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From: ironjustice on 30 Jun 2008 13:44

---

On Jun 30, 10:19 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com>
wrote: imatinib <<

Polycythemia the first line recommended treatment is .. bloodletting.
Gleevec results in 75% remission rate in polycythemia.

Someone buying an expensive .. bridge .. ?
Some can't even afford the .. bridge .. ?

Gleevec, the cost: $3,100
Cost of cancer drugs crushes all but hope
Updated 7/11/2006 10:50 AM ET

By Liz Szabo, USA TODAY
When Tom Reek was diagnosed with a rare leukemia at age 65, doctors
said he might live only another three years. Today, Reek is thriving
at age 72, thanks to a drug called Gleevec.
"I used to kid around and say that I feel like Clark Kent," says Reek,
who lives on Long Island, N.Y., and volunteers as a peer counselor
with other patients, including youngsters. "It's like a gift from God
to be able to work with these children."

The only downside to Gleevec, Reek says, is the cost: $3,100 a month.
Reek went back to work four years ago as a truck driver, delivering
blood tests and lab results to medical offices. With insurance, his
pills cost only about $50 a month.

Since Gleevec was approved in 2001, researchers have hoped that every
new cancer therapy would copy its success: a convenient pill that lets
patients live for years with relatively few serious side effects.
Though experts say few of the new "targeted" therapies come close to
that ideal, they do have one thing in common with Gleevec: They're all
incredibly expensive.

PRESCRIPTION COSTS: Prices soar for cancer drugs

Some doctors are questioning whether targeted therapies — designed to
turn cancer into a chronic disease by silencing growth signals inside
malignant cells — are worth the expense to individuals and taxpayers.

Most new cancer drugs improve survival by only a few weeks or months,
says researcher Leonard Saltz of New York's Memorial Sloan-Kettering
Cancer Center. Although Erbitux, for example, costs almost $10,000 a
month, studies have not shown that it helps colorectal cancer patients
live longer.

"There is a real question whether insurance ought to pay for a drug
like that," says Ezekial Emanuel, chairman of clinical bioethics at
the National Institutes of Health clinical center. "If you pay for
something that doesn't have a big impact, you could lose out on
treatments that really do work.

"We can cure testicular cancer. We can cure Hodgkin's disease. You
don't want to skimp on that."

Canada has decided that Erbitux isn't worth the money. Last month,
Bristol-Myers Squibb Canada announced that it won't sell Erbitux there
because it couldn't get "an appropriate price for its product
reflecting the value of the innovation it brings."

Today's prices seem especially high, given that the new targeted
therapies don't actually cure cancer, says Jerome Kassirer, former
editor of The New England Journal of Medicine and author of On the
Take: How Medicine's Complicity with Big Business Can Endanger Your
Health

"Families could end up spending their fortunes for what turns out to
be a minor benefit," Kassirer says.

As the number of targeted therapies increase, more patients are facing
this decision. Almost 200,000 patients could soon be eligible for the
drug Avastin if it's approved for lung and breast cancers, two of the
most common malignancies, according to Genentech.

David Johnson, former president of the American Society of Clinical
Oncology, says a few of his patients are turning down care because of
the cost. Johnson, who has treated cancer for 25 years, notes, "That
never used to happen."

All those years in medicine, though, also have made Johnson optimistic
about targeted therapies, in spite of their high prices. A handful of
his lung cancer patients have done remarkably well on Tarceva, he
says, although patients overall live only two months longer than those
on placebos.

"Some folks tend to hype any therapy that is new," Johnson says.
"Reality always tends to center us."

Although he is glad new cancer drugs are available, Saltz says,
doctors had hoped that targeted drugs would replace chemotherapy,
making cancer treatment gentler.

But unlike Gleevec, many of the new drugs work only when combined with
chemo, he says. Adding drugs such as Erbitux and Avastin to older
therapies increases costs as well as side effects.

Patients today still don't live very long on most of the new
medications. Survival for patients with advanced colon cancer has
increased from one year to about two years over the past decade, Saltz
says. Patients with only two years to live may see that as major
progress, he says.

"The drug companies have been trying to put the word 'breakthrough' in
my mouth since 1995," Saltz says. "But it's far too flattering to say
we've made significant progress. ... The vast majority of targeted
drugs are a long way from what we hoped they would be."

Industry leaders defend their prices. Officials from Bristol-Myers
Squibb Co., which sells Erbitux, note that patents offer companies a
limited amount of time to recoup their investments.

Tony Plohoros, a company spokesman, says the company respects the
decisions of patients who opt not to use Erbitux. "That is a personal
decision up to each individual patient and their loved ones," Plohoros
says.

Administrators at public hospitals with limited budgets, such as
Atlanta's Grady Hospital, have to make hard choices, says Otis
Brawley, director of Grady Health System's Georgia Cancer Center for
Excellence. Grady doctors also are considering limiting the use of
Erbitux, Brawley says.

"We are constantly asking ourselves: Are we buying drugs that we
really ought not to be buying?" says Brawley, a professor at Atlanta's
Emory School of Medicine. "Are we going to bankrupt ourselves buying
Avastin so we won't be around to treat other people?"

Posted 7/10/2006 9:30 PM ET
--------------------------
Hello,
My monthly refill of Gleevec (800mg/day) is now $5,910, which is up
about $1,000 over last month. I'm interested in what anyone else is
paying, and if the cost has gone up recently.

Fred.

http://ubb-lls.leukemia-lymphoma.org/ubb/Forum17/HTML/000325.html


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


> On Jun 30, 9:01 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com> wrote:
> Imatinib mesylate <<
>
> Isn't this special that the drug used to treat **polycythemia** is
> also VERY effective in arthritis .. lupus .. diabetes .. multiple
> sclerosis .. ?
>
> "Imatinib mesylate produces 75% lasting remissions in polycythemia"
>
> Nihon Rinsho Meneki Gakkai Kaishi. 2007 Jun ;30 (3):165-73 17603257
> (P,S,E,B) Imatinib mesylate as a novel therapeutic drug for systemic
> rheumatic diseases.
>
> [My paper] Hideto Kameda
> Division of Rheumatology/Clinical Immunology, Department of Internal
> Medicine, Saitama Medical Center, Saitama Medical University.
> Platelet-derived growth factor (PDGF) is a topic in the
> pathophysiology of various systemic rheumatic diseases.
> For example, autoantibody against PDGF receptor was identified in
> patients with systemic sclerosis.
> Imatinib mesylate has been well tolerable and widely used for chronic
> myeloid leukemia and gastrointestinal stromal tomor.
> Imatinib also inhibits the activation of c-Abl, which is a key
> downstream molecule of transforming growth factor-beta signaling, and
> PDGF receptors.
> Thus, imatinib effectively suppresses the activation and proliferation
> of fibroblasts, mesangial cells and smooth muscle cells.
> Therefore, imatinib may overcome the limitation of current therapeutic
> strategy with corticosteroids and immunosuppressive agents for
> refractory diseases
>
> -------------------------------
>
> Imatinib mesylate both prevents and treats the arthritis induced by
> type II collagen antibody in mice
> Journal Modern Rheumatology
>
> ORIGINAL ARTICLE
> Imatinib mesylate both prevents and treats the arthritis induced by
> type II collagen antibody in mice
> Kensuke Koyama1, 2 , Kyosuke Hatsushika1, Takashi Ando1, Michitomo
> Sakuma1, Masanori Wako1, Ryohei Kato3, Hirotaka Haro2, Hajime
> Sugiyama2, Yoshiki Hamada2, Hideoki Ogawa4 and Atsuhito Nakao1, 4
>
> (1)  Department of Immunology, Faculty of Medicine, University of
> Yamanashi, Yamanashi, Japan
> (2)  Department of Orthopaedic Surgery, Faculty of Medicine,
> University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi 409-3898,
> Japan
> (3)  Department of Human Pathology, Faculty of Medicine, University of
> Yamanashi, Yamanashi, Japan
> (4)  Atopy Research Center, Juntendo University School of Medicine,
> Tokyo, Japan
>
> Received: 08 February 2007  Accepted: 01 May 2007  Published online:
> 20 August 2007
>
> Abstract  Rheumatoid arthritis (RA) is a chronic inflammatory disease
> that is associated with joint destruction.
> Imatinib mesylate (imatinib) is an inhibitor that specifically targets
> a set of protein tyrosine kinase, such as abl, c-kit, and platelet-
> derived growth factor receptor (PDGFR) and it is widely used to treat
> chronic myeloid leukemia (CML).
> The purpose of the present study is to determine whether imatinib can
> provide benefit in the arthritis induced by anti-collagen type II
> antibody (CAIA) in mice, a model that provides an opportunity to study
> the effector inflammatory phase of arthritis without involving the
> priming phase of the immune responses.
> Mice treated with intraperitoneal administration of imatinib (1 or 10
> mg/kg) prior to the development of CAIA displayed significant
> reductions in the severity of CAIA as assessed by arthritis score,
> histology, and synovial PDGF and vascular endothelial growth factor
> expression.
> In addition, treatment of the mice that had developed CAIA with
> intraperitoneal administration of imatinib (1 or 10 mg/kg) inhibited
> the progression of arthritis as assessed by those parameters.
> These results suggest that imatinib prevents and treats CAIA.
> Imatinib may thus have both a preventive and therapeutic potential for
> the joint inflammation at the effector stage of RA.
> Key words  Anti-collagen type II antibody-induced arthritis (CAIA) -
> Imatinib mesylate - Rheumatoid arthritis
>
>  Kensuke Koyama
> Email: vesupanomus...(a)yahoo.co.jp
>
> ---------------------------------------------------------------------------­-----
>
> Update on the treatment of polycythemia vera with recombinant
> interferon alfa or imatinib mesylate
> Journal Current Hematologic Malignancy Reports
>
> Update on the treatment of polycythemia vera with recombinant
> interferon alfa or imatinib mesylate
> Richard T. Silver1
>
> (1)  New York-Presbyterian Hospital/Weill Cornell Medical Center, 1300
> York Avenue, Box 581, New York, NY 10021, USA
>
> Published online: 15 April 2007
>
> Abstract  Polycythemia vera is a myeloproliferative disease, which, if
> untreated, leads to thrombohemorrhagic complications and eventually to
> progressive myelofibrosis, anemia, and splenomegaly. Two newly
> available drugs, interferon alfa and imatinib mesylate, may alter the
> course of this disease. Used as single agents, each produces lasting
> remissions in about 75% of patients with polycythemia vera. Of
> significance, change in JAK2 expression has been reported after
> treatment with both agents.
>
>  Richard T. Silver
> Email: rtsi...(a)med.cornell.edu
>
> Publisher Current Medicine Group LLC
> ISSN 1558-8211 (Print) 1558-822X (Online)
> Issue Volume 2, Number 1 / February, 2007
> DOI 10.1007/s11899-007-0006-2
>
> ---------------------------------------------------------------------------­-----
>
> Published as doi: 10.1096/fj.06-6910com.
> (The FASEB Journal. 2007;21:618-628.)
> © 2007 FASEB
>
> Amelioration of diabetes by imatinib mesylate (Gleevec®): role of ß-
> cell NF-B activation and anti-apoptotic preconditioning
> Robert Hägerkvist, Stellan Sandler, Dariush Mokhtari and Nils Welsh
> Department of Medical Cell Biology, Uppsala University, Biomedicum,
> Uppsala, Sweden
>
> 1Correspondence: Department of Medical Cell Biology, Uppsala
> University, Biomedicum, P.O. Box 571, SE-75123 Uppsala, Sweden. E-
> mail: Nils.We...(a)medcellbiol.uu.se06-6910com
>
> It was recently reported that tyrosine kinase inhibitor imatinib
> mesylate (Gleevec®) improves Type 2 diabetes, possibly by decreasing
> insulin resistance.
> However, as both Type 2 and Type 1 diabetes are characterized by ß-
> cell dysfunction and death, we investigated whether imatinib
> counteracts diabetes by maintaining ß-cell function.
> We observed that imatinib counteracted diabetes in two animal models,
> the streptozotocin-injected mouse and the nonobese diabetes mouse, and
> that this was paralleled by a partial preservation of the ß-cell
> mass.
> In addition, imatinib decreased the death of human ß-cells in vitro
> when exposed to NO, cytokines, and streptozotocin.
> The imatinib effect was mimicked by siRNA-mediated knockdown of c-Abl
> mRNA. Imatinib enhanced ß-cell survival by promoting a state similar
> to ischemic preconditioning, as evidenced by NF-B activation,
> increased NO and reactive oxygen species production, and
> depolarization of the inner mitochondrial membrane.
> Imatinib did not suppress islet cell death in the presence of an NF-B
> inhibitor, suggesting that NF-B activation is a necessary step in the
> antiapoptotic action of imatinib.
> We conclude that imatinib mediates ß-cell survival and that this could
> contribute to the beneficial effects observed in diabetes.
> —Hägerkvist, R., Sandler, S., Mokhtari, D., Welsh, N. Amelioration of
> diabetes by imatinib mesylate (Gleevec®): role of ß-cell NF-B
> activation and anti-apoptotic preconditioning.
>
> Key Words: pancreatic islet • c-Abl • NO
> --------------------------http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1564430
>
> In addition to potentially providing benefit in RA, it is anticipated
> that imatinib could also provide efficacy in other autoimmune
> diseases. A patient with psoriasis exhibited clinical improvement
> following treatment with imatinib for a concomitant malignancy (55).
> Imatinib ameliorated glomerulonephritis in MRL/lpr mice, and this
> effect was attributed to inhibition of PDGFR (56). Mast cells, which
> are potently inhibited by imatinib, have been suggested to contribute
> to pathogenesis of multiple sclerosis, autoimmune skin diseases, and
> inflammatory bowel disease (15). TNF-α is a driver of autoimmune
> tissue injury in a spectrum of autoimmune diseases, including RA,
> Crohn disease, psoriasis, and multiple sclerosis (57). Although
> imatinib-mediated inhibition of macrophage TNF-α production, mast cell
> activation and TNF-α release, and autoreactive B and T lymphocyte
> activation could provide benefit in many autoimmune diseases,
> imatinib’s ability to inhibit PDGFR makes it particularly suited for
> the treatment of RA and other diseases in which fibrotic processes
> play a central role in pathogenesis.
>
> In conclusion, we have shown that imatinib potently treats CIA and
> inhibits multiple signal transduction pathways that drive pathogenic
> cellular responses in RA. Our results provide further rationale for
> prospective clinical trials to determine whether imatinib provides
> efficacy in RA and other autoimmune diseases. Selective tyrosine
> kinase inhibition by imatinib and other pharmacologic agents (58)
> represents a promising and powerful strategy for the treatment of RA
> and other inflammatory diseases.
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On Jun 30, 8:39 am, ironjustice <ironjust...(a)cashette.com> wrote:
> > elevated serum homocysteine <<
>
> > Silent Cerebral Infarction Reported in 10% of Healthy People
>
> > DALLAS -- June 26, 2008 -- A recent study found that about 10% of the
> > apparently healthy middle-aged participants with no symptoms of stroke
> > were injured from silent cerebral infarction (SCI) researchers report
> > in Stroke: Journal of the American Heart Association.
>
> > "The findings reinforce the need for early detection and treatment of
> > cardiovascular risk factors in midlife," said co-author of the study,
> > Sudha Seshadri, MD, Boston University School of Medicine, Boston,
> > Massachusetts. "This is especially true since SCIs have been
> > associated with an increased risk of incident stroke and cognitive
> > impairment."
>
> > Researchers evaluated magnetic resonance imaging (MRI) from about
> > 2,000 people aged an average
>
> ...
>
> read more »- Hide quoted text -
>
> - Show quoted text -

From: ironjustice on 30 Jun 2008 14:50

---

On Jun 30, 10:44 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com>
wrote: thrombosis <<

Curious thing here is ,, there was a question of "the hemolysis in
blood donor bags" someone ventured .. "add arginine to offset the
hemolysis".

-------------------------------------------

Arginine Butyrate Heals Sickle Cell Leg Ulcers

Jane Salodof MacNeil

Dec. 10, 2002 (Philadelphia) — Researchers working with an
experimental drug for sickle cell anemia noticed an unexpected side
effect: the incidental healing of debilitating leg ulcers in seven
patients.

That serendipitous observation led to a 25-patient phase II study in
which treatment with the compound, arginine butyrate, healed 17 of 37
leg ulcers. In contrast, among 24 ulcers that received standard local
care for wounds, complete healing was documented for one ulcer.

Several of the participants had suffered with large open sores for
decades, according to investigator Susan Perrine, MD, of Boston
University School of Medicine in Massachusetts. One woman had leg
ulcers for 30 years, Dr. Perrine reported in a presentation here at
the American Society of Hematology annual meeting.

The investigator showed dramatic before and after photographs of legs
from several patients who benefited from the treatment. The mean
initial area of ulcers in the arginine butyrate arm of the study was
50.8 cm2 — nearly twice the 26.4 cm2 in the control group.

Within three months of treatment, the area had been reduced by 53% in
patients who received arginine butyrate, but the area was reduced by
9% in the control arm. Dr. Perrine said the researchers don't know why
the compound heals these ulcers.

H. Grant Prentice, MD, of the London Clinic in the U.K., called the
study "extremely important." The former head of hematology at the
Royal Free Hospital in London, Dr. Prentice said the most common
therapy for leg ulcers associated with sickle cell disease is
hydroxyurea. "It's not very effective, and the patients don't like to
take it," he told Medscape.

About 25% of sickle cell patients suffer from leg ulcers, according to
an earlier study of 2,000 patients that Dr. Perrine cited at the start
of her talk. In the United States, she said, the typical sickle cell
ulcer lasts as long as three years; in the Caribbean more than nine
years is common. Even if they are cured, between a quarter and a half
of these ulcers will recur.

Despite their prevalence, the ulcers are not well known, even in the
sickle cell community, according to Dr. Perrine. They tend to occur in
adults, she said, explaining she had little experience with them
because she works in pediatrics.

Patients in the treatment arm of the trial received 500 mg/kg of
arginine butyrate six hours a day three days a week for twelve weeks.
Although hydroxyurea is used, she said there is no standard regimen
for these sores. The control group was treated aggressively according
to local standards for wound healing, but no particular protocol was
used in the six-center study.

Although the study ended after three months, patients were allowed to
continue for 16 weeks if their ulcers were closing with arginine
butryate. Within five to seven months, a 10-fold increase in wound
healing was reported.

Dr. Perrine said the investigators plan to seek funds for a phase III
trial. The pilot study was conducted with support from the U.S. Food
and Drug Administration's orphan drug program, she said. Arginine
butryate is an experimental compound and is not yet commercially
available.

ASH 44th Annual Meeting: Abstract 26. Presented Dec. 8, 2002.

Reviewed by Gary D. Vogin, MD

Jane Salodof MacNeil is a freelance writer for Medscape.
Conference Coverage
44th Annual Meeting of the American Society of Hematology

-------------------

THE IDEA THAT DRUGS MIGHT SAFELY SWITCH ON NONWORKING GENES RECEIVED
ABOOST FROM RESEARCHERS DEVELOPING TREATMENTS FOR A GROUP OF GENETIC
BLOODDISORDERS

THE BLOOD DISORDERS INVOLVE RED BLOOD CELLS' FAILURE TO PRODUCE
HEMOGLOBIN OR PRODUCTION OF A DEFECTIVE FORM OF THE OXYGEN CARRYING
PROTEIN.
THE DISORDERS INCLUDE SICKLE CELL ANEMIA WHICH MOSTLY AFFLICTS
AFRICAN AMERICANS AND COOLEY'S ANEMIA WHICH MOSTLY AFFLICTS ITALIANS
GREEKS AND OTHER MEDITERRANEAN GROUPS.

BLOOD SPECIALISTS HAVE BEEN TRYING FOR A DECADE TO FIND A NEW WAY TO
TREAT THESE DISORDERS BY TURNING ON A HEMOGLOBIN GENE THAT ORDINARILY
QUITS WORKING AFTER BIRTH.
THE FEW DRUGS THAT HAVE PULLED OFF THIS TRICK HAVE BEEN
TOO TOXIC FOR THE LIFETIME USE THAT THE ANEMIC PATIENTS WOULD REQUIRE.

NOW A TEAM OF RESEARCHERS IN OAKLAND CALIF REPORTED PRELIMINARY
RESULTS IN WHICH A FOOD ADDITIVE A FATTY ACID CALLED ARGININE BUTYRATE
APPEARED TO STIMULATE THE NONWORKING GENE TO BEGIN MAKING NORMAL
HEMOGLOBIN IN SIX PATIENTS THEIR REPORT APPEARS IN THIS WEEK'S ISSUE
OF THE NEW ENGLAND JOURNAL OF MEDICINE.

THE MAIN PROBLEM IS THAT THE DRUG MUST BE GIVEN INTRAVENOUSLY BUT ONE
OF THE RESEARCHERS SAID AN ORAL FORM OF THE DRUG IS BEING DEVELOPED.

THE TWO ANEMIAS ARE IDEAL CANDIDATES FOR GENE ACTIVATION THERAPY.
BOTH INVOLVE DEFECTS IN HEMOGLOBIN THE IRON CONTAINING PROTEIN THAT
RED BLOOD CELLS USE TO CARRY OXYGEN TO BODY TISSUES.
OF THE TWO GENES CAPABLE OF MAKING HEMOGLOBIN ONE FUNCTIONS ONLY
DURING FETAL LIFE WHEN THE FETUS MUST PULL OXYGEN CARRYING BLOOD
ACROSS THE PLACENTA.
THIS FETAL GENE TURNS OFF AFTER BIRTH AND A SECOND ADULT GENE TAKES
OVER.

IN COOLEY'S ANEMIA ALSO KNOWN AS BETATHALASSEMIA THE DEFECTIVE ADULT
GENE PRODUCES LITTLE OR NO HEMOGLOBIN.
THOSE BORN WITH THE DEFECT MUST RECEIVE REPEATED BLOOD TRANSFUSIONS TO
SURVIVE.
IF THE FETAL GENE COULD BE REAWAKENED AND PUT BACK TO WORK THE
PATIENT'S RED CELLS WITH A NEW ENDOWMENT OF PERFECTLY FUNCTIONAL FETAL
HEMOGLOBIN WOULD ENLARGE REDDEN
AND REGAIN VIABILITY EXPLAINED H FRANKLIN BUNN IN AN EDITORIAL
COMMENTINGON THE NEW RESEARCH.
DR BUNN WHO IS AT THE BRIGHAM AND WOMEN'S HOSPITAL IN
BOSTON IS ALSO WORKING ON GENESWITCHING TREATMENTS FOR THE
BLOODDISORDERS

IN SICKLECELL ANEMIA THE ADULT HEMOGLOBIN GENE FUNCTIONS BUT IS
DEFECTIVE AND THE DEFECTIVE HEMOGLOBIN IT PRODUCES LEADS TO A RIGID
SICKLE SHAPED RED BLOOD CELL.
THIS SICKLING EFFECT DOESN'T OCCUR IF FETAL HEMOGLOBIN IS ALSO
PRESENT.

IN THE LATEST RESEARCH ALL SIX PATIENTS THREE WITH COOLEY'S ANEMIA AND
THREE WITH SICKLECELL ANEMIA EXPERIENCED INCREASES IN FETAL HEMOGLOBIN
PRODUCTION FOLLOWING INFUSIONS OF AN ULTRAPURE FORM OF ARGININE
BUTYRATE REPORTED A TEAM OF RESEARCHERS HEADED BY SUSAN P PERRINE OF
CHILDREN'S
HOSPITAL OAKLAND RESEARCH INSTITUTE IN OAKLAND CALIF.
THE TEAM INCLUDEDSCIENTISTS FROM A HALF DOZEN MEDICAL CENTERS IN THE
US AND CANADA.

INCREASES IN THE OUTPUT OF FETAL HEMOGLOBIN RANGED FROM 6 TO 45 ABOVE
PRETREATMENT LEVELS THE RESEARCHERS REPORTED.
IN TWO PATIENTS THE PRODUCTION OF FETAL HEMOGLOBIN CONTINUED FOR A
MONTH AFTER TREATMENT STOPPED.
SIDE EFFECTS WERE ALMOST NONEXISTENT THEY SAID.

THE RESULTS ALTHOUGH HIGHLY PRELIMINARY INDICATE THAT THE
ADMINISTRATION OF ARGININE BUTYRATE REPRESENTS A NOVEL AND POTENTIALLY
EFFECTIVE THERAPY FOR THESE PREVALENT MOLECULAR DISORDERS THE REPORT
DECLARED.

IN A TELEPHONE INTERVIEW DR PERRINE SAID SHE HAD TO COMPOUND THE
ARGININE BUTYRATE USED IN THE TEST.
THE TEAM SHE SAID HAS SINCE DEVELOPED SOME VARIATIONS OF THE FATTY
ACID THAT COULD BE GIVEN ORALLY.
THE RESEARCHERS HOWEVER ARE LOOKING FOR A DRUG MANUFACTURER WHO WOULD
TAKE OVER DEVELOPMENT
OF THE DRUGS AND TAKE THEM THROUGH THE US FOOD AND DRUG ADMINISTRATION
PROCESSES FOR MARKETING

Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


> On Jun 30, 10:19 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com>
> wrote: imatinib <<
>
> Polycythemia the first line recommended treatment is .. bloodletting.
> Gleevec results in 75% remission rate in polycythemia.
>
> Someone buying an expensive .. bridge .. ?
> Some can't even afford the .. bridge .. ?
>
> Gleevec, the cost: $3,100
> Cost of cancer drugs crushes all but hope
> Updated 7/11/2006 10:50 AM ET
>
> By Liz Szabo, USA TODAY
> When Tom Reek was diagnosed with a rare leukemia at age 65, doctors
> said he might live only another three years. Today, Reek is thriving
> at age 72, thanks to a drug called Gleevec.
> "I used to kid around and say that I feel like Clark Kent," says Reek,
> who lives on Long Island, N.Y., and volunteers as a peer counselor
> with other patients, including youngsters. "It's like a gift from God
> to be able to work with these children."
>
> The only downside to Gleevec, Reek says, is the cost: $3,100 a month.
> Reek went back to work four years ago as a truck driver, delivering
> blood tests and lab results to medical offices. With insurance, his
> pills cost only about $50 a month.
>
> Since Gleevec was approved in 2001, researchers have hoped that every
> new cancer therapy would copy its success: a convenient pill that lets
> patients live for years with relatively few serious side effects.
> Though experts say few of the new "targeted" therapies come close to
> that ideal, they do have one thing in common with Gleevec: They're all
> incredibly expensive.
>
> PRESCRIPTION COSTS: Prices soar for cancer drugs
>
> Some doctors are questioning whether targeted therapies — designed to
> turn cancer into a chronic disease by silencing growth signals inside
> malignant cells — are worth the expense to individuals and taxpayers.
>
> Most new cancer drugs improve survival by only a few weeks or months,
> says researcher Leonard Saltz of New York's Memorial Sloan-Kettering
> Cancer Center. Although Erbitux, for example, costs almost $10,000 a
> month, studies have not shown that it helps colorectal cancer patients
> live longer.
>
> "There is a real question whether insurance ought to pay for a drug
> like that," says Ezekial Emanuel, chairman of clinical bioethics at
> the National Institutes of Health clinical center. "If you pay for
> something that doesn't have a big impact, you could lose out on
> treatments that really do work.
>
> "We can cure testicular cancer. We can cure Hodgkin's disease. You
> don't want to skimp on that."
>
> Canada has decided that Erbitux isn't worth the money. Last month,
> Bristol-Myers Squibb Canada announced that it won't sell Erbitux there
> because it couldn't get "an appropriate price for its product
> reflecting the value of the innovation it brings."
>
> Today's prices seem especially high, given that the new targeted
> therapies don't actually cure cancer, says Jerome Kassirer, former
> editor of The New England Journal of Medicine and author of On the
> Take: How Medicine's Complicity with Big Business Can Endanger Your
> Health
>
> "Families could end up spending their fortunes for what turns out to
> be a minor benefit," Kassirer says.
>
> As the number of targeted therapies increase, more patients are facing
> this decision. Almost 200,000 patients could soon be eligible for the
> drug Avastin if it's approved for lung and breast cancers, two of the
> most common malignancies, according to Genentech.
>
> David Johnson, former president of the American Society of Clinical
> Oncology, says a few of his patients are turning down care because of
> the cost. Johnson, who has treated cancer for 25 years, notes, "That
> never used to happen."
>
> All those years in medicine, though, also have made Johnson optimistic
> about targeted therapies, in spite of their high prices. A handful of
> his lung cancer patients have done remarkably well on Tarceva, he
> says, although patients overall live only two months longer than those
> on placebos.
>
> "Some folks tend to hype any therapy that is new," Johnson says.
> "Reality always tends to center us."
>
> Although he is glad new cancer drugs are available, Saltz says,
> doctors had hoped that targeted drugs would replace chemotherapy,
> making cancer treatment gentler.
>
> But unlike Gleevec, many of the new drugs work only when combined with
> chemo, he says. Adding drugs such as Erbitux and Avastin to older
> therapies increases costs as well as side effects.
>
> Patients today still don't live very long on most of the new
> medications. Survival for patients with advanced colon cancer has
> increased from one year to about two years over the past decade, Saltz
> says. Patients with only two years to live may see that as major
> progress, he says.
>
> "The drug companies have been trying to put the word 'breakthrough' in
> my mouth since 1995," Saltz says. "But it's far too flattering to say
> we've made significant progress. ... The vast majority of targeted
> drugs are a long way from what we hoped they would be."
>
> Industry leaders defend their prices. Officials from Bristol-Myers
> Squibb Co., which sells Erbitux, note that patents offer companies a
> limited amount of time to recoup their investments.
>
> Tony Plohoros, a company spokesman, says the company respects the
> decisions of patients who opt not to use Erbitux. "That is a personal
> decision up to each individual patient and their loved ones," Plohoros
> says.
>
> Administrators at public hospitals with limited budgets, such as
> Atlanta's Grady Hospital, have to make hard choices, says Otis
> Brawley, director of Grady Health System's Georgia Cancer Center for
> Excellence. Grady doctors also are considering limiting the use of
> Erbitux, Brawley says.
>
> "We are constantly asking ourselves: Are we buying drugs that we
> really ought not to be buying?" says Brawley, a professor at Atlanta's
> Emory School of Medicine. "Are we going to bankrupt ourselves buying
> Avastin so we won't be around to treat other people?"
>
> Posted 7/10/2006 9:30 PM ET
> --------------------------
> Hello,
> My monthly refill of Gleevec (800mg/day) is now $5,910, which is up
> about $1,000 over last month. I'm interested in what anyone else is
> paying, and if the cost has gone up recently.
>
> Fred.
>
> http://ubb-lls.leukemia-lymphoma.org/ubb/Forum17/HTML/000325.html
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On Jun 30, 9:01 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com> wrote:
> > Imatinib mesylate <<
>
> > Isn't this special that the drug used to treat **polycythemia** is
> > also VERY effective in arthritis .. lupus .. diabetes .. multiple
> > sclerosis .. ?
>
> > "Imatinib mesylate produces 75% lasting remissions in polycythemia"
>
> > Nihon Rinsho Meneki Gakkai Kaishi. 2007 Jun ;30 (3):165-73 17603257
> > (P,S,E,B) Imatinib mesylate as a novel therapeutic drug for systemic
> > rheumatic diseases.
>
> > [My paper] Hideto Kameda
> > Division of Rheumatology/Clinical Immunology, Department of Internal
> > Medicine, Saitama Medical Center, Saitama Medical University.
> > Platelet-derived growth factor (PDGF) is a topic in the
> > pathophysiology of various systemic rheumatic diseases.
> > For example, autoantibody against PDGF receptor was identified in
> > patients with systemic sclerosis.
> > Imatinib mesylate has been well tolerable and widely used for chronic
> > myeloid leukemia and gastrointestinal stromal tomor.
> > Imatinib also inhibits the activation of c-Abl, which is a key
> > downstream molecule of transforming growth factor-beta signaling, and
> > PDGF receptors.
> > Thus, imatinib effectively suppresses the activation and proliferation
> > of fibroblasts, mesangial cells and smooth muscle cells.
> > Therefore, imatinib may overcome the limitation of current therapeutic
> > strategy with corticosteroids and immunosuppressive agents for
> > refractory diseases
>
> > -------------------------------
>
> > Imatinib mesylate both prevents and treats the arthritis induced by
> > type II collagen antibody in mice
> > Journal Modern Rheumatology
>
> > ORIGINAL ARTICLE
> > Imatinib mesylate both prevents and treats the arthritis induced by
> > type II collagen antibody in mice
> > Kensuke Koyama1, 2 , Kyosuke Hatsushika1, Takashi Ando1, Michitomo
> > Sakuma1, Masanori Wako1, Ryohei Kato3, Hirotaka Haro2, Hajime
> > Sugiyama2, Yoshiki Hamada2, Hideoki Ogawa4 and Atsuhito Nakao1, 4
>
> > (1)  Department of Immunology, Faculty of Medicine, University of
> > Yamanashi, Yamanashi, Japan
> > (2)  Department of Orthopaedic Surgery, Faculty of Medicine,
> > University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi 409-3898,
> > Japan
> > (3)  Department of Human Pathology, Faculty of Medicine, University of
> > Yamanashi, Yamanashi, Japan
> > (4)  Atopy Research Center, Juntendo University School of Medicine,
> > Tokyo, Japan
>
> > Received: 08 February 2007  Accepted: 01 May 2007  Published online:
> > 20 August 2007
>
> > Abstract  Rheumatoid arthritis (RA) is a chronic inflammatory disease
> > that is associated with joint destruction.
> > Imatinib mesylate (imatinib) is an inhibitor that specifically targets
> > a set of protein tyrosine kinase, such as abl, c-kit, and platelet-
> > derived growth factor receptor (PDGFR) and it is widely used to treat
> > chronic myeloid leukemia (CML).
> > The purpose of the present study is to determine whether imatinib can
> > provide benefit in the arthritis induced by anti-collagen type II
> > antibody (CAIA) in mice, a model that provides an opportunity to study
> > the effector inflammatory phase of arthritis without involving the
> > priming phase of the immune responses.
> > Mice treated with intraperitoneal administration of imatinib (1 or 10
> > mg/kg) prior to the development of CAIA displayed significant
> > reductions in the severity of CAIA as assessed by arthritis score,
> > histology, and synovial PDGF and vascular endothelial growth factor
> > expression.
> > In addition, treatment of the mice that had developed CAIA with
> > intraperitoneal administration of imatinib (1 or 10 mg/kg) inhibited
> > the progression of arthritis as assessed by those parameters.
> > These results suggest that imatinib prevents and treats
>
> ...
>
> read more »- Hide quoted text -
>
> - Show quoted text -

From: ironjustice on 30 Jun 2008 15:02

---

On Jun 30, 11:50 am, ironjustice <ironjust...(a)aol.com> wrote: Arginine
butyrate <<

This would be your plant food.

"Effects of short-chain fatty acids on head and neck squamous"

"Arginine butyrate and α-lipoic acid are the most effective in
suppressing growth"

Titre du document / Document title
Differential effects of short-chain fatty acids on head and neck
squamous carcinoma cells
Auteur(s) / Author(s)
KRISHNA Srinivasan (1) ; BROWN Neil (1) ; FALLER Douglas V. (2) ;
SPANJAARD Remco A. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Otolaryngology-Head and Neck Surgery, Cancer
Research Center, Boston University School of Medicine, Boston,
Massachusetts, ETATS-UNIS
(2) Department of Medicine, Cancer Research Center, Boston University
School of Medicine, Boston, Massachusetts, ETATS-UNIS

Résumé / Abstract
Objectives/Hypothesis:
Head and neck squamous cell carcinoma (HNSCC) is a major cause of
mortality. Despite advances in therapeutic modalities, recurrences and
second primaries are commonly observed.
Biological agents that can suppress growth of tumors that are
otherwise difficult to treat are greatly needed.
The present study examined the effects of short-chain fatty acids on
HNSCC cell lines.
Study Design:
The effects of short-chain fatty acids on HNSCC cells was examined
using tissue culture and immunoblotting techniques.
Methods:
The effects of four short-chain fatty acids, arginine butyrate, α-
methyl hydrocinnamic acid, 2,2-dimethylbutyrate, and α-lipoic acid,
were evaluated on four HNSCC cell lines (FaDu, SCC9, SCC25, and
Detroit-562).
Proliferation assays were performed by means of spectrophotometric
techniques. Histone deacetylase activity was assessed by identifying
the amount of acetylated histone H4.
Involucrin expression was determined to assess cellular
differentiation.
Results:
Inhibition of cellular proliferation was determined after 5 days of
incubation with increasing doses with short-chain fatty acids.
Arginine butyrate and α-lipoic acid were most effective in suppressing
growth. Arginine butyrate demonstrated strong histone deacetylase
inhibition in FaDu cells, while not inducing cellular
differentiation.
The short-chain fatty acid α-lipoic acid demonstrated weak histone
deacetylase inhibition but was the only short-chain fatty acid that
induced involucrin expression in at least two of the cell lines.
Histone deacetylase inhibitory activity or induction of involucrin
expression correlated with suppression of cell growth.
Conclusions:
Short-chain fatty acids have variable effects on HNSCC cells.
Arginine butyrate and α-lipoic acid are the most effective in
suppressing growth and appear to do so through different biochemical
mechanisms.
These compounds warrant further research as chemotherapeutic or
chemopreventive agents in HNSCC.
Revue / Journal Title
The Laryngoscope ISSN 0023-852X CODEN LARYA8
Source / Source
2002, vol. 112, no4, pp. 645-650 (46 ref.)
Langue / Language
Anglais

Editeur / Publisher
Lippincott, Hagerstown, MD, ETATS-UNIS (1896) (Revue)

Mots-clés anglais / English Keywords
ENT disease ; Malignant tumor ; Cell culture ; Cell line ; Biological
effect ; Experimental study ; Immunoblotting assay ; Fatty acids ;
Short chain ; Head and neck ; Squamous cell carcinoma ;
Mots-clés français / French Keywords
ORL pathologie ; Tumeur maligne ; Culture cellulaire ; Lignée
cellulaire ; Effet biologique ; Etude expérimentale ; Méthode
immunoblotting ; Acide gras ; Chaîne courte ; Tête cou ; Carcinome
épidermoïde ;
Mots-clés espagnols / Spanish Keywords
ORL patología ; Tumor maligno ; Cultivo celular ; Línea celular ;
Efecto biológico ; Estudio experimental ; Western blotting ; Acido
graso ; Cadena corta ; Cabeza cuello ; Carcinoma epidermoide ;
Localisation / Location
INIST-CNRS, Cote INIST : 3102, 35400010053073.0100


Copyright 2007 INIST-CNRS. All rights reserved

Toute reproduction ou diffusion même partielle, par quelque procédé ou
sur tout support que ce soit, ne pourra être faite sans l'accord
préalable écrit de l'INIST-CNRS.
No part of these records may be reproduced of distributed, in any form
or by any means, without the prior written permission of INIST-CNRS.

Nº notice refdoc (ud4) : 13609728


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk



> On Jun 30, 10:44 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com>
> wrote: thrombosis <<
>
> Curious thing here is ,, there was a question of  "the hemolysis in
> blood donor bags" someone ventured .. "add arginine to offset the
> hemolysis".
>
> -------------------------------------------
>
> Arginine Butyrate Heals Sickle Cell Leg Ulcers
>
> Jane Salodof MacNeil
>
> Dec. 10, 2002 (Philadelphia) — Researchers working with an
> experimental drug for sickle cell anemia noticed an unexpected side
> effect: the incidental healing of debilitating leg ulcers in seven
> patients.
>
> That serendipitous observation led to a 25-patient phase II study in
> which treatment with the compound, arginine butyrate, healed 17 of 37
> leg ulcers. In contrast, among 24 ulcers that received standard local
> care for wounds, complete healing was documented for one ulcer.
>
> Several of the participants had suffered with large open sores for
> decades, according to investigator Susan Perrine, MD, of Boston
> University School of Medicine in Massachusetts. One woman had leg
> ulcers for 30 years, Dr. Perrine reported in a presentation here at
> the American Society of Hematology annual meeting.
>
> The investigator showed dramatic before and after photographs of legs
> from several patients who benefited from the treatment. The mean
> initial area of ulcers in the arginine butyrate arm of the study was
> 50.8 cm2 — nearly twice the 26.4 cm2 in the control group.
>
> Within three months of treatment, the area had been reduced by 53% in
> patients who received arginine butyrate, but the area was reduced by
> 9% in the control arm. Dr. Perrine said the researchers don't know why
> the compound heals these ulcers.
>
> H. Grant Prentice, MD, of the London Clinic in the U.K., called the
> study "extremely important." The former head of hematology at the
> Royal Free Hospital in London, Dr. Prentice said the most common
> therapy for leg ulcers associated with sickle cell disease is
> hydroxyurea. "It's not very effective, and the patients don't like to
> take it," he told Medscape.
>
> About 25% of sickle cell patients suffer from leg ulcers, according to
> an earlier study of 2,000 patients that Dr. Perrine cited at the start
> of her talk. In the United States, she said, the typical sickle cell
> ulcer lasts as long as three years; in the Caribbean more than nine
> years is common. Even if they are cured, between a quarter and a half
> of these ulcers will recur.
>
> Despite their prevalence, the ulcers are not well known, even in the
> sickle cell community, according to Dr. Perrine. They tend to occur in
> adults, she said, explaining she had little experience with them
> because she works in pediatrics.
>
> Patients in the treatment arm of the trial received 500 mg/kg of
> arginine butyrate six hours a day three days a week for twelve weeks.
> Although hydroxyurea is used, she said there is no standard regimen
> for these sores. The control group was treated aggressively according
> to local standards for wound healing, but no particular protocol was
> used in the six-center study.
>
> Although the study ended after three months, patients were allowed to
> continue for 16 weeks if their ulcers were closing with arginine
> butryate. Within five to seven months, a 10-fold increase in wound
> healing was reported.
>
> Dr. Perrine said the investigators plan to seek funds for a phase III
> trial. The pilot study was conducted with support from the U.S. Food
> and Drug Administration's orphan drug program, she said. Arginine
> butryate is an experimental compound and is not yet commercially
> available.
>
> ASH 44th Annual Meeting: Abstract 26. Presented Dec. 8, 2002.
>
> Reviewed by Gary D. Vogin, MD
>
> Jane Salodof MacNeil is a freelance writer for Medscape.
> Conference Coverage
> 44th Annual Meeting of the American Society of Hematology
>
> -------------------
>
> THE IDEA THAT DRUGS MIGHT SAFELY SWITCH ON NONWORKING GENES RECEIVED
> ABOOST FROM RESEARCHERS DEVELOPING TREATMENTS FOR A GROUP OF GENETIC
> BLOODDISORDERS
>
> THE BLOOD DISORDERS INVOLVE RED BLOOD CELLS' FAILURE TO PRODUCE
> HEMOGLOBIN OR PRODUCTION OF A DEFECTIVE FORM OF THE OXYGEN CARRYING
> PROTEIN.
> THE DISORDERS INCLUDE SICKLE CELL ANEMIA WHICH MOSTLY AFFLICTS
> AFRICAN AMERICANS AND COOLEY'S ANEMIA WHICH MOSTLY AFFLICTS ITALIANS
> GREEKS AND OTHER MEDITERRANEAN GROUPS.
>
> BLOOD SPECIALISTS HAVE BEEN TRYING FOR A DECADE TO FIND A NEW WAY TO
> TREAT THESE DISORDERS BY TURNING ON A HEMOGLOBIN GENE THAT ORDINARILY
> QUITS WORKING AFTER BIRTH.
> THE FEW DRUGS THAT HAVE PULLED OFF THIS TRICK HAVE BEEN
> TOO TOXIC FOR THE LIFETIME USE THAT THE ANEMIC PATIENTS WOULD REQUIRE.
>
> NOW A TEAM OF RESEARCHERS IN OAKLAND CALIF REPORTED PRELIMINARY
> RESULTS IN WHICH A FOOD ADDITIVE A FATTY ACID CALLED ARGININE BUTYRATE
> APPEARED TO STIMULATE THE NONWORKING GENE TO BEGIN MAKING NORMAL
> HEMOGLOBIN IN SIX PATIENTS THEIR REPORT APPEARS IN THIS WEEK'S ISSUE
> OF THE NEW ENGLAND JOURNAL OF MEDICINE.
>
> THE MAIN PROBLEM IS THAT THE DRUG MUST BE GIVEN INTRAVENOUSLY BUT ONE
> OF THE RESEARCHERS SAID AN ORAL FORM OF THE DRUG IS BEING DEVELOPED.
>
> THE TWO ANEMIAS ARE IDEAL CANDIDATES FOR GENE ACTIVATION THERAPY.
> BOTH INVOLVE DEFECTS IN HEMOGLOBIN THE IRON CONTAINING PROTEIN THAT
> RED BLOOD CELLS USE TO CARRY OXYGEN TO BODY TISSUES.
> OF THE TWO GENES CAPABLE OF MAKING HEMOGLOBIN ONE FUNCTIONS ONLY
> DURING FETAL LIFE WHEN THE FETUS MUST PULL OXYGEN CARRYING BLOOD
> ACROSS THE PLACENTA.
>  THIS FETAL GENE TURNS OFF AFTER BIRTH AND A SECOND ADULT GENE TAKES
> OVER.
>
> IN COOLEY'S ANEMIA ALSO KNOWN AS BETATHALASSEMIA THE DEFECTIVE ADULT
> GENE PRODUCES LITTLE OR NO HEMOGLOBIN.
> THOSE BORN WITH THE DEFECT MUST RECEIVE REPEATED BLOOD TRANSFUSIONS TO
> SURVIVE.
> IF THE FETAL GENE COULD BE REAWAKENED AND PUT BACK TO WORK THE
> PATIENT'S RED CELLS WITH A NEW ENDOWMENT OF PERFECTLY FUNCTIONAL FETAL
> HEMOGLOBIN WOULD ENLARGE REDDEN
> AND REGAIN VIABILITY EXPLAINED H FRANKLIN BUNN IN AN EDITORIAL
> COMMENTINGON THE NEW RESEARCH.
> DR BUNN WHO IS AT THE BRIGHAM AND WOMEN'S HOSPITAL IN
> BOSTON IS ALSO WORKING ON GENESWITCHING TREATMENTS FOR THE
> BLOODDISORDERS
>
> IN SICKLECELL ANEMIA THE ADULT HEMOGLOBIN GENE FUNCTIONS BUT IS
> DEFECTIVE AND THE DEFECTIVE HEMOGLOBIN IT PRODUCES LEADS TO A RIGID
> SICKLE SHAPED RED BLOOD CELL.
> THIS SICKLING EFFECT DOESN'T OCCUR IF FETAL HEMOGLOBIN IS ALSO
> PRESENT.
>
> IN THE LATEST RESEARCH ALL SIX PATIENTS THREE WITH COOLEY'S ANEMIA AND
> THREE WITH SICKLECELL ANEMIA EXPERIENCED INCREASES IN FETAL HEMOGLOBIN
> PRODUCTION FOLLOWING INFUSIONS OF AN ULTRAPURE FORM OF ARGININE
> BUTYRATE REPORTED A TEAM OF RESEARCHERS HEADED BY SUSAN P PERRINE OF
> CHILDREN'S
> HOSPITAL OAKLAND RESEARCH INSTITUTE IN OAKLAND CALIF.
> THE TEAM INCLUDEDSCIENTISTS FROM A HALF DOZEN MEDICAL CENTERS IN THE
> US AND CANADA.
>
> INCREASES IN THE OUTPUT OF FETAL HEMOGLOBIN RANGED FROM 6 TO 45 ABOVE
> PRETREATMENT LEVELS THE RESEARCHERS REPORTED.
> IN TWO PATIENTS THE PRODUCTION OF FETAL HEMOGLOBIN CONTINUED FOR A
> MONTH AFTER TREATMENT STOPPED.
> SIDE EFFECTS WERE ALMOST NONEXISTENT THEY SAID.
>
> THE RESULTS ALTHOUGH HIGHLY PRELIMINARY INDICATE THAT THE
> ADMINISTRATION OF ARGININE BUTYRATE REPRESENTS A NOVEL AND POTENTIALLY
> EFFECTIVE THERAPY FOR THESE PREVALENT MOLECULAR DISORDERS THE REPORT
> DECLARED.
>
> IN A TELEPHONE INTERVIEW DR PERRINE SAID SHE HAD TO COMPOUND THE
> ARGININE BUTYRATE USED IN THE TEST.
> THE TEAM SHE SAID HAS SINCE DEVELOPED SOME VARIATIONS OF THE FATTY
> ACID THAT COULD BE GIVEN ORALLY.
> THE RESEARCHERS HOWEVER ARE LOOKING FOR A DRUG MANUFACTURER WHO WOULD
> TAKE OVER DEVELOPMENT
> OF THE DRUGS AND TAKE THEM THROUGH THE US FOOD AND DRUG ADMINISTRATION
> PROCESSES FOR MARKETING
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On Jun 30, 10:19 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com>
> > wrote: imatinib <<
>
> > Polycythemia the first line recommended treatment is .. bloodletting.
> > Gleevec results in 75% remission rate in polycythemia.
>
> > Someone buying an expensive .. bridge .. ?
> > Some can't even afford the .. bridge .. ?
>
> > Gleevec, the cost: $3,100
> > Cost of cancer drugs crushes all but hope
> > Updated 7/11/2006 10:50 AM ET
>
> > By Liz Szabo, USA TODAY
> > When Tom Reek was diagnosed with a rare leukemia at age 65, doctors
> > said he might live only another three years. Today, Reek is thriving
> > at age 72, thanks to a drug called Gleevec.
> > "I used to kid around and say that I feel like Clark Kent," says Reek,
> > who lives on Long Island, N.Y., and volunteers as a peer counselor
> > with other patients, including youngsters. "It's like a gift from God
> > to be able to work with these children."
>
> > The only downside to Gleevec, Reek says, is the cost: $3,100 a month.
> > Reek went back to work four years ago as a truck driver, delivering
> > blood tests and lab results to medical offices. With insurance, his
> > pills cost only about $50 a month.
>
> > Since Gleevec was approved in 2001, researchers have hoped that every
> > new cancer therapy would copy its success: a convenient pill that lets
> > patients live for years with relatively few serious side effects.
> > Though experts say few of the new "targeted" therapies come close to
> > that ideal, they do have one thing in common with Gleevec: They're all
> > incredibly expensive.
>
> > PRESCRIPTION COSTS: Prices soar for cancer drugs
>
> > Some doctors are questioning whether targeted therapies — designed to
> > turn cancer into a chronic disease by silencing growth signals inside
> > malignant cells — are worth the expense to individuals and taxpayers.
>
> > Most new cancer drugs improve survival by only a few weeks or months,
> > says researcher Leonard Saltz of New York's Memorial Sloan-Kettering
> > Cancer Center. Although Erbitux, for example, costs almost $10,000 a
> > month, studies have not shown that it helps colorectal cancer patients
> > live longer.
>
> > "There is a real question whether insurance ought to pay for a drug
> > like that," says Ezekial Emanuel, chairman of clinical bioethics at
> > the National Institutes of Health clinical center. "If you pay for
> > something that doesn't have a
>
> ...
>
> read more »- Hide quoted text -
>
> - Show quoted text -

From: ironjustice on 3 Jul 2008 01:26

---

On Jun 30, 12:02 pm, ironjustice <ironjust...(a)aol.com> wrote:
thrombosis <<

"Iron markedly accelerates thrombus formation"

(Circulation. 2003;107:2601.)
© 2003 American Heart Association, Inc.

--------------------------------------------------------------------------------

Basic Science Reports


Chronic Iron Administration Increases Vascular Oxidative Stress and
Accelerates Arterial Thrombosis
Sharlene M. Day, MD; Damon Duquaine, BS; Lakshmi V. Mundada, MS; Rekha
G. Menon, MD; Bobby V. Khan, MD, PhD; Sanjay Rajagopalan, MD; William
P. Fay, MD
From the University of Michigan Medical School, Division of
Cardiology, Ann Arbor (S.M.D., D.D., L.V.M., S.R., W.P.F.); and Emory
University School of Medicine, Division of Cardiology, Atlanta, Ga
(R.G.M., B.V.K.).

Correspondence to Sharlene M. Day, MD, University of Michigan Medical
Center, 7301 MSRB III, 1150 W Medical Center Dr, Ann Arbor, MI
48109-0644. E-mail sday(a)umich.edu

Background— Iron overload has been implicated in the pathogenesis of
ischemic cardiovascular events. However, the effects of iron excess on
vascular function and the thrombotic response to vascular injury are
not well understood.

Methods and Results— We examined the effects of chronic iron dextran
administration (15 mg over 6 weeks) on thrombosis, systemic and
vascular oxidative stress, and endothelium-dependent vascular
reactivity in mice. Thrombus generation after photochemical carotid
artery injury was accelerated in iron-loaded mice (mean time to
occlusive thrombosis, 20.4±8.5 minutes; n=10) compared with control
mice (54.5±35.5 minutes, n=10, P=0.009). Iron loading had no effect on
plasma clotting, vessel wall tissue factor activity, or ADP-induced
platelet aggregation. Acute administration of DL-cysteine, a reactive
oxygen species scavenger, completely abrogated the effects of iron
loading on thrombus formation, suggesting that iron accelerated
thrombosis through a pro-oxidant mechanism. Iron loading enhanced both
systemic and vascular reactive oxygen species production. Endothelium-
dependent vasorelaxation was impaired in iron-loaded mice, indicating
reduced NO bioavailability.

Conclusions— Moderate iron loading markedly accelerates thrombus
formation after arterial injury, increases vascular oxidative stress,
and impairs vasoreactivity. Iron-induced vascular dysfunction may
contribute to the increased incidence of ischemic cardiovascular
events that have been associated with chronic iron overload.


Key Words: thrombosis • free radicals • arteries


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


> On Jun 30, 11:50 am, ironjustice <ironjust...(a)aol.com> wrote: Arginine
> butyrate <<
>
> This would be your plant food.
>
> "Effects of short-chain fatty acids on head and neck squamous"
>
> "Arginine butyrate and α-lipoic acid are the most effective in
> suppressing growth"
>
> Titre du document / Document title
> Differential effects of short-chain fatty acids on head and neck
> squamous carcinoma cells
> Auteur(s) / Author(s)
> KRISHNA Srinivasan (1) ; BROWN Neil (1) ; FALLER Douglas V. (2) ;
> SPANJAARD Remco A. (1) ;
> Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
> (1) Department of Otolaryngology-Head and Neck Surgery, Cancer
> Research Center, Boston University School of Medicine, Boston,
> Massachusetts, ETATS-UNIS
> (2) Department of Medicine, Cancer Research Center, Boston University
> School of Medicine, Boston, Massachusetts, ETATS-UNIS
>
> Résumé / Abstract
> Objectives/Hypothesis:
> Head and neck squamous cell carcinoma (HNSCC) is a major cause of
> mortality. Despite advances in therapeutic modalities, recurrences and
> second primaries are commonly observed.
> Biological agents that can suppress growth of tumors that are
> otherwise difficult to treat are greatly needed.
> The present study examined the effects of short-chain fatty acids on
> HNSCC cell lines.
> Study Design:
> The effects of short-chain fatty acids on HNSCC cells was examined
> using tissue culture and immunoblotting techniques.
> Methods:
> The effects of four short-chain fatty acids, arginine butyrate, α-
> methyl hydrocinnamic acid, 2,2-dimethylbutyrate, and α-lipoic acid,
> were evaluated on four HNSCC cell lines (FaDu, SCC9, SCC25, and
> Detroit-562).
> Proliferation assays were performed by means of spectrophotometric
> techniques. Histone deacetylase activity was assessed by identifying
> the amount of acetylated histone H4.
> Involucrin expression was determined to assess cellular
> differentiation.
> Results:
> Inhibition of cellular proliferation was determined after 5 days of
> incubation with increasing doses with short-chain fatty acids.
> Arginine butyrate and α-lipoic acid were most effective in suppressing
> growth. Arginine butyrate demonstrated strong histone deacetylase
> inhibition in FaDu cells, while not inducing cellular
> differentiation.
> The short-chain fatty acid α-lipoic acid demonstrated weak histone
> deacetylase inhibition but was the only short-chain fatty acid that
> induced involucrin expression in at least two of the cell lines.
> Histone deacetylase inhibitory activity or induction of involucrin
> expression correlated with suppression of cell growth.
> Conclusions:
> Short-chain fatty acids have variable effects on HNSCC cells.
> Arginine butyrate and α-lipoic acid are the most effective in
> suppressing growth and appear to do so through different biochemical
> mechanisms.
> These compounds warrant further research as chemotherapeutic or
> chemopreventive agents in HNSCC.
> Revue / Journal Title
> The Laryngoscope   ISSN 0023-852X   CODEN LARYA8
> Source / Source
> 2002, vol. 112, no4, pp. 645-650 (46 ref.)
> Langue / Language
> Anglais
>
> Editeur / Publisher
> Lippincott, Hagerstown, MD, ETATS-UNIS (1896) (Revue)
>
> Mots-clés anglais / English Keywords
> ENT disease ; Malignant tumor ; Cell culture ; Cell line ; Biological
> effect ; Experimental study ; Immunoblotting assay ; Fatty acids ;
> Short chain ; Head and neck ; Squamous cell carcinoma ;
> Mots-clés français / French Keywords
> ORL pathologie ; Tumeur maligne ; Culture cellulaire ; Lignée
> cellulaire ; Effet biologique ; Etude expérimentale ; Méthode
> immunoblotting ; Acide gras ; Chaîne courte ; Tête cou ; Carcinome
> épidermoïde ;
> Mots-clés espagnols / Spanish Keywords
> ORL patología ; Tumor maligno ; Cultivo celular ; Línea celular ;
> Efecto biológico ; Estudio experimental ; Western blotting ; Acido
> graso ; Cadena corta ; Cabeza cuello ; Carcinoma epidermoide ;
> Localisation / Location
> INIST-CNRS, Cote INIST : 3102, 35400010053073.0100
>
> Copyright 2007 INIST-CNRS. All rights reserved
>
> Toute reproduction ou diffusion même partielle, par quelque procédé ou
> sur tout support que ce soit, ne pourra être faite sans l'accord
> préalable écrit de l'INIST-CNRS.
> No part of these records may be reproduced of distributed, in any form
> or by any means, without the prior written permission of INIST-CNRS.
>
> Nº notice refdoc (ud4) : 13609728
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On Jun 30, 10:44 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com>
> > wrote: thrombosis <<
>
> > Curious thing here is ,, there was a question of  "the hemolysis in
> > blood donor bags" someone ventured .. "add arginine to offset the
> > hemolysis".
>
> > -------------------------------------------
>
> > Arginine Butyrate Heals Sickle Cell Leg Ulcers
>
> > Jane Salodof MacNeil
>
> > Dec. 10, 2002 (Philadelphia) — Researchers working with an
> > experimental drug for sickle cell anemia noticed an unexpected side
> > effect: the incidental healing of debilitating leg ulcers in seven
> > patients.
>
> > That serendipitous observation led to a 25-patient phase II study in
> > which treatment with the compound, arginine butyrate, healed 17 of 37
> > leg ulcers. In contrast, among 24 ulcers that received standard local
> > care for wounds, complete healing was documented for one ulcer.
>
> > Several of the participants had suffered with large open sores for
> > decades, according to investigator Susan Perrine, MD, of Boston
> > University School of Medicine in Massachusetts. One woman had leg
> > ulcers for 30 years, Dr. Perrine reported in a presentation here at
> > the American Society of Hematology annual meeting.
>
> > The investigator showed dramatic before and after photographs of legs
> > from several patients who benefited from the treatment. The mean
> > initial area of ulcers in the arginine butyrate arm of the study was
> > 50.8 cm2 — nearly twice the 26.4 cm2 in the control group.
>
> > Within three months of treatment, the area had been reduced by 53% in
> > patients who received arginine butyrate, but the area was reduced by
> > 9% in the control arm. Dr. Perrine said the researchers don't know why
> > the compound heals these ulcers.
>
> > H. Grant Prentice, MD, of the London Clinic in the U.K., called the
> > study "extremely important." The former head of hematology at the
> > Royal Free Hospital in London, Dr. Prentice said the most common
> > therapy for leg ulcers associated with sickle cell disease is
> > hydroxyurea. "It's not very effective, and the patients don't like to
> > take it," he told Medscape.
>
> > About 25% of sickle cell patients suffer from leg ulcers, according to
> > an earlier study of 2,000 patients that Dr. Perrine cited at the start
> > of her talk. In the United States, she said, the typical sickle cell
> > ulcer lasts as long as three years; in the Caribbean more than nine
> > years is common. Even if they are cured, between a quarter and a half
> > of these ulcers will recur.
>
> > Despite their prevalence, the ulcers are not well known, even in the
> > sickle cell community, according to Dr. Perrine. They tend to occur in
> > adults, she said, explaining she had little experience with them
> > because she works in pediatrics.
>
> > Patients in the treatment arm of the trial received 500 mg/kg of
> > arginine butyrate six hours a day three days a week for twelve weeks.
> > Although hydroxyurea is used, she said there is no standard regimen
> > for these sores. The control group was treated aggressively according
> > to local standards for wound healing, but no particular protocol was
> > used in the six-center study.
>
> > Although the study ended after three months, patients were allowed to
> > continue for 16 weeks if their ulcers were closing with arginine
> > butryate. Within five to seven months, a 10-fold increase in wound
> > healing was reported.
>
> > Dr. Perrine said the investigators plan to seek funds for a phase III
> > trial. The pilot study was conducted with support from the U.S. Food
> > and Drug Administration's orphan drug program, she said. Arginine
> > butryate is an experimental compound and is not yet commercially
> > available.
>
> > ASH 44th Annual Meeting: Abstract 26. Presented Dec. 8, 2002.
>
> > Reviewed by Gary D. Vogin, MD
>
> > Jane Salodof MacNeil is a freelance writer for Medscape.
> > Conference Coverage
> > 44th Annual Meeting of the American Society of Hematology
>
> > -------------------
>
> > THE IDEA THAT DRUGS MIGHT SAFELY SWITCH ON NONWORKING GENES RECEIVED
> > ABOOST FROM RESEARCHERS DEVELOPING TREATMENTS FOR A GROUP OF GENETIC
> > BLOODDISORDERS
>
> > THE BLOOD DISORDERS INVOLVE RED BLOOD CELLS' FAILURE TO PRODUCE
> > HEMOGLOBIN OR PRODUCTION OF A DEFECTIVE FORM OF THE OXYGEN CARRYING
> > PROTEIN.
> > THE DISORDERS INCLUDE SICKLE CELL ANEMIA WHICH MOSTLY AFFLICTS
> > AFRICAN AMERICANS AND COOLEY'S ANEMIA WHICH MOSTLY AFFLICTS ITALIANS
> > GREEKS AND OTHER MEDITERRANEAN GROUPS.
>
> > BLOOD SPECIALISTS HAVE BEEN TRYING FOR A DECADE TO FIND A NEW WAY TO
> > TREAT THESE DISORDERS BY TURNING ON A HEMOGLOBIN GENE THAT ORDINARILY
> > QUITS WORKING AFTER BIRTH.
> > THE FEW DRUGS THAT HAVE PULLED OFF THIS TRICK HAVE BEEN
> > TOO TOXIC FOR THE LIFETIME USE THAT THE ANEMIC PATIENTS WOULD REQUIRE.
>
> > NOW A TEAM OF RESEARCHERS IN OAKLAND CALIF REPORTED PRELIMINARY
> > RESULTS IN WHICH A FOOD ADDITIVE A FATTY ACID CALLED ARGININE BUTYRATE
> > APPEARED TO STIMULATE THE NONWORKING GENE TO BEGIN MAKING NORMAL
> > HEMOGLOBIN IN SIX PATIENTS THEIR REPORT APPEARS IN THIS WEEK'S ISSUE
> > OF THE NEW ENGLAND JOURNAL OF MEDICINE.
>
> > THE MAIN PROBLEM IS THAT THE DRUG MUST BE GIVEN INTRAVENOUSLY BUT ONE
> > OF THE RESEARCHERS SAID AN ORAL FORM OF THE DRUG IS BEING DEVELOPED.
>
> > THE TWO ANEMIAS ARE IDEAL CANDIDATES FOR GENE ACTIVATION THERAPY.
> > BOTH INVOLVE DEFECTS IN HEMOGLOBIN THE IRON CONTAINING PROTEIN THAT
> > RED BLOOD CELLS USE TO CARRY OXYGEN TO BODY TISSUES.
> > OF THE TWO GENES CAPABLE OF MAKING HEMOGLOBIN ONE FUNCTIONS ONLY
> > DURING FETAL LIFE WHEN THE FETUS MUST PULL OXYGEN CARRYING BLOOD
> > ACROSS THE PLACENTA.
> >  THIS FETAL GENE
>
> ...
>
> read more »- Hide quoted text -
>
> - Show quoted text -

From: Harvey R. Stone on 3 Jul 2008 08:17

---

Reported for being off topic in Alt.support.arthritis,,,, cross posting
after being warned not to do it.

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On Jun 30, 12:02=C2=A0pm, ironjustice <ironjust...(a)aol.com> wrote:
thrombosis <<

"Iron markedly accelerates thrombus formation"

(Circulation. 2003;107:2601.)
=C2=A9 2003 American Heart Association, Inc.

---------------------------------------------------------------------------=
-----

Basic Science Reports


Chronic Iron Administration Increases Vascular Oxidative Stress and
Accelerates Arterial Thrombosis
Sharlene M. Day, MD; Damon Duquaine, BS; Lakshmi V. Mundada, MS; Rekha
G. Menon, MD; Bobby V. Khan, MD, PhD; Sanjay Rajagopalan, MD; William
P. Fay, MD
=46rom the University of Michigan Medical School, Division of
Cardiology, Ann Arbor (S.M.D., D.D., L.V.M., S.R., W.P.F.); and Emory
University School of Medicine, Division of Cardiology, Atlanta, Ga
(R.G.M., B.V.K.).

Correspondence to Sharlene M. Day, MD, University of Michigan Medical
Center, 7301 MSRB III, 1150 W Medical Center Dr, Ann Arbor, MI
48109-0644. E-mail sday(a)umich.edu

Background=E2=80=94 Iron overload has been implicated in the pathogenesis o=
f
ischemic cardiovascular events. However, the effects of iron excess on
vascular function and the thrombotic response to vascular injury are
not well understood.

Methods and Results=E2=80=94 We examined the effects of chronic iron dextra=
n
administration (15 mg over 6 weeks) on thrombosis, systemic and
vascular oxidative stress, and endothelium-dependent vascular
reactivity in mice. Thrombus generation after photochemical carotid
artery injury was accelerated in iron-loaded mice (mean time to
occlusive thrombosis, 20.4=C2=B18.5 minutes; n=3D10) compared with control
mice (54.5=C2=B135.5 minutes, n=3D10, P=3D0.009). Iron loading had no effec=
t on
plasma clotting, vessel wall tissue factor activity, or ADP-induced
platelet aggregation. Acute administration of DL-cysteine, a reactive
oxygen species scavenger, completely abrogated the effects of iron
loading on thrombus formation, suggesting that iron accelerated
thrombosis through a pro-oxidant mechanism. Iron loading enhanced both
systemic and vascular reactive oxygen species production. Endothelium-
dependent vasorelaxation was impaired in iron-loaded mice, indicating
reduced NO bioavailability.

Conclusions=E2=80=94 Moderate iron loading markedly accelerates thrombus
formation after arterial injury, increases vascular oxidative stress,
and impairs vasoreactivity. Iron-induced vascular dysfunction may
contribute to the increased incidence of ischemic cardiovascular
events that have been associated with chronic iron overload.


Key Words: thrombosis =E2=80=A2 free radicals =E2=80=A2 arteries


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

"ironjustice" <teamtanner(a)hotmail.com> wrote in message
news:9d51be37-5f04-4068-ae3d-23d3d76a387f(a)l64g2000hse.googlegroups.com...
On Jun 30, 12:02 pm, ironjustice <ironjust...(a)aol.com> wrote:
thrombosis <<

"Iron markedly accelerates thrombus formation"

(Circulation. 2003;107:2601.)
� 2003 American Heart Association, Inc.

--------------------------------------------------------------------------------

Basic Science Reports


Chronic Iron Administration Increases Vascular Oxidative Stress and
Accelerates Arterial Thrombosis
Sharlene M. Day, MD; Damon Duquaine, BS; Lakshmi V. Mundada, MS; Rekha
G. Menon, MD; Bobby V. Khan, MD, PhD; Sanjay Rajagopalan, MD; William
P. Fay, MD
From the University of Michigan Medical School, Division of
Cardiology, Ann Arbor (S.M.D., D.D., L.V.M., S.R., W.P.F.); and Emory
University School of Medicine, Division of Cardiology, Atlanta, Ga
(R.G.M., B.V.K.).

Correspondence to Sharlene M. Day, MD, University of Michigan Medical
Center, 7301 MSRB III, 1150 W Medical Center Dr, Ann Arbor, MI
48109-0644. E-mail sday(a)umich.edu

Background- Iron overload has been implicated in the pathogenesis of
ischemic cardiovascular events. However, the effects of iron excess on
vascular function and the thrombotic response to vascular injury are
not well understood.

Methods and Results- We examined the effects of chronic iron dextran
administration (15 mg over 6 weeks) on thrombosis, systemic and
vascular oxidative stress, and endothelium-dependent vascular
reactivity in mice. Thrombus generation after photochemical carotid
artery injury was accelerated in iron-loaded mice (mean time to
occlusive thrombosis, 20.4�8.5 minutes; n=10) compared with control
mice (54.5�35.5 minutes, n=10, P=0.009). Iron loading had no effect on
plasma clotting, vessel wall tissue factor activity, or ADP-induced
platelet aggregation. Acute administration of DL-cysteine, a reactive
oxygen species scavenger, completely abrogated the effects of iron
loading on thrombus formation, suggesting that iron accelerated
thrombosis through a pro-oxidant mechanism. Iron loading enhanced both
systemic and vascular reactive oxygen species production. Endothelium-
dependent vasorelaxation was impaired in iron-loaded mice, indicating
reduced NO bioavailability.

Conclusions- Moderate iron loading markedly accelerates thrombus
formation after arterial injury, increases vascular oxidative stress,
and impairs vasoreactivity. Iron-induced vascular dysfunction may
contribute to the increased incidence of ischemic cardiovascular
events that have been associated with chronic iron overload.


Key Words: thrombosis . free radicals . arteries


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk


> On Jun 30, 11:50 am, ironjustice <ironjust...(a)aol.com> wrote: Arginine
> butyrate <<
>
> This would be your plant food.
>
> "Effects of short-chain fatty acids on head and neck squamous"
>
> "Arginine butyrate and ?-lipoic acid are the most effective in
> suppressing growth"
>
> Titre du document / Document title
> Differential effects of short-chain fatty acids on head and neck
> squamous carcinoma cells
> Auteur(s) / Author(s)
> KRISHNA Srinivasan (1) ; BROWN Neil (1) ; FALLER Douglas V. (2) ;
> SPANJAARD Remco A. (1) ;
> Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
> (1) Department of Otolaryngology-Head and Neck Surgery, Cancer
> Research Center, Boston University School of Medicine, Boston,
> Massachusetts, ETATS-UNIS
> (2) Department of Medicine, Cancer Research Center, Boston University
> School of Medicine, Boston, Massachusetts, ETATS-UNIS
>
> R�sum� / Abstract
> Objectives/Hypothesis:
> Head and neck squamous cell carcinoma (HNSCC) is a major cause of
> mortality. Despite advances in therapeutic modalities, recurrences and
> second primaries are commonly observed.
> Biological agents that can suppress growth of tumors that are
> otherwise difficult to treat are greatly needed.
> The present study examined the effects of short-chain fatty acids on
> HNSCC cell lines.
> Study Design:
> The effects of short-chain fatty acids on HNSCC cells was examined
> using tissue culture and immunoblotting techniques.
> Methods:
> The effects of four short-chain fatty acids, arginine butyrate, ?-
> methyl hydrocinnamic acid, 2,2-dimethylbutyrate, and ?-lipoic acid,
> were evaluated on four HNSCC cell lines (FaDu, SCC9, SCC25, and
> Detroit-562).
> Proliferation assays were performed by means of spectrophotometric
> techniques. Histone deacetylase activity was assessed by identifying
> the amount of acetylated histone H4.
> Involucrin expression was determined to assess cellular
> differentiation.
> Results:
> Inhibition of cellular proliferation was determined after 5 days of
> incubation with increasing doses with short-chain fatty acids.
> Arginine butyrate and ?-lipoic acid were most effective in suppressing
> growth. Arginine butyrate demonstrated strong histone deacetylase
> inhibition in FaDu cells, while not inducing cellular
> differentiation.
> The short-chain fatty acid ?-lipoic acid demonstrated weak histone
> deacetylase inhibition but was the only short-chain fatty acid that
> induced involucrin expression in at least two of the cell lines.
> Histone deacetylase inhibitory activity or induction of involucrin
> expression correlated with suppression of cell growth.
> Conclusions:
> Short-chain fatty acids have variable effects on HNSCC cells.
> Arginine butyrate and ?-lipoic acid are the most effective in
> suppressing growth and appear to do so through different biochemical
> mechanisms.
> These compounds warrant further research as chemotherapeutic or
> chemopreventive agents in HNSCC.
> Revue / Journal Title
> The Laryngoscope ISSN 0023-852X CODEN LARYA8
> Source / Source
> 2002, vol. 112, no4, pp. 645-650 (46 ref.)
> Langue / Language
> Anglais
>
> Editeur / Publisher
> Lippincott, Hagerstown, MD, ETATS-UNIS (1896) (Revue)
>
> Mots-cl�s anglais / English Keywords
> ENT disease ; Malignant tumor ; Cell culture ; Cell line ; Biological
> effect ; Experimental study ; Immunoblotting assay ; Fatty acids ;
> Short chain ; Head and neck ; Squamous cell carcinoma ;
> Mots-cl�s fran�ais / French Keywords
> ORL pathologie ; Tumeur maligne ; Culture cellulaire ; Lign�e
> cellulaire ; Effet biologique ; Etude exp�rimentale ; M�thode
> immunoblotting ; Acide gras ; Cha�ne courte ; T�te cou ; Carcinome
> �pidermo�de ;
> Mots-cl�s espagnols / Spanish Keywords
> ORL patolog�a ; Tumor maligno ; Cultivo celular ; L�nea celular ;
> Efecto biol�gico ; Estudio experimental ; Western blotting ; Acido
> graso ; Cadena corta ; Cabeza cuello ; Carcinoma epidermoide ;
> Localisation / Location
> INIST-CNRS, Cote INIST : 3102, 35400010053073.0100
>
> Copyright 2007 INIST-CNRS. All rights reserved
>
> Toute reproduction ou diffusion m�me partielle, par quelque proc�d� ou
> sur tout support que ce soit, ne pourra �tre faite sans l'accord
> pr�alable �crit de l'INIST-CNRS.
> No part of these records may be reproduced of distributed, in any form
> or by any means, without the prior written permission of INIST-CNRS.
>
> N� notice refdoc (ud4) : 13609728
>
> Who loves ya.
> Tom
>
> Jesus Was A Vegetarian!http://tinyurl.com/2r2nkh
>
> Man Is A Herbivore!http://tinyurl.com/4rq595
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On Jun 30, 10:44 am, "ironjust...(a)aol.com" <ironjust...(a)aol.com>
> > wrote: thrombosis <<
>
> > Curious thing here is ,, there was a question of "the hemolysis in
> > blood donor bags" someone ventured .. "add arginine to offset the
> > hemolysis".
>
> > -------------------------------------------
>
> > Arginine Butyrate Heals Sickle Cell Leg Ulcers
>
> > Jane Salodof MacNeil
>
> > Dec. 10, 2002 (Philadelphia) - Researchers working with an
> > experimental drug for sickle cell anemia noticed an unexpected side
> > effect: the incidental healing of debilitating leg ulcers in seven
> > patients.
>
> > That serendipitous observation led to a 25-patient phase II study in
> > which treatment with the compound, arginine butyrate, healed 17 of 37
> > leg ulcers. In contrast, among 24 ulcers that received standard local
> > care for wounds, complete healing was documented for one ulcer.
>
> > Several of the participants had suffered with large open sores for
> > decades, according to investigator Susan Perrine, MD, of Boston
> > University School of Medicine in Massachusetts. One woman had leg
> > ulcers for 30 years, Dr. Perrine reported in a presentation here at
> > the American Society of Hematology annual meeting.
>
> > The investigator showed dramatic before and after photographs of legs
> > from several patients who benefited from the treatment. The mean
> > initial area of ulcers in the arginine butyrate arm of the study was
> > 50.8 cm2 - nearly twice the 26.4 cm2 in the control group.
>
> > Within three months of treatment, the area had been reduced by 53% in
> > patients who received arginine butyrate, but the area was reduced by
> > 9% in the control arm. Dr. Perrine said the researchers don't know why
> > the compound heals these ulcers.
>
> > H. Grant Prentice, MD, of the London Clinic in the U.K., called the
> > study "extremely important." The former head of hematology at the
> > Royal Free Hospital in London, Dr. Prentice said the most common
> > therapy for leg ulcers associated with sickle cell disease is
> > hydroxyurea. "It's not very effective, and the patients don't like to
> > take it," he told Medscape.
>
> > About 25% of sickle cell patients suffer from leg ulcers, according to
> > an earlier study of 2,000 patients that Dr. Perrine cited at the start
> > of her talk. In the United States, she said, the typical sickle cell
> > ulcer lasts as long as three years; in the Caribbean more than nine
> > years is common. Even if they are cured, between a quarter and a half
> > of these ulcers will recur.
>
> > Despite their prevalence, the ulcers are not well known, even in the
> > sickle cell community, according to Dr. Perrine. They tend to occur in
> > adults, she said, explaining she had little experience with them
> > because she works in pediatrics.
>
> > Patients in the treatment arm of the trial received 500 mg/kg of
> > arginine butyrate six hours a day three days a week for twelve weeks.
> > Although hydroxyurea is used, she said there is no standard regimen
> > for these sores. The control group was treated aggressively according
> > to local standards for wound healing, but no particular protocol was
> > used in the six-center study.
>
> > Although the study ended after three months, patients were allowed to
> > continue for 16 weeks if their ulcers were closing with arginine
> > butryate. Within five to seven months, a 10-fold increase in wound
> > healing was reported.
>
> > Dr. Perrine said the investigators plan to seek funds for a phase III
> > trial. The pilot study was conducted with support from the U.S. Food
> > and Drug Administration's orphan drug program, she said. Arginine
> > butryate is an experimental compound and is not yet commercially
> > available.
>
> > ASH 44th Annual Meeting: Abstract 26. Presented Dec. 8, 2002.
>
> > Reviewed by Gary D. Vogin, MD
>
> > Jane Salodof MacNeil is a freelance writer for Medscape.
> > Conference Coverage
> > 44th Annual Meeting of the American Society of Hematology
>
> > -------------------
>
> > THE IDEA THAT DRUGS MIGHT SAFELY SWITCH ON NONWORKING GENES RECEIVED
> > ABOOST FROM RESEARCHERS DEVELOPING TREATMENTS FOR A GROUP OF GENETIC
> > BLOODDISORDERS
>
> > THE BLOOD DISORDERS INVOLVE RED BLOOD CELLS' FAILURE TO PRODUCE
> > HEMOGLOBIN OR PRODUCTION OF A DEFECTIVE FORM OF THE OXYGEN CARRYING
> > PROTEIN.
> > THE DISORDERS INCLUDE SICKLE CELL ANEMIA WHICH MOSTLY AFFLICTS
> > AFRICAN AMERICANS AND COOLEY'S ANEMIA WHICH MOSTLY AFFLICTS ITALIANS
> > GREEKS AND OTHER MEDITERRANEAN GROUPS.
>
> > BLOOD SPECIALISTS HAVE BEEN TRYING FOR A DECADE TO FIND A NEW WAY TO
> > TREAT THESE DISORDERS BY TURNING ON A HEMOGLOBIN GENE THAT ORDINARILY
> > QUITS WORKING AFTER BIRTH.
> > THE FEW DRUGS THAT HAVE PULLED OFF THIS TRICK HAVE BEEN
> > TOO TOXIC FOR THE LIFETIME USE THAT THE ANEMIC PATIENTS WOULD REQUIRE.
>
> > NOW A TEAM OF RESEARCHERS IN OAKLAND CALIF REPORTED PRELIMINARY
> > RESULTS IN WHICH A FOOD ADDITIVE A FATTY ACID CALLED ARGININE BUTYRATE
> > APPEARED TO STIMULATE THE NONWORKING GENE TO BEGIN MAKING NORMAL
> > HEMOGLOBIN IN SIX PATIENTS THEIR REPORT APPEARS IN THIS WEEK'S ISSUE
> > OF THE NEW ENGLAND JOURNAL OF MEDICINE.
>
> > THE MAIN PROBLEM IS THAT THE DRUG MUST BE GIVEN INTRAVENOUSLY BUT ONE
> > OF THE RESEARCHERS SAID AN ORAL FORM OF THE DRUG IS BEING DEVELOPED.
>
> > THE TWO ANEMIAS ARE IDEAL CANDIDATES FOR GENE ACTIVATION THERAPY.
> > BOTH INVOLVE DEFECTS IN HEMOGLOBIN THE IRON CONTAINING PROTEIN THAT
> > RED BLOOD CELLS USE TO CARRY OXYGEN TO BODY TISSUES.
> > OF THE TWO GENES CAPABLE OF MAKING HEMOGLOBIN ONE FUNCTIONS ONLY
> > DURING FETAL LIFE WHEN THE FETUS MUST PULL OXYGEN CARRYING BLOOD
> > ACROSS THE PLACENTA.
> > THIS FETAL GENE
>
> ...
>
> read more �- Hide quoted text -
>
> - Show quoted text -

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