluripotent Stem Cells, Stem Cell Reports (2018). DOI: 10.1016/j.stemcr.2017.12.012

Targeting olfactory receptors by agonists, aromas, microbiota or digital scents : Myth or Reality?

The olfactory receptor (OR) is the first protein that recognizes odorants in the olfactory signal pathway and it is present in over 1,000 genes. Olfactory receptors are G protein-coupled receptors which serve important sensory functions beyond their role as odorant detectors in the olfactory epithelium. Olfactory receptors detect volatile chemicals that lead to the initial perception of smell in the brain. 

Most ORs are extensively expressed in the nasal olfactory epithelium where they perform the appropriate physiological functions that fit their location.

However, recent whole-genome sequencing shows that ORs have been found outside of the olfactory system, suggesting that ORs may play an important role in the ectopic expression of non-chemosensory tissues.

The ectopic expressions of ORs and their physiological functions have attracted more attention recently since MOR23 and testicular hOR17-4 have been found to be involved in skeletal muscle development, regeneration, and human sperm chemotaxis, respectively. Olfr1393, as a regulator of renal glucose handling, is specifically expressed in the kidney proximal tubule, which is the site of renal glucose reabsorption. Olfr1393 knockout mice exhibit urinary glucose wasting and improved glucose tolerance, despite euglycemia and normal insulin levels.

As the outermost barrier of the body, the skin is exposed to multiple environmental factors, including temperature, humidity, mechanical stress, and chemical stimuli such as odorants. Keratinocytes, the major cell type of the epidermal layer, express a variety of different sensory receptors that enable them to react to various environmental stimuli and process information in the skin. Recently, the identification of a novel type of chemoreceptors in human keratinocytes, the olfactory receptors OR2AT4, and identified Sandalore, a synthetic sandalwood odorant, as an agonist of this receptor. Sandalore induces strong Ca(2+) signals in cultured human keratinocytes, which are mediated by OR2AT4, as demonstrated by receptor knockdown experiments using RNA interference. The activation of OR2AT4 induces a cAMP-dependent pathway and phosphorylation of extracellular signal-regulated kinases (Erk1/2) and p38 mitogen-activated protein kinases (p38 MAPK). Moreover, the long-term stimulation of keratinocytes with Sandalore positively affected cell proliferation and migration, and regeneration of keratinocyte monolayers in an in vitro wound scratch assay. OR 2AT4 is involved in human keratinocyte re-epithelialization during wound-healing processes.

The Gut Microbiota and Olfactory Receptors are one of the intriguing phenomenons. How Gut microbiota communicate with the brain, skin, kidney, liver…? How they activate OR? What kind of agonist? This is one of questions which will be discussed.

The Digital Olfaction science needs the understanding of how to activate and modulate these multi-locations ORs. Why our nose is everywhere? Can a Digital aroma activate skin OR? A multi-disciplinary collaboration is urgently needed between experts of olfactory receptors and the digital science.

Finally, a strategic question is how digital olfaction world will establish non-verbal communication between us (our Olfactory Receptors) and the artificial systems (robots, connected devices…)?

EDEAS, Marvin

University of Paris Descartes, INSERM 1016, Institut Cochin, Paris, France

More than 150 leaders working is skin and all skin-related fields will join Porto Skin Challenges 2018

The audience of Porto Skin Ageing & Challenges will be composed by academics and industrials coming from all around the world. Among the participants:

AHAVA Dead Sea Laboratories
Rousselot
Laboratoires M&L
UNESP
Monteloeder SL
Oriflame Cosmetics
Chanel
Philips
Mibelle Group Mifa
Arterra Bioscience srl
Laboratoires Clarins
Merck
Beiersdorf AG

Unilever
Lycotec
DSM Nutritional Products
ID bio
InternationalaMicrobiology Department
L’Oréal Research and Innovation
Laboratoires Pierre Fabre Dermo-Cosmétique
Greentech
L’Oréal Active Cosmetics
Symrise AG
Walgreens Boots Alliance
CLR – Berlin
Dow Slicones Belgium
Provital SA
ROQUETTE Frères
SEDERMA
IFF-Lucas Meyer Cosmetics
Vichy Laboratoires
Symrise Ibérica
Greensea
Procter & Gamble International Operations
University of Manchester
Oriflame R&D
Clariant
Devan Micropolis, SA
Inovapotek
Allergan
Prestige et Collections International
Ashland
Unilever R&D
Nestle Skin Health
SAFIC-ALCAN
SEPPIC
Technion
University of Namur
University of Rouen Normandy
Okayama University of Science

Université Pierre et Marie Curie
China Medical University
Chung-Ang University
Medical University of Bialystok
Newcastle University
Pennsylvania State University
Saarland University
Université du Havre
Tokyo Medical & Dental University
Stanford University
Doshisha University
The University of Bradford
University of Ferrara
Zhejiang University
Albstadt-Sigmaringen University of Applied Sciences
Biodonostia Health Research Institute
CEA
Université Grenoble Alpes
Department Dermatology Saint Jacques Hospital
EstheMedis
University of Coimbra

Miguel Hernández University
Public Health England
Université Paris-Sud
University College London
BOKU – University of Natural Resources and Life Sciences Vienna
Université du Havre
Moscow state University
Winogradsky Institute of Microbiology
Wojskowy Instytut Higieny i Epidemiologii
The Francis Crick Institute

The Hebrew University
The Hong Kong University of Science and Technology
Eastman Dental Institute
Hong Kong University of Science and Technology
UCL
Adolphe Merkle Institute
University of Fribourg
Dow Slicones Belgium
Jagiellonian University
Medical University of Bialystok
Medical University of Warsaw
Universität Innsbruck
University of Porto
University Brasil
Institut Cochin
Leibniz Research Institute for Environmental Medicine
University of Ferrara
University of Exester
Centre de Recherche en Cancérologie de Lyon
Johns Hopkins University School of Medicine
University of Tübingen
Swansea University
and many more…

 
It is a non-exhaustive list of attendees, and we remind you that you can join all these leaders and save if you register before January 31, midnight by clicking here.
 
For more information: www.skin-challenges.com
 

Bacteria in the gut modulates response to immunotherapy in melanoma

Bacteria in the gut modulates response to immunotherapy in melanoma
The group performed fecal microbiome transplant (FMT) studies from responding patients on PD-1 blockade (R) or from non-responding patients (NR). In these studies, mice receiving FMT from R had enhanced systemic and anti-tumor immunity, with more immune cells in the tumor and in the gut of the transplanted animals. Conversely, mice receiving FMT from NR had poor anti-tumor immunity and a paucity of immune cells in the gut. Credit: Dr. Luigi Nezi

Bacteria that live in the human digestive tract can influence how cancer responds to immunotherapy, opening a new avenue for research to improve treatment, a team led by researchers at The University of Texas MD Anderson Cancer Center reports in the journal Science

Patients with metastatic melanoma treated with anti-PD1 checkpoint blockade have their disease controlled longer if they have a more diverse population of bacteria in the gut or an abundance of certain types of bacteria, according to the team’s analysis of to assess patients’ gut microbiomes.

“You can change your microbiome, it’s really not that difficult, so we think these findings open up huge new opportunities,” said study leader Jennifer Wargo, M.D., associate professor of Surgical Oncology and Genomic Medicine. “Our studies in patients and subsequent mouse research really drive home that our gut microbiomes modulate both systemic and anti-tumor immunity.”

Wargo and colleagues are working with the Parker Institute for Cancer Immunotherapy to develop a clinical trial that combines checkpoint blockade with microbiome modulation.

Research has shown that a person’s microbiome is a modifiable risk factor that can be targeted by diet, exercise, antibiotic or probiotic use or transplantation of fecal material, said lead co-first author Vancheswaran Gopalakrishnan, Ph.D.

Immune checkpoint blockade drugs that free the body’s own immune system to attack cancer help around 25 percent of metastatic melanoma patients, and those responses are not always durable. Research focuses on extending the impact of these drugs.

To assess the impact of the microbiome, Wargo and colleagues analyzed buccal swabs – tissue samples from inside the cheek—and fecal samples of patients treated with anti-PD1 therapy that blocks the PD1 protein on T cells, which acts as a brake on the immune system. They conducted 16S rRNA and whole genome sequencing to determine diversity, composition and functional potential of the buccal and fecal microbiomes.

While the team found no substantial differences in response or progression based on buccal samples, analysis of fecal samples of 30 patients who responded to treatment and 13 who did not told a different story.

  • Patients with higher diversity of bacteria in their digestive tract had longer median progression-free survival (PFS), defined at the time point where half of studied patients have their disease progress. While the patient group with high diversity had not reached median PFS (more than half had not progressed), those with intermediate and low diversity had median PFS of 232 and 188 days respectively.
  • Notable compositional differences existed in the gut microbiome of patients who responded versus those who did not, with the Ruminococcaceae family enriched in responders and the Bacteroidales order enriched in non-responders. Patients who had a high abundance of the genus Faecalibacterium (of the Ruminococcaceae family and Clostridiales order) in their gut had significantly prolonged PFS (median not reached), compared to patients who had a low abundance (median PFS of 242 days)
  • Abundance of Bacteroidales was associated with more rapid disease progression, with high abundance within the gut microbiome associated with significantly reduced PFS (median 188 days), compared to low abundance (median PFS of 393 days).

Additional analysis showed that responding patients with high levels of the beneficial Clostridiales/Ruminococcaceae had greater T cell penetration into tumors and higher levels of circulating T cells that kill abnormal cells. Those with abundant Bacteriodales had higher levels of circulating regulatory T cells, myeloid derived suppressor cells and a blunted cytokine response, resulting in dampening of anti-tumor immunity.

A favorable microbiome also was associated with increased antigen processing and presentation by the immune system at the tumor site.

To investigate causal mechanisms, the team transplanted fecal microbiomes from responding patients and non-responding patients via fecal microbiome transplant (FMT) into germ-free mice. Those receiving transplants from responding had significantly reduced tumor growth as well as higher densities of beneficial T cells and lower levels of . They also had better outcomes when treated with immune checkpoint blockade.

Wargo and colleagues note that there is still much to learn about the relationship between the and cancer treatment, so they urge people not to attempt self-medication with probiotics or other methods.

News source: medicalxpress.com

Researchers find factor that delays wound healing

New research carried out at The University of Manchester has identified a bacterium—normally present on the skin that causes poor wound healing in certain conditions.

Pseudomonas aeruginosa and its variants are associated with delays in .

Damage to a receptor that allows the body to recognise the is associated with a change in the balance of the community of bacteria present normally on the skin. And according to Dr Sheena Cruickshank, the shift in balance has an enormous impact on the ability of the wound to heal.

The study was carried out at Manchester and co-led by Dr Cruickshank and Dr Matthew Hardman, who is now at now at The University of Hull. The bacterium has previously been associated with wound infections, and such infection is a major complication of that fail to heal. At least one in 10 people will develop a wound that heals poorly.

The research, published in the Journal of Investigative Dermatology and funded by the Medical Research Council, casts new light on why one in 10 people will develop a which does not heal well.

The research was carried out using mice that were previously shown to heal poorly. The mice lack the receptor Nod2 that recognises bacterial components and has been shown to help regulate the host response to bacteria. The team found that mice lacking Nod2 had more Pseudomonas aeruginosa than , which is associated with delayed wound healing.

The bacteria also caused normal mice to heal poorly. The team says the findings are also applicable to humans as Pseudomonas aeruginosa is associated with that heal poorly in people. Dr Cruickshank said, “There is an urgent need to understand the bacterial communities in our skin and why so many of us will develop wounds that do not heal.

“Wounds can be caused by a multitude of factors from trauma to bed sores, but infection is a complication that can, on occasion, lead to life-threatening illness. Many people are struggling with wounds that heal poorly, but this new study suggests that the types of bacteria present may be responsible for our failure to heal, which is important for considering how we manage wound treatment.”

Explore further: Bacteria on the skin: New insights on our invisible companions

More information: Helen Williams et al. Cutaneous Nod2 Expression Regulates the Skin Microbiome and Wound Healing in a Murine Model, Journal of Investigative Dermatology (2017). DOI: 10.1016/j.jid.2017.05.029

Topical gel made from oral blood pressure drugs shown effective in healing chronic wounds

An international team of researchers led by Johns Hopkins has shown that a topical gel made from a class of common blood pressure pills that block inflammation pathways speeds the healing of chronic skin wounds in mice and pigs.

A report of the findings, published Oct. 16 in the Journal of Investigative Dermatology, marks efforts to seek approval from the U.S. Food and Drug Administration (FDA) to use the gel application in treatment-resistant skin among diabetics and others, particularly older adults.

“The FDA has not issued any new drug approval for in the past 10 years,” says Peter Abadir, M.D., associate professor of medicine at the Johns Hopkins University School of Medicine and the paper’s first author. “Using medicines that have been available for more than two decades, we think we have shown that this class of medicines holds great promise in effectively healing that are prevalent in diabetic and aged patients.”

Chronic wounds, defined as skin injuries that fail to heal in a timely manner and increase the risk of infection and tissue breakdown, accounted for more than 100 million hospital visits in United States hospitals in 2008, according to Abadir.

In recent years, attention has turned to the skin’s renin-angiotensin system (RAS), which is involved in the skin’s inflammatory response, collagen deposition and signaling necessary for wound healing. Studies show that the RAS system is abnormally regulated in diabetic and older adults.

Abadir and colleagues experimented with gel formulations of angiotensin II receptor antagonists, or blockers, a long-standing class of drugs that includes losartan and valsartan, prescribed to treat hypertension. The drugs block RAS and increase wound blood flow, and the goal was to apply the gels directly to wounds, increasing wound tissue level of the drugs that promote faster healing.

Abadir and colleagues first tested 5 percent topical losartan on mice in three different phases of wound healing: group 1 treatment, for up to three days post-wound infliction to target the inflammatory phase; group 2 treatment, starting on day seven after wound infliction to target the proliferative/remodeling (later) phase of tissue healing; and group 3 treatment, starting the first day of wound infliction until closure to treat all wound healing phases. A fourth group was kept back as a control and given standard care and a placebo. Mice in group 2 experienced the most accelerated wound healing rate.

Next, Abadir and colleagues compared the effects of different concentrations of losartan and valsartan on young diabetic and aged mice during the proliferation/remodeling phase of wound healing, which involves the regrowth of normal tissue.

The results showed that valsartan was more effective in accelerating wound healing than losartan, without any significant difference in healing time between valsartan doses. Overall, 1 percent valsartan had the greatest impact on total closure compared with the other agents, and 10 percent losartan led to the worst wound healing, which Abadir says may be attributed to toxicity.

Wound. Credit: Johns Hopkins Medicine

Final results showed that half of all mice that received 1 percent valsartan achieved complete wound healing, while only 10 percent of the mice given the placebo did.

Driven by 1 percent valsartan’s promising results in mice, the researchers tested its effects on wounds among aged, diabetic pigs, as pig skin has more similar properties to human skin.

Compared with pigs in the placebo group, wounds that received 1 percent valsartan healed much more quickly, and all 12 wounds were closed by day 50, compared with none of the placebo-treated wounds, the researchers say.

Of note, Abadir says, a low concentration (1 to 50 nanomoles) of valsartan was detected in the pigs’ blood near the beginning of treatment, and none was detected later in the treatment course, suggesting that the drug acts locally on the tissues where it’s absorbed, rather than affecting the entire body.

For comparison, oral ingestion of valsartan generally yields 4,000 to 5,000 nanomoles in the blood level for a human. This suggests that topical application of valsartan will not be absorbed into the bloodstream and could have unintended physiological effects, such as those that affected blood pressure, body weight or kidney function.

Finally, to determine the quality of 1 percent valsartan’s biological effects on wound repair—not just rate of repair—Abadir and colleagues examined collagen content and tensile strength in the pigs’ skin. Pigs treated with valsartan had a thicker epidermal layer (the outermost layer of the skin) and dermal collagen layer, as well as a more organized collagen fiber arrangement, all of which indicate 1 percent valsartan application leads to stronger healing skin, Abadir says.

“Our strategy for specifically targeting the biology that underlies chronic wounds in diabetics and older adults differs greatly from other approaches to wound care thus far. The topical gel likely enables a cascade of positive biological effects that facilitates and accelerates chronic wound ,” says Jeremy Walston, M.D., professor of medicine and the paper’s senior author.

“Now that we’ve proven efficacy in animals, we’re moving on to the next stage of FDA-required testing in humans. Hopefully, this medication will be available for public use in a few years, if further research bears out our results,” adds Walston. Walston and colleagues envision that the medication could one day also be used to treat scars, wrinkles and other skin problems.

Twenty-nine million Americans have diabetes and 1.7 million are newly diagnosed each year. Of this group, approximately 900,000 will develop annually. With an aging population and incidence of diabetes increasing rapidly across the globe. Abadir estimates the total number of diabetic foot ulcers to be more than 20 million per year, with an estimated total cost of $25 billion annually in the U.S. alone.

More information: Peter Abadir et al, Topical Reformulation of Valsartan for Treatment of Chronic Diabetic Wounds, Journal of Investigative Dermatology (2017). DOI: 10.1016/j.jid.2017.09.030

News source: www.medicalxpress.com