Immunology

Researcher aims to promote diversity as member of global academy – UM Today

April 21, 2020

A UM faculty member who studies immune cells in her lab and promotes diversity in science has been selected for membership in a prestigious worldwide organization.

Dr. Janilyn Arsenio, assistant professor of internal medicine and immunology in the Max Rady College of Medicine, has been honoured with admission to the Global Young Academy (GYA).

Arsenio holds a Canada Research Chair in systems biology of chronic inflammation. She is one of four Canadians among this years 40 GYA inductees, who represent 30 countries.

The GYA brings together outstanding early-career researchers for international dialogue and collaboration. Members, who are typically in their 30s, are selected for their scientific excellence and commitment to service. Each member joins the academy for a term of five years.

The academy undertakes projects in a number of areas, from promoting science education and outreach to improving the research environment.

Its a group of young scientists who share a motivation to improve the scientific culture, Arsenio says. I applied because Im really passionate about promoting equity, diversity and inclusion in science.

As a visible minority academic woman in science, I feel a personal responsibility to advocate for that. Im a member of Canadian and American organizations like the Society for Canadian Women in Science and Technology and the Association for Women in Science, and this is an opportunity to interact on a more international level.

The Winnipeg-born Arsenio, who is of Filipino heritage, earned her bachelors degree in microbiology and her PhD in medical microbiology and infectious diseases at UM. She did four years of postdoctoral research, primarily in immunology, at the University of California San Diego before joining the UM faculty in 2017.

While in California, she learned techniques for analyzing the genetic material of individual cells. She brought that expertise to her lab at UMs Manitoba Centre for Proteomics and Systems Biology, making it the first lab in the province to enter the field of single-cell genomics.

Arsenio studies, at the molecular level, how immune cells behave in response to infection, chronic inflammation and disease. Were trying to understand how cells change to become functional protectors of the immune system, versus how their functions are lost during disease, she says.

The professor is vice-chair of Women in Science: Development, Outreach and Mentoring (WISDOM), a Manitoba organization based in the Rady Faculty of Health Sciences that works to address the under-representation of women in science, particularly in leadership. She also serves on the equity, diversity and inclusion committee of the Rady Faculty.

Arsenios previous honours include the American Association of Immunologists Young Investigator Award, which she received in 2016.

Her formal induction into the Global Young Academy was to have been at the academys 2020 conference and annual general meeting in India this June. Because of the COVID-19 crisis, the gathering has been converted to an e-conference. Hopefully, the new members will interact online, and we can meet in person at the 2021 meeting in Japan, Arsenio says.

Although she has studied infectious diseases, the scientist says its surreal to experience an outbreak on the scale of COVID-19. You learn about this during your training, but you never think that youll live through a pandemic, she says.

Like all lab scientists in the Rady Faculty, Arsenio has closed her lab and put her experiments on hold because of the pandemic.

Its very difficult to have to pause your research, she says. But were doing what we have to do for everyones well-being.

ALISON MAYES

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Researcher aims to promote diversity as member of global academy - UM Today

Immunology

High-throughput production of tetramer assay probes used for COVID-19 – Drug Target Review

The developers of a novel method to create immunological assay probes for screening T cells has leveraged their new protocol against COVID-19.

Researchers have developed a method that enables them to create libraries containing hundreds of molecular probes for tetramer assays in only days, whereas previous protocols required a week to produce a single probe. The team suggest their process opens up new opportunities for immunological research, development of cancer immunotherapies and assessment of immune responses from patients with COVID-19.

Tetramer assays are an immunological test used to detect and analyse the T cells in a blood sample. T cells each recognise and bind to a specific antigen like a viral protein and bind to them, identifying them to the immune system. However, where antibodies bind directly to antigens on the surface of a pathogen, T cells only bind to antigens expressed on the surface of antigen presenting cells, like macrophages and dendritic cells.

As a result, antibody assays are relatively simple and T-cell assays are more complex; requiring the probes for the latter to be formed of antigens incorporated into a molecular complex that mimics how they are presented in vivo, where they are bound to tetramers of major histocompatibility complex (MHC) proteins.

This diagram outlines a workflow for preparing and using a library of peptide-loaded MHC multimers for assessment of T cell repertoires in patient blood samples [credit: Overall et al., Nature Communications, 2020].

Corresponding author of the study published in Nature Communications, Nikolaos Sgourakis, assistant professor of chemistry and biochemistry at the University of California (UC) Santa Cruz has been studying how protein fragments are selected and bound to MHC proteins in cells for years, a process which requires molecular chaperones. The new protocol is based on his research which indicates that molecular chaperones can eject antigens that have low affinity for the MHC protein tetramers, in favour of antigens with higher affinity.

Sgourakis designed a placeholder peptide for use in preparing large quantities of pre-loaded MHC complexes. When incubated with a high-affinity antigen, the placeholder is displaced, a reaction that can be performed in a high-throughput system with large numbers of antigens.

Its a force multiplier, enabling us to perform these reactions at high throughput, Sgourakis said. A lot of groups are working on similar methodologies, all of which have their pros and cons. This technology has the advantage of using the same system that cells use naturally and we can combine it very elegantly with existing single-cell analytical tools.

The researchers originally used the new method to develop libraries of probes for assessing T-cell responses to neuroblastoma and designing cancer immunotherapies. However, since the emergence of COVID-19, the team have been exploring ways to apply the technology to address the challenges of the novel coronavirus. With a viral infection, there are many different fragments of the viral proteins that an infected cell can display and the researchers say it is important for drug design to determine which of these peptides elicit a strong immune response.

Based on the coronavirus genome, we can predict all the possible peptides, synthesise them, load them onto MHC tetramers and do a fishing expedition to find which ones are recognised by the T cells in blood samples from patients, Sgourakis explained. Certain peptides are immunodominant, ie, they steer the immune response and those are the ones we want to discover so we can potentially use them in a vaccine.

Sgourakis explained that the tetramer assays could also answer one of the biggest questions surrounding COVID-19: why is there so much variability in the severity of this disease?

According to Sgourakis, the approach can be used to compare the T-cell repertoires of different cohorts of patients. It is known that as people age their T-cell repertoire declines, resulting in a weaker immune response to pathogens, which may explain why older people are more vulnerable to COVID-19. Sgourakis said: We can use this technology to screen patients and see what the gaps are in their T-cell repertoires and maybe use this as a diagnostic for which patients will need more intensive treatment.

This research was in close collaboration with researchers at the New York Genome Center and the University of Pennsylvanias Childrens Hospital and Perelman School of Medicine, all US.

Related topicsAnalytical techniques, Assays, Cell-based assays, Disease research, Drug Development, Immunology, Protein, Proteomics, Research & Development, Screening, t-cells

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High-throughput production of tetramer assay probes used for COVID-19 - Drug Target Review

Immunology

Vivoryon Therapeutics Starts Development Program for Meprin Protease Inhibitors with Intended Therapeutic Use in Fibrosis, Cancer and Alzheimer’s…

HALLE (SAALE) / MUNICH and LEIPZIG, Germany, 16 April 2020 Vivoryon Therapeutics AG (Euronext Amsterdam: VVY, ISIN DE0007921835) announced today that the Company has entered into a research collaboration with the Fraunhofer Institute for Cell Therapy and Immunology (IZI) and acquired related patents from the Institute for a meprin protease inhibitor and assay platform. Under the guidance of PD Dr. Stephan Schilling, the Department of Drug Design and Target Validation will work together with Vivoryon to advance first-in-class small molecule meprin inhibitors. This collaboration will combine Vivoryons expertise in translating basic research into marketable small molecule therapeutics with the departments focus on discovery and development of new therapeutics that target putative pathologic post-translational modifications.

The metal-dependent proteases, meprin alpha and meprin beta, are emerging targets in kidney protection, fibrotic diseases, cancer and Alzheimers disease. Increased meprin expression and their mislocalization has been associated with tissue damage and collagen deposition in fibrosis, which can result in the loss of organ function. Meprin-targeted protease inhibitors thus have the potential to not only target symptoms, but also treat a range of indications including acute and chronic kidney disease and multiple organ fibrosis.

Dr. Michael Schaeffer, CBO at Vivoryon Therapeutics AG noted:The IP estate we have acquired from Fraunhofer IZI expands our current drug development portfolio and places us in a leading position to explore the full potential of meprin protease inhibitors. As a company, our goal is to consistently seek out opportunities that can further strengthen our pipeline with the ultimate vision of delivering novel therapies to patients in need. By working with Dr. Schilling and his team we are set to advance meprin inhibitors very quickly towards clinical testing in indications like fibrotic diseases or cancer.

PD Dr. Stephan Schilling, Head of Protein and Drug Biochemistry Unit at Fraunhofer Institute for

Cell Therapy and Immunology added:As the roles and functionality of meprin alpha and beta continue to become more distinguished through research, it is clear these metalloproteases represent interesting novel targets that could be developed into therapeutics for a variety of indications. As such, I am delighted that with this collaboration the groundbreaking research of our institute will eventually be translated into clinical programs by an experienced drug development company.

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For more information, please contact:

Vivoryon Therapeutics AG

Dr. Ulrich Dauer, CEO

Email:contact@vivoryon.com

Fraunhofer Institute for Cell Therapy and Immunology

Jens Augustin, Head of Press and Public Affairs

E-Mail:presse@izi.fraunhofer.de

Trophic Communications

Gretchen Schweitzer / Joanne Tudorica

Tel: +49 172 861 8540 / +49 176 2103 7191

Email:Trophic@vivoryon.com

About Vivoryon Therapeutics AG

With 20+ years of unmatched understanding in identifying post-translational modifying enzymes that play critical roles in disease initiation and progression, Vivoryons scientific expertise has facilitated the creation of a discovery and development engine for small molecule therapeutics. This platform has demonstrated success by developing a novel therapeutic in type 2 diabetes. In its current programs Vivoryon Therapeutics is advancing its lead product, PQ912, in Alzheimers disease and its entire portfolio of QPCT and QPCTL inhibitors in oncology and other indications.

http://www.vivoryon.com

About Fraunhofer-Gesellschaft

The Fraunhofer-Gesellschaft, headquartered in Germany, is the worlds leading applied research organization. With its focus on developing key technologies that are vital for the future and enabling the commercial exploitation of this work by business and industry, Fraunhofer plays a central role in the innovation process. As a pioneer and catalyst for groundbreaking developments and scientific excellence, Fraunhofer helps shape society now and in the future. Founded in 1949, the FraunhoferGesellschaft currently operates 74 institutes and research institutions throughout Germany. The majority of the organizations 28,000 employees are qualified scientists and engineers, who work

with an annual research budget of 2.8 billion euros. Of this sum, 2.3 billion euros is generated through

contract research.

http://www.izi.fraunhofer.de

Forward Looking Statements

Information set forth in this press release contains forward-looking statements, which involve a number of risks and uncertainties. The forward-looking statements contained herein represent the judgment of Vivoryon Therapeutics AG as of the date of this press release. Such forward-looking statements are neither promises nor guarantees but are subject to a variety of risks and uncertainties, many of which are beyond our control, and which could cause actual results to differ materially from those contemplated in these forward-looking statements. We expressly disclaim any obligation or undertaking to release publicly any updates or revisions to any such statements to reflect any change in our expectations or any change in events, conditions or circumstances on which any such statement is based.

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Vivoryon Therapeutics Starts Development Program for Meprin Protease Inhibitors with Intended Therapeutic Use in Fibrosis, Cancer and Alzheimer's...

Immunology

Could genetics explain why some COVID-19 patients fare worse than others? – Live Science

Certain genetic differences might separate people who fall severely ill with COVID-19 from those who contract the infection but hardly develop a cough, a new preliminary study suggests.

The research is still in its early days, though, experts say.

The immune system can react to viruses thanks, in part, to specific genes that help cells spot unfamiliar bugs when they enter the body. The genes, known as human leukocyte antigen (HLA) genes, contain instructions to build proteins that bind to bits of a pathogen; those proteins serve as warning flags to alert immune cells. The immune cells, once trained to recognize these bits, jumpstart the process of building antibodies to target and destroy the invasive germ.

Within each individual, HLA genes code for three different classes of proteins; in other words, HLAs come in a variety of flavors, and depending on which HLAs you have, your body may be better or worse equipped to fight off certain germs including SARS-CoV-2, the virus that causes COVID-19.

In a new study, published April 17 in the Journal of Virology, researchers used computer models to predict which combination of HLAs might be best at binding SARS-CoV-2, and which might be worst.

If certain HLAs can bind well to a large proportion of the virus's proteins, "we expect there to be a more protective immune response," authors Abhinav Nellore and Dr. Reid Thompson, who lead a computational biology research group at the Oregon Health and Science University, told Live Science in an email. A better bind means that the viral proteins are more likely to be presented to immune cells and prompt the production of specific antibodies, the authors said.

"If the interaction is not stable, you will not have a proper [immune] response," said Dr. Shokrollah Elahi, an associate professor in the Department of Dentistry and adjunct associate professor in the Department of Medical Microbiology and Immunology at the University of Alberta, who was not involved in the study.

Related: 10 deadly diseases that hopped across species

But a stable bond, alone, does not guarantee the best immune response, Elahi added. If an HLA binds a viral protein that happens to be critical for the germ to replicate and survive, the subsequent antibody activity will likely target the virus more effectively than that prompted by a less important protein, Elahi said.

"This is an issue we did not address in our analysis," the authors noted. Instead, the team focused on predicting how well different HLA types could bind to bits of SARS-CoV-2. Their analysis identified six HLA types with a high capacity to bind different SARS-CoV-2 protein sequences, and three with a low capacity to do so. Specifically, a HLA type known as HLA-B*46:01 had the lowest predicted capacity to bind to bits of SARS-CoV-2.

The same HLA type cropped up in a 2003 study published in the journal BMC Medical Genetics, which assessed patients infected with SARS-CoV, a closely related coronavirus that caused an outbreak of severe acute respiratory syndrome in the early 2000s. The study found that, in a group of patients of Asian descent, the presence of HLA-B*46:01 was associated with severe cases of the infection. In their paper, the research group noted that more clinical data would be needed to confirm the connection and the same goes for the new study of SARS-CoV-2, Nellore and Thompson said.

"The most substantial limitation of our study is that this was conducted entirely on a computer and did not involve clinical data from COVID-19 patients," the authors said. "Unless and until the findings we present here are clinically validated, they should not be employed for any clinical purposes," they added.

"In the body, we have so many things interacting," Elahi said. HLAs represent just one piece of a large, intricate puzzle that comprises the human immune system, he said. To better understand the variety of immune responses to COVID-19, Elahi and his research group aim to assess markers of immune system activity in infected patients and also catalog the ratio of immune cell types present in their bodies. While taking age, sex and other demographic factors into account, these so-called immunological profiles could help pinpoint when and why the illness takes a turn in some patients.

The clinical data could be assessed in parallel with genetic data gathered from the same patients, Elahi added. Similarly, Nellore and Thompson said that "COVID-19 testing should be paired with HLA typing, wherever [and] whenever possible," to help determine how different HLA types relate to symptom severity, if at all. Partnerships with genetic testing companies, biobanks and organ transplant registries could also offer opportunities to study HLA types in larger populations of people, they said.

"We cannot in good conscience predict at this point who will be more or less susceptible to the virus because we have not analyzed any clinical outcomes data with respect to HLA type to know that any of our predictions are valid," the authors said. If future studies support the notion that some HLA genes protect people from the virus, while others place patients at greater risk, those in the latter group could be first in line for vaccination, they added.

"In addition to prioritizing vaccinating the elderly or those with preexisting conditions, one could prioritize vaccinating people with HLA genotypes that suggest the SARS-CoV-2 virus is more likely to give them worse symptoms."

The authors went on to analyze how well HLAs can bind SARS-CoV-2 as compared with other coronaviruses, such as those that cause the common cold and infect humans often. They identified several viral bits shared between SARS-CoV-2 and at least one of these common viruses, suggesting exposure to one germ could somewhat protect the body against the other.

"If someone was previously exposed to a more common coronavirus and had the right HLA types ... then it is theoretically possible that they could also generate an earlier immune response against the novel SARS-CoV-2," the authors said. On the other hand, exposure to a similar virus could leave the body ill-equipped to fight off the new one, if, for instance, "the body is using an old set of tools that aren't ideally suited to address the new problem," the authors said.

Originally published on Live Science.

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Could genetics explain why some COVID-19 patients fare worse than others? - Live Science

Immunology

Outlook 2020: ‘Passionate about helping to train the next generation of physicians, scientists,’ Judith James says – Oklahoman.com

Name: Dr. Judith James, 52.

Career highlights: Oklahoma Medical Research Foundation vice president of Clinical Affairs; member and program chair, Arthritis & Clinical Immunology Research Program; Lou C. Kerr Endowed Chair in Biomedical Research; associate vice provost for Clinical and Translational Science; George Lynn Cross Professor of Research, professor of medicine, professor of pathology, adjunct professor of microbiology and immunology, Oklahoma University Health Sciences Center.

Community impact: As a leader in the Oklahoma Shared Clinical Translational Resources, James helps oversee partnerships between 29 entities within the state whose mission is to improve health and health outcomes. Along with universities, the program includes tribal health services.

James also works with the Cherokee Nation and the Chickasaw Nation at outreach clinics to improve tribal members with rheumatic diseases.

Life philosophy and advice to young women: "I am incredibly passionate about helping to train the next generation of physician and physician scientists," James said. "When I started in medical school, less than 30% of my class was female. And now we're close to 50%. And so I hope that I will encourage, inspire, motivate and facilitate their ability to think about how they can help improve the health and research training, for everyone. But especially for women."

Dale Denwalt, Staff writer

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Outlook 2020: 'Passionate about helping to train the next generation of physicians, scientists,' Judith James says - Oklahoman.com

Immunology

New research gives further evidence that autoimmunity plays a role in Parkinsons disease – Newswise

Newswise LA JOLLAA new study co-led by scientists at the La Jolla Institute for Immunology (LJI) adds increasing evidence that Parkinsons disease is partly an autoimmune disease. In fact, the researchers report that signs of autoimmunity can appear in Parkinsons disease patients years before their official diagnosis.

The research could make it possible to someday detect Parkinsons disease before the onset of debilitating motor symptomsand potentially intervene with therapies to slow the disease progression.

The study, published in the April 20, 2020, issue of Nature Communications, was co-led by LJI professor Alessandro Sette, Dr. Biol. Sci, and Professor David Sulzer, Ph.D., of the Columbia University Medical Center.

Scientists have long known that clumps of a damaged protein called alpha-synuclein build up in the dopamine-producing brain cells of patients with Parkinsons disease. These clumps eventually lead to cell death, causing motor symptoms and cognitive decline.

Once these cells are gone, theyre gone. So if you are able to diagnose the disease as early as possible, it could make a huge difference, says LJI research assistant professor Cecilia Lindestam Arlehamn, Ph.D., who served as first author of the new study.

A 2017 study led by Sette and Sulzer was the first to show that alpha-synuclein can act as a beacon for certain T cells, causing them to mistakenly attack brain cells and potentially contribute to the progression of Parkinsons. This was the first direct evidence that autoimmunity could play a role in Parkinsons disease.

The new findings shed light on the timeline of T cell reactivity and disease progression. The researchers looked at blood samples from a large group of Parkinsons disease patients and compared their T cells to a healthy, age-matched control group. They found that the T cells that react to alpha-synuclein are most abundant when patients are first diagnosed with the disease. These T cells tend to disappear as the disease progresses, and few patients still have them ten years after diagnosis.

The researchers also did an in-depth analysis of one Parkinsons disease patient who happened to have blood samples preserved going back long before his diagnosis. This case study showed that the patient had a strong T cell response to alpha-synuclein ten years before he was diagnosed with Parkinsons disease. Again, these T cells faded away in the years following diagnosis.

This tells us that detection of T cell responses could help in the diagnosis of people at risk or in early stages of disease development, when many of the symptoms have not been detected yet, says Sette. Importantly, we could dream of a scenario where early interference with T cell responses could prevent the disease from manifesting itself or progressing.

Sulzer added, One of the most important findings is that the flavor of the T cells changes during the course of the disease, starting with more aggressive cells, moving to less aggressive cells that may inhibit the immune response, and after about 10 years, disappearing altogether. It is almost as if immune responses in Parkinsons disease are like those that occur during seasonal flu, except that the changes take place over ten years instead of a week.

In fact, already therapies exist to treat inflammation from autoreactive T cells, and these TNF therapies are associated with lower incidence of Parkinsons disease. Going forward, the researchers are especially interested in using a tool called a T cell-based assay to monitor patients already at risk for Parkinsons to see if they could benefit from TNF therapies. These patients include people with REM sleep disorders and certain genetic mutations.

The researchers hope to study more Parkinsons patients and follow them over longer time periods to better understand how T cell reactivity changes as the disease progresses.

The study, titled -Synuclein-specific T cell reactivity is associated with preclinical and early Parkinsons disease, was supported by the National Institutes of Healths (NIH) National Institute of Neurological Disorders and Stroke (R01NS095435, P50NS108675), the NIH National Institute on Aging (P50AG08702), the Parkinsons Foundation, the Michael J. Fox Foundation, JPB Foundation, William F. Richter Foundations, and the UCSD-LJI Program in Immunology.

Additional study authors included Rekha Dhanwani, John Pham, Rebecca Kuan, April Frazier, Juliana Rezende Dutra, Elizabeth Phillips, Simon Mallal, Mario Roederer, Karen S. Marder, Amy W. Amara, David G. Standaert, Jennifer G. Goldman, Irene Litvan, and Bjoern Peters.

DOI: 10.1038/s41467-020-15626-w

About La Jolla Institute for Immunology

The La Jolla Institute for Immunology is dedicated to understanding the intricacies and power of the immune system so that we may apply that knowledge to promote human health and prevent a wide range of diseases. Since its founding in 1988 as an independent, nonprofit research organization, the Institute has made numerous advances leading toward its goal: life without disease.

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New research gives further evidence that autoimmunity plays a role in Parkinsons disease - Newswise

Anatomy

Bolton 1-3 Reading FC: The Anatomy Of A Perfect Away Day – The Tilehurst End

Its an age-old conversation topic for football fans that can easily fill an evening in the pub, or multiple for the die-hard. Whats your favourite ever away game?

Reading fans are pretty blessed in this regard. The obvious answers include Southampton and West Ham away in 2012, the play-off demolition of Cardiff a year earlier, and the Bryniesta inspired beating Liverpool in the FA Cup.

But every fan has their personal favourites, those perfect days that rest in the lower tiers of Reading folklore. Mine include the 3-1 promotion six-pointer win at Birmingham in 2008, the 1-1 draw at Old Trafford earned by our second-string XI in the 2006/07 FA Cup. And then theres Bolton.

On April 21, 2007, 13 years ago as I sit here today, Steve Coppells side found themselves 1-0 down to Bolton at the Reebok Stadium with 83 minutes on the clock. On the face of it, this isnt a particularly impressive prologue to a Lazarus-esque tale.

But Reading were dreaming of Europe in their first season of Premier League football, and Sam Allardyces side were a major rival with established faces such as Nicolas Anelka, Kevin Nolan and El Hadji-Diouf in their ranks. It was also a chance to see how the other half lives. A decade-and-a-half earlier, Bolton were not an intrinsically bigger team and their rise in that period set the blueprint for the Royals own ambitions - having featured something of a fork in the road 12 years earlier.

The hosts had generally been the better team for those 83 minutes. Anelkas second-half opener came via an unfortunate attempted block from Nicky Shorey but couldnt really be argued with. Readings best chance came in an agonising goalmouth scramble that suggested a typically tough day in the life of a small fish in a big pond.

Then the last six minutes happened. Kevin Doyles frankly rude insistence on running at goal brought an errant leg from Abdoulaye Meite. That was the thing about that Reading team, they didnt care who you played for, they just turned up and beat you. They didnt know they were born. The Irishman picked himself up to slot home the equaliser.

Bolton keeper Jussi Jaaskelainen prepared to take a goal kick a minute later and took his time, earning a hounding from his own supporters desperate to re-take the lead. If only they knew what he knew. In the 89th minute, a cross from the right floated over to Doyle whose brazen arrogance allowed time for the ball to settle perfectly on the six-yard line, Bolton studs stabbing at his heels, before belting it home.

Reading had the lead but the fun wasnt over. Shorey tricked his way down the left wing and a perfect cross was only inches over the head of a hat-trick hunting Doyle. That left Shane Long with a free header to make it 3-1. Little did he know Stephen Hunt was barrelling in at 100mph, blinkers on, to headbutt the ball into the back of the net.

The atmosphere in the away end was next level. Its best shown by the photo at the top of this article as Doyle celebrates the equaliser, I can see 13-year-old me and my dad celebrating, split by the fan in the row above whose somehow been lifted six feet in the air. The final whistle rang around a suddenly empty Reebok Stadium - sending the home fans back down the stairs early being one of the finest and most unique joys of following football on the road.

There was still one Bolton fan looking on in disbelief, as the boxer Amir Khan stood in his executive box near the away end, and received hundreds of playful taunts by joyous visitors singing of a dream European Tour. It was also our first win on their turf since a certain day in 1995, a memory no doubt resonating in the minds of many that day.

For myself, 2006/07 was my first season on the road with Reading and Im sure Ive never beaten the W3 D1 L1 record I witnessed that campaign. With our family connections up north, my mum had come up with us and visited the retail park next door during the game. All that loud cheering, she was worried we had received a battering... until we told her it was the away end going bananas.

It is also timely that the anniversary of that beautiful Lancastrian day lands on an equally lovely day in our very different world. On these football-less times, memories like these remind us why we all cant wait to do it all again.

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Bolton 1-3 Reading FC: The Anatomy Of A Perfect Away Day - The Tilehurst End

Anatomy

How Trolls World Tour Lets the Dogs Out – The New York Times

In Anatomy of a Scene, we ask directors to reveal the secrets that go into making key scenes in their movies. See new episodes in the series each Friday. You can also watch our collection of more than 150 videos on YouTube and subscribe to our YouTube channel.

A few decades worth of earworms are jammed into less than two minutes in this moment from the animated sequel Trolls World Tour, now available on demand. The sequence has Poppy (voiced by Anna Kendrick) and Branch (Justin Timberlake) on a journey that takes them to the land of country music. They try to improve the gloomy moods of the residents with a pop medley that includes Wannabe, Gangnam Style and Who Let the Dogs Out, among others.

Narrating the scene, the director Walt Dohrn discusses trying to get Kendrick and Timberlake excited about performing this hyperkinetic montage, using a choreographer for the dance bits and creating fun sight gags with his story artists.

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How Trolls World Tour Lets the Dogs Out - The New York Times

Anatomy

Grey’s anatomy boss on Meredith and Deluca’s fate – Andover Leader

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Greys Anatomy is an American medical drama TV series which premieres on American broadcasting company (ABC).

This is a series that focuses on surgical interns, attending doctors and residents as they develop into seasoned doctors while maintaining their personal lives and relationships at the same time. There have been a total of whopping 16 seasons of this series.

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This series always provides plenty of drama and season 16 has been no exception, particularly the season finale.

Put on a Happy Face was not intended to be the season finale, but premiered as one, as four planned episodes couldnt be produced due to the COVID-19 pandemic. Although, it served enough excitement to be one.

The major highlight of this episode was seeing Meredith Grey(Ellen Pompeo) and Andrew DeLuca(Giacomo Gianniotti) working out to figure out why Richard Webber(James Pickens Jr.) has been experiencing hallucinations.

They come to know that the reason for his condition was Cobalt poisoning from a hip replacement surgery. They enlisted Dr. Lincoln to remove the Cobalt that would send Webber on the road to recovery.

The question which arises is will their professional team up turn them up for their romance again which ended in catastrophe last time? Krista Vernoff, the showrunner of the series has hinted the same.

I will be fascinated to see how that storytelling emerges in season 17 because this story played in a way that I didnt picture, she reported Deadline. You know, you write a thing, and then the actors play it, and then it gets all put together, and then you know what the story is. You dont know how its going to play when you write it. Its been amazing for me to watch this story this season.

But if Meredith and DeLuca revive their romance, its not going to be easy. Because theres already a spark between Meredith and Cormac Hayes. Vernoff has said that theres hope for them as well.

I feel like Giacomo has been so compelling, and DeLuca has risen so much, and simultaneously, Hayes has been really compelling and feels very much like Merediths equal, she told. At this point, Im not even sure which couple Im rooting for, and thats always an exciting thing, she said.

Although Vernoff didnt reveal whether the reports of a major character dying in the intended season finale were true, she gave a clue to fans that how they can work it out.

Ironically, when fans watch episodes 15 and 16 of Station 19, they will probably have a feeling of some of what we had planned, she teased. She hinted.

For much such related news and latest updates, stay tuned.

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Grey's anatomy boss on Meredith and Deluca's fate - Andover Leader

Anatomy

Jesse Williams’ Ex Aryn Drake-Lee Talks About Her Split from the ‘Grey’s Anatomy’ Star – Showbiz Cheat Sheet

Most know Jesse Williams as the hunky plastic surgeon on ABCs iconic show Greys Anatomy. Fans of Williams may not realize that the actor is also the father of two kids daughter Sadie, 6, and son Maceo, 4.

The Greys star went through a somewhat public divorce from wife Aryn Drake-Lee in 2017. Williams ex spoke about their split in May in an interview with People.

In 2017, Williams filed for divorce from Drake-Lee after five years of marriage, though the couple had been together for over a decade. The actor somewhat addressed rumors that the split was caused by his infidelity.

I was in a relationship 13 years, 13 real years, not 5 years, not 7 years 13 years, Williams said in July 2017, according to People. All of a sudden [expletive] are writing think-pieces that I somehow threw a 13-year relationship. Like, the most painful experience Ive had in my life like with a person Ive loved with all of my heart that I threw a person and my family in the trash because a girl I work with is cute.

After a court battle over child support for their two children, Williams was ordered to pay his ex $50,629 for their two children in addition to the $50,695 a month he was ordered to pay Drake-Lee forspousal support, as reported by Entertainment Tonight.

Last year, Drake-Lee broke her silence on her divorce from the Greys star, revealing the difficulty of her life being radically changed by their split.

When the divorce process started I had two nursing babies, and I am the one that ran our household, Drake-Lee told People in May. And for our children, and for the creation of the businesses that we built together when I left my career in New York for us to move to California to pursue his, and then as a result built it I knew, as the one that was really holding it all together, that I didnt have a lot of room to fall, even though I was falling.

The mom of two shared that she felt abandoned by the people the couple had formed relationships with over the years. I was in a place where I needed the support that was going to help to ground me, Drake-Lee said. Most everybody I had spent the eight years here in LA with all went with him.

Drake-Lee noted that she never felt comfortable with the show business environment, where Williams was becoming more entrenched.

Hollywood and I bump heads. It was never my value system, and it was never something that I was striving for, she said. It never felt comfortable for me because of how superficial it was. And then that all became abundantly clear when everybody left.

Despite the painful breakup, Drake-Lee focuses on the positive changes the split brought about for her life.

It was a blessing in disguise because it was a real slap in the face to see who was around us and why, and at that point it became very clear, she explained. And it cleared a pathway for me to make a shift and get back onto a path that was more in alignment with how I wanted to live my life.

Drake-Lee also moved on to connect with people who shared her perspective and overall mindset. I was able to really find people that were more in alignment with my values in how they are living their lives and how they want to raise their children, she said. I found community.

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Regarding the tabloid fodder that made headlines of her divorce from Williams, Drake-Lee downplayed many of the stories. Much of what they say is wrong, she revealed. But Im not interested in a tit-for-tat, because thats just never ending. People believe what they want to believe because its easy.

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Jesse Williams' Ex Aryn Drake-Lee Talks About Her Split from the 'Grey's Anatomy' Star - Showbiz Cheat Sheet