Guest column: It’s time to come to terms with our racist past – Press Herald

Much has been said of late about protests, as they have sprung up all over the country. Perhaps the most disturbing of all the commentary has been the idea that protest is somehow unpatriotic or illegal. This could not be further from the truth. The people who hold in such high regard the Second Amendment right to bear arms, totally overlook the First Amendment Freedom of Assembly and Petition. The founding fathers felt that it was so important they stated that Congress shall make no law respecting an establishment of religion, or prohibiting the free exercise thereof; or abridging the freedom of speech, or of the press, or the right of the people peaceably to assemble, and to petition the Government for a redress of grievances.

This amendment means that people have a right to gather in the public square and complain about the government. Somehow the president has persisted in labeling all protest he doesnt like as leftist riots by unpatriotic looters and thugs. This is not only unfair, it misses the point entirely. Marching, waving flags or signs, and making speeches have been widely accepted as constitutional First Amendment rights, even though we may not like or agree with the messages. This administration allows all manner of behaviors by people who agree with his right white American agenda but considers even the most passive protest by people of color dangerous.

There is a difference between exercising the freedom to protest and civil or criminal acts of vandalism. One does not equal the other. In any large gathering, there may be people who act out following their own agenda, maybe even using the protest to cover their own criminal actions. Often, they want to discredit the legitimate message of the protesters and may have been sent by opposing groups for that purpose. People protesting the ongoing and systematic racism and brutality by the police are angry, and it is a righteous anger born of centuries of mistreatment and abuse. Why are angry, gun-toting white people seen as patriots exercising their free speech, while unarmed shouting black people are seen as violent? Perhaps it says more about our guilt for centuries of treating them like livestock or imbeciles in order to protect our fragile sense of superiority.

We tried to enslave the native people and failing that, we tried to destroy them with disease and wars. We pushed them onto reservations, took their children away to whiten them, and dismantled their culture. We brought Chinese people to America to build the railroads and when we were done with them threw them out or killed them. We tore apart Black families for our own purposes and kept them in chains so they could neither fight nor flee. When the slaves were finally freed we still kept them in their place with Jim Crow laws and segregation, out of fear, because we knew in our hearts none of it was justifiable. After the nearly century and a half that black men have had the right to vote, we are still actively trying to keep them away from the polls in numerous states. It is a curious thing that the same people who cheered when Iraqis turned out in such large numbers to vote for their new democracy, dont want whole segments of American citizens to vote at all.

For 400 years white people have seen Native Americans, Blacks, Asians, Hispanics and anyone different as not American, regardless of their citizenship. But they are citizens, and they have as much right to speak, assemble, vote, be angry, and even carry weapons, as any other law-abiding citizen. Yet somehow they have not been treated equally under the law. Its well past the time we came to terms with our bigoted racist past and accepted that.

Susan Chichetto lives in Bath.

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Guest column: It's time to come to terms with our racist past - Press Herald

Texas Election: What to know about the congressional race to replace U.S. Rep. Will Hurd – El Paso Times

Here's what to know about the primary runoff in Texas. Wochit

One of the most competitive congressional races in the country is in El Paso's backyard.

The race for outgoing U.S. Rep. Will Hurd'sseat is in full swing, and on July 14 Republican voters in the district will decide who should represent their party on the November General Election ballot.

Republicans Tony Gonzalesand Raul Reyes are in a runoff for a district that spans much of the Texas-Mexico border and includes part of El Paso. Early voting in the race is ongoing and ends July 10.

The runoff election day is Tuesday, July 14.

Republicans Tony Gonzales (left) and Raul Reyes (right) are in a runoff for Congressional District 23.(Photo: Contributed)

Hurd, R-Helotes, announced last year that he wouldn't seek reelection to the House seat he won by a narrow margin in 2018.

That opened the doors for a crowded primaryin March. Gonzales, a Navy veteran, and Reyes, anAir Force veteran, garnered the most votes in the pool of nine candidates.

Gonzales received28.11% of the votes district wide, followed by Reyes who received 23.31%. In El Paso County, Reyes received37.97% of the votes and Gonzales 28.48%.

Congressional District 23 has flipped between being represented by Republicans and Democrats in the past. It's been held by a Republicansince Hurd took office in 2015, but Democrats are working to flip it.

Hurd, who has crossed party lines and criticizedPresident Donald Trump in the past, won his reelection for a two-year term in 2018 by less than 1,000 votes.

His opponent, Democrat Gina Ortiz Jones, a former Air Force intelligence officer, won the Democratic primary in 2020 and is on the November ballot.

Gina Ortiz Jones(Photo: Courtesy of the Gina Ortiz Jones campaign)

"This is one of themost competitive districts in the country, so all eyes are going to be on it," said Brandon Rottinghaus, a University of Houston political science professor. "It is a district which has been purple ... Republicans have been successful in part because Will Hurd was a popular figure in the area."

Hurd receivedattention in 2017for a"bipartisan road trip"with then U.S. Rep. Beto O'Rourke, D-El Paso. O'Rourke left Congress after his failed bid to upset U.S. Sen. Ted Cruz in 2018.

President Donald Trump chimed in on Twitter July 3 in the race for Texas 23rd Congressional District, announcing his endorsement of Gonzales.

Tony Gonzales will be a GREAT Congressman for Texas!, Trump wrote on Twitter. A Navy veteran, he is Strong on the Economy, Life and the Second Amendment. We need him to defeat the Radical Left in November. Tony has my Complete and Total Endorsement!

Gonzales, who has also been endorsedby Hurd, retweeted the post, thanking the president for his support.

Lets win in November! he said in the tweet.

Trump's endorsement comes just days after Sen. Cruz, R-Texas, announced his support for Reyes in the election. In an advertisement, Cruz casts Reyes as one of the "conservative warriors" needed in the House.

"President Trump needs more congressmen like Col. Reyes," Cruz says in the advertisement. "Leaders who won't surrender our border, our sovereignty, our way of life."

Jones predicted that Trump's endorsement would get Gonzalesthrough to November in a Friday tweet.

"Well, meet my likely opponent," Jones said in the tweet. "I'm a proud first-gen American, daughter of a single mom, and Iraq and Air Force veteran. And unlike him, I'm running in #TX23 to fight for affordable health care, good jobs, and an economy that works for everyone."

TheDemocratic Congressional Campaign Committee maintained that while the endorsement may help Gonzales in July, it could hurt him in November. In 2016, the district went for Clinton by just over 3 percentage points,though Hurd was elected in the congressional race.

With this toxic endorsement in a pro-Clinton and pro-Biden district, Tony Gonzales is now the overwhelming favorite to win on July 14 and lose on November 3,"DCCCspokesman Avery Jaffe said in the statement.

Reyes paints Gonzales as the establishment candidate who would be a "continuum of the legacy of Will Hurd."

Reyes' key policy issues include the Second Amendment and border security. He's for "zero red flag laws and no more infringement on the Second Amendment" and his an advocate for the construction of a border wall. He also wants to "bring jobs to district 23," including El Paso.

"We would be a powerhouse in Congress, fighting for the people, to get things really done," Reyes said.

Gonzales maintained he'sthe candidatewho can bring togethermembers of the RepublicanParty. He pointed to endorsements from Hurd, U.S. Reps. Kevin McCarthy, R-California, and Dan Crenshaw, R-Houston, asexamples.

Economic growth, advocating for veterans healthcare and helping veterans transition into the workforce are areas of interest for Gonzales. Border security is also a focus of his campaign, citing a need for resources to keep communities safe, "whether that's added technology" or "resources to DHS, ICE, Border Patrol and elsewhere."

"The biggest thing that distinguishes me from Reyes, is I can unite the party," Gonzales said.

Eleanor Dearmanmay be reached at361-244-0047;edearman@elpasotimes.com; @EllyDearman on Twitter.

Read or Share this story: https://www.elpasotimes.com/story/news/politics/2020/07/08/texas-election-republicans-runoff-replace-will-hurd-district-23/5383216002/

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Texas Election: What to know about the congressional race to replace U.S. Rep. Will Hurd - El Paso Times

POLITICO Playbook: White House weighing another swing at DACA – Politico

The Supreme Court said the Trump administration repealed the DACA program incorrectly last time, and gave the White House a road map for a do-over. | Win McNamee/Getty Images

THE BUZZ IN THE WHITE HOUSE is that, at some point over the next week or so, there is a plan in place to resubmit paperwork to do away with DACA. Remember: The Supreme Court said the administration repealed it incorrectly last time, and gave the White House a road map for a do-over.

OF COURSE, this will elicit head slaps from many corners of the Republican Party, but it follows in line with the TRUMP ADMINISTRATIONS consistent political belief that they are somehow at risk of losing their base.

-- NEW THE UNITED STATES CONFERENCE OF MAYORS has sent the president a letter urging him to fully maintain the Deferred Action for Childhood Arrivals (DACA) program until Congress passes legislation that would enable Dreamers people who have lived in America since they were children and built their lives here to earn lawful permanent residence and eventually American citizenship, if they meet certain criteria. Full letter, led by Louisville, Ky., Mayor Greg Fischer

TAKE THREE!! TRY TO PUT THIS ON A BUMPER STICKER! SEAN HANNITY had President DONALD TRUMP on his show Thursday night, and again tried to get him to lay out his second-term agenda. REMEMBER: HANNITY has asked the president before, and so did ERIC BOLLING. Both times, the answer was panned as jumbled and underwhelming.

HANNITY: I asked you a question in Wisconsin and you got criticized for the answer. I want to ask you again. You are now asking America in 117 days to give you a second term as president of the United States. Lets -- what is your second-term agenda?

TRUMP: First of all, I didnt know it was criticized for that answer because its a simple question. First of all, were going to defeat the invisible enemy, and we are well on our way. And again, I told you, the mortality rate is tenfold down. Were going to rebuild the economy, were going to bring back jobs from all of these foreign lands that have stolen our jobs on horrible trade deals. We are going to continue to make great trade deals.

Were going to finish rebuilding our wall. Were going to finish, were going to have that -- its going to be almost complete by the end of this year, shortly thereafter its finished. Its made a tremendous difference. You see, were doing record numbers on the border. Very few people are able to get through. Were rebuilding with our military. Weve rebuilt the military. $2.5 trillion. We are fixing up the VA for our vets. The job weve done there, between choice and accountability.

We have choice, where they go out and get a doctor. If they are sick, they dont have to wait for five weeks, six weeks, two weeks. So we are doing great with the vets, and the vets are loving Trump. We are protecting our Second Amendment, so. We need more judges and more justices. You see that now with the Supreme Court more than ever. And the next president, Ive had two, the next president is going to be able to pick two or three or one or whatever, but a lot of justices. And that means everything, whether its for life or other things, I mean it means so much.

But protecting the Second Amendment, getting more judges. All of the things that weve done, nobodys done what this administration has done in the first three and a half years. Nobodys even come close. When you look at everything that were doing. Now what were doing is working on lowering drug prices and knocking out special interests, because its not easy. Were fighting for choice. We did it for the veterans and now we are doing it for school too. One choice in school so a parent can take their child to a school of their choice, and thats happening -- very good, very, very well.

And we have many things we are doing and many things that we have already completed, and you cant do more than what weve done. I think weve set records. We actually set a record on judges. We are going to be, by the time of the end of this year, we will be up to almost 300 federal judges, and thats a record. Thats incredible, including D.C.

-- BIDEN LAYS OUT HIS AGENDA: Biden releases U.S.-centered economic plan, challenging Trumps America First agenda, by WaPos Sean Sullivan and Jeff Stein

Good Friday morning.

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The numbers are in private equity invests in every state and every congressional district around the country. Last year alone, private equity invested $700 billion in 4,841 businesses around the country. Does your state rank in the top 20? Click here to read the report.

THE FOLKS AT THE RNC ARE QUITE SENSITIVE to the notion that their convention this summer in Jacksonville, Fla., may be in trouble. But all publicly available evidence would suggest that, in fact, it is in trouble, and to think otherwise would be burying your head in the sand.

ABOUT A HALF DOZEN SENATE REPUBLICANS have suggested they wont go, and even more have cast doubt on the convention or said that they havent made their mind up. RNC-ALIGNED REPUBLICANS say its two months away, and its too early to make any determinations about the prospect of a large-scale gathering in hard-hit Florida. There are reports of efforts to study holding it outdoors. In August. In Florida.

ON THURSDAY, THE RNC and TRUMP were dealt another blow. APPEARING IN KENTUCKY, Senate Majority Leader MITCH MCCONNELL was asked if he would be attending the convention in Jacksonville this summer. He said he didnt have any idea whether the event would even be happening.

-- MCCONNELL: Well, I think the convention is a challenging situation. And a number of my colleagues have announced that theyre not going to attend, and well have to wait and see how things look in late August and determine whether or not you can safely convene that many people. The clip

AND THEN THERES THIS GREAT ANNIE KARNI and PATRICIA MAZZEI story on A15 of the NYT today, which suggests the Republican governor of Florida is trying to sabotage the convention because of a beef he has with a consultant!

-- NYT: DeSantis Is Said to Quietly Hinder Fund-Raising for Trump Convention: [Gov. Ron] DeSantis, a Republican, has directed his top fund-raiser, Heather Barker, to tell donors not to give to the convention because of a personal dispute between the governor and Susie Wiles, his former campaign manager who is serving as an informal adviser to the convention planners, according to multiple people familiar with his actions.

Ms. Wiles is a veteran Republican operative who led Mr. Trumps Florida team in 2016 and who ran Mr. DeSantiss 2018 campaign for governor. Mr. DeSantiss relationship with Ms. Wiles soured over his suspicion that she had leaked embarrassing information.

NEW THE WHITE HOUSE is launching a rapid-response Twitter account to try to drive messages and make announcements. @WHRapidResponse is now live, and will be manned by the White House communications shop, under the direction of KAYLEIGH MCENANY and ALYSSA FARAH.

-- FIRST TWEET: @WHRapidResponse at 12:01 a.m.: Follow @WHRapidResponse as we cut through the bias and provide real-time updates on the historic accomplishments of President @realDonaldTrumps administration!

MERIDITH MCGRAW: The White Houses new briefing strategy: Short, with lots of commentary: The White Houses ever-mutating press conferences have found a new form. Theyre short, with frequent prepared commentary and press critiques.

Its a format that has taken shape under new White House press secretary Kayleigh McEnany, who took over her role in April. McEnany initially chose to resurrect the concept of semi-regular briefings in the White Houses press room which had sat unused for over a year under her predecessors. But her briefings, often announced at the last minute, have since clocked in, on average, 25 minutes. And on occasion, they have been scheduled right before President Donald Trumps official events, giving McEnany a pre-planned stopping point.

The strategy has extended to President Donald Trump himself. The president has, in recent weeks, cut back his own free-for-all press conferences from early 2020 taking questions just five times in June from a group of reporters. Instead, Trump has been gathering reporters for a self-described press conference or news conference, only to make long speeches straight into the TV camera before walking off without taking any questions.

For the White House, the tactic has given the administration the opportunity to use the cameras in the room to project its message, surrounded by reporters who arent able to ask many follow-up questions. And it has changed how the White House has conveyed information during two ongoing crises the coronavirus pandemic and the protests against police brutality and racial injustice. POLITICO

TRUMPS FRONTS: NYT, banner headline: PRESIDENT IS NOT ABOVE THE LAW, JUSTICES DECIDE The NYT also fronted a Shane Goldmacher/Jim Tankersley story with this headline: Biden Puts Economy at the Center of His Attack WSJ N.Y. POST

CANDACE OWENS RAISING MONEY FOR HERSELF! OWENS -- a conservative activist -- is sending text message solicitations to raise money for herself, through an LLC called Candace Owens LLC. The solicitation says: Hi its Candace Owens. The Black Lives Matter movement is getting more power by the day and we must stop them. Stand with me. That directs to this page, which raises money for the LLC. Paid for by Candace Owens LLC and not authorized by any candidate or candidates committee, the page reads.

-- WHAT MAKES THIS UNIQUE is it looks like a campaign advertisement, but its not. Its directing money not to a campaign committee, but rather to a corporation.

SCOOP A NEW WHISTLEBLOWER BETSY WOODRUFF SWAN: A top terrorism fighters dire warning

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CORONAVIRUS RAGING

-- NYT: U.S. Hits Another Record for New Coronavirus Cases: Officials across the United States reported more than 59,880 cases on Thursday, setting a single-day record for the sixth time in 10 days, according to a New York Times database. The surge has been driven largely by states in the South and the West that were among the first to ease restrictions established during the viruss initial wave in the spring. At least six states set single-day case records on Thursday: Alabama, Idaho, Missouri, Montana, Oregon and Texas.

The numbers were especially striking in Texas, which set a record for the fourth consecutive day with more than 10,900 cases. Nearly one in 10 of them were in Hidalgo County, which consists of over a thousand square miles of scrub and urban sprawl on the Mexico border.

-- WAPO: CDC feels pressure from Trump as rift grows over coronavirus response, by Lena Sun and Josh Dawsey: The June 28 email to the director of the Centers for Disease Control and Prevention was ominous: A senior adviser to a top Health and Human Services Department official accused the CDC of undermining the President by putting out a report about the potential risks of the coronavirus to pregnant women.

The adviser, Paul Alexander, criticized the agencys methods and said its warning to pregnant women reads in a way to frighten women as if the President and his administration cant fix this and it is getting worse.

As the country enters a frightening phase of the pandemic with new daily cases surpassing 57,000 on Thursday, the CDC, the nations top public health agency, is coming under intense pressure from President Trump and his allies, who are downplaying the dangers in a bid to revive the economy ahead of the Nov. 3 presidential election. In a White House guided by the presidents instincts, rather than by evidence-based policy, the CDC finds itself forced constantly to backtrack or sidelined from pivotal decisions.

-- LAT: Coronavirus hospitalizations jump 97% in Orange County in less than a month, by Hannah Fry: The number of patients hospitalized with confirmed coronavirus infections reached new heights Thursday in Orange County jumping 97% over the past three weeks an indicator that health experts say makes it clear the virus is spreading more rapidly in the region.

County health officials on Thursday reported that 691 patients were being hospitalized with confirmed coronavirus infections. Seven days earlier, 556 people were hospitalized. A week prior there were 437 people in hospitals, and a week before that there were 351. The spike has prompted hospitals countywide to begin to prepare for a surge of sick patients, said Orange County Health Care Agency Director Dr. Clayton Chau.

-- NPR: Bolivian President Tests Positive For Coronavirus

MARC CAPUTO: Trump advisers fracture over Roger Stone pardon: Roger Stone is headed to prison next week unless Donald Trump intervenes. And a chorus of outside allies is pressing the president to do just that over the wishes of White House and campaign aides who dont like Stone and think Trump has nothing to gain by helping him.

Both camps expect Trump will at least split the difference by commuting Stones sentence, according to interviews with nine sources familiar with the discussions. A commutation would keep Stone from behind bars without wiping his record clean.

KNOWING ELISSA SLOTKIN TIM ALBERTA: Elissa Slotkins Reluctant War with Donald Trump: She cannot hope to win reelection this fall without persuading a significant number of voters in Michigans 8th Congressional District to split their tickets four more years for Trump, two more years for her and every feud with the White House is equivalent to a few more straight-party ballots being punched.

Whether Slotkin can have it both ways, speaking her mind about the president and winning over some of his supporters, may well determine not only her fate but the fate of Democrats in swing districts and battleground states across the country.

Slotkin didnt want it to be this way. She envisioned another hyperlocal campaign, like the one she ran in 2018, building consensus around kitchen-table issues and eluding perceptions of partisanship. But if her first two years in Congress taught her anything, its that sooner or later, everyone has to pick a side. There is no middle ground when it comes to Donald Trump.

Hes forcing my hand, Slotkin tells me a day after the tweetstorm, resignation dripping from her voice. Hes doing things and saying things that call upon me to think about my fundamental oath of office.

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This is big private equity invested in 4,841 American companies last year alone. See where your community ranks.

TRUMPS FRIDAY -- The president will depart the White House at 9:30 a.m. en route to Miami. He will head to U.S. Southern Command in Doral, where hell receive a briefing on enhanced counternarcotics operations at 12:35 p.m. and deliver remarks. Afterward, he will head to Iglesia Doral Jesus Worship Center for a roundtable on supporting Venezuelans.

TRUMP will leave at 3:20 p.m. and fly to Fort Lauderdale, Fla., for an event at a private residence in Hillsboro Beach, Fla. He will depart at 6:35 p.m. and return to Washington, arriving back at the White House at 9:45 p.m.

TV TONIGHT -- PBS Washington Week with Bob Costa: Yamiche Alcindor, Cleve Wootson Jr., Eamon Javers and Paula Reid Joan Biskupic.

SUNDAY SO FAR

Gray TV

Full Court Press with Greta Van Susteren: President Donald Trump.

NBC

Meet the Press: Maryland Gov. Larry Hogan. Panel: Anna Palmer, Kristen Welker and George Will.

ABC

This Week: Panel: Chris Christie, Rahm Emanuel, Amanda Carpenter and Zerlina Maxwell.

CBS

Face the Nation: Phoenix Mayor Kate Gallego Terry Shaw Scott Gottlieb Tom Wyatt New battleground tracker for Texas, Florida and Arizona.

FOX

Fox News Sunday: Thomas Inglesby. Panel: Karl Rove, Jane Harman and Josh Holmes. Power Player: Vanilla Beane.

Sinclair

America This Week With Eric Bolling: Horace Lorenzo Anderson Sr. HUD Secretary Ben Carson Rep. Devin Nunes (R-Calif.) Rep. Brian Babin (R-Texas). Panel: Ameshia Cross and Sebastian Gorka.

PHOTO DU JOUR: Police in Seoul, South Korea, on Friday carry the alleged body of Mayor Park Won-soon, who was reportedly found dead after leaving a will-like message for his daughter. A sexual harassment legal complaint involving him was reported to have been filed Wednesday. | Chung Sung-Jun/Getty Images

ERIK PRINCE STILL PUSHING ON AFGHANISTAN DAILY WIRE: Top Security Expert Points To History To Show How Trump Can Successfully End The War In Afghanistan

JOSH GERSTEIN: Trump poised to run out political clock on emoluments suits: A key lawsuit over spending by foreign entities at President Donald Trumps businesses appears likely to remain on hold until the fall, effectively blocking what appeared to be the best vehicle for the presidents critics to demand details of such spending in advance of the November election.

A federal appeals court Thursday extended a stay on fact-finding in the lawsuit so the Justice Department can ask the Supreme Court to order dismissal of the suit, filed in 2017 by the State of Maryland and the Washington, D.C., government.

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VALLEY TALK LEAH NYLEN: California investigating Google for potential antitrust violations: California has opened its own antitrust probe into Google, intensifying the pressure on the search giant already in the middle of investigations by the Justice Department and a host of other states, according to three people with knowledge of the inquiry.

The move by California's attorney general comes as Google has come under increasing scrutiny from both Congress and foreign regulators for its market conduct and acquisitions that have turned it into the world's top search engine and the most profitable online advertising company.

In September, attorneys general from 48 states, Puerto Rico and the District of Columbia announced an antitrust investigation into Google focused on the companys dominance of the advertising technology market. Over the past 10 months, that investigation led by Texas has expanded into other aspects of the companys business, including its conduct in the search market.

California which houses Googles headquarters in Mountain View was the most notable holdout in the multi-state group, and Democratic Attorney General Xavier Becerra has repeatedly declined to answer questions about why the state wasnt a participant. The California antitrust probe is a separate investigation from the multi-state effort, two of the individuals said. All of the individuals spoke on condition of anonymity to talk openly about a confidential probe. Alabama is now the only state that is not investigating the company. POLITICO

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ON THE BORDER -- Arrests at U.S. Border With Mexico Jumped 40% in June, by WSJs Michelle Hackman: The number of migrants arrested at the southern border jumped by 40% in June from the prior month, according to figures released by U.S. Customs and Border Protection. The jump in numbers came at a time when the Trump administration is immediately turning back most migrants at the border for the duration of the coronavirus pandemic. Arrests of migrants surged to 30,300 last month, including about 27,000 people who were turned back under the new policy.

MEDIAWATCH -- Trump Appointee Might Not Extend Visas for Foreign Journalists at V.O.A., by NYTs Pranshu Verma and Edward Wong: As many as 100 foreign citizens working in the United States as journalists for the Voice of America, a government-funded news outlet, might not have their visas extended once they expire, according to people familiar with the planning.

Michael Pack, the new chief executive for the U.S. Agency for Global Media, has indicated he may not approve extensions for any journalist holding a J-1 visa, which allows foreign citizens to temporarily work in the United States in ways that promote cultural exchanges.

The decision could be a blow to the news-gathering and global-broadcasting abilities of the V.O.A., which operates independently but is funded by the government. Foreign journalists on the specialty visa are often recruited to work there because they are able to translate American news reports into difficult languages like Swahili or Mandarin and can do reporting using those languages. NYT

Send tips to Eli Okun and Garrett Ross at [emailprotected].

TRANSITIONS -- Gina Reis is now video director for Mark Kellys Senate campaign in Arizona. She previously was a video producer/editor for Pete Buttigiegs campaign. Mikka Kei Macdonald is joining Community Change as a senior digital organizer. She previously was associate director for campaigns at the Hub Project.

WELCOME TO THE WORLD -- Eduardo Lerma, COS for Rep. Veronica Escobar (D-Texas), and Johanna Lerma, a registered nurse at MedStar Georgetown Hospital, welcomed Noemi Soledad Lerma early Thursday morning. Pic

BIRTHDAY OF THE DAY: Kyle Griffin, senior producer for MSNBCs The Last Word. What hes been reading: Im reading Station Eleven by Emily St. John Mandel. Its not for the faint of heart. Its about a fictional flu pandemic. Im a glutton for punishment when it comes to extracurriculars, but its interesting to compare the book to our real-world experiences. Her writing is clear and vivid -- she knows how to paint a bleak picture. And as a TV news writer, Im a sucker for the teases she writes at the end of each chapter. Playbook Q&A

BIRTHDAYS: CDC Director Robert Redfield is 69 Rep. Elissa Slotkin (D-Mich.) is 44 Rep. Tom McClintock (R-Calif.) is 64 ... Rep. Brian Mast (R-Fla.) is 4-0 ... Rep. Dan Newhouse (R-Wash.) is 65 ... State Department spokeswoman Morgan Ortagus (h/t Katie Martin) Megan Ortagus (h/ts Sam Vinograd) Sam Stein of The Daily Beast and MSNBC Sarah Boxer Alex Angelson of Michael Best Strategies Ben Napier is 3-0 Katie Pavlich is 32 POLITICOs Chris Cadelago, Matt Daily, Catherine Boudreau, John Appezzato and Ashley Afranie-Sakyi Melanie Seitz David Dinkins is 93 Julianna Smoot, co-founder of WaterWorks (h/t Jon Haber) Rena Shapiro, head of politics and public affairs at a4 Media Sam Harper, VP of comms at SoundExchange Eli Yokley, Morning Consult political reporter Quibis Shawna Thomas Karen Hinton

Kenny Day (h/t Tim Burger) former Rep. Ron Klein (D-Fla.), now chair of the Jewish Democratic Council of America, is 63 former Rep. Russ Carnahan (D-Mo.) is 62 (h/t Mitchell Rivard) former Rep. Phil Gingrey (R-Ga.) is 78 Hazel Rosenblum-Sellers, who just accepted a job at NEWCO Strategies, is 23 (h/t Claire Goldberg) Emil Caillaux Rob Bogart White & Cases Keir Whitson is 51 Kayla Maree Sanders Remley Johnson is 29 ... WSJs Heather Haddon ... Phillip Hedayatnia ... Jamie Lockhart ... Peter Bondi Barbara Goldberg Goldman is 71 Christine Turner ... Caroline Ciccone ... CUNY Board Chairman Bill Thompson ... Ian Rivera ... Amanda Woloshen Glass ... Kevin Call ... Bill Roberts ... Sarah Hodgkins ... Caroline Gransee ... Clay Haynes ... Chris Terris ... Finlay Lewis is 82 ... Elie Jacobs ... Monty Warner ... Elizabeth Bartz ... Chuck Lewis ... Jeff Mitchell

A message from the American Investment Council:

The numbers are in. The American Investment Council released its annual Top States and Districts Report, which ranks the countrys top twenty states and Congressional districts in total private equity capital and the number of companies receiving investment in 2019.

Private equity invested over $700 billion last year in diverse communities and industries across the country, helping to rescue, build, or grow 4,841 businesses. Private equity firms provided capital to a broad range of industries, from financial services and healthcare to technology and consumer businesses.

Drew Maloney, President and CEO of The American Investment Council, released the following statement:

Our 2019 Top States and Districts Report underscores how private equity is unlocking critical capital in every state and Congressional district across the United States. The figures in this report are more than just numbers. They represent jobs, economic security, and well-being for millions of Americans.

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POLITICO Playbook: White House weighing another swing at DACA - Politico

Impact of Covid-19 on Nootropics Market Expected to Witness the Highest Growth 2027 with Top Key Players Company1, Company2, Company3, Company4, etc -…

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The report also emphasizes the initiatives undertaken by the companies operating in the market including product innovation, product launches, and technological development to help their organization offer more effective products in the market. It also studies notable business events, including corporate deals, mergers and acquisitions, joint ventures, partnerships, product launches, and brand promotions.

In market segmentation by manufacturers, the report covers the following companies-

Accelerated Intelligence Inc., AlternaScript; HVMN, Onnit Labs, Inc., Peak Nootropics, Teva Pharmaceutical Industries, Purelife bioscience Co., Ltd., United Pharmacies, SupNootropic bio co., Ltd.

Nootropics product types, applications, geographies, and end-user industries are the key market segments that are comprised in this study. The report speculates the prospective growth of the different market segments by studying the current market standing, performance, demand, production, sales, and growth prospects existing in the market.

Application Outlook (Revenue in Million USD; 20162026)

Distribution Channel Outlook (Revenue in Million USD; 20162026)

The regional segmentation includes the present and forecast demand for the Nootropics Market in North America, Europe, Asia Pacific, Latin America, and Middle East & Africa. It covers the individual application segments of the market in each region.

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Get to know the business better:The global Nootropics market research is carried out at the different stages of the business lifecycle from the production of a product, cost, launch, application, consumption volume and sale. The research offers valuable insights into the marketplace from the beginning including some sound business plans chalked out by prominent market leaders to establish a strong foothold and expand their products into one thats better than others.

The global Nootropics market report answers some important questions for you:

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The research report by Reports and Data analyzes and forecasts the Nootropics Market at the global and regional levels. The market has been projected in terms of volume and price for the forecast period. The report also sheds light on the various opportunities within the market.

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Impact of Covid-19 on Nootropics Market Expected to Witness the Highest Growth 2027 with Top Key Players Company1, Company2, Company3, Company4, etc -...

Nootropics Market Growth By Manufacturers, Type And Application, Forecast To 2026 – 3rd Watch News

New Jersey, United States,- Market Research Intellect sheds light on the market scope, potential, and performance perspective of the Global Nootropics Market by carrying out an extensive market analysis. Pivotal market aspects like market trends, the shift in customer preferences, fluctuating consumption, cost volatility, the product range available in the market, growth rate, drivers and constraints, financial standing, and challenges existing in the market are comprehensively evaluated to deduce their impact on the growth of the market in the coming years. The report also gives an industry-wide competitive analysis, highlighting the different market segments, individual market share of leading players, and the contemporary market scenario and the most vital elements to study while assessing the global Nootropics market.

The research study includes the latest updates about the COVID-19 impact on the Nootropics sector. The outbreak has broadly influenced the global economic landscape. The report contains a complete breakdown of the current situation in the ever-evolving business sector and estimates the aftereffects of the outbreak on the overall economy.

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Leading Nootropics manufacturers/companies operating at both regional and global levels:

The report also inspects the financial standing of the leading companies, which includes gross profit, revenue generation, sales volume, sales revenue, manufacturing cost, individual growth rate, and other financial ratios.

Industrial Analysis:

The Nootropics market report is extensively categorized into different product types and applications. The study has a separate section for explaining the cost of raw material and the revenue returns that are gained by the players of the market.

The segmentation included in the report is beneficial for readers to capitalize on the selection of appropriate segments for the Nootropics sector and can help companies in deciphering the optimum business move to reach their desired business goals.

In Market Segmentation by Types of Nootropics, the report covers-

In Market Segmentation by Applications of the Nootropics, the report covers the following uses-

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The Nootropics market report provides successfully marked contemplated policy changes, favorable circumstances, industry news, developments, and trends. This information can help readers fortify their market position. It packs various parts of information gathered from secondary sources, including press releases, web, magazines, and journals as numbers, tables, pie-charts, and graphs. The information is verified and validated through primary interviews and questionnaires. The data on growth and trends focuses on new technologies, market capacities, raw materials, CAPEX cycle, and the dynamic structure of the Nootropics market.

This study analyzes the growth of Nootropics based on the present, past and futuristic data and will render complete information about the Nootropics industry to the market-leading industry players that will guide the direction of the Nootropics market through the forecast period. All of these players are analyzed in detail so as to get details concerning their recent announcements and partnerships, product/services, and investment strategies, among others.

Sales Forecast:

The report contains historical revenue and volume that backing information about the market capacity, and it helps to evaluate conjecture numbers for key areas in the Nootropics market. Additionally, it includes a share of each segment of the Nootropics market, giving methodical information about types and applications of the market.

Reasons for Buying Nootropics Market Report

This report gives a forward-looking prospect of various factors driving or restraining market growth.

It renders an in-depth analysis for changing competitive dynamics.

It presents a detailed analysis of changing competition dynamics and puts you ahead of competitors.

It gives a six-year forecast evaluated on the basis of how the market is predicted to grow.

It assists in making informed business decisions by performing a pin-point analysis of market segments and by having complete insights of the Nootropics market.

This report helps the readers understand key product segments and their future.

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In the end, the Nootropics market is analyzed for revenue, sales, price, and gross margin. These points are examined for companies, types, applications, and regions.

To summarize, the global Nootropics market report studies the contemporary market to forecast the growth prospects, challenges, opportunities, risks, threats, and the trends observed in the market that can either propel or curtail the growth rate of the industry. The market factors impacting the global sector also include provincial trade policies, international trade disputes, entry barriers, and other regulatory restrictions.

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Smart Pills Technology Market Thriving Growth Over Forecast 2020 with Leading Players Proteus Digital Health, Chongqing Jinshan Science &…

Due to the pandemic, we have included a special section on the Impact of COVID 19 on the Smart Pills Technology Market which would mention How the Covid-19 is affecting the Smart Pills Technology Industry, Market Trends and Potential Opportunities in the COVID-19 Landscape, Covid-19 Impact on Key Regions and Proposal for Smart Pills Technology Players to Combat Covid-19 Impact.

Smart Pills Technology is a revolutionary technological advance that has diminished the gap between healthcare and digital technology. Smart pills or Nootropics are basically medical devices and small embedded electronic components such as cameras, sensors, and trackers. This electronic medical appliance can be easily swallowed and offers a comprehensive evaluation of the gastrointestinal tract (GIT).

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Report Consultant has recently added a new Report on Smart Pills Technology Market into its largest Database. It gives the complete report on trends, growth, and opportunity, restraint. Along with this, it delivers a comprehensive description of the key players of different regions.

Leading Players Smart Pills Technology Market:

Proteus Digital Health, Chongqing Jinshan Science & Technology Group, CapsoVision, IntroMedic, Given Imaging, Olympus Corporation

Market Segmentation: The market is segmented on the basis of type, application, and region.

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Smart Pills Technology Market Thriving Growth Over Forecast 2020 with Leading Players Proteus Digital Health, Chongqing Jinshan Science &...

How Disneylands Galaxys Edge fits into the Star Wars universe – OCRegister

A new book from Lucasfilm and Walt Disney Imagineering explains how the Star Wars planet at the heart of the Galaxys Edge themed land in Disneyland fits into the vast universe of a galaxy far, far away.

The new Travelers Guide to Batuu serves as an in-world travel guide to the Black Spire Outpost village on the Star Wars planet of Batuu, the setting for the 14-acre lands at Disneyland in Anaheim and Disneys Hollywood Studios in Florida.

Disneyland remains closed until further notice amid the COVID-19 pandemic. Disneys Hollywood Studios in Florida home to Batuu East is set to reopen on Tuesday, July 15.

SEE ALSO: Brook and Robin Lopez will get to ride Disney World coasters during NBA bubble season

The backstory and the residents of Black Spire Outpost and Batuu help frame the adventures that play out in Star Wars: Galaxys Edge. Delving deeper into the geography and history of the planet in the Travelers Guide to Batuu helps peel back additional layers in Galaxys Edge and offers hints at stories yet to be told in the Star Wars themed lands.

A galactic map in the Travelers Guide to Batuu places the Galaxys Edge planet on the western reaches of the outer rim of the fictional Star Wars universe.

It is precisely this location that has shaped the planets history, according to Travelers Guide to Batuu. Before advanced hyperspace capabilities, Batuus position made it a bustling fueling stop for ships heading into Wild Space. With the advances in technology and well-charted hyperlanes, most modern travelers choose to bypass Batuu, resulting in the planet becoming a crossroads for adventurers and a haven for those who prefer life in the shadows.

SEE ALSO: Downtown Disney now selling coronavirus masks with Mickey Mouse, Hulk and Baby Yoda characters

Black Spire Outpost the planets small but most populous settlement sits in the Surabat River Valley near the neighboring villages of Galma, Surabat and Peka.

Galma is a short shuttle ride from Black Spire Outpost.

To many it feels undeveloped as most of the structures here have been scavenged and repurposed, according to Travelers Guide to Batuu. Broken-down speeders and ships serve as homes and workshops for the resourceful mechanics who live here today.

Galma is known as a haven for illegal podracing and the gambling that surrounds the outlawed sport.

These activities attract a criminal element and I do not recommend it for most off-worlders, according to the book. Gambling on these activities is a quick way to lose all your credits and you do not want to be in debt to anyone who frequents this district.

SEE ALSO: These are the 26 Downtown Disney shops and restaurants that will reopen Thursday

The tiny town of Surabat offers few modern conveniences.

The hardy residents, though isolated, build sturdy homes that sit nestled against the base of the beautiful spires and mountains, according to Travelers Guide to Batuu. Weather here is more harsh than other parts of Batuu with strong winds throughout the year.

Like the rest of Batuu, Surabat is distinguished by the towering petrified spires that dot the landscape.

It remains a favorite jumping-off point for mountain hikers and thrill-seekers looking to climb the ancient spires, according to the book. Many who live here sustain themselves as lichen harvesters, bravely climbing the spires to collect valuable golden lichen.

SEE ALSO: How will Disneyland keep fans from getting too close to Mickey Mouse?

Peka is known for its simple huts and log cabins built from native trees.

I find the residents here welcoming and sociable to visitors, willing to share their modest, family-oriented lives with those who pass through, according to Travelers Guide to Batuu.

Peka residents survive off the land and the river that runs past the community.

Many work as fishermen and farmers, some even offering to take off-worlders on fishing excursions that let you catch and cook your own lunch on the banks of the flowing river, according to the book.

SEE ALSO: Which Disneyland shows and attractions will remain closed when the park reopens?

Batuu is a short hyper-space hop to a number of nearby planets in the Star Wars galaxy.

For Star Wars fans, the forest moon of Endor from Return of the Jedi is likely the best-known destination in the Batuu region of the galaxy.

The lush forest planet of Takodana had been the perfect planet for a day trip before Maz Kanatas castle was destroyed in The Force Awakens.

SEE ALSO: How Disneyland will enforce mandatory mask rule when park reopens

A short commute to Bakura offers the closest big city to Batuu. Mokivj is known for its beautiful sunsets and ten moons, but catastrophic lava flows have devastated the planet.

The unfortunately named Gannaria is a refuge for smugglers involved in the illegal spice trade. The mountainous planet of Rattatak is home to warlords and gladiatorial societies.

Yakorki attracts thousands each year for the annual Fungi Fest. High tides cover the white sand beaches of Zaddja each night. The remote planet of Umme is a haven for big-game safaris.

The new Travelers Guide to Batuu offers recommendations on where to eat, shop and sightsee during a visit to Galaxys Edge while providing backstories for the characters and locations in the Star Wars themed land.

The Travelers Guide to Batuu is ostensibly penned by Eloc Throno, a galactic historian and travel writer who has also written guides to Tatooine, Mustafar and other Star Wars destinations. The book also credits Lucasfilm creative executives Pablo Hidalgo and Matt Martin as well as Walt Disney Imagineering managing story editor Margaret Kerrison who all had a hand in developing the backstory for Galaxys Edge.

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How Disneylands Galaxys Edge fits into the Star Wars universe - OCRegister

TVA offers incentives to businesses, schools that install virus-killing technology – WKRN News 2

The Tennessee Valley Authority is offering incentives to businesses and schools that install virus killing UV technology.

UVC light is a short wavelength ultraviolet light used around the world to disinfect air in hospitals and laboratories. Studies show it is 99.9 percent lethal to bacteria, fungi, viruses and other microorganisms. Amid the COVID-19 pandemic, TVA says the same technology is ideal for schools, offices and retail locations to help keep people healthy.

As the largest public power provider in America, a key focus for TVA is helping to keep our children and the public safe by supporting technologies that are proven to kill viruses, said Jason Snyder, manager, TVA EnergyRight. Schools and businesses realize they need solutions to purify indoor air, and we want to help them install it as they reopen.

According to Snyder, a TVA Preferred Partners Network professional can install germicidal lights into the ductwork of many existing commercial HVAC systems. Customers who use TVAs provider network can receive a $30 per ton incentive toward the adoption of approved UV technologies that directly combat COVID-19.

Contact your local power company or visit TVAs websitehttps://energyright.com/business-industry/incentives/for more information.

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TVA offers incentives to businesses, schools that install virus-killing technology - WKRN News 2

Microsofts solution to Zoom fatigue is to trick your brain – MIT Technology Review

Very rarely are you standing two feet away from a person and staring at them for an hour like that, unless youre getting in conflict or about to mate, he says. When you have faces staring at you like this, the arousal response kicks in, that fight-or-flight mode. If youre in fight-or-flight mode all day, its taxing to do these meetings.

Microsoft hopes Together Mode will make videoconferencing feel less taxing. In Zooms gallery mode, for example, it can be hard to figure out who is speaking and who wants to speak. Together Mode solves this, in theory, by putting a participant in the same seat on everyones screen. That means if a person pipes up in the upper right hand corner of the virtual room, everyones gaze moves at about the same time to focus on that person; if someone interrupts from the middle, heads and eyes shift in that direction. In internal tests, Microsoft claims, users felt less fatigued and more focused in Together Mode.

But whether Together Mode encourages quieter or often ignored members of a team to speak up is yet to be seen. Despite the promise of a more democratic virtual platform, women have had a more difficult time making their voices heard. Teams, Meet, and Zoom have all incorporated a hand-raising function to help, and guides for supporting female colleagues in this setting have become increasingly common.

I think Together Mode gives people the tools to do better, but it doesnt guarantee people will be better, says Jaron Lanier, a research scientist at Microsoft whos considered a world expert in mixed reality.

Another nagging issue is, well, your face. In a demo, I found myself trying to adjust my seating so that I would not appear too big or too small, something Lanier claims is helpful in democratizing participation. But it meant I often lost track of the discussion as I self-consciously corrected my posture. And perhaps self-consciousness is the root of the problem to begin with.

The ideal technology would let you disappear so you would stop being aware of yourself, says Amber Davisson, an associate professor of communication at Keene State College. Davisson, who researches the intersection of intimacy, communication, and technology, says the way videoconferencing tries to emulate meetings contrasts with how humans normallyinteract.

When Im sitting in my class and teaching, Im not looking at myself, she says. [Videoconferencing] is anxiety-causing and we can never relax; were way too aware of ourselves. The best technology would eliminate your face so you can look at everyone and they can look at you, and you dont see yourself.

One thing Davisson says is working in Together Modes favor is the non-personal background and predictable seating layout. Personalized Zoom backgrounds can be fun, but Davisson says having an agreed-upon, bland background like the ones offered by Together Mode eliminates the brains confusion of personal and professional.

That conceptof delineating work and home as the two spaces coalesceis ultimately the challenge of videoconferencing during a pandemic. We need a safe place to fall apart, and we used to think that was home, she says. But we do work and school in our homes now. Our only private space has been invaded, and its a lot for our brains to compute.

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Microsofts solution to Zoom fatigue is to trick your brain - MIT Technology Review

Boost in Technology Driving the Traffic Management Systems Market Globally – 3rd Watch News

Global Information & Communication Technologies (ICT) Sector Outlook

The global digital ecosystem has been continuously evolving over the last few years. The worldwide ICT sector has witnessed some key disruptions of late and governments of various economies are devising and implementing smart and inclusive regulations to govern sector penetration and facilitate technology connectivity to all parts of the world. Even as the world of technology prepares for a massive revolution with unimaginable advancements powered by machine intelligence, here are some of the key drifts presently trending the global ICT sector:

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Research Methodology

FMI utilizes robust methodology and approach to arrive at market size and related projections. The research methodology for this report is based on 3 dimensional model. We conduct about 45-60 min duration detailed interviews with product manufacturers; apart from this we also collect market feedback from industry experts. To validate this data, we interact with senior panel members having more than 10 years of experience in relevant field. The panel members help in validating the findings and fill the gaps if any. In addition, we leverage on our existing pool of information, paid database and other valid information sources available in public domain. Usually industry interactions extend to more than 50+ interviews from market participants across the value chain.

Data Collection

FMI collects data from secondary sources including company annual reports, association publications, industry presentations, white papers, and company press releases apart from these we leverage over paid database subscriptions and industry magazines to collect market information and developments in exhaustive manner. After being done with desk research, detailed questionnaire and discussion guide is formulated to initiate primary research with key industry personnel; the discussion aims at collecting key insights, growth perspectives, prevalent market trends and quantitative insights including market size and competition developments. Both of these research approaches help us in arriving at base year numbers and market hypothesis.

Download Methodology of this Report @ https://www.futuremarketinsights.com/askus/rep-gb-6469Data Validation

In this phase, FMI validates the data using macro and micro economic factors. For instance, growth in electricity consumption, industry value added, other industry factors, economic performance, growth of top players and sector performance is closely studied to arrive at precise estimates and refine anomalies if any.

Data Analysis and Projection

Data analysis and projections were made based on proprietary research frameworks and statistical analysis, which was further validated from industry participants. These frameworks include Y-o-Y growth projections, macro-economic factor performance, market attractiveness analysis, key financial ratios, and others.

For public companies we capture the data from company website, annual reports, investor presentations, paid databases. While for privately held companies, we try to gather information from the paid databases (like Factiva) and based on the information we gather from databases we estimate revenue for the companies. In addition, the team tries to establish primary contact with the companies in order to validate the assumptions or to gather quality inputs.

Standard Report Structure

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Market Taxonomy

The global traffic management system market has been segmented into the following:

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Boost in Technology Driving the Traffic Management Systems Market Globally - 3rd Watch News

Micron Waste Completes Acquisition of Covid Technologies and Appoints Harveer Singh Sidhu to Board of Directors – Canada NewsWire

VANCOUVER, BC, July 10, 2020 /CNW/ -Micron Waste Technologies Inc. ("Micron" or the "Company") (CSE: MWM) (OTC: MICWF) (Frankfurt: 7FM2) (OTCQB: MICWF), is pleased to announce that, further to its news releases on April 20, 2020, and May 19, 2020, the Company has completed the acquisition (the "Acquisition") of all of the issued and outstanding shares of Covid Technologies Inc. ("Covid Technologies") pursuant to the terms of a share exchange agreement, effective May 18, 2020 (the "Definitive Agreement") among the Company, Covid Technologies, and the securityholders of Covid Technologies.

Pursuant to the terms of the Definitive Agreement and in consideration of the Acquisition, the Company issued to the former Covid Technologies securityholders:

Additionally, effective upon closing of the Acquisition, Harveer Singh Sidhu was appointed to the Company's board of directors.

About Covid Technologies

Covid Technologies is preparing to deliver much needed personal protective equipment ("PPE") by providing Canadian-made, high quality, vapour barrier technology (masks, protective garments), that provide protection from biological hazards, pathogens, and suberbugs.

About Micron

Micron is a well-funded industrial/technology company with a manufacturing facility in Delta, BC. Micron is currently developing waste digesters using proprietary technology. Micron's waste digester business is focused on the cannabis and food industry with its Cannivore, Organivore and Pharmavore waste digesters. The Company will continue its research and development of its waste digester business alongside its PPE manufacturing business.

Micron is a public company with listings on the CSE: MWM, OTC: MICWF, and in Frankfurt: 7FM2.

ON BEHALF OF THE BOARD OF DIRECTORS

"Kal Malhi"

Kal Malhi, Chairman

The Canadian Stock Exchange does not accept responsibility for the adequacy or accuracy of this release.

FORWARD LOOKING STATEMENTS:The forward-looking information contained in this press release is made as of the date of this press release and, except as required by applicable law, the Company does not undertake any obligation to update publicly or to revise any of the included forward-looking information, whether as a result of new information, future events or otherwise, except as may be required by law. By its very nature, such forward-looking information requires the Company to make assumptions that may not materialize or that may not be accurate. This forward-looking information is subject to known and unknown risks and uncertainties and other factors, which may cause actual results, levels of activity and achievements to differ materially from those expressed or implied by such information.

SOURCE Micron Waste Technologies Inc.

For further information: Kal Malhi, [emailprotected]

https://micronwaste.com

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Micron Waste Completes Acquisition of Covid Technologies and Appoints Harveer Singh Sidhu to Board of Directors - Canada NewsWire

Work from home in Barbados: Caribbean island considering Barbados Welcome Stamp to let tourists work there remotely for 12 months – The Scotsman

LifestyleTravelWork from home in Barbados: Caribbean island considering Barbados Welcome Stamp to let tourists work there remotely for 12 months

Friday, 10th July 2020, 2:35 pm

The Barbados government has come up with a plan to help its tourism industry while giving UK residents the chance to escape the new daily routine of working from home.

The Caribbean island says it will offer British nationals who work remotely the chance to make Barbados their home for a year, under a new Barbados Welcome Stamp scheme.

Prime Minister Mia Mottley created the scheme to increase the country's GDP and boost the tourism industry on the island.

When will the scheme start?

The scheme is in the first stages of development and therefore hasn't been finalised yet.

Mottley has also not yet revealed when the scheme will be open for applicants, so those who are interested will need to keep their eyes peeled.

However, Barbados will start welcoming international travellers from Sunday 12 July.

Those who choose to visit the island will have to undergo mandatory tests for Covid-19 upon arrival and will need to isolate until the test results are provided.

How would the scheme work?

The initiative would allow international arrivals to live on the island while working remotely at their current jobs.

Prime Minister Mia Mottley said the Barbados Welcome Stamp scheme would allow persons to come and work from here overseas, digitally so, so that persons dont need to remain in the countries in which they are.

However those who wish to make Barbados their permanent home, will have to do so in another way, as the scheme only permits you to remain on the island for 12 months.

How has Barbados handled the coronavirus crisis?

If you love the idea of spending your work days on the beach, rather than the sofa, but are worried about the safety aspects of living in Barbados, here are some reassuring facts:

The number of coronavirus cases and fatalities is extremely low in comparison to that of the UK, with only 98 recorded infections and seven deaths.

Safety measures currently in place to protect the country, include mandatory face masks for all incoming visitors as well as coronavirus testing at the airports.

Barbados has now relaxed some of its restrictions and lifted its curfews.

It is now allowing social events with up to 500 people, as well as spectator sporting events, however it has introduced social distancing rules whereby people must remain at least three feet apart.

The UK government included Barbados in its list of approved nations announced last week, meaning that tourists arriving in the UK from the Carribean island would not need to go into a 14 day quarantine.

Prime Minister Mottley said in a statement, "You don't need to work in Europe, or the US or Latin America if you can come here and work for a couple months at a time; go back and come back.

"The government is committed to working with you on the promotion of new concepts like the 12-month Barbados Welcome Stamp, being able to open our borders to persons travelling and making it as hospitable as ever for all of us, and making it available for Barbadians from every walk of life to believe that for special occasions, or just for so, that they can come out and be a part of this wonderful exercise."

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Work from home in Barbados: Caribbean island considering Barbados Welcome Stamp to let tourists work there remotely for 12 months - The Scotsman

New Pirates of the Caribbean Movie Will Reference Johnny Depp and Captain Jack Sparrow on One Condition – GameRant

Disney will allow the new Pirates of the Caribbean movies to reference Captain Jack Sparrow and Johnny Depp if the actor's current press dies down.

Back in 2018, UK publisher The Sun described Johnny Depp known best for playingCaptain Jack Sparrow in Pirates of the Caribbean as a "wife-beater" in one of their prints. It did so in reference to accusations Depp's ex-wife Amber Heard threw at him during their infamous divorce back in 2015-2017. Depp decided to retaliate against this by suing The Sun, and his libel case begins this week.

Amidst all of this, Disney has announced that it has plans to create anewPirates of the Caribbeanmovie starring Margot Robbie. The film will feature an all-female main cast and be completely separate from the previously announced Pirates of the Caribbean reboot helmed by the series original writer, Ted Elliott.

RELATED:Birds of Prey Director Cathy Yan Fought to Keep Controversial Scene in the Film

Jerry Bruckheimer, the producer of the originalPirates of the Caribbeantrilogy and its two sequels, would like to reference Johnny Depp and Sparrow in the upcoming Margot Robbie spin-off. But Disney is apparently hesitating in allowing it because of Depp's past being in the spotlight again. It seems the company will only give the green light if Depp's press dies down a bit.

It's worth noting that Amber Heard is on tape admitting that she's the one who abusedJohnny Depp. Overall, the situation is somewhat similar to that of James Gunn's when he was under fire for some questionable tweets he made in the past. Disney felt it needed to distance itself from Gunn because of the controversy surrounding him. Hopefully, Depp will get the chance to move on the same way Gunn was allowed to.

MORE:Birds of Prey Director Reveals Which Batman Villain Will Join Harley Quinn in Potential Sequel

Source: Hollywood Reporter

Batman Gotham Knights Title Leak May Solidify Other Rumors

For as long as his terrible memory can recall, Jametrious has had a love for the art of storytelling and its resulting creations. His passions led him to Full Sail University, where studying and producing creative media allowed him to goof his way to a BFA in Creative Writing. Now a certified professional man-child, Jametrious spends his time playing and writing about video games. He favors action-RPGs over most, but hell pretty much play anything that features mindless action wrapped up in an intriguing story. You can follow him on twitter @J_Broson for updates.

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New Pirates of the Caribbean Movie Will Reference Johnny Depp and Captain Jack Sparrow on One Condition - GameRant

COVID-19 Daily Update 7-11-2020 – 5 PM – West Virginia Department of Health and Human Resources

The West Virginia Department of Health andHuman Resources (DHHR) reports as of 5:00 p.m., on July 11,2020, there have been 204,914 total confirmatorylaboratory results received for COVID-19, with 4,146 totalcases and 96 deaths.

DHHR has confirmed the death of a 68-yearold female from Ohio County. Itis with great sadness that we report the loss of this West Virginian and sendcondolences to her family, said Bill J. Crouch, DHHR Cabinet Secretary.

Inalignment with updated definitions from the Centers for Disease Control andPrevention, the dashboard includes probable cases which are individuals that havesymptoms and either serologic (antibody) or epidemiologic (e.g., a link to aconfirmed case) evidence of disease, but no confirmatory test.

CASESPER COUNTY (Case confirmed by lab test/Probable case):Barbour(19/0), Berkeley (512/19), Boone (33/0), Braxton (5/0), Brooke (23/1), Cabell(192/6), Calhoun (4/0), Clay (12/0), Fayette (79/0), Gilmer (13/0), Grant(18/1), Greenbrier (71/0), Hampshire (42/0), Hancock (38/3), Hardy (45/1),Harrison (115/0), Jackson (148/0), Jefferson (248/5), Kanawha (398/12), Lewis(21/1), Lincoln (9/0), Logan (36/0), Marion (105/3), Marshall (62/1), Mason(24/0), McDowell (8/0), Mercer (62/0), Mineral (63/2), Mingo (28/2), Monongalia(510/14), Monroe (14/1), Morgan (19/1), Nicholas (20/1), Ohio (140/0),Pendleton (15/1), Pleasants (4/1), Pocahontas (36/1), Preston (77/16), Putnam(85/1), Raleigh (73/3), Randolph (185/2), Ritchie (2/0), Roane (12/0), Summers(2/0), Taylor (22/1), Tucker (6/0), Tyler (10/0), Upshur (24/1), Wayne (123/1),Webster (1/0), Wetzel (34/0), Wirt (6/0), Wood (175/9), Wyoming (7/0).

Ascase surveillance continues at the local health department level, it may revealthat those tested in a certain county may not be a resident of that county, oreven the state as an individual in question may have crossed the state borderto be tested. Such is the case of Brooke, Jefferson,McDowell, and Preston counties in this report.

Please visit the dashboard at http://www.coronavirus.wv.gov for more detailed information.

Additional report:

Toincrease COVID-19 testing opportunities, the Governor's Office, the HerbertHenderson Office of Minority Affairs, WV Department of Health and HumanResources, WV National Guard, local health departments, and community partners providedfree COVID-19 testing for residents in counties with high minority populationsand evidence of COVID-19 transmission.

The two-day testing resulted in 5,826 individuals tested: 807in Marshall County; 262 in Mercer County; 2,955 in Monongalia County; 730 inPreston County; 301 in Wayne County; and 771 in Upshur County. Please notethese are considered preliminary numbers.

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COVID-19 Daily Update 7-11-2020 - 5 PM - West Virginia Department of Health and Human Resources

Covid-19 vaccine trials: Here’s how to volunteer – CNN

The website will handle registration for the four large vaccine studies that are expected to start this summer and fall, and any others that follow.

The US Department of Health and Human Services announced the website Wednesday, along with the appointment of the Fred Hutchinson Cancer Research Center in Seattle as the coordinating center for vaccine clinical trials run by the Covid-19 Prevention Network, which is funded by the National Institutes of Health.

"That's the target, but those target dates move up and down. They won't let a site start until they're absolutely ready. Some could start on July 27, and others on August 8," del Rio said.

Despite the delay, the Covid-19 vaccine trials are moving at an unprecedented speed, as researchers try to accomplish in months what usually takes years.

Del Rio said he enrolls six or seven study subjects a week in a typical clinical trial, but for the Covid vaccine trial he'll try to enroll that number in a day. Eventually, he aims to have a total of 750 study subjects at three Atlanta-area sites.

He noted that he still has not yet received approval from Emory's Institutional Review Board to begin the trial, a requirement before moving forward.

"This is the most complicated research study I've ever done, and we need to do it in record time," del Rio said, noting that he is still hiring staff and securing facilities for the trial.

Dr. Richard Novak, another clinical trial veteran agrees.

"I've been doing vaccine trials for 25 years, but this is the largest I've ever committed to and I just don't have enough staff and I don't have enough space," said Novak, who will be leading the Moderna trial at the University of Illinois at Chicago.

What researchers are looking for

On the new website, anyone interested in joining a vaccine study can fill out a quick questionnaire.

There will be more than 100 sites in the United States and abroad, and after registering on the website, your information will be sent to the study site closest to you.

Several of the questions are designed to assess how likely you are to become infected and sick with Covid-19, including your race, what kind of work you do and how many people you come into contact with on a daily basis.

Based on those answers, you might be rejected. People who don't get out much, and who wear a mask when they do leave home, would not make the best study subjects.

That's because the point of the study is to see if the vaccine protects people from getting sick with Covid-19. If people who mostly stay home get vaccinated, and they don't get sick with Covid-19, it's hard to know if the vaccine protected them or if their lifestyle kept them away from the virus in the first place.

That's why researchers are looking for people in communities that have been hardest hit by coronavirus.

"We need people who are black and brown and representative of harder hit communities by the pandemic," said Dr. Carl Fichtenbaum, medical director of the Moderna trial at University of Cincinnati Health.

The doctors say they'll recruit at churches and other organizations in those communities, as well as in workplaces such as factories and meatpacking plants where workers are at high risk of getting sick with Covid-19.

The researchers are also aiming to have 40% of the study subjects over age 65 or with underlying conditions, such as hypertension, lung disease, diabetes and morbid obesity, since they're more likely to become ill with Covid-19, Novak said.

Tens of thousands of volunteers needed

Moderna has finished a safety trial with more than 100 study subjects, but it has not yet published the results. These later phase trials monitor safety and focus on whether the vaccine protects against becoming ill from the coronavirus.

Novak said volunteers for the Moderna trial will receive two injections spaced a month apart. About half the study volunteers will receive two doses of the vaccine, and the other half will receive placebos -- a shot that has no therapeutic value. Neither the doctors nor the volunteers will know who's getting which shot.

The volunteers will have appointments seven times throughout the two-year course of the study, where they will have blood drawn and their noses swabbed to check for Covid-19 infection.

Volunteers will keep a weekly diary of their symptoms and will speak on the phone with study staff to discuss how they're feeling.

"It has to be done really meticulously, because that's a key part of clinical research," Novak said. "The data has to be impeccable."

Either way, tens of thousands of volunteers will need to step up for the studies.

"I want to emphasize to people that you will be part of something special, even if the answer is that this does not work," Fichtenbaum said. "That's a very important scientific answer because we need to know what works [and] what won't work."

CNN's John Bonifield and Dana Vigue contributed to this story.

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Covid-19 vaccine trials: Here's how to volunteer - CNN

Michigan tops 600 new COVID-19 cases for 3rd time this week – The Detroit News

Michigan confirmed 28 coronavirus deaths Saturday and 653 new cases.

The deaths announced Saturday include22 prior deaths identified during a record review, the state said.

Michigan has seen growth in the number of new cases of the disease COVID-19 in the last three weeks. Saturdaywas the third time this week the single-day case count topped 600, which hadn't happened since May.

The average number of new cases for the past seven days ending Friday is up to 451 a day from an average of 349 a day for the previous seven-day period, according to state data.

The state recorded 15 deaths Friday and 612 new cases Friday, as Gov. Gretchen Whitmer issued a mask mandatein an attempt to stem the virus' spread in the state.

While reported deaths and hospitalizations due to the disease remain relatively low, that could change in the coming weeks, health leaders warned Thursday.

Michigan had a six-week high for newly confirmed infections last week, surpassing 2,500 cases during the week ending July 4. In addition to the 612 cases confirmed Friday, the state reported 10 probable cases.

The state health department had confirmed 68,948 cases of COVID-19. When probable cases are added, Michigan's case total reaches 75,685, and the death toll is 6,313.

The 3,415 new cases reported this week are a seven-week high. The last time Michigan reported more than 3,000 new cases in a week was May 17-23 when 3,861 cases were reported.

While more testing is being done to help confirm new cases, the rate of positive tests continues to trend upward. About 3.5% of the tests done this week have come back positive, according to data through Saturday. It's the highest percentage for positive tests since the beginning of June, but still well below the positive percentages in April, when the virus peaked in Michigan.

This weeks reported death toll is a four-week high, according to the states data.

The state's hardest-hit city, Detroit, has a total of 11,936 confirmed cases and 1,461 deaths, according to city-data released Saturday.

The statewide death rate from the virus is 8.8%, dropping from 9.8% last week.

As of Friday,53,867 have recovered from the virus.

srahal@detroitnews.com

Twitter: @SarahRahal_

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Michigan tops 600 new COVID-19 cases for 3rd time this week - The Detroit News

Wisconsin reports record number of COVID-19 cases for third day in a row at 926 new cases – Post-Crescent

For the third day in a row, Wisconsin health officials reported a record number of new COVID-19 cases.

The state Department of Health Services reported 926 new cases on Saturday, following two previous record-setting days. On Friday, 845 new cases were reported and on Thursday, the state announced 754 new cases. Last Saturday, July 4, kicked off the record-setting week when738 cases were reported.

The926positive cases reported Saturday account for 7.7% of the 12,019tests processed since Friday, according to the state health department. As of Saturday,35,679 Wisconsinites have tested positive for COVID-19.

The state health department also reported seven more COVID-19 deaths, bringing the state's total to 821.

Statewide, 264people with COVID-19 were hospitalized as of Saturday morning, which is 29 morepeople than last Saturday, according to theWisconsin Hospital Association. Of those patients, 75are in the intensive care unit. Another 155hospitalized patients are waiting for the results of a COVID-19 test.

In total, 3,793 people in Wisconsin have had to be hospitalized due to COVID-19, or around 11% of all cases.

RELATED:Bars and coronavirus don't mix. Will Wisconsin's drinking culture ever be the same?

RELATED:Claire Hornby is 10, has brain cancer; now COVID is complicating the ordeal

As of Saturday, there are 6,944active COVID-19 casesin Wisconsin, or 19% of all confirmed cases. Another 79%of people have recovered and the remaining 2% of people have died, according to the state health department.

County activity ratings as of Wednesday, July 8, are as follows. Parentheses reflect a change in the activity level from last week's ratings.

Globally, there have been more than 12.5 million confirmed cases of COVID-19, with the United States accounting for around 3.2 million cases, according to Johns Hopkins University. More than 134,000 people in the U.S. have died.

Contact Natalie Brophy at (715) 216-5452 or nbrophy@gannett.com. Followher on Twitter @brophy_natalie.

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Wisconsin reports record number of COVID-19 cases for third day in a row at 926 new cases - Post-Crescent

Immunophenotyping of COVID-19 and influenza highlights the role of type I interferons in development of severe COVID-19 – Science

Abstract

Although most SARS-CoV-2-infected individuals experience mild coronavirus disease 2019 (COVID-19), some patients suffer from severe COVID-19, which is accompanied by acute respiratory distress syndrome and systemic inflammation. To identify factors driving severe progression of COVID-19, we performed single-cell RNA-seq using peripheral blood mononuclear cells (PBMCs) obtained from healthy donors, patients with mild or severe COVID-19, and patients with severe influenza. Patients with COVID-19 exhibited hyper-inflammatory signatures across all types of cells among PBMCs, particularly up-regulation of the TNF/IL-1-driven inflammatory response as compared to severe influenza. In classical monocytes from patients with severe COVID-19, type I IFN response co-existed with the TNF/IL-1-driven inflammation, and this was not seen in patients with milder COVID-19. Interestingly, we documented type I IFN-driven inflammatory features in patients with severe influenza as well. Based on this, we propose that the type I IFN response plays a pivotal role in exacerbating inflammation in severe COVID-19.

Currently, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), is spreading globally (1, 2), and the World Health Organization (WHO) has declared it a pandemic. As of June 2, 2020, more than 6.1 million confirmed cases and more than 376,000 deaths have been reported worldwide (3).

SARS-CoV-2 infection usually results in a mild disease course with spontaneous resolution in the majority of infected individuals (4). However, some patients, particularly elderly patients develop severe COVID-19 infection that requires intensive care with mechanical ventilation (4, 5). The mortality rate for COVID-19 in Wuhan, China, is estimated to be 1.4% (5). Although this rate is lower than that of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), which are caused by other human pathogenic coronaviruses (6), it is much higher than that of influenza, a common respiratory viral disease requiring hospitalization and intensive care in severe cases.

In severe cases of COVID-19, a hyper-inflammatory response, also called a cytokine storm, has been observed and is suspected of causing the detrimental progression of COVID-19 (7). Circulating levels of pro-inflammatory cytokines, including TNF and IL-6, are increased in severe cases (8). Gene expression analyses have also shown that IL-1-related pro-inflammatory pathways are highly up-regulated in severe cases (9). In a murine model of SARS-CoV infection, a delayed, but considerable type I IFN (IFN-I) response promotes the accumulation of monocytes-macrophages and the production of pro-inflammatory cytokines, resulting in lethal pneumonia with vascular leakage and impaired virus-specific T-cell responses (10).

Immune dysfunction is also observed in patients with COVID-19. In severe cases, the absolute number of T cells is reduced (8, 11), and the T cells exhibit functional exhaustion with the expression of inhibitory receptors (12, 13). However, hyper-activation of T cells as reflected in the up-regulation of CD38, HLA-DR, and cytotoxic molecules was also reported in a lethal case of COVID-19 (14). Immune dysfunction in patients with severe COVID-19 has been attributed to pro-inflammatory cytokines (15).

In the present study, we performed single-cell RNA-seq (scRNA-seq) using peripheral blood mononuclear cells (PBMCs) to identify factors associated with the development of severe COVID-19 infection. By comparing COVID-19 and severe influenza, we report that the TNF/IL-1-driven inflammatory response was dominant in COVID-19 across all types of cells among PBMCs, whereas the up-regulation of various interferon-stimulated genes (ISGs) was prominent in severe influenza. When we compared the immune responses from patients with mild and severe COVID-19 infections, we found that classical monocytes from severe COVID-19 exhibit IFN-I-driven signatures in addition to TNF/IL-1-driven inflammation.

PBMCs were collected from healthy donors (n=4), hospitalized patients with severe influenza (n=5), and patients with COVID-19 of varying clinical severity, including severe, mild, and asymptomatic (n=8). PBMCs were obtained twice from three (the subject C3, C6, and C7) of the eight COVID-19 patients at different time points during hospitalization. PBMC specimens from COVID-19 patients were assigned to severe or mild COVID-19 groups according to the National Early Warning Score (NEWS; mild < 5, severe 5) evaluated on the day of whole blood sampling (16). In NEWS scoring, respiratory rate, oxygen saturation, oxygen supplement, body temperature, systolic blood pressure, heart rate, and consciousness were evaluated (16). Severe influenza was defined when hospitalization was required irrespective of NEWS score. Patients with severe influenza were enrolled from December 2015 to April 2016, prior to the emergence of COVID-19. The severe COVID-19 group was characterized by significantly lower lymphocyte count and higher serum level of C-reactive protein than the mild COVID-19 group on the day of blood sampling (Fig. S1A). Multiplex real-time PCR for N, RdRP, and E genes of SARS-CoV-2 was performed, and there was no statistical difference in Ct values for all three genes between two groups (Fig. S1B). Demographic information is provided with experimental batch of scRNA-seq in Table S1 and clinical data in Table S2 and S3.

Employing the 10X Genomics scRNA-seq platform, we analyzed a total of 59,572 cells in all patients after filtering the data with stringent high quality, yielding a mean of 6,900 UMIs per cell and detecting 1,900 genes per cell on average (Table S4). The transcriptome profiles of biological replicates (PBMC specimens in the same group) were highly reproducible (Fig. S1C), ensuring the high quality of the scRNA-seq data generated in this study.

To examine the host immune responses in a cell type-specific manner, we subjected 59,572 cells to t-distributed stochastic neighbor embedding (tSNE) based on highly variable genes using the Seurat package (17) and identified 22 different clusters unbiased by patients or experimental batches of scRNA-seq (Fig. 1A, Fig. S1D). These clusters were assigned to 13 different cell types based on well-known marker genes and two uncategorized clusters (Fig. 1B and C, and Table S5). In downstream analysis, we only focused on 11 different immune cell types, including IgG- B cell, IgG+ B cell, effector memory (EM)-like CD4+ T cell, non-EM-like CD4+ T cell, EM-like CD8+ T cell, non-EM-like CD8+ T cell, natural killer (NK) cell, classical monocyte, intermediate monocyte, non-classical monocyte, and dendritic cell (DC) after excluding platelets, red blood cells (RBCs), and two uncategorized clusters. The subject C8 (asymptomatic case) was also excluded due to a lack of replicates. In hierarchical clustering, most transcriptome profiles from the same cell type tended to cluster together, followed by disease groups, suggesting that both immune cell type and disease biology, rather than technical artifacts, are the main drivers of the variable immune transcriptome (Fig. S1E).

(A) tSNE projections of 59,572 PBMCs from healthy donors (HDs) (4 samples, 17,590 cells), severe influenza (FLU) patients (5 samples, 10,519 cells), COVID-19 patients (asymptomatic: 1 sample, 4,425 cells; mild COVID-19: 4 samples, 16,742 cells; severe COVID-19: 6 samples, 10,296 cells) colored by group information. (B) Normalized expression of known marker genes on a tSNE plot. (C) tSNE plot colored by annotated cell types. EM: effector memory, NK cell: natural killer cell, DC: dendritic cell, RBC: red blood cell. (D) Proportion of cell types in each group excluding Uncategorized 1, Uncategorized 2, RBC, and Platelet. The colors indicate cell type information. (E) Boxplots showing the fold enrichment in cell type proportions from mild COVID-19 (n=4), severe COVID-19 (n=6), and FLU (n=5) patients compared to the HD group (mild COVID-19 vs. HD: n=16, severe COVID-19 vs. HD: n=24, FLU vs. HD: n=20). For the boxplots, the box represents the interquartile range (IQR) and the whiskers correspond to the highest and lowest points within 1.5IQR. Uncategorized 1 (relatively high UMIs per cells and presence of multiple marker genes), Uncategorized 2 (B cell-like and high expression of ribosomal protein genes), RBC, and Platelet were excluded. Two-sided KolmogorovSmirnov (KS) tests were conducted for each cell type between the disease and HD group. *p<0.05, **p<0.01, and ***p<0.001.

As a feature of immunological changes, we investigated the relative proportions of immune cells among PBMCs in the disease groups compared to the healthy donor group (Fig. 1D and E, and Fig. S1F). Unlike the limited changes in mild COVID-19, significant changes were observed in both influenza and severe COVID-19 across multiple cell types among PBMCs. In severe COVID-19, the proportion of classical monocytes significantly increased whereas those of DCs, non-classical monocytes, intermediate monocytes, NK cells, EM-like CD8+ T cells, and EM-like CD4+ T cells significantly decreased (Fig. 1E). In severe influenza, the proportion of classical monocytes significantly increased whereas those of DCs, non-EM-like CD4+ T cells, EM-like CD4+ T cells, IgG+ B cells, and IgG- B cells significantly decreased. We validated the proportions of immune cell subsets from scRNA-seq by flow cytometry analysis. The relative proportions of total lymphocytes, B cells, CD4+ T cells, CD8+ T cells, NK cells, and total monocytes from scRNA-seq significantly correlated with those from flow cytometry analysis (Fig. S1G).

In order to compare the effect of infection between diseases, we performed hierarchical clustering based on relative gene expression changes against the healthy donor group. Unexpectedly, all types of cells among PBMCs were clustered together according to the disease groups instead of cell-types (Fig. 2A). Further investigation of the variable genes based on K-means clustering supported COVID-19-specific up- or down-regulated gene expression patterns across all types of cells among PBMCs (Fig. S2A). These results indicate that, in COVID-19, peripheral blood immune cells may be influenced by common inflammatory mediators regardless of cell type. Despite distinct transcriptional signatures between COVID-19 and influenza, severe COVID-19 and influenza shared transcriptional signatures in all types of monocytes and DCs (black boxed region in Fig. 2A), possibly reflecting common mechanisms underlying the innate immune responses in severe influenza and severe COVID-19.

(A) Hierarchical clustering using the Pearson correlation coefficient (PCC) of a normalized transcriptome between diseases in cell type resolution (n = 33). The color intensity of the heat map indicates the PCC values. The color bars above the heat map indicate the cell type and disease group. The black box indicates the cell types that highly correlate between the severe COVID-19 and FLU groups. (B) Illustration of the enrichment p-values for the select GO biological pathways (n = 49) of differentially expressed genes (DEGs) in COVID-19 and FLU patients (left 6 columns: DEGs for COVID-19 and FLU groups compared to HD, right 2 columns: DEGs between COVID-19 and FLU groups). (C) tSNE plot of representative gene expression patterns for GBP1 (FLU specific), CREM (COVID-19 specific), and CCL3 (COVID-19/FLU common). (D) Top, dendrogram from WGCNA analysis performed using relative normalized gene expression between the COVID-19 and FLU groups for the genes belonging to the select biological pathways in (B) (n=316). Bottom, heat map of relative normalized gene expression between the COVID-19 and FLU groups. The color bar (left) indicates cell type information clustered by hierarchical clustering based on the PCC for relative normalized gene expression. Modularized gene expression patterns by WGCNA are shown together (G1, n=10; G2, n=147; G3, n=27; G4, n=17; G5, n=12; G6, n=64; G7, n=34; G8, n=5).

Next, we sought to identify relevant biological functions in disease-specific up- or down-regulated genes in terms of the GO biological pathways. First, we combined both mild and severe COVID-19 as a COVID-19 group and identified disease-specific changes in genes for each cell type compared to the healthy donor group using model-based analysis of single cell transcriptomics (MAST) (18). NFKB1, NFKB2, IRF1, and CXCR3 were specifically up-regulated in COVID-19, and CXCL10, STAT1, TLR4, and genes for class II HLA and immunoproteasome subunits were specifically up-regulated in influenza (Table S6). TNF, TGFB1, IL1B, and IFNG were commonly up-regulated. When we directly compared COVID-19 and influenza, NFKB1, NFKB2, and TNF were up-regulated in COVID-19, whereas STAT1, TLR4, and genes for immunoproteasome subunits were up-regulated in influenza. For each group of differentially expressed genes (DEGs), we identified the top 10 enriched GO biological pathways and collected them to demonstrate p-value enrichment in each group of DEGs (Fig. 2B). Both distinct and common biological functions were identified as illustrated by inflammatory response genes being highly active in both COVID-19 and influenza, but genes for transcription factors, including inflammatory factors (i.e., NFKB1/2, and STAT4) were up-regulated in COVID-19. In contrast, a limited response in genes associated with the IFN-I and -II signaling pathways, T-cell receptor pathways, and adaptive immune response was observed in COVID-19 compared to influenza. Such disease-specific gene expression patterns were exemplified at single cell resolution by GBP1 (IFN--mediated signaling pathway) being specifically up-regulated in influenza, CREM (positive regulation of transcription) being specifically up-regulated in COVID-19, and CCL3 (inflammatory response) being commonly up-regulated (Fig. 2C and Table S7).

We expanded our analysis in a cell type specific manner by conducting weighted gene correlation network analysis (WGCNA) (19) for the collected genes associated with Fig. 2B. We identified several modular expression patterns (Fig. 2D and Table S8). In the COVID-19 group, NFKB1/2, JUN, and TNF were modularized in CD8+ T and NK cells (G6 and G7 in Fig. 2D), and IL1B, NFKBID, and OSM were modularized in all types of monocytes and DCs (G3 in Fig. 2D). In the influenza group, GBP1, TAP1, STAT1, IFITM3, OAS1, IRF3, and IFNG were modularized in all types of T cells and NK cells (G2 in Fig. 2D), and CXCL10 and TLR4 were modularized in all types of monocytes and DCs (G5 and part of G6 in Fig. 2D). Consistently, the DEGs between COVID-19 and influenza were dominant in CD8+ T cells and all types of monocytes (Fig. S2B).

To uncover disease-specific transcriptional signatures in CD8+ T cells, we performed sub-clustering analysis from EM-like and non-EM-like CD8+ T cell clusters using Seurat (17). Each disease group-specifically enriched sub-clusters compared to the two other groups were identified in the non-EM-like CD8+ T cell cluster (Fig. 3A). Of the six sub-clusters from the non-EM-like CD8+ T cell cluster, cluster 1 and cluster 3 were significantly enriched in the influenza and COVID-19 groups, respectively (Fig. 3B and C, and S3A). Clusters with the high expression of PPBP, a marker of platelets, were excluded in following analysis (e.g., cluster 6 in Fig. S3A). Intriguingly, up-regulated genes in cluster 1 and cluster 3 were associated with previously defined gene sets for influenza A virus infection and SARS-CoV infection, respectively (Fig. S3B) (20). We also found that the cluster 3-specific up-regulated genes reflect activation of immune response, including CD27, RGS1, CCL5, SELL, and RGS10 (Fig. S3C and Table S9). Protein interaction network analysis of selected top 30 up-regulated genes in each cluster based on STRING v11 (21) revealed the up-regulation of PRF1, GNLY, GZMB, and GZMH in cluster 1 and the up-regulation of GZMK, GZMA, CXCR3, and CCL5 in cluster 3 (Fig. 3D, green). STAT1, TAP1, PSMB9, and PSME2, which are up-regulated preferentially by IFN-, were overexpressed only in influenza-specific cluster 1 (Fig. 3D, blue). We validated these data by intracellular staining for granzyme B and PMA/ionomycin-stimulated intracellular cytokine staining for IFN-. The percentages of granzyme B+ and IFN-+ cells among CD8+ T cells were significantly higher in the influenza group than in the COVID-19 group (Fig. S3D). Of the seven representative GO biological pathways for the pro-inflammatory and IFN responses, pathways for responses to IFN-I and -II were more associated with influenza-specific cluster 1, whereas pathways for the response to TNF or IL-1 were more prominent in COVID-19-specific cluster 3 (Fig. 3E).

(A) tSNE plot of the non-EM-like CD8+ T cell subpopulations in all groups (left, n=6,253), COVID-19 (top right, n=2,653), FLU (middle right, n=1,452), and HD (bottom right, n=2,148) colored by cluster information. (B, C) Boxplots showing the proportion of individual sub-clusters from the non-EM-like CD8+ T cell cluster within each group (COVID-19, n=10; FLU, n=5; HD, n=4). The proportions follow normal distribution as tested by the Shapiro-Wilk normality test except the proportion of cluster 3 in the COVID-19 group (p=0.04). Cluster 1 and cluster 3 were highly enriched in the FLU and COVID-19 group, respectively. Two-sided Welchs t test p-values were 4.4E-03 between COVID-19 and FLU in cluster 1, 3.5E-02 between FLU and HD donor in cluster 1, 8.6E-03 between COVID-19 and FLU in cluster 3, and 5.8E-3 between COVID-19 and HD in cluster 3. *p<0.05, **p<0.01. (D) STRING analysis using the top 30 up-regulated genes in cluster 1 (left) and cluster 3 (right). (E) Bar plots showing enrichment p-values of eight representative GO biological pathways for pro-inflammation and interferon in cluster 1 or cluster 3-specific up-regulated genes (cluster 1, n=66; cluster 3, n=183).

We performed sub-clustering analysis from all three types of monocyte clusters to find COVID-19-specific sub-clusters. However, there was no COVID-19-specifically enriched sub-cluster (Fig. S4A and B). Next, we further focused on classical monocytes considering their crucial roles for inflammatory responses. We investigated DEGs between influenza and COVID-19 to seek COVID-19-specific transcriptional signatures in classical monocytes (Fig. 4A). Interestingly, TNF and IL1B, major genes in the inflammatory response, were identified as COVID-19-specific and commonly up-regulated genes, respectively. To better characterize the transcriptional signatures in classical monocytes, we performed K-means clustering of up-regulated genes in at least one disease group compared to the healthy donor group. We identified five different clusters of up-regulation (Fig. 4B and Table S10): genes in cluster 1 are commonly up-regulated in all disease groups, cluster 2 is influenza-specific, cluster 3 is associated with mild/severe COVID-19, cluster 4 is associated with influenza and severe COVID-19, and cluster 5 is severe COVID-19-specific.

(A) Venn diagram of differentially expressed genes (DEGs) in COVID-19 and FLU compared to HD. The representative genes are shown together. (B) K-means clustering of DEGs between all pairs of FLU, mild COVID-19, and severe COVID-19 (n=499). The color indicates the relative gene expression between the diseases and HD. The representative genes are shown together. (C) Bar plots showing the average log10(p-value) values in enrichment analysis using the perturbed genes of four different cell lines listed in L1000 LINCS for up-regulated genes in cluster 2 (C2, left) and cluster 3 (C3, right). Error bars indicate standard deviation. (D) Combined enrichment scores were compared between C2 and C3 for the gene sets of the type I IFN response (left; GSE26104) and TNF response (right; GSE2638, GSE2639). **p<0.01. Each dot indicates an individual subject. (E) Bar plots showing the average log10(p-value) values in the enrichment analysis using the perturbed genes listed of four different cell lines in L1000 LINCS for up-regulated genes in cluster 4 (C4, left) and cluster 5 (C5, right). Error bars indicate standard deviation (C and E).

We examined each cluster-specific genes by gene set enrichment analysis (GSEA) using cytokine-responsive gene sets originated from each cytokine-treated cells (LINCS L1000 ligand perturbation analysis in Enrichr) (22). COVID-19-specific cluster 3 genes were enriched by TNF/IL-1-responsive genes whereas influenza-specific cluster 2 genes were enriched by IFN-I-responsive genes in addition to TNF/IL-1-responsive genes (Fig. 4C), indicating that the IFN-I response is dominant in influenza compared to COVID-19. We confirmed this result by analyzing cluster-specific genes with cytokine-responsive gene sets originated from other sources (Fig. 4D). Unexpectedly, cluster 4 and 5 exhibited strong associations with IFN-I-responsive genes, in addition to TNF/IL-1-responsive genes (Fig. 4E), indicating that severe COVID-19 acquires IFN-I-responsive features in addition to TNF/IL-1-inflammatory features.

Next, we directly compared classical monocytes between mild and severe COVID-19. When we analyzed DEGs, severe COVID-19 was characterized by up-regulation of various ISGs, including ISG15, IFITM1/2/3, and ISG20 (Fig. 5A). Both TNF/IL-1-responsive genes and IFN-I-responsive genes were enriched in severe COVID-19-specific up-regulated genes (Fig. 5B). We measured plasma concentrations of TNF, IL-1, IL-6, IFN-, IFN-, and IL-18 in a larger cohort of COVID-19 patients. Among these cytokines, IL-6 and IL-18 were significantly increased in severe COVID-19 compared to mild COVID-19 whereas there was no difference in plasma concentrations of the other cytokines between the two groups (Fig. S5A). These results indicate that cytokine-responsive gene signatures cannot be simply explained by a few cytokines because of overlapped effects of cytokines.

(A) Volcano plot showing DEGs between mild and severe COVID-19 groups. Each dot indicates individual gene, colored by red when a gene is significant DEG. (B) Bar plot showing the average log10(p-value) values in enrichment analysis using the perturbed genes of four different cell lines listed in L1000 LINCS for up-regulated genes in the severe COVID-19 group. Error bars indicate standard deviation. (C) Trajectory analysis of classical monocytes from specimens obtained at two different time points in a single COVID-19 patient (mild: C7-2, 1,197 cells; severe: C7-1, 631 cells). The color indicates cluster information (left) or the severity of COVID-19 (right). (D) Relative expression patterns of representative genes in the trajectory analysis are plotted along the Pseudotime. The color indicates the relative gene expression calculated by Monocle 2. (E) Bar plots showing the average log10(p-value) values in the enrichment analysis using the perturbed genes of four different cell lines in L1000 LINCS for up-regulated genes in cluster 3 (left) and cluster 1 (right). Error bars indicate standard deviation. (F) Comparison of combined enrichment scores between cluster 3 and cluster 1 for the gene sets from systemic lupus erythematosus (SLE) (n=16) and rheumatoid arthritis (RA) (n=5). ***p<0.001; ns, not significant. (G) GSEA of up-regulated genes in cluster 3 (left) and cluster 1 (right) to the class 1 gene module of monocyte-derived macrophages by Park et al. (2017). NES: normalized enrichment score, FDR: false discovery rate.

To further investigate the characteristics of severe COVID-19, we performed a trajectory analysis with Monocle 2 (23) using two internally well-controlled specimens (one severe and one mild) in which both PBMC samples were collected from a single patient (the subject C7) with COVID-19. Trajectory analysis aligned classical monocytes along the disease severity with cluster 1 and cluster 3 corresponding to later and earlier Pseudotime, respectively (Fig. 5C). Representative genes in cluster 1 was enriched in the severe stage and highly associated with the both IFN-I and TNF/IL-1-associated inflammatory response (Fig. 5D, Fig. S5B, and Table S11). GSEA confirmed that both the IFN-I response and TNF/IL-1 inflammatory response were prominent in cluster 1, but not in cluster 3 (Fig. 5E). Cluster 1 exhibited a significantly higher association with a gene set from systemic lupus erythematosus, which is a representative inflammatory disease with IFN-I features, than cluster 3 (Fig. 5F, left), but was not significantly associated with a gene set from rheumatoid arthritis (Fig. 5F, right).

We obtained additional evidence of the IFN-I-potentiated TNF inflammatory response in severe COVID-19 by analyzing a gene module that is not responsive to IFN-I, but associated with TNF-induced tolerance to TLR stimulation. Park et al. previously demonstrated that TNF tolerizes TLR-induced gene expression in monocytes, though TNF itself is an inflammatory cytokine (24). They also showed that IFN-I induces a hyper-inflammatory response by abolishing the tolerance effects of TNF, and defined a gene module responsible for the IFN-I-potentiated TNF-NF-B inflammatory response as class 1 (24). This gene module was significantly enriched in cluster 1, but not in cluster 3 (Fig. 5G), which suggests that the IFN-I response may exacerbate hyper-inflammation by abolishing a negative feedback mechanism.

Finally, we validated IFN-I response and inflammatory features using bulk RNA-seq data obtained using post-mortem lung tissues from patients with lethal COVID-19 (25). Although the analysis was limited to only two patients without individual cell-type resolution, in genome browser, up-regulation of IFITM1, ISG15, and JAK3 and down-regulation of RPS18 were observed commonly in post-mortem COVID-19 lung tissues and classical monocytes of severe COVID-19 (Fig. 6A). In the analysis with cytokine-responsive gene sets, both the IFN-I response and TNF/IL-1-inflammatory response were prominent in the lung tissues (Fig. 6B). DEGs in the lung tissues were significantly associated with cluster 4, which is commonly up-regulated in both influenza and severe COVID-19, and cluster 5, which is specific to severe COVID-19 in Fig. 4B (Fig. 6C). These genes were also significantly associated with the cluster 1 identified in the trajectory analysis, but not with cluster 3 (Fig. 6D). When gene sets were defined by DEGs between mild and severe COVID-19, the DEGs in post-mortem lung tissues were significantly associated with genes up-regulated specifically in severe COVID-19 (Fig. 6E).

(A) UCSC Genome Browser snapshots of representative genes. (B) Bar plot showing the average log10(p-value) values from the enrichment analysis using the perturbed genes of four different cell lines in L1000 LINCS for up-regulated genes (n= 386) in post-mortem lung tissues compared to biopsied healthy lung tissue. Error bars indicate standard deviation. (C) GSEA of significantly up- and down-regulated genes in post-mortem lung tissues for gene sets originated from up-regulated genes in C2 (n=96), C3 (n=143), C4 (n=218), and C5 (n=30) of Fig. 4B. (D and E) GSEA of significantly up- and down-regulated genes in post-mortem lung tissues for gene sets originated from the top 200 up-regulated genes in cluster 3 (left) and cluster 1 (right) from the trajectory analysis in Fig. 5C (D), and from gene sets originated from the top 200 up-regulated genes in classical monocytes of mild (left) and severe (right) COVID-19 (E).

Severe COVID-19 has been shown to be caused by a hyper-inflammatory response (7). Particularly, inflammatory cytokines secreted by classical monocytes and macrophages are considered to play a crucial role in severe progression of COVID-19 (26). In the current study, we confirmed the results from previous studies by showing that the TNF/IL-1 inflammatory response is dominant in COVID-19 although a small number of patients were enrolled. However, we also found that severe COVID-19 is accompanied by the IFN-I response in addition to the TNF/IL-1 response. These results indicate that the IFN-I response might contribute to the hyper-inflammatory response by potentiating TNF/IL-1-driven inflammation in severe progression of COVID-19.

In the current study, we carried out scRNA-seq using PBMCs instead of specimens from the site of infection, e.g., lung tissues or bronchoalveolar lavage (BAL) fluids. However, hierarchical clustering based on relative changes to the healthy donor group showed that all types of cells among PBMCs were clustered together according to the disease groups as shown in Fig. 2A, indicating that there is disease-specific global impact across all types of cells among PBMCs. This finding suggests that peripheral blood immune cells are influenced by common inflammatory mediators regardless of cell type. However, we could not examine granulocytes in the current study because we used PBMCs, not whole blood samples for scRNA-seq.

In transcriptome studies for cytokine responses, we often analyze cytokine-responsive genes rather than cytokine genes themselves. However, we cannot exactly specify responsible cytokine(s) from the list of up-regulated genes because of overlapped effects of cytokines. For example, up-regulation of NF-B-regulated genes can be driven by TNF, IL-1 or other cytokines, and up-regulation of IFN-responsive genes can be driven by IFN-I or other interferons. In the current study, we designated the IFN-I response because many up-regulated IFN-responsive genes were typical ISGs.

Recently, Wilk et al. also performed scRNA-seq using PBMCs from COVID-19 patients and healthy controls (27). Similar to our study, they found IFN-I-driven inflammatory signatures in monocytes from COVID-19 patients. However, they did not find substantial expression of pro-inflammatory cytokine genes such as TNF, IL6, IL1B, CCL3, CCL4 and CXCL2 in peripheral monocytes from COVID-19 patients whereas we detected the up-regulation of TNF, IL1B, CCL3, CCL4 and CXCL2 in the current study. Moreover, they found a developing neutrophil population in COVID-19 patients that was not detected in our study. These discrepant results might be due to different platforms for scRNA-seq. Wilk et al. used the Seq-Well platform whereas we used the 10X Genomics platform that is more generally used. We also note that recent scRNA-seq analyses of COVID-19 sometimes lead to unrelated or contradictory conclusions to each other despite the same platform (28, 29). Although it often occurs in unsupervised analysis of highly multi-dimensional data, more caution will be required in designing scRNA-seq analysis of COVID-19, including definition of the severity and sampling time points.

Recently, Blanco-Melo et al. examined the transcriptional response to SARS-CoV-2 in in vitro infected cells, infected ferrets, and post-mortem lung samples from lethal COVID-19 patients and reported that IFN-I and -III responses are attenuated (25). However, we noted that IFN-I signaling pathway and innate immune response genes were relatively up-regulated in post-mortem lung samples from lethal COVID-19 patients compared to SARS-CoV-2-infected ferrets in their paper. Given that SARS-CoV-2 induces only mild disease without severe progression in ferrets (30), we interpret that IFN-I response is up-regulated in severe COVID-19 (e.g., post-mortem lung samples from lethal COVID-19 patients), but not in mild COVID-19 (e.g., SARS-CoV-2-infected ferrets). Indeed, severe COVID-19-specific signatures discovered in our current study were significantly enriched in the publically available data of post mortem lung tissues from the Blanco-Melo et al.s study although the analysis was limited to only two patients without individual cell-type resolution (Fig. 6). In a recent study, Zhou et al. also found a robust IFN-I response in addition to pro-inflammatory response in BAL fluid of COVID-19 patients (31). Moreover, up-regulation of IFN-I-responsive genes has been demonstrated in SARS-CoV-2-infected intestinal organoids (32).

Although IFN-I has direct antiviral activity, their immunopathological role was also reported previously (33). In particular, the detrimental role of the IFN-I response was elegantly demonstrated in a murine model of SARS (10). In SARS-CoV-infected BALB/c mice, the IFN-I response induced the accumulation of pathogenic inflammatory monocytes-macrophages and vascular leakage, leading to death. It was proposed that a delayed, but considerable IFN-I response is critical for the development of acute respiratory distress syndrome and increased lethality during pathogenic coronavirus infection (6, 34).

Currently, the management of patients with severe COVID-19 relies on intensive care and mechanical ventilation without a specific treatment because the pathogenic mechanisms of severe COVID-19 have not yet been clearly elucidated. In the current study, we demonstrated that severe COVID-19 is characterized by TNF/IL-1-inflammatory features combined with the IFN-I response. In a murine model of SARS-CoV infection, timing of the IFN-I response is a critical factor determining outcomes of infection (6, 10). Delayed IFN-I response contributes to pathological inflammation whereas early IFN-I response controls viral replication. Therefore, we propose that anti-inflammatory strategies targeting not only inflammatory cytokines, including TNF, IL-1, and IL-6, but also pathological IFN-I response needs to be investigated for the treatment of patients with severe COVID-19.

Patients diagnosed with COVID-19 were enrolled from Asan Medical Center, Severance Hospital, and Chungbuk National University Hospital. SARS-CoV-2 RNA was detected in patients nasopharyngeal swab and sputum specimens by multiplex real-time reverse-transcriptase PCR using the Allplex 2019-nCoV Assay kit (Seegene, Seoul, Republic of Korea). In this assay, N, RdRP, and E genes of SARS-CoV-2 were amplified, and Ct values were obtained for each gene. SARS-CoV-2-specific antibodies were examined using the SARS-CoV-2 Neutralization Antibody Detection kit (GenScript, Piscataway, NJ) and were positive in all COVID-19 patients in convalescent plasma samples or the last plasma sample in a lethal case. Hospitalized patients diagnosed with influenza A virus infection by a rapid antigen test of a nasopharyngeal swab were also enrolled from Asan Medical Center and Chungbuk National University Hospital from December 2015 to April 2016, prior to the emergence of COVID-19. Patients clinical features, laboratory findings, and chest radiographs were collected from their electronic medical records at each hospital. This study protocol was reviewed and approved by the institutional review boards of all participating institutions. Written informed consent was obtained from all patients.

Peripheral blood mononuclear cells (PBMCs) were isolated from peripheral venous blood via standard Ficoll-Paque (GE Healthcare, Uppsala, Sweden) density gradient centrifugation, frozen in freezing media, and stored in liquid nitrogen until use. All samples showed a high viability of about 90% on average after thawing. Single-cell RNA-seq libraries were generated using the Chromium Single Cell 3 Library & Gel Bead Kit v3 (10X genomics, Pleasanton, CA) following the manufacturers instructions. Briefly, thousands of cells were separated into nanoliter-scale droplets. In each droplet, cDNA was generated through reverse transcription. As a result, a cell barcoding sequence and Unique Molecular Identifier (UMI) were added to each cDNA molecule. Libraries were constructed and sequenced as a depth of approximately 50,000 reads per cell using the Nextseq 550 or Novaseq 6000 platform (Illumina, San Diego, CA).

The sequenced data were de-multiplexed using mkfastq (cellranger 10X genomics, v3.0.2) to generate fastq files. After de-multiplexing, the reads were aligned to the human reference genome (GRCh38; 10x cellranger reference GRCh38 v3.0.0), feature-barcode matrices generated using the cellranger count, and then aggregated by cellranger aggr using default parameters. The following analysis was performed using Seurat R package v3.1.5 (17). After generating the feature-barcode matrix, we discarded cells that expressed <200 genes and genes not expressed in any cells. To exclude low-quality cells from our data, we filtered out the cells that express mitochondrial genes in >15% of their total gene expression as described in previous studies (29, 35, 36). Doublets were also excluded, which were dominant in the cluster Uncategorized 1. Although there was a high variability in the number of UMIs detected per cell, majority of cells (90.5%) were enriched in a reasonable range of the UMIs (1,000 - 25,000), and 59% of cells with less than 1,000 UMIs were platelet or RBC excluded in downstream analysis. In each cell, the gene expression was normalized based on the total read count and log-transformed. To align the cells originating from different samples, 2000 highly variable genes from each sample were identified by the vst method in Seurat R package v3.1.5 (17). Using the canonical correlation analysis (CCA), we found anchors and aligned the samples based on the top 15 canonical correlation vectors. The aligned samples were scaled and principal component analysis (PCA) conducted. Finally, the cells were clustered by unsupervised clustering (0.5 resolution) and visualized by tSNE using the top 15 principal components.

To identify marker genes, up-regulated genes in each cluster relative to the other clusters were selected based on the Wilcoxon rank sum test in Seurats implementation with >0.25 log fold change compared to the other clusters and a Bonferroni-adjusted p < 0.05 (Table S4). By manual inspection, among the 22 different clusters, 20 were assigned to 11 known immune cell types, RBCs which are characterized by HBA1, HBA2, and HBB, and platelets. The clusters characterized by similar marker genes were manually combined as one cell type. The two remaining clusters were assigned to Uncategorized 1 and Uncategorized 2 because they had no distinct features of known cell types. Based on the distribution of UMI counts, the cluster Uncategorized 1 was featured by relatively high UMIs per cell compared to other clusters and presence of higher expression of multiple cell type marker genes. The cluster Uncategorized 2 was featured by a B cell-like signatures and high expression of ribosomal protein genes, not recommended to be further analyzed according to the 10X platform guideline. In these aspects, RBCs, platelets, Uncategorized 1, and Uncategorized 2 were excluded in downstream analysis.

To check the reproducibility of biological replicates (individuals within a same group), we calculated the Spearmans rank correlation coefficient for UMI counts that were merged according to each individual. The correlation coefficients of all individual pairs within the same group were visualized by a boxplot (COVID-19, n=45; FLU, n=10; HD, n=6).

In Fig. S1E, to investigate the similarity of the transcriptomes between cell types across diseases, we merged the UMI counts of each cell type according to healthy donor, influenza, mild COVID-19, and severe COVID-19. Next, the UMI counts for each gene were divided by the total UMI count in each cell type and multiplied by 100,000 as the normalized gene expression. Based on a median expression value >0.5, we calculated the relative changes in gene expression divided by the median value for each gene. Hierarchical clustering analysis was performed based on the PCC of the relative change in gene expression.

In Fig. 2A and Fig. S2A, to compare the highly variable gene expression among mild and severe COVID-19 and influenza relative to healthy donors, the normalized gene expression used in Fig. S1E was divided by the values in the healthy donor group. We selected the highly variable genes in terms of the top 25% standard deviation followed by log2-transformation (pseudo-count =1). In Fig. 2A, hierarchical clustering analysis was performed based on the PCCs of the selected highly variable genes. For Fig. S2A, to investigate the expression patterns of the selected highly variable genes (n=6,052), K-means clustering (k=50) was performed based on Euclidean distance. We manually ordered the clusters and visualized them as a heat map, revealing four distinct patterns: influenza-specific (n=1,046), COVID-19 specific (n=1,215), influenza/COVID-19 common (n=1,483), and cell type-specific (n=2,308).

To investigate the dynamic changes in cell type composition, we calculated the proportion of cell types in each individual. As a control, we calculated the relative variation in each cell type composition between all pairs of healthy donors. Similarly, for each disease group, we calculated the relative variation in each cell type by dividing the fraction of the cell type in individual patient by that of individual healthy donor. After log2-transformation, we conducted statistical analysis using the relative variation in composition between the control and disease groups using a two-sided KolmogorovSmirnov test.

For any two transcriptome profiles, to identify DEGs, we utilized the model-based analysis of single cell transcriptomics (MAST) algorithm in Seurats implementation based on a Bonferroni-adjusted p<0.05 and a log2 fold change > 0.25.

In Fig. 2B, the DEGs in COVID-19 and influenza compared to healthy donors or COVID-19 compared to influenza were identified at cell type resolution. All DEGs were combined according to the disease groups for further analysis. The overlapping up or down DEGs between COVID-19 and influenza compared to healthy donors were defined as Common up or Common down. The specific DEGs in COVID-19 or influenza were assigned as COVID-19 up/down or FLU up/down, respectively. In addition, COVID-19-specific up- or down-regulated genes compared to influenza were assigned as COVID-19>FLU or FLU>COVID-19, respectively. The Gene Ontology analysis was performed by DAVID. For each group of DEGs, the top 10 enriched GO biological pathways were selected, resulting in 49 unique GO biological pathways across all groups. The -log10(p-values) are shown as a heat map in Fig. 2B.

The weighted gene correlation network analysis (WGCNA) was conducted with the genes listed in the top 10 GO biological pathways of COVID-19 up, FLU up, and Common up defined in Fig. 2B. The normalized gene expression values of the genes in COVID-19 were divided by the values in influenza and log2-transformed (pseudo-count =1). We used default parameters with the exception of soft threshold =10 and networkType = signed when we constructed a topological overlap matrix. The modular gene expression patterns were defined using cutreeDynamic with a minClusterSize of 5. We visualized the modular gene expression pattern as a heat map in which the cell types were ordered according to hierarchical clustering with the default parameters of hcluster in R.

To find disease-specific subpopulations, each immune cell type was subjected to the subclustering analysis using Seurat. Briefly, the highly variable genes (n=1000) were selected based on vst and then scaled by ScaleData in Seurat with the vars.to.regress option to eliminate variation between individuals. The subpopulations were identified by FindClusters with default parameters, except resolution (non-EM-like CD8+ T cells, 0.3; classical monocytes, 0.2); the inputs were the top eight principal components (PCs) obtained from PCA of the scaled expression of the highly variable genes. The subpopulations were visualized by tSNE using the top eight PCs.

The trajectory analysis was performed with 2000 highly variable genes in classical monocytes across mild (C7-2) and severe (C7-1) COVID-19 as defined by the vst method in Seurat. The following analysis was performed using Monocle2. Briefly, the input was created from the UMI count matrix of the highly variable genes using the newCellDataSet function with default parameters, except expressionFamily = negbinomial.size. The size factors and dispersion of gene expression were estimated. The dimension of the normalized data was reduced based on DDRTree using reduceDimension with default parameters, except scaling = FALSE, which aligned the cells to the trajectory with three distinct clusters.

To determine genes that gradually changed along the trajectory, we identified the DEGs using MAST between clusters 1 and 3, which represent the severe stage and mild stage, respectively. The expression patterns of representative DEGs were visualized along the Pseudotime after correction with estimated size factors and dispersion for all genes.

In Fig. 4B, we performed K-means clustering of DEGs among all pairs of mild COVID-19, severe COVID-19, and influenza. The log2-transformed relative gene expression of DEGs compared to healthy donors was subjected to K-means clustering (k=10). Here, we used up-regulated DEGs in at least one disease group compared to the healthy donor group. We manually assigned five clusters based on gene expression patterns.

The transcriptome profiles of post-mortem lung tissues from two lethal cases of COVID-19 and biopsied heathy lung tissues from two donors were downloaded from a public database (GSE147507). The DEGs were identified using DESeq2 based on a Bonferroni-adjusted p < 0.05 and a log2 fold change > 1.

Enrichr, the web-based software for gene set enrichment analysis (GSEA) was used for LINCS L1000 ligand perturbation analysis (22), virus perturbation analysis, and disease perturbation analysis from the GEO database. Combined score was calculated as a parameter of enrichment as the log(p-value) multiplied by the z-score from the Fisher exact test. GSEA 4.0.3 software was used to conduct the GSEA when a ranked list of genes was available (Fig. 5G, Fig. 6C-E) (37). Results for IFN--responsive genes were not presented because those were considerably overlapped with IFN--responsive genes, which are typical ISGs. The normalized enrichment score and FDR-q value were calculated to present the degree and significance of enrichment.

Cryopreserved PBMCs were thawed, and dead cells were stained using the Live/Dead Fixable Cell Stain kit (Invitrogen, Carlsbad, CA). Cells were stained with fluorochrome-conjugated antibodies, including anti-CD3 (BV605; BD Biosciences), anti-CD4 (BV510; BD Biosciences), anti-CD8 (BV421; BD Biosciences), anti-CD14 (PE-Cy7; BD Biosciences), anti-CD19 (Alexa Fluor 700; BD Biosciences), and anti-CD56 (VioBright FITC; Miltenyi Biotec). For staining with anti-granzyme B (BD Biosciences), cells were permeabilized using a Foxp3 staining buffer kit (eBioscience).

For intracellular cytokine staining of IFN-, PBMCs were stimulated with phorbol 12-myristate 13-acetate (PMA, 50 ng/ml) (Sigma Aldrich) and ionomycin (1 g/ml) (Sigma Aldrich). Brefeldin A (GolgiPlug, BD Biosciences) and monesin (GolgiStop, BD Biosciences) were added 1 hour later. After another 5 hours of incubation, cells were harvested for staining with the Live/Dead Fixable Cell Stain kit, anti-CD3, anti-CD4, and anti-CD8. Following cell permeabilization, cells were further stained with anti-IFN- (Alexa Fluor 488; eBioscience).

Flow cytometry was performed on an LSR II instrument using FACSDiva software (BD Biosciences) and the data analyzed using FlowJo software (Treestar, San Carlos, CA).

Cytokines were measured in plasma samples, including IFN-, IL-18 (ELISA, R&D Systems, Minneapolis, MN), IL-1 (Cytometric bead array flex kit, BD Biosciences, San Jose, CA), TNF, IL-6, and IFN- (LEGENDplex bead-based immunoassay kit, BioLegend, San Diego, CA).

We performed the KS test to compare the distributions of two groups without assuming that the distributions follow normality. Welchs t test was conducted to compare the two distributions after confirming the normality of the distributions using the Shapiro-Wilk normality test. A Wilcoxon signed rank test was conducted to compare the differences between two groups with paired subjects. The Mann-Whitney test was performed to compare the means of two groups. Statistical analyses were performed using Prism software version 5.0 (GraphPad, La Jolla, CA). p<0.05 was considered significant.

immunology.sciencemag.org/cgi/content/full/5/49/eabd1554/DC1

Fig. S1. Clinical characteristics and assessment of the quality of scRNA-seq results.

Fig. S2. Transcriptome features of highly variable genes.

Fig. S3. Characterization of disease-specific CD8+ T-cell subpopulations.

Fig. S4. Subpopulation analysis of classical monocytes.

Fig. S5. STRING analysis of up-regulated genes in cluster 1 obtained from the trajectory analysis of classical monocytes.

Table S1. Experimental batches of scRNA-seq.

Table S2. Clinical characteristics of severe influenza patients.

Table S3. Clinical characteristics of COVID-19 patients.

Table S4. The scRNA-seq results.

Table S5. A list of marker genes for each cluster.

Table S6. A list of DEGs and associated biological pathways in Fig. 2B.

Table S7. Cell types in which the GBP1, CREM, and CCL3 were upregulated in Fig. 2C.

Table S8. A list of genes in each module obtained from WGCNA in Fig. 2D.

Table S9. A list of up-regulated genes in non-EM-like CD8+ T-cell subpopulations.

Table S10. A list of genes included in each cluster defined by K-mean clustering of classical monocytes.

Table S11. A list of genes up-regulated in early and late Pseudotime.

This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Immunophenotyping of COVID-19 and influenza highlights the role of type I interferons in development of severe COVID-19 - Science

Georgia Governor And The Mayor Of Atlanta In Turf War Over COVID-19 Restrictions – NPR

Georgia Gov. Brian Kemp holds a protective mask while speaking during a 'Wear A Mask' tour stop in Dalton, Georgia, earlier this month. Bloomberg/Bloomberg via Getty Images hide caption

Georgia Gov. Brian Kemp holds a protective mask while speaking during a 'Wear A Mask' tour stop in Dalton, Georgia, earlier this month.

Georgia's governor and the mayor of the state's capital and largest city are at odds over COVID-19 restrictions, with Atlanta Mayor Keisha Lance Bottoms announcing a return to tough measures to control a spike in coronavirus infections and Gov. Brian Kemp insisting that her order is "non-binding and legally unenforceable."

Bottoms, a Democrat, announced Friday that she was bringing Atlanta back to Phase 1 reopening the most restrictive post-lockdown measures that require all residents to stay home except for essential trips.

The mayor's order came on the same day that Georgia announced a record-breaking one-day spike in coronavirus, logging 4,400 new confirmed cases. Health authorities in Atlanta's Fulton County says about half of the new cases in Georgia in the past two weeks have occurred in the city.

But Kemp, a Republican, quickly dismissed the mayor's directive, saying on Friday that it didn't supersede his own, more relaxed, statewide order issued at the end of June.

"Mayor Bottoms' action today is merely guidance both non-binding and legally unenforceable," Kemp said in a statement.

"As clearly stated in the Governor's executive order, no local action can be more or less restrictive, and that rule applies statewide," the governor said.

"Once again, if the Mayor actually wants to flatten the curve in Atlanta, she should start enforcing state restrictions, which she has failed to do," he said. "We ask citizens and businesses alike to comply with the terms of the Governor's order, which was crafted in conjunction with state public health officials. These common-sense measures will help protect the lives and livelihoods of all Georgians."

Earlier this week, Bottoms had issued a directive for Atlanta residents to wear masks in public, and Kemp responded similarly to that order. Although the governor launched a "Wear A Mask" campaign to encourage their use, he has declined to make it mandatory.

Bottoms told the Atlanta Journal-Constitution on Wednesday that she had the authority to enforce the mask restrictions the way she would enforce any other city ordinance.

The cities of Savannah, East Point and Athens, Kemp's hometown, have enacted similar mask directives.

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Georgia Governor And The Mayor Of Atlanta In Turf War Over COVID-19 Restrictions - NPR

COVID-19: City of Lubbock reports 144 new cases, 8 additional recoveries on Saturday – KLBK | KAMC | EverythingLubbock.com

by: News Release & Posted By Staff | newsweb@everythinglubbock.com

(Nexstar Media Group/EverythingLubbock.com Staff)

LUBBOCK, Texas (NEWS RELEASE) The following is a news release from the City of Lubbock:

As of 4:00 p.m. on Saturday, July 11, 2020, the City of Lubbock confirmed 144 new cases of Coronavirus (COVID-19) and 8 recoveries. The total number of cases in Lubbock County is 3,668: 1,950 active, 1,650 listed as recovered and 60 deaths.

Walgreens, at602 Avenue Q, will operate a COVID-19 drive-thru testing sitestarting on Friday, July 17.The drive-thru will be openfrom 9:00 a.m. 5:00 p.m., seven days a week. Visitors need to take a COVID-19 assessment test before they will be given an appointment time to be tested. The assessment can be found atwww.walgreens.com/COVID19testing.

In a recent proclamation, Governor Greg Abbott limited outdoor gatherings to 10 people, unless approved by a mayor or county judge. If citizens, or organizations, would like to have their event considered for approval they can download a form atwww.mylubbock.us/lubbocksafe. They can then send the form toLubbockSafe@mylubbock.us. Those seeking approval are asked to submit their request at least 10 days before the event.

(News release from the City of Lubbock)

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COVID-19: City of Lubbock reports 144 new cases, 8 additional recoveries on Saturday - KLBK | KAMC | EverythingLubbock.com