Mesenchymal stem cells in the treatment of spinal cord …
By LizaAVILA
World J Stem Cells. 2014 Apr 26; 6(2): 120133.
Venkata Ramesh Dasari, Krishna Kumar Veeravalli, Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, IL 61656, United States
Dzung H Dinh, Department of Neurosurgery and Illinois Neurological Institute, University of Illinois College of Medicine at Peoria, Peoria, IL 61656, United States
Correspondence to: Dzung H Dinh, MD, Department of Neurosurgery and Illinois Neurological Institute, University of Illinois College of Medicine at Peoria, One Illini Drive, Peoria, IL 61605, United States. ude.ciu@hnidd
Telephone: +1- 309-6552642 Fax: +1-309-6713442
Received 2013 Oct 30; Revised 2014 Feb 19; Accepted 2014 Mar 11.
With technological advances in basic research, the intricate mechanism of secondary delayed spinal cord injury (SCI) continues to unravel at a rapid pace. However, despite our deeper understanding of the molecular changes occurring after initial insult to the spinal cord, the cure for paralysis remains elusive. Current treatment of SCI is limited to early administration of high dose steroids to mitigate the harmful effect of cord edema that occurs after SCI and to reduce the cascade of secondary delayed SCI. Recent evident-based clinical studies have cast doubt on the clinical benefit of steroids in SCI and intense focus on stem cell-based therapy has yielded some encouraging results. An array of mesenchymal stem cells (MSCs) from various sources with novel and promising strategies are being developed to improve function after SCI. In this review, we briefly discuss the pathophysiology of spinal cord injuries and characteristics and the potential sources of MSCs that can be used in the treatment of SCI. We will discuss the progress of MSCs application in research, focusing on the neuroprotective properties of MSCs. Finally, we will discuss the results from preclinical and clinical trials involving stem cell-based therapy in SCI.
Keywords: Spinal cord injury, Mesenchymal stem cells, Bone marrow stromal cells, Umbilical cord derived mesenchymal stem cells, Adipose tissue derived mesenchymal stem cells
Core tip: Despite our deeper understanding of the molecular changes that occurs after the spinal cord injury (SCI), the cure for paralysis remains elusive. In this review, the pathophysiology of SCI and characteristics and potential sources of mesenchymal stem cells (MSCs) that can be used in the treatment of SCI were discussed. We also discussed the progress of application of MSCs in research focusing on the neuroprotective properties of MSCs. Finally, we discussed the results from preclinical and clinical trials involving stem cell-based therapy in SCI.
Traumatic spinal cord injury (SCI) continues to be a devastating injury to affected individuals and their families and exacts an enormous financial, psychological and emotional cost to them and to society. Despite years of research, the cure for paralysis remains elusive and current treatment is limited to early administration of high dose steroids and acute surgical intervention to minimize cord edema and the subsequent cascade of secondary delayed injury[1-3]. Recent advances in neurosciences and regenerative medicine have drawn attention to novel research methodologies for the treatment of SCI. In this review, we present our current understanding of spinal cord injury pathophysiology and the application of mesenchymal stem cells (MSCs) in the treatment of SCI. This review will be more useful for basic and clinical investigators in academia, industry and regulatory agencies as well as allied health professionals who are involved in stem cell research.
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July 13th, 2015
Haematopoietic stem cells and early lymphoid progenitors …
By Sykes24Tracey
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July 12th, 2015
Non-Small Cell Lung Cancer Treatment – National Cancer …
By daniellenierenberg
General Information About Non-Small Cell Lung Cancer (NSCLC)
NSCLC is any type of epithelial lung cancer other than small cell lung cancer (SCLC). The most common types of NSCLC are squamous cell carcinoma, large cell carcinoma, and adenocarcinoma, but there are several other types that occur less frequently, and all types can occur in unusual histologic variants. Although NSCLCs are associated with cigarette smoke, adenocarcinomas may be found in patients who have never smoked. As a class, NSCLCs are relatively insensitive to chemotherapy and radiation therapy compared with SCLC. Patients with resectable disease may be cured by surgery or surgery followed by chemotherapy. Local control can be achieved with radiation therapy in a large number of patients with unresectable disease, but cure is seen only in a small number of patients. Patients with locally advanced unresectable disease may achieve long-term survival with radiation therapy combined with chemotherapy. Patients with advanced metastatic disease may achieve improved survival and palliation of symptoms with chemotherapy, targeted agents, and other supportive measures.
Estimated new cases and deaths from lung cancer (NSCLC and SCLC combined) in the United States in 2014:[1]
Lung cancer is the leading cause of cancer-related mortality in the United States.[1] The 5-year relative survival rate from 1995 to 2001 for patients with lung cancer was 15.7%. The 5-year relative survival rate varies markedly depending on the stage at diagnosis, from 49% to 16% to 2% for patients with local, regional, and distant stage disease, respectively.[2]
NSCLC arises from the epithelial cells of the lung of the central bronchi to terminal alveoli. The histological type of NSCLC correlates with site of origin, reflecting the variation in respiratory tract epithelium of the bronchi to alveoli. Squamous cell carcinoma usually starts near a central bronchus. Adenocarcinoma and bronchioloalveolar carcinoma usually originate in peripheral lung tissue.
Anatomy of the respiratory system.
Smoking-related lung carcinogenesis is a multistep process. Squamous cell carcinoma and adenocarcinoma have defined premalignant precursor lesions. Before becoming invasive, lung epithelium may undergo morphological changes that include the following:
Dysplasia and carcinoma in situ are considered the principal premalignant lesions because they are more likely to progress to invasive cancer and less likely to spontaneously regress.
In addition, after resection of a lung cancer, there is a 1% to 2% risk per patient per year that a second lung cancer will occur.[3]
NSCLC is a heterogeneous aggregate of histologies. The most common histologies include the following:
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July 11th, 2015
Sickle-cell disease – Wikipedia, the free encyclopedia
By Sykes24Tracey
Sickle-cell disease (SCD), also known as sickle-cell anaemia (SCA) and drepanocytosis, is a hereditary blood disorder, characterized by an abnormality in the oxygen-carrying haemoglobin molecule in red blood cells. This leads to a propensity for the cells to assume an abnormal, rigid, sickle-like shape under certain circumstances. Sickle-cell disease is associated with a number of acute and chronic health problems, such as severe infections, attacks of severe pain ("sickle-cell crisis"), and stroke, and there is an increased risk of death.
Sickle-cell disease occurs when a person inherits two abnormal copies of the haemoglobin gene, one from each parent. Several subtypes exist, depending on the exact mutation in each haemoglobin gene. A person with a single abnormal copy does not experience symptoms and is said to have sickle-cell trait. Such people are also referred to as carriers.
The complications of sickle-cell disease can be prevented to a large extent with vaccination, preventive antibiotics, blood transfusion, and the drug hydroxyurea/hydroxycarbamide. A small proportion requires a transplant of bone marrow cells.
Almost 300,000 children are born with a form of sickle-cell disease every year, mostly in sub-Saharan Africa, but also in other parts of the world such as the West Indies and in people of African origin elsewhere in the world. In 2013 it resulted in 176,000 deaths up from 113,000 deaths in 1990.[1] The condition was first described in the medical literature by the American physician James B. Herrick in 1910, and in the 1940s and 1950s contributions by Nobel prize-winner Linus Pauling made it the first disease where the exact genetic and molecular defect was elucidated.
Sickle-cell disease may lead to various acute and chronic complications, several of which have a high mortality rate.[2]
The terms "sickle-cell crisis" or "sickling crisis" may be used to describe several independent acute conditions occurring in patients with SCD. SCD results in anemia and crises that could be of many types including the vaso-occlusive crisis, aplastic crisis, sequestration crisis, haemolytic crisis, and others. Most episodes of sickle-cell crises last between five and seven days.[3] "Although infection, dehydration, and acidosis (all of which favor sickling) can act as triggers, in most instances, no predisposing cause is identified."[4]
The vaso-occlusive crisis is caused by sickle-shaped red blood cells that obstruct capillaries and restrict blood flow to an organ resulting in ischaemia, pain, necrosis, and often organ damage. The frequency, severity, and duration of these crises vary considerably. Painful crises are treated with hydration, analgesics, and blood transfusion; pain management requires opioid administration at regular intervals until the crisis has settled. For milder crises, a subgroup of patients manage on NSAIDs (such as diclofenac or naproxen). For more severe crises, most patients require inpatient management for intravenous opioids; patient-controlled analgesia devices are commonly used in this setting. Vaso-occlusive crisis involving organs such as the penis[5] or lungs are considered an emergency and treated with red-blood cell transfusions. Incentive spirometry, a technique to encourage deep breathing to minimise the development of atelectasis, is recommended.[6]
Because of its narrow vessels and function in clearing defective red blood cells, the spleen is frequently affected.[7] It is usually infarcted before the end of childhood in individuals suffering from sickle-cell anemia. This spleen damage increases the risk of infection from encapsulated organisms;[8][9] preventive antibiotics and vaccinations are recommended for those lacking proper spleen function.
Splenic sequestration crises are acute, painful enlargements of the spleen, caused by intrasplenic trapping of red cells and resulting in a precipitous fall in hemoglobin levels with the potential for hypovolemic shock. Sequestration crises are considered an emergency. If not treated, patients may die within 12 hours due to circulatory failure. Management is supportive, sometimes with blood transfusion. These crises are transient, they continue for 34 hours and may last for one day.[10]
Acute chest syndrome (ACS) is defined by at least two of the following signs or symptoms: chest pain, fever, pulmonary infiltrate or focal abnormality, respiratory symptoms, or hypoxemia.[11] It is the second-most common complication and it accounts for about 25% of deaths in patients with SCD, majority of cases present with vaso-occlusive crises then they develop ACS.[12][13] Nevertheless, about 80% of patients have vaso-occlusive crises during ACS.
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July 11th, 2015
Non-small cell lung cancer | University of Maryland …
By JoanneRUSSELL25
Description
An in-depth report on the causes, diagnosis, treatment, and prevention of non-small cell lung cancer (NSCLC).
Lung cancer - non-small cell; NSCLC
Risk:
Treatment:
Although lung cancer accounts for only 15% of all newly-diagnosed cancers in the United States, it is the leading cause of cancer death in U.S. men and women. It is more deadly than colon, breast, and prostate cancers combined. About 160,000 patients die from lung cancer each year. Death rates have been declining in men over the past decade, and they have about stabilized in women.
The lungs are two spongy organs surrounded by a thin moist membrane called the pleura. Each lung is composed of smooth, shiny lobes: the right lung has three lobes, and the left has two. About 90% of the lung is filled with air. Only 10% is solid tissue.
The major features of the lungs include the bronchi, the bronchioles, and the alveoli. The alveoli are the microscopic blood vessel-lined sacks in which oxygen and carbon dioxide gas are exchanged.
Lung cancer develops when genetic mutations (changes) occur in a normal cell within the lung. As a result, the cell becomes abnormal in shape and behavior, and reproduces endlessly. The abnormal cells form a tumor that, if not surgically removed, invades neighboring blood vessels and lymph nodes and spreads to nearby sites. Eventually, the cancer can spread (metastasize) to locations throughout the body.
The two major categories of lung cancer are small cell lung cancer and non-small cell lung cancer. Most lung cancers are non-small cell cancer, the subject of this report. Less common cancers of the lung are known as carcinoids, cylindromas, and certain sarcomas (cancer in soft tissues). Some experts believe all primary lung cancers come from a single common cancerous (malignant) stem cell. As it copies itself, that stem cell can develop into any one of these cancer types in different people.
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July 11th, 2015
Peripheral-blood stem cells versus bone marrow from …
By Dr. Matthew Watson
See comment in PubMed Commons below N Engl J Med. 2012 Oct 18;367(16):1487-96. doi: 10.1056/NEJMoa1203517. Anasetti C, Logan BR, Lee SJ, Waller EK, Weisdorf DJ, Wingard JR, Cutler CS, Westervelt P, Woolfrey A, Couban S, Ehninger G, Johnston L, Maziarz RT, Pulsipher MA, Porter DL, Mineishi S, McCarty JM, Khan SP, Anderlini P, Bensinger WI, Leitman SF, Rowley SD, Bredeson C, Carter SL, Horowitz MM, Confer DL; Blood and Marrow Transplant Clinical Trials Network. Collaborators (182)
Horowitz MM, Carter SL, Confer DL, DiFronzo N, Wagner E, Merritt W, Wu R, Anasetti C, Logan BR, Lee SJ, Waller EK, Weisdorf DJ, Wingard JR, Couban S, Anderlini P, Bensinger WI, Leitman SF, Rowley SD, Carter SL, Karanes C, Horowitz MM, Confer DL, Allen C, Colby C, Gurgol C, Knust K, Foley A, King R, Mitchell P, Couban S, Pulsipher MA, Ehninger G, Johnston L, Khan SP, Maziarz RT, McCarty JM, Mineishi S, Porter DL, Bredeson C, Anasetti C, Lee S, Waller EK, Wingard JR, Cutler CS, Westervelt P, Woolfrey A, Logan BR, Carter SL, Lee SJ, Waller EK, Anasetti C, Logan BR, Lee SJ, Stadtmauer E, Wingard J, Vose J, Lazarus H, Cowan M, Wingard J, Westervelt P, Litzow M, Wu R, Geller N, Carter S, Confer D, Horowitz M, Poland N, Krance R, Carrum G, Agura E, Nademanee A, Sahdev I, Cutler C, Horwitz ME, Kurtzberg J, Waller EK, Woolfrey A, Rowley S, Brochstein J, Leber B, Wasi P, Roy J, Jansen J, Stiff PJ, Khan S, Devine S, Maziarz R, Nemecek E, Huebsch L, Couban S, McCarthy P, Johnston L, Shaughnessy P, Savoie L, Ball E, Vaughan W, Cowan M, Horn B, Wingard J, Silverman M, Abhyankar S, McGuirk J, Yanovich S, Ferrara J, Weisdorf D, Faber E Jr, Selby G, Rooms LM, Porter D, Agha M, Anderlini P, Lipton J, Pulsipher MA, Pulsipher MA, Shepherd J, Toze C, Kassim A, Frangoul H, McCarty J, Hurd D, DiPersio J, Westervelt P, Shenoy S, Agura E, Culler E, Axelrod F, Chambers L, Senaldi E, Nguyen KA, Engelman E, Hartzman R, Sutor L, Dickson L, Nademanee A, Khalife G, Lenes BA, Eames G, Sibley D, Gale P, Antin J, Ehninger G, Newberg NR, Gammon R, Montgomery M, Mair B, Rossmann S, Wada R, Waxman D, Ranlett R, Silverman M, Herzig G, Fried M, Atkinson E, Weitekamp L, Bigelow C, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Miller JP, Price T, Young C, Hilbert R, Oh D, Cable C, Smith JW, Kalmin ND, Schultheiss K, Beck T, Lankiewicz MW, Sharp D.
Randomized trials have shown that the transplantation of filgrastim-mobilized peripheral-blood stem cells from HLA-identical siblings accelerates engraftment but increases the risks of acute and chronic graft-versus-host disease (GVHD), as compared with the transplantation of bone marrow. Some studies have also shown that peripheral-blood stem cells are associated with a decreased rate of relapse and improved survival among recipients with high-risk leukemia.
We conducted a phase 3, multicenter, randomized trial of transplantation of peripheral-blood stem cells versus bone marrow from unrelated donors to compare 2-year survival probabilities with the use of an intention-to-treat analysis. Between March 2004 and September 2009, we enrolled 551 patients at 48 centers. Patients were randomly assigned in a 1:1 ratio to peripheral-blood stem-cell or bone marrow transplantation, stratified according to transplantation center and disease risk. The median follow-up of surviving patients was 36 months (interquartile range, 30 to 37).
The overall survival rate at 2 years in the peripheral-blood group was 51% (95% confidence interval [CI], 45 to 57), as compared with 46% (95% CI, 40 to 52) in the bone marrow group (P=0.29), with an absolute difference of 5 percentage points (95% CI, -3 to 14). The overall incidence of graft failure in the peripheral-blood group was 3% (95% CI, 1 to 5), versus 9% (95% CI, 6 to 13) in the bone marrow group (P=0.002). The incidence of chronic GVHD at 2 years in the peripheral-blood group was 53% (95% CI, 45 to 61), as compared with 41% (95% CI, 34 to 48) in the bone marrow group (P=0.01). There were no significant between-group differences in the incidence of acute GVHD or relapse.
We did not detect significant survival differences between peripheral-blood stem-cell and bone marrow transplantation from unrelated donors. Exploratory analyses of secondary end points indicated that peripheral-blood stem cells may reduce the risk of graft failure, whereas bone marrow may reduce the risk of chronic GVHD. (Funded by the National Heart, Lung, and Blood Institute-National Cancer Institute and others; ClinicalTrials.gov number, NCT00075816.).
Survival after Randomization in the Intention-to-Treat Analysis
The P value is from a stratified binomial comparison at the 2-year point. The P value from a stratified log-rank test was also not significant. A total of 75 patients in each group were still alive at 36 months.
N Engl J Med. 2012 October 18;367(16):10.1056/NEJMoa1203517.
Outcomes after Transplantation, According to Study Group
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July 8th, 2015
ProgeniDerm Anti-Senescence Skin Stem Cell Serum …
By NEVAGiles23
ProgeniDerm Anti-Senescence Skin Stem Cell Serum encourages new epidermal cell growth while protecting and prolonging the cell life of existing skin cells. Wrinkle depth is reduced, hyperpigmentation lightened, and collagen/elastin fibers become thicker and stronger. The ratio of older skin cells to younger skin cells is reversed. Skin looks visibly younger.
Elegantly formulated with fruit-derived Malus Domestica Fruit Stem Cell Extract, ProgeniDerm protects against chromosomal damage that signals skin cells to undergo apoptosis (cell death). Often this signal is sent prematurely due to free radical damage caused by UV light, smoke, stress, etc. With protection against this damage, existing skin cells live longer and more new cells are created.
The Malus Domestica Fruit Stem Cell Extract in ProgeniDerm restores aging skin stem cells regenerative properties. In-vitro and in-vivo testing showed that this new extract:
The ultimate result: skin that regains its ability to repair itself and regenerate new skin cells within two weeks. Substantially greater numbers of new epithelial cells are formed. Enzymes are released that protect cells from damage that shorten the skin cell life cycle. The addition of chondrus crispus (red seaweed/algae extract) and palmitoyl oligopeptide in a hyaluronic acid base combine to make our ProgeniDerm Anti-Senescence Skin Stem Cell serum a powerful new tool against premature aging.
Note: Epidermal skin stem cell DNA/chromosomal protection is the newest, most exciting direction for anti-aging products currently. Cellular Skin Rx is proud to be able to provide a serum containing this cutting-edge, naturally-derived extract to our customers. Now that peptides are firmly established as helpful to the skin for relaxing, firming, and reducing inflammation, using naturally-derived fruit stem cell extracts to prevent damage at the most basic cellular level is taking skin care to a whole new realm. You will see more and more of this approach to maintaining a younger complexion moving forward -with Cellular Skin Rx proudly providing you with products that incorporate these new Active Ingredients That Work.
After applying antioxidant serum of your choice, apply twice daily including eye area.
Combining with antioxidant serums such as C+ Firming serum or CSRx Antioxidant Complex yields best results.
Two weeks to gorgeous skin routine: Each morning use CSRx Antioxidant Defense Complex then C+ Firming serum, follow with ProgeniDerm Anti-Senescence Skin Stem Cell Serum, then any wrinkle-relaxers/firming products/moisturizers/sunscreen you regularly use. Each night use Age-Limit Advanced Refinishing serum or Ultra-Gentle Enzyme Surface Peel, then apply ProgeniDerm again. In just two weeks, you will see a visible difference in your skin tone, color, and texture.
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CVM Stem Cell Study Benefits Dogs with Spinal Cord Injuries
By JoanneRUSSELL25
Tobi is a six-year-old cocker spaniel whose hind legs were paralyzed after he suffered a herniated disc in his spine. Although Tobi will never fully regain the use of his legs, he has benefitted from a clinical trial involving stem cell transplantation in dogs that is currently underway at North Carolina State University.
See video presentation: Stem cell treatments for paralyzed dogs.
Dr. Natasha Olby, professor of neurology at the NC State College of Veterinary Medicine, specializes in researching treatments for long-term paralysis in dogs. According to Dr. Olby, even in the case of severe spinal cord injury all may not be lost in terms of spinal cord function there may still be salvageable, living nerves and nerve fibers, or axons, bridging the site of the injury that could still transmit signals if they had a little help.
Obviously, researchers would love to be able to replace all the lost neurons and axons and restore normal connections in a damaged spinal cord. But that sort of treatment is not yet possible. On the other hand, targeting surviving nerves and axons that are still crossing the site of the injury and restoring their conductivity is more attainable.
Often, these damaged nerves have lost the myelin sheath, fatty material that coats axons and allows them to conduct signals. Dr. Olby wants to restore the myelin sheath to these surviving axons by taking fat cells from the patient and turning them into stem cells that can be combined with nerve cells and injected into the site of the damage, regrowing the sheath. Even though she is still in the early stages of a randomized clinical trial, the results thus far are encouraging.
Dogs like Tobi will not be the only beneficiaries of Dr. Olbys research. If the therapy produces positive results in dogs, then translating the treatment to humans is a natural next step. And in humans, even very small improvements have the capacity to radically transform quality of life.
Even if this procedure produced an effect in a person as small as giving him or her partial control of one finger, that could allow the patient to use a computer, which opens up a whole new world of possibilities in terms of communication and interaction with the outside world, Dr. Olby says.
-- Tracey Peake
Dr. Olbys research is funded by the Morris Animal Foundation and is one of the clinical trials underway in the Neurology Service within the Randall B. Terry, Jr. Companion Animal Veterinary Medical Center. For more information on the clinical trial, visit the "call for patients" web page.
Posted Feb. 14, 2012
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July 3rd, 2015
Stem Cell vs. Bone Marrow Transplant: Whats the …
By NEVAGiles23
With Brigham and Womens Hospital and Boston Childrens Hospital, Dana-Farber has performed thousands of stem cell/bone marrow transplants for adult and pediatric patients with blood cancers and other serious illnesses.
Whats the difference between these two terms? As it turns out, the only real distinction is in the method of collecting the stem cells.
Lets start with the basics.
Stem cells are versatile cells with the ability to divide and develop into many other kinds of cells.
Hematopoietic stem cells produce red blood cells, which deliver oxygen throughout the body; white blood cells, which help ward off infections; and platelets, which allow blood to clot and wounds to heal.
While chemotherapy and/or radiation therapy are essential treatments for the majority of cancer patients, high doses can severely weakenand even wipe outhealthy stem cells. Thats where stem cell transplantation comes in.
Stem cell transplantation is a general term that describes the procedures performed by the Adult Stem Cell Transplantation Program at Dana-Farber/Brigham and Womens Cancer Center and the Pediatric Stem Cell Transplantation Program at Dana-Farber/Boston Childrens Cancer and Blood Disorders Center.
Stem cells for transplant can come from bone marrow or blood.
When stem cells are collected from bone marrow and transplanted into a patient, the procedure is known as a bone marrow transplant. If the transplanted stem cells came from the bloodstream, the procedure is called a peripheral blood stem cell transplantsometimes shortened to stem cell transplant.
Whether you hear someone talking about a stem cell transplant or a bone marrow transplant, they are still referring to stem cell transplantation. The only difference is where in the body the transplanted stem cells came from. The transplants themselves are the same.
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July 3rd, 2015
Sickle cell disease | University of Maryland Medical Center
By NEVAGiles23
Description
An in-depth report on the causes, diagnosis, and treatment of sickle cell disease.
Sickle cell anemia
What is Sickle Cell Disease?
Sickle cell disease is an inherited blood disorder in which the body produces abnormally shaped red blood cells. In sickle cell disease, the hemoglobin in red blood cells clumps together. This causes red blood cells to become stiff and C-shaped. These sickle cells block blood and oxygen flow in blood vessels. Sickle cells break down more rapidly than normal red blood cells, which results in anemia.
What Causes Sickle Cell Disease?
Sickle cell disease is a genetic disorder. People who have sickle cell disease are born with two sickle cell genes, one from each parent. If one normal hemoglobin gene and one sickle cell gene are inherited, a person will have sickle cell trait. People who have sickle cell trait do not develop sickle cell disease, but they are carriers who can pass the abnormal gene on to their children.
Complications of Sickle Cell Disease
Sickle cell disease can block the flow of blood in arteries in many parts of the body, causing many complications. The hallmark of sickle cell disease is the sickle cell crisis, which causes sudden attacks of severe pain. Acute chest syndrome, which is triggered by an infection or by blockage of blood vessels in the lungs, is another common and serious occurrence. Additional medical complications include:
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July 3rd, 2015
Radiation Therapy for Cancer – National Cancer Institute
By NEVAGiles23
What is radiation therapy?
Radiation therapy uses high-energy radiation to shrink tumors and kill cancer cells (1). X-rays, gamma rays, and charged particles are types of radiation used for cancer treatment.
The radiation may be delivered by a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body near cancer cells (internal radiation therapy, also called brachytherapy).
Systemic radiation therapy uses radioactive substances, such as radioactive iodine, that travel in the blood to kill cancer cells.
About half of all cancer patients receive some type of radiation therapy sometime during the course of their treatment.
How does radiation therapy kill cancer cells?
Radiation therapy kills cancer cells by damaging their DNA (the molecules inside cells that carry genetic information and pass it from one generation to the next) (1). Radiation therapy can either damage DNA directly or create charged particles (free radicals) within the cells that can in turn damage the DNA.
Cancer cells whose DNA is damaged beyond repair stop dividing or die. When the damaged cells die, they are broken down and eliminated by the bodys natural processes.
Does radiation therapy kill only cancer cells?
No, radiation therapy can also damage normal cells, leading to side effects.
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July 3rd, 2015
Cardiovascular Stem Cell Therapy
By JoanneRUSSELL25
Stem Cell Clinical Research & Deployment Cardiovascular & Pulmonary Conditions
The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use ofAdult Autologous Adipose-derived Stem Cells (ADSCs) for clinical research and deployment for numerous Cardiovascular and Pulmonary disorders, inclusive of:
Cardiovascular conditions include medical problems involving the heart and vascular system (the arterial and venous blood vessels). The most common cardiovascular condition is atherosclerotic coronary artery disease (ASCVD), which especially affects the coronary arteries and is the leading cause of heart attacks and death worldwide; and Congestive Heart Failure (CHF).
Other common cardiovascular conditions involve the cardiac muscle (CHF), cardiac valves, and heart rhythm. Many patients are typically treated with a multitude of medications; many patients require surgical interventions such as coronary angioplasty, coronary artery bypass, or other surgeries. Often patients, despite maximum therapy with medications and surgery, continue to suffer pain, discomfort, disability and have marked restrictions in their normal daily living activities.
The Manhattan Regenerative Medicine Medical Group is proud to be part of the only Institutional Review Board (IRB)-based stem cell treatment network in the United States that utilizes fat-transfer surgical technology. We have an array of ongoing IRB-approved protocols, andwe provide care for patients with a wide variety of disorders that may be treated with adult stem cell-based regenerative therapy.
The Manhattan Regenerative Medicine Medical Group offers IRB approved protocols and investigational use of Autologous Adult Adipose Derived Stem Cells (ADSCs) for clinical research and deployment for numerous cardiovascular conditions. These ADSCs cells are derived from fat an exceptionally abundant source of stem cells that has been removed during our mini-liposuction office procedure. The source of the regenerative stem cells actually comes from stromal vascular fraction (SVF) a protein rich segment from processed adipose tissue. SVF contains a mononuclear cell line (predominantly autologous mesenchymal stem cells), macrophage cells, endothelial cells, red blood cells, and important growth factors that facilitate the stem cell process and promote their activity. Our technology allows us to isolate high numbers of viable cells that we can deploy during the same surgical setting.
The SVF and stem cells are then deployed back into the patients body via injection or IV infusion on an outpatient basis; the total procedure takes less than two hours; and only local anesthesia is used. Not all cardiovascular problems respond to stem cell therapy, and each patient must be assessed individually to determine the potential for optimal results from this regenerative medicine process.
The Manhattan Regenerative Medicine Medical Group is committed not only to providing a high degree of quality care for our patients with cardiovascular problems but we are also highly committed to clinical stem cell research and the advancement of regenerative medicine. At the Miami Stem Cell Treatment Center we exploit anti-inflammatory, immuno-modulatory and regenerative properties of adult stem cells to mitigate cardiovascular conditions which are otherwise lethal to our bodies.
Myocardial infarction (heart attack) is responsible for significant cardiac muscle destruction and impairment due to ischemia (lack of blood flow). This can lead to further or recurrent restriction of blood flow thereby causing re-current infarct and pain on exertion (or even rest) known as chronic angina. Chronic angina causes restriction of daily activities of everyday living and is plagued with chest pain, chest pressure, and depression. This problem is caused most commonly by coronary artery disease which is very common in the United States and associated with significant morbidity and mortality.
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Cardiovascular Stem Cell Therapy
IPS Cell Therapy
By raymumme
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Stem Cell Research is an amazing field right now, and promises to be a powerful and potent tool to help us live longer and healthier lives. Just last month, for example, Stem Cell Therapy was used to restore sight in patients with severe retinal deterioration, allowing them to see clearer than they had in years, or even decades.
Now, there is another form of Stem Cell Treatment on the horizonthis one of a very different form. Stem Cells have now been used as a mechanism to deliver medical treatment designed to eliminate cancer cells, even in hard to reach places. One issue with current cancer treatments is that, treatments that are effective at treating tumors on the surface of the brain cannot be performed safely when the tumor is deeper within the brains tissues.
Stem Cells have the fantastic ability to transform into any other kind of cell within the human body, given the appropriate stimulation. As of today, most of these cells come from Embryonic Lines, but researchers are learning how to backwards engineer cells in the human body, reverting them back to their embryonic state. These cells are known as Induced Pluripotent Stem Cells.
How Does This Stem Cell Cancer Treatment Work?
Using genetic engineering, it is possible to create stem cells that are designed to release a chemical known as Pseudomonas Exotoxin, which has the ability to destroy certain tumor cells in the human brain.
What is Pseudomonas Exotoxin?
Pseudomonas Exotoxin is a compound that is naturally released by a form of bacteria known as Pseudomonas Aeruginosa. This chemical is toxic to brain tumor cells because it prevents polypeptides from growing longer, essentially preventing the polypeptides from growing and reproducing. When used in a specific manner, this toxin has the ability to destroy cancerous and malignant tissue without negatively impacting healthy tissue. In addition to its potential as a cancer treatment, there is also evidence that the therapy could be used for the treatment of Hepatitis B.
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Stem Cells for Heart Cell Therapies – National Center for …
By JoanneRUSSELL25
Abstract
Myocardial infarctioninduced heart failure is a prevailing cause of death in the United States and most developed countries. The cardiac tissue has extremely limited regenerative potential, and heart transplantation for reconstituting the function of damaged heart is severely hindered mainly due to the scarcity of donor organs. To that end, stem cells with their extensive proliferative capacity and their ability to differentiate toward functional cardiomyocytes may serve as a renewable cellular source for repairing the damaged myocardium. Here, we review recent studies regarding the cardiogenic potential of adult progenitor cells and embryonic stem cells. Although large strides have been made toward the engineering of cardiac tissues using stem cells, important issues remain to be addressed to enable the translation of such technologies to the clinical setting.
Heart disease is a significant cause of morbidity and mortality worldwide. In the United States, heart failure is ranked number one as a cause of death, affecting over 5 million people and with more than 500,000 new cases diagnosed each year.1 The health care expenditures associated with heart failure were $26.7 billion in 2004 and are estimated to $33.2 billion in 2007. Although significant progress has been made in mechanical devices and pharmacological interventions, more than half of the patients with heart failure die within 5 years of initial diagnosis. Wide application of heart transplantation is severely hindered by the limited availability of donor organs. To this end, cardiac cell therapy may be an appealing alternative to current treatments for heart failure.
Recent investigations focusing on engineering cells and tissues to repair or regenerate damaged hearts in animal models and in clinical trials have yielded promising results. Considering the limited regenerative capacity of the heart muscle, renewable sources of cardiomyocytes are highly sought. Cells suitable for myocardial engineering should be nonimmunogenic, should be easy to expand to large quantities, and should differentiate into mature, fully functional cardiomyocytes capable of integrating to the host tissue. Adult progenitor cells (APCs) and embryonic stem cells (ESCs) have extensive proliferative potential and can adopt different cell fates, including that of heart cells. The recent advances in the fields of stem cell biology and heart tissue engineering have intensified efforts toward the development of regenerative cardiac therapies. In this article, we review findings pertaining to the cardiogenic potential of major APC populations and of ESCs (). We also discuss significant challenges in the way of realizing stem cellbased therapies aiming to reconstitute the normal function of heart.
Potential sources of stem/progenitor cells for cardiac repair. ESCs derived from the inner cell mass of a blastocyst can be manipulated ex vivo to differentiate toward heart cells. APCs residing in various tissues such as the BM and skeletal muscle may ...
Bone marrow (BM) is a heterogeneous tissue comprising of multiple cell types, including minute fractions of mesenchymal stem cells (MSCs; 0.0010.01% of total cells2) and hematopoietic stem cells (HSCs; 0.71.5cells/108 nucleated marrow cells3). The heterogeneity of BM makes challenging the identification of a subpopulation of cells capable of cardiogenesis, and studies of BM celltocardiac cell transdifferentiation should be examined through this prism.
The notion that BM-derived cells may contribute to the regeneration of the heart was first illustrated when dystrophic (mdx) female mice received BM cells from male wild-type mice.4 More than 2 months after the transplantation, tissues of the recipient mice were histologically examined for the presence of Y-chromosome+ donor cells. Besides the skeletal muscle, donor cells were identified in the cardiac region, suggesting that circulating BM cells contribute to the regeneration of cardiomyocytes.
Further supporting evidence was provided by Jackson et al.5 in studies using a side population (SP) of cells characterized by their intrinsic capacity to efflux Hoechst 33342 dye through the ATP-binding Bcrp1/ABCG2 transporter. The cells were isolated from the BM fraction of HSCs of Rosa26 mice constitutively expressing the -galactosidase reporter gene (LacZ). After SP cells were injected into mice with coronary occlusioninduced ischemia, cells coexpressing LacZ and cardiac -actinin were identified around the infarct region with a frequency of 0.02%. Endothelial engraftment was more prevalent (3.3%). The observed improvement in myocardial function may thus be attributed to the potential of BM cells to give rise to a rather endothelial progeny. This may be a parallel to cardiovascular progenitors from differentiating ESCs giving rise to cardiomyocytes, and endothelial and vascular smooth muscle lineages.6,7
Orlic et al.8 also reported the regeneration of infarcted myocardium after transplantation of lineage-negative (LIN)/C-KIT+ BM cells from transgenic mice constitutively expressing enhanced green fluorescent protein (eGFP). Cells were injected in the contracting wall close to the infarct area. Nine days after transplantation, an impressive 68% of the infarct was occupied by newly formed myocardium with eGFP+ cells displaying cardiomyocyte markers such as troponin, MEF2, NKX2.5, cardiac myosin, GATA-4, and -sarcomeric actin. Similar outcomes were reported by the same group9 when mouse C-KIT+ (but not screened for LIN) BM cells were transplanted.
Although these findings led to the conclusion that BM cells can repopulate a damaged heart, work by other investigators has casted doubt on this assertion. Balsam et al.10 noted that mice with infarcts receiving BM LIN/C-KIT+, C-KIT-enriched or THY1.1low/LIN/stem cell antigen-1 (SCA-1+) cells exhibited improved ventricular function. However, donor cells expressed granulocyte but not heart cell markers 1 month after injection. In another study,11 HSCs carrying a nuclear-localized LacZ gene flanked by the cardiac -myosin heavy chain promoter were delivered into the periinfarct zone of mice 5h after coronary artery occlusion. One to 4 weeks later, LacZ+ cells were absent in heart tissue sections from 117 mice that received HSCs. Similarly, no eGFP+ cells were detected in the infarcted hearts of mice infused with BM cells constitutively expressing eGFP. Finally, Nygren et al.12 in similar transplantation experiments observed only blood cells (mainly leukocytes) originating from BM HSCs in the infarcted myocardium without evidence of transdifferentiation of donor cells to cardiomyocytes.
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July 1st, 2015
Cancer – Wikipedia, the free encyclopedia
By Dr. Matthew Watson
Cancer i, also known as a malignant tumor or malignant neoplasm, is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] Not all tumors are cancerous; benign tumors do not spread to other parts of the body.[2] Possible signs and symptoms include: a new lump, abnormal bleeding, a prolonged cough, unexplained weight loss, and a change in bowel movements among others.[3] While these symptoms may indicate cancer, they may also occur due to other issues.[3] There are over 100 different known cancers that affect humans.[2]
Tobacco use is the cause of about 22% of cancer deaths.[1] Another 10% is due to obesity, a poor diet, lack of physical activity, and consumption of ethanol (alcohol).[1] Other factors include certain infections, exposure to ionizing radiation, and environmental pollutants.[4] In the developing world nearly 20% of cancers are due to infections such as hepatitis B, hepatitis C, and human papillomavirus.[1] These factors act, at least partly, by changing the genes of a cell.[5] Typically many such genetic changes are required before cancer develops.[5] Approximately 510% of cancers are due to genetic defects inherited from a person's parents.[6] Cancer can be detected by certain signs and symptoms or screening tests.[1] It is then typically further investigated by medical imaging and confirmed by biopsy.[7]
Many cancers can be prevented by not smoking, maintaining a healthy weight, not drinking too much alcohol, eating plenty of vegetables, fruits and whole grains, being vaccinated against certain infectious diseases, not eating too much red meat, and avoiding too much exposure to sunlight.[8][9] Early detection through screening is useful for cervical and colorectal cancer.[10] The benefits of screening in breast cancer are controversial.[10][11] Cancer is often treated with some combination of radiation therapy, surgery, chemotherapy, and targeted therapy.[1][12] Pain and symptom management are an important part of care. Palliative care is particularly important in those with advanced disease.[1] The chance of survival depends on the type of cancer and extent of disease at the start of treatment.[5] In children under 15 at diagnosis the five year survival rate in the developed world is on average 80%.[13] For cancer in the United States the average five year survival rate is 66%.[14]
In 2012 about 14.1 million new cases of cancer occurred globally (not including skin cancer other than melanoma).[5] It caused about 8.2 million deaths or 14.6% of all human deaths.[5][15] The most common types of cancer in males are lung cancer, prostate cancer, colorectal cancer, and stomach cancer, and in females, the most common types are breast cancer, colorectal cancer, lung cancer, and cervical cancer.[5] If skin cancer other than melanoma were included in total new cancers each year it would account for around 40% of cases.[16][17] In children, acute lymphoblastic leukaemia and brain tumors are most common except in Africa where non-Hodgkin lymphoma occurs more often.[13] In 2012, about 165,000 children under 15 years of age were diagnosed with cancer. The risk of cancer increases significantly with age and many cancers occur more commonly in developed countries.[5] Rates are increasing as more people live to an old age and as lifestyle changes occur in the developing world.[18] The financial costs of cancer have been estimated at $1.16 trillion US dollars per year as of 2010.[19]
Cancers are a large family of diseases that involve abnormal cell growth with the potential to invade or spread to other parts of the body.[1][2] They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth, and will often form a mass or lump, but may be distributed diffusely.[20][21]
Six characteristics of cancer have been proposed:
The progression from normal cells to cells that can form a discernible mass to outright cancer involves multiple steps known as malignant progression.[22][23]
When cancer begins, it invariably produces no symptoms. Signs and symptoms only appear as the mass continues to grow or ulcerates. The findings that result depend on the type and location of the cancer. Few symptoms are specific, with many of them also frequently occurring in individuals who have other conditions. Cancer is the new "great imitator". Thus, it is not uncommon for people diagnosed with cancer to have been treated for other diseases, which were assumed to be causing their symptoms.[24]
Local symptoms may occur due to the mass of the tumor or its ulceration. For example, mass effects from lung cancer can cause blockage of the bronchus resulting in cough or pneumonia; esophageal cancer can cause narrowing of the esophagus, making it difficult or painful to swallow; and colorectal cancer may lead to narrowing or blockages in the bowel, resulting in changes in bowel habits. Masses in breasts or testicles may be easily felt. Ulceration can cause bleeding that, if it occurs in the lung, will lead to coughing up blood, in the bowels to anemia or rectal bleeding, in the bladder to blood in the urine, and in the uterus to vaginal bleeding. Although localized pain may occur in advanced cancer, the initial swelling is usually painless. Some cancers can cause a buildup of fluid within the chest or abdomen.[24]
General symptoms occur due to distant effects of the cancer that are not related to direct or metastatic spread. These may include: unintentional weight loss, fever, being excessively tired, and changes to the skin.[25]Hodgkin disease, leukemias, and cancers of the liver or kidney can cause a persistent fever of unknown origin.[24]
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June 30th, 2015
Bone marrow or stem cell transplants for AML | Cancer …
By Sykes24Tracey
Having someone elses marrow or stem cells is called a donor transplant, or an allogeneic transplant. This is pronounced al-lo-jen-ay-ik.
The donors bone marrow cells must match your own as closely as possible. The most suitable donor is usually a close relative, such as a brother or sister. It is sometimes possible to find a match in an unrelated donor. Doctors call this a matched unrelated donor (MUD). To find out if there is a suitable donor for you, your doctor will contact The Anthony Nolan Bone Marrow Register and other UK based and international bone marrow registers.
To make sure that your donors cells match, you and the donor will have blood tests. These are to see how many of the proteins on the surface of their blood cells match yours. This is called tissue typing or HLA matching. HLA stands for human leucocyte antigen.
Once you have a donor and are in remission, you have high dose chemotherapy either on its own or with radiotherapy. A week later the donor goes into hospital and their stem cells or marrow are collected. You then have the stem cells or bone marrow as a drip through your central line.
If you've had a transplant from a donor, there is a risk of graft versus host disease (GVHD). This happens because the transplanted stem cells or bone marrow contain cells from your donor's immune system. These cells can sometimes recognise your own tissues as being foreign and attack them. This can be an advantage because the immune cells may also attack any leukaemia cells left after your treatment.
Acute GVHD starts within 100 days of the transplant and can cause
If you develop GVHD after your transplant, your doctor will prescribe medicines to damp down this immune reaction. These are called immunosuppressants.
Chronic GVHD starts more than 100 days after the transplant and you may have
Your doctor is likely to suggest that you stay out of the sun because GVHD skin rashes can often get worse in the sun.
There is detailed information about graft versus host disease in the section about coping physically with cancer.
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June 26th, 2015
Prostate Cancer Treatment – National Cancer Institute
By raymumme
General Information About Prostate Cancer Key Points Prostate cancer is a disease in which malignant (cancer) cells form in the tissues of the prostate. Signs of prostate cancer include a weak flow of urine or frequent urination. Tests that examine the prostate and blood are used to detect (find) and diagnose prostate cancer. Certain factors affect prognosis (chance of recovery) and treatment options. Prostate cancer is a disease in which malignant (cancer) cells form in the tissues of the prostate.
The prostate is a gland in the male reproductive system. It lies just below the bladder (the organ that collects and empties urine) and in front of the rectum (the lower part of the intestine). It is about the size of a walnut and surrounds part of the urethra (the tube that empties urine from the bladder). The prostate gland makes fluid that is part of the semen.Enlarge
Anatomy of the male reproductive and urinary systems, showing the prostate, testicles, bladder, and other organs.
Prostate cancer is found mainly in older men. In the U.S., about 1 out of 5 men will be diagnosed with prostate cancer.
These and other signs and symptoms may be caused by prostate cancer or by other conditions. Check with your doctor if you have any of the following:
Other conditions may cause the same symptoms. As men age, the prostate may get bigger and block the urethra or bladder. This may cause trouble urinating or sexual problems. The condition is called benign prostatic hyperplasia (BPH), and although it is not cancer, surgery may be needed. The symptoms of benign prostatic hyperplasia or of other problems in the prostate may be like symptoms of prostate cancer.
Normal prostate and benign prostatic hyperplasia (BPH). A normal prostate does not block the flow of urine from the bladder. An enlarged prostate presses on the bladder and urethra and blocks the flow of urine.
The following tests and procedures may be used:
Digital rectal exam (DRE). The doctor inserts a gloved, lubricated finger into the rectum and feels the prostate to check for anything abnormal.
Transrectal ultrasound. An ultrasound probe is inserted into the rectum to check the prostate. The probe bounces sound waves off body tissues to make echoes that form a sonogram (computer picture) of the prostate.
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June 23rd, 2015
Spinal Cord Injury | Canadian Stem Cell Foundation
By daniellenierenberg
Are there stem cell therapies available for spinal cord injury?
To our knowledge, no stem cell therapy has received Health Canada or U.S. Food and Drug Administration approval for treatment of spinal cord injury at this time. Patients who are researching their options may come across companies with Web sites or materials that say otherwise and offer fee-based stem cell treatments for curing this disease. Many of these claims are not supported by sound scientific evidence and patients considering these therapies are encouraged to review some of the links below before making crucial decisions about their treatment plan.
For the latest developments read our blog entrieshere.
For moreabout stem cell clinical trials for spinal cord injuryclick here. For printed version:http://goo.gl/ZpNLg)
The basis of using stem cells to treat spinal cord injury would be as a source of new cells and products that could prevent further spinal cord damage, restore nerve function, generate new nerve cells and guide the regrowth of severed nerve fibres. Stem cells have an unparalleled regenerative capacity with the flexibility to grow into hundreds of different cell types and make factors that can support a range of physiological functions. Researchers are evaluating which types of stem cells are the best for growing neurons and other support cells in the brain, and making factors that promote nerve function. They want to develop strategies that transplant the support cells that wrap myelin insulation around nerve fibres to conduct electrical signals. A steady supply of these cells grown from stem cells could be a tremendous asset for studies that are exploring how to restore nerve function across damaged spinal cords.
Two main strategies for using stem cells to treat spinal cord injury are being explored: exogenous and endogenous repair (exo meaning outside the body and endo meaning inside the body). In exogenous repair the required cells are first grown from stem cells in the laboratory and then transplanted into patients. In endogenous repair stem cells are transplanted into the patient and the outcome depends on the bodys ability to coax the stem cells to grow into the required cells. Either way, the goal is to use stem cells to improve nerve function. There are no existing therapies that are able to repair spinal cord injuries.
Many research teams around the globe are working to develop stem cell therapies for spinal cord injury. Their common goals are to identify which stem cells are best suited for the job, which signals will be able to coax them into becoming neurons or support cells, and which large scale lab methods are effective at ramping up the production of the required cells.
The discovery of neural stem cells in Canada in 1992 kindled great hope among that stem cells could someday be used to regenerate the damage caused by spinal cord injury. Until around 1998, it was believed that the brain could not repair itself by regenerating new neurons. We now know that patients who have partial lesions to the spinal cord do experience a degree of spontaneous recovery arising from the ability of the brain to reorganize new connections. These observations spurred researchers to test their theories in animal models of spinal cord injury, and the positive results have provided the proof of principle that stem cells can potentially improve function after spinal cord injury.
Stem cell research is continuing on a number of different avenues and some of the successful stops along the way have yielded early Phase 1and 2 clinical trials for spinal cord injury. These trials are very small, mostly testing the safety of putting adult stem cells into patients. The results should yield information about the viability of this kind of therapy, but further clinical trials will be required to answer the question of whether a stem cell therapy can improve nerve function. For patients, the answer to that question is still many years away.
A North American clinical trial is using adult neural stem cell injections to treat spinal cord injury. Find out morehere.
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June 20th, 2015
Tuberculosis bacteria hide in the low oxygen niches of …
By JoanneRUSSELL25
A new study from the Forsyth Institute is helping to shed light on latent tuberculosis and the bacteria's ability to hide in stem cells. Some bone marrow stem cells reside in low oxygen (hypoxia) zones. These specialized zones are secured as immune cells and toxic chemicals cannot reach this zone. Hypoxia- activated cell signaling pathways may also protect the stem cells from dying or ageing. A new study led by Forsyth Scientist Dr. Bikul Das has found that Mycobacterium tuberculosis (Mtb) hijack this protective hypoxic zone to hide intracellular to a special stem cell type. The study was published online on June 8th in the American Journal of Pathology.
Mtb, the causative organism of tuberculosis, infects nearly 2.2 billion people worldwide and causes 1.7 million annual deaths. This is largely attributed to the bacteria's ability to stay dormant in the human body and later resurface as active disease. Earlier research at Forsyth revealed that Mtb hides inside a specific stem cell population in bone marrow, the CD271+ mesenchymal stem cells. However, the exact location of the Mtb harboring stem cells was not known.
"From our previous research, we learned that cancer stem cells reside in the hypoxic zones to maintain self-renewal property, and escape from the immune system" said Bikul Das, MBBS, PhD, Associate Research Investigator at the Forsyth Institute, and the honorary director of the KaviKrishna laboratory, Guwahati, India. "So, we hypothesized that Mtb, like cancer, may also have figured out the advantage of hiding in the hypoxic area."
To test this hypothesis, Dr. Das and his collaborators at Jawarharlal Nehru Univeristy (JNU), New Delhi, and KaviKrishna Laboratory, Indian Institute of Technology, Guwahati, utilized a well-known mouse model of Mtb infection, where months after drug treatment, Mtb remain dormant for future reactivation. Using this mouse model of dormancy, scientists isolated the special bone marrow stem cell type, the CD271+ mesenchymal stem cells, from the drug treated mice. Prior to isolation of the stem cells, mice were injected with pimonidazole, a chemical that binds specifically to hypoxic cells. Pimonidazole binding of these cells was visualized under confocal microscope and via flow cytometry. The scientists found that despite months of drug treatment, Mtb could be recovered from the CD271+ stem cells. Most importantly, these stem cells exhibit strong binding to pimonidazole, indicating the hypoxic localization of the stem cells. Experiments also confirmed that these stem cells express a hypoxia activated gene, the hypoxia inducible factor 1 alpha (HIF-1 alpha).
To confirm the findings in clinical subjects, the research team, in collaboration with KaviKrishna Laboratory, the team isolated the CD271+ stem cell type from the bone marrow of TB infected human subjects who had undergone extensive treatment for the disease. They found that not only did the stem cell type contain viable Mtb, but also exhibit strong expression of HIF-1alpha. To their surprise, the CD271+ stem cell population expressed several fold higher expression of HIF-1alpha than the stem cell type obtained from the healthy individuals.
"These findings now explain why it is difficult to develop vaccines against tuberculosis," said Dr. Das. "The immune cells activated by the vaccine agent may not be able to reach the hypoxic site of bone marrow to target these "wolfs-in-stem-cell-clothing".
The success of this international collaborative study is now encouraging the team to develop a Forsyth Institute/KaviKrishna Laboratory global health research initiative to advance stem cell research and its application to global health issues including TB, HIV and oral cancer, all critical problems in the area where KaviKrishna Laboratory is located.
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Das is the co-senior and co-corresponding author of the study, Rakesh Bhatnagar, PhD, professor of biotechnology, JNU, New Delhi, is the co-senior author of the study. Ms. Jaishree Garhain, a PhD student of Dr. Das and Dr. Bhatnagar, is the first author of the study. Other members of the team are Ms. Seema Bhuyan, Dr. Deepjyoti Kalita, and Dr. Ista Pulu. The research was funded by the KaviKrishna Foundation (Sualkuchi, India), the Laurel Foundation (Pasadena, California), and Department of Biotechnology, India.
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June 20th, 2015
cardiovascular disease :: Cardiac stem cells | Britannica.com
By LizaAVILA
Cardiac stem cells, which have the ability to differentiate (specialize) into mature heart cells and therefore could be used to repair damaged or diseased heart tissue, have garnered significant interest in the development of treatments for heart disease and cardiac defects. Cardiac stem cells can be derived from mature cardiomyocytes through the process of dedifferentiation, in which mature heart cells are stimulated to revert to a stem cell state. The stem cells can then be stimulated to redifferentiate into myocytes or endothelial cells. This approach enables millions of cardiac stem cells to be produced in the laboratory.
In 2009 a team of doctors at Cedars-Sinai Heart Institute in Los Angeles, California, reported the first attempted use of cardiac stem cell transplantation to repair damaged heart tissue. The team removed a small section of tissue from the heart of a patient who had suffered a heart attack, and the tissue was cultured in a laboratory. Cells that had been stimulated to dedifferentiate were then used to produce millions of cardiac stem cells, which were later reinfused directly into the heart of the patient through a catheter in a coronary artery. A similar approach was used in a subsequent clinical trial reported in 2011; this trial involved 14 patients suffering from heart failure who were scheduled to undergo cardiac bypass surgery. More than three months after treatment, there was slight but detectable improvement over cardiac bypass surgery alone in left ventricle ejection fraction (the percentage of the left ventricular volume of blood that is ejected from the heart with each ventricular contraction).
Stem cells derived from bone marrow, the collection of which is considerably less invasive than heart surgery, are also of interest in the development of regenerative heart therapies. The collection and reinfusion into the heart of bone marrow-derived stem cells within hours of a heart attack may limit the amount of damage incurred by the muscle.
There are many types of arterial diseases. Some are generalized and affect arteries throughout the body, though often there is variation in the degree they are affected. Others are localized. These diseases are frequently divided into those that result in arterial occlusion (blockage) and those that are nonocclusive in their manifestations.
Atherosclerosis, the most common form of arteriosclerosis, is a disease found in large and medium-sized arteries. It is characterized by the deposition of fatty substances, such as cholesterol, in the innermost layer of the artery (the intima). As the fat deposits become larger, inflammatory white blood cells called macrophages try to remove the lipid deposition from the wall of the artery. However, lipid-filled macrophages, called foam cells, grow increasingly inefficient at lipid removal and undergo cell death, accumulating at the site of lipid deposition. As these focal lipid deposits grow larger, they become known as atherosclerotic plaques and may be of variable distribution and thickness. Under most conditions the incorporation of cholesterol-rich lipoproteins is the predominant factor in determining whether or not plaques progressively develop. The endothelial injury that results (or that may occur independently) leads to the involvement of two cell types that circulate in the bloodplatelets and monocytes (a type of white blood cell). Platelets adhere to areas of endothelial injury and to themselves. They trap fibrinogen, a plasma protein, leading to the development of platelet-fibrinogen thrombi. Platelets deposit pro-inflammatory factors, called chemokines, on the vessel walls. Observations of infants and young children suggest that atherosclerosis can begin at an early age as streaks of fat deposition (fatty streaks).
Atherosclerotic lesions are frequently found in the aorta and in large aortic branches. They are also prevalent in the coronary arteries, where they cause coronary artery disease. The distribution of lesions is concentrated in points where arterial flow gives rise to abnormal shear stress or turbulence, such as at branch points in vessels. In general the distribution in most arteries tends to be closer to the origin of the vessel, with lesions found less frequently in more distal sites. Hemodynamic forces are particularly important in the system of coronary arteries, where there are unique pressure relationships. The flow of blood through the coronary system into the heart muscle takes place during the phase of ventricular relaxation (diastole) and virtually not at all during the phase of ventricular contraction (systole). During systole the external pressure on coronary arterioles is such that blood cannot flow forward. The external pressure exerted by the contracting myocardium on coronary arteries also influences the distribution of atheromatous obstructive lesions.
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June 19th, 2015