Womb quality linked to cot death - 7 citations about toxins in placenta, etc

[Guest guest]

" In addition, the findings lend vital weight to previous work that shows

the vast majority of cases of multiple cot deaths are not caused by

child abuse. " It provides supportive evidence that most cot deaths are

not murder, they are deaths from natural causes, " says . "

I agree with the not murder part when it comes to the parent. I call it

murder though by the drug companies and medical system.

I would say NOT deaths from natural causes, but deaths from VACCINES and

other toxins in highly susceptible families

Sheri

[seven citations follow the news article]

From Binstock

* * * *

16 December 2005; | doi:10.1038/news051212-15

Womb quality linked to cot death

Poor conditions may explain multiple infant deaths.

Ainsworth

http://www.nature.com/news/2005/051212/full/051212-15.html

The seeds of sudden infant death syndrome seem to be planted in part by

conditions in the mother's womb. The finding shows it is not just genetic

factors that determine whether babies are predisposed to the tragic

condition. And although it will not change doctors' advice to parents, it

may shed some light on the causes of these mysterious deaths.

Cot death, or sudden infant death syndrome (SIDS), is the name for the

unexplained death of a baby, usually in its sleep. The condition strikes 1

in 2,000 babies in the developed world.

Most cases are isolated. But it is known that a woman who has had one baby

die from SIDS is five times more likely than other women to have a second

baby die. This was once thought to cast suspicion on a mother's ability to

care for her children. But it is now accepted that there are biological

reasons for this recurrence, although it hasn't been clear what these are.

Brothers and sisters

To investigate, a team led by Gordon , an obstetrician at the

University of Cambridge, UK, studied the medical records of more than a

quarter of a million women in Scotland. They compared three groups: those

who had given birth to two surviving children; those whose first baby had

died from SIDS, but whose second child did not; and those who first child

did not die, but whose second baby did.

They found that the babies of women whose first baby had died of SIDS were

two to three times more likely to be smaller than usual and delivered

early. What's more, women whose first baby was alive, but born small or

early, were at increased risk of having a subsequent child die from SIDS.

They publish their results in the

Lancet<http://www.nature.com/news/2005/051212/pf/051212-15_pf.html#B1>1.

Stunted growth and pre-term delivery are signs that the babies have

experienced a poor environment in the womb. So the findings suggest that an

inferior environment can make babies more vulnerable to SIDS, says .

" These women are tending to give birth to babies that are, on the whole,

less healthy than the general population, " he says.

The team then looked at why these women tended to have such complications.

They were more likely to smoke, and to be unmarried, very young and living

in areas of high deprivation.

Jigsaw puzzle

Although no one knows for sure precisely why the womb environment matters

for cot death, it is possible that it affects the development of the part

of the nervous system that controls breathing, says . " But the long

and the short of it is that these ideas are in the realm of speculation. "

, a trustee of the Foundation for the Study of Infant Deaths

and a paediatrician at Kingston Hospital, London, says the work is an

important contribution to piecing together the causes of SIDS. " This whole

thing is a jigsaw and all the bits are being fitted together, " he says.

The work will also help target information to the right people. All parents

are told how to reduce cot death: doctors recommend that they do not smoke

and put their baby to sleep on its back. But it is now especially important

to focus on parents whose previous babies were born early or small, says

.

In addition, the findings lend vital weight to previous work that shows the

vast majority of cases of multiple cot deaths are not caused by child

abuse. " It provides supportive evidence that most cot deaths are not

murder, they are deaths from natural causes, " says .

References

* G. C. S., Wood A. M., G. C. S., Pell J. P, Dobbie R., et

al. The Lancet, 366. 2107 - 2111 (2005).

© 2004 Nature Publishing Group

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

A mere sampling of the available citations regarding toxins in amniotic

fluid, cord blood, breast milk, placenta - of humans:

1: <javascript:AL_get(this, 'jour', 'Biosci Biotechnol Biochem.');>Biosci

Biotechnol Biochem. 2005 Oct;69(10):1836-47.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pu

bmed_pubmed & from_uid=16244432>Related Articles,

<javascript:PopUpMenu2_Set(Menu16244432);>Links

<http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3580 & uid=16244432

& db=pubmed & url=http://joi.jlc.jst.go.jp/JST.JSTAGE/bbb/69.1836?from=PubMed>C

lick here to read

Distribution of PCDDs/PCDFs and Co-PCBs in human maternal blood, cord

blood, placenta, milk, and adipose tissue: dioxins showing high toxic

equivalency factor accumulate in the placenta.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Suzuki+G%22%5BAuthor%5D>Suzuki G,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Nakano+M%22%5BAuthor%5D>Nakano M,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Nakano+S%22%5BAuthor%5D>Nakano S.

Department of Bioresource Science, Obihiro University of Agriculture and

Veterinary Medicine, Obihiro City, Hokkaido, Japan.

To assess levels of dioxin background contamination and transfer of dioxins

from mothers to unborn children and infants, concentrations of

polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans

(PCDFs), and coplanar-polychlorinated biphenyls (Co-PCBs) were measured in

human samples from expectant and nursing mothers living in Nara, Japan. The

average toxic equivalency quantities (TEQs) of PCDDs/PCDFs and Co-PCBs from

circulating maternal blood, cord blood, placenta, milk taken 3-10 d after

delivery, milk taken one month after delivery, and adipose tissue were 26

and 9.3, 15 and 2.3, 31 and 1.2, 16 and 5.4, 18 and 8.8, and 16 and 7.7

pg-TEQ/g-fat, respectively. Among the various PCDD/PCDF congeners,

1,2,3,7,8-PeCDD and 2,3,4,7,8-PeCDF contributed most heavily to the TEQs of

all maternal samples. Among the various Co-PCB congeners, 3,3',4,4',5-PeCB

(#126), 2,3,3',4,4',5-HxCB (#156), and 2,3',4,4',5-PeCB (#118) contributed

most heavily to the TEQs of all maternal samples. But, the concentrations

and relative percentages of congeners differed among the various samples,

suggesting that congeners showing high toxic equivalency factor accumulate

in the placenta.

PMID: 16244432 [PubMed - in process]

----------

2: <javascript:AL_get(this, 'jour', 'Environ Res.');>Environ Res. 2005 Aug

2; [Epub ahead of print]

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pu

bmed_pubmed & from_uid=16081062>Related Articles,

<javascript:PopUpMenu2_Set(Menu16081062);>Links

<http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3048 & uid=16081062

& db=pubmed & url=http://linkinghub.elsevier.com/retrieve/pii/S0013-9351%2805%2

900082-4>Click here to read

Maternal and umbilical cord blood levels of mercury, lead, cadmium, and

essential trace elements in Arctic Canada.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

++J%22%5BAuthor%5D> J,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Houseman+J%22%5BAuthor%5D>Houseman J,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Seddon+L%22%5BAuthor%5D>Seddon L,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

McMullen+E%22%5BAuthor%5D>McMullen E,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Tofflemire+K%22%5BAuthor%5D>Tofflemire K,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Mills+C%22%5BAuthor%5D>Mills C,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Corriveau+A%22%5BAuthor%5D>Corriveau A,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Weber+JP%22%5BAuthor%5D>Weber JP,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Leblanc+A%22%5BAuthor%5D>Leblanc A,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

+M%22%5BAuthor%5D> M,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

son+SG%22%5BAuthor%5D>son SG,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Van+Oostdam+J%22%5BAuthor%5D>Van Oostdam J.

Government of the Northwest Territories (GNWT), Department of Health and

Social Services, Yellowknife, NT, Canada.

Maternal and umbilical cord blood levels of mercury (Hg), lead (Pb),

cadmium (Cd), and the trace elements copper (Cu), zinc (Zn), and selenium

(Se) are reported for Inuit, Dene/Metis, Caucasian, and Other nonaboriginal

participants from Arctic Canada. This is the first human tissue monitoring

program covering the entire Northwest Territories and Nunavut for multiple

contaminants and establishes a baseline upon which future comparisons can

be made. Results for chlorinated organic pesticides and PCBs for these

participants have been reported elsewhere. Between May 1994 and June 1999,

523 women volunteered to participate by giving their written informed

consent, resulting in the collection of 386 maternal blood samples, 407

cord samples, and 351 cord:maternal paired samples. Geometric mean (GM)

maternal total mercury (THg) concentrations ranged from 0.87mug/L (SD=1.95)

in the Caucasian group of participants (n=134) to 3.51mug/L (SD=8.30) in

the Inuit group (n=146). The GM of the Inuit group was 2.6-fold higher than

that of the Dene/Metis group (1.35mug/L, SD=1.60, n=92) and significantly

higher than those of all other groups (P<0.0001). Of Inuit women

participants, 3% (n=4) were within Health Canada's level of concern range

(20-99mug/L) for methylmercury (MeHg) exposure. Of Inuit and Dene/Metis

cord samples, 56% (n=95) and 5% (n=4), respectively, exceeded 5.8mug/L

MeHg, the revised US Environmental Protection Agency lower benchmark dose.

GM maternal Pb was significantly higher in Dene/Metis (30.9mug/L or

3.1mug/dL; SD=29.1mug/L) and Inuit (31.6mug/L, SD=38.3) participants

compared with the Caucasian group (20.6mug/L, SD=17.9) (P<0.0001). Half of

all participants were smokers. GM blood Cd in moderate smokers (1-8

cigarettes/day) and in heavy smokers (>8 cigarettes/day) was 7.4-fold

higher and 12.5-fold higher, respectively, than in nonsmokers. The high

percentage of smokers among Inuit (77%) and Dene/Metis (48%) participants

highlights the need for ongoing public health action directed at tobacco

prevention, reduction, and cessation for women of reproductive age. Pb and

THg were detected in more than 95% of all cord blood samples, with GMs of

21 mug/L and 2.7mug/L, respectively, and Cd was detected in 26% of all cord

samples, with a GM of 0.08mug/L. Cord:maternal ratios from paired samples

ranged from 0.44 to 4.5 for THg, from 0.5 to 10.3 for MeHg, and 0.1 to 9.0

for Pb. On average, levels of THg, MeHg, and Zn were significantly higher

in cord blood than in maternal blood (P<0.0001), whereas maternal Cd, Pb,

Se, and Cu levels were significantly higher than those in cord blood

(P<0.0001). There was no significant relationship between methylmercury and

selenium for the range of MeHg exposures in this study. Ongoing monitoring

of populations at risk and traditional food species, as well as continued

international efforts to reduce anthropogenic sources of mercury, are

recommended.

PMID: 16081062 [PubMed - as supplied by publisher]

----------

3: <javascript:AL_get(this, 'jour', 'Placenta.');>Placenta. 2005

May;26(5):361-71.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pu

bmed_pubmed & from_uid=15850640>Related Articles,

<javascript:PopUpMenu2_Set(Menu15850640);>Links

<http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3048 & uid=15850640

& db=pubmed & url=http://linkinghub.elsevier.com/retrieve/pii/S0143-4004%2804%2

900242-5>Click here to read

Human placenta: a human organ for developmental toxicology research and

biomonitoring.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Myllynen+P%22%5BAuthor%5D>Myllynen P,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Pasanen+M%22%5BAuthor%5D>Pasanen M,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Pelkonen+O%22%5BAuthor%5D>Pelkonen O.

Department of Pharmacology and Toxicology, University of Oulu, PO Box 5000,

FIN-90014 Oulu, Finland.

<mailto:paivi.k.myllynen@...>paivi.k.myllynen@...

Pregnant mothers are exposed to a wide variety of foreign chemicals. This

exposure is most commonly due to maternal medication, lifestyle factors,

such as smoking, drug abuse, and alcohol consumption, or occupational and

environmental sources. Foreign compounds may interfere with placental

functions at many levels e.g. signaling, production and release of hormones

and enzymes, transport of nutrients and waste products, implantation,

cellular growth and maturation, and finally, at the terminal phase of

placental life, i.e. delivery. Placental responses may also be due to

pharmaco-/toxicodynamic responses to foreign chemicals, e.g. hypoxia. On

the other hand, placental xenobiotic-metabolizing enzymes can detoxify or

activate foreign chemicals, and transporters either enhance or prevent

cellular accumulation and transfer across the placenta. The understanding

of what xenobiotics do to the placenta and what the placenta does to the

xenobiotics should provide the basis for the use of placenta as a tool to

investigate and predict some aspects of developmental toxicity. This review

aims to give an update of the fate and behavior of xenobiotics in the

placenta from the viewpoint of xenobiotic-metabolizing enzymes and

transporters. Their response levels will be described according to

gestational status and methods used. The effects of foreign chemicals on

placental metabolizing enzymes will be discussed. Also, interactions in the

transporter protein level will be covered. The role of the placenta in

contributing to developmental effects and fetotoxicity will be examined.

The toxicological effects of maternal medications, smoking, and

environmental exposures (dioxins, pesticides) as well as some possibilities

for biomonitoring will be highlighted.

Publication Types:

* <javascript:AL_get(this, 'ptyp', 'Review');>Review

PMID: 15850640 [PubMed - indexed for MEDLINE]

----------

4: <javascript:AL_get(this, 'jour', 'Pediatr Allergy Immunol.');>Pediatr

Allergy Immunol. 2005 Mar;16(2):104-12.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pu

bmed_pubmed & from_uid=15787866>Related Articles,

<javascript:PopUpMenu2_Set(Menu15787866);>Links

<http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3046 & uid=15787866

& db=pubmed & url=http://www.blackwell-synergy.com/openurl?genre=article & sid=nl

m:pubmed & issn=0905-6157 & date=2005 & volume=16 & issue=2 & spage=104>Click here to

read

Putative regulatory T cells are impaired in cord blood from neonates with

hereditary allergy risk.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Haddeland+U%22%5BAuthor%5D>Haddeland U,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Karstensen+AB%22%5BAuthor%5D>Karstensen AB,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Farkas+L%22%5BAuthor%5D>Farkas L,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Bo+KO%22%5BAuthor%5D>Bo KO,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Pirhonen+J%22%5BAuthor%5D>Pirhonen J,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Karlsson+M%22%5BAuthor%5D>Karlsson M,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Kvavik+W%22%5BAuthor%5D>Kvavik W,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Brandtzaeg+P%22%5BAuthor%5D>Brandtzaeg P,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Nakstad+B%22%5BAuthor%5D>Nakstad B.

Laboratory for Immunohistochemistry and Immunopathology (LIIPAT), Institute

of Pathology, University of Oslo, Rikshospitalet University Hospital, Oslo,

Norway.

The hygiene hypothesis implies that the increasing prevalence of allergy in

'westernized' countries is explained by reduced bacterial exposure in early

life, but the underlying mechanism remains elusive. We therefore wanted to

study the effect of bacterial lipopolysaccharide (LPS) on the generation of

regulatory T (T®) cells in neonates, and to analyze differences between

neonates with allergy risk because of a family history of atopy (FH+) and

controls without such hereditary risk (FH-). Cord blood mononuclear cells

from the FH+ and FH- groups were stimulated with beta-lactoglobulin in the

presence of LPS. T-cell phenotypes suggestive of T® cells [CD25+,

CD25high and integrin (CD103+)], and the intracellular proliferation

antigen Ki-67 were quantified by flow cytometry. Release of the

immunosuppressive cytokine transforming growth factor beta1 (TGF-beta1)

from its inactive complex was determined by enzyme-linked immunosorbent

assay. The analyses revealed the generation of T-cell phenotypes suggestive

of T® cells including a CD25high T-cell subset which was inversely

related to T-cell proliferation (r=-0.54, p<0.05) and to activation-induced

release of TGF-beta1 (r=-0.80, p<0.001). The CD25high T-cell subset tended

to be impaired in the FH+ group (% of CD3+ T cells: FH+, 5.1% vs. FH-,

12.6%), and notably, the FH+ group showed a significantly reduced capacity

for generation of both CD25+ (FH+, 16.2% vs. FH-, 34.9%; p<0.01) and T

cells (FH+, 2.1% vs. FH-, 3.9%; p<0.05). Our findings suggested that

early-life exposure to a dietary antigen in the presence of LPS might

modulate the immune system by generating T® cells. This capacity was

impaired in neonates with hereditary allergy risk, but clinical follow-up

will be required to determine a possible effect on allergy emergence.

Copyright © 2005 Blackwell Munksgaard

PMID: 15787866 [PubMed - indexed for MEDLINE]

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5: <javascript:AL_get(this, 'jour', 'Pediatr Dev Pathol.');>Pediatr Dev

Pathol. 2003 Nov-Dec;6(6):484-94.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pu

bmed_pubmed & from_uid=15018448>Related Articles,

<javascript:PopUpMenu2_Set(Menu15018448);>Links

Amniotic sac infection syndrome features fetal lung neuroendocrine cell

hyperfunction.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Saad+AG%22%5BAuthor%5D>Saad AG,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Heffelfinger+S%22%5BAuthor%5D>Heffelfinger S,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Stanek+J%22%5BAuthor%5D>Stanek J.

Department of Pathology and Laboratory Medicine, University of Cincinnati

College of Medicine, 231 Albert Sabin Way, P.O. Box 670529, Cincinnati, OH

45267-0529, USA.

Neuroendocrine cells (NEC) are abundant in fetal and neonatal lungs, but

reduced in infants with hyaline membrane disease. Perinatal neuroendocrine

cell hyperplasia (NCH) has been reported in the hypoplastic lung in

diaphragmatic hernia, bronchopulmonary dysplasia, and -Mikity

syndrome. Since we are unaware of any reports on NCH in fetal inflammatory

conditions, this report addresses the NEC in fetuses with congenital

pneumonia. Twenty-one fetuses/neonates with congenital pneumonia, autopsied

between 1995 and 2001, were compared to 21 fetuses without a congenital

infection matched for gestational age. Lung sections were immunostained for

chromogranin, bombesin, calcitonin, and synaptophysin. Proportions of

immunopositive cells lining 20 consecutive bronchioles calculated from

digital images were significantly higher in the study than the control

group for chromogranin (1.8 vs. 0.8%, P = 2.4 E-06), calcitonin (1.2 vs.

0.7%, P = 0.005), and bombesin (1.1 vs. 0.7%, P = 0.005). There was no

difference in synaptophysin (11.7% vs. 12.6%, P = 0.07). The absence of

significant differences in the synaptophysin ratio excludes simple NCH in

the study group. The synchronous increase in three neurohormones is

indicative of NEC hyperfunction, due to either altered enzymatic

inactivation by neutral endopeptidase, known to be reduced in adult lung

inflammation, or by an increase in expression of the neurohormone genes.

These data indicate that NEC hyperfunction may be responsible for the

deranged fetal/neonatal lung function and circulatory adaptation, and

contribute to the lethality of the amniotic sac infection syndrome.

PMID: 15018448 [PubMed - indexed for MEDLINE]

----------

6: <javascript:AL_get(this, 'jour', 'Am J Physiol Regul Integr Comp

Physiol.');>Am J Physiol Regul Integr Comp Physiol. 2004

Jun;286(6):R1024-9. Epub 2004 Feb 26.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pu

bmed_pubmed & from_uid=14988088>Related Articles,

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<http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3051 & uid=14988088

& db=pubmed & url=http://ajpregu.physiology.org/cgi/pmidlookup?view=long & pmid=1

4988088>Click here to read

Maternal LPS induces cytokines in the amniotic fluid and corticotropin

releasing hormone in the fetal rat brain.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Gayle+DA%22%5BAuthor%5D>Gayle DA,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Beloosesky+R%22%5BAuthor%5D>Beloosesky R,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Desai+M%22%5BAuthor%5D>Desai M,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Amidi+F%22%5BAuthor%5D>Amidi F,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Nunez+SE%22%5BAuthor%5D>Nunez SE,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Ross+MG%22%5BAuthor%5D>Ross MG.

Department of Obstetrics and Gynecology, Harbor-University of California

Los Angleles Medical Center and Research and Education Institute, Torrance,

CA 90502, USA. <mailto:dgayle@...>dgayle@...

Perinatal infections are a risk factor for fetal neurological pathologies,

including cerebral palsy and schizophrenia. Cytokines that are produced as

part of the inflammatory response are proposed to partially mediate the

neurological injury. This study investigated the effects of intraperitoneal

injections of lipopolysaccharide (LPS) to pregnant rats on the production

of cytokines and stress markers in the fetal environment. Gestation day 18

pregnant rats were treated with LPS (100 microg/kg body wt i.p.), and

maternal serum, amniotic fluid, placenta, chorioamnion, and fetal brain

were harvested at 1, 6, 12, and 24 h posttreatment to assay for LPS-induced

changes in cytokine protein (ELISA) and mRNA (real-time RT-PCR) levels. We

observed induction of proinflammatory cytokines interleukin (IL)-1 beta,

IL-6, and tumor necrosis factor-alpha (TNF-alpha) as well as the

anti-inflammatory cytokine IL-10 in the maternal serum within 6 h of LPS

exposure. Similarly, proinflammatory cytokines were induced in the amniotic

fluid in response to LPS; however, no significant induction of IL-10 was

observed in the amniotic fluid. LPS-induced mRNA changes included

upregulation of the stress-related peptide corticotropin-releasing factor

in the fetal whole brain, TNF-alpha, IL-6, and IL-10 in the chorioamnion,

and TNF-alpha, IL-1 beta, and IL-6 in the placenta. These findings suggest

that maternal infections may lead to an unbalanced inflammatory reaction in

the fetal environment that activates the fetal stress axis.

PMID: 14988088 [PubMed - indexed for MEDLINE]

----------

7: <javascript:AL_get(this, 'jour', 'Environ Health Perspect.');>Environ

Health Perspect. 2003 Dec;111(16):1952-7.

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Comment in:

*

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=A

bstract & list_uids=14674393>Environ Health Perspect. 2003 Dec;111(16):A896-7.

*

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=A

bstract & list_uids=15471711>Environ Health Perspect. 2004

Oct;112(14):A794-5; author replies A795-7.

Oct;112(14):A794-5; author replies A795-7.

<http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3040 & uid=14644672

& db=pubmed & url=http://ehpnet1.niehs.nih.gov/members/2003/6433/6433.html>Clic

k here to read

<http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3494 & uid=14644672

& db=pubmed & url=http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed & p

ubmedid=14644672>Click here to read

In vitro activation of cord blood mononuclear cells and cytokine

production in a remote coastal population exposed to organochlorines and

methyl mercury.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Bilrha+H%22%5BAuthor%5D>Bilrha H,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Roy+R%22%5BAuthor%5D>Roy R,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Moreau+B%22%5BAuthor%5D>Moreau B,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Belles%2DIsles+M%22%5BAuthor%5D>Belles-Isles M,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Dewailly+E%22%5BAuthor%5D>Dewailly E,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & term=%22

Ayotte+P%22%5BAuthor%5D>Ayotte P.

Rheumatology-Immunology Research Unit, CHUQ-Laval University Medical

Center, Quebec City, Quebec, Canada.

Remote coastal populations that rely on seafood for subsistence often

receive unusually high doses of organochlorines and methyl mercury.

Immunosuppression resulting from prenatal exposure to organochlorines has

been reported in wildlife species and humans. In this study, we assessed

lymphocyte activation and associated cytokine secretion in 47 newborns from

a remote maritime population living on the Mid and Lower North Shore

regions of the St. Lawrence River (Quebec, Canada; subsistence fishing

group) and 65 newborns from nearby urban settings (reference group). Cord

blood samples were collected for organochlorine and mercury analyses and

also to isolate cord blood mononuclear cells (CBMCs) for the in vitro

assessment of cytokine production and expression of surface markers after

mitogenic stimulation (CD4(+)CD45RO(+), CD8(+)CD45RO(+), CD3(+)CD25(+), and

CD8(+)HLA-DR(+)). Blood mercury and plasma concentrations of

polychlorinated biphenyls (PCBs),

1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (p,p'-DDE), and

hexachlorobenzene (HCB) were significantly higher in the subsistence

fishing group than in the reference group (p < 0.001). No difference was

observed between the two groups regarding subsets of lymphocytes showing

markers of activation. In vitro secretion of cytokines by CBMCs after

mitogenic stimulation was lower in the subsistence fishing group than in

the reference group (p < 0.05). Moreover, we found an inverse correlation

between tumor necrosis factor-alpha (TNF-alpha) secretion and plasma PCB,

p,p'-DDE, and HCB concentrations (p < 0.05). Our data support a negative

association between TNF-alpha secretion by CBMCs and prenatal

organochlorine exposure. If the relationship between organochlorine and

TNF-alpha secretion is causal, it would suggest a role for this important

proinflammatory cytokine in mediating organochlorine-induced immunotoxicity

in infants developmentally exposed to these compounds.

PMID: 14644672

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

Sheri Nakken, R.N., MA, Classical Homeopath

Vaccination Information & Choice Network, Nevada City CA & Wales UK

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