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Genetics

BRIEF-Interleukin Genetics to explore strategic alternatives, reduce workforce – Reuters

Morning News Call - India, July 4

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BRIEF-Interleukin Genetics to explore strategic alternatives, reduce workforce - Reuters

Genetics

Can genetics play a role in education and well-being? – USC News

When Daniel Benjamin was just beginning his PhD program in economics in 2001, he attended a conference with his graduate school advisers. They took in a presentation on neuroeconomics, a nascent field dealing with how the human brain goes about making decisions.

Afterward, as they took a stroll outside, they couldnt stop talking about what they had learned, how novel and intriguing it was. What would be next, they wondered. What would come after neuroeconomics?

The human genome project had just been completed, and we decided that even more fundamental than the brain would be genes, and that someday this was going to matter a lot for social science, said Benjamin, associate professor (research) of economics at the USC Dornsife College of Letters, Arts and Sciences Center for Economic and Social Research (CESR). Indeed, his excitement that day was the foundation of a visionary academic path.

Fast forward to today. Genoeconomics is now an emerging area of social science that incorporates genetic data into the work that economists do. Its based on the idea that a persons particular combination of genes is related to economic behavior and life outcomes such as educational attainment, fertility, obesity and subjective well-being.

Theres this rich new source of data that has only become available recently, said Benjamin, also co-director of the Social Science Genetic Association Consortium, which brings about cooperation among medical researchers, geneticists and social scientists.

Collecting genetic data and creating the large data sets used by economists and other social scientists have become increasingly affordable, and new analytical methods are getting more and more powerful as these data sets continue to grow. The big challenge, he said, is figuring out how scientists can leverage this new data to address a host of important policy questions.

Were ultimately interested in understanding how genes and environments interact to produce the kinds of outcomes people have in their lives, and then what kinds of policies can help people do better. That is really what economics is about and were trying to use genetics to do even better economics.

Only a handful of economists are working with genetics, but this brand of research is perfectly at home at CESR. The center, founded three years ago, was conceived as a place where visionary social science could thrive and where research could be done differently than in the past.

Being in a place where thats the shared vision is pretty rare, said econometrician Arie Kapteyn, professor (research) of economics and CESR director. Theres no restriction on which way you want to go or what you want to do. It doesnt mean that there are no restrictions on resources, but its the opportunity to think about your vision of whats really exciting in social science research. Then being able to actually implement it is absolutely fantastic.

The mission of CESR is discovering how people around the world live, think, interact, age and make important decisions. The centers researchers are dedicated to innovation and combining their analysis to deepen the understanding of human behavior in a variety of economic and social contexts.

What we try to do is mold a disciplinary science in a very broad sense, Kapteyn said. Because todays problems in society, theyre really all multidisciplinary.

Case in point: Benjamins work combining genetics and economics.

The flagship research effort for Benjamins CESR research group deals with genes and education. In a 2016 study, the team identified variants in 74 genes that are associated with educational attainment. In other words, people who carry more of these variants, on average, complete more years of formal schooling.

Benjamin hopes to use this data in a holistic way to create a predictive tool.

Were also creating methods for combining the information in a persons entire genome into a single variable that can be used to partially predict how much education a persons going to get.

Daniel Benjamin

Rather than just identifying specific genes, he said, were also creating methods for combining the information in a persons entire genome into a single variable that can be used to partially predict how much education a persons going to get.

The young field of genoeconomics is still somewhat controversial, and Benjamin is careful to point out that individual genes dont determine behavior or outcome.

The effect of any individual gene on behavior is extremely small, Benjamin explained, but the effects of all the genes combined on almost any behavior were interested in is much more substantial. Its the combined information of many genes that has predictive power, and that can be most useful for social scientists.

While the cohort of researchers actively using the available genome-wide data in this way is still somewhat limited, Benjamin says it is growing quickly.

I think across the social sciences, researchers are seeing the potential for the data, and people are starting to use it in their work and getting excited about it, but right now its still a small band of us trying to lay the foundations.

Were putting together huge data sets of hundreds of thousands of people approaching a million people in our ongoing work on educational attainment because you need those really big sample sizes to accurately detect the genetic influences.

As CESR works to improve social welfare by informing and influencing decision-making in the public and private sectors, big data such as Benjamins is a growing part of that process, according to Kapteyn.

What big data reflects is the fact that nowadays there are so many other ways in which we can learn about behavior, he said. As a result, I think well see many more breakthroughs and gain a much better understanding of whats going on in the world and in social science than in the past.

I think were really at the beginning of something pretty spectacular. What we are doing is really only scratching the surface theres so much more that can be done.

More stories about: Big Data, Economics, Research

Report comes as the university nears the opening of USC Village, the largest economic development project in the history of South Los Angeles.

The USC Dornsife Economics Department launches the USC Economics Review to spotlight students research.

The program at USC Dornsife offers tailored training in preparation for Fall Career Fair.

Conference covers methods of prompting change in human behavior for the public good.

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Can genetics play a role in education and well-being? - USC News

Immunology

Immunology, one cell at a time : Nature News & Comment – Nature.com

Amir Giladi & Ido Amit

Single-cell genomics can identify unique immune cells (red) involved in Alzheimer's disease.

For more than a century, scientists have tried to characterize the different functions of the 10 trillion to 50 trillion cells of the human body from neurons, which can reach 1 metre in length, to red blood cells, which are around 8 micrometres wide. Such efforts have helped to identify important cell types and pathways that are involved in human physiology and pathology.

But it has become apparent that the research tools of the past few decades fail to capture the full complexity of cell diversity and function. (These tools include fluorescent tags fused to antibodies that bind to specific proteins on the surfaces of cells, known as cell-surface markers, and sequencing in bulk of the RNA or DNA of thousands of seemingly identical cells.) This failure is partly because many cells with completely different functions have similar shapes or produce the same markers.

Single-cell genomics is transforming the ability of biologists to characterize cells. The new techniques that have emerged aim to capture individual cells and determine the sequences of the molecules of RNA and DNA that they contain. The shift in approach is akin to the change in how cells and molecules could be viewed during the 1980s, following advances in microscopy and the tagging and sorting of cells.

In the past five years, several groups of biologists, including our own laboratory, have gone from measuring the expression of a few genes in a handful of cells to surveying thousands of genes in hundreds of thousands of cells from intact tissues. New cell types1, 2, cellular states and pathways are being uncovered regularly as a result.

Our lab was one of the first to study the immune system using single-cell genomics. The tools are particularly suited to this task because the heterogeneity and plasticity of cells are integral to how the immune system works the nature of each agent that could attack the body being impossible to know ahead of time.

Exploiting single-cell genomics fully will require scientists and clinicians to make experimental and analytical adjustments. In particular, we must be ready to jettison assumptions about cell types and cellular states, and to rebuild representations of cellular networks.

The cells of the immune system, which patrol the blood and dwell in tissues, have many functions. They protect the body from pathogens and cancer, and orchestrate metabolism and the formation of organs. They are involved in almost every activity that regulates the bodys internal environment, from the development and remodelling of tissues to the clearance of dying cells and debris. So their dysfunction can cause many problems. For instance, deregulated immune cells can attack healthy cells and cause autoimmune conditions such as lupus, type 1 diabetes or multiple sclerosis.

A first step towards harnessing the immune system for therapeutic use is to characterize the types of cell that occupy a specific area (such as the surroundings of a tumour). Another is to map the unique processes and pathways that the cells are involved in, the genes they express and the cells interactions and responses to environmental cues. Over the past 40 years, meticulous approaches based on genetic labelling have enabled researchers to identify dozens of types and functions of immune cells. For example, the use of antibodies fused to fluorescent tags that bind to and flag specific cell-surface markers established the basic taxonomy of immune cells including several types of T cells, B cells, monocytes and granulocytes. Such studies also kick-started the search for treatments known as immunotherapies, which harness the body's natural defences to fight disease.

Increasingly, however, these techniques hint that the world of immune cells is more complex than current categories allow. Immune cells seem to change their functions depending on their surroundings. For instance, macrophages (as identified by their cell-surface markers) might have one function in the gut yet a completely different one in the brain3. Also, molecular markers cannot fully describe the functional diversity of cells in different immune contexts. For example, a group of immune cells that suppresses the immune response around tumours (myeloid-derived suppressor cells) has been shown to express markers from both monocytes and granulocytes4.

In short, conventional methods based on populations of cells are proving too blunt a tool with which to tease apart complex immune assemblies5.

In the past five years, technologies for capturing single cells have improved dramatically. Some approaches rely on placing cells inside miniature vessels, one at a time; others capture individual cells inside droplets of oil. Meanwhile, bioinformaticians have built algorithms for representing multidimensional data, identifying distinct cellular states and modelling the transitions between such states6.

Thanks to these developments, researchers can now capture hundreds of thousands (or even millions) of cells and accurately measure the DNA, RNA or protein content of each (see Scale up). Gene-editing tools such as the CRISPRCas9 system can be used to introduce a specific mutation into the genome of one cell, and then a different alteration into the next7. Thus, the function of dozens of genes can be inferred from just one experiment by reading the resulting RNA barcode in parallel with the single-cell genetic information.

With such measurements, researchers can potentially record the functional states of many cells at once8. They can also probe the ancestry of individual cells9 or identify mutations in a particular cells DNA, as well as track communication between cells. In other words, single-cell genomics allows researchers to build an accurate representation of the entire make-up of a tissue10, such as a specific organ or a tumour, or of a multicellular process such as the immune systems response to an infection. Importantly, it enables them to do this without making prior assumptions based on, for instance, the participating cell types and their characteristics.

About 20 labs worldwide have fully embraced single-cell genomics, and even more are trying out the approach. In the past few years, numerous papers have been published that describe new types of immune cell and previously unknown pathways involved in various conditions.

For instance, 15 subtypes of innate lymphoid cell, which are similar to T cells but do not express the T-cell receptor, have been identified in the gut11. Different progenitors of immune-cell lineages have been uncovered in the bone marrow12. Specific types of immune cell have been associated with particular stages of tumour growth13, 14. And various types of microglial cell have been identified in the brain during development.

Last month, our lab reported the discovery of a new type of immune cell in the brain, disease-associated microglia (DAM)15. Our experiments indicate that DAM break down dead cells and protein aggregates called plaques in the brains of mice engineered to express mutated proteins associated with Alzheimers disease.

More than a decade of population-based assays, including cell sorting using specific cell-surface markers and bulk RNA sequencing, had failed to flag these cells. Only by individually sequencing the RNA of each of the immune cells in a sample of brain were we able to find a rare subpopulation of microglia that may open up fresh approaches to treating Alzheimers disease.

It is early days for single-cell genomics. But already, a number of important lessons can be learnt from the experiences of our lab and those of others.

First, it is clear that many of the current categories of immune cells, such as T cells or monocytes, encompass heterogeneous populations. To probe cellular complexity, researchers must therefore cast their nets wide, and try to collect all immune cells within a tissue or region of interest. This is a very different approach from that used with methods based on cell-surface markers, which aim to obtain as pure a sample as possible.

Second, success will depend, in part, on the extent to which researchers preserve the states of cells and the original composition of a tissue. Cell stress or death should be minimized to ensure that tissue preparation does not favour specific cell types. (Some are more sensitive to heat stress, for example, than others.)

Single-cell genomics will soon be commonplace in basic and applied immunology research.

Third, bioinformaticians will need to develop scalable and robust algorithms to cope with greater numbers of cells, conflicting or overlapping programs of gene expression and fleeting developmental stages.

Fourth, after researchers have characterized all of the immune cells in a sample, they will need to find molecular markers that can be used to either enrich or deplete certain cell types in further samples. Tissues comprise trillions of cells with myriad molecular characteristics and functions, and the types or states of these cells may vary in abundance by many orders of magnitude. For instance, in the brains of healthy mice, our newly identified population of DAM makes up less than 0.01% of cells15. Thus, repeated unbiased sampling to characterize rare populations will keep on accumulating cells that are not those of interest.

Other experimental, computational and statistical approaches can help to overcome this problem. Importantly, once a rare population of cells is identified using single-cell genomics, they can be purified and experiments conducted only on them. In our recent study, for instance, we used cell-surface markers to isolate DAM and then assessed their role in Alzheimers disease using various techniques, including fluorescent labelling.

A fifth lesson regards a considerable drawback of current single-cell technologies. They capture snapshots of dynamic systems, in which cells are devoid of important context spatial, temporal, clonal and epigenetic. Without knowing where a profiled cell came from, who its neighbours were or what it developed from, it is hard to model complex processes such as tissue formation or a tumours interaction with nearby immune cells.

One way around this problem might be to combine several layers of information from the same cell. Genetic fluorescent labelling, for instance, can be used to track changes in the state of a cell over time or to find exactly where it is in a tissue.

Ultimately, textbook definitions and long-held beliefs about cellular identities, such as the distinction between cell type and cell state, will almost certainly need to be rethought. Some classifications of subgroups based on extra markers may prove helpful in the short term, but can quickly become unwieldy. For example, instead of being able to refer to T-helper (TH) cells, researchers must now refer to one of about a dozen subcategories, including TH1 cells and TH2 cells16. And such an approach may continue to overlook the true functional complexity of the immune ecosystem.

A more workable solution may be for researchers to replace rigid classifications with assemblies of gene-expression programs (see Genetic microscope). These elaborate gene maps could represent all cell types and states, including those from different physiological and pathological contexts. Such maps would allow biologists to define cells not just by one fate, lineage or function, but by the combination of all of these. It would also allow these functional entities to be compared across organisms.

Claire Welsh/Nature

Single-cell genomics will soon be commonplace in basic and applied immunology research. This is thanks to efforts to make the tools affordable, standardized and accessible to academia, the biotech industry and the clinic. We predict that, within a decade, blood samples or biopsies will be routinely sent for single-cell genomic analysis, and the entire immune composition of patients analysed and compared with all known healthy and diseased states.

Also likely to undergo rapid transformation is our understanding of tumours and tumour stem cells, processes such as neuronal development, metabolic disorders and neural function.

Almost every scientific breakthrough has originated from a new measurement or observation that enabled scientists to come up with new hypotheses and merge them into unifying theories. Robert Hookes observation of cells as units of multicellular organisms, James Watson and Francis Cricks discovery of the 3D structure of DNA and Edwin Hubbles detection of galaxies beyond the Milky Way could not have been achieved without new ways of seeing.

The molecular microscope of single-cell genomics is already adding to our knowledge of cell types and gene pathways. But for single-cell genomics to tell us something truly new about the blueprint of humans, we will have to address how individual cells communicate to achieve shared goals.

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Immunology, one cell at a time : Nature News & Comment - Nature.com

Cell Biology

‘Cellular mosh pit’ helps researchers understand tissue formation – Phys.Org

July 3, 2017 by Grant Hill

Researchers led by the University of Dundee have developed a way of exploring a 'cellular mosh pit' that may shed light on processes such as embryo development, wound healing and cancer growth.

Working with colleagues at the University of Aberdeen, they have developed the Active Vertex Model (AVM), a new computational model that allows scientists to examine in greater depth than ever before how cells move in a variety of biological processes.

Epithelial tissues, such as the skin or lining of the internal organs, act as barriers to the environment. To form an effective barrier, cells in epithelia have to be closely packed together. These epithelial tissues are formed and shaped during embryonic development, while not disrupting the tissue's connectivity.

This is achieved via carefully orchestrated exchanges between neighbours so-called cell intercalations. These intercalations also play key roles during tissue repair and regeneration. The mechanisms behind intercalations a process of fundamental importance for proper tissue function are not fully understood.

The AVM will allow much larger areas of individual cells to be studied, almost 10 times the size previously possible. This will provide scientists with a greater understanding of these active systems and the mechanics of tissues, something has previously been likened to watching fans mosh away at gigs.

"Understanding the emergence of collective behaviour of cells in tissues is what our model is interested in explaining," said lead author Dr Rastko Sknepnek, a lecturer in Physics within Dundee's Division of Computational Biology. "This behaviour has hallmarks of an active system. Active systems can be a school of fish, a developing embryo or even a mosh pit at a rock concert, which is quite a well-known analogy among people working in this area.

"Each person in a mosh pit has their own choice on where to move but is also affected by those around them. If you compare the biology we are interested in with this scenario, each person is like a cell, and we have built a model that can look at the activity and movement of the people in the mosh pit."

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The AVM combines the physics of active systems, which is credited with describing behaviours of systems such as flocks of birds, schools of fish and human crowds, with the Vertex Model commonly used to study mechanical properties of epithelial tissues. The AVM not only allows for very efficient computations but also incorporates the cell intercalation events in a natural way.

The interdisciplinary project combined the biological expertise of Professor Kees Weijer, from the University's School of Life Sciences, with the modelling knowledge of Dr Sknepnek and Dr Silke Henkes, a lecturer in Physics at the Institute for Complex Systems and Mathematical Biology at the University of Aberdeen. Much of the work was carried out by Daniel Barton, a postgraduate student in Dr Sknepnek's lab.

The next stage of the project will see the research team apply the model to Professor Weijer's research on cell and tissue dynamics during embryogenesis, the process by which the embryo forms and develops.

"We will now carry out work with existing biological research that will to improve the model further," said Dr Sknepnek. "We want to work with other researchers to expand the model to other systems, in particular curved surfaces such as those found in the gut."

Owing to its efficiency, the AVM will allow researchers to explore cell motion patterns over previously inaccessible sizes, while retaining the resolution of individual cells. This may help understand how collectives of cells organise and control their behaviour at the scale of the entire tissue, providing new insights into processes such as development of embryos and cancer metastasis.

The AVM is publicly available under a non-restrictive open source licence and can downloaded at https://github.com/sknepneklab/SAMoS.

The research was funded by BBSRC and is published in the latest edition of the journal PLoS Computer Biology.

Explore further: Physical basis of tissue coordination uncovered

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An engineer at Washington University in St. Louis discovered a model in which the mechanics of the cells' environment can predict their movement, a finding thatultimately could mean confining cell transition in tumors and ...

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Physiology

The Five Secrets Of Lifelong Health – FemaleFirst.co.uk

3 July 2017

The media today can make you think that living a long, healthy (and happy!) life is quite complicated. There are diet wars, exercise wars, and competing tips on how to have a successful date, sex life, marriage or family. The boring (but fabulous) truth, is that it is actually fairly simple. And at the same time, completely particular to YOU. As human animals, our physiology is 10,000 years old, but life in the industrialized, digital modern world is quite new. The key to making choices that extend your health and your life is to get in touch with what your body was made forthe evolutionary health that your physiology thrives in.

We are made to move

And this is the other key, that you are unique! Genetically unique and socially and environmentally unique. You need to be bodywise, to listen to YOUR bodys needs and responses when considering competing health advice or making decisions about what to have for dinner or when to go to bed. With body intelligence (your BQ) as your navigational guide and your bodys earth-adapted physiology as your map, it is simple to make choices that help your body (and your life) hum with vibrancy and wellness.

Here are the Five Secrets to Lifelong Evolutionary Health that every major health advocate can agree upon, and that you can decide upon according to your own body intelligence.

Here are the principles of a healthy diet according to the worlds longest lived peoples.

Let your body guide you as to which grains and how many carbohydrates make you feel energetic and happy, or whether meat or dairy products agree with your digestion. Listen to your body and let it guide you to YOUR healthy diet, within these evolutionary guidelines.

The average person in modern societies sleeps 6.5 hours and we need, on average, 8! How much sleep does your body intelligence say you need to wake up rested and refreshed? Adequate sleep reduces pain, anxiety, depression, infections and weight gain. Sleep is your most important anti-aging activity.

We are made to move. How can you be more active in your everyday life and what kind of activities does your body wisdom lead you to? Dancing? Biking? Yoga? Exercise is the best treatment for depression, high blood pressure and the best prevention for heart disease and stroke.

Loneliness will kill you faster than cigarettes. What kinds of love and affection does your body crave? Cuddling with friends (or your dog!)? Hot sex with your lover? Sweet, affectionate family time with kids, siblings, parents or grandparents? How can you get a regular dose of love and affection in your life? Love truly is our greatest healer, halving the risk of heart attack and reducing your risk of cancer, stroke and all chronic disease.

A sense of pupose can extend your life by 50%what are you committed to? What kinds of creativity, service or work make create peace, satisfaction or excitement inside you?

If you use your body intelligence to guide you in these five evolutionary fundamentals of health, you will live long and prosper, and benefit the world as well. Blessings on your bodywise path!

BodyWise: Discovering Your Body's Intelligence for Lifelong Health and Healing by Dr Rachel Carlton Abrams is published by Bluebird and priced 12.99

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The Five Secrets Of Lifelong Health - FemaleFirst.co.uk

Physiology

Mark Hargreaves Receives 2017 ACSM Citation Award … – https://ryortho.com/ (press release) (subscription)

Tracey Romero Mon, July 3rd, 2017 Print this article Mark Hargreaves, Ph.D., FACSM

Mark Hargreaves, Ph.D., FACSM, a professor of physiology at the University of Melbourne in Australia received the 2017 American College of Sports Medicine Citation Award at the associations recent annual meeting in Denver, Colorado.

Hargreaves was awarded for his contributions to sports medicine and exercise sciences research. His main research focus has been on better understanding the cellular mechanisms that regulate muscle metabolism during exercise and what effect training and nutritional manipulations may have on those mechanisms. His research has been funded by the Australian Sports Commission, the National Health and Medical Research Council of Australia, the Australian Research Council and the Diabetes Australia Research Trust.

Citation Award winners are selected for their leadership and contributions in the areas of research and scholarship, clinical care, administrative services or educational services, said Walter Thompson, FASCM, president of the American College of Sports Medicine (ACSM) in a press release. We are happy to recognize Dr. Hargreaves tremendous accomplishments. Hargreaves work has been published in more than 120 peer-reviewed journals and 65 book chapters and invited reviews, and has been cited more than 5,600 times. He has also received the American College of Sports Medicines Young Investigator Award and the Australian Physiological Societys McIntyre Prize, both in 1994.

One of the most recent studies he participated in, which was published in the June issue of the Journal of Science & Medicine in Sport, evaluated the physical activity training in Australian medical school. The researchers found that while most schools included some physical activity training, they did not always include national strength recommendations.

Hargreaves has served on the ACSMs board of trustees as a foreign corresponding editor of Medicine & Science in Sports & Exercise, associate editor of Exercise and Sport Sciences Reviews and consulting editor of the Journal of Applied Physiology. He received his masters degree in exercise physiology from Ball State University in 1984 and his Ph.D. in physiology from the University of Melbourne in 1989.

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Embryology

Age has an effect on male fertility – study | DESTINY Magazine – DestinyConnect

A recent study reveals that women aren't the only ones who have to worry about a ticking biological clock

Women deal with the stigma of infertility issues in most societies. Manywomen of a certain age know the feeling of being told that their biological clock is ticking by well meaning relatives. However, a new study shows that a mans age also has a role to play in fertility. A recent Harvard Universitystudy, which is being presented atthe third annual meeting of theEuropean Society of Human Reproduction and Embryology in Geneva, Switzerland, shows that male fertility declines with age.

Our study found an independent effect of male age on the cumulative incidence of live birth, said investigator Dr Laura Dodge from the Beth Israel Deaconess Medical Center and Harvard Medical School in Boston, USA.

Researchers looked at 19 000 cycles in 7 753 couples over a four-year period in Boston.

In couples with a female partner aged under 30, a male partner aged 40-42 was associated with a significantly lower cumulative birth rate (46%) than a male partner aged 30-35 (73%). Similarly, in couples with a female partner aged 35-40 years, live birth rates were higher with a younger partner than with an older male partner, the researchers found.

Oneof the reasons for decreased fertility as men get older is genetic damage to the sperm.

Globally infertility is a significantproblem. A 2015 report, titledA unique view on male infertility around the globe,found that48,5 million couples around the world experience infertility and men contribute to an estimated 20%-30% of issues.

The burden of fertility often falls on women because of dominant patriarchal norms.

In an interview with DESTINY, Rhandzu Tshivhasi (34), who has been married to her husband for 10 years, said when people speculate on why the couple have not yet conceived, she finds it easier to be the one to admit she is infertile.

When a man is infertile, he is looked down upon. You find that other men actually laugh at him like its his fault, but its not, she said.

The Harvard study found that in some cases, women couldbenefit from having younger partners.

For women aged 30-35, having a older partner is associated with approximately 11% relative decreases in cumulative incidence of live birth from 70% to 64% when compared to having a male partner within the same age band, the researchers found.

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Age has an effect on male fertility - study | DESTINY Magazine - DestinyConnect

Embryology

Australian invention modernises IVF – CNW – Canada NewsWire (press release)

GENEVA, July 3, 2017 /CNW/ -- The European Society of Human Reproduction and Embryology's Annual Meeting in Geneva has today heard that a world first Australian invention has modernised one of the key IVF processes by automating and standardising steps that are currently performed manually.

Genea Biomedx's Gavi automates key stages of vitrification - the process of freezing IVF patients' embryos for use in later cycles or whilst awaiting results from genetic screening.

In Australia, the leading technology is exclusive to Genea clinics meaning only Genea patients have access to Gavi and its vitrification outcomes.

Results presented today show clinical outcomes of day five embryos vitrified using the Gavi system are comparable to the traditional manual CRYOTOP system. Gavi also offers time savings through standardising what is traditionally a highly manual process which is subject to environment and human variation.

"In IVF labs across the world, vitrification is currently undertaken many times each day, requiring a high level of manual dexterity and leading to variations between embryologists and clinics in the way embryos are handled and the outcomes achieved," Genea Biomedx General Manager Dr Tammie Roy said.

She added, "we know that the more experience an embryologist has in the manual process the better the outcomes. By implementing Gavi and therefore standardising the vitrification process, every embryo in the lab is treated exactly the same way despite the embryologist's level of experience".

In the Genea clinics that were assessed for this study the Gavi system provided immediate high level survival rates thus demonstrating the potential to reduce the learning curve that is experienced by embryologists in the manual process.

Vitrification of embryos is an essential component of an effective assisted conception program. Genea Medical Director, Associate Professor Mark Bowman said, "at Genea, most patients are likely to have more than one viable embryo so preserving extra embryos for patients to complete their family or try again is imperative." He added, "it's all part of our commitment to getting women pregnant in the least number of stimulated cycles."

Full media release here: http://geneabiomedx.com/Content/Files/MEDIA-RELEASE_Genea-Biomedx-GAVI_ESHRE_FINAL_Genev.aspx

Media Contact at ESHRE

Sophie Hegarty M: +61447 111 190 E: sophie.hegarty@geneabiomedx.com

* The selection of this abstract for publication in the press programme does not imply endorsement by ESHRE of the products and/or services

SOURCE Genea

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Australian invention modernises IVF - CNW - Canada NewsWire (press release)

Anatomy

Anatomy of a Goal: Villalba’s Dagger – Massive Report

Welcome to the Anatomy of a Goal, where each week we dissect one goal (or near goal) from the previous weeks Columbus Crew SC match.

For match 19 of the 2017 MLS Season, we take a look at Hector Villalbas 64th minute goal that put Atlanta United up 2-0 as part of their win over Crew SC on Saturday.

Here is a look at the finish from the Atlanta winger.

Though Columbus dominated possession for much of the first half, the team never really threatened Atlanta. Usually possession oriented, the Five Stripes were happy to lose the possession battle with the Black and Gold, instead focusing on long balls into open spaces. Just like Nathaniel Marhefka predicted in his lineup preview, Atlanta exploited the space vacated by Crew SCs attack-minded right winger and right fullback. Villalbas second goal is a direct result of the Five Stripes getting into the vacant space on the Columbus defensive right.

As usual, Nate absolutely nailed his focal area when he said to expect a tug-of-war between [Harrison] Afful and [Ethan] Finlay for Crew SC & [Yamil] Asad and [Greg] Garza for Atlanta United.

Atlantas second goal begins with their No. 10, Miguel Almiron, receiving the ball just inside the Black and Golds defensive half. Marked by Wil Trapp, Almiron has three options. He can continue his dribble, make a quick pass straight ahead to Greg Garza, or play a long pass to Yamil Asad into the space behind Harrison Afful.

Almiron opts for the more difficult pass over the top. Asad has already begun his run and will easily beat Afful, who gets caught sitting back on his heels.

Asad is by Afful before the ball hits the ground. If Asad is able to cleanly play the ball then hell have an easy chance on goal.

Lucky for Crew SC, Asad badly misplays the ball. Instead of letting the ball run ahead of him, the midfielder attempts to control the ball as it lands, sending it behind him. Defender Josh Williams, just to the right of Asad, does a good job to get near the Atlanta attacker, causing him to take that extra touch.

With the ball heading away from the Columbus goal, both Afful and Williams are in position to make a quick clearance before Asad can recover. Striker Josef Martinez has his own idea, and quickly moves toward the loose ball. Somehow, Martinez beats both Williams and Afful, neither of whom try to play the ball. Instead, both Black & Gold defenders act surprised at the misplay by Asad and fall back on defense rather than playing the ball back up the field.

Meanwhile, Artur, just beside the referee, hustles back.

Having beaten Afful and Williams to the ball, Martinez can either continue his dribble up the field, play a pass to Garza running up the wing or slot a pass to Asad. The pressure from Artur and Williams will force Martinez to play the ball out to Garza on the wing, away from his own goal.

As Garza receives the ball and is marked by Afful, he will fire a cross into the Crew SC goal box. Atlanta has three players (from left to right: Martinez, Asad and Villalba) in the area to receive Garzas cross. Three Columbus defenders (from left to right: Williams, Jonathan Mensah and Jukka Raitala) are in good positions to deny the Five Stripes attackers.

Williams is in the perfect position to win Garzas cross and sends a headed ball out to the top of the 18-yard box. Jonathan makes an awkward hop at the ball, but provides cover were Williams to miss his clearance.

This is an excellent bit of defensive coverage from the Black & Gold, calmly marking Atlantas attackers and clearing out a goal-scoring opportunity. Sadly, the Crew SC defense will be let down by their inability to stop the next cross.

That red highlighted blur is Almiron, who ran in from the midfield to win Williamss clearance right in front of Kekuta Manneh. Either by lack of communication or lack of awareness, Manneh totally missed Almiron running right toward the ball. Had he notice Almiron before the Atlanta attacker won the ball, Manneh could have made a clearance or quick pass to a wide open Trapp.

Having won the ball, Almiron will drive directly at Artur.

If Artur can slow or dispossess Almiron, he will have multiple passing options to start a counterattack. If Almiron beats Artur, Columbus will face another defensive scramble.

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As the above video shows, Artur halfheartedly stabs at Almiron and is beaten by the Five Stripes attacker, setting up an Atlanta cross.

Having blown by Artur, Almiron, with a difficult angle on goal, faces immediate pressure from Williams. The Five Stripes No. 10 will likely have to send a cross into the box.

Just below Almiron is Asad, who is not yet marked by Trapp and is wide open for a slotted pass to his feet. Martinez is available at the near post, but is marked by, the taller Jonathan. Villalba is at the top of the 18, and should be marked by Raitala if he makes a move toward goal.

As Almiron chips in his cross, the Black & Gold have Atlantas two options covered. Almirons decision to cross has taken Asad out of the immediate picture, and he will likely be pressured by Trapp if the ball pops out. Jonathan lets Martinez in behind him, but has six inches on the Atlanta striker. Raitala is aware of Villalbas position and has him covered. . . for now.

From the side angle, you can see that most of Atlantas attackers are covered. If Almiron were able to turn his hips quickly enough, he would have an easy pass right to the feet of Asad. However, things change as soon as the ball is played.

Just before the ball is played, Martinez floats a few feet behindJonathan. As the ball floats into the face of the goal, the center back fails to find Martinez and misjudges where the ball will land, allowing the shorter Martinez to contest him for a header. Raitala, unsure of what to do, sprints back toward the goal, leaving Villalba totally alone.

Comparing this image to the image above, you can see that Raitala has moved about two yards toward the goal, and is standing on the top line of the 6-yard box.

Though Jonathan misjudged the ball, he is able to contest Martinezs header, deflecting the ball out into the path of Villalba. Seeing the ball bounce out, Raitala oddly decides to keep heading toward the goal and plants his feet right on the goal line.

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In the above video, you can clearly see Raitala sprint back toward his goal like he thinks the ball is heading right into the net. It seems Raitala thought that he needed to cover the back post of the goal, which seems odd given Steffen not having come off his line and Jonathan being in position to deflect the cross.

With his main defensive threat inexplicably standing on the goal line, Villalba moves toward the ball headed right into his path. Jonathan is forced to scramble into Villalbas path.

Villalba has ample time to settle the bouncing ball as Jonathan scrambles to defend.

Jonathan is able to get in a decent position but is just a half second too late to block Villalbas shot . . .

. . . and Atlanta takes a 2-0 lead.

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Anatomy of a Goal: Villalba's Dagger - Massive Report

Physiology

Anatomy and physiology of ageing 6: the eyes and ears – Nursing Times

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John Knight is senior lecturer in biomedical science; Chris Wigham is senior lecturer in interprofessional studies; Yamni Nigam is associate professor in biomedical science; all at the College of Human Health and Sciences, Swansea University.

The special senses sight, hearing, smell, touch and balance allow us to perceive the world and communicate. Like all body systems, they undergo age-related changes that negatively affect their function. Physiological changes to the eyes and ears mean older people gradually see, hear and balance less well. The changes also increase the risk of conditions such as cataracts, age-related macular degeneration, and conductive and sensory hearing loss. This sixth article in our series on the effects of age on the body describes what happens to the eyes and ears.

Knight J et al (2017) Anatomy and physiology of ageing 6: the eyes and ears. Nursing Times [online]; 113: 7, 39-42.

The special sense organs the eyes, ears, nose, tongue detect information coming from the environment, such as light, sound, smells and tastes, which is then relayed to the brain where it is processed into meaningful sensations. Diminished acuity of the special senses reduces our ability to perceive the world and communicate. All the senses go through an age-related decline, but the most dramatic changes are seen in the eyes and ears. This sixth article in this series on the effects of ageing on the different body systems examines the age-related changes in the eyes and ears.

Vision is affected by the ageing of the internal and external structures of the eye. Its decline is gradual and linear, and detectable changes begin in the third decade of life. The main changes are outlined in Fig 1.

Anatomy and physiology fig 1

Anatomy and physiology fig 1

The retro-orbital fat, which protects and cushions the eye, atrophies with age, causing the eyeball to recede into its socket (enophthalmos). As a result, eyelid tissues become lax and the levator muscles in the eyelids weaken, causing the eyelids to droop (ptosis). Drooping eyelids can gradually obstruct the upper field of vision.

Sinking eyeballs and drooping eyelids often lead to the conjunctiva lining the eyelids (tarsal conjunctiva) failing to sufficiently lubricate the front of eye (cornea). This can result in an air space developing between the lid and the cornea, particularly at night, potentially leading to epithelial breakdown (Sobel and Tienor, 2013; Liang et al, 2011).

In some people, the weakening of the muscles supporting the eyelids and loosening of the eyelids result in the eyelashes turning inwards (entropion) and irritating the corneas surface, which could lead to ulceration. A significant weakening of the muscles supporting the lower eyelids can result in them flopping away from the eyeball (ectropion), which can then dry out and become irritated. Symptoms of entropion and ectropion can be relieved by anti-inflammatory eye drops or artificial tears, while surgery to tighten the skin and muscles of the eyelid can provide permanent relief (Garrity, 2016).

With age, the lacrimal glands produce fewer tears, while the composition of tears changes, and the wetting efficiency and stability of the tear film is reduced. This leads to dry eye syndrome in up to 14% of the over-65s. Irritation, grittiness and pain can ensue and affect many activities, such as reading or watching television. Persistent irritation can make the cornea less sensitive, which in turn can diminish the ability to detect injury or infection. Many people find the use of artificial tears effective (NHS Choices, Dry Eye Workshop, 2007).

Throughout life, equatorial lens cells divide and new cell layers are added to the outside of the lens. Since the lens cannot grow in size (if it did it would soon outgrow the eyeball), its cells must be compressed, which results in the lens becoming increasingly dense and inflexible. The lens, therefore, becomes progressively less able to change shape to be able to focus light on the retina.

Presbyopia is the age-related reduction in the ability to see near objects. It typically presents as an inability to read text positioned close to the eye and generally develops in the 40s and 50s. Presbyopia results from a reduction in the ability of the intraocular lens to change shape. The distance from the eye at which print can be read (near point) increases from about 10cm at the age of 20 to over 100cm by the age of 70. Most people manage presbyopia by using correcting reading glasses (Boyd, 2016).

New lens cells continue to be produced throughout life, so the lens continues to increase in density. This can cause particular light frequencies to be absorbed and the lens to take on a yellowish hue, affecting contrast sensitivity and the accurate perception of colours.

When the concentration of proteins in the lens becomes very high, precipitation occurs. This is seen as a cataract. Thescattering of the light causes a glare or a halo effect when looking at bright lights. As the densest area of the lens is the centre, this is where age-related cataracts are most commonly seen.

Cataracts can make it difficult to see in certain circumstances for example, when driving at night. They can also interfere with the ability of certain wavelengths of light to enter the eye, thereby reducing colour perception: people with cataracts may wear garish clothing due to their compromised colour vision.

Individuals with poorly controlled diabetes are at much greater risk of developing cataracts because increased blood glucose encourages the build-up of damaging levels of sorbitol in the lens (Knight et al, 2017).

Cataracts are managed by removing the lenss contents from the capsular bag and placing a small intraocular lens inside the capsule to provide refractive power. The power of the intraocular lens can be chosen to suit the patients wishes and lifestyle (Truscott, 2003).

One role of the pupils is to regulate the amount of light entering the eye. With age, their diameter decreases, reducing the admittance of light. Age also has a negative effect on the pupils ability to adapt to changes in light intensity for example, when going from light to dark. Adapting to the dark requires the photosensitive cells of the retina to regenerate the photopigment rhodopsin; this is considerably delayed with age, which contributes to night-vision problems.

These changes increase older peoples risk of falls and other accidents, for example, when leaving a brightly lit bathroom to walk up or down a flight of poorly lit stairs (Rukmini et al, 2017; Turner and Mainster, 2008; Bitsios et al, 1996).

The eye consists of two hollow chambers separated by the lens. The anterior chamber is filled with a watery fluid (aqueous humor) and the posterior chamber with a jelly-like material (vitreous humor). The composition of the vitreous humor can change from a gel to liquid with age and, in some people, it shrinks, collapses and separates from the retina. This posterior vitreous detachment often manifests as discrete opacities (floaters) or sheering patterns in the field of vision (Bishop et al, 2004).

With age, cone photoreceptor cells in the fovea, which provide high-quality colour vision, begin to die, eventually resulting in age-related macular degeneration (ARMD). This is thought to be caused by changes to the cells of the retinal pigment epithelium (RPE), which lies next to, and maintains, the photoreceptor cells.

There are two types of ARMD: dry (90% of cases) and wet (10%). Dry or atrophic ARMD is characterised by a gradual bilateral loss of vision as the RPE degenerates. Wet or exudative ARMD is caused by the growth of new blood vessels in the space between photoreceptors and RPE (subretinal space) and the leakage of serous fluid from these new vessels. Wet AMRD has a more rapid onset and causes more severe loss of vision.

In ARMD, pale yellow-white elevated spots called drusen appear on the retinal surface, distorting vision and reducing visual acuity. Their appearance steadily increases after the age of 60 years. ARMD accounts for half of all visual impairments among people aged 75 and over (AMD.org; National Eye Research Centre; Forrester et al, 2001).

The ear is the organ of hearing but also plays the major role in our sense of balance. Problems with hearing are the most common sensory disorder associated with ageing. At age 61-70 years, around a third of people develop problems understanding speech if there is ambient background noise, and in those aged 85 years and over this rises to around 80% (Sogebi, 2015). Age-related changes to the ear are shown in Fig 2.

Anatomy and physiology fig 2

Anatomy and physiology fig 2

The auricle (pinna) collects sound waves and directs them through the ear canal (auditory meatus) to the eardrum. With age, the pinna often becomes larger and features more external hair on the tragus and lower helix; these changes are more often seen in men. The pinna becomes increasingly dry and scaly in both sexes.

The auditory meatus produces earwax (cerumen), which moistens the ear canal and is mildly antiseptic, helping to keep the ear free from infection. Unless compressed and pushed inwards by implements such as cotton buds, cerumen gradually works its way out (the ears are often described as self-cleaning).

With age, the ceruminous glands become less active and produce less earwax, which can lead to the auditory meatus becoming increasingly dry and prone to infection. The cartilaginous components that form the walls of the auditory meatus can lose elasticity, degrade and sometimes collapse, which increases the likelihood of ear canal collapse (Howarth and Shone, 2006). A drier environment and ear canal collapse both increase the likelihood of cerumen accumulation and obstruction, commonly resulting in conductive hearing loss. Older people may need to use earwax softeners before having excess wax removed by micro-suction at audiology clinics or by syringing at GP surgeries.

The middle ear consists of the ear drum (tympanic membrane) and a hollow, air-filled chamber spanned by three tiny bones (auditory ossicles):

The tympanic membrane vibrates in harmony with the sound waves collected by the outer ear, and these vibrations are transmitted and amplified across the middle ear by the three auditory ossicles. With age, the tympanic membrane becomes less vascular and begins to thin and stiffen (Liu and Chen, 2000; Weinstein, 2000). In older people, the tiny synovial joints between the three auditory ossicles are often stiff and calcified, leading to less efficient conduction and amplification of sound waves.

The air-filled chamber of the middle ear is connected to the back of the pharynx by the auditory or Eustachian tube: this ensures the pressure is kept relatively equal on both sides of the eardrum to prevent pressure building up and damaging the tympanic membrane. The musculature lining the auditory tube often undergoes age-related atrophy, which may interfere with the tubes opening during swallowing, thereby increasing the risk of pressure differences between the two sides of the eardrum.

The inner ear consists primarily of the:

The cochlear is a fluid-filled, spiral-shaped organ that receives sound waves directly from the stirrup. Sound waves travel rapidly through the fluid of the cochlear and are detected by special sensory receptor cells called hair cells. These relay auditory signals to the cochlear nerve, which delivers them to the auditory cortex of the brain, where they are perceived as sound. Our sense of hearing is most acute at the age of 10 years and gradually declines thereafter.

Almost everyone experiences a deterioration in hearing as they age, and currently there is no way of preventing or reversing these age-related changes. Presbycusis is the sum of all conditions that lead to decreased hearing sensitivity with age; it can be accelerated by exposure to loud noise, conditions that impair cardiovascular function and nerve damage (Parham et al, 2011). Presbycusis is usually associated with a progressive degeneration of the hair cells and neurones in the cochlea.

It has been suggested that a lifetime exposure to loud noises cumulatively damages hearing. Indeed, some people living in isolated, non-industrial communities in Africa and India have little age-related hearing loss. Inheritance of certain genes, increased exposure to free radicals and toxins, and decreasing blood supply to the inner ear (Danner and Harris, 2003) contribute to presbycusis and the rate at which it develops. A slowing in the brains processing of auditory information is another contributing factor.

Presbycusis is particularly associated with a declining ability to hear high frequencies, which are important for interpreting speech. As a result, older people find it increasingly difficult to follow and join in conversations, especially when competing background sounds (for example, from television or music) are present. This can restrict interactions and contribute to loneliness and social isolation (Parham et al, 2011).

Tinnitus is the hearing of a noise often a ringing, buzzing, humming or whooshing in the absence of any external sound; it is occasionally reported as having a musical quality. The condition has a variety of causes, including:

However, the major cause of tinnitus might be the lack of sensory input reaching the auditory cortex of the brain. Tinnitus has been compared to phantom sensations perceived in a non-existent limb after amputation: in some people, the sounds associated with tinnitus persist even after the cochlear nerve has been severed (Danner and Harris, 2003). As ageing is associated with a loss of sensory hair cells, the resultant reduction in sensory input to the brain may explain why prebycusis and tinnitus often coexist.

There is mounting evidence that exposure to loud sounds throughout life can both accelerate age-related hearing loss and increase the risk of tinnitus. It is a concern to audiologists that growing numbers of young people attend loud concerts and listen to loud music through headphones for long periods this is likely to accelerate their hearing loss and lead to hearing problems and deafness much earlier in life (Kujawa and Liberman, 2006).

The ability to balance the body at rest (static balance) and when moving (dynamic balance) relies on a complex interplay between different sensory systems including sight, touch and the vestibular system of the inner ear. To trigger the intricate motor coordination of skeletal muscles required to maintain balance, various regions of the brain need to quickly process a large and continuous input from these sensory systems (Horak, 2006).

The vestibular system of the inner ear consists of a labyrinth containing semicircular canals and their hair cells, and the otolith organs (utricle and saccule). All are key in maintaining balance. With age, the vestibular apparatus progressively loses hair cells some people aged 70 years or over experience up to 40% reduction in hair cells in the semi-circular canals (Rauch et al, 2001).

Other notable changes are the progressive fragmentation and degeneration of the otoliths (tiny stones made of calcium carbonate), particularly in the saccule. The number of vestibular nerve cells also diminishes from around the age of 60 years. These changes mean that, with age, our sense of balance becomes impaired and we may experience dizziness. Poor balance and dizziness, together with frailty and reduced reaction times, contribute to the risk of falls a major concern in older people. Each year an estimated 20-40% of those aged 65 and over fall at home (Shupert and Horak, 2017).

While little can be done to avoid the effects of ageing on sight and hearing, it is vital to encourage older people to have regular eye and hearing tests (Box 1). This means appropriate glasses and/or hearing aids can be dispensed, and common age-related pathologies such as cataracts, ARMD, and conductive and sensory hearing loss can be diagnosed early. Many people now have their eyes and hearing tested by high-street optometrists in addition to relying on GP referrals.

People who have diabetes and hypertension need tests more often because both conditions can adversely affect sight and hearing. People with a family history of glaucoma should also be encouraged to undergo regular testing because this condition (which is not part of the normal ageing process) can be hereditary.

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Anatomy and physiology of ageing 6: the eyes and ears - Nursing Times