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Katie Sharify had six days to decide: would she let her broken body become experimental territory for a revolutionary new approacheven if it was unlikely to do her any good? The question was barely fathomable. She had only just regained consciousness. A week earlier, she had been in a car crash that damaged her spine, leaving her with no sensation from the chest down. In the confusion and emotion of those first few days, the family thought that the treatment would fix Katie's mangled spinal cord. But that was never the goal. The objective, in fact, was simply to test the safety of the treatment. The misunderstanding a cure, and then no cure -- plunged the 23-year-old from hope to despair. And yet she couldn't let the idea of this experimental approach go.

Just days after learning that she would never walk again, that she would never know when her bladder was full, that she would not feel it if she broke her ankle, she was thinking about the next girl who might lie in this bed with a spinal injury. If Katie walked away from this experimental approachwhat would happen to others that came after her?

Her medical team provided a crash course in stem cell therapy to help Katie think things through. In this case the team had taken stem cells obtained from a five-day old embryo and converted them into cells that support communication between the brain and body. Those cells would be transplanted into the injured spines. Earlier experiments in animal models suggested that, once in place, these cells might help regenerate a patient's own nerve tissue. But before scientists could do the experiment, they needed to make sure the technique they were using was safe by using a small number of cells, too few to likely have any benefit. And that's why they wanted Katies help in this CIRM-funded trial. They explained the risks. They explained that she was unlikely to derive any benefit. They explained that she was just a step along the way. Even so, Katie agreed. She became the fifth patient in what's called a Phase I trial: part of the long, arduous process required to bring new therapies to patients. Shortly after she was treated the trial stopped enrolling patients for financial reasons.

That was in 2011. Since then, she has been through an intensive physical therapy program to increase her strength. She went back to college. She tried skiing and surfing. She learned how to make life work in this new body. But as she rebuilt her life she wondered if taking part in the clinical trial had truly made a difference.

"I was frustrated at first. I felt hopeless. Why did I even do this? Why did I even bother?" But soon she began to see how small advances were moving the science forward. She learned the steep challenges that await new therapies. Then in 2014, she discovered that the research she participated in was deemed to be safe and is about to enter its next phase, thanks to a $14.3 million grant from CIRM to Asterias Biotherapeutics. "This has been my wish from day one," Katie says.

"It gives me so much hope to know there is an organization that cares and wants to push these therapies forward, that wants to find a cure or a treatment," she says. "I don't know what I would do if I thought nobody cared, nobody wanted to take any risks, nobody wanted to put any funding into spinal cord injuries.

"I really have to have some ray of hope to hold onto, and for me, CIRM is that ray of hope."

For more information about CIRM-funded spinal cord injury research, visit our fact sheet.

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Stories of Hope: Spinal Cord Injury | California's Stem ...

Spinal Cord Stem Cells Comments Off on Stories of Hope: Spinal Cord Injury | California’s Stem … | February 7th, 2018

Engineered human stem cells have been used to enable paraplegic rats to walk independently and regain sensory perception. The implanted rats had some healing in their spinal cords.

Led by Dr. Shulamit Levenberg, of the Technion-Israel Institute of Technology, the researchers implanted human stem cells into rats with a complete spinal cord transection. The stem cells, which were derived from the membrane lining of the mouth, were induced to differentiate into support cells that secrete factors for neural growth and survival.

The work involved more than simply inserting stem cells at various intervals along the spinal cord. The research team also built a three-dimensional scaffold that provided an environment in which the stem cells could attach, grow and differentiate into support cells. This engineered tissue was also seeded with human thrombin and fibrinogen, which served to stabilize and support neurons in the rats spinal cord.

5 of 12 rats (42%) treated with the induced constructs demonstrated BBB scores exceeding 17, a compiled reflection of improved coordinated gait, plantar placement, weight support, recovery of toe clearance, trunk stability, and predominant parallel paw and tail position, suggesting regained cortical motor control.

The induced constructs promoted remarkable recovery in 42% of the rats, and show no efficacy in the remainder of the rats within the same group. This binary effect compels further investigation, since understanding of the underlying mechanisms causing substantial improvement in some animals and no practical improvement in others can render this method into an effective treatment.

Spinal cord injury (SCI), involving damaged axons and glial scar tissue, often culminates in irreversible impairments. Achieving substantial recovery following complete spinal cord transection remains an unmet challenge. Here, we report of implantation of an engineered 3D construct embedded with human oral mucosa stem cells (hOMSC) induced to secrete neuroprotective, immunomodulatory, and axonal elongation-associated factors, in a complete spinal cord transection rat model. Rats implanted with induced tissue engineering constructs regained fine motor control, coordination and walking pattern in sharp contrast to the untreated group that remained paralyzed (42 vs. 0%). Immunofluorescence, CLARITY, MRI, and electrophysiological assessments demonstrated a reconnection bridging the injured area, as well as presence of increased number of myelinated axons, neural precursors, and reduced glial scar tissue in recovered animals treated with the induced cell-embedded constructs. Finally, this construct is made of bio-compatible, clinically approved materials and utilizes a safe and easily extractable cell population. The results warrant further research with regards to the effectiveness of this treatment in addressing spinal cord injury.

Frontiers in Neuroscience Implantation of 3D Constructs Embedded with Oral Mucosa-Derived Cells Induces Functional Recovery in Rats with Complete Spinal Cord Transection.

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Overview

A spinal cord injury damage to any part of the spinal cord or nerves at the end of the spinal canal (cauda equina) often causes permanent changes in strength, sensation and other body functions below the site of the injury.

If you've recently experienced a spinal cord injury, it might seem like every aspect of your life has been affected. You might feel the effects of your injury mentally, emotionally and socially.

Many scientists are optimistic that advances in research will someday make the repair of spinal cord injuries possible. Research studies are ongoing around the world. In the meantime, treatments and rehabilitation allow many people with spinal cord injuries to lead productive, independent lives.

Your ability to control your limbs after a spinal cord injury depends on two factors: the place of the injury along your spinal cord and the severity of injury to the spinal cord.

The lowest normal part of your spinal cord is referred to as the neurological level of your injury. The severity of the injury is often called "the completeness" and is classified as either of the following:

Additionally, paralysis from a spinal cord injury may be referred to as:

Your health care team will perform a series of tests to determine the neurological level and completeness of your injury.

Spinal cord injuries of any kind may result in one or more of the following signs and symptoms:

Emergency signs and symptoms of a spinal cord injury after an accident may include:

Anyone who experiences significant trauma to his or her head or neck needs immediate medical evaluation for the possibility of a spinal injury. In fact, it's safest to assume that trauma victims have a spinal injury until proved otherwise because:

Spinal cord injuries may result from damage to the vertebrae, ligaments or disks of the spinal column or to the spinal cord itself.

A traumatic spinal cord injury may stem from a sudden, traumatic blow to your spine that fractures, dislocates, crushes or compresses one or more of your vertebrae. It also may result from a gunshot or knife wound that penetrates and cuts your spinal cord.

Additional damage usually occurs over days or weeks because of bleeding, swelling, inflammation and fluid accumulation in and around your spinal cord.

A nontraumatic spinal cord injury may be caused by arthritis, cancer, inflammation, infections or disk degeneration of the spine.

The central nervous system comprises the brain and spinal cord. The spinal cord, made of soft tissue and surrounded by bones (vertebrae), extends downward from the base of your brain and is made up of nerve cells and groups of nerves called tracts, which go to different parts of your body.

The lower end of your spinal cord stops a little above your waist in the region called the conus medullaris. Below this region is a group of nerve roots called the cauda equina.

Tracts in your spinal cord carry messages between the brain and the rest of the body. Motor tracts carry signals from the brain to control muscle movement. Sensory tracts carry signals from body parts to the brain relating to heat, cold, pressure, pain and the position of your limbs.

Whether the cause is traumatic or nontraumatic, the damage affects the nerve fibers passing through the injured area and may impair part or all of your corresponding muscles and nerves below the injury site.

A chest (thoracic) or lower back (lumbar) injury can affect your torso, legs, bowel and bladder control, and sexual function. A neck (cervical) injury affects the same areas in addition to affecting movements of your arms and, possibly, your ability to breathe.

The most common causes of spinal cord injuries in the United States are:

Although a spinal cord injury is usually the result of an accident and can happen to anyone, certain factors may predispose you to a higher risk of sustaining a spinal cord injury, including:

At first, changes in the way your body functions may be overwhelming. However, your rehabilitation team will help you develop the tools you need to address the changes caused by the spinal cord injury, in addition to recommending equipment and resources to promote quality of life and independence. Areas often affected include:

Bladder control. Your bladder will continue to store urine from your kidneys. However, your brain may not be able to control your bladder as well because the message carrier (the spinal cord) has been injured.

The changes in bladder control increase your risk of urinary tract infections. The changes also may cause kidney infections and kidney or bladder stones. During rehabilitation, you'll learn new techniques to help empty your bladder.

Skin sensation. Below the neurological level of your injury, you may have lost part of or all skin sensations. Therefore, your skin can't send a message to your brain when it's injured by certain things such as prolonged pressure, heat or cold.

This can make you more susceptible to pressure sores, but changing positions frequently with help, if needed can help prevent these sores. You'll learn proper skin care during rehabilitation, which can help you avoid these problems.

Circulatory control. A spinal cord injury may cause circulatory problems ranging from low blood pressure when you rise (orthostatic hypotension) to swelling of your extremities. These circulation changes may also increase your risk of developing blood clots, such as deep vein thrombosis or a pulmonary embolus.

Another problem with circulatory control is a potentially life-threatening rise in blood pressure (autonomic hyperreflexia). Your rehabilitation team will teach you how to address these problems if they affect you.

Respiratory system. Your injury may make it more difficult to breathe and cough if your abdominal and chest muscles are affected. These include the diaphragm and the muscles in your chest wall and abdomen.

Your neurological level of injury will determine what kind of breathing problems you may have. If you have a cervical and thoracic spinal cord injury, you may have an increased risk of pneumonia or other lung problems. Medications and therapy can help prevent and treat these problems.

Fitness and wellness. Weight loss and muscle atrophy are common soon after a spinal cord injury. Limited mobility may lead to a more sedentary lifestyle, placing you at risk of obesity, cardiovascular disease and diabetes.

A dietitian can help you eat a nutritious diet to sustain an adequate weight. Physical and occupational therapists can help you develop a fitness and exercise program.

Following this advice may reduce your risk of a spinal cord injury:

Drive safely. Car crashes are one of the most common causes of spinal cord injuries. Wear a seat belt every time you drive or ride in a car.

Make sure that your children wear a seat belt or use an age- and weight-appropriate child safety seat. To protect them from air bag injuries, children under age 12 should always ride in the back seat.

Dec. 19, 2017

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Spinal cord injury - Symptoms and causes - Mayo Clinic

Spinal Cord Stem Cells Comments Off on Spinal cord injury – Symptoms and causes – Mayo Clinic | December 21st, 2017

Stem cell research is often controversial but it has also led to incredible medical progress in recent years.

Stem cell research is at defining moment. Although it can be controversial and does raise a lot of important ethical issues, this area of medical science has been characterised by a number of important advances, ever since the first embryonic stem cells were isolated from mice in the 1980s. In the near future, it could reshape the way we treat some of the worlds most debilitating diseases.

Stem cells have already been used as treatment for a number of years think bone marrow transplant and they have the potential to help with many other medical conditions. They could also prove crucial for scientists wishing to understand more about human biology and development.

Studies using stem cells have benefited from important media coverage in recent years and many of them hailed as breakthroughs. However, the reality is often more complex, and a number of scientific and ethical challenges often stand in the way of successes in animal models being replicated in humans.

IBTimes UK takes a look at what stem cell research is, what it is used for and what the future looks like.

Stem cells could be defined as building block cells that have not yet differentiated into one cell type and could develop into many different cell types. Stem cells can continue to divide almost indenitely.

There are two main types of stem cells: embryonic stem cells and adult stem cells.

Embryonic stem cells were first isolated in mice in the early 1980s at the University of Cambridge. All developing embryos contains a number of stem cells that can go on to develop into different cell types. In humans, these cells can be isolated from around five days after the egg has been fertilised around 50 to 100 stem cells are present at that stage.

These cells are isolated from embryos that have been donated by couples who have been through IVF and have extra embryos left which were not used during the treatment.

Stem cells are also found in adults, particularly in the bone marrow, the blood, the eyes, the brain and the muscles. They are also known as somatic stem cells.

They can also differentiate into other cells, but into a much more limited number than embryonic stem cells. They range from cells that are able to form different kinds of tissues to more specialised cells that form just some of the cells of a particular tissue or organ. They also have the ability to divide and reproduce indefinitely.

19th Place: Dr Gist F Croft, Lauren Pietilla, Stephanie Tse, Dr. Szilvia Galgoczi, Maria Fenner, Dr Ali H. Brivanlou, Rockefeller University, Brivanlou Laboratory New York, New York, USA: Human neural rosette primordial brain cells, differentiated from embryonic stem cells Confocal, 10x (Dr Gist F Croft, Lauren Pietilla, Stephanie Tse, Dr. Szilvia Galgoczi, Maria Fenner, Dr Ali H. Brivanlou)

Scientists have also found a way to make induced pluripotent stem cells cells taken from any adult tissue and genetically modified to behave like an embryonic stem cell (and thus able to differentiate into any cell type). The term pluripotant refers to the fact that the stem cells can produce almost all of the cells in the body.

To create these induced pluripotent stem cells, researchershave learnt to reprogramme the genes of human adult cells. A major 2007 US study, found that introducing 14 genes could reprogramme the cells to become stem cells, and the researchers then narrowed this down to four genes. Subsequent studies have built on this knowledge to find new, safer ways to turn adult cells into pluripotant stem cells.

Stem cells are already used to help a number of patients around the world. For nearly 50 years, they have been used in the form of bone marrow transplants.

Indeed, bone marrow contains stem cells that can produce many different blood cells. A bone marrow transplant can be used to treat people with blood cancers or genetic blood disorders, such as sickle cell anaemia. The stem cell turn into healthy blood cells that can help the patient. Some hospitals also use stem cells to grow skin grafts for patients with life-threatening burns. It is also possible to receive a stem cell therapy based on limbal stem cells (in the eye) to repair damaged corneas.

Stem cells are also very useful for scientists conducting basic research on diseases, as they can be used to model a large number of conditions. Recent studies have used stem cells to model the nerve cells that are lost in Alzheimers disease or to model deafness or Autism Spectrum disorder.

Scientists have gained a better understanding of blood stem cells (Alden Chadwick/Flickr)

A number of treatment using stem cells has been tested by researchers around the world. A type of patients that could be helped by stems cells are those suffering from spinal cord injuries. Stem cell therapy for spinal cord repair could be used to promote the growth of nerve cells directly or to transplant cells that protect the nerves and help them function.

One of most important studies in this area was published in October 2010. tested the used embryonic stem cells on patients in the US who had sustained a spinal cord injury in the previous 14 days. Preliminary findings were encouraging.

Studies have also been conducted to assess the safety and efficacy of stem cells in helping patients who suffered a stroke. The idea is that stem cells could help in rehabilitation after a persons brain has been damaged by the stroke. Stem cells have also been investigated to treat diseases such as MS, diabetes and to reverse ageing.

Beyond clinical trials, which still remain limited in number, many of the preliminary research opens up a number of very interesting perspectives. One of the main area of interest is growing organs in the lab from tissues created from stem cells. These organs may one day be used for transplantation in humans.

Recently, stem cells have been shown to present an interest to improve fertility treatments with the creation of a new technique in mice in-vitro gametogenesis. The idea is to create eggs and sperm using pluripotant stem cells.

By La Surugue

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Spinal Cord Stem Cells Comments Off on What are stem cells and how will they be used to treat the … | November 25th, 2017

Spinal cord injury is the injury to the spinal cord, a very serious form of trauma with enduring effects on the patients daily life. The spinal cord is approximately 18 inches long and extends from brain base at the neck and ending just above the buttocks. It has numerous nerves known as upper motor neurons (UMNs) and is responsible for transmitting signals back and forth from the brain to different parts on the body.Human beings are in a position to feel pain and move their limbs because messages are sent via the spinal cord, therefore if the spinal cord is damaged some or all of these impulses may not be sent.

Usually, a spinal cord injury happens as a result of an impulsive accident or event, we list here some of the most common causes of spinal cord injury:

An aggressive attack like being stabbed or shot Diving into very shallow water and hitting the bottom Trauma to the face, head, back or the neck region during a motor accident Falling from a very high height Electrical accident Injuries while engaging in sports Severe twist of the torso middle portion

1) Incomplete spinal cord injuries; the spinal cord is partially affected and in this case, the patient retains some functions depending on the degree of the injury. Some of the common types of partial spinal cord include anterior cord syndrome, central cord syndrome and brown-sequard syndrome.

2) Complete spinal cord injuries; this type occurs when the spinal cord is fully damaged and there is no function below the level of injury. However, with proper treatment and physical therapy, it is possible for a patient to regain some functions.

Challenges walking Loss of control of bladder or bowels Difficulties moving arms and legs Headaches Unconsciousness Pain, pressure, and stiffness in the neck/or back region Spreading numbness feelings Unnatural head positioning Signs of shock Loss of libido Loss of fertility Bedsores How are spinal cord injuries diagnosed?

Usually, physicians examine patients for spinal cord injuries based on factors like the location, type and the symptoms of the injury. However, no single test can assess 100% these injuries; instead, doctors depend on a number of protocols such as:

Clinical evaluation; the doctor will keenly observe your symptoms, carry out blood tests, ask detailed questions about your condition and follow your eye movement Imaging tests; the doctor may request a magnetic reasoning imaging or radiological imaging to view the spinal column, spinal cord, and brain

Stem cells are found in all multi-cellular organisms and are well known for their remarkable ability to differentiate into almost any other type of cell. Therefore depending on the disease, stem cells can be transplanted into the patient to assist renewal and regeneration of the previously dying cells.This principle is now being used for a spinal cord injury using stem cells; it assists patients with the recovery process and restores their physiological and sensory ability.Currently, no stem cell therapy has been approved as a complete cure for spinal injuries. Stem cell therapy is used to improve conditions and symptoms whilst allowing the patient to enjoy a better quality of life after injury.

Exogenous and endogenous repair.While in exogenous repair the stem cells are first grown in the lab and then injected into the patient, in endogenous repair stem cells are injected into the injured site and the results depend on the bodys ability to change stem cells into the needed cells.

Adult neural stem cells can differentiate into different cell types. Consequently, researchers are taking advantage of this regenerative ability and are trying to come up with ways to reintroduce the bodys own stem cells into the damaged spinal cord. Research in rats shows that transplanting oligodendrocyte (support cells that make myelin) and astrocyte (boost nerve function) precursors from the neural stem cells can protect axons and reduce motor neuron damage.

Embryonic stem cells are the best type of stem cells and researchers are developing ways to turn embryonic stem cells into oligodendrocyte which have successfully repaired neural functions in animal models. However, using the same approach in a clinical trial is very challenging; it is close to impossible to make oligodendrocyte without also making other unasked for cells.

Induced Pluripotent Stem cells (IPs) are just like embryonic stem cells and can be made from the skin or any other tissue cell. They are easily reachable and offer a great source of cells that match the patients profile, hence theres no chance of rejection.

By combining the Anti CD2 human clonal antibodies and Anti-cytokines monoclonal antibodies, we create injections. This helps to reduce the inflammation, axonal degeneration and to prevent demyelination. Lysis functions of leukocyte cells get enhanced as well.

Spinal laser therapyIV laser therapyIV OxygenShock Wave TherapyPeptides injectionsPhysiotherapyEnzymes & Nutrition

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Spinal Cord Stem Cells Comments Off on Spinal Cord Injury Treatment with Stem Cells – Stem Cells … | October 3rd, 2017

What Is Quadriplegia?

Paralysis can be either partial, periodic, complete, or incomplete. Paralysis of both the arms and legs has been traditionally been called quadriplegia. Quad comes from the Latin for four and plegia comes from the Greek for inability to move. Currently the term tetraplegia is becoming more popular, but it means the same thing. Tetra is from the Greek for inability to move.

The primary cause of quadriplegia is a spinal cord injury, but other conditions such as cerebral palsy and strokes can cause a similar appearing paralysis. The amount of impairment resulting from a spinal cord injury depends on the part of the spinal cord injured and the amount of damage done. Injury to the spinal cord can be devastating because the spinal cord and the brain are the main parts of the central nervous system, which sends messages throughout your body.

When the spinal cord is injured the brain cannot properly communicate with it and so sensation and movement are impaired. The spinal cord is not the spine itself; it is the nerve system encased in the vertebrae and discs which make up the spine.

Quadriplegia occurs when the neck area of the spinal cord is injured. The severity of the injury and the place it occurred at determine the amount of function a person will maintain. A major spinal cord injury may interfere with breathing as well as with moving the limbs. A patient with complete quadriplegia has no ability to move any part of the body below the neck; some people do not even have ability to move the neck.

Sometimes people with quadriplegia can move their arms, but have no control over their hand movements. They cannot grasp things or make other motions which would allow them a little independence. New treatment options have been able to help some of these patients regain hand function.

Quadriplegia causes many complications which will need careful management:

Immediate treatment of quadriplegia consists of treating the spinal cord injury or other condition causing the problem. In the case of a spinal cord injury, you will immobilized with special equipment to prevent further injury, while medical personnel work to stabilize your heart rate, blood pressure, and over all condition. You may be intubated to assist your breathing. This means that flexible tube carrying oxygen will be inserted down your throat. Imaging tests will be used to determine the extent of your injury.

Surgery may be needed to relieve pressure on the spine from bone fragments or foreign objects. Surgery may also be used to stabilize the spine, but no form of surgery can repair the damaged nerves of the spinal cord. Unfortunately, the nerve damage caused by the initial spinal cord injury has a tendency to spread. The reasons for this tendency are not completely understood by researchers, but it is related to spreading inflammation as blood circulation decreases and blood pressure drops.

The inflammation causes nerve cells not directly in the injured area to die. A powerful corticosteroid, methylprednisolone (Medrol) can sometimes help prevent the spread of this damage if it is given within eight hours of the original injury; however, methylprednisolone can cause serious side effects and not all doctors are convinced that it is beneficial.

Rehabilitation for quadriplegia once consisted primarily of training to learn how to deal with your new limitations. Passive physical therapy was given to help prevent the muscles from atrophying. Today, many new options are offering quadriplegia patients new hope. These new options combine older methods with new technology with encouraging results.

While passive physical therapy once consisted solely of the therapists manipulating the patients arms and legs in an effort to increase circulation and retain muscle tone, today therapists can use electrodes to stimulate the patients muscles and give them an optimal workout. This technology is called functional neuromuscular stimulation (FNS). FNS stimulates the intact peripheral nerves so that the paralyzed muscles will contract.

The contractions are stimulated using either electrodes that have been placed on the skin or that have been implanted. With FNS, the patient may ride a stationary bicycle to improve muscle and cardiac function and prevent the muscles from atrophying. An implantable FNS system has been used to help people with some types of spinal injury regain use of their hands.

This is an option for people with quadriplegia, who have some voluntary use of their arms. The shoulders position controls the stimulation to the hands nerves, allowing the individual to pick up objects at will. Tendon transfer is another option which allows some people with quadriplegia more use of the arms and hands. This complicated surgery transfers a nonessential muscle with nerve function to the shoulder or arm to help restore function. FNS may be used in conjunction with tendon transfer.

Other forms of treatments for quadriplegia are still in the experimental stage. Many clinical trials of new treatment options are run every year. If you or a loved one suffers from quadriplegia, you may want to consider one of these trials. Ask your doctor to help you find a suitable trial.

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Spinal Cord Stem Cells Comments Off on Quadriplegia | Types of Paralysis | Brain and Spinal Cord … | September 22nd, 2017

Treatment

The Stem Cell treatment performed at our clinics is a painless medical procedure where Stem Cells (cellular building blocks) are usually administered intravenously and subcutaneously (under the skin). The whole procedure takes approximately one hour and has no known negative side effects.

Following the treatment, the Fetal Stem Cells will travel throughout the body, detecting damaged cells and tissue and attempts to restore them. The Fetal Stem Cells can also stimulate existing normal cells and tissues to operate at a higher level of function, boosting the bodys own repair mechanisms to aid in the healing process. These highly adaptive cells then remain in the body, continually locating and repairing any damage they encounter.

As with any medical treatment, safety should be of the highest priority. The Stem Cells used in our treatment undergo extensive screening for possible infection and impurities.

Utilizing tests more sophisticated than those regularly used in the United States for Stem Cell research and transplant. Our testing process ensures we use only the healthiest cells to enable the safest and most effective Fetal Stem Cell treatment possible. And, unlike other types of Stem Cells, there is no danger of the bodys rejection of Fetal Stem Cells due to the fact they are immune privileged. This means that you can give the cells to any patient without matching, use of immunosuppressive drugs and without rejection. This unique quality eliminates the need for drugs used to suppress the immune system, which can leave a patient exposed to serious infections.

With over 4,000 patients treated, Stem Cell Of America has achieved positive results with a wide variety of illnesses, conditions and injuries. Often, in cases where the diseases continued to worsen, our patients have reported substantial improvements following the Stem Cell treatment.

Patients have experienced favorable developments such as reduction or elimination of pain, increased strength and mobility, improved cognitive function, higher tolerance for chemotherapy, and quicker healing and recovery.

To view follow up letters from patients, please visit the patient experiences page on our website.

All statements, opinions, and advice on this page is provided for educational information only. It is not a substitute for proper medical diagnosis and care. Like all medical treatments and procedures, results may significantly vary and positive results may not always be achieved. Please contact us so we may evaluate your specific case.

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Spinal Cord Stem Cells Comments Off on Stem Cell of America – Breakthrough Stem Cell Treatments … | September 20th, 2017

I can see him in his glass-fronted Cambridge office from the foosball table in the light-filled central atrium. Hes standing there talking to a visitor and seems to be finishing up. This entire side of the third floor in MITs new Media Lab building is partitioned with glass, and professor Hugh Herr and his colleagues and whatever madness theyre up to in their offices and the open, gadget-filled, lower-floor lab are on display. Several people, myself included, are peering down, hoping to see a bit of magic.

Months ago, when I e-mailed Herr to propose writing an article about him, I told him about my rare bone cancer and resulting partial paralysis below the waist as a way to explain my interest in his work. Though I didnt tell him this, I also harbored a secret wish that he could help me. People write to Herr, a 52-year-old engineer and biophysicist, daily about his inspiring example. Theyve heard him promise an end to disability. They have conditions that medicine cant fix and futures they cant stand to consider. Theyre wishing for his intervention, wanting of hope. Crossing his threshold, Im the lucky one. Im here.

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Herr welcomes me into his office, a clean, well-ordered space. Theres a round glass table with a laptop on it, a handful of hard office chairs, and a pair of prosthetic legs Herr designed that are arranged like statuary behind us, one in either corner. Above us on a wall looms a large mounted photograph of another pair of prosthetics. These are hand-carved from solid ash, with vines and flowers and six-inch heels. The real-life legs were famously worn by a friend of Herrs, the amputee track-and-field athlete and actress Aimee Mullins.

I have hobbled into Herrs office with a dented $20 stock metal cane on one side and a foot-lifting Blue Rocker brace on the other. (The dent is from my recently firing the cane at the wall.) I had imagined Herr noticing the cane and asking more about my story to see how he could fix me, like he has fixed so many others. The moment I realize that the meeting Id imagined isnt the meeting were going to haveIm here as a reporter, not a friend or patient, after allI start to stammer. Herr deftly resets the conversation by suggesting we look at his computer.

On it are the PowerPoint slides of his next big project, a breathtaking $100 million, five-year proposal focused on paralysis, depression, amputation, epilepsy, and Parkinsons disease. The work will be funneled through Herrs new brainchild, MITs Center for Extreme Bionics, a team of faculty and researchers assembled in 2014 that he codirects. After exploring various interventions for each condition, Herr and his colleagues will apply to the FDA to conduct human trials. One to-be-explored intervention in the brain might, with the right molecular knobs turned, augment empathy. If we increase human empathy by 30 percent, would we still have war? Herr asks. We may not.

As he continues with the presentation hes been giving to technologists, engineers, health researchers, and potential donorslast December alone, he keynoted in Dubai, Istanbul, and Las Vegaseach revolutionary intervention he mentions yields a boyish grin and a look that affirms: Yes, you heard that right. In a talk I hear him give a few weeks later, hell dare to characterize incurable paralysis as low-hanging fruit. In his outspoken willingness to fix everything, even things that some argue should be left alone, he knows how he sounds. If half the audience is frightened and the other half is intrigued, I know Ive done a good job, he says.

Herr on a 5.12 route on Arizonas Mount Lemmon in 1986. (Beth Wald/Aurora)

Herr calmly ticks off one condition after another. He shows me an animation of an innovative surgery that will restore an amputees lost proprioception, giving a person the ability to feel and control a prosthetic as if it were their own limb. In another slide, of a paralyzed man in a bulky walk-assisting exoskeleton suit, he asks me to imagine a futuristic treatment that uses light to control cells in muscle tissue. Then he presents a video clip of a rat with a severed spinal cord dragging around its paralyzed hind legs.

Having dragged my mostly unresponsive left leg around for two years, I think I know something about the rodents life. In the next clip, however, that rat, just 90 days later, is walking on all fours. A team at the MIT center led by Herrs colleague Robert Langer successfully regrew the rats spinal cord by implanting a dissolvable scaffold seeded with neural stem cells. In Herrs world, the limbless can be whole again, the paralyzed can walk. Making the extraordinary seem ordinary is maybe the whole point.

Herr himself is proof positive. Trim, fit, and handsome, he is the showpiece for the Center for Extreme Bionics. Im kind of what theyre selling, he says. The fuss over Herr has been building for decades but reached new levels in 2014, courtesy of his TED Talk, which has now been viewed in excess of 7.3 million times. In it, Herr describes the horrific 1982 winter climbing accident in New Hampshires White Mountains during which he suffered severe frostbite, leading to the amputation of both legs below the knee. Then 17, Herr was told hed never climb again. Instead, he rebuilt himself almost immediately, willfully reshaping his artificial legs and realizing that he wasnt handicapped, the technology was.

By hacking his prosthetic devices for his vertical world, he was able to quickly return to climbing, becoming the first athletedecades before Oscar Pistoriusto blur the line between para and not. His accomplishments landed him on the cover of Outside a year after his accident, something that sticks with him not because of the many accolades other climbers bestowed on him, or even the controversy it reignited around the tragic death of one of his rescuers, but because of the questions the article raised about how far Herr would be able to go. I was a sad case. I was going to end up in this machine shop, disabled, Herr recalls of the piece, pausing to let the perceived insult ripen in his mind. Yeah, its a real sad story.

The triumphant, fully realized man in the TED Talk is a marvel. His outrage at the unnecessary suffering from disability is fiercely personal. What first-time viewers like me invariably fixate on is the way Herr gracefully owns the stage. Hes wearing pants that end above the knee, revealing shimmering high-tech silver and black prosthetics. Herr is focused on what hes saying, not what his artificial legs are doing. The crime of physical impairment is that it often steals from a persons sense of self. If you didnt look below his knees, youd never guess that Herr is missing half of each leg. He walks through the world the way we all would hope to.

He has effectively ended his disability, or at least the perception of it, just as he said he would. Inspired by his accident, he earned a masters degree in mechanical engineering at MIT in 1993, followed by a Ph.D. at Harvard in biophysics. Ever since, Herr has produced a string of breakthrough products, starting with a computer-controlled artificial knee in 2003. In 2004, he created the biomechatronics group at MIT, a now 40-person R&D lab drawing on the fields of biology, mechanics, and electronics to restore function to those whove lost it. Three years later, the team produced a powered ankle-foot prosthesis that allows an amputee to walk with speed and effort comparable to those with biological legs. Called the emPower, the apparatus weighs a few pounds and houses 12 sensors, three computers, tensioning springs, and muscle-tendon actuators. The ankle system is manufactured by a private company Herr started called BionX.

Last year, Herr advanced another of his labs goals, to improve human performance beyond what nature intends by creating a brace-like exoskeleton device that reduces the metabolic cost of walking. The implications for people who want to get places fasteror perhaps a soldier trying to conserve energy on a long marchare vast.

In the near future, Herr and his colleagues at the MIT center are committed to, among other things, reversing paralysis. Herrs goal is to develop a synthetic spinal cord thataids the damaged original. A prosthesis, in other words.

In his office, Herr draws up his pant leg and rolls down a silicone sleeve to show me a newly developed fabric that lines the socket of his prosthetic and cushions the problematic intersection between the biological stump and the man-made limb. The exquisitely comfortable fitdigitally derived, he explains, but highly personalis something he delights over with a savoring gush.

With our first meeting nearing its end, I grow distracted thinking about the wounded few Herr has smiled upon. In 2014, he worked on a bionic prosthetic for the dancer Adrianne Haslet-Davis, who lost her left leg in the Boston Marathon bombing. Currently, hes working with Hari Budha Magar, a double-amputee former Gurkha soldier who plans to climb Mount Everest in 2018, and also Jim Ewing, an old New Hampshire climbing buddy. Ewing was climbing a wall on vacation in the Cayman Islands in 2014 when he fell with his teen daughter on belay. She couldnt brake the rope, and he plummeted some 60 feet, shattering his pelvis and left foot on impact.

The dancer, the Gurkha, the climber, and Herr himself are examples of what he often describes as the millions of humans who might appear broken but are not. Haslet-Davis, on a bionic limb embedded with dance intelligence, brilliantly performed the rumba again, and Ewing underwent a pioneering amputation procedure developed by Herrs biomechatronics team in partnership with MIT colleague and surgeon Matthew Carty, who performed the operation at Brigham and Womens Faulkner Hospital, to prepare Ewing for an advanced prosthesis. Magar will be outfitted with short prosthetics to reduce leg drag and sophisticated crutches for speed as he attempts Everest history.

The stories Herr tells, the future he sees, the beautifully functioning artificial limb before meits all I can do not to show him my atrophied left leg and ask for his godlike intervention to fix what I know is broken. But I dont, not yet.

When I wrote Herr to tell him about my interest in his work, I summarized my case history. I explained how in the summer of 2014, I found myself with increasingly debilitating nerve and lower-back pain. When I finally got an MRI, I learned that I had an extremely rare bone cancer called chordoma that had spread from my lower lumbar vertebrae into my right hip flexor. Radiation and a difficult multi-stage surgery successfully removed the softball-size tumor, but months later, possibly due to a loss of blood to the spinal cord, Id yet to regain sensation or strength in my hips and legs. The doctors didnt know if it was permanent, but the prognosis didnt look good.

Jim Ewing and his robotic prosthetic. (Boston Globe/Getty)Aimee Mullins. (Lynn Johnson/Getty)Mountaineer Hari Budha Magar. (Himalayan Ski Trek)

Id expected a rapid, maybe even exceptional recovery. I am an athlete and adventurer who has had the good fortune to do a lot of cool stuff over the years. Id become a whitewater guide, climbed Grand Teton, raced the hill climb at Mount Washington on foot and by bike, and mountain-biked half the 3,000-mile-plus Great Divide route. I expected to complete the other half someday.

Id progressed from a walker to a cane, from a recumbent tricycle to a pedal-assist e-bike. Then my nerve regeneration halted. In May 2015, after the surgery, Id contacted Boston neurologist Bill David for muscle and nerve testing. An avid cyclist and kindredspirit, hed hopefully stuck needles into my skin every six months to chart my recovery. Late last year, he confirmed what I had already sensed. Short of a miracle, Id gone about as far as I could. I really wish that we had met on a mountain or river as opposed to a medical clinic, David said.

Id negotiated several stages of recovery, but the one I feared most was right nowat the end, my future fixed. Ive been coming to grips with who I am as an incomplete paraplegic and figuring out how to make the best version of this new person, I wroteto Herr.

Id imagined a stirring epilogue to our encounters, a moment perhaps when a radical trial arose and a crazy volunteer was needed. To be closer to the person I once was, I would try anythinginjected viruses, exoskeletal suits, implants. When I got together with a close friend for lunch, I told her how the story with Herr was progressing, and how the limbs he created were so advanced that Id read about people wanting them even though their leg complications didnt medically require amputation. She listened carefully. Let me ask you something, she said. Would you, um, get your legs cut off?

Exactly when in his childhood Hugh Herr decided to become the worlds best climber is impossible to pinpoint, but the goal was nurtured during family road trips across the West. He and his older brothers climbed, fished, and hiked in the American and Canadian Rockies, whetting the youthful Herrs appetite for adventure. The Shawangunk Mountains in New York were a four-and-a-half-hour drive from the Herrs home in Lancaster, Pennsylvania. The Gunks were an emerging mecca in the seventies, and Herr quickly established himself as a prodigy, climbing this stuff when I was 11 that only adults had done, and at 15 that no one else had done, he says.

When he and Jeff Batzer, a friend from Lancaster, drove to New Hampshires Mount Washington in January 1982 for a weekend ice-climbing outing, it wasnt to do anything audacious. Theyd attempt a classic route in Huntingtons Ravine, and maybe, depending on the weather and avalanche conditions, summit Mount Washington before racing down for the 12-hour drive home. Herr was a 17-year-old junior in high school, his friend Batzer, 20.

The decision to tack on the summit of Washington turned out to be a tragic mistake. They left a sleeping bag and bivy sack behind to reduce weight but encountered howling winds and blizzard conditions near the top, and they ended up losing their way, mistakenly descending into a different valley from where theyd come.

After four days trekking through a storm in deep snow and below-freezing temperatures to find their way out, Herr was no longer able to walk. Early on in the odyssey, he had punched through a frozen streambed into shin-deep water, soaking his boots and pants, and was suffering from severe frostbite. In Second Ascent, a biography by Alison Osius, Herr said that he had reconciled himself to death when a backcountry snowshoer saw some of Batzers tracks and followed them to a makeshift shelter the two were bivouacked in. The climbers were evacuated to a nearby hospital in Littleton, where doctors treated both for hypothermia and frostbite. Herrs legs were in terrible shape. At the hospital, he learned that doctors might not be able to save them and that a member of his search party, a 28-year-old climbing-school instructor named Albert Dow, had been killed in an avalanche. Two months later, doctors amputated Herrs legs four inches below the knee. Batzers fingers on his right hand were amputated, along with his left foot and the toes on his right foot.

I asked my doctor after the amputation what Id be able to do with my new body, Herr recalls. The doctor said, What do you want to do? I said I wanted to drive a car, ride my bike, and climb. The doctor said youll be able to drive a car, but with hand controls. He said I would not be able to ride a bike or return to climbing.

Herr did all of the above within a year. He worked closely with his prosthetist on one pair of artificial legs after another and tinkered on his own in the machine shop of a vocational school hed begun attending in 1981. He soon figured out that he could hack his artificial limbs to suit the requirements of particular climbing routes. He built limbs that extended or shortened his stature; he carved out feet with wedge ends to slice into crevices. He began to knock off routes that he hadnt been able to do previously, including leading an ascent of Vandals at Skytop, the first 5.13 on the East Coast. It ignited a new controversy: that his adaptations were a form of cheating. Herr likes to tell audiences that he invited his affronted rivals to chop off their own legs.

Some people were bitter and angry about the accident, says Jim Ewing, a summer roommate of Herrs in the 1980s, and with Hugh coming back and climbing so well, they started making up excuses, saying things like, He can stand on a dime, his feet dont get sore, he doesnt have calf fatigue. Id just look at these people and think, By God, you havent seen this guy crawl to the toilet in the middle of the night because he doesnt have his legs on. He is handicapped; it is a handicap. People had no idea.

The 1982 rescue. (Jim Cole/AP)Herr in the hospital. (Jim Cole/AP)Herr in 1984. (Peter Lewis)

While there was a lot of media attention about Herrs accident, he kept private the struggles and self-doubt he faced after he lost his legs. When he returned to New Hampshire to climb again 18 months later, the unease from locals over Dows death and Herrs resurgence was palpable.

The harsh early views of Herr didnt soon go away. When I asked him what he thought when the American Alpine Club last year honored him at a celebratory awards evening in Denver, he said he was stunned. They had named him a new inductee of the Hall of Mountaineering Excellence for lasting contributions on and off the mountain. It shocked me, he said. The initial story line of the accident was that these young, irresponsible, incompetent climbers caused the death of an experienced, beloved local climber. That narrative went on for a very long time. So for two decades at least, I wouldnt even expect the American Alpine Club to invite me to be in the audience.

When Herr talks about Albert Dow, who he never met, its with the fondness of a friend. That was Albert! he recounts about Dows insistence that he go looking for Herr and Batzer because hed want someone to do the same for him. Last year, Herr told a Reddit audience that he strives to honor Dow. I hate the idea that his death somehow enabled me to live so I could do good work, he says. What I like is that his kindness and who he wasand his sacrificeinspired me to work really hard.

In 1985, Herr free-climbed New Hampshires exceptionally steep and unprotected Stage Fright, with his friend Jim Surette on belay. It was a significant and life-threatening milestone, and afterward Herr had a dream that set his new path. He describes a nightmare in which Surette, bunking on a neighboring couch, throws off his covers to reveal mangled, bloody, amputated legs. We both go Aaah! in the dream, says Herr, but then I turn to Jimmy and say, Dont worry, Jimmy, its just a dream. Im the one without legs. Prior to that, in all my dreams I would be running and jumping, and I would have my biological legs. It was the first time my brain recognized my new state.

Some mightve interpreted the nightmare with melancholy, an attempt to come to terms with a sorrowful lifelong condition. Herr saw it as a beautiful vision.

The auditorium is full at the Princeton, New Jersey, headquarters of the Robert Wood Johnson Foundation, all 150 in attendance looking stage left as Herr introduces an image of himself in a New Hampshire hospital room decades earlier. What do you see? he asks.

It is Herr in the moments after his legs have been amputated. The 17-year-old is gazing down at a white sheet and the outline of his stumps. The audience is riveted.

What do you see? he asks again. I see a new beginning, he declares. I see beauty.

Herr, who prefers to use the term unusual instead of handicapped or disabled, often says that he wouldnt want his biological legs back. He loves the legs he started building after the accident and has steadily improved upon for the past several decades.

His meteoric rise in academia is almost as improbable as his comeback to elite climbing. I actually graduated from high school not being able to take 10 percent of 100, he says. I had no idea what a percent was. His older brothers were all in construction. He understood that the family trade was unavailable to him, so he shut himself away and applied the same obsessive focus to science that hed once reserved for climbing. He read everything he could find and enrolled at the local college, Millersville University.

Wed watch all these films of animals locomoting to try to learn about motion, says Don Eidam, his first adviser at Millersville and an unapologetic superfan who writes a newsletter about Herr. Hed put all these ideas on my blackboard, and the chalk would literally be disintegrating. Hed call me at midnight with an idea. Ive never met anyone so committed or intense.

In 1991, Herr became the first student from Millersville to be accepted at MIT. The academic degrees, innovations, and honors have since overflowed. He is the holder or coholder of over 100 patents. The powered prosthesis he developed for ankle-foot amputees was the product of a special mind with a special motivation. By copying the behavior of a biologically intact leg, Herr and his biomechatronics lab were able to create a breakthrough replacement. In 2011, Time crowned him the leader of the bionic age. Last year he won Europes top prize for inventors, the prestigious Princess of Asturias Award.

In Hughs mind, he has not successfully innovated until people are able to benefit from his innovation, says Tyler Clites, a Harvard-MIT student who has worked in Herrs lab for six years. He has said to me, Look, Tyler, Ive invented hundreds of times, but Ive only ever innovated twice. The two items, his prosthetic knee and the ankle-foot, are the only ones commercially available to others.

The idea of an endlessly upgradable human is something Herr feels in his bones. I believe in the near future, in a decade or two, when you walk down the streets of Boston, youll routinely see people wearing bionic systems, Herr told ABC News in a 2016 interview. In 100 years, he thinks the human form will be unrecognizable. The inference is that the abnormal will be normal, beauty rethought and reborn. Unusual people like Herr will have come home.

At a small luncheon after his talk in New Jersey, the organizers ask me to say a few words about my condition. I give a five-minute recap of my struggles with cancer, the spinal-cord complication, and my up-and-down recovery. It is my first time speaking publicly about my situation. As I do, I sneak a glance or two at Herr. I wonder what he thinks hearing me tell my story. He is sitting immediately to my right, raking through a towering salad.

There is no clear signal from him, but I leave feeling that Ive pulled ever so slightly into his orbit. I am also beginning to understand the weight he bears of being a savior. A friend who saw his impassioned SXSW talk in 2015 told me how she raced up to thank him afterward, only to encounter a different guy. He was polite but aloof. She was put off, but I think I understand. The man has to set boundaries. He cant save everybody.

You might say that Herrs the sort of disrupter the research world needs, or you might say hes overpromising. One spinal-cord-injury scientist I spoke with wasnt so sure that a bold tech solution is the answer in a field long focused on the biology of nerve regeneration.

Nicholas Negroponte, the cofounder and former director of the MIT Media Lab, says Herrs sense of humor helps him handle any negative commentary. Its particularlyimportant when you do and say risky things, some of which invite harsh criticism, he says. You smile and keep going, because you know youre right.

A week after his talk in New Jersey, Herr and I meet up at a seafood restaurant near his MIT office. I arrive 30 minutes early, wanting to get situated. Having lived with my disability for some time now, I understand that I cant just sweep in like I used to. Herr, to my surprise, given his packed schedule, arrives ten minutes early.

Bomb survivor Adrianne Haslet-Davis. (Michael Dwyer/AP)

Herr told me earlier that he rarely pushes himself on climbs anymore. He proudly mentioned his two preteen, homeschooled daughters, who are avid hikers and spend almost every weekend with Herrs former wife, Patricia Ellis Herr, in the White Mountains happily exhausting themselves. They long ago summited Mount Washington and have high-pointed in 46 of the 50 states.

Herr and I talk at length about some of the people he has worked with and why. The Haslet-Davis project took a group from his biomechatronics lab 200 days to create the prosthetic, counting down to the 2014 TED Talk. She said she wanted to dance again. I really related, he says. He told himself, Im an MIT professor, I have resources. The timeline was tight enough that there was a TED Talk plan A (with her) and plan B (without). As everyone knows who has watched the video, Herrs team hit its deadline. Haslet-Davis unforgettably danced again, and there wasnt a dry eye because of it.

But as incredible as the moment was, its a source of frustration that the prosthetic cant be permanently handed over to Haslet-Davis. While Herr would love to give it to her, its a prototype that would cost millions to reproduce. As for Herrs climbing buddy Jim Ewing, thats a similarly uncertain situation. Months after Ewing had his foot amputated, he was fitted with a newly designed ankle-foot prosthetic that responds to his brain waves and allows him to feel his appendage. It is also a prototype that Ewing will eventually have to return.

Haslet-Davis and Ewing understood that they were part of a research project and wouldnt be able to keep the prototypes. Meanwhile, Herrs knee and ankle prosthetics, which cost tens of thousands of dollars, arent yet widely covered by insurance and remain too expensive for most who have a need for them. Herr has been in discussions with insurers to try and change that. According to Amputee Coalition of America estimates, there are 185,000 new lowerextremity amputations annually in the U.S. By contrast, there are only 1,700 emPower ankles in circulation right now. About half of them are worn by vets, paid for through reimbursements covered by the Department of Veterans Affairs.

Herrs work is important and coming from a good place, says Alisha Sarang-Sieminski, an associate professor of bioengineering at the Massachusetts-based Franklin W. Olin College of Engineering, a school involved in numerous projects related to lower-cost accessibility design. But people have different needs for different contexts. Also, so much of the high tech is really not accessible to very many people financially. Should people keep building them? Definitely. Should we also explore basic solutions? Yes.

Still, Ewings pioneering amputation is a huge success for Herrs group, the Brigham and Womens surgical team, and, most notably, Ewing. When I visited him at a climbing gym near Portland, Maine, he was planning a trip back to the Cayman Islands. For Ewing, the amputation has reduced the acute pain he used to feel in his biological foot and dramatically changed his outlook. He says that after his accident, he contemplated suicide. Being alive isnt enough, he says. Breathing isnt enough. I had to do something. Hugh understood my motivation probably better than I did.

Herr hadnt seen Ewing for years when he got an e-mail from him asking for advice about his foot. He was in a bad place, says Herr. Also, I really felt for his daughter. I know guilt so well, that poor girl.

Ewing says that the way hed set up the ropes is to blame for his daughters inability to brake the fall. Though she has returned to climbing at the gym and bouldering, she wasnt interested in rope climbing in the accidents aftermath, and Ewing worried that hed ruined the sporta passion theyd shared for yearsfor her.

Meanwhile, the gift Herr has given Ewing is exceptional. It might be the first time Herr is not the most technologically advanced lower-limb amputee. Herr often describes himself and others facing disabilities as astronauts testing new life-enabling technologies. As for his own legs, Herr wants to go even further but would need to leave the U.S. to undergo the operation he has in mind. Id love to do it, he says, without revealing any details about the procedure. Im just weighing the risk. I definitely dont want to go backwards.

In the short term, hes using a newly designed set of titanium legs and pushing forward on his work, noting hoped-for funding this year from the military to show we can synthetically take over a paralyzed limb. Herr then asks about my rehabilitation experience. This is finally my chance, I think, to ask if theres anything he can do for me.

I tell him that I identify with amputees and often wonder how some people without legs are more adept than some of us with them. Every time I watch a person with artificial legs walking, I selfishly wonder, Why not me? Why not us? Herr says they have some good ideas but acknowledges that the field has been way more successful in the amputation arena than with spinal-cord injuries. Its hard, he says.

While Herr has complete autonomy selecting projects in his lab, his interventions are rare, and they dont happen unless the time and circumstances are right. Often, people ask for help and I dont have the resources or the solution, he says. Exceptions like Haslet-Davis and Ewing come from feeling deeply about it and being in the position to make it happen.

I realize talking to Herr that its not my story thats weak, its the technology. Id incorrectly understood his comment about an imminent cure. Paralysis is lowhanging fruit in that its a condition they can impact in ten to twenty years instead of fifty. There are no toys to play with in Herrs lab closet. Not yet.

Before Herr and I wrap up our last visit, I ask what hed do if he were at an impasse. Its clear, at least to me, that Im talking about myself. Being a scientist, he focuses on process. He says he throws everything and anything at a problem. He visualizes each idea as a rock and starts turning them over. He mentions an acquaintance who came to see him earlier in the day who was struggling with depression. Herr started in, imagining at hyperspeed all the places the person might go and hadnt yet. Acupuncture? No? Meditation? No? Are you running? No? What medications have you tried? One? One! Theres like 20 antidepressants! Go, go, go! he says he wanted to plead. He chuckles at his overexuberance, but his belief is real. This can be solved!

When I say goodbye to Herr and watch him bound down from the upper level of the restaurant to the rain-drenched sidewalk, Im struck by a malaise. Maybe its the rain. Maybe its the opportunity lost. Maybe its the way he flipped a switch on his emPower ankle and raced effortlessly into the street. But then I think about Herr turning over one rock at a time and the span of possibilities he presented to help with depression. Im not out of options. There are hundreds of researchers working on a paralysis cure, and I immediately think of a world map I saw recently on a website with dozens of bright red circles representing centers of innovation. I can hear the words of my neurologist, who on my last visit leaned in with something else when he said goodbye. Keep moving, he urged. Theres even a clinic in New Hampshire I heard about where theyve produced exceptional walking recoveries using a robotic gait trainer available nowhere else in the U.S.

I begin to wonder, was Herrs story about his depressed acquaintance allegorical? An on-the-spot intervention? Had I just been, ever so lightly, smiled upon, too?

Longtime Outside contributor Todd Balf is the author of The Last River. Guido Vitti is anOutsidecontributing photographer.

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The $100 Million Plan to End Paralysis - Outside Magazine

Spinal Cord Stem Cells Comments Off on The $100 Million Plan to End Paralysis – Outside Magazine | September 7th, 2017

by David M. Panchision*

Diseases of the nervous system, including congenital disorders, cancers, and degenerative diseases, affect millions of people of all ages. Congenital disorders occur when the brain or spinal cord does not form correctly during development. Cancers of the nervous system result from the uncontrolled spread of aberrant cells. Degenerative diseases occur when the nervous system loses functioning of nerve cells. Most of the advances in stem cell research have been directed at treating degenerative diseases. While many treatments aim to limit the damage of these diseases, in some cases scientists believe that damage can be reversed by replacing lost cells with new ones derived from cells that can mature into nerve cells, called neural stem cells. Research that uses stem cells to treat nervous system disorders remains an area of great promise and challenge to demonstrate that cell-replacement therapy can restore lost function.

The nervous system is a complex organ made up of nerve cells (also called neurons) and glial cells, which surround and support neurons (see Figure 3.1). Neurons send signals that affect numerous functions including thought processes and movement. One type of glial cell, the oligodendrocyte, acts to speed up the signals of neurons that extend over long distances, such as in the spinal cord. The loss of any of these cell types may have catastrophic results on brain function.

Although reports dating back as early as the 1960s pointed towards the possibility that new nerve cells are formed in adult mammalian brains, this knowledge was not applied in the context of curing devastating brain diseases until the 1990s. While earlier medical research focused on limiting damage once it had occurred, in recent years researchers have been working hard to find out if the cells that can give rise to new neurons can be coaxed to restore brain function. New neurons in the adult brain arise from slowly-dividing cells that appear to be the remnants of stem cells that existed during fetal brain development. Since some of these adult cells still retain the ability to generate both neurons and glia, they are referred to as adult neural stem cells.

These findings are exciting because they suggest that the brain may contain a built-in mechanism to repair itself. Unfortunately, these new neurons are only generated in a few sites in the brain and turn into only a few specialized types of nerve cells. Although there are many different neuronal cell types in the brain, we now know that these new neurons can quot;plug inquot; correctly to assist brain function.1 The discovery of these cells has spurred further research into the characteristics of neural stem cells from the fetus and the adult, mostly using rodents and primates as model species. The hope is that these cells may be able to replenish those that are functionally lost in human degenerative diseases such as Parkinson's Disease, Huntington's Disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease), as well as from brain and spinal cord injuries that result from stroke or trauma.

Scientists are applying these new stem cell discoveries in two ways in their experiments. First, they are using current knowledge of normal brain development to modulate stem cells that are harvested and grown in culture. Researchers can then transplant these cultured cells into the brain of an animal model and allow the brain's own signals to differentiate the stem cells into neurons or glia. Alternatively, the stem cells can be induced to differentiate into neurons and glia while in the culture dish, before being transplanted into the brain. Much progress has been made the last several years with human embryonic stem (ES) cells that can differentiate into all cell types in the body. While ES cells can be maintained in culture for relatively long periods of time without differentiating, they usually must be coaxed through many more steps of differentiation to produce the desired cell types. Recent studies, however, suggest that ES cells may differentiate into neurons in a more straightforward manner than may other cell types.

Figure 3.1. The NeuronWhen sufficient neurotransmitters cross synapses and bind receptors on the neuronal cell body and dendrites, the neuron sends an electrical signal down its axon to synaptic terminals, which in turn release neurotransmitters into the synapse that affects the following neuron. The brain neurons that die in Parkinson's Disease release the transmitter dopamine. Oligodendrocytes supply the axon with an insulating myelin sheath.

2001 Terese Winslow

Second, scientists are identifying growth (trophic) factors that are normally produced and used by the developing and adult brain. They are using these factors to minimize damage to the brain and to activate the patient's own stem cells to repair damage that has occurred. Each of these strategies is being aggressively pursued to identify the most effective treatments for degenerative diseases. Most of these studies have been carried out initially with animal stem cells and recipients to determine their likelihood of success. Still, much more research is necessary to develop stem cell therapies that will be useful for treating brain and spinal cord disease in the same way that hematopoietic stem cell therapies are routinely used for immune system replacement (see Chapter 2).

The majority of stem cell studies of neurological disease have used rats and mice, since these models are convenient to use and are well-characterized biologically. If preliminary studies with rodent stem cells are successful, scientists will attempt to transplant human stem cells into rodents. Studies may then be carried out in primates (e.g., monkeys) to offer insight into how humans might respond to neurological treatment. Human studies are rarely undertaken until these other experiments have shown promising results. While human transplant studies have been carried out for decades in the case of Parkinson's disease, animal research continues to provide improved strategies to generate an abundant supply of transplantable cells.

The intensive research aiming at curing Parkinson's disease with stem cells is a good example for the various strategies, successful results, and remaining challenges of stem cell-based brain repair. Parkinson's disease is a progressive disorder of motor control that affects roughly 2% of persons 65 years and older. Triggered by the death of neurons in a brain region called the substantia nigra, Parkinson's disease begins with minor tremors that progress to limb and bodily rigidity and difficulty initiating movement. These neurons connect via long axons to another region called the striatum, composed of subregions called the caudate nucleus and the putamen. These neurons that reach from the substantia nigra to the striatum release the chemical transmitter dopamine onto their target neurons in the striatum. One of dopamine's major roles is to regulate the nerves that control body movement. As these cells die, less dopamine is produced, leading to the movement difficulties characteristic of Parkinson's disease. Currently, the causes of death of these neurons are not well understood.

For many years, doctors have treated Parkinson's disease patients with the drug levodopa (L-dopa), which the brain converts into dopamine. Although the drug works well initially, levodopa eventually loses its effectiveness, and side-effects increase. Ultimately, many doctors and patients find themselves fighting a losing battle. For this reason, a huge effort is underway to develop new treatments, including growth factors that help the remaining dopamine neurons survive and transplantation procedures to replace those that have died.

The strategy to use new cells to replace lost ones is not new. Surgeons first attempted to transplant dopamine-releasing cells from a patient's own adrenal glands in the 1980s.2,3 Although one of these studies reported a dramatic improvement in the patients' conditions, U.S. surgeons were only able to achieve modest and temporary improvement, insufficient to outweigh the risks of such a procedure. As a result, these human studies were not pursued further.

Another strategy was attempted in the 1970s, in which cells derived from fetal tissue from the mouse substantia nigra was transplanted into the adult rat eye and found to develop into mature dopamine neurons.4 In the 1980s, several groups showed that transplantation of this type of tissue could reverse Parkinson's-like symptoms in rats and monkeys when placed in the damaged areas.The success of the animal studies led to several human trials beginning in the mid-1980s.5,6 In some cases, patients showed a lessening of their symptoms. Also, researchers could measure an increase in dopamine neuron function in the striatum of these patients by using a brain-imaging method called positron emission tomography (PET) (see Figure 3.2).7

The NIH has funded two large and well-controlled clinical trials in the past 15 years in which researchers transplanted tissue from aborted fetuses into the striatum of patients with Parkinson's disease.7,8 These studies, performed in Colorado and New York, included controls where patients received quot;shamquot; surgery (no tissue was implanted), and neither the patients nor the scientists who evaluated their progress knew which patients received the implants. The patients' progress was followed for up to eight years. Unfortunately, both studies showed that the transplants offered little benefit to the patients as a group. While some patients showed improvement, others began to suffer from dyskinesias, jerky involuntary movements that are often side effects of long-term L-dopa treatment. This effect occurred in 15% of the patients in the Colorado study.7 and more than half of the patients in the New York study.8 Additionally, the New York study showed evidence that some patients' immune systems were attacking the grafts.

However, promising findings emerged from these studies as well. Younger and milder Parkinson's patients responded relatively well to the grafts, and PET scans of patients showed that some of the transplanted dopamine neurons survived and matured. Additionally, autopsies on three patients who died of unrelated causes, years after the surgeries, indicated the presence of dopamine neurons from the graft. These cells appeared to have matured in the same way as normal dopamine neurons, which suggested that they were acting normally in the brain.

Figure 3.2. Positron Emission Tomography (PET) images from a Parkinson's patient before and after fetal tissue transplantation. The image taken before surgery (left) shows uptake of a radioactive form of dopamine (red) only in the caudate nucleus, indicating that dopamine neurons have degenerated. Twelve months after surgery, an image from the same patient (right) reveals increased dopamine function, especially in the putamen. (Reprinted with permission from N Eng J Med 2001;344(10) p. 710.)

Researchers in Sweden followed the severity of dyskinesia in patients for eleven years after neural transplantation and found that the severity was typically mild or moderate. These results suggested that dyskinesias were due to effects that were distinct from the beneficial effects of the grafts.9 Dyskinesias may therefore be related to the ways that transplantation disturbs other cells in the brain and so may be minimized by future improvements in therapy. Another study that involved the grafting of cells both into the striatum (the target of dopamine neurons) and the substantia nigra (where dopamine neurons normally reside) of three patients showed no adverse effects and some modest improvement in patient movement.10 To determine the full extent of therapeutic benefits from such a procedure and confirm the reliability of these results, this study will need to be repeated with a larger patient population that includes the appropriate controls.

The limited success of these studies may reflect variations in the fetal tissue used for transplantation, which is of limited quantity and can not be standardized or well-characterized. The full complement of cells in these fetal tissue samples is not known at present. As a result, the tissue remains the greatest source of uncertainty in patient outcome following transplantation.

The major goal for Parkinson's investigators is to generate a source of cells that can be grown in large supply, maintained indefinitely in the laboratory, and differentiated efficiently into dopamine neurons that work when transplanted into the brain of a Parkinson's patient. Scientists have investigated the behavior of stem cells in culture and the mechanisms that govern dopamine neuron production during development in their attempts to identify optimal culture conditions that allow stem cells to turn into dopamine-producing neurons.

Preliminary studies have been carried out using immature stem cell-like precursors from the rodent ventral midbrain, the region that normally gives rise to these dopamine neurons. In one study these precursors were turned into functional dopamine neurons, which were then grafted into rats previously treated with 6-hydroxy-dopamine (6-OHDA) to kill the dopamine neurons in their substantia nigra and induce Parkinson's-like symptoms. Even though the percentage of surviving dopamine neurons was low following transplantation, it was sufficient to relieve the Parkinson's-like symptoms.11 Unfortunately, these fetal cells cannot be maintained in culture for very long before they lose the ability to differentiate into dopamine neurons.

Cells with features of neural stem cells have been derived from ES-cells, fetal brain tissue, brain tissue from neurosurgery, and brain tissue that was obtained after a person's death. There is controversy about whether other organ stem cell populations, such as hematopoietic stem cells, either contain or give rise to neural stem cells

Many researchers believe that the more primitive ES cells may be an excellent source of dopamine neurons because ES-cells can be grown indefinitely in a laboratory dish and can differentiate into any cell type, even after long periods in culture. Mouse ES cells injected directly into 6-OHDA-treated rat brains led to relief of Parkinson-like symptoms. Further investigation showed that these ES cells had differentiated into both dopamine and serotonin neurons.12 This latter type of neuron is generated in an adjacent region of the brain and may complicate the response to transplantation. Since ES cells can generate all cell types in the body, unwanted cell types such as muscle or bone could theoretically also be introduced into the brain. As a result, a great deal of effort is being currently put into finding the right quot;recipequot; for turning ES cells into dopamine neuronsand only this cell typeto treat Parkinson's disease. Researchers strive to learn more about normal brain development to help emulate the natural progression of ES cells toward dopamine neurons in the culture dish.

The recent availability of human ES cells has led to further studies to examine their potential for differentiation into dopamine neurons. Recently, dopamine neurons from human embryonic stem cells have been generated.13 One research group used a special type of companion cell, along with specific growth factors, to promote the differentiation of the ES cells through several stages into dopamine neurons. These neurons showed many of the characteristic properties of normal dopamine neurons.13 Furthermore, recent evidence of more direct neuronal differentiation methods from mouse ES cells fuels hope that scientists can refine and streamline the production of transplantable human dopamine neurons.

One method with great therapeutic potential is nuclear transfer. This method fuses the genetic material from one individual donor with a recipient egg cell that has had its nucleus removed. The early embryo that develops from this fusion is a genetic match for the donor. This process is sometimes called quot;therapeutic cloningquot; and is regarded by some to be ethically questionable. However, mouse ES cells have been differentiated successfully in this way into dopamine neurons that corrected Parkinsonian symptoms when transplanted into 6-OHDA-treated rats.14 Similar results have been obtained using parthenogenetic primate stem cells, which are cells that are genetic matches from a female donor with no contribution from a male donor.15 These approaches may offer the possibility of treating patients with genetically-matched cells, thereby eliminating the possibility of graft rejection.

Scientists are also studying the possibility that the brain may be able to repair itself with therapeutic support. This avenue of study is in its early stages but may involve administering drugs that stimulate the birth of new neurons from the brain's own stem cells. The concept is based on research showing that new nerve cells are born in the adult brains of humans. The phenomenon occurs in a brain region called the dentate gyrus of the hippocampus. While it is not yet clear how these new neurons contribute to normal brain function, their presence suggests that stem cells in the adult brain may have the potential to re-wire dysfunctional neuronal circuitry.

The adult brain's capacity for self-repair has been studied by investigating how the adult rat brain responds to transforming growth factor alpha (TGF), a protein important for early brain development that is expressed in limited quantities in adults.16 Injection of TGF into a healthy rat brain causes stem cells to divide for several days before ceasing division. In 6-OHDAtreated (Parkinsonian) rats, however, the cells proliferated and migrated to the damaged areas. Surprisingly, the TGF-treated rats showed few of the behavioral problems associated with untreated Parkinsonian rats.16 Additionally, in 2002 and 2003, two research groups isolated small numbers of dividing cells in the substantia nigra of adult rodents.17,18

These findings suggest that the brain can repair itself, as long as the repair process is triggered sufficiently. It is not clear, though, whether stem cells are responsible for this repair or if the TGF activates a different repair mechanism.

Many other diseases that affect the nervous system hold the potential for being treated with stem cells. Experimental therapies for chronic diseases of the nervous system, such as Alzheimer's disease, Lou Gehrig's disease, or Huntington's disease, and for acute injuries, such as spinal cord and brain trauma or stoke, are being currently developed and tested. These diverse disorders must be investigated within the contexts of their unique disease processes and treated accordingly with highly adapted cell-based approaches.

Although severe spinal cord injury is an area of intense research, the therapeutic targets are not as clear-cut as in Parkinson's disease. Spinal cord trauma destroys numerous cell types, including the neurons that carry messages between the brain and the rest of the body. In many spinal injuries, the cord is not actually severed, and at least some of the signal-carrying neuronal axons remain intact. However, the surviving axons no longer carry messages because oligodendrocytes, which make the axons' insulating myelin sheath, are lost. Researchers have recently made progress to replenish these lost myelin-producing cells. In one study, scientists cultured human ES cells through several steps to make mixed cultures that contained oligodendrocytes. When they injected these cells into the spinal cords of chemically-demyelinated rats, the treated rats regained limited use of their hind limbs compared with un-grafted rats.19 Researchers are not certain, however, whether the limited increase in function observed in rats is actually due to the remyelination or to an unidentified trophic effect of the treatment.

Getting neurons to grow new axons through the injury site to reconnect with their targets is even more challenging. While myelin promotes normal neuronal function, it also inhibits the growth of new axons following spinal injury. In a recent study to attempt post-trauma axonal growth, Harper and colleagues treated ES cells with a combination of factors that are known to promote motor neuron differentiation.20 The researchers then transplanted these cells into adult rats that had received spinal cord injuries. While many of these cells survived and differentiated into neurons, they did not send out axons unless the researchers also added drugs that interfered with the inhibitory effects of myelin. The growth effect was modest, and the researchers have not yet seen evidence of functional neuron connections. However, their results raise the possibility that signals can be turned on and off in the correct order to allow neurons to reconnect and function properly. Spinal injury researchers emphasize that additional basic and preclinical research must be completed before attempting human trials using stem cell therapies to repair the trauma-damaged nervous system.

Since myelin loss is at the heart of many other degenerative diseases, oligodendrocytes made from ES cells may be useful to treat these conditions as well. For example, scientists recently cultured human ES cells with a combination of growth factors to generate a highly enriched population of myelinating oligodendrocyte precursors.21,22 The researchers then tested these cells in a genetically-mutated mouse that does not produce myelin properly. When the growth factor-cultured ES cells were transplanted into affected mice, the cells migrated and differentiated into mature oligodendrocytes that made myelin sheaths around neighboring axons. These researchers subsequently showed that these cells matured and improved movement when grafted in rats with spinal cord injury.23 Improved movement only occurred when grafting was completed soon after injury, suggesting that some post-injury responses may interfere with the grafted cells. However, these results are sufficiently encouraging to plan clinical trials to test whether replacement of myelinating glia can treat spinal cord injury.

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is characterized by a progressive destruction of motor neurons in the spinal cord. Patients with ALS develop increasing muscle weakness over time, which ultimately leads to paralysis and death. The cause of ALS is largely unknown, and there are no effective treatments. Researchers recently have used different sources of stem cells to test in rat models of ALS to test for possible nerve cell-restoring properties. In one study, researchers injected cell clusters made from embryonic germ (EG) cells into the spinal cord fluid of the partially-paralyzed rats.24 Three months after the injections, many of the treated rats were able to move their hind limbs and walk with difficulty, while the rats that did not receive cell injections remained paralyzed. Moreover, the transplanted cells had migrated throughout the spinal fluid and developed into cells that displayed molecular characteristics of mature motor neurons. However, too few cells matured in this way to account for the recovery, and there was no evidence that the transplanted cells formed functional connections with muscles. The researchers suggest that the transplanted cells may be promoting recovery in some other way, such as by producing trophic factors.

This possibility was addressed in a second study in which scientists grew human fetal CNS stem cells in culture and genetically modified them to produce a trophic factor that promotes the survival of cells that are lost in ALS. When grafted into the spinal cords of the ALS-like rats, these cells secreted the desired growth factor and promoted the survival of the neurons that are normally lost in the ALS-like rats.25 While promising, these results highlight the need for additional basic research into functional recovery in ALS disease models.

Stroke affects about 750,000 patients per year in the

U.S. and is the most common cause of disability in adults. A stroke occurs when blood flow to the brain is disrupted. As a consequence, cells in affected brain regions die from insufficient amounts of oxygen. The treatment of stroke with anti-clotting drugs has dramatically improved the odds of patient recovery. However, in many patients the damage cannot be prevented, and the patient may permanently lose the functions of affected areas of the brain. For these patients, researchers are now considering stem cells as a way to repair the damaged brain regions. This problem is made more challenging because the damage in stroke may be widespread and may affect many cell types and connections.

However, researchers from Sweden recently observed that strokes in rats cause the brain's own stem cells to divide and give rise to new neurons.26 However, these neurons, which survived only a couple of weeks, are few in number compared to the extent of damage caused. A group from the University of Tokyo added a growth factor, bFGF, into the brains of rats after stroke and showed that the hippocampus was able to generate large numbers of new neurons.27 The researchers found evidence that these new neurons were actually making connections with other neurons. These and other results suggest that future stroke treatments may be able to coax the brain's own stem cells to make replacement neurons.

Taking an alternative approach, another group attempted transplantation as a means to treat the loss of brain mass after a severe stroke. By adding stem cells onto a polymer scaffold that they implanted into the stroke-damaged brains of mice, the researchers demonstrated that the seeded stem cells differentiated into neurons and that the polymer scaffold reduced scarring.28 Two groups transplanted human fetal stem cells in independent studies into the brains of stroke-affected rodents; these stem cells not only survived but migrated to the damaged areas of the brain.29,30 These studies increase our knowledge of how stem cells are attracted to diseased areas of the brain.

There is also increasing evidence from numerous animal disease models that stem cells are actively drawn to brain damage. Once they reach these damaged areas, they have been shown to exert beneficial effects such as reducing brain inflammation or supporting nerve cells. It is hoped that, once these mechanisms are better understood, this stem cell recruitment can potentially be exploited to mobilize a patient's own stem cells.

Similar lines of research are being considered with other disorders such as Huntington's Disease and certain congenital defects. While much attention has been called to the treatment of Alzheimer's Disease, it is still not clear if stem cells hold the key to its treatment. But despite the fact that much basic work remains and many fundamental questions are yet to be answered, researchers are hopeful that repair for once-incurable nervous system disorders may be amenable to stem cell based therapies.

Considerable progress has been made the last few years in our understanding of stem cell biology and devising sources of cells for transplantation. New methods are also being developed for cell delivery and targeting to affected areas of the body. These advances have fueled optimism that new treatments will come for millions of persons who suffer from neurological disorders. But it is the current task of scientists to bring these methods from the laboratory bench to the clinic in a scientifically sound and ethically acceptable fashion.

Notes:

* Chief, Developmental Neurobiology Program, Molecular, Cellular & Genomic Neuroscience Research Branch, Division of Neuroscience and Basic Behavioral Science, National Institute of Mental Health, National Institutes of Health, Email: panchisiond@mail.nih.gov

Chapter 2|Table of Contents|Chapter 4

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Repairing the Nervous System with Stem Cells | stemcells ...

Spinal Cord Stem Cells Comments Off on Repairing the Nervous System with Stem Cells | stemcells … | September 5th, 2017

NEW YORK--(BUSINESS WIRE)--Americord, the fastest growing cord blood bank in the country, and a leader in the advancement of umbilical cord blood, cord tissue, and placental tissue banking, has expanded customer options to now offer placental tissue banking as a stand-alone service.

As one of the only companies to offer placental tissue banking, Americord believes in the importance of offering new mothers an opportunity to preserve their stem cells for potential future use. We are therefore launching placental tissue banking as a stand-alone service, without the need to bank umbilical cord blood.

While many families have embraced Americords cord blood and tissue bundles, some have expressed interest in storing only placental tissue, commented Erin Willigan, Vice-President of Marketing at Americord. We wanted to respond to their desire to select individual services that best fit their budget and future plans.

Placental tissue contains mesenchymal stem cells (MSCs) that are a genetic match to the mother. These stem cells are multipotent, meaning that they can differentiate into many different types of cells, including organ and muscle tissue, skin, bone, cartilage, and fat cells. The placenta uses these stem cells to grow and function during pregnancy. After baby is delivered, stem cells from the placenta can be collected and stored for potential future use.

Due to their ability to multiply and become many different types of tissue, MSCs hold great promise for regenerative treatments. Over 50 clinical trials are currently researching therapeutic uses for MSCs, including treatments for Type 1 Diabetes, Alzheimers, and spinal cord injuries.

About Americord Registry LLC (Americord)

Americord Registry LLC is a leader in the advancement of umbilical cord blood, cord tissue and placenta tissue banking. Americord collects, processes, and stores newborn stem cells from umbilical cord blood for future medical or therapeutic use, including the treatment of more than 80 blood diseases such as sickle cell anemia and leukemia. Founded in 2008, Americord is registered with the FDA and operates in all 50 states. The companys laboratory is CLIA Certified, accredited by the AABB and complies with all federal and state guidelines and applicable licenses. Americord is headquartered in New York, NY. For more information, visit http://www.americordblood.com.

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Americord Offers New Option for Banking Placental Tissue - Business Wire (press release)

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Human neural stem cells are derived via fluorescence-activated cell sorting (FACS) from donated fetal brain tissue. Credit: Hal X. Nguyen and Aileen J. Anderson

A new study in mice published in The Journal of Neuroscience details a potential therapeutic strategy that uses stem cells to promote recovery of motor activity after spinal cord injury.

The transplantation of neural stem cells could help promote repair of an injured spinal cord, but the interaction between donor cells and the resident cells that are part of the body's immune response to injury is not well understood.

Hal Nguyen, Aileen Anderson and colleagues found that mice receiving stem cells derived from donated human brain tissue required depletion of a specific population of immune cells in order to improve the mice's ability to walk along a glass plate. Although the donor cells survived equally when transplanted immediately or 30 days after injury, their location and cell type changed with time. These results suggest that immune cells populating the spinal cord at different time points after injury affect the ability of stem cells to promote functional recovery.

Human neural stem cell replicates itself during mitosis in vitro. Credit: Hal X. Nguyen and Aileen J. Anderson

Explore further: Stem cell scarring aids recovery from spinal cord injury

More information: "Systemic neutrophil depletion modulates the migration and fate of transplanted human neural stem cells to rescue functional repair," Journal of Neuroscience (2017). DOI: 10.1523/JNEUROSCI.2785-16.2017

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Using donor stem cells to treat spinal cord injury

Spinal Cord Stem Cells Comments Off on Using donor stem cells to treat spinal cord injury | September 3rd, 2017

CINCINNATI -- Ryan Custer tearfully thanked the community for their support at his prayer service Sunday.

I cant thank you guys enough, he said in front of a standing ovation at Elder High Schools Fieldhouse.

Custer, an Elder grad and Wright State freshman, suffered a traumatic spinal injury at a large party in April after he tried to jump into a shallow, makeshift pool.

Family and friends welcomed Custer home on Wednesday. He had been been recovering and undergoing therapy at University of Cincinnati Medical Center. He also traveled to Chicago to be considered for a stem cell study at Rush University.

Doctors injected 20 million stem cells into Custers neck, and HBO has been following his progress.

Ryans brother, Nick Custer, thanked the West Side community for being so uplifting to his family.

It means the world to us. It just shows you what a special kid Ryan is as a 19-year-old kid going through this, its just overwhelming support, he said.

Nick said Ryan will continue rehabilitation in Cincinnati, and he said Ryan is looking forward to the start of Wright States season.

Ryan wants to get back to the team as soon as possible, and they all want him to come back and help however he can. He misses them, definitely, Nick said.

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Ryan Custer, Elder grad injured at Oxford party, thanks community for their support - WCPO

Spinal Cord Stem Cells Comments Off on Ryan Custer, Elder grad injured at Oxford party, thanks community for their support – WCPO | September 3rd, 2017

GABRIELLA FIORINO

We trust our doctors with our lives. However, what is the reaction when some medical professionals allow unsanitary measures and diseases to break out into the population? Four institutions in the U.S. came under fire recently by the FDA for improperly handling microbiological organisms and exposing the public to smallpox after conducting unapproved techniques, endangering hundreds of lives.

The FDA identified four medical centers in California and Florida as utilizing unapproved stem cell therapies for those with cancer and other serious illnesses. One of the institutes, California Stem Cell Treatment Centers, applied a method developed by StemImmune Inc., which consisted of injecting clients with a mixture of the smallpox vaccine and stem cells. Dr. Mark Berman, co-founder of the California center, described their methods as cutting edge therapy for stage-4 cancer patients, as reported by the Los Angeles Times.

The consequences of such methods are worrisome; as the FDA claims exposure to the smallpox vaccine significantly increases the risk of life-threatening complications, including heart inflammation. Perhaps even more troubling is the fact that individuals in contact with those receiving the vaccine may develop similar symptoms, possibly infecting hundreds of others. The FDA is currently investigating how StemImmune Inc. received shipments of the vaccine, as the product is unavailable on the market.

The Stem Cell Clinic of Sunrise, Florida is another facility under investigation by the FDA for taking improper sanitary measures to prevent contamination during their therapies. According to the agency, the clinic refused to permit entry of an FDA inspector without an appointment, which is a violation of federal law. This refusal would not be the first time the Florida institution came under fire. According to the New England Journal of Medicine, three clients suffering from macular degeneration sustained blindness following treatment at the facility.

A variety of sources derive stem cells, including bone marrow, blood, umbilical cords, and controversially, human embryos. These products aid in the development and restoration of healthy human tissue, and help battle cancer, heart disease, and Parkinsons disease, as noted by the University of Utah. These products are also employed for spinal cord injuries, indicating critical applications, as the central nervous system does not naturally permit neuro-regeneration following damage. Excitingly, organs growth for those requiring life-saving transplants is another possible advancement.

These innovations are not without consequences, however. According to the Mayo Clinic, some may develop graft-versus-host disease, a condition in which a donors stem cells attack the patients tissues and organs, possibly leading to death. Risks of brain tumor development are also an increased possibility for those receiving injections in the spinal cord, as abnormal tissue growth may result.

As the FDA investigates unsound practices by the four institutes endangering the lives of hundreds, Americans should not be misled regarding stem cell therapies. Through proper sanitary measures, their uses are a huge medical development, comprising a myriad of medical advantages. Liberty Nation will keep readers up to date regarding the actions of the FDA against the four clinics.

Gabi is a Biomedical Sciences major and manages a Cognitive Neuroscience Research Lab at the University of Central Florida. A Libertarian, Gabi says shes surrounded on by whiny, wannabe anti-capitalists, posting about their victimhood on Facebook.Although leftists often confuse her with privileged white girls, Gabi is Puerto Rican and Italian.Make sense of that, liberals!

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Stem Cells and "Mishandling" Smallpox - Liberty Nation - Liberty Nation (registration) (blog)

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01 Sep 2017

A paper in the September 1 Nature claims a cadre of rogue microglia are all it takes to orchestrate neurodegeneration. Researchers led by Frederic Geissmann and Omar Abdel-Wahab of Memorial Sloan Kettering Cancer Center in New York, and Marco Prinz of the University of Freiburg in Germany, induced a somatic mutation in about 10 percent of microglia that switched on ERK kinase signaling. The mice later developed a severe neurodegenerative disease that paralyzed them. The researchers determined that damaging inflammation caused by the mutated microglia was likely to blame. The findings raise the possibility that similar somatic mutations in people are responsible for a rare neurodegenerative disease that occurs inchildren.

This is a great paper for many reasons, commented Bart De Strooper of the Dementia Research Institute in the U.K. I am particularly excited about the concept of acquired genetic mosaicism as a cause of neurodegenerative disorder. The paper also shows that microglia mutations can be directly causative inneurodegeneration.

Most famous for their role in causing cancer, somatic mutations can spontaneously arise in any cell, sometimes giving it a proliferative edge. Mutations in the RAS-MEK-ERK signaling pathway, for example, can cause diseases called histiocytoses if they arise in the myeloid cell lineage, which gives rise to blood and immune cells, including macrophages and microglia. Histiocytoses manifest in different ways, including leukemias, other tumors, and malfunctions in multiple organs. Mysteriously, a small fraction of carriers also get a neurodegenerative disease that manifests between childhood and middle age, with symptoms such as cerebellar ataxia and tremor (Lachenal et al., 2006; Wnorowski et al., 2008). The reason for the neurodegeneration has been amystery.

Geissmann and colleagues speculated it could be caused by microglia descended from erythro-myeloid progenitor cells (EMPs) harboring the same RAS-MEK-ERK somatic mutations. EMPs arise in the embryonic yolk sac early in development, and give rise to microglia in the brain and macrophages in other tissues (Perdiguero et al., 2014; Feb 2015 conference news).In contrast, circulating monocytes are continually replenished by hemotopoietic stem cells (HSCs) in the bonemarrow.

Doomed During Development? Histiocytoses arise from somatic mutations in hematopoietic stem cells (HSCs, left) or in erythro-myeloid progenitor (EMP) cells (right), which give rise to macrophages and microglia. The mutant microglia may cause inflammation, leading to neurodegeneration. [Courtesy of Tarnawsky and Yoder, Nature, News & Views,2017.]

To find out if somatic mutations in EMPs could beget microglia that trigger neurodegeneration, first author Elvira Mass and colleagues induced a somatic mutation that causes histiocytoses into mice. They chose the V600E variant of the BRAF gene, a substitution that switches on ERK signaling. The researchers generated transgenic mice carrying an inducible copy of the mutated BRAF gene, which could only be switched on via tamoxifen-induced Cre recombination in EMPs. This also turned on yellow fluorescent protein so the researchers could identify the cells. At embryonic day 8.5, they injected pregnant mice with a teeny dose of the drug to ensure that only a fraction of the embryos EMPs would express the mutation. About 10 percent of tissue resident macrophages, including microglia, in the resulting offspring expressed V600E BRAF at one month ofage.

The mutant microglia took up their positions in the brain, but were different from their normal counterparts from the get-go. Those carrying the V600E BRAF expressed elevated markers of proliferation, ERK signaling, and inflammation. In one-month-old mice, these feisty microglia had yet to cause trouble, but by four months of age, the researchers noticed neurological symptoms in the mice, including loss of hind limb reflexes and shortened stride. At seven months, 90 percent of the animals were affected and by nine months 60 percent of the mice had full hind limb paralysis. These symptoms, similar to cerebellar ataxia, are common in people with cerebral histiocytoses. Feeding the mice a BRAF inhibitor starting at one month of age drastically delayed onset and slowedprogression.

Compared to wild-type mice (left), animals with induced BRAF mutations in their EMPs had an expansion of mutant microglia expressing YFP in their spinal cord (middle). Microglia also expressed the activation marker CD68 (top) and phosphorylated ERK (bottom). [Courtesy of Mass et al., Nature2017.]

The researchers next searched for pathological changes that could have triggered the disorder. In month-old mice, the researchers found signs of elevated microglial and astrocyte activation, but not neuronal death. Oddly, by immunohistochemistry using the 22C11 antibody, the researchers noticed deposits of amyloid precursor protein (APP) in the inflamed areas, a phenomenon that Geissmann attributed to release of the membrane protein from newly damaged axons. In six-month-old animals, large clusters of activated, phagocytic microglia carrying the BRAF mutation crowded in the thalamus, brain stem, cerebellum, and spinal cord. These same regions were rife with synaptic and neuronal loss, demyelination, and astrogliosis. The mutant microglia had a small proliferative advantage compared with their wild-type counterparts, but Geissmann attributed the bulk of the neuronal damage to the activation of the cells, rather than their expansion. Treatment with a BRAF inhibitor mitigated theseresponses.

Gene expression analysis of mutant microglia taken from paralyzed mice revealed the differential expression of around 8,000 genes, 80 percent of which were upregulated compared to microglia from control mice. These genes included a bevy of pro-inflammatory mediators, including cytokines, phagocytosis boosters, matrix proteins, and growthfactors.

For some reason, the thalamus, brain stem, cerebellum, and spinal cord were uniquely vulnerable to the presence of the V600E BRAF mutant cells. Tissue macrophages carrying the mutation also expanded in the liver, spleen, kidney, and lung, even more so than in the brain, but did not cause damage in those regions. Geissmann speculated that differences in the tissue microenvironment could play a role in this selective vulnerability. For example, normal liver macrophages are in a near constant state of activation, Geissmann said, so the organ is equipped to deal with them. Perhaps the posterior part of the brain is unaccustomed to constant microglial activation, he said. Indeed, chronic microglial activation occurs during AD as well, and appears to ultimately inflict damage, rather than helpfulresponses.

Finally, the researchers investigated whether patients with histiocytoses also had abnormal microglia. They analyzed postmortem brain tissue from three patients with Erdheim-Chester disease (ECD), and conducted gene expression analysis on brain biopsies from one person with Langerhans cell histiocytosis (LCH), and another with juvenile xanthogranuloma (JXG). All of these patients had neurodegenerative disease associated with their histiocytoses, which were all caused by BRAF V600E mutations. In the ECD samples, the researchers spotted abundant activated microglia gathered at sites of neuronal loss, astrogliosis, and demyelination. Compared with data from five control samples, gene expression analysis on the JXG and LCH samples revealed an upregulation of genes in the MAPK pathway, including multiple pro-inflammatorycytokines.

The findings support the idea that activated microglia wreak havoc in the brain and cause neurodegeneration in people withhistiocytoses.

For a somatic mutation to have an effect, affected cells must propagate sufficiently. EMPs proliferate during early development, making it a prime time for mutant clones to multiply, Geissmann said. Perhaps the number of mutant clones born during the EMP stage would suffice to harm neurons, he said. However, if microglia are also bestowed with a proliferative edge, this would likely exacerbate the damage, he added. Either way, Geissmann proposed that inhibitors of ERK signaling might thwart neurodegeneration when mutant microglia areinvolved.

In an accompanying editorial, Stefan Tarnawsky and Mervin Yoder at Indiana University in Indianapolis noted opportunities for better diagnosis in this scenario. When somatic mutations occur in EMPs during early development, macrophages in many regions of the body will likely carry the mutations, not just microglia in the brain. This suggests that it might be possible to collect macrophage samples from more easily accessible, non-CNS tissues to look for biomarkers when diagnosing microglia-related disease, theywrote.

What about somatic mutations that might arise later in life, when tissue resident macrophages or microglia are already nestled into their permanent residences? Though recent studies reported that microglia are relatively long-lived cells, they proliferate in response to threats (Aug 2017 news),perhaps setting the stage for expansion of mutant cells, Geissmann speculated. That said, beyond people with histiocytoses, the contribution of somatic mutations in microglia to neurodegenerative disease is unclear. De Strooper and others have reported that genetic mosaicism in neurons could cause neurodegeneration (Jul 2015 news). A major impediment to studying this phenomenon is that somatic mutations that arise in the brain go undetected in standard genomic sequencing.JessicaShugart

No Available Further Reading

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Somatic SNAFUCan a Few Mutant Microglia Cause Neurodegenerative Disease? - Alzforum

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You might feel a bit down if you watch the news. Who wouldnt?

Angry people might be grabbing headlines and making you wonder about the future, but the antidote is all around you.

Talk to some of your neighbours. Chances are, no matter what they look like or where theyre originally from, youll find theyre actually pretty decent people just like you.

The little improvements we all try to make may not register much, but the accumulation of them all eventually does.

And if theres one tangible piece of proof that the world is changing for the better, its Lucas Lindner.

2016 was not a kind year for 22-year-old Lucas.

Last May he lost control of his pickup truck when a deer ran out on the road. The front passenger tire blew out. The truck rolled, throwing him out of the window.

When he woke up in the hospital, he was paralysed from the neck down. He was just heading to the grocery store on a Wisconsin Sunday morning.

It was an accident that could happen to anyone, to a friend or relative.

Normally, people like Lucas have no hope of restoring motor control of their bodies ever again.

In the United States, this awful story plays out 17,000 times every year. There are a quarter of a million people in the country with paralysis.

But Lucas story is working out a little bit differently.

Lucas was airlifted to Froedtert Hospital, a teaching hospital of the Medical College of Wisconsin.

There, Dr. Shekar N. Kurpad, professor of neurosurgery, applied 15 years of research into cell transplantation for spinal cord injury.

The procedure revolutionary and so were the cells Dr. Kurpad used.

The new procedure used cells that were developed over many years by researchers at a two companies leading the way in regenerative medicine.

Researchers at these companies have discovered how to grow stem cells and make them reliable for transplantation use.

On doctor, in fact, who Ive researched extensively, has been called the father of regenerative medicine.

Ive had the pleasure of meeting with him on a number of occasions.

Whenever I am in the San Francisco Bay Area, I try to visit him to learn whats going on in the field.

And from what Ive seen the therapeutic potential is hard to understate.

And were starting to see the results in people like Lucas Lindner.

Hes still wheelchair-bound we have a lot more to learn but he now has fine motor skills in his upper body. Thats extraordinary in cases like his.

Lucass miraculous improvement is due to newly designed pluripotent stem cells They are called pluripotent because they have the power to transform into any other cell type in the body.

And this Bay Area doctors company has accumulated the technology to make that happen.

Over the next few months, well get more clinical data from patients being treated with the full 20 million-cell dose and potentially more great news of restored motor function.

The recent headlines may have been about a few angry people rioting and hating each other, but the real important news is this

Recently, when the Cincinnati Reds played the Milwaukee Brewers, Lucas threw out the opening pitch.

Many U.S. presidents and other famous people have thrown pitches, but no pitch has been as historic as this one. And the advances I highlighted today are the reason why.

As this therapy matures and gets closer to market, I believe it will make a big impact on shares of companies in this space.

Which means the right-timed move in the upcoming months means a huge potential windfall of cash for you.

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A year ago he was paralysed from the neck down then this happened - The Daily Reckoning

Spinal Cord Stem Cells Comments Off on A year ago he was paralysed from the neck down then this happened – The Daily Reckoning | September 1st, 2017

Spinal injuries are oftenpermanent, but new research suggests such injuries may be healed, at least in part.Researchers were able to stimulate limb function in paralyzed mice by implanting human stem cells into theirspinal cords. We're not close to repeating the test in people, but the study shows it may be possible some day with further research.

The University of California-San Diego team grafted human neural stem cells (NSCs) into the spinal cord injuries of mice who were purposely injuredto impair the use of their front legs. The stem cells grew slowly, yet steadily, over the course of 18 months, retaining their original function despite being in a strange and challenging environment for an extended period of time. Whats more, eventually the rodents were able to use their front legs again.

"The bottom line is that clinical outcome measures for future trials need to be focused on long time points after grafting," said study researcher Mark Tuszynskiin a recent statement. Relying on shorter time frames might produce misleadingly negative results considering how long it takes neural stem cells to develop, he added.

For the study, the team used H9 human NSCs, which are a type of stem cell derived from human embryonic stem cells, as commonly used in scientific research, the statement reported. They then grafted these human stem cells into the spinal injuries of mice. The researchers observed the rodents recovery over the course of 18 months, noting that significant cellgrowth did occur soon after grafting, and continued up to a year after the initial implantation.

The most important observation was that these cells were able to continue to do what they were designed to doregrow neural cellsdespite the fact that they were transplanted into an entirely different species. This suggests the cells have resilience and similar experiments mayalso work in human subjects.

Before you get too excited about these results, the researchers emphasized that there were a number of caveats. First, humans and mice are entirely different species, and though the results observed in the rodents are promising, we don't know if they could be repeated in people.

Also, the researchers observed that some astrocytes, star-shaped neural cells associated with electrical impulse transmission, did migrate from the original implantation site to other areas of the rodents. These brain cells are classified as glial cells, which are noted to lead to devastating and difficult to treat cancers when they are dysregulated, Harvard University reported. However, there were no tumors or abnormal growths observed in the mice in the study and the researchers are trying to figure out way to make sure cancer doesn't develop.

Ultimately, the team believe that these results stand as a good foundation on which to buildfurther research.

Success, it would seem, will take time," concluded Tuszynski.

Source: Lu P, Ceto S, Wang Y, et al. Prolonged human neural stem cell maturation supports recovery in injured rodent CNS. The Journal of Clinical Investigation . 2017

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Stem Cell Graft Repairs Spinal Cord Injury, Helps Paralyzed Mice ... - Medical Daily

Spinal Cord Stem Cells Comments Off on Stem Cell Graft Repairs Spinal Cord Injury, Helps Paralyzed Mice … – Medical Daily | August 31st, 2017

A brain cell replacement therapy reduced Parkinsons disease symptoms in monkeys, Japanese researchers report in a study released Wednesday. The positive result boosts prospects to test the therapy in people.

The goal is to implant neurons derived from stem cells into the brains of Parkinsons patients, a project pursued by scientists in San Diego, New York, Britain and Sweden as well as in Japan. If all goes well, the neurons will function as replacements for those destroyed in the disease.

In addition, human testing of a related brain cell therapy from Carlsbads International Stem Cell Corp. is already under way in Australia.

While treatments exist for the movement disorders caused by Parkinsons, none of them actually halt progression. Replacing the brain cells destroyed in Parkinsons holds the promise of actually reversing the disease.

Moreover, success with Parkinsons could pave the way to treating many other neurodegenerative diseases, such as ALS (Lou Gehrigs disease) and perhaps Alzheimers, along with brain and spinal cord injuries. These afflictions cost hundreds of billions annually, and most importantly, produce immense suffering in patients and caregivers.

Years of extensive research are required before any such therapy can be tried in people. Testing in monkeys or other primates is often regarded as the last step before human treatment can be contemplated.

The study was published in the journal Nature. Its senior author was Jun Takahashi, a prominent stem cell researcher at Kyoto University in Kyoto, Japan. Go online to j.mp/parkips for the study.

There is precedent to suggest the therapy might work. Beginning decades ago, brain cells taken from human fetuses have been implanted into the brains of Parkinsons patients, with mixed results. Some patients experienced improved movement control. But others gained nothing, or experienced uncontrolled movements.

Scientists in the field say using stem cells should provide improved results. Stem cells can be made in greater quantity than the limited number of fetal brain cells available. In addition, the stem cells and neurons made from them can be analyzed for quality before implantation.

The study was praised by regenerative medicine researcher Tilo Kunath at the University of Edinburgh, in comments provided by the UK Science Media Centre.

This is extremely promising research demonstrating that a safe and highly effective cell therapy for Parkinsons can be produced in the lab, Kunath said.

Such a therapy has the potential to reverse the symptoms of Parkinsons in patients by restoring their dopamine-producing neurons. The next stage will be to test these therapies in a first-in-human clinical trial.

In the study, researchers produced neurons that secrete dopamine, a neurotransmitter deficient in Parkinsons disease. These neurons were made from human stem cells derived from both healthy people and those with Parkinsons.

The researchers then implanted the human neurons into 10 monkeys whose own dopamine-making neurons had been destroyed. The monkeys were given immunosuppressive drugs to prevent rejection of the human cells.

The human neurons integrated into the brains of the monkeys and functioned as dopamine-making neurons. The monkeys improved in movement ability, save for one monkey that became ill and was euthanized. Both cells from healthy and Parkinsons patients were effective.

A companion study in Nature Communications demonstrated a method of immune-matching the cells to reduce the immune response. Takahashi was also senior author of that study. Go online to j.mp/ipsimmune for the study.

Both studies used artificial embryonic stem cells, called induced pluripotent stem cells (IPS). These act-alike cells are not derived from embryos, but are genetically reprogrammed from adult cells, usually skin cells.

The IPS cells appear to act virtually identically to embryonic stem cells, but dont raise the ethical objections many have to using embryonic stem cells. These cells were invented in 2006 by a team led by Shinya Yamanaka, a co-author of the Nature Communications study.

Moreover, the cells can be made from the patients themselves, which is not expected to cause an immune reaction. This is the approach taken by the San Diego team, including scientists at The Scripps Research Institute.

Carlsbads International Stem Cell Corp. uses a different approach. It starts with unfertilized, or parthenogenetic, human egg cells. These are grown into immature neurons that are implanted. The cells are expected to grow not only into dopamine-making neurons, but other kind of brain cells that preserve the remaining neurons.

The Australian clinical trial has gathered evidence of safety, and continued testing is under way determine efficacy.

The Nature study dovetails with research by the San Diego group, Summit for Stem Cell, (www.summitforstemcell.org), including scientists at The Scripps Research Institute and doctors at Scripps Health.

The group proposes to treat Parkinsons patients with neurons grown from their own IPS cells. The scientists have received funding from the California Institute for Regenerative Medicine, the states stem cell agency.

The studies support the personalized approach that we are taking for a neuron replacement therapy for Parkinson's disease patients, said Jeanne Loring and Andres Bratt-Leal, stem cell scientists at The Scripps Research Institute.

Two points from the studies should be highlighted, Loring and Bratt-Leal said by email.

Parkinson's disease is a late-onset disorder, they said. That means that there was nothing wrong with the neurons that people with Parkinson's were born with. Few PD patients have a family history of the disease, which suggests that genetic mutations did not cause their disease.

So for the great majority of patients, transplantation of their own neurons is a promising approach to relieving symptoms, without having to take expensive and risky immunosuppressive drugs, they said.

The Summit for Stem Cell scientists are members of an international partnership of laboratories developing neuron replacement therapies for Parkinsons, called GForce PD.

Takahashi belongs to the partnership, as do scientists in the UK, Sweden and New York. These use both embryonic and IPS stem cells. The Summit for Stem Cell effort is the only one using patient-matched IPS cells, Loring and Bratt-Leal said.

Brain cells reprogrammed to make dopamine, with goal of Parkinsons therapy

Parkinson's stem cell therapy shows signs of safety

Parkinson's therapy funded by California's stem cell agency

Dopamine-making neurons can be chemically controlled in animal model of Parkinson's

Stem cell clinical trial for Parkinson's begins

Summit for Stem Cell

bradley.fikes@sduniontribune.com

(619) 293-1020

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Brain cell replacement for Parkinson's boosted by monkey study - The San Diego Union-Tribune

Spinal Cord Stem Cells Comments Off on Brain cell replacement for Parkinson’s boosted by monkey study – The San Diego Union-Tribune | August 31st, 2017

Researchers at the University of California San Diego and at the San Diego Veterans Administration Medical Center have shown that human neural stem cells (NSCs) grafted onto the spinal cord injuries of mice produced a functional recovery after one year. The team has shown that the NSCs continue to grow slowly and steadily even18 months after implantation.

The study is published in the Journal of Clinical Investigation and set out to answer how long it would take for the cells to mature inside the rodents. Mice and humans have a very different pace when it comes to cell biology.

"The NSCs retained an intrinsic human rate of maturation despite being placed in a traumatic rodent environment," lead author Professor Paul Lu said in a statement. "That's a finding of great importance in planning for human clinical trials."

The researchers were worried that the animal model would not reflect the how this approach might in the future work in humans. For example, pregnancies last 21 days in mice and 280 days in humans. And the weight of a toddlers brain is comparable with that of a 20-day-old mouse.

"Most NSC grafting studies have been short-term, measuring survival times in weeks to a few months," added co-author Professor Mark Tuszynski. "That's not enough time to fully measure the growth and maturation rate of human NSCs or what changes might occur farther out from the original grafting. These are important considerations, not just for the basic science of stem cell biology, but for the practical design of translational human trials using NSCs for spinal cord injuries."

The researchers report that the cells maintained their natural maturation pace even though they were in a foreign environment. Thats why it took several months for the lesions to begin healing. The scientists noted that improvement in the mice mobility only happened after more mature nerve cells formed. As the grafts aged, they displayed the expected pruning and cell redistribution activities that help the development of fewer but more mature cells.

"The bottom line is that clinical outcome measures for future trials need to be focused on long time points after grafting," said Tuszynski. "We need to take into account the prolonged developmental biology of neural stem cells. Success, it would seem, will take time."

The team noticed that none of the implanted NSCs migrated from the graft but some supportive astrocytes cells did, which could be a potential safety concern. No tumors or anomalous formation were created by these cells and modified grafting should fix the problem. A better understanding of this approach, so that the results can be carefully assessed, is required before we can even think to try it on humans.

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Human Stem Cells Repair Spinal Cord Injuries In Mice At Human Biological Rate - IFLScience

Spinal Cord Stem Cells Comments Off on Human Stem Cells Repair Spinal Cord Injuries In Mice At Human Biological Rate – IFLScience | August 30th, 2017

The FDAs commissioner Scott Gottlieb has pledged to crack down on unscrupulous actors attempting to treat patients with potentially dangerous or unproven stem cell therapies.

According to Gottlieb, these companies are able to promote, unproven, illegal and expensive treatments that offer little hope and could pose health risks to vulnerable patients, based on the clinical promise of regenerative medicine.

The crackdown comes after a number of shocking incidents in the US, including the case of three women who went blind following bogus treatment at a Florida clinic.

In a statement the FDA said it is stepping up enforcement to separate unscrupulous companies from those offering genuine treatments approved and backed with genuine medical evidence.

At the same time it will offer those with regenerative medicine products a less burdensome regulatory process although the regulator noted that in some cases individualised treatments fall outside the FDAs remit.

Gottlieb noted the FDA must tread a fine line, separating new medical products from those that are tailor-made by surgeons in such a way that they are not subject to its regulation.

The announcement comes after the US Marshals Service, on behalf of the FDA seized five vials of smallpox vaccine from California-based StemImmune.

The San Diego biotech was using the vaccinia virus vaccine to create an unapproved stem cell product, from cells derived from body fat.

This was being injected intravenously and directly into patients tumours potentially causing fatal health problems in unvaccinated people as the virus can cause inflammation and swelling of the heart.

The FDA also wrote to another operator, Floridas Stem Cell Clinic, raising issues about poor manufacturing standards. An inspection found the clinic was processing body fat into stem cells and administering directly into spinal cords of patients with illnesses such as Parkinsons disease, amyotrophic lateral sclerosis, and pulmonary fibrosis.

This autumn, Gottlieb said he will issue guidance documents outlining a new, efficient, process to evaluate safety and effectiveness of stem cell therapies.

The guidance will also implement provisions of the 21st Century Cures Act relating to regenerative medicine.

A compliance policy will give current product developers a very reasonable grace period to consult with the FDA so that they can meet required standards aside from outliers potentially harming public health.

Gottlieb said: We cant let a small number of unscrupulous actors poison the well for the good science that holds the promise of changing the contours of human illness and altering the trajectory of medicine and science.

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FDA cracks down on bogus cell therapy firms - pharmaphorum

Spinal Cord Stem Cells Comments Off on FDA cracks down on bogus cell therapy firms – pharmaphorum | August 30th, 2017

Here are some of the latest health and medical news developments, compiled by the editors of HealthDay:

Another Outbreak of Salmonella Traced to Pet Turtles

Thirty-seven people across 13 states have contracted salmonella infection from contact with pet turtles, the U.S. Centers for Disease Control and Prevention announced Tuesday.

The agency has for years warned Americans that reptiles such as turtles can be a potent source of the potentially dangerous bacterium, which attacks the gastrointestinal system.

In fact, the CDC notes that "since 1975, the FDA has banned selling and distributing turtles with shells less than 4 inches long as pets because they are often linked to salmonella infections, especially in young children."

In the the latest outbreak, illnesses began to appear on March 1 and diagnoses continued until Aug. 3, the agency said. No deaths have yet been reported, but 16 people have required hospitalization. The CDC says the outbreak may not yet be over.

The agency's advice? "Do not buy small turtles as pets or give them as gifts. All turtles, regardless of size, can carry Salmonella bacteria even if they look healthy and clean."

Federal Prisons Must Now Make Free Tampons, Pads Available

New policy from the Federal Bureau of Prisons (FBP) now requires that all facilities make feminine hygiene products, such as tampons and pads, available for free to prisoners who need them.

In an email memo issued earlier in August, FBP spokesman Justin Long said that "wardens have the responsibility to ensure female hygiene products such as tampons or pads are made available for free in sufficient frequency and number. Prior to the (memo), the type of products provided was not consistent, and varied by institution."

Andrea James is a former lawyer and founder of the National Council for Incarcerated and Formerly Incarcerated Women and Girls. In 2010 and 2011, she served 18 months in a federal prison.

Speaking with CNN, James recalled tough choices made by prisoners involving feminine hygiene products, which the prisoners themselves had to pay for.

"We were paid 12 cents an hour [for in-prison work]," she said, and that wage could be spent on other things, such as phone calls. "That's the choice. Do I buy the tampons or do I call my children?"

According to CNN, the new policy arrives a month after Democratic Senators Cory Booker, Elizabeth Warren, Dick Durbin and Kamala Harris introduced the Dignity for Incarcerated Women Act into Congress. Among other issues, the Act requires that women in prisons have access to multiple sizes of free tampons, pads and liners. Long said the new announcement had nothing to do with the proposed law, however.

In a statement, Harris said she applauded the memorandum, adding, "too many women reside in prison and jail facilities that don't support basic hygiene or reproductive health, and that's just not right."

FDA: Serious Problems at Florida Stem Cell Clinic

A Florida stem cell clinic has been cited by the U.S. Food and Drug Administration for what the agency describes as serious problems that could pose health risks to patients.

The agency said Monday that it has cited US Stem Cell Clinic, of Sunrise, for marketing stem cell products without FDA approval and for "significant deviations from current good manufacturing practice requirements," including some that could affect the "sterility of their products, putting patients at risk."

"Stem cell clinics that mislead vulnerable patients into believing they are being given safe, effective treatments that are in full compliance with the law are dangerously exploiting consumers and putting their health at risk," FDA Commissioner Dr. Scott Gottlieb said in a news release.

The FDA said it recently inspected US Stem Cell Clinic and found that it was processing fat tissue into stem cells derived from body fat and administering the product both intravenously or directly into the spinal cord of patients to treat a variety of serious health problems. Those problems included Parkinson's disease, amyotrophic lateral sclerosis (Lou Gehrig's disease), chronic obstructive pulmonary disease (COPD) and heart disease, among others.

The FDA said it hasn't approved any biological products made by US Stem Cell Clinic for any use.

During an inspection, FDA investigators also found evidence of "significant deviations from current good manufacturing practices" in the production of at least 256 lots of stem cell products. Those deviations included "failure to establish and follow appropriate written procedures designed to prevent microbiological contamination of products purporting to be sterile, which puts patients at risk for infections."

US Stem Cell Clinic also tried to hamper the FDA's investigation during a recent inspection "by refusing to allow entry except by appointment and by denying FDA investigators access to employees," the agency said.

Interfering with an FDA inspection is a violation of federal law, the agency said.

The FDA said it wants to hear from US Stem Cell Clinic within 15 working days, detailing how the problems cited in the agency warning letter will be fixed. If the problems aren't corrected, the company faces such enforcement actions as seizure, injunction or prosecutions, the agency said.

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Health Highlights: Aug. 29, 2017 - Bloomington Pantagraph

Spinal Cord Stem Cells Comments Off on Health Highlights: Aug. 29, 2017 – Bloomington Pantagraph | August 30th, 2017