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‘Grey’s Anatomy’ recap: ‘Who Is He (And What Is He to You)?’ – EW.com

Posted on March 17, 2017 by Fredricko

'Grey's Anatomy' recap: 'Who Is He (And What Is He to You)?'
EW.com
Here's one thing you should know: Jackson doesn't make promises he can't keep. He makes this known in his various monologues throughout this episode, where he and April jet off to Montana for a quick trip to perform surgery on a couple of kids who can ...
Grey's Anatomy Season 13 Episode 16: "Who Is He (And What Is He To You)?"Refinery29
'Grey's Anatomy' Stars Jesse Williams and Sarah Drew on April and Jackson's Big Step ForwardHollywood Reporter
Grey's Anatomy Recap: #Japril Goes to MontanaVulture
E! Online -Daily Mail -TVLine
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The anatomy of a comeback: How Central’s chaotic, wacky second-half surge sparked a DI title win (photos) – MassLive.com

Posted on March 19, 2017 by ev1

SPRINGFIELD Sharaya Haines caught fire.

And then the MassMutual Center nearly did too.

Central girls basketballs 61-45 Division I state championship win over Braintree its first state title since 2007 was sparked by a chaotic, dramatic and occasionally perplexing second-half surge. The Golden Eagles erased a 10-point deficit, overcame injuries to two separate guards, endured a stop-and-go third quarter devoid of flow due to a barrage of fouls and whistles by the referees.

They then waited for seven minutes early in the fourth quarter while the fire alarm yes, the fire alarm went off inside the MassMutual Center, halting play.

At the center of all of the chaos was Haines, who scored all of her game-high 17 points in the second half, pouring in four 3-pointers.

She was a tremendous help, fellow senior Ishanna Brown said. I think her shooting threes sparked some energy and our success tonight. It was really big. She stepped up.

But before Haines could play the hero role, propelling Central to a win in front of its hometown crowd, it needed to break out of its malaise.

The early comeback

Central trailed 30-20 at halftime and was fortunate the deficit wasnt larger.

It scored just eight points over the games first 15 minutes before finding life at the end of the first half. Coach Erik Maurer said his team wasnt rotating defensively like hes accustomed to and was taken aback by Braintrees early run. It was addressed in the locker room at halftime.

The Golden Eagles quickly made up ground.

They opened the second half on an 8-0 run, cutting the deficit, before Braintrees Mackenzie Moore drilled a 3-pointer. Phyness Baldwin and Haines answered with back-to-back 3s, and suddenly, Central had a one-point lead, finally awakening a dormant pro-Central crowd.

Brown also played a significant role in keying the run, pulling down two rebounds and firing outlet passes that led to scores, and forcing two steals within the first 1:40 of the second half.

Central also had to deal with key injuries to Makayla Thompson and Jaliena Sanchez. Thompson dislocated her right shoulder at the beginning of the third quarter, missing over four minutes of game time. An MIAA doctor popped it back in and Thompson, who has dislocated the shoulder before, said she was ready to return to the game.

She was needed.

Midway through the quarter, Sanchez was fouled on a fast-break layup, crashing to the floor on her right hip. She writhed in pain and could not put weight on it, requiring two assistants to carry her off the floor. Alayah Sweeney took Sanchezs free throws officially ending the sophomore guards day and Sanchez was later wheeled out of the arena on a stretcher.

It made us angry, Haines said, but we still stayed focused. We played the rest of the game for her.

Haines lights it up

Haines embodied that focus as well as any player on the roster, shaking off a scoreless first half to score 11 points in the third quarter, including the teams final seven points of the quarter. Central took a 38-36 lead into the fourth quarter.

Then Brown scored three points to open the quarter. Haines followed, sandwiching two 3-pointers around a Makayla Rudder put-back layup, and suddenly Central had a 49-41 lead with 4:47 left.

Then the wonkiness.

The fire alarm went off.

Emergency lights flashed throughout the arena as an automated voice recording alerted fans to an emergency situation. The majority of the fans in the MassMutual Center remained in their seats, and the players stayed at their benches, more perplexed than anything.

The Central girls handled the situation well. After all, at that point, they were used to stoppages, as officials frustratingly halted play several times in the third quarter to confer at the scoring table.

It was really tough, there was just so much built up inside, Brown said. We werent getting calls we wanted, we had to fight through it all. Those bad calls, it brought something out of us, and made us come to the realization that we needed to step up because we werent going to get any calls

Maurer thought his team relaxed as the game became more chaotic.

I thought that we loosened up a little bit when everything started to happen the way that it did, he said. We started to joke on the bench. The girls were kind of laughing about things. Even with a couple of the injuries we had. It allowed the girls to take a little bit of a breath.

After a seven-minute delay, the alarm was turned off and play resumed. Central promptly went on a 7-1 run, and the game was theirs.

We knew the first half, it wasnt our best half, Thompson said. Over in the locker room, we talked about everything to improve, weve got each others back, believe in each other, keep shooting shots. Got back out there second half, trust each other and we got it. We came back and we won.

For Haines, who has withstood shooting slumps before, it was a rewarding stretch. Maurer regularly chides Haines to shoot more often if her shot becomes available. By the fourth quarter of Saturdays win, Haines was stepped into 3-pointers off the dribble, looking as comfortable as ever behind the arc.

He joked with her to only stop shooting if she missed three 3-pointers in a row.

I was feeling pretty confident, Haines said, so sometimes I feel like they are all going to go in.

It felt like, at least in the second half, they did.

Originally posted here:
The anatomy of a comeback: How Central's chaotic, wacky second-half surge sparked a DI title win (photos) - MassLive.com

Anatomy Of A Decision, Part 1: The C-Suite – Yahoo Finance

Posted on March 21, 2017 by ev1

Professional networking leader GLG has produced a new series of videos focused on decision making in the business world. As part of the series, GLG has interviewed a number of business leaders to ask about what considerations go into making important decisions.

In the first installment, GLG speaks with former Pfizer Inc. (NYSE: PFE) CEO Jeff Kindler.

Kindler said a key ingredient in his meteoric rise was an open mind.

The Importance Of An Open Mind

I started saying I should be open to whatever comes along, Kindler said. And that led me down all kinds of different paths I never would have predicted.

Kindler joined Pfizer as the pharma giants general council, but he admits that he had always had ambitions to be CEO. Once he assumed the role, he was presented with an opportunity to work with former President Barack Obama on the Affordable Care Act (ACA).

Kindler said many of the provisions being discussed at the time were politically polarizing but would have been universally bad for the pharmaceutical industry. Rather than fight the change, Kindler and a handful of other pharma CEOs decided to take a more constructive approach.

We formed a small group of five of us who were CEOs of different companies in pharmaceuticals with different interests and a different focus, and we decided that within the right boundaries, if we could achieve acceptable policy solutions, we would support the bill, Kindler recalled.

To this day, there are people who dont like what we did, even within the pharmaceutical industry. But my view is I got attacked by both the Wall Street Journal and the New York Times editorial page, and I think when that happens you know youre in the sweet spot.

Lessons Learned

Kindler sees his participation in the process as a valuable lesson in the power of compromise. While the pharmaceutical industry made a number of financial sacrifices as part of the process, he and his colleagues were also able help shape the bill to maximize potential industry benefits.

Kindler said the success of Obamacare to this day depends on perspective. In terms of increasing health insurance coverage, the program was a complete success. In terms of fixing the underlying problems of rising healthcare costs, Kindler believes Obamacare hasnt delivered.

He closed the interview by discussing one key regret he has about his time as CEO.

I think I fell prey to something thats in human nature, which is I didnt block enough time for personal development. I think a lot of [people] that are Type A personalities end up in big jobs, and theyre so focused on both the fact that they have achieved that and the things that they need to do on it that they... just dont pay attention enough to the things that are of long-term importance.

Kindler said time management, prioritization and mentorship were three of the biggest challenges of such an important professional role.

TV’s 15 Best Musical Episodes, Ranked (Plus the One Absolute Worst) – TVLine

Posted on March 17, 2017 by ev1

TVLine

TV's 15 Best Musical Episodes, Ranked (Plus the One Absolute Worst)
TVLine
Grey's Anatomy: Song Beneath the Song (Season 7, Episode 18) First of all, stop rolling your eyes. This is a gut-wrenching hour of television, anchored by powerful performances from Sara Ramirez whose character's life remains in limbo after a near ...

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‘Grey’s Anatomy’ Star Jesse Williams: Trump a ‘Pig’ – Breitbart News

Posted on March 17, 2017 by Danzig

Asked by TMZ how Trump is doing with racial injustice in America, theGreysAnatomyactor replied: Hes not.

Hes a pig whos trying to make sure that he galvanizes as much fear as possible, particularly against black, brown immigrants, and Muslims, Williamstold TMZ.

Concerning Trumps law enforcement policy agenda, Williams cited a series of police-involved shooting statistics.

There were more killings at the hands of police this February than January and February of last year,211 murders at the hands of police this year so far,the actor said.

Williamshas spoken out against Trump before.

In September, the actor and activist appeared in Joss Whedons Important political PSA alongside Avengers stars Robert Downey Jr. and Scarlett Johansson to urge people to vote for former Democratic presidential candidate Hillary Clinton.

Last year, the actor wasthe subject of a petition calling for his firing from Greys Anatomy following hisracially-charged acceptance speech at the BET Awards,during which hevilified police officers and accused white people of appropriating and then profiting from black culture.

Williams alsoprotested in Ferguson, Missouriafter the shooting of Michael Brown in 2014. Helatersaid on CNNsState of the Unionthat theres a complete double standard and a complete different experience that a certain element of this country has the privilege of being treated like human beings, and the rest of us are not treated like human beings, period.

FollowJerome Hudsonon Twitter:@jeromeehudson

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'Grey's Anatomy' Star Jesse Williams: Trump a 'Pig' - Breitbart News

‘Grey’s Anatomy’ 3/2/2017 Why Didn’t the Show Air? – Closer … – Closer Weekly

Posted on March 4, 2017 by Fredricko

Closer Weekly

'Grey's Anatomy' 3/2/2017 Why Didn't the Show Air? - Closer ...
Closer Weekly
Many #TGIT fans were totally confused last night when a new episode of Grey's didn't air on ABC on Thursday, March 2. Thankfully, it wasn't a TV glitch the hit ...
'Grey's Anatomy' Season 13 Episode 15 Spoilers Tease Meredith's ...Counsel & Heal
Gray's Anatomy Season 13: Episode 15, when will it be broadcast ...The Siver Times
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The anatomy of heartbreak – The Kathmandu Post

Posted on March 4, 2017 by Danzig

What I felt for her was profound and real. I felt every bit of it as much as the hunger that stings my stomach and as much as the anger that blinds me. Yes, it was that real and strong. I know how genuine it was

Mar 5, 2017- The intensity of your love defines the intensity of your heartbreak. The deeper your love, the more unfathomable is your heartbreak. The shallower your love, the more fleeting your heartbreak is.

Perhaps, my love was far too deep. If not, why would I take forever to recover from our abrupt end? Why would I take forever to move on? Why would I take this long to be the person I knew I was supposed to be in the real world? How would I even know my love was deep when, in fact, I wasnt even there? All there was is the love itself. I was the love. Yes, I was love itself.

A heart breaks when your grand expectation from someone seems impossible to be met. A heart breaks when the utopian universe inside your head starts collapsing before it even sees the light of the day. A heart breaks when you surrender your soul to someone who is utterly soulless. A heart breaks when your heart starts beating more for someone else, and less for yourself. A heart breaks when you start thinking and feeling more for someone else, and less for yourself.

A heart breaks when you handcuff yourself to your love, kneel down before your beloved and surrender yourself completely only to become disregarded. A heart breaks when your own existence escapes your memory. A heart breaks not because it is fragile, but because you have been clumsy with it. I have been clumsy, very clumsy.

For the first time in my life, I had developed genuine feelings for somebody. For the first time in my life, I was experiencing the joy of being and sharing my life with someone. For the first time in my life, I felt like if there was someone at all for me out there, it had to be her and nobody else.

But, maybe she could never see the authenticity in my love. Perhaps, she also thought of me as someone fake.

It kills you when your unconditional love is unappreciated. It maddens you when your utmost care goes unacknowledged. It suffocates you when your admiration is mocked. It hurts you when you become a clown in the most beautiful pair of eyes you have ever seen.

And its all real, every bit of pain. It is as real as the air you are breathing now.

Every winter, as I soak in the snow standing in the middle of a street, hands spread wide open, head bent backward and my two little teary eyes looking into the sky, I think of her. I let her memory envelop me. Every single snow flake reminds me of her.

Even when I try to shake off the snow, there never is enough energy in my body. It just seems to escape me. As I get home, fully covered in snow, I cant help but collapse on my bed. The snow leaves my clothes to melt on the sheets, soaking it in all its glory. I feel like I am laying on a pond, perhaps drowning in one. It is then that I start bawling like a baby. Why should the snow melt into water? Why should anything leave its state of being to become something else? Why did love leave me so soon?

She loved snow. She loved watching snowfall from her balcony. She loved the sound of silence as the entire city quietly snuggled under a blanket of snow. She knew that it was a myth that no two snowflakes are exactly the same. She pretended that she knew all the hundred names that Eskimos had for snow.

She loved snow, just like I did. She knew of snow, as much as I did. It was the snow that brought us together. Our mutual fondness for it invoked conversations and sparked an untold chemistry between us. It was because of the snow that we started opening up to each other, little by little.

Yes, it is strange, but arent all the beautiful things?

When you heart breaks, your ego bruises too. What if my ego is steering my heart, telling it how to feel? What if it is not the heart, but the ego? What if it is not love, but my pride that has been torn apart?

If I tackle this mindfully, love shouldnt be so hard. Maybe there is no such this as a heart break. Hearts never break. Hearts dont hurt. Hearts function perfectly until they stop functioning altogether. Perhaps, when we talk of heartbreak we are talking of our imagination not taking shape. May be when we talk about heartbreak, we are talking of our subtle agendas regarding somebody not being met. Perhaps we are talking about the sudden collapse of our countless expectations and our incapability of loving ourselves in the first place.

Heartbreak has nothing to do with the heart or with love. Maybe even when we cant control how we love, we can decide how we feel about heartbreak. Love is inevitable, heart break is optional. So what should I do now, who should I blame?

It looks like with my heart still intact, heartbreak is just a notion I inventedan emotional play maybe? Is this heartbreak just another excuse to escape from the now, from the reality? Is it my way of justifying why I have failed to love myself in the first place? Is it my way of feeding my ego-telling myself nobody will ever love her like I did?

I have been thinking how she doesnt deserve my love; is this tool of superiority complex? Am I trying to prove something here? Am I demanding more than I should here? Should I demand or prove something at all? Do I really need to claim that I love someone; do I really need to seek for credit? Cant I just love-without any anticipation or greed? The answer escapes me.

Once upon a time, on a beautiful evening I remember saying to her: You are the wind that blows my mind and the silence that soothes my heart. You are the beauty that blinds my eyes and the beast that scares my soul. You are the root that grows underground and the branch that grows towards the sky. You are the question I ask and the answer I find. You are the chaos to my thoughts and the order of my heartbeats. You are the yin and you are the yang. You are the contradiction that confuses me, and the ultimate truth that relieves me. That is why you are so beautiful, so intriguing.

What happened to that statement and all those words? Did I even mean every single thing? Could they have been as meaningless and as empty as I feel right now? Perhaps, she understood it long before I did.

Come to think of it, she loved herself more than anyone else. She was so much in love with herself that my so-called unconditional love didnt amount to anything. She knew how to live every single moment of her life and on her own to the fullest. She was a free soul who didnt entertain any kind of entanglement. She was a rebel who questioned everything and enjoyed basking in the glory of lifes mysteries. She was someone who dared to be nave and perhaps just herself. She was someone who could maintain her curiosity passionately.

Thats the reason why her eyes always twinkled. She was utterly blissful in her own being. She was a peaceful soul.

Thats the reason why everyone around her experienced peace. She was always joyful and that is why being around her was so intoxicating.

She was a dream that you wanted to hold on to. Thats why I loved her, and thats why I lost her.

I remember how she always pushed me to love myself first, when all I wanted to do was love her. Maybe she waited for me to love myself while I thought I could only do so if she loved me back.

The power of your ego defines the intensity of your heartbreak. The deeper your ego, the more unfathomable is your heartbreak. The shallower your ego, the more fleeting your heartbreak is. Look! Its snowing again.

Published: 05-03-2017 09:09

The anatomy of a scheduled loss – Golden State of Mind

Posted on March 10, 2017 by Fredricko

Last night, the Golden State Warriors fell to the Boston Celtics (99-86) in the sixth game of a nightmare eight-game stretch that has been dubbed the hardest part of the Warriors schedule. Golden State clearly ran out of gas as Boston dominated the fourth quarter.

To get an idea of what the Warriors have been facing, we take a look at the realities of their grueling itinerary.

After defeating the Brooklyn Nets at home, the Warriors started this killer stretch with a flight across the country to Philadelphia. From there they made their way west to Washington and Chicago, back east to New York, south to Atlanta and back across the country to California for their most recent game against Boston. Theyre now on their way back east to play a back-to-back in Minnesota and then in San Antonio before returning home.

If you do the math on this trip it sounds like a horrible version of The Twelve Days of Christmas: Over 9,500 miles traveled, 10 days, eight games total, seven away, six time zone changes, two sets of back-to-backs sing with me now and a tragic MCL sprain.

Anyone who has traveled over time zones knows it can be an unpleasant experience. You feel groggy, slow and disoriented. This is because your body is telling you that its one time, while your environment is telling you its a completely different time.

We can naturally adjust to this discrepancy as our internal clocks catch up to external environmental clues, but it usually takes a couple days. NBA players have no such luxury. As a result, theyre often forced to play games with their internal clocks out of rhythm. Hardly a recipe for success.

Sleep schedules are often disrupted when traveling across time zones. A 2011 Stanford University study was conducted on eleven members of the Stanford mens basketball team. Baseline data was collected on the players while they maintained their typical sleep schedules. Then a period of extended sleep was instituted where the subjects would get at least 10 hours of sleep per night.

Impressively, with the increase in sleep, the subjects also had faster reaction times and faster sprint times. They also had, get this, an increase in free-throw and three-point shooting percentages of nine percent.

Unfortunately, lack of sleep can have essentially the opposite effect on performance. So traveling across the country while playing an intense sport on the biggest stage is going to take its toll, to say the least.

Obviously, the act of playing basketball is itself a tall task. Players will run over three miles during the course of a game, mostly at a dead sprint. On average, a player will have 1,000 changes of movement patterns per game each change occurring about every two seconds all from explosive bursts from their muscles.

Along with the physical aspects of the sport comes the mental fatigue. Being locked in and engaged during a game takes a significant amount of mental energy.

Not to mention that the Warriors are one of the most scrutinized teams in the league right now and every move, good or bad, is analyzed to death. The players know this better than anyone; and while they might not care what anyone else thinks, that doesnt mean it doesnt take mental fortitude to deal with all the talk.

Given the difficulty of this stretch of games, the result of last nights game against the Celtics shouldnt come as a huge surprise. So far, theyre 3-3 since the start of their most recent road trip 2-3 since losing Durant and with a back-to-back left, the Warriors still have a lot more work to do before they can return home for a nice home stand.

History tells us that in an 82-game season, there are always going to be scheduled losses. I mean, the game against the San Antonio Spurs has scheduled loss written all over it! But the reality is that every team has a killer stretch of games at some point during the season and they just have to deal with it. For the Warriors, that time is now. Its just unfortunate that it has coincided with the loss of a key player, but thats the NBA.

You can chalk it up to the schedule, to the grind, to fatigue or to any other reason, but in the end, a loss is a loss. All the Warriors can do is look to the next game and work on getting better.

Yes, theyre tired. Yes, theyre a man down. And, yes, theyre not playing very well at the moment. So, as a fan, its sometimes hard to watch. But Klay Thompson put it best when he said this:

Eyes on the prize, people.

Lets go Dubs.

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The anatomy of a scheduled loss - Golden State of Mind

Nature up close: A giraffe’s anatomy is a study in superlatives – the tallest terrestrial animals on Earth, with a neck six feet long, and strong legs…

Posted on February 13, 2020 by Danzig

By "Sunday Morning" contributing videographer Judy Lehmberg.

I come from a pretty small family, so when my father married a South African woman with a large extended family, I was delighted. They are an interesting bunch: Russian Jews, some of whom survived the German concentration camps during World War II, and some like my step-mother's father, who fought in that war and lived to be 98 years old. Not long after I first met him, he asked me about the animals in Yellowstone National Park which they had visited on one of their trips to the U.S. He knew I was a biologist, so he asked where all the large animals were in the park.

I had to think a minute. Didn't he see the bison, elk, moose, pronghorn antelope, mule deer, two species of bears and the wolves? Yes, he said he say them, but where were the rest of them?

Then it hit me. Those are the only large animals in Yellowstone, and he was comparing them to his experiences in Kruger National Park and other African parks and reserves.

He was right. The continental U.S. has a measly 490 species of mammals, while Africa has 4,700. Granted the continent of Africa is huge by comparison, but that is almost ten times the number of mammal species than are in the U.S.

Africa has 90 species of antelope; the U.S. has zero. (Contrary to their name, American pronghorn are not true antelope.) We fair better in the bird department with a little more than 2,000 species in all of North America, which is similar to the total number in all of Africa. But Kenya alone has over 1,100 species, and Africa has the Sahara Desert where very few birds live full time. And then there are the strange-looking animals like elephants, rhinos, hippos and giraffes animals that are pretty difficult to explain strictly from an evolutionary standpoint. They all look like they were made by committees that couldn't agree on anything.

The giraffes are the most graceful of the "committee" species. They move almost as if they are trying to hold an invisible stack of books on their head. They aren't all that graceful-looking when they lean down to get a drink of water, but even just standing still and eating Acacia leaves, they seem to emit a graceful, peaceful air. How they eat those leaves is hard to understand when you notice the plant's three-inch-long thorns, but they don't seem to bother the giraffes a bit. They must have really tough tongues.

Their general anatomy is a study in superlatives. They are the tallest terrestrial animals on Earth. Even though they only have seven neck, or cervical, vertebra (the same as humans), their neck is six feet long and weighs 600 pounds. Their legs are six feet long, and their feet are 12 inches across, which along with strong leg bones helps them support their immense weight (in males, that's up to 3,000 pounds). Their heart is about two feet long and weighs around 25 pounds, and their lungs can hold up to 12 gallons of air.

Although males can be aggressive towards each other (more on that in a minute), they don't defend a territory or even live in consistent family groups. Sometimes a group of giraffes is all females and their young, sometimes they are all male, and sometimes the group is a mix of ages and both sexes. They are more fluid than many species, as group members tend to come and go from one group to another. No one seems to know what triggers them to move, or to return.

No one really knows why a giraffe's neck is so long. Before Charles Darwin proposed his theory of organisms inheriting characteristics (what we now know as genes) from their parents, some people thought animals acquired characteristics during their lifetimes and then passed those characteristics to their offspring. For several thousand years, that theory was believed by everyone from Hippocrates and Aristotle to, most famously, Jean-Baptiste Lamarck, and became known as "Lamarckian evolution." Lamarck used giraffes as an example. He believed they stretched their necks to reach higher leaves, and passed those stretched necks to their offspring. He was wrong. For many years biology teachers have taught that giraffes who happened to be born with slightly-longer necks could reach higher leaves, thereby outcompeting their shorter-necked friends and relatives and successfully pass those genes on to the next generation.

That may very well be true, as the fossil record shows giraffe necks have elongated, especially in the last seven million years. But it is virtually impossible to say why their necks got longer. Maybe it was because longer-necked individuals could reach higher leaves. But there could be at least one other explanation.

Male giraffes sometimes fight to win the right to mate with a female. They all fight the same way, by swinging their necks and hitting the other giraffe, usually trying to knock it off balance, causing it to fall, which can result in their death. They can also do a good bit of damage with their horns if a blow lands hard enough. I've never seen them fight to the death, but I have seen fights that lasted several minutes and didn't always have an obvious winner. Maybe males with longer, thicker necks are more successful at mating, and therefore pass those genes on to their offspring?

My favorite thing about giraffes is that they attract oxpeckers, birds that land on giraffes and other herbivorous animals in Africa, and pick parasites off them. I have no idea why, but oxpeckers seem particularly attracted to giraffes. I love to watch them run their beaks systematically through a giraffe's fur like a single-tinged comb, feeling for ticks and other parasites. Sometimes the giraffe will twitch its skin and the oxpeckers fly off, but sometimes they will hold their ears really still so an oxpecker can go in and grab whatever parasites are in there.

Judy Lehmberg is a former college biology teacher who now shoots nature videos.

‘Grey’s Anatomy’ Star Ellen Pompeo Takes Fans Behind the Scenes of the Popular Show – Closer Weekly

Posted on March 4, 2017 by Fredricko

Closer Weekly

'Grey's Anatomy' Star Ellen Pompeo Takes Fans Behind the Scenes of the Popular Show
Closer Weekly
Grey's Anatomy fans were stoked when the show's star Ellen Pompeo gave them a sneak-peek at her life on set. In the series of Instagram clips on Thursday, March 2, the 47-year-old actress gave a detailed behind-the-scenes look at the popular medical ...

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'Grey's Anatomy' Star Ellen Pompeo Takes Fans Behind the Scenes of the Popular Show - Closer Weekly

Anatomy of a difficult marriage – The New Indian Express

Posted on March 4, 2017 by ev1

Historical lovers, courtesy researchers and biographers, cant act coy in death. Claretta: Mussolinis Last Lover by RJB Bosworth details the grand passion between Italys prime minister Benito Mussolini and Claretta Petacci, all the way down to that unforgettable portrait of their butchered bodies hung upside down in Piazzale Loreto. Sheela Reddys Mr and Mrs Jinnah: The Marriage That Shook India chronicles a liaison closer home, but no less doomed.

If Mussolini was 49 to Clarettas 20, Mohammad Ali Jinnah was 40 to Ruttie Petits 16. Ruttie, a social butterfly in her gauze saris and backless blouses, romances a reticent and charismatic politician whom no one, not even her, called by his first name. He was her J.

Despite their elopement and Muslim-Parsi tag, the Jinnahs too had to contend with domestic ennui. The man from Karachi and the girl from Bombay fall for each other in haste but they repent in exquisite leisure.

While Motilal Nehru escapes having a son-in-law from another caste, Sir Dinshaw Petit was tricked into revealing his doublespeak when Jinnah asked him his opinion on inter-caste marriage and, after ascertaining his support for it, requested his daughters hand and the father refused.

It was Ruttie who chased after Jinnah and nothing stopped them from being one of the historys tempestuous couples. Prominent figures are part-narrators, like Sarojini Naidu, whose letters, maternal advice and perceptive insight into the matrimonial disaster between two such dissimilar people via letters to daughters Padmaja and Leilamani are a testimony to the timeline.

Ruttie sashays off the pages with great panache. Jinnah hardly blinked when his first wife, Emi Bai, died but Rutties death changes the tone of his silence. He had shaved off his moustache to marry hera precondition she laid downand been a most indulgent husband, letting her shop infinitely, getting out of his car to buy her roadside chaat, handing only child over to nannies so Ruttie could gallivant around. But couldnt give her what she wanted most, his time.

He was grooming himself for destiny, she was dressing up for him. It was her sparkling mischief against his staidness, her pout against his stiff upper lip. Naturally, they suffered. The same woman who told the court: Mr Jinnah has not abducted me... I abducted him, when her father sued him for kidnap, much later, when not a star was left in her eyes, told Sarojini he could never satisfy her mind and soul.

Sarojini documented Rutties changing persona in a letter to her daughter: There is something hard and cold about it all paint, powder, bare back...

Bedridden with discontent, Rutties body seemed unable to rise to the ordeal of breaking free even after she mentally fled the marriage. She kept her only daughter nameless through sheer lack of interest.

Since the book bats for Ruttieit is all about her desire, her disappointments and her deaththe reader awaits a husbandly version. One cant help wonder what Jinnahs matrimonial take might have been. It is not the first time a childish, high-strung flibbertigibbet wife drove mad a man inherently disinterested in coochie-coo.

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Anatomy of a difficult marriage - The New Indian Express

Film review: The anatomy of a comeback in Panga – Livemint

Posted on January 24, 2020 by Danzig

For such an unhurried film, Panga has a bracingly violent start. All of Bhopal is sleeping, except for Prashant (Jassie Gill), whos getting kicked by his wife, Jaya (Kangana Ranaut), in bed. These arent light kicks either. Ranaut isnt an actor given to half-measures and Id wager Gill left the set that day with more than a few bruises. Not only are the kicks satisfyingly hard, they have a certain rhythm and coil to them. Theyre athlete kicks.

Its a nice detail, because Jaya is an athlete, or at least was one. A national-level kabaddi player, she quit the sport to take care of her son, born prematurely and with low immunity. She never returned to kabaddi, working instead at a railway ticket counter and investing all her energy in her precocious school-going child and loving husband. She feels a pang now and then, but tells herself that neither her umar (age shes 32) nor kamar (waistline) would allow a return to the game.

In Ashwiny Iyer Tiwaris first film, 2016's Nil Battey Sannata, a working mother joins her daughters school so she can first learn and then tutor her in math. Panga, too, has a mother risking embarrassment for her child: once the boy learns that Jaya left kabaddi for him, he badgers his father to persuade her to make a comeback. In a montage scored with an Annu Kapoor comic number, Jaya starts training again, with the intention of giving up in a month. But when the time comes, she cant. She left kabaddi, but kabaddi never left her.

Its barely a surprise when the super-supportive Prashant an endearing, if slightly wishful, creation insists she try and make her way back to the national team. Tiwari and co-writer Nikhil Mehrohtra carefully unpeel the various levels of social indoctrination that someone like Jaya must overcome before they can follow their dreams, not only practical problems (Prashant is inept around the house) but her own guilt at what in her mind amounts to abandoning her child.

For a sports film, this is a timely idea to be grappling with (Sultan, in 2016, also dealt with it). There are more prominent Indian women athletes today than perhaps ever before, and some like Mary Kom and Sania Mirza have returned to their sports after becoming parents. But in a more general sense, the film is an empathetic look at the social cost of continuing with ones life after marriage and children. That Jaya should consider herself lucky that she actually is lucky, as shes told by several women to get to do the thing shes good at, is one of the more poignant reiterations of this film.

Nitesh Tiwari is credited with additional dialogue and screenplay, and theres a hint of Dangals unnecessary villain in the figure of national team captain, who for no reason keeps slighting Jaya. I can see why the film tries to introduce a late-stage antagonist, though; Panga is easy-going to a fault. Its not often one gets to say this about a Hindi film, but there are moments when it could really use some drama. The kabaddi isnt badly executed but because the film takes its time building to Jayas comeback, the final championship is both rushed and predictable.

After a series of high-strung, if often brilliant, performances in Rangoon, Simran, Manikarnika and Judgmentall Hai Kya, its a relief to see Ranaut play in a more down-to-earth style. Jaya is more comfortable in her skin than Rani Mehra, but Queen does come to mind: its the same homemade-sweater-wearing, chaat-eating, cautiously progressive middle-class milieu. Gill does little but look lost and smile broadly a surprisingly winsome strategy. Richa Chadha, in a very Richa Chadha role as an outspoken coach and friend of Jayas, is supremely relaxed. She even gets to do a little shout-out to her own line from Gangs of Wasseypur: Ghoor kaahe rahe ho?" The best adaptation of a famous line, though, is by a character whos there in just one scene, the doctor who tells Jaya, Ab goli kha".

Skeletal system 1: the anatomy and physiology of bones – Nursing Times

Posted on January 28, 2020 by Danzig

Bones are an important part of the musculoskeletal system. This article, the first in a two-part series on the skeletal system, reviews the anatomy and physiology of bone

The skeletal system is formed of bones and cartilage, which are connected by ligaments to form a framework for the remainder of the body tissues. This article, the first in a two-part series on the structure and function of the skeletal system, reviews the anatomy and physiology of bone. Understanding the structure and purpose of the bone allows nurses to understand common pathophysiology and consider the most-appropriate steps to improve musculoskeletal health.

Citation: Walker J (2020) Skeletal system 1: the anatomy and physiology of bones. Nursing Times [online]; 116: 2, 38-42.

Author: Jennie Walker is principal lecturer, Nottingham Trent University.

The skeletal system is composed of bones and cartilage connected by ligaments to form a framework for the rest of the body tissues. There are two parts to the skeleton:

As well as contributing to the bodys overall shape, the skeletal system has several key functions, including:

Bones are a site of attachment for ligaments and tendons, providing a skeletal framework that can produce movement through the coordinated use of levers, muscles, tendons and ligaments. The bones act as levers, while the muscles generate the forces responsible for moving the bones.

Bones provide protective boundaries for soft organs: the cranium around the brain, the vertebral column surrounding the spinal cord, the ribcage containing the heart and lungs, and the pelvis protecting the urogenital organs.

As the main reservoirs for minerals in the body, bones contain approximately 99% of the bodys calcium, 85% of its phosphate and 50% of its magnesium (Bartl and Bartl, 2017). They are essential in maintaining homoeostasis of minerals in the blood with minerals stored in the bone are released in response to the bodys demands, with levels maintained and regulated by hormones, such as parathyroid hormone.

Blood cells are formed from haemopoietic stem cells present in red bone marrow. Babies are born with only red bone marrow; over time this is replaced by yellow marrow due to a decrease in erythropoietin, the hormone responsible for stimulating the production of erythrocytes (red blood cells) in the bone marrow. By adulthood, the amount of red marrow has halved, and this reduces further to around 30% in older age (Robson and Syndercombe Court, 2018).

Yellow bone marrow (Fig 1) acts as a potential energy reserve for the body; it consists largely of adipose cells, which store triglycerides (a type of lipid that occurs naturally in the blood) (Tortora and Derrickson, 2009).

Bone matrix has three main components:

Organic matrix (osteoid) is made up of approximately 90% type-I collagen fibres and 10% other proteins, such as glycoprotein, osteocalcin, and proteoglycans (Bartl and Bartl, 2017). It forms the framework for bones, which are hardened through the deposit of the calcium and other minerals around the fibres (Robson and Syndercombe Court, 2018).

Mineral salts are first deposited between the gaps in the collagen layers with once these spaces are filled, minerals accumulate around the collagen fibres, crystallising and causing the tissue to harden; this process is called ossification (Tortora and Derrickson, 2009). The hardness of the bone depends on the type and quantity of the minerals available for the body to use; hydroxyapatite is one of the main minerals present in bones.

While bones need sufficient minerals to strengthen them, they also need to prevent being broken by maintaining sufficient flexibility to withstand the daily forces exerted on them. This flexibility and tensile strength of bone is derived from the collagen fibres. Over-mineralisation of the fibres or impaired collagen production can increase the brittleness of bones as with the genetic disorder osteogenesis imperfecta and increase bone fragility (Ralston and McInnes, 2014).

Bone architecture is made up of two types of bone tissue:

Also known as compact bone, this dense outer layer provides support and protection for the inner cancellous structure. Cortical bone comprises three elements:

The periosteum is a tough, fibrous outer membrane. It is highly vascular and almost completely covers the bone, except for the surfaces that form joints; these are covered by hyaline cartilage. Tendons and ligaments attach to the outer layer of the periosteum, whereas the inner layer contains osteoblasts (bone-forming cells) and osteoclasts (bone-resorbing cells) responsible for bone remodelling.

The function of the periosteum is to:

It also contains Volkmanns canals, small channels running perpendicular to the diaphysis of the bone (Fig 1); these convey blood vessels, lymph vessels and nerves from the periosteal surface through to the intracortical layer. The periosteum has numerous sensory fibres, so bone injuries (such as fractures or tumours) can be extremely painful (Drake et al, 2019).

The intracortical bone is organised into structural units, referred to as osteons or Haversian systems (Fig 2). These are cylindrical structures, composed of concentric layers of bone called lamellae, whose structure contributes to the strength of the cortical bone. Osteocytes (mature bone cells) sit in the small spaces between the concentric layers of lamellae, which are known as lacunae. Canaliculi are microscopic canals between the lacunae, in which the osteocytes are networked to each other by filamentous extensions. In the centre of each osteon is a central (Haversian) canal through which the blood vessels, lymph vessels and nerves pass. These central canals tend to run parallel to the axis of the bone; Volkmanns canals connect adjacent osteons and the blood vessels of the central canals with the periosteum.

The endosteum consists of a thin layer of connective tissue that lines the inside of the cortical surface (Bartl and Bartl, 2017) (Fig1).

Also known as spongy bone, cancellous bone is found in the outer cortical layer. It is formed of lamellae arranged in an irregular lattice structure of trabeculae, which gives a honeycomb appearance. The large gaps between the trabeculae help make the bones lighter, and so easier to mobilise.

Trabeculae are characteristically oriented along the lines of stress to help resist forces and reduce the risk of fracture (Tortora and Derrickson, 2009). The closer the trabecular structures are spaced, the greater the stability and structure of the bone (Bartl and Bartl, 2017). Red or yellow bone marrow exists in these spaces (Robson and Syndercombe Court, 2018). Red bone marrow in adults is found in the ribs, sternum, vertebrae and ends of long bones (Tortora and Derrickson, 2009); it is haemopoietic tissue, which produces erythrocytes, leucocytes (white blood cells) and platelets.

Bone and marrow are highly vascularised and account for approximately 10-20% of cardiac output (Bartl and Bartl, 2017). Blood vessels in bone are necessary for nearly all skeletal functions, including the delivery of oxygen and nutrients, homoeostasis and repair (Tomlinson and Silva, 2013). The blood supply in long bones is derived from the nutrient artery and the periosteal, epiphyseal and metaphyseal arteries (Iyer, 2019).

Each artery is also accompanied by nerve fibres, which branch into the marrow cavities. Arteries are the main source of blood and nutrients for long bones, entering through the nutrient foramen, then dividing into ascending and descending branches. The ends of long bones are supplied by the metaphyseal and epiphyseal arteries, which arise from the arteries from the associated joint (Bartl and Bartl, 2017).

If the blood supply to bone is disrupted, it can result in the death of bone tissue (osteonecrosis). A common example is following a fracture to the femoral neck, which disrupts the blood supply to the femoral head and causes the bone tissue to become necrotic. The femor
al head structure then collapses, causing pain and dysfunction.

Bones begin to form in utero in the first eight weeks following fertilisation (Moini, 2019). The embryonic skeleton is first formed of mesenchyme (connective tissue) structures; this primitive skeleton is referred to as the skeletal template. These structures are then developed into bone, either through intramembranous ossification or endochondral ossification (replacing cartilage with bone).

Bones are classified according to their shape (Box1). Flat bones develop from membrane (membrane models) and sesamoid bones from tendon (tendon models) (Waugh and Grant, 2018). The term intra-membranous ossification describes the direct conversion of mesenchyme structures to bone, in which the fibrous tissues become ossified as the mesenchymal stem cells differentiate into osteoblasts. The osteoblasts then start to lay down bone matrix, which becomes ossified to form new bone.

Box 1. Types of bones

Long bones typically longer than they are wide (such as humerus, radius, tibia, femur), they comprise a diaphysis (shaft) and epiphyses at the distal and proximal ends, joining at the metaphysis. In growing bone, this is the site where growth occurs and is known as the epiphyseal growth plate. Most long bones are located in the appendicular skeleton and function as levers to produce movement

Short bones small and roughly cube-shaped, these contain mainly cancellous bone, with a thin outer layer of cortical bone (such as the bones in the hands and tarsal bones in the feet)

Flat bones thin and usually slightly curved, typically containing a thin layer of cancellous bone surrounded by cortical bone (examples include the skull, ribs and scapula). Most are located in the axial skeleton and offer protection to underlying structures

Irregular bones bones that do not fit in other categories because they have a range of different characteristics. They are formed of cancellous bone, with an outer layer of cortical bone (for example, the vertebrae and the pelvis)

Sesamoid bones round or oval bones (such as the patella), which develop in tendons

Long, short and irregular bones develop from an initial model of hyaline cartilage (cartilage models). Once the cartilage model has been formed, the osteoblasts gradually replace the cartilage with bone matrix through endochondral ossification (Robson and Syndercombe Court, 2018). Mineralisation starts at the centre of the cartilage structure, which is known as the primary ossification centre. Secondary ossification centres also form at the epiphyses (epiphyseal growth plates) (Danning, 2019). The epiphyseal growth plate is composed of hyaline cartilage and has four regions (Fig3):

Resting or quiescent zone situated closest to the epiphysis, this is composed of small scattered chondrocytes with a low proliferation rate and anchors the growth plate to the epiphysis;

Growth or proliferation zone this area has larger chondrocytes, arranged like stacks of coins, which divide and are responsible for the longitudinal growth of the bone;

Hypertrophic zone this consists of large maturing chondrocytes, which migrate towards the metaphysis. There is no new growth at this layer;

Calcification zone this final zone of the growth plate is only a few cells thick. Through the process of endochondral ossification, the cells in this zone become ossified and form part of the new diaphysis (Tortora and Derrickson, 2009).

Bones are not fully developed at birth, and continue to form until skeletal maturity is reached. By the end of adolescence around 90% of adult bone is formed and skeletal maturity occurs at around 20-25 years, although this can vary depending on geographical location and socio-economic conditions; for example, malnutrition may delay bone maturity (Drake et al, 2019; Bartl and Bartl, 2017). In rare cases, a genetic mutation can disrupt cartilage development, and therefore the development of bone. This can result in reduced growth and short stature and is known as achondroplasia.

The human growth hormone (somatotropin) is the main stimulus for growth at the epiphyseal growth plates. During puberty, levels of sex hormones (oestrogen and testosterone) increase, which stops cell division within the growth plate. As the chondrocytes in the proliferation zone stop dividing, the growth plate thins and eventually calcifies, and longitudinal bone growth stops (Ralston and McInnes, 2014). Males are on average taller than females because male puberty tends to occur later, so male bones have more time to grow (Waugh and Grant, 2018). Over-secretion of human growth hormone during childhood can produce gigantism, whereby the person is taller and heavier than usually expected, while over-secretion in adults results in a condition called acromegaly.

If there is a fracture in the epiphyseal growth plate while bones are still growing, this can subsequently inhibit bone growth, resulting in reduced bone formation and the bone being shorter. It may also cause misalignment of the joint surfaces and cause a predisposition to developing secondary arthritis later in life. A discrepancy in leg length can lead to pelvic obliquity, with subsequent scoliosis caused by trying to compensate for the difference.

Once bone has formed and matured, it undergoes constant remodelling by osteoclasts and osteoblasts, whereby old bone tissue is replaced by new bone tissue (Fig4). Bone remodelling has several functions, including mobilisation of calcium and other minerals from the skeletal tissue to maintain serum homoeostasis, replacing old tissue and repairing damaged bone, as well as helping the body adapt to different forces, loads and stress applied to the skeleton.

Calcium plays a significant role in the body and is required for muscle contraction, nerve conduction, cell division and blood coagulation. As only 1% of the bodys calcium is in the blood, the skeleton acts as storage facility, releasing calcium in response to the bodys demands. Serum calcium levels are tightly regulated by two hormones, which work antagonistically to maintain homoeostasis. Calcitonin facilitates the deposition of calcium to bone, lowering the serum levels, whereas the parathyroid hormone stimulates the release of calcium from bone, raising the serum calcium levels.

Osteoclasts are large multinucleated cells typically found at sites where there is active bone growth, repair or remodelling, such as around the periosteum, within the endosteum and in the removal of calluses formed during fracture healing (Waugh and Grant, 2018). The osteoclast cell membrane has numerous folds that face the surface of the bone and osteoclasts break down bone tissue by secreting lysosomal enzymes and acids into the space between the ruffled membrane (Robson and Syndercombe Court, 2018). These enzymes dissolve the minerals and some of the bone matrix. The minerals are released from the bone matrix into the extracellular space and the rest of the matrix is phagocytosed and metabolised in the cytoplasm of the osteoclasts (Bartl and Bartl, 2017). Once the area of bone has been resorbed, the osteoclasts move on, while the osteoblasts move in to rebuild the bone matrix.

Osteoblasts synthesise collagen fibres and other organic components that make up the bone matrix. They also secrete alkaline phosphatase, which initiates calcification through the deposit of calcium and other minerals around the matrix (Robson and Syndercombe Court, 2018). As the osteoblasts deposit new bone tissue around themselves, they become trapped in pockets of bone called lacunae. Once this happens, the cells differentiate into osteocytes, which are mature bone cells that no longer secrete bone matrix.

The remodelling process is achieved through the balanced activity of osteoclasts and osteoblasts. If bone is built without the appropriate balance of osteocytes, it results in abnormally thick bone or bony spurs. Conversely, too much tissue loss or calcium depletion can lead to fragile bone that is more susceptible to fracture. The larger
surface area of cancellous bones is associated with a higher remodelling rate than cortical bone (Bartl and Bartl, 2017), which means osteoporosis is more evident in bones with a high proportion of cancellous bone, such as the head/neck of femur or vertebral bones (Robson and Syndercombe Court, 2018). Changes in the remodelling balance may also occur due to pathological conditions, such as Pagets disease of bone, a condition characterised by focal areas of increased and disorganised bone remodelling affecting one or more bones. Typical features on X-ray include focal patches of lysis or sclerosis, cortical thickening, disorganised trabeculae and trabecular thickening.

As the body ages, bone may lose some of its strength and elasticity, making it more susceptible to fracture. This is due to the loss of mineral in the matrix and a reduction in the flexibility of the collagen.

Adequate intake of vitamins and minerals is essential for optimum bone formation and ongoing bone health. Two of the most important are calcium and vitamin D, but many others are needed to keep bones strong and healthy (Box2).

Box 2. Vitamins and minerals needed for bone health

Key nutritional requirements for bone health include minerals such as calcium and phosphorus, as well as smaller qualities of fluoride, manganese, and iron (Robson and Syndercombe Court, 2018). Calcium, phosphorus and vitamin D are essential for effective bone mineralisation. Vitamin D promotes calcium absorption in the intestines, and deficiency in calcium or vitamin D can predispose an individual to ineffective mineralisation and increased risk of developing conditions such as osteoporosis and osteomalacia.

Other key vitamins for healthy bones include vitamin A for osteoblast function and vitamin C for collagen synthesis (Waugh and Grant, 2018).

Physical exercise, in particular weight-bearing exercise, is important in maintaining or increasing bone mineral density and the overall quality and strength of the bone. This is because osteoblasts are stimulated by load-bearing exercise and so bones subjected to mechanical stresses undergo a higher rate of bone remodelling. Reduced skeletal loading is associated with an increased risk of developing osteoporosis (Robson and Syndercombe Court, 2018).

Bones are an important part of the musculoskeletal system and serve many core functions, as well as supporting the bodys structure and facilitating movement. Bone is a dynamic structure, which is continually remodelled in response to stresses placed on the body. Changes to this remodelling process, or inadequate intake of nutrients, can result in changes to bone structure that may predispose the body to increased risk of fracture. Part2 of this series will review the structure and function of the skeletal system.

Bartl R, Bartl C (2017) Structure and architecture of bone. In: Bone Disorder: Biology, Diagnosis, Prevention, Therapy.

Danning CL (2019) Structure and function of the musculoskeletal system. In: Banasik JL, Copstead L-EC (eds) Pathophysiology. St Louis, MO: Elsevier.

Drake RL et al (eds) (2019) Grays Anatomy for Students. London: Elsevier.

Iyer KM (2019) Anatomy of bone, fracture, and fracture healing. In: Iyer KM, Khan WS (eds) General Principles of Orthopedics and Trauma. London: Springer.

Moini J (2019) Bone tissues and the skeletal system. In: Anatomy and Physiology for Health Professionals. Burlington, MA: Jones and Bartlett.

Ralston SH, McInnes IB (2014) Rheumatology and bone disease. In: Walker BR et al (eds) Davidsons Principles and Practice of Medicine. Edinburgh: Churchill Livingstone.

Robson L, Syndercombe Court D (2018) Bone, muscle, skin and connective tissue. In: Naish J, Syndercombe Court D (eds) Medical Sciences. London: Elsevier

Tomlinson RE, Silva MJ (2013) Skeletal blood flow in bone repair and maintenance. Bone Research; 1: 4, 311-322.

Tortora GJ, Derrickson B (2009) The skeletal system: bone tissue. In: Principles of Anatomy and Physiology. Chichester: John Wiley & Sons.

Waugh A, Grant A (2018) The musculoskeletal system. In: Ross & Wilson Anatomy and Physiology in Health and Illness. London: Elsevier.

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Skeletal system 1: the anatomy and physiology of bones - Nursing Times

9 Grey’s Anatomy Actors Who Acted Like Total Jerks On Set (11 Surprising Sweethearts) – TheThings

Posted on December 23, 2019 by Danzig

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9 Grey's Anatomy Actors Who Acted Like Total Jerks On Set (11 Surprising Sweethearts) - TheThings

Anatomy of a Motherboard – TechSpot

Posted on January 6, 2020 by Danzig

You might have a desktop PC at work, school, or home. You might use one to work out tax returns or play the latest games; you might even be into building and tweaking computers. But how well do you know the components that make up a PC? Take the humble motherboard -- it sits there, quietly keeping everything running, and rarely gets the same attention as the CPU or graphics card.

Motherboards are remarkably important though, and full of really cool technology. So let's go all Grey's Anatomy, and dissect the motherboard -- breaking down its various parts and seeing what each bit does!

Let us begin with the main role of a motherboard. In essence, it serves two purposes:

There are other things a motherboard does (e.g. holds the components in place, or provides feedback as to how well everything is functioning) but the aforementioned aspects are critical to how a PC operates, that almost every other part that makes up the motherboard, is related to these two things.

Nearly every motherboard used in a standard desktop PC today will have sockets for the central processing unit (CPU), memory modules (nearly always a type of DRAM), add-in expansion cards (such a graphics card), storage, input/ouputs, and a means to communicate with other computers and systems.

Standard motherboards initially differ in terms of their size, and there are industry-wide standards that manufacturers tend to adhere to (and plenty of others that don't). The main sizes you're likely to come across are:

You can see a far more comprehensive list on Wikipedia but we'll just stick to standard ATX for simplicity, because the differences generally lie in the number of sockets available to be powered and connected; a bigger motherboard permits more sockets.

A motherboard is simply a big electronic printed circuit board, with lots of connectors to plug things into and hundreds, if not thousands, of feet of electrical traces that run between the various sockets. Theoretically, the board isn't needed: you could connect everything together by using a huge mass of wires. The performance would be terrible, though, as the signals would interfere with one another, and there would be notable power losses by using this method, too.

We'll begin our breakdown by using a typical ATX motherboard. The image below corresponds to an Asus Z97-Pro Gamer and its appearance, features, and functions can be found in dozens more like it.

The only problem with the picture (other than the motherboard being quite... umm... well, used) is that there are a lot of visible components, making it trickier to spot everything clearly.

Let's strip it all away and look at a simplified diagram to begin with (below).

That's better, but there is still a lot of sockets and connectors to talk about! Let's start near the top, with the most important one of all.

The diagram has a structure labelled LGA1150. This is the name used by Intel to describe the socket used to hold many of their CPUs. The letters, LGA, stand for Land Grid Array, a common type of packaging technology for CPUs and other integrated circuits.

LGA systems have lots of little pins in the motherboard, or in a socket on the board, to provide power and communications to the processor. You can see them in the picture below:

The metal bracket holds the CPU in place but it's getting in the way of seeing the pins clearly, so let's move it to one side.

Remember the name for this? LGA1150. The number is for how many pins there are in this socket. We'll explore the connections for a CPU in another article, but for now we'll just point out that motherboards for other CPUs will have more or fewer pins.

In general, the more capable the CPU (in terms of number of cores, amount of cache, etc), the more pins will be found in the socket. A large number of these connections will be used to send and receive data to the next important feature on a motherboard.

The sockets or slots that are always the closest to the CPU are those that hold DRAM modules, aka system memory. These are connected directly to the CPU and nothing else on the motherboard. The number of DRAM slots depend mostly on the CPU, as the controller for the memory is built into the central processor.

In the example we're looking at, the CPU that fits into this motherboard has 2 memory controllers, with each one handling 2 sticks of memory - hence there are 4 sockets in total. You can see that, on this motherboard, the memory sockets are colored in way to let you know which ones are managed by which controller. They're commonly called memory channels, so channel #1 handles the 2 black connectors, and channel #2 the grey ones.

This CPU/motherboard combination uses DDR3 SDRAM (double data rate version 3, synchronous dynamic random access memory) chips and each socket holds one SIMM or DIMM. The 'IMM' part stands for Inline Memory Module; the S and D refers to where the module has one side filled with chips or both sides (single or dual).

Along the bottom edge of the memory module are lots of gold plated connectors, and this type of memory has 240 of them in total (120 each side). These provide the power and data signals for the chips.

A single DIMM of DDR3 SDRAM. Image: Crucial

Bigger modules would allow you to have more memory, but the whole setup is limited by the pins on the CPU (almost half of the 1150 pins in this example are dedicated to handle these memory chips) and space for all of the traces or electrical wires in the motherboard.

The computer industry has stuck with using 240 pins on memory modules since 2004 and shows no signs of changing any time soon. To improve memory performance, the chips simply run faster with each new version released. In the example we're looking at, the CPU's memory controllers can each send and receive 64 bits of data per clock cycle. So with two controllers, the memory sticks will having 128 pins dedicated to transferring information. So why 240 pins?

Each memory chip on the DIMM (16 in total, 8 per side) can transfer 8 bits per clock cycle. That means each chip needs 8 pins, just for data transfers; however, two chips share the same data pins, so only 64 of the 240 are data ones. The remaining 176 pins are required for timing and reference purposes, transmitting the addresses of the data (location of where the data is on the module), controlling the chips, and providing electrical power.

So you can see that having more than 240 pins won't necessarily make things better!

System memory is connected directly to the central processor to boost performance, but there are other sockets on the motherboard that are wired a bit like this (and for the same reason). They use a connection technology called PCI Express (PCIe, for short) and every modern CPU has a PCIe controller built into it.

These controllers can handle multiple connections (typically referred to as lanes), even though it is a 'point-to-point' system, meaning that the lanes in the socket aren't shared with any other device. In our example, the CPU's PCI Express controller has 16 lanes.

The image below shows 3 sockets: the top two are PCI Express, while the bottom one is a much older system called PCI (related to PCIe, but a lot slower). The little one at the top is labelled PCIEX1_1 because it is a single lane socket; the one below it is a 16 lane socket.

If you scroll back up and look at the whole motherboard again, you can see that there are:

But if the CPU's controller only has 16 lanes, what's going on? First of all, only PCIEX16_1 and PCIEX16_2 are connected to the CPU - the third one, and the two single lane sockets are connected to another processor on the motherboard (more about that in a moment). Secondly, if both sockets were filled with devices that use 16 PCIe lanes, then the CPU will only dedicate 8 lanes to each.

This is the case of all CPUs today; they have a limited number of lanes, so as more devices get connected to the CP
U, each one gets a smaller number of lanes to work with.

Different CPU and motherboard configurations have their own way of handling of this. For example, Gigabyte's B450M Gaming motherboard has one PCIe 16 lane socket, one PCIe 4 lane socket and a M.2 socket that uses 4 PCIe lanes. With only 16 lanes available from the CPU, using any two sockets will force the larger x16 one to be capped to 8 lanes.

So what kind of things use those sockets? The most common choices are:

You can see the difference between the connectors in the image above. The graphics card sports the longer 16 lane one, compared to the sound card's little 1-lane setup. The latter has far less data to transfer than the former, so it doesn't need all those extra lanes.

In our motherboard example, like all others, has lots more sockets and connections to manage, and so the CPU gets a helping hand from another processor.

If we go back 15 years or so, and look at motherboards from that era, there were two additional chips built into them to support the CPU. Together, they were called a chip set (usually concatenated to chipset), and individually they were called the Northbridge (NB) and Southbridge (SB) chips.

The former handled the system memory and graphics card, the latter processed the data and instructions for everything else.

The above image, of an ASRock 939SLI32 motherboard, clearly shows the NB/SB chips - they're both hidden under aluminum heatsinks, but the one closest to the CPU socket in the middle of the image is the Northbridge. A few years after this product was around, both Intel and AMD released CPUs that had the NB integrated into the central processor.

The Southbridge, though, has remained separate and is likely to be so for the foreseeable future. Interestingly, both CPU manufacturers have stopped calling it the SB and often refer to it as the chipset (Intel's proper name for it is the PCH, platform controller hub), even though it's just a single chip!

On our more modern example from Asus, the SB is also covered with a heatsink, so let's pop it off and have a look at the extra processor.

This chip is an advanced controller, handling multiple types and numbers of connections. Specifically, it's an Intel Z97 chipset and offers the following features:

It also has an integrated network adapter, an integrated sound chip, a VGA display output, and a whole host of other timing and controlling systems. Other motherboards will have more basic/advanced chipsets (providing more PCIe lanes, for example) but in general, most chipsets offer the same kind of features.

For this particular motherboard, this is the processor that handles the single lane PCIe slots, the third 16 lane slot, and the M.2 slot. Like many newer chipsets, it handles all of these different connections by using a set of high speed ports that can be switched to PCI Express, USB, SATA, or networking, depending on what is connected at the time. This, unfortunately, places a limit on how many devices plugged into the motherboard, despite all those sockets.

In the case of our Asus motherboard, the SATA ports (used to attach hard drives, DVD burners, etc) are grouped as shown above because of this limitation. The block of 4 ports in the middle use the chipset's standard USB connections, whereas the two on the left use some of these high speed connections.

So if you use the ones on the left, then the chipset will have fewer connections for other sockets. The same is true for the USB 3.0 ports. There is support for up to 6 devices, but 2 of these ports will also eat into the high speed connections.

The M.2 socket, used to connect SSD storage, uses the fast system, too (along with the third 16 lane PCI Express slot on this motherboard); however, on some CPU/motherboard combinations, the M.2 sockets connect directly to the CPU, as many newer products have more than 16 PCIe lanes to distribute and use.

Along the left hand side of our motherboard, there is a row of connectors generally called the I/O set (input/output) and in this instance, the Southbridge chip (or chipset) only handles a few of them:

The CPU's integrated graphics processor handles the HDMI and DVI-D sockets (bottom middle) but the rest are managed by additional chips. Most motherboard have a raft of extra little processors to manage all kinds of things, so let's have a look at some of those.

CPUs and chipsets have a limit to what they can support or connect to, so most motherboard manufacturers offer products with extra features, thanks to the use of other integrated circuits. This might be to provide extra SATA ports, for example, or provide connections for older devices.

The Asus motherboard we've been looking at is no different. For example, the Nuvoton NCT6791D chip handles all of the little connectors for fans and the temperature sensors built into the board; the Asmedia ASM1083 processor next to it manages the two legacy PCI sockets, because the Intel Z97 chip has no such capability.

Although Intel's chipset has a built-in network adapter, it uses some of those valuable high speed connections, so Asus added another Intel chip (an I218V) to manage the red ethernet socket we saw in the I/O set. The above image does no justice to how small this chip is: it's just 0.24 inches (6 mm) square!

The stadium-shaped silver metal thing is a type of quartz crystal oscillator -- it provides a low frequency timing signal, for the networking chip to stay synchronized.

Something else that this motherboard offers as an extra is a chip to handle audio. Yes, the Intel chipset has its own integrated sound processor, but it's been bypassed for the same kind of reasons that Asus have added a separate networking chip and that most people add a graphics card to replace the integrated graphics processor in the CPU. In other words, the extra chip is just better!

Not all of the extra chips on the motherboard are about replacing integrated ones, many are there to manage or control the operation of the board in general.

These little chips are PCI Express switches and help the CPU and Southbridge manage the 16 lane PCIe connectors, when they need to distribute the lanes to more devices.

Motherboards with the ability to overclock CPUs, chipsets, and system memory are now commonplace, and many come with extra integrated circuits to manage this. In our example board, highlighted in red, Asus is using its own design called the TPU ('TurboV Processing Unit') that adjusts clock speeds and voltages to a fine level of control and adjustment.

The little Pm25LD512 device next to it, highlighted in blue, is a flash memory chip that stores the clock and voltage settings when the motherboard is powered off, so you don't have to redo them, every time you power up the PC.

Every single motherboard has at least one flash memory device, though, and this is for storing the motherboard's BIOS (the basic hardware initialization operating system that gets everything going before loading Windows, Linux, macOS, etc).

This Winbond chip is just 8 MB in size but that's more than enough to hold all of the software needed. This kind of flash memory is designed to use very little power when in use and hold onto its data for decades.

When you switch on the PC, the contents of the flash memory are copied directly to the CPU's cache or system memory, and then run from there, for maximum performance. However, the one thing that this memory can't hold onto is time.

This motherboard, like every other one around, uses a CR2032 cell to power a simple timing circuit, that keeps track of the data and time for the motherboard. Of course, the power of a cell doesn't last forever and once it's flat, the motherboard will default to a starting time/date in the flash memory.

And speaking of power, there are more connectors for that, too!

To provide the voltage and current required to run the motherboard and many of the devices attach
ed to it, the computer's power supply unit (PSU) will have a number of standard connectors for this purpose. The main one is a 24-pin ATX12V version 2.4 socket.

The amount of current that can be drawn from the pins depends on the PSU, but the voltages are industry set to +3.3, +5, and +12 volts.

The bulk of the current for the CPU is drawn off the 12 volt pins, but for modern high-end systems, it's not enough. To get around this problem, there is an additional 8-pin power connector that provides another four set of 12V pins to be used.

The connectors from the PSU have color coded wires to help identify what each wire is for, but the sockets on the motherboard don't tell you very much. Here's a diagram for the two power sockets:

The +3.3V, +5, and +12V lines supply power to the various components on the motherboard itself, and also powers the CPU, DRAM, and any devices plugged into the extension sockets such as the USB or PCI Express slots. Anything using the SATA ports need power directly from the PSU, though, and PCI Express sockets can only provide up to 75W. If the device needs more juice than that -- lots of graphics cards do -- then they'll need to be hooked up to the PSU directly, too.

However, there's a larger problem than having enough 12V pins: CPUs don't run on that voltage.

For example, the Intel CPUs designed to run on this Asus Z97 motherboard run off voltages between 0.7 and 1.4 volts. It's not a fixed voltage, because today's CPUs vary how much voltage they're running on to save power and reduce heat; so when idling on the desktop, the CPU can tootle away with less than 0.8 volts. Then with all the cores fully loaded and working away, it rises to 1.4 volts or more.

Power supply units are designed to convert mains AC voltage (110 or 230, depending on the country) into fixed DC voltages, so additional circuits must be used to drop them lower and vary them as required. These circuits are called voltage regulation modules (VRMs, for short) and can be easily spotted on any motherboard.

Each VRM is typically comprises 4 components:

You can read more about how they work on Wikichip, but let's briefly go through a few things. Each VRM is usually called a phase and multiple phases are required, because one alone can't supply enough current for a modern CPU (our motherboard has 8 VRMs, called an 8-phase system).

The VRMs are usually managed by a separate chip, that monitors the device, and switches the modules as for the required voltage. These are called multiphase pulse width modulator controllers; Asus calls theirs an EPU! All of these things get quite hot when they're working away, so they're often covered by a metal heatsink to help dissipate the waste energy.

Continue reading here:
Anatomy of a Motherboard - TechSpot

Grey’s Anatomy Season 13’s Gag Reel Is Here to Help You Start … – E! Online

Posted on August 22, 2017 by Danzig

The struggle is real, Grey's Anatomy fans.

We've still got over a month before we can check back in with the good doctors of Grey Sloan Memorial Hospital to see how they're recovering after last season's (literally) explosive finale.Our impatience over waiting for the two-hour season 14 premiere may be growing stronger, but we've got a new way to distract ourselves from our Grey's hunger pangs: The season 13 gag reel.

Exclusive to E! News, and available as a bonus feature on the season 13 DVD set (in stores August 29), this year's reel has all of your faves cutting loose and cracking up. There's Ellen Pompeo continually referring to Dr. Webber as the "Director of Admissions" despite knowing full-well that's not his title, and Justin Chambers stumbling over the usually easily pronounceable phrase "surgical consult." Not to be outdone, Jesse Williams begins saying lines that aren't even his, while an extra full-on breaks a table in one scene.

"We still doing the TV show?" Chandra Wilson asks hysterically.

When the show returns for season 14, some of the laughter from the gag reel just might be making its way into the final cut, Jessica Capshaw recently admitted to E! News. When asked how the hospital was handling the events of the finale, she had this to offer:"I think it's in a recovery and I think it's not only in a recovery, but it's in sort of like a moment where you find your placeand you gain a little traction and then you move positively and forward-ly on. We did a table read for both the firstand second episodes, and they are righteously hysterical. They're so much fun and very sort of going back to firstand second season Grey's. It's very funny. It's very irreverent and funny and sort of on its side. I think it'swhat you remember and love about the beginning of the original group."

Whose flub has you cracking up the most? Sound off in the comments below!

Grey's Anatomy: The Complete 13th Season hits shelveson Tuesday, Aug. 29, while Season 14 premieres Thursday, Sept. 28 at 8 p.m. on ABC.

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Grey's Anatomy Season 13's Gag Reel Is Here to Help You Start ... - E! Online

Wisconsin football: Is there hope for a Badgers win over Ohio State? – Bucky’s 5th Quarter

Posted on December 6, 2019 by Danzig

Well, your B1G West champion No. 8 Wisconsin Badgers (10-2 overall, 7-2 B1G) take on the No. 1 Ohio State Buckeyes (12-0 overall, 9-0 B1G) tomorrow in the B1G championship game.

The Badgers are pretty serious underdogs here, as the Buckeyes are about 16.5 point favorites. If Wisconsin pulls off the upset, this could very well be the biggest victory in program history.

Lets take a look at some of the common aspects of big upsets and how the Badgers may or may not be up to the task.

Before we get into the details, lets talk about how people are feeling heading into this one. Before the first Ohio State game and earlier this week, I posted a twitter poll, which of course is known for scientific accuracy.

Anyways, the tool was consistent from six weeks ago to now, so it is interesting to compare the poll results. We asked the same question both times with the same options: How are #Badgers fans feeling about Saturdays football game against OSU? Optimism - Apathy - Dread - Other. And, here are the results.

A quick Chi-Squared test confirms (p-value = .001) that this data suggests fan sentiment has shifted in the last month and a half. However, this shift has been rather small. Folks seem to be slightly more apathetic, less optimistic and are not dreading this game quite as much, but the ordinal ranking of the responses remain the same.

You can run through the twitter replies yourself, but here are a few highlights from our followers written responses to the poll:

Wisconsin is in a really strange spot. It has definitely earned a spot in the top 10, but absolutely nobody outside of Wisconsin is giving the Badgers a chance. The gap between Wisconsin and Ohio State is not as big as the gap between Virginia and Clemson, but both games appear impossible on paper.

Alright, so if Wisconsin is going to pull this thing off, what is it going to need to do? Well, Im done with grad school now, so why not start off with a literature review because I have not been punished enough.

I dont know why I thought the anatomy of an upset was clever, but when I googled it, I found hundreds of articles.

Im unique, just like everyone else.

After wading through a ton of nonsense, I found four resources that did a nice job talking about what has to go right for an underdog to win.

College Football Nerds bring this up all the time on their channel (although they are not alone in these resources). They point out a common mistake coaches make: trying to keep the game close.

Warning: paragraph about chess incoming.

This is the exact same thing in chess. The clearer the game is, the stronger player knows how to play you. Weaker chess players often try to play conservatively to avoid big mistakes, but instead the stronger player makes small improvements over forty moves and ends up with an insurmountable advantage. The one time I beat a Grandmaster, it was because I played an aggressive opening and keep the game dynamic. My position was worse, but I gave the GM opportunities to make mistakes.

We are done talking about chess now.

This is the key here: you have to give the other team opportunities to make mistakes. If you curl up into a ball, you may keep the game artificially close, but you will never have a chance to actually score more points. If you play ultra-aggressive, youll tend to lose by more points, but one out of ten times the stars will align and you will find an edge.

College Football Nerds assessed the October 26 meeting between Wisconsin and Ohio State as an overly-passive strategy, saying that Wisconsin relied on Jonathan Taylor too much and died a death by a thousand cuts. They also noticed that Taylor ran the ball more than Coan threw it against Ohio State. Further, they contrasted that with the Minnesota game when Coan threw the ball more than Taylor ran it.

My colleague Tyler Hunt thinks that Wisconsin will indeed be more aggressive this time around:

In this game, I expect the Badgers to continue with the aggressive to give themselves a shot. Punts and field goals arent going to win this game, so when the opportunity calls, take your shots.

I want to believe this, I really do. However, I perceive that Paul Chryst gets most aggressive against teams like Michigan and Minnesota that are closer in ability to Wisconsin, and he becomes more passive against teams like Illinois, Northwestern and Ohio State. Basically, I perceive Chryst coaching more aggressively against teams within one standard deviation of the Badgers and less aggressive against teams further away from Wisconsin in ability for better or worse.

Further, Chryst might decide that Wisconsins best realistic outcome is a Rose Bowl. In this case, he might try to just shorten the game and keep it close. Hunt noted this as well:

Sure Wisconsin can try to keep it close to back into a Rose Bowl, or they can be aggressive and let the chips fall where they may. I fully expect the Badgers to do the latter, and I cannot wait to see it. Shock the world boys.

Im not as optimistic that Wisconsin will go all-out, but I sure hope Tyler is right. We will know early on what kind of game this is.

I am not the expert in this, or else I would be making hundreds of thousands a year as an offensive coordinator. However, I will try ton take a stab at this.

I think the key mismatch is finding ways to get Taylor the ball out in space, preferably with one-on-one coverage by a linebacker. Its clear that Wisconsin has struggled to get Taylor into these situations out of conventional run plays, so Chryst will need to use Taylor in some new packages.

Lets go off the wall here. How about Wisconsin running spread looks out of the 22 personnel with Taylor lined out wide and maybe Mason Stokke, Nakia Watson or Garret Groshek in the backfield? Or, how about 11 personnel that lines up five wide?

Feel free to comment how these are stupid ideas, but I think its this type of thinking that could produce a successful game if it is filtered through a smarter schematic mind than mine.

In Football Study Halls series on anatomy of an upset, Bill Connelly looked at two big upsets form 2007: Appalachian States victory over Michigan and UL-Monroes victory over Alabama. Additionally, Ian Boyd added a piece to the series on Houstons 2016 upset win over Oklahoma.

The key thing to learn about these posts is each game went quite differently. For some turnovers were key, for some it wasnt. For some total yardage was important, for some it wasnt. And so on, and so on.

However, each of these upsets featured consistent success by the underdog in obvious passing situations.

Thats it. Success on obvious passing situations is important.

Moving on.

Ohio State is going to out-gain Wisconsin. If Wisconsin gains 150 yards in a quarter, you want that 150 yards to be mostly spread between few significant plays instead of being sprinkled over five 30-yard drives that end in punts or field goals.

Further, turnovers can neutralize Ohio States offensive production. A fifty yard drive becomes a thought experiment when it ends in a fumble.

You probably knew this, but turnovers and explosive plays are important.

Again, Ohio State is going to out-gain Wisconsin. When Ohio State makes it into the red zone, Wisconsin has to force several field goals.

Ohio State averages 4.8 red zone scoring attempts each game. Ohio State is the second best team in the country in terms of red zone touchdown percentage at 86%. That means, on average Ohio State scores 30.91 red zone points per game.

This is an easy stat to turn aroundit only takes a handful of successful defensive plays to change Ohio States effective red zone touchdown percentage.

First, Wisconsin needs to not allow any scores without Ohio State coming through the red zone. Next, it needs to cut Ohio States red zone touchdown percentage from 86% to about 25%. While the percentage drop is significant, that is only three more red zone stops over the course of
a game. That is difficult yet achievable.

Assume Ohio State makes it into the red zone five times against Wisconsin. If Ohio State follows its season average for red zone production, that would turn into 31 Buckeye points. However, if Wisconsin can make four red zone stops instead of only one, that drops Ohio State down to 19 red zone points.

Three extra red zone stops would decrease Ohio States scoring by 12 points, which is almost 75% of the spread.

Each of these findings are about increasing variance: upwards for Wisconsin (taking more chances, success on passing downs and turnovers) and downwards for Ohio State (field goals instead of turnovers and strange mismatches).

Its a million-to-one shot, but its a chance Wisconsin gets to take.

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Wisconsin football: Is there hope for a Badgers win over Ohio State? - Bucky's 5th Quarter

Greys Anatomy Contributed To Public Awareness Of Sexual Assault Report – Deadline

Posted on December 6, 2019 by Danzig

An Oklahoma State University study has concluded that an episode of ABCs Greys Anatomy medical drama contributed to heightened public awareness of sexual assault.

The study,published in the journalJAMA Internal Medicine earlier this month, claimed that the March episode, Silent All These Years,helped raise the profile of the group RAINN (Rape, Abuse, and Incest National Network). A key was the call-out by series star Ellen Pompeo at the end of the episode, encouraging victims to call the organizations hotline.

The OKU research found that searches for the terms RAINN spiked by 41 percent and rape by 8 percent following the episodes airing. On Twitter, tweets with sexual assault hotline and RAINN increased by more than 1,000 percent. Beyond social media, calls to RAINN increased by 43 percent in the 48 hours after the episode, the organization claimed.

In the episode, a patient named Abby (played by Khalilah Joi) was sexually assaulted, but reluctant to report the crime because she feared not being believed.

Abby was eventually convinced to undergo a sex assault forensic exam. As Abby is wheeled into surgery to fix a tear in her diaphragm, all the female hospital employees line the hallway to the OR, shielding a skittish Abby from males.

Watch the video of that clip above.

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Greys Anatomy Contributed To Public Awareness Of Sexual Assault Report - Deadline

Caitlin Johnstone: Anatomy of an Alt-Left Conspiracy Nut – The Daily Banter

Posted on June 12, 2017 by Danzig

The Daily Banter

Caitlin Johnstone: Anatomy of an Alt-Left Conspiracy Nut
The Daily Banter
Caitlin Johnstone: Anatomy of an Alt-Left Conspiracy Nut. We take you inside the mind Caitlin Johnstone, a member of the Alt-Left movement dedicated to spreading vile conspiracy theories and atrocious journalism. Avatar: Ben Cohen; Author: Ben Cohen ...

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Caitlin Johnstone: Anatomy of an Alt-Left Conspiracy Nut - The Daily Banter

Review: Anatomy of Ferguson, From a Shooting to Activism – New York Times

Posted on August 12, 2017 by ev1

Photo Brittany Ferrells activism in Ferguson, Mo., is a focal point of the documentary Whose Streets? Credit Autumn Lin/Magnolia Pictures

Whose Streets?, a documentary about the unrest and activism in Ferguson, Mo., in the wake of the 2014 police shooting of Michael Brown, an unarmed black teenager, is choppy, sometimes unfocused, and in every respect the opposite of slick. Its directors, Sabaah Folayan and Damon Davis, are novice filmmakers, true; but I also suspect this movies form is deliberate, part of its message. This is direct and frequently powerful filmmaking that doesnt much care about meeting my aesthetic standards.

A preview of the film.

Whose Streets? takes off from the night Mr. Brown was shot. One of the movies subjects is David Whitt, a resident of the apartment complex on the street where the shooting took place, who is moved to take his video camera onto the streets to record police action as rioting started. Another thread follows Brittany Ferrell and Alexis Templeton, a couple navigating parenthood and school, and putting themselves at considerable risk as they lead and participate in demonstrations like one in which they formed a human chain to block traffic on a highway.

The movie is punctuated with quotes by black historical figures Martin Luther King Jr.s observation that a riot is the language of the unheard is particularly resonant. Much of the footage is from low-resolution video cameras and cellphones; the most professional-looking material here is from a television interview with Officer Darren Wilson, who shot Mr. Brown, in which he says, You cant perform the duties of a police officer and have racism in you. This is shown in the same section that features on-the-fly shots of off-duty St. Louis police officers puffing their chests at activists at a town hall meeting. Another wrenching scene shows a protester trying to address a black female officer, the only person of color in a defensive line of cops; she holds her position even as tears fill her eyes.

Whose Streets?

Directors Sabaah Folayan, Damon Davis

Stars Brittany Ferrell, Tef Poe, Kayla Reed, Tory Russell, Alexis Templeton

Rating R

Running Time 1h 30m

Genre Documentary

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Review: Anatomy of Ferguson, From a Shooting to Activism - New York Times

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