the body is derived directly from the pancreas. The specialized cells within the pancreas that secrete insulin are known as beta cells (β cells). In type 1 diabetes, the β cells are destroyed by an autoimmune response from the body, resulting in the decreased production of insulin by the body. The most successful interventions within the pancreas target these β cells, as a means to replace the inoperative cells with fully functioning substitutes. This will, hopefully, result in a full recovery of the individuals suffering from type 1 diabetes.
Prior to the advent of the mainstream feasibility of stem cells, scientists were relegated to simply transplanting the β cells of healthy individuals into the pancreases of those suffering from diabetes. Although the patients did show signs of insulin independence after the initial transplantation, it did not last. Due to the transient effects of the transplantation, multiple transplantations were required to produce the effects of insulin independence on a steady basis. However, a shortage of viable donors for the transplantation as well as an immune rejection on the part of the transplant recipients has stalled this avenue of research.
Stem cells have proven to possibly be a suitable replacement for these β cell transplantation therapies. Research in recent years has shown that it is possible to grow insulin-producing cells from embryonic stem cells. This is a very promising development in the search for a cure for type 1 diabetes. The research thus far has shown that it is possible to take murine embryonic stem cells and coax them into insulin-producing cells, ex vivo. These newly formed cells are subsequently reintroduced into the pancreases of diabetic mice and have shown to improve insulin efficiency within their bodies.
It is advantageous to upscale this method of manufacturing insulin-producing cells to the human level for a variety of reasons. First and foremost, a constant reserve of stem cell–derived pancreatic cells would do away with any need for multiple donors. This would expedite the transplantation process, vastly improving clinical outcomes.
Furthermore, embryonic stem cells are in essence a blank slate. Their undifferentiated qualities are a means to circumvent any adverse immune response that may be elicited from the transplant recipient’s body upon the cells. Growing these cells outside the body isolates them from adopting the unique histocompatibility markers that are so readily adopted by cells produced from within the body. Hence, when these cells are transplanted into an individual suffering from diabetes, that individual’s body will implant upon these cells markers that are inherently unique to that body. This process leaves no room for an immune rejection to the cells on the part of the patient’s body.
Years of research are still ahead to further elucidate any current unforeseen repercussions of this intervention. Positive showings in mice models are reassuring for the future of this avenue of research. A much wider consensus among the greater scientific community must be reached before large-scale human trials can begin. This burgeoning field of study is ever rapidly expanding, though; the leaps that have been made in the past 20 years may very well be outshined by advances that could be seen in the next five years.
Cardiovascular Disease
The Centers for Disease Control and Prevention (CDC) estimates that roughly 600,000 people die of heart disease every year. By the numbers, cardiovascular disease is the leading cause of death in the United States. Immeasurable leaps have been made in combating the disease over the past 25 years, and with the help of better prognostic tools, outcomes have steadily become more and more positive. However, the prevalence of the disease will increase in the coming years. Similar to diabetes, cardiovascular disease is a disease of affluence. As medicine progresses and effectively reduces the mortality rates of many acute communicable diseases, the fight against chronic illnesses comes to the forefront.
Cardiovascular disease is a term that refers to any disease that involves the heart and/or the blood vessels. The leading causes of cardiovascular disease are atherosclerosis and hypertension. Atherosclerosis is a term used to describe the thickening of arterial walls by the accumulation of cholesterol and triglycerides, ultimately leading to a full occlusion of the vessel. In laymen’s terms, hypertension is simply high blood pressure found within the arteries. If it is not addressed appropriately, hypertension places an undue amount of strain on the heart, culminating in heart disease.
As is indicative of other diseases of affluence, cardiovascular disease and its direct causes are a result of a sedentary lifestyle. Therefore, it should come as no surprise that the most immediate prevention for the onset of the disease is the adoption of healthier living habits. A daily regimen of exercise and a diet filled with foods low in fat are all positive means to prevent the occurrence of cardiovascular disease.
However, genetics is also a huge factor in the onset of cardiovascular disease. It is well known that thousands of seemingly healthy individuals are struck by heart attacks every year. Therefore, more research is warranted on the environment within the body post–myocardial infarction (MI). Prevention can only do so much. Sometimes a heart attack is inevitable, but it no longer is a death sentence.
In the world of interventional cardiologists, “Time is muscle.” From the moment of the initial heart attack, every second matters. Breakthroughs in the field of catheterization have allowed physicians to enter the heart and clear a path through the most occluded of vessels. However, no matter how early a heart attack is addressed, ischemic damage will always result.
Ischemia is a term used to describe any situation where the blood flow to a particular part of the body is impaired. A heart attack results in ischemia of the heart. The size and extent of the ischemic damage done to the heart is dependent upon the severity of the heart attack itself and the amount of time that transpires prior to any form of intervention being administered. A prolonged absence of oxygen to the myocardium will ultimately result in diminished heart function, and herein lies the major component in the fight against cardiovascular disease.
The diminished function of the heart seen after a heart attack does not improve over time. One indicator of heart function that sheds a great deal of light on the overall integrity and efficiency of the heart is the ejection fraction (EF). Simply put, it is the ratio of the volume of blood pumped out of the left and right ventricles during each heartbeat. A normal EF has a range of roughly 55–70 percent. In the event of a heart attack, that range can severely dip. Currently, there are no practical means to reverse the trend in ischemic damage. Management with medication will lead to a somewhat normal lifestyle, but the risk of congestive heart failure (CHF) always surrounds any heart attack victim.
Stem cells provide a revolutionary means to reinvigorate dead myocardium to a point of functionality that nearly mirrors the state of the heart pre-MI. The ability of stem cells to differentiate into nearly any cell line allows for innumerable opportunities of intervention, especially in the case of cardiovascular disease. Two specific types of stem cells have been linked to improved function in the heart post-MI in murine models. Those types are hematopoietic and umbilical cord blood stem cells.
Hematopoietic stem cells are derived from bone marrow deposits, while umbilical cord blood stem cells are derived from the cord blood of infants. In early murine models, both types of these stem cells have shown to be able to differentiate into adult cardiac cells. The administration of these newly derived cardiac cells into ischemic regions of the heart has shown to produce an increase in the ejection fraction of mice.
A novel clinical study performed by cardiologists at Cedars-Sinai Hospital in 2009 has provided the scientific community with some of the first tangible results of a stem cell therapy for cardiovascular disease. The study was revolutionary in scale and also in simplicity. Healthy cardiac progenitor cells were extracted from heart attack patients via a minimally invasive catheter procedure. This small portion of cells was then allowed to grow outside the body in a cultured dish. After roughly 20 to 25 days of growth, the cells were deemed confluent, after which the cells were reintroduced into the hearts of the patients, and the patients were monitored over the course of six months. All in all, the patients showed an increase in heart functionality. Outcomes were good, with no real signs of adverse effects. This particular study is the beginning of an entire field of research that will utilize stem cells and the possibility of directly infusing them into zones of ischemia within the infarcted heart.
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