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Glutamatergic drugs exacerbate symptomatic behavior in a transgenic model of comorbid Tourette's syndrome and obsessive-compulsive disorder.

 

McGrath MJ, Campbell KM, Parks CR, Burton FH.

Department of Pharmacology, University of Minnesota, 6-120 Jackson Hall, 321 Church St. S.E., Minneapolis, MN 55455, USA.

 

We previously created a transgenic mouse model of comorbid Tourette's syndrome and obsessive-compulsive disorder (TS+OCD), by expressing a neuropotentiating cholera toxin (CT) transgene in a subset of dopamine D1 receptor-expressing (D1+) neurons thought to induce cortical and amygdalar glutamate output. To test glutamate's role in the TS+OCD-like disorder of these transgenic mice (D1CT-7 line), the effects of glutamate receptor-binding drugs on their behavior were examined. MK-801, a non-competitive NMDA receptor antagonist that indirectly stimulates cortical-limbic glutamate output, aggravated a transgene-dependent abnormal behavior (repetitive climbing and leaping) in the D1CT-7 mice at doses insufficient to induce stereotypies, and more readily induced stereotypies and limbic seizure behaviors at high doses. NBQX, a seizure-inhibiting AMPA receptor antagonist, reduced only the MK-801-dependent stereotypic and limbic seizure behavior of D1CT-7 mice, but not their transgene-dependent behaviors. These data imply that TS+OCD-like behavior is mediated by cortical-limbic glutamate, but that AMPA glutamate receptors are not an essential part of this behavioral circuit. Our findings lead to the prediction that the symptoms of human Tourette's syndrome and obsessive-compulsive disorder are elicited by excessive forebrain glutamate output.PMID: 10980239 [PubMed - indexed for MEDLINE]

 

http://www.whale.to/a/blaylock5.html

 

SNIP

 

Our knowledge of this process opens up new avenues for treatment as well as prevention of excitotoxic injury to the nervous system. For example, there are many nutritional ways to improve CNS antioxidant defenses and boost neuronal energy generation, as well as improve membrane fluidity and receptor integrity. By using selective glutamate blocking drugs or nutrients, one may be able to alter some of the more devastating effects of Parkinson's disease. For example, there is evidence that dopamine deficiency causes a disinhibition (overactivity) of the subthalamic nucleus and that this may result in excitotoxic injury to the substantia nigra.(22) By blocking the glutamatergic neurons in this nucleus, one may be able to reduce this damage. There is also evidence that several nutrients can significantly reduce excitotoxicity. For example, combinations of coenzyme Q10 and niacinamide have been shown to protect against striatal excitotoxic lesions. Methylcobolamine, phosphotidylserine, picnogenol and acetyl-L-carnitine all protect against excitotoxicity as well.

 

Of particular concern is the toxic effects of these excitotoxic compounds on the developing brain. It is well recognized that the immature brain is four times more sensitive to the toxic effects of the excitatory amino acids as is the mature brain. This means that excitotoxic injury is of special concern from the fetal stage to adolescence. There is evidence that the placenta concentrates several of these toxic amino acids on the fetal side of the placenta. Consumption of aspartame and MSG containing products by pregnant women during this critical period of brain formation is of special concern and should be discouraged. Many of the effects, such as endocrine dysfunction and complex learning, are subtle and may not appear until the child is older. Other hypothalamic syndromes associated with early excitotoxic lesions include immune alterations and violence dyscontrol.

 

Over 100 million American now consume aspartame products and a greater number consume products containing one or more excitotoxins. There is sufficient medical literature documenting serious injury by these additives in the concentrations presently in our food supply to justify warning the public of these dangers. The case against aspartame is especially strong.

 

Kim, I believe this info relates to your post on ADHD. Your original article is here: http://www.cbn.com/cbnnews/news/050928a.aspx

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Laurensmom,

 

I had looked at that study before too. In fact I have some things saved (kind of the ole "one thing led to another" and pretty soon I was in info overload :blink: )

 

Is there anything here that catches your eye?

 

I was looking at glutamate in relationship to alum. I mixed powered soy formula for my boys as infants. Used tap water, which I always boiled. I concentrated the amt. of fluoride and alum that was present in the drinking water, along with what was contained in the soy formula (which is know to be high :wub: in soy) by boiling the water like that. Alum. salts are used in the purification process in many water treatment plants.

 

Our local news paper recently had a huge front page article on how awful our water quality here is. The bottem line was, be careful what you wish for (clean water) because the cost will go up greatly.

 

Anyway, here is some of the stuff that I had saved. One is a study that was done subsequent to the one you posted, by the same guys, I believe.

 

http://content.febsjournal.org/cgi/content...act/267/10/3049

 

Effects of aluminum on activity of Krebs cycle enzymes and glutamate dehydrogenase in rat brain homogenate

 

P. Zatta1, E. Lain2 and C. Cagnolini2

1 CNR Center on Metalloproteins, and 2 Department of Pharmacological Sciences, University of Padova, Italy

 

Correspondence to P. Zatta, CNR Center on Metalloproteins, Department of Biology, University of Padova, Viale G. Colombo 3, 35131, Padova, Italy. Fax: + 39 49 827 6330; Tel.: + 39 49 827 6331; E-mail: zatta@cribi1.bio.unipd.it

 

Aluminum is a neurotoxic agent for animals and humans that has been implicated as an etiological factor in several neurodegenerative diseases and as a destabilizer of cell membranes. Due to its high reactivity, Al3+ is able to interfere with several biological functions, including enzymatic activities in key metabolic pathways. In this paper we report that, among the enzymes that constitute the Krebs cycle, only two are activated by aluminum: -ketoglutarate dehydrogenase and succinate dehydrogenase. In contrast, aconitase, shows decreased activity in the presence of the metal ion. Al3+ also inhibits glutamate dehydrogenase, an allosteric enzyme that is closely linked to the Krebs cycle. A possible correlation between aluminum, the Krebs cycle and aging processes is discussed.

 

Keywords: aluminum; Krebs cycle; Alzheimer's disease; neurodegeneration; metal ions.

 

 

http://www.ncbi.nlm.nih.gov/entrez/query.f...st_uids=1070064

 

Van Woert MH, Jutkowitz R, Rosenbaum D, Bowers MB Jr.

Haloperidol, a dopamine receptor blocking agent, is the most effective therapy for Tourette's syndrome. In five patients with Tourette's syndrome, we found in the CSF an elevated probenecid-induced accumulation of HVA, the major metabolite of dopamine. This supports the hypothesis that Tourette symptoms are related to an increased firing of dopaminergic neurons in the central nervous system; haloperidol relieves these symptoms by blocking dopamine receptors. Some similarities of Tourette's syndrome to Lesch-Nyhan's syndrome prompted us to compare these two disorders, obtaining data from a large number of Tourette patients. In a questionnaire completed by 114 patients with Tourette's syndrome, the incidence of self-destructive behavior was 43%, a family history of gout or hyperuricemia was present in 27%, and 11% had a family history of Tourette's syndrome or tics. We propose that Tourette's syndrome could be a genetic disorder of purine metabolism which may result in neurotransmitter abnormalities such as an increased brain

dopamine turnover.

 

http://www.ncbi.nlm.nih.gov/entrez/query.f...p;dopt=Abstract

 

1. Hyperuricemia is common among the gouty relatives as reported by others (8-11). It is of interest to note that serum urate fluctuates periodically. Hyperuricemia is not necessarily maintained in a steady state throughout the years. Thus a single determination of serum uric acid can be misleading. 2. Development of gout from asymptomatic hyperuricemia is often correlated with the degree of hyperuricemia as observed from population or family studies (12-14). The data presented indicate that unequivocal hyperuricemia is more often accompanied by excessive excretion of uric acid, diminished excretion of ammonia and abnormally high plasma glutamic acid. All are undoubtedly important risk factors for gout. 3. The elevated glutamate could be due to a deficiency of glutamic dehydrogenase, as postulated by Pagliara and Goodman (15). In presence of intracellular accumulation of glutamate in glutamic dehydrogenase deficiency, renal production of ammonium may be reduced due to its inhibitory action on glutaminase 1. As a result of a renal block of ammonia formation, the glutamine in surplus may be diverted for uric acid synthesis. 4. Long-term studies indicate serum urate in most hyperuricemia relatives of gout can be modified by environmental factors, such as diet, weight and changes of life style. When hyperuricemia is under better control, the potential hazard of developing symptomatic gout may be circumvented.

 

PMID: 7424621 [PubMed - indexed for MEDLINE]

 

http://content.febsjournal.org/cgi/content...act/267/10/3049

 

Effects of aluminum on activity of Krebs cycle enzymes and glutamate dehydrogenase in rat brain homogenate

P. Zatta1, E. Lain2 and C. Cagnolini2

1 CNR Center on Metalloproteins, and 2 Department of Pharmacological Sciences, University of Padova, Italy

 

Correspondence to P. Zatta, CNR Center on Metalloproteins, Department of Biology, University of Padova, Viale G. Colombo 3, 35131, Padova, Italy. Fax: + 39 49 827 6330; Tel.: + 39 49 827 6331; E-mail: zatta@cribi1.bio.unipd.it

 

Aluminum is a neurotoxic agent for animals and humans that has been implicated as an etiological factor in several neurodegenerative diseases and as a destabilizer of cell membranes. Due to its high reactivity, Al3+ is able to interfere with several biological functions, including enzymatic activities in key metabolic pathways. In this paper we report that, among the enzymes that constitute the Krebs cycle, only two are activated by aluminum: -ketoglutarate dehydrogenase and succinate dehydrogenase. In contrast, aconitase, shows decreased activity in the presence of the metal ion. Al3+ also inhibits glutamate dehydrogenase, an allosteric enzyme that is closely linked to the Krebs cycle. A possible correlation between aluminum, the Krebs cycle and aging processes is discussed.

 

Keywords: aluminum; Krebs cycle; Alzheimer's disease; neurodegeneration; metal ions.

 

 

 

http://www.springerlink.com/content/gwbn78m9hqwv43q3/

 

Research Article

Inactivation of human glutamate dehydrogenase by aluminum

S.-J. Yang1, 2, J.-W. Huh1, J. E. Lee3, S. Y. Choi4, T. U. Kim2 and S.-W. Cho1

 

(1) Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, 138-736 Seoul, 388-1 Poongnap-dong, Songpa-ku, Korea

(2) Department of Medical Technology, College of Health Science, Yonsei University, 222-701 Wonju, Korea

(3) Department of Anatomy, Yonsei University College of Medicine, 150-752 Seoul, Korea

(4) Department of Genetic Engineering, Division of Life Sciences, Hallym University, 200-702 Chunchon, Korea

 

 

Abstract Aluminum inactivated glutamate dehydrogenase (GDH) by a pseudo-first-order reaction at micromolar concentrations. A double-reciprocal plot gave a straight line with a kinact of 2.7 min-1 and indicated the presence of a binding step prior to inactivation. The inactivation was strictly pH dependent and a marked increase in sensitivity to aluminum was observed as the pH decreased. At a pH higher than 8.5, no inactivation was observed. The completely inactivated GDH contained 2 mol of aluminum per mole of enzyme subunit monomer. When preincubated with enzyme, several chelators such as citrate, NaF, N-(2-hydroxyethyl) ethylenediaminetriacetic acid or ethylenediaminetriacetic acid efficiently protected the enzyme against the aluminum inactivation. In a related experiment, only citrate and NaF released the aluminum from the completely inactivated aluminum-enzyme complex and fully recovered the enzyme activity. Ferritin, NADP+, or nerve growth factor did not show any effects on the recovery of the aluminum-inactivated GDH activity. The dissociation constant for the aluminum-enzyme complex was calculated to be 5.3 M. Although aluminum has been known to form a complex with nucleotides, no such effects were observed in the inactivation of GDH by aluminum as determined using GDHs mutated at the ADP-binding site, NAD+-binding site or GTP-binding site. Circular dichroism studies showed that the binding of aluminum to the enzyme induced a decrease in helices and sheets and an increase in random coil. Therefore, inactivation of GDH by aluminum is suggested to be due to the conformational change induced by aluminum binding. These results suggest a possibility that aluminum-induced alterations in enzymes of the glutamate system may be one of the causes of aluminum-induced neurotoxicity.

Glutamate dehydrogenase - aluminum - glutamate - chelator - conformational change

 

Received 25 July 2003; received after revision 27 August 2003; accepted 15 September 2003

 

http://www.blackwell-synergy.com/doi/abs/1...1998.70041609.x

 

Abstract: Humans are exposed to aluminum from environmental sources and therapeutic treatments. However, aluminum is neurotoxic and is considered a possible etiologic factor in Alzheimer's disease and other neurological disorders. The molecular mechanism of aluminum neurotoxicity is not understood. We tested the effects of aluminum on the glutamate-nitric oxide-cyclic GMP pathway in cultured neurons. Neurons were exposed to 50 µM aluminum in culture medium for short-term (4 h) or long-term (8–14 days) periods, or rats were prenatally exposed, i.e., 3.7% aluminum sulfate in the drinking water, during gestation. Chronic (but not short-term) exposure of neurons to aluminum decreased glutamate-induced activation of nitric oxide synthase by 38% and the formation of cyclic GMP by 77%. The formation of cyclic GMP induced by the nitric oxide-generating agent S-nitroso-N-acetylpenicillamine was reduced by 33%. In neurons from rats prenatally exposed to aluminum but not exposed to it during culture, glutamate-induced formation of cyclic GMP was inhibited by 81%, and activation of nitric oxide synthase was decreased by 85%. The formation of cyclic GMP induced by S-nitroso-N-acetylpenicillamine was not affected. These results indicate that chronic exposure to aluminum impairs glutamate-induced activation of nitric oxide synthase and nitric oxide-induced activation of guanylate cyclase. Impairment of the glutamate-nitric oxide-cyclic GMP pathway in neurons may contribute to aluminum neurotoxicity.

 

http://www.ncbi.nlm.nih.gov/entrez/query.f...t_uids=10357247

 

1: Eur J Pharmacol. 1999 Apr 29;371(2-3):103-11. Links

Differential response of cortical-limbic neuropotentiated compulsive mice to dopamine D1 and D2 receptor antagonists.Campbell KM, McGrath MJ, Burton FH.

Department of Pharmacology, University of Minnesota, Minneapolis 55455, USA.

 

We previously created transgenic mice in which dopamine D1 receptor-expressing (D1+) neurons in regional subsets of the cortex and amygdala express a neuropotentiating cholera toxin (CT) transgene. These 'D1CT' mice engage in complex biting, locomotor and behavioral perseverance-repetition abnormalities that resemble symptoms of human compulsive disorders associated with cortical-limbic hyperactivity. Because excessive cortical-limbic stimulation of striatal motor pathways may play a critical role in causing compulsive disorders, we examined the responsiveness of D1CT mice to dopamine D1 and D2 receptor antagonists. D1CT mice were found to be largely resistant to the cataleptic action of the D1 receptor antagonist SCH23390. The abnormal repetitive leaping of D1CT mice was similarly unaffected by SCH23390. In contrast, the D1CT mice displayed supersensitivity to cataleptic induction by the D2 receptor antagonist sulpiride. These data are consistent with the hypothesis that complex compulsions are mediated by chronic excessive corticostriatal (and/or amygdalostriatal) glutamatergic stimulation of the striatal direct and indirect motor pathways.

 

 

http://www.msgtruth.org/foodfor.htm

 

MSG is a nervous system stimulant.

 

Recent research at Johns Hopkins directly ties nervous system stimulation to the immune system.

 

The FDA admits that MSG has been proven to induce asthma attacks in certain individuals.

 

Asthma deaths have increased with the increased use of MSG in the US food supply.

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

 

 

Healthy Skepticism Library number: 10018

Publication type: journal article

 

Tanne JH.

Investigators will review conflicts of interest at NIH

BMJ 2007 Apr 14;334(7597):767

http://www.bmj.com/cgi/content/full/334/7597/767-a

 

Abstract:

Daniel Levinson, inspector general of the US Department of Health and Human Services, has said that his office will reopen 103 cases of conflicts of interest among scientists at the US National Institutes of Health (NIH).

 

The investigation will be carried out by the inspector general's Special Investigations Unit, staffed by five criminal investigators.

 

Mr Levinson's office was active in prosecuting Lester Crawford, the former head of the Food and Drug Administration, who was fined nearly $90 000 (£46 000; 67 000) for falsely reporting he had sold stock in companies regulated by the FDA while he still owned the shares (BMJ 2007;334:492, doi: 10.1136/bmj.39142.592130.DB)

 

The special unit will also investigate conflicts of interest among about 40 000 scientific teams at about 2000 universities, medical centres, and non-profit institutions that receive research grants from NIH, potentially a much bigger problem. The NIH's rules on conflicts of interest do . . .

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interesting...

 

April 27, 2007

 

Studies Reveal an Immune System Regulator

 

By NICHOLAS WADE

http://www.nytimes.com/2007/04/27/us/27immune.html

 

Scientists working independently in Cambridge, England, and Cambridge,

Mass., have discovered an unexpected regulatory network that

affects the

entire immune system.

 

 

http://www.kvue.com/news/top/stories/04260...m.103abb48.html

 

Perchlorate showing up in nation's milk supply

 

 

We want to be clear: we are not suggesting anyone should avoid milk, or any other foods out of fear over perchlorate contamination. At this point, doctors are only urging consumers to become more educated about the risks of environmental hazards in the foods you eat. If you have questions, you should talk with your doctor
.

 

I wish we had a "rolling on the floor laughing," smiley.

 

If I have to read this phrase one more time, I'm going to barf.

 

Ask my Dr. about supplements and medication interactions...he doesn't know. Ask about an out of range result on a blood profile...doesn't know.....ask about Perchlorate...don't think so.

 

I think it's about time, they stopped making Dr.s carry the burden, of patients having the illusion that Dr.s know everything. It's not realistic, and it's not a safe assumption.

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http://www.jsonline.com/story/index.aspx?id=597586

 

Research triggers conflict concerns

Booming private industry serves drug companies and government clients

By SUSANNE RUST and CARY SPIVAK

srust@journalsentinel.com

Posted: April 28, 2007

The medical research company hired by the federal government four years ago to update its list of carcinogens moved quickly to add a virus to the list while two of its clients were developing vaccines to combat that same virus.

 

 

 

 

http://www.sunjournal.com/story/209824-3/b...young_So_toxic/

 

So young. So toxic

 

It doesn't take a lifetime of unhealthy living to accumulate toxins in

your body. Ask 30-year-old Mainer Hannah Pingree, House majority leader in

the Legislature and a walking chemical soup. She's not alone.

 

By Jessica Alaimo , Staff Writer

Sunday, April 29, 2007

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New fears over additives in children's food

 

Potential link to behaviour problems prompts advice to parents over diet

 

Felicity Lawrence

Tuesday May 8, 2007

The Guardian

http://www.guardian .co.uk/food/ Story/0,, 2074346,00. html

 

Food safety experts have advised parents to eliminate a series of

additives from their children's diet while they await the publication of a

new study that is understood to link these ingredients to behaviour

problems in youngsters.

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http://www.boston.com/business/globe/artic...ken_from_china/

 

WASHINGTON -- In China, some farmers try to maximize the output from their

small plots by flooding produce with unapproved pesticides, pumping

livestock with antibiotics banned in the United States, and using human

feces as fertilizer to boost soil productivity. But the questionable

practices don't end there: Chicken pens are frequently suspended over

ponds where seafood is raised, recycling chicken waste as a food source

for seafood, according to a leading food safety expert who served as a

federal adviser to the Food and Drug Administration.

 

 

http://www.nytimes.com/2007/05/09/business...ess/09food.html

 

SHANGHAI, May 8 — A second industrial chemical that American regulators

have identified as a pet food contaminant may have been intentionally

added to animal feed by producers seeking larger profits, according to

interviews Tuesday with chemical industry officials.

 

 

Washington Post Staff Writer

Wednesday, May 9, 2007; A03

http://www.washingtonpost.com/wp-dyn/conte...7050801060.html

 

The tainted Chinese ingredient that was incorporated into U.S. pet food

and later made its way into chicken and pig feed was neither wheat gluten

nor rice protein as advertised, but was seriously contaminated wheat

flour, government investigators said yesterday.

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http://www.foxnews.com/story/0,2933,275736,00.html

 

The ingredient has been the subject of concern on cancer, because when mixed with Vitamin C, it turns into a carcinogenic substance called benzene, the Independent reported.

 

and

 

"These chemicals have the ability to cause severe damage to DNA in the mitochondria to the point that they totally inactivate it: they knock it out altogether,"

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June 5, 2007

 

The Disorder Is Sensory; the Diagnosis, Elusive

 

By BENEDICT CAREY

http://www.nytimes.com/2007/06/05/health/p...amp;oref=slogin

 

DENVER — Almost every parent of young children has heard an anguished cry

or two (or 200) something like:

 

“This shirt is scratchy, this shirt is scratchy, get it off!”

 

 

 

http://www.dailymail.co.uk/pages/live/arti...in_page_id=1965

 

Using pesticides on house plants could more than double your risk of developing a brain tumour, a study suggests

 

The findings come a week after British researchers warned that using

pesticides while gardening could increase the risk of Parkinson's disease

by more than 40 per cent.

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http://www.huffingtonpost.com/david-kirby/...ur_b_51224.html

 

David Kirby| BIO

See You In (Vaccine) Court

9 Comments | Posted June 7, 2007 | 07:05 PM (EST)

 

 

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

 

Read More: Breaking Living Now News

 

 

 

On Monday, one of the most important legal proceedings in American medical history will get underway at the U.S. Court of Federal Claims in Washington. There, a special panel of three judges will begin hearing evidence to support -- and refute -- the hypothesis that mercury in vaccines and/or the live-virus measles-mumps-rubella shot caused autism or autism-like symptoms in some American children.

 

 

Monday will mark the first time ever that evidence of autistic harm from childhood vaccines is examined and cross-examined in a court of law. This is far from a slam dunk case for either side, and the stakes - professional, financial, emotional -- could not be more intense.

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Silly me, I thought these studies were done before mass marketing and wide spread use

 

Toxicology. 2007 May 26; [Epub ahead of print]

 

Effect of an acute 900MHz GSM exposure on glia in the rat brain: A

time-dependent study.

 

Brillaud E, Piotrowski A, de Seze R.

 

INERIS, Unité de Toxicologie Expérimentale, Parc Technologique ALATA, BP

no. 2, 60550 Verneuil-en- Halatte, France.

 

Because of the increasing use of mobile phones, the possible risks of

radio frequency electromagnetic fields adverse effects on the human brain

has to be evaluated. In this work we measured GFAP expression, to evaluate

glial evolution 2, 3, 6 and 10 days after a single GSM exposure (15min,

brain averaged SAR=6W/kg, 900MHz signal) in the rat brain. A statistically

significant increase of GFAP stained surface area was observed 2 days

after exposure in the frontal cortex and the caudate putamen. A smaller

statistically significant increase was noted 3 days after exposure in the

same areas and in the cerebellum cortex. Our results confirm the

Mausset-Bonnefont et al. study [Mausset-Bonnefont, A.L., Hirbec, H.,

Bonnefont, X., Privat, A., Vignon, J., de Seze, R., 2004. Acute exposure

to GSM 900MHz electromagnetic fields induces glial reactivity and

biochemical modifications in the rat brain. Neurobiol. Dis. 17, 445-454],

showing the existence of glial reactivity after a 15min GSM acute exposure

at a brain averaged SAR of 6W/kg. We conclude to a temporary effect,

probably due to a hypertrophy of glial cells, with a temporal and a

spatial modulation of the effect. Whether this effect could be harmful

remains to be studied.

 

PMID: 17624651

 

Well, what significance could a few swollen glial cells have anyway?

 

http://en.wikipedia.org/wiki/Glial_cell

 

Recent findings in the hippocampus and cerebellum have indicated that glia are also active participants in synaptic transmission, regulating clearance of neurotransmitter from the synaptic cleft, releasing factors such as ATP which modulate presynaptic function, and even releasing neurotransmitters themselves.

 

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

 

 

http://www.latimes.com/features/health/la-...1,1093654.story

 

John Bucher, associate director of the National Toxicology Program, which oversees

the reproductive health center, said the panel gave the most

weight to neurological effects in children, infants and fetuses because

studies consistently have found those effects when newborn animals are

exposed to low doses similar to what people encounter. Bucher said that

because the science remains uncertain, it is up to individuals to decide

whether they want to avoid products containing BPA.

 

 

http://www.star-telegram.com/state_news/story/187556.html

 

By SCOTT STREATER

Star-Telegram Staff Writer

 

Congress has taken the first steps toward blocking a Bush administration

policy that many say will make it difficult for residents and public

health officials to track industrial pollution.

 

 

http://www.dailymail.co.uk/pages/live/fema...picbox&ct=5

 

Girls entering puberty by the age of six - but are drugs the answer?

 

By LOIS ROGERS - More by this author » Last updated at 10:01am on 7th

August 2007

 

Some girls now enter puberty as early as six - with toxic chemicals widely

held to blame. But are new drugs to hold back the years really the right

answer?:

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Oh good greif, we love brown rice here. This article mentions the use of rice milk too.

 

http://www.telegraph.co.uk/earth/main.jhtm...9/eababy129.xml

 

'Dangerous' levels of arsenic in 10pc of rice

 

He said that brown rice, favoured by macro-biotic, healthfood fans, had even higher levels of arsenic. Bran from the United States used as a food supplement had levels approaching Britain's food standard of one part per million, set in 1959.

 

"That is incredibly high," he added.

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