Thursday, February 26, 2009

TNF blocker pills, creams? Yes!

Remicade in a pill? Oral Enbrel? Humira as a cream? TNF alpha blocker eye drops to stop Behcet's? Yes, all of that is coming. As soon as the FDA gets out of the way and lets it happen.

Research and Markets: TNF Antagonists: Most Successful with Plenty of Competition in the Pipeline
Feb 24, 2009 - Research and Markets

( has announced the addition of the "Competitor Analysis: TNF Antagonists & Agonists" report to their offering.
The present Competitive Intelligence Report about Tumor Necrosis Factor (TNF) and TNF receptor antagonists and agonists used to treat TNF-mediated inflammatory diseases such as rheumatoid arthritis or to treat cancer, respectively, provides a competitor evaluation in the field of R&D projects with TNF Antagonists & Agonists as of February 2009.

TNF blockers are the commercially most successful single-target group of biologic therapies. 2008 sales of the four approved brands were US$16.35 bln with double digit growth rates due to indication expansion and new market entrants. Abbott's fully human antibody Humira recorded 2008 sales growth of 48% over the previous year which may explain why competitors with the established brands Enbrel and Remicade also have fully human anti-TNF antibodies in their pipeline. Forthcoming patent expiries also may have encouraged to develop next generation anti-TNF antibodies. Clinical indications approved for therapy with TNF blockers include rheumatoid arthritis (RA) and juvenile RA, ankylosing spondylitis, psoriatic arthritis, psoriasis in adults and in children, Crohn's disease and pediatric Crohn's disease, and ulcerative colitis.

As in other cases, a clinically validated target with commercial success attracts companies to exploit and leverage their new technologies. Next generations of TNF blockers may bring orally bioavailable versions, locally applied TNF blockers, antagonists with higher binding affinities or better tissue penetration due to smaller size. At least 15 clinical stage and 19 preclinical stage are under evaluation in various indications including ophthalmic use, osteoarthritis, Behcet's disease, organ transplantation, cutaneous sarcoidosis, oral mucositis, atopical dermatitis and sepsis.

The report includes a compilation of marketed products and their sales in 2008 and current active projects in research and development of TNF antagonists and agonists. In addition, the report lists company-specific product portfolios and R&D pipelines of TNF antagonists and agonists.

Competitor projects are listed in a tabular format providing information on:

Drug Codes,
Target / Mechanism of Action,
Class of Compound,
Product Category/Therapeutic Area,
R&D Stage and
additional comments with a hyperlink leading to the source of information.
Competitor Analysis: TNF Antagonists & Agonists
Sales of TNF Antagonists in 2008

More B cell news

B cells as targets for asthma as well as autoimmune? Turning off select B cell clones and turning off allergy? or autoimmune disease? All is becoming possible. Rituxan is good first step in B cell depletion, but much better is coming. Read below.

Contact: Tom Rickey
University of Rochester Medical Center
A worm-and-mouse tale: B cells deserve more respect

By studying how mice fight off infection by intestinal worms – a condition that affects more than 1 billion people worldwide – scientists have discovered that the immune system is more versatile than has long been thought. The work with worms is opening a new avenue of exploration in the search for treatments against autoimmune diseases like diabetes and asthma, where the body mistakenly attacks its own tissues.

The findings, reported by scientists who performed the work at the Trudeau Institute in Saranac Lake, N.Y., and who are now at the University of Rochester Medical Center, appear in the March issue of the journal Immunity. The article was published online Feb. 26.

The research focuses mainly on B cells, one of many types of immune cells that the body maintains to fight off invaders like bacteria, viruses, and parasites. Besides B cells, there are T cells, macrophages, neutrophils, monocytes, mast cells and others, all working in concert to keep an organism healthy. The cells cruise our bodies, looking to eliminate infectious threats before they become a serious risk to our health.

For many years, scientists believed that the major job of B cells was to identify foreign invaders and tag them with antibodies, marking the microbe for destruction by the immune system. But scientists are discovering that B cells do much more, resulting in new information about our immune system that could be useful for developing more effective vaccines and better treatments for many types of disease.

In the past few years, Frances Lund, Ph.D., professor of Medicine in the Division of Allergy/Immunology and Rheumatology at the University of Rochester Medical Center, has found an array of unexpected functions for B cells. In the laboratory, she has found that B cells produce chemical signaling molecules known as cytokines that spur other immune cells in the body to action. Her team has also shown that B cells are crucial for presenting to T cells snippets of proteins from invaders, so that the T cells can recognize the invader, a crucial step that allows T cells to mature into useful cells which can then fight an infection efficiently.

In the new paper, Lund's team tested how the findings actually translate by watching closely as an organism – in this case, a mouse – actually fights off infection by a parasite. They chose to study the intestinal parasite Heligmosomoides polygyrus, a bright red worm about one-third of an inch long that infects mice.

It's a cousin of the scores of worms that infect more than 1 billion people worldwide. Roundworms, hookworms, pinworms, and others – these and other worms cause fatigue, diarrhea, nausea, and death.

"Nematodes – worms – sicken a lot of people, they can cause severe malnutrition, and they play havoc with the immune system, making many people more vulnerable to other threats, such as malaria," said Lund, whose project was funded by the National Institute of Allergy and Infectious Diseases.

The team not only verified the additional actions of B cells that they've discovered in the laboratory, but, importantly, they showed that these functions are crucial for the organism to fight off infection.

Lund's team showed that the chemical messengers produced by B cells, such as interleukin-2 and tumor necrosis factor, are necessary for the immune system to protect mice against Heligmosomoides polygyrus. The team also showed that B cells must be present in order for T cells to mature and operate properly.

"It's long been dogma that B cells need the help of T cells to make antibody. That's in all the textbooks," said Lund. "Now work from our laboratory and others shows that it's a two-way street, that T cells need the help of B cells also."

B cells' effects on T cells may open a new window on such diseases as lupus, asthma, multiple sclerosis, and diabetes, where doctors know that T cells are active. Maybe manipulating B cells offers a new way to affect the activity and survival of the T cells that cause disease.

The work also brings up the possibility of more targeted treatments than current treatments, which generally affect all B cells. Lund has found that different B cells produce different collections of chemical signaling molecules. Someday, instead of having a drug that simply targets all B cells, it may be possible to target a specific type of cell, cutting down side effects and making a treatment more effective.

"It may be that only certain B cells play a role in damaging immune responses. If we can narrow down the group of cells at the root of the problem, we may be able to find important new targets for improving treatment," said Lund.

The paper is dedicated in memory of author Frank Sprague, who was a technical associate at Trudeau and performed many of the experiments.

The first authors of the paper, who share equal credit, are post-doctoral associate Wojciech Wojciechowski, now at Rochester, and former post-doctoral associate David P. Harris, now with Lexicon Genetics. Other authors in addition to Sprague include technicians Betty Mousseau and Kim Kusser, now at Rochester; former technician Melissa Makris; Markus Mohrs and Katja Mohrs of Trudeau; Tasuko Honjo of Kyoto University; and Troy Randall, Ph.D., professor of Medicine at the University of Rochester Medical Center.

Most of the research described in the paper was done by Lund's group at the Trudeau Institute, before the group moved to Rochester last summer.

Contact: Cathleen Genova
Cell Press
Busy Bs: Lymphocyte uses multiple mechanisms to shape immune response

New research expands our understanding of how a type of immune cell called a B lymphocyte enables the immune system to mount a successful defense against an intestinal parasite. The study, published by Cell Press online in the journal Immunity on 26 February, provides some intriguing insight into the variety of mechanisms implemented by B cells to protect the host from infection.

B cells are critical cells of the immune system that produce antibodies (Abs) to help rid the body of harmful pathogens. This type of immunity, called "humoral immunity", is complemented by "cellular immunity" which is mediated by T lymphocytes. Research has shown that B cells do not just produce Abs but can regulate the immune response in many other ways as well. B cells produce critical regulatory chemicals called cytokines and there is some evidence that B cells may amplify T cell dependent immune responses.

An earlier study by Dr. Frances E. Lund from the Department of Medicine at the University of Rochester indicated that specific types of B cells may promote the maturation of T cells. To gain insight into the mechanisms used by B cells, Dr. Lund and colleagues performed a series of experiments to examine whether cytokine-producing B cells are required for protection against the intestinal parasite, Heligmosomoides polygyrus (Hp).

The researchers found that B cells were required for protection against Hp and that B cells mediate protection, in part, by producing Abs. In addition, B cells promoted the production and long-term maintenance of an essential type of T cell, called T helper 2 cells (Th2), which are known to be critical for protection from Hp. Importantly, the influence of B cells on the Th2 cells was independent of antibody production.

The researchers went on to show that B cell-derived cytokines interleukin-2 and tumor necrosis factor ? were required both for effective Ab and for Th2 cell responses to Hp. Therefore, in addition to Ab production, B cells also make a critical contribution to the immune response to this pathogen by regulating T cells.

"Our findings fill an important gap as they show for the first time that multiple cytokines made by B cells regulate both humoral and cellular protective immune responses to infectious organisms," says Dr. Lund. "In addition to protective effects, we also suggest that cytokine-producing B cells may play a role in damaging immune responses, such as reactions to allergens and autoantigens. Therefore, B cell subsets may represent future targets for many types of therapeutics to treat allergy, asthma and autoimmunity."

The researchers include Wojciech Wojciechowski, Trudeau Institute Inc., Saranac Lake, NY, University of Rochester, Rochester NY; David P. Harris, Trudeau Institute Inc., Saranac Lake, NY, Lexicon Genetics, The Woodlands, TX; Frank Sprague, Trudeau Institute Inc., Saranac Lake, NY, Betty Mousseau, Trudeau Institute Inc., Saranac Lake, NY, University of Rochester, Rochester NY, Melissa Makris, Trudeau Institute Inc., Saranac Lake, NY, Kim Kusser, Trudeau Institute Inc., Saranac Lake, NY, University of Rochester, Rochester NY, Tasuko Honjo, Kyoto University, Yoshida-Konoe, Sakyo-Ku, Kyoto, Japan, Katja Mohrs, Trudeau Institute Inc., Saranac Lake, NY, Markus Mohrs, Trudeau Institute Inc., Saranac Lake, NY, Troy Randall, University of Rochester, Rochester NY, and Frances E. Lund, Trudeau Institute Inc., Saranac Lake, NY, University of Rochester, Rochester NY.

Tuesday, February 24, 2009

FDA fails to protect us and Americans know it

The American public now realizes how incompetent the FDA bureaucrats are at protecting our foods. Hopefully soon they will realize that FDA incompetence also is keeping sick Americans from having access to clinical trial cures. FDA bureaucrats, through incompetence or something more sinister, have delayed breakthrough medications and cures for years even decades. Prime example is Ustekinumab. Other examples are HuMax CD-20. The biggest breakthrough since the discovery of Penicillin is the discovery of a universal blood and immune stem cell formulation that allows any patient's immune system, no matter what HLA type, to accept these universal cells (Prochymal by Osiris). Prochymal should be in shot gun try it against everything trials for a hundred different autoimmune and blood disorders. That it is not, indicates complete lack of imagination on part of FDA and complete lack of understanding of the breakthroughs in stem cell technology that are here now.

Here is the article indicating the American public's complete distrust in the FDA:

U of Minnesota study finds confidence in food safety plunges in wake of peanut butter contamination

Fewer than one in four consumers now believe the US food supply is safer than it was a year ago

Fewer than one in four consumers now believe the U.S. food supply is safer than it was a year ago, according to new data from the University of Minnesota's Food Industry Center.

After January's national salmonella outbreak, just 22.5 percent of consumers in the study said they were confident the food supply is safer than a year ago, the lowest reading since the study began in May 2008. Eight people died and more than 500 have become ill in the most recent outbreak, which may have originated in a Georgia peanut plant and spread through peanut-butter products sold nationwide.

The drop in confidence mirrors a similar drop last June, when a salmonella outbreak later traced to jalapeno peppers sickened nearly 1,500 people. The study involves continuously tracking consumer confidence in food supply safety via a weekly online survey of about 175 consumers from across the nation. The consumers are selected each week by a national market research company.

Several measures are being collected on an ongoing basis to monitor consumer concerns, expectations and perceptions of the safety of the food supply from natural/accidental contamination, and the defense of the food supply from deliberate contamination from an act of terrorism. These measures soon will be used to develop a composite food confidence indicator similar to the Consumer Sentiment Index that measures overall consumer confidence.

The indicator is unique because of its continuous tracking feature, said Jean Kinsey, director of the Food Industry Center. Consumers' response to food-borne illnesses and recalls helps inform the design of food safety strategies and regulations, and consumer confidence "is critical to their peace of mind as well as to the economic health of the entire food industry."

The ongoing study is conducted jointly with the Louisiana State University AgCenter and is funded by the National Center for Food Protection and Defense.

Saturday, February 21, 2009

FDA delays another breakthrough--increased "workload" extends review

The lazy FDA bureaucrats have again delayed a new drug for which there is NO alternative on the market today. They say they have "an increased workload" so they have to "extend the review." Poor babies. Sick Americans suffer while FDA bureaucrats take two hour lunches. It is now FIFTY YEARS since the drug was discovered. Let's hear for the heroes at the FDA.

Here is the article:

Hemispherx plays the FDA waiting game
February 20, 2009 — 12:17pm ET By
Calisha Myers

Hemispherx Biopharma says the FDA, citing an increased workload, has extended its review for Ampligen for the treatment of chronic fatigue syndrome. No drug candidate has received FDA approval for the treatment of chronic fatigue syndrome, but supporters remain confident in the drug's potential.

Kim McCleary, president and CEO of the Chronic Fatigue and Immune Dysfunction Syndrome Association of America, tells the Philadelphia Business Journal that the group remains optimistic that the FDA will find Hemispherx's data sufficient for an approval. "If it is approved, it is expected to be quite expensive," McCleary said. "[Ampligen] has shown to be effective in certain subsets of the condition... If they get an approval, we think other companies will follow them in and it will lead to more research."

It has taken Hemispherx some time to get to this stage. The company began as HEM--a Maryland-based contract services company that primarily provided research services for the NIH and NASA. It was reorganized into a drug development company in the 1980s. Since then, the company has fired and rehired its CEO (who co-invented Ampligen), battled with a Wall Street shortseller after going public and avoided an alleged hostile takeover, the Business Journal reports.

The original compound for Ampligen was discovered at Merck in the 1960s. The drug candidate Ampligen has has been under development for over three decades and has been studied as a treatment for a range of diseases, including AIDS, cancer and the avian flu.
As of September 30, Hemispherx had an accumulated deficit of $182.5 million, according to its latest SEC report.

Smoking as a Cause of Autoimmune Disease

Smoking can be a "trigger" for autoimmune disease specifically Multiple Sclerosis. There is an article below makes that association.

The question is why? No one knows the answer for sure, just like no one knows what triggers autoimmune disease to start in otherwise healthy people.

However it is known that identical twins do not both get an autoimmune disease at the same time or one might not get an autoimmune disesease the other has at all.

There are many instances of identical twins with one affected and the other not. One identical twin goes his/her whole long life with no sign of autoimmune and the other twin is horribly affected for decades before dying. Identical twins have identical genes, so how could this happen?

Epigenetics. This is a newly discovered environmental effect on our genes as we age.

Infection or CHEMICALS cause permanent changes to our genes during our lifetimes by turning off or on certain of our genes. These changes can be measured. Studies that measure these changes have been done on identical twins. It seems that twins are most similar at birth. The older identical twins get the more differences in gene expression they have. Gene expression is a measure of which genes are turned on and turned off. Environmental insults cause epigenetic changes to our genes which are seen as changes in gene expression.

Cigarette smoke is one such environmental insult. There are many others. You can pretty much guess what they are pesticides, cleaning chemicals, environmental smoke, diesel exhaust, etc.

Good news is there are proven medication that can reverse epigenetic changes. (HDAC is one.)These meds are in clinical trials for cancer right now.

Bad news the FDA is delaying the approval of this revolution in reversing epigenetic changes with red tape causing clinical trials to be too specific and too long lasting. The interference is no different than the FDA throws at the stem cell revolution and at new more effective autoimmune disease modifying drugs like ustekinumab.

Here are the articles. The first is about cigarette smoking associated with MS. The next about how lung cancer rates drop when cigarette smoking drops. The third is about President Obama's struggle to stop smoking.

Contact: Jenine Anderson
American Academy of Neurology
Young smokers increase risk for multiple sclerosis
Young Smokers Increase Risk for Multiple Sclerosis

SEATTLE – People who start smoking before age 17 may increase their risk for developing multiple sclerosis (MS), according to a study released today that will be presented at the American Academy of Neurology's 61st Annual Meeting in Seattle, April 25 to May 2, 2009.
The study involved 87 people with MS who were among more than 30,000 people in a larger study. The people with MS were divided into three groups: non-smokers, early smokers (smokers who began before age 17), and late smokers (those who started smoking at 17 or older), and matched by age, gender, and race to 435 people without MS.

Early smokers were 2.7 times more likely to develop MS than nonsmokers. Late smokers did not have an increased risk for the disease. More than 32 percent of the MS patients were early smokers, compared to 19 percent of the people without MS.

"Studies show that environmental factors play a prominent role in multiple sclerosis," said study author Joseph Finkelstein, MD, PhD, of Johns Hopkins University School of Medicine, in Baltimore, MD, which conducted the study in collaboration with Veterans Affairs MS Center for Excellence. "Early smoking is an environmental factor that can be avoided."
The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as multiple sclerosis, restless legs syndrome, Alzheimer's disease, narcolepsy, and stroke.

For more information about the American Academy of Neurology, visit
The AAN 61st Annual Meeting, the world's largest gathering of neurology professionals, takes place April 25 to May 2, 2009, in Seattle. Visit for more information.
Editor's Note: Study authors are available for interviews. Please contact Jenine Anderson, or Jay Mac Bride,

To access 2009 AAN Annual Meeting abstracts available February 25, 2009, visit

Experts predict 20 per cent drop in lung cancer rate

Published: Thursday, 19-Feb-2009

Cancer Reserach UK experts are predicting that lung cancer rates will drop by nearly a fifth over the next 20 years, according to new figures.

Successful anti-smoking measures - such as the tobacco advertising ban and the legislation making public places smokefree - have meant the number of smokers has continued to drop.

But, although lung cancer rates will continue to fall - from around 50 people per 100,000 to around 40 by 2024 - the overall number of people diagnosed with the disease looks set to increase.

People living longer, combined with the delay between smoking and the onset of lung cancer means cases in the UK are expected to rise from around 38,500 to more than 41,600 by 2024.
Smoking causes around 90 per cent of lung cancers so as smoking rates have fallen so has the rate of lung cancer. The difference in lung cancer trends for men and women is dramatically mirrored by the smoking patterns for each sex.

More men than women have been diagnosed with lung cancer since records began. This is because more men have smoked. By 2024 women's lung cancer rate will drop, reflecting the female smoking rate falling by half between the mid-70s and today. But, the number of women diagnosed in the UK each year is expected to increase from around 15,500 today to more than 18,000 by 2024.

Men's lung cancer rates were highest in the early 1970s with more than 150 men in every 100,000 diagnosed with lung cancer. This reflected the peak in smoking rates in the 1940s and 50s. Even though the male lung cancer rate is set to drop by more than a quarter between now and 2024 the number of cases diagnosed in the future will remain similar to those diagnosed today - around 22,000.

Professor Max Parkin, co-author of the report, said: "These predictions are based on what we know to date about the current figures and trends for lung cancer. We can see that lung cancer rates should continue to drop but the number of cases will increase.

"This increase will mostly be in women which reflects the peak rates of smoking among women back in the 1970s. Lung cancer is unique in that we can track the reduction in cases with a reduction in the number of people exposed to a specific product - cigarette smoke. As fewer people smoke we should see a lower rate of the disease."

Jean King, Cancer Research UK's director of tobacco control, said: "These figures highlight just how effective tobacco control measures can be and how important it is for work to continue in this area. We know that nine in ten cases of lung cancer are caused by smoking but that one in five people still smoke, so it's vital we all work to protect future generations from this scourge.

"We want to see tobacco products put out of sight and out of mind in the upcoming tobacco control legislation. We would like a commitment from the government to introduce a comprehensive and well funded tobacco control strategy - one that stops young people from beginning an addiction that kills half of all long term smokers, and fully supports smokers to quit."


Obama on front lines in battle to stop smoking
Experts say his efforts to quit illustrate how difficult it is.
By Victoria Stagg Elliott, AMNews staff. Posted Jan. 19, 2009.

Physicians and other smoking-cessation advocates have found a high-profile illustration of the challenges of quitting tobacco: President-elect Barack Obama.

"His honesty should help a lot of people, because it's just not that easy to quit smoking," said Anthony Atkins, MD, a family physician and director of minority health and community outreach for the Lima Community Health Center in Lima, Ohio.

Obama has smoked intermittently for years, tried to quit several times and chewed nicotine gum, according to a report on his health compiled by his primary care physician, David L. Scheiner, MD, and released in May 2008 by his presidential campaign. According to more recent news reports, he still lights up occasionally but has pledged to respect the ban on smoking in the White House. To those who work on smoking issues, his situation is a very public example of how difficult quitting can be and how much effort it can require.

"He has not given up, and people should not give up or feel that they are failures if they do not quit smoking on the first or second or third attempt. They should just continue to try until they get it," said Carolyn Barley Britton, MD, president of the National Medical Assn.

Many physicians also hope he will be a role model for African-American men in particular. This demographic group tends to smoke more than do white males, although the numbers for white and black women are comparable. African-Americans experience a disproportionate rate of disease associated with tobacco use. The reason for this is unclear, but data from the National Cancer Institute's Surveillance Epidemiology and End Results indicate that African-Americans are 17% more likely than Caucasians to develop lung cancer.

Many experts praised Obama for taking all the right steps, even if it appears he has not yet been successful.

"This is an incredible opportunity to help educate the majority of smokers in America who want to quit, and those who have tried to quit and have failed, that this is a chronic medical condition and there are evidence-based treatments available," said Michael C. Fiore, MD, MPH, director of the Center for Tobacco Research and Intervention at the University of Wisconsin in Madison.

The American Medical Association encourages physicians to use practice guidelines to help patients with smoking cessation, such as Treating Tobacco Use and Dependence: 2008 Update.
Dr. Fiore chaired the panel that authored the document, which was released in May 2008 by the U.S. Public Health Service. It recognized tobacco dependence as a chronic disease that often requires more than one intervention and several attempts to quit.

African-Americans are 17% more likely than Caucasians to develop lung cancer.

The Update also advocates using existing treatments to improve the chance of success.
In addition, anti-smoking advocates are optimistic that Obama's personal experience with attempting to give up tobacco will trigger more interest in legislation amenable to reducing the number of smokers.

"My hope is that his firsthand knowledge of the power of tobacco will influence his administration in confronting tobacco dependence in our society," Dr. Fiore said.
According to the report on Obama's health, he exercises regularly and eats a balanced diet. His blood pressure is 90/60 and his pulse 60 beats per minute. His triglycerides are 44, total cholesterol 173, HDL cholesterol 68 and LDL cholesterol 96. Dr. Scheiner rated his health as excellent.

The print version of this content appeared in the Jan. 26, 2009

Friday, February 20, 2009

Ustekinumab found effective AGAIN! FDA STILL DELAYS!

Ustekinumab was found effective in yet another study.

When will the bureaucrats at the FDA approve its use?

The FDA bureaucratic cowards will not tell. I have personally written and asked the FDA three times. Three times they have sent me a form email with NO INFORMATION.

Also notice in the article that the Mengele monsters at the FDA required a placebo group of psoriasis patients to suffer so that "pretty numbers" could be had in this study. Not every study needs "pretty numbers' of a placebo group. Especially not in WELL KNOWN diseases whose disease progression has been well studied and long known.

Thursday, February 19, 2009

FDA requires Patients to Die for "Pretty Numbers" in Rituxan study

The following article is primarily about the fact that giving Rituxan more than one time for patients with B cell cancers prolongs their lives but hidden in the middle of it is a couple of lines about clinical trials required by the Mengeles at the FDA that required patients to die in order for the FDA to accept the findings of a clinical trial.

Patients were divided into three groups chemotherapy only, Rituxan only, and Rituxan plus chemotherapy. One of those groups was a DEATH CAMP group. Can you tell which one?

It was the chemotherapy alone. Clinical trials with those chemotherapy agents were done YEARS AGO. The results are in and known. There is no reason to redo those trials. The patients live a little longer than no treatment but they die and they die on average in a certain number of months that WAS ALREADY KNOWN. It was determined in clinical trials YEARS AGO.

The FDA required patients with fatal B cell cancer whose average number of months of remaining life was already known to take those less than ideal chemotherapy drugs alone and to die so FDA bureaucrats could have pretty numbers. PLACEBO GROUPS ARE DEATH CAMP GROUPS. The FDA bureaucrats who require these pretty numbers are MURDERERS.

Do you suppose the people who died for the FDA to have pretty numbers had families and friends who were devastated? Well what does it matter, requiring redundant trials to find the same thing again and again is what the FDA bureaucrats are good at. The most awful part is the bureaucrats who require patients to die always get promoted and never get demoted or fired. It is time to change the culture of death at the FDA.

Read the article below:

Rituximab Should Be Used for Maintenance in Follicular Lymphoma

Zosia Chustecka
Medscape Medical News 2009. © 2009 Medscape
February 18, 2009 — Rituximab should be used for maintenance therapy in patients with relapsed or refractory follicular lymphoma after successful induction therapy because it significantly improves survival.

This is the conclusion from a new meta-analysis of 5 trials, involving more than 1000 patients, published in the February 18 issue of the Journal of the National Cancer Institute.
"This meta-analysis demonstrates for the first time, to our knowledge, that rituximab maintenance therapy improves overall survival and disease control," say the researchers, headed by Liat Vidal, MD, from the Rabin Medical Center, in Petah-Tikva, Israel.

"Rituximab should be used for patients with relapsed follicular lymphoma after successful induction treatment," Dr. Vidal told Medscape Oncology. Such use is not currently recommended in guidelines, but many physicians are already doing this, he said.

Already Established in First-Line Treatment

Rituximab is already established in the first-line treatment of follicular lymphoma, for which it is often used in combination with chemotherapy. As reported by Medscape Oncology, a recent editorial in the Journal of Clinical Oncology (2008;26:4537-4538) said it was "time to declare a giant leap forward," because patients with follicular lymphoma are now living longer than ever and rituximab has been a major contributor to the progress that has been made in the treatment of this disease.

However, the question of what to do when a patient relapses or becomes refractory has not had a clear answer. Dr. Vidal and colleagues point out that individual trials exploring rituximab use in this situation have shown a prolongation of remission and of the progression-free interval, but have not yielded any clear evidence of an impact on overall survival. As a result, rituximab maintenance for follicular lymphoma is not recommended in treatment guidelines, such as those issued by the National Comprehensive Cancer Network, they point out.

Now, however, Dr. Vidal and colleagues have shown a clear survival advantage from the meta-analysis of 5 trials that they performed. The trials involved 1143 patients, but survival data were available for only 985 patients.

Patients who received rituximab maintenance had significantly better overall survival that those who did not (hazard ratio [HR] for death, 0.60; 95% confidence interval [CI], 0.45–0.79).
However, patients taking rituximab were twice as likely to have an infection-related adverse effect (HR, 1.99; 95% CI, 1.21–3.27), and some of the infections reported in these patients were life-threatening, Dr. Vidal and colleagues report. "The higher rate of infections should be taken into consideration when making treatment decisions," they say.

Survival Advantage Seen With Both Schedules

The 5 trials in the meta-analysis used various drug combinations and administration schedules, but the type of rituximab maintenance schedule had no effect on overall survival, the researchers note.

At the time when the clinical trials were initiated, rituximab was not yet established as a standard in first-line treatment, so some patients received it in their induction regimen and others did not. Some patients were treated with first-line rituximab alone, some with rituximab and chemotherapy, and some with chemotherapy alone. (these patients died months earlier than the other two arms of the clinical trial)

In addition, the maintenance regimens varied. In 3 trials, rituximab was administered weekly for 4 consecutive weeks (4 doses) every 6 months, whereas in the 2 other trials, a single infusion of rituximab was administered every 2 to 3 months. The duration of treatment varied from 8 to 9 months to 2 years.

"Our results suggest that rituximab maintenance therapy for up to 2 years, either as 4 weekly infusions every 6 months or as a single infusion every 2 to 3 months, should be added to standard therapy of patients with relapsed or refractory follicular lymphoma after successful induction treatment," Dr. Vidal and colleagues conclude.

This study was performed as part of, and with the support of, the Cochrane Hematological Malignancies Group of the Cochrane Collaboration. Dr. Vidal disclosed no relevant financial relationships. Two of his coauthors, Martin Dreyling, MD, from the Univeritat Munchen-Grobhadern, in Germany, and Michele Ghielmini, MD, from the Swiss Group for Clinical Cancer Research, in Bern, Switzerland, report receiving research funding and either consultancy fees or speaker honorarium from Roche, the manufacturer of rituximab.
J Natl Cancer Inst. 2009:101:248-255.

Re-booting immune system ends autoimmune disease

It has been known for ten years or so that 're-booting' the immune system can cure various inflammatory autoimmune diseases--Crohn's, RA, psoriasis, PsA, MS, diabetes type I etc. But it is a bit dangerous. Some patient's die. Here is an article from Spain which describes the procedure well. There are many places in the United States that will also do this procedure. Google to find a place near you. I recall several places. Fred Hutchins Cancer Center Seattle, a couple of places in Boston, maybe UCLA--anyway here is the article:

(The therapy described is NOT new contrary to the line in the article below. Instead it is old technology. It is a decade or more old.

The truly new and revolutionary new therapy is Prochymal--living immune adult stem cells from many many donors. These cells live inside of the patient and make the missing regulatory signals that settle down the immune system.

With the autogolous stem cell therapy below, the "bad guy" cells are temporarily eliminated. They may stay gone for life or they may be regenerated in just a few weeks (esp for Lupus patients) before the disease returns.

Autologous Stem Cell therapy is a temporary re-boot and it does not provide a source of regulatory cells or their cytokine products that would keep the disease from ever returning. Prochymal on the other had DOES provide those regulatory cells.

I currently do NOT recommend this "cure" because of the significant death rate, the cost, and the fact that a MUCH BETTER alternative is in phase II clinical trials right now in the United States. That is PROCHYMAL by Osiris.

All inflammatory autoimmune patients should have Prochymal ACCESS NOW!!!!!)

Contact: Maria Trenzado
IDIBAPS - Institut d'Investigacions Biomèdiques August Pi i Sunyer
New therapy with stem cells to treat Crohn's disease

• When drugs don't work and surgery is not possible, transplanting stem cells from the patient's own bone marrow is an effective alternative for the treatment of this chronic disease.
• The procedure has been tested successfully in the US and Italy, where total remission of the disease has been shown in 80% of cases, and considerable improvement in quality of life in the remaining 20% of cases. Since August 2008, Hospital Clínic has used this therapy in a total of 6 patients.
• In Spain, this disease affects 1% of the population between 18 and 40 years of age and each year approximately 2000 new cases are diagnosed. This regenerative therapy constitutes a new focus on the use of stem cells in intestinal diseases.

Barcelona, February 19, 2009. Cellular therapy with stem cells is revolutionizing the focus of treatment of many serious diseases. Replacing the cells of damaged tissue with other new cells from the same patient is already a reality. This is the basis of cellular therapy and regenerative medicine, the latest great advance in biomedicine.

In this line, Hospital Clínic, Barcelona is leading the world in the application of an innovative cellular therapy that uses stem cells to treat Crohn's disease, a chronic genetic disease that affects 1% of the population in Spain and which has considerable impact on the quality of life of the patients. The procedure is based on an autologous bone-marrow transplant (when patients receive a transplant of their own stem cells) and now constitutes a treatment option to cure an intestinal disease that sometimes does not successfully respond to drugs and requires highly complex surgery that does not provide a cure.

Hospital Clínic, Barcelona is one of the few hospitals in the world to apply this new therapeutic option for patients with Crohn's disease, and it does so with the guarantee of success experienced in the US and Italy, where the technique has been tested with excellent results: in an average follow-up period of 6 years, 80% of transplant patients are in a phase of total remission of the disease and the remaining 20% have shown considerable improvement following the transplant, and are now responding favorably to drugs. Dr. Julián Panés and Dr. Elena Ricart over the Gastroenterology Department of Hospital Clínic, Barcelona are the driving force behind this therapy in Spain and began to implement regenerative cellular therapy in patients with Crohn's disease in August 2008. To date, a total of 6 patients are benefiting from this new treatment, of whom 3 I've already completed the process and are in the follow-up face, and a further 3 are at different stages of therapy. The transplant requires several weeks of admission to hospital before patients receive their own cells.

The success of autologous stem-cell transplants in Crohn's disease is possible thanks to the joint collaboration of the gastroenterology and hematology departments and of the hemotherapy and hemostasis department, as the procedure is the same as that carried out in bone-morrow transplants to cure leukemia or myeloma. Thus, when a case is detected, the professionals from the different departments of Hospital Clinic, Barcelona supervise each of the phases of the process to autologous Transplant. In this case, Dr. Panés and Dr. Ricart from the gastroenterology department work together with Dr. Montserrat Rovira from the hematology department of the Catalan hospital and with Dr. Enric Carreras, the head of this department, to provide joint monitoring of the patients. Dr. Pedro Marín of the hemotherapy and hemostasis department of Hospital Clínic, together with Dr. Miquel Lozano, are responsible for guiding the patients through the process of cryopreservation and collection of stem cells before the final transplant.

Cellular Therapy as a Strategy to Combat Crohn's Disease.

Crohn's disease, together with ulcerative colitis, is included in what is called irritable bowel disease. It is a chronic genetic disease that occurs when the immune system loses tolerance to the patient's own intestinal flora, leading to an abnormal inflammatory response that continues over time. The results are inflammation and ulceration in different areas of the digestive tract, leading to the symptoms. The disease progresses in the form of unpredictable and variable outbreaks throughout the patient's life and the severity of the symptoms varies according to the level of involvement of the intestines and the patient's response to the assigned treatment. It is a disease that usually affects young people between the ages of 18 and 40 years, and approximately 2000 new cases are diagnosed in Spain every year. Diagnosis is often difficult because it presents symptoms similar to those of other diseases of the digestive tract: abdominal pain, diarrhea, vomiting, nausea, fever, general malaise, etc. Patients' quality of life is conditioned by the severity of the disease and, in the most severe cases, prevents them from leading a normal life, with a very high level of suffering due to the acuteness and frequency of the intestinal symptoms.

Hospital Clínic de Barcelona is one of the few hospitals in the world to instate cellular therapy using autologous stem-cell transplantation. In the US, the treatment has been tested on 12 patients with severe Crohn's disease, of whom 11 have had very good results; in Italy, the treatment has been applied to 4 patients, 3 of whom are also showing excellent progress following the transplant. As Hospital Clínic, 6 patients with Crohn's disease are already included in the process and, following the international examples, increasing numbers of patients are expected to choose this option to treat the disease in a state that was, to date, practically untreatable.

In severe cases involving recurrent outbreaks (reactivation of the disease several times throughout the patient's life), Crohn's disease presents several treatment options. Firstly, doctors choose to use corticosteroids and immunosuppressant and biological drugs to control the inflammatory process and prevent complications of the disease such as stenosis (narrowing of the intestinal lumen) or fistulas (openings from the intestinal lumen to other organs, such as the intestine, bladder, vagina, or skin). However, over the course of the disease, as much as 70% of severe patients require surgery to remove segments affected by the disease, due to failure of the pharmacologic approach. The surgery is occasionally very aggressive for the patient, as it is sometimes necessary to remove the entire colon or large sections of the small intestine, thereby considerably affecting the absorption of food by the intestine, with a resulting deterioration in quality of life and body image (colostomy bag). For this reason, new treatments are being developed for patients in whom this solution has not been an option to date.
Autologous Stem-Cell Transplant: Phases of the Procedure.

When the case is detected (that does not respond to drugs or surgery), the patient undergoes an autologous stem-cell transplant, which is a bone-morrow transplant in which the immune system is reset to prevent it from attacking the intestinal flora. The process lasts approximately 2 months and consists of 6 phases:

1. Initial Chemotherapy (Cyclophosphamide + G-CSF). In this initial phase, leukopenia or reduction of the number of leukocytes (immune-system cells) in the blood is induced in the patient.

2. Migration of Stem-Cells to the Blood. Following the previous immunosuppression, the organism reacts by releasing stem cells from the bone marrow into the blood; these are the cells which will later be used for the transplant.

3. Collection of Stem Cells by means of Apheresis. Apheresis is a technique that separates components of the blood. Here, the stem cells that previously migrated from the bone marrow are separated.

4. Cryopreservation of Stem Cells. When the stem cells have been collected by apheresis, they are frozen and preserved until ready for transplant.

5. Second Chemotherapy. In this phase, total leukopenia is induced; that is, the immune system is left devoid of leukocytes, ready to be reset with the stem-cell transplant.

6. Autologous Stem-Cell Transplant. The patient receives the transplant by means of transfusion with his or her own stem cells. The immune system is reset, leading to remission or reduction of the abnormal inflammatory process of Crohn's disease.

Autoimmune Induced Fatigue Cause Found

My son, Paul, has psoriasis, psoriatic arthritis, and ankylosing spondylitis. He is tired all the time. He used to be a ball of non stop energy--running to his college classes at UCSD instead of taking the slow tram. Now especially as he gets closer to needing his next Remicade infusion, he gets more and more tired.

Many have observed that autoimmune disease causes a kind of chronic fatigue. Although our physician often feel it is important to try to motivate autoimmune sufferers to exercise more and get on with their lives. There is a reason for patients to be so tired and listless. The attempts at humiliation and scorn by our physician friends really is counter productive. I wish every physician who treated autoimmune patients would read the following article:

How Inflammatory Disease Causes Fatigue
19 Feb 2009

New animal research in the February 18 issue of The Journal of Neuroscience may indicate how certain diseases make people feel so tired and listless.

Although the brain is usually isolated from the immune system, the study suggests that certain behavioral changes suffered by those with chronic inflammatory diseases are caused by the infiltration of immune cells into the brain.

The findings suggest possible new treatment avenues to improve patients' quality of life.

Chronic inflammatory diseases like rheumatoid arthritis, inflammatory bowel disease, psoriasis, and liver disease cause "sickness behaviors," including fatigue, malaise, and loss of social interest.

However, it has been unclear how inflammation in other organs in the body can impact the brain and behavior.

The researchers found that in mice with inflamed livers, white blood cells called monocytes infiltrated the brain.

These findings support previous research demonstrating the presence of immune cells in the brain following organ inflammation, challenging the long-held belief that the blood-brain barrier prevents immune cells from accessing the brain.

"Using an experimental model of liver inflammation, our group has demonstrated for the first time the existence of a novel communication pathway between the inflamed liver and the brain," said the study's senior author Mark Swain, MD, Professor of Medicine at the University of Calgary.

Swain and his colleagues found that liver inflammation triggered brain cells called microglia to produce CCL2, a chemical that attracts monocytes. When the researchers blocked CCL2 signaling, monocytes did not enter the brain despite ongoing inflammation in the liver.

Liver inflammation also stimulated cells in the blood to make an immune chemical (TNFα).
(blog editor note: This is why Paul's mood gets better after an infusion with a TNFalpha blocker like Remicade--sorry I had to write alpha as I do not know how to make the greek letter, alpha, with my keyboard)

When the researchers blocked the signaling of this immune chemical, microglia produced less CCL2, and monocytes stayed out of the brain.

In the mice with inflamed livers, preventing the entry of monocytes into the brain reduced sickness behaviors; mice showed more mobility and social interaction. These findings suggest that people with chronic inflammatory diseases may benefit from treatments that limit monocyte access to the brain.

"Sickness behavior significantly impacts quality of life. Our findings further our understanding and may generate potential new avenues for treatment of these often crippling symptoms," said Swain.

"The brain is the master coordinator of many of our bodies' defense responses, so it must be able to sense injury and inflammation in distant body organs. This study starts to explain the peripheral communication signals that activate the brain," said Nancy Rothwell, PhD, DSc, at the University of Manchester, an expert on brain inflammation who is unaffiliated with the study.

-------Article adapted by Medical News Today from original press release.---------------------

The research was supported by the Canadian Institutes of Health Research, the Canadian Liver Foundation, and the Alberta Heritage Foundation for Medical Research. The Journal of Neuroscience is published by the Society for Neuroscience, an organization of more than 38,000 basic scientists and clinicians who study the brain and nervous system. Source: Todd Bentsen Society for Neuroscience
Article URL:
Main News Category: Neurology / NeuroscienceAlso Appears In: Arthritis / Rheumatology, Biology / Biochemistry, Immune System / Vaccines,

Wisconsin finds treatment for deadly medicine induced PML

PML is a deadly disease of the brain that was unknown before the advent of new autoimmune medications that help autoimmune disease but cripple the patient's immune system in some way. PML is an occult brain virus that many of us carry in our bodies. It is harmless to us unless our bodies loose the ability to fight it. Several really good autoimmune meds can trigger it in carriers. At first it was nearly 100% fatal and the VERY few survivors were left with mental deficits. Patients taking Tysabri, Rituxan and now Raptiva have come down with the disease.

Now good news, a Wisconsin hospital has found a way to eliminate the medicine that cripples the patient's immune system allowing PML to develop. The pull the blood serum (yellow fluid red blood cells float in) and replace it with donated serum. This procedure helps in two ways. One it reduces greatly the amount of medicine causing the problem. Two it introduces serum from healthy donors whose serum may have PML fighting antibodies in it as well as autoimmune fighting antibodies. IVIG--intravenous immunoglobin (serum) is one treatment for autoimmune disease.

Good news patients with PML now have a real chance to survive. Bad news is they can no longer take the medicine that was helping their autoimmune disease or any other med associated with allowing PML to break out as they will continue to carry the virus.

We need permanent cures for autoimmune disease. We need stem cells cures used in ALL patients now. Prochymal by Osiris is the fist of these. All patients especially those surviving PML should have ACCESS NOW! Prochymal is made of precursor immune cells. They live inside recipients body and make the regulatory cells and cytokines we need to get healthy again and stay healthy for years if not for life.

First article below is about Wisconsin breakthrough in PML treatment. (BROWN)

Second article is about Raptiva causing PML. (BLUE)
Source: Aurora St. Luke's Medical Center
Wednesday, February 18, 2009

Researchers at Aurora St. Luke's Medical Center have developed a technique that counteracts an unusual, but serious, side effect from natalizumab (Tysabri®), a drug that fights multiple sclerosis (MS).

The side effect is a brain virus called progressive multifocal leukoencephalopathy (PML).
"This virus looks like a multiple sclerosis relapse," Dr. Bhupendra Khatri says. "It rapidly destroys the white matter of the brain. Now we know exactly how to respond if this virus emerges."

The response is a series of plasma exchanges that filter the drug out of the blood stream, allowing the immune system to recover and fight the virus.

Multiple sclerosis is a disease where the body's immune system attacks the protective sheath surrounding the nerves. Natalizumab suppresses the immune system to slow or halt the progression of the disease. However, if the patient contracts PML, the immune system is not strong enough to combat the infection, so the drug needs to be removed from the body quickly.

Dr. Khatri, medical director of Aurora's Regional MS Center is lead author of the study published in the Feb. 3 issue of Neurology, the official publication of the American Academy of Neurology.

In the study 12 multiple sclerosis patients on natalizumab underwent three plasma exchange sessions over a five-day or an eight-day period. By replacing the drug-infused plasma with clean fluid, Dr. Khatri and his team were able to get 92 percent of the drug out of patients' bodies over a span of eight days instead of the 12 weeks it would take with no treatment.

Debra Goodwin, a clinical research nurse who worked on the study and a multiple sclerosis patient herself, says the discovery gives new hope to those with the disease who take natalizumab.

"If something were to go wrong, now there is a demonstrated method to remove the drug from the body and help the patient fight PML," Goodwin says.
The National Multiple Sclerosis Society estimates 400,000 people in the United States have MS. There is no cure for multiple sclerosis though there are several drugs that can slow or stop its progress. Symptoms can include blurred vision, loss of coordination and short-term or long-term memory loss.

Aurora Health Care is a not-for-profit health care provider and a national leader in efforts to improve the quality of health care. Aurora offers care at sites in more than 90 communities throughout eastern Wisconsin.
Aurora's online newsroom:
The Regional MS Center:
CONTACT: Myrle Croasdale, +1-414-649-3917, or pager, +1-414-222-4332,, for Aurora St. Luke's Medical Center
Web site:


FDA Advises Public of Serious Adverse Event with Psoriasis Drug Raptiva

The U.S. Food and Drug Administration today issued a public health advisory concerning three confirmed, and one possible report of progressive multifocal leukoencephalopathy (PML), a rare brain infection, in patients using the psoriasis drug Raptiva (efalizumab). Three of those patients have died. All four patients were treated with the drug for more than three years. None of the patients were receiving other treatments that suppress the immune system.

The FDA is reviewing this latest information. The agency will take appropriate steps to:
• ensure that the risks of Raptiva do not outweigh its benefits;
• that patients prescribed Raptiva are clearly informed of the signs and symptoms of PML; and
• that health care professionals carefully monitor patients for the possible development of PML.

PML is caused by a virus that affects the central nervous system. PML usually occurs in people whose immune systems have been severely weakened. It leads to an irreversible decline in neurologic function and death. Symptoms may include unusual weakness, loss of coordination, changes in vision, difficulty speaking and personality changes. There is no known effective prevention or treatment.

Psoriasis is a chronic disease, for which a number of effective therapeutic options are available, including four other approved biologic agents, ultraviolent light therapy, and the drugs cyclosporine, acitretin, and methotrexate. Generally, treatment for psoriasis patients involves a rotation of therapies.

In October 2008, the product labeling for Raptiva was revised to highlight in a boxed warning the risks of life-threatening infections, including PML. At that time, the FDA directed Genentech, the manufacturer, to develop a risk evaluation and mitigation strategy (REMS) to include a medication guide to educate patients about the drug’s risks.

The FDA strongly recommends that health care professionals carefully monitor patients on Raptiva, as well as those who have discontinued the drug, for any signs or symptoms of neurologic disease, and that they periodically reassess the benefits of continued treatment. Patients should be aware of the symptoms of PML and contact their health care professionals immediately if they experience any such symptoms.

Raptiva is a once-weekly injection approved for adults with moderate to severe plaque psoriasis who are candidates for systemic (whole body) therapy or phototherapy. The drug works by suppressing T-cells (blood cells that help fight infection) in the immune system. These cells, when activated, migrate to the skin and cause inflammation which results in the red, inflamed and scaly patches of skin, which is associated with psoriasis. By suppressing T-cells, Raptiva decreases the function of the immune system which increases a patient’s susceptibility to infections.

Health care professionals and consumers may report serious adverse events (side effects) or product quality problems with the use of this product to the FDA's MedWatch Adverse Event Reporting program online, by regular mail, fax or phone.

--Regular Mail: use postage-paid FDA form 3500 available at: and mail to MedWatch, 5600 Fishers Lane, Rockville, MD 20852-9787
--Fax: (800) FDA-0178
--Phone: (800) FDA-1088

Read the FDA’s 2009 Public Health Advisory

Breast feeding relieves autoimmune disease?

Below is an article describing a small study that seems to indicate that there is a protective effect for mothers with Multiple Sclerosis to breast feed babies. It seems to indicate that breast feeding without taking meds is more beneficial for the moms than not breastfeeding and resuming meds immediately after birth. Interesting. However the numbers of mothers looked at is small so no definite conclusions can be drawn.

I wonder if the breast feeding affect is found in women who have other autoimmune diseases as well? Too bad the authors of the study did not also look at mothers with diabetes type I, RA, SLE, psoriasis and other autoimmune disease. What helps one autoimmune condition often helps other autoimmune conditions as well especially the ones caused by out of control inflammatory responses (type I diabetes, psoriasis, PsA, RA, MS).

Here is the article:

Can breastfeeding reduce multiple sclerosis relapses?

SEATTLE – Women who have multiple sclerosis may reduce their risk of relapses after pregnancy if they breastfeed their babies, according to a study released today that will be presented at the American Academy of Neurology's 61st Annual Meeting in Seattle, April 25 to May 2, 2009.

For the study, researchers followed 32 pregnant women with MS and 29 pregnant women without MS during each trimester and up to a year after they gave birth. The women were interviewed about their breastfeeding and menstrual period history.

A total of 52 percent of the women with MS did not breastfeed or began supplemental formula feedings within two months of giving birth. Of those, 87 percent had a relapse after pregnancy compared to 36 percent of women with MS who breastfed exclusively for at least two months after pregnancy.

Sixty percent of the women reported their main reason for not breastfeeding exclusively was to start taking MS treatments again. Women who began taking MS treatments within the first two months after giving birth had significantly higher risk of suffering a relapse than women with MS who did not start taking medications early, regardless of whether they breastfed. Those who breastfed exclusively got their menstrual periods back later than the women who did not breastfeed or began early supplemental feedings.

"Our findings call into question the benefit of choosing not to breastfeed or stopping breastfeeding early in order to start taking MS therapies," said study author Annette Langer-Gould, MD, PhD, of Stanford University in California, and a member of the American Academy of Neurology. "Larger studies need to be done on whether women should delay taking MS medications in order to breastfeed."
The study was supported by the National Institutes of Health and the Wadsworth Foundation.
The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as multiple sclerosis, restless legs syndrome, Alzheimer's disease, narcolepsy, and stroke.

For more information about the American Academy of Neurology, visit
The AAN 61st Annual Meeting, the world's largest gathering of neurology professionals, takes place April 25 to May 2, 2009, in Seattle. Visit for more information.
Editor's Note: Study authors are available for interviews. Please contact Jenine Anderson, or Jay Mac Bride,

To access 2009 AAN Annual Meeting abstracts available February 25, 2009, visit

Linda Powers blasts FDA as "not balanced" or "open minded"

Linda Powers of Toucan Capital has blasted the FDA's "lack of balance" between science and the needs of the patients. She says the FDA "is guardian of safety and effectiveness" of new medications and therapies but it is "supposed to do it in a balanced way that reflects the needs of the public and the country's health care system". She further rightly points out that the FDA bureaucrats are not "open minded" and should not make the same requirements over and over again at each different level of regulatory hurtle."

Our poorly educated and timid friends at the FDA find it so much safer for their own personal jobs to require the very same tests be done over and over again in clinical trial after clinical trial. What's proven in Phase I trials must be demonstrated again in Phase II trials and again in Phase III trials. This unnecessary repetition in not only enormously expensive, it is time consuming and much, much worse pointlessly time wasting while Americans are suffering and dying. While my son, Paul, sits in pain in a wheel chair.

In her podcast at the Genetic Engineering website she says that there are over 200 clinical trials of stem cells going on right now. These trials are showing remarkable success. Yet are being relentlessly delayed by FDA red tape.

If American patients understood the revolution of cures that is here right now waiting to be used, they would sweep the FDA bureaucrats out of the way.

Once patients are allowed access to these REGENERATIVE THERAPIES the demand for the therapies will drive a multi-trillion dollar industry. That industry and those high paying jobs are going to happen one way or the other. Those jobs can be here in the United States or they can be in China, India, Dominican Republic or other countries.

Most of these tens of thousands of jobs would be require only a high school diploma and pay between $40,000 and $70,000. There would also be a plethora of better paying jobs into the high six figure range if that industry is allowed to start here. These jobs could drive economic recovery in America. But only if the FDA bureaucrats get out of the way.

Here her podcast at:

She refers to Prochymal by Osiris in the podcast when she takes about mesenchymal stem cells that stop Graft versus Host Disease. She says that GvHD kills 50% of patients who develop it in the first hundred days after symptoms start. GvHD happens ONLY to bone marrow transplant recipients. The new bone marrow contains a new immune system as bone marrow is maker of all immune and blood cells and components.

The new transplanted immune system sometimes attacks the new host (transplantee--patient who got the transplant). As the new immune system attacks the transplantee it dissolves away the tissues of the poor patient. It is kind of like having every possible autoimmune disease at once. Prochymal stops this process virtually 100% of the time. There is nothing else like it on the market, not even close.

As you know if a drug or procedure can stop GvHD, it can stop autoimmune disease. Prochymal offers the real possibility of a life time cessation of all autoimmune symptoms. In addition because it is made of precursors of bone marrow cells it also has the potential of ending any blood disease that is caused by missing blood components like aplastic anemia or hemophilia.

Saturday, February 14, 2009

The FDA--Incompetent? Corrupt? Flies in your tomato soup

The incompetent or corrupt FDA bureaucrats who refuse to approve new revolutionary medications like ustekinumab also are given the job or protecting our food (except meat--The USDA "inspects" meat.). It seems the FDA is equally incompetent and corrupt in their job of food inspection as they are at approving new medications to relieve suffering.

Read the article below. Then enjoy your tomato soup.

New York Times
February 13, 2009
Op-Ed Contributor
The Maggots in Your Mushrooms

THE Georgia peanut company at the center of one of our nation’s worst food-contamination scares has officially reached a revolting new low: a recent inspection by the Food and Drug Administration discovered that the salmonella-tainted plant was also home to mold and roaches.
You may be grossed out, but insects and mold in our food are not new. The F.D.A. actually condones a certain percentage of “natural contaminants” in our food supply — meaning, among other things, bugs, mold, rodent hairs and maggots.

In its (falsely) reassuringly subtitled booklet “The Food Defect Action Levels: Levels of Natural or Unavoidable Defects in Foods That Present No Health Hazards for Humans,” the F.D.A.’s Center for Food Safety and Applied Nutrition establishes acceptable levels of such “defects” for a range of foods products, from allspice to peanut butter.

Among the booklet’s list of allowable defects are “insect filth,” “rodent filth” (both hair and excreta pellets), “mold,” “insects,” “mammalian excreta,” “rot,” “insects and larvae” (which is to say, maggots), “insects and mites,” “insects and insect eggs,” “drosophila fly,” “sand and grit,” “parasites,” “mildew” and “foreign matter” (which includes “objectionable” items like “sticks, stones, burlap bagging, cigarette butts, etc.”).

Tomato juice, for example, may average “10 or more fly eggs per 100 grams [the equivalent of a small juice glass] or five or more fly eggs and one or more maggots.” Tomato paste and other pizza sauces are allowed a denser infestation — 30 or more fly eggs per 100 grams or 15 or more fly eggs and one or more maggots per 100 grams.

Canned mushrooms may have “over 20 or more maggots of any size per 100 grams of drained mushrooms and proportionate liquid” or “five or more maggots two millimeters or longer per 100 grams of drained mushrooms and proportionate liquid” or an “average of 75 mites” before provoking action by the F.D.A.

The sauerkraut on your hot dog may average up to 50 thrips. And when washing down those tiny, slender, winged bugs with a sip of beer, you might consider that just 10 grams of hops could have as many as 2,500 plant lice. Yum.

Giving new meaning to the idea of spicing up one’s food, curry powder is allowed 100 or more bug bits per 25 grams; ground thyme up to 925 insect fragments per 10 grams; ground pepper up to 475 insect parts per 50 grams. One small shaker of cinnamon could have more than 20 rodent hairs before being considered defective.

Peanut butter — that culinary cause célèbre — may contain approximately 145 bug parts for an 18-ounce jar; or five or more rodent hairs for that same jar; or more than 125 milligrams of grit.
In case you’re curious: you’re probably ingesting one to two pounds of flies, maggots and mites each year without knowing it, a quantity of insects that clearly does not cut the mustard, even as insects may well be in the mustard.

The F.D.A. considers the significance of these defects to be “aesthetic” or “offensive to the senses,” which is to say, merely icky as opposed to the “mouth/tooth injury” one risks with, for example, insufficiently pitted prunes. This policy is justified on economic grounds, stating that it is “impractical to grow, harvest or process raw products that are totally free of non-hazardous, naturally occurring, unavoidable defects.”

The most recent edition of the booklet (it has been revised and edited six times since first being issued in May 1995) states that “the defect levels do not represent an average of the defects that occur in any of the products — the averages are actually much lower.” Instead, it says, “The levels represent limits at which F.D.A. will regard the food product ‘adulterated’ and subject to enforcement action.”

Bugs in our food may not be so bad — many people in the world practice entomophagy — but these harmless hazards are a reminder of the less harmless risks we run with casual regulation of our food supply. For good reason, the F.D.A. is focused on peanut butter, which the agency is considering reclassifying as high risk, like seafood, and subjecting it to special safety regulations. But the unsettling reality is that despite food’s cheery packaging and nutritional labeling, we don’t really know what we’re putting into our mouths.

Soup merits little mention among the products listed in the F.D.A.’s booklet. But, given the acceptable levels for contaminants in other foods, one imagines that the disgruntled diner’s cri de coeur — “Waiter, there’s a fly in my soup!” — would be, to the F.D.A., no cause for complaint.

E. J. Levy is a professor of creative
writing at the University of Missouri.

Pregnancy cure for autoimmune

Pregnancy seems to turn off various forms of autoimmune disease at least temporarily. Weeks or months after delivery the disease usually returns. Lots of research is ongoing to figure out what turns off the autoimmune disease in pregnant women and how to duplicate it as a therapy. Below is an abstract of one set of experiments. Read and enjoy.

Suppression of experimental autoimmune encephalomyelitis using estrogen receptor-selective ligands
by: Merle M Elloso, Kristen Phiel, Ruth A Henderson, Heather A Harris, Steven J Adelman
J Endocrinol, Vol. 185, No. 2. (1 May 2005), pp. 243-252.

Estrogens have been shown to modulate disease activity in experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis.

Consistent with these findings, the severity of disease is reduced in pregnant women with multiple sclerosis when levels of estrogens are high.

Estrogens bind to two known estrogen receptors (ER), ERalpha and ERbeta. The relative contribution of these receptors to estrogen-mediated suppression of EAE was explored using ER-selective ligands. The ER antagonist ICI 182 780 reversed the suppressive effects of 17beta-estradiol (E2), demonstrating that the protective effects of E2 on disease are dependent upon ER signaling.

Treatment of SJL mice with the ERalpha-selective agonist proteolipid protein (PPT) prior to the induction of disease resulted in suppression of clinical symptoms of disease, whereas treatment with an ERbeta-selective agonist (WAY-202041) had no effect.

Treatment of mice with PLP peptide 139-151 (PPT) was also associated with decreased immune responses associated with disease. Consistent with its lack of effect on disease, the ERbeta agonist had minimal effects on immune responses.

The use of selective estrogen receptor modulators (SERMs) in this model was also explored, and we show that raloxifene and WAY-138923 were also effective in suppressing disease.

These results demonstrate the beneficial effects of estrogen receptor ligands, in particular ERalpha-selective ligands, and may have implications in the development of therapeutic strategies for multiple sclerosis. 10.1677/joe.1.06063

Friday, February 13, 2009

Ustekinumab helps Psoriatic Arthritis, FDA still delays approval

Here is another article about the effectiveness of blocking IL-23. Right now there are no IL-23 blockers on the market. Ustekinumab would be the first. In the article below clinical trial results have been releasedishowing it to help PsA as well as psoriasis (not to mention Graft versus Host Disease), yet the FDA still delays approval.

No approval means no access for sufferers like my son. Way to go FDA. Keep it up. Who is paying you guys off?

Read the article below and then wonder why this drug hasn't been rushed to approval instead of delayed time and again by the FDA bureaucrats.

Ustekinumab has already been shown (September 2008) to give better results for psoriasis than Enbrel in head to head trials.

It was recommended by 100% of the outside panel (June 2008) who reviewed the results of the clinical trials.

It has been TWO YEARS since "stunning results" were released at the conclusion of phase II clinical trials.

Still FDA will not approve it.

My son still has NO ACCESS to the drug. He has been turned down four different times for clinical trials as he is too sick.

He has been turned down for a compassionate use individual trial by Centocor.

How long must he wait and suffer? What does a father have to do to get his suffering son access?

The article:

Tufts University, Health Sciences

Investigational study of ustekinumab in the treatment of psoriatic arthritis

published BOSTON (Feb. 11, 2009) – A group of patients suffering from potentially debilitating psoriatic arthritis showed significant and prolonged improvement after treatment with ustekinumab, according to data from a randomized, double-blind, placebo-controlled study in patients with moderate to severe psoriatic arthritis (PsA). The Phase 2 study was published in the British medical journal The Lancet.

"This is a positive development for patients living with the joint pain and swelling that characterizes the disease, even as more research is needed to further test the efficacy of this treatment in psoriatic arthritis," said Alice Gottlieb, MD, Chairperson of the Department of Dermatology at Tufts Medical Center and lead author of the study.

Tufts Medical Center was among several academic medical centers which participated in the study. Tufts Medical Center is a 451-bed hospital in Boston and the primary teaching hospital for Tufts University School of Medicine.

Ustekinumab is a human immunoglobulin monoclonal antibody that is also being studied for treatment of patients with moderate-to-severe plaque psoriasis. Researchers conducting the study published in The Lancet reported that at week 12 of the study, 42 percent of patients given 63 or 90 mg of the drug at weeks 0, 1, 2 and 3 showed significant improvement in their pain, stiffness and other symptoms defined by the American College of Rheumatology (ACR20) score compared with 14 percent of patients who received placebo (NOTE THE EVIL USE OF A PLACEBO GROUP. This research was done at Tufts in the United States under the guidelines of the criminals at the FDA. The FDA motto: LET THEM SUFFER WITHOUT MEDICATION SO WE CAN GET PRETTY NUMBERS for our study. Outrageous!) at the same time points (P < n="3)">

Big Pharma money and Corruption, Corruption, Corruption

How much corruption is there in the medical research industry?
How much does the apparent wide spread corruption slow down cures?

How much control of advocacy groups, clinical trial regulations, and drug approvals does Big Pharma have?

How many cures have been delayed?

Do the big Pharma ads on the web pages of advocacy groups and the underwriting of advocacy group conventions and magazines mean that advocacy group first priority is not cures but pleasing its Big Pharma sponsors and advertisers?

If a cure could come faster than a Big Pharma advertiser and underwriter wanted which direction would the officers of the advocacy group go?

Where does the majority of the money come from that pays the salaries of paid staff at advocacy groups?

Do FDA bureaucrats have a reason for the delays in cures?
Are there financial incentives for FDA bureaucrats to slow some cures so that more money can be made on the older, soon to be outdated and less effective treatments already FDA approved?

Who are advocacy groups really working for?

All of the above questions should be asked and answers demanded. The questions sound paranoid. Too paranoid to even write down, yet I keep wondering why amazing research discoveries are not making it to patients?

I would never have said the questions aloud let alone written them here until I read the following article about the massive corruption/scandal regarding which articles are published in major medical journals and which articles are the most cited. (The more citations the more likely authors are to get promotions and additional lucrative grants.)

Could there be a sinister reason that Ustekinumab has been delayed?

Read the article below and then decide for yourself whether or not it is time to engage in a little paranoia.

Publication Of Flu Vaccines Studies In Prestigious Journals Are Determined By The Sponsor

13 Feb 2009

Industry-sponsored studies on influenza vaccines are published in journals with higher rankings (impact factors) and are cited more than studies with other sponsors, but this is not because they are bigger or better, finds a study published on today.

Tom Jefferson and colleagues at the Cochrane Vaccine Field in Italy identified and assessed 274 studies on influenza vaccines and analysed their methodological quality, prestige of the host journals (impact factor) and citation rates in the scientific literature. They found no relationship between study quality, publication in prestige journals or their subsequent citation in other articles. They also found that influenza vaccine studies are of poor quality and those with conclusions in favour of the vaccines are of significantly lower methodological quality.

The single most important determinant of where the studies were published or how much they were cited was sponsorship.

Those partially or wholly funded by industry had higher visibility.

The researchers also found no relationship between journal impact factor and the quality of the influenza vaccine studies it publishes, suggesting that the impact factor is not the robust quality indicator that publishers suggest and confirming some of the widely expressed doubts on its appropriateness as a means of rewarding researchers with promotions and funds.

Dr Jefferson concludes: "The study shows that one of the levers for accessing prestige journals is the financial size of your sponsor. Pharmaceutical sponsors order many reprints of studies supporting their products, often with in-house translations into many languages. They will also purchase publicity space on the journal. Many publishers openly advertise these services on their website. It is time journals made a full disclosure of their sources of funding."

"Research: Relation of study quality, concordance, take home message, funding, and impact in studies of influenza vaccines: systematic review." BMJ Online Medical Journal

Ustekinumab stops Graft versus Host Disease

Researchers at the Wisconsin Cancer Center have shown that blocking IL-23 stops Graft versus Host Disease (GvHD). Interesting since GvHD is basically an out of control autoimmune reaction caused by the replacement of a patient's immune system (bone marrow) with a new one that attacks the patient's body. Ustekinumab stops GVHD. Ustekinumab stops psoriasis--an autoimmune disease. What a coincidence! NOT.

Another coincidence no matter how good Ustekinumab is no dying GvHD patient will have access. Why? The coincidence is the FDA will not put into effect rules to allow it, just like they would not approve it for psoriasis.

Let the patients suffer and die. Hey Hey Hey, we don't care. We are the FDA.

Two years after Ustekinumab showed "stunning results" in clinical trials the FDA has not approved it for suffering Americans. Nine months ago (June 2008) it was unanimously recommended for approval by an outside panel of experts. What did the FDA do? Of course they DELAYED. Four months ago clinical trial results showing it to be MORE EFFECTIVE than the number one medication for psoriasis were released. What did the FDA do? More DELAY. Even today, February 13, no approval and more DELAY.

Now we know it could save even more lives. Those poor patients who had bone marrow transplants to try to save their lives but whose new bone marrow (immune system) is dissolving their bodies(GvHD) in a most horrible way.

Ustekinumab could end their horrible suffering and save their lives, but the rules of the FDA will not allow its use. Hooray for the FDA!

Here is the article:

Bone Marrow Transplant Patients May Benefit From New Immune Research

12 Feb 2009

Bone marrow transplant (BMT) researchers at The Medical College of Wisconsin Cancer Center in Milwaukee may have found a mechanism that could preserve the leukemia-killing effects of a transplant graft, while limiting the damage donor immune cells might do to the recipient host's vital organs.

"Our results suggest that targeting of interleukin 23, (IL-23), an immune substance secreted by donor marrow cells, may be a viable way to limit graft-versus-host-disease without limiting graft-versus-leukemia activity," says lead researcher Rupali Das, Ph.D.

The study was presented at the national BMT Tandem Meetings in Tampa, Fla., Feb. 11, 2009, and was among those receiving the highest scores from the abstract review committee.

Dr. Das is a postdoctoral fellow in pediatric hematology/oncology at the Medical College in the laboratory of William R. Drobyski, M.D., professor of medicine in neoplastic diseases, and principal investigator of this study.

Dr. Drobyski practices at Froedtert Hospital.

In a recent study, the researchers found that donor mice with marrow cells incapable of producing IL-23, provided protection from graft-versus-host damage to the recipient's colon, but not to other organs.

They then conducted studies in which mice with leukemia received T cells from the marrow and spleen of IL-23-deficient donor mice. The recipient mice not only had longer survival times than those receiving T-cells from IL-23-producing mice, but also showed no evidence of leukemia.

Mice transplanted with T cells capable of producing IL-23 all died of graft versus host disease.

The study was funded by the Midwest Athletes Against Childhood Cancer (MACC) Fund, a major donor that has been supporting cancer research at the Medical College since 1976, and the National Institutes of Health's National Heart, Blood and Lung Institute.Medical College of Wisconsin8701 Watertown Plank Rd.MilwaukeeWI 53226United States