text:
AJ Allmendinger wins Xfinity race at rain-soaked Charlotte
Published: Sat, October 10, 2020 6:36 PM Updated: Sat, October 10, 2020 6:36 PM
AJ Allmendinger stands beside his trophy after winning a NASCAR Xfinity Series auto race at Charlotte Motor Speedway in Concord, N.C., Saturday, Oct. 10, 2020. (AP Photo/Nell Redmond)
CONCORD, N.C. (AP) — AJ Allmendinger splashed his way through a torrential rainstorm that turned Charlotte Motor Speedway into a slip-and-slide Saturday to win the Xfinity Series race on the hybrid road course-oval "Roval."
Allmendinger won for the second time this season in 10 starts for Kaulig Racing. He's easily the most experienced NASCAR driver at both road course racing and driving in wet conditions — Allmendinger has a long career in multiple formulas, including sports cars and open-wheel, which both race in the rain.
"I don't know what we just witnessed," Allmendinger said. "I was complaining the whole race. That was miserable. Crazy. Those conditions, to me, it's not a lot of fun.
"I thought at times it was dangerous, the hydroplaning. At times I thought we should have stopped it."
Allmendinger's victory in near darkness on a soaking wet track ended a sloppy race marred by multiple slides through standing water. It was an elimination race for the Xfinity Series playoffs and Harrison Burton, Brandon Brown, Michael Annett and Riley Herbst were knocked from title contention.
Allmendinger had a short celebration before he had to transition to NBC Sports' booth to call IMSA's debut on Charlotte's purpose-built Roval. While he was in victory lane, the soaking wet fans still in attendance loudly chanted "AJ! AJ! AJ!" as Allmendinger was shown on Charlotte's massive video board that illuminated the infield.
"In the infield with no lights, and the world's biggest jumbotron blaring, I mean, you couldn't see anything," Allmendinger said. "I was just guessing where the corners were and just praying that when you hit the puddles you don't go off the racetrack."
Allmendinger and Xfinity Series championship leader Chase Briscoe, the defending Roval winner, had a spirited race for the victory. Briscoe took the lead from Allmendinger with four laps remaining in regulation but Allmendinger grabbed it back at the start of overtime.
As Allemendinger surged to the front, Briscoe spun and slipped to an 18th-place finish.
"Driver mistake," Briscoe said. "In conditions like this you've got to be 100%. I tried to go 110 and it bit me. That one is going to sting for a long time."
It began to rain mere minutes after the race began and the wet conditions immediately disrupted the action. Drivers began sliding all over the track, into walls, and some struggled to get their windshield wipers working.
NASCAR had to stop the race for nearly 40 minutes as track dryers attempted to sweep standing water from the surface, and while it temporarily improved conditions, heavy rain later simply soaked the track again.
There were 10 cautions and six different leaders, including Noah Gragson who spun while out front in an eventful afternoon. He was later shoved off the course by Riley Herbst and during the delay vowed his revenge.
"I don't really get mad," he said. "I get even."
Gragson still finished second and was followed by Daniel Hemric to give JR Motorsports a pair of Chevrolets on the podium.
Alex Labbe was fourth followed by Ross Chastain as Chevrolet drivers swept the first five positions.
Austin Cindric was the highest-finishing Ford driver in sixth, followed by Cody Ware, Jade Buford, Michael Annett and Brandon Jones in a Toyota.
CommentsAJ Allmendinger wins Xfinity race at rain-soaked Charlotte


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Weeks After Modi-Xi Summit, US Officials In Arunachal, Dharamsala
These visits come just weeks after Chinese President Xi Jinping visited India for the second informal summit.
Published: 28 Oct 2019, 11:00 PM IST
The US ambassador to India, Kenneth Juster, on Monday, 28 October, visited Tawang in Arunchal Pradesh, an area which is claimed entirely by China in an unresolved land dispute.
At the same time, the US ambassador for religious freedom, Sam Brownback, was in Dharamsala to share the stage with the Tibetan leader Dalai Lama.
These visits come just weeks after Chinese President Xi Jinping visited India from 11 to 12 October to take part in the second informal summit with Prime Minister Narendra Modi.
Taliban Says New Intra-Afghan Peace Talks to Be Held in China
Juster is in Arunachal Pradesh to attend the three-day Tawang Festival, a mega event that draws hundreds of tourists every year.
It is great to be in Tawang as the Chief Guest for the Tawang Festival. #USIndiaDosti https://t.co/0h22s1z3vA
— Ken Juster (@USAmbIndia) October 28, 2019
Pema Khandu, chief minister of Arunachal Pradesh, had earlier welcomed the ambassador in a Twitter post, "Welcome to Ambassador Mr. Kenneth I. Juster and Consul General Patti Hoffman for Tawang Festival."
Beijing had raised objection after the former US ambassador to India Richard Verma had visited Tawang in 2016, according to Livemint.
Brownback visited Dharamsala in Himachal Pradesh to meet Dalai Lama and attend the 60th anniversary event honouring the Tibetan Institute for Performing Arts.
Here in #Dharamsala to share the stage with His Holiness the @DalaiLama for the 60th Anniversary event honoring the Tibetan Institute for Performing Arts. We celebrate the rich and vibrant Tibetan heritage & vow to continue to advance #religiousfreedom on their behalf. pic.twitter.com/6lFeDJyJtE
— Ambassador Sam Brownback (@IRF_Ambassador) October 28, 2019
During his visit, he tweeted, "They (Tibetans) have not only endured but defied attacks by those who sought to revise, restrict, and erase their unique heritage."
Dharamsala is the refuge of the 14th Dalai Lama, the religious leader of Tibet, who fled to India to escape Chinese persecution.
Reminded today of the rich history of the Tibetans. They are a beacon of hope for #religiousfreedom for all. They have not only endured but defied attacks by those who sought to revise, restrict, and erase their unique heritage. Today we stand in honor and celebration of them. pic.twitter.com/GdqBwRnYOp
The second India-China summit had ended on a positive note. Jinping had said he was overwhelmed by India's hospitality and said it was a memorable experience. He said that PM Modi's idea of an informal summit was a very good one.
China is yet to respond to the US officials' visits.
(With inputs from Livemint)
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redpajama_set_name: RedPajamaCommonCrawl


text:
Q: Visual Studio 2010 "Publish" does not copy Razor view files When using the built-in Publish feature of Visual Studio 2010 with a web application that includes Razor views (.cshtml or .vbhtml), the publish service does not copy the Razor view files.
This occurs both on a local "File System" publish as well as a remote publish using Web Deploy, using the November 9 Release Candidate.
Are there any known workarounds?

A: (This answer is mostly if someone finds this through google etc)
As @Ted Ballou pointed out you need to change output type to Content. This can be quite cumbersome if you, like me, have 100+ files in different subfolders.
Especially since you can't update multiple files at once if there's a folder included in the selection.
Instead of changing through the GUI, open the project file and modify the settings directly.
In YourProject.csproj change  items like:
<None Include="Views\Foo\Bar.cshtml />
to
<Content Include="Views\Foo\Bar.cshtml" />

I used the following Regular Expression to replace all files:
Search for: <None Include="(.+)\.cshtml" />
Replace with: <Content Include="$1.cshtml" />
Now Visual Studio should treat all your changed cshtml as Content on publish.

A: You need to set the build action to "Content" under properties.
Edit: You have to do this on each of the files that aren't being copied over.
Edit 2: I did some poking around, and found a forum posting over at msdn, sounds like you can edit the registry, or create a pkdef file.
http://social.msdn.microsoft.com/Forums/en/vsxprerelease/thread/c0212d15-96c4-455d-b7e1-d299c5ef384a

redpajama_set_name: RedPajamaStackExchange


Phoenix Ariz. – CBRE announced today that Steve Julius and Jesse Goldsmith, who together specialize exclusively in the sale and purchase of retail investment properties in Arizona, have been promoted to First Vice President with CBRE Capital Markets, Retail. The team will continue to focus on advising a diverse mix of private and institutional investors on their long-term real estate and investment strategies.
In December, Chase Dorsett joined the team as sales associate. Mr. Dorsett, who began his career at CBRE in 2016 as a retail researcher, is responsible for conducting market analyses, providing financial underwriting and pitching for new business.
CBRE Group, Inc. (NYSE:CBRE), a Fortune 500 and S&P 500 company headquartered in Los Angeles, is the orld's largest commercial real estate services and investment firm (based on 2017 revenue). The company has more than 80,000 employees (excluding affiliates), and serves real estate investors and occupiers through approximately 450 offices (excluding affiliates) worldwide. CBRE offers a broad range of integrated services, including facilities, transaction and project management; property management; investment management; appraisal and valuation; property leasing; strategic consulting; property sales; mortgage services and development services. Please visit our website at www.cbre.com.


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Q: How can I enable keep-alive on flask running behind uwsgi? I am running a python(3.6) with Flask. It runs behind uwsgi. I need to enable keep-alive on this app so I added --so-keepalive parameter on uwsgi command like below:
uwsgi \
  --uid uwsgi \
  --master \
  --http :8080 \
  --enable-threads \
  --so-keepalive \
  --wsgi-file api/uwsgi.py

and when inspect the request response header, keep-alive doesn't appear. It only appears on the request header. The response header is:
HTTP/1.1 200 OK
Content-Type: application/json
Content-Length: 99

I use curl to test the connection:
curl -Iv http://localhost:9301/v2/health  --next http://localhost:9301/v2/health

*   Trying ::1...
* TCP_NODELAY set
* Connected to localhost (::1) port 9301 (#0)
> HEAD /v2/health HTTP/1.1
> Host: localhost:9301
> User-Agent: curl/7.64.1
> Accept: */*
>
< HTTP/1.1 200 OK
HTTP/1.1 200 OK
< Content-Type: application/json
Content-Type: application/json
< Content-Length: 5
Content-Length: 5

<
* Connection #0 to host localhost left intact
* Found bundle for host localhost: 0x7fb4db60b7d0 [can pipeline]
* Could pipeline, but not asked to!
* Connection 0 seems to be dead!
* Closing connection 0
* Hostname localhost was found in DNS cache
*   Trying ::1...
* TCP_NODELAY set
* Connected to localhost (::1) port 9301 (#1)
> GET /v2/health HTTP/1.1
> Host: localhost:9301
> User-Agent: curl/7.64.1
> Accept: */*
>
< HTTP/1.1 200 OK
< Content-Type: application/json
< Content-Length: 5
<
"OK"
* Connection #1 to host localhost left intact
* Closing connection 1

And you can see that it creates two connections #0 and #1. It doesn't seem to use keep-alive connection on my server.
I wonder is keep-alive enabled on my application? How can I enable it?

A: you should use http11_socket parame, such as
http11-socket = 0.0.0.0:8080
add-header = Connection: Keep-Alive

please refer https://uwsgi-docs.readthedocs.io/en/latest/HTTP.html


The Activejet brand came into existence in 2002 and has been an important ingredient of our success story ever since. We are a national leader in Poland in terms of product sales and brand awareness, a fact confirmed on countless occasions by various consumer surveys. We hold BSI and TUV Rheinland certificates. Both organisations additionally monitor our manufacturing processes.
Since the very birth of Activejet as a brand, we have focused on our integrated and long-term approach to its growth and maintaining the best world-class standards of quality, innovation and advanced technology.
During the 20 years of ACTION's history we have achieved the top rank in sales on the Central and Eastern-European market, which we attribute, among other initiatives, to the constant development of the Activejet brand, based on the company's know-how and its state-of-the-art logistics facilities.
We have been present on the market since 2002, which means we have many years' experience in creating innovative solutions in the field of printer consumables.
In our operations we follow a long-term development strategy. We put emphasis on quality and broad availability of our products. We also keep expanding our portfolio by adding the most sought after models. Our products undergo regular testing and checks to make sure they will meet the requirements of even the most demanding end users.
We hold international certificates awarded by the international certification organisation BSI and the German TUV Rheinland, which additionally monitor our manufacturing processes.
We offer the best print quality – thanks to the innovative solutions our products are unique for their top quality and high performance. In the recent years Activejet has won more top ranks in quality tests on the Polish market than any other company.
Our leading market position is confirmed by independent surveys. According to IDC, the international market research, analysis and advisory firm, Activejet is the no. 1 brand in terms of the quantity of non-OEM consumables sold, both in the segment of inkjet cartridges as well as in that of laser toner cartridges.
Activejet: The e-Quality of 2017!


I've been spending a lot of time on the area golf courses in preparation of the upcoming Southport-Oak Island Area Golf Classic taking place early next month. It's being held at the Oak Island Golf Club at Caswell Beach on May 4 and I'm planning on entering this year. This will be a new experience for me because I generally just play golf with friends and family on all the courses in our area and haven't entered any tournaments.
There are more than 30 golf courses in Brunswick County available for me to practice on and the truth is, I've gotten pretty good. I feel rather confident going into my first golf classic, but I can't let it get to my head. I've heard it said that the toughest part of playing golf is right between your ears. Based on my own experience, I've found that to be true.
With all of these courses to play you'd think I would wait for a tournament closer to home. The Southport-Oak Island area actually has seven of the best courses in Brunswick County. Some of my favorites are the two George Cobb traditional courses at Bald Head Island Golf Club and Oak Island Golf Club. I found them both to be challenging enough as to improve my game overall.
Some of the other courses I've played in that area and thoroughly enjoyed are The Lakes Country Club in Boiling Spring Lakes and the three courses in St. James Plantation — The Founders, The Players, and The Members. If you ever get the chance to play the Fred Couples designed Carolina National in Winding River Plantation near Sunset Harbor don't pass it up! It's a winning course with challenges that will make you a better player, just like it did me!


text:
Mendiswe Mzamane is set to take legal action against ENSafrica after the law firm allegedly agreed to represent her company while it sat on the panel of the enterprise she was suing. Photo: File
ENSafrica set to be sued for accepting a case knowing it represents both parties
By Aishah Cassiem Jul 1, 2021
A BUSINESSWOMAN is set to take legal action against one of Africa's biggest law firms, for allegedly agreeing to represent her company, taking her money and confidential information, and thereafter backing out while knowing it was on the panel of the Small Enterprise Finance Agency (Sefa) which was a respondent in the case.
Mendiswe Mzamane's small black-owned business, Razoscan, was one of many approved loans for businesses from historically disadvantaged communities, but alleged corruption from Sefa left her with a major company loss when the entity allegedly gave her R3 million to a Greek national in 2015.
Mzamane said she was searching for trustworthy firms to assist her in retrieving her money from Sefa when she finally approached Edward Nathan Sonnenbergs (ENSafrica) in December 2018 to represent her.
ENSafrica allegedly also failed to inform her that it was part of a group of 70 law firms on Sefa's panel, until earlier this year after two other firms declined to represent her due to being on the same panel.
She said the sad part was that while she was in financial difficulties, she had to go through a fund-raising exercise to pay the firm R50 000.
How Sefa helped Greek national fraudulently retrieve R2m from black business
Private Security Sector Provident Fund rot exposed
1 774 service providers under investigation for PPE corruption spree, SIU report reveals
In a January email sent to Mzamani by ENSafrica's George van Niekerk, the latter argued that the matter had a long and tortuous history.
"Clearly there has been a complete breakdown in the relationship. It does not appear to me that it can be mended, and in these circumstances, I think your interests will be better served by appointing other attorneys. Having come to this view, we will refund your deposit of R50 000," he said.
Even though ENSafrica has since reimbursed Mzamane, she said she was concerned that the firm could have played her in favour of Sefa and was sitting with her confidential information which could ruin her case in the Pretoria high court.
ENSafrica chief operating officer Lee Mendelsohn said: "You will no doubt appreciate that much of the detail which you are seeking from us is confidential and, as such, we are not permitted to share it with anybody. You are of course at liberty to request it directly from the persons/entities concerned, as you appear to have done.
"We can, however, confirm that we were on record for Mzamane in the matter to which you refer for some time, after which we ceased to act for her, for reasons entirely unrelated to those referred to by you.
"We can confirm that we are not and were not at any time relevant to Mzamane's matter, on the legal panel of Sefa. We would caution you not to be drawn into publishing what are clearly false allegations," he said.
However, Mzamane said the firm was lying, as they were in fact representing her at the same time as being on Sefa's panel, as she made contact with ENSafrica only in December 2018, and finally made payment for services last year.
"They should have clearly known that they were on Sefa's panel at that time before taking on my matter, as several other firms who I approached for help recently immediately declined me due to being on the panel. So, why did they choose to not warn me, like the others?" she asked.
ENSafrica was listed as the 70th service provider, one of the chosen legal entities on the panel of external legal attorneys for Sefa, for a period of three years, as published in 2018.
Mzamane said she was laying criminal charges against Sefa and ENSafrica over the matter. She had written to the Legal Practice Council (LPC) and Pretoria high court Judge President Dunstan Mlambo.
LPC communication manager Sthembiso Mnisi said Mzamane was within her rights to report the legal practitioners for misconduct.
Sefa did not respond to the questions pertaining to the matter after several calls and emails, and while ENSafrica had responded, at the time of publication they did not respond to questions around the allegations of a possible irregular bidding process.


Reading Women travel up to the midlands on Thursday evening to face fourth placed Birmingham City in a televised Women's Super League 1 clash. The 19:45 kick-off at Solihull Moors FC will be live on BT Sport 2.
The game will see the Royals looking for a first league victory of the season, with Reading having picked up points on the road earlier in the campaign. Kelly Chambers' side earned a 1-1 draw at Sunderland and were held by Notts County in a 2-2 thriller at Meadow Lane.
Last time out on the 2nd of May, Reading drew 1-1 with the Black Cats at home, coming from a goal down at Adams Park to earn a point. Helen Ward scored from the spot for the Royals after Sunderland's Megan Beer handled the ball inside the area, giving Reading a 74th minute equaliser.
A win for Reading could see them lifted as high as 5th in the WSL1 table, going ahead of the likes of Liverpool, Notts County and Sunderland.
In recent weeks Birmingham have been in good form, and are unbeaten in three in the league, having earned a 1-0 win away at Notts County in their last WSL1 outing. Defender Emily Westwood headed home the only goal of the game, as Birmingham came away with a deserved victory, setting up what should be an entertaining clash with the Royals tomorrow evening.
For any fans looking to follow the Royals up to Solihull on Thursday evening, click here for ticket information.


text:
Birth Name: Parker Posey
Born: November 08, 1968	in Baltimore, Maryland, USA
Parker Posey is an American film and television actress, best known for her supporting roles in many independent feature films such as "Party Girl", "Kicking and Screaming", and "The House of Yes", which led to her nickname "Queen of the Indies".
Adam & Steve (2005)
Event, The (2003)
Basquiat (1996)
Drama, History
Doom Generation, The (1995)
Action, Comedy, Crime, Drama


text:
When and where John Digweed was born?
January 1, 19671967-01-01
Log in and Edit
Biography (wiki)
Thomas John Digweed (born 1 January 1967) is a British DJ, record producer and actor. DJ Magazine voted him World No 1 DJ in 2001. As well as achieving success as a solo act, he has collaborated with Sasha as Sasha & John Digweed, and with Nick Muir as Bedrock.
Digweed began DJing at the age of 15, and made a name for himself in his home town of Hastings, where he put on successful club nights, the most famous of which were his successful raves on Hastings Pier, where the likes of Carl Cox and The Prodigy performed. His breakthrough came in 1993, when he sent a mixtape demo to Geoff Oakes, founder of the Renaissance nightclub in Mansfield, who played it to fellow DJ Alexander Coe (aka Sasha). The two DJs struck up a long-term friendship and working relationship, despite Sasha twice failing to turn up for gigs that Digweed had booked him for in Hastings.
In partnership with Sasha, Digweed is known for promoting progressive house and notable for producing the first commercial compilation for a nightclub, when they released their 1994 compilation of mixes from Renaissance entitled Renaissance: The Mix Collection. Until then, mixtapes from clubs had only been circulated by DJs on an amateur basis. The Renaissance CD was the first time that a compilation CD had been planned strategically for marketing, from artwork to promotion. The two DJs famously followed this up with their Northern Exposure compilations and those on Global Underground.
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How tall and how much weigh John Digweed?
5 ft 10 in / 177 cm
165 lb / 75 kg
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text:
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7 DPO Symptoms: What to Expect
By Inito
Verified By Add user
7 DPO, or 7 Days Post Ovulation, is exactly what it sounds like – the seventh day after ovulation (the release of a mature egg from the ovary). If you are trying to conceive and have had intercourse during your fertile days, you may be waiting for a sign that you are pregnant. But what exactly happens at 7 DPO? Read on for all the details about what to expect.
What happens at 7 DPO?
Throughout the entire menstrual cycle, there are lots and lots of hormonal changes that occur. All of these changes work to get the body ready for a potential pregnancy. At 7 days post ovulation, a lot of these very important events have already happened.
Ovulation is the release of a mature egg from the ovary. The ovary releases the egg into the abdomen very close to the fallopian tube. It then begins to travel down the fallopian tube towards the uterus.
Fertilization is when a single sperm cell joins with the mature egg after ovulation. This usually occurs in the fallopian tube within the first 24 hours after ovulation.
The fertilized egg, now called a zygote, travels down toward the uterus. The zygote divides in half over and over again until it is a ball of hundreds of cells known as a blastocyst.
Implantation of the fertilized egg into the uterine wall may or may not have occurred. This process usually happens between day 6 and day 10 after ovulation.
If implantation has already occurred, the cells in the little embryo are busy dividing and growing into a baby. They also develop into the other structures needed for pregnancy.
If not; don't worry! Implantation occurs most frequently between days 5 and 7 after ovulation.
What are possible 7 DPO Symptoms?
If implantation has already occurred, some women do experience early pregnancy symptoms. Here are some of the most common 7 DPO symptoms that women experience:
Cramping: Some women experience mild abdominal or pelvic cramping. This is caused by the implantation of the fertilized egg into the uterine wall. Many women report that they are similar to menstrual cramps, but are often less intense or painful.
Spotting: Implantation spotting is another possible symptom that women can experience at 7 DPO. At implantation, small blood vessels can rupture, which can cause light vaginal bleeding or spotting. This spotting is usually lighter than a period and light brown to red or pink in color. Implantation bleeding also tends to be shorter than a period and lasts only a day or two.
Mood swings: Newly pregnant women are often subject to mood swings: happy one minute, crying the next, and angry the next. Changing hormone levels are responsible for this lovely symptom.
Breast tenderness: One of the most common early pregnancy signs is breast enlargement and tenderness. Nipple soreness and sensitivity is also a common symptom in early pregnancy. Both are caused by rising progesterone levels.
Increased urination: Even though it's way too early for a growing babe to push on the bladder and cause more frequent bathroom trips, increased urination is still common in early pregnancy. This is most often thanks to, you guessed it again, hormonal changes.
Headaches: Changing hormone levels can lead to headaches, and in some women, even dizziness or lightheadedness.
Food cravings or aversions: That old wives' tale about craving ice cream and pickles may not be too far off. Many women report craving strange foods during their pregnancy. Other women also mention having strong food aversions to certain foods or food smells.
Nausea/vomiting: Nausea and vomiting in early pregnancy is known as morning sickness, but in reality it can be all-day sickness. Many women have said that they realized they were pregnant only because of persistent nausea/vomiting.
Fatigue: Early pregnancy fatigue is nothing to joke about. It can be debilitating, and for some women, starts before their missed period.
Increased sense of smell: Early hormone changes can make a pregnant woman extremely sensitive to smells, even odors that didn't bother them before. This often accompanies food aversions, as cooking smells can be especially triggering.
All of these symptoms are the result of changing progesterone levels. Here's the thing though; rising progesterone levels are also present normally in the days leading up to your period. So, a lot of these symptoms can occur with early pregnancy or with plain-old, regular PMS.
How can you tell the difference? Unfortunately, there's no real reliable way to know whether your symptoms are from a pregnancy or just your body getting ready for your period.
Are pregnancy tests reliable at 7 DPO?
It depends on a ton of different factors, though 7DPO is quite early for a test to give a positive result. The primary factor to keep in mind is whether pregnancy has actually occurred yet.
If implantation has not happened, which if you remember, occurs most often between days 5 and 7, the pregnancy test will not be positive.
Another factor is the test and its sensitivity. Home pregnancy tests look for the pregnancy hormone called human chorionic gonadotropin (hCG). Some early pregnancy tests can detect very low levels of this hormone. Other tests need a higher amount of hCG to register as a positive result. If your hormone levels aren't high enough, the test won't give you a positive result, even if you are pregnant.
When is the best time to take a pregnancy test?
The best and most reliable time to take a pregnancy test is with a missed period. HCG hormone levels will be most likely to be high enough to be detected by most pregnancy tests.
That said, it's pretty hard for many women to wait the whole two weeks without taking a test. In this case, the answer really depends on your test. Is it one specifically designed to be used a certain number of days before a missed period? If so, go ahead! But just be aware that you could still get a false negative if your hormone levels aren't high enough to register as a positive.
What if I get a negative pregnancy test at 7 DPO?
Don't panic! There's still a good chance that it is showing a negative result only because the hormone levels aren't high enough. Wait a couple of days and try taking the test again. Try to stay busy and remind yourself that 7 DPO symptoms and pregnancy testing aren't reliable just yet. There is still hope!
7 DPO is also known as 7 days past ovulation.
Implantation occurs 5-7 days past ovulation.
Some women experience early pregnancy symptoms at 7 DPO, like cramping, bleeding, headache, mood swings, breast/nipple tenderness, or nausea and vomiting.
It is unlikely that early pregnancy tests will be positive at 7 DPO, but some very sensitive tests may register a positive result.
If you get a negative pregnancy test at 7 DPO, retest in a few days.
Use the Inito Fertility Monitor to keep track of your progesterone levels post ovulation.
Article Source:
Early pregnancy symptoms by days past ovulation (DPO). Retrieved from https://www.medicalnewstoday.com/articles/322723
Pregnancy: Am I pregnant? Retrieved from https://my.clevelandclinic.org/health/articles/9709-pregnancy-am-i-pregnant
Can You Have a Period and Be Pregnant?
How Long After Miscarriage Do You Get Your Period?
Can You Ovulate More Than Once in a Month?
What to know if you think you've bruised your cervix
How To Know If You Are Ovulating Late? A Simple Guide For Women
LH Levels & Surges: What Does a 'Normal' LH Level Look Like?
Estrogen Dominance and How Does it Affect the Body?
Does Sex Delay Your Period?
Using Ovulation Tests with PCOS: Can You Trust the Accuracy?
Ovulation Symptoms: How Do You Really Know?
Can You Have a Miscarriage from Stress?
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The City of Durango is now offering vendors the option to receive payment by ACH (Automatic Clearing House). Using this method of payment, funds will be received electronically within in two business days.
If a vendor chooses this method of payment, after an electronic transfer is made, the vendor will receive an email confirmation showing the invoice number and the amount the City is paying.
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Medical Dictionaries in the 21st Century
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Walter Mitty syndrome
Home » Media Medicine » Literary figures, real and fictional » Walter Mitty syndrome
Walter Mitty syndromeJoe Segen2016-12-07T01:42:05+00:00
Walter Mitty
Walter Mitty syndrome is a condition of unknown frequency or magnitude in which a person indulgences himself in daydreams that he–or to be fair, she–has a heroic persona that he or she lacks in real life.
Comment The syndrome obtains its name from James Thurber's short story, The Secret Life of Walter Mitty, first published in The New Yorker (1939), about a milquetoast of a man who is browbeaten into quiet submission by an overbearing wife. Walter imagines in succession that he is a pilot of a Navy flying boat in a storm; a surgeon performing a one-of-a-kind procedure; a deadly assassin, and a Royal Air Force pilot volunteering for a suicide mission to bomb an ammunition dump. At the story's end, Mitty imagines himself facing a firing squad, to quote Thurber, …inscrutable to the last. Walter Mitty syndrome is a commonly used vehicle in fiction. Hollywood took a crack at it in 1949 with Danny Kaye (see movie poster) and in 2013 with Ben Stiller.
References http://www.esquire.com/blogs/culture/real-secret-life-walter-mitty
http://en.wikipedia.org/wiki/The_Secret_Life_of_Walter_Mitty
Copyright © 2016 - 2018 Joe Segen, MD


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import sys
import superscp_tool
import node_data_manager
from pathmanager import node
from pathmanager import paths

def usage(argv):
    show="usage:\n\
            insertLinks {fname}: read link data from fname file and insert into system\n\
            superscp {source_file/dir}  {target_ip}  {target_dir}: scp file or dir to target host\n\
            "
    print(show)

if __name__ == '__main__':
    node.restore()
    paths.restore()
    cmds = {
            'insertLinks': node_data_manager.insert_data,
            'superscp': superscp_tool.superscp
    }

    if len(sys.argv) < 2:
        usage(None)
        sys.exit(1)
    cmds.get(sys.argv[1], usage)(sys.argv)

redpajama_set_name: RedPajamaGithub


From the Central Laboratory of the Netherlands Red Cross Blood Transfusion Service and Laboratory for Experimental and Clinical Immunology, University of Amsterdam, Amsterdam; and Academic Medical Centre, Amsterdam, The Netherlands.
We analyzed a genetic polymorphism of Fcγ receptor IIIa (CD16) that is present on position 158 (Phe or Val) in the membrane-proximal, IgG-binding domain. With a polymerase chain reaction–based allele-specific restriction analysis assay we genotyped 87 donors and found gene frequencies of 0.57 and 0.43 for FcγRIIIA-158F and −158V, respectively. A clear linkage was observed between the FcγRIIIA-158F and −48L genotypes on the one hand and the FcγRIIIA-158V and −48H or −48R genotypes on the other hand (χ2 test; P < .001). To determine the functional consequences of this FcγRIIIa-158V/F polymorphism, we performed IgG binding experiments with natural killer (NK) cells from genotyped donors. All donors were also typed for the recently described triallelic FcγRIIIa-48L/R/H polymorphism. NK cells were treated with lactic acid to remove cell-associated IgG. FcγRIIIaNK158F bound significantly less IgG1, IgG3, and IgG4 than did FcγRIIIaNK-158V, irrespective of the FcγRIIIa-48 phenotype. Moreover, freshly isolated NK cells from FcγRIIIa-158VV individuals carried significantly more cytophilic IgG than did NK cells from FcγRIIIa-158FF individuals. In addition, CD16 monoclonal antibody (MoAb) MEM154 bound more strongly to FcγRIIIa-158V, compared with -158F, again independently of the FcγRIIIa-48 phenotype. The binding of MoAb B73.1 was not influenced by the FcγRIIIa-158V/F polymorphism, but proved to depend solely on the amino acid present at position 48 of FcγRIIIa. In conclusion, the previously reported differences in IgG binding among the three FcγRIIIa-48L/R/H isoforms are a consequence of the linked, biallelic FcγRIIIa-158V/F polymorphism at amino-acid position 158.
Previously, Ravetch and Perussia described a polymorphism in the membrane-proximal domain of FcγRIIIa.13 A nucleotide substitution at position 559 of FcγRIIIA predicts either a valine or a phenylalanine at amino-acid position 158 of FcγRIIIa. Because the IgG binding site is most probably located in this part of FcγRIIIa,14 ,15 we determined the gene frequency and functional consequences of this polymorphism in the context of the recently described FcγRIIIa-48L/R/H polymorphism. As expected, a clear although incomplete linkage was observed between the two polymorphisms. Moreover, we found that the previously described differences in binding between the FcγRIIIa-48 isoforms of IgG and of some of the CD16 monoclonal antibodies (MoAbs) are attributable to the FcγRIIIa-158 phenotype.
MoAbs.Anti-pan FcγRIII (CD16) MoAbs used were CLBFcRgran1 (mIgG2a) and MEM154 (mIgG1). B73.1 (mIgG1) reacts with NA1-FcγRIIIb and with FcγRIIIa,16 and was kindly provided by Dr B. Perussia (Thomas Jefferson University, Philadelphia, PA). MEM154 was obtained through the 5th Leukocyte Typing Workshop. Phycoerythrin (PE)-labeled Leu19 (CD56; mIgG1) was purchased from Becton Dickinson (San Jose, CA). Fluorescein isothiocyanate (FITC)-conjugated goat–antimouse Ig and irrelevant control MoAbs of the IgG1 and IgG2a subclasses were from the Central Laboratory of the Netherlands Red Cross Blood Transfusion Service (CLB), Amsterdam, The Netherlands.
Isolation of cells.Fresh, EDTA-anticoagulated blood from healthy volunteers was diluted with two volumes of phosphate-buffered saline (PBS) and was centrifuged over a Ficoll gradient (Pharmacia Fine Chemicals AB, Uppsala, Sweden) with a specific gravity of 1.076 g/mL. Peripheral blood mononuclear cells (PBMC) were obtained from the interphase and were washed twice with PBS, containing 0.2% (wt/vol) bovine serum albumin (BSA).
Flow cytometry.PBMC were incubated with CD16 MoAbs for 25 minutes at room temperature. The cells were washed with PBS/BSA, and were incubated with FITC-labeled goat–antimouse-Ig for 25 minutes at room temperature. Free F(ab′ )2 regions of the conjugate were blocked with a mixture of irrelevant mIgG1 and mIgG2a. Thereafter, the cells were incubated with PE-labeled CD56. Only CD56+ lymphocytes were analyzed in a FACScan flowcytometer (Becton Dickinson).
FcγRIIIA-48L/R/H genotyping.Genotyping for the FcγRIIIA-48L/R/H polymorphism was performed as previously described,17 with a polymerase chain reaction (PCR)-based allele-specific restriction analysis assay. Briefly, a 91-bp FcγRIIIA-specific fragment containing the polymorphic site was amplified from genomic DNA and digested with Mnl I. Digested fragments were electrophoresed in 10% acryl amide gels, stained with ethidium bromide, and visualized with UV light. Homozygous FcγRIIIA-48LL individuals showed 40-bp, 34-bp, and 17-bp bands, whereas PCR fragments of individuals carrying no or only one FcγRIIIA-48L allele showed a 51-bp band. The genotype of these latter individuals was determined by direct sequencing of the amplified fragments, using one of the PCR primers, end-labeled with 32P (Amersham International, Buckinghamshire, UK), with the Life Technologies cycle sequencing kit, following the instructions of the manufacturer (Life Technologies, Gaithersburg, MD).
FcγRIIIA-158V/F genotyping.Genotyping of the FcγRIIIA-158V/F polymorphism was performed by means of a (nested) PCR-based allele-specific restriction analysis assay. Two FcγRIIIA gene-specific primers (sense A013: 5′-ATA TTT ACA GAA TGG CAC AGG-3′; antisense A012: 5′-GAC TTG GTA CCC AGG TTG AA-3′; italic characters denote mismatches that were introduced to increase specificity) were used to amplify a 1.2-kb fragment containing the polymorphic site. This PCR assay was performed with 5 ng of genomic DNA, 150 ng of each primer, 200 μmol/L of each dNTP, and 2 U of Taq DNA polymerase (Promega, Madison, WI), diluted in a buffer recommended by the manufacturer in a total volume of 50 μL in a Perkin Elmer Cetus cycler (Norwalk, CT). The first PCR cycle consisted of 10 minutes denaturation at 95°C, 11/2 minute primer annealing at 56°C, and 11/2 minute extension at 72°C. This was followed by 35 cycles in which the denaturing time was decreased to 1 minute. The last cycle was followed by 8 minutes at 72°C to complete extension. The sense primer in the second PCR contained a mismatch that created an NlaIII restriction site only in FcγRIIIA-158V-encoding DNA (A014: 5′-atc aga ttc gAT CCT ACT TCT GCA GGG GGC AT-3′; uppercase characters denote annealing nucleotides, lowercase characters denote nonannealing nucleotides), the antisense primer was chosen just 5′ of the fourth intron (A016: 5′-acg tgc tga gCT TGA GTG ATG GTG ATG TTC AC-3′ ). This "nested" PCR was performed with 1 μL of the amplified fragment, 150 ng of each primer, 200 μmol/L of each dNTP, and 2 U of Taq DNA polymerase, diluted in the recommended buffer. The first cycle consisted of 5 minutes' denaturing at 95°C, 1 minute primer annealing at 64°C, and 1 minute extension at 72°C. This was followed by 35 cycles in which the denaturing time was 1 minute. The last cycle was followed by 91/2 minutes at 72°C to complete extension. The 94-bp fragment was digested with NlaIII, and digested fragments were electrophoresed in 10% polyacrylamide gels, stained with ethidium bromide, and visualized with UV light. Cycle sequencing of first-round fragments to check for specificity was performed with 32P end-labeled primer A016 with the Life Technologies cycle sequencing kit. Genomic DNA of individuals whose FcγRIIIa encoding cDNA sequence was known were used to optimize the PCR assay.
IgG-binding experiments.Quantification of IgG binding to natural killer (NK) cells of genotyped donors was performed as previously described.17 In short, mononuclear cells were pretreated with 0.1% (wt/vol) lactic acid (pH 3.9) to remove NK-cell–associated IgG. This treatment did not alter FcγRIIIa expression as measured with CD16 MoAb CLBFcRgran1 (not shown). The cells were incubated with saturating amounts of human IgG subclasses purified from sera of patients suffering from multiple myeloma. The antibodies were at least partially aggregated, because binding to PMN was observed with the IgG1 and IgG3 preparations (not shown). After washing, bound IgG was detected by FITC-labeled F(ab′ )2 fragments of goat–antihuman-IgG (Kallestad, South Austin, TX), and NK cells were identified with PE-labeled CD56. Only CD56+ lymphocytes were analyzed in a FACScan flowcytometer.
Statistical analysis.The data were analyzed with the Student's t-test and the χ2-test. Data with different standard deviations (SDs) were compared with the Welch's approximate t-test. P values below .05 were considered significant.
FcγRIIIA-158V/F genotyping.An FcγRIIIA-derived fragment containing the polymorphic site was amplified from genomic DNA with two FcγRIIIA gene-specific primers. Subsequently, a nested PCR was performed in which an NlaIII restriction site was created only in the FcγRIIIA-158V allele. Figure 1 shows digestion of the 94-bp PCR fragment with NlaIII. In lanes 1 to 3, PCR fragments from homozygous FcγRIIIA-158FF donors are not digested by NlaIII. In lanes 4 to 6, three bands of 94 bp, 61 bp, and 33 bp are visible, indicating the FcγRIIIA-158VF heterozygosity of these individuals. Although the fragments in lanes 7 to 9 were from homozygous FcγRIIIA-158VV donors, a 94-bp band of low intensity remained, which was not removed by longer digestion, higher enzyme concentrations, or use of isoschizomer Nsp I. The 94-bp band in these donors was not a result of amplification of FcγRIIIB fragments due to unspecificity of the first-round PCR, because the FcγRIIIB gene carries a G at nucleotide position 559, which results in digestion by NlaIII. Direct sequencing of several first-round PCR products confirmed the FcγRIIIA gene specificity of the assay and the FcγRIIIA-158 genotype of the donors. Genotyping of 87 healthy white individuals yielded gene frequencies of 0.57 and 0.43 for FcγRIIIA-158F and −158V, respectively.
NlaIII restriction analysis of the 94-bp FcγRIIIA-specific fragment, containing the polymorphic nucleotide 559. A 1.2-kb FcγRIIIA-specific fragment was amplified from genomic DNA, followed by a nested PCR. The sense primer of this nested PCR contained a mismatch that introduced a NlaIII restriction site only in the FcγRIIIA-158V (559G) allele. Homozygous FcγRIIIA-158FF fragments were not digested (lanes 1 through 3). Three bands (94 bp, 61 bp, and 33 bp) were visible in heterozygous individuals, whereas homozygous FcγRIIIA-158VV fragments were maximally digested (lanes 7 through 9). A 92-bp fragment of low intensity remained in homozygous 559G fragments (lanes 7 through 9).
Table 1 displays the correlation between the FcγRIIIa-48 and the FcγRIIIa-158 phenotypes. A clear linkage was observed between the FcγRIIIA-158V/F and the FcγRIIIA-48L/R/H polymorphisms (χ2-test, P < .001). All FcγRIIIA-158FF individuals were homozygous FcγRIIIA-48LL, whereas all donors with heterozygous FcγRIIIA-48LR or −48LH genotypes carried at least one FcγRIII-158V allele.
Binding of CD16 MoAbs to NK cells of genotyped donors.To determine the influence of the FcγRIIIa-158V/F and -48L/R/H polymorphisms on the binding of a panel of CD16 MoAbs, we investigated binding patterns by NK cells of genotyped donors (Table 2). The binding of MoAb CLBFcRgran1 was not significantly different among NK cells from all donors. In contrast, FcγRIIIa-158VF-positive NK cells from donors homozygous positive for FcγRIIIa-48L bound more MEM154 than did NK cells of FcγRIIIa-158FF-positive donors (Welch's approximate t-test, P =.01). In turn, FcγRIIIa-158VF NK cells from donors who had only one FcγRIIIA-48L allele bound less MEM154 than did FcγRIIIa-158VV NK cells (P = .04).
Comparison of NK cells of FcγRIIIa-158VF phenotyped donors who were either homozygous FcγRIIIa-48LL, or heterozygous -48LR or -48LH showed different binding patterns with MoAb B73.1. NK cells positive for the FcγRIIIa-48R or -48H isoforms showed reduced binding of B73.1 compared with FcγRIII-48LL homozygous NK cells (P = .05). Binding of MoAb MEM154 was equal among these donors. Three FcγRIIIa-158VV individuals who were either homozygous FcγRIIIA-48RR or −48HH were tested. Binding of MEM154 to cells of these donors was equal compared to the binding to NK cells from FcγRIIIa-158VV individuals with a heterozygous FcγRIIIa-48 phenotype, whereas the binding of B73.1 was diminished (Table 2).
Binding of IgG subclasses by FcγRIIIaNK-158 isoforms in the context of FcγRIIIaNK-48 phenotype.To determine the functional consequences of the FcγRIIIa-158V/F polymorphism, we compared the IgG binding capacity of NK cells from genotyped donors. We studied the differences in IgG binding between individuals who had different FcγRIIIA-158V/F genotypes, but were identical regarding the FcγRIIIA-48L/R/H genotype. Preincubation of PBMC with F(ab′ ) fragments of CD16 MoAb CLBFcRgran1 reduced the binding of IgG to less than 10% of control values, indicating that the interaction was FcγRIIIa-mediated (data not shown). As shown in Table 3, lactic acid-treated homozygous FcγRIIIa-48LL NK cells from individuals heterozygous at position 158 of FcγRIIIa bound more IgG3 than did NK cells from FcγRIIIa-158FF phenotyped donors (P = .02). Although a trend was observed, the difference in binding of IgG1 was not statistically significant. In one single experiment, NK cells from the one available donor who was homozygous FcγRIIIA-48LL as well as −158VV bound more IgG3 than did FcγRIIIA-8LL-matched homozygous FcγRIIIA-158FF or heterozygous donors, without clear differences in binding of IgG1 (data not shown). In individuals who were heterozygous for the FcγRIIIa-48L/R/H polymorphism, FcγRIIIa-158VV-positive NK cells bound more IgG1 compared with FcγRIIIa-158VF-positive NK cells (Table 3; Welch's approximate t-test, P = .03). For these donors, the differences in binding of IgG3 were not statistically significant, although a trend was observed. When we determined the levels of NK-cell–associated IgG of freshly isolated NK cells, we observed that FcγRIIIa-158FF-positive cells carried less IgG than did FcγRIII-158VV-positive cells. Comparing NK cells from donors of the same FcγRIIIa-48L/R/H phenotype, we observed a trend toward higher levels of cytophilic IgG bound by FcγRIIIa-158VF and -158VV-positive cells, as compared with FcγRIIIa-158FF-positive cells (Table 3). The levels of NK-cell–associated IgG of FcγRIIIa-48LL and -158VF-positive NK cells did not significantly differ from that of FcγRIIIa-48LR or -48LH NK cells of the same -158VF phenotype.
To exclude any effect of the triallelic FcγRIIIa-48L/R/H polymorphism on IgG binding, we compared FcγRIIIa-48LLpositive NK cells with FcγRIIIa-48LR-or -48LH-positive NK cells from donors who were all heterozygous FcγRIIIa-158VF. As shown in Table 3, no statistically significant differences were observed in either the amount of NK-cell–associated IgG or in the binding of IgG subclasses to lactic acid–treated NK cells. Therefore, we depicted the results of IgG-binding experiments, comparing FcγRIIIa-158FF NK-cells with FcγRIIIa-158VV NK cells, disregarding the FcγRIIIa-48 phenotype (Fig 2). Significant differences in levels of IgG1 (P = .007), IgG3 (.005), IgG4 (.02), and cytophilic IgG (.004) were observed.
FcγRIIIaNK-158V binds more IgG than does FcγRIIIaNK-158F. IgG binding by NK cells from individuals either homozygous FcγRIIIA-158FF (▪) or homozygous FcγRIIIA-158VV (□) was compared, irrespective of the FcγRIIIa-48L/R/H genotype. At least three different donors of each genotype were tested. The level of cytophilic IgG and the binding of IgG1, IgG3, and IgG4 was significantly higher in NK cell from FcγRIIIA-158VV individuals (P < .05 in all cases).
Recently we identified a triallelic polymorphism in the membrane-distal Ig-like domain of FcγRIIIa, in which a leucine, an arginine, or a histidine can be present at amino acid position 48.17 In the present report, we functionally characterized a previously described genetic polymorphism of FcγRIIIA, encoding either a phenylalanine (F ) or a valine (V) at amino acid position 158 in the membrane-proximal Ig-like loop of FcγRIIIa.13 We determined that the gene frequencies for FcγRIIIA-158F and FcγRIIIA-158V were 0.57 and 0.43, respectively. The FcγRIIIA-158F genotype was shown to be clearly linked to the FcγRIIIA-48L genotype, whereas the FcγRIIIA-158V was found to be linked to FcγRIIIA-48R and −48H. A linkage between allotypes of the FcγRIIIA-158V/F and the FcγRIIIA-48L/R/H polymorphisms was expected because the two polymorphisms are located within the same gene.
The membrane-proximal domain, carrying the FcγRIIIa-158V/F polymorphism, is generally accepted to contain the IgG-binding site in FcγRs, and experiments with mutants of FcγRIIIb showed that the membrane-proximal loop is essential for IgG binding in FcγRIIIb.14 ,15 To study the functional consequences of the FcγRIIIa-158V/F polymorphism in the context of the FcγRIIIa-48L/R/H polymorphism, we performed IgG binding experiments with NK cells from genotyped donors. NK cells from homozygous FcγRIIIa-158VV-positive individuals bound more IgG1 and IgG3 than did FcγRIIIa-158FF-positive NK cells, irrespective of the amino acid present on position 48 of the receptor. NK cells of FcγRIIIa-158VF heterozygous donors showed intermediate levels of IgG binding, indicating a gene-dosis effect. These data indicate that the donor-dependent differences in IgG binding of FcγRIIIa isoforms are attributable to the FcγRIIIa-158 polymorphism and not to the FcγRIIIa-48L/R/H polymorphism, as we previously suggested.17 Due to the linkage between the two FcγRIIIA polymorphisms, the FcγRIIIa-48LL-positive donors described in our previous work were all homozygous FcγRIIIa-158FF and therefore their NK cells showed low IgG binding. In contrast, the tested FcγRIIIa-48LR or -48LH-positive donors all carried one or two FcγRIIIa-158V alleles and therefore bound high levels of IgG.
Vance et al20 described a donor-dependent difference in binding of CD16 MoAb 3G8 and monomeric IgG to NK cells. Although we did not observe clear differences in 3G8 binding among our donors (not shown), our IgG binding experiments suggest that the polymorphism described by these investigators might be the result of different FcγRIIIa-158V/F phenotypes.
The clinical consequences of our findings remain to be established. A higher affinity for IgG could result in higher clearance of immune complexes in patients suffering from (auto)immune disease. On the other hand, a higher amount of cytophilic IgG might imply a decreased availability of FcγRIIIa and, thus, obstruction of receptor-immune complex interaction. Recently we23 and others18 separately described children with a homozygous FcγRIIIA-48HH genotype suffering from recurrent viral infections. We genotyped the two unrelated patients from the former study and found that they were both homozygous FcγRIIIA-158VV. Previous work has suggested that cytophilic IgG on NK cells has inhibitory effects on natural cytotoxicity.24 ,25 It is tempting to speculate that in the described pediatric patients, NK cells are loaded with a high amount of FcγRIIIa-158V-bound IgG, thereby hampering a proper antiviral response.
We thank Dr E. De Vries (Department of Pediatrics of the University Hospital Leiden, Leiden, The Netherlands) for providing the patient samples.
Supported by Grant No. 900-512-092 from the Netherlands Organization for Scientific Research (NWO).
Address reprint requests to Masja de Haas, PhD, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands.
. Fcγ receptors of phagocytes. J Lab Clin Med 1995;126:330.
. Role of neutrophil FcγRII (CD32) and FcγRIIIb (CD16) polymorphic forms in phagocytosis of human IgG1- and IgG3-opsonized bacteria and erythrocytes. Immunology 1994;83:624.
. Fcγ receptor III on human neutrophils. Allelic variants have functionally distinct capacities. J Clin Invest 1990;85:1287.
. Allelic polymorphisms of human Fcγ receptor IIA and Fcγ receptor IIIB. Independent mechanisms for differences in human phagocyte function. J Clin Invest 1992;89:1274.
. Fcγ receptor IIIb enhances Fcγ receptor IIa function in an oxidant dependent and allele-sensitive manner. J Clin Invest 1995;95:2877.
. On the interaction of IgG subclasses with the low-affinity FcγRIIa (CD32) on human monocytes, neutrophils and platelets. J Clin Invest 1992;90:1537.
. Fcγ receptor IIa (CD32) heterogeneity in patients with recurrent bacterial respiratory tract infections. J Infect Dis 1994;170:854.
. Fcγ Receptor IIa (CD32) polymorphism in fulminant meningococcal septic shock in children. J Infect Dis 1994;170:848.
. Single amino acid mutation of Fc receptor is associated with the development of heparin-induced thrombocytopenia. Br J Haematol 1995;91:761.
. FcγRIIa (CD32): A potential marker defining susceptibility to localized juvenile periodontitis. J Periodontol 1996;67:323.
. Skewed distribution of IgG Fc recptor IIa (CD32) polymorphism is associated with renal disease in systemic lupus erythematosus patients. Arthritis Rheum 1995;39:1832.
. FcγRIIA alleles are heritable risk factors for Lupus nephritis in African-Americans. J Clin Invest 1996;97:1348.
. Alternative membrane forms of FcγRIII (CD16) on human NK cells and neutrophils: Cell-type specific expression of two genes which differ in single nucleotide substitutions. J Exp Med 1989;170:481.
. Membrane-proximal Ig-like domain of FcγRIII (CD16) contains residues critical for ligand binding. J Immunol 1994;152:4466.
. The IgG binding site of human FcγRIIIB receptor involves CC' and FG loops of the membrane-proximal domain. J Biol Chem 1996;271:3659.
. Human natural killer cells analyzed by B73.1, a monoclonal antibody blocking Fc receptor functions. I. Characterization of the lymphocyte subset reactive with B73.1. J Immunol 1983;130:2133.
. A triallelic Fcγ receptor type IIIA polymorphism influences the binding of human IgG by NK cell FcRIIIa. J Immunol 1996;156:2948.
. Identification of an unusual Fcγ receptor IIIa on natural killer cells in a patient with recurrent infections. Blood 1996;88:3022.
. The binding epitopes of human CD16 (FcγRIII) monoclonal antibodies. Implications for ligand binding. J Immunol 1996;157:1576.
. Binding of monomeric human IgG defines an expression polymorphism of FcγRIII on large granular lymphocyte/natural killer cells. J Immunol 1993;151:6429.
. Molecular basis of Fc receptor function. Adv Immunol 1994;57:1.
. A novel role for the Fc receptor gamma subunit: Enhancement of FcγR ligand affinity. J Exp Med 1996;183:2227.
. Natural killer (NK) cell deficiency associated with an epitope-deficient Fcγ receptor type IIIA (CD16-II). Clin Exp Immunol 1996;103:408.
. Inhibition of human natural killer cell activity by cytophilic immunoglobulin G. J Immunol 1982;128:1031.
. Regulation of human natural cytotoxicity by IgG. Characterization of the structural site on monomeric IgG responsible for inhibiting natural killer cell activity. Mol Immunol 1987;24:743.
Koene, H. R., Kleijer, M., Algra, J., Roos, D., E.G.Kr. von dem Borne, A., & de Haas, M. (1997). FcγRIIIa-158V/F Polymorphism Influences the Binding of IgG by Natural Killer Cell FcγRIIIa, Independently of the FcγRIIIa-48L/R/H Phenotype. Blood, 90(3), 1109-1114. Accessed April 19, 2019. Retrieved from http://www.bloodjournal.org/content/90/3/1109.


The Branched Chain Amino Acids Leucine, Isoleucine, and Valine are so called because the side chains of these amino acids (the part of the molecule that differentiates the amino acids) are made up of non-linear (branching) carbon chains. BCAAs are essential amino acids, meaning that they must be consumed in the diet (rather than manufactured in the body) and constitute more than one-third of the amino acid composition of skeletal muscle. As a dietary supplement, BCAAs help support increased muscle metabolism and increased energy production, making them an ideal recovery aid following intense exercise.✝ True Nutrition's BCAA Capsules are derived from fermented plant-based ingredients, and are entirely vegan-friendly!
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text:
Bernie Madoff was arrested 10 years ago — here's what his life is like in prison
Dec. 11, 2018, 2:16 PM
Bernie Madoff is one of the biggest white-collar criminals in history.
For about a decade, he's been serving a 150-year sentence in federal prison for offenses related to a major Ponzi scheme.
In the video above, Harvard professor Eugene Soltes explains what Madoff's life is like behind bars.
Eugene Soltes is a professor at Harvard Business School as well as the author of " Why They Do It," which focuses on white-collar crime. He spent seven years speaking with some of the biggest white-collar criminals in history including Bernie Madoff. Here he discusses what Madoff's life is like behind bars.
Eugene Soltes: Life for Bernie Madoff in prison isn't as bad as you would expect perhaps. He's actually very well respected in prison. To the extent that you're going to go to prison, people respect people who have done bigger things, and there is no bigger white-collar offender than Bernie Madoff.
So people look up to him as the financial guru. The person you go to to actually get financial advice.
One of Madoff's jobs in prison has been running the commissary. So, it's the place where inmates go to purchase a variety of food items. Things like ramen noodles, a variety of flavors, or to buy a pair of sneakers, flip-flops to wear in the shower, or maybe even a watch.
Bernie lives a pretty simple life now, being stuck in prison but he's a voracious reader. There is no one that reads the paper more carefully, listens to every radio show, digests every piece of news more carefully than Bernie does about himself and his case. But he actually spends a significant amount of time meeting with lawyers. He has appointments every, every week with lawyers flying in from around the world that are actually trying to better understand his case in part to look at some of the proceeds and some of the receivership about getting money back.
Produced by Eames Yates
EDITOR'S NOTE: This video was originally published May 22, 2017.
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Orange you glad I found a stablized Vitamin C serum in the Hylamide C25 Booster?
When I decided to delve into the world of Hylamide, it was because of the SubQ Anti-Age serum that was so highly raved. Personally though, I didn't notice significant enough results to join in the raves, even though I do think that it's a decent product.
When I made my order though, I wanted to get something else – since I was shipping the serum all the way from Canada, I might as well ship something else along with it! And that something was the Hylamide C25 Booster Stabilized Vitamin C Booster serum.
I didn't come across many reviews for it at the time. Perhaps it was new (about 6 months back or so) but I was curious, as I'd just been told by a friend about how effective using vitamin c had been for brightening and clarifying her complexion. The thing about Vitamin C though, is that it is quite unstable, so oxidises quite quickly, nullifying it's antioxidant properties.
This Hylamide C25 Booster however, claimed to be a stabilized version of a vitamin C, which allows them to package it into a clear bottle (most products that contain vitamin c come in brown/dark bottles), and to not oxidise, therefore keeping it effective. The key ingredient here is 25% Etyhyl Ascorbic Acid that's stabilized, and the ingredient list that you'll see below is impressively short!
I haven't used a "whitening" or correcting skincare product in quite a while, as I'm sure the regulars would have noticed. I used to, back in the day, but I soon wised up to the fact that they were all far too drying for my skin. So these days, I turn away offers to try this new whitening/brightening range and that new range. I'm just past all that.
Which isn't to say that I don't have a problem with skin pigmentation. If you've ever seen my bare faced pictures (which you will have, if you're a regular) then you know I have a problem, but I'm not obsessed about it. So, why try this one from Clinique, you may wonder.
The short answer, is that the Clinique Even Better Clinical Dark Spot Corrector (formerly known as Derma White) was the one product that gave me noticeable (and very impressive) results the first time I tried it, back in the day. It was so effective for me, that I went through about 3 bottles of it, and told everyone about it. Worked for some, didn't work for others. But I eventually changed my whole skincare regimen and stopped using it.
But this year, Clinique has upgraded the formula so the product is now called the Even Better Clinical Dark Spot Corrector & Optimizer. It's still a serum, and it still targets dark spots and evens out complexion, but with an added ingredient extracted from Gyokuro, very expensive green tea from tea leaves plucked from tea leaves grown in the shade, that is packed with antioxidants and anti-irritants, to optimize the product efficacy. This helps calm the skin and prevent the exacerbation of formation of pigmentation.


text:
The Thatcher effect or Thatcher illusion is a phenomenon where it becomes more difficult to detect local feature changes in an upside-down face, despite identical changes being obvious in an upright face.  It is named after the then British prime minister Margaret Thatcher, on whose photograph the effect was first demonstrated. The effect was originally created in 1980 by Peter Thompson, Professor of Psychology at the University of York.

Overview
The effect is illustrated by two originally identical photos, which are inverted.  The second picture is altered so that the eyes and mouth are vertically flipped, though the changes are not immediately obvious until the image is viewed upright.

The Thatcher effect is thought to be due to specific psychological cognitive modules involved in face perception which are tuned especially to upright faces.  Faces seem unique despite the fact that they are  very similar.  It has been hypothesized that we develop specific processes to differentiate between faces that rely as much on the configuration (the structural relationship between individual features on the face) as the details of individual face features, such as the eyes, nose and mouth.

There is evidence that rhesus monkeys as well as chimpanzees experience the Thatcher effect, raising the possibility that some brain mechanisms involved in processing faces may have evolved in a common ancestor more than 30 million years ago.

The basic principles of the Thatcher effect in face perception have also been applied to biological motion. The local inversion of individual dots is hard, and in some cases, nearly impossible to recognize when the entire figure is inverted.

Further investigations

The Thatcher illusion has also been useful in revealing the psychology of face recognition. Typically, experiments using the Thatcher illusion look at the time required to see the inconsistent features either upright or inverted. Such measures have been used to determine the nature of the processing of holistic facial images.

By looking at the intermediate angles between upright and inverted, studies have explored the gradual or sudden appearance of the illusions. Sensitivity to the Thatcher illusion has been found in children, including children with autism.

However, people with congenital prosopagnosia have been shown to exhibit an overall much weaker response to the illusion compared to people without such condition. Their response time was shown to be weakly and linearly affected by the grotesque face's orientation. This last observation suggests that the part of the brain responsible for "configural processing" in face recognition is the fusiform face area of the cortex, which is affected in both the congenital and the acquired condition.

References

External links

 Thatcher illusion demonstration
 Open University YouTube Thatcher illusion demonstration
 BBC article on the Thatcher illusion
 Windows utility for "thatcherizing" the face in the webcam (open source)

Psychological effects
Vision
Optical illusions
Margaret Thatcher
Face perception

redpajama_set_name: RedPajamaWikipedia


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International Hippie
www.InternationalHippie.com
voters have to know
Well i am not sure about anyone else if i am voting for you i wanna know everything ....including packing of any kind .....not gonna fly ....means you are dishonest.....maybe joe has got something to hide ....oh well it will not be the first time a president has lied ....or the last ....!!!!!!its politics .......
Biden Says Voters 'Don't Deserve' to Know His Position on Court Packing
National Review• October 10, 2020
Joe Biden on Friday again refused to state whether he would attempt to pack the Supreme Court if elected president, saying in an interview that voters "don't deserve" to know his position on the issue.
Some Democrats have suggested the party attempt to pack the Supreme Court, or increase the number of justices on the bench, if the party wins the presidency and a Senate majority in the November elections. The proposal comes as Republicans attempt to confirm Judge Amy Coney Barrett to the court, solidifying a 6-3 conservative majority.
Biden and running mate Senator Kamala Harris (D., Calif.) have repeatedly refused to state whether they support packing the court. However, Biden was again pressed on the issue during an interview by reporter Ross DiMattei of KTNV, a Las Vegas ABC affiliate.
Biden gets pressed on court-packing in every interview, but this answer to @KTNV is new:@RossDiMattei: "Don't the voters deserve to know-"@JoeBiden: "No they don't deserve- I'm not gonna play his game. He'd love… that to be the discussion instead of what he's doing now." pic.twitter.com/BpIxTrborp
— Andrew Solender (@AndrewSolender) October 10, 2020
DiMattei said the question of court packing was the "number-one issue" viewers have asked him about.
"Sir, don't the voters deserve to know…" DiMattei asked.
"No they don't deserve—I'm not gonna play [President Trump's] game," Biden responded, adding that Trump would "love that to be the discussion instead of what he's doing now."
Biden said at a Friday press conference that voters would only know his position on court packing after the election.
These rioters........................
Listen ....its all fun and games till someone gets fucked.......proper fucked ......and 5 people died .......i am pretty sure that wa...
I am not a fan of weddings ....although they are good for a laugh .....one way or another .....because the men get to look stupid in a pengu...
Voting scam
Like most things in life .......voting is a scam .....indoctrination ......brainwashing .......its fear dusguised. As a task to let human ...
I do hope we stop getting shit from china .....that's all it is...... pure cheap shit ....it might be worth paying a little extra for ...
Guest book.............................
VINYL RECORD SHOP .......
internationalhippie
.......this picture has me elegance to Anthony weiner. other than its a new York bagel company. ....how ever. the bagels. are. good. and tasty .....and the coffee. is. great. .
200 million dollars
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Bring a touch of nostalgia and style into your kitchen or office break room with this Checkmate Spice Salt and Pepper Holder. Designed for chess players and fans alike, this centerpiece is sure to please with it's classic eye appeal. Crafted from highly detailed polyresin, this Chess Salt and Pepper Holder is built to last for years. Even if the Chess Team is the best team on your campus, you can still represent your School Colors!
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