What's UP is NOW down?
randall
Is susan right beyond our ability to perceive her brightness?
and / or
Can we ALL turbo out our brains some MORE?
Is the PSOR upstream of genes or due to HPA-axis?
And what, if anything of SFB in our ileum?
Time will tell and so will ...<i>
http://www.examiner.com/x-10848-SF-Natural-Health-Examiner~y2009m11d13-Adrenal-BurnOut
Healing From ‘Adrenal Burn-Out”
By Nancy Gardner PHD
Our adrenal glands govern our fight and flight mechanism that protect
us by stimulating up our bodies to move quick, think quick and get out
of danger! It is meant for emergencies not for us to be running hyper-
adrenal 24/7. It’s no wonder that many of us have chronic fatigue and
are exhausted. Many diseases that are caused by inflammation like
colitis, arthritis, psoriasis, tonsillitis, etc., are causes because
exhausted adrenals cannot produce the cortisone needed to alleviate
inflammation.
<sniP>
So, is it really TRUE we simply need to heal our adrenals?
or is their a gene in our future?
Or a few hundred of them?
Comprehensive transcriptional profiling of human epidermis,
reconstituted epidermal equivalents, and cultured keratinocytes using
DNA microarray chips.
Lee DD, Zavadil J, Tomic-Canic M, Blumenberg M.
The Departments of Dermatology and Biochemistry, The NYU Cancer
Institute, New York University School of Medicine, New York, NY, USA.
Because of its accessibility, skin has been among the first organs
analyzed using DNA microarrays; psoriasis, melanomas, carcinomas,
chronic wound biopsies, and epidermal keratinocytes in culture have
been intensely investigated. Skin has everything: stem cells,
differentiation, signaling, inflammation, diseases, cancer, etc. Here
we provide step-by-step instructions for bioinformatics analysis of
transcriptional profiling of skin. Specifically, we describe the use
of GCOS and RMA programs for initial normalization and selection of
differentially expressed genes, DAVID and LOLA programs for annotation
of genes, and statistically relevant identification of over- and under-
represented functional and biological categories in identified gene
sets, L2L and Venn diagrams for comparing multiple lists of genes, and
oPOSSUM for identification of statistically over-represented
transcription factor binding sites in the promoter regions of gene
sets. The work can be a primer for researchers embarking on skinomics,
the comprehensive analysis of transcriptional changes in the skin.
PMID: 19908006
================
What about our brains?
Top mine off with extra LEADed formula 1 please.
And it's
Good for alzheimers? Right on Ronnie...
Maybe we can get the prez on it?
Don't bow down unless he bows first. LOL
Why don't you apologize for the bombs they droPPed on US first?
And find out why a second bomb was needed?
Get those liberal brain cells working...
Good luck with that.
SuPPlements can only do so much. <W>
The wisdumb of leftright and light and dark in a yin/yang duality.
Be ONE in the eternal NOW
Or be duo in the infernal then... LOL
FDR II and their still selling depression as a GOOD, UP, LIGHT thing.
LOL
Light uP your yin yang cells perhaPs?
http://www.wellnessresources.com/health/articles/can_carnosine_help_shaky_nerves_memory/
Can Carnosine Help Shaky Nerves & Memory?
Saturday, November 14, 2009 - Byron J. Richards, CCN
Carnosine is an antioxidant that is highly concentrated in your brain,
heart, and muscles. A new study shows that it becomes depleted during
brain aging, especially in regions of your brain associated with
memory problems (hippocampus) and nerve tremors (substantia nigra).
Upon exposure to stress your brain activates its defense system, which
includes a variety of antioxidants. In this research scientists
looked into the activation of an enzyme called Carnosinase, which
requires carnosine in order to work. The researchers showed that in
the aging brain stress increased and antioxidants struggled to keep
up. The lower the antioxidants, the worse the brain stress and
consequent aging.
One method of coping is to increase carnosinase activity, which
eventually depletes carnosine. This is part of the key antioxidant
system in your brain that must work properly – which is why carnosine
is needed.
While every area of the brain was susceptible to this problem of
increased stress and decreased antioxidants, this was especially
important to the hippocampus (memory) and substantia nigra (nerve
transmission). The substantia nigra is rich in dopamine transmitters
and is the area of the brain affected by Parkinson’s. To a lesser
extent, the shaky extremities that often occur during aging are a
clear sign of inadequate antioxidants for the amount of stress an
individual is under. Carnosine may be able to help.
<sniP>
--------
And take some ALC with carnosine?
Sure... stop the tau proteins dead in your track.
Brain tangles when locked to one paradigm can obstruct clear
vision...s
http://www.wellnessresources.com/health/articles/acetyl-l-carnitine_prevents_alzheimers_brain_tangles/
Acetyl-L-Carnitine Prevents Alzheimer’s Brain Tangles
Friday, November 13, 2009 - Byron J. Richards, CCN
Acetyl-l-carnitine has long been regarded as an important nutrient for
memory. A new study shows that it stabilizes tau proteins, which if
over-excited produce brain tangles that lead to Alzheimer’s.
Tau proteins are heavily involved in the structure of nerve cells and
are found throughout your nervous system. When they are working
properly they support nerve stability, However, if they become over-
excited (hyperphosphorylated) they begin to assemble nerves in a
chaotic and tangled form. Thus, one goal of nerve health and memory
is to keep tau proteins functioning properly.
Scientists have figured out a chemical injection into the nerves that
hyperphosphorylates tau proteins leading to brain tangles and memory
decline – an animal model mimicking one key aspect of Alzheimer’s. In
the new study the scientists found that giving acetyl-l-carnitine to
animals for two weeks prior to injection prevented the formation of
brain tangles and memory decline.
Since the accumulation of brain tangles is common during aging, even
happening prior to noticeable memory decline, acetyl-l-carnitine is a
top choice for brain anti-aging and memory.
<sniP>
-----------
Get the BRAIN and body stress helper
The nutrients in Stress Helper are Acetyl-L-Carnitine (ALC),
Pantethine, and Carnosine.
http://www.wellnessresources.com/products/stress_helper.php
=============
http://www.life-enhancement.com/article_template.asp
Nicotinamide Restores Cognition in Alzheimer’s Disease
Reduces Alzheimer’s tau lesions and memory loss in mice
By Will Block
Memory is a way of holding onto the things you love,
the things you are, the things you never want to lose.
— The Wonder Years
[...]
Mapping Uncharted Waters
Previous research suggests that vitamins such as Vitamin E, Vitamin C,
vitamin B6, Vitamin B12, and folic acid may help people lower their
risk of developing Alzheimer’s disease. Also helpful may be omega-3
fatty acids, choline, galantamine, turmeric, green tea, quercetin, and
lithium. But nothing, until now, has suggested that any nutrient or
combination of nutrients—let alone any drug—can reverse the cognitive
decline associated with any of the dementias, including Alzheimer’s.
Consequently, nicotinamide may be mapping uncharted waters.
Other trials with nicotinamide have shown that it possesses benefits
for some diabetics and those with certain skin conditions because of
its anti-inflammatory properties.
Nicotinamide is a water soluble member of the B vitamin group. Also
known as niacinamide, nicotinamide is the amide of nicotinic acid
(vitamin B3), also known as niacin. In vivo, niacin is converted to
nicotinamide and although the two are identical in their vitamin
functions, nicotinamide does not have the same pharmacologic effects
of niacin, which may affect the liver negatively in some individuals.
Unlike niacin, nicotinamide does not reduce cholesterol or cause
flushing. In cells, niacin forms the coenzymes nicotinamide adenine
dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate
(NADP). Although the pathways for nicotinamide and nicotinic acid are
very similar. NAD+ and NADP+ are coenzymes in a wide variety of
enzymatic oxidation-reduction reactions.
Nicotinamide belongs to a class of compounds called histone
deacetylase (HDAC) inhibitors, which have been shown to protect the
central nervous system in rodent models of Parkinson’s and
Huntington’s diseases and amyotrophic lateral sclerosis. Clinical
trials are underway to learn whether HDAC inhibitors help ALS and
Huntington’s patients.*
<snIP>
=============
http://www.genengnews.com/news/bnitem.aspx?name=67992118
Scripps team shows diet switching can activate brain's stress system,
lead to 'withdrawal' symptoms
EUREKALERT
Contact: Keith McKeown
kmck...@scripps.edu
858-784-8134
Scripps Research Institute
Vicious circle of compulsive eating and anxiety can result
LA JOLLA, CA, November 9, 2009 - In research that sheds light on the
perils of yo-yo dieting and repeated bouts of sugar-bingeing,
researchers from The Scripps Research Institute have shown in animal
models that cycling between periods of eating sweet and regular-
tasting food can activate the brain's stress system and generate
overeating, anxiety, and withdrawal-like symptoms.
The research is being published in an advance, online Early Edition of
the journal Proceedings of the National Academy of Sciences (PNAS) the
week of November 9, 2009.
"When many people diet, they try to avoid fattening foods that taste
good, but ultimately end up going back to their regular eating
habits," said senior author Eric Zorrilla, Ph.D., an associate
professor and member of the Pearson Center for Alcoholism and
Addiction Research and Harold L. Dorris Neurological Research
Institute at Scripps Research. "We found that rats cycled in this way
between palatable food and less tasty, but otherwise acceptable, food,
begin to binge on the sweet food, stop eating their regular food, and
show withdrawal-like behaviors often associated with drug addiction.
As in addiction to drugs or ethanol, the brain's stress system is
involved in each of these changes."
"Our research suggests that this eating pattern leads to a vicious
circle," explained Pietro Cottone, Ph.D., who is co-first author of
the paper with Valentina Sabino, Ph.D.; both are former postdoctoral
fellows at Scripps Research who are now assistant professors and co-
directors of the Laboratory of Addictive Disorders at Boston
University School of Medicine. "The more you cycle this way, the more
likely it is you cycle again. Having a 'free day' in your diet
schedule is a risky habit."
Seeking Pleasure, Avoiding Pain
According to the U.S. Department of Health and Human Services, about
two-thirds of the adult population of the United States is overweight
or obese, conditions that cost the country an estimated $117 billion
in terms of medical expenses and lost productivity. Understanding the
factors that underpin overeating and that undermine attempts at weight
loss is important for addressing this major public health concern.
Instead of focusing on the positive motivation derived from eating
pleasurable foodwhich had previously been the gist of much research in
the fieldthe Scripps Research team took a new tack and focused on the
questions of whether negative reinforcement, which is thought to drive
compulsive drug intake, may play a similar role in excessive eating
and whether the brain's stress system was involved in this process.
Cottone explained, "For example, I can be motivated to work hard
because I get praise from my bossthat's positive reinforcement.
Conversely, I can work hard to avoid being firedthat's negative
reinforcement. Similarly, I can either eat a lot for the pleasure of
eating, or I can eat a lot to relieve the stress of not having certain
foods. We wanted to know if negative factors were involved."
To examine this question, the researchers divided the rats into two
groups. The first group was fed alternating cycles of five days of
regular chow and two days of sweet chow. The second group ate only
regular-tasting food. The amount of food consumed was not restricted
for either group.
When the researchers examined the results, they found that the two
groups showed different patterns of behavior. When the diet-cycled
rodents were fed regular chow, they put less effort into obtaining the
previously acceptable food, ate less, and were more likely to avoid
anxiety-provoking situations. When they returned to a diet of sweet
food, their anxiety-related behaviors returned to normal, but they ate
more than they needed. The control group showed none of these effects.
A Diet that Causes Stress
Next, the researchers looked at the involvement of the brain's stress
systemwhich had been shown to contribute to patterns of drug and
alcohol binging and withdrawalin underpinning these behaviors.
To do this, the team measured levels of stress-related corticotropin-
releasing factor (CRF) mRNA and peptide in an area of the brain known
as the central amygdala, which is involved in fear, anxiety, and
stress responses. Indeed, the researchers found that the diet-cycled
group on normal chow displayed five times the control group's levels
of CRF. Only when the diet-cycled group was fed sweet food did CRF
levels return to normal.
"CRF is a key stress neuropeptide," said Cottone. "In observing the
activation of the amygdaloid CRF system during abstinence from sweet
foods, we understood the causes of recurrent dieting failures."
Zorrilla pointed out that the increase in stress was due to the
withdrawal state, rather than to outside factors.
"People will often say they are eating bad foods or fail a diet
because they 'are stressed,'" he said. "Our findings suggest that
intermittently eating sweet food changes the brain's stress system so
that you might feel stressed, even though nothing that terrible has
happened. In other words, you might be self-medicating stress-like
symptoms of abstinence with that piece of pie. Or, the adaptations in
your brain stress system might make you more reactive to otherwise
minor stressors."
To confirm these results and to see whether blocking CRF could reverse
some of the effects of diet cycling, the researchers turned to a
compound called R121919 (a small molecule CRF1 receptor antagonist).
When administered to the diet-cycled rats, the compound blunted the
bingeing on sweet chow, as well as the lackluster pursuit of regular
chow and the anxiety-associated behaviors during this part of the diet
cycle. As in similar studies modeling alcoholism, on a molecular level
diet-cycled rats showed greater sensitivity to the ability of the CRF1
receptor antagonist to reduce central amygdala synaptic transmission
of the neurotransmitter GABA, which plays an important role in
regulating neuronal excitability.
"We believe we may have identified part of the neurochemical basis
underlying behavioral adaptations that can result from yo-yo dieting,"
said Zorrilla. "The mechanism corresponds to what is colloquially
known as the 'dark side' of addiction to drugs of abuse or ethanol,
supporting the idea that the brain shows addiction-like adaptations to
intermittent eating of palatable food."
An Unhealthy Cycle
While many questions remain, the study helps explain how a pattern yo-
yo dieting can be established and why it is usually ineffective in
promoting weight loss. The study also underlines the health risks of
such an eating pattern, as activation of the brain's stress system has
been linked not only to emotional disorders, but also to conditions
such as heart disease.
"The findings suggest that frequent dieting with frequent relapse is
worse than dieting by itself," said Cottone.
In addition, the research opens the door to potential development of a
drug therapy to assist people escape an unhealthy cycle of eating.
###
In addition to Zorrilla, Cottone, and Sabino, the paper, "CRF system
recruitment mediates dark side of compulsive eating," was authored by
Marisa Roberto, Michal Bajo, Lara Pockros, Jennifer B. Frihauf, Eva M.
Fekete, Bruno Conti, and George Koob of Scripps Research; Luca Steardo
of the University of Roma La Sapienza (Rome, Italy); Kenner C. Rice of
the National Institute on Drug Abuse of the National Institutes of
Health (NIH); and Dimitri E. Grigoriadis of Neurocrine Biosciences.
This research was supported by the NIH's National Institute of
Diabetes and Digestive and Kidney Diseases, National Institute on Drug
Abuse, and National Institute on Alcohol Abuse and Alcoholism, as well
as the Pearson Center for Alcoholism and Addiction Research at Scripps
Research.
About The Scripps Research Institute
<sniP>
=====================
Super duper mister pooPer, LPS and IL-10 STUFF in the same deal no
less. LOL
Why, why do i cry for MORE IL-10?
Duh, it makes the Th1 skew go down. But till now
that action doesn't work accordingly to plan.
Is it bcause of SFB's?
Could be till the trial is run.
Which big pharma hopes is NEVER. LOL
But on the other hand
http://www.eurekalert.org/pub_releases/2009-11/joci-imi110409.php
Interstitial macrophages: immune cells that prevent asthma
Microbe-derived molecules able to stimulate the immune system are
omnipresent in the air, and the presence of one such molecule (LPS)
promotes asthma in some individuals. What prevents inhalation of LPS
from promoting asthma in the majority of individuals is not well
understood. However, Fabrice Bureau and colleagues, at the University
of Liège, Belgium, have now ascribed this function in mice to a
population of lung immune cells known as lung interstitial macrophages
(IMs). Surprisingly, this is the first in vivo function described for
these cells.
The way in which airborne LPS promotes asthma is by inducing lung
immune cells known as DCs to initiate Th2 immune responses towards
normally innocuous allergens. In the study, mouse IMs were found to
produce high levels of the soluble immune factor IL-10, to inhibit LPS-
induced DC activation in an IL-10–dependent manner, and to prevent the
induction of Th2 responses directed towards innocuous allergens
following exposure to LPS and the allergen.
Importantly, mice in which IMs had been depleted developed severe
asthmatic reactions to innocuous airborne allergens inhaled with low
doses of LPS. The authors therefore conclude that IMs help prevent
airborne LPS from promoting allergy in mice and suggest that they
might have a similar function in humans; determining whether
inhibition or dysfunction of IMs contributes to the development of
asthma in humans is likely to be an area of future investigation.
###
=======================
With autoimmune conditions like psoriasis you need more Treg's to turn
off the self attack.
Right... how do we do it easily?
Not enough info on that but it's coming slowly.
I did it. Then again my brain is working and knows how brown cow.
it's the sweet whey... :)
You have to BUY the FARM and own it....
Not avoid your ownership by blaming everyone but
the guy in the oval office mirror. LOL
www.ncbi.nlm.nih.gov/pubmed/19203092
Resuscitating adaptive Tregs with combination therapies?
Bresson D, von Herrath M.
Developmental Immunology-3, La Jolla Institute for Allergy and
Immunology, La Jolla, CA 92037, USA.
Induction of 'adaptive' regulatory T cells (Tregs) using islet-
specific antigen vaccinations has been shown to prevent disease in
various animal models for type 1 diabetes (T1D). Even though
translation from bench to bedside has been unsuccessful so far, this
non-invasive approach is the Holy Grail to safely achieve immune
tolerance in humans. We will discuss here the fact that every immune
response appears to contain a balance of adaptive effector and Treg
cells. The evolution of these population and their antigen
specificities over time during diabetes development will determine at
which time and route a given islet antigen can be chosen to augment
such adaptive Tregs most efficiently. Their 'resuscitation' will be
crucial for long-term tolerance and homeostasis in the islet micro-
environment, which is ultimately needed for a cure from T1D. Recent
insight from our studies shows that short-term creation of a systemic
milieu that favours Treg propagation, as it occurs after systemic
administration of non Fc-binding anti-CD3, can strongly enhance this
process. We propose that combination therapies with anti-CD3 or
similar systemic immune modulators that lower effector cells and
enhance Tregs with vaccines that induce adaptive Tregs will be a
crucial step in developing successful immune-based intervention in
T1D.
PMID: 19203092
=================
http://www.physorg.com/news177180535.html
Researchers Study Whether Psychosocial Interventions Ease Psoriasis
November 11, 2009 (PhysOrg.com) -- The National Center for
Complementary and Alternative Medicine has awarded University of
Rochester Medical Center researchers $2.5 million to investigate the
impact of psychological interventions on attacks of psoriasis and the
intensity of the disease.
Researchers will measure and track the biological markers of the
disease in the skin lesions that are the hallmark of psoriasis and
also in the blood of volunteers who have participated in programs
designed to improve daily living.
Psoriasis appears to have a strong psychoneuroimmunological component
to it, such that signals from the brain may exacerbate the disease,
and the disease itself may induce psychological distress, said Jan
Moynihan, Ph.D., director of the Rochester Center for Mind-Body
Research and principal investigator for the study.
“We want to determine whether increasing psychological well-being
results in measurable decreases in inflammation,” said Moynihan, a
professor of Psychiatry. “We want to see if positive changes in
psychological well-being affect actual psoriatic lesions and which
immune mechanisms are the targets.”
Researchers plan to recruit 200 Rochester-area residents with
psoriasis to take part in the study, which will test the effects of
two interventions, Mindfulness Based Stress Reduction and Living Well.
Psoriasis is a chronic inflammatory disease of the skin that affects
about 7.5 million people in the United States. The disease causes
silvery scales and red patches that are sites of inflammation and
excessive production of skin cells.
In many people with psoriasis, psychological or life stress precedes
flare-ups of the disease, according to Moynihan.
Research also suggests that stress is associated with increased
production of many of the proinflammatory proteins called cytokines
that are involved in psoriasis, including interleukin-6 and tumor
necrosis factor-alpha. Researchers will test skin lesions and blood
for these cytokines and other markers.
Participants in the study will take part in one of two interventions.
Mindfulness Based Stress Reduction, a program developed at the
University of Massachusetts Medical Center, uses meditation and yoga
to develop a calm, non-judgmental awareness and acceptance of the
present moment. Living Well is a didactic intervention that includes
seminars on relevant topics, including sleep, nutrition and the
importance of exercise. It will be led by a team of wellness educators
and researchers.
Psoriasis patients could benefit from these low-cost, adjunctive
psychological interventions that are intended to decrease
psychological distress, but which may also ameliorate the skin disease
and inflammatory processes by interrupting the connection between the
stress response and flare-ups of psoriasis.
“We have the opportunity to use new technology to look at the
molecular biology of this disease. We hope to elucidate new ways that
the brain can direct our immune responses,” Moynihan said.
======================
How come none of these folks have psoriasis?
WE know there are 94 psoriatic arthritis subjects and some of them
have it.
So?
Well does that mean you can't get TNF *BLOCKERs* (Their words JRStern
and not mine)
unless you have PsA?
www.ncbi.nlm.nih.gov/pubmed/19904485
The use of tumour necrosis factor alpha-blockers in daily routine. An
Austrian consensus project.
Leeb BF, Böttcher E, Brezinschek HP, Czerwenka C, Herold M,
Hitzelhammer H, Mayrhofer F, Puchner R, Rainer F, Rintelen B, Schirmer
M, Stuby U, Bröll H.
Karl Landsteiner-Institute for Clinical Rheumatology, First and Second
Department of Medicine, Center for Rheumatology,
Lower Austria, State Hospital Stockerau, Landstrasse 18, Stockerau,
2000, Austria, burkha...@stockerau.lknoe.at.
To define relevant disease parameters and their respective limits
indicating the initiation of TNF-alpha-blockers in individual
patients. Subsequently, to analyze retrospectively patients with
rheumatoid arthritis (RA), psoriatic arthritis (PsA) or ankylosing
spondylitis (AS), who started TNF-alpha inhibition in 2006. Points to
consider, regarded relevant for individual treatment decisions as well
as their assessment methods, were ascertained by experts' consensus
applying the Delphi technique. Subsequently, these parameters'
thresholds with respect to the initiation of a TNF-alpha-blocker were
identified. Thereafter, the rheumatologists representing 12 centres
all over Austria agreed to retrospectively analyze their patients
started on a TNF-alpha-blocker in 2006. Experts' opinion regarding
disease parameters relevant to initiate TNF-alpha-blockers in RA
patients only slightly differed from those applied in clinical trials,
but the parameters' threshold values were considerably lower. For PsA
patients, some differences and for AS patients, considerable
differences between experts' opinion and clinical studies appeared,
which held also true for decisive parameters' means and thresholds.
Six hundred and fifty patients, started on TNF-blockers in 2006, could
be analyzed retrospectively, 408 RA patients (53.3 years mean, 340
females), 93 PsA patients (48.9 years mean, 59 males) and 149 AS
patients AS (42.2 years mean, 108 males), representing approximately
25% of all Austrian patients initiated on a TNF-blocker in this
respective year. Far more individualized, patient-oriented treatment
approaches, at least in part, are applied in daily routine compared
with those derived from clinical trials or recommendations from
investigative rheumatologists.
PMID: 19904485
What stands out is a study on usage since 2006?
Doesn't it take closer to five years for the PML to set in?
http://www.usrecallnews.com/2009/03/new-raptiva-warnings-risk-of-pml-brain-disease.html
============================
Which opportunistical bug kills psoriatics who USE to much TNF-
blockers and aids/hiv folks
via their brains?
PML is that pain in the brain.
http://www.aidsmap.com/en/news/2FA46F26-2F9F-4365-BA5D-CEB89C2C11B2.asp
Progressive multifocal leukoencephalopathy (PML) as a cause of serious
central nervous system (CNS) complications and death among people with
HIV has increased since the introduction of antiretroviral therapy
(ART), according to several presentations made last month at the
Second HIV Infection and Central Nervous System: Developed and
Resource-Limited Settings meeting in Venice
<sniP>
So why are aids/hiv patients getting it?
Easy... they can't make TNF to eat the JC virus?
Holy Christ man... so it's JC and viral?
Right and when a psoriatic blocks to much TNF they functionally create
the aids/hiv situation and the virus takes over.
So what is this JC virus?
http://en.wikipedia.org/wiki/Progressive_multifocal_leukoencephalopathy
Progressive multifocal leukoencephalopathy (PML), also known as
progressive multifocal leukoencephalitis, is a rare and usually fatal
viral disease that is characterized by progressive damage (-pathy) or
inflammation of the white matter (leuko-) of the brain (-encephalo-)
at multiple locations (multifocal). It occurs almost exclusively in
people with severe immune deficiency, e.g. transplant patients on
immunosuppressive medications, patients receiving certain kinds of
chemotherapy, patients recieving Natalizumab (Tysabri)[1] for multiple
sclerosis, psoriasis patients on long-term Efalizumab (Raptiva)[2] or
AIDS patients.
It is caused by the JC virus.
http://en.wikipedia.org/wiki/Progressive_multifocal_leukoencephalopathy#Cause
The cause of PML is a type of polyomavirus called the JC virus (JCV),
after the initials of the patient from whose tissue the virus was
first successfully cultured. The virus is widespread, with 86% of the
general population presenting antibodies, but it usually remains
latent, causing disease only when the immune system has been severely
weakened.
Prior to the advent of effective antiretroviral therapy, as many as 5
percent of people with AIDS eventually developed PML.[3] It is unclear
why PML occurs more frequently in AIDS than in other immunosuppressive
conditions; some research suggests that the effects of HIV on brain
tissue, or on JCV itself, make JCV more likely to become active in the
brain and increase its damaging inflammatory effects.[4]
Contributing causes
There are case reports of PML being caused by pharmacological agents,
although there is some speculation this could be due in part to the
existing impaired immune response or 'drug combination therapies'
rather than individual drugs. These include efalizumab, rituximab,[5]
infliximab,[6] natalizumab,[7] chemotherapy,[8] corticosteroids,[9]
and various transplant drugs such as tacrolimus.[10]
<sniP>
-------------------
Christ all mighty we all have this virus. Or nearly all of us.
I wonder if atheist get it?
Maybe if you believe in nothing your protected?
Good question.... or maybe you can believe in modified nothing?
Light is light and dark is... and your in the twilight zone? LOL
===========
Smad smack DOWN?
TGF smad2 smad3 smad4
http://www.signaling-gateway.org/update/featured/index.html
Cancer biology: The benefit of being single
TGFβ signaling drives single cell motility and stimulates hematogenic
metastasis in breast cancer cells.
<sniP>
===========
http://www.signaling-gateway.org/molecule/query
Homeodomain-interacting protein kinase 2 (HIPK2) is a promiscuous,
predominantly nuclear-localized serine/threonine protein kinase. HIPK2
has been implicated in the regulation of fundamental signaling
networks that govern transcriptional regulation, differentiation and
development, as well as DNA damage signaling and apoptosis. This broad
range of cellular responses is orchestrated by HIPK2 through the
functional regulation of key signaling molecules in the p53, Wnt,
transforming growth factor β (TGF-β), bone morphogenetic protein (BMP)
and hypoxia pathways.
Alternative names for this molecule: Hipk2; Homeodomain interacting
protein kinase 2; Homeodomain-interacting protein kinase 2; Stank
<sniP>
============
randall....