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Human Behavior

We call it panic, the world calls it preparedness – Pakistan Today

It was a warm day of July 2015 in Hawaii, when we Fellows of the Crisis Management Course at APCSS role-played handling of a health epidemic with potential to be pandemic in South Asian Region. To our utter surprise we as crisis managers had to communicate with Border Control Forces, the Health Minister, National Security Officers, the Police, the Fire Department, the Finance Ministry, the Military officials of the affected country and its neighbors, and above all the Prime Minister along with his bureaucracy, and the border security of neighborly countries. What the heck had we to do with all these stiff collar people, we thought. We were the national crisis management team to deal with crisis-specific stuff only, but now with Covid-19 termed a pandemic by the WHO, it all seems so true!

The mock-up opened avenues unknown to us, making us realize how close knitted disaster management is to human and international security. It did enable us to realize that making consented decisions an all-inclusive approach taking all stakeholders on board, is the answer to hindrances, both human and situational in crises. At the policymaking level understanding the importance of information dissemination and risk communication as a safety weapon, like a missile in war, is absolutely vital.

The first coronavirus case was reported on 26 February in Karachi. The evidence suggest the source was imported not indigenous, and now we have reports of cases being transmitted within communities, which is alarming as economic factors and inability to earn a living might be a precipitating factor for political unrest starting from the lowest income earning population. Today, with infected cases crossing, 2400 Pakistan needs to realize that earthquake 2005 was an eye opener for the world as a whole, but as it was restricted to Pakistan, the world rushed for help. Covid-19 has affected the whole world, made health systems collapse and left corpses to pick so the international help scenario might not be the same as in 2005. A recent analysis by Foreign Policy argues that Covid-19 might be a precipitating factor for political unrest in economically weak states as the world is facing its own economic crisis. The report warns that with main aid providers busy in their own countries, there is serious risk that economically weak states may face debt, deaths, mass unemployment and political unrest due to economic collapse leading to toppling governments around the world.

In a crisis no one person is Aristotle and its OK to build a team and learn, thats how we converted the adversity into opportunity in past and only group approach involving all stake holders is the answer, you dont need to hire people to trace experts already working in government. We need to get going, the sooner we realize this, the better it will be for Pakistan

With the Army now actively participating, we are hopeful to get real data which is necessary for further planning. Keeping in view the unknown nature of this virus and its ability to adapt and change, we cannot purely depend on kneejerk reactions but must understand that this virus is amongst us and here to stay for a while. With rapid growth capability, remaining dormant in many, thus infecting others without the host knowing he or she is a carrier and likely relapse of cured population after months, it poses a unique challenge to think innovatively keeping in view the cultural, social and economic fabric of our society. Are we ready for the future?

Comparing our reaction versus the worlds, we saw while the Australian Government took a fairly aggressive approach, making the National Response Strategy keeping the worst-case scenario in mind, saying it was better to be prepared that to avoid fear as we are attacked by an entity we do not know much about, we on the other hand focused on not scaring the masses, thus no proactive awareness campaigns were seen initially. The world made nearly 100 academic journals, societies, institutes, and companies data on COVID-19 available free of cost available, for the outbreaks duration. I wonder how many of us took advantage of this research covering social, economic, psychological and political impacts of the pandemic and sharing input with policy makers to make consented and long-term decisions? Unfortunately we are still stuck at fight-alone mode.

Another example, as the virus could affect employees, NASA charted out a four-stage response plan for Civil Servants. Using a predictive model for disease, each stage caters for severity and frequency of spread and discusses a four-point agenda from access to center, health and safety of employees, meetings and events and travel of employees so that even if the situation gets really bad, work does not suffer. The good thing is the plan refers to Center of Disease Control which has updated Travel details warnings and awareness, meaning all relevant departments are well synchronized. Can we learn and implement by replicating an already good plan making changes suited to our cultural and social needs? Have we spelled out a COVID-19 strategy for government and private office employees knowing most of the lower staff comes to work by bus?

Other examples are of John Hopkins University giving public access to its live database worldwide, the Royal College of Obstetricians recommending social distancing for pregnant women, while chemical and biological journals are tracking the virus plasma to hinder its growth. All this has gone open-source, so a world of knowledge is right there to take, learn and prevent the disease, but you need a team for that. Do we have a database and names of experts of disaster managers in the country? Where are the trained teams who handled earthquake 2005? Do we know past strategies and policies, tried and tested for previous disasters stacked somewhere in stores? Or are we re-inventing the wheel? If so will COVID-19 wait?

A tried and tested cluster approach must be taken with short-, medium- and long-term goals. Clusters could include, Health, Livelihood, Security, Water and Power, Sanitation, Risk Communication Awareness and Community Engagement, Gender and Vulnerable Groups (including women and children stranded in jails), Economic Revival and Stability, Agriculture and Research and Knowledge Management (not medical, but from a human behavior and change perspective). On War footing each Cluster should prepare action plans with short-, medium- and long-term measures while a research group has to back them up with latest research and the media should be made partner in Crisis Management.

In a crisis no one person is Aristotle and its OK to build a team and learn, thats how we converted the adversity into opportunity in past and only group approach involving all stake holders is the answer, you dont need to hire people to trace experts already working in government. We need to get going, the sooner we realize this, the better it will be for Pakistan.

The writer is Fellow of the Asia Pacific Center for Security Studies Hawaii on Crisis Management

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We call it panic, the world calls it preparedness - Pakistan Today

Human Behavior

Model behavior: Estimates of COVID-19 spread all over the place – FOX 9

Developing a definitive model for COVID-19 is a difficult task.

MINNEAPOLIS (FOX 9) - There is no COVID-19 crystal ball, so health officials and the public alike are eager to learn about mathematical projections of how the virus will spread. But the predictions can vary dramatically, because models are not magic. Its hard when what you want is the certainty of a high school math test, but thats not what we have, said Maggie Koerth, a science journalist based in Minneapolis.

COVID-19 models vary. Here's why.

Koerth details the technical difficulties in developing a COVID-19 model in a story calledWhy Its So Fricking Hard To Make A Good Covid-19 Model for the statistical web site FiveThirtyEight.She said it is called a novel virus for a reason. This is all new.None of these models is the right model. Theyre all going to be different, said Koerth. Youre not waiting for one model to prove the other wrong, theyre just offering a range of possible outcomes.The problem, as Koerth explains, is that every model is based on assumptions, that are based on other assumptions and variables, which rely on incomplete data from other counties or other cities in the U.S.Koerth said there is no standard top down reporting of epidemiological data in the U.S., so it is difficult to compare apples to apples.In Minnesota, a model developed by the Minnesota Health Department (MDH) and the University of Minnesota School of Public Health, predicted that with mitigation efforts, like a stay-at-home order and social distancing, the pandemic in Minnesota would peak in June with two million people infected, and tens of thousands could die. MDH said this model has state specific demographic and health data. Health Commissioner Jan Malcolm said the model was initially run ten days ago, and they plan on re-running the model soon with updated data.A separate model, developed by the Institute for Health Metrics and Evaluation (IHME) at the University of Washington, indicated the pandemic would peak sooner in Minnesota, but would be less severe. The IHME model predicted the peak in Minnesota would arrive in April, killing slightly more than a thousand people. That model relied on mortality data and is being updated daily.A model from the Harvard Global Health Institute laid out multiple scenarios for the Twin Cities based on the percentage of the community infected, predicting that a moderate outbreak with 40 percent infected over 12 months would mean 214,000 patients, overwhelming the health care system.One of the earliest and most models for the U.S. was from Londons Imperial College, and predicted if the U.S. did nothing, 81 percent would become infected and 2.2 million would die. With mitigation effects, there would be half the number of deaths, according to the model.

FOX 9's Tom Lyden interviews science journalist Maggie Koerth on why different models for COVID-19 depict different outcomes.

At its most simplistic, the formula for such a model could fit on a napkin: infection rate x fatality rate x susceptible population = the number who will die. The reality is a much bigger, more complicated data set, with some relatively unknown or hard to predict variables.The biggest obstacle for any model may be the moving target of an infection rate, which is largely unknown in the U.S. because there has been so little surveillance testing.Even a fatality rate is not a straightforward figure, but can vary dramatically by age, health conditions, and available hospital capacity. There are, in fact, multiple fatality rates in a given population.There is also the symptomaticity ratio, which is how many of those who test positive for COVID-19 are displaying symptoms and how many are asymptomatic. That number is key to understanding asymptomatic spreaders and super spreader events.Koerth said the Diamond Princess cruise ship offered a unique opportunity to study a confined group that was more widely tested. Research on the Diamond Princess revealed that only half of those testing positive were symptomatic, the others were asymptomatic, a much larger percentage of asymptomatic carriers than researchers had expected. It is also unknown how many of those who recover from COVID-19 will have immunity, or how long they will be contagious. Koerth said here are still questions about the virus itself: How long can it survive on a surface? How far can it travel in the air?Finally, all the models are now considering various mitigation efforts, like a stay-at-home order, that are highly dependent on human behavior, which can change over time. One thing you can take away is this is a moving target and youre not going to get a clear answer, said Koerth, who said each model is simply providing a range and trajectory. But she understands there is a strong psychological need for answers, from the public and policy makers, and the science is still not exact. Its asking people to be at ease with the unknown, with some scary stuff, but thats about the best thats available right now.

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Model behavior: Estimates of COVID-19 spread all over the place - FOX 9

Human Behavior

Liberation during the coronavirus pandemic – The Ecologist

The SARS-CoV-2 virus and subsequent COVID-19 disease is present in nearly every country and has of today infected more870,000 people globally. However, withoutinternational public lockdowns routine testingthis figure would be much higher.

When new pandemics occur an almost immediate reaction is to pinpoint the blame on someone, or something.

Despite not knowing the exact origin of the virus, one fact is for certain COVID-19 is a zoonotic disease that began in humans when it was directly transmitted from a non-human animal, to a human one.

Zoonotic

Early claims of snake or bat origin were frequent in the media, and more recently the pangolin otherwise known as the most highly trafficked animal in the world seems to be center stage.

Zoonotic diseases can have no negative impacts in certain species and deadly impacts in others, and blame is unjustly given to non-human animals when there is no intent behind the cause. In other words, whether the origin lies in a snake, bat, pangolin or any other species, any blame that we may feel towards that species is unnecessary.

Finding the origin of COVID-19 may be essential to finding a cure, however it is not essential to limiting the spread of the disease, which we can do by changing our behaviour.

The industrialisation of the farming sector has led to ever increasing numbers of animals who are reared for food, numbers almost impossible to imagine. Despite what we would like to think, these animals often live their whole lives in cramped conditions where disease spreads quickly, easily and lethally.

Adding fuel to the fire is stress, which reduces immune system capabilities and increases disease susceptibility. As we know, stress can be both physical and mental, and these feelings are as present in farmed animals as they are in us.

The threat that products from animals have to human health is vast. Campylobacter has been described by the World Health Organisation as the most important food borne pathogens, but this doesnt originate from a seemingly exotic animals. Approximately 50-75 percent of the chickens on sale in the UK are infected with Campylobacter, which lead to 700,000 reported cases and a NHS cost of over 710 million annually.

Disease outbreaks

But we are not alone on this planet, and outbreaks of disease affect more than just humans. Avian pathogenic E. coli, commonly spread by poor hygiene in cramped conditions, causes disease in chickens which is described as causing significant economic losses [to the] industry worldwide.

But this loss is far beyond just economic value in the UK alone at least 10 million chickens die unnecessarily from outbreaks.

Little is known about the pain they suffer during the disease, but with fatality rates so high we can make our own assumptions. Researchers in the field have described Avian pathogenic E. coli as not well understood and others have expressed concern of this developing into a zoonotic disease - consumer demand for products from animals at rock bottom prices could potentially speed up this process.

A vegan diet, which excludes all forms products from animals, can greatly reduce the risk of zoonotic disease outbreaks. This nutritious and kind diet has been recognised by both the British Dietetic Association and the American Academy of Nutrition and Dietetics as being suitable for every age and stage of life.

The Vegan Society has extensive online sources to ensure you are meeting micronutrient such as B12 -and macronutrient such as protein targets which are suited to your individual needs.

Of course, a vegan diet alone will not stop the spread of zoonotic diseases. Consider for a moment, that if you come into close contact with any other person, then there is a chance of catching an infectious disease.

We are all animals. So, when you come into close contact with any non-human animal, again there is the chance of catching an infectious disease and vice versa. The overwhelming majority of individuals say they love animals, but to love animals we must do this in ways which respect their natural ways of life.

Time for reflection

Non-human animals are not here to entertain, feed or clothe us. They are not here for cosmetic or pharmaceutical purposes. Yet within these industries, large numbers of non-human animals are mass bred to live short and painful lives in environments where the spread of zoonotic disease is a continuous threat to both the species bred within them and the workers in each industry.

In this time of uncertainty, where many countries around the world have gone into lockdown, millions of individuals are using this as a moment to reflect on their lives and the world we live in.

We should be working towards a liberated world in which no non-human animals are artificially bred for any human purposes. This is because non-human animals are entitled to live for their own sake, following their own natural behaviours in their natural habitats.

Most humans share the value, 'it is wrong to cause harm unnecessarily'. But many of us are currently taught to be ignorant of the harm which artificially breeding non-human animals causes.

Now is a good time to reflect upon the harms which our non-human animal exploitation industries cause to all the non-human animals involved, and to us as humans as well.

This Author

Louisianna Waring is the insight and commercial policy officer at The Vegan Society. She has a background in both food policy and animal science and is passionate about animal rights. Interested in veganism and the environment? Why not take the seven-day planet-saving vegan pledge atwww.vegansociety.com/plateup

More information about zoonotic diseases can be found in the Compassion in World Farming and World Society for the Protection of Animals report.

Also anticipated is the release of an upcoming feature length documentary exploring the nature of disease and its link with human behavior, produced by Keegan Kuhn (What the Health) and directed by Alex Lockwood (73 Cows).

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Liberation during the coronavirus pandemic - The Ecologist

Neuroscience

Psychedelics should be used to treat depression – The Ecologist

Psychedelic drugs such as LSD and magic mushrooms should be used to treat depression and alcoholism, a new study has claimed.

According to the report, published in the scientific journal Cell, such psychedelics are an effective tool against a number of mental health conditions but have become an unfortunate victim of the global war on drugs.

The now-banned drugs were regularly used as treatments around the world until about 50 years ago.

Neuroplastic

Now, the government's former chief drugs adviser Professor David Nutt is among the team of scientists behind the study who are calling for "the resurrection of research into the neuroscience and therapeutic application of psychedelics".

"It (would rectify) decades of global research paralysis that emerged as collateral damage from the war on drugs," they write.

The study claims that brain imaging has revealed the "powerful neuroplastic changes" of psychedelics can have numerous long-term benefits for people suffering from a variety of mental health conditions.

"What is now needed is a combined, multi-level, multidisciplinary program of research into the mechanisms underpinning these findings," the report says.

This Author

Brendan Montague is editor of The Ecologist.

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Psychedelics should be used to treat depression - The Ecologist

Biochemistry

Former University of Birmingham Professor Michael Wakelam dies after suspected coronavirus infection – University of Birmingham

Mike Wakelam served as Professor of Molecular Pharmacology in the Institute of Cancer Studies from 1993-2007

The University of Birmingham was devastated to hear the news of the death of Professor Michael Wakelam, a former member of staff and an alumnusof the College of Medical and Dental Sciences.

Michael Wakelam died from respiratory complications arising from a suspected Covid-19 infection.

Michael Wakelam served as Professor of Molecular Pharmacology in the Institute of Cancer Studies from 1993-2007 before leaving to become director of the Babraham Institute, Cambridge.

Micheal's links to the University of Birmingham go beyond his teaching and research as he had also obtained his BSc in Medical Biochemistry (1977) and PhD in Biochemistry (1980) from Birmingham as well. Before taking up his post in 1993 at the University, Michael had pursued post-doctoral research at the University of Konstanz in Germany and Imperial College London as a Beit Memorial Fellow. In 1985 he was appointed as a lecturer in Biochemistry at the University of Glasgow.

Michael Wakelam also was a Honorary Professor at the University of Birmingham, as well as a Honorary Professor of Lipid Signalling in the Cambridge University Clinical School. He also served as a visiting Professor at Kings College London and as a Fellow of the Royal Society of Biology and a member of the Academia Europaea. In 2018 Mike received the Morton Lectureship from the Biochemical Society.

Paying tribute to Michael Wakeham, Professor David Adams, Pro-Vice-Chancellor and the Head of College of Medical and Dental Sciences said:

"The College of Medical and Dental Sciences was devastated to hear last night about the death of Professor Michael Wakelam from a suspected Covid-19 infection. Mikes links to Birmingham go even further back as he was an undergraduate and then PhD student in Biochemistry here. Those of you who knew Mike will remember him not only as a superb scientist but also as a warm, supportive and highly collaborative colleague, Mike will be greatly missed. Our thoughts go out to his wife Jane and sons Alex and Patrick."

Michael Wakelam had over twenty years research experience in the area of cell signalling and communication; a major focus of his research was upon the use and development of advanced lipidomics methodologies in determining the functions of individual lipid molecular species in the regulation of signalling pathways in normal and cancer cells and in inflammatory responses.

Michael Wakelam is survived by his wife Jane and their two sons Alex and Patrick.

For more information or interviews, please contact:Hasan Salim Patel, Communications Manager (Arts, Law and Social Sciences) or contact the press office out of hours on +44 (0)7789 921 165.

The University of Birmingham is ranked amongst the worlds top 100 institutions. Its work brings people from across the world to Birmingham, including researchers, teachers and more than 6,500 international students from over 150 countries.

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Former University of Birmingham Professor Michael Wakelam dies after suspected coronavirus infection - University of Birmingham

Biochemistry

To divide or not to divide? The mother cell may decide – CU Boulder Today

When do cells decide to divide? For 40 years, the textbook answer has been that this decision occurs in the first phase of a cells existence right after a mother cell divides to become daughter cells.

But researchers at CU Boulder have found that its actually the mother cell that determines if its daughter cells will divide. The finding, explained in a new study out today in Science, sheds new light on the cell cycle using modern imaging technologies, and could have implications for cancer drug therapy treatments.

We see something different than what's in the textbooks, said Sabrina Spencer, senior author of the paper and assistant professor of biochemistry.

Cells choose to divide based on the amount of mitogens, or growth factors, they sense in their environment. The availability of mitogens drives the signal to proliferate: duplicate cellular contents and divide into two daughter cells. This is all part of the cell cycle.

Cancer cells can enter the cell cycle even if growth factors aren't there, said Spencer. Thats part of why they proliferate so much the cell cycle becomes dysregulated and growth continues unchecked.

Sabrina Spencer points to a specific cell in an image on a screen, which contains a population of cells expressing fluorescent reporters. (Credit: BioFrontiers Institute, CU Boulder)

Better understanding of why and when cells choose to proliferate, could help scientists tailor or expand the timing of cancer drug therapies.

In their experiments, the researchers found that rather than daughter cells deciding on their own whether to divide, they committed to another cell cycle or not immediately after division of the mother cell. This implies the decision was made in the previous cell cycle, because the daughter cells were already born on one path or another, according to Spencer.

That got us thinking that maybe all the sensing of the environment is actually happening in the mother cell cycle, said Spencer.

Previous textbook experiments had to first remove all growth factors in order to synchronize the cells cycling, which perturbs cell cycle behavior. But this new research used time lapse microscopy and cell tracking technologies, which allowed the scientists to film cells doing their own thing, on their own time.Doing the experiment this way led to very different results, said Spencer.

The researchers tracked thousands of cells across 48 hours, using computational cell tracking which can track the same cell through hundreds of sequential images.

Even 10 years ago, very few labs could track cells even for a couple of hours, said Spencer.

A mother cell divides into two daughter cells, and the daughter cell is trying to decide if it is going to divide again. The answer is that it depends on the mother cells history of growth factor signaling. (Credit: Sabrina Spencer)

When do cells care about mitogen (growth factors)? In the textbook model, researchers found that the daughter cell cared in the first phase of the cell cycle about mitogen. From this new research, CU Boulder scientists found that cells are actually sensing mitogen during the entirely of the mother cell cycle. (Credit: Sabrina Spencer)

Their next question was: when in the mother cell cycle does a cell decide if its daughter cells will divide?

To answer this, the researchers removed and replaced the growth factors which give the signal for the cell to divide for several hours at different phases in the mother cell cycle.

They found that the longer these growth factors were removed in the mother cell, the less likely the daughter cells were to divide. If the growth factors were removed for more than nine hours, none of the daughter cells ended up dividing.

We found that no matter when you blocked this signaling, cells can sense it, said Mingwei Min, first author and postdoctoral researcher in the Department of Biochemistry and BioFrontiers Institute. And not only can they sense it, they can remember that information for many hours, all the way through to the daughter cell cycle.

If cells are continually sensing growth factor signaling as this new paper found instead of only in the first phase of the daughter cycle, cancer drugs may have a longer window than previously believed to provide therapeutic effects.

But how are cells remembering the availability of growth factors? The key lies in a protein known as Cyclin D.

Normally, Cyclin D rises up in the second half of the cell cycle in the mother cell. But when growth factors were removed and replaced in the experiment, there was less Cyclin D at the end of the mother cell cycle, the study found.

And without as much Cyclin D, the daughter cells have less of the thing they need to be able to divide.

The fact that cells can store memory or integrate past history of growth factor availability is a new finding, said Spencer. The combination of fluorescent sensor design, long-term time-lapse microscopy, and cell tracking is really our forte that enabled this discovery.

Additional authors on this paper include Yao Rong and Chengzhe Tian of the Department of Biochemistry and the BioFrontiers Institute at CU Boulder.

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To divide or not to divide? The mother cell may decide - CU Boulder Today

Biochemistry

Artificial proteins that function as molecular logic gates – Tech Explorist

Scientists at the University of Washington School of Medicine have devised artificial proteins that can regulate gene expression inside human T-cells. Whats interesting, these proteins can function as molecular logic gates, tools are used to program the behavior of more complex systems.

Senior author David Baker, professor of biochemistry at the UW School of Medicine and director of the Institute for Protein Design, said,Bioengineers have made logic gates out of DNA, RNA and modified natural proteins before, but these are far from ideal. Our logic gates built from de novo designed proteins are more modular and versatile, and can be used in a wide range of biomedical applications.

Whether electronic or biological, logic gates sense and respond to signals in predetermined ways. One of the simplest is the AND gate; it produces output only when one input AND another are present.

For example, when typing on a keyboard, pressing the Shift key AND the A key produces an uppercase letter A. Logic gates made from biological parts aim to bring this level of control into bioengineered systems.

With the right gates operating inside living cells, inputs such as the presence of two different moleculesor one and not the othercan cause a cell to produce a specific output, such as activating or suppressing a gene.

Lead author Zibo Chen, a recent UW graduate student, said,The whole Apollo 11 Guidance Computer was built from electronic NOR gates. We succeeded in making protein-based NOR gates. They are not as complicated as NASAs guidance computers, but are a key step toward programming complex biological circuits from scratch.

Enlisting a patients immune in the battle against cancer growth has worked for specific types of the disease. In any case, focusing on strong tumors with this so-called CAR-T cell therapy approach has demonstrated challenging.

Scientists think part of the reason has to do with T cell exhaustion. Genetically altered T cells can fight for only so long before they stop working. There may be a way around this. With protein logic gates that respond to exhaustion signals, the team from UW Medicine hopes to prolong the activity of CAR T cells.

Chen said,Longer-lived T cells that are better programmed for each patient would mean more effective personalized medicine.

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Artificial proteins that function as molecular logic gates - Tech Explorist

Biochemistry

Letter to the Editor: Let there be music – Mount Desert Islander

To the Editor:

All acrossthe world, people are turning to music to help them cope and connect with others during the COVID-19 pandemic. First, we saw a plethora of handwashing songs and parodies. Next came the viral videos of people in Italy singing to each other from their balconies. The Facebook group, Quarantine Karaoke, has over 400,000 followers. Musicians are posting live concerts from home and choirs are sharing virtual group songs.

So many of us, unable to connect with each other in physical space, are doing so through music. It makes sense. Coronavirus fears have us feeling anxious, isolated and perhaps even depressed. We seem to intrinsically know that music can help us, in concrete and specific ways, withall ofthese feelings.

Making music encourages group cohesion and bonding. To music with others, people need to work together in a cooperative, synchronized manner. Research shows that when we make music together, people feel more bonded, more trusting and may even start tosynchronizeheartbeats.

Music also has a direct impact on our physiology and biochemistry. Making music reduces levels of the stress hormone cortisol and modulates levels of dopamine and serotonin, all which help improve mood.

One thing that excites me about the musical explosion happening right now is that music is being made byeveryone. Not just the professionals, but everyone. This is the way that music once was. Music was shared around the piano, in the legion hall, across the fire and on the front porch. Singing once was a part of everyday life and now, perhaps it is again.

So please, keep the music going. And when this current crisis passes, remember how important music was in helping us get through this. Remember it the next time your local school system wants to cut music programs from the budget, or community arts organizations come asking for donations. Professional musicians, music therapists, teachers, and community music groups are being financially devastated by the loss of paid work. Yet, the music goes on. Because what else can we do? We are human beings, we will persevere, and there will be music.

Carla Tanguay

Mount Desert

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Letter to the Editor: Let there be music - Mount Desert Islander

Genetics

Genes and genetics explained – Better Health Channel

Your chromosomes contain the blueprint for your body your genes. Almost every cell in the human body contains a copy of this blueprint, mostly stored inside a special sac within the cell called the nucleus. Chromosomes are long strands of a chemical substance called deoxyribonucleic acid (DNA).

A DNA strand looks like a twisted ladder. The genes are like a series of letters strung along each edge. These letters are used like an instruction book. The letter sequence of each gene contains information on building specific molecules (such as proteins or hormones both essential to the growth and maintenance of the human body).

Although every cell has two copies of each gene, each cell needs only certain genes to be switched on in order to perform its particular functions. The unnecessary genes are switched off.

Sometimes, a gene contains a change that disrupts the genes instructions. A change in a gene can occur spontaneously (no known cause) or it can be inherited. Changes in the coding that makes a gene function can lead to a wide range of conditions.

Humans typically have 46 chromosomes in each cell of their body, made up of 22 paired chromosomes and two sex chromosomes. These chromosomes contain between 20,000 and 25,000 genes. New genes are being identified all the time.

The paired chromosomes are numbered from 1 to 22 according to size. (Chromosome number 1 is the biggest.) These non-sex chromosomes are called autosomes.

People usually have two copies of each chromosome. One copy is inherited from their mother (via the egg) and the other from their father (via the sperm). A sperm and an egg each contain one set of 23 chromosomes. When the sperm fertilises the egg, two copies of each chromosome are present (and therefore two copies of each gene), and so an embryo forms.

The chromosomes that determine the sex of the baby (X and Y chromosomes) are called sex chromosomes. Typically, the mothers egg contributes an X chromosome, and the fathers sperm provides either an X or a Y chromosome. A person with an XX pairing of sex chromosomes is biologically female, while a person with an XY pairing is biologically male.

As well as determining sex, the sex chromosomes carry genes that control other body functions. There are many genes located on the X chromosome, but only a few on the Y chromosome. Genes that are on the X chromosome are said to be X-linked. Genes that are on the Y chromosome are said to be Y-linked.

Parents pass on traits or characteristics, such as eye colour and blood type, to their children through their genes. Some health conditions and diseases can be passed on genetically too.

Sometimes, one characteristic has many different forms. For example, blood type can be A, B, AB or O. Changes (or variations) in the gene for that characteristic cause these different forms.

Each variation of a gene is called an allele (pronounced AL-eel). These two copies of the gene contained in your chromosomes influence the way your cells work.

The two alleles in a gene pair are inherited, one from each parent. Alleles interact with each other in different ways. These are called inheritance patterns. Examples of inheritance patterns include:

The most common interaction between alleles is a dominant/recessive relationship. An allele of a gene is said to be dominant when it effectively overrules the other (recessive) allele.

Eye colour and blood groups are both examples of dominant/recessive gene relationships.

The allele for brown eyes (B) is dominant over the allele for blue eyes (b). So, if you have one allele for brown eyes and one allele for blue eyes (Bb), your eyes will be brown. (This is also the case if you have two alleles for brown eyes, BB.) However, if both alleles are for the recessive trait (in this case, blue eyes, bb) you will inherit blue eyes.

For blood groups, the alleles are A, B and O. The A allele is dominant over the O allele. So, a person with one A allele and one O allele (AO) has blood group A. Blood group A is said to have a dominant inheritance pattern over blood group O.

If a mother has the alleles A and O (AO), her blood group will be A because the A allele is dominant. If the father has two O alleles (OO), he has the blood group O. For each child that couple has, each parent will pass on one or the other of those two alleles. This is shown in figure 1. This means that each one of their children has a 50 per cent chance of having blood group A (AO) and a 50 per cent chance of having blood group O (OO), depending on which alleles they inherit.

Figure 1 -Fathers blood group(OO, group O)

AO

(group A)

AO

(group A)

The combination of alleles that you have is called your genotype (e.g. AO). The observable trait that you have in this case blood group A is your phenotype.

If a person has one changed (q) and one unchanged (Q) copy of a gene, and they do not have the condition associated with that gene change, they are said to be a carrier of that condition. The condition is said to have a recessive inheritance pattern it is not expressed if there is a functioning copy of the gene present.

If two people are carriers (Qq) of the same recessive genetic condition, there is a 25 per cent (or one in four) chance that they may both pass the changed copy of the gene on to their child (qq, see figure 2.) As the child then does not have an unchanged, fully functioning copy of the gene, they will develop the condition.

There is also a 25 per cent chance that each child of the same parents may be unaffected, and a 50 per cent chance that they may be carriers of the condition.

Figure 2 -Father (carrier)

QQ(unaffected)

Qq(carrier)

Recessive genetic conditions are more likely to arise if two parents are related, although they are still quite rare. Examples of autosomal recessive genetic conditions include cystic fibrosisand phenylketonuria (PKU).

Not all genes are either dominant or recessive. Sometimes, each allele in the gene pair carries equal weight and will show up as a combined physical characteristic. For example, with blood groups, the A allele is as strong as the B allele. The A and B alleles are said to be co-dominant. Someone with one copy of A and one copy of B has the blood group AB.

The inheritance pattern of children from parents with blood groups B (BO) and A (AO) is given in figure 3.

Each one of their children has a 25 per cent chance of having blood group AB (AB), A (AO), B (BO) or O (OO), depending on which alleles they inherit.

Figure 3 -Fathers blood group -(group B)

AB

(group AB)

AO

(group A)

A cell reproduces by copying its genetic information then splitting in half, forming two individual cells. Occasionally, an alteration occurs in this process, causing a genetic change.

When this happens, chemical messages sent to the cell may also change. This spontaneous genetic change can cause issues in the way the persons body functions.

Sperm and egg cells are known as germ cells. Every other cell in the body is called somatic (meaning relating to the body).

If a change in a gene happens spontaneously in a persons somatic cells, they may develop the condition related to that gene change, but wont pass it on to their children. For example, skin cancer can be caused by a build-up of spontaneous changes in genes in the skin cells caused by damage from UV radiation. Other causes of spontaneous gene changes in somatic cells include exposure to chemicals and cigarette smoke. However, if the gene change occurs in a persons germ cells, that persons children have a chance of inheriting the altered gene.

About half of the Australian population will be affected at some point in their life by a condition that is at least partly genetic in origin. Scientists estimate that more than 10,000 conditions are caused by changes in single genes.

The three ways in which genetic conditions can arise are:

Having a genetic susceptibility to a condition does not mean that you will develop the condition. It means that you are at increased risk of developing it if certain environmental factors, such as diet or exposure to chemicals, trigger its onset. If these triggering conditions do not occur, you may never develop the condition.

Some types of cancer are triggered by environmental factors such as diet and lifestyle. For example, prolonged exposure to the sun is linked to melanoma. Avoiding such triggers means significantly reducing the risks.

Related parents are more likely than unrelated parents to have children with health problems or genetic conditions. This is because the two parents share one or more common ancestors and so carry some of the same genetic material. If both partners carry the same inherited gene change, their children are more likely to have a genetic condition.

Related couples are recommended to seek advice from a clinical genetics service if their family has a history of a genetic condition.

If a family member has been diagnosed with a genetic condition, or if you know that a genetic condition runs in your family, it can be helpful to speak to a genetic counsellor.Genetic counsellors are health professionals qualified in both counselling and genetics. As well as providing emotional support, they can help you to understand a genetic condition and what causes it, how it is inherited (if it is), and what a diagnosis means for you and your family.

Genetic counsellors are trained to provide information and support that is sensitive to your family circumstances, culture and beliefs.

Genetic services in Victoria provide genetic consultation, counselling, testing and diagnostic services for children, adults, families, and prospective parents. They also provide referral to community resources, including support groups, if needed.

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Genes and genetics explained - Better Health Channel

Genetics

Unlocking the Genetics of Autism Spectrum Disorder – TMC News – Texas Medical Center News

Cason McKee was diagnosed with autism when he was 3 years old.

Both of his parents worked with autistic children in the Texas school system, so they saw it coming.

Early on, when we first started noticing a difference in him, he was a typical 18-month old, said Shannon McKee, Casons mother. But between 18 months and 2 years, he started to lose his language and his interest in language. It happened gradually.

At Casons second birthday party, McKee realized that her son wasnt engaging with his friends. He doesnt even carethat his friends are here, she thought.

A light bulb went off in my head, she said.

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Casons diagnosis of ASD (autism spectrum disorder) unleashed a host of questions for Shannon and Michael McKee, who began searching for the best therapies and pro- grams for their son. Once they got a grasp on their own situation, it became increasingly important for them to help other families who had received an ASD diagnosis. One of the best ways to do that, they realized, was to participate in research that could unlock some of the genetic mysteries surrounding the disorder, which affects communication and social interaction.

In 2016, the McKees were among the first families to enroll in the national SPARK for Autism study, a landmark project that aims to accelerate the pace of autism research and answer myriad genetic questions about the disorder.

More specifically, that 50,000 actually refers to triosto an individual with autism and both biological parents, Kochel explained. To date, SPARK has enrolled close to 23,000 families in a database that allows investigators to search for and identify genetic trends and similarities.

Its open to everyone, Kochel said. Basically, families enroll online. It takes about 20 to 30 minutes. They have the option to consent to providing a genetic sample.

For families who consent, a saliva kit is mailed to their home, with instructions for its use and return. Families also consent to whether or not they want to see the results of a genetic finding, if one is made.

Today, there are over 1,000 genes that have been associated with autism, and part of what SPARK is doing is to help identify more genetic causes of autism, Kochel said. We do know that autism is largely caused by genetic factors, yet when you go to get a clinical genetic test today, only a fraction of kids come back with a finding. But we still believe that theres more there, genetically, and were look- ing for it. Its just going to take some time.

SPARK hopes to identify small groups of people diagnosed with ASD who have the same genetic differencesdifferences researchers didnt know about before.

The study is a way for us to help identify those people and get them together and think about what would be valuable to learn about this particular group, Kochel said. We call it a genet- ics first approach. We might then have next-step studies that would convene those folks and say: You all have the same genetic difference. Can we work with you to see what else is similar with you? It might be certain medical conditions or other psychiatric diagnoses, things like that.

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Unlocking the Genetics of Autism Spectrum Disorder - TMC News - Texas Medical Center News