Netflix’s speed-watching trial joins a long history of content cramming, but may be bad for artists and viewers – ABC News

Updated December 09, 2019 08:15:43

When it was announced in October that Netflix was trialling a new variable playback option that would allow viewers to watch their titles sped up (or slowed down), filmmakers reacted with dismay.

Judd Apatow, director and screenwriter of Knocked Up and Funny People, tweeted: "Leave them as they were intended to be seen."

Filmmakers Brad Bird (The Incredibles), Peter Ramsey (Spider-Man: Into the Spider-Verse) and Peyton Reed (Ant-Man) also piled on.

"Having worked a lot in large-scale TV, it's kind of like sitting in a theatre audience and yelling out to the directors and the actors to 'hurry up!' it feels that rude as a concept," says Thomas M Wright, an Australian actor (Top of The Lake) and filmmaker (Acute Misfortune).

In fact, browser plugins that allow viewers to adjust the speed that they watch Netflix (and other video content) already exist.

Melbourne university student Seraphya told Stop Everything! that he watches YouTube videos at triple speed and Netflix at double speed.

"If you watch faster, you get to watch more shows," he says.

And speeding through video content seems like a natural evolution in one sense; first there was speed reading, then came speed listening, after podcasts and audiobooks invaded our phones.

Seraphya, a bioinformatics student, jacks up his podcast listening to triple speed.

"I'm listening for both knowledge and entertainment, and it's just boring to listen at single speed," he says.

He's also not particularly fazed by the concerns of content creators, pointing out that "we now know from musical historians that Beethoven was meant to be much faster than we currently generally perform it at so there's no use getting stuck with what was intended, because what was intended doesn't last".

Seraphya has attention deficit hyperactivity disorder (ADHD) but says that speed listening and watching actually calms him down, the stimulation allowing his brain to focus.

Emma, undertaking her teaching masters in Adelaide, ramps up her speed to dial down her FOMO: "I feel like there is so much to be seen and not enough time to see it in, so when I get the opportunity I do tend to ramp the speed up."

She recently watched historical action thriller Hotel Mumbai and Swedish fantasy Border "between x1.4 and x1.6 speed".

She's likely to use Netflix's faster playback option, but she believes "some things that are really stressful and distressing shouldn't be watched at speed", pointing to Netflix miniseries Unbelievable, based on a true story of rape and injustice, as an example.

"There will always be things I listen to at 1.0 speed, the things that I love," Emma says.

"It's irrational and personal, but isn't everybody's relationship to what they consume?"

Ian, a public servant in Queensland, listens to most podcasts on double speed and sometimes watches YouTube videos sped up, but says he won't be speeding through Netflix.

"I don't think I would do it for television shows I think they usually have particular production values that I don't think would be helped by watching them at a faster rate."

Director Thomas M Wright recognises that not all television is "carefully crafted" and some directors wouldn't be concerned by the idea of viewers speed-watching their work.

"But cinema takes years and people are actually orchestrating a completely false reality, and in order to do that it takes extraordinary investment and extraordinary care and the idea of that being trampled over for convenience is absurd," he says.

"Cinema for me is a machine of empathy and there's something that dies, the more people atomise it."

Joel Werner, host and producer of ABC podcast Sum of All Parts, understands why listeners speed up some podcast content but draws a line.

"I think watching a really good TV series or a really good movie, or listening to a really immersive audio documentary, it's an experience, right?"

"It's taking you to a different world, it's putting you in someone else's shoes, it's giving you a perspective on life that you didn't have before and I just don't think you can get any of that nuance when you listen at double the speed it was intended to be listened at," Werner says.

"So the theory on speed reading is it's more of a skim than a read," says Jared Cooney Horvath, an educational neuroscientist from The University of Melbourne.

Dr Horvath says that our ability to speed read is limited by the foveal spot at the back of the eye, "which essentially determines what you can focus on.

"If something isn't in that spot, then bad news, you're not going to be reading it and unfortunately, it's a very small spot."

When you combine our small foveal spots with the fact you need to move your eyes across a page to read, he says that even a speed reader would still take 10-20 seconds to read an average page of text.

While many seem to draw the line at narrative-based or fictional content, Dr Horvath says that "because of the way narratives are constructed, especially creative narratives, that's when you might be able to get away with it [skim reading]".

That's because fiction involves a degree of "redundancy" (repetition and references to characters, plot points and settings) which enables readers to make sense of a book while skimming through it.

But if you speed through nonfiction or anything you're planning to learn information from, "you get almost nothing out of it because you don't have these little points to use as kind of references," says Dr Horvath.

"Without that 'redundancy' you have nothing to hang your hat on. You get to the end and your comprehension is just trash."

The good news for speed-demons? Dr Horvath says that for speed listening and watching, anything up to x1.25 speed is "fine" in terms of recall and comprehension.

"As soon as you go above that, prepare to start just dropping key facts and that's just fact recall. Comprehension is [about] now how do you piece those facts together into a story."

As you recall fewer facts, Dr Horvath says your "comprehension tanks" compared to someone listening to or watching something on normal speed.

"When you're breastfeeding with your mother, you get a very certain chemical signature that spreads through your body which we think is a signature of bonding," Dr Horvath says.

"It turns out when you're lost in a narrative you get that same signature, so you're bonding. So when people say 'I love Dostoyevsky,' they're not being flippant, you're bonding with the author at that moment."

If you speed through a book, you risk losing the depth and engagement required to bond with the work.

Even so as long as the current glut of content exists, there are going to be people willing to sacrifice depth of engagement in favour of skimming as much of it as they can.

Dr Horvath traces the problem of "information overload" to the advent of the printing press, pinning this as the moment we were faced with a major decision between depth and breadth.

"The vast majority of people pick broad: 'I just want to listen to as many podcasts, watch as many shows, make sure I get everything'. And it's neither right nor wrong," he says.

But if you choose to speed through all three seasons of Stranger Things in one evening, don't expect it to make much of an impact.

"Deep learning is predicated on thinking," says Dr Horvath.

"You have to embed these memories and you have to give yourself time to think about them."

Rather than speed-watching, Dr Horvath suggests: "If you watch a show don't binge it, spend a day not watching the show, thinking about the episode you just watched, predicting what's going to come next."

"That's the deep thinking that makes the show resonate."

Topics:arts-and-entertainment,film-movies,film,television,popular-culture,books-literature,neuroscience,australia,united-states

First posted December 07, 2019 06:25:33

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Netflix's speed-watching trial joins a long history of content cramming, but may be bad for artists and viewers - ABC News

Longhorn Laureates – UT News | The University of Texas at Austin

University of Texas professor John Goodenough will receive the Nobel Prize in Chemistry tomorrow at a ceremony in Sweden.

Goodenough won the award for his part in developing the lithium-ion battery, which powers most cell phones, electric cars and other portable electronic devices. At 97-years-old, he is the oldest person to ever win a Nobel Prize.

Hes not the first Longhorn laureate, of course.

Eight UT professors and alumni have won a Nobel Prize. Their pioneering work proves that what starts here really does change the world. They include:

Hermann Joseph Muller, a UT professor from 1920 to 1932, won the 1946 Nobel Prize in Physiology or Medicine. He was the first to show that radiation from X-rays could cause gene mutations and played a key role in early efforts to promote public awareness of the dangers of radiation.

Ilya Prigogine, a former UT professor, won the 1977 Nobel Prize in Chemistry. He showed how complex structures, such as life on Earth, could arise despite a law of physics that says all physical systems tend to become less organized over time. His research could also help explain the growth of cities and the dynamics of traffic jams.

UT professor Steven Weinbergwon the 1979 Nobel Prize in Physics. He proposed a theory unifying two fundamental forces of nature that led to the development of what is known as the Standard Model of particle physics the model that predicted the existence of the Higgs boson God particle. Weinberg is considered by many to be the preeminent living theoretical physicist.

UT alumnus E. Donnall Thomas, B.A.41, M.A. 43, won the 1990 Nobel Prize in Physiology or Medicine. Known as the father of bone marrow transplantation, he showed bone marrow could be successfully transplanted to treat illnesses such as leukemia, a discovery that paved the way for the use of organ and cell transplants as a way to treat diseases.

UT alumnus John Maxwell J.M. Coetzee, Ph.D. 69, won the 2003 Nobel Prize in Literature. One of the most award-winning English-language authors alive, he was the first to win the prestigious Booker prize twice for The Life & Times of Michael K in 1983 and Disgrace in 1989. The Swedish Academy praised the universal and humanistic character of his literary work.

Photo courtesy of Rockefeller University

UT alumnus Michael W. Young won the 2017 Nobel Prize in Physiology or Medicine. He shared the award with Jeffrey Hall and Michael Rosbash for research that led to the understanding of how plants, animals and humans synchronize their biological clocks with the Earths rotation. The three researchers analyzed genes of fruit flies and discovered that genes accumulated a specific protein at night that gradually degraded during daylight hours. Read more here.

UT alumnus James Allison, B.A. 69, Ph.D. 73, won the 2018 Nobel Prize in Physiology or Medicine. Allison, who is chairman of immunology at MD Anderson Cancer Center, shared the award with Tasuku Honjo of Kyoto University for discovering a new way to attack cancer by releasing the brakes on immune cells, a major landmark in the fight against cancer.Allisons pioneering work in immunotherapy has saved countless lives and turnedonce untreatable diagnoses into ones that are now treatable and beatable. Read more here.

John Goodenough, a professor in the Cockrell School of Engineering, won the Nobel Prize in Chemistry for his part in developing the lithium-ion battery, which powers most portable electronic devices, including cell phones and laptop computers. The lithium-ion battery can also store significant energy from solar and wind power, which has allowed for the development of new clean energy technologies. Goodenough won the award jointly with Stanley Whittingham of the State University of New York at Binghamton and Akira Yoshino of Meijo University. In the words of the Nobel Foundation, Through their work, they have created the right conditions for a wireless and fossil fuel-free society, and so brought the greatest benefit to humankind. Read more on the lithium-ion battery here.

Original post written by Kylie Fitzpatrick and updated by Ellie Breed, University Communications.

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Could the Monarch butterfly help us to understand seasonal depression? – Health Europa

Understanding the findings to translate day length encoding into seasonal physiological and behavioural responses in animals.

Biologists at Texas A&M University are making strides in understanding biological clock function in several model organisms and translating these studies into broader implications for human health, such as understanding seasonal depression.

The Merlin Laboratory in the Texas A&M Department of Biology has found genetic evidence linking circadian clock genes and clock-regulated molecular pathways to the Monarch butterflys uncanny ability to sense the changes in day length, or photoperiod an environmental cue that signals them to migrate and triggers the reproductive dormancy they exhibit in the process.

Their work establishes a clear connection between clock genes and the vitamin A pathway within the brain of this iconic insect.

The Merlin Labs study, published in theProceedings of the National Academy of Sciences, not only provides genetic proof for the photoperiod-clock connection but also demonstrates for the first time that it also regulates a critical vitamin A pathway necessary for seasonal responses.

Texas A&M biologist and 2017 Klingenstein-Simons Fellow Christine Merlin, said: Nearly all organisms adapt to the seasons by adjusting their physiology and behaviour to changes in day length, or photoperiod.

Despite decades of research, the molecular and genetic mechanisms by which changes in photoperiod are sensed and translated into seasonal changes in animal physiology and behaviour have remained poorly understood.

While much remains to be learned, our findings pave the way for understanding the mechanisms by which vitamin A operates in the brain to translate day length encoding into seasonal physiological and behavioural responses in animals.

Given that seasonal changes associated with this pathway have also been reported in the mammalian brain, it is tantalising to speculate that the function of vitamin A in animal photoperiodism may be evolutionary conserved.

If this turns out to be the case, our work in the Monarch could have implications for better understanding seasonal changes in the human brain that could lead to ailments such as seasonal depression.

For the past six years, Merlins lab within the Texas A&M Center for Biological Clocks Research has been using the majestic Monarch as a model to study animal migration, the role of circadian clocks in regulating daily and seasonal animal physiology and behaviour, and the evolution of the animal clockwork.

Aided by CRISPR/Cas9 technology, her group already has succeeded in altering key biological clock-related genes in the Monarch in order to study their impact on daily circadian rhythms and seasonal migratory responses.

One of the complications the Merlin lab had to overcome in the study is that vitamin A is necessary for visual function of the Monarchs compound eyes, meaning that their ninaB1 full-body knockouts would be rendered blind. As a fail-safe, Merlins team had to find a non-genetic way to eliminate the potential function of the compound eyes as a possible tie-back to the lack of photoperiodic responses observed in these new mutant butterflies.

Merlin said: We had to be creative, so we turned to arts and crafts experiments.

By painting the compound eyes of wild-type adult butterflies with black paint, we demonstrated that visual function was not necessary for photoperiodic responses, thereby supporting the idea that the vitamin A function in the brain and not the eyes is responsible for photoperiodic sensing and responses.

Merlin says the study raises interesting questions regarding the pathways possible involvement in any number of intriguing scenarios, including the production of a deep-brain photoreceptor for photoperiodic sensing, the seasonal regulation of a retinoic acid-mediated transcriptional program, and/or the seasonal plasticity of the clock neuronal circuitry in the brain.

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7th Pay Commission news today: Get salary upto Rs 67,700 in this sarkari institution, apply at aiimsjodhpur… – Zee Business

7th Pay Commission news today: All India Institute of Medical Sciences (AIIMS), Jodhpur has invited applications for over 110 posts of Senior Resident. Candidates can apply for the posts through online registration of application on AIIMS, Jodhpur website, http://www.aiimsjodhpur.edu.in. Interested candidates need to check the eligibility criteria and apply before December 30, 2019. Interestingly, the selected candidates will be paid as per 7th pay commission report based salary system.

7th Pay Commissionpay scale:For Senior Resident (Medical) candidates the pay scale is Rs 18,750 + 6,600 (Grade Pay) + NPA (Non Practicing Allowance) plus other usual allowance or revised pay scale as per 7th CPC as applicable. (Level 11 of the Matrix (Pre-revised PB 3, entry pay of the Rs 67,700per month + NPA plus other usual allowance admissible under rules).

Notably, NPA is applicable for only Medical candidates.

Vacancy details:Anesthesiology and Critical Care, MD / DNB (Anaesthesiology)Anatomy, MD / MS / DNB (Anatomy) / M.Sc. (Anatomy) with PhDBiochemistry, MD / DNB (Biochemistry) / M.Sc. (Biochemistry) with PhDBurns & Plastic Surgery, M.Ch./DNB (Burn & Plastic Surgery)Cardiology, DM/DNB (Cardiology)Cardiothoracic Surgery, M.Ch./DNB (CTVS)Community Medicine and Family Medicine, MD/DNB (Community Medicine / PSM)Dentistry (Endodontics), MDS (Endodontics)Diagnostic and Interventional Radiology, MD/DNB (Radiology)Endocrinology & Metabolism, DM/DNB (Endocrinology)Forensic Medicine & Toxicology, MD/DNB (Forensic Medicine)Gastroenterology, DM/DNB (Gastroenterology)General Medicine, MD/DNB (General Medicine)General Surgery, MS/DNB (General Surgery)Medical Oncology / Haematology, DM/DNB (Medical Oncology) / DM / DNB (Haematology)Microbiology, MD/DNB (Microbiology)Neonatology, MD/DNB (Paediatrics)/DM/DNB (Neonatology)Nephrology, DM/DNB (Nephrology)Neurology, DM/DNB (Neurology)Nuclear Medicine, MD/DNB (Nuclear Medicine)Orthopaedics, MS/DNB (Orthopaedics)Obstetrics and Gynaecology, MS/MD/DNB (Obs. & Gynaecology)Paediatric Surgery, M.Ch/DNB (Paediatric Surgery)Paediatrics, MD/DNB (Paediatrics)Pathology / Lab. Medicine, MD/DNB (Pathology)Pharmacology, MD/DNB (Pharmacology)Physical Medicine and Rehabilitation, MD/DNB (PMR)Physiology, MD/DNB (Physiology) / M.Sc. (Physiology) with PhDPsychiatry, MD/DNB (Psychiatry)Radiotherapy, MD/DNB (Radiotherapy)Surgical Gastroenterology, M.Ch/DNB (Surgical Gastroenterology)Surgical Oncology, M.Ch/DNB (Surgical Oncology)Transfusion Medicine and Blood Bank, MD/DNB (Transfusion Medicine / Pathology)Trauma & Emergency (Medical), MD/DNB (Medicine/Geriatric Medicine/Emergency Medicine)Trauma & Emergency (Surgical), MS/DNB (General Surgery)/M.Ch (Trauma Surgery and Critical Care)Urology, M.Ch/DNB (Urology)

Application Fees:For General/OBC category candidates the application fees is Rs 1,000/- + transaction charges as applicable. For SC/ST category the application fees are Rs 800. Note that the payment should be made online only.

Candidates can also check the official notice from the official website or else from this linkhere.

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Selection Process:Selection will be on the basis of MCQ based written examination and Interview. Candidates will be called for Interview in the ratio of 1:6 i.e. for one post, only six candidates will be called for the interview.

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7th Pay Commission news today: Get salary upto Rs 67,700 in this sarkari institution, apply at aiimsjodhpur... - Zee Business

How to live longer: Women who exercise have healthier hearts – Today.com

Women who exercise appear to live longer: Those who are very fit run a much lower risk of dying from heart disease, cancer and other common causes compared to those who are less active, a new study suggests. They new report is considered important because it's one of the few exercise studies that focus on benefits for women.

Spanish researchers found that compared to the fittest women, those with poor capacity for exercise were nearly four times more likely to die from heart disease, according to the study presented at EuroEcho 2019, the annual meeting of the European Association of Cardiovascular Imaging.

The fittest women in the study were able to manage the equivalent of walking up four flights of stairs in about 45 seconds, or walking up three flights very fast, said the studys lead author Dr. Jesus Peteiro, a cardiologist at the University Hospital A Coruna.

Prior to Peteiros research, information on the benefits of exercise in women had been scant as many studies have focused on men.

Peteiro believes there is hope even for women who don't workout if they are willing to make a change now. While gym memberships may work for some, its too easy to let those lapse, he said in an email.

Women were considered fit if they could walk fast up four flights of stairs or very fast up three flights without stopping to catch their breath.

We think that it is more important to change the lifestyle than to merely join a fitness club for a time, Peteiro said. For changing lifestyle we mean to change the daily routine to make it more active. For instance, commuting to work by walking, cycling or public transport always leads to more exercise than taking your car."

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Also, walking up stairs at home or work instead of using the elevator can help.

To take a closer look at how a womans fitness might impact her longevity, Peteiro and his colleagues turned to data that had been collected on 4,714 adult women with an average age of 64 who had been referred for a heart disease test that involves working out on a treadmill.

The women were asked to walk, and then run if they could, with increasing intensity until they couldnt go any longer. Images of the womens hearts were generated during the test.

The women were declared fit if they could work out at 10 metabolic equivalents or METs equal to walking fast up four flights of stairs or very fast up three flights without stopping to catch their breath.

One question Peteiro cant answer is what the fit women did to get in shape. That information wasnt in their records, he said.

The women who achieved 10 METs or more were compared to those who couldnt make 10 METs.

Over the next four and a half years, there were 345 deaths from heart disease, 164 from cancer and 203 from other causes.

The annual rate of death from heart disease was nearly four times higher among women who didn't exercise compared to those who were fit, 2.2% versus 0.6%, while the annual rate of cancer deaths among women with poor exercise tolerance was double that of the fit women, 0.9% versus 0.4%.

The annual rate of death from other causes was more than four times higher in those with poor exercise capacity compared to those who were fit, 1.4% versus 0.3%.

The new research adds to what is already known about exercise and longevity, but heralds as one of the few landmark studies that focus solely on women, said lcilma Fergus, director of cardiovascular disparities at The Mount Sinai Hospital in New York.

While many existing guidelines indicate that physical activity is an important first step, this study does help to quantify how much more of a benefit can be achieved by exercise, especially vigorous exercise, Fergus said in an email.

The new study underscores the importance of regular exercise for all of us, said Kerry Stewart, a professor of medicine and director of clinical and research physiology at Johns Hopkins Medicine.

The vast majority of evidence suggests that 30 minutes a day of moderate exercise will produce health benefits and lower the risk of many diseases, including cardiovascular disease, cancer, hypertension, diabetes and arthritis, Stewart said, adding that just being thin isnt enough to protect against these diseases.

There is research in men showing that those who were able to maintain a high level of fitness had the lowest risk of cardiovascular disease, Stewart said. And those who worked at becoming fit lowered their risk of heart disease, whereas those who started out in very good shape, but lost fitness over time were more at risk.

Linda Carroll is a regular contributor to NBCNews.com and Today.com. She is also the co-author ofOut of the Clouds: The Unlikely Horseman and The Unwanted Colt who Conquered the Sport of Kings.

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AbbVie and Scripps Research Enter Research Partnership in Cancer, Immunology, Neurology and Fibrosis – BioSpace

Illinois-based AbbVie and La Jolla, California-based The Scripps Research Institute entered into a broad research collaboration in oncology, immunology, neurology and fibrosis.

Based on our strong switchable CAR-T alliance launched in 2018, we feel the expanded relationship with AbbVie represents a robust path forward for some of our programs, complementing a diverse ecosystem of innovation weve created over the past several years at Scripps to advance life-changing therapies, said Peter Schultz, chief executive officer of Scripps Research and Calibr, its drug discovery division.

Under the terms of the 2018 agreement, AbbVie paid Calibr an upfront license fee and picked up exclusive access to Calibrs switchable CAR-T platform for up to four years. The plan was to develop T-cell therapies against solid tumor targets chosen by AbbVie. AbbVie had the option to develop more cell therapies toward its targets and license existing Calibr cell therapy programs in hematological and solid cancers, including Calibrs lead programs.

In the new collaboration, in addition to the initial programs, Scripps will offer AbbVie a certain number of preclinical programs each year to be included in the partnership. They will work together in parallel to advance CD3 bispecifics against cancer targets picked by AbbVie

Under the terms of the deal, Scripps will run preclinical R&D, and in some cases, Phase I clinical trials. AbbVie will have an exclusive option to continue development and possible commercialization activities.

Once AbbVie chooses to exercise its option on any given program, it will pay Scripps additional payments that include option exercise fees, success-based development and commercial milestone payments, and tiered royalties. At hitting a milestone, AbbVie will make an undisclosed upfront payment as well as near-term milestone payments.

The best way to develop transformational medicines is through collaborations that bring together the brightest minds, said Mohit Trikha, vice president and head of oncology early development at AbbVie. This partnership with Scripps Research will collaboratively advance next generation programs, build stronger relationships with proven and emerging scientific leaders, and most importantly help us advance novel medicines for patients.

Trikha added, We are eager to partner with Scripps on these assets as they enter the clinic over the next few years as Scripps has one of the strongest track records of any academic institution when it comes to advancing novel medicines for patients.

Although neither organization released financial terms, they did say the partnership requires antitrust review. Under the law, reports The San Diego Union-Tribune, antitrust review has to be conducted for deals exceeding $84.4 million.

The Tribune notes, A deal of that size will bolster the La Jolla biomedical science institutes troubled finances for several years, and perhaps much longer. And if approved cancer therapies result, the payout could be gigantic.

The early work will be on an immuno-oncology treatment for lymphoma, which Calibr plans to launch in the clinic in 2020.

What were developing is a fully controllable, universal switchable CAR-T cell platform that allows a physician fine control over the activation and specificity of the CAR-T cells, Travis Young, director of protein sciences at Calibr told The Tribune.

At the moment, there are two CAR-T products approved, Novartis Kymriah and Gilead Sciences Yescarta. Both are quite effective in certain patient populations, but the process is expensive and time-consuming, requiring immune cells be collected from the patient, engineered to focus on the patients specific cancer, then be infused back into the patient. A number of companies are working on off-the-shelf CAR-T, that would not require the specific engineering catered to each patient.

CAR-T and other immunotherapy approaches also have high risks of immune reactions, although Novartis and Gilead have both developed protocols for minimizing or dealing with them. Scripps argues that their type of CAR-T improves over these, particularly in terms of safety, convenience and versatility.

These antibody-based switches bridge the CAR-T cells to the target cell. And so, by forming that bridge, they develop an immunological synapse, which redirects the CARs very specifically towards the target cells, said Young.

They also claim they can control the intensity of the response by varying the number of antibodies infused, would should minimize the adverse immune reactions.

The Tribune notes that in recent years Scripps has reported annual deficits that have hit as high as $20 million. The company currently has a drug in early clinical trials for osteoarthritis and is prepping another for prostate cancer, which it is hoping to partner with a company for commercialization.

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AbbVie and Scripps Research Enter Research Partnership in Cancer, Immunology, Neurology and Fibrosis - BioSpace

Impact of Induced Syncytia Formation on the Oncolytic Potential of Myx | OV – Dove Medical Press

Chase Burton, Mee Y Bartee, Eric Bartee

Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA

Correspondence: Eric BarteeDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Ave, Charleston, SC, USAEmail bartee@musc.edu

Introduction: Cancer has become one of the most critical health issues of modern times. To overcome the ineffectiveness of current treatment options, research is being done to explore new therapeutic modalities. One such novel treatment is oncolytic virotherapy (OV) which uses tumor tropic viruses to specifically target and kill malignant cells. While OV has shown significant promise in recent clinical trials, the therapeutic use of viruses poses a number of unique challenges. In particular, obtaining effective viral spread throughout the tumor microenvironment remains problematic. Previous work has suggested this can be overcome by forcing oncolytic viruses to induce syncytia formation.Methods: In the current work, we generated a series of recombinant myxoma viruses expressing exogenous fusion proteins from other viral genomes and examined their therapeutic potential in vitro and in vivo.Results: Similar to previous studies, we observed that the expression of these fusion proteins during myxoma infection induced the formation of multinucleated syncytia which increased viral spread and lytic potential compared to non-fusogenic controls. Contrary to expectations, however, the treatment of established tumors with these viruses resulted in decreased therapeutic efficacy which corresponded with reduced viral persistence.Discussion: These findings indicate that enhanced viral spread caused by syncytia formation can actually reduce the efficacy of OV and supports a number of previous works suggesting that the in vitro properties of viruses frequently fail to predict their in vivo efficacy.

Keywords: myxoma virus, syncytia, fusogenic, oncolytic virotherapy, lung cancer

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Impact of Induced Syncytia Formation on the Oncolytic Potential of Myx | OV - Dove Medical Press

Research casts new light on the role of the immune… – ScienceBlog.com

New research by scientists at Harvard Medical School has found that nerves in the guts of mice do not merely sense the presence ofSalmonellabut actively protect against infection by this dangerous bacterium by deploying two lines of defense.

The study,published Dec. 5 inCell, casts in a new light the classic view of the nervous system as a mere watchdog that spots danger and alerts the body to its presence. The results show that by directly interfering withSalmonellas ability to infect the intestines, the nervous system is both a detector of danger and a defender against it.

Our results show the nervous system is not just a simple sensor-and-alert system, said neuro-immunologistIsaac Chiu, the studys lead investigator and assistant professor of immunology in the Blavatnik Institute at Harvard Medical School. We have found that nerve cells in the gut go above and beyond. They regulate gut immunity, maintain gut homeostasis and provide active protection against infection.

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Specifically, the experiments reveal that pain-sensing neurons embedded in the small intestine and beneath cells called Peyers patches are activated by the presence ofSalmonella, a foodborne bacterium responsible for a quarter of all bacterial diarrheal disease worldwide.

Once activated, the nerves use two defensive tactics to prevent the bug from infecting the intestine and spreading throughout the rest of the body. First, they regulate the cellular gates that allow microorganisms and various substances to go in and out of the small intestine. Second, they boost the number of protective gut microbes called SFB (segmented filamentous bacteria), which are part of the microbiome in the small intestine.

Bacteria get on our nerves

Under normal conditions, Peyers patchesclusters of lymphatic and immune tissue found exclusively on the wall of the small intestinescan the environment, sample substances and determine what can go into the intestine. To perform this function, Peyers patches are studded with microfold cells, or M cells, which are cellular channels that open and close to regulate influx of substances and microorganisms into the intestine. M cells are the major entry points thatSalmonellaand other dangerous bacteria exploit to invade the small intestine. To do so, theSalmonellabacterium injects into the gut transcription factors that stimulate intestinal cells to become M cells. Next, Salmonella latches onto sugars sitting atop the M cellsthe cellular gatesand uses its tentacles to prop the gates open. The bacterium then wiggles its way into the intestine.

To understand the role of pain-sensing gut neurons in infection protection, researchers compared how mice with and without them responded toSalmonella. One group of mice had intact gut neurons, another group had these neurons genetically disabled or deleted, and yet another cohort had them chemically disabled.

Experiments showed that in the presence ofSalmonella, gut neurons fire back by releasing a neurochemical called CGRP, which slows down M cell differentiation, thereby reducing the number of entry points that Salmonella can use. Additionally, the experiments show, gut neurons launch another form of defense. By releasing CGRP, they boost the presence of SFB microbesmicroorganisms that, among performing other beneficial functions, also guard againstSalmonellainvasion. Precisely how they do so remains unclear, but Chiu and colleagues say one plausible mechanism may be that SFB uses its tiny little hooks to attach itself to the intestinal wall and form a repellent coating that shields against the disease-causing bacteria.

Both defense mechanisms functioned reliably in mice with intact gut neurons. Not so, however, in animals that lacked these gut neurons. Indeed, intestinal biopsies from mice with inactivated neurons showed their Peyers patches more densely infiltrated by Salmonella at a greater rate than animals with intact neurons. The neuron-deficient animals also had fewer protective SFB microbes in their guts. Not surprisingly, these mice got sick fromSalmonellaat a greater rate and had more widespread disease than mice with intact nerve fibers.

It is becoming increasingly clear that the nervous system interacts directly with infectious organisms in various ways to affect immunity, Chiu said. Bacteria literally do get on our nerves.

The findings are in line with past research by Chius group showing a powerful three-way interplay between infection and the nervous and the immune systems. But in contrast to the new findings, the previous work showed that the nervous system can, at times, be exploited by infectious organisms to their advantage. For example, Chius previousresearchfound that nerves in the lungs can alter immune response in serious lung infections with the bacteriumStaphylococcus aureus, commonly known as staph. In anotherstudy, Chius team discovered that the bacterium that can cause flesh-eating disease hijacks nerves as a way to dampen immune defenses and weaken the bodys defenses.

A diverse repertoire

The new findings add to a growing body of knowledge showing that the nervous system has a repertoire far broader than signaling to and from the brain.

Our findings illustrate an important cross talk between the nervous system and the immune system, said study first author Nicole Lai, research fellow in immunology in the Chiu lab. It is clearly a bidirectional highway with both systems sending messages and influencing each other to regulate protective responses during infection.

Indeed, the gut contains so many nerves that it has often been called the second brain. As an alert system designed to warn the body of looming threats, the nervous system acts ultrafast. Thus, the new findings, the researchers said, suggest that evolution has taken advantage of this feature for added protection.

If you think about it, the nervous systems involvement in immunity is an evolutionarily smart way to protect the gut from infection by repurposing an existing feature, Chiu said.

The researchers say their findings could also help explain previous observations showing that the use of opioidswhich silence pain-sensing nerve fibersand other nerve-modulating drugs can make people more prone to infections.

If you dial down nerve signaling in an effort to reduce pain, you may be inadvertently also dampening their protective abilities, Chiu said. Our observations support that idea.

The interaction between gut neurons and gatekeeping M cells represents an area ripe for future research, the team said, because M cellsthe molecular gates of the small intestineare also exploited by other organisms that cause serious human disease, including the bacteriaE. coli, ShigellaandYersinia, as well as prions, self-propagating clumps of misfolded protein that can cause rare but universally fatal neurodegenerative conditions.

The results also point to a possible therapeutic pathway that involves modulating nerve signaling either for boosting gut immunity or intestinal inflammation.

The idea would be that if we could somehow stimulate these protective gut neurons or mimic their activity with a drug, we could activate the immune response and increase the bodys ability to fend off infection, Chiu said.

Other researchers included Melissa Musser, Felipe Pinho-Ribeiro, Pankaj Baral, Amanda Jacobson, Pingchuan Ma, David Potts, Zuojia Chen, Donggi Paik, Salima Soualhi, Yiqing Yan, Aditya Misra, Kaitlin Goldstein, Valentina Lagomarsino, Anja Nordstrom, Kisha Sivanathan, Antonia Wallrapp, Vijay Kuchroo, Roni Nowarski, Michael Starnbach, Hailian Shi, Neeraj Surana, Dingding An, Chuan Wu, Jun Huh, and Meenakshi Rao.

This work was supported by National Institutes of Health grants DP2AT009499 and K08 AI108690, National Institute of Allergy and Infectious Diseases grant R01AI130019, NIH grant R01 DK110559, the Chan-Zuckerberg Initiative, Harvard Digestive Disease Center, National Institute of Diabetes and Digestive and Kidney Diseases (grant K08 DK110532), National Multiple Sclerosis Society (Career Transition award TA3059-A-2), and Whitehead Scholar award and Translating Duke Health Scholar award.

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University community mourns the death of Stephen Benedict, professor of microbiology – KU Today

LAWRENCE The University of Kansas has lost a longtime faculty member to a battle with cancer. Stephen Benedict, professor of microbiology, died Dec. 2 in Lawrence. He was 72.

Professor Benedict was a dedicated researcher and an inspirational and award-winning teacher to his many hundreds of students during his long career at KU, said Chancellor Douglas A. Girod. On behalf of the entire university, I offer my sincere condolences to his family, his friends and all who knew him throughout his time at KU.

Benedict came to KU in 1990 as an assistant professor of pharmacology & toxicology and later moved to the Department of Molecular Biosciences. Benedict was named full professor in 2008, a position he held until his death.

He touched the lives of many hundreds of KU undergraduates, said Susan Egan, professor and chair of the Department of Molecular Biosciences. Among Benedicts career honors were numerous awards recognizing his influence on students. Those honors included the Kemper Teaching Award, the Robert Weaver Graduate Mentoring Award, the J. Michael Young Academic Advisor Award, the Chancellors Club Teaching Professorship and the Mortar Board Outstanding Educator Award.

Moreover, Benedict was voted Favorite Biology Professor from among nearly 50 biology faculty members five times over the past 15 years, Egan said.

Benedicts research interests centered on immune-related disorders specifically related to T-cells. He published nearly 90 academic papers, received six U.S. patents and made numerous service contributions to the field, from serving on grant review panels for the National Institutes of Health to serving as associate editor of the Journal of Immunology.

Steves loss will be felt widely among the KU community and far beyond, Egan said. He will be remembered for the deep caring he showed for his students, his positivity and his tremendous sense of humor.

A celebration of life service is planned for Jan. 18, 2020, in Lawrence.

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Advaite Inc. Enters into Exclusive License Option Agreement with the George Washington University for Novel AMES Negative HDAC6 Inhibitor Technology -…

CHICAGO, Dec. 9, 2019 /PRNewswire/ -- Advaite Inc., a Chicago, IL based oncology-focused biotech company developing novel therapeutics and diagnostics to help patients suffering from debilitating diseases, has announced that it has entered into an exclusive license option agreement with the George Washington University with respect to the intellectual property of a novel AMES Negative HDAC6 inhibitor. Histone Deacetylases modulate a multitude of cellular processes and are part of the regulation of cellular pathways involved in anti-tumor immunologic responses. Selective inhibition of HDAC6 slows tumor growth in various cancer models. Under terms of this agreement, Advaite has the option to exclusively license intellectual property covering methods of use and pharmaceutical compositions.

"We look forward to future success by advancing the development of this novel HDAC6 inhibitor to treat a multitude of cancers, to ease suffering and extend life. This epigenetic regulator can have a potentially enormous therapeutic effect on patients who continue to suffer from debilitating cancer, as there is a great need for therapies that deliver an effective response, and specifically ones which are not limited by their toxicity profile. George Washington University's expertise with HDACs provide a perfect relationship for Advaite to advance truly viable, state of the art, impactful technology," said Karthik Musunuri, CEO & Co-Founder of Advaite.

"The quest for newer and more effective ways of treating cancer has now led to an extensive focus on the involvement of the immune system and its capacity to recognize and engage tumor cells. Recent findings from several research groups have demonstrated that ultra-selective HDAC6 inhibitors have the unique capacity of remodeling of the cellular composition of tumors, favoring the recognition and killing of cancer cells by the immune system. Our novel HDAC6 inhibitor has shown to have reduced toxic effects, thus clearly differentiating from previous HDAC inhibitors used in the clinic," said Alejandro Villagra, Ph.D., Member of the Immunology and Microbial Oncology Research Program at the GW Cancer Center and Assistant Professor of Biochemistry and Molecular Medicine at the GW School of Medicine and Health Sciences.

About Advaite

Advaite Inc. is a biotech company focused on developing novel therapeutics and diagnostics to help patients suffering from a variety of debilitating diseases, primarily within the oncology space. Advaite strives to maintain a patient centric approach in developing healthcare innovations. For more information, please visit http://www.advaite.com.

Forward Looking Statement

This press release includes statements that are "forward-looking statements," within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. While Advaite has based any forward looking statements contained herein on its current expectations, the information on which such expectations were based may change. These forward-looking statements rely on a number of assumptions concerning future events and are subject to a number of risks, uncertainties, and other factors, many of which are outside ofAdvaite's control.

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Advaite Inc. Enters into Exclusive License Option Agreement with the George Washington University for Novel AMES Negative HDAC6 Inhibitor Technology -...