OCASCR scientist Lin Liu at work. Photo provided.

Working together, scientists from Oklahoma State University, the University of Oklahoma Health Sciences Center and the Oklahoma Medical Research Foundation are advancing adult stem cell research to treat some of todays most devastating diseases.

Under the umbrella of the Oklahoma Center for Adult Stem Cell Research (OCASCR), created with funding from the Oklahoma Tobacco Settlement Endowment Trust, these scientists have amassed groundbreaking findings in one of the fastest growing areas of medical research.

We have made exciting progress, said OCASCR scientist Lin Liu, director of the Oklahoma Center for Respiratory and Infectious Diseases and director of the Interdisciplinary Program in Regenerative Medicine at Oklahoma State University.

We can convert adult stem cells into lung cells using our engineering process in petri dishes, which offers the possibility to repair damaged lung tissues in lung diseases, said Liu, whose research primarily focuses on lung and respiratory biology and diseases.

Using our engineered cells, we can also reverse some pathological features. These studies give us hope for an eventual application of these cells in humans.

Adult stem cells in the body are capable of renewing themselves and becoming various types of cells.

Until recently, stem cell treatments were largely restricted to blood diseases. However, new studies suggest many other types of adult stem cells can be used for medical treatment, and the Oklahoma Center for Adult Stem Cell Research was created to promote this branch of research.

OCASCR scientist Lin Liu and his team discussing their work. Photo provided.

Liu said the discipline provides hope for many ailments.

What most fascinated me in stem cell research is the hope that we may be able to use stem cells from our own body; for example, bone marrow or fat tissues to cure lung diseases, Liu said.

It is impossible to know exactly which diseases will respond to treatments.However, results of early experiments suggest many diseases should benefit from this type of research, including lung, heart, Alzheimers and Parkinsons diseases, as well as cancer, diabetes and spinal cord injuries. The field is often referred to as regenerative medicine, because of the potential to create good cells in place of bad ones.

While the application of stem cells can be broad, Liu hopes that his TSET-funded work will help develop treatments for diseases caused by tobacco use.

The goal of my research team is to find cures for lung diseases, Liu said. One such disease is chronic obstructive pulmonary disease (COPD).

COPD is the third leading cause of death in the country and cigarette smoking is the leading cause of COPD.

Cigarette smoking is also a risk factor for another fatal lung disease, idiopathic pulmonary fibrosis (IPF), which has a mean life expectancy of 3 to 5 years after diagnosis, he added.

There is no cure for COPD or IPF. The current treatments of COPD and IPF only reduce symptoms or slow the disease progression.

Using OCASCR/TSET funding, my team is researching the possibility to engineer adult stem cells using small RNA molecules existing in the body to cure COPD, IPF and other lung diseases such as pneumonia caused by flu, Liu said.

This is vital research, considering that more than11 million peoplehave been diagnosed with COPD, but millions more may have the disease without even knowing it, according to the American Lung Association.

Despite declining smoking rates and increased smokefree environments, tobacco use continues to cause widespread health challenges and scientists will continue working to develop treatments to deal with the consequences of smoking.

We need to educate the public more regarding the harms of cigarette smoking, Liu said. My research may offer future medicines for lung diseases caused by cigarette smoking.

Under the umbrella of the Oklahoma Center for Adult Stem Cell Research (OCASCR), created with funding from the Oklahoma Tobacco Settlement Endowment Trust, these scientists have amassed groundbreaking findings in one of the fastest growing areas of medical research. Photo provided.

Liu has been conducting research in the field of lung biology and diseases for more than two decades.

However, his interests in adult stem cell therapy began in 2010 when OCASCR was established through a grant with TSET, which provided funding to Oklahoma researchers for stem cell research.

I probably would have never gotten my feet into stem cell research without OCASCR funding support, he said. OCASCR funding also facilitated the establishment of the Interdisciplinary Program in Regenerative Medicine at OSU.

These days, Liu finds himself fully immersed in the exciting world of adult stem cell research and collaborating with some of Oklahomas best scientific minds.

Dr. Liu and his colleagues are really thriving. It was clear seven years ago that regenerative medicine was a hot topic and we already had excellent scientists in the Oklahoma, said Dr. Paul Kincade, founding scientific director of OCASCR. All they needed was some resources to re-direct and support their efforts. OSU investigators are using instruments and research grants supplied by OCASCR to compete with groups worldwide. TSET can point to their achievements with pride.

The Oklahoma Center for Adult Stem Cell Research represents collaboration between scientists all across the state, aiming to promote studies by Oklahoma scientists who are working with stem cells present in adult tissues.

The center opened in 2010 and has enhanced adult stem cell research by providing grant funding for researchers, encouraging recruitment of scientists and providing education to the people of Oklahoma.

We are fortunate that the collaboration at the Oklahoma Center for Adult Stem Cell Research is yielding such positive results, said John Woods, TSET executive director. This research is leading to ground breaking discoveries and attracting new researchers to the field. TSET is proud to fund that investments for Oklahomans.

Funding research is a major focus for TSET and it comes with benefits reaching beyond the lab. For every $1 TSET has invested at OCASCR, scientists have been able to attract an additional $4 for research at Oklahoma institutions, TSET officials said.

TSET also supports medical research conducted by the Stephenson Cancer Center and the Oklahoma Tobacco Research Center.

For more information, visit http://www.ocascr.org.

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Genetic profiling can guide stem cell transplantation for patients with ... Science Daily A single blood test and basic information about a patient's medical status can indicate which patients with myelodysplastic syndrome (MDS) are likely to benefit ... and more »

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(WXYZ) - When we get sick, it's common for us to reach for some medicine or maybe even have surgery to deal with disease or pain, but what if you could use your own healthy cells to fight back instead?

Right now, there's a procedure being performed in metro Detroit where healthy stem cells are stored so they can be reintroduced to your system and potentially have life changing or life saving benefits.

Dr. Michael Schenden is the first plastic surgeon in the US to perform the Forever Labs stem cell collection. He starts by harvesting her bone marrow to save those healthy stem cells.

"They should be available for many, many different medical applications is a wonderful thing," says Dr. Schenden.

The company behind this procedure is based in Ann Arbor and it's called Forever Labs.

We're told about 30 people have decided to store their stem cells this way. Sonja Michelsen is one of them. She had her daughter in her early 40s and felt like storing her own stem cells could pay off in the future.

"I want to be able to be here with her throughout her life," she says.

She knows there's no guarantee banking her stem cells will help her in the future, but she sees it as an investment that could pay off if her health takes a turn.

"To have that peace of mind that you do have something to use down the road .. is huge," she says.

Steven Clausnitzer is CEO of Forever Labs. He says by re-introducing your own healthy cells, you may be able to fight disease in the future.

"There are a number of ways people are already using these cells. Maybe the most promising .. orthopedic surgeons .. are reintroducing them into joints in lieu of surgery," he says.

Clausnitzer says there are about 500 clinical trials right now that are using stem cells that, one day, may be able to treat everything from osteoarthritis to multiple scleroses to cardiovascular disease.

This kind of stem cell banking is a 15 minute outpatient procedure. It starts with a local anesthetic in the lower back.

He says the number of your stem cells diminishes with age, as does their therapeutic quality.

"My stem cells were stored at 38. I'm going to turn 40 this year. I rest assured knowing I have my 38-year-old stem cells rendered biologically inert. They're no longer aging .. even as I do," says Clausnitzer.

Mark Katakowski is president of Forever Labs. He says his research showed him the rejuvenating and healing power of stem cells in animals. He believes it can have the same effect in humans.

He says the best time to store the stem cells is when you're young.

"There's a slower decline between 20 and 40 years-old and then it picks up. When you put them in the right place at the right time, they can actually improve recovery in a bunch of therapeutic applications," he says.

Katakowski says there's no limit as to how long they can be stored.

Should a person pass away, their stored stem cells would be destroyed unless arrangements have been made for them to be given to a family member.

At this point, the procedure is not FDA approved. The Forever Labs stem cell collection isn't covered by insurance. It costs around $3,500 to have the procedure done and $250 a year for storage.

The company says it plans to bring the first clinical trials for longevity to market in the next 7-10 years, once there is a large enough differential time between when our first clients stored their cells and can then reintroduce.

It says its goal is that its clientele will be able to participate in the first longevity based human trials utilizing autologous stem cell treatments of healthy individuals.

To learn more about Forever Labs, go to: https://www.foreverlabs.co/

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Can storing your stem cells be the key to fighting disease and living longer? - WXYZ

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OCASCR scientist Lin Liu at work. Photo provided.

Working together, scientists from Oklahoma State University, the University of Oklahoma Health Sciences Center and the Oklahoma Medical Research Foundation are advancing adult stem cell research to treat some of todays most devastating diseases.

Under the umbrella of the Oklahoma Center for Adult Stem Cell Research (OCASCR), created with funding from the Oklahoma Tobacco Settlement Endowment Trust, these scientists have amassed groundbreaking findings in one of the fastest growing areas of medical research.

We have made exciting progress, said OCASCR scientist Lin Liu, director of the Oklahoma Center for Respiratory and Infectious Diseases and director of the Interdisciplinary Program in Regenerative Medicine at Oklahoma State University.

We can convert adult stem cells into lung cells using our engineering process in petri dishes, which offers the possibility to repair damaged lung tissues in lung diseases, said Liu, whose research primarily focuses on lung and respiratory biology and diseases.

Using our engineered cells, we can also reverse some pathological features. These studies give us hope for an eventual application of these cells in humans.

Adult stem cells in the body are capable of renewing themselves and becoming various types of cells.

Until recently, stem cell treatments were largely restricted to blood diseases. However, new studies suggest many other types of adult stem cells can be used for medical treatment, and the Oklahoma Center for Adult Stem Cell Research was created to promote this branch of research.

OCASCR scientist Lin Liu and his team discussing their work. Photo provided.

Liu said the discipline provides hope for many ailments.

What most fascinated me in stem cell research is the hope that we may be able to use stem cells from our own body; for example, bone marrow or fat tissues to cure lung diseases, Liu said.

It is impossible to know exactly which diseases will respond to treatments.However, results of early experiments suggest many diseases should benefit from this type of research, including lung, heart, Alzheimers and Parkinsons diseases, as well as cancer, diabetes and spinal cord injuries. The field is often referred to as regenerative medicine, because of the potential to create good cells in place of bad ones.

While the application of stem cells can be broad, Liu hopes that his TSET-funded work will help develop treatments for diseases caused by tobacco use.

The goal of my research team is to find cures for lung diseases, Liu said. One such disease is chronic obstructive pulmonary disease (COPD).

COPD is the third leading cause of death in the country and cigarette smoking is the leading cause of COPD.

Cigarette smoking is also a risk factor for another fatal lung disease, idiopathic pulmonary fibrosis (IPF), which has a mean life expectancy of 3 to 5 years after diagnosis, he added.

There is no cure for COPD or IPF. The current treatments of COPD and IPF only reduce symptoms or slow the disease progression.

Using OCASCR/TSET funding, my team is researching the possibility to engineer adult stem cells using small RNA molecules existing in the body to cure COPD, IPF and other lung diseases such as pneumonia caused by flu, Liu said.

This is vital research, considering that more than11 million peoplehave been diagnosed with COPD, but millions more may have the disease without even knowing it, according to the American Lung Association.

Despite declining smoking rates and increased smokefree environments, tobacco use continues to cause widespread health challenges and scientists will continue working to develop treatments to deal with the consequences of smoking.

We need to educate the public more regarding the harms of cigarette smoking, Liu said. My research may offer future medicines for lung diseases caused by cigarette smoking.

Under the umbrella of the Oklahoma Center for Adult Stem Cell Research (OCASCR), created with funding from the Oklahoma Tobacco Settlement Endowment Trust, these scientists have amassed groundbreaking findings in one of the fastest growing areas of medical research. Photo provided.

Liu has been conducting research in the field of lung biology and diseases for more than two decades.

However, his interests in adult stem cell therapy began in 2010 when OCASCR was established through a grant with TSET, which provided funding to Oklahoma researchers for stem cell research.

I probably would have never gotten my feet into stem cell research without OCASCR funding support, he said. OCASCR funding also facilitated the establishment of the Interdisciplinary Program in Regenerative Medicine at OSU.

These days, Liu finds himself fully immersed in the exciting world of adult stem cell research and collaborating with some of Oklahomas best scientific minds.

Dr. Liu and his colleagues are really thriving. It was clear seven years ago that regenerative medicine was a hot topic and we already had excellent scientists in the Oklahoma, said Dr. Paul Kincade, founding scientific director of OCASCR. All they needed was some resources to re-direct and support their efforts. OSU investigators are using instruments and research grants supplied by OCASCR to compete with groups worldwide. TSET can point to their achievements with pride.

The Oklahoma Center for Adult Stem Cell Research represents collaboration between scientists all across the state, aiming to promote studies by Oklahoma scientists who are working with stem cells present in adult tissues.

The center opened in 2010 and has enhanced adult stem cell research by providing grant funding for researchers, encouraging recruitment of scientists and providing education to the people of Oklahoma.

We are fortunate that the collaboration at the Oklahoma Center for Adult Stem Cell Research is yielding such positive results, said John Woods, TSET executive director. This research is leading to ground breaking discoveries and attracting new researchers to the field. TSET is proud to fund that investments for Oklahomans.

Funding research is a major focus for TSET and it comes with benefits reaching beyond the lab. For every $1 TSET has invested at OCASCR, scientists have been able to attract an additional $4 for research at Oklahoma institutions, TSET officials said.

TSET also supports medical research conducted by the Stephenson Cancer Center and the Oklahoma Tobacco Research Center.

For more information, visit http://www.ocascr.org.

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A 45-year-old Salina man who was diagnosed with leukemia in November is being honored by a bone marrow registration drive Saturday being held at his church.

This is open to the whole community we want to stress that, said Linda Ourada, a member of the health ministry committee at St. Mary Queen of the Universe Catholic Church Parish Center, 230 E. Cloud. The drive will be held from 10 a.m. to 2 p.m. Saturday at the parish center.

Its possible that Phong Vos sister is a match for him, said Vos wife, Mary Pham.

More blood work is planned to determine if the match is close enough. In the meanwhile, the effort to sign up possible donors for Vo or anyone else who needs a bone marrow or peripheral blood stem cell donation is planned.

Pam Welsh, of Salina, said that more than a decade ago, she had her cheek swabbed during a bone marrow registration drive when a Bennington woman needed a match. She said she was called about a year later and told she was one of three people who were a possible match for a patient. She said she went to Salina Regional Health Center to have blood drawn for further testing.

I was given a choice if I wanted to continue in the process, she said. There was never any pressure.

She said that after the blood tests showed she was a good match for the patient, a nurse came to her house to give her shots to boost her stem cell count. Then she and a friend drove to a Wichita hospital, where she underwent an outpatient procedure during which her blood was drawn from one arm and passed through a machine that filtered out blood stem cells before the blood was returned to her other arm. Welsh said the procedure took one day, and then she took the next day off to recover. All expenses were paid by DKMS, an international organization that fights blood cancer and blood disorders, she said.

She said she found out that her blood was given to a 55-year-old man with some form of leukemia. She was told he was still alive when DKMS contacted her for a five-year checkup.

Although she never met him, Welsh said that for her there was a huge reward in knowing that I was able to help this man knowing that I gave him more years.

Its just a good feeling, she said.

Pham said Vo started feeling ill in October and has since undergone chemotherapy at Via Christi Hospital in Wichita and the University of Kansas Medical Center in Kansas City. However, the leukemia has persisted.

Pham, who works for Schwans, has lived in Salina since her grandparents and an aunt, who had lived here since 1975, acted as her sponsors when she immigrated from Vietnam about 21 years ago. She met Vo, who moved here in the late 1990s, at work, and they were married at St. Marys. They have four sons, ages 11, 11, 10 and 8, who have missed their father during his long hospital stays.

When my husband got sick, I was panicked, and I was like, What do I need to do? I dont know what to do, Pham said. Soon she was told about DKMS, which will attempt to match potential donors who register at the Salina drive with Vo and other patients.

The bone marrow registration process for DKMS is simple, said Linda Ourada, who is helping to organize the event.

Its not like drawing blood, Ourada said. People get this mixed up with a blood drive. Theres no blood involved.

A swab is taken from the inside of the cheek, which is then sent for DNA analysis and entered into a global donor computer registry that already includes information about 7 million potential donors.

Every day in the United States, there are 14,000 people waiting for this blood stem cell donation, and only 30 percent get a family match, so that leaves 70 percent out there looking for a suitable donation from someone like us, Ourada said.

Ourada said that in 2012, more than 250 people registered and nine potential matches were contacted for further testing during a bone marrow drive at the church to honor a St. Louis family with Salina ties who had four boys with a rare form of blood cancer.

There is no cost to register as a donor, although monetary donations are being accepted to cover the approximately $65 in costs associated with registering each possible donor.

Potential donors must be between the ages of 18 and 55, in general good health and be willing to donate should their marrow be matched with a person who needs it. Further details about weight and height requirements or other limiting factors can be found at dkmsamericas.org.

The donation process may be accomplished one of two ways, depending on the patients needs. The preferred method is a blood transfusion, but for some patients, an actual bone marrow graft is necessary. The marrow is harvested through a hollow needle from a hip bone in an outpatient surgical procedure.

Bone marrow could be used to treat blood cancers, anemias, genetic disorders and other life-threatening ailments.

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This post was originally published on this site New Facility at Sunnybrook Part of Plan to Expand Care for People with Blood Diseases

Ontario is investing in a new facility at Sunnybrook Health Sciences Centre that will offer specialized treatment for people with blood cancers such as leukemia.

Premier Kathleen Wynne was at Sunnybrook in Toronto Tuesday to announce the governments support for a new Complex Malignant Haematology (CMH) site. Sunnybrook will become the second hospital in the Greater Toronto Area along with Princess Margaret Cancer Care to provide a full range of potentially life-saving CMH services, including stem cell transplants.

Ontario is also improving treatment for people with blood diseases by:

Investing to improve care for people with blood cancers and disorders is part of our plan to build a better Ontario by providing patients with faster access to the right health care.

Kathleen Wynne: Premier of Ontario

Stem cell transplants can help lessen the terrible toll that cancer takes on families. We are providing support so hospitals can offer more patients access to a life-saving treatment and the chance for a new lease on life.

Dr. Eric Hoskins: Minister of Health and Long-Term Care

Today marks a major milestone for Ontario patients needing stem cell transplants. With this investment, patients will have better access to timely service and state-of-the-art treatment, but most importantly, more patients will be able to receive stem cell transplants right here in Ontario.

Dr. Barry McLellan: President and CEO, Sunnybrook Health Sciences Centre

This is a life-saving investment. We are grateful to the Ontario government for the funding to provide care and build a new state-of-the-art facility for patients who are afflicted with this serious illness.

Michael Sherar: President and CEO, Cancer Care Ontario; Co-convener, Complex Malignant Hematology Hematopoietic Cell Therapy Consultation Group

Sunnybrook Health Sciences Centre is an important and valued partner in Ontarios cancer care system. The addition of a new Complex Malignant Haematology site is a critical step in our efforts to ensure that patients receive timely access to transplant services in Ontario.

Source Government of Ontario press release

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Using stem cells and gene therapy to treat orcure disease may still sound like science fiction, but a scientific meeting here last week emphasizedall the fronts onwhich it is moving closer and closer to fact.

Were entering a new era in medicine, said Lloyd Minor, MD, dean of the School of Medicine, in his opening remarks at the first annual symposium of the schools new Center for Definitive and Curative Medicine. Stanford researchersare poised to use stem cells and gene therapy to amelioratea wide swath of diseases, from common diagnoses such as diabetes and cancerto rare diseases ofthe brain, blood, skin, immune system and other organs. Ultimately, the goal is to create one-time treatments that can provide lifetime cures; hence the definitive and curative part of the centers name. Stanford is a leader in this branch of medical research, Minor said, addingThis is a vital component of our vision for precision health.

Stanford has a long history of leading basic-science discoveries in stem cell biology, andis now engaged in studyingmany different ways those discoveries couldbenefit patients, saidMaria Grazia Roncarolo, MD, who leads the new center.Our job is to produce clinical data so compelling that industry will pick up the product and take it to the next stage, Roncaraolo told the audience.

Among otherevent highlights:

More coverage of the days events is available in a story from the San Jose Mercury News that describeshowAnthonyOro, MD, PhD, and his colleagues are fighting epidermolysis bullosa, a devastating genetic disease of the skin. Oro closed his talk with a slightly goofy photo of a man getting a spray tan. It got a laugh, but his point was serious: Our goal for the cell therapy of the future is spray-on skin to correct a horrible genetic disease.

Ambitious? Yes. Science fiction? In the future, maybe not.

Previously: One of the most promising minds of his generation: Joseph Wu takes stem cells to heart,Life with epidermolysis bullosa: Pain is my reality, pain is my normaland Rat-grown mouse pancreases reverse diabetes in mice, say researchers Photo of Matthew Porteus courtesy of Stanford Childrens

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The 2017 Australian of the Year award went to Professor Alan Mackay-Sim for his significant career in stem cell science.

The prize was linked to barbeque-stopping headlines equating his achievements to the scientific equivalent of the moon landing and paving the road to recovery for people with spinal cord injuries.

Such claims in the media imply that there is now a scientifically proven stem cell treatment for spinal cord injury. This is not the case.

For now, any clinic or headline claiming miracle cures should be viewed with caution, as they are likely to be trading on peoples hope.

Why stem cells for spinal cord injury?

Put simply, injury to the spinal cord causes damage to the nerve cells that transmit information between the brain and the rest of the body.

Depending on which part of the spine is involved, the injury can affect the nerves that control the muscles in our legs and arms; those that control bowel and bladder function and how we regulate body temperature and blood pressure; and those that carry the sensation of being touched. This occurs in part because injury and subsequent scarring affect not just the nerves but also the insulation that surrounds and protects them. The insulation the myelin sheath is damaged and the body cannot usually completely replace or regenerate this covering.

Stem cells can self-reproduce and grow into hundreds of different cell types, including nerves and the cells that make myelin. So the blue-sky vision is that stem cells could restore some nerve function by replacing missing or faulty cells, or prevent further damage caused by scarring.

Studies in animals have applied stem cells derived from sources including brain tissue, the lining of the nasal cavity, tooth pulp, and embryos (known as embryonic stem cells).

Dramatic improvements have been shown on some occasions, such as rats and mice regaining bladder control or the ability to walk after injury. While striking, such improvement often represents only a partial recovery. It holds significant promise, but is not direct evidence that such an approach will work in people, particularly those with more complex injuries.

What is happening now in clinical trials?

The translation of findings from basic laboratory stem cell research to effective and safe treatments in the clinic involves many steps and challenges. It needs a firm scientific basis from animal studies and then careful evaluation in humans.

Many clinical studies examining stem cells for spinal repair are currently underway. The approaches fit broadly into two categories:

using stem cells as a source of cells to replace those damaged as a result of injury

applying cells to act on the bodys own cells to accelerate repair or prevent further damage.

One study that has attracted significant interest involves the injection of myelin-producing cells made from human embryonic stem cells. Researchers hoped that these cells, once injected into the spinal cord, would mature and form a new coating on the nerve cells, restoring the ability of signals to cross the spinal cord injury site. Preliminary results seem to show that the cells are safe; studies are ongoing.

Other clinical trials use cells from patients own bone marrow or adipose tissue (fat), or from donated cord blood or nerves from fetal tissue. The scientific rationale is based on the possibility that when transplanted into the injured spinal cord, these cells may provide surrounding tissue with protective factors which help to re-establish some of the connections important for the network of nerves that carry information around the body.

The field as it stands combines years of research, and tens of millions of dollars of investment. However, the development of stem cell therapies for spinal cord injury remains a long way from translating laboratory promise into proven and effective bedside treatments.

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February 08, 2017 09:45 ET | Source: BioRestorative Therapies, Inc.

MELVILLE, N.Y., Feb. 08, 2017 (GLOBE NEWSWIRE) -- BioRestorative Therapies, Inc. ("BRT" or the Company") (OTCBB:BRTX), a life sciences company focused on stem cell-based therapies, today announced that it has received clearance by the U.S. Food and Drug Administration (FDA) to commence a Phase 2 clinical trial using its lead cell therapy candidate, BRTX-100, to treat chronic lower back pain due to degenerative disc disease related to protruding/bulging discs.

The Phase 2 clinical trial is a 72 patient, randomized, double-blind, controlled, multi-center study designed to evaluate safety and efficacy of a single dose of BRTX-100 in treating chronic lower lumbar disc disease. BRTX-100 will be administered via intradiscal injection into one disc of a subject with chronic lumbar disc disease and whose pain is not responsive to conservative treatment measures (e.g., oral medication, epidural injections and physical therapy). The primary goal of the treatment is to both reduce pain and increase function in these patients.

In January 2017, the Company had submitted an Investigational New Drug Application (IND) to the FDA to obtain clearance to commence this clinical trial using BRTX-100. BRTX-100 is a product formulated using a patients own cell population (autologous), which consists of hypoxic (low oxygen) cultured mesenchymal stem cells (MSCs) that are optimized for specific use for a non-surgical, conservative intradiscal procedure that can be performed in a physicians office.

"We are excited to be able to begin our clinical development of BRTX-100 with this Phase 2 clinical trial," saidMark Weinreb, President and Chief Executive Officer of BioRestorative Therapies. This treatment has the potential to positively impact millions of Americans suffering from chronic lumbar disc disease as an alternative to surgery. We believe that this technology can be truly transformative and addresses a large market underserved by current therapies.

About BioRestorative Therapies, Inc.

BioRestorative Therapies, Inc. (www.biorestorative.com) develops therapeutic products using cell and tissue protocols, primarily involving adult stem cells. Our two core programs, as described below, relate to the treatment of disc/spine disease and metabolic disorders:

Disc/Spine Program (brtxDISC): Our lead cell therapy candidate, BRTX-100, is a product formulated from autologous (or a persons own) cultured mesenchymal stem cells collected from the patients bone marrow. We intend that the product will be used for the non-surgical treatment of protruding and bulging lumbar discs in patients suffering from chronic lumbar disc disease. The BRTX-100 production process involves collecting a patients bone marrow, isolating and culturing stem cells from the bone marrow and cryopreserving the cells. In an outpatient procedure, BRTX-100 is to be injected by a physician into the patients damaged disc. The treatment is intended for patients whose pain has not been alleviated by non-invasive procedures and who potentially face the prospect of surgery.

Metabolic Program (ThermoStem): We are developing a cell-based therapy to target obesity and metabolic disorders using brown adipose (fat) derived stem cells to generate brown adipose tissue (BAT). BAT is intended to mimic naturally occurring brown adipose depots that regulate metabolic homeostasis in humans. Initial preclinical research indicates that increased amounts of brown fat in the body may be responsible for additional caloric burning as well as reduced glucose and lipid levels. Researchers have found that people with higher levels of brown fat may have a reduced risk for obesity and diabetes.

Forward-Looking Statements

This press release contains "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, and such forward-looking statements are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. You are cautioned that such statements are subject to a multitude of risks and uncertainties that could cause future circumstances, events or results to differ materially from those projected in the forward-looking statements as a result of various factors and other risks, including those set forth in the Company's Form 10-K filed with the Securities and Exchange Commission. You should consider these factors in evaluating the forward-looking statements included herein, and not place undue reliance on such statements. The forward-looking statements in this release are made as of the date hereof and the Company undertakes no obligation to update such statements.

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Ally Little described the past month of her life as a nightmare from which she just cant wake up.

On Dec. 22, the University of Southern Maine soccer player learned she had a rare and life-threatening disease in which her bone marrow stops producing healthy blood cells. However, the words severe aplastic anemia meant nothing to Little at the time.

Its really hard because I didnt know what this was before I had it, said Little, a 20-year-old sophomore from Stoneham, Massachusetts. No one has really heard of aplastic anemia or what the treatment is.

A bone marrow transplant is the cure for this disease, and Little has yet to find a matching donor. Littles teammates have organized a bone marrow donor registry drive from 9 a.m. to 1 p.m. Wednesday at Abromson Mezzanine at the USM Portland campus and from 2:30 to 5:30 p.m. at Costello Complex at the Gorham campus.

Diagnosed during winter break, Little broke the news to her teammates on social media.

It hit home, said USM womens soccer coach Lisa Petruccelli. This is really the first time someone their age at this juncture is struggling with something like this.

Littles initial symptoms didnt seem serious. She started getting pounding headaches around Thanksgiving, but she had gotten headaches before. Physical activities such as skiing or working out for soccer became unusually exhausting, which Little attributed to dehydration. She didnt go to her doctor until she noticed blood in her stool.

(Aplastic anemia) is believed to be an autoimmune system gone wrong, said Paul Scribner, Senior Director of Patient Advocacy Programs with the Aplastic Anemia and MDS International Foundation (AAMDS). The disease usually results from the destruction of bone marrow stem cells by the immune system. Other symptoms include infections and the tendency to bruise and bleed easily. With such innocuous warning signs, Scribner said a lot of people find out when they go to their doctor because theyre feeling run down.

After bloodwork, Little was told that her results were very abnormal. She spent the next few days in the hospital undergoing tests while doctors prepared her for the worst case scenario leukemia.

That was obviously horrifying, Little said. We didnt find out until about three days later that it was severe aplastic anemia.

Aplastic anemia is rare and can occur at any age. In the United States, about 600 to 900 people are diagnosed each year, according to AAMDS. The disease is considered severe when all three types of blood cells red blood cells (carry oxygen), white blood cells (fight infections) and platelets (help blood to clot) are very low in number.

I was kind of relieved it wasnt cancer, Little said. Then, doctors explained to me that its really not that good. It was devastating.

Little couldnt go back to school. With her compromised immune system, crowds are off limits. She cant play contact sports or do anything that could put her at risk of internal bleeding. She gets blood transfusions every week, and she can tell when shes due for another by the dizziness and headaches she gets. The long-term risk of too many transfusions, Scribner said, is iron overload.

Most days, I feel OK, Little said. I dont really feel sick, which is good. But its hard to remember I cant do certain things.

Little is buying time until she can get a bone marrow transplant. Bone marrow is the spongy tissue inside of the bones that produces the bodys blood cells. She didnt find a match among her family or with Be The Match a national bone marrow registry that contains 22.5 million adult donors.

Registering at the drive is simple. Potential donors must be between 18-44 years old and fill out basic paperwork and get their cheek swabbed to have their tissue type added to the registry a process that takes just a few minutes. After that, they will remain registered until age 61, unless they withdraw.

However for those in need of bone marrow finding a perfect match is not so easy.

Think about Megabucks and how hard it is to match that, said Jackie McLoon, Assistant Account Executive with Rhode Island Blood Center as well as a bone marrow donor. McLoon, a representative with Be the Match, has helped the USM soccer team organize its drive. Everyday, there are donors getting added to the database. Hopefully, her match shows up one of these days.

Only 30 percent of patients in need of a marrow transplant have a matching donor in their family. Be The Match helps the 14,000 patients a year who suffer from leukemia, lymphoma or a variety of bone marrow functioning diseases. McLoon said a protein called human leukocyte antigen (HLA) is used to match patients with donors, and potential matches will then undergo bloodwork to determine if they would be a good fit. Only about 1 in 500 registrants go on to actually donate marrow.

There are 10 things that they are supposed to match, Little said. They think one of my 10 is very rare.

But her teammates are optimistic. On Saturday, they attended a home basketball game clad in T-shirts adorned with the phrase: All for Ally. They gushed about Littles kind personality and reminisced about all the times they crashed in her room.

Shes the best teammate ever. Shes so sweet oh my god, I love her, said Jessica Preble, a sophomore on the team. If you ask anything of her, shell drop everything and do it.

This team is kind of used to bad things happening to our girls, said Dayna Staffiere, noting that one of their teammates lost her dad at sea last season when the cargo ship El Faro sank after encountering Hurricane Joaquin. It just brings us all closer.

When Little isnt at the hospital, shes usually working on her online classes or walking her dog. She said the support from family, friends and her soccer team is what keeps her going.

Were the ones who are supposed to be strong for her, but shes so strong for us, Preble said. Just a cheek swab and some paperwork could help save her life.

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USM women's soccer players organize bone marrow drive for teammate with rare disease - Press Herald

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An act of kindness can change your life in a positive way. But how much better would it be if that same act ends up changing someone elses life in an amazing way too? Jillian Altenburg can answer that.

It will change me for the better, but I am even happier I have the ability to change someone elses life for the better, Jillian said.

This month, Jillian will go through a bone marrow donor procedure for a little child struggling with leukemia. Not only will this change Jillian forever, but it gives a small child a new chance at life.

Jillian, the daughter of Gary Altenburg and Lori Altenburg, is a Cut Bank High School 2013 graduate. She will be part of another graduation this May when she receives her nursing degree from the MSU-BSN college of nursing program in Great Falls.

Jillian first learned about being a bone marrow donor while in her freshman year of college at MSU-Bozeman. It was during one of my classes we heard about a child who was looking for a bone marrow match and after class the organization called Be the Match was introduced to us.

Be the Match is an organization that matches bone marrow donors to patients in need of a bone marrow transplant. Jillian became a potential donor that day after class when she had her cheek swabbed and entered into the program.

It was a few years before she heard anything from Be the Match, but this past December Jillian received a call saying she could be a match for a patient needing bone marrow.

I didnt know if I was the only match or if there were other potential matches too, Jillian stated. They asked me to do some blood work and they said it usually takes 60 days to determine if I would be a perfect match. But it only took a week for them to get back to me and let me know I was a perfect match for this little child with leukemia.

It was then that things started happening fast for Jillian. They told me that the child was in remission and that there is a window of time to do the procedure, so they gave me the date it would be done and where I needed to be for the procedure and explained what would be happening. And Be the Match would be picking up the tab for everything.

According to Jillian, there are two ways to collect bone marrow. One of those is by putting needles in my arm to gather stem cells. The other is by cutting a slit on both sides of my pelvis and inserting a hollow needle into the bone to pull out what they need. Normally they can take up to six cups of bone marrow, but with this being a child needing the bone marrow, they probably will not need that much.

After the procedure, Jillian will be discharged but will need to stay close to the hospital for another night in a hotel to make sure all is okay. Once that is determined, she can return home.

They say the procedure is painful and I will be sore. But ever since I learned I was a match, there was no choice in this for me. I actually feel like the lucky one, having this opportunity to help this child, Jillian said.

Within seven days of harvesting Jillians bone marrow, the child will receive the bone marrow that is so desperately needed for survival. During that time, Jillian should feel better and better each day. And within two weeks of having made the donation, Jillians body will have replaced the bone marrow taken from her.

Even though Be the Match tells all their potential donors that they can opt out of the program at any time, that was not an option for Jillian. Once they start prepping the patient to receive a bone marrow transplant, they really dont want people to say they have changed their minds. I have no intention of doing that anyway. When they called me, it was not a decision I had to think about. I knew I was going to do it. It feels good to be able to help someone and change their life for the better, she said.

The day Jillian shared the news with her mom Lori, that she was a potential bone marrow match for someone, Lori said, I got that warm, fuzzy feeling, but as we spoke longer it turned to worry, mostly for this child who has had to deal with these awful circumstances. I knew Jillian would be fine. She is strong, very physically fit and young. She has everything going for her in being a good donor.

Lori will be accompanying Jillian when she has the procedure done and will be there for her all the way through to recovery. We have always teased Jillian that she is still attached to her moms umbilical cord, so we both know I have to go, even though I know it doesnt stretch quite that far, laughed Lori.

Lori admitted she did not know Jillian had even put her name into the Be the Match program. We have lost many loved ones due to cancer, with number one being Jillians Grama Nancy (Loris mom). Even so, when I got the call from Jillian that she was contacted by the Be the Match program because she was a possible bone marrow match, it was very, very surprising. But I feel super proud and very blessed that she was chosen. To say I am not a little nervous would be a fib, but she will be in good hands and we know friends and family are praying for her and the child who will receive the donation, Lori shared.

For a year following the transplant, Jillian will not know the name of the child she made the donation to. I can find out through Be the Match how this little one is doing, but for up to a year they want me to remain anonymous. After a year, we can have contact.

As Jillian said, she knew without a doubt, she would be going through this procedure the minute she was called and told she was a perfect match. And while she admitted she is a little scared, she countered that with, It will be worth it.

There are two lives being changed with one procedure. Jillians life will be forever changed by this. And the young child? With Jillians donation, there is hope that many years can be added to that young little life.

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Jillian Altenburg: Sharing her gift of lifeand bone marrowwith young leukemia patient - Cut Bank Pioneer Press

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Physicians at the Johns Hopkins Kimmel Cancer Center report they have successfully treated 16 patients with a rare and lethal form of bone marrow failure called severe aplastic anemia using partially matched bone marrow transplants followed by two high doses of a common chemotherapy drug. In a report on the new transplant-chemo regimen, published online Dec. 22, 2016, in Biology of Blood and Marrow Transplantation, the Johns Hopkins team says that more than a year after their transplants, all of the patients have stopped taking immunosuppressive drugs commonly used to treat the disorder and have no evidence of the disease.

"Our findings have the potential to greatly widen treatment options for the vast majority of severe aplastic anemia patients," according to Robert Brodsky, M.D., professor of medicine and oncology at the Johns Hopkins Kimmel Cancer Center and an author of the report.

Results of the small clinical trial have already prompted the organization of a larger national trial being led by Amy DeZern, M.D., an assistant professor of oncology and medicine at the Johns Hopkins Kimmel Cancer Center, with plans to involve patients at 25 medical centers across the country.

Diagnosed in about one in 250,000 people each year, aplastic anemia occurs when one's own immune system damages blood-making bone marrow cells, which gradually stop producing red and white blood cells and platelets.

Patients must receive frequent blood transfusions, take multiple medicines to suppress the autoimmune response that damages the marrow, take other drugs to prevent infections, and limit contact with the outside world to avoid infection and even minor injury. Over the long term, most patients eventually die of infections.

When immunosuppressive therapy fails to keep the disease in check -- in as many as 30 to 40 percent of patients -- doctors usually prescribe a drug called eltrombopag, which is used in a variety of blood disorders to increase platelets. The drug, according to the Johns Hopkins experts, works only in about 30 percent of patients and usually leads to a partial, not complete, response.

Brodsky and DeZern say that the only curative treatment is a bone marrow transplant, but few patients have donors who are "fully matched" -- sharing the same collection of immune-stimulating proteins that decorate every cell in the body.

In an effort to overcome the donor shortage and offer transplant to more patients, DeZern, Brodsky and their colleagues enrolled 16 patients between 11 and 69 years of age in this study from July 2011 through August 2016.

Each of the patients had failed to respond to immunosuppressive therapy or other drug treatments. None had access to a related fully matched bone marrow donor but did have an available and willing donor who was a half match. Three patients used unrelated donors.

After administering a cocktail of drugs designed to suppress their immune system and prevent rejection of the donor marrow, the patients received half-matched bone marrow transplants, some from siblings or parents, and others from unrelated donors.

Three and four days after their transplants, the patients received high doses of the chemotherapy drug cyclophosphamide. For the next year, or slightly longer, they remained on immunosuppressive medications, including tacrolimus, then stopped taking them.

Within weeks of their transplants, tests showed that each of the patients' red and white blood cell and platelet counts had returned to normal levels without the need for blood transfusions. Once immunosuppressive therapy was stopped, none of the patients required further treatment related to their disease, the Johns Hopkins team reported.

Although 13 patients were able to discontinue immunosuppressive drugs a year after their transplant, three developed mild graft-versus-host disease (GVHD), a common complication of bone marrow transplants that occurs when immune cells in the transplant attack the newly transplanted cells. Two patients had mild GVHD that appeared on their skin, and one patient's GVHD occurred in the mouth and skin. After a few extra months of immunosuppressive therapy, their GVHD subsided, and they also were able to stop taking these medications.

Ending all therapy related to their disease has been life-changing for the patients, says DeZern. "It's like night and day," she says. "They go from not knowing if they have a future to hoping for what they'd hoped for before they got sick. It's that transformative."

Successful transplants using partial match donors, Brodsky says, open up the transplant option to nearly all patients with this condition, especially minority patients. Seven of the 16 patients treated at Johns Hopkins self-identified as nonwhite.

A full sibling only has a 25 percent chance of being a full match. However, 100 percent of parents and 50 percent of siblings or half-siblings are half matches, regardless of ethnicity. The average person in the United States has about four half matches or better. "Now, a therapy that used to be available to 25 to 30 percent of patients with severe aplastic anemia is potentially available to more than 95 percent," says Brodsky.

The idea of using cyclophosphamide after a partial-match transplant was first pioneered decades ago by Johns Hopkins Kimmel Cancer Center experts. Brodsky says the drug destroys patient's diseased immune system cells but does not harm the donor's blood stem cells, which create new disease-free blood cells in the patient.

Bone marrow transplants are costly -- sometimes exceeding more than $300,000. However, Brodsky and DeZern say that full and half-matched transplants are life-saving for many, and there is cost-saving potential when aplastic anemia patients can avoid a lifetime of immunosuppressive therapy, hospitalizations, medications and blood transfusions.

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16 aplastic anemia patients free of disease after bone marrow transplant and chemo - Science Daily

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Louisville, Ky. man saves stranger's life

Julia Rose, WHAS 1:17 PM. EST February 07, 2017

Eric Gurevich and Ron Dreben

LOUISVILLE (WHAS11) -- It's hard to believe that up until a few months ago, Eric Gurevich and Ron Dreben were total strangers.

I got to see him for the first time and I just gave him this big bear hug and he was crying and his wife was there and his 81-year-old mother was there, Gurevich said.

That bear hug was years in the making but the two were bonded long before as blood brothers.

Because he received those, he was kind of given a new lease on life, Gurevich said.

Gurevich lives in Louisville. He donated his stem cells to Dreben who lives in Washington D.C. in 2014, one, quick decision that changed the lives of two people. Gurevich remembers the call from the organization Gift of Life like it was yesterday.

They said that there was a 54-year-old man with MDS and his life was dire and I am the only potential match, Gurevich said.

Without hesitation, he hopped on a plane from Louisville to D.C. and a week later started the donation process. Despite some concerns from family members who weren't totally sold on the idea of him undergoing the major medical procedure for a man he didn't even know, Gurevich says his decision was a no-brainer.

You're a little kid and you dream of being a superhero or helping someone or saving someone's life and you get this call. You get an opportunity. How could you not? Gurevich said.

He says donating 1.5 billion stem cells is painless, just like the cheek swab he did back in 2008, the reason he was even a possible match for Dreben.

Didn't think anything of it, got my cheek swabbed and then forgot about it pretty much the next day, Gurevich said.

That cheek swab was taken on his Birthright trip to Israel, a once in a lifetime opportunity that he never expected to lead to another once in a life time journey.

Gurevichs stem cell donation saved Dreben's life and for a full year after the transplant, they wondered about one another. By law, they weren't allowed to know each other's identities but that didn't stop them from exchanging cards and small gifts.

Eric Gurevich donated his stem cells to Dreben who lives in Washington D.C. in 2014, one, quick decision that changed the lives of two people.

He sent me a magnet that says 'life is a journey not a destination' and I have it right on my fridge and I think about him just about every day, Gurevich said.

Finally, after more than a year, the pair met face to face in Miami in November, a moment captured in a picture and forever captured in their hearts.

When you donate to a stranger you always wonder, you know who is on the other side and I was just so grateful that it was him, Gurevich said.

Gurevich says he and Dreben text each other often, sending pictures of their families back and forth and they plan to meet up again in the future.

If you're interested in becoming a potential stem cell or bone marrow donor with Gift of Life, you can find more information here: http://www.giftoflife.org.

There are also two local organizations dedicated to stem cell research and transplants: sharingamericasmarrow.com & nationalstemcellfoundation.org.

( 2017 WHAS)

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Ky. man saves stranger's life with stem cell transplant - WHAS11.com

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Globalnews.ca

Quebec family hopes to raise awareness for patients in need with stem cell registry drive Globalnews.ca Natasha Camacho-Gomes (middle right, standing) organized a bone marrow registry drive Saturday, Feb. 4, 2017 to raise awareness for patients in need. Her Fianc Kevin Butterfill is one of those patients. He was diagnosed with leukemia in January.

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Quebec family hopes to raise awareness for patients in need with stem cell registry drive - Globalnews.ca

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The 2017 Australian of the Year award went to Professor Alan Mackay-Sim for his significant career in stem cell science.

The prize was linked to barbeque-stopping headlines equating his achievements to the scientific equivalent of the moon landing and paving the road to recovery for people with spinal cord injuries.

Such claims in the media imply that there is now a scientifically proven stem cell treatment for spinal cord injury. This is not the case.

For now, any clinic or headline claiming miracle cures should be viewed with caution, as they are likely to be trading on peoples hope.

Put simply, injury to the spinal cord causes damage to the nerve cells that transmit information between the brain and the rest of the body.

Depending on which part of the spine is involved, the injury can affect the nerves that control the muscles in our legs and arms; those that control bowel and bladder function and how we regulate body temperature and blood pressure; and those that carry the sensation of being touched. This occurs in part because injury and subsequent scarring affect not just the nerves but also the insulation that surrounds and protects them. The insulation the myelin sheath is damaged and the body cannot usually completely replace or regenerate this covering.

Stem cells can self-reproduce and grow into hundreds of different cell types, including nerves and the cells that make myelin. So the blue-sky vision is that stem cells could restore some nerve function by replacing missing or faulty cells, or prevent further damage caused by scarring.

Studies in animals have applied stem cells derived from sources including brain tissue, the lining of the nasal cavity, tooth pulp, and embryos (known as embryonic stem cells).

Dramatic improvements have been shown on some occasions, such as rats and mice regaining bladder control or the ability to walk after injury. While striking, such improvement often represents only a partial recovery. It holds significant promise, but is not direct evidence that such an approach will work in people, particularly those with more complex injuries.

The translation of findings from basic laboratory stem cell research to effective and safe treatments in the clinic involves many steps and challenges. It needs a firm scientific basis from animal studies and then careful evaluation in humans.

Many clinical studies examining stem cells for spinal repair are currently underway. The approaches fit broadly into two categories:

using stem cells as a source of cells to replace those damaged as a result of injury

applying cells to act on the bodys own cells to accelerate repair or prevent further damage.

One study that has attracted significant interest involves the injection of myelin-producing cells made from human embryonic stem cells. Researchers hoped that these cells, once injected into the spinal cord, would mature and form a new coating on the nerve cells, restoring the ability of signals to cross the spinal cord injury site. Preliminary results seem to show that the cells are safe; studies are ongoing.

Other clinical trials use cells from patients own bone marrow or adipose tissue (fat), or from donated cord blood or nerves from fetal tissue. The scientific rationale is based on the possibility that when transplanted into the injured spinal cord, these cells may provide surrounding tissue with protective factors which help to re-establish some of the connections important for the network of nerves that carry information around the body.

The field as it stands combines years of research, and tens of millions of dollars of investment. However, the development of stem cell therapies for spinal cord injury remains a long way from translating laboratory promise into proven and effective bedside treatments.

Each case is unique in people with spinal cord injury: the level of paralysis, and loss of sensation and function relate to the type of injury and its location. Injuries as a result of stab wounds or infection may result in different outcomes from those incurred as a result of trauma from a car accident or serious fall. The previous health of those injured, the care received at the time of injury, and the type of rehabilitation they access can all impact on subsequent health and mobility.

Such variability means caution needs to accompany claims of man walking again particularly when reports relate to a single individual.

In the case that was linked to the Australian of the Year award, the actual 2013 study focused on whether it was safe to take the patients own nerves and other cells from the nose and place these into the damaged region of the spine. While the researchers themselves recommended caution in interpreting the results, accompanying media reports focused on the outcome from just one of the six participants.

While the outcome was significant for the gentleman involved, we simply do not know whether recovery may have occurred for this individual even without stem cells, given the type of injury (stab wounds), the level of injury, the accompanying rehabilitation that he received or a combination of these factors. It cannot be assumed a similar outcome would be the case for all people with spinal injury.

Finding a way to alleviate the suffering of those with spinal cord injury, and many other conditions, drives the work of thousands of researchers and doctors around the globe. But stem cells are not a silver bullet and should not be immune from careful evaluation in clinical trials.

Failure to proceed with caution could actually cause harm. For example, a paraplegic woman who was also treated with nasal stem cells showed no clinical improvement, and developed a large mucus-secreting tumour in her spine. This case highlights the need for further refinement and assessment in properly conducted clinical trials before nasal stem cells can become part of mainstream medicine.

Its also worth noting that for spinal cord injury, trials for recovery of function are not limited to the use of stem cells but include approaches focused on promoting health of surviving nerves (neuroprotection), surgery following injury, nerve transfers, electrical stimulation, external physical supports known as exoskeletons, nanotechnology and brain-machine interfaces.

Ultimately, determining which of these approaches will improve the lives of people with spinal injury can only be done through rigorous, ethical research.

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Yes there's hope, but treating spinal injuries with stem cells is not a reality yet - The Conversation AU

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BUCKEYE, AZ - As the saying goes: "blood is thicker than water." But when it comes to bone marrow, it is truer than ever especially because family is usually the only people to turn to for a match.

But, one Buckeye family is finding that the phrase could not be more perfectfor them because a brother has been serving as the lifeline for his sibling over the last few years.

Gloria Mesquias calls her 11-year-old son, Shaun, "the warrior."

"He takes every jab he gets and just rolls through," said Mesquias.

Shaun's 13-year-old brother Malik is called "the hero."

"They are actually like night and day, "Mesquias said. "They're brothers."

The three of them, and other supportive family members, have spent months at Phoenix Children's Hospital. Shaun has a condition where his body isn't producing new blood cells.

"He was diagnosed with severe aplastic anemia," Mesquias said.

That happened when he was just about 1 year old. Ever since then, he's been in and out of the hospital.

But, Malikhas served as a bone marrow and stem cell donor to his b brother not once, not twice but, three different times.

And the fight for this little warrior, is not over yet. If his treatment goes well over the next few days, he will have a fourth surgery on Wednesday; another stem cell transplant.

Mesquias doing this all as a single mother. She also has a 5-year-old daughter, who has not seen Shaun since before Christmas.

"She understand;she gets it," Mesquias explained. "She knows brother is sick and she knows mom is here with Shaun."

But, while she tries to keep it together, all of the stress and days away from home are weighing on Mesquias. But, it's something she will never let her family see.

"At night time, I can go in the restroom and cry my eyes out or ball my face out in the pillow," Mesquias said. "But, I just don't do it in front of him."

So, the boys' Buckeye teacher, Carrie Brown, has also taken action to try and do something special for the family.

"She would never ask for help," Brown said. "She's not that kind of person. So, I just thought that this was one thing that I could do to relieve some of the worry that she has and to give her a little bit of comfort."

Brown started a GoFundMe page to try and help the family who has given so much to each other.

And Mesquias said she is making sure all of them get out of that hospital together.

"He has his moments too where he says he wants to go home," Mesquias explained. "And... I'm like, 'I'm not going home until you're going home. So, we're good."

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Buckeye boy donates bone marrow to sick brother - ABC15 Arizona - ABC15 Arizona

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By filling out a form, and swabbing his mouth, Harlee O'Watch could save a life.

"To find a match, because the list of donors is so low, is really unlikely," said the 22-year-old.

O'Watch is one of four young adults from Carry the Kettle First Nation who registered with the OneMatch program, which connects donors with people in need of bone marrow or stem cell transplants.

A problem for the 14 indigenous people currently waiting for a match is that, out of the 17,000 people on the Canadian registry, fewer than one per cent are indigenous.

"It doesn't give me much hope if I ever get sick and need a blood transfusion or bone marrow transplant, said OWatch.

It doesn't give me much hope because, if there's no potential matches, I'm going to die, bottom line, and I don't want to die."

Robyn Henwood works for Canadian Blood Services, which runs OneMatch. She covers Alberta to Northern Ontario and the Northwest Territories, including the Prairies, and visited Carry the Kettle to recruit. A match requires a genetic twin and indigenous people are only in Canada.

"It does get more complicated [with] these different ethnic backgrounds. . . even within First Nations that get brought into it, said Henwood.

The chances of finding a match becomes that much more difficult."

This means someone who is Cree cannot donate to someone who is Mohawk, she said.

In the past year, Canadian Blood Services has visited less than 12 reserves to help find matches for indigenous people. Carry the Kettle is Henwoods third community.

"We have been leaving messages and voicemails, not getting a lot of response back, she said.

I'm hoping a new technique will work. Things like this, this is so important to spread our message."

According to Indigenous and Northern Affairs Canada, more than 50 per cent of indigenous people live in urban centres. And yet, Henwood says finding indigenous donors in cities is also a struggle.

"Trying to get someone to sign up and commit for the next 30 to 40 years, to potentially save a stranger's life is not an easy thing to do," she said.

Henwood says informing indigenous people about one match will empower more to donate. Until then, the chance of survival for those waiting on the registry is low.

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Program seeks to boost bone marrow, stem cell donations from indigenous people - CTV News

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ANDREW and Judy Kim are still searching the globe for a donor for their two-year-old son after he was diagnosed with a rare genetic condition.

The couple's son Alastair was diagnosed with chronic granulomatous disorder (CGD) in February last year.

Mr and Mrs Kim launched an appeal for help in September but the search is still on for a matching donor and their son still needs hospital treatment.

The life-threatening condition wipes out his immune system, meaning even the most minor infections leave him seriously ill.

A course of genetic therapy treatment to help him fight infections has been launched and Alastair has been treated at Oxford Children's Hospital and Great Ormond Street Hospital in London.

The only hope of a permanent cure lies in a bone marrow stem cell donor but it needs to be a 90 per cent genetic match and the family is calling for more East Asians to sign up as donors.

Mr Kim, 37, a medical research engineer, said: "It is not easy to find a match and we pray every day that it will work out.

"We have to make sure that Alastair does not get a cut because it could get infected and he does not have the ability to fight off bacteria.

"That could cascade down the line to something very dangerous for him.

"If we get ill then we have to stay away from him he loves our dog Choco Pie but he is not allowed to stroke her.

"We are doing our best to stay positive and raise awareness about his condition."

Mr and Mrs Kim, who live near Longworth with their other son Micah, five, have already searched the international register of more than four million donors but without success.

They are both of Korean descent so a matching donor will most likely be of Korean, Japanese or Chinese heritage.

The number of East Asians on international donor registers is very limited of the 617,000 registered donors in the UK just 0.5 per cent are east Asian.

The couple, who moved to Oxfordshire from Chicago nine years ago, are now appealing for people around the world, particularly East Asians, to order a free kit through a website they have set up, and take a two-minute home test to see if they could help.

Alastair has had numerous infections since he was born in September 2014.

He spent the first year-and-a-half of his life in and out of hospital but CGD is so rare, doctors never thought to test him for it but eventually a doctor at the John Radcliffe Hospital in Oxford decided to test Alastair for the condition.

The couple desperately want to find a matching donor, but also want to increase the number of East Asians on the donor register.

The couple have run several blood drives at Mrs Kim's office at Oxford University and at Harwell Oxford.

More than 90 people came forward and of those, five were able to donate blood that helped Alastair to fight infections.

Mr Kim added: "At a couple of blood drives we have found matches for other people and hopefully one day a match will found for Alastair."

To join the register go to allysfight.com

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Search goes on for bone marrow match for little Longworth lad ... - Oxford Mail

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CCR5 Identifiers Aliases CCR5, CC-CKR-5, CCCKR5, CCR-5, CD195, CKR-5, CKR5, CMKBR5, IDDM22, C-C motif chemokine receptor 5 (gene/pseudogene) External IDs OMIM: 601373 MGI: 107182 HomoloGene: 37325 GeneCards: CCR5 Targeted by Drug aplaviroc, cenicriviroc, maraviroc, vicriviroc[1] Orthologs Species Human Mouse Entrez Ensembl UniProt RefSeq (mRNA) RefSeq (protein) Location (UCSC) Chr 3: 46.37 46.38 Mb Chr 9: 124.12 124.15 Mb PubMed search [2] [3] Wikidata View/Edit Human View/Edit Mouse

C-C chemokine receptor type 5, also known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines. This is the process by which T cells are attracted to specific tissue and organ targets. Many forms of HIV, the virus that causes AIDS, initially use CCR5 to enter and infect host cells. Certain individuals carry a mutation known as CCR5-32 in the CCR5 gene, protecting them against these strains of HIV.

In humans, the CCR5 gene that encodes the CCR5 protein is located on the short (p) arm at position 21 on chromosome 3. Certain populations have inherited the Delta 32 mutation resulting in the genetic deletion of a portion of the CCR5 gene. Homozygous carriers of this mutation are resistant to M-tropic strains of HIV-1 infection.[4][5][6][7][8][9]

The CCR5 protein belongs to the beta chemokine receptors family of integral membrane proteins.[10][11] It is a G proteincoupled receptor[10] which functions as a chemokine receptor in the CC chemokine group.

CCR5's cognate ligands include CCL3, CCL4 (also known as MIP 1 and 1, respectively), and CCL3L1.[12][13] CCR5 furthermore interacts with CCL5 (a chemotactic cytokine protein also known as RANTES).[12][14][15]

CCR5 is predominantly expressed on T cells, macrophages, dendritic cells, eosinophils and microglia. It is likely that CCR5 plays a role in inflammatory responses to infection, though its exact role in normal immune function is unclear. Regions of this protein are also crucial for chemokine ligand binding, functional response of the receptor, and HIV co-receptor activity.[16]

HIV-1 most commonly uses the chemokine receptors CCR5 and/or CXCR4 as co-receptors to enter target immunological cells.[17] These receptors are located on the surface of host immune cells whereby they provide a method of entry for the HIV-1 virus to infect the cell.[18] The HIV-1 envelope glycoprotein structure is essential in enabling the viral entry of HIV-1 into a target host cell.[18] The envelope glycoprotein structure consists of two protein subunits cleaved from a Gp160 protein precursor encoded for by the HIV-1 env gene: the Gp120 external subunit, and the Gp41 transmembrane subunit.[18] This envelope glycoprotein structure is arranged into a spike-like structure located on the surface of the virion and consists of a trimer of three Gp120-Gp41 hetero-dimers.[18] The Gp120 envelope protein is a chemokine mimic.[17] It lacks the unique structure of a chemokine, however it is still capable of binding to the CCR5 and CXCR4 chemokine receptors.[17] During HIV-1 infection, the Gp120 envelope glycoprotein subunit binds to a CD4 glycoprotein and a HIV-1 co-receptor expressed on a target cell- forming a heterotrimeric complex.[17] The formation of this complex stimulates the release of a fusogenic peptide inducing the fusion of the viral membrane with the membrane of the target host cell.[17] Because binding to CD4 alone can sometimes result in gp120 shedding, gp120 must next bind to co-receptor CCR5 in order for fusion to proceed. The tyrosine sulfated amino terminus of this co-receptor is the "essential determinant" of binding to the gp120 glycoprotein.[19] Co-receptor recognition also include the V1-V2 region of gp120, and the bridging sheet (an antiparallel, 4-stranded sheet that connects the inner and outer domains of gp120). The V1-V2 stem can influence "co-receptor usage through its peptide composition as well as by the degree of N-linked glycosylation." Unlike V1-V2 however, the V3 loop is highly variable and thus is the most important determinant of co-receptor specificity.[19] The normal ligands for this receptor, RANTES, MIP-1, and MIP-1, are able to suppress HIV-1 infection in vitro. In individuals infected with HIV, CCR5-using viruses are the predominant species isolated during the early stages of viral infection,[20] suggesting that these viruses may have a selective advantage during transmission or the acute phase of disease. Moreover, at least half of all infected individuals harbor only CCR5-using viruses throughout the course of infection.

CCR5 is the primary co-receptor used by gp120 sequentially with CD4. This bind results in gp41, the other protein product of gp160, to be released from its metastable conformation and insert itself into the membrane of the host cell. Although it hasn't been finalized as a proven theory yet, binding of gp120-CCR5 involves two crucial steps: 1) The tyrosine sulfated amino terminus of this co-receptor is an "essential determinant" of binding to gp120 (as stated previously) 2) Following step 1., there must be reciprocal action (synergy, intercommunication) between gp120 and the CCR5 transmembrane domains [19]

CCR5 is essential for the spread of the R5-strain of the HIV-1 virus.[21] Knowledge of the mechanism by which this strain of HIV-1 mediates infection has prompted research into the development of therapeutic interventions to block CCR5 function.[22] A number of new experimental HIV drugs, called CCR5 receptor antagonists, have been designed to interfere with the associative binding between the Gp120 envelope protein and the HIV co-receptor CCR5.[21] These experimental drugs include PRO140 (CytoDyn), Vicriviroc (Phase III trials were cancelled in July 2010) (Schering Plough), Aplaviroc (GW-873140) (GlaxoSmithKline) and Maraviroc (UK-427857) (Pfizer). Maraviroc was approved for use by the FDA in August 2007.[21] It is the only one thus far approved by the FDA for clinical use, thus becoming the first CCR5 inhibitor.[19] A problem of this approach is that, while CCR5 is the major co-receptor by which HIV infects cells, it is not the only such co-receptor. It is possible that under selective pressure HIV will evolve to use another co-receptor. However, examination of viral resistance to AD101, molecular antagonist of CCR5, indicated that resistant viruses did not switch to another coreceptor (CXCR4) but persisted in using CCR5, either through binding to alternative domains of CCR5, or by binding to the receptor at a higher affinity. However, because there is still another co-receptor available, this indicates that lacking the CCR5 gene doesn't make one immune to the virus; it simply implies that it would be more challenging for the individual to contract it. Also, the virus still has access to the CD4. Unlike CCR5, which the body apparently doesn't really need due to those still living healthy lives even with the lack of/or absence of the gene (as a result of the delta 32 mutation), CD4 is critical in the bodies defense system (fighting against infection).[23] Even without the availability of either co-receptors (even CCR5), the virus can still invade cells if gp41 were to go through an alteration (including its cytoplasmic tail), resulting in the independence of CD4 without the need of CCR5 and/or CXCR4 as a doorway.[24]

CCR5-32 (or CCR5-D32 or CCR5 delta 32) is an allele of CCR5.[25][26]

CCR5 32 is a 32-base-pair deletion that introduces a premature stop codon into the CCR5 receptor locus, resulting in a nonfunctional receptor.[27][28] CCR5 is required for M-tropic HIV-1 virus entry.[29] Individuals homozygous for CCR5 32 do not express functional CCR5 receptors on their cell surfaces and are resistant to HIV-1 infection, despite multiple high-risk exposures.[29] Individuals heterozygous for the mutant allele have a greater than 50% reduction in functional CCR5 receptors on their cell surfaces due to dimerization between mutant and wild-type receptors that interferes with transport of CCR5 to the cell surface.[30] Heterozygote carriers are resistant to HIV-1 infection relative to wild types and when infected, heterozygotes exhibit reduced viral loads and a 2-3-year-slower progression to AIDS relative to wild types.[27][29][31] Heterozygosity for this mutant allele also has shown to improve one's virological response to anti-retroviral treatment.[32] CCR5 32 has an (heterozygote) allele frequency of 10% in Europe, and a homozygote frequency of 1%.

The CCR5 32 allele is notable for its recent origin, unexpectedly high frequency, and distinct geographic distribution,[33] which together suggest that (a) it arose from a single mutation, and (b) it was historically subject to positive selection.

Two studies have used linkage analysis to estimate the age of the CCR5 32 deletion, assuming that the amount of recombination and mutation observed on genomic regions surrounding the CCR5 32 deletion would be proportional to the age of the deletion.[26][34] Using a sample of 4000 individuals from 38 ethnic populations, Stephens et al. estimated that the CCR5-32 deletion occurred 700 years ago (275-1875, 95% confidence interval). Another group, Libert et al. (1998), estimated the age of the CCR5 32 mutation is based on the microsatellite mutations to be 2100 years (700-4800, 95% confidence interval). On the basis of observed recombination events, they estimated the age of the mutation to be 2250 years (900-4700, 95% confidence interval).[34] A third hypothesis relies on the north-to-south gradient of allele frequency in Europe which shows that the highest allele frequency occurred in Nordic regions such as Iceland, Norway and Sweden and lowest allele frequency in the south. Because the Vikings historically occupied these countries, it may be possible that the allele spread throughout Europe was due to the Viking dispersal in the 8th to 10th century.[35] Vikings were later replaced by the Varangians in Russia, which migrated East which may have contributed to the observed east-to-west cline of allele frequency.[33][35]

HIV-1 was initially transmitted from chimpanzees (Pan troglodytes) to humans in the early 1900s in Southeast Cameroon, Africa,[36] through exposure to infected blood and body fluids while butchering bushmeat.[37] However, HIV-1 was effectively absent from Europe until the late 1980s.[38] Therefore, given the average age of roughly 1000 years for the CCR5-32 allele, it can be established that HIV-1 did not exert selection pressure on the human population for long enough to achieve the current frequencies.[33] Hence, other pathogens have been suggested agents of positive selection for CCR5 32. The first major one being bubonic plague (Yersinia pestis), and later, smallpox (Variola major). Other data suggest that the allele frequency resulted as a negative selection pressure as a result of pathogens that became more widespread during Roman expansion.[39] The idea that negative selection played a role in its low frequency is also supported by experiments using knockout mice and Influenza A, which demonstrated that the presence of the CCR5 receptor is important for efficient response to a pathogen.[40][41]

Several lines of evidence suggest that the CCR5 32 allele evolved only once.[33] First, CCR5 32 has a relatively high frequency in several different Caucasian populations but is comparatively absent in Asian, Middle Eastern and American Indian populations,[26] suggesting that a single mutation occurred after divergence of Caucasians from their African ancestor).[26][27][42] Second, genetic linkage analysis indicates that the mutation occurs on a homogenous genetic background, implying that inheritance of the mutation occurred from a common ancestor.[34] This was demonstrated by showing that the CCR5 32 allele is in strong linkage disequilibrium with highly polymorphic microsatellites. More than 95% of CCR5 32 chromosomes also carried the IRI3.1-0 allele, while 88% carried the IRI3.2 allele. By contrast, the microsatellite markers IRI3.1-0 and IRI3.2-0 were found in only 2 or 1.5% of chromosomes carrying a wild-type CCR5 allele.[34] This evidence of linkage disequilibrium supports the hypothesis that most, if not all, CCR5 32 alleles arose from a single mutational event. Finally, the CCR5 32 allele has a unique geographical distribution indicating a single Northern origin followed by migration. A study measuring allele frequencies in 18 European populations found a North-to-South gradient, with the highest allele frequencies in Finnish and Mordvinian populations (16%), and the lowest in Sardinia (4%).[34]

In the absence of selection, a single mutation would take an estimated 127,500 years to rise to a population frequency of 10%.[26] Estimates based on genetic recombination and mutation rates place the age of the allele between 1000 and 2000 years. This discrepancy is a signature of positive selection.

It is estimated that HIV-1 entered the human population in Africa in the early 1900s,[36] symptomatic infections were not reported until the 1980s. The HIV-1 epidemic is therefore far too young to be the source of positive selection that drove the frequency of CCR5 32 from zero to 10% in 2000 years. In 1998, Stephens et al. suggested that bubonic plague (Yersinia pestis) had exerted positive selective pressure on CCR5 32.[26] This hypothesis was based on the timing and severity of the Black Death pandemic, which killed 30% of the European population of all ages between 1346 and 1352.[43] After the Black Death, there were less severe, intermittent, epidemics. Individual cities experienced high mortality, but overall mortality in Europe was only a few percent.[43][44][45] In 1655-1656 a second pandemic called the "Great Plague" killed 15-20% of Europes population.[43][46] Importantly, the plague epidemics were intermittent. Bubonic plague is a zoonotic disease, primarily infecting rodents and spread by fleas and only occasionally infecting humans.[47] Human-to-human infection of bubonic plague does not occur, though it can occur in pneumonic plague, which infects the lungs.[48] Only when the density of rodents is low are infected fleas forced to feed on alternative hosts such as humans, and under these circumstances a human epidemic may occur.[47] Based on population genetic models, Galvani and Slatkin (2003) argue that the intermittent nature of plague epidemics did not generate a sufficiently strong selective force to drive the allele frequency of CCR5 32 to 10% in Europe.[25]

To test this hypothesis, Galvani and Slatkin (2003) modeled the historical selection pressures produced by plague and smallpox.[25] Plague was modeled according to historical accounts,[49][50] while age-specific smallpox mortality was gleaned from the age distribution of smallpox burials in York (England) between 1770 and 1812.[44] Smallpox preferentially infects young, pre-reproductive members of the population since they are the only individuals who are not immunized or dead from past infection. Because smallpox preferentially kills pre-reproductive members of a population, it generates stronger selective pressure than plague.[25] Unlike plague, smallpox does not have an animal reservoir and is only transmitted from human to human.[51][52] The authors calculated that if plague were selecting for CCR5 32, the frequency of the allele would still be less than 1%, while smallpox has exerted a selective force sufficient to reach 10%.

The hypothesis that smallpox exerted positive selection for CCR5 32 is also biologically plausible, since poxviruses, like HIV, are viruses that enter white blood cells by using chemokine receptors.[53] By contrast, Yersinia pestis is a bacterium with a very different biology.

Although Caucasians are the only population with a high frequency of CCR5 32, they are not the only population that has been subject to selection by smallpox, which had a worldwide distribution before it was declared eradicated in 1980. The earliest unmistakable descriptions of smallpox appear in the 5th century A.D. in China, the 7th century A.D. in India and the Mediterranean, and the 10th century A.D. in southwestern Asia.[52] By contrast, the CCR5 32 mutation is found only in European, West Asian, and North African populations.[54] The anomalously high frequency of CCR5 32 in these populations appears to require both a unique origin in Northern Europe and subsequent selection by smallpox.

Research has not yet revealed a cost of carrying the CCR5 null mutation that is as dramatic as the benefit conferred in the context of HIV-1 exposure. In general, research suggests that the CCR5 32 mutation protects against diseases caused by certain pathogens but may also play a deleterious role in postinfection inflammatory processes, which can injure tissue and create further pathology.[55] The best evidence for this proposed antagonistic pleiotropy is found in flavivirus infections. In general many viral infections are asymptomatic or produce only mild symptoms in the vast majority of the population. However, certain unlucky individuals experience a particularly destructive clinical course, which is otherwise unexplained but appears to be genetically mediated. Patients homozygous for CCR5 32 were found to be at higher risk for a neuroinvasive form of tick-borne encephalitis (a flavivirus).[56] In addition, functional CCR5 may be required to prevent symptomatic disease after infection with West Nile virus, another flavivirus; CCR5 32 was associated with early symptom development and more pronounced clinical manifestations after infection with West Nile virus.[57]

This finding in humans confirmed a previously-observed experiment in an animal model of CCR5 32 homozygosity. After infection with West Nile Virus, CCR5 32 mice had markedly increased viral titers in the central nervous system and had increased mortality[58] compared with that of wild-type mice, thus suggesting that CCR5 expression was necessary to mount a strong host defense against West Nile virus.

CCR5 32 can be beneficial to the host in some infections (e.g., HIV-1, possibly smallpox), but detrimental in others (e.g., tick-borne encephalitis, West Nile virus). Whether CCR5 function is helpful or harmful in the context of a given infection depends on a complex interplay between the immune system and the pathogen.

A genetic approach involving intrabodies that block CCR5 expression has been proposed as a treatment for HIV-1 infected individuals.[59] When T-cells modified so they no longer express CCR5 were mixed with unmodified T-cells expressing CCR5 and then challenged by infection with HIV-1, the modified T-cells that do not express CCR5 eventually take over the culture, as HIV-1 kills the non-modified T-cells. This same method might be used in vivo to establish a virus-resistant cell pool in infected individuals.[59]

This hypothesis was tested in an AIDS patient who had also developed myeloid leukemia, and was treated with chemotherapy to suppress the cancer. A bone marrow transplant containing stem cells from a matched donor was then used to restore the immune system. However, the transplant was performed from a donor with 2 copies of CCR5-32 mutation gene. After 600 days, the patient was healthy and had undetectable levels of HIV in the blood and in examined brain and rectal tissues.[5][60] Before the transplant, low levels of HIV X4, which does not use the CCR5 receptor, were also detected. Following the transplant, however, this type of HIV was not detected either, further baffling doctors.[5] However, this is consistent with the observation that cells expressing the CCR5-32 variant protein lack both the CCR5 and CXCR4 receptors on their surfaces, thereby conferring resistance to a broad range of HIV variants including HIV X4.[61] After over six years, the patient has maintained the resistance to HIV and has been pronounced cured of the HIV infection.[6]

Enrollment of HIV-positive patients in a clinical trial was started in 2009 in which the patients' cells were genetically modified with a zinc finger nuclease to carry the CCR5-32 trait and then reintroduced into the body as a potential HIV treatment.[62][63] Results reported in 2014 were promising.[9]

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CCR5 - Wikipedia

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Session Tracks

Conference Series invites all the participants from all over the world to attend"8th European Immunology Conference, June 29-July 01, 2017 Madrid, Spain, includesprompt keynote presentations, Oral talks, Poster presentations and Exhibitions.

European ImmunologyConferenceis to gathering people in academia and society interested inimmunologyto share the latest trends and important issues relevant to our field/subject area.Immunology Conferencesbrings together the global leaders in Immunology and relevant fields to present their research at this exclusive scientific program. TheImmunology Conferencehosting presentations from editors of prominent refereed journals, renowned and active investigators and decision makers in the field of Immunology.European Immunology ConferenceOrganizing Committee also invites Young investigators at every career stage to submit abstracts reporting their latest scientific findings in oral and poster sessions.

Track:1Cellular Immunology

The study of the molecular and cellular components that comprise the immune system, including their function and interaction, is the central science ofimmunology. The immune system has been divided into a more primitive innate immune system and, in vertebrates, an acquired oradaptive immune system

The field concerning the interactions among cells and molecules of the immunesystem,and how such interactions contribute to the recognition and elimination of pathogens. Humans possess a range of non-specific mechanical and biochemical defences against routinely encountered bacteria, parasites, viruses, and fungi. The skin, for example, is an effective physical barrier to infection. Basic chemical defences are also present in blood, saliva, and tears, and on mucous membranes. True protection stems from the host's ability to mount responses targeted to specific organisms, and to retain a form of memory that results in a rapid, efficient response to a given organism upon a repeat encounter. This more formal sense of immunity, termed adaptive immunity, depends upon the coordinated activities of cells and molecules of the immune system.

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Track: 2Inflammatory/Autoimmune Diseases

Autoimmune diseasescan affect almost any part of the body, including the heart, brain, nerves, muscles, skin, eyes, joints, lungs, kidneys, glands, the digestive tract, and blood vessels.

The classic sign of an autoimmune disease is inflammation, which can cause redness, heat, pain, and swelling. How an autoimmune disease affects you depends on what part of the body is targeted. If the disease affects the joints, as inrheumatoid arthritis, you might have joint pain, stiffness, and loss of function. If it affects the thyroid, as in Graves disease and thyroiditis, it might cause tiredness, weight gain, and muscle aches. If it attacks the skin, as it does in scleroderma/systemic sclerosis, vitiligo, andsystemic lupus erythematosus(SLE), it can cause rashes, blisters, and colour changes. Many autoimmune diseases dont restrict themselves to one part of the body. For example, SLE can affect the skin, joints, kidneys, heart, nerves, blood vessels, and more. Type 1 diabetes can affect your glands, eyes, kidneys, muscles, and more.

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Track: 3T-Cells and B-Cells

T cell: A type of white blood cell that is of key importance to the immune system and is at the core of adaptive immunity, the system that tailors the body's immune response to specific pathogens. The T cells are like soldiers who search out and destroy the targeted invaders. Immature T cells (termed T-stem cells) migrate to the thymus gland in the neck, where they mature and differentiate into various types of mature T cells and become active in the immune system in response to a hormone called thymosin and other factors. T-cells that are potentially activated against the body's own tissues are normally killed or changed ("down-regulated") during this maturational process.There are several different types of mature T cells. Not all of their functions are known. T cells can produce substances called cytokines such as the interleukins which further stimulate the immune response. T-cell activation is measured as a way to assess the health of patients withHIV/AIDSand less frequently in other disorders. T cell are also known as T lymphocytes. The "T" stands for "thymus" -- the organ in which these cells mature. As opposed to B cells which mature in the bone marrow.B cells, also known asBlymphocytes, are a type of white bloodcellof the lymphocyte subtype. They function in thehumoral immunitycomponent of the adaptive immune system by secreting antibodies. Many B cells mature into what are called plasma cells that produce antibodies (proteins) necessary to fight off infections while other B cells mature into memory B cells. All of the plasma cells descended from a single B cell produce the same antibody which is directed against the antigen that stimulated it to mature. The same principle holds with memory B cells. Thus, all of the plasma cells and memory cells "remember" the stimulus that led to their formation. The maturation of B cells takes place in birds in an organ called the bursa of Fabricus. B cells in mammals mature largely in the bone marrow. The B cell, or B lymphocyte, is thus an immunologically important cell. It is not thymus-dependent, has a short lifespan, and is responsible for the production ofimmunoglobulins.It expresses immunoglobulins on its surface.

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Track: 4Cancer and Tumor Immunobiology

The tumour is an important aspect of cancer biology that contributes to tumour initiation, tumour progression and responses to therapy. Cells and molecules of the immune system are a fundamental component of the tumour microenvironment. Importantly,therapeutic strategies for cancer treatmentcan harness the immune system to specifically target tumour cells and this is particularly appealing owing to the possibility of inducing tumour-specific immunological memory, which might cause long-lasting regression and prevent relapse in cancer patients.The composition and characteristics of the tumour microenvironment vary widely and are important in determining the anti-tumour immune response.Immunotherapyis a new class ofcancer treatmentthat works to harness the innate powers of the immune system to fight cancer. Because of the immune system's unique properties, these therapies may hold greater potential than current treatment approaches to fight cancer more powerfully, to offer longer-term protection against the disease, to come with fewer side effects, and to benefit more patients with more cancer

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Track: 5 Vaccines

A vaccine is a biological preparation that improves immunity to a particular disease. A vaccine typically contains an agent that resembles a disease-causing microorganism, and is often made from weakened or killed forms of the microbe, its toxins or one of its surface proteins. The agent stimulates the body's immune system to recognize the agent as foreign, destroy it, and "remember" it, so that the immune system can more easily recognize and destroy any of these microorganisms that it later encounters. There are two basictypes of vaccines: live attenuated and inactivated. The characteristics of live and inactivatedvaccinesare different, and these characteristics determine how thevaccineis used. Liveattenuatedvaccinesare produced by modifying a disease-producing (wild) virus or bacteria in a laboratory.

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Track: 6Immunotherapy

Immunotherapy,also called biologic therapy, is a type of cancer treatment designed to boost the body's natural defences to fight the cancer. It uses materials either made by the body or in a laboratory to improve, target, or restore immune system function. Immunotherapy is treatment that uses certain parts of a persons immune system to fight diseases such as cancer. This can be done in a couple of ways:1)Stimulating your own immune system to work harder or smarter to attack cancer cells2)Giving you immune system components, such as man-made immune system proteins. Some types of immunotherapy are also sometimes called biologic therapy or biotherapy.

In the last few decadesimmunotherapyhas become an important part of treating some types of cancer. Newer types of immune treatments are now being studied, and theyll impact how we treat cancer in the future. Immunotherapy includes treatments that work in different ways. Some boost the bodys immune system in a very general way. Others help train the immune system to attack cancer cells specifically. Immunotherapy works better for some types of cancer than for others. Its used by itself for some of these cancers, but for others it seems to work better when used with other types of treatment.

Many different types of immunotherapy are used to treat cancer. They include:Monoclonal antibodies,Adoptive cell transfer,Cytokines, Treatment Vaccines, BCG,

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Track: 7Neuro Immunology

Neuroimmunology, a branch of immunologythat deals especially with the inter relationships of the nervous system and immune responses andautoimmune disorders. It deals with particularly fundamental and appliedneurobiology,meetings onneurology,neuropathology, neurochemistry,neurovirology, neuroendocrinology, neuromuscular research,neuropharmacologyand psychology, which involve either immunologic methodology (e.g. immunocytochemistry) or fundamental immunology (e.g. antibody and lymphocyte assays).

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Track: 8Infectious Diseases and Immune System

Infectious diseases are caused by pathogenic microorganisms, such as bacteria, viruses, parasites or fungi; the diseases can be spread, directly or indirectly, from one person to another.Zoonotic diseasesare infectious diseases of animals that can cause disease when transmitted to humans. Some infectious diseases can be passed from person to person. Some are transmitted by bites from insects or animals. And others are acquired by ingesting contaminated food or water or being exposed to organisms in the environment. Signs and symptoms vary depending on the organism causing the infection, but often include fever and fatigue. Mild complaints may respond to rest and home remedies, while some life-threatening infections may require hospitalization.

Many infectious diseases, such as measles andchickenpox, can be prevented by vaccines. Frequent and thorough hand-washing also helps protect you from infectious diseases

There are four main kinds of germs:

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Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; 3nd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 19thInternational Conference on Immunology (ICI) Sept 14-17, 2017, Berlin, Germany; Modelling Viral Infections and Immunity (E1) , May 1 - 4, 2017 | Estes Park, Colorado, USA; 7thInternational Conference on Allergy, Asthma and Clinical Immunology; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand

Track: 9Reproductive Immunology,

Reproductive immunologyrefers to a field of medicine that studies interactions (or the absence of them) between the immune system and components related to thereproductivesystem, such as maternal immune tolerance towards the fetus, orimmunologicalinteractions across the blood-testis barrier. The immune system refers to all parts of the body that work to defend it against harmful enemies. In people with immunological fertility problems their body identifies part of reproductive function as an enemy and sendsNatural Killer (NK) cellsto attack. A healthy immune response would only identify an enemy correctly and attack only foreign invaders such as a virus, parasite, bacteria, ect.

The concept of reproductive immunology is not widely accepted by all physicians.Those patients who have had repeated miscarriages and multiple failed IVF's find themselves exploring it's possibilities as the reason. With an increased amount of success among treating any potential immunological factors, the idea of reproductive immunology can no longer be overlooked.The failure to conceive is often due to immunologic problems that can lead to very early rejection of the embryo, often before the pregnancy can be detected by even the most sensitive tests. Women can often produce perfectly healthy embryos that are lost through repeated "mini miscarriages." This most commonly occurs in women who have conditions such asendometriosis, an under-active thyroid gland or in cases of so called "unexplained infertility." It has been estimated that an immune factor may be involved in up to 20% of couples with otherwiseunexplained infertility. These are all conditions where abnormalities of the womans immune system may play an important role.

RelatedImmunology Conferences|Immunologists Meetings|Conference Series LLC:

9thworld congress & expo on Immunology, Oct 02-04, 2017, Toronto, Canada; 3rdAntibodies and Bio Therapeutics Congress, November 02-03, 2017 Las Vegas, USA; Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; 3nd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 18th International Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; British Society for Immunology Congress, Dec 06-09, 2016, Liverpool, United Kingdom; 7thInternational Conference on Allergy, Asthma and Clinical Immunology; Cancer Immunology and Immunotherapy: Taking a Place in Mainstream Oncology (C7), March 19 - 23, 2017, Whistler, British Columbia, Canada

Track:10Auto Immunity,

Autoimmunityis the system ofimmuneresponses of an organism against its own cells and tissues. Any disease that results from such an aberrantimmuneresponse is termed an autoimmune disease.

Autoimmunity is present to some extent in everyone and is usually harmless. However, autoimmunity can cause a broad range of human illnesses, known collectively as autoimmune diseases. Autoimmune diseases occur when there is progression from benign autoimmunity to pathogenicautoimmunity. This progression is determined by genetic influences as well as environmental triggers. Autoimmunity is evidenced by the presence of autoantibodies (antibodies directed against the person who produced them) and T cells that are reactive with host antigens.

Autoimmune disorders

An autoimmune disorder occurs whenthe bodys immune systemattacks and destroys healthy body tissue by mistake. There are more than 80 types of autoimmune disorders.

Causes

The white blood cells in the bodys immune system help protect against harmful substances. Examples include bacteria, viruses,toxins,cancercells, and blood and tissue from outside the body. These substances contain antigens. The immune system producesantibodiesagainst these antigens that enable it to destroy these harmful substances. When you have an autoimmune disorder, your immune system does not distinguish between healthy tissue and antigens. As a result, the body sets off a reaction that destroys normal tissues. The exact cause of autoimmune disorders is unknown. One theory is that some microorganisms (such as bacteria or viruses) or drugs may trigger changes that confuse the immune system. This may happen more often in people who have genes that make them more prone toautoimmune disorders.

An autoimmune disorder may result in:

A person may have more than one autoimmune disorder at the same time. Common autoimmune disorders include:

RelatedImmunology Conferences|Immunologists Meetings|Conference Series LLC:

9thworld congress & expo on Immunology, Oct 02-04, 2017, Toronto, Canada; 3rdAntibodies and Bio Therapeutics Congress, November 02-03, 2017 Las Vegas, USA; Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; 3nd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 18th International Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; British Society for Immunology Congress, Dec 06-09, 2016, Liverpool, United Kingdom; 7thInternational Conference on Allergy, Asthma and Clinical Immunology; Cancer Immunology and Immunotherapy: Taking a Place in Mainstream Oncology (C7), March 19 - 23, 2017, Whistler, British Columbia, Canada

Track: 11Costimmulatory pathways in multiple sclerosis

Costimulatory moleculescan be categorized based either on their functional attributes or on their structure. The costimulatory molecules discussed in this review will be divided into (1)positive costimulatory pathways:promoting T cell activation, survival and/or differentiation; (2)negative costimulatory pathways:antagonizing TCR signalling and suppressing T cell activation; (3) as third group we will discuss themembers of the TIM family, a rather new family of cell surface molecules involved in the regulation of T cell differentiation and Treg function.Costimulatory pathways have a critical role in the regulation of alloreactivity. A complex network of positive and negative pathways regulates T cell responses. Blocking costimulation improves allograft survival in rodents and non-human primates. The costimulation blocker belatacept is being developed asimmunosuppressivedruginrenal transplantation.

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3rdAntibodies and Bio Therapeutics Congress, November 02-03, 2017 Las Vegas, USA; Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 3rd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 2nd Autoimmunity Conference, Nov 9-10, 2017 Madrid, Spain; Integrating Metabolism and Immunity , May 29 - June 2, 2017 | Dublin, Ireland; American Academy of Allergy, Asthma & Immunology (AAAAI) Annual Meeting, March 03-06, 2017, Atlanta, Georgia

Track: 12Autoimmunity and Therapathies

Autoimmunityis the system ofimmuneresponsesof an organism against its own cells and tissues. Any disease that results from such an aberrantimmuneresponse is termed an autoimmune disease.

Autoimmunity is present to some extent in everyone and is usually harmless. However, autoimmunity can cause a broad range of human illnesses, known collectively as autoimmune diseases.Autoimmune diseasesoccur when there is progression from benign autoimmunity to pathogenic autoimmunity. This progression is determined by genetic influences as well as environmental triggers. Autoimmunity is evidenced by the presence of autoantibodies (antibodies directed against the person who produced them) and T cells that are reactive with host antigens.

Current treatments for allergic and autoimmune disease treat disease symptoms or depend on non-specific immune suppression. Treatment would be improved greatly by targeting the fundamental cause of the disease, that is the loss of tolerance to an otherwise innocuous antigen in allergy or self-antigen in autoimmune disease (AID). Much has been learned about the mechanisms of peripheral tolerance in recent years. We now appreciate that antigen presenting cells (APC) may be either immunogenic or tolerogenic, depending on their location, environmental cues and activation state

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3rdAntibodies and Bio Therapeutics Congress, November 02-03, 2017 Las Vegas, USA; Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 3rd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 2nd Autoimmunity Conference, Nov 9-10, 2017 Madrid, Spain; Integrating Metabolism and Immunity , May 29 - June 2, 2017 | Dublin, Ireland; American Academy of Allergy, Asthma & Immunology (AAAAI) Annual Meeting, March 03-06, 2017, Atlanta, Georgia

Track: 13DiagnosticImmunology

Diagnostic Immunology. Immunoassays are laboratory techniques based on the detection of antibody production in response to foreign antigens. Antibodies, part of the humoral immune response, are involved in pathogen detection and neutralization.

Diagnostic immunology has considerably advanced due to the development of automated methods.New technology takes into account saving samples, reagents, and reducing cost.The future of diagnosticimmunologyfaces challenges in the vaccination field for protection against HIV and asanti-cancer therapy. Modern immunology relies heavily on the use of antibodies as highly specific laboratory reagents. The diagnosis of infectious diseases, the successful outcome of transfusions and transplantations, and the availability of biochemical and hematologic assays with extraordinary specificity and sensitivity capabilities all attest to the value of antibody detection.Immunologic methods are used in the treatment and prevention ofinfectious diseasesand in the large number of immune-mediated diseases. Advances in diagnostic immunology are largely driven by instrumentation, automation, and the implementation of less complex and more standardized procedures.

Examples of such processes are as follows:

These methods have facilitated the performance of tests and have greatly expanded the information that can be developed by a clinical laboratory. The tests are now used for clinical diagnosis and the monitoring of therapies and patient responses. Immunology is a relatively young science and there is still so much to discover. Immunologists work in many different disease areas today that include allergy, autoimmunity, immunodeficiency, transplantation, and cancer.

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3nd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 19thInternational Conference on Immunology (ICI) Sept 14-17, 2017, Berlin, Germany; Modelling Viral Infections and Immunity (E1) , May 1 - 4, 2017 | Estes Park, Colorado, USA; 7thInternational Conference on Allergy, Asthma and Clinical Immunology; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand

Track: 14Allergy and Therapathies

Although medications available for allergy are usually very effective, they do not cure people of allergies. Allergenimmunotherapyis the closest thing we have for a "cure" for allergy, reducing the severity of symptoms and the need for medication for many allergy sufferers. Allergen immunotherapy involves the regular administration of gradually increasing doses of allergen extracts over a period of years. Immunotherapy can be given to patients as an injection or as drops or tablets under the tongue (sublingual).Allergen immunotherapy changes the way the immune system reacts to allergens, by switching off allergy. The end result is that you become immune to the allergens, so that you can tolerate them with fewer or no symptoms. Allergen immunotherapy is not, however, a quick fix form of treatment. Those agreeing to allergen immunotherapy need to be committed to 3-5 years of treatment for it to work, and to cooperate with your doctor to minimize the frequency of side effects.Allergen immunotherapyis usually recommended for the treatment of potentially life threatening allergic reactions to stinging insects. Published data on allergen immunotherapy injections shows that venom immunotherapy can reduce the risk of a severe reaction in adults from around 60 % per sting, down to less than 10%. In Australia and New Zealand,venom immunotherapyis currently available for bee and wasp allergy. Jack Jumper Ant immunotherapy is available in Tasmania for Tasmanian residents. Allergen immunotherapy is often recommended for treatment ofallergic rhinitis

RelatedImmunology Conferences|Immunologists Meetings|Conference Series LLC:

Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; 3nd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 19thInternational Conference on Immunology (ICI) Sept 14-17, 2017, Berlin, Germany; Modelling Viral Infections and Immunity (E1) , May 1 - 4, 2017 | Estes Park, Colorado, USA; 7thInternational Conference on Allergy, Asthma and Clinical Immunology; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand

Track: 15Technological Innovations inImmunology

Immunology is the branch of biomedical sciences concerned with all aspects of the immune system in all multicellular organisms. Immunology deals with physiological functioning of the immune system in states of both health and disease as well as malfunctions of the immune system in immunological disorders like allergies, hypersensitivities, immune deficiency, transplant rejection andautoimmune disorders.

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9thworld congress & expo on Immunology, Oct 02-04, 2017, Toronto, Canada; 3rdAntibodies and Bio Therapeutics Congress, November 02-03, 2017 Las Vegas, USA; Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 3rd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 2nd Autoimmunity Conference, Nov 9-10, 2017 Madrid, Spain; Integrating Metabolism and Immunity , May 29 - June 2, 2017 | Dublin, Ireland; American Academy of Allergy, Asthma & Immunology (AAAAI) Annual Meeting, March 03-06, 2017, Atlanta, Georgia

Track:16Antigen Processing

Antigen processingis an immunologicalprocessthat prepares antigensfor presentation to special cells of the immune system called T lymphocytes. It is considered to be a stage ofantigenpresentation pathways. The process by which antigen-presenting cells digest proteins from inside or outside the cell and display the resulting antigenic peptide fragments on cell surface MHC molecules for recognition by T cells is central to the body's ability to detect signs of infection or abnormal cell growth. As such, understanding the processes and mechanisms of antigen processing and presentation provides us with crucial insights necessary for the design ofvaccines and therapeutic strategiesto bolster T-cell responses.

RelatedImmunology Conferences|Immunologists Meetings|Conference Series LLC:

3rdAntibodies and Bio Therapeutics Congress, November 02-03, 2017 Las Vegas, USA; Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 3rd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 2nd Autoimmunity Conference, Nov 9-10, 2017 Madrid, Spain; Integrating Metabolism and Immunity , May 29 - June 2, 2017 | Dublin, Ireland; American Academy of Allergy, Asthma & Immunology (AAAAI) Annual Meeting, March 03-06, 2017, Atlanta, Georgia

Track: 17Immunoinformatics and Systems Immunology

Immunoinformaticsis a branch ofbioinformaticsdealing with in silico analysis and modelling of immunological data and problems Immunoinformatics includes the study and design of algorithms for mapping potential B- andT-cell epitopes, which lessens the time and cost required for laboratory analysis of pathogen gene products. Using this information, an immunologist can explore the potential binding sites, which, in turn, leads to the development of newvaccines. This methodology is termed reversevaccinology and it analyses the pathogen genome to identify potential antigenic proteins.This is advantageous because conventional methods need to cultivate pathogen and then extract its antigenic proteins. Although pathogens grow fast, extraction of their proteins and then testing of those proteins on a large scale is expensive and time consuming. Immunoinformatics is capable of identifying virulence genes and surface-associated proteins.

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9thworld congress & expo on Immunology, Oct 02-04, 2017, Toronto, Canada; 3rdAntibodies and Bio Therapeutics Congress, November 02-03, 2017 Las Vegas, USA; Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; 3nd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 18th International Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; British Society for Immunology Congress, Dec 06-09, 2016, Liverpool, United Kingdom; 7thInternational Conference on Allergy, Asthma and Clinical Immunology; Cancer Immunology and Immunotherapy: Taking a Place in Mainstream Oncology (C7), March 19 - 23, 2017, Whistler, British Columbia, Canada

Track: 18Rheumatology

Rheumatology represents a subspecialty in internal medicine and pediatrics, which is devoted to adequate diagnosis andtherapy of rheumatic diseases(including clinical problems in joints, soft tissues, heritable connective tissue disorders, vasculitis and autoimmune diseases). This field is multidisciplinary in nature, which means it relies on close relationships with other medical specialties.The specialty of rheumatology has undergone a myriad of noteworthy advances in recent years, especially if we consider the development of state-of-the-art biological drugs with novel targets, made possible by rapid advances in the basic science of musculoskeletal diseases and improved imaging techniques.

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Molecular Immunology & Immunogenetics Congress, March 20-21, 2017 Rome, Italy; 3nd International Congress on Neuroimmunology and Therapeutics, September 18-19, 2017 Philadelphia, USA; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand; Annual Meeting on Immunology and Immunologist, July 03-05, 2017 Malyasia, Kuala lumpur; 19thInternational Conference on Immunology (ICI) Sept 14-17, 2017, Berlin, Germany; Modelling Viral Infections and Immunity (E1) , May 1 - 4, 2017 | Estes Park, Colorado, USA; 7thInternational Conference on Allergy, Asthma and Clinical Immunology; 18thInternational Conference on Immunology (ICI) Dec 12-13, 2016, Bangkok, Thailand

Track: 19Nutritional Immunology

Nutritional immunologyis an emerging discipline that evolved with the study of the detrimental effect of malnutrition on the immune system. The clinical and public health importance of nutritional immunology is also receiving attention. Immune system dysfunctions that result from malnutrition are, in fact, NutritionallyAcquired Immune Deficiency Syndromes(NAIDS). NAIDS afflicts millions of people in the Third World, as well as thousands in modern centers, i.e., patients with cachexia secondary to serious disease, neoplasia or trauma. The human immune system functions to protect the body against foreign pathogens and thereby preventing infection and disease. Optimal functioning of the immune system, both innate and adaptive immunity, is strongly influenced by an individuals nutritional status, with malnutrition being the most common cause of immunodeficiency in the world. Nutrient deficiencies result in immunosuppression and dysregulation of the immune response including impairment of phagocyte function and cytokine production, as well as adversely affecting aspects of humoral and cell-mediated immunity. Such alterations in immune function and the resulting inflammation are not only associated with infection, but also with the development of chronic diseases including cancer, autoimmune disease, osteoporosis, disorders of the endocrine system andcardiovascular disease.

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