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Coronavirus’s Genetics Not Changing Much, And That Bodes Well For A Vaccine : Shots – Health News – NPR

Internationally, scientists now have on file the genomes of more than 47,000 different samples of the virus that causes COVID-19 up from just one in January. Here's a transmission electron micrograph of SARS-CoV-2 virus particles (orange) isolated from a patient. National Institute of Allergy and Infectious Diseases/National Institutes of Health hide caption

Internationally, scientists now have on file the genomes of more than 47,000 different samples of the virus that causes COVID-19 up from just one in January. Here's a transmission electron micrograph of SARS-CoV-2 virus particles (orange) isolated from a patient.

Scientists are monitoring the virus that causes COVID-19 for genetic changes that could make a vaccine ineffective. But so far, they're not seeing any.

"There's nothing alarming about the way the coronavirus is mutating or the speed at which it's mutating," says Emma Hodcroft, a molecular epidemiologist at the University of Basel in Switzerland. "We don't think this will be a problem [for vaccines] in the short term."

"To date, there have been very few mutations observed," says Peter Thielen, a senior scientist at Johns Hopkins Applied Physics Laboratory. "And any mutations that we do see are likely not having an effect on the function of the virus itself."

That's good news for scientists working to produce an effective vaccine by the end of the year. And it reflects the enormous quantity of genetic information on SARS-CoV-2, the virus that causes COVID-19, that researchers have amassed since the virus appeared in China late last year.

In January, scientists were limited to just one whole genome sequence of the virus. "Today we have over 47,000 coronavirus genomes that have been submitted to international databases," Thielen says.

New genomes are added every day by teams of scientists from around the world. And each time a new one arrives, it gets a close examination, Thielen says.

"What we're looking for in the data is similarity between the virus that first emerged and the genome that had been deposited and any changes that have occurred in the virus," he says. And overall, the viruses circulating today look remarkably similar to the ones first identified in China.

There had been concern about mutations because SARS-CoV-2 is a type of virus capable of quickly changing its genes. But unlike many similar viruses, the coronavirus uses a proofreading system to catch any errors in the genetic code when it begins generating copies of itself.

"The targets for vaccine design today remain the same as we would have designed them in January."

Peter Thielen, Johns Hopkins Applied Physics Laboratory

"So if there's a change, it will actually make a correction at a specific location," Thielen says.

Vaccine developers have been especially concerned about genetic locations that affect something called a spike protein. It's a structure on the surface of the coronavirus that allows it to invade cells.

Spike proteins also give the virus its distinctive appearance and account for its name. Scientists who first viewed a coronavirus through an electron microscope were reminded of the solar corona.

The candidates for a coronavirus vaccine now under development are all designed to teach the immune system to recognize these spike proteins. So far, Thielen says, that's looking like a good strategy.

"The targets for vaccine design today remain the same as we would have designed them in January," he says.

Some other well-known viruses have proved less amenable to the strategy of using the same vaccine from year to year. Influenza, for example, is constantly altering its surface proteins in ways that require annual vaccine updates for each strain that's making the rounds that year.

"Flu just really loves to change these parts," Hodcroft says. "And that's why we can end up with such different flus from season to season."

Measles represents a virus at the other extreme its genome has stayed fairly consistent over the years, at least in the ways that trigger immunity in people after infection. That means children today still get a measles vaccine that was developed in the 1960s, and it provides immunity for a lifetime.

Hodcroft says she thinks SARS-CoV-2 is likely to fall somewhere between the flu and measles when it comes to making a vaccine.

"I think in the short term we'll find something," she says. "The big question is whether this is something we'll be able to vaccinate once and then you never have to get it again, or will it be something you'll have to get every couple of years to keep your immunity up to date."

Scientists are uncertain because the coronavirus is still so new, Hodcroft says.

"We haven't really seen the full diversity of how the virus can mutate," she says. "It gathers mutations over time. We can't speed up time, so we just have to wait and see."

At the moment, though, vaccine developers have more pressing concerns than mutations. First, they'll have to demonstrate that they can produce vaccines that are both safe and effective. Then they'll have to make huge quantities.

"It's not a small feat to manufacture a vaccine for billions of people and then to get it to all of those people," Hodcroft says.

That will take months, she says, in addition to the months required to develop a vaccine in the first place.

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Coronavirus's Genetics Not Changing Much, And That Bodes Well For A Vaccine : Shots - Health News - NPR

China to Fast-Track Coronavirus Vaccine Trial Based on Advanced Genetics Technology – The Wall Street Journal

A research institute run by Chinas military received approval to conduct human clinical trials of a new Covid-19 vaccine developed using advanced genetics technology, in a notable breakthrough for Chinas quickly developing pharmaceutical industry.

The approval comes as other Chinese drugmakers move to expand testing of more traditional coronavirus vaccines outside China.

The...

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PCOS subtypes associated with distinct genetic variations, finds study – News-Medical.Net

Researchers working on a National Institutes of Health (NIH) funded study found that polycystic ovary syndrome (PCOS) has distinct subtypes that are associated with genetic variations. Their study titled, "Distinct subtypes of polycystic ovary syndrome with novel genetic associations: An unsupervised, phenotypic clustering analysis," is published in the journal PLOS Medicine.

This study was funded by the NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Diabetes and Digestive and Kidney Diseases.

PCOS affects a large number of women, and authors of the study explain it as a "common, complex genetic disorder." They write that as many as 15 percent of women of reproductive age group suffer from this condition, and several diagnostic criteria can help in confirming the condition in a patient.

In women with PCOS, some of the common symptoms include irregular or missing periods, lack of or infrequent ovulation, raised levels of male sex hormones androgens in blood and associated features such as hirsutism or excessive facial hair. On ultrasound investigation, small cysts are detected on the surface of the ovaries. These women are at risk of being overweight and obese and may develop heart disease and type 2 diabetes and metabolic syndrome with time.

Image Credit: Marochkina Anastasiia / Shutterstock

There are several diagnostic criteria for the detection of PCOS. These are mainly based on expert opinions and consensus. Several controversies exist in these diagnostic criteria for PCOS, the team wrote.

There is a variation of physical features and physical symptoms among patients with PCOS. These are called phenotypic variations. In a recent study across populations with European ancestry, it was noted that the genetic makeup of women suffering from PCOS was distinctly similar despite being labeled using different diagnostic criteria. They write that this suggests that these diagnostic criteria "do not identify biologically distinct disease subtypes."

The objective of this study was thus to "test the hypothesis that there are biologically relevant subtypes of PCOS." Researcher Andrea Dunaif, MD, Chief of the Hilda and J. Lester Gabrilove Division of Endocrinology, Diabetes and Bone Disease at the Mount Sinai Health System, explained, "We're starting to make headway on what causes PCOS. It's very frustrating for patients because it's poorly understood, and patients often see several physicians before PCOS is diagnosed." Dunaif added, "Through genetics, we're beginning to understand the condition and may have specific targeted therapies in the not-too-distant future."

Study participants were a genotypical cohort. The biochemical data and the genotype data from these women was obtained from the "PCOS genome-wide association study (GWAS)." They made connections with the genotypes and the phenotypic or physical subtypes of the condition. A total of 893 women were included in the study. Their age range was between 25 and 32 years, and body mass index was between 28.2 and 41.5. These genotypic clusters were replicated in another cohort, which were not genotyped. Here there were 263 PCOS cases with an age range of 24 to 33 years and BMI ranging between 28.4 and 42.3.

On clustering analysis, the team found two distinct subtypes of PCOS. These were

On genotyping the initial cohort and dividing them into the two types of PCOS, several genetic characteristics were detected. The findings were:

A separate predictive model was developed to see if the cases tended to cluster in families. They found that 73 women with PCOS within an age range of 25 and 33 and BMI range of 27.8 and 42.3 kg/m2, usually "tended to cluster in families and that carriers of previously reported rare variants in DENND1A". The team wrote that this gene variant is known to regulate the synthesis of androgens or male hormones in the body.

The authors said that this initial study was conducted only among women with European ancestry who were diagnosed based on the National Institutes of Health (NIH) criteria. More extensive studies with a wide-ranging population would be more conclusive.

The researchers wrote that they "found reproducible reproductive and metabolic subtypes of PCOS," and these subtypes were "associated with novel, to our knowledge, susceptibility loci." They wrote that these subtypes had distinct genetic architecture.

Dr. Dunaif said, "In contrast to classifying disorders based on expert opinion, this is a very powerful objective approach to categorizing syndromes like PCOS into distinct subtypes with different causes, treatment, and clinical outcomes."

The team wrote, "Women with PCOS may be poorly served by being grouped under a single diagnosis because PCOS subtypes may differ in responses to therapy and in long-term outcomes."

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Researchers identify novel genetic variants linked to Type 2 diabetes – Penn: Office of University Communications

After examining the genes of more than 200,000 people all over the world who have Type 2 diabetes, researchers from thePerelman School of MedicineandtheVeterans Health Administrations (VHA)Corporal Michael J. Crescenz Veterans Affairs Medical Center found hundreds of genetic variants never before linked to the disease. The study also identified gene variants that vary by ethnicity, as well as variants tied to conditions related to Type 2 diabetes like coronary heart disease and chronic kidney disease. This expansive genetic investigation, the largest of its kind, has the potential to dramatically impact care for millions of people worldwide who suffer from this disease. The study is published inNature Genetics.

Using data from the worlds biggest biobanktheMillion Veteran Program (MVP)in the VHAplus the DIAGRAM Consortium, the UK Biobank, the Penn Medicine Biobank, and Biobank Japan, the researchers analyzed a study population of 1.4 million people around the world, of which almost 230,000 people had Type 2 diabetes. From there, they broke down the genetic makeup of those hundreds of thousands of people and found 558 independent genetic variants that are differentially distributed between people with and without Type 2 diabetes, 21 being European-ancestry-specific and seven African American-ancestry specific. Of the 588 variants found, 286 had never before been discovered.

Researchers then set out to see if certain genetic variants among this group of people could be tied to specific Type 2 diabetes-related diseases.

Ultimately, three were linked to coronary heart disease, two to acute ischemic stroke, four to retinopathy, two to chronic kidney disease, and one to neuropathy, saysMarijana Vujkovic, a biostatistician at both the Perelman School of Medicine, VHAs CMCVAMC and a co-leader for the VHAs national MVP Cardiometabolic Working Group. Building on this research, the scientific community can assess which of the surrounding genes nearby the identified genetic variants is likely to be the causal gene that alters the risk of Type 2 diabetes, and that could lead to early interventions to limit controllable risks of developing the condition.

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Senior Farewell: With appreciation for my first 18 years in Washington … and the four more years to come – Yakima Herald-Republic

Ive thought about writing this article for four years. One might assume I had an outline carefully prepared and ready to go, but such is not the case.

In my musings, I pictured my senior farewell article to be the capstone of four years of Unleashed, high school and extracurriculars, and my childhood in the Yakima Valley. But, I was wrong.

I had planned (loudly at times) to leave the state of Washington. College was going to be my ticket out of this mountain-dotted landscape we call home. I spent years envisioning what college would be like someplace far from here. I was enamored by the unknown. I couldnt have dreamed that 2020 would be so full of the unknown, even the unimaginable, no matter your physical location.

March brought a cacophony of unexpected events. My senior year went online, and I decided I would call the University of Washington my home for the next four years. Yes, you read that right: I will be attending college in-state, defying all of my expectations. As I delve into the inner workings of the brain as a neuroscience major, I hope to also deepen my understanding of the many reasons that make Washington a wonderful state to live. So, this farewell isnt a farewell at all; instead, its a documented account of why Im excited to live in the Pacific Northwest for four more years.

To start, I need to express my gratitude for my fellow Unleashed writers and this program as a whole. This group of brilliant reporters (including the alumni) are the most sincere and spirited lovers of the Yakima area I have ever met. My peers articles on community events and their experiences living in this Valley are endearing.

Next, thank you to my teachers who expressed, with great ardor, their love of the Yakima Valley. I am proud to be a Selah Viking.

Lastly, here is a list of the things I am grateful to have experienced in my first 18 years in the state of Washington:

Quarantine has taught me to embrace life with an open mind and heart. I am excited to spend time exploring this beautiful state Ive grown up in.

So, I have to be a fatalist: Attending the University of Washington wasnt what I imagined, but it is exactly where I need to be (except when Im back home visiting Yakima, of course).

Anna Ergeson is a 2020 graduate of Selah High School and a four-year member of the Yakima Herald-Republics Unleashed program. She plans to enroll this fall at the University of Washington as a presidential scholar majoring in neuroscience.

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Senior Farewell: With appreciation for my first 18 years in Washington ... and the four more years to come - Yakima Herald-Republic

Sosei Heptares and AbbVie Announce New Discovery Collaboration Targeting Inflammatory Diseases – PharmiWeb.com

Tokyo, Japan and London, UK, 25 June 2020 Sosei Group Corporation (the Company; TSE: 4565) announces that it has entered into an exclusive discovery collaboration and option-to-license agreement with AbbVie (NYSE: ABBV), a research-based global biopharmaceutical company, to discover, develop and commercialize novel medicines that modulate G protein-coupled receptor (GPCR) targets of interest to AbbVie. The collaboration will initially focus on discovery of novel small molecules targeting inflammatory and autoimmune diseases.

Dr. Malcolm Weir, Executive Vice Chairman of Sosei Heptares, said: We are delighted to begin this new partnership with AbbVie, which further extends the application of our technology to novel and exciting targets, and we look forward building a close working relationship as the programs advance. Collaborating with leading pharmaceutical companies is a core element of our successful value-generating strategy. The ability to combine our unique technology and structure-based discovery and early development capabilities, particularly around challenging drug targets, with AbbVies extensive therapeutic area, development and global commercialization expertise is a powerful approach to creating new improved therapeutics for inflammatory and autoimmune diseases.

Dr. Lisa Olson, Vice President, Discover Immunology, AbbVie, said: Continued innovation across Immunology remains a key AbbVie priority. Combining AbbVies more than two decades of expertise in Immunology with researchers developing cutting-edge technologies best positions us to offer patients new hope for advanced, next-generation treatment for autoimmune diseases.

Sosei Heptares will apply its proprietary StaR technology and GPCR-focused Structure-based Drug Design (SBDD) capabilities and fund R&D activities through the completion of Investigational New Drug (IND)-enabling studies. AbbVie may then pay license fees to exercise its exclusive license options and assume responsibility for global development and commercialization.

Under the terms of the agreement, Sosei Heptares is eligible to receive up to US$32 million in upfront and near-term milestone payments, as well as potential option, development and commercial milestones of up to $377 million, plus tiered royalties on global commercial sales.

AbbVie has the option to expand the collaboration up to a total of four targets.

About AbbVie

AbbVie's mission is to discover and deliver innovative medicines that solve serious health issues today and address the medical challenges of tomorrow. We strive to have a remarkable impact on people's lives across several key therapeutic areas: immunology, oncology, neuroscience, eye care, virology, women's health and gastroenterology, in addition to products and services across its Allergan Aesthetics portfolio. For more information about AbbVie, please visit us at http://www.abbvie.com. Follow @abbvie on Twitter, Facebook, Instagram, YouTube and LinkedIn.

About Sosei Heptares

We are an international biopharmaceutical group focused on the discovery and early development of new medicines originating from our proprietary GPCR-targeted StaR technology and structure-based drug design platform capabilities. We are advancing a broad and deep pipeline of novel medicines across multiple therapeutic areas, including CNS, immuno-oncology, gastroenterology, inflammation, and other rare/specialty indications.

We have established partnerships with some of the worlds leading pharmaceutical companies, including AbbVie, AstraZeneca, Genentech (Roche), Novartis, Pfizer and Takeda, and additionally with multiple emerging biotechnology companies. Sosei Heptares is headquartered in Tokyo, Japan with R&D facilities in Cambridge, UK.

Sosei Heptares is the corporate brand and trademark of Sosei Group Corporation, which is listed on the Tokyo Stock Exchange (ticker: 4565). Sosei, Heptares, the logo and StaR are trademarks of Sosei Group companies.

For more information, please visit https://www.soseiheptares.com/

LinkedIn: @soseiheptaresco | Twitter: @soseiheptaresco | YouTube: @soseiheptaresco

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One-time treatment generates new neurons, eliminates Parkinson’s disease in mice – University of California

Xiang-Dong Fu, PhD, has never been more excited about something in his entire career. He has long studied the basic biology of RNA, a genetic cousin of DNA, and the proteins that bind it. But a single discovery has launched Fu into a completely new field: neuroscience.

For decades, Fu and his team at University of California San Diego School of Medicine studied a protein called PTB, which is well known for binding RNA and influencing which genes are turned on or off in a cell. To study the role of a protein like PTB, scientists often manipulate cells to reduce the amount of that protein, and then watch to see what happens.

Several years ago, a postdoctoral researcher working in Fus lab was taking that approach, using a technique called siRNA to silence the PTB gene in connective tissue cells known as fibroblasts. But its a tedious process that needs to be performed over and over. He got tired of it and convinced Fu they should use a different technique to create a stable cell line thats permanently lacking PTB. At first, the postdoc complained about that too, because it made the cells grow so slowly.

But then he noticed something odd after a couple of weeks there were very few fibroblasts left. Almost the whole dish was instead filled with neurons.

In this serendipitous way, the team discovered that inhibiting or deleting just a single gene, the gene that encodes PTB, transforms several types of mouse cells directly into neurons.

More recently, Fu and Hao Qian, PhD, another postdoctoral researcher in his lab, took the finding a big step forward, applying it in what could one day be a new therapeutic approach for Parkinsons disease and other neurodegenerative diseases. Just a single treatment to inhibit PTB in mice converted native astrocytes, star-shaped support cells of the brain, into neurons that produce the neurotransmitter dopamine. As a result, the mices Parkinsons disease symptoms disappeared.

The study is published June 24, 2020 inNature.

Researchers around the world have tried many ways to generate neurons in the lab, using stem cells and other means, so we can study them better, as well as to use them to replace lost neurons in neurodegenerative diseases, said Fu, who is a Distinguished Professor in the Department of Cellular and Molecular Medicine at UC San Diego School of Medicine. The fact that we could produce so many neurons in such a relatively easy way came as a big surprise.

There are several different ways to mimic Parkinsons disease in mice. In this case, the researchers applied a dopamine look-a-like molecule to poison neurons that produce dopamine. As a result, the mice lose dopamine-producing neurons and develop symptoms similar to Parkinsons disease, such as movement deficiencies.

The treatment works like this: The researchers developed a noninfectious virus that carries an antisense oligonucleotide sequence an artificial piece of DNA designed to specifically bind the RNA coding for PTB, thus degrading it, preventing it from being translated into a functional protein and stimulating neuron development.

Antisense oligonucleotides, also known as designer DNA drugs, are a proven approach for neurodegenerative and neuromuscular diseases study co-author, Don Cleveland, PhD, pioneered the technology, and it now forms the basis for a Food and Drug Administration (FDA)-approved therapy for spinal muscular atrophy and several other therapies currently in clinical trials. Cleveland is chair of the Department of Cellular and Molecular Medicine at UC San Diego School of Medicine and member of the Ludwig Institute for Cancer Research, San Diego.

The researchers administered the PTB antisense oligonucleotide treatment directly to the mouses midbrain, which is responsible for regulating motor control and reward behaviors, and the part of the brain that typically loses dopamine-producing neurons in Parkinsons disease. A control group of mice received mock treatment with an empty virus or an irrelevant antisense sequence.

In the treated mice, a small subset of astrocytes converted to neurons, increasing the number of neurons by approximately 30 percent. Dopamine levels were restored to a level comparable to that in normal mice. Whats more, the neurons grew and sent their processes into other parts of brain. There was no change in the control mice.

By two different measures of limb movement and response, the treated mice returned to normal within three months after a single treatment, and remained completely free from symptoms of Parkinsons disease for the rest of their lives. In contrast, the control mice showed no improvement.

I was stunned at what I saw, said study co-author William Mobley, MD, PhD, Distinguished Professor of Neurosciences at UC San Diego School of Medicine. This whole new strategy for treating neurodegeneration gives hope that it may be possible to help even those with advanced disease.

What is it about PTB that makes this work? This protein is present in a lot of cells, Fu said. But as neurons begin to develop from their precursors, it naturally disappears. What weve found is that forcing PTB to go away is the only signal a cell needs to turn on the genes needed to produce a neuron.

Of course, mice arent people, he cautioned. The model the team used doesnt perfectly recapitulate all essential features of Parkinsons disease. But the study provides a proof of concept, Fu said.

Next, the team plans to optimize their methods and test the approach in mouse models that mimic Parkinsons disease through genetic changes. They have also patented the PTB antisense oligonucleotide treatment in order to move forward toward testing in humans.

Its my dream to see this through to clinical trials, to test this approach as a treatment for Parkinsons disease, but also many other diseases where neurons are lost, such as Alzheimers and Huntingtons diseases and stroke, Fu said. And dreaming even bigger what if we could target PTB to correct defects in other parts of the brain, to treat things like inherited brain defects?

I intend to spend the rest of my career answering these questions.

Co-authors of the study include: Jing Hu, Dongyang Zhang, Zhengyu Liang, Fan Meng, Xuan Zhang, Yuanchao Xue, Steven F. Dowdy, Neal K. Devaraj, UC San Diego; Xinjiang Kang, Peking University, Liaocheng University; Roy Maimon, UC San Diego and Ludwig Institute for Cancer Research; and Zhuan Zhou, Peking University.

Funding for this research came, in part, from the National Institutes of Health (grants GM049369 and GM052872), Ludwig Institute for Cancer Research and Nomis Foundation, and Larry Hillblom Foundation.

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One-time treatment generates new neurons, eliminates Parkinson's disease in mice - University of California

Stanford professor says rise in COVID-19 cases is proof that virus is tracking human behavior – KRON4

STANFORD, Calif. (KRON) There are several factors behind the rise in COVID-19 cases, including testing, contact tracing, and people interacting more as shelter-in place orders get relaxed.

But as we continue to track the virus a Stanford University professor says the new numbers are proof that the coronavirus is also tracking us.

I think the virus is tracking peoples behavior, Dr. Robert Siegel said.

Stanford University professor of microbiology and immunology Dr. Robert Siegel

says wear your mask, accounting for the recent rise in COVID-19 case numbers like this.

The virus would be very happy if we all went back and started socializing, Dr. Siegel said.

In other words, says Dr. Siegel, the virus doesnt care about what matters to people and that is the key to reopening.

The reopening is not working perfectly because as things open people are being more lax in their behavior like fewer people wearing masks, Dr. Siegel said.

Its called mask fatigue or quarantine fatigue.

Dr. Siegel points out that new cases are not spiking among one high risk group in particular, health care workers.

People are very carefully watching health care providers and their rate of infection is really, really low so they have a high exposure but they are being very careful and they are not getting infected, Dr. Siegel said.

If anything, Dr. Siegel says more testing is showing the recent uptick in cases is real.

He says there is scant evidence warmer weather has made much of a difference.

The key is, we have to continue to do the public health measures of wearing masks, social distancing and washing hands, using hand sanitizers and basically being smart, Dr. Siegel said.

Dr. Siegel says outsmarting the coronavirus starts with admitting that its still here and what you can do could save your life or someone elses life.

The virus is still very much present and you just have to look at the numbers, we are breaking records every day so in terms of risky behavior, you are more at risk for being in social settings without a mask than you ever were, Dr. Siegel said.

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Racism: Its foundations may not be what you think they are – Washington Daily News – thewashingtondailynews.com

I recently received an email from the son of a Greenville friend who lives in Florida. The son was moved by the murder of George Floyd to initiate a new local program to reduce acts of racial prejudice through education, in hopes that education would change human behavior.

I applaud his efforts to make a difference. Would that more Americans would be stirred by the murders of black men to reduce racial hatred and prejudice. But I fear that education, alone, will is insufficient to address Americas original sin. It is difficult for me to imagine that after 400 years of prejudice and exploitation of African Americans in the land of the free there remains anyone unaware of the cruelty and viciousness with which black persons have been treated.

In 2016, Ibram X. Kendi addressed these issues in his National Book Award for Non-Fiction, Stamped from the Beginning. Kendis book traces the history of racist ideas in America, from colonial times to the present. During a recent book tour, he explained why education, alone, is inadequate for reducing racism: If the fundamental problem is ignorance and hate, then your solutions are going to be focused on education, and love and persuasion. But the actual foundation of racism is not ignorance and hate, but self-interest, particularly economic and political and cultural.

Self-interest, he added, drives racist policies that benefit that self-interest. When the policies are challenged because they produce inequalities, racist ideas spring up to justify those policies. Hate flows freely from there.

The first slaves to step foot on what would become American soil did so in the English settlement of Jamestown, Virginia, in 1619. Over the next decades, 400,000 more slaves joined them in the cotton, tobacco and sugar fields of southern planters interested in increasing profits. And what better way to cut costs than free labor?

By the 1800s, slavery had become the economic engine of the South, making it possible for planters to reap enormous profits. Self-interest motivated the heirs of those planters to succeed from the Union in 1860. And self-interest moved their descendants to deny civil rights to African Americans during the Jim Crow era.

In fact, throughout American history, racism has been used intentionally to preserve the privileged positions of white Americans. Since the very founding of the Republic, discrimination has been justified by those who benefit from it by appeals to pseudo-science, scriptures and other self-serving rationalizations that the black race is inferior by nature in intellect; that Africans were created by God to serve white Europeans; that the Bible supports slavery; that African Americans cannot compete with whites in school or work; that blacks are inherently violent and non-law abiding; and that all black men secretly desire to rape white women.

All of that, of course, is bunk. There is no verifiable evidence that Africans were or have ever been less intelligent than Europeans. Verses in the Bible that purport to legitimize slavery were cherry-picked and abused by Christian racists interested in providing scriptural cover for their right to own other human beings. Given a fair chance, there is no reason African Americans cannot compete with their white counterparts in school and work. Black neighborhoods are not more dangerous than white neighborhoods and neither are black people. And, to the consternation of members of the KKK and other white supremacist groups, black men do not rape white women near as often as white men do.

Prejudice against non-white peoples in America has existed for so long that it has become institutionalized. Practically every economic, political, social and, yes, religious institution in the USA continues to support racist policies, to varying degrees. Since the first European settlers landed on the shores of Virginia in 1608, the superiority of white European culture has been encoded in our customs, traditions and laws.

From housing to healthcare, policing to education, and banking to employment, America is a racist system that knows exactly what it is doing and does it successfully every day.

We cant educate our way out of something as structural, deeply embedded and systemic as American racism. No amount of education or love can eradicate the cancer that has been eating away at the body politic of America for more than 400 years.

On the contrary, efforts to reduce racism demand both honest recognition and our participation in a systemic response that changes the political, economic, social, cultural and religious policies that are the foundation of Americas foulest bias.

Polk Culpepper is a former Episcopal priest, retired lawyer and resident of Washington.

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Racism: Its foundations may not be what you think they are - Washington Daily News - thewashingtondailynews.com

HBO Max’s magical and action-packed "Adventure Time" special is a tribute to heroic resistance – Salon

While watching the first installment ofHBO Max'sfour hour-long specials"Adventure Time: Distant Lands,"based on Pendleton Ward'sfantasy animated seriesthat ran on Cartoon Network, I was reminded of an episode from the show's fifth season. In the episode titled "BMO," the sentientgaming console voiced by Niki Yangaccidentally deletes their entire coresystemdrivers.sys during a round of routine maintenance. In order to operate as normal, BMO explains to Finn (Jeremy Shada) and Jake (John DiMaggio) that they'll need to trek out to the MO factory where BMO was "born."

Disguises are donned and shenanigans ensue, until BMO is finally reunited with their creator, Moseph "Moe" Mastro Giovanni, who proceeds to fix them. Moe reveals that BMO is very special. They were built as a companion for the child he never ended up having.

Moe explains, "I made BMO to be more."

In "Distant Lands," helmed by executive producer Adam Muto,BMO fully embraces that element of their design in their own special way. After 10 seasons of serving as a sidekick to Finn and Jake (albeit it an incredibly adorable and well-loved one), BMO steps into the role of hero by fighting the power of a broken system led by a corrupt ruler a narrative that is both universally timeless and incredibly timely.

BMO is happily shuttling through spacearmed with potatoes and a song about potatoes:"They're better than tomatoes!" on a mission to terraform Mars when they're suddelny thrown off course. BMO ends up on The Drift, a debilitated space station powered on-and-off by questionable energy sources and inhabited by colonies of scavengers. Watch the first four minutes below:

Thesociety is built on selling bits of valuable scrap to Hugo (Randall Park), a sketchy former Earthling who masterminds many of The Drift's mechanisms. BMO's crash-landingdestroys some valuable scrapping equipment that two groups The Great Elves and Shell People are feuding over, which then turns the conflict on BMO.

Before they can retaliate, BMO is swept up by Y4 (later renamed Y5), a young bunny-like creature (Glory Curda), who initially contemplates selling them to Hugo. But after BMO's quick thinking helps residents repair a breach and earns them the self-styled title ofsheriff, Y5 decides to become their playmate/deputy.

Together, they spend their days assisting Drift residents with day-to-day disasters like saving space beetles from drowning or wrangling space lard whileY5 is visibly weighed down by a sense of impending doom, as well as the vocal disapproval of her parents, who work for Hugo. As The Drift is becoming more and more unstable, it becomes increasingly apparent that Hugo is less of a reliable leader and more of a smarmy politician using the labor of the station's residents for his own selfish gain.

Inevitably, Y5 has to determine her own loyalties, while BMO remains undeterred from fighting against the injustice at play on The Drift.

"Even when things look really, really stupid, we still have to try," BMO says.

In this case, what is viewed as "stupid" on The Drift is voicing dissent especially as a child or a member of a marginalized community even when the people around you are apathetically falling in line.

And in this world, that so-called stupidityultimately makes a big difference.

"Adventure Time" has always succeeded in communicating a message without being moralistic, and this installment of "Distant Lands" is no different. This is partially because of, despite the absurdist environments, the show's very real depiction of human behavior and political machinations. When I watched Hugo boarding an escape pod despite cries of injustice, I couldn't help but think of Donald Trump retreating to the White House bunker while thousands took to the streets to protest racial inequality.

But just because "justice," however you define it, may not be immediately achieved, "Distant Lands" shows, through its depiction of BMO, that it's still something for which people should fight. "This robot expends energy in ways that yield it no benefit," observes Y5 at one point, perfectly encapsulating the generous heroism woven throughout the "Adventure Time" canon.

It's an almost childishly idealistic way to approach the universe, but after watching "Distant Lands," I realize that our world needs more BMOs because by embracing the philosophy to "be more," change can happen.

Thefirst installment of "Adventure Time: Distant Lands" is available to stream now on HBO Max. No release date has been announced for the following specials.

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HBO Max's magical and action-packed "Adventure Time" special is a tribute to heroic resistance - Salon