Month of Birth and Vitamin D3 Autoimmune Ramifications -- Smoking and Ai -- Mir-223 -- Flavonoid Baicalin (TCM Meds!) & Skin -- Cigs/Kidney Disease and Autoimmunity

[randall]

hi


Another obit today but...

Well..

First.


What month of the YEAR were you BORN?

Do you have MS or some autoimmune condition like psoriasis due to THAT
MONTH's birth, perhaPs?

What month was MS afflicted Mouseketeer Annette Funicello born?


I don't KNOW!


YET... what... or...


Could it be a vitamin D3 difference of getting an auto-immune
condition says this next STUDY:


And is that the reason for more people in Northern Latitudes getting
an autoimmune condition versus people born around tropical regions?

Coudn 't they have done a meta-analysis of data?


http://www.eurekalert.org/pub_releases/2013-04/qmuo-mob040513.php
Month of birth impacts on immune system development

Newborn babies' immune system development and levels of vitamin D have
been found to vary according to their month of birth, according to new
research.

The research, from scientists at Queen Mary, University of London and
the University of Oxford, provides a potential biological basis as to
why an individual's risk of developing the neurological condition
multiple sclerosis (MS) is influenced by their month of birth. It also
supports the need for further research into the potential benefits of
vitamin D supplementation during pregnancy.

Around 100,000 people in the UK have MS, a disabling neurological
condition which results from the body's own immune system damaging the
central nervous system. This interferes with the transmission of
messages between the brain and other parts of the body and leads to
problems with vision, muscle control, hearing and memory.

The development of MS is believed to be a result of a complex
interaction between genes and the environment.

A number of population studies have suggested that the month you are
born in can influence your risk of developing MS. This 'month of
birth' effect is particularly evident in England, where the risk of MS
peaks in individuals born in May and drops in those delivered in
November. As vitamin D is formed by the skin when it is exposed to
sunlight, the 'month of birth' effect has been interpreted as evidence
of a prenatal role for vitamin D in MS risk.

In this study, samples of cord blood – blood extracted from a newborn
baby's umbilical cord – were taken from 50 babies born in November and
50 born in May between 2009 and 2010 in London.

The blood was analysed to measure levels of vitamin D and levels of
autoreactive T-cells. T-cells are white blood cells which play a
crucial role in the body's immune response by identifying and
destroying infectious agents, such as viruses. However some T-cells
are 'autoreactive' and capable of attacking the body's own cells,
triggering autoimmune diseases, and should be eliminated by the immune
system during its development. This job of processing T-cells is
carried out by the thymus , a specialised organ in the immune system
located in the upper chest cavity.

The results showed that the May babies had significantly lower levels
of vitamin D (around 20 per cent lower than those born in November)
and significantly higher levels (approximately double) of these
potentially harmful autoreactive T-cells, compared to the sample of
November babies.

Co-author Dr Sreeram Ramagopalan, a lecturer in neuroscience at Barts
and The London School of Medicine and Dentistry, part of Queen Mary,
said: "By showing that month of birth has a measurable impact on in
utero immune system development, this study provides a potential
biological explanation for the widely observed "month of birth" effect
in MS. Higher levels of autoreactive T-cells, which have the ability
to turn on the body, could explain why babies born in May are at a
higher risk of developing MS.

"The correlation with vitamin D suggests this could be the driver of
this effect. There is a need for long-term studies to assess the
effect of vitamin D supplementation in pregnant women and the
subsequent impact on immune system development and risk of MS and
other autoimmune diseases."

###
The research letter is published today in the journal JAMA Neurology.
<snip>

160 hits : Ramagopalan SV[Author]
http://www.ncbi.nlm.nih.gov/pubmed/?term=Ramagopalan+SV%5BAuthor%5D

#4 of 160 most likely led to the above..

http://www.ncbi.nlm.nih.gov/pubmed/23519972
Association of vitamin D and multiple sclerosis in India.
Pandit L, Ramagopalan SV, Malli C, D'Cunha A, Kunder R, Shetty R.
Mult Scler. 2013 Mar 21.
PMID: 23519972

And #6 has been a theme around this group:

http://www.ncbi.nlm.nih.gov/pubmed/23448218
Epstein-Barr virus and multiple sclerosis: association or causation?
Pakpoor J, Giovannoni G, Ramagopalan SV.
Expert Rev Neurother. 2013 Mar;13(3):287-97. doi: 10.1586/ern.13.6.
PMID: 23448218


<snip>

So we LOST ... de ja vu for me and you:

Annette Funicello, Mouseketeer and Beach Movie Actress, Dies at 70
(multiple sclerosis)
http://www.nytimes.com/2013/04/09/movies/annette-funicello-mouseketeer-dies-at-70.html?pagewanted=all

[...] Ask the birds and ask the bees

And ask the stars above

Who’s their favorite sweet brunette;

You know, each one confesses:

Annette! Annette! Annette!
<snip>

Who get's MS? And are MICE good models for a cure?

And what if mom and DAD smoked CIGs like a chimney?

http://www.sciencedaily.com/releases/2013/04/130408152955.htm
Smoking May Negatively Impact Kidney Function Among Adolescents
Apr. 8, 2013 — Exposure to tobacco smoke could negatively impact
adolescent kidney function;
<snip... see below for rest of this story .. ***>

55,806 hits for: multiple sclerosis -pubmed:
http://www.ncbi.nlm.nih.gov/pubmed/?term=Multiple+sclerosis


Hit #1 of 55,806: Baicalein and stopPing fat mayHAM so on EASTER we
rise from the lame or dead... Hole sanna in the highest.


http://www.ncbi.nlm.nih.gov/pubmed/23559003
Cell Death Dis. 2013 Apr 4;4:e569. doi: 10.1038/cddis.2013.86.
Inhibition of 12/15-lipoxygenase by baicalein induces microglia PPARβ/
δ: a potential therapeutic role for CNS autoimmune disease.

Xu J, Zhang Y, Xiao Y, Ma S, Liu Q, Dang S, Jin M, Shi Y, Wan B, Zhang
Y.

Source
1] Shanghai Institute of Immunology, Institutes of Medical Sciences,
Shanghai Jiao Tong University School of Medicine, Shanghai, China [2]
Key Laboratory of Stem Cell Biology, Institute of Health Sciences,
Shanghai Institutes for Biological Sciences, Chinese Academy of
Sciences and Shanghai Jiao Tong University School of Medicine,
Shanghai, China.

Abstract
12/15-Lipoxygenase (12/15-LO) is an enzyme that converts
polyunsaturated fatty acids into bioactive lipid derivatives. In this
study, we showed that inhibition of 12/15-LO by baicalein (BA)
significantly attenuated clinical severity of experimental autoimmune
encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).
Inhibited migration of autoimmune T cells into the central nervous
system (CNS) by BA treatment could be attributed to reduced activation
of microglia, which was indicated by suppressed phagocytosis, and
decreased production of proinflammatory cytokines and chemokines in
the CNS. We further observed that inhibition of 12/15-LO with BA led
to increased expression of peroxisome proliferator-activated receptor
(PPAR)β/δ in microglia of EAE mice. This was confirmed in vitro in
primary microglia and a microglia cell line, BV2. In addition, we
demonstrated that BA did not affect 12/15-LO or 5-lipoxygenase (5-LO)
expression in microglia, but significantly decreased 12/15-LO products
without influencing the levels of 5-LO metabolites. Moreover, among
these compounds only 12/15-LO metabolite 12-hydroxyeicosatetraenoic
acid was able to reverse BA-mediated upregulation of PPARβ/δ in BV2
cells. We also showed that inhibition of microglia activation by PPARβ/
δ was associated with repressed NF-κB and MAPK activities. Our
findings indicate that inhibition of 12/15-LO induces PPARβ/δ,
demonstrating important regulatory properties of 12/15-LO in CNS
inflammation. This reveals potential therapeutic applications for MS.

PMID: 23559003

419 of 55,806 have Th17
http://www.ncbi.nlm.nih.gov/pubmed/?term=Multiple+sclerosis+Th17

8399 of 55,806 have autoimmune
http://www.ncbi.nlm.nih.gov/pubmed/?term=Multiple+sclerosis+autoimmune

WOW one hit for: MS and TMAO - pubmed
http://www.ncbi.nlm.nih.gov/pubmed/?term=Multiple+sclerosis+tmao

And here is #1 of ONE, no LESS:


http://www.ncbi.nlm.nih.gov/pubmed/21481905
Rev Neurol (Paris). 2011 Jun-Jul;167(6-7):541-4. doi: 10.1016/j.neurol.
2010.08.015. Epub 2011 Apr 8.
[L-carnitine treatment and fish odor syndrome: an unwaited adverse
effect].

[Article in French]
Rocher F, Caruba C, Broly F, Lebrun C.

Source
Centre Régional de Pharmacovigilance de Nice, CHU de Nice, Hôpital
Cimiez, 4 avenue Victoria, BP 1179, 06003 Nice cedex 1, France.
Roch...@chu-nice.fr
Abstract
INTRODUCTION:
Levocarnitine treatment is usually well tolerated, with essentially
dose-dependent diarrhea as the main induced adverse effect.
CASE REPORT:
We report a case of fish odor syndrome during levocarnitine treatment
which resolved after levocarnitine discontinuation.

CONCLUSION:
This adverse effect seems to be correlated with excedent carnitine
intake and might be expressed when the elimination pathway becomes
saturated or in a situation of deficiency enzymatic metabolism.

PMID: 21481905

Oh no... as NO is nitric oxide... hide the NO or hide your pride
behind the heartBREAK

But dear annette had hid from society when the MS hit.

With psoriasis you wear a sweater on the hotter days and that's why
it's called a SWEAT er er er..


ok so run it tar blabby..

ok i will it, id squidster.


and look..

236 hits : ER autoimmune -pubmed
http://www.ncbi.nlm.nih.gov/pubmed/?term=ER+autoimmune

it's a GOOD juan..# 1 and 2 both'

http://www.ncbi.nlm.nih.gov/pubmed/23557796
hsBAFF promotes proliferation and survival in cultured B lymphocytes
via calcium signaling activation of mTOR pathway.
Ke Z, Liang D, Zeng Q, Ren Q, Ma H, Gui L, Chen S, Guo M, Xu Y, Gao W,
Zhang S, Chen L.
Cytokine. 2013 Apr 1. doi:pii: S1043-4666(13)00113-0. 10.1016/j.cyto.
2013.03.011. [Epub ahead of print]
PMID: 23557796


http://www.ncbi.nlm.nih.gov/pubmed/23554479
J Neurosci. 2013 Apr 3;33(14):5980-91. doi: 10.1523/JNEUROSCI.
1636-12.2013.
Oligodendrocyte-Specific Activation of PERK Signaling Protects Mice
against Experimental Autoimmune Encephalomyelitis.

Lin W, Lin Y, Li J, Fenstermaker AG, Way SW, Clayton B, Jamison S,
Harding HP, Ron D, Popko B.

Source
Department of Cell Biology & Neuroscience, University of South Alabama
College of Medicine, Mobile, Alabama 36688, Department of Comparative
Medicine, University of South Alabama College of Medicine, Mobile,
Alabama 36688, Department of Neurology, University of Chicago,
Chicago, Illinois 60637, and University of Cambridge Metabolic
Research Laboratories and NIHR Cambridge Biomedical Research Centre,
Cambridge CB20QQ, United Kingdom.

Abstract
There is compelling evidence that oligodendrocyte apoptosis, in
response to CNS inflammation, contributes significantly to the
development of the demyelinating disorder multiple sclerosis and its
animal model, experimental autoimmune encephalomyelitis (EAE).
Therefore, approaches designed to protect oligodendrocytes would
likely have therapeutic value. Activation of pancreatic endoplasmic
reticulum kinase (PERK) signaling in response to endoplasmic reticulum
(ER) stress increases cell survival under various cytotoxic
conditions. Moreover, there is evidence that PERK signaling is
activated in oligodendrocytes within demyelinating lesions in multiple
sclerosis and EAE. Our previous study demonstrated that CNS delivery
of the inflammatory cytokine interferon-γ before EAE onset protected
mice against EAE, and this protection was dependent on PERK signaling.
In our current study, we sought to elucidate the role of PERK
signaling in oligodendrocytes during EAE. We generated transgenic mice
that allow for temporally controlled activation of PERK signaling, in
the absence of ER stress, specifically in oligodendrocytes. We
demonstrated that persistent activation of PERK signaling was not
deleterious to oligodendrocyte viability or the myelin of adult
animals. Importantly, we found that enhanced activation of PERK
signaling specifically in oligodendrocytes significantly attenuated
EAE disease severity, which was associated with reduced
oligodendrocyte apoptosis, demyelination, and axonal degeneration.
This effect was not the result of an altered degree of the
inflammatory response in EAE mice. Our results provide direct evidence
that activation of PERK signaling in oligodendrocytes is
cytoprotective, protecting mice against EAE.

PMID: 23554479


And taking pathways from each we get

40 hits: mTor + perk
http://www.ncbi.nlm.nih.gov/pubmed/?term=perk+mtor

Looked like all are cancer abstracts but only half:

22 of 40 have keyword: cancer
http://www.ncbi.nlm.nih.gov/pubmed/?term=perk+mtor+cancer


=======================


217 hits: mir-223
http://www.ncbi.nlm.nih.gov/pubmed/?term=mir-223

8 hits : skin mir-223
http://www.ncbi.nlm.nih.gov/pubmed/?term=skin+mir-223


3 of 8 are :psoria*
http://www.ncbi.nlm.nih.gov/pubmed/?term=skin+mir-223+psoria*


#1 of 217

more is better or a better situation:

http://www.ncbi.nlm.nih.gov/pubmed/23559634
Characterization of Levels and Cellular Transfer of Circulating
Lipoprotein-Bound MicroRNAs.
Wagner J, Riwanto M, Besler C, Knau A, Fichtlscherer S, Röxe T, Zeiher
AM, Landmesser U, Dimmeler S.
Arterioscler Thromb Vasc Biol. 2013 Apr 4. [Epub ahead of print]
PMID: 23559634


#2 of 217


http://www.ncbi.nlm.nih.gov/pubmed/23557915
Eur J Dermatol. 2013 Apr 5.
Down-regulation of miR-223 contributes to the formation of Gottron's
papules in dermatomyositis via the induction of PKCɛ

Inoue K, Jinnin M, Yamane K, Makino T, Kajihara I, Makino K, Honda N,
Nakayama W, Fukushima S, Ihn H.

Source
Department of Dermatology and Plastic Surgery, Faculty of Life
Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto, 860-8556, Japan.

Abstract
Background: Dermatomyositis (DM) is characterized by skin
manifestations accompanying and preceding muscle weakness. Gottron's
papules, one of the skin manifestations, are of great diagnostic value
because they are specific to DM. However, the pathogenesis of
Gottron's papules remains unclear. Objectives: We investigated the
expression pattern of miRNAs in Gottron's papules of DM patients and
evaluated the possibility that miRNAs play a role in its pathogenesis.
Materials and methods: miRNAs were extracted from skin tissues and
sera of patients with DM, clinically amyopathic DM (CADM) and healthy
controls. To identify pathogenic miRNAs, we performed miRNA PCR array
analysis. The results were confirmed by in situ hybridization,
immunohistochemistry, immunoblotting and transient transfection of
siRNAs or miRNA inhibitors. Results: PCR array analysis using tissue
miRNAs demonstrated the miR-223 level was markedly decreased in
Gottron's papules of DM and CADM in vivo, but not in psoriasis skin.
The protein expression of PKCɛ, a predicted target of miR-223, was
increased in DM/CADM skin. The transfection of a specific inhibitor of
miR-223 in keratinocytes led to up-regulation of the PKCɛ protein, and
resulted in increased cell proliferation. On the other hand, cell
numbers were significantly decreased when cells were transfected with
siRNA for PKCɛ. The serum miR-223 concentration was decreased in DM/PM
patients, particularly in CADM patients, compared with healthy
controls. Conclusions: A decreased miR-223 expression and the
subsequently increased PKCɛ levels may therefore play a key role in
the pathogenesis of Gottron's papules.

KEYWORDS:
autoimmune disease, collagen disease, keratinocyte, microRNA, serum

PMID: 23557915

#3 of 217

http://www.ncbi.nlm.nih.gov/pubmed/23554741
J Biomed Res. 2012 Mar;26(2):125-34. doi: 10.1016/
S1674-8301(12)60022-0.
Baicalin modulates microRNA expression in UVB irradiated mouse skin.

Xu Y, Zhou B, Wu D, Yin Z, Luo D.

Source
Department of Dermatology, the First Affiliated Hospital of Nanjing
Medical University, Nanjing, Jiangsu 210029, China.

Abstract
This study aimed to evaluate the effects of baicalin on ultraviolet
radiation B (UVB)-mediated microRNA (miRNA) expression in mouse skin.
We determined miRNA expression profiles in UVB irradiated mice,
baicalin treated irradiated mice, and untreated mice, and conducted
TargetScan and Gene Ontology analyses to predict miRNA targets. Three
miRNAs (mmu-miR-125a-5p, mmu-miR-146a, and mmu-miR-141) were
downregulated and another three (mmu-miR-188-5p, mmu-miR-223 and mmu-
miR-22) were upregulated in UVB irradiated mice compared with
untreated mice. Additionally, these miRNAs were predicted to be
related to photocarcinogenesis, hypomethylation and apoptosis. Three
miRNAs (mmu-miR-378, mmu-miR-199a-3p and mmu-miR-181b) were
downregulated and one (mmu-miR-23a) was upregulated in baicalin
treated mice compared with UVB irradiated mice, and they were
predicted to be related to DNA repair signaling pathway. These
deregulated miRNAs are potentially involved in the pathogenesis of
photodamage, and may aid treatment and prevention of UVB-induced
dermatoses.

KEYWORDS:
baicalin, microRNA, microarray, photodamage, ultraviolet radiation B

PMID: 23554741



http://en.wikipedia.org/wiki/Baicalin
Baicalin is a flavone, a type of flavonoid. It is found in several
species in the genus Scutellaria, including Scutellaria lateriflora
(blue skullcap). There are 10 mg/g baicalin in Scutellaria
galericulata (common skullcap) leaves.[1] Baicalin is the glucuronide
of baicalein.

It is a component of Chinese medicinal herb Huang-chin (Scutellaria
baicalensis) and one of the chemical ingredients of Sho-Saiko-To, an
herbal supplement.
Baicalin is a known prolyl endopeptidase inhibitor,[2] induces
apoptosis in pancreatic cancer cells,[3] and affects the GABA
receptors

http://en.wikipedia.org/wiki/Baicalein
http://en.wikipedia.org/wiki/Scutellaria_baicalensis


http://en.wikipedia.org/wiki/Sho-Saiko-To
Sho-Saiko-To or SST (Japanese: 小柴胡湯), also known as Minor Bupleurum
Formula and Xiao Chai Hu Tang in Chinese小柴胡汤, is a herbal supplement,
believed to enhance liver health. Sho-Saiko-To is a widely used
prescription drug in Japan and is a listed formula in Japanese Kampo.
There are currently ongoing clinical trials for Sho-Saiko-To at
University of California, San Diego and Memorial Sloan-Kettering
Cancer Center. The active ingredients of Sho-Saiko-To discovered so
far include: Baicalin, Baicalein, Glycyrrhizin, Saikosaponins,
Ginsenosides, Wogonin, Gingerol.
<snip>


5 hits for: baicalin - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=Baicalin&start=0&scoring=d&hl=en&

************


rest of the cig kidney story:

from above:
[...] this is according to a new study led by a team of researchers at
the Johns Hopkins Bloomberg School of Public Health and the Johns
Hopkins Children's Center. They examined the association between
exposure to active smoking and kidney function among U.S. adolescents
and found the effects of tobacco smoke on kidney function begin in
childhood. The results are featured in the April 2013 issue of
Pediatrics.

"Tobacco use and exposure to secondhand tobacco smoke are major health
problems for adolescents, resulting in short-term and long-term
adverse health effects," said Ana Navas-Acien, MD, PhD, senior author
of the study and an associate professor with the Bloomberg School's
Department of Environmental Health Sciences. "In this nationally
representative sample of U.S. adolescents, exposure to tobacco,
including secondhand smoke and active smoking, was associated with
lower estimated glomerular filtration rates -- a common measure of how
well the kidneys are working. In addition, we found a modest but
positive association between serum cotinine concentrations, a
biomarker of tobacco exposure, among first-morning albumin to
creatinine ratio. These findings further support the conclusion that
tobacco smoke may damage the kidneys."

Using a cross-sectional study of 7,516 adolescents ages 12 to 17, the
authors assessed participant tobacco use and exposure to secondhand
smoke through self-reported data from a home questionnaire and serum
cotinine. Participants who reported having smoked "at least one day"
in the last month or "at least one cigarette" in the last month, or
those who had serum cotinine concentrations over 10 ng/ml were
classified as active smokers. Secondhand smoke exposure was defined as
non-active smokers who reported living with at least one person who
smoked, or who had cotinine levels greater than or equal to 0.05 ng/
ml, but less than or equal to 10 ng/ml even if they reported not
living with a smoker. Participants with serum cotinine levels below
0.05 ng/ml, not living with a smoker and not smoking in the last
month, were classified as unexposed to tobacco.

Earlier studies examining U.S. adolescent tobacco exposure have
indicated more than 600,000 middle school students and 3 million high
school students smoke cigarettes and 15 percent of non-smoking
adolescents report exposure to secondhand smoke at home. Among
adolescents, active smoking has been associated with increased asthma
risk, reduced lung function and growth, early atherosclerotic lesions
and increased cancer risk as well as premature mortality in adulthood.
According to Centers for Disease Control and Prevention, smoking is
also a risk factor for several autoimmune diseases, including Crohn's
disease and rheumatoid arthritis.

"Small changes in the distribution of estimated glomerular filtration
rate levels in the population could have a substantial impact in
kidney-related illness, as it is well known for changes in blood
pressure levels and hypertension-related disease. Evaluating potential
secondhand smoke exposure and providing recommendations to minimize
exposure should continue to be incorporated as part of children's
routine medical care," noted Jeffrey Fadrowski, MD, MHS, co-author of
the study and an assistant professor in Pediatric Nephrology at the
Johns Hopkins School of Medicine.

"Tobacco as a chronic kidney disease risk factor is of great concern
given the high prevalence of use and the chronicity that most often
accompanies this exposure. Protecting young people from active smoking
is essential since nearly 80 percent of adults who smoke begin smoking
by 18 years of age," said Navas-Acien.
<snip>

Journal Reference:
Esther García-Esquinas, Lauren F. Loeffler, Virginia M. Weaver,
Jeffrey J. Fadrowski, and Ana Navas-Acien. Kidney Function and Tobacco
Smoke Exposure in US Adolescents. Pediatrics, 2013 DOI: 10.1542/peds.
2012-3201d
http://dx.doi.org/10.1542/peds.2012-3201d



randall... holy TUNA batman...pass the sushi... please & hold the..
epigenesis MADman!

[Bohgosity BumaskiL]

Another reason month of birth could affect Vitamin D3, iz that month
of birth probably affects how long a baby gets breastfed.
If born in November, for instance, a mother might find little to do
(say outside), but care for her baby. That would last for about six
months, which should be the minimum, but seems to be about normal in
western culture, where people who give out free formula from Nestle
are not drawn and quartered.
_______
http://www.incultureparent.com/2011/02/breastfeeding-land-genghis-khan