Findings from animal study have implications for disorders such as chronic obstructive pulmonary disease

IMAGE:Adult lung cells regenerating: Type 1 cells are green. Type 2 cells are red. New Type 2 derived from Type 1 cells are yellow. Nuclei are blue view more

Credit: Jon Epstein, MD & Rajan Jain, MD, Perelman School of Medicine at the University of Pennsylvania, and Christina Barkauskas & Brigid Hogan, Duke University

PHILADELPHIA - A new collaborative study describes a way that lung tissue can regenerate after injury. The team found that lung tissue has more dexterity in repairing tissue than once thought. Researchers from the Perelman School of Medicine at the University of Pennsylvania and Duke University, including co-senior authors Jon Epstein, MD, chair of the department of Cell and Developmental Biology, and Brigid L.M Hogan, Duke Medicine, along with co-first authors Rajan Jain, MD, a cardiologist and instructor in the Department of Medicine and Christina E. Barkauskas, also from Duke, report their findings in Nature Communications

"It's as if the lung cells can regenerate from one another as needed to repair missing tissue, suggesting that there is much more flexibility in the system than we have previously appreciated," says Epstein. "These aren't classic stem cells that we see regenerating the lung. They are mature lung cells that awaken in response to injury. We want to learn how the lung regenerates so that we can stimulate the process in situations where it is insufficient, such as in patients with COPD [chronic obstructive pulmonary disease]."

The two types of airway cells in the alveoli, the gas-exchanging part of the lung, have very different functions, but can morph into each other under the right circumstances, the investigators found. Long, thin Type 1 cells are where gases (oxygen and carbon dioxide) are exchanged - the actual breath. Type 2 cells secrete surfactant, a soapy substance that helps keep airways open. In fact, premature babies need to be treated with surfactant to help them breathe.

The team showed in mouse models that these two types of cells originate from a common precursor stem cell in the embryo. Next, the team used other mouse models in which part of the lung was removed and single cell culture to study the plasticity of cell types during lung regrowth. The team showed that Type 1 cells can give rise to Type 2 cells, and vice-versa.

The Duke team had previously established that Type 2 cells produce surfactant and function as progenitors in adult mice, demonstrating differentiation into gas-exchanging Type 1 cells. The ability of Type I cells to give rise to alternate lineages had not been previously reported.

"We decided to test that hypothesis about Type 1 cells," says Jain. "We found that Type 1 cells give rise to the Type 2 cells over about three weeks in various models of regeneration. We saw new cells growing back into these new areas of the lung. It's as if the lung knows it has to grow back and can call into action some Type 1 cells to help in that process."

This is one of the first studies to show that a specialized cell type that was thought to be at the end of its ability to differentiate can revert to an earlier state under the right conditions. In this case, it was not by using a special formula of transcription factors, but by inducing damage to tell the body to repair itself and that it needs new cells of a certain type to do that.

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One type of airway cell can regenerate another lung cell type

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Newswise PHILADELPHIA A new collaborative study describes a way that lung tissue can regenerate after injury. The team found that lung tissue has more dexterity in repairing tissue than once thought. Researchers from the Perelman School of Medicine at the University of Pennsylvania and Duke University, including co-senior authors Jon Epstein, MD, chair of the department of Cell and Developmental Biology, and Brigid L.M Hogan, Duke Medicine, along with co-first authors Rajan Jain, MD, a cardiologist and instructor in the Department of Medicine and Christina E. Barkauskas, also from Duke, report their findings in Nature Communications.

Its as if the lung cells can regenerate from one another as needed to repair missing tissue, suggesting that there is much more flexibility in the system than we have previously appreciated, says Epstein. These arent classic stem cells that we see regenerating the lung. They are mature lung cells that awaken in response to injury. We want to learn how the lung regenerates so that we can stimulate the process in situations where it is insufficient, such as in patients with COPD [chronic obstructive pulmonary disease].

The two types of airway cells in the alveoli, the gas-exchanging part of the lung, have very different functions, but can morph into each other under the right circumstances, the investigators found. Long, thin Type 1 cells are where gases (oxygen and carbon dioxide) are exchanged the actual breath. Type 2 cells secrete surfactant, a soapy substance that helps keep airways open. In fact, premature babies need to be treated with surfactant to help them breathe.

The team showed in mouse models that these two types of cells originate from a common precursor stem cell in the embryo. Next, the team used other mouse models in which part of the lung was removed and single cell culture to study the plasticity of cell types during lung regrowth. The team showed that Type 1 cells can give rise to Type 2 cells, and vice-versa.

The Duke team had previously established that Type 2 cells produce surfactant and function as progenitors in adult mice, demonstrating differentiation into gas-exchanging Type 1 cells. The ability of Type I cells to give rise to alternate lineages had not been previously reported.

We decided to test that hypothesis about Type 1 cells, says Jain. We found that Type 1 cells give rise to the Type 2 cells over about three weeks in various models of regeneration. We saw new cells growing back into these new areas of the lung. Its as if the lung knows it has to grow back and can call into action some Type 1 cells to help in that process.

This is one of the first studies to show that a specialized cell type that was thought to be at the end of its ability to differentiate can revert to an earlier state under the right conditions. In this case, it was not by using a special formula of transcription factors, but by inducing damage to tell the body to repair itself and that it needs new cells of a certain type to do that.

The team is also applying the approaches outlined in this paper to cells in the intestine and skin to study basic ideas of stem cell maintenance and differentiation to relate back to similar mechanisms in the heart. They also hope to apply this knowledge to such other lung conditions as acute respiratory distress syndrome and idiopathic pulmonary fibrosis, where the alveoli cannot get enough oxygen into the blood.

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Limber Lungs: One Type of Airway Cell Can Regenerate Another Lung Cell Type

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NYC, NY (PRWEB) April 13, 2015

NYC Health & Longevity Center is now offering outpatient stem cell therapy to help patients avoid joint replacement in all extremities. The treatments are performed by a Board Certified physician, with most patients being able to avoid or delay the need for surgery. Simply call (844) GET-STEM for more information and scheduling with stem cell therapy NYC trusts.

Millions of joint replacements are performed in the US annually for degenerative arthritis of the knee, hip, shoulder, elbow, wrist and ankle. While these are mostly effective, they are not risk free procedures and should be avoided as long as possible. In addition, the implants placed are not meant to last forever.

With stem cell therapy now being commercially available, individuals now have access to the most cutting-edge procedures with the potentially to actually regenerate damaged tissue. This includes cartilage, ligament and tendon.

The stem cell procedures are performed by a Board Certified Anti-Aging doctor with considerable experience in both the stem cell procedures along with prolotherapy too.

The stem cell material comes from amniotic fluid that is obtained from consenting donors after a scheduled C-section, which is then processed at an FDA regulated lab. No fetal tissue or embryonic stem cells are used, eliminating any ethical concerns. Amniotic fluid causes no rejection, and has a very high amount of stem cells, growth factors and anti-inflammatory effects. The overall result is typically tremendous pain reduction and functional improvements that are long lasting.

Stem cell therapy for arthritis is performed on an outpatient basis, with absolutely minimal risk. The procedure takes less than a half hour, with patients able to return to desired activities quickly.

Along with degenerative arthritis, the stem cell procedures also help rheumatoid arthritis along with tendonitis of the rotator cuff, Achilles, elbow and knee. Athletes benefit from typically being able to avoid surgery and get back their sport much faster than with conventional treatments.

For more information on stem cell therapy at NYC Health & Longevity Center for extremity arthritis of the hips, knees, shoulders, elbow, wrist or ankle, call (844) GET-STEM.

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NYC Health & Longevity Center Now Offering Stem Cell Therapy to Avoid Joint Replacement

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Accelerating the Promise of Personalized Medicine
CNN #39;s Chief Medical Correspondent Dr. Sanjay Gupta extends his "60 Minutes Overtime" conversation with renowned Dr. Patrick Soon-Shiong, who is developing the revolutionary approach to cancer...

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Personalized Medicine for Melanoma Aims at Keeping the Immune System Awake
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U.S. Stem Cell Clinic: What Conditions Can Be Treated?
tem cells have the unique attribute to form many different types of tissue including bone, cartilage, and muscle. They are naturally anti-inflammatory and can therefore help in the body #39;s...

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Who We Are at World Stem Cells, LLC

Advanced stem cell treatments offered by Would Stem Cells, LLC a patient management company for qualified patients at the medical facilities World Stem Cells Clinic, http://worldstemcellsclinic.comin Cancun provides an opportunity for a better quality of life. The clinic and laboratory were designed, built and are operated under the stringent guidelines as established by USFederal Regulations Title 21, Subpart C, 211-42 through 211-58,and the US Federal Drug Administrations Good Tissue Practice (cGTP)regulations for pharmaceutical, biologics and clinical laboratories. The strict adherence to these established guidelines and policies guarantees the highest quality of clinical care and stem cell treatment safety for you. Check out our clinic locations at http://worldstemcells.com/locations.html

What Is Done

World Stem Cells Clinics medical staff and clinical physicians will examine you and review all available medical records, radiology films, CT scans and other diagnostic information to assess if stem cell therapy will be a helpful primary treatment or adjunctive therapy for your specific condition.

Then, the medical doctors meet and confer with the research scientists for a pre-treatment planning meeting. This Stem cell treatment planning conference takes advantage of decades of the staffs clinical experience, your current condition, your available social support system, full review of your medical history as well as an inclusion and consideration of any recently published research literature on stem cell treatments. In other words, you are provided a detailed, systematic and entirely unique treatment care plan for his or her needs.

Creating the best treatment

Sorry, they do not perform a one or two day treatment as it would not be medically sound and could not provide the benefits or safety that the World Stem Cells Clinic treatment schedule gives (please do not be fooled). Your Stem Cell Treatment at World Stem Cells Clinic takes 5 days to complete as the treatments are comprehensive and designed to maximize the benefits and safety you derive from the process.

How Is It Done

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Theres been a lot of talk lately about how spider silk is this crazy wonder material that may soon find its way into everything from electronics to ultra-strong fabrics. Now, theres another reason to be excited about spider silk: doctors might one day use the stuff to grow you a new heart.

Growing new organs and tissues outside the body is the bleeding edge of biomedical research. Just imagine: if doctors could grow replacement hearts or kidneys from a patients own stem cells, that patient would no longer have to face the agonizing prospect of waiting to find a suitable donor. The risk of organ rejection would become nil. But theres a lot of R&D to be done before we get there. One initial challenge has been finding a scaffold material to grow organ tissues onsomething thats non-toxic, will not impede cell growth, and will not, itself, be rejected by the body. That, it turns out, is a pretty tall order.

But, as described in a study published recently in PLOS ONE, genetically engineered fibers of spidrointhe protein that builds cobweb strandsmight just fit the bill when it comes to human heart tissue. Spidroin fibers have already proven themselves a useful substrate for growing tendons and cartilages. Researchers at the Moscow Institute for Physics and Technology decided to see whether spidroin grown in the lab via genetically modified yeast cells can also be used to grow cardiomycetes, the cells that form heart tissue.

Heart tissue cells grown on a matrix and stained with fluorescent markers via Alexander Teplenin et al. / PLOS ONE

For their experiments, the researchers seeded a spidroin fiber matrix with neonatal rat cardiomycetes. Within 3 to 5 days, a layer of cardiac cells had formed. Follow-up tests determined that this tissue was able to contract synchronously and conduct electrical impulses, just like normal heart tissue should

Itll probably be some years yet before were growing full human hearts on any sort of artificial scaffold, but its exciting to see that progress is being made toward that goal. If the idea of an artificial heart thats stitched together with spider webs sounds a bit creepy, know this: those fibers are five times stronger than steel and twice as elastic as nylon. If anything, it sounds like an upgrade.

Read the full open-access scientific paper at PLOS ONE.

Top image via Shutterstock

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In The Future, Spider Silk May Help Grow Your Replacement Heart

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Next month Mr Brown and his wife will attend the wedding in the United States as very special guests.

He joined the Anthony Nolan register in the late 1980s when his baby son Michael - now 33 - was being treated for cancer.

A few years later, in 1991, he received a call to tell him that he was a match for a patient in the USA who was in desperate need of a transplant.

Mr Brown agreed to donate and travelled to the Harley Street Clinic in London to make the lifesaving donation.

He gave his bone marrow on the morning of May 17, 1991, and it was immediately picked up by a courier who flew over to the USA on Concorde, on a journey of more than 3,500 miles, which allowed the patient to have his transplant that evening.

Mr Brown said: It was so rewarding after making the donation, I went round with a huge smile on my face for six months.

Following the donation, the sales manager learned that his bone marrow had gone to a 44-year-old man called Rick Haines who lived in Delaware and who was suffering from aplastic anaemia.

Afterwards, Mr Haines, an engineer in the motor industry, contacted Mr Brown to thank him.

Mr Haines, now 68, explained that he had feared he would not live to see his young daughter walk down the aisle, and a deal was struck.

Donor organs from cancer patients should be transplanted despite risks

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Bone marrow donation ends in a wedding promise

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Stem Cell Therapy For Pain - Columbia Pain Management, Hood River OR
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Meet #39;Cookie: #39; Healing Through Stem-Cell Therapy
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The U.S. Stem Cell Clinic is founded on the principle belief that the quality of life for our patients can be improved through stem cell therapy. We are dedicated to providing safe and effective...

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last revised December 20, 2000 Management of Patients with Sickle Cell Disease An Overview Contents Background Nature of the Problem Modulators of SCD Severity Origin of the Sickle Mutation Management of Acute Problems Pain Acute chest syndrome Infection Bone marrow necrosis Stroke Splenic sequestration crisis Aplastic crisis Hepatic sequestration crisis Priapism Management of Chronic Problems Pain Anemia infection prophylaxis Avascular bone necrosis Osteomyelitis skin ulcers Renal dysfunction Retinopathy Heart Pregnancy Newer Therapies Hydroxyurea Erythropoietin Butyrate Clotrimazole Nitric Oxide FluocorTM Bone marrow transplantation Gene replacement therapy References Background Nature of the Problem Sickle cell disease (SCD) results from the substitution of a valine residue for glutamic acid at position 6 in the beta-subunit of hemoglobin (Ingram, 1956). With a few minor exceptions, people with only one gene for hemoglobin S (Hb S) are phenotypically normal (sickle trait). People who inherit two Hb S genes from their parents have sickle cell disease. Deoxygenated Hb S tends to polymerize non-covalently into long strands that deform the erythrocyte, giving the characteristic "sickle cell" morphology (Eaton and Hofrichter, 1990). Hb S with bound oxygen (e.g., in the arterial circulation) does not polymerize.

The mechanism by which these changes in the physical properties of the hemoglobin molecule produce the clinical manifestations of the disease is not unequivocally proven. The most widely accepted hypothesis is that erythrocytes deform as they release their oxygen in the capillaries and are trapped in the microcirculation (Eaton et al., 1976) (Kaul et al., 1989). The blockade of blood flow produces areas of tissue ischemia, leading to the myriad of clinical problems seen with sickle cell disease. Although a good deal of indirect evidence supports this theory, definitive proof that this is the pathophysiologic mechanism in sickle cell disease is lacking.

Recently, investigators have focused on other factors outside the red cell that could contribute to the manifestations of sickle cell disease. Hebbel and colleagues first showed that sickle erythrocytes adhere abnormally to vascular endothelial cells. Their observations were confirmed and extended by other workers. The endothelial cells may abnormally express adhesion receptors, perhaps in response to activators released from sickle red cells (e.g., reactive oxygen species). Other investigators have focused on leucocytes and platelets which might also contribute to disturbed blood flow in sickle cell disease. The involvement of multiple components of the blood in the manifestations of sickle cell disease makes understanding the pathophysiology more difficult. On the other hand, these additional modulators could be targeted by new therapies, with diminution in the severity of sickle cell symptoms.

Sickle cell disease is extremely varied in its manifestations (Ballas, 1991) (Wethers, 1982). This includes both the organ systems that are affected as well as the severity of the affliction. A study of the natural history of sickle cell disease indicated that about 5% of patients account for nearly one-third of hospital admissions (Platt et al., 1991). A significant number of patients with the disease have few admissions and live productive and relatively healthy lives. The average life-span of people with sickle cell disease is shorter than normal, however, reflecting increased mortality due to the complications of the disease.

Patients with sickle cell disease who also have hereditary persistence of fetal hemoglobin (HPFH) often have few if any symptoms (Stamatoyannopoulos et al., 1975). In these individuals, Hb F usually comprises greater than 20% of the hemoglobin in the erythrocytes. Patients may be partially protected from the ravages of sickle cell disease with even lower levels of Hb F. Unfortunately, few patients with SCD have Hb F levels of greater than 10 or 11% in the absence of HPFH.

Fetal Hb disrupts the polymerization of deoxy-Hb-S (Goldberg et al., 1977). Since polymerization of deoxy-Hb-S is the signal event in the pathogenesis of SCD, fetal Hb effectively prevents disease manifestation. The distribution of Hb F among RBCs is also important. In hereditary persistence of fetal hemoglobin (HPFH), Hb F exists at high levels in all red cells. All red cells are equally protected from sickling. In the absence of HPFH, patients with high levels of Hb F have a heterogeneous distribution of fetal hemoglobin between cells. An over simplified example is a patient in whom half the cells have 30% Hb F and half have 0%. The patient would have 15% Hb F overall. However, half the cells would sickle and occlude flow through the microcirculation. These deformed cells would block the flow of the normally shaped high Hb F cells. The patient would experience all the manifestations of sickle cell disease.

The relationship of stroke risk to high blood velocity in the intracranial arteries is discussed below.

No clear explanation exists for the differences in average severity between the haplotypes. The mutations in the flanking region could secondarily affect severity by altering Hb F expression in the cells. This is only a hypothesis, however. The patterns of severity apply only to populations. Broad overlap in the clinical patterns prevents the use of haplotypes to predict the clinical course in a particular person. Usually, people with sickle cell disease outside Africa (e.g., blacks in the United States) or India have mixed haplotypes for their sickle cell genes. Analysis of haplotype in this setting is even less likely to provide clinically useful information.

Hb S is common in some areas of the Mediterranean basin, including regions of Italy, Greece, Albania and Turkey (Boletini et al., 1994) (Schiliro et al., 1990). Haplotype analysis shows that the Hb S in these areas originated in Africa. The genes probably moved along ancient trading routes between wealthy kingdoms in western Africa and the trade centers in the Mediterranean basin. The high levels of Hb S attained in some areas reflects partial protection against protection against malaria provided by sickle cell trait (see below).

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B1 Genetic Engineering (AQA)
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