text:
Otis Smith Kansas City chiefs?
Asked by Celestine Adella Little
Asked in National Football League (NFL), Athletes
What NFL team does Otis Hudson play for?
Otis Hudson plays for the Kansas City Chiefs.
What position does Otis Hudson play?
Otis Hudson plays Guard for the Kansas City Chiefs.
Asked in Kansas City Chiefs, American Revolution, Wolfgang Amadeus Mozart
Who climbed out a window in 1965 to begin playing for the Kansas City Chiefs?
Otis Taylor - who was being snuck out of a hotel before the Dallas Cowboys could talk to him about being drafted by them in the NFL.
Asked in Washington Redskins, Football - American, National Football League (NFL)
8 Which Kansas City Chiefs players have been inducted in the NFL Hall of Fame?
Len Dawson Ed Budde Otis Taylor Willie Lanier Bobby Bell Buck Buchanon
When was Otis Smith born?
Otis Smith was born on January 30, 1964.
When was Otis M. Smith born?
Otis M. Smith was born in 1922.
When did Otis M. Smith die?
Otis M. Smith died in 1994.
Asked in Football - American, Kansas City Chiefs
Who has wore number 35 for the Kansas City Chiefs?
Some players who have worn number 35 for the Dallas Texans/Kansas City Chiefs franchise include linebacker Smokey Stover (1960-66), fullback Jim Otis (1971-72), running back Horace Belton (1978-80), All-Pro fullback Christian Okoye (1987-92), safety William White (1994-96), and reserve linebacker Larry Atkins (1999-2000).
How old is Otis Smith?
Otis Smith is 47 years old (birthdate: January 30, 1964).
What is Otis Smith's birthday?
Asked in Baseball History
How many games did baseball player Amos Otis play as designated hitter for the Kansas City Royals in 1973?
Amos Otis played in 14 games at designated hitter for the Kansas City Royals in 1973, starting in none of them. , equivalent to 0 errors per game (estimate based on total games played in).
What were the fielding stats for baseball player Amos Otis playing at designated hitter for the Kansas City Royals in 1974?
Amos Otis played in 2 games at designated hitter for the Kansas City Royals in 1974, starting in none of them. , equivalent to 0 errors per game (estimate based on total games played in).
Asked in Kansas City Royals, Baseball History
How many games did baseball player Amos Otis playing at designated hitter for the Kansas City Royals in 1978?
Amos Otis played in just one game at designated hitter for the Kansas City Royals in 1978 and did not start. , equivalent to 0 errors per game (estimate based on total games played in).
When was Otis Garth born?
Otis Garth was born on July 1, 1901, in Toledo, Kansas, USA.
Asked in Explorers and Expeditions, Amelia Earhart
Who was Amelia Earhart's mother?
SHe was Amelia "Amy" Otis Earhart of Atchison, Kansas
Asked in Amelia Earhart
Who was Amelia Earhart related to?
She was related to the Otis family, well known in Kansas.
What players wore jersey number 89 in Kansas City Chiefs history?
The most famous number 89 in Kansas City Chiefs history would be All-Pro wide receiver Otis Taylor (1965-75). Others include wide receiver Henry Marshall (1976-87), wide receiver/kick returner Pete Mandley (1989-90), tight end Keith Cash (1992-96), wide receiver Andre Rison (1997-99), tight end Jason Dunn (2000-07), wide receiver Chris Chambers (2009) and wide receiver Jonathan Baldwin (2011-current as of August 2012).
Asked in Actors & Actresses
What movie and television projects has Jim Otis been in?
Jim Otis has: Played Himself - St. Louis Cardinals Fullback in "The NFL on CBS" in 1956. Played Himself - New Orleans Saints Fullback in "The NFL on CBS" in 1956. Played Himself - St. Louis Cardinals Fullback in "NFL Monday Night Football" in 1970. Played Himself - Kansas City Chiefs Fullback in "NFL Monday Night Football" in 1970. Played himself in "ESPN SportsCentury" in 1999.
What were the fielding stats for baseball player Amos Otis playing at outfield for the Kansas City Royals in 1977?
Amos Otis played in 140 games at outfield for the Kansas City Royals in 1977, starting in 129 of them. He played for a total of 3544 outs, equivalent to 131.26 9-inning games. He made 326 putouts, had 10 assists, and committed 3 errors, equivalent to .023 errors per 9-inning game. He had no double plays.
What were the fielding stats for baseball player Amos Otis playing at right field for the Kansas City Royals in 1981?
Amos Otis played in just one game at right field for the Kansas City Royals in 1981 and started. He played for a total of 24 outs, equivalent to .89 9-inning games. He made 3 putouts, had no assists, and committed no errors, equivalent to 0 errors per 9-inning game. He had no double plays.
Amos Otis played in 159 games at outfield for the Kansas City Royals in 1970, starting in 158 of them. He played for a total of 4241 outs, equivalent to 157.07 9-inning games. He made 388 putouts, had 15 assists, and committed 4 errors, equivalent to .025 errors per 9-inning game. He had 6 double plays.
Amos Otis played in 137 games at outfield for the Kansas City Royals in 1972, starting in all of them. He played for a total of 3570 outs, equivalent to 132.22 9-inning games. He made 351 putouts, had 6 assists, and committed 3 errors, equivalent to .023 errors per 9-inning game. He had 3 double plays.


Gaps in coverage for sexual and reproductive health services for girls and women may be hurting broader development objectives, say experts from the United Nations Population Fund. Here's why governments in Asia Pacific need to make these issues a priority in health coverage.
Mai was 17 years old when she and her boyfriend became sexually active. Because unmarried adolescents in their country cannot access contraception without parental consent, they decided to make do without. Not long after, Mai became pregnant.
Stories like Mai's are all too common in the Asia-Pacific region, where access to comprehensive sexual and reproductive health services remains uneven. Despite significant progress in some countries toward achieving universal health coverage—a priority of the United Nations Sustainable Development Goals (SDGs)—a key component of women's health is falling through the cracks. Until sexual and reproductive health services, including family planning, are offered more widely and fully covered under health financing schemes, efforts to provide health care to all who need it will continue to come up short.
Today, many governments in the Asia-Pacific consider some sexual and reproductive health services to be beyond the scope of their health financing priorities. Unfortunately, this has the effect of maintaining and reinforcing the very barriers to sustainable development that universal health coverage was meant to remove—in particular, improving health outcomes for the poor and vulnerable, and preventing people from falling into poverty to pay for the health services they need.
When public health systems do not cover critical services—for example, cervical cancer screening—people are forced either to forego those services or to pay out of pocket for them. Out-of-pocket expenditures already account for a substantial share of total health-care payments in the Asia-Pacific region, reaching as high as 60 per cent in some countries. And, in some parts of the region, this share has actually been increasing. Health-care debt thus continues to trap people and communities in poverty.
Efforts to promote universal health coverage must be complemented and reinforced by initiatives to ensure access to sexual and reproductive health services. To reduce maternal illness and death, women and girls need easy and consistent access to contraception, maternal health services, and sexually transmitted infection and cancer screening and treatment. Vulnerable groups such as adolescents, migrant workers, and indigenous populations have the greatest need for affordable sexual and reproductive health care; complex eligibility requirements for health financing schemes must be scrapped if coverage is to be sufficiently improved.
Until sexual and reproductive health services, including family planning, are offered more widely and fully covered under health financing schemes, efforts to provide health care to all who need it will continue to come up short.
Anderson E. Stanciole is a Health Economics Advisor and Federica Maurizio is Health Economics and SRHR Analyst at the United Nations Population Fund (UNFPA) Asia-Pacific Regional Office in Bangkok.


What does the best available science say about the role multivitamins may play in heart disease, cancer, and longevity?
About one in three Americans takes a multivitamin. Is that helpful, harmful, or just harmless—a waste of money? In 2011, the Iowa Women's Health Study reported that multivitamin use was "associated with a higher risk of total mortality"—meaning, in effect, women who took a multivitamin appeared to be paying to live shorter lives. But this was an observational study, meaning they didn't split them up into two groups, and put half on multivitamins to see who lived longer. They just followed a large population of women over time, and found those that happened to be taking multivitamins were more likely to die. But, maybe, they were taking multivitamins because they were sick? The researchers didn't find any evidence of that. But, ideally, we'd have a randomized, double-blind, placebo-controlled trial—thousands of people followed for over a decade; half given a multivitamin, and half a placebo, and see what happens. And, that's what we got the following year, in 2012. The Harvard Physicians' [Health] Study II. And, after a decade, no effect on heart attack, stroke, or mortality.
The accompanying editorial concluded that multivitamins are a "distraction from effective [cardiovascular disease] prevention. The message needs to remain simple and focused:" heart disease can be largely prevented by healthy lifestyle changes.
They did, however, find that for men with a history of cancer, the multivitamin appeared to be protective against getting cancer again—though there was no significant difference in cancer mortality, or cancer protection, in those who've never had cancer before. Still, though, that's pretty exciting. It is just one study, though. Ideally, we'd have, like, twenty of these placebo-controlled trials, and then compile all the results together.
And, that's what we got in 2013—"a meta-analysis of randomized controlled trials." Twenty-one of them, covering more than 90,000 individuals, and—"no influence…on…mortality" either way. Some found more cancer mortality; some found less cancer mortality; but all and all, it was a wash.
And, that was heralded as good news. I mean, after the Iowa Women's Health Study came out, we were worried multivitamins could be harming millions of people. But, instead, they don't appear to have much effect either way. The accompanying editorial asked, "Should meta-analyses trump observational studies?" I mean, Iowa Women's Health Study followed tens of thousands of women for nearly twenty years. Well, what if we put all the studies together—the big observational studies, along with the experimental trials? And, that's what we got in December 2013—concluding that multivitamins appear to offer "no consistent evidence" of benefit for heart disease, cancer, or living longer.
Why, though? Aren't vitamins and minerals good for us? Well, "[o]ne explanation for this result could be that [our bodies] are so complex that the effects of supplementing [a few] components is generally ineffective or actually does harm." Maybe, we should get our nutrients in the way nature intended.
The accompanying editorial concluded "Enough is Enough; [we should] Stop Wasting [our] Money on Vitamin and Mineral Supplements." Americans spend billions on such supplements. "A better investment in health would be eating more fruits and vegetables." Imagine if we instead spent those billions on healthy food?
This is not the aisle we should be getting our nutrients from. With the money we save on pills, we can buy more of the best multivitamins on earth.
J. M. Gaziano, H. D. Sesso, W. G. Christen, V. Bubes, J. P. Smith, J. MacFadyen, M. Schvartz, J. E. Manson, R. J. Glynn, J. E. Buring. Multivitamins in the prevention of cancer in men: the Physicians' Health Study II randomized controlled trial. JAMA. 2012 308(18):1871 - 1880.
H. D. Sesso, W. G. Christen, V. Bubes, J. P. Smith, J. MacFadyen, M. Schvartz, J. E. Manson, R. J. Glynn, J. E. Buring, J. M. Gaziano. Multivitamins in the prevention of cardiovascular disease in men: the Physicians' Health Study II randomized controlled trial. JAMA. 2012 308(17):1751 - 1760.
E. Guallar, S. Stranges, C. Mulrow, L. J. Appel, E. R. Miller. Enough is enough: Stop wasting money on vitamin and mineral supplements. Ann Intern Med. 2013 159(12):850 - 851.
M. Cully. Prevention. Multivitamins do not reduce the risk of cardiovascular disease. Nat Rev Cardiol. 2013 10(1):7.
S. M. Chang. Should meta-analyses trump observational studies? Am. J. Clin. Nutr. 2013 97(2):237 - 238.
S. Rautiainen, L. Wang, J. M. Gaziano, H. D. Sesso. Who uses multivitamins? A cross-sectional study in the Physicians' Health Study. Eur J Nutr. 2013 [Epub ahead of print].
L. Anekwe. Daily multivitamins do not protect against cardiovascular events, finds study. BMJ. 2012 345:e7599.
R. Vogt. The importance of translating research skillfully to benefit the public. Arch. Intern. Med. 2012 172(5):449; author reply 449-450.
E. M. Lonn. Multivitamins in prevention of cardiovascular disease. JAMA. 2012 308(17):1802-1803.
F. Greenway, K. Fujioka, Y. Yu. Vomiting from multivitamins: A potential drug interaction. Am J Ther. 2011 18(6):453 - 457.
S. P. Fortmann, B. U. Burda, C. A. Senger, J. S. Lin, E. P. Whitlock. Vitamin and Mineral Supplements in the Primary Prevention of Cardiovascular Disease and Cancer: An Updated Systematic Evidence Review for the U.S. Preventive Services Task Force. Ann. Intern. Med. 2013 159(12):824-838.
J. Mursu, K. Robien, L. J. Harnack, K. Park, D. R. Jacobs Jr. Dietary supplements and mortality rate in older women: The Iowa Women's Health Study. Arch. Intern. Med. 2011 171(18):1625 - 1633.
R. F. Redberg. Vitamin supplements: More cost than value. Arch. Intern. Med. 2011 171(18):1634 - 1635.
Comparte "Should We Take a Multivitamin?"
I've previously addressed multivitamins in Are Multivitamins Good for You? and Multivitamin Supplements & Breast Cancer (with a follow-up in my Q&A post, Is multivitamin use really associated with an increased risk of breast cancer?). I also touched on potential risks in Dietary Theory of Alzheimer's.
With the exception of vitamins D and B12 (see Vitamin Supplements Worth Taking), we should strive to get our nutrients from produce, not pills (see Produce, not Pills, to Increase Physical Attractiveness).
Next, I cover all the new science on fish oil supplements in Is Fish Oil Just Snake Oil?


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Flu season: Send sick people home, employers' group manager says
The AM Show 02/07/2019
With flu season in full swing, an employers' group is calling on employers to send staff home if they show symptoms of an illness.
A large number of influenza cases are being reported, with the Canterbury District Health Board (CDHB) saying late last month that it was treating between 35 and 48 patients in Christchurch hospital every day with the illness or symptoms.
The number of influenza vaccines handed out also far exceed the number distributed at this point last year, and Paul Jarvie, the Employers and Manufacturers Association (EMA) employment relations and safety manager, says it's impacting employers.
"We are getting quite a few calls through our call centre that people are having the flu and it is quite hard on them," Jarvie told The AM Show.
"We hear from [the Ministry of Health] that the flu virus has come down earlier, which is unexpected, but it is also very aggressive, so people are getting the flu, but getting it very quickly and badly.
"I think people are taking more and more leave as they are getting sicker."
The flu is quite a serious problem and you shouldn't underestimate it.
Jarvie said his message to employers was that "if people are sick, then send them home".
"We don't want sick people at work… It is actually infecting other people.
When you sneeze, you are sneezing at about 130km/h and it blows it out about 3 metres. It is better to stay home during the first week and rest up," he said.
Cutting off the spread of illness was important to ensuring businesses can get back to running as normal quicker without sick people bringing down productivity.
"Anytime an employee is away, you lose productivity, and given that our country is made up of a very large number of small employers, having one person away really hurts.
"If you are a large employer then there is a lot more ability for the company to have some back-up, so it is about productivity."
While the law does allow employers to require a medical certificate from an employee's doctor, Jarvie said most employers are happy to take the worker's word for it as long as that isn't abused.
Last month, Pharmac said that the number of vaccines distributed was already higher than the number of vaccines distributed in 2016 and 2017, and nearly as many as the total of last winter, when 1.3 million were given out.
The AM Show / Newshub reporter Jamie Ensor

redpajama_set_name: RedPajamaCommonCrawl


text:
Good Reads, Ocean Navigator
The Outlaw Ocean: Journeys Across the Last Untamed Frontier
Ocean Navigator January 2, 2020 January 26, 2022
The Outlaw Ocean:
Journeys Across the Last Untamed Frontier
by Ian Urbina
Alfred A. Knopf, New York
The basic premise of The Outlaw Ocean by Ian Urbina is a riff on the classic logic problem referred to commonly as "the prisoner's dilemma." We have treaties that protect the oceans and the people who sail upon them. And we have enforcement protocol for these treaties. But, while collectively we have incentive to enforce the treaties — thereby protecting our collective welfare (the cleanliness and health of the oceans' ecosystems, the health of the fish and mammals that swim in them) — no one has incentive to single-handedly enforce them. Why should one nation's coast guard or fisheries police spend resources fighting malefactors on the high seas when there is no direct benefit to this one nation? The result is not surprising: No one enforces them, or they are enforced sparingly and in limited, largely ineffectual ways.
Ian Urbina, a journalist for The New York Times, spent four years researching and writing this important book, documenting modern-day slavery, prostitution, pillaging of the ocean's fisheries, the unchecked slaughter of whales, quasi-legal vigilantism, and overwhelming pollution in the form of plastics and oil. Because of the layers of corporate protection and the fiction of flags of convenience, shipowners can largely do as they please, using one nation's laws against another or simply flouting all law, domestic or international, by hiding in the vastness of the high seas and reaping the harvest with impunity.
The following passage illustrates the current predicament:
"Over the years, I'd spoken to dozens of industry consultants, lawyers, insurers and ship operators, and they often contended that the industry was not unified enough to solve problems like debt bondage, human trafficking, wage theft or seafarer abandonment. In fact, they often told me, there was no industry to speak of, certainly not one that could act efficiently or with consensus to tackle such thorny problems. There was, instead, just lots of independent ships and fleets, flying a plethora of different flags, they said. What was striking to me, however, was that when it came to issues like countering Somali piracy, resisting unions, standardizing port protocol, countering terrorism threats, or resisting measures that might put large fisheries off-limits or impose stricter pollution or wage rules, these industries were surprisingly efficient and united.
"The unfortunate truth was that, in much of the maritime world, the law protects a ship's cargo better than its crew."
There are a few heroes in the book, namely the intrepid marauders at the Sea Shepherd Conservation Society and, surprisingly, the government and coast guard officers of Indonesia and other seafaring nations, whose recent efforts prove modestly effective at stemming illegal fishing that is often violent (and always chaotic). Toward the end of the book, Urbina concludes: "Through time, humanity's capacity, both legally and scientifically, for extracting life from the oceans has greatly surpassed our ability to protect it."
But the book is unavoidably nihilistic in tone and substance. Without immediate and collective action to address the urgent and myriad crises faced by our oceans, we're all just a group of selfish prisoners, distrustful of one another, destroying our world and headed to hell together.
Previous PostSea anchor assists ocean cleanup
Next PostNational Sailing Hall of Fame inducts new members


text:
Two Cabinet members fêted Kuwait at their boss's hotel
Trump Cabinet members Ross and Carson fêted Kuwait at Trump's hotel
Last night Commerce Secretary Wilbur Ross and HUD Secretary Ben Carson attended the Kuwaiti embassy in the United States' national day celebration at the Trump Hotel D.C., according to a person who attended the event and social-media postings.
It marks the second year in a row Ross was present, and apparently the second consecutive night he visited his boss's hotel (Ross is currently embroiled in ethics scandals). While no pictures of Ross there have surfaced yet, a person at the Kuwaiti party confirmed his presence to 1100 Pennsylvania. Carson was last spotted at the hotel earlier this month.
An attendee who spoke with 1100 Pennsylvania estimated 200 to 300 people attended the event. In addition to Ross, this guest spotted Deputy Secretary of State for the Bureau of Educational and Cultural Affairs, Marie Royce, and military members from the United States and other countries.
Also in attendance, of course, was Ambassador Salem Al-Sabah and his wife, Rima.
A flight officer in U.S. Navy, Angela Domingos, was at the commander-in-chief's hotel to attend a foreign government's party. "Yes this is my job 😆," she wrote.
And here are some other photos a guest shared privately with 1100 Pennsylvania:
Trump, Inc. spent a night at the Trump Hotel D.C.
For today's Trump, Inc. from ProPublica and WNYC, hosts Ilya Marritz and Meg Cramer "spent a night at President Donald Trump's hotel in Washington, D.C.—and we met lots of interesting people":
"How a Nigerian Presidential Candidate Hired a Trump Lobbyist and Ended Up in Trump's Lobby"
The episode does an excellent job capturing the issues regarding President Trump's ownership of the hotel. As will be clear seconds after hitting that play button, I was there with them and feel like I fulfilled my destiny by drawing an explicit-language warning from public radio. Check out the 1100 Pennsylvania from the following morning for more details about what we saw, along with pictures and video:
Nigerian presidential candidate Atiku Abubakar checks in to Trump's hotel
And some postscripts:
turns out a second Nigerian presidential candidate was at the Trump Hotel D.C. that same weekend, as were three elected Nigerian government officials who were part of Atiku's entourage
Atiku held a town-hall meeting for Nigerian diaspora and members of his party at the hotel
this morning we learned that Atiku lost his bid for election
Campaign expenditure
The Republican National Committee spent another $2,487.90 at Trump properties, mostly the D.C. hotel, in January 2019.
Other noteworthy sightings
The president of lobbying firm the Da Vinci Group, Mark Smith, a Trump Hotel D.C. regular, had a lovely evening with the CEO of Avella Specialty Pharmacy, John Musil, and a staff assistant for U.S. Sen. Mike Enzi (R–WY), Sean Joseph Cullen Smith (who's the son of the lobbyist mentioned at the beginning of this entry).
The national president of the American Association of Healthcare Administrative Management, John Currier, dined at BLT Prime, which is one of his favorite restaurants in D.C. He ate with Paul Miller, a managing partner of Miller/Wenhold Capitol Strategies, "your government affairs and association management firm." Miller also "started the National Institute for Lobbying and Ethics where he currently serves as president."
The managing partner of Coast to Coast strategies ("Where business and government comes together") and a former chairman of the Michigan GOP, Saulius Saul Anuzis, was completely shocked by his surprise party at the hotel.
Russian singers Victoria Sukhareva and Артём Старченко enjoyed a wonderful evening.
Four-time kickboxing world champion Emory Andrew Tate III inked an endorsement deal for digital products in the hotel's lobby.
"Former acting Attorney General Matthew Whitaker has agreed to meet a second time with House lawmakers to clarify public testimony he gave earlier this month, the chairman of the House Judiciary Committee said." By Dustin Volz for The Wall Street Journal.
"What Michael Cohen's testimony will tell us about Trump's business, bluster, and wealth" by Adam Davidson for The New Yorker
"The Trump SoHo Hotel was struggling to survive. Then it dropped its name" by Nikki Ekstein for Bloomberg
Donald Trump Jr. came to the aid of Trump Hotel D.C. regular, Raheem Kassam.
Trump Realty advertised the "unique opportunity" of renting a home adjacent to Mar-a-Lago. Asking price: $100,000 per month.
House investigations, current status (latest change, Feb. 27, 2019)
Intelligence—On Feb. 6, chair Rep. Adam Schiff (D–CA) issued a statement that said his committee would investigate links or coordination between the Russian government/related foreign actors and individuals associated with Trump's businesses, as well as if foreign actors sought to compromise or hold leverage over Trump's businesses. During an interview with NBC's "Meet the Press" on Feb. 10, Schiff said the committee will investigate Trump's relationship with Deutsche Bank, a major lender to the Trump Organization. Earlier, on Jan. 24, the committee sent an inquiry to Deutsche Bank AG on its ties to Trump, according to the bank.
UPDATED Oversight and Reform—Chair Rep. Elijah Cummings's (D–MD) staff "has already sent out 51 letters to government officials, the White House, and the Trump Organization asking for documents related to investigations that the committee may launch," according to CBS News on Jan. 13. In a Feb. 15 letter to White House Counsel Pat Cipollone, Cummings said the committee received documents showing a White House attorney and one of Trump's personal attorneys provided "false information" to the Office of Government Ethics regarding Michael Cohen's "hush-money payments." A Feb. 20 memo from the majority laid out the scope for the Feb. 27 hearing with Michael Cohen. Topics include the Trump Hotel D.C. And, according to The Wall Street Journal, "Cohen also will make public some of Mr. Trump's private financial statements and allege that Mr. Trump at times inflated or deflated his net worth for business and personal purposes, including avoiding paying property taxes." And "Cohen will also discuss a check he received in March 2017 for a $35,000 installment that was signed by Trump Organization Chief Financial Officer Allen Weisselberg and Donald Trump Jr., the president's eldest son."
Transportation and Infrastructure subcommittee on Economic Development, Public Buildings, and Emergency Management—Transportation committee chair Rep. Peter DeFazio (D–OR) and subcommittee chair Dina Titus (D–NV) sent a letter to GSA administrator Emily Murphy on Jan. 22 asking for all communication between the GSA and members of the Trump family dating back to 2015, an explanation of how the hotel calculates its profits, profit statements since the hotel opened in 2016, any guidance from the White House regarding the lease, and whether or not Ivanka Trump and Jared Kushner are recused from participating in decisions regarding the property. GSA has "sent a partial response and the subcommittee is reviewing it," according to a senior House staffer familiar with the situation. When hearings begin, it is likely that Murphy will be the first person called to testify, according to a person familiar with the subcommittee's plans.
Ways and Means subcommittee on Oversight—The subcommittee held its first hearing on "legislative proposals and tax law related to presidential and vice-presidential tax returns" on Feb. 7. "We will ask the question: Does the public have a need to know that a person seeking the highest office in our country obeys tax law?" said chair Rep. John Lewis (D–GA). Experts in tax law testified.
Legal cases, current status (latest change, Feb. 22, 2019)
Official capacity—On Dec. 20, 2018, the 4th U.S. Circuit Court of Appeals ruled it would hear the president's appeal of district court rulings that allowed the case to proceed to discovery, and the appellate court halted discovery in the case. Discovery had started Dec. 3 and was scheduled to run through Aug. 2, 2019, with the AGs having subpoenaed the Trump Organization, including its Scottish golf courses; the U.S. Departments of Agriculture, Commerce, Defense, and Treasury and the GSA; and the state of Maine. Oral arguments on the appeal are scheduled for March 19. The AGs filed their brief opposing the president's appeal on Feb. 6, stating, "The President is not entitled to an order requiring the district court to certify for interlocutory review its denial of his motion to dismiss. No court has ever issued such relief." Trump's DOJ attorneys replied on Feb. 21: "Plaintiffs fundamentally err, substantively and procedurally."
196 Democratic senators and representatives' emoluments lawsuit—On Sept. 28, Judge Emmet G. Sullivan ruled that the legislators have standing to sue. Trump's Justice Department attorneys filed an interlocutory appeal on Oct. 22. On Jan. 30, 2019, the plaintiffs' filed a notice of supplemental authority, notifying the court of the GSA inspector general's report that criticized GSA for failing to consider if the Trump Hotel D.C.'s lease was in compliance with the Constitution after Donald Trump became president. Two days later, the president's attorneys argued that the IG's conclusion was not inconsistent with Trump's argument, but that the judge should ignore that report anyway because the IG has no expertise in interpreting or applying the foreign emoluments clause.
Cork's unfair competition lawsuit—Judge Richard J. Leon dismissed the case on Nov. 26, 2018, writing "Cork has failed to state a claim for unfair competition under D.C. law." On Dec. 10, Cork's attorneys filed a notice of appeal and on Jan. 10, 2019 they submitted a statement of issues to be raised. The next steps, which don't yet have a timeline, include setting a briefing schedule and both sides filing appellate briefs.
Due to a formatting error, yesterday's 1100 Pennsylvania was published with a couple of broken links. The web version has been corrected and those links are
"Trump's Biggest Potential Conflict Of Interest Is Hiding In Plain Sight" by Dan Alexander and Matt Drange for Forbes
"At President Trump's hotel in New York, revenue went up this spring—thanks to a visit from big-spending Saudis" by David A. Fahrenthold and Jonathan O'Connell for The Washington Post
"They think they know you, Lionel Messi" by Rowan Ricardo Phillips for The Paris Review
Thanks for reading. If you like what you see, tell someone—and support this work by becoming a paying member ($5/month or $50/year). If you've been forwarded this newsletter, subscribe for yourself at zacheverson.substack.com. Questions? Read our FAQ/manifesto. Tips or feedback? Contact me, Zach Everson, securely via email at 1100Pennsylvania@protonmail.com or on Signal at 202.804.2744.


text:
Marriage Equality Support on the Rise
Apr 29, 2009 by Rev. Candace Chellew in Society
Despite the ridiculous fear mongering of those opposed to marriage equality for same-gender partners, the population at large gets it. A new NY Times/CBS poll shows the highest support yet for marriage equality – 42 percent now support it, up from just 33 percent last month:
Twenty-eight percent say same sex couples should have no legal recognition — down from 35 percent in March — while 25 percent support civil unions, but not marriage, for gay couples.
As has historically been the case on this issue, liberals are more likely to support same sex marriage. Sixty-nine percent support the idea, while conservatives generally favor either civil unions (28 percent) or no legal recognition (44 percent).
That means 67 percent support either marriage equality or civil unions for LGBT people. If that doesn't denote a tipping point on this issue, I'm not sure what will! Great news!
Rev. Candace Chellew
Whosoever founder and Editor Emeritus Rev. Candace Chellew (she/her) is the author of Bulletproof Faith: A Spiritual Survival Guide for Gay and Lesbian Christians. She earned her masters of theological studies at Emory University's Candler School of Theology, was ordained by Gentle Spirit Christian Church in December 2003, and trained as a spiritual director through the Omega Point program of the Episcopal Diocese of Atlanta. She serves as the spiritual director of Jubilee! Circle in Columbia, S.C., and blogs at Motley Mystic.
Tagged with: marriage


text:
package org.lastaflute.web.validation.exception;

import org.lastaflute.core.exception.LaSystemException;

/**
 * @author jflute
 */
public class ValidationSuccessAttributeNotFoundException extends LaSystemException {

    private static final long serialVersionUID = 1L;

    public ValidationSuccessAttributeNotFoundException(String msg) {
        super(msg);
    }

    public ValidationSuccessAttributeNotFoundException(String msg, Throwable cause) {
        super(msg, cause);
    }
}

redpajama_set_name: RedPajamaGithub


text:
EU plays central role in landmark deal on CO2 standard for aircraft emissions
The European Commission has welcomed the agreement reached recently (8.2) within the International Civil Aviation Organisation (ICAO) on the first ever-global standard to cap CO2 emissions from aircraft.
"This agreement is an important step to curb aviation emissions," said EU Commissioner for Transport Violeta Bulc. "An ambitious climate policy is an integral part of the Commission's plan to create an Energy Union, and a priority of the new Aviation Strategy. The EU played a central role in brokering this deal, as it did at the COP21 in Paris. I hope this will create further momentum for the creation of a Global Market-Based Measure to offset CO2 emissions from international aviation, which we hope to achieve this autumn at the ICAO General Assembly."
Commissioner Bulc referred to United Nation's conference on climate change last December in Paris where 195 nations signed a climate agreement to cut fossil fuel use. The agreement set an ambitious goal of limiting the rise of temperature to below 2 degrees Celsius above pre-industrial levels, a mark which could be a tipping point for climate change.
Meeting in Montreal, the ICAO's Committee on Aviation and Environmental Protection (CAEP) agreed on a CO2 standard, which will guide the certification of aircraft towards greater fuel-efficiency. The new environmental measure was unanimously recommended by the 170 international experts in the committee.
For large new aircraft types, a very ambitious standard was agreed, to incentivize ever-greater fuel efficiency performance of future aircraft fleets. For such aircraft types, the standard will apply as of 2020. By 2028, existing aircraft types will also have to apply the new standard. Over the period until 2040, the CO2 standard could help save up to 650 million tonnes of CO2.
The proposed global standard is especially stringent where it will have the greatest impact: for larger aircraft. Operations of aircraft weighing over 60 tonnes account for more than 90% of international aviation emissions. They also have access to the broadest range of emissions reduction technologies, which the standard recognizes.
"Our sector presently accounts for less than two percent of the world's annual CO2 emissions, but we also recognize that the projected doubling of global passengers and flights by 2030 must be managed responsibly and sustainably," said Olumuyiwa Benard Aliu, President of the ICAO Council.
The agreement concluded six years of international negotiations. It will be brought before the 39th ICAO Assembly in September for political endorsement, and is expected to be formally adopted by the ICAO Council in early 2017.


Does CYP2D6 Genotyping have a Role in Guiding Tamoxifen Therapy?
Inter-individual variability to drug response is a major concern in the field of oncology. In the era of "targeted" therapy, optimal treatment outcomes can be achieved by more individualized initial dosing and/or alternative treatment according to the patient's genetic make-up. Although several genes are responsible for the interindividual variability in drug metabolism and response, the Cytochrome P450 enzymes are the most widely validated and clinically utilized. Pharmacogenetic testing of CYP2D6 alleles was the first FDA approved test due to its involvement in the metabolism of a wide range of drugs such as the anti-cancer drug tamoxifen (Nolvadex®), to which clinical response varies widely among patients.
Identifying determinants and predictors of the variable response or non-response to tamoxifen can facilitate therapeutic dose measurement or even determine the choice of alternative agents (e.g. aromatase inhibitors). Several clinical trials have shown that genetic variants associated with slower metabolism of tamoxifen may lead to lower than expected blood levels of its pharmacologically active metabolites and thus shorter recurrence-free survival. CYP2D6 genotyping can be clinically useful for selecting adjuvant therapy, improving the clinical outcome of tamoxifen and potentially reducing overall costs of treatment. However, CYP2D6 phenotypebased recommendations for tamoxifen have not been developed and guidelines linking the CYP2D6 status to personalized oncologic care do not exist and therefore clinicians' uptake of the testing has remained very low. Large prospective randomized clinical trials are required to assess whether CYP2D6 genotype can robustly predict treatment outcome of tamoxifen and improve overall survival.
Tamoxifen, a selective oestrogen receptor modulator, has been the mainstay for the therapy and prevention of recurrence in pre-menopausal women with oestrogen receptor-positive breast cancers for almost 40 years. Tamoxifen decreases the risk of relapse by half and the mortality rate by nearly a third in patients with ER (+) breast cancer which count for approximately 80% of all breast cancers [ 1-3]. While aromatase inhibitors are more effective for treating post-menopausal patients with ER (+) breast cancer, tamoxifen was approved by the FDA for metastatic breast cancer and as an alternative to aromatase inhibitors for the chemoprevention in post-menopausal women [4-6]. Hence, tamoxifen remains the gold standard for ER (+) breast cancer. However, tamoxifen efficacy varies widely, many breast cancer patients with adjuvant tamoxifen remain free of recurrence but 30-50% suffer relapse [7-10].
The pro-drug, tamoxifen, is extensively metabolised by CYP2D6 into therapeutically-active moieties, 4-hydroxytamoxifen and endoxifen; their affinity for the oestrogenreceptors is ~100-fold greater than tamoxifen and their antioestrogenic potency in suppressing ER-dependent cell proliferation is 30-100-fold stronger than tamoxifen [ 6,9,11-15].
Although factors underlying the ineffectiveness of tamoxifen are yet to be fully defined, these active metabolites play a key role in the high degree of interindividual differences in response to tamoxifen therapy [7-10].
Tamoxifen is metabolised via two routes; 4-hydroxylation and N-demethylation which account for ~7% and ~92% of tamoxifen metabolism, respectively. The 4-hydroxylation pathway, which is catalysed primarily via CYP2D6, leads immediately to the formation of 4-hydroxy-tamoxifen. Ndemethylation results in the formation of N-desmethyltamoxifen and is catalysed mainly via CYP3A4/5, and is followed by CYP2D6-mediated secondary metabolism to endoxifen (Figure 1). However, endoxifen can be formed from both N-desmethyl-tamoxifen and 4-hydroxy-tamoxifen and it has been found to play a more significant antiproliferative role than 4-hydroxy-tamoxifen in breast cancer [13,16-19]. Thus, it has been hypothesised that single nucleotide polymorphisms (SNPs) in the highly-polymorphic CYP2D6 can affect tamoxifen biotransformation and therefore may have the potential to predict the clinical outcome of tamoxifen therapy [9,19,20].
Figure 1: Tamoxifen metabolism in humans.
More than 100 variants, including more than 20 poor metaboliser alleles, with significant interethnic differences were identified [16,21,22] (Table 1).
Table 1: Allelic frequencies of CYP2D6 variant in selected population.
CYP2D6 different genotypes have been associated with four predicted phenotypes based on their CYP2D6 enzymatic function: poor (PM), intermediate (IM), extensive (EM) and ultra-rapid (UM) metabolizers (Table 2).
Table 2: CYP2D6 enzymatic function.
The widely-accepted criteria used to evaluate pharmacogenetic tests are: analytical validity, clinical validity and clinical utility .
The heterogeneity at the CYP2D6 locus and the high homology of CYP2D6 locus with its pseudogenes render analyzing CYP2D6 using the widely available short-read "nextgeneration" sequencing platforms to identify duplicated alleles immensely challenging. Nevertheless, clinical "nextgeneration" sequencing and genotyping pipelines have been developed and validated for CYP2D6 pharmacogenetic testing. For example, microarray technology-based genotyping for common CYP2D6 alleles can be optimal with sensitivity and specificity up to 100% [6,24].
While comparative double-blinded trials showed no correlation between tamoxifen plasma concentrations and clinical response in women treated with tamoxifen , plasma levels of endoxifen in those with reduced CYP2D6 activity were found to be considerably low in comparison with those whose CYP2D6 activity is normal [6,16,17,26]. However, since tamoxifen efficacy is dependent upon multiple factors, one of which may be endoxifen plasma level, the variability in clinical outcome of tamoxifen therapy cannot always be explained by CYP2D6 genotype. Furthermore, the precise clinical role of endoxifen in the overall efficacy of tamoxifen is debatable. Endoxifen plasma concentrations cannot be regarded as a surrogate outcome for clinical response and the association between endoxifen concentrations and breast cancer outcomes should be confirmed . Some drug models suggest that both tamoxifen and endoxifen overwhelm oestrogen receptors and therefore small concentrations of endoxifen may be needed to block oestrogen receptors suggesting that variations in endoxifen plasma concentrations may not affect this mechanism . However, endoxifen and other tamoxifen metabolites were proposed to have different mechanisms in modulating hormone receptors . The interpatient variability of tamoxifen metabolism and clinical outcomes in breast cancer may also result from genetic variation in enzymes involved in tamoxifen metabolism such as CYP3A, or resistance to chronic tamoxifen treatment due to activation of somatic mutations in the estrogenic receptor (ESR1) [2,30,31].
Various studies regarding treatment outcomes in the adjuvant and/or metastatic settings have reported that those with genetically impaired CYP2D6 appear to have experienced significantly higher rate of breast cancer recurrence and mortality than those with normal CYP2D6 enzymatic activity [ 10,20,32-38], suggesting that variants associated with reduced function alleles (e.g.*4/*10/*41) are robust predictors of tamoxifen's antitumoral efficacy [10,20,34,37]. Moreover, findings from a prospective study found that CYP2D6 polymorphisms were strongly associated with Ki-67 response, implying that CYP2D6 genetic variation is an important predictor for efficacy of tamoxifen in women with breast cancer . However, Ki-67 response has not yet been validated as a surrogate marker for tamoxifen efficacy.
Most of these studies were retrospective [33,34,39] and therefore liable to substandard documentation. The prospective studies [20,32], however, were also retrospective in nature since CYP2D6 genotyping has been performed after the relapse had eventuated. Nonparametric analyses and substantial overlaps in the patients' data were also reported in the following studies [10,33-35]. Nevertheless, two prospective yet small studies [36,38] and two large trials (n>1300) [35,40] have reported statistically strong correlation between CYP2D6 genotype and clinical outcome in patients with breast cancer taking tamoxifen. Although some studies assessed overall survival outcomes [34,39], the trials were mostly non-randomized and failed to show a statistically significant correlation between overall survival and CYP2D6 genotype and whether this association varies by therapy type. In the metastatic setting, however, a significant association was observed but the study was small and the evidence was equivocal and limited . The small sample size and the low coverage of alleles genotyped in most of these studies have diminished the reliability of the tests and reduced the ability to identify false positive results. The insufficient allelic coverage can cause patient misclassification. However, it can be argued that a clear bias toward positive results was observed with higher allelic coverage . Furthermore, the inclusion of ER/PR-negative patients, who do not response to tamoxifen, might have resulted in underestimation of the impact of genotype on clinical outcome and potentially false negative results in some studies [28,41]. These studies have also assumed that CYP2D6 genotype has no impact on clinical outcomes in women with breast cancer who are not taking tamoxifen. The apparent disparity in the ethnic composition, sample size, study design, methodologies, therapeutic regimens, adherence to treatment, co-treatments with CYP2D6 inhibitors and the inconsistent inclusion criteria of the majority of these trials can partly explain the controversial results and render comparison difficult. This has been further complicated by the inconsistent genotype-phenotype assignment and extensive heterogeneity in definition of outcome, as many measured the recurrence or disease-free survival but only a very few assessed the overall survival. More importantly, none of these studies has suggested detailed therapeutic paradigms, or addressed the potential consequences of CYP2D6 testing-based guidance on individuals with phenotypes determined incorrectly.
In contrast, two studies (n=226 and n=677) reported conflicting findings and demonstrated significantly reverse association between clinical outcome of tamoxifen and low activity CYP2D6 genotype [42,43]. It can, however, be argued that using a high dose of tamoxifen in these trials [42,43] might have normalized the low CYP2D6 activity in PMs and IMs. Analyses from two of the most influential large prospective randomized studies (n=1243 and n=588), BIG 1-98 and ATAC, found a near-null correlation between CYP2D6 genotype and breast cancer prognosis in tamoxifen-treated women, and provided statistically strong evidence of the opposite [7,44]. However, this null association was also unexplainably observed in the patients receiving tamoxifen in combination with other anti-tumour agents . It has been suggested that the DNA extracted from formalin-fixed paraffinembedded tumour tissues used in these studies instead of germline DNA [7,44] has potentially led to erroneous genotyping due to the presence of loss of heterozygosity (LOH) at the unstable CYP2D6 locus in breast tumour DNA. This bias was detected by the massive deviation from Hardy-Weinberg equilibrium (i.e. expected versus observed allelic frequencies) [ 46-49]. However, departure from Hardy-Weinberg equilibrium has not been reported in several trials using DNA derived from breast tumour–infiltrated tissues . Even though germline DNA was used or blood samples with (LOH) were excluded, no positive association between genetic variations of CYP2D6 and tamoxifen efficacy was observed [51-53]. Therefore, results from the abovementioned studies [7,44] can be considered valid and should be included in evaluating the value of CYP2D6 genotyping in tamoxifen therapy [38,50,54-56].
To date, there are no standards to validate quality of pharmacogenetic association. "Validation of a true pharmacogenetic association, demonstration of so-called 'clinical validity', should be conducted in prospective clinical studies that are larger, have more homogeneous patients and treatment and systematically collect outcomes data" .
Even though it has been recognized that there are certain circumstances in which CYP2D6 genotyping can be helpful for tamoxifen dose adjustment or consideration of alternative treatment , CYP2D6 testing is not currently recommended for women for whom tamoxifen treatment is being considered.
Several studies provided evidence that doubling the tamoxifen dose to 40mg/day, which may have normalized impaired metabolism, was clearly associated with an increased concentration of endoxifen in IMs [27,42,43,58,59]. Nevertheless, endoxifen plasma levels remained considerably low in PMs taking 40 mg/day  and several studies showed that CYP2D6 metabolizer status was not a reliable predictor of individualizing tamoxifen optimal dose . Recently, it has been, however, found that adjusted doses of tamoxifen to 80 and 40 mg for poor and intermediate CYP2D6 metabolizers, respectively, had achieved therapeutic endoxifen levels in approximately 90% of patients. However, inter-patient variability remained [61-63]. Thus, it is still debatable whether patients benefit from the dose escalation of tamoxifen. Interestingly, recent data showed that the PM status did not affect the clinical outcomes in majority of the patients . Furthermore, studies showed that CYP2D6 genotype alone can only partly explain the interindividual variability among patients treated with tamoxifen and that tamoxifen treatment cannot be individualized only by CYP2D6 genotype suggesting other genes involved in the metabolism of tamoxifen should be considered [30,65-69]. Therefore, a definitive exposureresponse effect remains debated and additional research is needed to determine whether CYP2D6 PMs phenotypes or even patients with low endoxifen plasma levels will achieve better clinical outcomes with increased dose of tamoxifen.
In spite of the fact that CYP2D6 genotyping test for tamoxifen treatment might be appropriate to optimize treatment outcome in specific patients , at present, it is still not generally recommended. The analysis of the existing literature and current evidence seem to be insufficient to justify the clinical utilization of CYP2D6 pharmacogenetic test to effectively guide dose and decision making in women with breast cancer for whom tamoxifen is being considered. Hence, it seems to be immensely challenging to reach consensus whether tamoxifen treatment should be based on the CYP2D6 testing and whether CYP2D6 genotyping approach is reliable and accurate in predicting treatment outcomes. For reliable implementation of CYP2D6 genotyping, large prospective studies of uniformly-treated women which establish evidence that the predictive capability of CYP2D6 testing exceeds the current approaches are required. Strategies such as therapeutic drug monitoring (TDM) and approaches based on phenotyping or direct measurements of endoxifen concentrations or even more recently administering chemical compounds that are unaffected by CYP2D6 metabolism such as Z-endoxifen have proved to be more useful and effective than CYP2D6 genotyping to individualize tamoxifen therapy. However, their value must be validated in prospective clinical studies as well [63,70-73].
American Society of Clinical Oncology clinical practice (ASCO) guidelines and the National Comprehensive Cancer Network (NCCN) recommendations: Because of the controversial findings from the two above-mentioned big studies, BIG 1–98 and ATAC trial, in which no relationship was found between the CYP2D6 genotype and breast cancer recurrence, the committee of the American Society of Clinical Oncology clinical practice (ASCO) and the National Comprehensive Cancer Network (NCCN) do not recommend CYP2D6 genotype testing to personalize tamoxifen therapy and therefore CYP2D6 allelic status should not be used to guide adjuvant endocrine therapy. Although no definitive conclusion was made with regard to the interaction between CYP2D6 inhibitors and tamoxifen, NCCN and ASCO recommend that concomitant use of CYP2D6 inhibitors and tamoxifen should be avoided due to drug-drug interactions [74-76].
The FDA recommendations: Initial findings from retrospective studies prompted the FDA Advisory Committee in 2006 to recommend re-labelling tamoxifen to state that PMs patients have a high incidence of recurrence in comparison with other genotypes [34,77]. Since then, several studies have reported conflicting and highly discordant results [7,44,70,78]. At present, the FDA does not recommend the pharmacogenetic testing for CYP2D6 and current FDA label of tamoxifen does not refer to CYP2D6 genotyping [79,80].
PharmaGKB and the Dutch pharmacogenetics working group recommendations: For CYP2D6 poor (PMs) and intermediate (IMs) metabolizers, alternative drugs are recommended for treating postmenopausal patients with breast cancer and concurrent use of CYP2D6 inhibitors with tamoxifen to be avoided .
As genotyping costs drop and CYP2D6 genotyping has the potential to guide hormone therapy, one may inevitably anticipate a wide adoption of the test in clinical setting. However, the existing evidence does not support a statistically strong correlation between variant genotypes of CYP2D6 and breast cancer outcomes. The discrepant and conflicting findings regarding the influence of CYP2D6 genotype on clinical outcomes with tamoxifen have caused perplexity among regulatory bodies and health professionals.
Even if the evidence was consistent for a strong association between CYP2D6 genotype and treatment outcomes, at best, reimbursement decisions by governmental or insurance schemes are based partly on evidence of cost-effectiveness. Therefore, the major challenges that are hindering the adoption of CYP2D6 genotyping include the relatively small proportion of non-response to tamoxifen, cost implications of testing and availability of alternative drugs that may exceed the benefits achieved by tamoxifen therapy. One could argue that it is unethical not to offer CYP2D6 pharmacogenetic screening prior to initiation of tamoxifen to women who might take it for 5 or 10 years, since it is known that certain women indeed will not respond to a standard dose of it. However, to achieve convincing evidence of clinical validity, large scale prospective randomized trials are warranted to robustly and quantitatively demonstrate that knowledge of the patient's CYP2D6 genotype can improve overall survival or reduce overall treatment cost in clinical practice. Further functional analysis is also required to elucidate the biological mechanisms underlying the metabolism and efficacy of tamoxifen and to further our understanding of the association between CYP2D6 phenotype and long-term clinical outcome.
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Spitman AS, Moes DJ, Gelderblom H, Dezentje VO, Swen JJ, et al. (2017) Effect of CYP3A4* 22, CYP3A5* 3, and CYP3A combined genotypes on tamoxifen metabolism. Eur J Clin Pharmacol.
Sutiman N, Lim JS, Muerdter TE, Singh O, Cheung YB, et al. (2016) Pharmacogenetics of UGT1A4, UGT2B7 and UGT2B15 and their influence on tamoxifen disposition in Asian breast cancer patients. Clinical Pharmacokinetics 55: 1239-1250.
Schroth W, Winter S, Mürdter T, Schaeffeler E, Eccles D, et al. (2017) Improved prediction of endoxifen metabolism by CYP2D6 genotype in breast cancer patients treated with tamoxifen. Front Pharmacol 8: 582.
Bertholee D, Maring JG, Van Kuilenburg AB (2017) Genotypes affecting the pharmacokinetics of anticancer drugs. Clinical Pharmacokinetics 56: 317-337.
Novillo A, Romero-Lorca A, Gaibar M, Rubio M, Fernández-Santander A (2017) Tamoxifen metabolism in breast cancer treatment: Taking the focus off the CYP2D6 gene. Pharmacogenomics Journal 17: 109-111.
Del Re M, Citi V, Crucitta S, Rofi E, Belcari F, et al. (2016) Pharmacogenetics of CYP2D6 and tamoxifen therapy: Light at the end of the tunnel?. Pharmacological Res 107:398-406.
Binkhorst L, Mathijssen RH, Jager A, Van Gelder T (2015) Individualization of tamoxifen therapy: much more than just CYP2D6 genotyping. Cancer Treat Rev 41: 289-299.
Goetz MP, Suman VJ, Reid JM, Northfelt DW, Mahr MA, et al. (2017) First-in-human phase I study of the tamoxifen metabolite Z-endoxifen in women with endocrine-refractory metastatic breast cancer. J Clin Oncol 30: JCO2017733246.
Koolen SL, Bins S, Mathijssen RH (2016) Individualized tamoxifen dose escalation. Clin Cancer Res 22: 6300-.
Harris LN, Ismaila N, McShane LM, Andre F, Collyar DE, et al. (2016) Use of biomarkers to guide decisions on adjuvant systemic therapy for women with early-stage invasive breast cancer: American Society of Clinical Oncology clinical practice guideline. J Clin Oncol 34: 1134-1150.
Gradishar WJ, Anderson BO, Blair SL, Burstein HJ, Cyr A, et al. (2014) Breast cancer version 3.2014J Natl Compr Canc Netw 12: 542-590.
Damkier P, Kjærsgaard A, Barker KA, Cronin-Fenton D, Crawford A, et al. (2017) CYP2C19* 2 and CYP2C19* 17 variants and effect of tamoxifen on breast cancer recurrence: Analysis of the International Tamoxifen Pharmacogenomics Consortium dataset. Scientific Reports 7: 7727.


text:
Q: Chartkick - Stacked vertical graph in percentage I am building a vertical percentage graph following the google instruction: https://developers.google.com/chart/interactive/docs/gallery/barchart#StackedBars
This is how it should look like:

However, this is how it look right now.

I am using the same data as the one of google.
my_graph_controllers
@data = [
        ['Genre', 'Fantasy & Sci Fi', 'Romance', 'Mystery/Crime', 'General',
         'Western', 'Literature', { role: 'annotation' } ],
        ['2010', 10, 24, 20, 32, 18, 5, ''],
        ['2020', 16, 22, 23, 30, 16, 9, ''],
        ['2030', 28, 19, 29, 30, 12, 13, '']
      ]

view/my_graph.html.erb
<head>
<%= javascript_include_tag "https://www.gstatic.com/charts/loader.js" %>
<%= javascript_include_tag 'application' %>
</head>

<div class="container">

  <%= bar_chart @data, isStacked: true, isStacked: "percentage" %>

</div>

assets/javascripts/application.js
//= require rails-ujs
//= require_tree .
//= require Chart.bundle
//= require chartkick
//= require highcharts

gemfile
gem "chartkick"

A: So the trick is to transform the data a bit.
@data = [
      {
        name: "Fantasy & Sci Fi",
        data: [["2010", 10], ["2020", 16], ["2030", 28]]
      },
      {
        name: "Romance",
        data: [["2010", 24], ["2020", 22], ["2030", 19]]
      },
      {
        name: "Mystery/Crime",
        data: [["2010", 20], ["2020", 23], ["2030", 29]]
      }
    ]

And this works like a charm then:
<%= bar_chart @data, stacked: true %>

I have found the answer in an older question over here.
However, if you want to do the percentage stack, you need to use the library hash for that.
<%= bar_chart @data, adapter: 'google', library: { isStacked: 'percent' } %>

P.s. Notice that it should be either true or 'percent' for the isStacked. More information here.

redpajama_set_name: RedPajamaStackExchange


text:
namespace blink {
namespace {

WebMessagePayload DecodeWithV8(const TransferableMessage& message) {
  base::test::TaskEnvironment task_environment;
  WebMessagePayload result;

  v8::Isolate::CreateParams params;
  params.array_buffer_allocator =
      v8::ArrayBuffer::Allocator::NewDefaultAllocator();
  v8::Isolate* isolate = v8::Isolate::New(params);
  {
    v8::HandleScope scope(isolate);
    v8::TryCatch try_catch(isolate);

    v8::Local<v8::Context> context = v8::Context::New(isolate);
    v8::Context::Scope lock(context);

    v8::ValueDeserializer deserializer(isolate, message.encoded_message.data(),
                                       message.encoded_message.size());
    deserializer.SetSupportsLegacyWireFormat(true);
    if (message.array_buffer_contents_array.size() == 1) {
      // Prepare to transfer ArrayBuffer first. This does not necessary mean the
      // result type is ArrayBuffer.
      mojo_base::BigBuffer& big_buffer =
          message.array_buffer_contents_array[0]->contents;
      v8::Local<v8::ArrayBuffer> message_as_array_buffer =
          v8::ArrayBuffer::New(isolate, big_buffer.size());
      memcpy(message_as_array_buffer->GetBackingStore()->Data(),
             big_buffer.data(), big_buffer.size());
      deserializer.TransferArrayBuffer(0, message_as_array_buffer);
    }
    EXPECT_TRUE(deserializer.ReadHeader(context).ToChecked());

    v8::Local<v8::Value> value =
        deserializer.ReadValue(context).ToLocalChecked();
    if (value->IsString()) {
      v8::Local<v8::String> js_str = value->ToString(context).ToLocalChecked();
      std::u16string str;
      str.resize(js_str->Length());
      js_str->Write(isolate, reinterpret_cast<uint16_t*>(&str[0]), 0,
                    str.size());
      result = str;
    }
    if (value->IsArrayBuffer()) {
      auto js_array_buffer = value.As<v8::ArrayBuffer>()->GetBackingStore();
      std::vector<uint8_t> array_buffer_contents;
      array_buffer_contents.resize(js_array_buffer->ByteLength());
      memcpy(array_buffer_contents.data(), js_array_buffer->Data(),
             js_array_buffer->ByteLength());
      result = array_buffer_contents;
    }
  }
  isolate->Dispose();
  delete params.array_buffer_allocator;

  return result;
}

TransferableMessage EncodeWithV8(const WebMessagePayload& message,
                                 const bool transferable = false) {
  TransferableMessage transferable_message;
  base::test::TaskEnvironment task_environment;
  std::vector<uint8_t> result;

  v8::Isolate::CreateParams params;
  params.array_buffer_allocator =
      v8::ArrayBuffer::Allocator::NewDefaultAllocator();
  v8::Isolate* isolate = v8::Isolate::New(params);
  {
    v8::HandleScope scope(isolate);
    v8::TryCatch try_catch(isolate);

    v8::Local<v8::Context> context = v8::Context::New(isolate);
    v8::Context::Scope lock(context);
    v8::ValueSerializer serializer(isolate);
    serializer.WriteHeader();

    if (const auto* str = absl::get_if<std::u16string>(&message)) {
      v8::Local<v8::String> message_as_value =
          v8::String::NewFromTwoByte(
              isolate, reinterpret_cast<const uint16_t*>(str->data()),
              v8::NewStringType::kNormal, str->size())
              .ToLocalChecked();
      EXPECT_TRUE(serializer.WriteValue(context, message_as_value).ToChecked());
    } else if (const auto* array_buffer =
                   absl::get_if<std::vector<uint8_t>>(&message)) {
      v8::Local<v8::ArrayBuffer> message_as_array_buffer =
          v8::ArrayBuffer::New(isolate, array_buffer->size());
      memcpy(message_as_array_buffer->GetBackingStore()->Data(),
             array_buffer->data(), array_buffer->size());
      if (transferable) {
        serializer.TransferArrayBuffer(0, message_as_array_buffer);
      }
      EXPECT_TRUE(
          serializer.WriteValue(context, message_as_array_buffer).ToChecked());

      mojo_base::BigBuffer big_buffer(*array_buffer);
      transferable_message.array_buffer_contents_array.push_back(
          mojom::SerializedArrayBufferContents::New(std::move(big_buffer)));
    } else {
      NOTREACHED();
    }

    std::pair<uint8_t*, size_t> buffer = serializer.Release();
    result = std::vector<uint8_t>(buffer.first, buffer.first + buffer.second);
    free(buffer.first);
  }
  isolate->Dispose();
  delete params.array_buffer_allocator;

  transferable_message.owned_encoded_message = std::move(result);
  transferable_message.encoded_message =
      transferable_message.owned_encoded_message;
  return transferable_message;
}

void CheckStringEQ(const absl::optional<WebMessagePayload>& optional_payload,
                   const std::u16string& str) {
  EXPECT_TRUE(optional_payload);
  auto& payload = optional_payload.value();
  EXPECT_TRUE(absl::holds_alternative<std::u16string>(payload));
  EXPECT_EQ(str, absl::get<std::u16string>(payload));
}

void CheckVectorEQ(const absl::optional<WebMessagePayload>& optional_payload,
                   const std::vector<uint8_t>& buffer) {
  EXPECT_TRUE(optional_payload);
  auto& payload = optional_payload.value();
  EXPECT_TRUE(absl::holds_alternative<std::vector<uint8_t>>(payload));
  const auto& vec = absl::get<std::vector<uint8_t>>(payload);
  EXPECT_EQ(buffer.size(), vec.size());
  for (size_t i = 0; i < buffer.size(); ++i)
    EXPECT_EQ(buffer[i], vec[i]);
}

TEST(StringMessageCodecTest, SelfTest_ASCII) {
  std::u16string message = u"hello";
  CheckStringEQ(DecodeToWebMessagePayload(
                    EncodeWebMessagePayload(WebMessagePayload(message))),
                message);
}

TEST(StringMessageCodecTest, SelfTest_Latin1) {
  std::u16string message = u"hello \u00E7";
  CheckStringEQ(DecodeToWebMessagePayload(
                    EncodeWebMessagePayload(WebMessagePayload(message))),
                message);
}

TEST(StringMessageCodecTest, SelfTest_TwoByte) {
  std::u16string message = u"hello \u263A";
  CheckStringEQ(DecodeToWebMessagePayload(
                    EncodeWebMessagePayload(WebMessagePayload(message))),
                message);
}

TEST(StringMessageCodecTest, SelfTest_TwoByteLongEnoughToForcePadding) {
  std::u16string message(200, 0x263A);
  CheckStringEQ(DecodeToWebMessagePayload(
                    EncodeWebMessagePayload(WebMessagePayload(message))),
                message);
}

TEST(StringMessageCodecTest, SelfTest_ArrayBuffer) {
  std::vector<uint8_t> message(200, 0xFF);
  CheckVectorEQ(DecodeToWebMessagePayload(
                    EncodeWebMessagePayload(WebMessagePayload(message))),
                message);
}

TEST(StringMessageCodecTest, SelfToV8Test_ASCII) {
  std::u16string message = u"hello";
  CheckStringEQ(
      DecodeWithV8(EncodeWebMessagePayload(WebMessagePayload(message))),
      message);
}

TEST(StringMessageCodecTest, SelfToV8Test_Latin1) {
  std::u16string message = u"hello \u00E7";
  CheckStringEQ(
      DecodeWithV8(EncodeWebMessagePayload(WebMessagePayload(message))),
      message);
}

TEST(StringMessageCodecTest, SelfToV8Test_TwoByte) {
  std::u16string message = u"hello \u263A";
  CheckStringEQ(
      DecodeWithV8(EncodeWebMessagePayload(WebMessagePayload(message))),
      message);
}

TEST(StringMessageCodecTest, SelfToV8Test_TwoByteLongEnoughToForcePadding) {
  std::u16string message(200, 0x263A);
  CheckStringEQ(
      DecodeWithV8(EncodeWebMessagePayload(WebMessagePayload(message))),
      message);
}

TEST(StringMessageCodecTest, SelfToV8Test_ArrayBuffer) {
  std::vector<uint8_t> message(200, 0xFF);
  CheckVectorEQ(
      DecodeWithV8(EncodeWebMessagePayload(WebMessagePayload(message))),
      message);
}

TEST(StringMessageCodecTest, V8ToSelfTest_ASCII) {
  std::u16string message = u"hello";
  CheckStringEQ(DecodeToWebMessagePayload(EncodeWithV8(message)), message);
}

TEST(StringMessageCodecTest, V8ToSelfTest_Latin1) {
  std::u16string message = u"hello \u00E7";
  CheckStringEQ(DecodeToWebMessagePayload(EncodeWithV8(message)), message);
}

TEST(StringMessageCodecTest, V8ToSelfTest_TwoByte) {
  std::u16string message = u"hello \u263A";
  CheckStringEQ(DecodeToWebMessagePayload(EncodeWithV8(message)), message);
}

TEST(StringMessageCodecTest, V8ToSelfTest_TwoByteLongEnoughToForcePadding) {
  std::u16string message(200, 0x263A);
  CheckStringEQ(DecodeToWebMessagePayload(EncodeWithV8(message)), message);
}

TEST(StringMessageCodecTest, V8ToSelfTest_ArrayBuffer) {
  std::vector<uint8_t> message(200, 0xFF);
  CheckVectorEQ(DecodeToWebMessagePayload(EncodeWithV8(message)), message);
}

TEST(StringMessageCodecTest, V8ToSelfTest_ArrayBuffer_transferrable) {
  std::vector<uint8_t> message(200, 0xFF);
  CheckVectorEQ(DecodeToWebMessagePayload(EncodeWithV8(message, true)),
                message);
}

TEST(StringMessageCodecTest, Overflow) {
  const std::vector<uint8_t> kOverflowOneByteData{'"', 0xff, 0xff, 0xff, 0x7f};
  const std::vector<uint8_t> kOverflowTwoByteData{'c', 0xff, 0xff, 0xff, 0x7f};

  TransferableMessage one_byte_message;
  one_byte_message.owned_encoded_message = kOverflowOneByteData;
  one_byte_message.encoded_message = one_byte_message.owned_encoded_message;

  TransferableMessage two_byte_message;
  two_byte_message.owned_encoded_message = kOverflowTwoByteData;
  two_byte_message.encoded_message = two_byte_message.owned_encoded_message;

  EXPECT_FALSE(DecodeToWebMessagePayload(one_byte_message));
  EXPECT_FALSE(DecodeToWebMessagePayload(two_byte_message));
}

}  // namespace
}  // namespace blink


Barely three hours after the withdrawal of Dr. Obiageli Ezekwesili of the Allied Congress Party of Nigeria from the 2019 presidential race, the national chairman of the party, who is also her running mate, Alhaji Gani Galadima, on Thursday endorsed the re-election bid of President Muhammadu Buhari.
Galadima whose performance in the election debate for vice presidential candidates was seen to be very poor alleged that Ezekwesili entered the race because she was looking forward to becoming the Minister of Finance.
A source close to Galadima told our correspondent that by withdrawing from the presidential race, Ezekwesili had given Galadima a direct entry and opportunity he had been looking for to endorse Buhari.
"Galadima is not known and ACPN is not popular. By withdrawing from the race, the opportunity has now knocked at his door to endorse Buhari. This is what he has been looking for", a source in the party stated.
A statement issued by the party, signed by Galadima and the party's secretary, Chief Paul Isamade, read, "The reason for calling this press conference is to let the world know about the presidential aspiration of Dr. Oby Ezekwesili, which in actual fact, is not the truth. I have been put into confidence by one of her aide named Iyinoluwa Aboyeji that she only wanted to use the platform of the ACPN to negotiate to be Nigeria's finance minister," he said.


About Lugubrum: Flemish Black Metal horde playing 'Boersk Blekk Metle', which translates as farmer black metal. This term dates from their 'farmer'-era, when the band resided in Lovendegem, a small rural village. Now they moved to nearby city Ghent, resulting in less emphasis on the rural aspect.


text:
Калингаста — департамент в Аргентине в составе провинции Сан-Хуан.
 (3833) Калингаста — медленно вращающийся астероид, относящийся к группе астероидов, пересекающих орбиту Марса.

redpajama_set_name: RedPajamaWikipedia


text:
The Porta Maggiore Basilica is an underground basilica discovered in 1917 near Porta Maggiore in Rome. It is dated to the first century BC.  It is believed to have been the meeting place of the neo-Pythagoreans, and is the only historical site that has been associated with the neo-Pythagorean movement. This school of mystical Hellenistic philosophy preached asceticism and was based on the works of Pythagoras and Plato.  It was a precursor to the basilicas built during the Christian period, centuries later. It was opened to small groups of visitors in April 2015.

Discovery
It is  below the street level. The underground chamber was discovered accidentally in 1917 during the construction of a railway line from Rome to Cassino. An underground passage  caved in, revealing the hidden chamber.

History
The structure is thought to have been constructed by the Statilius family. The then head of the family, Titus Statilius Taurus, was accused by the Senate for what Tacitus in his Annals called "addiction to magical superstitions". He protested his innocence but eventually committed suicide in CE53.

Architecture

The basilica has three naves lined by six rock pillars and an apse. They are decorated with stucco images of centaurs, griffins and satyrs. Classical heroes such as Achilles, Orpheus, Paris and Hercules are also represented.

Originally the basilica was entered through a long downhill entrance from the Prenestina Street, and through a vestibule.

Opening
The basilica underwent several years of restoration work. In 1951, a concrete shell was constructed that enclosed the entire basilica. Air purifiers from IQAir in Switzerland have been installed to combat radon gas.

The 40ft-long basilica is now opened to visitors. The visiting groups are kept small because of the fragility of the monument. The temperature and humidity must be kept within a narrow range. It is open during 2nd and 4th Sunday of every month, and the tour must be prearranged.

References

External links
  La Basilica sotterranea di Porta Maggiore, Video, Adnkronos, Apr 24, 2015
Information on the Porta Prenestina from the LacusCurtius website.
 Pictures of the gate
 Porta Maggiore information
 Further information, and a map

Ancient basilicas in Rome
1917 archaeological discoveries
Buildings and structures completed in the 1st century BC

Subterranean buildings and structures


text:
Q: Unable to load react dev tools in electron I'm trying to load React and Redux dev tools in electron, so far Redux was loaded successfully, but React was not. I didn't see the React tab in Developer Tools. Here is my code:
main.js
const electron = require("electron");
const path = require("path");
const url = require("url");
const os = require("os");

const { app, BrowserWindow } = electron;

let win;

const installExtensions = async () => {
  const ses = win.webContents.session;
    // react dev tools
    ses.loadExtension(
      path.join(
        os.homedir(),
        ".config/google-chrome/Default/Extensions/fmkadmapgofadopljbjfkapdkoienihi/4.9.0_0"
      )
    );
    // redux dev tools
    ses.loadExtension(
      path.join(
        os.homedir(),
        ".config/google-chrome/Default/Extensions/lmhkpmbekcpmknklioeibfkpmmfibljd/2.17.0_0"
      )
    );
};

const createWindow = async () => {

  win = new BrowserWindow({
    webPreferences: {
      nodeIntegration: true,
      enableRemoteModule: true,
    },
  });
  win.maximize();

  await installExtensions();

  win.loadURL(
    url.format({
      pathname: path.join(__dirname, "index.html"),
      protocol: "file:",
      slashes: true,
    })
  );

  win.webContents.once("dom-ready", () => {
    win.webContents.openDevTools();
  });

  win.on("closed", () => {
    win = null;
  });
};

app.on("ready", createWindow);

app.on("window-all-closed", () => {
  if (process.platform !== "darwin") {
    app.quit();
  }
});

app.on("activate", () => {
  if (win === null) {
    createWindow();
  }
});

package.json
{
  "name": "electron-react-typescript",
  "version": "0.0.7",
  "description": "",
  "main": "/main.js",
  "scripts": {
    "start": "electron main.js"
  },
  "dependencies": {
    "electron": "^10.1.5",
    "electron-builder": "^22.9.1"
  }
}

I started the program using yarn start, here is the output:
yarn run v1.22.10
warning package.json: No license field
$ electron main.js
(node:8189) ExtensionLoadWarning: Warnings loading extension at /home/searene/.config/google-chrome/Default/Extensions/fmkadmapgofadopljbjfkapdkoienihi/4.9.0_0: Unrecognized manifest key 'browser_action'. Unrecognized manifest key 'minimum_chrome_version'. Unrecognized manifest key 'update_url'. Cannot load extension with file or directory name _metadata. Filenames starting with "_" are reserved for use by the system.
(node:8189) ExtensionLoadWarning: Warnings loading extension at /home/searene/.config/google-chrome/Default/Extensions/lmhkpmbekcpmknklioeibfkpmmfibljd/2.17.0_0: Unrecognized manifest key 'commands'. Unrecognized manifest key 'homepage_url'. Unrecognized manifest key 'page_action'. Unrecognized manifest key 'short_name'. Unrecognized manifest key 'update_url'. Permission 'notifications' is unknown or URL pattern is malformed. Permission 'contextMenus' is unknown or URL pattern is malformed. Permission 'tabs' is unknown or URL pattern is malformed. Cannot load extension with file or directory name _metadata. Filenames starting with "_" are reserved for use by the system.

I saw Redux in the developer tools, but I didn't find React. According to this github issue, the above warnings shouldn't block the loading of dev tools. I also tried re-opening dev-tools, no luck. How to solve it?

A: under webPreferences add
contextIsolation: false

for the loadExtension function add { allowFileAccess: true } as a 2nd argument.
That should make it work, as they changed the default of contextIsolation to be true in some version (I think 9.0.0),
and added allowFileAccess as an extention loading option for security.
You can make an isDev boolean to use for setting the allowFileAccess if needs be.