The Expedition 51 crew members are awaiting a new space shipment and getting ready for new science experiments. The crew is also preparing for the departure of a pair of International Space Station flight engineers.

The Falcon 9 rocket that will launch the SpaceX Dragon cargo craft to space is resting at its launch pad today at the Kennedy Space Center in Florida. Dragon will lift off Thursday at 5:55 p.m. EDT on a three-day trip to the stations Harmony module.

Inside the commercial space freighter is nearly 6,000 pounds of crew supplies, station hardware and science experiments. One of those experiments, Cardiac Stem Cells, will research how stem cells affect cardiac biology and tissue regeneration in space. The stations Microgravity Science Glovebox is being readied for the study which may provide insight into accelerated aging due to living in microgravity.

On Friday, cosmonaut Oleg Novitskiy will command the Soyuz MS-03 spacecraft to return him and European Space Agency astronaut Thomas Pesquet back to Earth after 196 days in space. The two crew members are packing their spacecraft with research samples, hardware and personal items for the near 3.5 hour ride home. The duo will undock from the Rassvet module at 6:47 a.m. EDT. They will then parachute to a landing in Kazakhstan at 10:10 a.m. (8:10 p.m. Kazakh time).

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Station Ramps Up for Cardiac Research Loaded on Dragon ... - Space Fellowship

COUNTLESS lives across the world could be saved by an Oxfordshire familys appeal to find a bone marrow donor for their little boy.

Two-year-old Alastair Ally Kim has Chronic Granulomatous Disorder (CGD), a life-threatening condition.

He has now become the fourth person in the world to start an experimental gene therapy course at Great Ormond Street Hospital.

In the meantime, his parents have spearheaded 200 international donor drives to find their son a match, signing up 7,000 would-be donors in the process - some of whom have since been matched with other patients.

Father Andrew Kim, 37, of Hinton Waldrist near Longworth, said: We want to use whatever momentum Allys story has to help someone else. We know that matches have come through our drives for other people. Its awesome that someone will benefit from all this.

On Thursday, May 25 family friend Cathy Oliveira organised a drive at the Oxford Universitys Old Road research building, signing up 80 staff members in a day.

Ms Oliveira said: When everything happened with Ally I wanted to show support in any way we could; this is directly beneficial not just for Ally but for others.

Allys CGD means his immune system is compromised and the tiniest infection could leave him seriously ill.

His only chance of a permanent cure is a bone marrow stem cell donation, with a match likely to be of Korean or East Asian origin.

In April the youngster and mum Judy Kim, 36, an Oxford University researcher, travelled to London for him to begin a pioneering new gene therapy treatment.

After a week of chemotherapy to wipe out Allys immune system, cells taken from him are modified in a lab and re-introduced to correct the disorder.

Mr Kim said: Bone marrow would give him back 100 per cent functionality and gene therapy is 10 to 15 per cent; its enough to live in the real world, and not be scared he will die every time he gets an infection.

It has been a roller-coaster of a year, but theres nothing to do but move forward. We are really excited at the thought of him being able to come home this summer.

Blood cancer charity DKMS supported last weeks donor drive in Oxford.

Senior donor recruitment manager Joe Hallet said: Around 30 per cent of patients in need of a blood stem cell donor will find a matching donor within their own family.

The remaining 70 per cent, like Ally, will need to find an unrelated donor to have a second chance of life, so events like these are crucial.

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Oxford University staff join bone marrow stem cell donor drive for ... - Oxford Mail

Blood stem cells are things of wonder: hidden inside each single cell is the power to reconstitute an entire blood system, like a sort of biological big bang.

Yet with great power comes greater vulnerability. Once these master cells are compromised, as in the case of leukemia and other blood disorders, treatment options are severely limited.

A bone marrow transplant is often the only chance for survival. The surgery takes a healthy donors marrowrich with blood stem cellsand reboots the patients blood system. Unfortunately, like organ transplants, finding a matching donor places a chokehold on the entire process.

According to Dr. George Daley at Harvard Medical School, a healthy sibling gives you a one in four chance. A stranger? One in a million.

For 20 years, scientists have been trying to find a way to beat the odds. Now, two studies published in Nature suggest they may be tantalizingly close to being able to make a limitless supply of blood stem cells, using the patients own healthy tissues.

"This step opens up an opportunity to take cells from patients with genetic blood disorders, use gene editing to correct their genetic defect and make functional blood cells," without depending on donors, says Dr. Ryohichi Sugimura at Boston Childrens Hospital, who authored one of the studies with Daley.

Using a magical mix of seven proteins called transcription factors, the team coaxed lab-made human stem cells into primordial blood cells that replenished themselves and all components of blood.

A second study led by Dr. Shahin Rafii, a stem cell scientist at Weill Cornell Medical College took a more direct route, turning mature cells from mice straight into genuine blood stem cells indiscernible from their natural counterparts.

This is the first time researchers have checked all the boxes and made blood stem cells, says Dr. Mick Bhatia at McMaster University, who was not involved in either study, That is the holy grail.

The life of a blood stem cell starts as a special cell nestled on the walls of a large blood vesselthe dorsal aorta.

Under the guidance of chemical signals, these cells metamorphose into immature baby blood stem cells, like caterpillars transforming into butterflies. The exact conditions that prompt this birthing process are still unclear and is one of the reasons why lab-grown blood stem cells have been so hard to make.

These baby blood stem cells dont yet have the full capacity to reboot blood systems. To fully mature, they have to learn to respond to all sorts of commands in their environment, like toddlers making sense of the world.

Some scientists liken this learning process to going to school, where different external cues act as textbooks to train baby blood stem cells to correctly respond to the body.

For example, when should they divide and multiply? When should they give up their stem-ness, instead transforming into oxygen-carrying red blood cells or white blood cells, the immune defenders?

Both new studies took aim at cracking the elusive curriculum.

In the first study, Daley and team started with human skin and other cells that have been transformed back into stem cells (dubbed iPSCs, or induced pluripotent stem cells). Although iPSCs theoretically have the ability to turn into any cell type, no one has previously managed to transform them into blood stem cells.

A lot of people have become jaded, saying that these cells dont exist in nature and you cant just push them into becoming anything else, says Bhatia.

All cells in an organism share the same genes. However, for any given cell only a subset of genes are turned into proteins. This process is what gives cells their identitiesmay it be a heart cell, liver cell, or blood stem cell.

Daley and team focused on a family of transcription factors. Similar to light switches, these proteins can flip genes on or off. By studying how blood vessels normally give birth to blood stem cells, they found seven factors that encouraged iPSCs to grow into immature blood stem cells.

Using a virus, the team inserted these factors into their iPSCs and injected the transformed cells into the bone marrow of mice. These mice had been irradiated to kill off their own blood stem cells to make room for the lab-grown human replacements.

In this way, Daley exposed the immature cells to signals in a blood stem cells normal environment. The bone marrow acts like a school, explains Drs. Carolina Guibentif and Berthold Gttgens at the University of Cambridge, who are not involved in the study.

It worked. In just twelve weeks, the lab-made blood stem cells had fully matured into master cells capable of making the entire range of cells normally found in human blood. Whats more, when scientists took these cells out and transplanted them into a second recipient, they retained their power.

This a major step forward compared with previous methods, says Guibentif.

In contrast, the second study took a more direct route. Rafii and team took cells lining a mouses vessels, based on the finding that these cells normally turn into blood stem cells during development.

With a set of four transcription factors, the team directly reprogrammed them into baby blood stem cells, bypassing the iPSC stage.

These factors act like a maternity ward, allowing the blood stem cells to be born, says Guibentif.

To grow them to adulthood, Rafii and team laid the cells onto a blanket of supporting cells that mimics the blood vessel nursery. Under the guidance of molecular cues secreted by these supporting cells, the blood stem cells multiplied and matured.

When transplanted into short-lived mice without a functional immune system, the cells sprung to action. In 20 weeks, the mice generated an active immune response when given a vaccine. Whats more, they went on to live a healthy 1.5 yearsroughly equivalent to 60 years old for a human.

Rafii is especially excited about using his system to finally crack the stem cell learning curriculum.

If we can figure out the factors that coax stem cells to divide and mature, we may be able to unravel the secrets of their longevity and make full-fledged blood stem cells in a dish, he says.

Calling both experiments a breakthrough, Guibentif says, this is something people have been trying to achieve for a long time.

However, she points out that both studies have caveats. A big one is cancer. The transcription factors that turn mature cells into stem cells endow them with the ability to multiply efficientlya hallmark of cancerous cells. Whats more, the virus used to insert the factors into cells may also inadvertently turn on cancer-causing genes.

That said, neither team found evidence of increased risk of blood cancers. Guibentif also acknowledges that future studies could use CRISPR in place of transcription factors to transform cells into blood stem cells on demand, further lowering the risk.

The techniques will also have to be made more efficient to make lab-grown blood stem cells cost efficient. Itll be years until human use, says Guibentif.

Even so, the studies deter even the most cynical of critics.

After 20 years, were finally tantalizingly close to generating bona fide human blood stem cells in a dish,"says Daley.

Image Credit: Pond5

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Limitless Lab-Grown Blood Is 'Tantalizingly Close' After 20 Years - Singularity Hub

In experiments in mice, UC San Francisco researchers have discovered that regulatory T cells (Tregs; pronounced tee-regs), a type of immune cell generally associated with controlling inflammation,directly trigger stem cells in the skin to promote healthy hair growth. Without these immune cells as partners, the researchers found, the stem cells cannot regenerate hair follicles, leading to baldness.

Our hair follicles are constantly recycling: when a hair falls out, a portion of the hair follicle has to grow back, saidMichael Rosenblum, M.D., an assistant professor of dermatology at UCSF and senior author on the new paper. This has been thought to be an entirely stem cell-dependent process, but it turns out Tregs are essential. If you knock out this one immune cell type, hair just doesnt grow.

The new study published online May 26 inCell suggests that defects in Tregs could be responsible for alopecia areata, a common autoimmune disorder that causes hair loss, and could potentially play a role in other forms of baldness, including male pattern baldness, Rosenblum said. Since the same stem cells are responsible for helping heal the skin after injury, the study raises the possibility that Tregs may play a key role in wound repair as well.

Normally Tregs act as peacekeepers and diplomats, informing the rest of the immune system of the difference between friend and foe. When Tregs dont function properly, we may develop allergies to harmless substances like peanut protein or cat dander, or suffer from autoimmune disorders in which the immune system turns on the bodys own tissues.

Like other immune cells, most Tregs reside in the bodys lymph nodes, but some live permanently in other tissues, where they seem to have evolved to assist with local metabolic functions as well as playing their normal anti-inflammatory role. In the skin, for example, Rosenblum and colleagues have previously shown that Tregs help establish immune tolerance to healthy skin microbes in newborn mice, and these cells also secrete molecules that help with wound healing into adulthood.

Rosenblum, who is both an immunologist and a dermatologist, wanted to better understand the role of these resident immune cells in skin health. To do this, he and his team developed a technique for temporarily removing Tregs from the skin. But when they shaved patches of hair from these mice to make observations of the affected skin, they made a surprising discovery. We quickly noticed that the shaved patches of hair never grew back, and we thought, Hmm, now thats interesting, Rosenblum said. We realized we had to delve into this further.

In the new research, led by UCSF postdoctoral fellow and first authorNiwa Ali,several lines of evidence suggested that Tregs play a role in triggering hair follicle regeneration.

First, imaging experiments revealed that Tregs have a close relationship with the stem cells that reside within hair follicles and allow them to regenerate: the number of active Tregs clustering around follicle stem cells typically swells by three-fold as follicles enter the growth phase of their regular cycle of rest and regeneration. Also, removing Tregs from the skin blocked hair regrowth only if this was done within the first three days after shaving a patch of skin, when follicle regeneration would normally be activated. Getting rid of Tregs later on, once the regeneration had already begun, had no effect on hair regrowth.

Tregs role in triggering hair growth did not appear related to their normal ability to tamp down tissue inflammation, the researchers found. Instead, they discovered that Tregs trigger stem cell activation directly through a common cell-cell communication system known as the Notch pathway. First, the team demonstrated that Tregs in the skin express unusually high levels of a Notch signaling protein called Jagged 1 (Jag1), compared to Tregs elsewhere in the body. They then showed that removing Tregs from the skin significantly reduced Notch signaling in follicle stem cells, and that replacing Tregs with microscopic beads covered in Jag1 protein restored Notch signaling in the stem cells and successfully activated follicle regeneration.

Its as if the skin stem cells and Tregs have co-evolved, so that the Tregs not only guard the stem cells against inflammation but also take part in their regenerative work, Rosenblum said. Now the stem cells rely on the Tregs completely to know when its time to start regenerating.

Rosenblum said the findings may have implications for alopecia areata, an autoimmune disease that interferes with hair follicle regeneration and causes patients to lose hair in patches from their scalp, eyebrows, and faces. Alopecia is among the most common human autoimmune diseases its as common as rheumatoid arthritis, and more common than type 1 diabetes but scientists have little idea what causes it.

After his team first observed hair loss in Treg-deficient mice, Rosenblum learned that the genes associated with alopecia in previous studies are almost all related to Tregs, and treatments that boost Treg function have been shown to be an effective treatment for the disease. Rosenblum speculates that better understanding Tregs critical role in hair growth could lead to improved treatments for hair loss more generally.

The study also adds to a growing sense that immune cells play much broader roles in tissue biology than had previously been appreciated, said Rosenblum, who plans to explore whether Tregs in the skin also play a role in wound healing, since the same follicle stem cells are involved in regenerating skin following injury.

We think of immune cells as coming into a tissue to fight infection, while stem cells are there to regenerate the tissue after its damaged, he said. But what we found here is that stem cells and immune cells have to work together to make regeneration possible.

Niwa Aliof UCSF was the lead author on the new study. Additional authors were Bahar Zirak,Robert Sanchez Rodriguez, Mariela L. Pauli,Hong-An Truong, Kevin Lai,Richard Ahn, Kaitlin Corbin, Margaret M. Lowe, PharmD,Tiffany C. Scharschmidt, M.D., Keyon Taravati, Madeleine R. Tan,Roberto R. Ricardo-Gonzalez, M.D., Audrey Nosbaum, M.D.,Wilson Liao, M.D., andAbul K. Abbas, MBBS, of UCSF; Frank O. Nestle, M.D., of Kings College London; Marta Bertoliniand Ralf Paus, M.D., of the University of Mnster in Germany; and George Cotsarelis, M.D., of the University of Pennsylvanias Perelman School of Medicine.

The work was primarily supported by the U.S. National Institutes of Health (K08-AR062064, DP2-AR068130, R21-AR066821), the Burroughs Wellcome Fund, a Scleroderma Research Foundation grant, the National Psoriasis Foundation and the Dermatology Foundation.

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A new baldness treatment? | University of California - University of California