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Trump Tweets Video With ‘White Power’ Chant, Then Deletes it

President Donald Trump on Sunday tweeted approvingly of a video showing one of his supporters chanting “white power,” a racist slogan associated with white supremacists. He later deleted the tweet and the White House said the president had not heard “the one statement” on the video.

The video appeared to have been taken at The Villages, a Florida retirement community, and showed dueling demonstrations between Trump supporters and opponents.

“Thank you to the great people of The Villages,” Trump tweeted. Moments into the video clip he shared, a man driving a golf cart displaying pro-Trump signs and flags shouts ‘white power.” The video also shows anti-Trump protesters shouting “Nazi,” “racist,” and profanities at the Trump backers.

“There’s no question” that Trump should not have retweeted the video and “he should just take it down,” Sen. Tim Scott, R-S.C., told CNN’s “State of the Union.” Scott is the only Black Republican in the Senate.

Shortly afterward, Trump deleted the tweet that shared the video. White House spokesman Judd Deere said in a statement that “President Trump is a big fan of The Villages. He did not hear the one statement made on the video. What he did see was tremendous enthusiasm from his many supporters.”

The president’s decision to highlight a video featuring a racist slogan comes amid a national reckoning over race following the deaths of George Floyd and other Black Americans. Floyd, a Black Minneapolis man, died after a white police officer pressed his knee into his neck for several minutes.

Protests against police brutality and bias in law enforcement have occurred across the country following Floyd’s death and there has also been a push to remove Confederate monuments, an effort Trump has opposed.

Trump’s tenure in office has appeared to have emboldened white supremacist and nationalist groups, some of whom have embraced his presidency. In 2017, Trump responded to clashes in Charlottesville, Virginia, between white nationalists and counter-protesters by saying there were “very fine people on both sides.”

 

Source: Voice of America

 

 

Pence Blames Younger People for Increase in US Coronavirus Cases

WASHINGTON – U.S. Vice President Mike Pence on Sunday mostly blamed young people for the sharp increase in recent days of the number of confirmed cases in the country, saying they are ignoring precautions to prevent the spread of the coronavirus.

Pence, in an interview on CBS’s “Face the Nation” show, said it is “inarguable” that increased testing in the U.S., with 500,000 per a day, has led to confirmation of more people with coronavirus infections. But he said “younger Americans have been congregating in ways that may have disregarded the guidance that we gave on the federal level for all the phases of reopening businesses.”

The number of coronavirus cases in the U.S. has risen sharply in recent days, particularly in a trio of states across southern tier of the U.S.:  Florida, Texas and Arizona, which are separated by hundreds of kilometers. In total, the U.S. reported more than 40,000 new cases Friday, a single-day record for reports of the pandemic in the U.S. over the last six months.

Pence has canceled political trips this coming week to both Florida and Arizona out of caution because of the increased number of cases in the two states.

Pence said the U.S. is better equipped medically to handle the hospitalization of more coronavirus patients than it was early in the year.

 

But he said President Donald Trump and he support measures taken by governors in Florida and Texas to again close bars to prevent people from gathering there, shoulder to shoulder, while ignoring frequent admonitions from health experts to wear masks and to socially distance from each other by at least two meters.

“It’s clear testing isn’t the only reason that we’re seeing more cases, but it’s a significant reason,” while adding, “It’s clear across the Sunbelt that there’s something happening, particularly among younger Americans.” Pence said.

But he said the Trump administration does not think it is necessary to impose national mandatory directives to wear a face mask.

Trump has rarely worn a mask, saying he does not think it is for him.

Health and Human Services Secretary Alex Azar told CNN that Trump’s unique circumstances are a reason why he doesn’t wear a mask.

He said Trump is regularly tested for coronavirus and that as a leader of the free world is in “very different circumstances than the rest of us.”

Azar urged Americans to take precautions for “public health.”

 

Pence has more frequently put on a mask, again on Sunday as he attended a church service in Dallas, Texas. He rejected the suggestion that Trump could help slow the spread of coronavirus by setting an example nationally by wearing a mask.

“We believe people should wear masks wherever social distancing is not possible, wherever it’s indicated by either state or local authorities,” Pence said.

But he added, “We believe that every state has a unique situation. One of the elements of the genius of America is the principle of federalism, of state and local control…we want to defer to governors, defer to local officials. And people should listen to them.”

In all, the U.S. has now recorded more than 2.5 million coronavirus cases and more than 125,000 deaths, both far and away the biggest national figures across the world. Health officials are predicting that tens of thousands more Americans will die in the coming months.

 

Source: Voice of America

 

 

Cell Publication Elucidates How SARS-CoV-2 Dramatically Rewires Important Cell Programming; Identifies Existing Therapeutics That May Fight COVID-19

Caco-2 cells

Fluorescence microscopy image of a two cell cluster of Caco-2 cells (human colon cells) infected with SARS-CoV-2 virus, the causative agent of COVID-19. Infected cells produce filopodia protrusions (white) extending out from the cell surface containing viral particles (M protein in red). Photo credits to Dr. Robert Grosse, CIBSS, University of Freiburg.

For the First Time, Images Show Rapid Spread of Infection May be Explained by Extensive Filopodia, Stringy Protrusions in Virally Infected Cells

Discoveries Emanate from QBI UCSF “Blueprint Map” Revealing how SARS-CoV-2 Hijacks Human Cells

SAN FRANCISCO, June 28, 2020 (GLOBE NEWSWIRE) — Pioneering a new paradigm in drug discovery by leveraging biological understanding of how a virus interacts with its host, an international team of researchers conducted a global analysis of proteins in human cells to determine mechanisms by which SARS-CoV-2 shifts cellular activity in infected cells. During the study, the researchers discovered for the first time that cells infected with SARS-CoV-2 exhibit filopodia, stringy arm-like extensions, which may explain rapid viral spread throughout the body.

Vero Cells

Electron microscopy image of Vero E6 cells infected with SARS-CoV-2 virus, the causative agent of COVID-19, produce filopodia protrusions (finger-like projections) extending out from the cell surface to enable budding of viral particles (circular spheres) and infection of nearby cells. Photo credits to Dr. Elizabeth Fischer, NIAID/NIH.

The quantitative study, ‘The Global Phosphorylation Landscape of SARS-CoV-2 Infection online now in Cell, builds upon a previously published novel “blueprint” of the 332 human proteins that interact with 27 SARS-CoV-2 viral proteins. In an extension of the blueprint, the scientists evaluated all human proteins that exhibited changes in phosphorylation. Phosphorylation, the addition of a phosphoryl group to a protein by an enzyme class called kinases, plays a pivotal role in the regulation of most cell processes including the production of the cytoskeleton, protein function, cell-to-cell communication, cell growth and cell death. The scientists collaborated with Zoic Labs to overlay this new phosphorylation information onto the interactive version of the previously published protein-protein interaction map.

“By conducting a systematic analysis of the changes in cell programming through phosphorylation when SARS-CoV-2 infects a cell, we identified several key factors that will not only inform the next areas of biological study but also therapies that may be repurposed to treat patients with COVID-19,” said Nevan Krogan, Ph.D., director of the Quantitative Biosciences Institute (QBI) at the School of Pharmacy at UC San Francisco, senior investigator at Gladstone Institutes, and lead investigator of the study. Key scientists from UCSF, QBI’s Coronavirus Research Group (QCRG), Gladstone, EMBL’s European Biosciences Institute (EMBL-EBI) in Cambridge, England, Icahn School of Medicine at Mount Sinai in New York, Institut Pasteur in Paris, University of Freiburg in Germany and NIH Rocky Mountain Laboratories in Montana participated in the research.

”Our understanding of how this virus co-opts human cells continues to be a fruitful source of key virus-host cell interactions, which are leading us to promising therapies already in existence that can disrupt the virus’ clever way of surviving and thriving within the body,” continued Dr. Krogan.

Phosphorylation of Viral and Human Host Proteins During Infection

The team determined that 40 of the 332 human proteins that interact with SARS-CoV-2 were significantly differentially phosphorylated in cells infected with SARS-CoV-2. In addition, they identified 49 human kinases, out of a total of 518, that showed changes – either upregulation or downregulation – of phosphorylation activity.

Vero Cells

Electron microscopy image of Vero E6 cells infected with SARS-CoV-2 virus, the causative agent of COVID-19, produce filopodia protrusions (red) extending out from the cell surface to enable budding of viral particles (yellow) and infection of nearby cells. Photo credits to Dr. Elizabeth Fischer, NIAID/NIH. Bouhaddou et al. © Elsevier 2020

The most strongly hijacked kinases include casein kinase II (CK2), kinases within the p38/MAP kinase (p38/MAPK) pathway, cyclin-dependent kinases (CDKs) and phosphatidylinositol 5-kinase (PIKFYVE), all of which fall within a set of cell signaling pathways. Because kinases possess certain structural features, they are very druggable targets with more than 500 compounds commercially available or in development.

Researchers then set out to evaluate whether existing compounds would inhibit SARS-CoV-2 in infected cells in which specific kinases had been manipulated by the virus.

“We employed state-of-the-art bioinformatics approaches to readily identify regulated kinases from sparse phosphorylation profiles, many of which are likely to be established drug targets with therapeutic potential,” commented Pedro Beltrao, Ph.D., group leader at EMBL’s European Bioinformatics Institute.

Specifically, the researchers found that:

  • CK2, a kinase that plays a key role in cytoskeleton formation, cell growth and proliferation as well as apoptosis (cell death), physically interacted with the SARS-CoV-2 viral N protein and was significantly more activated in virally infected cells. Using a CK2 inhibitor in the laboratory experiments eliminated the virus.
  • Several kinases within the p38/MAPK pathway respond to and control the production of potentially harmful pro-inflammatory cytokines including IL-6, IL-10 and TNF-alpha. Inhibiting p38/MAPK signaling in virally infected  suppressed the overproduction of inflammatory cytokines and directly impaired viral replication, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis.
  • CDKs are kinases that regulate cell cycle and DNA damage response. Cells infected with SARS-CoV-2 have significantly reduced CDK activities, which may facilitate viral replication. Inhibition of CDKs may halt viral replication.
  • PIKFYVE, a FYVE finger-containing phosphoinositide kinase that regulates cytoskeleton function, is targeted in a variety of different cancers. The compound apilimod that targets this kinase potently inhibited SARS-CoV-2 in the laboratory setting.

Repurposing Kinase Inhibitors for Treatment of COVID-19

The team triangulated changes in phosphorylation to specific protein kinase targets and identified 87 U.S. Food and Drug Administration (FDA) approved drugs and compounds in clinical trials or development. Based on an initial systematic review of these compounds, the researchers identified seven agents, primarily anti-cancer and anti-inflammatory compounds, that demonstrated antiviral activity in laboratory experiments: silmitasertib, gilteritnib, MAPK13-IN-1, SB203580, ralimetinib, apilimod and dinaciclib.

“We are encouraged by our findings that drugs targeting differentially phosphorylated proteins inhibited SARS-CoV-2 infection in cell culture,” said Kevan Shokat, Ph.D., professor in the department of Cellular and Molecular Pharmacology at UC San Francisco (UCSF). “We expect to build upon this work by testing many other kinase inhibitors while concurrently conducting gene knockout experiments with RNAi technologies to continue to identify both the underlying pathways and additional potential therapeutics that may intervene in COVID-19 effectively.”

Importantly, additional studies are needed to further characterize the anti-viral potential of the compounds identified through this analysis.

Filopodia on Virally Infected Cells Newly Discovered Through Advanced Imaging

Interestingly, while studying the impact of SARS-CoV-2 on CK2, high resolution imaging of virally infected cells produced by the NIH/NIAID/Rocky Mountain Laboratories and University of Freiburg revealed actin-rich filopodia containing viral proteins. Human CK2 and the viral N protein were found co-localized within the filopodia, suggesting that SARS-CoV-2 hijacks CK2 and co-opts it into creating these tentacle-like protrusions that poke holes in their neighboring cells.

Conversely, other viruses including vaccinia, Ebola and Marburg take over the host cell cytoskeleton to promote egress and rapid cell-to-cell spread. However, in SARS-CoV-2 infected cells, the filopodia exhibit longer tentacles and branches, enabling more aggressive transmission than some other viral infections.

“The distinct visualization of the extensive branching of the filopodia once again elucidates how understanding the biology of virus-host interaction can illuminate possible points of intervention in the disease,” continued Dr. Krogan. “Our data driven approach for drug discovery has identified a new set of drugs that have great potential to fight COVID-19, either by themselves or in combination with other drugs, and we are excited to see if they will help end this pandemic.”

About QBI: The Quantitative Biosciences Institute (QBI) is a University of California organized research unit reporting through the UCSF School of Pharmacy. QBI fosters collaborations across the biomedical and the physical sciences, seeking quantitative methods to address pressing problems in biology and biomedicine. Motivated by problems of human disease, QBI is committed to investigating fundamental biological mechanisms, because ultimately solutions to many diseases have been revealed by unexpected discoveries in the basic sciences. Learn more at qbi.ucsf.edu.

About UCSF: The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. UCSF Health, which serves as UCSF’s primary academic medical center, includes top-ranked specialty hospitals and other clinical programs, and has affiliations throughout the Bay Area. Learn more at ucsf.edu or see our Fact Sheet.

About Gladstone Institutes: To ensure our work does the greatest good, Gladstone Institutes focuses on conditions with profound medical, economic, and social impact—unsolved diseases. Gladstone is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease. It has an academic affiliation with UC San Francisco. Learn more at gladstone.org.

Authorship and funding: This work was funded by grants from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases, both part of the National Institutes of Health; the Defense Advanced Research Projects Agency; the Center for Research for Influenza Pathogenesis; the Centers of Excellence for Influenza Research and Surveillance of the National Institute of Allergy and Infectious Diseases; the Centers of Excellence for Integrative Biology of Emerging Infectious Diseases of the Agence Nationale de la Recherche (France); F. Hoffmann-LaRoche AG; Vir Biotechnology, Centre for Integrative Biological Signalling Studies (CIBSS), European Research Council (ERC) and the Ron Conway Family. Shokat is a Howard Hughes Medical Institute investigator. A complete list of authors and full funding information is available in the Cell paper.

Media Contacts

UCSF QBI                                                                    
Angela Bitting, Wheelhouse LSA
a.bitting@comcast.net
925-202-6211

UCSF
Pete Farley, UCSF Office of Communications
peter.farley@ucsf.edu
415-317-3781

Sylvia Wheeler, Wheelhouse LSA
swheeler@wheelhouselsa.com

Gladstone Institutes                    
Megan McDevitt, Gladstone Communications
megan.mcdevitt@gladstone.ucsf.edu
415-734-2019

Photos accompanying this announcement are available at

https://www.globenewswire.com/NewsRoom/AttachmentNg/9145af6f-0c38-4690-97a7-d60db05a6770

https://www.globenewswire.com/NewsRoom/AttachmentNg/96f65f4c-c1a8-4ed2-a504-a48019388204

https://www.globenewswire.com/NewsRoom/AttachmentNg/c3198fcf-1b2a-4bd0-a783-4d9026327c19

Cell Publication Elucidates How SARS-CoV-2 Dramatically Rewires Important Cell Programming; Identifies Existing Therapeutics That May Fight COVID-19

Caco-2 cells

Fluorescence microscopy image of a two cell cluster of Caco-2 cells (human colon cells) infected with SARS-CoV-2 virus, the causative agent of COVID-19. Infected cells produce filopodia protrusions (white) extending out from the cell surface containing viral particles (M protein in red). Photo credits to Dr. Robert Grosse, CIBSS, University of Freiburg.

For the First Time, Images Show Rapid Spread of Infection May be Explained by Extensive Filopodia, Stringy Protrusions in Virally Infected Cells

Discoveries Emanate from QBI UCSF “Blueprint Map” Revealing how SARS-CoV-2 Hijacks Human Cells

SAN FRANCISCO, June 28, 2020 (GLOBE NEWSWIRE) — Pioneering a new paradigm in drug discovery by leveraging biological understanding of how a virus interacts with its host, an international team of researchers conducted a global analysis of proteins in human cells to determine mechanisms by which SARS-CoV-2 shifts cellular activity in infected cells. During the study, the researchers discovered for the first time that cells infected with SARS-CoV-2 exhibit filopodia, stringy arm-like extensions, which may explain rapid viral spread throughout the body.

Vero Cells

Electron microscopy image of Vero E6 cells infected with SARS-CoV-2 virus, the causative agent of COVID-19, produce filopodia protrusions (finger-like projections) extending out from the cell surface to enable budding of viral particles (circular spheres) and infection of nearby cells. Photo credits to Dr. Elizabeth Fischer, NIAID/NIH.

The quantitative study, ‘The Global Phosphorylation Landscape of SARS-CoV-2 Infection online now in Cell, builds upon a previously published novel “blueprint” of the 332 human proteins that interact with 27 SARS-CoV-2 viral proteins. In an extension of the blueprint, the scientists evaluated all human proteins that exhibited changes in phosphorylation. Phosphorylation, the addition of a phosphoryl group to a protein by an enzyme class called kinases, plays a pivotal role in the regulation of most cell processes including the production of the cytoskeleton, protein function, cell-to-cell communication, cell growth and cell death. The scientists collaborated with Zoic Labs to overlay this new phosphorylation information onto the interactive version of the previously published protein-protein interaction map.

“By conducting a systematic analysis of the changes in cell programming through phosphorylation when SARS-CoV-2 infects a cell, we identified several key factors that will not only inform the next areas of biological study but also therapies that may be repurposed to treat patients with COVID-19,” said Nevan Krogan, Ph.D., director of the Quantitative Biosciences Institute (QBI) at the School of Pharmacy at UC San Francisco, senior investigator at Gladstone Institutes, and lead investigator of the study. Key scientists from UCSF, QBI’s Coronavirus Research Group (QCRG), Gladstone, EMBL’s European Biosciences Institute (EMBL-EBI) in Cambridge, England, Icahn School of Medicine at Mount Sinai in New York, Institut Pasteur in Paris, University of Freiburg in Germany and NIH Rocky Mountain Laboratories in Montana participated in the research.

”Our understanding of how this virus co-opts human cells continues to be a fruitful source of key virus-host cell interactions, which are leading us to promising therapies already in existence that can disrupt the virus’ clever way of surviving and thriving within the body,” continued Dr. Krogan.

Phosphorylation of Viral and Human Host Proteins During Infection

The team determined that 40 of the 332 human proteins that interact with SARS-CoV-2 were significantly differentially phosphorylated in cells infected with SARS-CoV-2. In addition, they identified 49 human kinases, out of a total of 518, that showed changes – either upregulation or downregulation – of phosphorylation activity.

Vero Cells

Electron microscopy image of Vero E6 cells infected with SARS-CoV-2 virus, the causative agent of COVID-19, produce filopodia protrusions (red) extending out from the cell surface to enable budding of viral particles (yellow) and infection of nearby cells. Photo credits to Dr. Elizabeth Fischer, NIAID/NIH. Bouhaddou et al. © Elsevier 2020

The most strongly hijacked kinases include casein kinase II (CK2), kinases within the p38/MAP kinase (p38/MAPK) pathway, cyclin-dependent kinases (CDKs) and phosphatidylinositol 5-kinase (PIKFYVE), all of which fall within a set of cell signaling pathways. Because kinases possess certain structural features, they are very druggable targets with more than 500 compounds commercially available or in development.

Researchers then set out to evaluate whether existing compounds would inhibit SARS-CoV-2 in infected cells in which specific kinases had been manipulated by the virus.

“We employed state-of-the-art bioinformatics approaches to readily identify regulated kinases from sparse phosphorylation profiles, many of which are likely to be established drug targets with therapeutic potential,” commented Pedro Beltrao, Ph.D., group leader at EMBL’s European Bioinformatics Institute.

Specifically, the researchers found that:

  • CK2, a kinase that plays a key role in cytoskeleton formation, cell growth and proliferation as well as apoptosis (cell death), physically interacted with the SARS-CoV-2 viral N protein and was significantly more activated in virally infected cells. Using a CK2 inhibitor in the laboratory experiments eliminated the virus.
  • Several kinases within the p38/MAPK pathway respond to and control the production of potentially harmful pro-inflammatory cytokines including IL-6, IL-10 and TNF-alpha. Inhibiting p38/MAPK signaling in virally infected  suppressed the overproduction of inflammatory cytokines and directly impaired viral replication, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis.
  • CDKs are kinases that regulate cell cycle and DNA damage response. Cells infected with SARS-CoV-2 have significantly reduced CDK activities, which may facilitate viral replication. Inhibition of CDKs may halt viral replication.
  • PIKFYVE, a FYVE finger-containing phosphoinositide kinase that regulates cytoskeleton function, is targeted in a variety of different cancers. The compound apilimod that targets this kinase potently inhibited SARS-CoV-2 in the laboratory setting.

Repurposing Kinase Inhibitors for Treatment of COVID-19

The team triangulated changes in phosphorylation to specific protein kinase targets and identified 87 U.S. Food and Drug Administration (FDA) approved drugs and compounds in clinical trials or development. Based on an initial systematic review of these compounds, the researchers identified seven agents, primarily anti-cancer and anti-inflammatory compounds, that demonstrated antiviral activity in laboratory experiments: silmitasertib, gilteritnib, MAPK13-IN-1, SB203580, ralimetinib, apilimod and dinaciclib.

“We are encouraged by our findings that drugs targeting differentially phosphorylated proteins inhibited SARS-CoV-2 infection in cell culture,” said Kevan Shokat, Ph.D., professor in the department of Cellular and Molecular Pharmacology at UC San Francisco (UCSF). “We expect to build upon this work by testing many other kinase inhibitors while concurrently conducting gene knockout experiments with RNAi technologies to continue to identify both the underlying pathways and additional potential therapeutics that may intervene in COVID-19 effectively.”

Importantly, additional studies are needed to further characterize the anti-viral potential of the compounds identified through this analysis.

Filopodia on Virally Infected Cells Newly Discovered Through Advanced Imaging

Interestingly, while studying the impact of SARS-CoV-2 on CK2, high resolution imaging of virally infected cells produced by the NIH/NIAID/Rocky Mountain Laboratories and University of Freiburg revealed actin-rich filopodia containing viral proteins. Human CK2 and the viral N protein were found co-localized within the filopodia, suggesting that SARS-CoV-2 hijacks CK2 and co-opts it into creating these tentacle-like protrusions that poke holes in their neighboring cells.

Conversely, other viruses including vaccinia, Ebola and Marburg take over the host cell cytoskeleton to promote egress and rapid cell-to-cell spread. However, in SARS-CoV-2 infected cells, the filopodia exhibit longer tentacles and branches, enabling more aggressive transmission than some other viral infections.

“The distinct visualization of the extensive branching of the filopodia once again elucidates how understanding the biology of virus-host interaction can illuminate possible points of intervention in the disease,” continued Dr. Krogan. “Our data driven approach for drug discovery has identified a new set of drugs that have great potential to fight COVID-19, either by themselves or in combination with other drugs, and we are excited to see if they will help end this pandemic.”

About QBI: The Quantitative Biosciences Institute (QBI) is a University of California organized research unit reporting through the UCSF School of Pharmacy. QBI fosters collaborations across the biomedical and the physical sciences, seeking quantitative methods to address pressing problems in biology and biomedicine. Motivated by problems of human disease, QBI is committed to investigating fundamental biological mechanisms, because ultimately solutions to many diseases have been revealed by unexpected discoveries in the basic sciences. Learn more at qbi.ucsf.edu.

About UCSF: The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. UCSF Health, which serves as UCSF’s primary academic medical center, includes top-ranked specialty hospitals and other clinical programs, and has affiliations throughout the Bay Area. Learn more at ucsf.edu or see our Fact Sheet.

About Gladstone Institutes: To ensure our work does the greatest good, Gladstone Institutes focuses on conditions with profound medical, economic, and social impact—unsolved diseases. Gladstone is an independent, nonprofit life science research organization that uses visionary science and technology to overcome disease. It has an academic affiliation with UC San Francisco. Learn more at gladstone.org.

Authorship and funding: This work was funded by grants from the National Institute of Mental Health and the National Institute of Allergy and Infectious Diseases, both part of the National Institutes of Health; the Defense Advanced Research Projects Agency; the Center for Research for Influenza Pathogenesis; the Centers of Excellence for Influenza Research and Surveillance of the National Institute of Allergy and Infectious Diseases; the Centers of Excellence for Integrative Biology of Emerging Infectious Diseases of the Agence Nationale de la Recherche (France); F. Hoffmann-LaRoche AG; Vir Biotechnology, Centre for Integrative Biological Signalling Studies (CIBSS), European Research Council (ERC) and the Ron Conway Family. Shokat is a Howard Hughes Medical Institute investigator. A complete list of authors and full funding information is available in the Cell paper.

Media Contacts

UCSF QBI                                                                    
Angela Bitting, Wheelhouse LSA
a.bitting@comcast.net
925-202-6211

UCSF
Pete Farley, UCSF Office of Communications
peter.farley@ucsf.edu
415-317-3781

Sylvia Wheeler, Wheelhouse LSA
swheeler@wheelhouselsa.com

Gladstone Institutes                    
Megan McDevitt, Gladstone Communications
megan.mcdevitt@gladstone.ucsf.edu
415-734-2019

Photos accompanying this announcement are available at

https://www.globenewswire.com/NewsRoom/AttachmentNg/9145af6f-0c38-4690-97a7-d60db05a6770

https://www.globenewswire.com/NewsRoom/AttachmentNg/96f65f4c-c1a8-4ed2-a504-a48019388204

https://www.globenewswire.com/NewsRoom/AttachmentNg/c3198fcf-1b2a-4bd0-a783-4d9026327c19

Aero-Engines Europe Virtual จะแทนที่งานอีเว้นท์สดในวันที่ 16-17 กันยายน

นิวยอร์ก, June 28, 2020 (GLOBE NEWSWIRE) — Aviation Week Network จะจัดงาน Aero-Engines Europe Virtual ซึ่งเป็นงานดิจิทัลที่ช่วยสร้างโอกาสในการจับคู่และสร้างเนื้อหาเพื่อการศึกษาที่มีคุณภาพสูง ในวันที่ 16-17 กันยายน  การตัดสินใจเชิงรุกเพื่อเปลี่ยนแปลงการประชุมประจำปีนี้ให้เป็นงานอีเว้นท์เสมือนเกิดขึ้นหลังการตรวจสอบข้อจำกัดของรัฐบาลและธุรกิจเกี่ยวกับการเดินทาง รวมถึงสุขภาพและความปลอดภัยของผู้เข้าร่วมประชุม  Aero-Engines Europe จะกลับมาในรูปแบบงานอีเว้นท์สดที่สตาวังเงร์ ประเทศนอร์เวย์ในวันที่ 15-16 กันยายน 2021

Aero-Engines Europe เป็นงานอีเว้นท์ชั้นนำที่มุ่งเน้นด้านแนวโน้มและประเด็นต่างๆ ที่เกี่ยวข้องกับชุมชน MRO ของเครื่องยนต์ในยุโรป ซึ่งได้รวบรวมผู้มีส่วนเกี่ยวข้องจากทั่วห่วงโซ่คุณค่ารวมถึง OEM, MRO, สายการบิน, ผู้ให้เช่าและซัพพลายเออร์  งานอีเว้นท์เสมือนนี้จะให้บริการเนื้อหาดิจิทัลและเครือข่าย รวมถึงฟอรั่มที่ชุมชนสายการบิน ผู้ให้เช่าเครื่องยนต์ ซัพพลายเออร์ OEM และ MRO สามารถเชื่อมต่อกับและจัดหาพันธมิตรทางธุรกิจใหม่และที่มีอยู่และแบ่งปันความรู้และแนวทางปฏิบัติที่ดีที่สุด

“เราเข้าใจดีว่า Aero-Engines Europe และซีรีส์งาน Aero-Engines Europe ทั้งหมดนั้นมีความสำคัญต่ออุตสาหกรรม และความพยายามที่ใช้ในการเตรียมงาน” Lydia Janow ผู้อำนวยการฝ่ายกิจกรรมของ Aviation Week Network กล่าว  “มันเป็นการตัดสินใจที่ไม่ง่ายเลยในการแทนที่งานอีเว้นท์สดด้วยงานอีเว้นท์เสมือน ดังนั้นในช่วงเวลาที่ยากลำบากนี้เราขอขอบคุณชุมชนของเราสำหรับความเข้าใจและการสนับสนุน เราตั้งใจที่จะดำเนินบทบาทของเราในการขับเคลื่อนอุตสาหกรรมของเราไปข้างหน้า เชื่อมต่อชุมชนของเราและธุรกิจการสนับสนุนเข้าด้วยกัน เราจะต้องก้าวไปด้วยกัน”

ทีมงานกิจกรรม Aviation Week กำลังดำเนินการรายละเอียดเพื่อสนับสนุนการเปลี่ยนแปลงนี้ และจะแบ่งปันการอัปเดตผ่านเว็บไซต์และแพลตฟอร์มสื่อสังคมออนไลน์ในอีกไม่กี่สัปดาห์ข้างหน้า

Informa ซึ่งเป็นบริษัทแม่ของ Aviation Week Network ได้พัฒนา AllSecure ชุดของมาตรฐานและแนวทางที่ได้รับการพัฒนาเพื่อนำเสนอบริการด้านสุขอนามัยและความปลอดภัยระดับสูงที่สุดในงานอีเว้นท์ทั้งหมดของ Informa งานอีเว้นท์ของ Aero-Engines และ MRO ที่กำลังจะจัดขึ้นทั้งหมดจะเป็นไปตามมาตรฐาน AllSecure ทำให้ผู้ร่วมงานมั่นใจได้ว่าพวกเขามีส่วนร่วมในสภาพแวดล้อมที่ปลอดภัยและได้รับการควบคุม

เกี่ยวกับ AVIATION WEEK NETWORK
Aviation Week Network เป็นผู้ให้บริการข้อมูลมัลติมีเดียรายใหญ่ที่สุดสำหรับอุตสาหกรรมการบิน การบินและอวกาศ และการป้องกันประเทศระดับโลก แก่มืออาชีพกว่า 1.7 ล้านคนทั่วโลก ผู้เชี่ยวชาญในอุตสาหกรรมพึ่งพา Aviation Week Network เพื่อช่วยให้พวกเขาเข้าใจตลาด ตัดสินใจ คาดการณ์แนวโน้ม และเชื่อมต่อกับผู้คนและโอกาสทางธุรกิจ ลูกค้าประกอบด้วยผู้ผลิตและซัพพลายเออร์ด้านการบินและอวกาศชั้นนำของโลก สายการบิน สนามบิน ผู้ประกอบการด้านการบิน ทหาร รัฐบาลและองค์กรอื่นๆ ที่ให้บริการในตลาดทั่วโลก กลุ่มผลิตภัณฑ์ของ Aviation Week Network ให้บริการด้านการสื่อสารมวลชนที่ได้รับรางวัล ข้อมูล ข่าวกรองและทรัพยากรเชิงวิเคราะห์ การแสดงสินค้าและการประชุมระดับโลก และบริการด้านการตลาดและโฆษณาที่มุ่งเน้นผลลัพธ์ ช่วยให้ลูกค้าของเราประสบความสำเร็จ

Aviation Week Network เป็นส่วนหนึ่งของ Informa Markets ซึ่งเป็นแผนกของ Informa PLC

เกี่ยวกับ INFORMA MARKETS
Informa Markets สร้างแพลตฟอร์มสำหรับอุตสาหกรรมและตลาดผู้เชี่ยวชาญเพื่อทำการค้า คิดค้น และเติบโต กลุ่มผลิตภัณฑ์ของเราประกอบด้วยอีเว้นท์และแบรนด์ B2B ระดับนานาชาติมากกว่า 550 รายการในตลาดรวมถึงผลิตภัณฑ์ดูแลสุขภาพและเภสัชกรรม โครงสร้างพื้นฐาน ธุรกิจก่อสร้างและอสังหาริมทรัพย์ แฟชั่นและเสื้อผ้า การต้อนรับ อาหารและเครื่องดื่ม และสุขภาพและโภชนาการและอื่นๆ เราเปิดโอกาสให้ลูกค้าและพันธมิตรทั่วโลกได้มีส่วนร่วม สัมผัส และทำธุรกิจผ่านนิทรรศการแบบตัวต่อตัว เนื้อหาดิจิทัลจากผู้เชี่ยวชาญ และโซลูชันข้อมูลที่สามารถดำเนินการได้ ในฐานะผู้จัดนิทรรศการชั้นนำของโลก เราได้นำตลาดผู้เชี่ยวชาญที่หลากหลายมาใช้ในชีวิตจริง ปลดล็อคโอกาสและช่วยให้พวกเขาเติบโตได้อย่างต่อเนื่องตลอด 365 วันในหนึ่งปี สำหรับข้อมูลเพิ่มเติม โปรดไปที่ www.informamarkets.com

Elizabeth Kelley Grace
Elizabeth@thebuzzagency.net
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