Similar to the human eyes, nose, and lips, the earlobes also have special features. Although the human ears look similar, there are minor structural differences that make each ear different from the other.

The major form of the gene that determines the shape of the earlobe is known as an allele. An allele is a gene which is found at a specific position on a chromosome. It has been established that all genes in our body have two copies; one from each parent.

Image Credit: Thiti Sukapan / Shutterstock

An earlobe is made up of connective tissues combined with a mixture of areola tissues and fat cells. Earlobes have a good blood supply which help in keeping them warm and maintaining balance. Majorly, there are two types of earlobes found in humans - free earlobes and attached earlobes.

Free Earlobes: Free earlobes are the most common form of lobes found. This type of earlobe is often large and hangs below the point of attachment to the head. This happens due to the influence of a dominant allele. If the genes from the parents get expressed by the dominant allele, then the child will be born with free earlobes.

In most cases, the allele is regnant to the free lobes compared to attached lobes. The free earlobe parents can also give birth to an attached earlobe child, depending on the reaction of the allele gene. If parents with free earlobes give birth to a baby with attached earlobes, it is certain that both of them had both a copy of the dominant and recessive allele.

Attached Earlobes: These types of earlobes are not rare, but are also not commonly found. Earlobes of such type are small in size and do not have hangs. They are attached directly to the side of the head. The structural formation of this kind of lobe is due to the absence of the dominant allele in the chromosomes. The recessive allele is expressed instead in the chromosomes to form an attached earlobe. It is not necessary that parents with attached earlobes should give birth only to the attached earlobe child.

Traits are the major factors that result from chromosome pairs and which, in turn, determine ones overall physical appearance. When alleles combine, some exert stronger influence down sythan the others. The stronger allele is responsible for the dominant traits. Dominant alleles are said to be found throughout an organism. If the dominant allele fails to show its presence, the recessive allele will be expressed. These are known as recessive traits. Although the traits vary, the size of the earlobes for both the traits remain the same. An average mans ear measures 6cm, while for a woman it is about 5cm, in which the earlobe size measures about 2cm.

Genetic conditions play an important role in the birth of a human being. People born with abnormal growth of organs are considered to be affected by the traits before their birth. The major conditions that cause irregular or abnormal growth include:

Birth disorders may be minor or severe and may occur at any stage during pregnancy. Most disorders affect the baby while in the womb, before the formation of the organs; however, not all genetic defects are caused by the transfer of gene from the parents. In many cases, the baby may be born with genetic disorders that the parents gene does not contain. Some defects are considered to be harmless, while some may require prolonged medical treatment.

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Genetics of Earlobes - News-Medical.net

By: IANS | New York | Published:July 4, 2017 10:51 pm Mutations in the gene called GDF5 resulted in shorter bones that led to a compact body structure while reducing the risk of bone fracture from falling. Thus, it also favoured early humans to better withstand frostbite. (Source: File photo)

A genetic change associated with shorter stature and increased risk of arthritis might have helped our ancestors survive the Ice Age, a study has showed. The findings showed that mutations in the gene called GDF5 resulted in shorter bones that led to a compact body structure while reducing the risk of bone fracture from falling. Thus, it also favoured early humans to better withstand frostbite as well as helped them migrate from Africa to colder northern climates between 50,000 and 100,000 years ago.

These advantages in dealing with chilly temperatures and icy surfaces may have outweighed the threat of osteoarthritis, which usually occurs after a prime reproductive age, the researchers said. The variant that decreases height is lowering the activity of GDF5 in the growth plates of the bone.

Interestingly, the region that harbours this variant is closely linked to other mutations that affect GDF5 activity in the joints, increasing the risk of osteoarthritis in the knee and hip, said Terence Capellini, Associate Professor at the Harvard University. For the study, published in the journal Nature, the team examined gene GDF5 first linked to skeletal growth in the early 1990s to learn more about how the DNA sequences surrounding GDF5 might affect the genes expression.

They identified a single nucleotide change that is highly prevalent in Europeans and Asians but rarely occurs in Africans. Introducing this nucleotide change into laboratory mice revealed that it decreased the activity of GDF5 in the growth plates of the long bones of foetal mice. The potential medical impact of the finding is very interesting because so many people are affected, said David Kingsley, Professor at the Stanford University.

This is an incredibly prevalent, and ancient, variant. Many people think of osteoarthritis as a kind of wear-and-tear disease, but theres clearly a genetic component at work here as well. Now weve shown that positive evolutionary selection has given rise to one of the most common height variants and arthritis risk factors known in human populations, Kingsley said.

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Genetics causing arthritis possibly helped humans survive Ice Age - The Indian Express

A new era of genome-based personalised medicine for cancer could be in place within five years under plans unveiled by the Chief Medical Officer.

The genomics dream outlined by Professor Dame Sally Davies would see millions of patients having all their DNA tested as genome sequencing becomes as routine as MRI or CT scans.

Ultimately, the future goal is for every cancer patient to have his or her whole genome sequenced, making the procedure as standard as blood tests and biopsies. People with rare diseases are also expected to benefit from having greater access to the technology, ending the years-long diagnostic odyssey of multiple tests and visits to different specialists.Whole genome sequencing involves unscrambling the entire book of genetic instructions that make us what we are, encompassing 3.2 billion letters of code.

Research suggests that in 60 per cent of cases, the genomes of cancer patients reveal actionable data personal mutations that can shape future treatment.

Tens of thousands of NHS patients have already had their DNA mapped, but the recommendations set out in Dame Sallys Generation Genome report aim to multiply the numbers many times over.

Dame Sally said: The age of precision medicine is now and the NHS must act fast to keep its place at the forefront of global science .

This technology has the potential to change medicine forever but we need all NHS staff, patients and the public to recognise and embrace its huge potential.

Genomic medicine has huge implications for the understanding and treatment of rare diseases, cancer and infections.

Currently, genetic testing of NHS patients in England is conducted via 25 regional laboratories and a plethora of smaller units operating along the lines of a cottage industry, Dame Sally said.

Her chief recommendation is to centralise all the labs and establish a national network providing equal access to the tests across the country.

Within government, a new National Genomics Board would be set up, chaired by a minister, to oversee the expansion and development of genomic services, taking into account new advances within the rapidly evolvingtechnology.

The Health Secretary, Jeremy Hunt, said he welcomed the report, pointing out that the UK had established itself as a world leader in genomics medicine. He added: Tens of thousands of patients across the country have already benefited from quicker diagnosis, precise treatment and care, and we will support the NHS to continue its relentless drive to push the boundaries of modern science.

Part of what made greater access to whole genome sequencing feasible was the rapidly falling cost of the tests, which has dropped from several thousand pounds to 680.

Reporting by John von Radowitz, Press Association

Achieving the genomics dream could make a huge difference to the 3.5 million adults and children with one of the 7,000 recognised rare diseases that could be treated far more quickly and more effective with genome testing.

Every persons genome contains 3.2 billion letters of genetic code, amounting to two terabytes of data. If it was printed your genome would fill a stack of books 61 metres high. Although officials now talk about personalised medicine, what they are trying to deliver is diagnosis and treatment related to the genomic signature of a particular patient.

This means giving the most effective drugs against cancer, using drugs which will cause fewer side effects, seeking new drugs and treatments and moving to personalised prevention. There will also be other applications, many of which we are not yet aware of, the report says.

In the case of cancer, tumour cells develop a different genome to normal cells. Comparing a patients normal and cancerous DNA can provide valuable clues about the best form of treatment, although this information is not set in stone. Cancers evolve rapidly and alter their DNA, which can make them resistant to treatments.

This is still much more to learn about genomes and their relation with treatment response, but once that knowledge base expands there should be much faster diagnosis of rare diseases which currently take on average four years to diagnose.

Paul Gallagher

Originally posted here:
NHS to offer personal cancer care based on patients' genetics - iNews

Throughout human existence it has been our nature to push the envelope. More speed. More power. More performance. Ingenuity combined with trial and error spawn new peaks in technology.

As we strive to stay ahead of the technological advancement curve, we sometimes forget about the interconnected systems that might need time and adjustment to catch up. Too much torque and the transmissions or drivelines wear out easily. Increases in output translate into greater input requirements and higher priced fuels. At some point, the law of diminishing returns kicks in, making that next increase to performance or production too costly and economically inefficient. Much of the same can be said of beef genetics.

It is amazing how much progress our industry has made in genomics in such little time. Genetic improvement is absolutely vital for every segment of our industry because it helps promote multiple elements linked to sustainability. However, producers need to be mindful of the inevitable trade-off that comes with a rapidly accelerated discovery curve.

Decades ago, the push for performance was inadvertently tied to frame. Mature size and calving difficulties almost singlehandedly devastated the marketability of many breeds. Though unintended, the consequences were still significant. It is no different than the push for muscle cars with powerful stances and large throaty motors that also guzzled fuel by the gallon.

Oddly enough, we have corrected cow size, yet cow maintenance or input cost remains a common issue. If you install a high performance racing engine in a car, it will require a grade of fuel of equal magnitude to perform up to its potential. Cheap, poor quality fuels simply wont do. The same is true for your cowherd. If you continue to select for growth and milk genetics, be prepared to adjust the feed input requirements that will follow. Our push to discover that next elite genetic package is changing the beef herd from independent foragers to concentrate dependents.

There are other phenotypic systems that desperately need to catch up with a hastily advancing genotype population. Evidence of this can be seen in the national beef herd by simply looking at their feet. The push to discover cattle that can be marketed as the next top genetic package for extreme calving ease, growth and marbling, is creating a significant gap in animal soundness.

Unintended consequences, arise under the strain of scientific and economic achievement. It will take time and discipline to bring traits like soundness up to speed.

I am by no means making an argument against genetic advancement. On the contrary, I am a firm believer in improvement and making wise use of all genetic selection tools. I simply see the road to change is not straight and narrow. It winds and turns with plenty of peaks and valleys, as well as, the occasional switch back. As a breeder, you need to understand the trade-offs that come with accelerated genetic selection. Can you afford to add that next unit of performance or milk? Or, should you keep pace just behind the curve and capture value as the rest of the systems catch up?

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Jared Wareham; The Genetic Paradox - CattleNetwork.com

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

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

TOKYO Japanese office equipment maker Konica Minolta Inc (4902.T) plans to acquire U.S. healthcare firm Ambry Genetics Corp to diversify its business, the Nikkei daily reported on Sunday.

The acquisition will likely cost around 100 billion yen ($890 million) and be Konica Minolta's most expensive, reflecting its ambition to branch out into healthcare as its printer business slows, the business daily reported without citing sources.

Konica Minolta will partner semi-government fund Innovation Network Corp of Japan (INCJ) to buy all shares of Ambry, a private firm that uses genetic data to screen for cancer, the Nikkei said.

Konica Minolta will own 60 percent of Ambry and INCJ the remainder, the newspaper reported.

Konica Minolta told Reuters nothing has been decided at this stage. INCJ did not respond to Reuters' requests for comment.

(Reporting by Leika Kihara; Editing by Christopher Cushing)

FRANKFURT German discount grocery chain Aldi North is planning to spend more than 5 billion euros ($5.71 billion) to revamp its stores around the world, which would be its biggest investment project ever, German weekly Bild am Sonntag reported, citing company sources.

JERUSALEM Flag carrier El Al Israel Airlines said on Sunday its board approved a plan by its Sun d'Or unit to buy smaller rival Israir from IDB Tourism.

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Japan's Konica Minolta plans to buy US cancer test firm: Nikkei - Reuters

Accelerated Genetics and Select Sires Inc. will be a merged cooperative.

According to a news release, the merger follows a June 22 vote by Accelerate Genetics officials. The vote green-lights an agreement recommended by both companies boards of directors. The smaller Accelerated Genetics has reported financial difficulty in the past. The larger Ohio-based Select Sires will acquire Accelerated Genetics assets, including a bull farm in Westby.

Both companies specialize in artificial insemination of cattle. The companies have an established working relationship that started in 2001 when the companies allied in international markets.

Accelerated Genetics has been searching for a partner who could enhance the business and move it forward, said Scott Dahlk, Accelerated Genetics Board chairman. Joining forces with Select Sires is a positive move for both the member-owners and producers worldwide.

The company said Accelerated Genetics assets, employees and sales representatives will be integrated into the organization. Both companies operate under the cooperative-business model and share similar structures, according to the company.

By working together we will be stronger, said David Thorbahn, Select Sires president and chief executive officer. The value and expertise gained by joining the people from both organizations allow us to offer our customers a broader genetics program in addition to an outstanding animal health product line. Its very exciting to work together, enabling our organizations the ability to expand genetic research, technical support, service, and programs with people who are passionate about the dairy and beef industries.

Link:
After vote, Accelerated Genetics slated to merge - La Crosse Tribune

Myriad Genetics, Inc.'s (NASDAQ: MYGN) strong run has caught investors attentions, however, JPMorgan analyst Tycho Peterson still doesn't see the stock being able to offset a decline in the hereditary cancer business.

Peterson maintained his Underweight rating and $16 price target.

While in the past, the esoteric LDT market was viewed as sitting at the nexus of the secular shift in healthcare towards personalized medicine, this vision has, in our view, run up against the reality that the LDT business model has a number of challenges, with many labs attempting to support a pharma model centered around heavy rep counts without the benefit of patent protection, Peterson said.

While Peterson expects the stock to fall to $16 - it trades around $25.60 per share - he noted the stock could still move in either direction.

Myriad represents, in our view, a significant opportunity, given near-term catalysts that could drive the stock meaningfully higher or lower, with the setting of FY18 guidance during F4Q earnings (including forward expectations for hereditary cancer) being the most significant upcoming event post-UNH renewal, he said.

However, with its core business in (arguably) structural decline and pipeline that could be long on potential, but short on near-term financial impact, Myriad is not an easy company to value. While we believe the pipeline is intriguing, we do not believe that it can offset what we expect to be a continued steady decline in the core hereditary cancer business.

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2017 Benzinga.com. Benzinga does not provide investment advice. All rights reserved.

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JPMorgan Checks In On Myriad Genetics Following 30% Rally - Benzinga

June 28, 2017

While the definitive causes remain unclear, several genetic and environmental factors increase the likelihood of autism spectrum disorder, or ASD, a group of conditions covering a "spectrum" of symptoms, skills and levels of disability.

Taking advantage of advances in genetic technologies, researchers led by Alex Nord, assistant professor of neurobiology, physiology and behavior with the Center for Neuroscience at the University of California, Davis, are gaining a better understanding of the role played by a specific gene involved in autism. The collaborative work appears June 26 in the journal Nature Neuroscience.

"For years, the targets of drug discovery and treatment have been based on an unknown black box of what's happening in the brain," said Nord. "Now, using genetic approaches to study the impact of specific mutations found in cases, we're trying to build a cohesive model that links genetic control of brain development with behavior and brain function."

The Nord laboratory studies how the genome encodes brain development and function, with a particular interest in understanding the genetic basis of neurological disorders.

Mouse brain models

There is no known specific genetic cause for most cases of autism, but many different genes have been linked to the disorder. In rare, specific cases of people with ASD, one copy of a gene called CHD8 is mutated and loses function. The CHD8 gene encodes a protein responsible for packaging DNA in cells throughout the body. Packaging of DNA controls how genes are turned on and off in cells during development.

Because mice and humans share on average 85 percent of similarly coded genes, mice can be used as a model to study how genetic mutations impact brain development. Changes in mouse DNA mimic changes in human DNA and vice-versa. In addition, mice exhibit behaviors that can be used as models for exploring human behavior.

Nord's laboratory at UC Davis and his collaborators have been working to characterize changes in brain development and behavior of mice carrying a mutated copy of CHD8.

"Behavioral tests with mice give us information about sociability, anxiety and cognition. From there, we can examine changes at the anatomical and cellular level to find links across dimensions," said Nord. "This is critical to understanding the biology of disorders like autism."

By inducing mutation of the CHD8 gene in mice and studying their brain development, Nord and his team have established that the mice experience cognitive impairment and have increased brain volume. Both conditions are also present in individuals with a mutated CHD8 gene.

New implications for early and lifelong brain development

Analysis of data from mouse brains reveals that CHD8 gene expression peaks during the early stages of brain development. Mutations in CHD8 lead to excessive production of dividing cells in the brain, as well as megalencephaly, an enlarged brain condition common in individuals with ASD. These findings suggest the developmental causes of increased brain size.

More surprisingly, Nord also discovered that the pathological changes in gene expression in the brains of mice with a mutated CHD8 continued through the lifetime of the mice. Genes involved in critical biological processes like synapse function were impacted by the CHD8 mutation. This suggests that CHD8 plays a role in brain function throughout life and may affect more than early brain development in autistic individuals.

While Nord's research centers on severe ASD conditions, the lessons learned may eventually help explain many cases along the autism spectrum.

Collaborating to improve understanding

Nord's work bridges disciplines and has incorporated diverse collaborators. The genetic mouse model was developed at Lawrence Berkeley National Laboratory using CRISPR editing technology, and co-authors Jacqueline Crawley and Jill Silverman of the UC Davis MIND Institute evaluated mouse behavior to characterize social interactions and cognitive impairments.

Nord also partnered with co-author Konstantinos Zarbalis of the Institute for Pediatric Regenerative Medicine at UC Davis to examine changes in cell proliferation in the brains of mice with the CHD8 mutation, and with Jason Lerch from the Mouse Imaging Centre at the Hospital for Sick Children in Toronto, Canada, to conduct magnetic resonance imaging on mouse brains.

"It's the act of collaboration that I find really satisfying," Nord said. "The science gets a lot more interesting and powerful when we combine different approaches. Together we were able to show that mutation to CHD8 causes changes to brain development, which in turn alters brain anatomy, function and behavior."

In the future, Nord hopes to identify how CHD8 packages DNA in neural cells and to determine the specific impacts to early brain development and synaptic function. Nord hopes that deep exploration of CHD8 mutations will ultimately yield greater knowledge of the general factors contributing to ASD and intellectual disability.

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Mouse brain models reveal insights into genetics of autism - News-Medical.net