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The number of people with myopia, aka short-sightedness (difficulty seeing objects in the distance), has increased dramatically in recent years in various regions of the world.

For example, in many cities in China more than 90% of university students are living with myopia. In pure numbers this is one of the largest epidemics humanity has even seen, far greater than the obesity epidemic.

The myopia boom was first noted in 1980s in the cities of East Asian countries such as Korea, Taiwan and Singapore. The cities of China followed soon afterwards, and a similar trend is being noted in Europe.

For most people, myopia is merely an inconvenience requiring correction with glasses, contact lenses or refractive surgery.

Notably, myopia is associated with an increased risk of blindness from retinal detachment, glaucoma and myopic macular degeneration. Risk of blindness increased with worsening severity of myopia and this is a major public health concern.

Researchers and parents of children developing myopia have looked for explanations and the latest suspect is the use of personal electronic devices.

But the myopia epidemic in Asia preceded the release of smart phones by many years (the first iPhone was released in 2007).

New technologies televisions in the 1960s, computers in the 1980s, laptops in the 1990s, and currently smartphones and tablets have all been blamed for causing myopia.

As far back as the 1600s, the German astronomer Johannes Kepler, who first identified concave lenses could correct myopia, is said to have attributed his short-sightedness to all his years of intense study of astronomical tables and so forth. But he might well have blamed Gutenbergs printed books (the latest technology at the time).

So what have researchers found so far?

Having parents with myopia increases a childs risk for myopia. But children can mimic their parents potentially myopia-inducing lifestyle such as near work that requires focusing on close-up objects and studying a lot inside as well as inherit their genes.

After years of debate over whether myopia is due to genetic or environmental factors (with reading and screen use suggested), we now know it is an interaction of both genes and environment.

Myopia does not result from a single gene defect; more than 160 interacting genes contribute to the risk of myopia.

What are the environmental triggers that would explain an epidemic?

Many studies have looked at possible risk factors but only a few have come out consistently around the world: near work, years in education and lack of time spent outdoors in daylight.

Untangling the interactions is a challenge because these factors are interrelated, with children who study more spending less time outdoors.

Despite decades of parents warning children, no study has shown that sitting too close to the television causes myopia.

In the past two years, five papers (1, 2, 3, 4 and 5) have looked at myopia and personal electronic devices. Some, but not all, have found an association between the amount of screen use and myopia. But this does not mean screen time itself causes myopia.

Instead of reading from books, children are reading more from screens and changing the nature of their near work. Rising rates of myopia are related to near work behaviours, rather than screen use in particular.

Children are also changing the way they use screens. The simple idea that screen use occurs indoors was completely overthrown by the Pokmon Go craze, as gamers headed outdoors with their smartphones in search of virtual treats.

In addition, we now have children using virtual reality goggles to play games or even study.

Australian guidelines recommend:

There is no rigorous scientific basis for these time limits in relation to visual health. But a recent study showed a large percentage of children exceeded these time limits.

Potential health issues relating to screen time are diverse. Sleep, posture, level of physical activity and behavioural issues are additional reasons for concern.

Unlike previous generations, most children today experience a lot of screen time. But we dont have consistent findings for use of television, computers, tablets, smart phones or even virtual reality goggles themselves as the main cause of myopia.

We clearly need some very large, well-conducted studies, where we directly measure the use of screen time across a wide range of health issues from infancy to young adulthood.

Some cities in China are trialling scheduled time spent outdoors at school to see if it prevents or decreases the progression of myopia in children.

In Australia, we need tailored messages to encourage kids to spend more time outdoors if they are inside reading or using screens too much.

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Short-sightedness in kids was rising long before they took to the screens - The Conversation AU

As Jesus passed by he saw a man blind from birth. His disciples asked him, "Rabbi, who sinned, this man or his parents, that he was born blind?" Jesus answered, "Neither he nor his parents sinned; it is so that the works of God might be made visible through him. We have to do the works of the one who sent me while it is day. Night is coming when no one can work. While I am in the world, I am the light of the world." When he had said this, he spat on the ground and made clay with the saliva, and smeared the clay on his eyes, and said to him, "Go wash in the Pool of Siloam" which means Sent. So he went and washed, and came back able to see. His neighbors and those who had seen him earlier as a beggar said, "Isn't this the one who used to sit and beg?" Some said, "It is," but others said, "No, he just looks like him." He said, "I am." So they said to him, "How were your eyes opened?" He replied, "The man called Jesus made clay and anointed my eyes and told me, 'Go to Siloam and wash.' So I went there and washed and was able to see." And they said to him, "Where is he?" He said, "I don't know." John 9: 1-1

Be on guard for the times when we are too confident about who God is.

Right before this story in Johns Gospel, Jesus was rejected by the Pharisees in the temple. He is unwanted and excluded.

And so Jesus approaches the one who is unwanted, excluded, and marginalized the man who was born blind.

The poor seek and find refuge with the other poor; the excluded with the excluded.

We see that the disciples are talking about the blind man, but they do not attempt to enter into a relationship with him. He is a nobody without a voice. No one seems to care about his hopes and needs.

People with disabilities are still sometimes treated as nobodies or as second-class citizens.

The disciples ask the question that every culture asks: Why is someone born with a disability?

Even today, the questions remain. Why us? What have we done? Why is God punishing us with illnesses and disabilities? What have I done to God that he would send me a catastrophe like this?

We often feel if people have success, wealth, and good families this is a sign they are blessed by God. Failure, broken relationships and bad health are signs of something wrong something bad in our lives.

But Jesus says: Neither this man nor his parents sinned; he was born blind so that Gods works might be revealed in him.

Each of us is born so Gods work may be accomplished in us. Each one of us has been created by God and for God. Each one of us has a vulnerable heart and yearns to love and be loved and valued. Each one of us has a mission. Disabled or not.

Jesus reveals this man born blind was made for love as well as me and you!

St. Paul confirms that, reminding us people with disabilities are chosen by God too.

In the first letter to the Corinthians he says: God has chosen the foolish of the world to shame the so-called wise. God has chosen what is weak in the world to shame strong. God has chosen what is low and despised, people who are nobodies, in order to reduce to nobodies those who are somebodies, so no one might boast in the presence of God.

That is very similar to the Copernican Revolution, which moved the center of the universe from Earth to the Sun.

We used to say we should do good for the poor, disabled, in need.

But it is they who are poor, disabled or ill who are doing good for us.

The people we are healing all in fact healing us.

They call us to love, they are awakening in us what is most precious: compassion.

Jesus calls himself the Light of the World in the context of the mans blindness. He spit and mixed his saliva with clay on purpose. This had great meaning, for when God made Adam, he made him of spit. Jesus is acting like God of the Old Testament: He gives the blind man new eyes and sight.

He is not just the Messiah, or just a prophet He is God! He is doing it on the Sabbath.

The Pharisees fail to realize this because of their tunnel vision; they call Jesus a sinner, and call the blind man a sinner, too that he was born in sin, which caused his blindness. But they are so wrong.

Jesus is teaching us the difference between true sight and true blindness. Jesus physical actions, miracles and manifestations are meant to point us toward the ones that are more invisible.

It is far better to be disabled, to be blind and ill and to live in the light of Gods mercy, love and tenderness.

On the Sabbath day, which is Sunday for most of us, consider visiting the sick and shut-in. Stop by the nursing home or hospital. Perhaps make time for someone you know, maybe even a friend, relative or neighbor who is disabled. The sick and suffering need you, but as the Gospel story tells us, we will receive blessings and graces from the least likely of places.

Father Mateusz Rudzik is a 32-year-old adventure-seeker, skateboarder, sky diver, rock climber, and Catholic priest. He is the pastor of St. Vincent de Paul Church in Tallassee and St. Joseph Church and School in Tuskegee.

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We are each created by and for God - Tallassee Tribune

By Chris LangeJanuary 9, 2020 12:00 pm

Applied Genetic Technologies Corp. (NASDAQ: AGTC) shares jumped by more than 50% on Thursday after the firm announced positive interim data from its midstage trial in X-linked retinitis pigmentosa (XLRP).

The study demonstrated that patients treated centrally with its product candidate demonstrated durable improvement in visual function six months after dosing.

The results reinforced the promising efficacy and safety results reported in September 2019 and will help to design the XLRP pivotal trial planned to be initiated by the end of 2020. The company also remains on track to report interim six-month data from the dose escalation cohorts of both of its ongoing trials in achromatopsia later this month.

At the six-month mark for the same nine centrally dosed patients:

Sue Washer, president and CEO of AGTC, commented:

These promising results further demonstrate that our XLRP candidate has tremendous potential to provide meaningful benefit to XLRP patients who today have no treatment options. The positive results observed to date give us confidence that the data as a whole will support advancement of our XLRP clinical program to a pivotal trial in 2020.

Shares were last seen up about 51% at $6.30, in a 52-week range of $2.52 to $7.12. The consensus price target is $12.42.

By Chris Lange

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How This Eye Study Is Making Waves - 24/7 Wall St.

Researchers at the University of New Hampshire have reported the first structural model for a key enzyme, and its activating protein, that can play a role in some genetically inherited eye diseases like retinitis pigmentosa and night blindness.

There has been substantial research on the biochemical pathway involving this enzyme, known as PDE6, but defining atomic-level models is important for locating PDE6 mutations in order to understand why they cause disease and how we can develop new therapeutic interventions to manage retinal diseases, said Rick Cote, director of Center of Integrated Biomedical and Bioengineering Research and principal investigator on the study.

Vision starts in the photoreceptor cells of the retina which contains rods, responsible for low light vision, and cones, which are active in brighter light and capable of color vision. When light is absorbed by the rods and cones, it triggers a pathway which activates the enzyme phosphodiesterase 6, or PDE6. This generates a nerve impulse to the brain that ultimately results in visual perception. Some genetically inherited eye diseases are caused by mutations to PDE6, or its activating protein, transducin, that can lead to disruptions of normal vision or even total blindness.

In the study, researchers reported how they were able to use chemical cross-linking combined with mass spectrometric analysis to resolve the structure of PDE6 in its nonactivated and transducin-activated states. This approach permitted visualization of flexible regions of individual PDE6 catalytic and inhibitory subunits that were poorly resolved in previous work as well as the overall molecular architecture of the activated protein complex.

Determining the structure of these visual signaling proteins has always been a challenge because of their complexity, said Michael Irwin, doctoral student in biochemistry and lead author. Having detailed structural information about how PDE6 is activated by transducin will help us understand the molecular causes of visual disorders and blinding diseases resulting from mutations in these proteins.

Current medical treatment for such genetically inherited retinal diseases may include gene therapy or drugs meant to inhibit the disease process. However, they are not always successful in restoring the balance of PDE6 and preventing blindness. Scientists believe that knowing the molecular structures of these visual signaling proteins and how they interact with each other can offer clues for the development of new drugs to both restore vision and prevent blindness.

Reference

Irwin et al. (2019) The molecular architecture of photoreceptor phosphodiesterase 6 (PDE6) with activated G protein elucidates the mechanism of visual excitation. Journal of Biological Chemistry. DOI: https://doi.org/10.1074/jbc.RA119.011002

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Protein Structure Associated with Inherited Retinal Diseases is Solved - Technology Networks

Catherine Payvandi, Community Music Published 2:23 p.m. CT Jan. 8, 2020

Josh Reynolds (Prince Yamadori), A. Scott Parry (Stage Director), Yulia Lysenko (Cio-Cio San), practice for CROpera's production of "Madama Butterfly"(Photo: Contributed photo)

There is little doubt that Giacomo Puccinis operas are among the worlds most loved. As the leading Italian opera composer of his generation, four of his twelve operas laBoheme, Tosca, Turnadot and Madama Butterfly are the most performed operas worldwide.

Cedar Rapids Opera Theatre will perform Puccinis Madama Butterfly January 17 at 7:30 pm and again January 19 at 2:30 pm. Free pre-opera talks will begin one hour before performance in the Encore Lounge of the Paramount Theatre, 123 3rd Ave. SE in Cedar Rapids. The opera is sung in Italian with English supertitles.

Part of Puccini's genius derives from his remarkable ability to depict the inner lives and feelings of his tragic heroines Mimi, Tosca, Turandot and Cio Cio San all are unforgettable heroines whose music accesses the soul and whose stories break your heart. But in Madama Butterfly, the intensity of storytelling, the gorgeous lyricism of the music, and sharpness of character are especially brought to life as we witness the incredible transformation of Puccinis Cio Cio San from an innocent young geisha into a towering image of strength.

The arc of her character development informs dramatic action her transformation from a young innocent to a bold and courageous woman who achieves mythic relevance is set forth against a backdrop of darkness and orchestral beauty. While the core of the opera is about conflict conflict between cultures, between idealism and reality the dramatic center of the opera has a universal message that speaks to evena modern audience.

Yulia Lysenko (Cio-Cio San) and Jeremy Brauner (Pinkerton), rehearse for CROpera's production of "Madama Butterfly."(Photo: Contributed photo)

Cio Cio San is a 15-year-old girl who falls in love with a man who promises her the world but who inevitably betrays her. The process of the opera is the unfolding of her character. She is a nave young geisha, who struggles to sustain her dream of happiness, but her innocence and willful blindness to the truth prevent her from achieving lasting joy. However, it is that blindness that prompts her to heroic action and which leads her to courageously choose death rather than accept a future tainted with dishonor.

While traditional opera commentary tends to focus on the operas historical context, and the clash between East and West the Cedar Rapids Opera Theatre production embraces more universal applications as it illuminates how idealism is crushed by what it most aspires to and demonstrates through dramatic counterpoint how irresponsible decisions have tragic consequences.

The opera is not just a story about the past or an exotic period piece. Instead, what emerges is the unfolding of a pattern of exploitation and selfdeception that renders universal relevance. And as such, that theme speaks to each of us in our own world.

The story of Cio Cio San, Pucinnis imaginary geisha, engenders an empathetic impulse we all feel. The beauty of Pucinnis dramatic hand is that while entering into the perspective of Cio Cio San, we recognize the doomed outcome shadowing her romantic hopes. She is like a butterfly beautiful and fragile with her dream of love but one who is ultimately pierced to the heart by betrayal.

Catherine Payvandi is a member of the Cedar Rapids Opera Theatre board of directors and is also an active community volunteer at Orchestra Iowa.She received her doctorate in English literature form the University of Iowa and has held faculty positions at Mt. Mercy University and Cornell College teaching writing and literature.

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Madama Butterfly offers up universal themes and tragedy - Iowa City Press-Citizen

TheJedi are a groupof legendary beings that can the Force. They can move things with their minds, they use laser beam swords, and theyre not supposed to give in to many strong emotions. Theyre put on this pedestal because theyre on the Light Side, but theyoftenhad their faults. While theStar Warsmovies dont show a lot of the bad side of the Jedi,The Clone Warscertainly did. And one of the most prominent displays of wrongdoing on the Jedis part was the falseaccusations against Ahsoka Tano.

Ahsoka, Anakin Skywalkers Padawan, was helping with the investigation into a bombing at the Jedi temple. She and Anakin had a lead and arrested a woman connected to the bomb. However, when Ahsoka went to visit her, to see if shed talk, an unseen Force-user strangled the woman. This was a way to frame Ahsoka since it looked like she Force-strangled her on video.

Afterward, the Republic militaryandthe Jedi didnt take Ahsokas word of innocence, even with a lack of evidence. All they had was that video, and Ahsoka did have an alibi for the actual bombing. And digging would have proven that she didnt know the woman beforehand. But thats the thing. The Jedi were wildly blind to the actual evils of the Republic and just handed Ahsoka over to the military for a trial. A trial that would have killed the Padawan if they found her guilty. No one on the Council outwardly stood up for her or the fact that they should have been able to sense whether she was lying. Not to mention the fact that Ahsoka showed no other signs of treason against the Jedi before. This blindness is partly why Palpatine was able to destroy them.

In Ahsokas first trial with the Jedi, Anakin yells, Youve already made your decision This meeting is just a formality! when Yoda is about to read their verdict. And its true. Before they even heard her speak, they had decided to ban her from the Order. This allowed the Republic to take over the trial, with Ahsoka now a non-Jedi, which Adjutant General Tarkin suggested.

The publics opinion on the Jedi was already changing, and then the bombing happened. They wanted a quick and lowkey investigation, so the public wasnt upset even more. Instead of standing by Ahsoka, they handed her over to a public trial that was out to kill her in order to relinquish the Jedi name from the bombing.

The bombing negatively swayed the publics opinion, but it also comes to light how much they disapprove of their involvement in the war. The Jedi were supposed to be peacekeepers, but instead, they aligned themselves to one sideandfought in the war. Its made clear in Season 3, Episode 10 Heroes on Both Sides, that the war has good people in the Republic and the Separatists. The Jedis involvement just made it seem like the Republic was the way to go.

When Anakin figures out Barriss Offee is the one that set up the bombing and framed Ahsoka, she makes some bold statements. Her remarks leave a sour note because they have some truth to them. She says that the Jedi were the ones responsible for this war and that theyve lost [their] way so much that theyre the villains. My attack on the temple was an attack onwhat the Jedi have become: an army fighting for the Dark Side.

Thats not the most diplomatic way to make a point. However, it hones in on what the publics feeling and mirrorssimilar disillusionment Anakinhas with the Order at this point and later down the line. Its also whyAhsoka leaves the Order. She says its because she cant trust them or herself, but the trial also showed how much the Jedi had fallen.

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Ahsoka's Choice To Leave The Jedi Exposed What Was Wrong With The Order - Showbiz Cheat Sheet

Nothing in life is stable or secure. One ventures out into the dark to watch the meteors rain across an evening sky. They streak in a most unpredictable fashion, mercurial, disappearing and re-emerging. They slide past the planetary axis. Their illuminations are intimate. There is a realization that the past can never rescue the present.

Watching the intermittent threads of light, one may be abjured to a frail existence. These falling stars in their mysterious showering, solicit the muses or catalyze dreams. We may not attribute our fates to these countless, heavenly fires, but in time, we will surely return to the minute dust from which we came.

What separates man from his fellow creatures is his intellect, his ability to think logically. It is the precise reason why we establish laws of order. Life exists as the product of endless failures and countless mutating engagements under the brow of the sun. Microscopic enablers created the universe of being and made the rhythm of existence complete, yet the lesser beings found themselves at the mercy of progress shifting pollutants. No Eden can exist as a utopia. All that is living is molded by the timeless rhythm of a cellular cosmos. It is the corruptive nature of the ego that has ravaged the garden within. It is the small life that instructs and is ultimately shunned as the planet warms.

One can come to an emotional crossroad when the light of intellect is diminished by ambiguous emotional stirrings of the heart. It may just be that the unexpected, brief illuminations from the heavens frame ones faith and enable one to feel the miraculous and unexpected creative energy of unknowing. The sparks of the synapses flicker through the universe of the soul like falling stars. Love is spawned in the horizon of light. Benevolence is un-prophesiable, yet always valid. Light falls out of the darkness where no law or political advantage can alter its journey.

Blindness often falls upon those that believe they see the world most clearly. Mankind is easily seduced and enslaved by the concept of authority. Millions adhere to dogma and fantical religiosities, rejecting the subtlety of the sublime. In a sense, humanity has forgotten its humaneness. Natural laws in the end usurp authority. It was written in the skies long ago, before men. I stand with my faith as the meteor rain moves through the shrouds of darkness. The spectacle lessens, and I hold my head in my hands pained by the fortissimo off these bewilderments.

I stand up and slowly walk back to the house, open the door and turn away, leaving the lost signatures to the immense night.

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End of the Line: The stars of wonder - Durango Telegraph

Published 12:20pm EST, Thursday, January 9, 2020

When Jared Kushner said, anti-Zionism is anti-Semitism, he was completely accurate.

Anyone who read President Trumps executive order knows it clearly states that it does not diminish or infringe upon the rights protected under any other provision of law, that is, the right to free speech. It does, however, provide a means to address anti-Semitism disguised as anti-Zionism that is destroying free speech on college campuses, where Jewish students and other supporters of Israel have been shouted down, defamed, vilified and physically menaced.

Zionism is the Jewish national movement of self-determination in the land of Israel, where Jews have lived for millennia, even while under occupation by Romans, Muslim Arabs and later Turks. Love of Zion, the biblical term for both the land of Israel and Jerusalem, is embedded in Jewish prayer, ritual, literature and culture.

A Human Rights Watch report found a systematic practice by both the Palestinian Authority and Hamas of arbitrary arrest and torture, and there have been no serious efforts to hold wrongdoers to account or any apparent change in policy or practice of Palestinians against their own people who dare to dissent.

Albert Einstein was a Zionist. Another Nobel laureate in physics, Steven Weinberg, has twice refused an invitation from a UK university because of boycotts against Israel. According to professor Weinberg, ... given the history of the attacks on Israel and the oppressiveness and aggressiveness of other countries in the Middle East and elsewhere, boycotting Israel indicated a moral blindness for which it is hard to find any explanation other than anti-Semitism.

Anti-Zionism is the camouflage worn by 21st century anti-Semitism.

Julia Lutch

Davis, Calif.

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Letter: Anti-Zionism is anti-Semitism - New Haven Register

Tips to help achieve a healthier you in 2020

By Sandra Crews, Health Strategist, UnitedHealthcare of Colorado

Now is the time of year when we typically take inventory of our lives and set new goals. Relationships, finances, careers and health are all important aspects that impact our overall wellbeing. For this New Year, consider making your health a top priority.

According to the recentAmericas Health Rankings Annual Report, the nations obesity rate continues to rise, with one in three adults now experiencing obesity. Colorado has the lowest obesity rate in the nation at 22.9%. The alarming national statistic may have serious health consequences such as diabetes which now impacts approximately 30 million adults and is the No. 1 cause of kidney failure, lower-limb amputations, and adult blindness, according to theCenters for Disease Control and Prevention.

There are many factors that play a role in your health, but one that you can control is making a commitment to start living a healthier lifestyle. Sure, there will be some bumps during your wellbeing journey, but your goal can be achievable and you deserve to reap the benefits.

Consider some helpful tips for achieving a healthier you in 2020.

Stay active

Regular exercise may help you live longer and may reduce your risks for a host of diseases. Try to aim for at least 2.5 hours of moderate aerobic activity a week, but if thats too challenging then start off with 15 minutes here and 15 minutes there. Every little bit counts. To be successful, your fitness program should become a part of your daily life.

Also, check with your health plan and employer to see if they offer wellness incentives. For example, UnitedHealthcaresGym Check-Inprogram enables participating employers to provide employees and their spouses the opportunity to each earn hundreds of dollars a year for visiting a fitness facility 12 days or more per month.

Eat healthier

Sure, its easier said than done, but good nutrition is a vital part of a healthier lifestyle. Experts say the healthiest diets are rich in fruits and vegetables, because these foods are full of healthful nutrients and fiber. Here are three simple tips to eating healthier: Go for more fruits and veggies; choose less meat and fat; and keep an eye on the size of your food portions. Just saying no, to the buffet can do wonders.

Reduce your stress

If youre feeling stressed, its important to unwind and relax by doing something you enjoy. Maybe its watching a movie, reading a book, or volunteering to give you time to recharge. Also, make time to connect with others. Maybe thats friends, family, a faith group or a hobby club. Its important that you dont isolate yourself after a stressful event. Remember, if you cannot get a handle on your stress, talk to your doctor. She or he may recommend a counselor who could help you find other ways to help reduce or manage the unhealthy stress in your life.

Team up with your doctor

Take time today to make an appointment with your doctor for your annual wellness visit and be sure to ask about preventive services such as health screenings and vaccines. Check with your health plan as many preventive services have no additional cost, as long they are delivered by care providers in your plans network. Your doctor will help you create a treatment plan to help manage any chronic conditions, such as asthma, diabetes and high blood pressure.

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Prioritize your health in the New Year - North Forty News

PARK CITY, Utah, Jan. 8, 2020 /PRNewswire/ --ZAND, the #1 natural lozenge brand in health food stores known for herbal-based immune support has announced the launch of the brand's first rapid immunity product, Immune Fast. This breakthrough new supplement delivers clinically supported immune support within two hours1 whenever and wherever you need it: at work, the airport, school, large gatherings, anywhere.

Simply put, ZAND's new Immune Fast producthelps boost your immune function, which is increasingly under stress in the modern world. So, if you're sick and tired of missing work or dragging yourself through the day feeling less than your best, then your immune system could use a boost. And nothing may work faster than Immune Fast.

Fluke or Happy Accident?

Uncovering the remarkable immune-boosting power of Immune Fast with EpiCor was what you might call "a happy accident." Made from yeast through a top-secret fermentation process, EpiCor is a patented ingredient created by Embria Health Sciences that was originally intended for use in agricultural products. But the company noticed that workers who manufactured the yeast cultures seemed to rarely, if ever, take any sick days. Why?

After conducting subsequent clinical studies, scientists were shocked to learn that EpiCor boosted immune cell activity within two hours.1

With that information in hand, scientists and health experts from ZAND took the patented ingredient and combined it with other immune helpers like vitamin C, zinc, echinacea, and elderberry to create convenient, fast-delivery chewable tablets that can do in two hours what other so-called "immunity helpers" can't do.

An Apple a Day But Maybe Better

"We believe people shouldn't have to sacrifice their preference for natural immune support products when they want to be proactive about boosting their immunity or when they feel off," said John D'Alessandro, chief marketing officer at Nutraceutical Corporation. "It is possible to have better-for-you products that are effective, and Zand Immune Fast delivers."

Immune Fast is now available to consumers at natural products stores and on Amazon for an SRP of $8.99 for the on-the-go 15 pack and $15.99 for the 30 pack.

About ZAND

Founded by a doctor of traditional Chinese medicine and a leading expert on dietary supplement regulations, ZAND is no stranger to premium herbal-based supplements. In fact, the company's Herbalozenges are the #1 seller in America.

The company continues to develop new herbal supplements using the best Eastern traditional philosophies combined with the latest scientific advances and produced prepared FDA-registered, state-of-the-art manufacturing facilities.

For more information, visitimmunefast.com and zand.com.

These statements have not been evaluated by theFDA. This product is not intended to diagnose, treat, cure or prevent any disease.

1. World Health Organization (WHO) monographs on selected medicinal plants; Vol. 1; 1999. Results observed with 500 mg dose of EpiCor in clinical study of 12 adults. Individual results may vary. EpiCor is a registered trademark of Embria Health Sciences. See https://www.immunefast.com/epicor/.

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An "On-the-Spot" Immune System Boost... Wherever and Whenever You Need It Most - P&T Community

A new study has revealed that the Siah2 protein is crucial to control Tregs in mice, which can reduce the effectiveness of immunotherapies.

Researchers have identified a new technique to improve the immune systems ability to fight cancer. Using mouse models they demonstrated that the Siah2 protein is essential to control T regulatory cells (Tregs), which can limit the effectiveness of currently used immunotherapies.

The study was conducted at the Sanford Burnham Prebys Medical Discovery Institute, in collaboration with NYU Langones Perlmutter Cancer Center, both US.

While Siah2 is involved in control of activities that govern cancer development, this study offers the first direct evidence for its role in the immune system, namely in anti-tumor immunity, says Dr Zeev Ronai, professor in Sanford Burnham Prebys Tumor Initiation and Maintenance Program and senior author of the study. Our study shows that a PD-1 inhibitor can be used to treat tumors that currently do not respond to this therapy, when administered in mice lacking the Siah2 gene, thereby offering a means to expand the effectiveness of immunotherapy. The findings also provide further justification for our efforts to find a drug that blocks Siah2.

In the study, the scientists used genetically engineered mice that did not produce the Siah2 protein and then introduced BRAF-mutant melanoma, a mutation that occurs in about half of human melanomas. This approach allowed the researchers to study the role of Siah2 in the tumours microenvironment, of which the immune system is a major component. In the absence of the Siah2 gene, the melanoma tumors receded, which contrasted to mice with the Siah2 gene, in which the tumour continued to grow. Giving these mice anti-PD-1 therapy effectively eliminated melanoma that otherwise resisted this therapy, demonstrating a new path to enhance the effectiveness of current immunotherapies.

The scientists discovered that in the Siah2 mutant mice, the tumours were infiltrated by killer but not Treg immune cells, indicating the immune system was more active in clearing the tumours. The lack of the Treg cells was attributed to reduced proliferation and recruitment into the tumour due to the role of Siah2 and its control of cell cycle regulatory proteins.

Ronai explains: In our study, mice lacking the Siah2 gene were able to mount an immune attack against melanoma. Moreover, the effectiveness of Siah2 in immunotherapy was demonstrated for cold tumors those that do not respond to immunotherapy which were effectively eliminated by a PD-1 blockade in Siah2-mutant mice.

The researchers say that their findings offer a new means to make immunotherapies more effective in individuals who do not respond to anti-PD-1 therapy.

The findings were published in Nature Communications.

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Siah2 protein discovered as a regulator of the immune system - Drug Target Review

All life on Earth has evolved to cope with a rotating planet which results in the predictable transition between day and night. The details differ between plants, fungi, bacteria and animals, but the consistent feature is a biological clock that allows the organism to anticipate the change and prepare for it.

In animals, the central clock that keeps track of night and day is in the brain where it receives light from the retina to keep synchronised with the light or dark. But all cells in the body have their own clocks. Because these biological clocks have a cycle that is close to 24 hours they are termed circadian (circa meaning about and dian, meaning day, from the Latin dies).

We now live with cheap, bright, artificial light, shift-work, sleep-deprivation and jet-lag all major challenges to the ancient circadian control mechanisms in our bodies. All these circadian and sleep challenges are associated with disease. But in our latest study, using mice, we discovered that infections at different times of the day cause different severity of disease.

Read more: The ancient clock that rules our lives and determines our health

Surprisingly, we found that the clock ticking in the cells of the immune system was responsible for the change in response to bacterial infection. In particular, specialised cells called macrophages, which are big cells that engulf and kill bacteria.

Macrophages, either growing in a dish or in a mouse, responded differently at different times of the day. And disabling the clock in these cells resulted in super macrophages, which moved faster and ate more bacteria than the normal macrophages.

We found that clockless macrophages protected mice from bacterial infection with many types of bacteria. A closer look at the macrophages revealed that the cells looked different, with a major change in the structural proteins that maintain the cell shape and are needed for cell movement and for eating bacteria. The change in the cells internal architecture, or cytoskeleton, became a focus of our studies.

We discovered that the macrophage circadian clock directly controlled the components of the cytoskeleton. We saw changes in the amount of cytoskeletal protein building blocks, and also in the activity of a master regulator of cytoskeletal change. This master regulator is a protein called RhoA.

RhoA is activated by bacterial contact and drives the macrophage to move and consume bacteria. We found that RhoA was active in the clockless macrophages even when no bacteria were present. When bacteria contacted the normal macrophages RhoA became active, but there was no further change in the clockless macrophages, as the RhoA was already active. So the clockless macrophages were always switched on, and so able to respond to bacterial attack more rapidly.

To find out how the clock was changing the behaviour of macrophages, we turned to the core clock mechanism. This comprises a small group of proteins that change in abundance through time, so allowing the cells to tell the time. We found that one of these clock factors, called BMAL1, was the essential link between the clock and the macrophage behaviour.

One of the major issues facing the modern world is the growing resistance of bacteria to antibiotics. There have been no new classes of antibiotics for 30 years. Bacterial resistance to antibiotics means that we have untreatable infections and face a future where surgery will become riskier.

Read more: What will happen when antibiotics stop working?

Finding new ways to enhance defence against bacteria is a high priority. Discovery of a circuit linking the clock to bacterial defence opens up a new route to reduce our reliance of the limited range of existing antibiotics. It may be possible to enhance natural defences to bacterial infection by targeting the clock.

The operation of the circadian clock can be altered by light exposure, by changing meal times, by genetic variability within human populations and by new drugs capable of regulating this system. One problem with targeting the clock with drugs is that the impact on other systems will be broad and the consequences hard to predict. But short-term intervention to boost immunity to infection may offer benefits, at low cost.

Similarly, reinforcing the circadian rhythm of high-risk people, in hospitals for example, by controlling lighting and meal times may boost immunity and prevent hospital-acquired infections.

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Body clock affects how the immune system works -- new findings - The Conversation UK

BEIJING Yisheng Biopharma Co. Ltd., of Beijing, said it has inked a pact with U.S. biotech Tavotek Biotherapeutics, of Ambler, Pa., to co-develop a combination therapy with Yishengs YS-ON-001/002 and Tavoteks Tavo-301/303, which the companies hope could prove a more efficacious cancer treatment than the popular anti-PD-1/PD-L1 monotherapies.

YS-ON-001 and YS-ON-002 are potent agonists of TLR3, MDA5 and RIG-I pathways. Meanwhile, Tavo-301/303 is a series of novel multispecific antibody-based immuno-oncology assets.

Our approach allows us to develop a combination therapy that can activate the immune system differently from PD-1/PD-L1-based molecules, Yishengs CEO David Shao told BioWorld.

He added that current immune-oncology approaches such as PD-1/PD-L1 antibodies as a single agent achieve only around 20% to 30% response rates in clinical settings.

By combining YS-ON-001/002 with multispecific antibodies like Tavo-301/303 directed against tumors, the two companies hope they can develop a first-in-class immunotherapy with potentially higher response rates.

We may find a very good application of this combination for different types of solid tumor, such as lung cancer, breast cancer and liver cancer, he said, adding that the two drug candidates can create synergy.

Shao also revealed to BioWorld that both companies aim to move this combination approach into clinical development in 2021, potentially in multiple countries, including China and the U.S.

Chinese biotechs have started to look beyond PD-1/PD-L1 antibodies as monotherapies, as the country has approved six of them so far and the craze for them has cooled down.

PD-1/PD-L1 antibodies as monotherapy is the first-generation approach. Right now, people are working on the second generation, such as bispecific antibodies, in order to improve the response rate for different tumor types, he added.

According to Yisheng, YS-ON-001 and YS-ON-002 have demonstrated promising effects in activating the innate and adaptive immune systems and modulating the tumor microenvironment. They can reduce the immunosuppressive effects of tumor microenvironments and enhance antitumor immune responses.

Currently in a phase I trial in China and Singapore, YS-ON-001 has shown a good safety profile to date. It also received orphan drug designations from the FDA for the treatment of pancreatic and liver cancers. The drug candidate can be delivered via intramuscular, subcutaneous or intratumoral injection.

In preclinical studies, YS-ON-001 was found to significantly increase the proportion of natural killer and natural killer T cells in addition to increasing CD4+ and CD8+ T-cell responses. The drug candidate also reduced the number of T regulatory cells and myeloid-derived suppressor cells in some tumor models.

Meanwhile, YS-ON-002 is in the IND-ready stage. It was found to significantly enhance the expression levels of PD-L1 in tumor cells, proving the rationale for combination therapy with PD-1 antibodies.

Yisheng has said it believes that YS-ON-001/002 could prove to be integral immunotherapy components of standard oncology care, joining other therapies such as chemotherapies, targeted therapies and checkpoint inhibitors or emerging immunotherapies for additive or synergistic treatment benefits.

Both compounds were developed using the companys PIKA immunomodulating technology, which augments both innate and adaptive immune responses through the TLR3, RIG-I and MDA5 pathways. Through TLR3, RIG-I and MDA-5 signaling, PIKA technology can enable the prompt production of interferon, cytokines, chemokines and co-stimulatory factors. Producing type I interferon using PIKA administration can facilitate antigen cross-presentation by dendritic cells, while augmenting CD4+ T-cell, CD8+ T-cell and natural killer cell responses. That makes PIKA-based therapeutics suitable for both antiviral and antitumor applications.

Our PIKA technology platform has achieved proof-of-concept results in phase I and phase II trials. It has demonstrated a good result in activating human immune system in clinical trials, Shao said.

He revealed to BioWorld that in the companys immune-oncology pipeline, a third drug candidate is being developed to target human papillomavirus-induced cancer.

What is intriguing is that Yisheng is better known as a vaccine maker, with four known assets in its vaccine pipeline.

Using the same PIKA technology platform, Yisheng has developed hepatitis B vaccine YS-HBV-001 and the PIKA rabies vaccine for accelerated protection against rabies infection.

Its most advanced asset is the YSJA rabies vaccine, which has been marketed already. It is also developing YS-HBV-002 for chronic hepatitis B treatment.

Its new U.S. partner, Tavotek, however, has kept a lower profile, with an undisclosed pipeline. It is known for extensive work on multispecific antibodies and advanced technology platforms with a focus on cancers, autoimmune conditions and infectious diseases.

Its Tavoselect platform, which the company used to develop Tavo-301/303, is designed to offer highly diversified human antibody sequences that can be utilized in different formats, such as multispecific antibodies. It is said to be able to capture and optimize the best candidates rapidly with NGS analyses and AI.

Tavotek also has three technology platforms for biologics, namely the Targeted Biologics Engineering Platform to develop monoclonal and multispecific antibodies against unique targets; the Tavo-Immune Modulator Platform to enable novel synthetic biologic design for auto-immune diseases and chronic viral infections; and the Multicyclic Intracellular Peptide Platform to develop unique multicyclic peptides with great potency targeting intracellular protein-protein interactions.

The partnership with Yisheng is the first that the U.S. biotech has unveiled, and the collaboration could go beyond oncology.

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Yisheng and Tavotek to co-develop combination therapy for cancer - BioWorld Online

Researchers with Rush University Medical Center injected tumors with flu vaccines, even some FDA-approved seasonal flu shots, and found that this attracted immune cells to attack the tumors. In the language of immuno-oncology, it turned cold tumors, which dont cause much of an immune reaction, hot. The research was published in the Proceedings of the National Academy of Sciences.

We wanted to understand how our strong immune responses against pathogens like influenza and their components could improve our much weaker immune response against some tumors, said Andrew Zloza, assistant professor in Rush Medical Colleges Department of Internal Medicine and senior author of the study.

Some immunotherapies against cancer leverage live pathogens, but they havent shown lasting effects in most patients or cancer types. Pulling data from a National Cancer Institute database, the research team found that lung cancer patients who had been hospitalized for a lung infection caused by influenza at the same time lived longer than lung cancer patients who had no flu. They ran experiments and found similar results in mice with tumors and flu lung infections.

However, there are many factors we do not understand about live infections, and this effect does not repeat in tumors where influenza infections do not naturally occur, like skin, Zloza said.

So they worked with an inactivated flu virus, which is basically a flu vaccine. A direct injection of this vaccine into the skin melanoma of the mice caused the tumors to either shrink or grow slower. It appears to increase the proportion of dendritic cells in the tumor, which are immune-stimulating cells. This resulted in an increase in CD8+ T-cells, which recognize and kill cancer cells.

In addition, injecting the vaccine into the skin melanoma tumor on one side of the body also reduced growth of a second skin tumor on the other side of the mouses body that had not been injected. This means that the vaccine, although dosed locally, had a systemic effect.

The researchers also observed similar systemic results in a mouse model of metastatic triple-negative breast cancer where it reduced the primary tumor but also the metastasis of the breast tumor to the lungs.

Based on this result, Zloza said, we hope that in patients, injecting one tumor with an influenza vaccine will lead to immune responses in their other tumors as well. Our successes with a flu vaccine that we created made us wonder if seasonal flu vaccines that are already FDA-approved could be repurposed as treatments for cancer.

He went on to add, Since these have been used in millions of people and have already been shown to be safe, we thought using flu shots to treat cancer could be brought to patients quickly.

And their experiments showed that they did. Additional experiments involved a mouse model called AIR-PDX, where they implanted tumor cells and immune cells from a cancer patient into a mouse that didnt have a functioning immune system of its own. This prevents the mouse from rejecting the implanted cells. They used a human lung tumor and a melanoma metastasis in their AIR-PDX models. What they found was that injecting the flu shot into the patient-derived tumors also caused them to shrink, while the untreated tumors continued to grow.

They also ran experiments using checkpoint inhibitors, a type of immuno-oncology treatment, such as Mercks Keytruda (pembrolizumab). The flu vaccines reduced cancer growth alone whether the tumor was responsive to checkpoint inhibitors or not. And when they combined the flu vaccine with a checkpoint inhibitor, they showed an even greater decrease in tumor growth.

These results propose that eventually both patients who respond and who do not respond to other immunotherapies might benefit from the injection of influenza vaccines into the tumor, and it may increase the small proportion of patients that are now long-term responders to immunotherapies, Zloza said.

The researchers used five different flu shots from the 2017-2018 flu season in their research, and four were effective in fighting tumors.

The next step is to plan clinical trials. Because the flu vaccine is already FDA approved, the study time may be shorter.

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Can a Flu Shot Be Used to Improve Cancer Immunotherapies? - BioSpace

Researchers at the University of Toronto have discovered how a brief disruption to a molecular pathway in the guts of mice before they are born can compromise immunity in adulthood to a common and often deadly intestinal virus.

The researchers found that in utero inhibition of molecular signalling in the lymphotoxin pathway, long known as important in the development of the immune system, prevented a robust antibody response in adult mice to rotavirus. In humans, rotavirus causes an estimated 215,000 deaths annually, mostly in the developing world.

That early disruption limits the ability of the immune system to later trigger and generate production of Immunoglobulin A (IgA) antibodies, the researchers showed. It also interferes with the nature and function of cells in the gut that support the antibody response, called mesenteric lymph node stromal cells.The research was recently published in the journal Science Immunology.

It was surprising that these non-immune stromal cells were so important to the immune response, saysJennifer Gommerman, a professor ofimmunologyin U of Ts Faculty of Medicine and principal investigator on the study.

It turns out that stromal cells affect the ability of immune B cells to produce IgA that neutralizes rotavirus. Were just beginning to understand the influence these stromal cells can have.

Gommerman says the findings highlight the growing importance of research on the environment in which immune cells function. We typically think of a lymph node as just a bag of lymphocytes, but there is also this supporting structure that clearly has an active role in shaping immunity.

The studys first author, post-doctoral researcherConglei Li, identified a broad subset of stromal cells that affect the immune response to rotavirus. But the key players are likely a subset of that subset, Gommerman says. New technology known as single-cell RNA sequencing should soon enable researchers to identify many more of those cells, she adds.

That work could, in turn, lead to a better understanding of the genetic and environmental factors that may undermine immunity to rotavirus in the developing world, where rotavirus vaccines are much less effective than in high-resource settings.

Gommerman says that while several dysfunctions in the immune system likely contribute to reduced immunity to rotavirus in low-income countries, the current study offers a hint that prevention may be possible.

The thinking would be that if youre pregnant in a resource-depleted area, you may take a dietary supplement at a specific point to ensure proper development of tissues that support immunity, and which enable a vaccine to be more effective, she says.

That kind of intervention is likely a long way off, adds Gommerman, and replicating her results in human pregnancy presents obvious ethical problems. A more immediate next step for her lab is a collaborative study on IgA immune responses to other pathogens such as norovirus, another highly contagious disease.

A focus on single pathogens is useful in studies of IgA, according to Gommerman, because so many factors can influence IgA response. If you simplify the system of study, you get more predictable kinetics and can ask more discrete questions, she says. Weve made a contribution with that approachon a question that has been percolating in several labs for years. That feels good.

The research received support from the Canadian Institutes of Health Research, Princess Margaret Cancer Foundation and the Swiss National Science Foundation.

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Molecular mechanism suggests new ways to bolster immunity to deadly rotavirus: U of T researchers - News@UofT

Borna disease virus 1 (BoDV-1) causes a bizarre and deadly neurological infection in horses, sheep and other domesticated mammals in parts of Germany, Switzerland, Liechtenstein and Austria. Borna disease was named after a city in eastern Germany where it once killed numerous horses in the late 19th century. Infected animals have been known to engage in strange behaviors, such as smashing their heads into things, as well aspipe smokingan informal term for when animals are eating hay and suddenly stop chewing mid-mouthful, with the uneaten portion protruding like a pipe. But the disease does not appear to spread between horses; they are thought to acquire it from shrews, which can live in hay and secrete or excrete fluids containing the virus.

About 14 years ago, researchers identified the bicolored white-toothed shrew as a reservoir hostan organism in which a virus replicates but does not usually cause illnessfor BoDV-1. Horses and sheep are considered dead-end hosts that cannot spread the pathogen. For decades, scientists had debated whether the virus is zoonotic, or capable of jumping from animals to humans. Several studies even suggested that it might be present in people with psychiatric disorders such as depression, schizophrenia and bipolar disorder. It was later shown, however, that the viral RNA sequences detected in these studies were likely the result of laboratory contamination, and research on human infections subsided.

But in 2015 a related type of bornavirus found in exotic squirrels was implicated in at least four human deaths. Then, between 2018 and 2019, scientists detected the classical bornavirus, BoDV-1, in five people in Germany who suffered serious or fatal encephalitis (brain inflammation caused by infection)three of whom were recipients of organ transplants and were taking drugs to suppress their immune system. Now, in a study published Tuesday in Lancet Infectious Diseases, researchers have reported eight additional cases of BoDV-1 infection in humans who died of encephalitis. The pathogen appears to have flown under the radar for decades, but the researchers say doctors should be considering it a potential cause in such deaths.

We now have eight more cases, and these provide additional material for a better understanding of the disease, says Martin Beer, head of the Institute of Diagnostic Virology at the Friedrich Loeffler Institute in Germany, who was co-senior author of the new study and was also part of the team that reported the squirrel bornavirus infections. The findings confirm that the virus can infect humans and cause deadly encephalitis. But the risk is, to our opinion, pretty low, Beer says.

Beer and his colleagues analyzed postmortem brain tissue from 56 patients in southeastern Germanys state of Bavaria between 1999 and 2019. The samples were tested for genetic material from BoDV-1, which the researchers verified by additional testing for antibodies to it. Seven out of nine patients who died of encephalitis of unknown cause at one diagnostic center later tested positive for the virus (one of these cases had been reported previously). An additional two cases that tested positive were also included in the analysis.

The results confirm the virus had caused eight new encephalitis cases; two of these were immune-compromised individuals who had received organ transplants, and six were not. Because other recipients of organs from the same donor did not test positive for the virus, researchers think the transplant recipients that died from the virus probably acquired it from being immune-compromised, not from the donor. The patients suffered symptoms including headache, fever and confusion, which later progressed to coma and ultimately death.

All of the patients lived in rural areas and worked or spent a lot of time outside. Most had also been around cats, which are known to catch shrews and sometimes present them to their owners. Beer and his team hypothesize that the patients were exposed to BoDV-1 this way or perhaps by inhaling dust containing dried shrew urine. Future research will be needed to determine the exact infection route, he says.

Once in a human or horse host, the virus is thought to cross the blood-brain barrier into the central nervous system, where it triggers the hosts immune system to attack brain tissue. Its not the virus killing the brain cell or nerve tissue, Beer explains. Its the [hosts] own immune system recognizing the infection and starting to kill parts of brain.

There is no known treatment for the disease, but researchers are exploring whether antivirals such as ribavirinwhich has been shown to kill a range of bornaviruses in cells grown in a dish and in animal studiescould be effective in treating BoDV-1 infections in humans. Beer and his colleagues have plans to test newer antivirals against the virus in animal studies.

I think its an excellent paper, says Norbert Nowotny, a professor of virology at the University of Veterinary Medicine, Vienna, who was not involved in the new study but was part of the group that discovered shrews were a reservoir host for the virus. This Borna disease is really a strange diseaseits not like a flu, he adds, noting that it does not cause epidemics. Its a single-animal disease, and it seems to be the same in humans.

The virus itself is somewhat unusual in that it has a very short genome and makes only a few proteins. It does not seem to infect many individualsbut when it does, it kills them very efficiently. Numerous other zoonotic viruses infect many people but are seldom deadly. Previous research has found that humans and most mammals actually have bornavirus sequences in their genomes, which may help organisms protect themselves against infection, some hypothesize.

Fortunately, the virus does not appear to be transmitted between humans. I think we are all happy that this is not a virus that can spread easily, Beer says. But in light of these new findings, doctors should consider BoDV-1 as a possible cause of encephalitis in areas where it has been known to infect humans and horses.

Read more from the original source:
Virus Spread by Shrews Linked to Human Deaths from Mysterious Brain Infections - Scientific American

CLEVELAND, Ohio Cleveland Clinic Childrens Hospital is seeing a significant rise in cases of respiratory syncytial virus, or RSV, an illness that causes respiratory tract infections in infants.

Most of the children hospitalized for RSV at the Clinic have been less than 2 years old, and some are as young as 6 months, said Dr. Camille Sabella, head of the Center for Pediatric Infectious Diseases at the childrens hospital.

In adults and older, healthy children, RSV symptoms are mild and typically mimic the common cold.

But RSV can cause severe infection in some people, especially premature babies, older adults, infants and adults with heart and lung disease, or anyone with a very weak immune system.

RSV is the most frequent cause of bronchiolitis inflammation of the small airway passages entering the lungs in infants and young children. The illness accounts for approximately 125,000 hospitalizations and 250 infant deaths every year in the United States, according to an American Academy of Pediatrics study.

The virus typically begins circulating in the fall, and peaks in January or February. This is prime season, Sabella said.

As of December, visits to the Clinics pediatric emergency department for flu and RSV were up 20% over December 2018, Sabella said. Numbers for RSV cases alone were not available.

The Clinic is also seeing a rise in flu cases, it reported Wednesday. Having peaks in both influenza and RSV results in more hospitalizations and emergency department visits, Sabella said.

At University Hospitals, the number of RSV cases declined for the week ending Jan. 4, as compared with previous weeks, the hospital system reported. Flu activity was also slightly lower from a peak seen during the week of Dec. 22-28.

Dr. Amy Ray, director of infection prevention at MetroHealth, said in a statement that the hospital system is seeing patients with symptoms that include fever, sore throat, cough and body aches. Many are being tested for both influenza and RSV.

The number of RSV diagnoses hit 80 five weeks ago and have been stable around 60 or 70 for the following four weeks, Ray said.

MetroHealth is still seeing widespread cases of flu. Flu season usually peaks around late January but its not certain when it will peak this year, Ray said.

Hospitals are not required to report cases of RSV to county health officials. However, the percentage of emergency department visits for congestion and/or cough was at an eight-year high last week, according to the Cuyahoga County Board of Health.

RSV spreads through direct person-to-person contact and can live on surfaces, Sabella said. Unlike the flu virus, the RSV virus does not survive in the air.

Premature babies or infants and adults who have chronic heart or lung problems may get a severe case of RSV, according to the Mayo Clinic website. Symptoms of severe RSV infection in infants include short, shallow and rapid breathing; cough; lack of appetite; tiredness; and irritability.

There is no vaccine to prevent RSV. Ways to stop the spread of the virus include disinfecting surfaces and shared toys, covering coughs and sneezes with an elbow, washing hands frequently and avoiding touching the face and eyes.

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WESTPORT, Conn.--(BUSINESS WIRE)--Intensity Therapeutics, Inc., a clinical-stage biotechnology company developing proprietary intratumoral immunotherapy products to kill tumors and increase immune system recognition of solid cancers, today announced that Lewis H. Bender, President and CEO, will be a featured panelist on the Developments in The Oncology Landscape panel at East/West CEO. The conference will take place January 11-12, 2020, the weekend before the 38th Annual J.P. Morgan Healthcare Conference, at the Four Seasons Hotel in San Francisco.

The panel, which will examine the next wave of innovations and developments in oncology, will be held on Sunday, January 12, 2020 from 1:45 p.m. to 2:15 p.m. PST.

About Intensity Therapeutics

Intensity Therapeutics, Inc. is a clinical-stage biotechnology company pioneering a new immune-based approach to treat solid tumor cancers. Intensity leverages its DfuseRxSM technology platform to create new, proprietary drug formulations that, following direct injection, rapidly disperse throughout a tumor and diffuse therapeutic agents into cancer cells. Intensitys product candidates have the potential to induce an adaptive immune response that not only attacks the injected tumor, but also non-injected tumors. The Company executed a Cooperative Research and Development Agreement (CRADA) with the National Cancer Institutes (NCI) Vaccine Branch in 2014. The Company is also collaborating with Merck Sharpe & Dohme to evaluate the combination of INT230-6, Intensitys lead product candidate, and KEYTRUDA (pembrolizumab), Mercks anti-PD-1 (programmed death receptor-1) therapy, in patients with advanced solid malignancies. For more information, please visit http://www.intensitytherapeutics.com and follow us on Twitter @IntensityInc.

Forward Looking Statements

This press release contains forward-looking statements regarding Intensity Therapeutics plans, future operations and objectives. Such statements involve known and unknown risks, uncertainties and other factors that may cause actual performance or achievements to be materially different from those currently anticipated. These forward-looking statements include, among other things, statements about the initiation and timing of future clinical trials.

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Intensity Therapeutics to Participate in East/West CEO Conference - Business Wire

Last year left us with this piece of bombshell news: He Jiankui, the mastermind behind the CRISPR babies scandal, has been sentenced to three years in prison for violating Chinese laws on scientific research and medical management. Two of his colleagues also face prison for genetically engineering human embryos that eventually became the worlds first CRISPRd babies.

The story isnt over: at least one other scientist is eagerly following Hes footsteps in creating gene-edited humans, although he stresses that he wont implant any engineered embryos until receiving regulatory approval.

Biotech stories are rarely this dramatic. But as gene editing tools and assisted reproductive technologies increase in safety and precision, were bound to see ever more mind-bending headlines. Add in a dose of deep learning for drug discovery and synthetic biology, and its fair to say were getting closer to reshaping biology from the ground upboth ourselves and other living creatures around us.

Here are two stories in biotech were keeping our eyes on. Although successes likely wont come to fruition this year (sorry), these futuristic projects may be closer to reality than you think.

The idea of human-animal chimeras immediately triggers ethical aversion, but the dream of engineering replacement human organs in other animals is gaining momentum.

There are two main ways to do this. The slightly less ethically-fraught idea is to grow a fleet of pigs with heavily CRISPRd organs to make them more human-like. It sounds crazy, but scientists have already successfully transplanted pig hearts into baboonsa stand-in for people with heart failurewith some recipients living up to 180 days before they were euthanized. Despite having foreign hearts, the baboons were healthy and acted like their normal buoyant selves post-op.

But for cross-species transplantation, or xenotransplants to work in humans, we need to deal with PERVsa group of nasty pig genes scattered across the porcine genome, remnants of ancient viral infections that can tag along and potentially infect unsuspecting human recipients.

Theres plenty of progress here too: back in 2017 scientists at eGenesis, a startup spun off from Dr. George Churchs lab, used CRISPR to make PERV-free pig cells that eventually became PERV-free piglets after cloning. Then last month, eGenesis reported the birth of Pig3.0, the worlds most CRISPRd animal to further increase organ compatibility. These PERV-free genetic wonders had three pig genes that stimulate immunorejection removed, and nine brand new human genes to make themin theorymore compatible with human physiology. When raised to adulthood, pig3.0 could reproduce and pass on their genetic edits.

Although only a first clinical propotype that needs further validation and refinement, eGenesis is hopeful. According to one (perhaps overzealous) estimate, the first pig-to-human xenotranplant clinical trial could come in just two years.

The more ethically-challenged idea is to grow human organs directly inside other animalsin other words, engineer human-animal hybrid embryos and bring them to term. This approach marries two ethically uncomfortable technologies, germline editing and hybrids, into one solution that has many wondering if these engineered animals may somehow receive a dose of humanness by accident during development. What if, for example, human donor cells end up migrating to the hybrid animals brain?

Nevertheless, this year scientists at the University of Tokyo are planning to grow human tissue in rodent and pig embryos and transplant those hybrids into surrogates for further development. For now, bringing the embryos to term is completely out of the question. But the line between humans and other animals will only be further blurred in 2020, and scientists have begun debating a new label, substantially human, for living organisms that are mainly human in characteristicsbut not completely so.

With over 800 gene therapy trials in the running and several in mature stages, well likely see a leap in new gene medicine approvals and growth in CAR-T spheres. For now, although transformative, the three approved gene therapies have had lackluster market results, spurring some to ponder whether companies may cut down on investment.

The research community, however, is going strong, with a curious bifurcating trend emerging. Let me explain.

Genetic medicine, a grab-bag term for treatments that directly change genes or their expression, is usually an off-the-shelf solution. Cell therapies, such as the blood cancer breakthrough CAR-T, are extremely personalized in that a patients own immune cells are genetically enhanced. But the true power of genetic medicine lies in its potential for hyper-personalization, especially when it comes to rare genetic disorders. In contrast, CAR-Ts broader success may eventually rely on its ability to become one-size-fits-all.

One example of hyper-tailored gene medicine success is the harrowing story of Mila, a six-year-old with Batten disease, a neurodegenerative genetic disorder that is always fatal and was previously untreatable. Thanks to remarkable efforts from multiple teams, however, in just over a year scientists developed a new experimental therapy tailored to her unique genetic mutation. Since receiving the drug, Milas condition improved significantly.

Milas case is a proof-of-concept of the power of N=1 genetic medicine. Its unclear whether other children also carry her particular mutationBatten has more than a dozen different variants, each stemming from different genetic miscodingor if anyone else would ever benefit from the treatment.

For now, monumental costs and other necessary resources make it impossible to pull off similar feats for a broader population. This is a shame, because inherited diseases rarely have a single genetic cause. But costs for genome mapping and DNA synthesis are rapidly declining. Were starting to better understand how mutations lead to varied disorders. And with multiple gene medicines, such as antisense oligonucleotides (ASOs) finally making a comeback after 40 years, its not hard to envision a new era of hyper-personalized genetic treatments, especially for rare diseases.

In contrast, the path forward for CAR-T is to strip its personalization. Both FDA-approved CAR-T therapies require doctors to collect a patients own immune T cells, preserved and shipped to a manufacturer, genetically engineered to boost their cancer-hunting abilities, and infused back into patients. Each cycle is a race against the cancer clock, requiring about three to four weeks to manufacture. Shipping and labor costs further drive up the treatments price tag to hundreds of thousands of dollars per treatment.

These considerable problems have pushed scientists to actively research off-the-shelf CAR-T therapies, which can be made from healthy donor cells in giant batches and cryopreserved. The main stumbling block is immunorejection: engineered cells from donors can cause life-threatening immune problems, or be completely eliminated by the cancer patients immune system and lose efficacy.

The good news? Promising results are coming soon. One idea is to use T cells from umbilical cord blood, which are less likely to generate an immune response. Another is to engineer T cells from induced pluripotent stem cells (iPSC)mature cells returned back to a young, stem-like state. A patients skin cells, for example, could be made into iPSCs that constantly renew themselves, and only pushed to develop into cancer-fighting T cells when needed.

Yet another idea is to use gene editing to delete proteins on T cells that can trigger an immune responsethe first clinical trials with this approach are already underway. With at least nine different off-the-shelf CAR-T in early human trials, well likely see movement in industrialized CAR-T this year.

Theres lots of other stories in biotech we here at Singularity Hub are watching. For example, the use of AI in drug discovery, after years of hype, may finally meet its reckoning. That is, can the technology actually speed up the arduous process of finding new drug targets or the design of new drugs?

Another potentially game-changing story is that of Biogens Alzheimers drug candidate, which reported contradicting results last year but was still submitted to the FDA. If approved, itll be the first drug to slow cognitive decline in a decade. And of course, theres always the potential for another mind-breaking technological leap (or stumble?) thats hard to predict.

In other words: we cant wait to bring you new stories from biotechs cutting edge in 2020.

Image Credit: Image by Konstantin Kolosov from Pixabay

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The Top Biotech Trends We'll Be Watching in 2020 - Singularity Hub

Yaser H Gholami, 1 4 Lee Josephson, 3 Eman A Akam, 5 Peter Caravan, 5 Moses Q Wilks, 3 Xiang-Zuo Pan, 3, 6 Richard Maschmeyer, 1 Aleksandra Kolnick, 3, 7 Georges El Fakhri, 3 Marc D Normandin, 3 Zdenka Kuncic, 1, 4, 8Hushan Yuan 3

1The University of Sydney, Faculty of Science, School of Physics, Sydney, NSW, Australia; 2Bill Walsh Translational Cancer Research Laboratory, The Kolling Institute, Northern Sydney Local Health District, Sydney, Australia; 3Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States; 4Sydney Vital Translational Cancer Research Centre, St Leonards, NSW, Australia; 5The Institute for Innovation in Imaging and the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, United States; 6Bouve College of Health Sciences, CaNCURE Program, Northeastern University, Boston, MA, USA; 7Internal Medicine Residency Program, Lahey Hospital and Medical Center, Burlington, MA, USA; 8The University of Sydney Nano Institute, Sydney, NSW, Australia

Correspondence: Hushan YuanGordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 149 13 th Street, Charlestown, MA 02129, USATel +1 617-643-1963Email hyuan@mgh.harvard.edu

Purpose: Using our chelate-free, heat-induced radiolabeling (HIR) method, we show that a wide range of metals, including those with radioactive isotopologues used for diagnostic imaging and radionuclide therapy, bind to the Feraheme (FH) nanoparticle (NP), a drug approved for the treatment of iron anemia.Material and methods: FH NPs were heated (120C) with nonradioactive metals, the resulting metal-FH NPs were characterized by inductively coupled plasma mass spectrometry (ICP-MS), dynamic light scattering (DLS), and r 1 and r 2 relaxivities obtained by nuclear magnetic relaxation spectrometry (NMRS). In addition, the HIR method was performed with [ 90Y]Y 3+, [ 177Lu]Lu 3+, and [ 64Cu]Cu 2+, the latter with an HIR technique optimized for this isotope. Optimization included modifying reaction time, temperature, and vortex technique. Radiochemical yield (RCY) and purity (RCP) were measured using size exclusion chromatography (SEC) and thin-layer chromatography (TLC).Results: With ICP-MS, metals incorporated into FH at high efficiency were bismuth, indium, yttrium, lutetium, samarium, terbium and europium (> 75% @ 120 oC). Incorporation occurred with a small (less than 20%) but statistically significant increases in size and the r 2 relaxivity. An improved HIR technique (faster heating rate and improved vortexing) was developed specifically for copper and used with the HIR technique and [ 64Cu]Cu 2+. Using SEC and TLC analyses with [ 90Y]Y 3+, [ 177Lu]Lu 3+ and [ 64Cu]Cu 2+, RCYs were greater than 85% and RCPs were greater than 95% in all cases.Conclusion: The chelate-free HIR technique for binding metals to FH NPs has been extended to a range of metals with radioisotopes used in therapeutic and diagnostic applications. Cations with f-orbital electrons, more empty d-orbitals, larger radii, and higher positive charges achieved higher values of RCY and RCP in the HIR reaction. The ability to use a simple heating step to bind a wide range of metals to the FH NP, a widely available approved drug, may allow this NP to become a platform for obtaining radiolabeled nanoparticles in many settings.

Keywords: nanomedicine, radiolabeling, radionuclide therapy, HIR, Feraheme

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A Chelate-Free Nano-Platform for Incorporation of Diagnostic and Thera | IJN - Dove Medical Press