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Category Archives: Transhuman News

Homo naledi genome: Will we ever find this elusive key to human evolution? – The Guardian

Posted: May 23, 2017 at 10:25 pm

Homo naledi may have lived at the same time as the first modern humans. Left: Neo skull of Homo naledi. Right: Omo 2 skull, one of the earliest modern humans. Photo credit: Wits University/ John Hawks Photograph: Wits University

Despite what many people believe, paradigm-shifting moments in science - where our understanding of a particular explanation is challenged by a single finding - are actually quite rare. But one happened in paleoanthropology on 9 May with the publication of three linked papers describing new fossils belonging to the enigmatic hominin Homo naledi.

Many people tend to think of human evolution as a very linear path: from primitive creatures more or less directly to ourselves. But for most of the history of evolution, there were multiple species of hominins running (or climbing) around the African landscape, each with their own unique physical adaptations to the challenges of survival. As with all evolutionary experiments, some of these adaptations proved more successful than others. Based on careful study of fossils spanning millions of years in Africa, paleoanthropologists thought they had a good understanding of how the experiments results unfolded. Human evolution wasnt a straight progression by any means, but more like a complicated bush, with branches leading off in many directions. Still, there were definite trends that made their way into our textbooks. Hominin lineages with some trait combinations died off without leaving any descendants. In the lineages that persisted, brains got bigger, legs longer, arms shorter, fingers less curved, teeth smaller.

It mostly made sense, and the new species discovered in a South African cave in 2015 seemed initially to fit within this paradigm. Homo naledi, as it was called, had some very primitive morphological features that meant it was likely very ancient indeed - possibly 2 million years ago, close to the root of our genus Homo.

But the recent discovery of a new set of H. naledi remains, in a separate chamber of the same cave system, and the first direct dates of the earlier H. naledi skeletons, has challenged this tidy story. Shockingly, the remains dated to just 236-335,000 years ago. This makes H. naledi very young: contemporaneous with early modern H. sapiens elsewhere in Africa. Yet, as the new fossils confirmed, H. naledi possessed a weird mosaic of primitive (ancient) and derived (more human-like) traits, such as small brain sizes (roughly a third of the size as ours: you can see the difference in the picture above) but human-like hands and limbs.

One reason this has paleoanthropologists in an uproar is that it means some features, such as small brain sizes, persisted long after they thought it possible. Berger et al. suggests that in light of this, we perhaps should be concerned about fossils which we have assigned to species on the basis of morphology rather than direct dates. If some remains have been misclassified, we may need to change our ideas about how different hominin lineages evolved. Another implication of these dates is that these hominins were around South Africa when stone tools began to be made. While they havent been found in association with any tools in the cave, we must still be open to the possibility that these small brained hominins could have made them. Finally, whether or not the H. naledi remains were deliberately buried inside the cave remains an extremely contentious issue among paleoanthropologists. These possibilities - both still unverified - pose a robust challenge for archaeologists to grapple with.

Notably, there are some things that these fossils wont change: 1) We are indeed the product of evolution (Im anticipating some of the comments on this post inevitably challenging evolution. Sorry guys, the evidence is incontrovertible and the fact that scientists change their minds as to the details when new discoveries are made speaks to the strength of the scientific process, not the weakness of the theory). 2) Humans originated in Africa, 3) There were multiple kinds of hominins co-existing for much of human evolution, 4) Humans are likely descended from H. erectus, with subsequent ancestry from some of the other kinds of hominins (Denisovans, Neanderthals, and probably others).

So where does H. naledi fit within the overall picture of human evolution in Africa? Its still unresolved. Berger et al. suggested three scenarios: First, H. naledi belongs to one of the lineages leading to H. habilis, H. rudolfensis, H. floresiensis, and A. sediba. Alternatively, H. naledi is younger - a sister lineage to the clade that contains H. erectus and the big-brained later hominins (including H. sapiens). The final scenario is that H. naledi is even younger still - a sister lineage to H. sapiens. Another possibility is that H. naledi is the result of hybridisation between two or more lineages, perhaps one related to humans and one related to Australopithecines.

The unusual combination of primitive and derived features of H. naledi make distinguishing between the above scenarios difficult without genetic evidence. If we could get a genome from one or more H. naledi individuals, we could determine the phylogenetic relationship between it and the big-brained hominins: H. sapiens and H. neanderthalensis (we dont yet know the brain size of Denisovans). This would tell us whether or not human populations had ancestry from this group (and perhaps others).

On a bioarchaeological level (assuming we could get DNA from multiple individuals in the cave), we could ask whether H. naledi individuals buried in the cave were close relatives, and whether there was a relationship between burial location and genetic relatedness. The answers to these questions might give us some insights into the social structure of the species, whether the individuals buried within the cave constituted a single population close in time, or whether there is detectable genetic change over time in the individuals within the cave. We could also use the molecular clock to estimate the time of divergence of H. naledi to the other hominins.

Ancient DNA could answer a lot of questions regarding H. naledis ancestry and relationships, but unfortunately were not there yet. While the dates of these fossils fit comfortably within the range at which we can obtain ancient DNA (currently up to ~560780,000 years ago), Berger et al. notes in their paper that attempts to obtain aDNA from H. naledi remains have thus far proven unsuccessful. One of the team members, Dr John Hawks, noted on twitter in a conversation with myself and others that three separate ancient DNA labs have actually made the attempt without any luck (ours at the University of Kansas wasnt one of them, for the record), but that they will keep trying.

This is an important reminder of just how difficult and frustrating ancient DNA research can be, and if theres anything I wish the interested public would know about it, its this: Behind the exciting news that comes out every month about this ancient genome or that lie scores of failed attempts, and the frustrated tears of many graduate students.

Ancient DNA preservation depends on many different variables, such as the temperature(s), UV radiation, and pH the remains have been subjected to, the type of bone, tooth, or tissue being sampled, and the amount of water, salinity, microbes, and oxygen present in the depositional context. This is why some very ancient bones will yield their genetic secrets, while ones just a few hundreds of years old wont no matter how hard you try. Furthermore, morphological preservation of bone doesnt always correspond with biomolecular preservation, and we cant necessarily know in advance whether DNA will be present in a skeleton before we attempt to recover it. Thus ancient DNA researchers must always be mindful about addressing important questions, be responsible about sampling fossils, and not commit too many resources (particularly money and time) to samples which wont work. Knowing when to stop working on a sample that wont yield DNA is almost as important as determining which samples to attempt in the first place.

Will we ever get a H. naledi genome? Based on the hints weve gotten so far, the odds dont look great. Just as with H. floresiensis, the other small-brained hominin that persisted until quite recently (50,000 years ago), their position in our family tree looks to remain unclear for a while - a lesson to us about how much we still have to learn. But if I werent relentlessly optimistic, I wouldnt have lasted long in the world of ancient DNA research. Perhaps it will just take a little more time and luck. Weve certainly seen these two variables in abundance throughout the remarkable story of H. naledis discovery.

Berger et al. Homo naledi and Pleistocene hominin evolution in subequatorial Africa. eLife 2017;6:e24234. DOI: http://dx.doi.org/10.7554/eLife.24234

Dirks PHGM et al. The age of Homo naledi and associated sediments in the Rising Star Cave, South Africa. eLife 2017;6:e24231 DOI: http://dx.doi.org/10.7554/eLife.24231

Hawks J et al. New fossil remains of Homo naledi from the Lesedi Chamber, South Africa. eLife 2017;6:e24232. DOI: http://dx.doi.org/10.7554/eLife.24232

Thompson JC. Human evolution: New opportunities rising. eLife 2017;6:e26775 DOI: http://dx.doi.org/10.7554/eLife.26775

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Discovery of an alga’s ‘dictionary of genes’ could lead to advances in biofuels, medicine – UCLA Newsroom

Posted: at 10:25 pm

Plant biologists and biochemists from UCLA, UC Berkeley and UC San Francisco have produced a gold mine of data by sequencing the genome of a green alga called Chromochloris zofingiensis.

Scientists have learned in the past decade that the tiny, single-celled organism could be used as a source of sustainable biofuel and that it produces a substance called astaxanthin, which may be useful for treating certain diseases. The new research could be an important step toward improving production of astaxanthin by algae and engineering its production in plants and other organisms.

The study is published online in the journalProceedings of the National Academy of Sciences.

Chromochloris zofingiensis is one of the most prolific producers of a type of lipids called triacylglycerols, which are used in producing biofuels.

Knowing the genome is like having a dictionary of the algas approximately 15,000 genes, said co-senior author Sabeeha Merchant, a UCLA professor of biochemistry. From there, researchers can learn how to put the words and sentences together, and to target our research on important subsets of genes.

C. zofingiensis provides an abundant natural source for astaxanthin, an antioxidant found in salmon and other types of fish, as well as in some birds feathers. And because of its anti-inflammatory properties, scientists believe astaxanthin may have benefits for human health; it is being tested in treatments for cancer, cardiovascular disease, neurodegenerative diseases, inflammatory diseases, diabetes and obesity. Merchant said the natural version has stronger antioxidant properties than chemically produced ones, and only natural astaxanthin has been approved for human consumption.

The study also revealed that an enzyme called beta-ketolase is a critical component in the production of astaxanthin.

Algae absorb carbon dioxide and derive their energy from sunlight, and C. zofingiensis in particular can be cultivated on non-arable land and in wastewater. Harnessing it as a source for renewable and sustainable biofuels could lead to new ways to produce clean energy, said Krishna Niyogi, co-senior author of the paper and a scientist at the Department of Energys Lawrence Berkeley National Laboratory.

Over the past decade-plus, Merchant said, research with algae, a small plant called rockcress, fruit flies and nematode worms all so-called model organisms has been advanced by other scientists determining their genome sequences.

They are called model organisms because we use what we learn about the operation of their cells and proteins as a model for understanding the workings of more complex systems like humans or crops, she said. Today, we can sequence the genome of virtually any organism in the laboratory, as has been done over the past 10 to 15 years with other model organisms.

Merchant, Niyogi and Matteo Pellegrini, a UCLA professor of molecular, cell and developmental biology and a co-author of the study, maintain a website that shares a wealth of information about the algas genome.

During the study, the scientists also used soft X-ray tomography, a technique similar to a CT scan, to get a 3-D view of the algae cells , which gave them more detailed insights about their biology.

Niyogi is also a UC Berkeley professor of plant and microbial biology and a Howard Hughes Medical Institute Investigator. The studys other authors are researchers Shawn Cokus and Sean Gallaher and postdoctoral scholar David Lopez, all of UCLA; postdoctoral fellow Melissa Roth, and graduate students Erika Erickson, Benjamin Endelman and Daniel Westcott, all of Niyogis laboratory; and Carolyn Larabell, a professor of anatomy, and researcher Andreas Walter, both of UC San Francisco.

The research was funded by the Department of Energys Office of Science, the Department of Agricultures National Institute of Food and Agriculture, the National Institute of General Medical Sciences of the National Institutes of Health, and the Gordon and Betty Moore Foundation.

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Discovery of an alga's 'dictionary of genes' could lead to advances in biofuels, medicine - UCLA Newsroom

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How about 2 million? DNAnexus joins AstraZeneca’s new genomics initiative – MedCity News

Posted: at 10:24 pm

In October 2013, DNAnexus and Baylor College of Medicine announced an ambitious ultra large-scalecollaboration to sequence and interpret3,751 whole genomes and 10,771 exomes. Some thought it was an impossible task.

Fast forward less than four years and DNAnexus is partnering on a new project with AstraZeneca to analyze two million genomes, with phenotypic data to boot.

The thing thats difficult to grasp from the outside is the velocity of knowledge gain in genomics. It is just amazing, marveled Richard Daly, CEO of DNAnexus. What people were doing two years ago is completely obsolete. And the tools they were using two years ago are obsolete.

Based in Mountain View, California, DNAnexus offers secure cloud-based platforms for research institutes, industry partners,andeven the U.S. government to massively increase their computing power. This, in turn, allows scientists to manage, access, and analyze sequencing data while collaborating with other groups around the world.

DNAnexus platform has scaled alongside the major genomics projects. But its not justthe volume of genomes sequenced that has risen dramatically over time. Daly noted by phone that the breadth of data being collected has also grown, as shown in AstraZenecas new undertaking.

The U.K.-based pharma companylaunched the initiative as well as an in-house Centre for Genomics Research in April 2016. Its aimis to build a bespoke database of genomic sequences using samples donated by patients in its global clinical trials. AstraZeneca has data from 500,000 participants amassed over the past 15 years and will add to that during the course of the 10-year study.

Importantly, the samples will also be matched with clinical notes and drug response data, meticulously collected through the course of its clinical trials. Merging genomic and phenotypic information is increasingly seen as the key to break into new layers of genomic complexity.

Even the basic sequencing techniques have advanced, Daly explained. Bioinformaticians have historically used reference genomes to do their base calling. In other words, genomes were interpreted in relation to a standard genome. Scientists soon realized that this approach was heavily biased in terms of ethnic diversity and error prone. Nowadays, scientists can draw on public databases of hundreds of thousands of genomes when they interpret the new results theyve obtained. Its another huge advance, which again requires huge technology gains.

As with Baylors 15,000-gemome project in 2013, AstraZenecas new initiative feels like a giant undertaking. But it will have help. Along with DNAnexus, collaborations withHuman Longevity, the Wellcome Trust Sanger Institute, and the Institute for Molecular Medicine Finland have also been announced.

Who knows where well be in ten years when this project wraps up.

Photo: farakos, Getty Images

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Got Eczema? Here’s Why You Might Want to Try an Elimination Diet – Health.com

Posted: at 10:24 pm

If you have eczema, I bet youre willing to do just about anything to soothe your itchy, irritated skin. Unfortunately, many of the topical remedies for this condition offer little relief. But an inside-out approach" focused on dietary changes may help considerably.

If you search for eczema diet online youll find a number of different protocols. But the standard approach is to begin with an elimination diet, which entails cutting out foods that may be triggering inflammation for at least four weeks, sometimes longer.

Most elimination diets start by nixing the top eight allergens: wheat; milk and milk products (think cheese and yogurt); eggs; soy; fish; shellfish; tree nuts (almonds, walnuts, pistachios); and peanuts. However, an elimination diet for eczema typically adds additional layers, such as all sugary and processed foods and anything artificial; gluten or possibly all grains; alcohol; caffeine; nightshade vegetables; seeds; and foods that are high in histamine.

Histamine causes an inflammatory response in the body, which is why anti-histamine medications are used for allergy relief. Some foods are high in histamine or trigger histamine release, including avocado, tomatoes, spinach, pickled or canned foods, pulses, nuts, cheese, chocolate, and vinegar.

RELATED: 15 Healthy Gluten-Free Recipes

By this point you may be thinking, Yikes, what can I eat on this plan? The good news is that an elimination diet isnt a forever diet. In the first phase, a number of foods are nixed. But after 30 or more days, the excluded foods are added back one at a time.

If the reintroduction doesnt result in the recurrence of symptoms, the food may be rotated back into the diet, although possibly not as a daily staple. Some of my clients find they don't tolerate dairy and gluten well, but can eat chickpeas, avocado, or nuts a few times a week without suffering a flare-up. What works for one person may be different for others.

It's also important to note that during the elimination phase, what you consume is just as important as what you dont. Eating anti-inflammatory, whole, fresh foods, and a diet balanced in macronutrients (protein, fat, and carbs) is essential. A nutritious diet not only supports immunity and supplies nutrients involved in skin maintenance and healing, it also improves the health of your gut, which is critical for immune function.

RELATED: 14 Inflammation-Fighting Foods

If you're considering trying an elimination diet, I cant overstate the value of working with a professional throughout the process. Some of my clients whove tried elimination diets on their own wound up with too few calories, or not enough protein or fat. Those imbalances can weaken immunity, prevent improvements, or even worsen eczema.

A dietitian can also help you identify hidden or sneaky sources of things that need to be eliminated. For example, while corn is a plant, its categorized as a grain, not a vegetable. So if youre going grain-free, you need to skip corn too.

Finally, a dietitian can help you meal plan, offer recipes, monitor your symptoms along the way, lend support, and guide you through the reintroduction phase. (You can search for an RD in your area through the the Academy of Nutrition and Dietetics online referral service.) An elimination diet is a big commitment. But identifying and managing your dietary eczema triggers has the potential to transform your skin, and your quality of life.

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That said, dietary changes are not a panacea. Eczema is a condition I struggle with myself, and even when my diet is spot on, I still get flare-ups. Mine are primarily triggered by stress, a lack of sleep, or both. In other words, diet alone isnt the only solution.

Bottom line: Because tests for food allergies and sensitivities can be imprecise (Ive personally had results come back as inconclusive while I was still battling flare-ups), an elimination diet is one of the most effective tools for uncovering precisely which foods are at the root of chronic inflammatory problems like eczema. But a healthy overall lifestyle that includes stress management (through techniques like meditation, acupuncture, and yoga), healthy sleep habits, and positive social support are also indispensable pillars of wellness.

Cynthia Sass isHealths contributing nutrition editor, a New York Times best-selling author, and consultant for the New York Yankees.

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My Eczema Makes Shopping Hell – Racked

Posted: at 10:24 pm

Id been eyeing the dress for a while. It was a red T-shirt dress with a simple cut and short sleeves, just as Id imagined it. Id been looking for a dress like this for ages, bored with all the dark colors in my wardrobe; this dress would liven up my style considerably. But I knew I wouldnt buy it. It was probably too expensive, I told myself, and I bet they wouldnt carry my size anyway.

Still, I needed proof that this dress wasnt meant for me, so I went inside the shop and touched it. It was just as I expected. The rough fabric was a shock to my fingers, and I knew it would be hell on the rest of my skin. This was not the first piece of clothing I couldnt buy because of my skin condition. It wouldnt be the last.

I have atopic dermatitis, also known as eczema. The National Eczema Association estimates that over 30 million Americans are affected by this skin condition. Symptoms include dry, itchy skin and rashes, which range from slightly annoying to basically hell. Eczema comes in several types, the most popular being contact eczema, and thats exactly the one I have. This particular type is not caused by anything I eat or inhale. Instead, it flares up at random moments throughout the year. Sometimes its better and sometimes its worse, but it never really goes away. There is no cure for atopic dermatitis. All I can do is to care for my skin and try not to scratch myself. I use special creams to relieve my symptoms, but that only takes me so far. And while I dont have to change my diet, I did have to change my lifestyle to work with the condition. That includes how I dress.

I was diagnosed as a teenager. First, I noticed ugly blotches on my hands and wrists. Then, they moved to my feet. I noticed that when I wore certain shoes on bare feet, they left itchy patches on my skin. Recently I noticed that it was getting worse, and I ended up getting rid of most those pairs, except for the few I wear with nicer outfits once in a while.

Then I went through my wardrobe and started cleaning it out. Everything with ruffles had to go. Ditto for lace, artificial fabrics, cinched tops, and tight skirts. Not that I ever wore them that much anyway. My wardrobe has now become emptier, and certainly more boring. And I feel ambivalent about that: On the one hand, I no longer have to worry whether a piece of clothing will cause my skin to break out. I can just put on whatever I grab first thing in the morning. But I really enjoy the look and feel of a nice piece of clothing. Id actually enjoy shopping for nice clothing if it wasnt for the fact that potential itchiness is always on my mind.

And there is the price issue, of course. Natural fabrics, which irritate my skin less, often cost more than artificial ones. Wool scratches, and cashmere, the only warm fabric I can wear, is expensive. I dont wear earrings because my skin only accepts gold. Anything else causes infection in my earlobes. A way out of it would be, of course, to not wear earrings, but I just happen to have a particular love for this piece of jewelry. I have a pair from all the countries Ive visited, and I love all of them. But theyre mostly not made of gold. Taking a moment to admire them from time to time is the best I can do.

Sometimes I wish I could just buy whatever clothing I want without having to wonder whether it will cause itchiness.

Sometimes I think of shopping like I think of drinking wine or coffee: I love the idea of it, but I dont actually like doing it. The images of luxury and pleasure they conjure appeal to me. In my mind, I often imagine going on shopping sprees, picking out the most adorable outfits. The reality couldnt be more different. Its getting excited about a piece of clothing, then realizing its way over your budget, it probably wont fit you, and even if it does, it will probably make your skin scream in protest.

There are a few go-to items I know I can always wear: jeans, cotton T-shirts and underwear, soft bras. In other words, things that have been part of my regular outfit for years. Maybe a part of me always intuitively knew to avoid certain fabrics and styles.

On one hand, having eczema makes my life easier. I dont face the same shopping choices that many women have because Im so focused on just feeling comfortable in my skin, in both the metaphorical and literal sense. The only thing I do is liberally slather myself up in body lotion. I dont know how to use most makeup products, and my morning routine consists of brushing my teeth, washing my face, putting on day cream, and getting dressed in the nearest jeans and T-shirt ensemble I can find. It saves me money as well.

But sometimes I wish I could just buy whatever clothing I want without having to wonder whether it will cause itchiness. I wish that I could go back to that store, take but one look at that perfect dress, and know that it could be mine.

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My Eczema Makes Shopping Hell - Racked

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Everything you need to know about eczema – DestinyConnect

Posted: at 10:24 pm

Entrepreneur and skin expert Roxy Marosa unpacks some of the causes of eczema and how to identify the skin condition

Marosa explains that eczema is classified as a condition that causes the skin to become irritated, red, itchy or inflamed.Its irritated, dry skin that looks like to has been bruised or discoloured, she says.

The severity of the skin condition differs from person to person while some people have mild cases, others have red, inflamed skin all over the body. Sometimes it can be so bad that when scratching, the skin cracks and bleeds, she says.

Symptoms of eczema include scratching, a very fine itchy rash, cracked skin, or discolouration of the skin inflamed. It usually shows up in softer parts of the skin like inside the elbow, behind the knees, the neck or even the face, she says.

Marosa says the causes of eczema vary. Environmental factors such as dry or cold weather play a role in triggering symptoms.

Some people suffer more in areas with dry summers, she says. In summer, the skin dries out to the point that it cracks and becomes constantly itchy, she says.

She further explains that even though eczema is a dry skin patch, its not aggravated by dry skin and can affect all skin types even oily skin.

The consumption of dairy products also contributes to eczema. Marosa adds that strong chemicals like chlorine can aggravate the condition. Eczema may be highly aggravated after swimming. You may find that eczema flares up due to the swimming pool chemicals, she says.

She says eczema can be treated and sometimes goes away on its own.

Marosaadds that chemical products, such as harsh soaps, should also be avoided. Gentle, hydrating cleaners that dont have chemicals are recommended. Use nourishing products.

Due to the unpredictable nature of eczema, Marosa says its important to pay attention to when you get flare-ups. Pay attention to what youre eating and when you experience problems, because youll become aware of what you need to cut from your diet, she says.

Try: Roxy Marosa Anti-Imflammotory Gel, R435

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Psoriasis treatment update: Woman discovers miracle cure in THIS natural cream product – Express.co.uk

Posted: at 10:23 pm

The woman was forced to wear lace gloves every day to work due to the crippling self-consciousness brought on by her psoriasis.

Pat Woodward, 60, an estate agent from Hampshire, suffered from psoriasis for over ten years.

Her hands were so sore and unsightly she would wear gloves to work.

However, she finally overcame the condition after finding a treatment when she least expected.

PAT WOODWARD

Pats hands are worst affected but she also has psoriasis on her legs and her scalp.

Having psoriasis on my hands affects every aspect of my life.

As obvious as it sounds, you need your hands for literally everything, from washing and dressing in the morning to eating, driving, typing or gripping a pen, and of course, for interacting with others.

Until very recently Pat would wear lace gloves to work, both for her benefit and also because she didnt want to make others feel uncomfortable.

Getty Images/Cultura RF

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Resist the itch - Eczema is almost always itchy no matter where it occurs on the body and although it may be tempting to scratch affected areas of the skin, this should be avoided as much as possible

PAT WOODWARD

Psoriasis can be very painful and having my hand squeezed by an unsuspecting stranger was often excruciating, Pat said.

The gloves would hide the layers of white, peeling, flaking skin, often cracked where my palms and knuckles were so dry my skin had split open.

Pat battled with different treatments for years.

She tried creams, mainly steroidal creams, from her doctor, but when these failed to work she begged to try stronger treatments.

My self-esteem was at an all-time low and I had started to suffer from depression, Pat said.

Doctors prescribed anti-depressants and continued to look at possible treatment plans, including light therapy, whilst family and friends suggested remedies including turmeric soap and beeswax creams, but nothing worked for any length of time.

Pat even tried three cancer-fighting drugs that break down the immune system, Methotrexate,Cyclosporineand Stelara.

PAT WOODWARD

However, the side-effects were horrendous.

From palpitations and general sickness to bowel disruptions so severe I actually thought I had cancer, and painful mouth ulcers, I felt dreadful, Pat said.

After my last course of skin injections in 2016, I asked my doctor not to put me forward for anymore.

Pat resolved herself to misery until she came across the cure to her condition completely by chance.

I was at a clients valuing her property when she asked me about my gloves. I went through the usual rigmarole of explaining why and what for, and she suggested I try Oregon grape root on my skin.

Ive had my fair share of tips and suggestions from well-meaning friends and family, but Oregon grape root was new to me.

I was immediately hopeful when I tried the Body & Hand Wash because for the first time in a long time my skin felt clean.

PAT WOODWARD

I was really keen to see an improvement in my hands. I applied a thick layer of Serum on these and wore with gloves overnight.

Pat claims the serum was immediately soothing and by morning her hands felt less tight.

After a few days she started to notice a visible difference too, the skin was less angry looking and after about four weeks, the thick flakes of white skin had reduced significantly and the deeper cracks had almost healed.

Pat has been using the Oregon Skincare range of products, designed especially to help combat the symptoms of psoriasis. The range costs from 7.95 and is available from http://www.skinshop.co.uk.

Guttate psoriasis is a sub-type of the skin condition psoriasis which is characterised by flakey, itchy skin and cannot be cured - although creams can quell the condition.

The Dermatology Clinic London's Dermatologist Dr Daniel Glass advised these two lifestyle factors could bring about a flare-up.

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Psoriasis treatment update: Woman discovers miracle cure in THIS natural cream product - Express.co.uk

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Galectin Therapeutics: Serendipity In Psoriasis, Strength In NASH … – Seeking Alpha

Posted: at 10:23 pm

Introduction

Galectin Therapeutics (NASDAQ:GALT) is a small biotechnology company based in Norcross, Georgia, focusing on the innovation of medicines that inhibit galectin molecules for the treatment of various diseases such as nonalcoholic steatohepatitis ("NASH"), skin cancer and plaque psoriasis. After a temporary nosedive in 2016, share price appreciated by approximately 80% for the past 52-weeks. It is highly likely that recent capital appreciation is reflective of the firm's increasing intrinsic value due to key developments. A notable catalyst was the positive data for the exploratory phase 2a trial, which suggests that lead molecule GR-MD-02 could be used to treat plaque psoriasis. Despite the firm's emphasis on NASH, this research shall focus on the potential therapeutic application of GR-MD-02 for plaque psoriasis.

Source: Google Finance

Plaque Psoriasis

As an autoimmune disease, plaque psoriasis is caused by the body's natural defense system going haywire, thus, causing the presence of well-demarcated red silvery scales on the skin surface. Due to its chronic nature, patients are placed on lifelong therapy. According to expert recommendations, the treatment for plaque psoriasis depends on the disease's severity. Patients with mild to moderate disease are prescribed with topical corticosteroid as the first-line agent. For moderate to severe cases without any contraindication, phototherapy serves as the therapeutic of choice. Those who failed the mentioned light treatment are managed with various approved systemic drugs such as steroid and methotrexate.

Source: Visualdx

The main setbacks for systemic therapies relate to their adverse effects. Nonetheless, doctors still employ such treatments, because the benefits outweigh the risks. In contrast to currently available medicine, GR-MD-02 potentially has a favorable efficacy and safety profile. As a new medicine in its own class, Galectin's lead molecule has a favorable chance of cutting into the multibillion-dollar psoriasis market. This is due to the fact that physicians tend to prescribe a unique therapeutic, especially one with a favorable safety profile like GR-MD-02, rather than another medicine amongst many approved drugs. In other words, GR-MD-02 would have a better chance of market success than a statin in development.

Another positive note for investors is that global data projected sales for psoriasis to increase from $6.6B in 2014 to $13.3B by 2024. If Galectin can cut into a small portion of this pie, the share price should increase multiple folds. And this would signify warranted optimism for shareholders.

Serendipitous Finding

Originally employed in the phase 2 trial for NASH patients, GR-MD-02 was found by chance to be efficacious for treating plaque psoriasis, which often occurs along with NASH. One patient with mild psoriasis participating in the NASH trial reported complete skin disease resolution for over a year. Another patient with moderate psoriasis reported the lesser use of her usual steroid medication. As a result, the aforesaid serendipitous finding prompted Galectin to commence the exploratory phase 2a.

Exploratory Phase 2a Trial

In March 2017, Galectin reported promising data for psoriasis in the aforementioned open-label exploratory phase 2a trial. Five patients employed in the study were infused with 8 mg/kg of GR-MD-02, a total of 13 infusions, for 24 weeks. No serious adverse events were found. All patients achieved an average PASI ("Psoriasis Area and Severity Index") reduction of over 50%, which is a measure of symptomatic improvement. The promising exploratory trial data prompted further development of GR-MD-02 for psoriasis treatment. Nonetheless, Galectin remains focused on innovating therapeutics for NASH.

"We are pleased by the results of our 24-week psoriasis trial demonstrating the safety and efficacy of GR-MD-02 in patients with moderate to severe plaque psoriasis," said Peter Traber, M.D., president, chief executive officer ("CEO"), and chief medical officer ("CMO"). "Moreover, the activity of GR-MD-02 in a human disease strongly associated with non-alcoholic steatohepatitis and increased galectin-3 expression suggests that our lead compound may also show significant activity in NASH, which remains the company's primary target."

As Dr. Traber suggested, the positive psoriasis data can foretell favorable outcome for the NASH trials. In addition, we strongly believe that it is intelligent to speculate trials data results for both NASH and psoriasis by analyzing GR-MD-02's mechanism of action.

Unique Mechanism of Action

Galectins are small molecules in the body that direct communication within the cells when being bound to glycoproteins found on cellular surface. In the disease processes that include inflammation, fibrogenesis, cancer formation, galectin's activity is heightened. Numerous research reports found the supporting role of galectin in the development of psoriasis in human. And it is hypothesized that lead molecule GR-MD-02 works by inhibiting galectin, thus, halting the disease process while stimulating the body to heal itself.

Source: Galectin

Focusing on Orphan Disease

In building its presence in the multibillion-dollars orphan disease market, Galectin is conducting two clinical trials, NASH-CX and NASH-FX for the treatment of NASH cirrhosis and NASH advanced fibrosis, respectively. Investing in orphan disease is seemingly the new trend for biopharmaceuticals investing. A firm can charge a premium price for a drug that treats rare ("orphan") diseases. And not only that this is viewed favorably by authority, the approach also ensures profitability for the company as well as the availability of lifesaving drugs for patients.

Source: Galectin

NASH asides, Galectin concurrently innovates GR-MD-02 for treating other fibrotic conditions, including lung, kidney, and heart. In addition, the named molecule is being studied for its applications together with other approved therapies ("Yervoy and Keytruda") to treat the dreaded skin cancer that is melanoma.

Adequate Funding

The majority of developing biotech firms operate in the red, as it takes substantial capital in the ballpark of more than a billion dollars to fund a drug from bench research to marketing. Hence, one can observe the increasing trend in operational cash flow that is needed to develop GR-MD-02 in the figure below.

Source: Morningstar

It is wise for biotech investors to note three key financial metrics. The first is that dilutive financing is not excess. The second is that debt to equity is not staggering. The third is whether the firm has adequate capital to fund their drugs to full development. That being said, Galectin increased its shares outstanding from 6M to 30M for the past decade, which is not unwarranted for a developing biopharma. It is a good sign that the firm's balance sheet is clean of long-term debts while there is only $3.8M borrowed for the short-term. As of March 2017, $13M in non-restricted cash and cash equivalents remain for operational spending. This amount is adequate to fund operation through the end of this year, which is sufficient for the reporting of NASH-CX's top line data.

Capable Management

With the strong track record of performance and many years of wisdom, Peter Traber, M.D. is the top-notch CEO and CMO to navigate this ship for Galectin shareholders. Prior to joining Galectin, Dr. Traber served as CEO of the prestigious medical schools: Baylor University and the University of Pennsylvania. As the former CMO at GlaxoSmithKline (NYSE:GSK), Dr. Traber knows the ins of the large and successful biopharma.

Due to his uniquely diverse background as a physician, executive and a molecular biology research scientist with over 100 original research publications, Dr. Traber has the differentiated wisdom to gauge whether a molecule can succeed in both clinical trials as well as in the market. After all, a doctor knows which medicine will be likely prescribed. Burdening with a total of roughly $1B to be invested in a developing drug, it is comforting for investors that Dr. Traber is the cream of the crops expert. The chief is highly likely to deliver the best capital appreciation for shareholders and hopes for countless patients worldwide.

Potential Risks

As alluded, it takes significant funding to innovate a molecule from bench research to marketing. The chance of success is less than 5%, as more than 95% of the drugs in development failed to make it to the market. Therefore, it is imperative for investors to be cognizant that investing in a developmental stage biopharma incurs substantial risks as well as upsides. During this lengthy process, any negative data or indication of negativity can cause significant stock depreciation. An unfavorable trial outcome can nose dive share price by more than 50%. Conversely, positive data could throttle share price in the North by leaps and bounds. Substantial risks, volatility, and rewards are inherent to biotech investing. And while some investors lost money in biopharma investing, shareholders of Exelixis (NASDAQ:EXEL) and Jazz Pharmaceuticals (NASDAQ:JAZZ) have enjoyed over 10-bagger and 100-bagger returns, respectively.

To minimize the risks and to maximize the rewards, investors should exercise a basket approach to biopharma investing. A good strategy is to invest in a group of firms with promising drugs-in-development, leading by expert management with a strong track record, and having adequate cash to run their drugs through the complete innovation process. Of note, investors only need a few successful firms like Exelixis and Jazz to compound outstanding returns for a small portfolio in the run.

Conclusion

After the mini recession in the biopharmaceutical industry in late 2015 through 2016, there is a sense of warranted optimism in the market. Of many bio firms enjoying the late 2016 to 2017 rebound, Galectin has promising data and deserves the consideration of serious biotech investors. This small capitalization firm has a unique lead therapeutic that leverages on the biology of galectin to potentially treat the orphan disease, namely NASH. Moreover, the data favors its application to other conditions, particularly psoriasis, due to the drug's promising efficacy and safety profile. Despite that it is highly difficult to gauge the success of an early stage drug, the positive data for psoriasis can mean favorable outcome for the NASH trials. Furthermore, it only takes a single blockbuster, a drug that sells more than one billion dollars annually, to turn a small capitalization firm into a powerful growth biopharma. All in all, our analytical research reveals highly asymmetric risks to rewards that can deliver multiple folds capital appreciation for investors in the long run and hopes for patients worldwide.

Disclosure: I am/we are long GALT.

I wrote this article myself, and it expresses my own opinions. I am not receiving compensation for it (other than from Seeking Alpha). I have no business relationship with any company whose stock is mentioned in this article.

Editor's Note: This article covers one or more stocks trading at less than $1 per share and/or with less than a $100 million market cap. Please be aware of the risks associated with these stocks.

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Galectin Therapeutics: Serendipity In Psoriasis, Strength In NASH ... - Seeking Alpha

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Researchers reveal potential target for the treatment of skin … – Medical Xpress

Posted: at 10:23 pm

May 22, 2017 TWEAK regulates inflammation in atopic dermatitis and psoriasis. Left: Normal skin. Middle: Skin inflammation in atopic dermatitis. Right: Blocking TWEAK reduces skin inflammation in atopic dermatitis. Credit: Courtesy of Dr. Daniel Sidler, La Jolla Institute for Allergy and Immunology

Superficially, psoriasis and atopic dermatitis may appear similar but their commonalities are only skin deep. Atopic dermatitis, also known as eczema, is primarily driven by an allergic reaction, while psoriasis is considered an autoimmune disease. Nevertheless, researchers at La Jolla Institute for Allergy and Immunology were able to pinpoint a common driver of skin inflammation in both diseases.

Their findings, published in the May 22, 2017 issue of Nature Communications, showed that TWEAK, a protein related to tumor necrosis factor (TNF), plays a major role in inducing pro-inflammatory signaling molecules that recruit immune cells to the skin. TNF is already a drug target in psoriasis.

"Atopic dermatitis and psoriasis are two distinct diseases that are induced by alternate immune responses and the factors involved are quite different," explains Michael Croft, Ph.D., professor and head in the Division of Immune Regulation, who led the research. "Showing that TWEAK is a critical mediator in both conditions, makes it a potential therapeutic target for the treatment of inflammatory skin diseases in general."

Over 30 million Americans have some form of atopic dermatitis, which typically develops during childhood but can occur at any age. Most people outgrow the itchy condition but some will continue to suffer from eczema in adulthood.

It is believed to result from a combination of genetics and environmental factors such as irritants and allergens that drive T lymphocytes to produce factors that cause abnormal changes in keratinocytes, the predominant cell type in the outermost layer of skin, as well as changes in other cells in the underlying dermis.

In psoriasis, T lymphocytes also drive an alteration in healthy keratinocytes, accelerating their life cycle. As a result, new keratinocytes move to the outer layer of skin faster than old skin cells can be sloughed off. The build-up of extra cells forms patches of red, itchy skin that are covered with silvery scales and can range from a few spots to major flare-ups that cover large swathes of skin.

"Atopic dermatitis and psoriasis are very common diseases and can have debilitating affects on people's daily lives," says the study's first author Daniel Sidler, M.D., Ph.D, formerly a postdoctoral researcher in the Croft lab and now a Primary Investigator at the University of Bern in Switzerland. "Understanding the molecular basis of these diseases is crucial before we can seek new treatments for these and other inflammatory skin diseases."

In their current study, Croft and his team, in collaboration with researchers at the biotechnology company Biogen, focused on TWEAK and its receptor, Fn14, which had previously been shown to participate in several inflammatory conditions such as inflammatory bowel disease, arthritis and lupus-like kidney disease. "TWEAK and its signaling receptor, Fn14, have emerged as a fundamental molecular pathway regulating tissue responses after acute tissue injury and in many different contexts of chronic injury and disease" said Linda Burkly, Ph.D., Senior Distinguished Investigator, VP, Biogen, Inc., and co-senior author on the current study.

When Sidler measured TWEAK signaling in skin, he found that the expression of both the receptor and ligand was upregulated in atopic dermatitis and psoriasis.

Keratinocytes and dermal fibroblasts, which form the connective tissue in skin, responded to increased TWEAK activity by producing a number of chemoattractive and pro-inflammatory factors commonly found in atopic dermatitis and psoriasis. It also amplified disease-specific cytokines, namely IL-13 and IL-17, further explaining why it can contribute to two fundamentally different diseases.

"TWEAK alone doesn't cause atopic dermatitis or psoriasis but it triggers the production of chemokines that recruit pathogenic inflammatory cells to the skin regardless of the condition," says Sidler. "Blocking TWEAK activity, alone or in combination with other treatments, may sufficiently control skin inflammation to clear up the debilitating symptoms and restore quality of life in severe cases of those diseases."

Explore further: Vitamin D levels not linked to asthma or dermatitis

More information: Daniel Sidler, Ping Wu, Rana Herro, Meike Claus, Dennis Wolf, Yuko Kawakami, Toshiaki Kawakami, Linda Burkly, and Michael Croft. "TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis", 2017. Nature Communications (2017). DOI: 10.1038/NCOMMS15395

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(HealthDay)Children aged 4 to 9 years with atopic dermatitis and with frequent use of emollients have increased urinary levels of low-molecular weight (LMW) phthalate metabolites and parabens, according to a study published ...

Scientists at Charit Universittsmedizin Berlin have discovered why patients with psoriasis are less susceptible to viral infections than patients suffering from atopic dermatitis (atopic eczema). The reason for this ...

Tohoku University Graduate School of Medicine and Tohoku Medical Megabank Organization (ToMMo) are pleased to announce the published results of a study into why air pollutants cause some people to be more susceptible to atopic ...

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Will this gene-editing tool cure the diseases of the future? – Sacramento Bee

Posted: at 10:23 pm

Sacramento Bee

Will this gene-editing tool cure the diseases of the future?
Sacramento Bee
We delete the gene, and we investigate what changes in behavior or physiology are the result of the deletion of that gene, Wood said. The results are being compared against human medical records, and this will find potential new models and sources ...

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Will this gene-editing tool cure the diseases of the future? - Sacramento Bee

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Category Archives: Transhuman News

Homo naledi genome: Will we ever find this elusive key to human evolution? – The Guardian

Discovery of an alga’s ‘dictionary of genes’ could lead to advances in biofuels, medicine – UCLA Newsroom

How about 2 million? DNAnexus joins AstraZeneca’s new genomics initiative – MedCity News

Got Eczema? Here’s Why You Might Want to Try an Elimination Diet – Health.com

My Eczema Makes Shopping Hell – Racked

Everything you need to know about eczema – DestinyConnect

Psoriasis treatment update: Woman discovers miracle cure in THIS natural cream product – Express.co.uk

Galectin Therapeutics: Serendipity In Psoriasis, Strength In NASH … – Seeking Alpha

Researchers reveal potential target for the treatment of skin … – Medical Xpress

Will this gene-editing tool cure the diseases of the future? – Sacramento Bee

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