Category Archives: California Stem Cells

California is one of six states that actively supports stem cell research. California Institute for Regenerative Medicine (CIRM) was formed in 2004 when voters approved proposition 71. The mission of CIRM is to accelerate stem cell treatments to patients with unmet medical needs. Research grant recipients include academic centers and medical companies focused on researching methods of transplantation, new drugs and improved diagnostics. With the goal of supporting research programs focused on creating cures, the institute is currently funding 43 clinical trials.

Before 2009, federal government funding restrictions prevented scientists from advancing stem cell research in the United States. Legislation such as proposition 71 was greatly needed to provide scientists with the financial support to pursue research for the advancement of stem cell and regenerative medicine. In the United State federal funding restricted the advancement of stem cell research while globally stem cell research continued with hundreds of studies published each year. The Stem Cells Transplant Institute in Costa Rica is one of the leaders is stem cell therapy.

To date, the only FDA approved stem cell therapies in the United States include bone marrow for bone marrow transplants and cord blood for certain blood disorders. Earlier this year, the FDA seized materials from one clinic in California that has been providing unapproved treatments to patients. On August 28, 2017, the FDA announced the agency will be pursuing clinics that offer unapproved stem cell therapies calling these clinics unscrupulous. Patients from California, interested in pursuing the potential benefits

of stem cells, can receive government approved stem cell therapy at the Stem Cells Transplant Institute in Costa Rica.

Stem cell treatment at the Stem Cells Transplant Institute is a safe, non-invasive, same-day procedure that takes only a few hours. You can experience the potential benefits of stem cell therapy by scheduling an appointment with the experts at the Stem Cells Transplant Institute. Delta and Alaska airlines offer non-stop flights from Los Angeles to San Jose, Costa Rica. Contact the experts at the Stem Cells Transplant Institute to see if stem cell therapy is right for you

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California Stem Cells Treatment, San Diego, San Francisco ...

Stem cells reside in adult bone marrow and fat, as wellas other tissues and organs of the body. These cells have a natural ability to repair damaged tissue, however in people with degenerative diseases they are not released quickly enough to fully repair damaged tissue. In the case of fat stem cells they may not be released at all. The process of actively extracting, concentrating and administering these stem cells has been shown in clinical trials to have beneficial effects in degenerative conditions. We offer patients and their doctors access to these therapies now.

We offer treatments using both autologous (your own) stem cells and/or third party donor cells. All of our stem cells are treated in a laboratory approved and regulated by COFEPRIS, or the Mexican equivalent of the US FDA.

Adult stem cells can be extracted from many areas of the body, including the bone marrow, fat, and peripheral blood. Once the cells have been harvested, they are sent to the lab where they are purified and assessed for quality before being reintroduced back in the patient. Stem cells isolated from the bone marrow or fat have the ability to become different cell types (i.e. nerve cells, liver cells, heart cells, and cartilage cells). Studies have also shown that these are capable of homing to and repairing damaged tissue. Animal studies have shown that these stem cells also secrete proteins and peptides that stimulate healing of damaged tissue, including heart muscle and spinal cord.

Fat stem cells are essentially sequestered and are not available to the rest of the body for repair or immune modulation.

Experimental studies suggest fat derived stem cells not only can develop into new tissues but also suppress pathological immune responses as seen in autoimmune diseases. In addition to orthopedic conditions, Stem Cell Institute has experience treating patients with Osteoarthritis, Rheumatoid Arthritis, Multiple Sclerosis, and other autoimmune diseases using fat derived stem cells.

The bone marrow stem cell is the most studied of the stem cells, since they were first discovered to in the 1960s. Originally used in bone marrow transplant for leukemias and hematopoietic diseases, numerous studies have now expanded experimental use of these cells for conditions such as peripheral vascular disease, diabetes, heart failure, and other degenerative disorders.

Umbilical cord stem cells reside in the umbilical cords of newborn babies. HUCT stem cells, like all post-natal cells, are considered to be adult stem cells.

Recently, the placenta has been shown to be a plentiful, non-controversial source of stem cells. It has a number of advantages over traditional methods of preparing stem cells. We have developed methods to harvest and employ stem cells from the placenta and the umbilical cord tissue so as to provide a safe non-controversial alternative to the harvesting of embryonic or fetal stem cells.

Embryonic stem cells, as their name suggests, are derived from embryos. Most embryonic stem cells are derived from embryos that develop from eggs that have been fertilized in vitroin an in vitro fertilization clinicand then donated for research purposes with informed consent of the donors.

For ethical and legal reasons we do not work with Fetal or embryonic stem cells.

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Stem cell treatments in Baja California

Just as good scientists are drawn to conclusions by solid data, the decision whether to spend another $345 million by Californias state-run stem-cell research project should be based on an objective analysis as to whether it would be cost-effective. A rigorous cost-benefit analysis is not only fiscally prudent, it avoids being drawn into the moral dilemmas posed by stem-cell research, especially with respect to cells from human embryos.

Created in 2004 with the passage of Proposition 71, the California Institute for Regenerative Medicine was authorized to spend $3 billion in bond proceeds. But as is typical with most bonds, the interest payments would double the cost to $6 billion. CIRM has made $2.4 billion in grants and used $255 million for administration and prepaid interest leaving $345 million remaining to disburse.

Should CIRM distribute the remaining $345 million (which, with interest, would amount to $690 million in repayment costs)? Should this remaining pool of funds be doled out?

According to the ballot pamphlet mailed to voters, proponents promised the bond proceeds would advance the cure and treatment of cancer, diabetes, heart disease, Alzheimers, Parkinsons, spinal cord injuries, blindness, Lou Gehrigs disease, HIV/AIDS, mental health disorders, multiple sclerosis, Huntingtons disease, and more than 70 other diseases and injuries.

But actual outcomes for these promised advances are speculative at best and nonexistent at worst.

Similar benefits were promised to the California economy to generate millions of new tax dollars.

In a Prop. 71 ad, actor Michael J. Fox, who has Parkinsons, urged, Vote yes on 71, and save the life of someone you love. Initiative backers also promised royalties to the state could be as much as $1.1 billion, thus providing a source of funds to pay off the bonds.

This past August, almost 13 years after Prop. 71 passed, CIRM announced it would cough up its first royalty check to the state on the new technologies it developed. Can anyone say bust?

With such a dismal record, this would be a good time to shut the spigot on issuing the remaining $345 million meaning some $690 million would be saved by state taxpayers. That money could be better spent on pensions, schools, roads, housing or better basic medical care for our residents.

And required bond payments include $313 million from the 2017-18 budget, which began on July 1, and another $309 million from the 2018-19 budget. Total: $622 million for just two years. No wonder the Democratic supermajority raised the gas tax to find money for roads.

Unbelievably, a recently proposed $5 billion initiative for the 2018 ballot to extend the subsidy effectively a second opinion on the project was dumped last June. Even supporters didnt think they could resell their snake oil.

When it seemed the new initiative might be advanced, the California Stem Cell Report ran an op-ed by Joe Rodota and Bernard Munos. CIRM has over-invested in academic research, and under-invested in translating that research into therapies that cure diseases and prolong heathy lives, they noted. California needs to right that balance.

But with the new initiative now moribund, CIRM therefore continues to operate as a kind of advanced high-school science project, instead of moving toward the cures promised to voters in Prop. 71.

Thats why Sen. John Moorlach (coauthor of this piece) sponsored Senate Constitutional Amendment 7. Requiring a two-thirds vote of both houses of the Legislature, it would have repealed Article XXXV of the California Constitution, which codified Prop. 71.

Gov. Jerry Brown, among others, has prudently warned of the coming inevitable recession. And recent federal data show jobs growth in the state rising at only a 1.2 percent annual rate. This should be a time for excising waste and terminating this disappointing abuse of taxpayer dollars.

Jon Coupal is the president of the Howard Jarvis Taxpayers Association. John Moorlach, R-Costa Mesa, is a state senator representing the 37th District.

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Take a scalpel to $345 million in Californias stem-cell ...

Diabetes exacts its toll on many Americans, young and old. For years, researchers have painstakingly dissected this complicated disease caused by the destruction of insulin producing islet cells of the pancreas. Despite progress in understanding the underlying disease mechanisms for diabetes, there is still a paucity of effective therapies. For years investigators have been making slow, but steady, progress on experimental strategies for pancreatic transplantation and islet cell replacement. Now, researchers have turned their attention to adult stem cells that appear to be precursors to islet cells and embryonic stem cells that produce insulin.

For decades, diabetes researchers have been searching for ways to replace the insulin-producing cells of the pancreas that are destroyed by a patient's own immune system. Now it appears that this may be possible. Each year, diabetes affects more people and causes more deaths than breast cancer and AIDS combined. Diabetes is the seventh leading cause of death in the United States today, with nearly 200,000 deaths reported each year. The American Diabetes Association estimates that nearly 16 million people, or 5.9 percent of the United States population, currently have diabetes.

Diabetes is actually a group of diseases characterized by abnormally high levels of the sugar glucose in the bloodstream. This excess glucose is responsible for most of the complications of diabetes, which include blindness, kidney failure, heart disease, stroke, neuropathy, and amputations. Type 1 diabetes, also known as juvenile-onset diabetes, typically affects children and young adults. Diabetes develops when the body's immune system sees its own cells as foreign and attacks and destroys them. As a result, the islet cells of the pancreas, which normally produce insulin, are destroyed. In the absence of insulin, glucose cannot enter the cell and glucose accumulates in the blood. Type 2 diabetes, also called adult-onset diabetes, tends to affect older, sedentary, and overweight individuals with a family history of diabetes. Type 2 diabetes occurs when the body cannot use insulin effectively. This is called insulin resistance and the result is the same as with type 1 diabetesa build up of glucose in the blood.

There is currently no cure for diabetes. People with type 1 diabetes must take insulin several times a day and test their blood glucose concentration three to four times a day throughout their entire lives. Frequent monitoring is important because patients who keep their blood glucose concentrations as close to normal as possible can significantly reduce many of the complications of diabetes, such as retinopathy (a disease of the small blood vessels of the eye which can lead to blindness) and heart disease, that tend to develop over time. People with type 2 diabetes can often control their blood glucose concentrations through a combination of diet, exercise, and oral medication. Type 2 diabetes often progresses to the point where only insulin therapy will control blood glucose concentrations.

Each year, approximately 1,300 people with type 1 diabetes receive whole-organ pancreas transplants. After a year, 83 percent of these patients, on average, have no symptoms of diabetes and do not have to take insulin to maintain normal glucose concentrations in the blood. However, the demand for transplantable pancreases outweighs their availability. To prevent the body from rejecting the transplanted pancreas, patients must take powerful drugs that suppress the immune system for their entire lives, a regimen that makes them susceptible to a host of other diseases. Many hospitals will not perform a pancreas transplant unless the patient also needs a kidney transplant. That is because the risk of infection due to immunosuppressant therapy can be a greater health threat than the diabetes itself. But if a patient is also receiving a new kidney and will require immunosuppressant drugs anyway, many hospitals will perform the pancreas transplant.

Over the past several years, doctors have attempted to cure diabetes by injecting patients with pancreatic islet cellsthe cells of the pancreas that secrete insulin and other hormones. However, the requirement for steroid immunosuppressant therapy to prevent rejection of the cells increases the metabolic demand on insulin-producing cells and eventually they may exhaust their capacity to produce insulin. The deleterious effect of steroids is greater for islet cell transplants than for whole-organ transplants. As a result, less than 8 percent of islet cell transplants performed before last year had been successful.

More recently, James Shapiro and his colleagues in Edmonton, Alberta, Canada, have developed an experimental protocol for transplanting islet cells that involves using a much larger amount of islet cells and a different type of immunosuppressant therapy. In a recent study, they report that [17], seven of seven patients who received islet cell transplants no longer needed to take insulin, and their blood glucose concentrations were normal a year after surgery. The success of the Edmonton protocol is now being tested at 10 centers around the world.

If the success of the Edmonton protocol can be duplicated, many hurdles still remain in using this approach on a wide scale to treat diabetes. First, donor tissue is not readily available. Islet cells used in transplants are obtained from cadavers, and the procedure requires at least two cadavers per transplant. The islet cells must be immunologically compatible, and the tissue must be freshly obtainedwithin eight hours of death. Because of the shortage of organ donors, these requirements are difficult to meet and the waiting list is expected to far exceed available tissue, especially if the procedure becomes widely accepted and available. Further, islet cell transplant recipients face a lifetime of immunosuppressant therapy, which makes them susceptible to other serious infections and diseases.

Before discussing cell-based therapies for diabetes, it is important to understand how the pancreas develops. In mammals, the pancreas contains three classes of cell types: the ductal cells, the acinar cells, and the endocrine cells. The endocrine cells produce the hormones glucagon, somatostatin, pancreatic polypeptide (PP), and insulin, which are secreted into the blood stream and help the body regulate sugar metabolism. The acinar cells are part of the exocrine system, which manufactures digestive enzymes, and ductal cells from the pancreatic ducts, which connect the acinar cells to digestive organs.

In humans, the pancreas develops as an outgrowth of the duodenum, a part of the small intestine. The cells of both the exocrine systemthe acinar cellsand of the endocrine systemthe islet cellsseem to originate from the ductal cells during development. During development these endocrine cells emerge from the pancreatic ducts and form aggregates that eventually form what is known as Islets of Langerhans. In humans, there are four types of islet cells: the insulin-producing beta cells; the alpha cells, which produce glucagon; the delta cells, which secrete somatostatin; and the PP-cells, which produce pancreatic polypeptide. The hormones released from each type of islet cell have a role in regulating hormones released from other islet cells. In the human pancreas, 65 to 90 percent of islet cells are beta cells, 15 to 20 percent are alpha-cells, 3 to 10 percent are delta cells, and one percent is PP cells. Acinar cells form small lobules contiguous with the ducts (see Figure 7.1. Insulin Production in the Human Pancreas). The resulting pancreas is a combination of a lobulated, branched acinar gland that forms the exocrine pancreas, and, embedded in the acinar gland, the Islets of Langerhans, which constitute the endocrine pancreas.

Figure 7.1. Insulin Production in the Human Pancreas. The pancreas is located in the abdomen, adjacent to the duodenum (the first portion of the small intestine). A cross-section of the pancreas shows the islet of Langerhans which is the functional unit of the endocrine pancreas. Encircled is the beta cell that synthesizes and secretes insulin. Beta cells are located adjacent to blood vessels and can easily respond to changes in blood glucose concentration by adjusting insulin production. Insulin facilitates uptake of glucose, the main fuel source, into cells of tissues such as muscle.

( 2001 Terese Winslow, Lydia Kibiuk)

During fetal development, new endocrine cells appear to arise from progenitor cells in the pancreatic ducts. Many researchers maintain that some sort of islet stem cell can be found intermingled with ductal cells during fetal development and that these stem cells give rise to new endocrine cells as the fetus develops. Ductal cells can be distinguished from endocrine cells by their structure and by the genes they express. For example, ductal cells typically express a gene known as cytokeratin-9 (CK-9), which encodes a structural protein. Beta islet cells, on the other hand, express a gene called PDX-1, which encodes a protein that initiates transcription from the insulin gene. These genes, called cell markers, are useful in identifying particular cell types.

Following birth and into adulthood, the source of new islet cells is not clear, and some controversy exists over whether adult stem cells exist in the pancreas. Some researchers believe that islet stem cell-like cells can be found in the pancreatic ducts and even in the islets themselves. Others maintain that the ductal cells can differentiate into islet precursor cells, while others hold that new islet cells arise from stem cells in the blood. Researchers are using several approaches for isolating and cultivating stem cells or islet precursor cells from fetal and adult pancreatic tissue. In addition, several new promising studies indicate that insulin-producing cells can be cultivated from embryonic stem cell lines.

In developing a potential therapy for patients with diabetes, researchers hope to develop a system that meets several criteria. Ideally, stem cells should be able to multiply in culture and reproduce themselves exactly. That is, the cells should be self-renewing. Stem cells should also be able to differentiate in vivo to produce the desired kind of cell. For diabetes therapy, it is not clear whether it will be desirable to produce only beta cellsthe islet cells that manufacture insulinor whether other types of pancreatic islet cells are also necessary. Studies by Bernat Soria and colleagues, for example, indicate that isolated beta cellsthose cultured in the absence of the other types of islet cellsare less responsive to changes in glucose concentration than intact islet clusters made up of all islet cell types. Islet cell clusters typically respond to higher-than-normal concentrations of glucose by releasing insulin in two phases: a quick release of high concentrations of insulin and a slower release of lower concentrations of insulin. In this manner the beta cells can fine-tune their response to glucose. Extremely high concentrations of glucose may require that more insulin be released quickly, while intermediate concentrations of glucose can be handled by a balance of quickly and slowly released insulin.

Isolated beta cells, as well as islet clusters with lower-than-normal amounts of non-beta cells, do not release insulin in this biphasic manner. Instead insulin is released in an all-or-nothing manner, with no fine-tuning for intermediate concentrations of glucose in the blood [5, 18]. Therefore, many researchers believe that it will be preferable to develop a system in which stem or precursor cell types can be cultured to produce all the cells of the islet cluster in order to generate a population of cells that will be able to coordinate the release of the appropriate amount of insulin to the physiologically relevant concentrations of glucose in the blood.

Several groups of researchers are investigating the use of fetal tissue as a potential source of islet progenitor cells. For example, using mice, researchers have compared the insulin content of implants from several sources of stem cellsfresh human fetal pancreatic tissue, purified human islets, and cultured islet tissue [2]. They found that insulin content was initially higher in the fresh tissue and purified islets. However, with time, insulin concentration decreased in the whole tissue grafts, while it remained the same in the purified islet grafts. When cultured islets were implanted, however, their insulin content increased over the course of three months. The researchers concluded that precursor cells within the cultured islets were able to proliferate (continue to replicate) and differentiate (specialize) into functioning islet tissue, but that the purified islet cells (already differentiated) could not further proliferate when grafted. Importantly, the researchers found, however, that it was also difficult to expand cultures of fetal islet progenitor cells in culture [7].

Many researchers have focused on culturing islet cells from human adult cadavers for use in developing transplantable material. Although differentiated beta cells are difficult to proliferate and culture, some researchers have had success in engineering such cells to do this. For example, Fred Levine and his colleagues at the University of California, San Diego, have engineered islet cells isolated from human cadavers by adding to the cells' DNA special genes that stimulate cell proliferation. However, because once such cell lines that can proliferate in culture are established, they no longer produce insulin. The cell lines are further engineered to express the beta islet cell gene, PDX-1, which stimulates the expression of the insulin gene. Such cell lines have been shown to propagate in culture and can be induced to differentiate to cells, which produce insulin. When transplanted into immune-deficient mice, the cells secrete insulin in response to glucose. The researchers are currently investigating whether these cells will reverse diabetes in an experimental diabetes model in mice [6, 8].

These investigators report that these cells do not produce as much insulin as normal islets, but it is within an order of magnitude. The major problem in dealing with these cells is maintaining the delicate balance between growth and differentiation. Cells that proliferate well do not produce insulin efficiently, and those that do produce insulin do not proliferate well. According to the researchers, the major issue is developing the technology to be able to grow large numbers of these cells that will reproducibly produce normal amounts of insulin [9].

Another promising source of islet progenitor cells lies in the cells that line the pancreatic ducts. Some researchers believe that multipotent (capable of forming cells from more than one germ layer) stem cells are intermingled with mature, differentiated duct cells, while others believe that the duct cells themselves can undergo a differentiation, or a reversal to a less mature type of cell, which can then differentiate into an insulin-producing islet cell.

Susan Bonner-Weir and her colleagues reported last year that when ductal cells isolated from adult human pancreatic tissue were cultured, they could be induced to differentiate into clusters that contained both ductal and endocrine cells. Over the course of three to four weeks in culture, the cells secreted low amounts of insulin when exposed to low concentrations of glucose, and higher amounts of insulin when exposed to higher glucose concentrations. The researchers have determined by immunochemistry and ultrastructural analysis that these clusters contain all of the endocrine cells of the islet [4].

Bonner-Weir and her colleagues are working with primary cell cultures from duct cells and have not established cells lines that can grow indefinitely. However the cells can be expanded. According to the researchers, it might be possible in principle to do a biopsy and remove duct cells from a patient and then proliferate the cells in culture and give the patient back his or her own islets. This would work with patients who have type 1 diabetes and who lack functioning beta cells, but their duct cells remain intact. However, the autoimmune destruction would still be a problem and potentially lead to destruction of these transplanted cells [3]. Type 2 diabetes patients might benefit from the transplantation of cells expanded from their own duct cells since they would not need any immunosuppression. However, many researchers believe that if there is a genetic component to the death of beta cells, then beta cells derived from ductal cells of the same individual would also be susceptible to autoimmune attack.

Some researchers question whether the ductal cells are indeed undergoing a dedifferentiation or whether a subset of stem-like or islet progenitors populate the pancreatic ducts and may be co-cultured along with the ductal cells. If ductal cells die off but islet precursors proliferate, it is possible that the islet precursor cells may overtake the ductal cells in culture and make it appear that the ductal cells are dedifferentiating into stem cells. According to Bonner-Weir, both dedifferentiated ductal cells and islet progenitor cells may occur in pancreatic ducts.

Ammon Peck of the University of Florida, Vijayakumar Ramiya of Ixion Biotechnology in Alachua, FL, and their colleagues [13, 14] have also cultured cells from the pancreatic ducts from both humans and mice. Last year, they reported that pancreatic ductal epithelial cells from adult mice could be cultured to yield islet-like structures similar to the cluster of cells found by Bonner-Weir. Using a host of islet-cell markers they identified cells that produced insulin, glucagon, somatostatin, and pancreatic polypeptide. When the cells were implanted into diabetic mice, the diabetes was reversed.

Joel Habener has also looked for islet-like stem cells from adult pancreatic tissue. He and his colleagues have discovered a population of stem-like cells within both the adult pancreas islets and pancreatic ducts. These cells do not express the marker typical of ductal cells, so they are unlikely to be ductal cells, according to Habener. Instead, they express a marker called nestin, which is typically found in developing neural cells. The nestin-positive cells do not express markers typically found in mature islet cells. However, depending upon the growth factors added, the cells can differentiate into different types of cells, including liver, neural, exocrine pancreas, and endocrine pancreas, judged by the markers they express, and can be maintained in culture for up to eight months [20].

The discovery of methods to isolate and grow human embryonic stem cells in 1998 renewed the hopes of doctors, researchers, and diabetes patients and their families that a cure for type 1 diabetes, and perhaps type 2 diabetes as well, may be within striking distance. In theory, embryonic stem cells could be cultivated and coaxed into developing into the insulin-producing islet cells of the pancreas. With a ready supply of cultured stem cells at hand, the theory is that a line of embryonic stem cells could be grown up as needed for anyone requiring a transplant. The cells could be engineered to avoid immune rejection. Before transplantation, they could be placed into nonimmunogenic material so that they would not be rejected and the patient would avoid the devastating effects of immunosuppressant drugs. There is also some evidence that differentiated cells derived from embryonic stem cells might be less likely to cause immune rejection (see Chapter 10. Assessing Human Stem Cell Safety). Although having a replenishable supply of insulin-producing cells for transplant into humans may be a long way off, researchers have been making remarkable progress in their quest for it. While some researchers have pursued the research on embryonic stem cells, other researchers have focused on insulin-producing precursor cells that occur naturally in adult and fetal tissues.

Since their discovery three years ago, several teams of researchers have been investigating the possibility that human embryonic stem cells could be developed as a therapy for treating diabetes. Recent studies in mice show that embryonic stem cells can be coaxed into differentiating into insulin-producing beta cells, and new reports indicate that this strategy may be possible using human embryonic cells as well.

Last year, researchers in Spain reported using mouse embryonic stem cells that were engineered to allow researchers to select for cells that were differentiating into insulin-producing cells [19]. Bernat Soria and his colleagues at the Universidad Miguel Hernandez in San Juan, Alicante, Spain, added DNA containing part of the insulin gene to embryonic cells from mice. The insulin gene was linked to another gene that rendered the mice resistant to an antibiotic drug. By growing the cells in the presence of an antibiotic, only those cells that were activating the insulin promoter were able to survive. The cells were cloned and then cultured under varying conditions. Cells cultured in the presence of low concentrations of glucose differentiated and were able to respond to changes in glucose concentration by increasing insulin secretion nearly sevenfold. The researchers then implanted the cells into the spleens of diabetic mice and found that symptoms of diabetes were reversed.

Manfred Ruediger of Cardion, Inc., in Erkrath, Germany, is using the approach developed by Soria and his colleagues to develop insulin-producing human cells derived from embryonic stem cells. By using this method, the non-insulin-producing cells will be killed off and only insulin-producing cells should survive. This is important in ensuring that undifferentiated cells are not implanted that could give rise to tumors [15]. However, some researchers believe that it will be important to engineer systems in which all the components of a functioning pancreatic islet are allowed to develop.

Recently Ron McKay and his colleagues described a series of experiments in which they induced mouse embryonic cells to differentiate into insulin-secreting structures that resembled pancreatic islets [10]. McKay and his colleagues started with embryonic stem cells and let them form embryoid bodiesan aggregate of cells containing all three embryonic germ layers. They then selected a population of cells from the embryoid bodies that expressed the neural marker nestin (see Appendix B. Mouse Embryonic Stem Cells). Using a sophisticated five-stage culturing technique, the researchers were able to induce the cells to form islet-like clusters that resembled those found in native pancreatic islets. The cells responded to normal glucose concentrations by secreting insulin, although insulin amounts were lower than those secreted by normal islet cells (see Figure 7.2. Development of Insulin-Secreting Pancreatic-Like Cells From Mouse Embryonic Stem Cells). When the cells were injected into diabetic mice, they survived, although they did not reverse the symptoms of diabetes.

Figure 7.2. Development of Insulin-Secreting Pancreatic-Like Cells From Mouse Embryonic Stem Cells. Mouse embryonic stem cells were derived from the inner cell mass of the early embryo (blastocyst) and cultured under specific conditions. The embryonic stem cells (in blue) were then expanded and differentiated. Cells with markers consistent with islet cells were selected for further differentiation and characterization. When these cells (in purple) were grown in culture, they spontaneously formed three-dimentional clusters similar in structure to normal pancreatic islets. The cells produced and secreted insulin. As depicted in the chart, the pancreatic islet-like cells showed an increase in release of insulin as the glucose concentration of the culture media was increased. When the pancreatic islet-like cells were implanted in the shoulder of diabetic mice, the cells became vascularized, synthesized insulin, and maintained physical characteristics similar to pancreatic islets.

( 2001 Terese Winslow, Caitlin Duckwall)

According to McKay, this system is unique in that the embryonic cells form a functioning pancreatic islet, complete with all the major cell types. The cells assemble into islet-like structures that contain another layer, which contains neurons and is similar to intact islets from the pancreas [11]. Several research groups are trying to apply McKay's results with mice to induce human embryonic stem cells to differentiate into insulin-producing islets.

Recent research has also provided more evidence that human embryonic cells can develop into cells that can and do produce insulin. Last year, Melton, Nissim Benvinisty of the Hebrew University in Jerusalem, and Josef Itskovitz-Eldor of the Technion in Haifa, Israel, reported that human embryonic stem cells could be manipulated in culture to express the PDX-1 gene, a gene that controls insulin transcription [16]. In these experiments, researchers cultured human embryonic stem cells and allowed them to spontaneously form embryoid bodies (clumps of embryonic stem cells composed of many types of cells from all three germ layers). The embryoid bodies were then treated with various growth factors, including nerve growth factor. The researchers found that both untreated embryoid bodies and those treated with nerve growth factor expressed PDX-1. Embryonic stem cells prior to formation of the aggregated embryoid bodies did not express PDX-1. Because expression of the PDX-1 gene is associated with the formation of beta islet cells, these results suggest that beta islet cells may be one of the cell types that spontaneously differentiate in the embryoid bodies. The researchers now think that nerve growth factor may be one of the key signals for inducing the differentiation of beta islet cells and can be exploited to direct differentiation in the laboratory. Complementing these findings is work done by Jon Odorico of the University of Wisconsin in Madison using human embryonic cells of the same source. In preliminary findings, he has shown that human embryonic stem cells can differentiate and express the insulin gene [12].

More recently, Itskovitz-Eldor and his Technion colleagues further characterized insulin-producing cells in embryoid bodies [1]. The researchers found that embryonic stem cells that were allowed to spontaneously form embryoid bodies contained a significant percentage of cells that express insulin. Based on the binding of antibodies to the insulin protein, Itskovitz-Eldor estimates that 1 to 3 percent of the cells in embryoid bodies are insulin-producing beta-islet cells. The researchers also found that cells in the embryoid bodies express glut-2 and islet-specific glucokinase, genes important for beta cell function and insulin secretion. Although the researchers did not measure a time-dependent response to glucose, they did find that cells cultured in the presence of glucose secrete insulin into the culture medium. The researchers concluded that embryoid bodies contain a subset of cells that appear to function as beta cells and that the refining of culture conditions may soon yield a viable method for inducing the differentiation of beta cells and, possibly, pancreatic islets.

Taken together, these results indicate that the development of a human embryonic stem cell system that can be coaxed into differentiating into functioning insulin-producing islets may soon be possible.

Ultimately, type 1 diabetes may prove to be especially difficult to cure, because the cells are destroyed when the body's own immune system attacks and destroys them. This autoimmunity must be overcome if researchers hope to use transplanted cells to replace the damaged ones. Many researchers believe that at least initially, immunosuppressive therapy similar to that used in the Edmonton protocol will be beneficial. A potential advantage of embryonic cells is that, in theory, they could be engineered to express the appropriate genes that would allow them to escape or reduce detection by the immune system. Others have suggested that a technology should be developed to encapsulate or embed islet cells derived from islet stem or progenitor cells in a material that would allow small molecules such as insulin to pass through freely, but would not allow interactions between the islet cells and cells of the immune system. Such encapsulated cells could secrete insulin into the blood stream, but remain inaccessible to the immune system.

Before any cell-based therapy to treat diabetes makes it to the clinic, many safety issues must be addressed (see Chapter 10. Assessing Human Stem Cell Safety). A major consideration is whether any precursor or stem-like cells transplanted into the body might revert to a more pluripotent state and induce the formation of tumors. These risks would seemingly be lessened if fully differentiated cells are used in transplantation.

But before any kind of human islet-precursor cells can be used therapeutically, a renewable source of human stem cells must be developed. Although many progenitor cells have been identified in adult tissue, few of these cells can be cultured for multiple generations. Embryonic stem cells show the greatest promise for generating cell lines that will be free of contaminants and that can self renew. However, most researchers agree that until a therapeutically useful source of human islet cells is developed, all avenues of research should be exhaustively investigated, including both adult and embryonic sources of tissue.

Chapter 6|Table of Contents|Chapter 8

Historical content: June 17, 2001

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7. Stem Cells and Diabetes | stemcells.nih.gov

CSL Behring, a Montgomery County-based global developer of biotherapeutic products, has entered into a deal to buy Calimmune Inc. for $91 million.

The deal also includes the potential for Calimmune to earn additional performance based milestone payments of up to $325 million over a period currently anticipated to be around eight years or more following the closing of the transaction. The transaction is expected to close within the next two weeks.

Calimmune, a biotechnology company specializing in hematopoietic stem cell gene therapy, has research and development facilities in Pasadena, Calif., and Sydney, Australia. [Hematopoietic stem cells are responsible for the production of all cellular blood components.]

The acquisition provides CSL Behring of King of Prussia, Pa., with Calimmunes pre-clinical asset, CAL-H, an experimental gene therapy for the treatment of sickle cell disease and beta-thalassemia. Officials at CSL Behring, a division of CSL Ltd. of Australia, said CAL-H complements CSL Behrings current product portfolio and its "deep expertise" in hematology.

To read the full story, click here.

For more business news, visit Philadelphia Business Journal.

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$91M Deal: CSL Acquires California Stem Cell Gene Therapy Developer - NBC 10 Philadelphia

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Our sense of smell is key to the enjoyment of food, so it may be no surprise that in experiments at the University of California, Berkeley, obese mice who lost their sense of smell also lost weight.

Whats weird, however, is that these slimmed-down but smell-deficient mice ate the same amount of fatty food as mice that retained their sense of smell and ballooned to twice their normal weight.

In addition, mice with a boosted sense of smell super-smellers got even fatter on a high-fat diet than did mice with normal smell.

The findings suggest that the odor of what we eat may play an important role in how the body deals with calories. If you cant smell your food, you may burn it rather than store it.

These results point to a key connection between the olfactory or smell system and regions of the brain that regulate metabolism, in particular the hypothalamus, though the neural circuits are still unknown.

This paper is one of the first studies that really shows if we manipulate olfactory inputs we can actually alter how the brain perceives energy balance, and how the brain regulates energy balance, said Cline Riera, a former UC Berkeley postdoctoral fellow now at Cedars-Sinai Medical Center in Los Angeles.

Humans who lose their sense of smell because of age, injury or diseases such as Parkinsons often become anorexic, but the cause has been unclear because loss of pleasure in eating also leads to depression, which itself can cause loss of appetite.

The new study, published this week in the journal Cell Metabolism, implies that the loss of smell itself plays a role, and suggests possible interventions for those who have lost their smell as well as those having trouble losing weight.

Sensory systems play a role in metabolism. Weight gain isnt purely a measure of the calories taken in; its also related to how those calories are perceived, said senior author Andrew Dillin, the Thomas and Stacey Siebel Distinguished Chair in Stem Cell Research, professor of molecular and cell biology and Howard Hughes Medical Institute Investigator. If we can validate this in humans, perhaps we can actually make a drug that doesnt interfere with smell but still blocks that metabolic circuitry. That would be amazing.

Riera noted that mice as well as humans are more sensitive to smells when they are hungry than after theyve eaten, so perhaps the lack of smell tricks the body into thinking it has already eaten. While searching for food, the body stores calories in case its unsuccessful. Once food is secured, the body feels free to burn it. Zapping olfactory neurons The researchers used gene therapy to destroy olfactory neurons in the noses of adult mice but spare stem cells, so that the animals lost their sense of smell only temporarily for about three weeks before the olfactory neurons regrew.

After UC Berkeley researchers temporarily eliminated the sense of smell in the mouse on the bottom, it remained a normal weight while eating a high-fat diet. The mouse on the top, which retained its sense of smell, ballooned in weight on the same high-fat diet.

The smell-deficient mice rapidly burned calories by up-regulating their sympathetic nervous system, which is known to increase fat burning. The mice turned their beige fat cells the subcutaneous fat storage cells that accumulate around our thighs and midriffs into brown fat cells, which burn fatty acids to produce heat. Some turned almost all of their beige fat into brown fat, becoming lean, mean burning machines.

In these mice, white fat cells the storage cells that cluster around our internal organs and are associated with poor health outcomes also shrank in size.

The obese mice, which had also developed glucose intolerance a condition that leads to diabetes not only lost weight on a high-fat diet, but regained normal glucose tolerance.

On the negative side, the loss of smell was accompanied by a large increase in levels of the hormone noradrenaline, which is a stress response tied to the sympathetic nervous system. In humans, such a sustained rise in this hormone could lead to a heart attack.

Though it would be a drastic step to eliminate smell in humans wanting to lose weight, Dillin noted, it might be a viable alternative for the morbidly obese contemplating stomach stapling or bariatric surgery, even with the increased noradrenaline.

For that small group of people, you could wipe out their smell for maybe six months and then let the olfactory neurons grow back, after theyve got their metabolic program rewired, Dillin said.

Dillin and Riera developed two different techniques to temporarily block the sense of smell in adult mice. In one, they genetically engineered mice to express a diphtheria receptor in their olfactory neurons, which reach from the noses odor receptors to the olfactory center in the brain. When diphtheria toxin was sprayed into their nose, the neurons died, rendering the mice smell-deficient until the stem cells regenerated them.

Separately, they also engineered a benign virus to carry the receptor into olfactory cells only via inhalation. Diphtheria toxin again knocked out their sense of smell for about three weeks.

In both cases, the smell-deficient mice ate as much of the high-fat food as did the mice that could still smell. But while the smell-deficient mice gained at most 10 percent more weight, going from 25-30 grams to 33 grams, the normal mice gained about 100 percent of their normal weight, ballooning up to 60 grams. For the former, insulin sensitivity and response to glucose both of which are disrupted in metabolic disorders like obesity remained normal.

Mice that were already obese lost weight after their smell was knocked out, slimming down to the size of normal mice while still eating a high-fat diet. These mice lost only fat weight, with no effect on muscle, organ or bone mass.

The UC Berkeley researchers then teamed up with colleagues in Germany who have a strain of mice that are supersmellers, with more acute olfactory nerves, and discovered that they gained more weight on a standard diet than did normal mice.

People with eating disorders sometimes have a hard time controlling how much food they are eating and they have a lot of cravings, Riera said. We think olfactory neurons are very important for controlling pleasure of food and if we have a way to modulate this pathway, we might be able to block cravings in these people and help them with managing their food intake.

Co-authors of the paper are Jens Brning, director of the Max Planck Institute for Metabolism Research in Cologne, Germany, and his colleagues Eva Tsaousidou, Linda Engstrm Ruud, Jens Alber, Hella Brnneke and Brigitte Hampel; Jonathan Halloran, Courtney Anderson and Andreas Stahl of UC Berkeley; Patricia Follett and Carlos Daniel de Magalhaes Filho of the Salk Institute for Biological Studies in La Jolla, California; and Oliver Hahn of the Max Planck Institute for Biology of Ageing in Cologne.

The work was supported by the Howard Hughes Medical Institute, the Glenn Center for Research on Aging and the American Diabetes Association.

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Smelling your food makes you fat - UC Berkeley

A state funded program created as the result of a bill by Pasadena-area State Senator Anthony Portantino which preserves blood stem cells found in the placenta and umbilical cord after childbirth for use in the treatment of a variety of blood cancers has received extended state funding.

On Thursday, AB 114 passed the State Senate and in that bill is a five-year extension of funding for the University of Californias Umbilical Cord Blood Collection Program (UCBCP). The current funding of this lifesaving cancer treatment effort is set to sunset on January 1, 2018.

The State Senate approved Governors proposal which was inserted in the State Budget by the State Senate Budget sub-committee chaired by Senator Anthony Portantino. Creation of the Cord Blood Collection Program was the first bill authored by Portantino when he entered the State Assembly in 2006.

Cord blood stem cells are left in the placenta and umbilical cord after a baby is born. These rich blood-forming cells are used to treat a variety of blood cancers such as Leukemia, Cycle Cell and Lymphoma. Cord blood is considered an essential alternative for patients who need a bone marrow transplant.

Despite its potential benefits, prior to Portantinos program umbilical cord blood was traditionally discarded as medical waste after a mother gives birth.

Since the UCBCP implementation in 2010, over 1,200 umbilical cord blood units have been added to the public registry. The University of California Davis currently reports 27 collected units under the UCBCP have been released for medical transplant. Cord Blood Stem Cells are statistically 100 times easier to match than bone marrow. About 1% of the public privately banks their familys stem cells after birth. The California program is an effort to capitalize on Californias diverse population and use that diversity to create a cord blood registry that can meet our populations health needs.

I am very excited that the legislature extended the funding for this important program in the fiscal 2017-2018 budget. The program was the result of the very first bill I introduced on my very first day in office as an Assemblymember. I am very pleased to be in a position today to extend the program for an additional five years. This will save a life and it feels pretty good to have played a part in that mission. commented Portantino.

Sen. Portantino represents nearly 930,000 people in the 25th Senate District, which includes Pasadena, Altadena, La Caada Flintridge, San Marino, Sierra Madre and South Pasadena.

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Pasadena Area State Senator Anthony Portantino's Signature California Umbilical Cord Blood Collection Program ... - Pasadena Now

Today, tracking the development of individual cells and spotting the associated factors under the microscope is nothing unusual. However, impairments like shadows or changes in the background complicate the interpretation of data. Now, researchers at the Technical University of Munich (TUM) and the Helmholtz Zentrum Mnchen have developed a software that corrects images to make hidden development steps visible.

When stem cells develop into specialized cells, this happens in multiple steps. But which regulatory proteins are active during the decisive branching on the development path? Using so-called time-lapse microscopy, researchers can observe individual cells at very high time resolutions and, using fluorescent labelling, they can recognize precisely which of these proteins appear when in the cell.

Once a stem cell has been identified, it can be closely observed over several days using cell-tracking software. Yet, this surveillance work often turns out to be difficult. The imaging data is frequently marred by irregular brightness and faded backgrounds in the time-lapse, explains Dr. Carsten Marr, heading the workgroup Quantitative Single Cell Dynamics at the Institute of Computational Biology (ICB) of the Helmholtz Zentrum Mnchen. This makes it difficult or impossible to detect proteins that are decisive when a cell opts for a specific development direction, so-called transcription factors.

Algorithms that filter out these kinds of artefacts exist, but they require either specifically prepared reference images, many images per dataset or complex manual adjustments. Furthermore, none of the existing methods correct alterations in the background over time, which hamper the quantification of individual cells.

Algorithm eliminates background changes Now, Dr. Tingying Peng, member of Dr. Carsten Marrs group at the Helmholtz Zentrum Mnchen and Professor Nassir Navab, head of the Chair for Computer Aided Medical Procedures and Augmented Reality at TU Munich, present an algorithm that corrects these artefacts using only a few images per dataset.

The software is called BaSiC and is freely available. It is compatible with many image formats commonly used in bioimaging, including mosaics pieced together from numerous smaller images and used, for example, to render large tissue regions. Contrary to other programs, however, explains Dr. Peng, BaSiC can correct changes in the background of time-lapse videos. This makes it a valuable tool for stem cell researchers who want to detect the appearance of specific transcription factors early on. Bringing significant details to light How well the new image correction program improves the analysis of individual stem cell development steps the scientists demonstrated with time-lapse videos of blood stem cells. They recorded the videos to observe cells over a six-day time span. At a certain point during this observation period undifferentiated precursor cells choose between two possible tacks of development that lead to the formation of different mature blood cells.

In images corrected using BaSiC, the researchers could identify a substantial increase in the intensity of a specific transcription factor in one of the two cell lines, while the amount of his protein in the other cell line remained unchanged. Without the image correction, the difference was not ascertainable.

Using BaSiC, we were able to make important decision factors visible that would otherwise have been drowned out by noise, says Nassir Navab. The long-term goal of this research is to facilitate influencing the development of stem cells in a targeted manner, for example to cultivate new heart muscle cells for heat-attack patients. The novel possibilities for observation are bringing us a step closer to this goal.

The BaSiC image correction program resulted from a close collaboration between the Chair of Mathematical Modeling of Biological Systems and the Chair of Computer Aided Medical Procedures & Augmented Reality at the Technical University of Munich and the Institute of Computational Biology (ICB) of the Helmholtz Zentrum Mnchen. Also involved were the Department of Biochemistry and Biophysics at the University of California in San Francisco (USA), as well as the Department of Biosystems Science and Engineering (D-BSSSE) at ETH Zrich and the Chair of Computer Aided Medical Procedure at Johns Hopkins University in Baltimore (USA).

This article has been republished frommaterialsprovided by the Technical University of Munich. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference:

Tingying Peng, Kurt Thorn, Timm Schroeder, Lichao Wang, Fabian J. Theis, Carsten Marr and Nassir Navab. BaSiC: A Tool for Background and Shading Correction of Optical Microscopy Images. Nature Communications 8, 14836 (2017) DOI: 10.1038/ncomms14836

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Clear View on Stem Cell Development - Technology Networks

By Vicki Ikeogu Monticello Times

Some days are better than others.

But lately, those days are rare and far between for Big Lake resident Kristi Hellen.

Ive never felt great, Hellen, 38, said. No, I never have great feeling days. Sometimes there would be a period 5 to 30 minutes a day that I would feel good. Now, thats down to just 5 to 10 minutes.

For the past 16 years the mystery surrounding Hellens crippling pain remained that, a mystery. Its been seven months since Big Lake resident Kristi Hellens chronic and crippling Lyme disease diagnosis. Hellen found two treatment options: One was taking a combination of medications, herbs and supplements for two years. The other was stem cell treatment at a clinic in California. Infusio Clinic in Beverly Hills, California, uses a patients own stem cells to help battle the disease. To cover the cost of the $35,350 for stem cell treatment, Hellen and her family have established a YouCaring site to thats raised just over $25,000 to date. Hellen will leave for her treatment Aug. 26. She will return to Big Lake on Sept. 11. (Submitted Photo)

Ive been diagnosed with depression, anxiety, chronic fatigue syndrome and fibromyalgia, Hellen said. Ive been on a few medications, but those would only make me feel like 20 percent better.

It wasnt until about a year ago and with the gentle persistence of a close friend that Hellen would get tested for a disease she feared: Lyme.

Those test results have since given Hellen something she hasnt had for almost two decades: hope.

Growing up in the Elk River and Zimmerman area, Hellen said she would spend a lot of time outdoors in her parents wooded yard.

We also would go to a cabin in Wisconsin, she said. And I would get bit by several ticks every year.

While none of those tick bites resulted in the trademark bullseye rash an early symptom of Lyme disease Hellen said during her teen years she would start getting severe migraine headaches. But it was nothing the avid dancer couldnt handle.

Until college. It was the summer after my freshman year in college, she said. My hands began hurting so much that I couldnt hold a pencil.

Hellen said she began feeling increasingly fatigued. Her back and neck began hurting to the point that she became immobile.

In my early 20s I had to move back home with my parents, she said. I physically was unable to take care of myself.

At that time, Hellen said she could push herself, forcing her body to retain some of her independence.

I so badly wanted to live a normal life, she said.

With the help and encouragement of her parents she started an in-home tutoring business. She even felt she had the strength to start dating.

Thats when I met my husband (Matt), Hellen said.

But dating while in crippling pain had its limitations.

After about five or seven dates I just didnt have enough energy to go out, Hellen said. So, a lot of our dates were him watching me rest.

But even still, Hellen said her then boyfriend stuck by her, eventually marrying her three years ago.

Our relationship is different than most, she said. My husband is a caregiver. And that can be hard at times for both of us. During this time, Hellen began questioning if her original diagnosis was accurate.

Hellen said she had been tested for Lyme disease at one point, but it came back negative. Dr. Glenn Nemec, a family medical practitioner with Stellis Health in Monticello, said that is a common issue with Lyme disease testing.

The tests that are currently out there, the tests that physicians use arent very good, he said. According to the Centers for Disease Control and Prevention those inaccuracies have to do with the length of time between the tick bite and when the testing is done.

The CDC finds that within the first few weeks of contracting Lyme disease, there is a higher likelihood of receiving a false negative on a blood test.

However, a second test, that can be administered approximately four to six weeks after contracting the disease, is likely to produce to clearer answer.

But that negative result Hellen had received wasnt enough to convince a good friend of hers who happens to suffer from chronic Lyme disease to encourage Hellen to get a second opinion.

With the assistance of a Lyme-Literate physician (a doctor who is specifically trained in identifying and treating Lyme disease) Hellens test results came back in November.

She had chronic Lyme disease.

Medicine as a body is not entirely convinced that Lyme disease is a chronic condition, Nemec said. There is some concern that the symptoms patients experience might not entirely be from the Lyme germ. There just isnt enough research out there.

Nemec did say there is a difference from acute Lyme disease and chronic Lyme disease (officially known as Post-treatment Lyme Disease Syndrome).

Nemec said there are three stages for acute Lyme disease.

The first stage, he said, can include the bullseye rash, but also presents symptoms like the flu. Most people will typically get the aches and pains, he said.

Acute Lyme disease can also progress into stage two which Nemec said can last for days or months.

During this stage people again have a lot of aches and pains and very sore muscles, he said. Stage three is when neurological problems can result.

On an average year, Nemec said he treats about a handful of people who test positive for Lyme disease. This year, with the warmer spring and ticks moving around a lot earlier, he anticipates seeing about 10 patients

However, with chronic Lyme disease, the CDC indicates those aches, pains and fatigue will last longer than six months.

Again, we are not entirely sure if that connection is genuine, Nemec said. The CDC indicates the medical communitys uncertainty with the link, adding that persistent symptoms might be a residual effect from the germ, not necessarily caused by Lyme.

But for Hellen, the symptoms aligned with the diagnosis.

When I was diagnosed I felt sad, she said. And then angry. Angry about the fact there isnt more knowledge about Lyme disease so I could have been diagnosed earlier. And now, feeling blessed that this has come to light. Now I finally have some direction as to where to seek treatment.

Its been seven months since Hellens chronic Lyme disease diagnosis.

Seven months of research. Seven months of searching for a treatment program that could give her back her life.

I basically found two options, Hellen said. One would be taking a combination of medications, herbs and supplements for two years. The other was stem cell treatment at a clinic in California.

Infusio Clinic in Beverly Hills, California, uses a patients own stem cells to help battle the disease.

Hellen said the two-week program would first help prepare her body for the treatment through IVs and other therapy methods.

Her stem cells would be harvested from her fat cells and then returned to her body at the end of the two weeks.

After about 100 days, Hellen would return to the clinic for a full assessment.

Ive talked with about 15 to 20 people who have done this type of treatment, Hellen said. Its a shorter recovery time and seems promising.

To cover the cost of the $35,350 for the treatment, Hellen and her family have established a YouCaring site to thats raised just over $25,000 to date.

Hellen will leave for her treatment on Aug. 26. She will return to Big Lake on Sept. 11. Yeah, Im nervous about how I will feel during the treatment, she said. They say the recovery will be tough. But to feel a little worse for a while to get my life back is so worth it.

Hellen has big plans for herself once she can fully walk again she has been bedridden and confined to a wheelchair for several years.

My parents have health issues, she said. My mom has fibromyalgia and my dad was just diagnosed with Stage-4 cancer, she said. So, I want to help them. But the very first thing I want to be able to do is go out on a date with my husband.

With tick season in full swing in Wright and Sherburne counties (considered to be a hot spot for Lyme disease according to Nemec) Hellen cautions all outdoor enthusiasts to be vigilant, especially when it comes to ticks.

If you have any symptoms at all get tested right away, she said. Educate yourself about Lyme disease and protect yourself.

Vicki Ikeogu is a freelance feature and business writer for the Monticello Times.

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Big Lake woman seeks stem cell treatment for chronic Lyme disease - Monticello Times

Ribosomes, which build a protein (black) from an RNA strand (blue), may specialize in making particular sets of proteins.

V. ALTOUNIAN/SCIENCE

By Mitch LeslieJun. 21, 2017 , 11:00 AM

The plant that built your computer isn't churning out cars and toys as well. But many researchers think cells' crucial protein factories, organelles known as ribosomes, are interchangeable, each one able to make any of the body's proteins. Now, a provocative study suggests that some ribosomes, like modern factories, specialize to manufacture only certain products. Such tailored ribosomes could provide a cell with another way to control which proteins it generates. They could also help explain the puzzling symptoms of certain diseases, which might arise when particular ribosomes are defective.

Biologists have long debated whether ribosomes specialize, and some remain unconvinced by the new work. But other researchers say they are sold on the finding, which relied on sophisticated analytical techniques. "This is really an important step in redefining how we think about this central player in molecular biology," says Jonathan Dinman, a molecular biologist at the University of Maryland in College Park.

A mammalian cell may harbor as many as 10 million ribosomes, and it can devote up to 60% of its energy to constructing them from RNA and 80 different types of proteins. Although ribosomes are costly, they are essential for translating the genetic code, carried in messenger RNA (mRNA) molecules, into all the proteins the cell needs. "Life evolved around the ribosome," Dinman says.

The standard view has been that a ribosome doesn't play favorites with mRNAsand therefore can synthesize every protein variety. But for decades, some researchers have reported hints of customized ribosomes. For example, molecular and developmental biologist Maria Barna of Stanford University in Palo Alto, California, and colleagues reported in 2011 that mice with too little of one ribosome protein have short tails, sprout extra ribs, and display other anatomical defects. That pattern of abnormalities suggested that the protein shortage had crippled ribosomes specialized for manufacturing proteins key to embryonic development.

Definitive evidence for such differences has been elusive, however. "It's been a really hard field to make progress in," says structural and systems biologist Jamie Cate of the University of California (UC), Berkeley. For one thing, he says, measuring the concentrations of proteins in naturally occurring ribosomes has been difficult.

In their latest study, published online last week in Molecular Cell, Barna and her team determined the abundances of various ribosome proteins with a method known as selected reaction monitoring, which depends on a type of mass spectrometry, a technique for sorting molecules by their weight. When the researchers analyzed 15 ribosomal proteins in mouse embryonic stem cells, they found that nine of the proteins were equally common in all ribosomes. However, four were absent from 30% to 40% of the organelles, suggesting that those ribosomes were distinctive. Among 76 ribosome proteins the scientists measured with another mass spectrometry-based method, seven varied enough to indicate ribosome specialization.

Barna and colleagues then asked whether they could identify the proteins that the seemingly distinctive ribosomes made. A technique called ribosome profiling enabled them to pinpoint which mRNAs the organelles were readingand thus determine their end products. The specialized ribosomes often concentrated on proteins that worked together to perform particular tasks. One type of ribosome built several proteins that control growth, for example. A second type churned out all the proteins that allow cells to use vitamin B12, an essential molecule for metabolism. That each ribosome focused on proteins crucial for a certain function took the team by surprise, Barna says. "I don't think any of us would have expected this."

Ribosome specialization could explain the symptoms of several rare diseases, known as ribosomopathies, in which the organelles are defective. In Diamond-Blackfan anemia, for instance, the bone marrow that generates new blood cells is faulty, but patients also often have birth defects such as a small head and misshapen or missing thumbs. These seemingly unconnected abnormalities might have a single cause, the researchers suggest, if the cells that spawn these different parts of the body during embryonic development carry the same specialized ribosomes.

Normal cells might be able to dial protein production up or down by adjusting the numbers of these specialized factories, providing "a new layer of control of gene expression," Barna says. Why cells need another mechanism for controlling gene activity isn't clear, says Cate, but it could help keep cells stable if their environment changes.

He and Dinman say the use of "state-of-the-art tools" makes the results from Barna's team compelling. However, molecular biologist Harry Noller of UC Santa Cruz doubts that cells would evolve to reshuffle the array of proteins in the organelles. "The ribosome is very expensive to synthesize for the cell," he says. If cells are going to tailor their ribosomes, "the cheaper way to do it" would entail modifying a universal ribosome structure rather than building custom ones.

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There are millions of protein factories in every cell. Surprise, they're not all the same - Science Magazine