8 replies to this topic

[kevin]

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Link:	http://www.eurekaler...h-ros111403.php
Date:	11-16-03
Author:	Amy Hoskins -br- amy@womens-health.org -br- 202-496-5011
Source:	Society for Women's Health Research
Title:	Research on spleen cells could yield potential cure for Type 1 diabetes

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Research on spleen cells could yield potential cure for Type 1 diabetes
Washington, D.C. -- Spleen cells may develop into insulin-producing pancreatic islet cells in adult animals, a breakthrough finding that could yield a potential cure for type 1 diabetes. Published in the Nov. 14 issue of Science, the finding stems from a study conducted by Denise Faustman, M.D., Ph.D., director of Massachusetts General Hospital (MGH) Immunobiology Laboratory and chair of the Society for Women's Health Research (SWHR) board of directors.

The finding builds on a 2001 study conducted by Faustman and a team of MGH researchers in which a treatment that cures advanced type 1 diabetes in mice was discovered. In discovering the biological mechanism behind that accomplishment, the researchers also have opened a potential new approach to replacing diseased organs and tissues using adult precursor cells.

"We have found that it is possible to rapidly regrow an adult organelle without the use of embryonic stem cells," said Faustman, the study's principal investigator. "By accomplishing effective, robust and durable regeneration of islets, this discovery opens up an entirely new approach to diabetes treatment."

Type 1 diabetes develops when the body's immune cells mistakenly attack the insulin-producing islet cells of the pancreas. As islet cells die, insulin production ceases, and blood sugar levels rise, damaging organs throughout the body. In their earlier study, Faustman's team directly attacked this process by retraining the immune system not to attack islet cells.

The researchers expected to follow that process, which eliminated the autoimmune basis of the animals' diabetes, with transplants of donor islet cells. However, they were surprised to find that most of the mice did not need the transplant: Their bodies were producing normal islet cells that were secreting insulin. [:o]

"The unanswered question from that study was whether this was an example of rescuing a few remaining islet cells in the diabetic mice or of regeneration of the insulin-secreting islets from another source," said Faustman, an associate professor of Medicine at Harvard Medical School. "We've found that islet regeneration was occurring and that cells were growing from both the recipient's own cells and from the donor cells."


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The Society for Women's Health Research is the nation's only not-for-profit organization whose mission is to improve the health of women through research, education and advocacy. Founded in 1990, the Society brought to national attention the need for the appropriate inclusion of women in major medical research studies and the need for more information about conditions affecting women disproportionately, predominately, or differently than men. The Society advocates increased funding for research on women's health; encourages the study of sex differences that may affect the prevention, diagnosis and treatment of disease; promotes the inclusion of women in medical research studies; and informs women providers, policy makers and media about contemporary women's health issues. Visit the Society's Web site at http://www.womens-health.org for more information.

[kevin]

vfb:

Type I diabetes is an 'autoimmune' disorder, as the article points out. The body attacks the islet cells for reasons which are not affected by diet and adjustments in sugar intake are not an effective treatment as they are in Type II. It usually strikes earlier in life as well, hence the name it is sometimes referred to as Juvenile Type I Diabetes.

[kevin]

A 'retard' doesn't fit the description.

The specific surface antigen which the T-cells recognize on the islets is unknown and I haven't read anything about lectins being the trigger, if you have any info on that I would appreciate a link. Lately, it is being thought to be in conjunction with viral infection (see below). Viruses are being implicated increasingly in conditions which they normally wouldn't have been thought of being involved in, but they can throw our biochemistry out pretty simply by turning a switch. Cancer of different types, Alzheimers, and certain neurological conditions are among the growing list.

If you are interested in any 'hard science studies' done on ANYTHING, you can visit http://www.pubmed.com and fill your boots by typing a search term. Even the abstracts are becoming less boring as time goes on.

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http://www.niaid.nih...ne.htm#diabetes

Immune-Mediated or Type 1 Diabetes Mellitus

Type 1 diabetes mellitus results from autoimmune destruction of the insulin-producing cells of the pancreas. Insulin is required by the body to keep the blood sugar (glucose) level under control. High levels of glucose are responsible for the symptoms and the complications of the disease. However, most of the insulin-producing cells are destroyed before the patient develops symptoms of diabetes. Symptoms include fatigue, frequent urination, increased thirst, and possible sudden confusion.

Type 1 diabetes mellitus is usually diagnosed before the age of 30 and may be diagnosed as early as the first month of life. Together with Type 2 diabetes (not considered an autoimmune disease), diabetes mellitus is the leading cause of kidney damage, loss of eyesight, and leg amputation. Close control of sugar levels decreases the rate at which these events occur. There is a genetic predisposition to Type 1 diabetes, which occurs in 1 out of 800 people in the United States. Among individuals who have a close relative with Type 1 diabetes, those at high risk for developing disease can be identified. Efforts are now under way to evaluate prevention strategies for these family members at risk.

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http://www.nlm.nih.g.....0risk factors

The exact cause of type 1 diabetes is not known. Type 1 diabetes accounts for 3% of all new cases of diabetes each year. There is 1 new case per every 7,000 children per year. New cases are less common among adults older than 20.

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http://www.drgreene.com/21_1068.html

Who gets it?
Type 1 diabetes most often strikes young people, especially between the ages of 5 and 7 (when viruses run through the schools), or at the time of puberty (when so many hormones change). For this reason, it used to be called juvenile-onset diabetes. This term has now been eliminated, since we now know that it can appear at any age.

People who get type 1 diabetes were born with a genetic predisposition to it. Not everyone born with this predisposition gets diabetes, however. In fact, if an identical twin has diabetes, the other twin only gets diabetes about half the time. Some predisposed individuals are exposed to something in the environment that triggers the diabetes. This is usually a viral infection. The virus misleads the body's immune system into making antibodies that attack its own pancreatic cells.

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[Mind]

Viruses are being implicated increasingly in conditions which they normally wouldn't have been thought of being involved in, but they can throw our biochemistry out pretty simply by turning a switch. Cancer of different types, Alzheimers, and certain neurological conditions are among the growing list.

And I thought the virus theory of cancer was nearly dead. You would think that after 30 years, billions of dollars, and miserable failure, the virus hunters would have given up. It is my opinion that the virus hunters hold too much sway in medical science. To them, every illness is caused by a virus.

Now, it may be that over a lifetime, viral damage or infection builds up to the point where certain diseases can be triggered (doubtful). The question then becomes, what then? What is there to do? Vaccinate against every single virus known to man. Don't laugh, I am sure there are some virus hunters out there thinking that would be a great idea.

[kevin]

Mind:

Some cancers are almost definitely caused by viral infection.

Human Papilloma Virus of which there are over 30 strains is ubiquitous in the human population. Strains 11 and 16 are almost certainly implicated in cervical cancer as well as a in the head and neck and ano-genital neoplasia. There are currently clinical trials with vaccines targeting the products (protein E7) of HPV integrated viral genomes which seem to be involved in the dysregulation of cellular differentiation and proliferation.

Check http://www.stressgen.com for an example of this. Normally our immune systems take care of viruses quite well, but for some, combinations of genetics, environment and it seems time, are enough to affect the pathways of cell division and form benign neoplasias which if the right circumstances occur can become malignant. This is pretty much guaranteed at this point for some cancers.

[chubtoad]

http://www.scienceda...40331005610.htm

Compound Shows Promise As Vaccine-like Drug For Preventing Type 1 Diabetes

Researchers have identified a compound that shows promise in animal studies of becoming the first effective drug for the prevention of type 1 diabetes, or insulin-dependent diabetes, which afflicts about one million people in the United States and is on the rise worldwide.

The synthetic compound, called ISO-1, appears to work by blocking a pathway involved in inflammation. If successful as a vaccine-like drug, it could ultimately save lives, reduce health care costs and help prediabetic people avoid a lifetime of insulin injections, the researchers say. Their work was described today at the 227th national meeting of the American Chemical Society, the world's largest scientific society.

"We believe this is the most promising compound to date for preventing type 1 diabetes," says study leader Yousef Al-Abed, Ph.D., an associate investigator at North Shore-Long Island Jewish Research Institute in Manhasset, N.Y. "If it works, it will be especially beneficial for young people, who often have a difficult time managing their diabetes with daily insulin injections."

The compound targets prediabetic individuals, defined as those who have blood markers — either antibodies or genetic markers — that are predictive of the disease. Using certain blood tests, many of these individuals can now be identified long before they actually develop type 1 diabetes (also known as juvenile diabetes). More testing is needed before the compound is ready for human use, which could be several years, say Al-Abed and his associates, who hope to develop the compound into a long-acting oral drug.

When ISO-1 was given via injection over a ten-day period to mice that were also given a chemical designed to induce a form of type 1 diabetes, ISO-1 completely protected them from developing the disease. By contrast, all of the mice treated only with the diabetes-inducing chemical developed the disease. In a similar controlled experiment, ISO-1 was given via injection to mice that were genetically bred to develop diabetes, preventing the onset of diabetes in 90 percent of the treated mice, the researchers say.

In both groups of mice receiving ISO-1, the animals continued to make insulin throughout the duration of their treatment and did not show any signs of adverse effects from the compound. The benefits were long-lasting, according to Al-Abed, since ISO-1 protected the animals from developing the disease for up to two months after the treatment was stopped.

The investigators believe that ISO-1 works by blocking a recently identified protein called macrophage migration inhibitory factor (MIF), which appears to play a major role in the cascade of inflammatory events leading to the destruction of pancreatic beta cells, which normally produce insulin, and the subsequent onset of the disease.

Although an increasing number of compounds are being designed to fight diabetes by targeting inflammation, the current study represents the first attempt to prevent type 1 diabetes by targeting the MIF protein, says Al-Abed, whose group first identified the protein as a possible target to fight the disease.

Because ISO-1 is a relatively small chemical compound, it could be easily developed into an oral drug that functions like a vaccine, says Al-Abed. He predicts that such a drug would only need to be taken a few times by prediabetic people in order to achieve long-lasting protection, perhaps a lifetime.

ISO-1 is being tested in animals to determine whether it will help in the actual treatment of ongoing type 1 diabetes and type 2 diabetes, the more common type. Results are not yet available from these tests, the researchers say.

There is currently no cure for diabetes. A few other research groups worldwide are attempting to develop vaccines to prevent type 1 diabetes, but none of the drug candidates has hit the market. The disease can be controlled and its complications minimized by following a healthy diet, getting exercise and taking prescribed medications as directed, according to health experts.

[chubtoad]

http://www.scienceda...40514031141.htm

Mechanism Found That May Protect Kidneys In Early Stages Of Diabetes

A group of Northwestern University researchers has identified what they believe is a built-in biological mechanism that prevents kidney damage in the early stages of diabetes associated with obesity.

Their study was led by Daniel Batlle, M.D., Earle, del Greco, Levin Professor of Nephrology and professor of medicine at Northwestern University Feinberg School of Medicine, and was published in the May issue of the journal Hypertension.

Batlle and colleagues assessed the activity of two enzymes, ACE (for angiotensin-converting enzyme) and ACE2, which play an important role in the control of blood pressure, in the kidneys of a young mouse model of obesity and diabetes. The mouse, called db/db, develops type 2, insulin-resistant diabetes and obesity at around four to seven weeks after birth and eventually manifests some, but not all, features of human diabetic nephropathy.

In eight-week old db/db mice, which were obese and had high levels of blood glucose but no evidence of diabetes-related kidney disease, the researchers found low levels of a substance known as ACE (for angiotensin-converting enzyme) and increased levels of a related enzyme, ACE2.

The significance of a reduction in ACE coupled with increased ACE2 production in the kidneys needs to be clarified, said Minghao Ye, research associate in medicine at the Feinberg School and first author on the study.

ACE is required for production of angiotensin II (AngII), which, among its actions, causes blood vessel constriction and sodium and water retention by the kidney, leading to hypertension and kidney damage.

ACE inhibitors, which block production of AngII, are commonly used to treat high blood pressure and heart failure, as well as to improve survival after a heart attack and slow progression of kidney disease in individuals with diabetes.

ACE2, which was recently discovered, prevents accumulation of AngII while promoting formation of another substance called Ang(1-7), which dilates blood vessels and helps eliminate excess water and sodium from the kidneys. ACE inhibitors do not block ACE2 production.

"Since AngII over-production is thought to play a pivotal role in the progression of diabetic nephropathy, we suggest that decreased renal ACE activity coupled with increased renal ACE2 expression may be protective for the kidneys in the early phases of diabetes by limiting the renal accumulation of AngII and possibly by favoring Ang(1-7) formation, as well," Batlle said.

Interestingly, the finding of a decrease in ACE activity and an increase in ACE2 expression in the young mouse model, is similar to a pattern seen after administering a kidney-protecting drug and ACE inhibitor called ramipril to diabetic rats, Batlle said.

Batlle said that an increased ACE2 level in the kidneys in early diabetes does not exclude the possibility of an ACE2 reduction later, during the course of the disease as kidney damage develops. He believes it is possible that with time decreased ACE2 expression with an increase in ACE may foster damage in diabetes.

"The significance of a reduction in ACE coupled with increased ACE2 production in the "kidneys needs to be further studied but there is every reason to believe that it can only be beneficial," Batlle said.

"We know that giving ACE inhibitors can protect against kidney disease, but we need to learn more about ACE2 in diabetes, obesity and hypertension," he said.

Kidney disease is among the most common complications of diabetes, affecting over 20 percent of the 17 million diabetic patients in the United States.

In addition to Ye, Batlle's co-researchers on the study were Jan Wysocki, Parveen Naaz, Mohammad Reza Salabat and Michael S. LaPointe of the Feinberg School.

[Cyto]

CellTran also aims to develop off-the-shelf products which can be used in the patient's home, avoiding visits to outpatient clinics altogether.

Not going to hold my breath. Kinda scares me too, feeling a little sick now... [lol]

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Innovative 'self healing' bandage to help diabetics

EPSRC Press Release
A revolutionary type of 'self healing' bandage that uses the patient's own cells is being developed. The technique has already been tried successfully on patients with diabetic ulcers and in the long-term could offer a more effective, quicker and cost efficient way of treating many types of slow-healing wounds such as pressure ulcers. The bandages are already available for patients with severe burns.

The bandages have been developed by CellTran Ltd., a spin-out company from the University of Sheffield. CellTran has grown from fundamental research funded by the Engineering and Physical Sciences Research Council (EPSRC).

Levels of diabetes in the UK are forecast to rise significantly in the years ahead. Chronic ulcers affect many diabetics, with sufferers often attending clinics for months or years to have their wounds dressed. CellTran offers an innovative but simple approach to healing diabetic ulcers and other slow-healing wounds, based on a combination of surface engineering and cell biology.

A small tissue sample is taken from a patient and a culture is grown from the cells in a laboratory. The cells are then placed on a membrane made from a medical-grade polymer. The membrane has been treated with a special cell-friendly coating, enabling skin cells to attach and grow on this surface. When cells are ready, the cell-membrane bandage is taken to the relevant clinic and used to dress the patient's wound instead of a standard bandage.

Because these cells belong to the patient, they are not rejected by the body but can actually transfer to the wound and grow. For particularly difficult wounds, the cells are applied every week. Early clinical studies have shown that weekly dressings enable these difficult wounds to heal in an average of eight weeks. Clinical trials are now under way, and the technique is also being used on other types of ulcer and on patients with extensive burns.

The underlying EPSRC-funded work at the University has focused on the development of surfaces that human cells will not only grow on but also transfer from to the patient's wound. It is also developing new approaches to culturing human skin cells without using animal derived products such as bovine serum.

The new bandages could take some pressure off healthcare budgets by reducing the need for long-term patient treatment. CellTran also aims to develop off-the-shelf products which can be used in the patient's home, avoiding visits to outpatient clinics altogether. Sheila MacNeil, CellTran's Research & Development Director and Professor of Tissue Engineering at the University of Sheffield, says; "we are moving the technology through to clinical use as quickly as we can and our objective is to make it as simple to use and as low-cost as possible".

[chubtoad]

http://www.bcm.edu/p...pe1diabetes.htm

New gene associated with type 1 diabetes

HOUSTON - (July 20, 2004) - A new gene mutation identified by researchers at Baylor College of Medicine in Houston is part of the constellation of genes associated with susceptibility to developing type 1 diabetes. It could also play a role in the devastating complications of diabetes such as kidney failure.

The gene called SUMO-4 contributes a portion of the risk of this form of diabetes, which typically strikes youngsters, said Drs. David Owerbach, Kurt Bohren and Kenneth Gabbay. Owerbach and Bohren are associate and assistant professors in the section of molecular diabetes and metabolism in the department of pediatrics at BCM, respectively. Gabbay is professor of pediatrics and head of the section.