Why Do Men Have Nipples? – ScienceAlert

It's a question that's been bothering humans for centuries, even before the theory of evolution was first conceived. Why do men and other male mammals have nipples if they don't feed their young? What's the point?

"I have received more than a dozen requests to explain how evolution could possibly produce such a useless structure," evolutionary biologist Stephen Jay Gould wrote in a journal column back in 1993.

After all, the vast majority of men never lactate, although there are a few exceptions which typically involve some hormonal problem. But when we think about traits from an evolutionary perspective, we often think in terms of 'What is this thing good for?'

It turns out that the case of male nipples somewhat contradicts that very question.

The short answer is that it's not necessarily a feature produced by evolution - instead, it's more like a feature that evolution didn't bother to get rid of, or possibly even couldn't.

"In my view of life ... male nipples are an expectation based on pathways of sexual differentiation in mammalian embryology," wrote Gould.

What he was referring to is the fact that all mammal embryos - male and female - start out looking exactly the same, with potential to develop into either sex.

But if the embryo has an XY chromosome set, after the first few weeks a gene called SRY kicks in, triggering the genetic switch that sends the embryo down the male development path.

But here's the thing - mammary glands start developing super-early, even before SRY can do its job. And so the precursors to breast tissue, nipples and all, are preserved even once an embryo becomes biologically male.

And it's not like having nipples is a costly feature to have. So even if evolution could rewire the developmental process to get rid of them for men, it's more likely that it just shrugged and let them be.

It's also a reminder that evolution is kinda messy. According to evolutionary biologist Rob Brooks from the University of New South Wales in Australia, several genes can be involved in the making of a trait, leaving it around even if it's not being selected for.

"Even for periods of time, something can be selected neither for nor against, and what you would expect under those circumstances is that the presence or absence of our traits will drift," Brooks told ScienceAlert.

So the answer seems pretty simple in the end. But exploring the question about male nipples also gives us a nice lesson about adaptive thinking in evolution.

People sometimes get carried away and try to find an evolutionary explanation for every trait they see. After all, when you understand the basic premise of evolution, it becomes a pretty compelling narrative.

"It's really tempting to [view traits as adaptive] because once you understand the adaptive logic, then you start - like with all confirmation bias - to see the signature of adaptation everywhere," says Brooks.

But just because a story is compelling, doesn't mean it's accurate. Sure, you could come up with some elaborate story on how male nipples must be attractive for females somehow, but it's much more plausible to consider the simple developmental wiring problem we explained above.

Gould himself was famously critical of "just-so stories" about natural selection, but bear in mind that they can be an excellent starting point for further experiments.

"Science is there to test the ideas, so adaptive storytelling is hugely important, because it's the source of our hypotheses," Brooks told ScienceAlert.

"If you don't come up with an adaptive story, then there's nothing to test."

Of course, in the case of male nipples, we don't need an adaptive story. Just treat them as accessories, guys.

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Why Do Men Have Nipples? - ScienceAlert

Center to advance tissue regeneration, stem cell discoveries – UIC News

The Center for Stem Cell and Regenerative Medicine will use a team-oriented, multidisciplinary approach, says Asrar Malik, head of pharmacology.

The College of Medicine launched a new center that focuses on understanding tissue regeneration and pioneering future developments in stem cell biology as a means to repair diseased organs and tissues.

The opening of the Center for Stem Cell and Regenerative Medicinewas commemorated Monday with a symposium on stem cell and regenerative medicine.

The center will partner with colleges and departments across the University of Illinois System.

Researchers in the new center will investigate the molecular signals that drive stem cells to mature into different cell types, such as blood, heart and blood vessel cells. The center will also study the epigenetic regulation of stem cells; determine the best approaches to transplant engineered cells, tissues and organs; and look for ways to efficiently produce the regenerative cells needed for novel treatments.

The center will use a team-oriented, multidisciplinary approach that incorporates experts in biochemistry, biophysics, bioengineering and the clinical sciences to investigate stem cell biology and tissue regeneration, said Asrar Malik, the Schweppe Family Distinguished Professor and head of pharmacology, who is guiding the effort.

A search has begun to recruit a director and additional faculty members, he said.

The current program in stem cell biology and regenerative medicine includes seven faculty members, most within the department of pharmacology, who together have more than $10 million in research grants from the National Institutes of Health.

The intent in the next few years will be to carry out additional recruitments with other departments, to build from this interdisciplinary foundation and capitalize on our strengths, Malik said.

Three new faculty members in pharmacology have joined the center in the last two years. Owen Tamplin studies stem cells in zebrafish; Kostandin Pajcini investigates the role of stem cells in the development of leukemia; and Jae-Won Shin engineers stem cells and tissues with an eye toward transplantation.

As the only dedicated stem cell and regenerative medicine center in Chicago with a focus on basic biology and translational science, it will affirm UICs leadership role in these fields and help attract additional talent, Malik said.

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Center to advance tissue regeneration, stem cell discoveries - UIC News

Pierre Coulombe, Ph.D. to lead UM Department of Cell & Developmental Biology – University of Michigan Health System News (press release)

ANN ARBOR, MI One of the oldest departments at the University of Michigan is about to get a new leader. The U-M Board of Regents today approved the appointment of Pierre A. Coulombe, Ph.D., to lead the Department of Cell and Developmental Biology in the Medical School.

Coulombe will become chair on August 1, and lead one of the nine basic science departments of Michigan Medicine, U-Ms academic medical center. The departments researchers study how structure governs function in cells and tissues throughout the body, and how complex arrays of signals are integrated to foster the proper development of tissues and organs. They also study stem cells, including embryonic stem cells, and train undergraduate, graduate and medical students in cell biology.

The department traces its roots back to 1854, soon after the founding of the Medical School, when it was known as the Department of Anatomy.

Coulombe comes to Michigan from Johns Hopkins University, where he chaired the Department of Biochemistry and Molecular Biology in the Bloomberg School of Public Health for nine years, and held the E.V. McCollum professorship as well as several joint appointments in the School of Medicine. At Hopkins, Coulombe was noted for at recruiting and nurturing junior faculty members to success, and developing robust training programs for graduate students and post-doctoral fellows. He was also instrumental in addressing the departments infrastructure needs.

To me, cell and developmental biology are critically important endeavors as one seeks to translate the wealth of knowledge acquired in biochemistry and molecular biology, along with the power of imaging techniques, into a better understanding of how organs and tissues form, and operate, under normal and disease conditions, he says. This knowledge is also important for developing novel therapies for human disease. U-M already is a formidable institution, and otherwise is making a substantial investment into biomedical research. Therefore, I am absolutely thrilled about the opportunity to lead Cell & Developmental Biology, and team up with my new colleagues in the department and at U-M, to fulfill this potential.

In addition to his appointment in Cell & Developmental Biology, Coulombe will have a joint appointment in the U-M Department of Dermatology. His research focuses on understanding how keratin proteins and the nanoscale filaments they form foster an optimal architecture and function in skin and related epithelia, and how disruption of these processes result in diseases ranging from inherited conditions to cancer.

A native of Montral, Qubec, Coulombe earned his undergraduate degree from the Universit du Qubec Montral and his Ph.D. in Pharmacology from Universit de Montral. He completed his postdoctoral fellowship in the Department of Molecular Genetics and Cell Biology & Howard Hughes Medical Institute at the University of Chicago before joining Johns Hopkins School of Medicine in 1992. He is the author of more than 140 peer-reviewed publications and one book, holds one patent, and has received multiple awards in recognition of his research and teaching endeavors.

For more about the U-M Department of Cell and Developmental Biology, visit https://medicine.umich.edu/dept/cell-developmental-biology.

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Pierre Coulombe, Ph.D. to lead UM Department of Cell & Developmental Biology - University of Michigan Health System News (press release)

Newly identified method of gene regulation challenges accepted … – Phys.Org

June 15, 2017

Researchers at the Stanford University School of Medicine have discovered an unexpected layer of the regulation of gene expression. The finding will likely disrupt scientists' understanding of how cells regulate their genes to develop, communicate and carry out specific tasks throughout the body.

The researchers found that cellular workhorses called ribosomes, which are responsible for transforming genes encoded in RNA into proteins, display a never-before-imagined variety in their composition that significantly affects their function. In particular, the protein components of a ribosome serve to tune the tiny machine so that it specializes in the translation of genes in related cellular pathways. One type of ribosome, for example, prefers to translate genes involved in cellular differentiation, while another specializes in genes that carry out essential metabolic duties.

The discovery is shocking because researchers have believed for decades that ribosomes functioned like tiny automatons, showing no preference as they translated any and all nearby RNA molecules into proteins. Now it appears that broad variation in protein production could be sparked not by changes in the expression levels of thousands of individual genes, but instead by small tweaks to ribosomal proteins.

'Broad implications'

"This discovery was completely unexpected," said Maria Barna, PhD, assistant professor of developmental biology and of genetics. "These findings will likely change the dogma for how the genetic code is translated. Until now, each of the 1 to10 million ribosomes within a cell has been thought to be identical and interchangeable. Now we're uncovering a new layer of control to gene expression that will have broad implications for basic science and human disease."

Barna is the senior author of the study, which will be published online June 15 in Molecular Cell. Postdoctoral scholars Zhen Shi, PhD, and Kotaro Fujii, PhD, share lead authorship. Barna is a New York Stem Cell Robertson Investigator and is also a member of Stanford's Bio-X and Child Health Research Institute.

The work builds upon a previous study from Barna's laboratory that was published June 1 in Cell. The lead author of that study was postdoctoral scholar Deniz Simsek, PhD. It showed that ribosomes also differ in the types of proteins they accumulate on their outer shells. It also identified more than 400 ribosome-associated proteins, called RAPs, and showed that they can affect ribosomal function.

Every biology student learns the basics of how the genetic code is used to govern cellular life. In broad strokes, the DNA in the nucleus carries the building instructions for about 20,000 genes. Genes are chosen for expression by proteins that land on the DNA and "transcribe" the DNA sequence into short pieces of mobile, or messenger, RNA that can leave the nucleus. Once in the cell's cytoplasm, the RNA binds to ribosomes to be translated into strings of amino acids known as proteins.

Every living cell has up to 10 million ribosomes floating in its cellular soup. These tiny engines are themselves complex structures that contain up to 80 individual core proteins and four RNA molecules. Each ribosome has two main subunits: one that binds to and "reads" the RNA molecule to be translated, and another that assembles the protein based on the RNA blueprint. As shown for the first time in the Cell study, ribosomes also collect associated proteins called RAPs that decorate their outer shell like Christmas tree ornaments.

'Hints of a more complex scenario'

"Until recently, ribosomes have been thought to take an important but backstage role in the cell, just taking in and blindly translating the genetic code," said Barna. "But in the past couple of years there have been some intriguing hints of a more complex scenario. Some human genetic diseases caused by mutations in ribosomal proteins affect only specific organs or tissues, for example. This has been very perplexing. We wanted to revisit the textbook notion that all ribosomes are the same."

In 2011, members of Barna's lab showed that one core ribosomal protein called RPL38/eL38 is necessary for the appropriate patterning of the mammalian body plan during development; mice with a mutation in this protein developed skeletal defects such as extra ribs, facial clefts and abnormally short, malformed tails.

Shi and Fujii used a quantitative proteomics technology called selected reaction monitoring to precisely calculate the quantities, or stoichiometry, of each of several ribosomal proteins isolated from ribosomes within mouse embryonic stem cells. Their calculations showed that not all the ribosomal proteins were always present in the same amount. In other words, the ribosomes differed from one another in their compositions.

"We realized for the first time that, in terms of the exact stoichiometry of these proteins, there are significant differences among individual ribosomes," said Barna. "But what does this mean when it comes to thinking about fundamental aspects of a cell, how it functions?"

To find out, the researchers tagged the different ribosomal proteins and used them to isolate RNA molecules in the act of being translated by the ribosome. The results were unlike what they could have ever imagined.

"We found that, if you compare two populations of ribosomes, they exhibit a preference for translating certain types of genes," said Shi. "One prefers to translate genes associated with cell metabolism; another is more likely to be translating genes that make proteins necessary for embryonic development. We found entire biological pathways represented by the translational preferences of specific ribosomes. It's like the ribosomes have some kind of ingrained knowledge as to what genes they prefer to translate into proteins."

The findings dovetail with those of the Cell paper. That paper "showed that there is more to ribosomes than the 80 core proteins," said Simsek. "We identified hundreds of RAPs as components of the cell cycle, energy metabolism, and cell signaling. We believe these RAPs may allow the ribosomes to participate more dynamically in these intricate cellular functions."

"Barna and her team have taken a big step toward understanding how ribosomes control protein synthesis by looking at unperturbed stem cells form mammals," said Jamie Cate, PhD, professor of molecular and cell biology and of chemistry at the University of California-Berkeley. "They found 'built-in' regulators of translation for a subset of important mRNAs and are sure to find more in other cells. It is an important advance in the field." Cate was not involved in the research.

Freeing cells from micromanaging gene expression

The fact that ribosomes can differ among their core protein components as well as among their associated proteins, the RAPs, and that these differences can significantly affect ribosomal function, highlights a way that a cell could transform its protein landscape by simply modifying ribosomes so that they prefer to translate one type of genesay, those involved in metabolismover others. This possibility would free the cell from having to micromanage the expression levels of hundreds or thousands of genes involved in individual pathways. In this scenario, many more messenger RNAs could be available than get translated into proteins, simply based on what the majority of ribosomes prefer, and this preference could be tuned by a change in expression of just a few ribosomal proteins.

Barna and her colleagues are now planning to test whether the prevalence of certain types of ribosomes shift during major cellular changes, such as when a cell enters the cell cycle after resting, or when a stem cell begins to differentiate into a more specialized type of cell. They'd also like to learn more about how the ribosomes are able to discriminate between classes of genes.

Although the findings of the two papers introduce a new concept of genetic regulation within the cell, they make a kind of sense, the researchers said.

"About 60 percent of a cell's energy is spent making and maintaining ribosomes," said Barna. "The idea that they play no role in the regulation of genetic expression is, in retrospect, a bit silly."

Explore further: In creation of cellular protein factories, less is sometimes more

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Again we're shocked to discover that the higher energy environment our solar system experiences, the greater the tightening and finite organizing we see at the cellular level. What will we find only to lose it as our system passes out of higher energy is astonishing. Looking thru this lens of higher energy in past cycles reforms myths into potential truths.

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Newly identified method of gene regulation challenges accepted ... - Phys.Org

Oley’s Rachel Stahl graduates with a Bachelor of Science in Biochemistry – Boyertown Berk Montgomery Newspapers

Rachel Stahl of Oley was among approximately 250 students who received diplomas at Marietta Colleges 180th graduation ceremony on Sunday, May 7, in the Dyson Baudo Recreation Center. Stahl completed requirements for the Bachelor of Science in Biochemistry.

Stahl is also a graduate of Oley Valley High School.

Robert Dyson 68, a businessman, philanthropist and racecar driver, delivered the commencement address to the Class of 2017.

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Oley's Rachel Stahl graduates with a Bachelor of Science in Biochemistry - Boyertown Berk Montgomery Newspapers

London fire: Anatomy of a high-rise horror – The Sydney Morning Herald

London:It began with a sudden, frantic knocking on a door, late at night.

On the fourth floor of Grenfell Tower, a block of flats in west London, pregnant Maryam Adam, 41, had been deep in sleep when the loud banging woke her. The clock told her it was just after a quarter to one in the morning.

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Fears the toll will rise with 12 confirmed dead and 78 taken to hospital after the massive blaze at the 24-storey Grenfell Tower in London.

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WARNING, DISTRESSING IMAGES: Two people died at the scene and five later died in hospital after an explosion near a kindergarten in east China's Jiangsu Province.

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A blimp at the US Open golf tournament in Wisconsin caught fire and crashed on Thursday.

Fears the toll will rise with 12 confirmed dead and 78 taken to hospital after the massive blaze at the 24-storey Grenfell Tower in London.

She went to the door. It was her neighbour, identified by one newspaper on Thursday as a 44-year old taxi driver from Ethiopia.

"He was shouting that his flat was on fire," Adam said.

She looked across the central corridor in the core of the 24-storey tower. A big bag of clothes sat outside the man's flat.

His door was open and through it she saw a "small" fire in his kitchen, she said later.

Another woman on the same floor, Aalya Moses, had a similar experience.

"There was no alarm, no sprinkler, just my neighbour who told everyone on my floor and the surrounding floors," she said. "If he hadn't told me I wouldn't have known."

Adam echoed the sentiment. "If he had not knocked, I don't know what would have happened."

They left the building, spooked. It was about 10 minutesto one in the morning on Wednesday, June 14.

Within an hour, the place would be an inferno.

This is a story that has many revisions to come.There will be surprise reunions and inevitable funerals. There will be police reports, fire reports and an inquest into the deaths: 17 at Thursday's count, a number that will rise over days and possibly weeks.

And there will be an official public inquiry into what happened and what can be learnt, what must be learntfrom a tragedy that, it appears, could have been and was foreseen, and could have been but wasn't prevented.

It was a pleasant night after a warm day. Many in Grenfell Tower had left their windows open to capture a light, cool night breeze.

The building benefited from new insulation, installed in a renovation that finished in 2016: a sleek aluminium composite cladding covering old, stained concrete.

That cladding was starting to catch fire.

Mahal Egal was another who got out from the fourth floor with his two small children, warned by a neighbour, among the first to evacuate.

He said the neighbour told him his fridge had exploded.

Leaving was against the building's fire safety advice. If residents knew there was a fire outside their flat, they were supposed to shut their door and wait for rescue.

Such buildings are designed to isolate fires. And with residents safe inside their flats, firefighters have more chance of running an orderly evacuation if it becomes necessary.

Indeed, this was reportedly the early advice that firefighters and 000 emergency operators were giving before an evacuation was ordered some time later. If this turns out to be the case, it could have been a fatal mistake firefighters and fire safety experts later said this fire spread faster than any high-rise blaze they had seen before.

Even as Egal left his flat, the first of many fire engines were arriving.

"At first it seemed controllable," he said, watching the fire from the outside. "At this point the fire was no higher than an average tree.

"But really quickly the fire started to rise, as the cladding caught fire."

There was already smoke inside the building, in the single central stairwell, he said.

He thought of his extended family and friends still inside the building, and he worried, and he watched the fire grow out of control, leaping eagerly up the building.

Within minutes it had climbed a dozen floors.

Witness Tanya Thompson said she saw it go "up like a firewall, straight up the side of the building" in about ten minutes. Another, Omar, said it was "like a piece of paper like dominos, fire and then fire and then fire. It was so quick and shocking."

Mickey (Michael) Paramasivan, 37, was woken on the seventh floor by the smell of burning plastic. He tucked his six-year-old daughter Thea into her dressing gown and they ran downstairs.

By the time they were outside "we looked up at the tower and it was like a horror movie", he said.

Mouna Elogbani was on the 11th floor with her husband and three children a friend called and warned her to get out. When they first opened the door to escape "flames burst into the house", she said. They managed to get out down the stairs.

On the 17th floor a man who identified himself on radio as "Methrob" was woken by fire sirens, grabbed his aunty and they started to make their way down.

"By the time that we got downstairs, the fire had gone all the way up and was just about reaching our windows," he said. "The whole side of the building was on fire. The cladding went up like a matchstick."

There are many more stories of narrow escapes. Other stories do not end well.

Jessica Urbano, 12, borrowed someone's phone as she hid in a stairwell with a group of friends making their way down from the 20th floor. She rang her mum.

"Jessica had been asleep in our flat when something woke her - I don't know if it was the smoke or a fire alarm - so she rang me at 1.39am as I was on my way home from work," Jessica's mum, Adriana, told the London Telegraph. "She said,''Mum where are you? Mummy come and get me'." Mrs Urbano urged Jessica to run down the stairs of the tower block and try to find a fire fighter to lead her to safety.

"I told her to get out of there as quickly as she could. I said 'run as fast as you can', but then the line cut out".

On Thursday Jessica was listed among the missing.

On the 14th floor, at 1.38am, ZainabDean phoned her brother Francis.

"She said there was a fire in the building," Francis said later. "She was very nervous and scared. She is a nervous person anyway. She said the fire service arrived and had told everyone to keep calm and to stay where she was."

Twenty minutes later, he got to the building and tried to get in to rescue his sister, but police stopped him.

After an hour, he was desperate with worry.

"I could see the building was going up in flames. I said Zainab you have to get out of the building it's not looking good. She said she didn't want to go down the stairs because there was too much smoke.

"But she tried anyway and then [her three-year-old son]Jeremiah collapsed in her arms."

Their last contact was at 3am.

"On the phone I just keep telling her they were coming to get her."

He handed his phone to a fireman. The fireman handed it back, saying "tell her you love her".

"I knew then to fear the worst. The phone went dead and I couldn't talk to her."

One firefighter was heard telling his crew "we're going in and we're going up".

"My firefighters battled through intense heat to reach some of the highest floors," said London Fire Brigade Commissioner Dany Cotton.

"I was looking at a building that was engulfed in fire where I knew members of the public were still trapped yet I was committing hundreds of firefighters into a building that to a lot of people looked terribly unsafe.

"My firefighters were desperate to get in there and desperate to rescue people, and we committed crew after crew into a very dangerous, very hot and very difficult situation because we had a passion to do as much as we could to rescue the people in there."

The firefighters were told to write their names and numbers on their helmets before they went in.

"It was like a war zone in there," said one. They rescued at least 65 people.

Another said they were "knee deep in debris and bodies" once they climbed past the 11th floor but they kept going up as high as they could, as far as their legs and oxygen canisters would taken them, touching and feeling their way along corridors and stairs, "sweeping and stamping" to check for obstacles or collapsed flooring.

Outside, the fire hoses simply couldn't reach the upper floors.

By the time the fire reached the top floors, the internal stairwell was ink-black with smoke and those remaining felt there was no escape.

Nura Jemal, mother of three on the 22nd floor, told a friend on the telephone "I'm so sorry, goodbye. Please forgive us. We are not going to make it."

The first victim of the fire to be name was Mohammed al-Haj Ali, 23, a Syrian refugee who came to the UK in 2014 and was studying civil engineering.

He had been in a flat on the 14th floor with his brother Omar.

"We smelled the smoke, opened the door, saw smoke," Omar said. "The smoke came inside. I've seen the fire around me."

They left the apartment together and headed for the stairs.

"I couldn't see anything, even my fingers," Omar said. "I thought I was going to die on those stairs. I was breathing smoke, lots of smoke."

Then, when he was almost out, "I looked behind me and I didn't see my brother."

"I called him [on the phone] and said 'where are you'? He said 'I'm in the flat'. I said 'why didn't you come?' He said 'no one brought me outside'."

There they stayed, Omar outside and Mohammed in. They spoke to the end.

"I was speaking to my brother [on the phone]he said 'I'm dying'. He said 'I cannot breathe'."

Among the lost are a 57-year-old man who told his wife and son to leave him behind, and has not been seen since, and Tony Disson, 66, whose phone fell silent at 4am after speaking to a friend and saying "tell my sons I love them".

Ali Jafari, 82, was escaping with his wife and daughter in the lift but got out at the 10th floor, unable to breathe, and did not get back in before the doors closed.

A mother lost her grip on her 12-year-old daughter's hand as they stumbled down the pitch-black stairwell. She spent Thursday travelling from hospital to hospital searching for her child.

Rania Ibrahim posted frightened videos on Snapchat and Facebook while trapped on the 23rd floor, the hallway outside impassable with smoke. Her last message was "guys, I can't get out".

But there were more survivors, too, emerging from the blaze in the arms of firefighters.

Natasha Elcock, trapped on the 12th floor with her six-year-old daughter, flooded the bathroom and kept her flat damp. After 90 minutes the fire crew told them to get out but they couldn't the door of the flat was too hot to open.

"The door was buckling and the windows bubbling and cracking, it was terrifying," she said.

Fire crews rescued her at 3am. She stepped over a body on the way out.

Schools inspector Marcio Gomes, 38, was told to stay put but by 4.30am the fire had engulfed the whole building, and fire crews were unable to make it up to them.

He wrapped his family up in wet towels and said, "There's no turning back, we have to go," he told the Sun.

"As soon as we opened the door all the smoke came in. We had no choice because the fire started coming in through the windows. We had to go down the stairs.

"You couldn't see anything. We didn't see people, we just felt people. We were just climbing over bodies."

He stayed on the line to the fire operator all the way down.

"They said 'keep going down, keep using your voice'."

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London fire: Anatomy of a high-rise horror - The Sydney Morning Herald

The anatomy of Beavers’ win streaks – Mail Tribune

By Bob LundebergMid-Valley Media Group

The two longest winning streaks in Division I baseball this year belong to Oregon State.

The top-seeded Beavers (54-4), who open the College World Series at noon Saturday against Cal State Fullerton (39-22), will take the field at TD Ameritrade Park in Omaha, Nebraska as winners of 21 consecutive games. OSU closed the regular season with 16 straight victories and has outscored opponents 44-9 during its five NCAA tournament games.

Earlier this year, the Beavers won a program-record 23 in a row from Feb. 25 to April 9, including a 12-0 start in Pac-12 play.

The two streaks have accounted for 44 of the teams 54 victories, another single-season school record. With a winning percentage of .931, OSU is on pace to break Arizona States 45-year-old all-time mark of .914 (the Sun Devils finished 64-6 in 1972).

Below is a breakdown of the Beavers winning streaks.

Streak 1, Feb. 25-April 9

Length: 23 games

Runs scored: 136 (5.9 per game)

Runs allowed: 49 (2.1 per game)

One-run games: 6

Shutouts: 6

A loss to Ohio State, which finished 148th in the NCAA RPI, dropped Oregon State to 5-1 early in the season.

The Beavers began the longest winning streak in school history with a 5-2 neutral-site victory over Nebraska, which later came to Oregon for the Corvallis Regional. OSU then got revenge against the Buckeyes to wrap up play in Surprise, Arizona before sweeping consecutive home series with UC Davis and Ball State.

Entering Pac-12 play 14-1 overall, the Beavers outscored Arizona State 16-1 during the three-game set to seize an immediate stranglehold on the conference standings. Starting pitchers Luke Heimlich (eight two-hit innings), Bryce Fehmel (eight innings, one run, four hits) and Jake Thompson (seven two-hit innings) were close to untouchable in the desert.

OSU picked up its first of six walk-off wins at Goss Stadium on March 24, knocking off Arizona 4-3 on a KJ Harrison single that plated Adley Rutschman. The Beavers trailed 3-1 entering the eighth.

One night later, OSU again overcame a deficit and walked off again when Preston Jones scored all the way from second on a wild pitch for a 5-4 win. A comfortable 11-7 decision in the series finale pushed the team to 20-1 overall and 6-0 in Pac-12 play.

The Beavers kept the streak alive with another come-from-behind effort, scoring three times in the ninth to steal a 4-3 victory at Saint Marys on March 28. Nick Madrigal collected the game-winning hit, a two-out, two-RBI single with the bases loaded.

Following another road sweep in which the Beavers outscored Stanford 25-8, OSU pulled out a 4-3 road decision at Portland for its 20th win in a row. Rutschmans two-run single in the sixth put the Beavers in front for good.

A home sweep of Utah including two more walk-offs left OSU 28-1 overall (12-0 Pac-12). Steven Kwan hit a game-winning single in the opener while a Rutschman sacrifice fly brought home Jack Anderson for a 5-4, 16-inning victory in Game 2.

The streak finally came to an end April 13, a 3-2 loss at Washington. But the Beavers fought back to win the final two games of the series.

Streak 2, April 30-current

Length: 21 games

Runs scored: 158 (7.5 per game)

Runs allowed: 41 (2.0 per game)

One-run games: 5

Shutouts: 6

After starting the year 28-1, the Beavers went just 5-3 during a two-week span from April 13-29. The rocky patch included a 7-5, 10-inning home loss to USC, which finished in the Pac-12 basement with Arizona State.

Oregon State came back to rout the Trojans 10-1 in the series finale, igniting a winning streak that has yet to end.

A midweek home victory over Oregon followed by a three-game sweep of California put the Beavers on the brink of the Pac-12 championship. After cruising past the Ducks in Game 1 of the Civil War conference series, Mitchell Verburg struck out Ryne Nelson with the bases loaded in the bottom of the ninth to seal a 5-4 victory and the outright Pac-12 title.

Verburgs heroics also delivered career win No. 1,000 for coach Pat Casey.

The Beavers blanked Oregon 1-0 to sweep the series and cruised by Portland two days later before coming out flat against Washington State May 19. Trailing 3-2 entering the ninth, Steven Kwan and Jack Anderson drew consecutive base-loaded walks off Cougars closer Scott Sunitsch for a true walk-off.

OSU went on to outscore Washington State 19-3 in the final two games of the series, finishing with the best record in conference history at 27-3.

The streak nearly ended again May 26 against Abilene Christian, the Beavers final regular-season opponent. Knotted at 4 in the bottom of the 11th, Anderson knocked in Andy Atwood with a single for the teams sixth walk-off of the year. Reliever Mitch Hickey proposed to his girlfriend on the Goss Stadium turf immediately following the game.

The Beavers entered the NCAA tournament with a 49-4 record and breezed through the Corvallis Regional, outscoring Holy Cross and Yale by a combined margin of 27-3. Two comfortable wins over Vanderbilt in the Corvallis Super Regional pushed the winning streak to 21 as OSU prepares for its CWS opener.

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The anatomy of Beavers' win streaks - Mail Tribune

The world’s worst haka: anatomy of the 1973 All Blacks fiasco – Telegraph.co.uk

The Haka has become one of the most beloved and inspirational spectacles in world sport.

New Zealanders talk passionately about its spiritual significance, the way it links them to their past and their ancestors, and its central place in their sporting culture.

Here, we examine how the Haka grew from this 1973 abomination against the Barbarians at Cardiff Arms Park.

Watch the video below, and then well examine it frame-by-frame, in excruciating detail.

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The world's worst haka: anatomy of the 1973 All Blacks fiasco - Telegraph.co.uk

High-Definition Immunology – Genetic Engineering & Biotechnology News

Once the libraries are sequenced, it is possible to pair the alpha and beta sequences from each individual cell. The 10x Genomics Cell Ranger bioinformatics pipeline assembles V(D)J short sequence reads into consensus alpha and beta chain annotated full-length paired V(D)J profiles.

The Cell Ranger pipeline filters the reads based on shared homology with germline V, D, J, constant segments and assembles the filtered reads within each barcode producing contigs, then annotates the contig sequences with the best germline V, D, J, constant, and UTR matches, detecting and translating the CDR3 sequence. It then groups cells into clonotypes, which share all productive CDR3 sequences, building a consensus for each chain in each clonotype.

To validate the Chromium Single Cell V(D)J Solution performance, the product was used to profile a variety of samples containing T cells. In one experiment, two samples of peripheral blood mononuclear cells (PBMCs) from the same healthy individual were sequenced to confirm that the two independently run samples would exhibit similar behavior. Since the samples came from a healthy individual with no known challenges to the immune system, researchers expected to see high T-cell diversity and low antigen specificity.

Cell Ranger software grouped the T cells into clonotypes and calculated the percent that each clonotype was represented in the sample. In the first sample, 2,809 clonotypes were detected, and 2,949 were detected in the second sample. As expected, no clonotype made up >0.5% of either sample, demonstrating a very high diversity and low specificity in the sample.

To determine antigen specificity, an experiment was performed using T cells exposed to the Epstein-Barr Virus (EBV) in cell culture (Figure 3). The EBV-specific T cells captured and sequenced by the Chromium System were sorted into clonotypes. It was found that 55% of the sequenced T cells shared one major alpha and beta chain, TRAV12-3:J20 (CDR3: CATQGSNDYKLSF), TRBV9:D1:J1-4 (CDR3: CASSTGQVATNEKLFF); 9% shared a second, unrelated clonotype, TRAV5:J15, TRBV14:D2:J2-1; 4% had two related clonotypes that shared a common beta chain3% with TRAV5:J15, TRBV29-1:D1:J1-4 and 1% with TRAV5:J23, TRBV29-1:D1:J1-4.

After the antigen specificities and frequencies of each of the four most dominant clonotypes were determined, limit-of-detection (LOD) experiments were performed using 1:99 dilutions of the EBV-specific T cells mixed into replicate samples of PBMCs from a healthy donor (Figure 3).

In this experiment, one would expect the most dominant clonotype (55%) from the EBV-specific T cells to be observed at a frequency of 0.55% when spiked into the PBMC background. Consistent with these expectations, 16 cells (0.4%) and 7 cells (0.3%) were found to express the major EBV-specific clonotype (TRAV12-3:J20, TRBV9:D1:J1-4) in the first and second spike-in replicates, respectively.

Interestingly, the Chromium V(D)J Solution was able to detect two cells (0.05%) and one cell (0.05%), respectively, of the second most abundant EBV-specific clonotype, resulting in an LOD of <0.1%. This limit of detection is likely to be pushed even lower as future experiments using more input T cells and greater sequencing depths enable the detection of even more rare known clonotypes.

The V(D)J Solution supports diverse basic and translational research studies of applied immunology and will ultimately accelerate our understanding of human health and disease. Particularly exciting application areas that will be propelled by the V(D)J Solution include T cellbased immunotherapies and with the addition of a planned B-cell-specific VDJ solution, vaccine development.

The V(D)J Solution will do this by enabling the identification of the true paired diversity of antigen receptors on a single-cell basis and thereby more effectively enable functional studies into the molecular genetic determinants of antigen specificity.

When coupled with assessments of immune repertoire diversity across experimental contexts of normal healthy tissues, longitudinal or case/control studies, and shared immune responses to common exposure histories, the V(D)J Solution will elucidate the adaptive immune system with greater resolution than ever before

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High-Definition Immunology - Genetic Engineering & Biotechnology News

DeepMind Asks: How Much Can Humans Teach AI? – Futurism

In BriefDeepMind is collaborating with humans so that its AI can learnusing human feedback instead of collecting rewards as it exploresits environment. This work will help AI systems perform moreeffectively and safely, and do what we want them to do. Humans Teaching Robots Artificial Intelligence (AI) has the potential to advance humanity and civilization than any technology that came before it. However, AI carries risks, and heavy responsibilities, with it. DeepMind, owned by Alphabet (Googles parent company), and OpenAI, a non-profit AI research company, are working to alleviate some of these concerns. They are collaborating with people (who dont necessarily have any special technical skills themselves) touse human feedback to teach AI. Not only because this feedback helps AIlearn more effectively, but also because the method providesimproved technical safety and control.

Not only because this feedback helps AIlearn more effectively, but also because the method providesimproved technical safety and control.

Among the first collaboration conclusions: AI learns by trial and error, and doesnt need humans to give it an end goal. This is good, because we already know that setting a goal thats even a little off can have disastrous results. In practice, the system used feedback to learn how to make a simulated robot do backflips.

The system is unusual because it learns by training the reward predictor, an agent from a neural network, instead of collecting rewards as it explores an environment. A reinforcement learning agent still explores the environment, but the difference is that clips of its behavior are then sent to a human periodically. That human then chooses the better behavior based on whatever the ultimate goal is. Its those human selectionsthat train the reward predictor, who in turn trains the learning agent. Finally, thelearning agent eventually learns how to improve its behavior enough to maximize its rewards which it can only do by pleasing the human.

This approach allows humans to detect and correct any behaviors that are undesirable, which ensures safety without being too burdensome for human stewards. Thats a good thing, because they need toreview about 0.1% of the agents behavior to teach it. That may not seem like much at first, butthat could well mean thousands of clips to review something the researchers are working on.

Human feedback can also help AI achieve superhuman results at least in some video games. Researchers are now parsing out why the human feedback system achieves wildly successful results with some tasks, average or even ineffective results with others.For example, no amount of human feedback could help the system master Breakout or Qbert. They are also working to fix the problem of reward hacking, in which early discontinuation of human feedback causes the system to game its reward function for bad results.

Understanding these problems is essential to building AI systems that behave as we intend them to safely and effectively. Other future goals may include reducing the amount of human feedback required, or changing the way its provided; perhaps eventually facilitatingface to face exchanges that offer the AI more opportunities to learn from actual human behavior.

Editors Note: This article has been updated to note the contributions made by OpenAI.

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DeepMind Asks: How Much Can Humans Teach AI? - Futurism