Tag Archives: environment

Genetics

Building ‘better’ astronauts through genetic engineering could be key to colonizing other planets – Genetic Literacy Project

Space exploration has long been a source of fascination. Since the stars first captured our attention, we have obsessed over that vast curtain of darkness that lies beyond our atmosphere. But to what end? What ultimate goal does mankind strive towards, if not the ability to visit and colonize other worlds?

Before we can take our first steps out into the universe, we have to answer a critical question: Do we have the ability to adapt to other environments very different from what we have on Earth to not only survive, but to thrive? Instead of focusing on how we might terraform other planets to suit us, perhaps we should consider how we might use genetic engineering to alter own bodies to suit those other planets.

As a jumping off point, lets consider the feasibility of using the popular gene-editing tool CRISPR to alter human physiology to tolerate parameters outside of Earths norms. If we take a look at common factors that are significant to human health, gleaned from our experience with space exploration, the most obvious choices for our attention are variations in gravity, atmospheric pressure and gas ratios, and solar radiation levels.

If we consider Mars as our template, because of its relative suitability for colonization, then we must compensate for two-thirds less gravity than Earth. A lack of gravity results in a number of ill effects on human health, including a decrease in bone mass and density over time, particularly in the large bones of the lower extremities, as well as the spine. While we do not have research showing the impact of living on a planet with one-third Earths gravity, we do know that we can expect losses in bone density somewhere under 1-2 percent per month, the amount lost in the microgravity environment of space.

For comparison, the elderly lose 1-1.5 percent per month in Earth gravity. Atmospheric pressure that is either too high or too low also results in complications; low atmospheric pressure results in less oxygen available and causes altitude sickness and possible death. Radiation levels from the sun are another variable that is well known to have upper and lower thresholds for optimal human health, where low levels can lead to vitamin D deficiency and high levels increase cell death and cancer.

It would stand to reason that the human body has a minimum threshold for healthy physiology as regards the environment in which it grows, develops and lives. To colonize other planets successfully, we must consider solutions to overcome these thresholds; for example: prostheses, domed colonies recreating an ideal or near ideal environment, or, as this author suggests, the permanent genetic alteration of humanity as a species. This applies to our four chosen variables of gravitational forces, atmospheric pressure, atmospheric gas ratios, and solar radiation levels. While science fiction might have us consider surgical and biomedical prostheses or the more far-fetched use of animal DNA to change ourselves for this purpose, the key to human adaptation for other planets lies in our own genetics and it may well be CRISPR, the use of the enzyme Cas9 for introduction of altered DNA sequences or CRISPRs to existing cells to change how those cells function, that will make this possible.

Human genetic variation provides a veritable treasure trove of adaptations if one looks at the less common but heritable variations that on Earth may seem irrelevant, nonessential, or even maladaptive, but on another planet could be essential to survival. One example of a gene that, with engineering, could help humanity adapt to higher or lower gravity is the LRP5 gene. Recent research into the LRP5 gene shows that mutations of the gene are responsible for both low bone density and elevated bone density in the case of the later, from increased bone formation. A family of individuals in Nebraska carrying the mutation for elevated bone density have never experienced broken bones even well into old age. A whole colony of such individuals or ones engineered to enhance this mutation further could be expected to fare much better during prolonged space travel in zero gravity as well as in the low gravity environment on a planet like Mars.

While an atmospheric pressure and gas makeup very similar to Earths would be required for humans to survive and thrive outside of a spacesuit, Nepals Sherpas, high altitude dwellers in Ethiopia, and the Collas people in the Central Andes , as well as the deep sea divers of Bajau, may provide a solution to living on planets with differences in atmospheric pressure and oxygen availability. The three groups of high-altitude dwellers appear to have separate adaptations for thriving in low oxygen environments. Recent research indicates that there are genetic mutations in each of these groups. Sherpas mutations allow for more efficient use of available oxygen and resistance to ill effects from hypoxia.

Sherpas experience less of an increase in red blood cells than others and therefore avoid the ill-effects caused, such as edema and brain swelling. Sherpas instead have mitochondria in their cells that make more efficient use of the available oxygen, as well as having more efficient anaerobic metabolism in the absence of oxygen. The Collas show genetic differences in genes that control heart morphology, as well as cerebral vascular flow, as a means to withstand an elevated hematocrit in response to high altitude living. The Amhara people living in high altitudes in Ethiopia unlike the Sherpas do have lower oxygen saturation and higher hemoglobin levels compared to lowland dwellers in the region.

Research has yet to determine what adaptation favors the Amhara, but several genes that may play a role have been isolated. Another group, the Bajau of Thailand, may have complementary genetic variations that help them resist hypoxia and survive the high pressures of deep sea diving. Researchers found them to have 50% larger spleens and also a gene, PDE10A, that controls a thyroid hormone thought to affect spleen size. Capitalizing on any of these genetic features would improve our ability to survive with a lower oxygen content atmosphere, perhaps on a newly terraformed Mars or under domes with oxygen rationing.

While we cannot yet determine how comparable an atmosphere we can create on Mars, it stands to reason that achieving an exact replica atmosphere to Earths could be difficult. An atmosphere that lets in less radiation could impede our production of vitamin D, while a thinner atmosphere would admit an excess of radiation. Vitamin D deficiency could perhaps be handled by supplementation, or instead addressed by increasing our cells response to ultraviolet light to increase vitamin D synthesis. On the other side of the coin, a thinner atmosphere opens us up to higher UVR, which would result in higher rates of skin cancer.

It would stand to reason that, while skin pigmentation has high cultural and historical significance, it could make our species more suitable for colonization of high radiation planets; darker skin with larger melanocytes that react proactively to UVA and UVB radiation through tanning and higher antioxidant and free-radical counteraction would be protective and provide an advantage if we are to branch out into our solar system and beyond. At the same time, this solution poses the problem of vitamin D production.

The answer could lie in isolating and using the genes responsible for East Asian populations lower skin pigmentation coupled with lower skin cancer rates than European populations. A study headed by Pennsylvania university has isolated gene mutations responsible for skin pigmentation differences, SLC24A5, MFSD12, OCA2, and HERC2, by studying African, South Asian Indian, and Australo-Melanesian populations, some of which are associated with vitiligo and a form of albinism common in African populations. These mutations that confer higher vitamin D production to Europeans are not present in East Asians, indicating a different mutation responsible, and, while both populations have higher vitamin D production than African populations, Europeans have a 10-20 percent higher rate of cancer than both Africans and East Asians. Further research into these genes could provide targets for CRISPR to modify the protective factors in our skin without sacrificing vitamin D production of potential colonists.

The question remains: is CRISPR a feasible route to including some of these adaptations to create a new, more suitable colonist? To answer this question we look at the current status of CRISPR research.

While some experiments using CRISPR gene editing were conducted in the technologys infancy, including the controversial creation of twin girls in China designed to be resistant to HIV, we are still quite a bit of research away from using CRISPR with high success rates and full confidence, especially considering the repercussions of rushing into human trials, including the death of trial participants and long-term side-effects of cancer, both of which have occurred in gene-therapy trials.

According to information revealed by the FDA and NIH, 691 trial volunteers died in gene-editing trials prior to the tragic and high-profile death of Jesse Gelsinger in a 1999 trial to treat his OTCD, a rare metabolic disorder. The death was blamed on ethical oversights and a rush to make gene editing pan out before it was ready. The result was a long period of gene-editing fear and oversight but also, in the case of James Wilson, director of the University of Pennsylvanias Institute for Human Gene Therapy responsible for the trials that led to Gelsingers death, greater caution in research methodology. He has put safety at the forefront of his research and asserts that even still the risks of gene editing with CRISPR and other methods brings enough risk to justify human trials only for those diseases that are severe and debilitating enough for patients to accept the risks of gene editing.

What does all this mean for our hypothetical future of using CRISPR to edit the DNA of human colonists for space colonization? Is the technology too far off to serve our purpose or fraught with too much risk? Is it beyond our knowledge and skill to accomplish? The answer to each of these questions is undoubtedly, no.

Weve had too much success in treating complex genetic conditions, like the creation of an immune system for Ashanthi Desilva born with severe combined immunodeficiency (SCVID). Weve unlocked too many keys to making gene therapy safer and more effective to discount the possibility of future use for the advancement of our species into harsher environments. While subsequent uses of gene therapy for SCVID resulted in development of Leukemia years later, further advancements in the research have revealed the need to find the best delivery system for each body system. Adeno-associated viruses, and lentiviruses are being looked at in place of the more aggressive adenovirus or retroviruses for delivery of DNA segments both of which are less likely to provoke an immune response and less likely to trigger cell death by way of the B35 gene in healthy cells, and later cancer.

Regardless of the work ahead and the bumpy road that gene therapy has traveled, vast potential remains at our fingertips whether it is through use of CRISPR or future gene therapy tools. It is a sure eventuality that we will one day have these skills at the ready to spread our species into other worlds, well-equipped to survive and thrive in harsher environments.

Cherrie Newman is a writer and student of human reproduction and biological sciences. She is the author of a science fiction novel series entitled Progeny under the pseudonym CL Fors. Follow her on her blogor on Twitter @clfors

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Building 'better' astronauts through genetic engineering could be key to colonizing other planets - Genetic Literacy Project

Human Behavior

The revenge of nature? – UCAN

The new coronavirus threatens the health of millions of people around the world if it spreads uncontrollably. Every precaution must be taken to prevent its spread and that means practicing greater personal and public hygiene and avoiding contact with people traveling from an infected area. We must show concern and never discriminate against anyone. Besides strict containment, strict personal hygiene, the washing of hands and clean surroundings can hold its spread. Public health officials must be prepared for an outbreak. The flu-like disease does not have a high fatality rate: only two people in every hundred die from it. People can get very sick with severe respiratory problems and yet recover. Others can have the virus but have no symptoms. Everywhere, including the Philippines, doctors and medical personnel have been briefed and advised on the potential health problem and we are reminded that prevention is better than cure. So, there is no need to panic or raise alarm, but intelligent planning, preparation and prevention are what is needed. Besides, most people are recovering from it with good medical care. The big hope is that the virus cannot survive in high temperatures, so bring on a hot summer everywhere, and with global warming we can expect that. The highest temperatures ever recorded in Australia and parts of Europe in 2019 are stunning. That is because of man-made climate change. That might kill off this deadly virus and tropical countries like the Philippines might be spared. The good news is the World Health Organization has announced that the virus may have reached its peak in China as fewer daily infections have been recorded. The coronavirus is also the result of ill-advised and illegal human behavior. We have seen the outbreak of many deadly diseases and viruses in recent decades. More viruses that are affecting humans are crossing over from other mammals and birds. Remember the avian flu? The human immunodeficiency virus is said to have crossed over from monkeys when people ate them as bush meat. Likewise, Ebola likely came from eating monkeys, they say. Then, we had the severe acute respiratory syndrome (SARS), said to have originated from bats, and today the 2019 coronavirus that possibly came from bats, too, although it is not yet proven. You might say these diseases are the revenge of nature. The natural world is striking back at the disastrous human exploitation of the rainforests, the oceans and all wildlife by driving them to extinction. There is destruction in almost every habitat in the developing world and in some parts of the developed world, too. Illegal trade and trafficking in many endangered animal species for huge profit could be the cause of coronavirus. China is a big market for endangered animals and thousands of animals are butchered each year, mostly in Africa, to provide elephant ivory for the China ornament trade, now banned but still thriving. In 2009, there was as many as 109,000 elephants in Tanzania but due to poaching and slaughter, there were only 43,000 left in 2014, a 60 percent loss according to government reports. There are even less today. In 1970, the number of rhino had decreased to 70,000 and as of today there are only 29,000 left on the planet. They are on the way to extinction like the white rhino by bandits killing them for their valuable horn for Chinese traditional medicine. Scientific research has shown the horn to have no more medicinal value than horses hooves. Hundreds of creatures are killed and collected to supply the demand for Chinese traditional medicine, most of which are ineffective, have no medical benefit and are unnecessary considering the huge advances in Chinese health care. The small ant-eating creature called the pangolin could be responsible for the jump of the 2019 coronavirus from animal to human. They are the most widely traded and trafficked creature stolen from the wild in Southeast Asia, India and Africa. They are now practically extinct in China because they killed them for food and their scales are used in traditional Chinese medicine. They have been found in the wild food market of Wuhan where the coronavirus first made the crossover leap from animal to humans. According to an investigative report by The Guardian, one shop was found to have for sale live animals such as "live wolf pups, golden cicadas, scorpions, bamboo rats, squirrels, foxes, civets, hedgehogs (probably porcupines), salamanders, turtles and crocodiles." All destined for the cooking pot, it seems. Bats are known carriers of many viruses and the forest dwelling pangolin could have picked up the virus from bats droppings on the forest floor, some speculate. This is a likely cross over for the virus. Or some human ate the bats. They are on sale in wildlife markets. Corrupt governments like that in Brazil allow traders and loggers to attack the last of the rai forests and destroy their natural beauty by cutting trees, driving out and killing their indigenous people and trafficking their wildlife. We can expect more health problems in the future. Nature will rebel just like the mighty storms and heatwaves caused by man-made climate change are coming back to hit us. Why cant we respect nature, preserve the forest, protect the environment and its wildlife? The answer is easy. It is because of human greed. It is an insatiable, unquenchable drive beyond control. To stop the greed and trafficking of wildlife and the crossover of animal-borne viruses to humans, the authorities worldwide must go after the traffickers and traders of wildlife. They must identify their bank accounts and confiscate their property, assets and money and jail the big-time traders. It is essential to ban all sale and trading in wildlife. Father Shay Cullen is an Irish missionary priest and founder of the Preda Foundation in the Philippines. He is a member of the Missionary Society of St. Columban. The views expressed in this article are those of the author and do not necessarily reflect the official editorial position of UCA News.

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The revenge of nature? - UCAN

Anatomy

Anatomy of a perfect cottage tips and trends from Parry Sound experts – parrysound.com

(Photos courtesy Schlager Inc.)

Peter Olyschlager, Schlager Inc.

Landscaping and hardscaping projects is a great way to enhance enjoyment of a property and increase its value. Flagstone patios and fire pits are really popular. They add to the outdoor living space of the cottage and are a nice area for family to get together and socialize. Its like creating an outdoor living room, but better! It also greatly adds the retail value of the cottage.

Granite is the product of choice with landscaping because it completely matches the natural environment. However, we often find limestone is a great option as well and can blend in naturally, depending on the style of cottage being built. Also, many man-made products have come a long way to complement the natural surroundings of cottage country.

Reputable contractors have the environment in mind. Using plants that are native to our area is important because it creates less waste by helping reduce water costs because they naturally adapt. They are better for our native wildlife species such as bees, butterflies and birds. Its important to use vegetation when possible to control run-off into the lakes; rather than clear-cut a property, maintain vegetation in place to filters pollutants. Also during construction, all measures must be taken to control run off into lakes and streams by using things such as silt curtains, and try to disturb as small of area as possible.

People often have to do costly and time-consuming backtracking when they hit roadblocks along the way because they did not first consult with all of the right contractors and municipalities before they begin their project. It is good to do thorough research before you begin, to know what permits you need and what bylaws exist, so you do not have to stop the work while waiting for these things to be sorted out. Hiring the right contractor is important and getting lots of information from them will help you keep things on track. Not to say there is never hiccups along the way, but you can plan and prepare to try and avoid them.

(Photos courtesy The Deck Store)

Stan Weiland, president, The Deck Store

Some of the deciding factors when it comes to selecting a decking material include budget, usage, exposure, environment, aesthetics, and personal preference. If a client wants a decking material that will last a long time and requires very little maintenance, a composite or PVC decking board would be the right choice. PVC decking performs great in pretty much all environments due to the fact there are no organic ingredients in the boards. Make sure the installer knows how to work with the plastic materials and understands how to fasten them to eliminate expansion and contraction issues.

For lower budgets, pressure-treated wood or cedar lumber are viable options but they tend to require more maintenance to keep them looking good. Also, the life span of a wood deck in some environments is only 10 years because the quality of the wood used for decking today is not up to the same standards as what was used 15-25 years ago; due to the high demand, younger trees are being harvested and the integrity of the material is not what it needs to be to last for any substantial amount of time. As well, it takes a lot of work to keep a wood deck looking nice I dont know too many people who enjoy spending their cottage time sanding and staining their wood decks.

Coming up with the right design is a process that involves getting to know the client and how they plan to use their outdoor space. We like to gather information using questions such as: How do you plan to use your deck (for dining, lounging, entertaining, access to the yard, sunbathing, evening cocktails, etc.)? How many people on average will be on the deck? Do you require privacy from any direction? Does it get hot on your deck and is shade needed? Are there any special features that you would like to see, such as borders, inlays, lights? Do you have a view that you would like to maintain?

(Photos courtesy Black Rock Landscaping)

Larry Martin, owner, Black Rock Landscaping

Trends are always evolving with gardening. Cottage country gardening is no different. Low maintenance gardens, which are practical for people who dont want to spend weekends gardening, are coming back in style right now. Also gaining in popularity again is the inclusion of some grass lawn areas for childrens activities. And combination gardens a healthy mixture of hardy perennials and shrubs are always a hit with people because they look great and are easier to maintain than purely flower gardens.

There is a lot of interest lately in preserving shorelines and near-shore areas because of their ecological importance. There are ways to beautify the waterfront and still maintain its natural function. Cleaning shorelines of dead limbs, debris and unwanted weeds provides a tidier appearance. Plant selectively with desired plants to give some colour to shoreline indigenous plants are best but do so with an eye towards maintaining natural appearance. Some common plants that can be used are iris, cotoneaster, daylilies, stephanandra, and hosta (if deer arent a problem) to name a few.

A lot of cottagers are adding raised beds into their designs because they offer a number of advantages. They are easier to maintain, offer a better planting base where soil is poor, accent an area that is plan and flat, and offer the opportunity raise and stack plants to different levels to show off different species.

People want to put planters on their docks to offer lake appeal, but there are valid concerns about chemicals entering the water from them. You can have flowering pots on your dock while still being environmentally friendly simply by using drip trays, which work well to collect excess water and fertilizer and also help to prevent deck stains.

(Photo courtesy Canadian Contracting Services)

Rick Zanussi, owner, Canadian Contracting Services

When it comes to a build, dont overlook the basement, where the use of ICF (insulated concrete form) is becoming the standard. This type of basement foundation provides many advantages. It gives incredible structure and an easily achieved level, plumb and square foundation. As important, a good quality ICF provides an incredible insulation value of R30. ICF foundations are certainly more expensive than a standard, uninsulated block foundation but the extra cost is well worth it. A solid, level and square foundation is the key building block to a quality build.

Electrical planning is paramount for providing all electrical needs a customer wants. Property owners should take the time to go through the entire build with the electrical subcontractor and builder, on site. Think about the layout of the Great Room, kitchen and bedrooms with respect to where you will or may need receptacles. The best rule of thumb is to install more receptacles than less.

Exterior windows and doors should never be skimped on. We encourage our customers to spend more to achieve more in R-value, weather resistance and longevity of windows and doors. Youll spend far more time gazing out windows at the cottage than at your permanent home you want to enjoy the cottage viewsso a good rule of thumb is to err towards larger windows rather than smaller.

In order to reduce stress and building-process issues, property owners need to spend the time to find the right builder. Never go with the cheapest builder you can find. A quality finished product is never achieved by being the least expensive. Your cottage must be built properly, meeting all structural, system, landscaping and aesthetic requirements. These are never accomplished unless you spend the money required to achieve them.

Owners need to research builders thoroughly. This takes time and effort, but is imperative to limit problems during the build. Take the time to find a builder with a very good reputation. Ask for contact information of previous customers and speak with them openly to determine their experience with the contractor. Ask builders how long their employees have been with them. These tradesmen are paramount for a quality build as they are the people who do the actual work and their qualifications and experience must be extensive.

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Anatomy of a perfect cottage tips and trends from Parry Sound experts - parrysound.com

Human Behavior

Let’s hear it for the skaters | Local – Crow River Media

If you're a fan of big hair, spandex, mullets and leg warmers, you're in for a flash to the past. "Back to the '80s" is the theme of the 40th annual ice show.

Sponsored by the Hutchinson Figure Skating Association and Hutchinson Parks, Recreation and Community Education, shows are 1 p.m. and 7 p.m. Saturday and 2 p.m. Sunday at Burich Arena.

A total of 104 skaters from tots to Freestyle 4 or higher will showcase their skills to popular '80s hits such as "Jesse's Girl," "Let's Hear It For The Boy," "Girls Just Wanna Have Fun" and "Holding Out For a Hero."

The audience is in for a treat when guest skaters Jaden Schwab, 17, and Estelle Schwab, 12, take the ice. They are the children of MiShaun Schmidt, an alumni of the Hutchinson Figure Skating program. The sister-and-brother duo skate with the St. Paul Figure Skating Club. They have competed nationally and internationally. Among their honors is winning the bronze medal in the Novice and Junior Challenge in Salt Lake City, and they also qualified for the 2020 U.S pair final at the novice level and are part of the U.S. Figure Skating 2020 National Developmental Team.

Back by popular demand is the dad/daughter skate. A group of 26 family units are performing to the song "Sweet Child of Mine."

While the skating takes center stage, recognition of milestones is important, too. This is the final skating show for four seniors: Khiana Knuth, Katarina Anderson, Halii Beilke and Anna Farley. Also presented will be the HFSA Most Improved Skater Awards. Allison Schwartz was recognized in 2019 in the Freestyle 1, 2, 3 category and Emma Staples was honored in the Freestyle 4 and Up category.

Joining them is the recipient of the PRCE Most Improved Skater Award, which looks at improved overall skating ability, attitude and good sportsmanship. Elizabeth Becker was the 2019 honoree. Also awarded is the I.C.E. Award, which is presented to a skater who displays integrity, commitment and enthusiasm for the love of skating and the skating program. The 2019 recipient was Emma Schwartz.

Khiana Knuth has been skating since she was 8 years old.

"I wanted to be on the ice," she said. "I liked the idea from watching hockey with my dad."

Knuth has stuck with it for nine years. The reason: It's calming.

"It relieves stress," she said. "It lets me blow off steam."

Knuth encourages others to consider skating as a hobby.

"It can be a laid back activity or you can make it highly competitive, so it's good for a variety of people," she said.

When she's not competing, Knuth enjoys spending time with her sister, Carrie, and cousin, Caydence, at private ice. Looking ahead, Knuth's college plans call for attending North Dakota State University where she plans to study psychology.

"Human behavior interests me," she said.

Knuth admits to having mixed emotions for the coming weekend.

"I'm excited and kind of sad it will be over," she said. "I'll miss having an hour a week where I can do my own thing, blow off steam and refresh."

The Hutchinson High School senior has been skating for 13 years, starting the sport at age 5.

"My mom was a skater and I followed in her footsteps," she said.

Beilke has stuck with it because she likes it and enjoys meeting other skaters.

"It's fun to do and a cool sport," she said.

Her favorite memories revolve around the rink where she has had fun making up moves with her friends. What she'll miss most: The shows.

"I'm sad about the last ice show," she said.

After graduation, Beilke will head to Marshall to attend Southwest Minnesota State University. She plans to study early childhood education with the goal of teaching first grade.

"The age group is cool," she said.

After this weekend's ice shows, Beilke will have more time for her other favorite activities: hanging out with friends, playing softball and photography.

Farley was introduced to skating as a 3-year-old toddler. It was a good fit because she has been skating for 14 years. She stayed with the sport as a way to make friends.

"I've built some really great friendships over the years skating," she said.

Like Knuth, Farley is feeling sad and excited about this weekend's ice shows.

"I'm going to miss being with my good friends I've known since I was little," she said.

That said, Farley admitted she was ready to move on to her next chapter. After graduating from HHS, she plans to head to the University of Minnesota Twin Cities where she will study architecture.

"I love the design appeal of it, the ability to build someone else's home," she said. "It's cool to design and build."

When she's isn't at the rink, Farley can be found at Iron Jungle Crossfit, running or hanging out with her friends. She's also enrolled at Ridgewater College.

When asked if she would recommend skating to others. Farley was quick to say "yes."

"It's a really good way to be involved in a sport and to make new friendships," she said.

It's not surprising Anderson's sport is ice skating. She is named after another skater, Katarina Witt, the German figure skater who earned two Olympic gold medals. Like Farley, Anderson has been skating since she was 3 years old.

"It's been fun for me," she said. "I feel graceful and angelic on the ice."

Anderson also said skating relieves stress.

"I don't have to worry about anything but to try and get the jump," she said.

Her future plans call for attending the University of Minnesota Duluth where she will study biology with a focus on wildlife or marine biology. She chose this career path because she loves animals and wants to help the environment.

When she isn't working on her skating skills, she can be found practicing karate and volunteering at Hutchinson Health. Anderson also plays trumpet in the high school band.

"I picked it up because it would be easy, but I was wrong," she said. "I participate in every band activity I can. I like jazz. I was in all-state this past week."

Anderson also juggles work for the city of Hutchinson and attending Ridgewater College as a PSEO student.

"I'm going to miss the every-day routine of rehearsal and hanging out with my friends," she said.

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Let's hear it for the skaters | Local - Crow River Media

Embryology

Shady Grove Fertility’s (SGF) Fairfax, VA IVF Center Reaches 1500 IVF and Egg Freezing Cycles in its First Full Year Open, Shares How SGF Labs Help…

Shady Grove Fertility Fairfax, VA IVF Center

FAIRFAX, Va. (PRWEB) February 26, 2020

SGF is the largest fertility center in Virginia, and has been serving Northern Virginia with highly specialized and personalized fertility care for over two decades. With seven locations in Northern Virginia, the addition of our newest physician, Nicole Doyle, M.D., brings our state total to 13 reproductive endocrinologists and 1 reproductive urologist. SGF Fairfaxs lab director recently shared just a few of the ways their lab is helping more people conceive.

SGFs embryologists have always undergone a rigorous and comprehensive training program, and at SGFs IVF Center in Fairfax, thats no exception. The SGF program takes 4 to 5 years to complete and requires trainees to progress through a robust series of mentorships, on-the-job training, and scaffolded exposure to different procedures. Our embryologists learn procedures in isolation, and practice them over and over and over again, often taking months to master each one before receiving the necessary clearance to perform the procedure unassisted, shared Jim Graham, MS, Laboratories Director.

SGF, a national network of IVF centers, completed over 15,000 IVF cycles in 2017, according to the Society for Assisted Reproductive Technologys (SART) latest preliminary data available.

The SGF Fairfax IVF Center is home to the ninth lab operated by SGF, joining the largest freestanding IVF laboratory in the United States in Rockville, Maryland as well as Towson, MD; Chesterbrook, PA; Manhattan, NY; Richmond, VA; Atlanta, GA; Tampa, FL; and Santiago, Chile.

The Fairfax office laboratory is accredited by the Joint Commission and operates under the leadership of nationally and internationally known Jim Graham, laboratories director and Michael J. Tucker, BSc, Ph.D., FIBiol, HCLD, director of Shady Grove Fertilitys IVF and embryology laboratories.

While our Fairfax lab is no different in following our already stringent training requirements, having increased space allows us to do even more training. Now, we have double the amount of equipment with which we can train new embryologists more effectively, and we can offer more frequent exposure to a variety of procedures, added Graham.

SGF is known for cultivating a culture of continuous innovation. We have always been dedicated to advancing our technical capacity and knowledge within the area of reproductive science. We dont wait for others in our field to figure out the latest techniques; we actively engage in research ourselves, shared Eric Levens, M.D., board certified reproductive endocrinologist and Medical Director of the Fairfax lab.

Within the Fairfax lab, SGF continually investigates new IVF techniques. If I had to summarize how determined we are to improving embryo cultures, Ive always said, even if our efforts result in one more pregnancy out of 1,000, our time was well spent, as we know that one more pregnancy means another family goes home happy as a result of our combined efforts, added Graham.

Like all SGF labs, the Fairfax IVF Center follows a system of both active and passive patient identification whereby team embryologists verify identities and maintain a one-patient-per-hood rule. This robust chain of custody procedure, which remains the gold-standard in reproductive medicine, has made it possible for SGF to increase its lab capacity and size without compromising the quality of patient care.

Another not so well known advantage that SGFs labs offer is isolated incubator spaces for embryos. The longer we can leave embryos undisturbed to develop, the more likely they are to become high-quality, viable embryos, added Graham. Thanks to a substantially increased number of isolated incubator spaces in the Fairfax lab, we can better leave cultures undisturbed.

The use of isolated chambers at SGF represents a major improvement in the IVF process. In many other labs around the nation, spaces are shared by multiple patientsmeaning the environment for one patients developing embryos would impact another each time an embryologist needs to access the embryos of another patient using the same space.

Because we can keep embryos in a more controlled, consistent environment, we can ensure optimal pregnancy rates for our patients, Graham adds.

Assisted reproductive technology continues to develop daily. Each year, new advancements in techniques, new tools to enhance success, and new procedures and protocols become available. SGF continues to not only develop our services, but also our science so that we can continue to deliver on our promise and provide patients the best possible support, adds Levens.

The SGF Fairfax IVF Center offers patients access to highly specialized, comprehensive fertility care, including fertility and ovarian reserve testing and diagnosis; semen analysis; hysterosalpingogram (HSG); low-tech fertility options; in vitro fertilization (IVF); donor egg, sperm, and embryo; genetic screening and testing; gestational carrier; egg freezing; fertility preservation for patients with cancer; and LGBTQ family building. To schedule an appointment with an SGF physician, please call the SGF New Patient Center at 1-888-761-1967 or submit this brief online form.

About Shady Grove Fertility (SGF)SGF is a leading fertility and IVF center of excellence with more than 85,000 babies born and counting. With 38 locations throughout FL, GA, MD, NY, PA, VA, D.C., and Santiago, Chile, we offer patients individualized care, accept most insurance plans, and make treatment affordable through innovative financial options, including treatment guarantees. More physicians refer their patients to SGF than any other center. Call 1-888-761-1967 or visit ShadyGroveFertility.com.

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Shady Grove Fertility's (SGF) Fairfax, VA IVF Center Reaches 1500 IVF and Egg Freezing Cycles in its First Full Year Open, Shares How SGF Labs Help...

Cell Biology

Here’s the Pro-Bernie Climate Scientist Op-Ed the Washington Post Wouldn’t Run – Gizmodo

On Sunday, the Washington Post published an opinion piece by Fred Hiatt, the opinion pages editor, entitled How Donald Trump and Bernie Sanders Both Reject the Reality of Climate Change. This false equivalence is, to put it bluntly, absolutely one of the most idiotic things I have ever seen.

Hiatts piece inexplicably attacks the climate plan Senator Bernie Sanders would implement as president (heres our analysis). While there are valid things to quibble with, Hiatt does a lot of hand waving bUt HoW wOuLd We PaY fOr It stuff and hand wringing over the idea that fossil fuel companies and the executives who run them should be prosecuted. He then turns to extensively quoting and paraphrase Patrick Pouyann, the chairman and CEO of Total, a [checks notes] large Paris-based oil giant currently being sued in France.

The whole post reads like an advertorial for Total (sample quote: Pouyann himself did not seem particularly hateful; on the contrary) and a carbon tax plan supported by the Climate Leadership Council, a group supported by Big Oil, including Total.

Both sidesing Trump and Sanders and credulously burbling out Big Oil talking points would be bad enough. But a group of scientists with the Sunrise Movement tweeted that the Post opinion section had previously rejected an op-ed they submitted defending Sanders climate plan and how seriously it takes the science. It was written in response to Joe Biden dismissing Sanders plan late last month, much as Hiatt did in his Sunday piece.

Earther reached out to Sunrise Scientists, and they shared their piece with us. Emails reviewed by Earther also confirm that a Washington Post editor explicitly declined to run the op-ed. Read the scientists article in full below, along with a list of authors who helped draft it.

Note: The letter is signed by the individual scientists and does not reflect the view of the institutions with which they are affiliated.

Joe Biden says Bernie Sanders Green New Deal is impossible.

We refuse that narrative. We are scientists here to refute Bidens claim that not a single, solitary scientist thinks that [Sanders Green New Deal would] work. Not only do we believe that it is possible for the U.S. to decarbonize electricity and transportation by 2030, we know that such a goal is imperative.

The Intergovernmental Panel on Climate Change, the worlds primary scientific authority on climate change, has been describing the immense harm that climate change will bring to the world and its peoples for decades. In 2018, it issued a report focused on the likely impacts of allowing global warming of 1.5. degrees Celsius (2.7 degrees Fahrenheit) above pre-industrial warming, concluding in its famously measured phrasing that the global impacts of such warming are going to be bad. One example: Any increase in global warming is projected to affect human health, with primarily negative consequences (high confidence). Nonetheless, limiting warming to 1.5 degrees Celsius can protect people and our planet from the most extreme anticipated consequences of climate change.

The planet has already warmed 0.8-1.2 degrees Celsius (1.4-2.2 degrees Fahrenheit), with an estimated future warming trajectory of 0.1-0.3 degrees Celsius (0.2-0.6 degrees Fahrenheit) per decade. Global mean sea level has already risen 89 inches (2124 centimeters) since 1880 and is expected to rise by another 10-30 inches (26 to 77 centimeters) by 2100 under a 1.5 degrees constraint, or more if we go past that. We are running out of time.

We know we must act. Constraining climate change in a way that is most protective of our planet, our families, and our homes requires cutting greenhouse gas emissions rapidly and permanently. We believe that Bernie Sanders Green New Deal proposal lays out a course of action that is matched to the scale of the challenge. It is possible. But we must commit wholeheartedly.

Sanders Green New Deal is informed by science, linking its targets and timelines to what the science tells us is critical for staving off the most devastating impacts of climate change. Just as importantly, it understands the challenge for what it is: A need to transform our economy to support a more sustainable, healthier future.

Accordingly, it addresses decarbonization systemically, focusing on where money needs to be spent, where social programs need to be implemented, and where people need support to do great things. The plan funds new, clean energy, leveraging successful New Deal models of public financing and control of power generation, and fully funds a just, five-year transition for workers in the fossil fuel industry.

The plan recognizes climate change as an emergency. It would make the U.S. a global leader on climate action, while ensuring funding for a just transition and industrialization of the developing world. And perhaps most importantly, the plan reflects that it is the American people who will make this happen. Thats why Sanders Green New Deal focuses on jobs, justice, and public ownership of the energy systems that we create and will be bolstered by other policy commitments like Medicare for All, student loan forgiveness, union empowerment, and other programs that recognize the power and dignity of all.

We know that it is possible to rise to the challenge of the climate crisis. And we know that Sanders Green New Deal is a commitment to people that recognizes that only together can we make this deeply ambitious and critically necessary plan work. As President John F. Kennedy said to Congress at the advent of the Space Race: I believe we possess all the resources and talents necessary. But the facts of the matter are that we have never made the national decisions or marshaled the national resources required for such leadership. We have never specified long-range goals on an urgent time schedule, or managed our resources and our time so as to insure their fulfillment.

It is again time to take urgent, visionary actions that rise to the challenge that we as scientists know is coming. It is time to commit to a Green New Deal.

Dr. Emily Grubert, Ph.D. in Environment and Resources from Stanford University

Dr. Eric Rehm, Senior Research Associate, UMI Takuvik/Arctic Remote Sensing at the Universit Laval

Dr. Dargan Frierson, Associate Professor of Atmospheric Sciences at University of Washington

Dr. Shannon Hateley, Ph.D. in Molecular and Cell Biology from the University of California, Berkeley

Dr. Peter Kalmus, Associate Project Scientist at the UCLA Joint Institute for Regional Earth System Science & Engineering

Matias Kaplan, PhD Candidate in Bioengineering at Stanford University

Isaac Larkin, PhD Candidate in Molecular Biology at Northwestern University

Yan Liu, BSc in Cell and Molecular Biology at San Francisco State University. Co-Founder and CEO, Biocaptivate

David Silverstone, PhD Candidate in Quantum Information Science at Yale University

Dr. Lucky Tran, PhD in Biology from Cambridge University

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Here's the Pro-Bernie Climate Scientist Op-Ed the Washington Post Wouldn't Run - Gizmodo

Cell Biology

Inflammation caused by radiation can promote survival of triple-negative breast cancer cells – News-Medical.net

While radiation is successfully used to treat breast cancer by killing cancer cells, inflammation caused as a side-effect of radiation can have a contrary effect by promoting the survival of triple-negative breast cancer cells, according to research published online in the International Journal of Radiation Biology by Jennifer Sims-Mourtada, Ph.D., director of Translational Breast Cancer Research at ChristianaCare's Helen F. Graham Cancer Center & Research Institute.

Accounting for 15-20% of all breast cancers, triple-negative breast cancer is faster growing than other types of breast cancers.

Dr. Sims-Mourtada's latest study, "Radiation induces an inflammatory response that results in STAT3-dependent changes in cellular plasticity and radioresistance of breast cancer stem-like cells," brings scientists closer to understanding the mechanisms behind this aggressive and hard-to-treat cancer. It shows that inflammation caused by radiation can trigger stem-cell-like characteristics in non-stem breast cancer cells.

"This is the good and the bad of radiation," Dr. Sims-Mourtada said. "We know radiation induced inflammation can help the immune system to kill tumor cells -- that's good -- but also it can protect cancer stem cells in some cases, and that's bad."

She added, "What's exciting about these findings is we're learning more and more that the environment the tumor is in - its microenvironment - is very important. Historically, research has focused on the genetic defects in the tumor cells. We're now also looking at the larger microenvironment and its contribution to cancer."

The term triple-negative breast cancer refers to the fact that the cancer cells don't have estrogen or progesterone receptors and also don't make too much of the protein called HER2. The cells test "negative" on all 3 tests. These cancers tend to be more common in women under age 40, who are African-American, Latina or who have a BRCA1 mutation.

My work focuses on cancer stem cells and their origination. They exist in many cancers, but they're particularly elusive in triple-negative breast cancer. Their abnormal growth capacity and survival mechanisms make them resistant to radiation and chemotherapy and help drive tumor growth."

Jennifer Sims-Mourtada, Ph.D., director of Translational Breast Cancer Research at ChristianaCare's Helen F. Graham Cancer Center & Research Institute

She and her team applied radiation to triple-negative breast cancer stem cells and to non-stem cells. In both cases, they found radiation induced an inflammatory response that activated the Il-6/Stat3 pathway, which plays a significant role in the growth and survival of cancer stem cells in triple-negative breast cancers. They also found that inhibiting STAT3 blocks the creation of cancer stem cells. Still unclear is the role IL-6/STAT3 plays in transforming a non-stem cell to a stem-cell.

For women living in Delaware, Dr. Sims-Mourtada's research is especially urgent: The rates of triple-negative breast cancer in the state are the highest nationwide.

At ChristianaCare, we are advancing cancer research to help people in our community today, while we also advance the fight against cancer nationwide. Dr. Sims-Mourtada's research is a dramatic step toward better treatments for triple-negative breast cancer."

Nicholas J. Petrelli, M.D., Bank of America endowed medical director of the Helen F. Graham Cancer Center & Research Institute

To advance her research on inflammation, last year Dr. Sims-Mourtada received a $659,538 grant from the Lisa Dean Moseley Foundation. The three-year grant will enable her and her team at the Cawley Center for Translational Cancer Research to continue investigating the role of cells immediately around a tumor in spurring the growth of triple-negative breast cancer and a possible therapy for this particularly difficult cancer.

"Our next step is to understand the inflammatory response and how we might inhibit it to keep new cancer stem cells from developing," Dr. Sims-Mourtada said.

Dr. Sims-Mourtada's research team previously identified an anti-inflammatory drug, currently used to treat rheumatoid arthritis, that has the potential to target and inhibit the growth of cancer stem cells and triple-negative breast cancer tumors. That research could set the stage for clinical investigation of the drug, alone or in combination with chemotherapy, to improve outcomes for patients with triple-negative breast cancer.

Source:

Journal reference:

Arnold, K.M., et al. (2020) Radiation induces an inflammatory response that results in STAT3-dependent changes in cellular plasticity and radioresistance of breast cancer stem-like cells. International Journal of Radiation Biology. doi.org/10.1080/09553002.2020.1705423.

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Inflammation caused by radiation can promote survival of triple-negative breast cancer cells - News-Medical.net

Immunology

Basic Immunology | The IBD Immunologist

The immune system, defined in the simplest terms, is the system in our bodies that defends us against infectious disease. However, our immune systems are far more complex. Not only does it defend us against pathogens, it is also responsible for protecting us against cancer, initiating allergy symptoms, and determining the state of our general health.

The Immune system itself is like a miniature world in our bodies, and it is populated with various immune cells that are supported by the cells making up the tissues and organs of the body. Each type of immune cell has its own specialized function. Some are good at fighting infectious bodies hand to hand like soldiers, while others are specialized at scouting, intelligence and recruitingother cell types during battle. During an immune response, the cells of the surrounding tissues also play their roles and, much like civilians in war, they fight, warn others, or die as a result of the battles.

I will do my best to introduce you to this exciting world in simple terms.

To put it quite simply, the Immune System is designed to protect you. Immunologist refer to the body often as self. This includes all the products of the body ranging from your tissues to the smallest secreted molecules. Life forms and molecules that interact with your body are considered non-self. The non-self life forms are parasites, bacteria and viruses as well as friendly intestinal bacteria. Common non-self molecules that we often encounter are food, pollen and chemical substances from our environments (like drugs, cleaning products and hygienic products)1.

Cells of the immune system are born from hematopoietic stem cells found deep in the bone marrow. Hematopoietic stem cells are immortal, capable of generating daughter cells, called progenitors that will later give rise to different type of immune cells. There are two main types of progenitors created, the myeloid progenitors and the lymphoid progenitors2.

Cells of Myeloid Progenitors

For immunologists, the mammalian body is divided into three main regions: the primary lymphoid areas, the secondary lymphoid areas and the periphery.

The primary lymphoid areas include the bone marrow and the thymus. The bone marrow, as we mentioned, is the site of immune cell generation2. The thymus, on the other hand, is the location of T cell development4. Lymphoid progenitor populations travel there from the bone marrow and produce a population of immature thymocytes. It is these thymocytes that give rise to the varied T cell populations.

The secondary lymphoid areas include the adenoids, tonsils, spleen, lymph nodes and lymphoid follicles found in the gastrointestinal system and the mucosa (areas adjacent to a mucus membrane). These areas house lymphocytes and support the development of an adaptive immune responses5-7.

The periphery includes all regions that are not included in the primary and secondary lymphoid areas. This includes areas like the skin, brain, joints, muscles and gastrointestinal/mucosal areas surrounding lymphoid follicles.

In order for an immune response to be initiated, there must be some kind of danger. This is a fairly simple idea, but it leads to the question: How is danger defined by the immune system? This question is actually one of the most exciting topics of immunology today. Simply put, danger is sensed by the immune system through two main avenues: the recognition of a pathogen-associated molecular pattern (PAMP)8 or through the release of cell molecules associated with trauma which are called danger-associated molecular patterns (DAMPs) or alarmins9. Examples of PAMPs would be cell wall lipoproteins of bacteria and an example of DAMPs would be ATP (adenosine triphosphate), a nucleotide used as an energy source in cells10.

PAMPs and DAMPs are recognized by the cells of the immune system and non-immune cells, through receptors located at the cell surface or internally8,9. PAMPs are also recognized by several non-cellular systems as well11,12. This recognition initiates the very first processes of an immune response called the innate immune response.

Immune cells, non-immune cells and non-cellular systems all participate in initiating an innate immune response. Why is it called innate? Its innate because it depends on intrinsic systems that are built into your body to recognize danger and there is no learning or adaptation involved.

In order to detect PAMPs or DAMPs, cells need tools to recognize them. These tools are protein receptors that can be found on the cell surface as well as internally. In general, they are called pattern recognition receptors or PRRs. These receptors come in families consisting of multiple members. Receptors that recognize PAMPs include the Toll-like receptors (TLRs), the C-type lectin receptors (CLRs), the NOD-like receptors (NLRs), RIG-I-like receptors (RLRs)8 and invariant T cell receptors13,14.

DAMP receptors are not so clear-cut. TLRs have been implicated15 as well as the receptor for advanced glycation endproducts (RAGE)15. Also the purinergic receptors that recognize ATP would also fall into this category10.

These receptors are found on most cells of the body. They recognize a variety patterns associated with a number of pathogens including virus-associated nucleic acids; bacterial-associated cell wall components, protein, ribosomal RNA and DNA; and protozoan-associated proteins8. The majority is found extracellularly, but a number are also found intracellularly. When stimulated they activate the transcription factor NFB, which is essential for activating a cells immune functions and set off a signal cascade via MAP kinase (a phosphorylating enzyme)8.

These receptors are specialized in recognizing carbohydrate structures, such as the sugar mannose, which is a common component of fungal cell walls16. Thus, these receptors are found on the cell surface. Though much of the literature involves their expression on immune cells, reports of CLR variants on non-immune cells can also be found17. On the phagocytic cells, it is known that they can participate in endocytosis, the engulfment of particles or pathogens and respiratory burst16. Some also appear to initiate signal cascades similar to TLRs leading to NFB and MAP kinase activation, but it also appears that they can work in concert with TLRs, enhancing or inhibiting their function16.

These receptors are found in the cytoplasm of cells. Traces of their expression is found in most organs of the body18 and it is probably safe to say that most immune cells express at least some members of the NLR family. These receptors are designed to detect intracellular bacteria and, possibly, endogenous stress molecules and allow the cell to produce one of the most potent inflammatory mediators, Interleukin (IL)-119.

Like NLRs, RLRs are also found in the cytoplasm of a cell. Instead of detecting bacterial products, these receptors help detect viral infection20. They do this by binding to RNA produced during viral replication. Working together with nucleic-acid detecting TLRs, they lead to NFB, MAP kinase activation and activation of Interferon regulatory factor (IRF) transcription factors20. The IRF transcription factors are necessary to produce cytokines specialized for the control of viral infections. Cytokines are small, secreted proteins used as messengers between cells, which alert surrounding immune cells about danger.

Areas of the body that come in contact with the outside world (skin, gastrointestinal and mucosal areas) are covered with an epithelial layer. Epithelial layers are composed mainly of cells called epithelial cells. These cells form an anatomical barrier and they have their own immune functions. When exposed to DAMPs or PAMPs, epithelial cells produce inflammatory cytokines 21. The cells of the epithelial layer are often the main cells involved in the first detection of pathogens and/or danger. The majority of cells in the body also have this capacity. Other cell types like muscle cells, adipocytes and fibroblasts are all outfitted with receptors to detect PAMPs and DAMPs8,22. Just like citizens of a city, they will alert the authorities if there are any problems.

Under epithelial layers are resident macrophages, neutrophils, dendritic cells, NK cells, mast cells and a number of T cell-related cells.

The name macrophage is derived from Greek, meaning large eaters. Their main function is to phagocytize (engulf) pathogens and particles. It does this by wrapping its plasma membrane around particles until they are enveloped and pinched off to form an endosome inside the cell. Once inside the cell, the endosome merges with a lysosome that contains enzymes and acids that can digest the contents. Macrophages also have the ability to generate a respiratory burst, which is a release of oxygen radicals that damage surrounding pathogens and cells. They also can alert and attract other immune cells through inflammatory cytokine release23.

Neutrophils are the main foot soldiers of the innate immune response and are certainly the most abundant. They also have a wide arsenal of tools to deal with invaders. Like macrophages, neutrophils can phagocytize particles, release a respiratory burst and produce inflammatory cytokines. Unlike macrophages, neutrophils have the internal caches of anti-microbial substances called granules24.

Dendritic cells are also phagocytic cells, but they have the special ability of initiating an adaptive immune response (will be discussed later). Unlike neutrophils and macrophages, Dendritic cells or DCs are not simple foot soldiers. Instead, they function more as spies and provide intelligence about invaders to T cells through a phenomenon called antigen presentation and through cytokine production25.

The NK stands for Natural Killer and the name implies their function. These cells, however, do not kill pathogens directly. Instead, these cells have the ability to recognize when other cells are harboring internal pathogens using special receptors and then kill them. Situations where this might occur is during viral and mycobacterial infections. These pathogens easily reside in host cells, finding ways to block lysosome fusion and their own destruction26.

Mast cells are the cells that are responsible for the classic signs of inflammation, which include redness, swelling and heat. Though well known for their association with allergy, they also can detect PAMPs and DAMPs through receptors and become immunologically active. Mast cells exert their functions mainly through cytokine and granule release. Unlike neutrophils, which release antimicrobial substances, mast cells release histamine and heparin. Histamine is well known for its vasodilator function and ability to allow fluid to leak between cells, causing redness and swelling. It also causes inflammatory itching by triggering neurons (unmyelinated C-fibers) responsible for the itch feeling. Heparin prevents blood coagulation27.

Most T cells are part of the adaptive immune response as they have adaptive T cell receptors (receptors that learn to recognize pathogens). NK T cells and T cells, however, use invariant T cell receptors (receptors that do not rearrange) or semi-invariant T cell receptors and participate in the innate immune response.

NK T cells are similar to the NK cells mentioned above. Not so much in function, but more in how they look. These cells share many of the same surface protein markers. NK T cells, however, do not kill compromised cells. Instead, they are quick cytokine producers. In doing so, they quickly notify all surrounding cells that there is problem when they recognize PAMPs presented to them via dendritic cells28.

The T cells are important for innate immune reactions and the adaptive immune response as they have invariant and variant T cell receptors. Their precise function remains unclear, but they can secrete cytokines and, like the NK T cells above, participate in alerting and strengthening local immune responses29.

Besides cells, there are also defenses in your body that are ready to react to pathogens as soon as they are encountered, much like booby traps. These systems rely on small proteins that are found within the bodily fluids.

The liver synthesizes the proteins of the complement system and they work in concert to aid in phagocytosis, bacteria lysing and immune cell attraction. One can visualize it as a self-assembling machine that starts to assemble as soon as the first proteins are bound and in place. The complement machine is known to be initiated by three different pathways: the classical pathway, the alternative pathway and the lectin pathway. The classical pathway is triggered when antibodies are bound to a pathogen. The alternative pathway is triggered when the victim is unable to block the cascade (normal cells can, while pathogens cannot). The lectin pathway uses free lectin proteins (lectins are proteins that bind sugars) to bind sugars associated with bacterial cell walls)11.

These proteins are also produced by the liver and especially during inflammation when pro-inflammatory cytokines are produced. Many are designed to coat pathogens and have chemotactic properties (have the ability to attract cells). Some inhibit microbial growth by sequestering iron from the environment. The lectins from the lectin pathway of complement activation are considered acute phase proteins30.

Often called defensins, these peptides function as natural antibiotics and our produced by cells that guard the external surfaces and internal surfaces such as the skin and the gastrointestinal system. In the skin, the main sources are keratinocytes, mast cells, neutrophils, sebocytes and eccine epithelial cells. In the intestines, one of the main producers are the Paneth cells of intestinal crypts31.

The adaptive immune response is what gives individuals long-term immunity to a pathogen after vaccination. Instead of relying on germ-line encoded receptors for the recognition of pathogens like the innate immune system, it depends on the development of receptors that can recognize any unique molecular characteristic of pathogens32. The molecules that can be recognized are called antigens. The classical definition of an antigen is any molecule that can provoke the development of antibodies. A better, and less-confusing, definition is a molecule that can be recognized by the adaptive immune system. The molecules are often protein peptides (small pieces of protein). But, they can also be sugars, lipids and other small molecules under the right circumstances. The main players of the adaptive immune response are the T cells (both T helper cells and cytotoxic T cells) and the B cells.

During the innate immune response, the first steps are taken to initiate an adaptive immune response. The main cells responsible for this step are the DCs that we described earlier25. As we mentioned before, DCs are a phagocytic cell type. This means that they have the ability to engulf pathogens/particles in endosomes and later fuse these vesicles to lysosomes for destruction. The process, however, does not stop here. Instead of just disposing of the pathogen/particle waste, the DC, instead, uses these parts to educate T helper cells about the pathogens. It does this by traveling from the location where it picked up its parcel to the local lymph node, where it finds T helper cells. Once there, it presents the pathogen-associated peptides on its surface using molecules called MHC class II molecules and provides information to T cells about how it should respond using surface molecules called co-stimulatory molecules and cytokines. Educating T helper cells is the first step towards initiating an adaptive immune response.

T helper cells or Th cells are crucial cells in the adaptive immune response and they are characterized by a surface protein called, CD4. They hold the key to initiating the functions of cytotoxic T cells33 and B cells34. Furthermore, they can also increase the efficacy of macrophages23.

Th cells interact with the MHC class II/peptide complexes presented by antigen presenting cells through its receptor, called the T cell receptor (TCR). If a T cell has never before seen antigen, it is called a nave T cell. In this situation, the T cell will need instruction from a professional antigen presenting cells, usually a DC, about how to perform its function. DCs do this through cell surface proteins call co-stimulatory molecules and through cytokine expression. This process is consists of three main signals. The first signal is the antigen recognition; the second signal is co-stimulation and the third cytokine exposure. This whole process is referred to as priming of the nave T cell. Once primed, the T cells begin to divide; a process that is referred to as expansion or proliferation35.

The most important set of co-stimulatory molecules is CD80 or CD86 on the DC and CD28 on the T cells. This second signal is necessary to tell the Th cell that there is a problem. If signal one is given without this second signal, the T cell will assume that the antigen is actually harmless and become non-responsive in a process called anergy36. Only a DC that has encountered a PAMP or another danger signal will express CD80 or CD86 on its surface reassuring the Th cell that there is, indeed, a problem.

Signal three is the secretion of cytokines of the DC. There are several cytokines important for Th cell eduction. They most important ones are IL-4, IL-12, IL-6, TGF and IL-10. Th cells will differentiate into different types of Th cells depending on which cytokines prevail. The main types of Th cells are T helper 1 (Th1) cells, T helper 2 (Th2) cells, T helper 17 (Th17) cells, and induced regulatory T cells (iTreg)35.

Each Th cell subtype has its own unique set of skills. One could almost see differentiation as an occupation. Just like an athlete will choose to develop her body and a scientist will choose to develop her mind. In humans, these choices are reflected at the level of gene transcription and protein expression. The athlete will stimulate muscle growth and the scientist develops the cerebral cortex of the brain. Its the same for Th cell differentiation. The four main subtypes of Th cells are listed. There are, however, rare forms that have been observed that are not listed and Th cells, much like humans, can fall into gray areas between the stereotypes.

The Th1 path is chosen when T cells are exposed to IL-12 during priming. Th1 cells are characterized by the production of the cytokine, interferon- (IFN) and the expression of the master transcription factor, T-bet. Th1 cells are experts at gearing the immune response towards to the control of internal pathogens like viruses and mycobacteria, which reside internally in macrophages. They perform this function by initiating cytotoxic T cell responses, helping macrophages to become more effective, by helping B cells to produce certain types of antibodies. These functions are executed, in part, through IFN exposure, however, some require cell-cell contact and will be explained in more detail later37.

Th2 cells are created during exposure to high amounts of IL-4. This leads to the expression of the Th2-associated master transcription factor, GATA3. Th2 cells are also characterized by the production of IL-4 (indeed, the same cytokine needed to create them). These cells are designed to skew the immune system towards a humoral immune response (antibody response) that can deal with parasite infection. Unfortunately, Th2 responses are also the ones associated with allergy development as well. Th2 cells do their work by effectively helping B cells and encouraging specific forms of antibodies. This is done through a combination of IL-4 exposure and cell-cell interactions37.

The Th17 subtype is the most recently described of the Th subtypes. It is most effective at controlling extracellular bacterial and fungi responses, like those found during intestinal food poisoning or during a yeast infection. Its creation is dictated by the cytokines IL-6 and TGF and this leads to the expression of the master transcription factor, RORt. Th17 cells produce the cytokine IL-17. IL-17 production is one of the main facilitators of their function and it encourages surrounding cells to increase neutrophil migration. Neutrophils are excellent phagocytic cells with many bacterial killing tools38.

To those just learning about the immune system, the existence of the following Th subtype may be confusing. iTreg are designed to counter the functions of other immune cells. Why? The reason is that immune responses are highly damaging to surrounding tissues and, without them, immune responses would spiral out of control.

That said; these cells are induced by DCs when they are exposed to high amounts of IL-10 or TGF. This causes the expression of the master transcription factor, Foxp3. In turn, iTreg produce IL-10 or TGF. IL-10 and TGF are what is called anti-inflammatory cytokines. They have the ability to limit the functions of immune cells. IL-10, for instance, lowers Th1 and Th17 responses and reduces macrophage efficacy. TGF encourages apoptosis (induced death of cells), prevents cell division and lowers phagocytosis39.

Th cells are not the only kind of T cell. Cytotoxic T cells (CTLs), characterized by the surface marker CD8, are not to be missed and are essential for the elimination of viral infections. The function of a CTL is found in its name. Cyto refers to cell and toxic means just how it sounds. These cells are cell toxic and kill other cells. In many ways, they are similar to the NK cells and NK T cells of the innate immune system. However, they do not use invariant receptors to recognize problems in other cells, but instead use an adaptive system.

CTLs, like Th cells, have a TCR. This means that they can detect unique peptides presented to them by other cells. In the case of Th cells, these are MHC class II molecules presented via DCs. In the case of CTLs, they are MHC class I molecules. During an infection, as we earlier mentioned, DCs will travel to the lymph node and present samples of the intruder to the T cells. This is also happens for CTLs. However, despite the presence of all the priming signals, priming will be suboptimal. CTLs need an additional signal, jokingly called the license to kill. This signal is given by a Th1 cell through the production of a cytokine called IL-2, which stimulates CTL expansion; and through an interaction between the Th1 cell and the DC via CD40 on the DC and CD40 ligand on the Th1 cell, which makes the DC more effective at priming CTLs33. Once a CTL is primed and active, it has the ability to kill.

As you can see, CTL activity is highly controlled to ensure that they react only to pathogen-associated peptides. The reason is that MHC class I can be expressed by every cell type in the body. MHC class I on a cell is like a sign advertising the health of the cell. The cell is constantly displaying samples of the proteins its making. If an active CTL recognizes one of these samples as being of viral origin, it kills that cell; eliminating a viral host.

The word humor means fluid in Latin and, therefore, humoral immune responses relate to non-cellular systems found in the bodily fluids. Weve already discussed non-cellular components of the innate immunity, however, in immunology most people are not referring to these non-cellular systems when they use the term humoral immune response. Instead, they are referring to the immune response mediated by antibodies and this is part of the adaptive immune response.

The cell behind antibody responses is the B cell. Nave B cells of the immune system produce rudimentary antibodies (see below) until other cells activate them. B cells, unlike the T cells, are not required to interact with DCs; instead B cells reside in lymphoid tissues and fish for antigens that they recognize using their B cell receptors or BCR. The BCR looks like a surface bound antibody and once it binds a molecule, the B cell engulfs it and much like the phagocytes, digests it. Just like the DC, the B cell will then present pieces of the antigen to Th cells using MHC class II molecules. Primed and activated Th cells, which recognize the presented peptides, are then able to help the B cell through a CD40-CD40 ligand interaction. The Th cell also provides cytokine signals to tell the B cell which kinds of antibodies it should make34.

This process is reminiscent of the priming process of Th cells. Signal one is the MHC class II/peptide and TCR interaction between the B cell and the T cell. Signal two is the costimulatory help provided by the T cell in the form of CD40-CD40 ligand interactions. And, signal three is the cytokine message provided by the T cell.

Helped B cells will then further differentiates into plasma cells, which can produce massive quantities of antibodies.

Antibodies, by themselves, cause very little harm. However, their strength lies in their ability to tag a molecule as harmful and block molecular functions. Antibodies enhance the functions of the innate immune system. They can bind to pathogens and particles to initiate the complement system and induce phagocytosis. They can also block/neutralize molecular interactions. Examples of this function would be an antibody that blocks the toxic effects of diphtheria toxin or antibodies the block viral binding sites to cells. Antibodies also interact directly with cells and can change their function by binding to specific antibody receptors found on the surfaces of immune cells40.

An Antibody is a small protein structure produced by B cells. It is also called an immunoglobulin (Ig). It looks like a Y and it is formed from four separate proteins. Each tip of the Y recognizes and sticks to the antigen, meaning that each antibody can bind two similar antigens. A single arm is called a Fab (Fragment, antigen binding) fragment. The base of the Y is called the Fc (Fragment constant) region and, while the Fab fragments dictate the specificity of the antigen binding, the Fc region dictates the type of antibody or isotype. The antibody isotype is dictated by the prevalent cytokines in the environment as well as additional danger signals that the B cell experienced while being helped by the Th cell41.

The first types of antibodies that a B cell can produce are IgM and IgD. The M and D refers to different classes of the Fc region. IgM is found as a pentamer, with five individual IgM antibodies bound by their Fc regions in the center forming a star. They are effective at complement activation. IgD is found as a monomer and its function is undefined. However, it has the ability to bind mast cells via an Fc receptor ( for D) and induce anti-microbial peptide secretion.

IgG antibodies are found as monomers and they are very potent at stimulating immune responses. They are capable of neutralization, inducing phagocytosis in macrophages and neutrophils via Fc receptors ( for G), activation of complement, and also the activation of NK cells (also via Fc receptors).

IgE antibodies are monomers. They are known to cause mast cell degranulation via binding of Fc receptors ( for E). They are induced during parasite infection and, unfortunately, also during allergy.

IgA is found as a dimer of two antibodies attached via their Fc regions. It is involved with mucosal defense: found in gastrointestinal system, the respiratory systems. They are particularly effective at neutralization of microbes and toxins.

Once the adaptive immune system has formed a response, the body has a long-term record of the invading pathogen in the form of long-lived plasma cells, memory T cells (not covered here) and antibodies. This is why vaccination is so important. It allows your body to create an adaptive immune response against an invader without having to truly become infected42.

When a body encounters a pathogen for the second time, its a completely different situation than the first encounter. During a second infection, T cells drawn to the inflammation site will have knowledge to help macrophages, recruit more neutrophils, and kill infected cells. Antibodies will be now present to assist complement activation, the phagocytosis of particles, and even kill microbes. The response will be quicker and more effective.

Though separating the two types of responses: innate and adaptive, helps with learning; it can also become an obstacle to seeing the immune response as a complex, dynamic system. It is important when looking at an immunological problem to consider the hosts previous history as it has so much influence on the immune response.

It is my sincere wish that this basic immunology overview helps with your understanding of the immune system. Keep in mind, that it is simplistic (skipping whole areas of immunological interest at times) and I have avoided adding too much terminology. If there are aspects that are particularly confusing, dont hesitate to mention them and I will do my best to update this document.top

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Basic Immunology | The IBD Immunologist

Human Behavior

Is it OK to want to be rich? – Fox Business

Council of Economic Advisers Chairman Tomas Philipson says homeownership among those 35 and under is steadily increasing.

Admit it...Money is something we all think about. Money is a reality that impacts all of our lives.

Common questions about money are:

All these questions are often bandied about and are definitely intriguing.

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So, when I was asked to write an op-edquestioning if its all right to want to be rich, I eagerly dove into this infinitely interesting topic.

In the 1960s famed psychologist, Eric Fromm wrote a cult classic called "To Have or To Be." In this book, he described those who measure their worth by money and possessions were immature. The better-adjusted individuals, Fromm noted, didnt have to equate their worth with money and acquired luxuries.

Even Sigmund Freud, "The father of psychoanalysis," wrote about our psychological relationship with money. Freud himself had difficulty talking about his own feelings toward money. He famously said, Money is like laughing gas to me, and did admit his mood was greatly impacted by his earnings.

You dont need to be an analyst to realize that money is often considered a taboo topic to discuss, which makes it even more challenging to identify as a topic to debate. What are our own personal feelings about how much money we want versus how much money we should want?

WHAT IS MARIAH CAREY'S NET WORTH?

Some find talking about money terribly vulgar, while others find it off-putting and socially gauche.

Those who are wealthy have been described in a myriad of ways and not always positively. This further complicates what we allow ourselves to approve of what we want financially. At its worst, wealth is seen to cloud moral judgment.

Psychologists who study the impact of wealth on human behavior found money can influence our thoughts and actions in ways we are not always aware of. Several studies have found that having wealth can be at odds with having compassion and empathy.

Researchers at UC Berkeley did an interesting study with faux money in a Monopoly game. They found that even play money can get people to behave with less regard for others. They followed two students who played Monopoly. The wealthier player over time started to act aggressively, move his pieces around more brashly, took up more space and even started taunting the other player who had less money.

Wealth can cause moral entitlement.

Even just thinking about money can lead to unethical behavior. Research conductedat Harvard and the University of Utah found participants were more likely to lie or behave immorally after being exposed to money-related words.

Given all of these findings about the feelings we have about money and what it means to be wealthy, why would people want to publicly admit they want to be rich? Still,there are many facets to money: its uses, its ownership, and how it affects the human personality.

In itself, there is nothing wrong with wanting to be rich. In fact, it makes perfect psychological sense.

Money is symbolic.

It is a symbol of competence, omnipotence, and prestige. It offers us a feeling of security and satisfaction and accomplishment.

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There is also an evolutionary component for wanting to be rich. The richer we are, the more likely we are to survive and thrive. When one is rich, you are better able to have control of your environment. You can be less dependent on the goodwill and social approval of others. It allows you to acquire what you want with greater ease.

When youre rich you may have fewer financial concerns. Having money means you can have more freedom and opportunities. Having wealth allows you to surround yourself with beautiful things and interesting experiences.

The rich can present themselves as refined and sophisticated. They can also share their personal aesthetics and taste with loved ones. Being rich can increase a sense of worthiness and self-importanceand help you to feel valued for these accomplishments.

In our culture, being wealthy is associated with success. Some believe being wealthy can innoculate you against ordinary human suffering. For others, being rich means being able to care for those they love. Being rich can be perceived as contributing to one'sfamilys intergenerational wealth. Money can further a sense of generosity allowing the wealthy to donate to causes and charities that benefit others.

Given all these perks, why wouldn't people want to be rich? Still, as with most things in life, its very important to know the why behind your financial goals.

For example, what do you believe being rich will do for you? Will the pursuit of wealth interfere with your ability to be happy in the present? Can you treat yourself well if you feel you dont achieve the riches you desire? And is there an understanding that there are different ways to be wealthy?

One can conclude that the desire to be rich is quite understandable. Its just important to make sure to never lose sight of your values and who you are.

To do good, be good and do notmake the pursuit of money the only benchmark of your value and success.

If you do this, then life can give you the best of all worlds.

Robi Ludwig Psy.D. is a nationally known psychotherapist, award-winning reporter, and author. She is a regular commentatoron CNN, HLN, Fox Business. She was arelationship contributor for Investigation Discover Network's "Scorned" and is currently the creator and host of Facebook Watch'sTalkingLive with Dr. Robi Ludwigin Times Square. She is on the Medical Advisory Board and a contributor for Bella Magazine. Dr. Ludwig has aprivate practice on the Upper East Side in New York City where she also resides with her family.

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Is it OK to want to be rich? - Fox Business

Human Behavior

Human behavior at the intersection of many sciences – Dailyuw

People frequently ask themselves, Why did I do that? Attempting to understand how we react to and interact with changing environments has resulted in years of research on human behavior.

Neurobiologists and psychologists study the biological basis of how the brain responds under certain situations. Social scientists like anthropologists explain what factors guide our behavior and engineers are taking all these studies to design tools that enforce human interaction, intelligence, and growth.

Human nature is complex, and interdisciplinary considerations may help us answer some interesting questions about how people think, remember, and behave.

Things that are good for one's health and longevity such as finding mates, food, and children; the dopamine reward or evaluation system is important to recall that success, Sheri Mizumori, a professor in the department of psychology who studies behavioral neuroscience, said.

Dopamine is known as the feel-good neurotransmitter, a chemical messenger that relays information between neurons. It is released by the brain when we eat food, exercise, and crave sex, helping reinforce desirable behaviors by encoding values of rewards. Psychologists and neurologists have studied this through animal models that help explain how humans access their own memory to guide their actions.

From a young age, babies learn that if an outcome is not what they want, they will change, Mizumori said. Much of the brain has evolved to be a predictor of outcomes.

Memory can be thought of as a repository of past experiences that did and did not work. When we are placed in a new situation, we use strategies we learned from previous experiences to guide our actions.

You are driving behavior based on memory and [guiding] behavior correctly the next time, Mizumori said.

The brain uses decision circuits that integrate information about past values from memory and evaluates it against our motivational, or internal, state. Understanding how the brain can switch behaviors or learn new ones is known as flexible decision making.

Theoretical psychologists study human behavior from a philosophical and social standpoint. A commonly known study argues if nature or nurture genetic or acquired influences behavior.

Maslows hierarchy of needs outlines a five-tier pyramid of deficiency and being needs. Once deficiency needs the first tier are met, people strive for self-fulfillment and personal growth, behaviors that encompass the fifth tier of the pyramid.

Depression is an interesting example of behavior at the intersection of social sciences and biology. Behavioral theory argues depression results from peoples interactions with the environment and psychodynamic theory states it stems from inwardly-directed anger or loss of self-esteem.

Conversely, Mizumori explained depression from a behavioral switch, or flexible decision-making standpoint.

Researchers in human centered design and engineering (HCDE) are attempting to design technologies that can support or prompt changes in peoples behaviors.

A lot of the research projects we explore are real-world-problem driven, Gary Hsieh, an associate professor in HCDE, said. How do we encourage users to eat healthier or exercise more? These are health-related problems aligned to behavior-related problems.

By studying the needs and values of certain groups, researchers like Hsieh are able to design technologies that encourage people to communicate and interact in welfare-improving ways. In a growing age of data, engineers and scientists are able to learn about people from social networks.

Data allows us to study people in ways that we could not before, Hsieh said. It ties in with the types of interventions and applications that we can build.

Human behavior presents unknown complexities that arise from cultural, social, internal, environmental, and biological factors. Being able to integrate all those is a challenge that many will be addressing for generations to follow.

Reach reporter Vidhi Singh at science@dailyuw.com. Twitter: @vidhisvida

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Human behavior at the intersection of many sciences - Dailyuw