Daily Archives: July 22, 2017

Key Parkinson’s Protein Gets Starring Research Role on International Space Station – Parkinson’s News Today

Posted: July 22, 2017 at 7:50 am

When a resupply mission lifts off in August bound for the International Space Station, it will be carrying an important cargo for researchers studying Parkinsons disease: aprotein consideredto be a key to potential future therapies.

Theleucine-rich repeat kinase 2(LRRK2) protein will be the focus of an experiment conducted on the Space Station.It is hoped that the microgravity conditions aboard the Space Station will allow growth of larger, more regular LRRK2 protein crystals, which would help scientists solve the proteins structure providing valuable information for thedesign of optimized therapies to fight Parkinsons disease (PD).

The experiment is the result of a partnership between theMichael J. Fox Foundation for Parkinsons Researchand the Center for the Advancement of Science in Space (CASIS).

Were thrilled that PD research has been selected to travel to the International Space Station and honored to partner with CASIS on behalf of the PD community here on Earth, said Michael J. Fox, the actor who started the foundation after he was diagnosed with Parkinsons, in a video message played at the International Space Station Research and Development Conference held in Washington, DC, July 17 20.

The SpaceX CRS-12 cargo resupply mission scheduled for liftoff in August will carry LRRK2 protein to the Space Station to be used in the Crystallization of LRRK2 Under Microgravity Conditions (CASIS PCG 7) experiment.

In its role as manager of the Space StationsU.S. National Laboratory, CASIS is responsible for coordinating transfer of scientific materials to and from theSpace Station and oversight of work conducted in the laboratory. The Michael J. Fox Foundation, which initiated this project, has supported earthside preparation of the protein for growth in space.

Advancing Understanding of LRRK2 as a Key Parkinsons Drug Target

LRRK2 is considered to be the greatest known genetic contributor to Parkinsons disease, according to the Michael J. Fox Foundation. Most Parkinsons cases are categorized as idiopathic of unknown cause with only about 10 percent of cases having been linked to a genetic cause. LRRK2 gene mutations are the most common cause of Parkinsonsin that minority, which represents only 1 to 2 percent of total Parkinsons cases.

However, LRRK2 mutations account for a much higher proportion of Parkinsonscases among people of certain ethnic groups, notably Ashkenazi Jews, North African Arab Berbers, and Basques, than they doin the general population.

The foundationnotes that while estimates vary, it is believed that mutated LRRK2 (predominantly the mutation scientists refer to as G2019S) account for some 15 to 20 percent of Parkinsons cases among Ashkenazi Jews, and about 40 percent of cases in North African Arab Berbers. Also, other genetic changes in LRRK2 have been found to increase risk of developing Parkinsons among people of other ethnic backgrounds, such as in Asians of Chinese descent.

Because LRRK2 protein function is heightened in people with Parkinsons disease, and is associated with a mutation in the LRRK2 gene, the foundation believes therapies targeting this gene could also accelerate development of treatments that can benefit a broader Parkinsons population.

However, one obstacle holding back this line of drug development is the limited understanding of LRRK2s exact structure. The foundationnotes that greater understanding of a proteins shape and structure can help developers design therapies more likely to engage a particular protein in treatment of disease.

Overcoming Gravitational Limitations

Earths gravitational field allows only low resolution versions of LRRK2 protein to be grown. However, the Crystallization of LRRK2 Under Microgravity Conditions (CASIS PCG 7) experiment will use automated biotechnology devices operating in the microgravity environment to grow larger, better-formed protein crystals with fewer defects that may yield higher resolution views of LRRK2. These will then be returned to Earth for postflight analysis.

Having a better detailed view of the precise shape and morphology of LRRK2s crystalline structure would help scientists better understand Parkinsons pathology, and accelerate development of LRRK2 inhibitor therapies designed to prevent, slow, or stop Parkinsons disease progression.

The unique environment of the International Space Station untethers research from restrictions imposed by gravity,CASIS president and executive director, Gregory H. Johnson, said in a press release. CASIS is glad to partner with The Michael J. Fox Foundation to explore the structure of this important piece of the Parkinsons puzzle.

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SpaceX’s Mars Plans Hit a Pothole. Up Next: the Moon? – WIRED

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Elon Musk speaks at the International Space Station Research and Development Conference in Washington, D.C. on July 19, 2017.

Aaron Bernstein/Reuters

Its been less than a year since Elon Musk announced his plans to settle humans on Mars during a talk in Guadalajara, Mexico. On stage at the International Astronautical Congress, the billionaire invoked the lore of Hitchhikers Guide to the Galaxy and Battlestar Galactica while describing a massive passenger ship loaded with the essentialsyou know, like a movie theater and a restaurant. SpaceX hoped to launch these breezy cruises to the red planet in the early 2030s.

Plot twist: Musk's original vision is no longer canon in his universe. On Wednesday, Musk took questions during a keynote discussion at the International Space Station R&D conference in Washington, DC. In between dad jokes about tunnel digging , a staple artificial intelligence threat assessment , and a spirited attempt to unpack the potential for interplanetary war, he candidly revealed a series of obstacles for SpaceX and its plan to build a city on Mars. SpaceX is rebooting its colonization plan, and may pivot to focus on a moon base that would aid that effort.

The Hawthorne, California-based spaceflight company has spent years touting propulsive landing technology for the next version of its Dragon spacecraft. SpaceX expected to equip the Dragon V2, rated for crew and cargo, with four small SuperDraco engines and deployable landing legs to allow for a guided surface touchdownfirst on the Earths surface, and then, maybe, on Mars. SpaceX was confident enough in the design to propose a variant of the vehicle Musk claimed would be able to land anywhere in the solar system.

The pitch for those uncrewed Red Dragon missions to Mars included a collaboration with NASA to gather landing data, test communications, and plan for potential contamination from Earth-based microbes. The space agency, of course, has its own boots-on-Mars ambitions, and hopes to send astronauts to the red planet aboard the Orion spacecraft by 2040. Musk would later compare Red Dragon launches to a train leaving the station, delivering cargo and science to Mars in preparation for a human mission.

But now, SpaceX has pulled the plug on its prologue to an interplanetary future.

Musk explained that Red Dragon was no longer in line with the evolving vision SpaceX has for getting to Marsspecifically, the part where you have to land on Mars . The company is hitting pause on the development of its propulsive landing technology on the Dragon V2 spacecraft. Musk argued that while the technology works, SpaceX would be put through the wringer trying to meet NASAs safety standards for landing a human crew on the ground. It doesnt seem like the right way to apply resources right now, Musk said. Im pretty confident that is not the right way, and that theres a far better approach. He later tweeted that SpaceX would still land with propulsive thrusters on Mars, but with a larger spacecraft.

SpaceX has had a busy year adding to its growing arsenal of recovered rockets while launching more times than any other year since its founding. The company also managed to re-fly both its Falcon 9 rocket and Dragon cargo capsule . In the flurry of praise surrounding rocket landings and Mars concepts, the fact that SpaceX has yet to attempt or complete a deep space mission of any kind still weighs on the companys future. Red Dragon would have been SpaceXs first toe into the deep end of the pool.

Its journey would have begun atop the triple-booster Falcon Heavy rocket, the famously-delayed launch vehicle that Musk claims has over twice the payload capability of a single Falcon 9 rocket, able to easily deliver 100,000 pounds to low-Earth orbit. At the ISS R&D conference, Musk invited the audience and those watching the livestream to witness the launch of the vehiclecurrently projected for this fallfrom Kennedy Space Center. But he followed with an uneasy disclaimer: Real good chance that vehicle doesnt make it to orbit.

That uncertainty doesnt bode well for Musks original Mars ambitions. Musk argued that the Falcon Heavy was impossible to test on the ground due to the machines complexity. And he said that development was far more difficult than SpaceX expected, admitting that the company was naive in its original projections. The simultaneous firing 27 orbital engines notwithstanding, launching a Falcon Heavy includes changing aerodynamics, heightened vibration, and an enormous thrust that pushes qualification levels of the flight hardware to the limit. Musk admitted on Wednesday that limited damage to former Apollo 11 Pad 39A would be a win in the aftermath of the Falcon Heavy test flight. Along with Musk, the audience laughed nervously.

According to Musks keynote this week, SpaceX is planning to scale down its Mars-bound spacecraft to a size suitable for a wider range of missionsmissions that would help pay for its development costs. A size reduction would certainly have a large economic impact on manufacturing, but savings could be augmented by focusing all efforts on a single reusable vehicle that could serve both low-Earth orbit and deep space. And Musk also offered that building a base on the moon is essential to getting the public excited about space again and would be an excellent stepping stone toward Mars.

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But is that a suggestion to another company? To NASA? Or is SpaceX going to unveil plans for a moon base as part of their updated Mars architecture?

Elon Musk has said that he would offer priority seating to NASA for missions to lunar orbit. SpaceX was the first private company to dock with the space station and the success between the federal space agency and the spaceflight company could point to a continuing partnership that expands beyond low Earth orbit. The ISS wont be around forever, and with NASA shifting toward deep space exploration, the opportunity to give the agency a lift is there. Especially if NASA wants to return to the moon.

But that doesnt mean SpaceX is abandoning its Mars ambitions; far from it. SpaceX owes much of its financial and development success to its partnership with NASA, and theres no doubt Musk will pursue that partnership beyond low-Earth orbit. That means that NASA astronauts could one day be flying on these deep space missions under lucrative taxpayer-funded contracts. Before then, SpaceX will have to fully prove its technology, along with life support systems and radiation protection for crewed missions.

Just a week ago, Musk dispatched SpaceX VP Tim Hughes to make the case for deep space in front of the Senate Subcommittee on Space, Science & Technology. Hughes used the success of SpaceX and NASAs commercial resupply missions and the governing Commercial Orbital Transportation Services program to make a case for partnership in deep space exploration. "To this day, Americas achievement of landing men on the moon and returning them safely to Earth likely represents humankinds greatest and most inspirational technological achievement, he said. Now, other nations like China seek to replicate an achievement America first accomplished 48 years ago. Maybe SpaceX can add private companies to the roster.

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C9ORF72 Throws a Wrench into DNA Repair Machinery | ALZFORUM – Alzforum

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21 Jul 2017

Hexanucleotide expansions in the C9ORF72 genethe most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementiamount a multipronged attack on the DNA repair system, according to a July 17 study in Nature Neuroscience. Researchers led by Mimoun Azzouz and Sherif El-Khamisy at the University of Sheffield in England reported that the repeat expansions trigger the formation of DNA-RNA hybrids, called R-loops, that break DNA. At the same time, the unusual dipeptide repeats (DPRs) translated from these expansions derail efforts to mend the damage. The researchers found evidence of broken DNA and a subpar repair response in mice expressing the expansions, and also in postmortem tissue from C9-ALS patients. They proposed that the onslaught of DNA damage in neurons ultimately leads to their demise, and that targeting the pathway could become a therapeuticstrategy.

DNA damage is a common hazard inside cells, and an extensive repair system exists to lessen its toll. Neurons are acutely dependent on this repair machinery, as they cannot easily wipe the slate clean through replication (see Pan et al., 2014).Making matters worse, oxidative DNA damage increases in the brain, and repair mechanisms start to falter with age and in the context of neurodegenerative disease (Sep 2011 news; Feb 2013 conference news).

Against this backdrop, El-Khamisy and colleagues wondered if an additional stressorC9ORF72 hexanucleotide expansionsmight add fuel to the fire. These expansions of the GGGGCC sequence exist in hundreds to thousands of copies in people with ALS/FTD. Both RNA foci formed from their transcription, and the DPRs generated by their translation, reportedly inflict damage on neurons. The researchers hypothesized that due to the expansions repetitive nature, and the abundance of GC repeats within them, the C9ORF72 expansions could be extremely prone to folding into R-loops, a type of DNA-RNA hybrid structure that can form during transcription (Aguilera and Garcia-Muse, 2012). R-loops are known triggers of double-stranded DNA breaks (Hamperl and Cimprich, 2014).

To learn if the expansions caused R-loops, first author Callum Walker and colleagues transfected the expansions into human fetal lung fibroblasts. Then they probed with antibodies specific to R-loops and phosphorylated histone H2AX, an established indicator of double-stranded breakages. Indeed, they found that cells expressing 102 repeats that could not be translatedand thus only formed RNA foci, not DPRsharbored elevated numbers of R-loops and breaks. This was also the case in cells transfected with constructs that did result in the translation of 34 or 69 DPRs. Notably, overexpression of senataxin, an RNA helicase known to resolve R-loops, reduced the number of breakages and even normalized the uptick in cell death the breakages triggered. Together, the findings suggested that the repeat expansions caused R-loops, which snapped DNA and harmedcells.

Cells transfected with dipeptide repeats (green) build up R-loops (red) in their DNA. [Courtesy of Walker et al., Nature Neuroscience2017.]

The researchers further wondered whether the repeat expansions would affect DNA repair. In both human fibroblasts and primary rat cortical neurons expressing the expansions, the researchers found the repair machinery to be profoundly hobbled. For starters, ataxia telangiectasia (ATM), the master DNA repair kinase, was hypophosphorylated and failed to activate when the researchers treated cells with DNA-damaging toxins. This led to a dismal nuclear recruitment of 53BP1, a factor that rejoins broken DNA, as well as subpar phosphorylation of another key ATM target,p53.

Through an extensive battery of biochemical and immunostaining experiments, the researchers zeroed in on the mechanisms that derailed the DNA repair machinery. The E3 ubiquitin ligase RN168 normally ubiquitylates histone H2A, an adornment that is needed to recruit 53BP1 to damaged DNA. However, in cells expressing the expansions, the researchers found RN168 tied up in p62 inclusions instead. This led to a reduction in ubiquitylated H2A and stymied 53BP1 recruitment. Interestingly, previous studies have reported that successful recruitment of 53BP1 to DNA helps sustain further ATM signaling (Lee et al., 2010). Therefore, RN168s entrapment in p62 inclusions could potentially derail the entire DNA repair process. In support of this idea, overexpression of RN168, or depletion of p62, restored 53BP1 recruitment and reduced the number of DNA breaks in cells expressing the repeatexpansions.

Strikingly, the researchers also observed R-loops, double-stranded breaks, and signs of weak ATM signaling in neurons from mice injected with viral vectors harboring the repeat expansions. These animals suffered a 20 percent loss in brainstem neurons, as well as motor deficits. The researchers proposed that DNA damage was the primary cause of this neurodegeneration, a hypothesis they will test by overexpressing senataxin and/or RN168 in the animals, El-Khamisy toldAlzforum.

The researchers also found evidence of DNA in disrepair in postmortem spinal cord tissue from ALS patients, which were wrought with R-loops, double-stranded DNA breaks, and signs of ATM signalingdefects.

Repeat Assault. In the proposed model, C9ORF72 repeat expansions damage DNA and thwart its repair. [Courtesy of Walker et al., Nature Neuroscience2017.]

The researchers proposed that C9ORF72 hexanucleotide expansions attacked DNA via two distinct, yet intertwined, pathways: through directly causing damage via R-loops, and by dismantling ATM-mediated DNA repair. El-Khamisy proposed that the repeat-laden RNA causes R-loops, while the DPRs manifest the p62 inclusions that sequester RN168 and disrupt repair. Interestingly, the latter pathway meshes with other recent findings implicating RN168 sequestration in p62 inclusions in the disruption of DNA repair (Wang et al., 2016).

Walkers findings dovetail with a previous study led by Li-Huei Tsai of MIT, which reported that the ALS gene FUS is recruited to DNA breaks and helps orchestrate repair (Sep 2013 news). The findings of the current paper are very consistent with ours, and together make a strong argument for the role of unrepaired DNA breaks in ALS, Tsaicommented.

This paper is particularly well done, commented Ray Truant of McMaster University in Hamilton, Canada. It really establishes ATM-mediated DNA repair as a common node in neurodegenerative disease, hesaid.

Truant recently reported that mutated huntingtin protein disrupted DNA repair (Maiuri et al., 2017). He added that as reactive oxidation builds in the brain with age, the efficiency of the DNA repair response could strongly influence the onset of neurodegenerative disease, a hypothesis supported by recent genome wide association studies (Bettencourt et al., 2016;Jones et al., 2017).

The study also provides researchers with a number of therapeutic targets, some of which may prove useful across neurodegenerative diseases, Truant added.JessicaShugart

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Who Killed Robin Brooks? DNA Technology Helps Paint Portrait of Killer – FOX40

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ROSEMONT -- Cold case investigators said Robin Brooks was raped and stabbed to death inside her apartment in the Rosemont area of Sacramento County more than 37 years ago.

Detectives have a full DNA profile of the suspected killer from his blood, but the case is still unsolved after all these years. But now, new technology is giving detectives a different way to look at the DNA and a glimpse at what the killer could possibly look like.

Its called DNA phenotyping. It sounds like science fiction, but this forensic method uses an unknown suspects DNA to create a composite sketch of the mystery persons physical characteristics.

Its not intended to be a photo ID, said Dr. Ellen Greytak over the phone to FOX40. Its a genetic witness in the absence of an eye witness.

Doctor Greytak works for Parabon NanoLabs, a Reston, Virginia-based biotech company that offers the tool called Snapshot. The Sacramento County Sheriffs Department has contracted the company to come up with two profiles of the suspected killer in Brooks unsolved murder case.

We have DNA, we have the person who did this, said retired Sacramento County sheriffs Detective Micki Links. There's no doubt about who it is. We just need their name.

The DNA profile of the suspected killer in Brooks case was put into all the criminal databases in 2004, but a match has never been made.

Links said she believes these two profiles will aid in the investigation by giving fading memories a look back at what the killers face may have looked like when he was 25. Another profile has the suspect aged to 56.

Links also shared new details on Robins whereabouts before her death.

For decades, investigators thought Brooks finished her shift at Donut Time off Keifer Boulevard and walked straight home to her apartment on Tallyho Drive. That apartment has been renamed the Garden Club Apartments.

But detectives said an informant, who has been cleared as a suspect, has come forward with a different timeline. He told them he saw Brooks at a house party somewhere off Roseport Way. The unnamed informant also told investigators Brooks went to the party after work and then went home.

The informant added that the party was made up of mostly teens, between 15 and 19 years old, many from Hiram Johnson High School and the nearby Lincoln Village.

You're not going to get away with this, said Links. I'm going to do whatever I can to find you, and make you pay for what you did.

Robins family is also still fighting for answers. Maria Arrick, Robins older sister, is offering up to a $10,000 reward for information that leads to the arrest of Brooks killer.

If you have any information regarding this case, please contact the Sacramento County Sheriffs Department main homicide line at (916) 874-5057. Or you can go to a special website set up for the victims of unsolved homicides in Sacramento County.

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Police: DNA links Decatur man to April burglary – The Decatur Daily

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A Decatur man was arrested Thursday after DNA collected from the scene of a burglary matched his DNA in the CODIS criminal DNA database, Decatur police said.

Eric Deondre Warner, 35, of 416 10th Ave. N.W., was charged Thursday with third-degree burglary, police said.

On Monday, DNA collected from the scene of the burglary matched with his DNA, which was on file in the CODIS database, police said.

On April 19, a burglary in the 400 block of Finley Drive N.W. was reported to police, reports show. The victim said items were taken from the home and it was "completely ransacked," according to reports.

Investigators were able to collect DNA evidence from the scene, which ultimately led to Warner being developed as a suspect, police said.

Warrants for Warner's arrest were obtained Thursday and were served on him in the Morgan County Jail, where he was incarcerated for other charges, police said.

Bail for his new burglary charge was set at $2,500.

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Removal of Aging Cells to Increase Longevity – Anti Aging News

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1167 1 Posted on Jul 21, 2017, 8 a.m.

Researchers find that a targeted removal of senescent cells could delay the onset of age-relateddegenerative joint conditions,such as osteoarthritis.

An international team of professional researchers joined forces to conduct a study that confirmed the targeted removal of senescent cells that collect in vertebrate tissue across the aging process contributes to delaying the onset of pathologies related to aging. The research was led by the Johns Hopkins University School of Medicine researcher Dr. Chaekyu Kim. He worked in tandem with the Johns Hopkins University School of Medicine's Dr. Ok Hee Jeon. Additional contributors from the University of California, Berkeley, the Mayo Clinic College of Medicine, the University Medical Center Groningen and the Buck Institute for Research on Aging and Unity Biotechnology, Inc. also played a part in the research. The findings were published this past April in the journal Nature Medicine.

About the Study

The research team presented a new pharmacologic candidate for the alleviation of degenerative joint conditions like osteoarthritis (OA) that are age-related. This occurs through the selective destroying of senescent cells known as SnCs. Such cells gather throughout the aging process in the body's vertebrate tissues. They are located at areas where age-related pathology occurs. Though such cells play an important role in the healing of wounds and repairing injured body sites, they might also lead to the onset of cancer within tissues. As an example, in particular joints like the knees and other cartilage tissues, SnCs are not always cleared from the area following the injury. This leads to the continuation of OA development.

In order to test the notion that SnCs might play a role in OA development, the researchers cut the anterior cruciate ligaments in young and old mice to a mimic a similar injury in human beings. The researchers applied injections of the experimental drug known as UBX0101 to remove SnCs following the anterior cruciate ligament transection surgery.

Preclinical studies in human and mice cells suggest removing SnCs dramatically decreases the development of post-traumatic OA as well as related pain. Removing SnCs also creates a prochondrogenic environment that allows for the growth of new cartilage and joint repair

The Findings

The findings suggest the selective removal of aged cells from the body's joints might decrease the development of post-traumatic OA. This selective removal might also allow for the growth of new cartilage and the repairing of joints. Aged mice did not show signs of any cartilage regeneration following the treatment applied through UBX0101 injections. The findings are relevant to human disease through validation with the use of chondrocytes isolated from patients who suffer from arthritis. The findings offer important insights into therapies keying in on the use of SnCs to treat trauma as well as degenerative joint disease related to the aging process.

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How Having Eczema on My Face Changed My LifeFor the Better – Health.com

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I have had eczema since I was a little girl, but it was neverterribly debilitating. I had some scratches on my neck, arms, and legs, but I never thought too much of it. And I was lucky to haveclear skin on my face. Other thana pimple here or there, my complexion was generally even and bright, andI neverneeded to use foundation.

That all changed this past May.Perhaps triggered by acombination ofpoor diet and taking too many medications, my eczema finally reared its ugly head in full force. Despite never having hadfacial eczemabefore, I started experiencing symptoms around my eyeswithin the next few months, it would consume my entire face, neck, arms, and upper legs.I ended up visiting countless doctors, starting a clean diet, and buying every product out there that claimed to be eczemas miracle cure.

I wish I could tell you that Im now free of eczema symptoms, butIhave a long ways to go. My face is still bright red, raw, and itchy. My legs and neck have inflammation, and I struggle to wake up every day feeling happy and healthy.

Did myskin issues make me feel down about myself at times? Sure. But succumbing to that way of thinking only made memore depressed.What has helped: understanding that my struggle with eczema is actually key to appreciating my life even more. Here, five ways the skin condition has helped me gain perspective and live a more fulfilling life.

RELATED: 9 Things You Should Never Do If You Have Eczema

1. I care less about looks. In the past, I couldn'tleave the house without eye makeup.In fact, I cant remember a time when I was able to confidently go outside without my trusty eyeliner. Now? I truly feel beautiful without makeup. Even when my facial eczema completely clearswhich I know it willI plan on wearing a lot less makeup than I used to. Im finally comfortable in my own skin.

2. In a strange way, I've become more confident. During my worst flares, when my face was red and sore, I found that I actually felt empowered. Sure, I cried and felt ugly at first. But I foundstrength from within to muster up thecourage to continue my day. Once that happened, I felt like I could take on anything.

3. Ibecame more empathetic. As clich as it might sound, I've realizedthat everyone is fighting their own battle. Sure, mine might be more noticeable, but I've become moreunderstanding that no one's life is all peaches and sunshine.

4. I focus more on health. I admittedly used to eat way too many cookies, cake, friesyou name it. As a result,I was constantly fatigued, no matter how many hours of sleep I got. Sinceimproving my diet by cutting out unnecessary sugarand consuming more leafy greens,I feel more alive. Another plus? I lost 10 pounds.

5. Iknow whos there for me. I didn'talways handle my eczema wellI avoided seeing people, I worked from home, and I didn'twant to look my boyfriend in the eye. But the experience has helped me realizewho truly loves me for me. My boyfriend, for example, continues to tell me Im beautiful every day. So whatif other people want to make comments or stare? They dont matter.

Have eczema, psoriasis, acne, or another conditionmessing with your confidence? Know that youre so much more than your skin, and you cant let it tell you how worthy you are. Do I still struggle with myself? Of course. But I now know that it willalways get better.

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Psoriasis Triggers & Types | Everyday Health

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Psoriasis, an autoimmune disease, affects about 7.5 million people in the United States.

Psoriasis is a disease that causes plaques, which are itchy or sore patches of thick, red, dry skin.

While any part of your body can be affected, psoriasis plaques most often occurs on the elbows, knees, scalp, back, face, palms, and feet.

Like other autoimmune diseases, psoriasis occurs when your immune system which normally attacks infectious germs begins to attack healthy cells instead.

According to the American Academy of Dermatology, about 7.5 million people in the United States have psoriasis, with the disease affecting Caucasians more than any other race.

The disease occurs about equally among men and women.

People with psoriasis generally see their first symptoms between 15 and 30 years of age; however, developing the disease between 50 and 60 years of age is also common.

Psoriasis patches can range from a few spots of dandruff-like scaling to major eruptions that cover large areas.

For some, psoriasis can clear up for months or even years at a time. This is known as remission.

Others experience psoriasis flares (or flare ups) in cyclical patterns; for instance, the disease will improve in the summer and worsen in the winter.

Psoriasis flares can be triggered by:

Stress: Stress is a major trigger for some people with psoriasis, either causing psoriasis to flare up for the first time or to make it worse after youve been diagnosed.

According to the National Psoriasis Foundation, a study of people who used light therapy for psoriasis found that listening to relaxation tapes during the therapy may help clear a psoriasis flare faster.

Cold weather: A trip to the Caribbean might be a good idea during the winter months if you have psoriasis and live in a cold climate,because the suns ultraviolet light turns off the skins immune system, which is overactive in people with psoriasis.

Dry skin: Anything that injures the skin can cause a psoriasis flare, including excessively dry skin.

The solution: Keep your skin moisturized. If youre allergic to the fragrances in moisturizers, use a product thats fragrance-free to avoid a rash.

Vaccinations: As with dry skin, puncturing the skin during a vaccination may cause a psoriasis flare, but thats no reason to skip a needed shot.

One thing to keep in mind: If youre on a potent psoriasis medication that suppresses your immune system (such as a biologic treatment), you shouldnt take a live vaccine. Your body may not be able to fight off a live virus because of the medication youre taking.

In that case, ask your doctor for a vaccine that contains a deactivated virus.

Beta blockers and lithium: Beta blockers to treat high blood pressure or lithium for a mental disorder can make psoriasis worse.

If you have high blood pressure, your doctor may be able to switch your medication to another drug that wont affect your psoriasis.

If youre taking lithium, your dermatologist may consider having you try light treatment or a topical therapy for psoriasis.

Upper-respiratory infections: Colds and other infections, especially strep throat, activate the immune system and can cause psoriasis to flare.

If you have psoriasis and develop a sore throat, get it treated and be sure to have a culture taken to check for strep. Long-term antibiotics may be an option for someone who has psoriasis and frequent sore throats.

Smoking: Theres some evidence that smoking can make psoriasis worse.

Diet: Studies havent shown any beneficial effects of taking nutritional supplements for psoriasis, but avoiding certain foods may reduce inflammation and help your psoriasis.

Additionally, studies have shown that many people with psoriasis may also have a gluten sensitivity, and eating a gluten-free diet can help reduce psoriasis symptoms.

In general, if you find that a certain food makes your psoriasis worse, try to avoid it.

Alcohol: For some people with psoriasis, having more than one or two drinks a day has been shown to cause psoriasis flares but the association is not a strong one. Flares from alcohol use could also be linked to psychological stress.

There are five types of psoriasis, yet people most often have only one type of psoriasis at a time. Each type has its own set of symptoms.

Most types of psoriasis go through cycles, flaring for a few weeks or months, then subsiding for a time or even going into complete remission.

Plaque psoriasis (also called psoriasis vulgaris) is the most common form. It appears as raised, red patches covered with a silvery white buildup of dead skin cells or scale.

The itchy, painful patches can crack and bleed, and commonly affect the scalp, knees, elbows, and lower back.

Guttate psoriasis often begins in childhood or young adulthood and is the second most common type of psoriasis.

Nearly 10 percent of people who get psoriasis develop guttate psoriasis, reports the National Psoriasis Foundation (NPF).

Inverse psoriasis, also known as intertriginous psoriasis, causes red lesions in folds of the body that may look smooth and shiny.

These lesions can occur on the genitals or areas near the genitals like the upper thighs and groin.

It's common for people with inverse psoriasis to have another type of psoriasis somewhere else on their body at the same time.

Pustular psoriasis causes white blisters of pus that surround red skin. The pus consists of white blood cells.

When pus-filled bumps cover the body, you may have bright-red skin and feel ill, exhausted, have a fever, chills, severe itching, rapid pulse, loss of appetite, or muscle weakness.

Erythrodermic psoriasis is a dangerous and rare form of the disease characterized by a widespread, fiery redness and exfoliation of the skin that causes severe itching and pain.

This type of psoriasis occurs once or more in 3 percent of people with psoriasis, according to the NPF.

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Psoriasis Triggers & Types | Everyday Health

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Cyndi Lauper showcases backstage psoriasis woes in Novartis’ new Cosentyx spot – FiercePharma

Posted: at 7:47 am

Cyndi Lauper is back to star in another round of Novartis psoriasis marketing.

The '80s pop music icon, who in 2015 partnered with the Swiss pharma giant and the National Psoriasis Foundation on a disease-awareness push, appears with two other real-life patients in Novartis latest Cosentyx spot.

RELATED:Novartis goes '80s with Cyndi Lauper-led psoriasis campaign

It was tough getting out there on stage, she narrates, as the camera shows her in her dressing room, trying to disguise her psoriasis with spray makeupand failing. The commercial weaves Laupers story with those of two other patients, shown struggling withunwanted attention aspeople around them stare at the red, flaky skin patches caused by the disease.

But the video spot takes a triumphant turn after Lauper declares that I found something that worked and keeps on working.

Never give up, she urges viewers, adding, clear skin can last as she rocks out on stage and then walks into a crowd of adoring fans.

RELATED:Novartis bolsters its home-turf advantage in psoriasis with Cosentyx DTC push

The new work is part of Novartis See Me campaign, which the company launched last year to play well with this patient base and further grow the brand, as then-pharma chief David Epstein told investors on an early 2016 conference call.

The new spot comes in the face of some new competition. Since the Basel-based drugmaker rolled out its first DTC effort in psoriasis, Eli Lillys Taltz, Valeants Siliq and, most recently, Johnson & Johnsons Tremfya have arrived on the next-gen psoriasis scene. Those rivals didn't stop Cosentyx from cracking the blockbuster barrier, though; it racked up $1.13 billion worldwide in 2016.

And asJohnson & Johnson execs recently reassured their own investors, theres still plenty of market share to go around. We believe it's only about 25% to 30% of the patients in that category [who] are actually on some of the newer agents, CEO Alex Gorsky said. So that in and of itselfrepresents a significant opportunity.

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Cyndi Lauper showcases backstage psoriasis woes in Novartis' new Cosentyx spot - FiercePharma

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Scientists provide insight into genetic basis of neuropsychiatric disorders – Medical Xpress

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July 21, 2017 Credit: CC0 Public Domain

A study by scientists at the Children's Medical Center Research Institute at UT Southwestern (CRI) is providing insight into the genetic basis of neuropsychiatric disorders. In this research, the first mouse model of a mutation in the arid1b gene was created and then used to show that growth hormone treatments reverse some manifestations of the mutation.

The ARID1B gene is one of the most commonly mutated genes in patients with intellectual disability and autism spectrum disorders, but scientists have not yet discerned if and how defects in the ARID1B gene contribute to these clinical manifestations. To understand how reduced levels of the protein product of the gene might cause these disorders, a team of researchers led by Dr. Hao Zhu and including graduate student Cemre Celen genetically modified mice to carry a mutation in one of two copies of the ARID1B gene. This mutation replicates the genetics of Coffin-Siris syndrome, a disorder that some patients with defects in the ARID1B gene have that is characterized by speech and social development problems, intellectual disability, and delayed physical growth.

The hope is that by understanding the molecular basis of Coffin-Siris syndrome, scientists will gain a deeper understanding of more common diseases involving intellectual and social impairment.

Scientists found mice with the mutated ARID1B gene exhibited the same type of physical and social changes seen in children with Coffin-Siris syndrome, such as abnormal brain development, muscle weakness, and increased anxiety and fear. The mice also displayed features consistent with autism spectrum disorder, such as social interaction abnormalities, repetitive behaviors, and abnormal "squeaks" or vocalizations. Further testing found these mice had lower-than-expected growth hormone and insulin-like growth factor (IGF1) levels in the blood, potentially explaining the small stature and delayed development seen in human patients. Treating mutant mice with growth hormones restored body size and muscle function, but did not significantly change the behaviors associated with the syndrome.

"These results suggest that growth hormone treatment could be a useful therapy for ARID1B patients. This is an interesting finding because we know some pediatricians already treat Coffin-Siris patients with growth hormones, although they were unaware that this response might be common to many people with ARID1B mutations," said Dr. Zhu, an Assistant Professor at CRI with joint appointments in Internal Medicine and Pediatrics at UT Southwestern Medical Center and a CPRIT Scholar in Cancer Research.

Dr. Zhu said he believes the study provides the scientific community with an important animal model to further investigate ARID1B's role in human brain disorders and will be a useful tool for therapeutic testing of potential treatments for autism, intellectual disability, and Coffin-Siris syndrome.

Explore further: Mice provide insight into genetics of autism spectrum disorders

More information: Cemre Celen et al. Arid1b haploinsufficient mice reveal neuropsychiatric phenotypes and reversible causes of growth impairment, eLife (2017). DOI: 10.7554/eLife.25730

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