metallothioneini s specifically up-regulated in response to neuronal injury

[Guest guest]

I thought these were interesting. There are many discussing metallothionein

impairment in autism and using supplements to raise levels. According to

these abstracts......metallothionein is upregulated in response to injury.

The majority of our children have dysfunctional brains but nothing

indicating injury. So does that mean those who are using high zinc or

other supplements to increase metallothionein are doing that by injuring the

brain or body?

J Neurochem. 2004 Jan;88(2):454-61.

Neuron-glia communication: metallothionein expression is specifically

up-regulated by astrocytes in response to neuronal injury.

Chung RS, Adlard PA, Dittmann J, Vickers JC, Chuah MI, West AK.

NeuroRepair Group, School of Medicine, University of Tasmania, Hobart,

Tasmania, Australia Institute for Brain Aging and Dementia, Gillespie

Neuroscience Research Facility, University of California Irvine, Gillespie,

Irvine, California, USA.

Recent data suggests that metallothioneins (MTs) are major neuroprotective

proteins within the CNS. In this regard, we have recently demonstrated that

MT-IIA (the major human MT-I/-II isoform) promotes neural recovery following

focal cortical brain injury.

To further investigate the role of MTs in cortical brain injury, MT-I/-II

expression was examined in several different experimental models of cortical

neuron injury. While MT-I/-II immunoreactivity was not detectable in the

uninjured rat neocortex, by 4 days, following a focal cortical brain injury,

MT-I/-II was found in astrocytes aligned along the injury site.

At latter time points, astrocytes, at a distance up to several hundred

microns from the original injury tract, were MT-I/-II immunoreactive.

Induced MT-I/-II was found both within the cell body and processes. Using a

cortical neuron/astrocyte co-culture model, we observed a similar MT-I/-II

response following in vitro injury. Intriguingly, scratch wound injury in

pure astrocyte cultures resulted in no change in MT-I/-II expression.

This suggests that MT induction was specifically elicited by neuronal

injury. Based upon recent reports indicating that MT-I/-II are major

neuroprotective proteins within the brain, our results provide further

evidence that MT-I/-II plays an important role in the cellular response to

neuronal injury.

PMID: 14690533 [PubMed - in process]

--------------------------------------------------------------------------------\

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

Ecotoxicology. 2003 Dec;12(6):475-83.

Gene expression profiling in ecotoxicology.

Snell TW, Brogdon SE, MB.

School of Biology, Georgia Institute of Technology, Atlanta, GA 30332-0230,

USA. terry.snell@...

Gene expression profiling is a powerful new end point for ecotoxicology and

a means for bringing the genomics revolution to this field. We review the

usefulness of gene expression profiling as an end point in ecotoxicology and

describe methods for applying this approach to non-model organisms. Since

genomes contain thousands of genes representing hundreds of pathways, it is

possible to identify toxicant-specific responses from this wide array of

possibilities.

Stressor-specific signatures in gene expression profiles can be used to

diagnose which stressors are impacting populations in the field. Screening

for stress-induced genes requires special techniques in organisms without

sequenced genomes. These techniques include differential display polymerase

chain reaction (DD PCR), suppressive subtractive hybridization PCR (SSH

PCR), and representational difference analysis.

Gene expression profiling in model organisms like yeast has identified

hundreds of genes that are up-regulated in response to various stressors,

including several that are well characterized (e.g., hsp78, metallothionein,

superoxide dismutase).

Using consensus PCR primers from several animal sequences, it is possible to

amplify some of these well characterized stress-induced genes from organisms

of interest in ecotoxicology. We describe how several stress-induced genes

can be grouped into cDNA arrays for rapidly screening samples.

PMID: 14680327 [PubMed - in process]

_________________________________________________________________

Check out the coupons and bargains on MSN Offers!

http://shopping.msn.com/softcontent/softcontent.aspx?scmId=1418

[Guest guest]

No, this says to me that metallothionein is increased by the body in response to

brain injury. Autistic brains haven't developed correctly, so they are injured,

even if it doesn't show up on an MRI. Therefore, those who are increasing their

MT production are perhaps helping the brain to heal. Kathy

metallothioneini s specifically up-regulated in response to

neuronal injury

I thought these were interesting. There are many discussing metallothionein

impairment in autism and using supplements to raise levels. According to

these abstracts......metallothionein is upregulated in response to injury.

The majority of our children have dysfunctional brains but nothing

indicating injury. So does that mean those who are using high zinc or

other supplements to increase metallothionein are doing that by injuring the

brain or body?

J Neurochem. 2004 Jan;88(2):454-61.

Neuron-glia communication: metallothionein expression is specifically

up-regulated by astrocytes in response to neuronal injury.

Chung RS, Adlard PA, Dittmann J, Vickers JC, Chuah MI, West AK.

NeuroRepair Group, School of Medicine, University of Tasmania, Hobart,

Tasmania, Australia Institute for Brain Aging and Dementia, Gillespie

Neuroscience Research Facility, University of California Irvine, Gillespie,

Irvine, California, USA.

Recent data suggests that metallothioneins (MTs) are major neuroprotective

proteins within the CNS. In this regard, we have recently demonstrated that

MT-IIA (the major human MT-I/-II isoform) promotes neural recovery following

focal cortical brain injury.

To further investigate the role of MTs in cortical brain injury, MT-I/-II

expression was examined in several different experimental models of cortical

neuron injury. While MT-I/-II immunoreactivity was not detectable in the

uninjured rat neocortex, by 4 days, following a focal cortical brain injury,

MT-I/-II was found in astrocytes aligned along the injury site.

At latter time points, astrocytes, at a distance up to several hundred

microns from the original injury tract, were MT-I/-II immunoreactive.

Induced MT-I/-II was found both within the cell body and processes. Using a

cortical neuron/astrocyte co-culture model, we observed a similar MT-I/-II

response following in vitro injury. Intriguingly, scratch wound injury in

pure astrocyte cultures resulted in no change in MT-I/-II expression.

This suggests that MT induction was specifically elicited by neuronal

injury. Based upon recent reports indicating that MT-I/-II are major

neuroprotective proteins within the brain, our results provide further

evidence that MT-I/-II plays an important role in the cellular response to

neuronal injury.

PMID: 14690533 [PubMed - in process]

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

Ecotoxicology. 2003 Dec;12(6):475-83.

Gene expression profiling in ecotoxicology.

Snell TW, Brogdon SE, MB.

School of Biology, Georgia Institute of Technology, Atlanta, GA 30332-0230,

USA. terry.snell@...

Gene expression profiling is a powerful new end point for ecotoxicology and

a means for bringing the genomics revolution to this field. We review the

usefulness of gene expression profiling as an end point in ecotoxicology and

describe methods for applying this approach to non-model organisms. Since

genomes contain thousands of genes representing hundreds of pathways, it is

possible to identify toxicant-specific responses from this wide array of

possibilities.

Stressor-specific signatures in gene expression profiles can be used to

diagnose which stressors are impacting populations in the field. Screening

for stress-induced genes requires special techniques in organisms without

sequenced genomes. These techniques include differential display polymerase

chain reaction (DD PCR), suppressive subtractive hybridization PCR (SSH

PCR), and representational difference analysis.

Gene expression profiling in model organisms like yeast has identified

hundreds of genes that are up-regulated in response to various stressors,

including several that are well characterized (e.g., hsp78, metallothionein,

superoxide dismutase).

Using consensus PCR primers from several animal sequences, it is possible to

amplify some of these well characterized stress-induced genes from organisms

of interest in ecotoxicology. We describe how several stress-induced genes

can be grouped into cDNA arrays for rapidly screening samples.

PMID: 14680327 [PubMed - in process]

_________________________________________________________________

Responsibility for the content of this message lies strictly with

the original author(s), and is not necessarily endorsed by or the

opinion of the Research Institute.

[Guest guest]

----Original Message Follows----

From: <evchk96@...>

Reply-

No, this says to me that metallothionein is increased by the body in

response to brain injury. Autistic brains haven't developed correctly, so

>they are injured, even if it doesn't show up on an MRI. >Therefore, those

who are increasing their MT production are perhaps helping the brain to

>heal. >Kathy

Kathy,

Do you have anything to validate that there's brain injury? As far as I'm

aware there is no credible science showing that they have the type of

antibodies that cause tissue damage. The elevated cytokines and other

immune abnormalities can certainly cause the brain to not function properly

without the need for any type of damage.

If there's no brain injury then there would be no reason for metallothionein

to be elevated.

Cheryl

Brain Behav Immun. 2004 Jan;18(1):1-6.

Innate immunity at the forefront of psychoneuroimmunology.

Dantzer R.

Integrative Neurobiology, Bordeaux, France.

robert.dantzer@...

The last 15 years of research in psychoneuroimmunology have been marked by a

renewed interest in the mechanisms of inflammation and participation of the

brain in these mechanisms.

Peripheral proinflammatory cytokines produced by activated accessory immune

cells act in the brain to trigger sickness, in the form of fever,

pituitary-adrenal axis activation, and sickness behavior.

Communication between the periphery and brain takes place via both neural

and humoral pathways. Recognition of the role of local production of

cytokines and their downstream messengers in the central nervous system

opens important new vistas for understanding and treating non-specific

neurovegetative and psychiatric symptoms of diseases. In this presidential

address, I present the main methodological and conceptual developments that

have allowed such progress.

PMID: 14651940 [PubMed - in process]

Brain Behav Immun. 2003 Apr;17(2):69-85.

Bi-directional immune-brain communication: Implications for understanding

stress, pain, and cognition.

Maier SF.

Department of Psychology and Center for Neuroscience, University of

Colorado, Campus box 345 80309-0345, Boulder, CO, USA.

smaier@...

The immune system and the central nervous system form a bi-directional

communication network. The critical roles of pro-inflammatory cytokines in

both the periphery and the nervous system are discussed. In the periphery,

these cytokines initiate the processes that signal the brain that immune

activation has occurred, and communicate this information over both neural

and blood-borne routes. The arrival of these signals in the central nervous

system induces a neural cascade that includes the de novo induction of

pro-inflammatory cytokines. The functions of these cytokines in the nervous

system are discussed, and it is argued that they play a key role in

regulating the neural control of immune processes in the periphery. In

addition, it is argued that these cytokines play a variety of other roles,

and some implications of the cytokine network for understanding stress,

behavior, sensory processing, mood, and cognition are described. The overall

argument is that because brain-mediated host defense involves behavioral,

sensory, mood, and cognitive alterations, immune activation, and immune

products such as the cytokines can have a pervasive effect on these

functions. Finally, these phenomena are placed in an evolutionary

perspective.

Publication Types:

Lectures

Physiol Behav. 2003 Nov;80(2-3):177-84. Related Articles, Links

Zymosan: induction of sickness behavior and interaction with

lipopolysaccharide.

Cremeans- JK, Newberry BH.

Department of Psychology, Kent State University, Kent, OH 44242, USA.

The yeast particulate zymosan (Zy) activates innate immune system cells and

induces cytokine secretion. There is also evidence that Zy can affect

biologic responses to bacterial lipopolysaccharide (LPS) and that the

pathways by which these two agents act upon immune cells are only partially

distinct. The present experiments assessed the ability of Zy to elicit

CNS-mediated sickness symptoms and to alter their responses to LPS. In

Experiment 1, Zy induced elements of the sickness behavior syndrome

dose-responsively in Long- rats, as indicated by reductions in

consumption of a highly palatable bait and in body temperature. In

Experiment 2, Zy exerted a priming effect, sensitizing animals to subsequent

LPS as measured by reductions in bait consumption, 24-h laboratory chow

intake, and body temperature. Experiment 3 failed to provide evidence for

LPS-to-Zy cross-tolerance but did indicate that the administration of Zy

disrupts previously acquired LPS tolerance. These results suggest that the

specifics of exposure to microbially derived innate immune activators have

to be taken into account in investigating the biologic bases of sickness

behaviors and developing models of coinfection.

PMID: 14637214 [PubMed - indexed for MEDLINE]

_________________________________________________________________

Find high-speed ‘net deals — comparison-shop your local providers here.

https://broadband.msn.com

[Guest guest]

No I don't, but studies have shown that there is increased neuronal growth as

evident by the large size heads (for a period of time) of a lot of kids with

autism and differences in the brains of people with autism, so how do we know

that the abnormal development isn't caused by some internal injury. I'm not

talking about a bump on the head type of injury, I'm talking about as the baby

is developing, if all of the proper mechanisms aren't in place or some

environmental insult (viruses, mercury, etc.) happened, there would be injury to

the brain. Kathy

Re: metallothioneini s specifically up-regulated in response

to neuronal injury

----Original Message Follows----

From: <evchk96@...>

Reply-

No, this says to me that metallothionein is increased by the body in

response to brain injury. Autistic brains haven't developed correctly, so

>they are injured, even if it doesn't show up on an MRI. >Therefore, those

who are increasing their MT production are perhaps helping the brain to

>heal. >Kathy

Kathy,

Do you have anything to validate that there's brain injury? As far as I'm

aware there is no credible science showing that they have the type of

antibodies that cause tissue damage. The elevated cytokines and other

immune abnormalities can certainly cause the brain to not function properly

without the need for any type of damage.

If there's no brain injury then there would be no reason for metallothionein

to be elevated.

Cheryl

Brain Behav Immun. 2004 Jan;18(1):1-6.

Innate immunity at the forefront of psychoneuroimmunology.

Dantzer R.

Integrative Neurobiology, Bordeaux, France.

robert.dantzer@...

The last 15 years of research in psychoneuroimmunology have been marked by a

renewed interest in the mechanisms of inflammation and participation of the

brain in these mechanisms.

Peripheral proinflammatory cytokines produced by activated accessory immune

cells act in the brain to trigger sickness, in the form of fever,

pituitary-adrenal axis activation, and sickness behavior.

Communication between the periphery and brain takes place via both neural

and humoral pathways. Recognition of the role of local production of

cytokines and their downstream messengers in the central nervous system

opens important new vistas for understanding and treating non-specific

neurovegetative and psychiatric symptoms of diseases. In this presidential

address, I present the main methodological and conceptual developments that

have allowed such progress.

PMID: 14651940 [PubMed - in process]

Brain Behav Immun. 2003 Apr;17(2):69-85.

Bi-directional immune-brain communication: Implications for understanding

stress, pain, and cognition.

Maier SF.

Department of Psychology and Center for Neuroscience, University of

Colorado, Campus box 345 80309-0345, Boulder, CO, USA.

smaier@...

The immune system and the central nervous system form a bi-directional

communication network. The critical roles of pro-inflammatory cytokines in

both the periphery and the nervous system are discussed. In the periphery,

these cytokines initiate the processes that signal the brain that immune

activation has occurred, and communicate this information over both neural

and blood-borne routes. The arrival of these signals in the central nervous

system induces a neural cascade that includes the de novo induction of

pro-inflammatory cytokines. The functions of these cytokines in the nervous

system are discussed, and it is argued that they play a key role in

regulating the neural control of immune processes in the periphery. In

addition, it is argued that these cytokines play a variety of other roles,

and some implications of the cytokine network for understanding stress,

behavior, sensory processing, mood, and cognition are described. The overall

argument is that because brain-mediated host defense involves behavioral,

sensory, mood, and cognitive alterations, immune activation, and immune

products such as the cytokines can have a pervasive effect on these

functions. Finally, these phenomena are placed in an evolutionary

perspective.

Publication Types:

Lectures

Physiol Behav. 2003 Nov;80(2-3):177-84. Related Articles, Links

Zymosan: induction of sickness behavior and interaction with

lipopolysaccharide.

Cremeans- JK, Newberry BH.

Department of Psychology, Kent State University, Kent, OH 44242, USA.

The yeast particulate zymosan (Zy) activates innate immune system cells and

induces cytokine secretion. There is also evidence that Zy can affect

biologic responses to bacterial lipopolysaccharide (LPS) and that the

pathways by which these two agents act upon immune cells are only partially

distinct. The present experiments assessed the ability of Zy to elicit

CNS-mediated sickness symptoms and to alter their responses to LPS. In

Experiment 1, Zy induced elements of the sickness behavior syndrome

dose-responsively in Long- rats, as indicated by reductions in

consumption of a highly palatable bait and in body temperature. In

Experiment 2, Zy exerted a priming effect, sensitizing animals to subsequent

LPS as measured by reductions in bait consumption, 24-h laboratory chow

intake, and body temperature. Experiment 3 failed to provide evidence for

LPS-to-Zy cross-tolerance but did indicate that the administration of Zy

disrupts previously acquired LPS tolerance. These results suggest that the

specifics of exposure to microbially derived innate immune activators have

to be taken into account in investigating the biologic bases of sickness

behaviors and developing models of coinfection.

PMID: 14637214 [PubMed - indexed for MEDLINE]

_________________________________________________________________

Find high-speed 'net deals - comparison-shop your local providers here.

https://broadband.msn.com

Responsibility for the content of this message lies strictly with

the original author(s), and is not necessarily endorsed by or the

opinion of the Research Institute.