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Thread: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

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    Default File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    Hello Avalon,
    I wanted to make a safe place where anyone who wants to share an autism research link can post that, and of course, discuss the papers posted.

    Since there are so many possible underlying factors being investigated, threads about autism often get derailed as people talk about more familiar assumptions and theories, and of course, the vaccination debate tends to darken some of those discussions for people who are unfamiliar with the more recent body of research in regards to de novo mutations and lack of evidence regarding whether autism is heritable.

    There was a paper in particular that I want you guys to read if and when you have time. The reason I want to talk about this here is that I trust most of you not only to leave this material safely here, but also to engage and to care about this issue, as people with autism and mental retardation often suffer a lot of discrimination when their families seek benefits from the state or federal gov'ts.

    The paper my spouse and I found is called:
    Quote
    Somatic Mutation, Genomic Variation,
    and Neurological Disease

    Annapurna Poduri, Gilad D. Evrony, Xuyu Cai, Christopher A. Walsh*

    http://www.walshlab.org/uploads/publ...viewpoduri.pdf

    Background: Genetic mutations that cause human disease are conventionally considered to be inherited from one’s parents and present in all somatic (body) cells. We do know, however, that most mutations that cause cancer arise somatically, and we are becoming increasingly aware of mutations that cause otherdiseases and that arise de novo, meaning they are undetectable inthe parents. Some such de novo mutations arise in the gamete of a parent, but some arise after fertilization during embryonic development,generating somatic mutations. Somatic mutations occur in several neurodevelopmental diseases associated with epilepsy, autism spectrum disorders, and intellectual disability, although their broader relevance for neurological disease is unknown.

    Advances: A key recent advance has been the increasing identification of somatic mutations in affected tissues. For example, somatic mutations in several genes (PIK3CA, AKT3, and mTOR) cause enlargement of just one hemisphere of the brain, a malformation called hemimegalencephaly that is highly associated with epilepsy.
    Quote A similar
    phenomenon occurs in the multisystem disorder
    tuberous sclerosis complex (TSC), a condition
    caused by mutations in the genes TSC1 and TSC2
    (33, 34), whose gene products form a protein complex together and regulate the mammalian target of rapamycin (mTOR) pathway;
    I am not going to post the whole document here and I respectfully ask that people try to copy/paste the specific parts of documents being referenced in conversation, in an effort to keep the total wordcount of the thread to a usable minimum while we talk about what's in the papers and how it affects our beliefs regarding the causation of autism.

    In regards to what I posted above from the document, I wanted to say, on my website Nuclearnuttery.com, I predicted about two years ago that autism and the mTOR pathway had something to do with each other. I had been reading about experimental vaccines and vaccine adjuvants that affect the mTOR pathway while allegedly having something to do with the AIDS cure. I wrote an article covering lots of different things, but when I found that bit about mTOR pathway, something inside told me it was a thing I needed to follow up on. And here it is, published in July 2013 LOL!

    I am actually quite hurt that my own research was taken offline. The autism articles on my website were getting 100s of reads per week at the end of the life of the blog.

    Please contribute any number of links you wish, hopefully most of them from the last few years if you don't mind, here for us to see and think about. I know for a fact that there are people out there who DO care and WANT to find a cure. It doesn't matter if eugenicists like J Craig Venter or Bill Gates would rather keep on reducing the numbers of useful people in the world. We are people too and we care more, so we are going to win against the corporations.

    I am looking forward to visiting this thread frequently and hope that anyone/everyone finds a link that will surprise me and give me food for thought. Most people don't have the knowledge to discuss these ideas, including me, but education is a process and we are all capable of learning more.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    the message i entered was too short as it was 100% quoted, lol

    Quote http://law-roundtable.uchicago.edu/s05.html
    THE UNIVERSITY OF CHICAGO LAW SCHOOL
    R O U N D T A B L E
    1 1 1 1 E A S T 6 0 T H S T R E E T
    C H I C A G O I L L I N O I S 6 0 6 3 7
    Return to Home Page
    1996 Symposium Abstracts

    Genetics and the Law: The Ethical, Legal, and Social Implications of Genetic Technology and Biomedical Ethics
    Quote http://www.walshlab.org/uploads/publ...viewpoduri.pdf

    Somatic Mutation, Genomic Variation,
    and Neurological Disease
    Annapurna Poduri, Gilad D. Evrony, Xuyu Cai, Christopher A. Walsh*
    Quote http://www.tcdb.org/search/index.php?query=&type=system

    The voltage-dependent L-type Ca2+ channel α-subunit-1C (L-type Cav1.2), CACNA1C (mutations cause Timothy's syndrome, a disorder associated with autism) (Splawski et al., 2006). The C-terminus of Cav1.2 encodes a transcription factor (Gomez-Ospina et al., 2006). Cav1.2 associates with the α-2, δ-1, β and γ subunits (Yang et al., 2011). The CRAC channel activator STIM1 binds and inhibits L-type voltage-gated calcium channel, Cav1.2 (Park et al., 2010). This channel appears to function as the molecular switch for synaptic transmission (Atlas 2013). Intramembrane signalling occurs with syntaxin 1A for catecholamine release in chromaffin cells (Bachnoff et al. 2013).

    Animals

    CACNA1C of Homo sapiens (2221 aas; Q13936)

    The voltage-dependent L-type Ca2 channel α-subunit-1H (T-type Cav3.2), CACNA1H (mutations can cause an increased propensity for autism spectrum disorders (ASD) characterized by impaired social interactions, communication skills and restricted and repetitive behaviors) (Splawski et al., 2006). Also called Cav3.2 or VSCC. Involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1H gives rise to T-type calcium currents, ''low-voltage activated'' currents blocked by nickel and mibefradil. Defective in Childhood Absence Epilepsy. Are permeated by divalent metal ions, such as Fe2 and Mn2 , and possibly Cd2 (Thévenod, 2010). Patented inhibitors of T-type calcium channels have been reviewed (Giordanetto et al. 2011).

    Animals

    CACNA1H of Homo sapiens (2353 aas; Q95180)
    Quote http://www.frontiersin.org/Cellular_...013.00028/full

    | doi: 10.3389/fncel.2013.00028
    Reversing autism by targeting downstream mTOR signaling

    Hansen Wang1* and Laurie C. Doering2*
    1Faculty of Medicine, University of Toronto, Toronto, ON, Canada
    2Department of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada
    A commentary on
    Autism-related deficits via dysregulated eIF4E-dependent translational control
    by Gkogkas, C. G., Khoutorsky, A., Ran, I., Rampakakis, E., Nevarko, T., Weatherill, D. B., et al. (2013). Nature 493, 371–377.
    Quote http://onlinelibrary.wiley.com/doi/1...omisedMessage=

    PRNP mutations in a series of apparently sporadic neurodegenerative dementias in China†

    Liu Zheng1,2, Jia Longfei1,2, Ye Jing1,2, Zhang Xinqing1,2, Song Haiqing1,2, Lv Haiyan1,2, Wang Fen1,2, Dong Xiumin1,2, Jia Jianping1,2,*
    Article first published online: 18 APR 2008

    DOI: 10.1002/ajmg.b.30761

    Copyright © 2008 Wiley-Liss, Inc.
    Quote http://www.autismspeaks.org/science/...-target-autism
    Science » Grant Search » Results » PI3K/mTOR signaling as a novel biomarker and therapeutic target in autism
    Search
    PI3K/mTOR signaling as a novel biomarker and therapeutic target in autism

    Status: Completed

    Investigator: Bassell, Gary

    Institution: Emory University

    Grant Amount: $100,000.00
    Quote https://sfari.org/funding/grants/abs...trum-disorders


    Home > Funding > Grant opportunities > Abstracts > Role of TSC/mTOR signaling pathway in autism and autism spectrum disorders
    Role of TSC/mTOR signaling pathway in autism and autism spectrum disorders
    Vijaya Ramesh, Ph.D.
    Massachusetts General Hospital


    For years, autism has been noted in individuals with tuberous sclerosis, leading researchers to speculate that the two disorders may develop after troubles in the same biological pathway. Vijaya Ramesh and her colleagues at Massachusetts General Hospital are pursuing this lead by investigating whether genes linked to tuberous sclerosis are also associated with autism spectrum disorders.

    The TOR pathway, which is named after a key protein that receives information on the cell surface, controls the growth of many cells and regulates the connections neurons make with each other. Mutations that remove regulators of the TOR pathway are associated with tuberous sclerosis. Ramesh hypothesizes that disruptions in this pathway may also cause the neuronal abnormalities that lead to autism.

    Ramesh and her colleagues are examining the genes of several components of the TOR pathway, looking for rare variations that are associated with autism. By narrowing their focus, the researchers will be able to analyze more samples drawn from the Simons Simplex Collection, with a greater attention to detail in the candidate genes. Once one mutation is linked to autism, the researchers can try to find the mutation among more people with autism to make the correlation stronger. The team will also perform assays in cultured neurons to see how the mutations affect TOR pathway activity.

    The investigators have adopted a two-tier pooling strategy wherein 10 DNA pools each of 300 patients (30 samples per pool) and 600 control samples (60 samples per pool) have been assembled. After completing sequencing of the 300 patient samples and 600 controls, the researchers plan to identify rare variations that are specific to autism samples. In future studies, they aim to confirm the identified variants in additional samples and validate these variants in functional assays using cultured neurons. This work will potentially identify novel pathways and strategies for autism treatment.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    And more on mTOR
    Quote http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075964/

    Rapamycin for treating Tuberous Sclerosis and Autism Spectrum Disorders
    Dan Ehninger and Alcino J. Silva

    Additional article information

    Abstract
    Tuberous sclerosis (TSC) is a genetic disorder caused by heterozygous mutations in the TSC1 or TSC2 genes and is associated with autism spectrum disorders (ASD) in 20–60% of cases. In addition, altered TSC/mTOR signaling is emerging as a feature common to a subset of ASD. Recent findings, in animal models, show that restoration of the underlying molecular defect can improve neurological dysfunction in several of these models, even if treatment is initiated in adult animals, suggesting that pathophysiological processes in the mature brain contribute significantly to the overall neurological phenotype in these models. These findings suggest that windows for therapeutic intervention in ASD may be wider than thought previously.

    Keywords: Tuberous sclerosis, TSC, mTOR, autism, ASD, rapamycin, pharmacology, treatment

    Quote http://medicalxpress.com/news/2013-0...disorders.html
    HomeNeuroscienceJune 3, 2013
    Researchers have found new role for mTOR in autism-related disorders
    by Shraddha Chakradhar

    (Medical Xpress)—Researchers have found a novel role for a protein that has been implicated in an autism-related disorder known as tuberous sclerosis complex (TSC).
    The disease, which affects 1 in about 8,000 children, manifests itself in the form of mental retardation in addition to severe epileptic episodes. The disease is caused by mutations in two tumor-suppressing proteins, TSC1 and TSC2.
    "Kids with this condition have benign tumors that grow all over the body," said Bernardo Sabatini, the Takeda Professor of Neurobiology at Harvard Medical School and senior author of the study, "but we wanted to know what happened in the brain."
    The researchers found that when mutations in TSC1 and TSC2 adversely affected a third protein, mTOR, this mutation increased brain activity, which can result in epileptic seizures.

    The findings were published in the May 8 issue of Neuron.
    A protein kinase, mTOR is responsible for controlling cell growth in many parts of the body and has been widely implicated in epilepsy and autism. TSC1 and TSC2 normally repress the activity of mTOR to keep cell growth in check. In the case of TSC, there are mutations in TSC1 or TSC2, and mTOR's ability to promote cell growth goes unchecked, resulting in tumors in regularly dividing cells.

    "But neurons don't divide," said Sabatini. "So it was important to note the changes in these non-dividing cells."
    The researchers hypothesized that mTOR's function in the brain related to homeostasis, the brain's ability to maintain a controlled level of electrical activity. When there's a lot of electrical activity, a negative feedback system switches on to suppress activity. Conversely, when levels are too low, other positive feedback pathways are engaged that bring the activity level back up.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    infantile spasms

    Quote http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075964/

    Epilepsy is also an important and common clinical feature of TSC and affects approximately 70–80% of subjects over their lifetime [90, 93]. Infantile spasms, a form of early childhood epilepsy, are diagnosed in approximately 50% of individuals with TSC [90, 93] and constitute a risk factor for ASD. Psychiatric disorders, including depression and anxiety, are also frequently encountered in TSC populations [13, 94].

    Quote http://community.babycenter.com/post...fantile_spasms

    Vaccines and Infantile Spasms

    Bookmark it

    SunkistSweete
    Posted 04/12/2011
    I posted this on the non-vaxing board too but I wanted to get a lot of opinions so Im posting here as well.

    My friend just called me and told me that her son was diagnosed with infantile spasms.� He just received his 6 month shots last week and started showing symtoms on Saturday.� She took him to the ped yesterday after he had a severe spasm and his eyes rolled back into his head and they sent her to the hosptial.� From what I have been able to research there is a link between the DTaP shot and infantile spasms, but of course doctors will deny this.� I had talked to her about vaccine dangers before he was born and she did not want to vaccinate, but her husband was totally opposed to that.� She has decided to discontinue vaccines and now that this has happened he agreed.� Does anyone have any information or evidence on the link between vaccines and infantile spasms or has anyone encountered this before with a vaxed child?

    --
    TTC #1 since 9/10 M/C 3/11/11 at 6 weeks 2 days

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    Thought you might be interested in Keri Riverra's success with autism. Search on her name or mms and autism. Some awesome testimonials. I'd put you some links but they probably wouldn't go anywhere.

    A total of 100 children have been recovered (ATEC score of 10 or below,) using the CD Autism parasite protocol published in Kerri Rivera´s new book Healing the Symptoms Known as Autism.

    CD = Chlorine Dioxide, the active ingredient of MMS1.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    http://www.autismspeaks.org/news/new...eatment-autism
    http://www.autismspeaks.org/science/...nsory-overload
    Quote However, these effects could be blocked by treating the PTEN-deficient mice with rapamycin, a powerful immune-system suppressant most commonly prescribed to prevent organ rejection. In examining the animal’s brain tissues, the researchers found that the drug prevented the abnormal increase in cell interconnections otherwise seen in PTEN-deficient mice (image above).

    “While this study is exciting, we need to know more before it would be appropriate to use rapamycin as a treatment for individuals with autism,” adds Joe Horrigan, M.D., Autism Speaks head of medical research. “Safety considerations are of paramount importance as rapamycin can increase susceptibility to infections and malignancies such as lymphoma. At present, it should be prescribed only by physicians experienced in immunosuppressive therapy.”

    http://clinicaltrials.gov/ct2/show/NCT01929642
    Quote Rapamycin for Autism Phenotype in TSC: A Feasibility Study (RAPT)
    This study is currently recruiting participants.
    Verified August 2013 by Hugo W. Moser Research Institute at Kennedy Krieger, Inc.
    Sponsor:
    Hugo W. Moser Research Institute at Kennedy Krieger, Inc.
    Information provided by (Responsible Party):
    Tanjala Gipson, Hugo W. Moser Research Institute at Kennedy Krieger, Inc.
    ClinicalTrials.gov Identifier:
    NCT01929642
    First received: August 7, 2013
    Last updated: August 28, 2013
    Last verified: August 2013
    History of Changes
    Full Text View Tabular ViewNo Study Results PostedDisclaimerHow to Read a Study Record
    Purpose
    The purpose of this study is to assess the feasibility and safety of administering sirolimus in participants with Tuberous Sclerosis Complex (TSC) and self-injury and to measure cognitive and behavioral changes, including reduction in autistic symptoms, self-injurious and aggressive behaviors, as well as improvements in cognition across multiple domains of cognitive function.
    http://www.ncbi.nlm.nih.gov/pubmed/23250422
    Quote Nat Commun. 2012;3:1292. doi: 10.1038/ncomms2295.
    Rapamycin reverses impaired social interaction in mouse models of tuberous sclerosis complex.
    Sato A, Kasai S, Kobayashi T, Takamatsu Y, Hino O, Ikeda K, Mizuguchi M.
    Source
    Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156 8506, Japan.
    Abstract
    Impairment of reciprocal social interaction is a core symptom of autism spectrum disorder. Genetic disorders frequently accompany autism spectrum disorder, such as tuberous sclerosis complex caused by haploinsufficiency of the TSC1 and TSC2 genes. Accumulating evidence implicates a relationship between autism spectrum disorder and signal transduction that involves tuberous sclerosis complex 1, tuberous sclerosis complex 2 and mammalian target of rapamycin. Here we show behavioural abnormalities relevant to autism spectrum disorder and their recovery by the mammalian target of rapamycin inhibitor rapamycin in mouse models of tuberous sclerosis complex. In Tsc2(+/-) mice, we find enhanced transcription of multiple genes involved in mammalian target of rapamycin signalling, which is dependent on activated mammalian target of rapamycin signalling with a minimal influence of Akt. The findings indicate a crucial role of mammalian target of rapamycin signalling in deficient social behaviour in mouse models of tuberous sclerosis complex, supporting the notion that mammalian target of rapamycin inhibitors may be useful for the pharmacological treatment of autism spectrum disorder associated with tuberous sclerosis complex and other conditions that result from dysregulated mammalian target of rapamycin signalling.
    PMID: 23250422 [PubMed - indexed for MEDLINE] PMCID: PMC3535343 Free PMC Article
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607786/
    Quote Reversing autism by targeting downstream mTOR signaling
    Hansen Wang and Laurie C. Doering

    Additional article information

    Autism spectrum disorders (ASDs) are a group of clinically and genetically heterogeneous neurodevelopmental disorders characterized by impaired social interactions, repetitive behaviors and restricted interests (Baird et al., 2006; Zoghbi and Bear, 2012). The genetic defects in ASDs may interfere with synaptic protein synthesis. Synaptic dysfunction caused by aberrant protein synthesis is a key pathogenic mechanism for ASDs (Kelleher and Bear, 2008; Richter and Klann, 2009; Ebert and Greenberg, 2013). Understanding the details about aberrant synaptic protein synthesis is important to formulate potential treatment for ASDs. The mammalian target of the rapamycin (mTOR) pathway plays central roles in synaptic protein synthesis (Hay and Sonenberg, 2004; Hoeffer and Klann, 2010; Hershey et al., 2012). Recently, Gkogkas and colleagues published exciting data on the role of downstream mTOR pathway in autism (Gkogkas et al., 2013) (Figure ​(Figure11).


    Previous studies have indicated that upstream mTOR signaling is linked to ASDs. Mutations in tuberous sclerosis complex (TSC) 1/TSC2, neurofibromatosis 1 (NF1), and Phosphatase and tensin homolog (PTEN) lead to syndromic ASD with tuberous sclerosis, neurofibromatosis, or macrocephaly, respectively (Kelleher and Bear, 2008; Bourgeron, 2009; Hoeffer and Klann, 2010; Sawicka and Zukin, 2012). TSC1/TSC2, NF1, and PTEN act as negative regulators of mTOR complex 1 (mTORC1), which is activated by phosphoinositide-3 kinase (PI3K) pathway (Kelleher and Bear, 2008; Auerbach et al., 2011; Sawicka and Zukin, 2012) (Figure ​(Figure1).1). Activation of cap-dependent translation is a principal downstream mechanism of mTORC1. The eIF4E recognizes the 5′ mRNA cap, recruits eIF4G and the small ribosomal subunit (Richter and Sonenberg, 2005; Hershey et al., 2012). The eIF4E-binding proteins (4E-BPs) bind to eIF4E and inhibit translation initiation.
    http://questioning-answers.blogspot....nd-autism.html
    http://asdresearchinitiative.wordpre...-mtor-pathway/
    Quote Autism , Epilepsy, Tuberous Sclerosis and the mTOR pathway
    Posted on March 2, 2013 by researchinitiative
    Autism, epilepsy and tuberous sclerosis complex: a functional model linked to mTOR pathway.

    http://www.ncbi.nlm.nih.gov/pubmed/23446718

    Hospital Infantil Universitario Nino Jesus, 28009 Madrid, Espana.

    Abstract

    INTRODUCTION.

    Tuberous sclerosis complex (TSC) is an autosomal dominant disorder that results from mutations in the TSC1 or TSC2 genes and is associated with hamartoma formation in multiple organ systems. Brain disorders are the origin of more frequent and severe problems and include infantile spasms, intractable epilepsy, brain tumors, cognitive disabilities, and autism. TSC1 or TSC2 encoded proteins modulate cell function via the mTOR signaling cascade and serve as keystones in regulating cell growth and proliferation.

    AIM.

    To review the etiopathogenic mechanisms and the natural course of the association of autism and epilepsy in TSC.

    DEVELOPMENT.

    Both the clinical and the neuroimaging findings of TSC, including early onset epilepsy and the localization of cortical tubers in the temporal lobes, and the molecular understanding of the mTOR signaling pathway, not only involved in cell growth, but also in synaptogenesis, synaptic plasticity and neuronal functioning, have suggested a multimodal origin of autism in these patients.

    CONCLUSIONS. A greater understanding of the pathogenetic mechanisms underlying autism in TSC could help in devising targeted and potentially more effective treatment strategies. Antagonism of the mTOR pathway with rapamycin and everolimus may provide new therapeutic options for these TSC patients.

    ——————-

    Neural connectivity abnormalities in autism: Insights from the tuberous sclerosis model.

    http://www.ncbi.nlm.nih.gov/pubmed/23445933

    Autism Spectrum Disorder (ASD) is a behavioral syndrome caused by complex genetic and non-genetic risk factors. It has been proposed that these risk factors lead to alterations in the development and ‘wiring’ of brain circuits and hence, the emergence of ASD.

    Although several lines of research lend support to this theory, etiological and clinical heterogeneity, methodological issues and inconsistent findings have led to significant doubts. One of the best established, albeit rare, causes of ASD is the genetic condition Tuberous Sclerosis Complex (TSC), where 40% of individuals develop ASD.

    A recent study by Peters and Taquet et al. analyzed electroencephalography (EEG) data using graph theory to model neural ‘connectivity’ in individuals with TSC with and without ASD and cases with ‘idiopathic’ ASD. TSC cases exhibited global under-connectivity and abnormal network topology, whereas individuals with TSC + ASD demonstrated similar connectivity patterns to those seen in individuals with idiopathic ASD: decreased long- over short-range connectivity.

    The similarity in connectivity abnormalities in TSC + ASD and ASD suggest a common final pathway and provide further support for ‘mis-wired’ neural circuitry in ASD. The origins of the connectivity changes, and their role in mediating between the neural and the cognitive / behavioral manifestations, will require further study. Please see related research article here http://www.biomedcentral.com/1741-7015/11/54.

    ———————–

    Brain functional networks in syndromic and non-syndromic autism: a graph theoretical study of EEG connectivity.

    http://www.ncbi.nlm.nih.gov/pubmed/23445896
    BACKGROUND:

    Graph theory has been recently introduced to characterize complex brain networks, making it highly suitable to investigate altered connectivity in neurologic disorders.

    A current model proposes autism spectrum disorder (ASD) as a developmental disconnection syndrome, supported by converging evidence in both non-syndromic and syndromic ASD. However, the effects of abnormal connectivity on network properties have not been well studied, particularly in syndromic ASD. To close this gap, brain functional networks of electroencephalographic (EEG) connectivity were studied through graph measures in patients with Tuberous Sclerosis Complex (TSC), a disorder with a high prevalence of ASD, as well as in patients with non-syndromic ASD.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    SV40 MAY BE CAUSING MTOR CHANGES IN AUTISM

    http://jvi.asm.org/content/79/11/6882

    Quote Effects of Simian Virus 40 Large and Small Tumor Antigens on Mammalian Target of Rapamycin Signaling: Small Tumor Antigen Mediates Hypophosphorylation of eIF4E-Binding Protein 1 Late in Infection
    Yongjun Yu, Sagar B. Kudchodkar, and James C. Alwine*
    + Author Affiliations

    Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania 19104-6142
    ABSTRACT

    We report that late in a simian virus 40 (SV40) infection in CV-1 cells, there are significant decreases in phosphorylations of two mammalian target of rapamycin (mTOR) signaling effectors, the eIF4E-binding protein (4E-BP1) and p70 S6 kinase (p70S6K). The hypophosphorylation of 4E-BP1 results in 4E-BP1 binding to eIF4E, leading to the inhibition of cap-dependent translation. The dephosphorylation of 4E-BP1 is specifically mediated by SV40 small t antigen and requires the protein phosphatase 2A binding domain but not an active DnaJ domain. Serum-starved primary African green monkey kidney (AGMK) cells also showed decreased phosphorylations of mTOR, 4E-BP1, and p70S6K at late times in infection (48 h postinfection [hpi]). However, at earlier times (12 and 24 hpi), in AGMK cells, phosphorylated p70S6K was moderately increased, correlating with a significant increase in phosphorylation of the p70S6K substrate, ribosomal protein S6. Hyperphosphorylation of 4E-BP1 at early times could not be determined, since hyperphosphorylated 4E-BP1 was present in mock-infected AGMK cells. Elevated levels of phosphorylated eIF4G, a third mTOR effector, were detected in both CV-1 and AGMK cells at all times after infection, indicating that eIF4G phosphorylation was induced throughout the infection and unaffected by small t antigen. The data suggest that during SV40 lytic infection in monkey cells, the phosphorylations of p70S6K, S6, and eIF4G are increased early in the infection (12 and 24 hpi), but late in the infection (48 hpi), the phosphorylations of mTOR, p70S6K, and 4E-BP1 are dramatically decreased by a mechanism mediated, at least in part, by small t antigen.

    FOOTNOTES

    Received 22 December 2004.
    Accepted 7 February 2005.
    ↵*Corresponding author. Mailing address: 314 Biomedical Research Building, 421 Curie Blvd., University of Pennsylvania, Philadelphia, PA 19104-6142. Phone: (215) 898-3256. Fax: (215) 573-3888. E-mail: alwine@mail.med.upenn.edu.

    http://en.wikipedia.org/wiki/SV40

    Quote SV40 is an abbreviation for Simian vacuolating virus 40 or Simian virus 40, a polyomavirus that is found in both monkeys and humans. Like other polyomaviruses, SV40 is a DNA virus that has the potential to cause tumors, but most often persists as a latent infection.

    SV40 became a highly controversial subject after it was revealed that millions were exposed to the virus after receiving a contaminated polio vaccine produced between 1955 and 1961.[1]
    http://www.ncbi.nlm.nih.gov/pubmed/20345322

    Quote J Neurovirol. 2010 Mar;16(2):141-9. doi: 10.3109/13550281003685839.
    Association of autism with polyomavirus infection in postmortem brains.
    Lintas C, Altieri L, Lombardi F, Sacco R, Persico AM.
    Source
    Laboratory of Molecular Psychiatry and Neurogenetics, University Campus Bio-Medico, Rome, Italy.
    Abstract
    Autism is a highly heritable behavioral disorder. Yet, two decades of genetic investigation have unveiled extremely few cases that can be solely explained on the basis of de novo mutations or cytogenetic abnormalities. Vertical viral transmission represents a nongenetic mechanism of disease compatible with high parent-to-offspring transmission and with low rates of disease-specific genetic abnormalities. Vertically transmitted viruses should be found more frequently in the affected tissues of autistic individuals compared to controls. Our initial step was thus to assess by nested polymerase chain reaction (PCR) and DNA sequence analysis the presence of cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV1), herpes simplex virus type 2 (HSV2), human herpes virus 6 (HHV6), BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) in genomic DNA extracted from postmortem temporocortical tissue (Brodmann areas 41/42) belonging to 15 autistic patients and 13 controls. BKV, JCV, and SV40 combined are significantly more frequent among autistic patients compared to controls (67% versus 23%, respectively; P < .05). The majority of positives yielded archetypal sequences, whereas six patients and two controls unveiled single-base pair changes in two or more sequenced clones. No association is present with the remaining viruses, which are found in relatively few individuals (N <or= 3). Also polyviral infections tend to occur more frequently in the brains of autistic patients compared to controls (40% versus 7.7%, respectively; P = .08). Follow-up studies exploring vertical viral transmission as a possible pathogenetic mechanism in autistic disorder should focus on, but not be limited to, the role of polyomaviruses.
    Comment in
    Polyomaviruses and autism: more than simple association? [J Neurovirol. 2010]
    PMID: 20345322 [PubMed - indexed for MEDLINE]
    Publication Types, MeSH Terms, Substances
    LinkOut - more resources

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    Here is one more for the file

    https://goodhealthhelpdesk.com/index...to-cure-autism

    Jul
    30

    It takes Guts to Cure Autism.
    Posted by Pedro Alvarez on 30 July 2013 07:06 PM



    Health News (Week 30 - 2013)
    By Robert Redfern

    Of course I am not talking about bravery or determination but a healthy digestive system.

    As well as Autism, I also include ADHD, ADD and Asperger’s – these are all other manifestations of a Gut/Brain disorder. The knowledge of this is not new (how the brain is linked to the gut). Hippocrates in ancient Greece said, “let food be thy medicine and medicine be thy food”.

    There have been many studies on Autism and the digestive system. James Adams -- director of just one Autism/Asperger's Research Program said "One of the reasons we started addressing this topic is the fact that autistic children have a lot of GI problems that can last into adulthood," and Krajmalnik-Brown (a researcher for the program) said: "Studies have shown that when we manage these problems, their behavior improves dramatically."

    There is no possible solution without a full diet change and this is especially difficult for Gut/Brain disorders as the determination needed to achieve a healthy gut is undermined by an abnormal fixation with unhealthy foods. Change is difficult for most human beings but it seems almost impossible for those with a Gut/Brain disorder or those caring for sufferers.

    Especially children.

    It is estimated that 15 years ago, around 1 in 10,000 kids had autism in the U.S.

    Now it is estimated to be 1 in 50.

    At this rate, what will it be in another 15 years’ time?

    I know I’ve suffered from many of the symptoms of a Gut/Brain disorder and still do if I fall off the ‘healthy food wagon’. Many people feel like they are suffering, but also find it isn’t easy to change their diet – even if their life depends upon it. That’s because it can be difficult for some to change a lifetime of poor dietary choices.

    The topic for this week’s newsletter came to me while watching a programme of a guy whose health was so bad he decided to consume only juiced vegetables and fruits for 60 days.

    Not only did he lose lots of weight, get off his prescription drugs and look much healthier but one of his employees in his business pointed out his thinking and clarity of decision making had considerably improved.

    I have no doubt that since he was only eating (juicing) raw fresh foods he was also taking in friendly bacteria as well as feeding the existing friendly bacteria which would accelerate his recovery (plus he had cut out dairy, carbs etc). Maybe the simple solution is to do anything we can to improve our gut, then everything after that may become much easier?

    Easy steps for a healthy Gut/Brain (all supported by studies), include:

    Taking a powerful Probiotic such as Prescript Assist, which can be opened and mixed with any food. Studies show the brain is affected positively with this
    Taking specific relaxation supplements such as RelaxWell, to help with the anxiety that change causes and for a more relaxed sleep (opened and mixed for easy use).
    Taking critical nutrients missing from the diet including Nascent Iodine Drops (4 drops x 4 times per day in a little water), and a good multivitamin such as Active Life (90 liquid vitamins in one)/MaxiVision containing selenium as a critical co-factor of Iodine.
    Taking Coconut Oil for its effective MCT's is helpful and is good for mixing in foods such as ‘Paleo cookies’.
    Krill Oil, Fish Oil complex or Hemp Oil for vegans.
    Ancient Minerals Magnesium OIL Lotion
    A better alternative is Magnesium Oil with added plant derived Melatonin (see studies at end)
    Diet is the one solution that will make the biggest change. The diet that makes a dramatic difference is the ‘My Really Healthy Foods’ diet. There are lots of other recipes on the internet and you can find them by searching on ‘Ketogenic’ recipes and ‘Paleo’ recipes.

    When it comes to children, get the mixing bowl out and start making the ‘Olivia's Choclate Brownies’ and ‘Ann’s Chocolate Cake’. There are many delicious desserts that will help to sweeten the change!

    Please help by sending me your ‘Really Healthy Foods’ ideas that a child suffering with Gut/Brain disorder may find acceptable. Email this directly to me.

    Questions and advice should come via Contact Me at the top, Robert’s Questions and then Next.


    With kind regards,


    Robert Redfern
    Nutritionalist, Author & Broadcaster
    www.GoodHealthHelpDesk.com


    PS.
    The initial cause of Gut/Brain disorders arises from lack of friendly bacteria available at birth or in the first year. It is also likely to be compounded by vaccinations, the latest studies confirm. The good news it is a dysfunction - not a life sentence.

    Studies:
    Iodine Deficiency Linked to Autisim In a number of countries with reported increases in autism there has been a concomitant increase in the prevalence of iodine deficiency.
    (3 4 5) Another line of evidence is the effect of iodine deficiency on brain development and the findings in some children with autism. Iodine deficiency during the prenatal period has been associated with a number of adverse effects on the brain resulting in a continuum of effects from mild to severe depending on the degree of iodine deficiency, from lowered IQ to severe mental retardation, i.e., cretinism. The mechanism of iodine deficiency is that insufficient levels of iodine lead to an imbalance in thyroid hormone metabolism with a decrease in circulating thyroxin (T4) in both the pregnant mother and the fetus. This results in irreversible changes in brain architecture such as less dense neural connections.
    (6) It has been reported that some children with autism have “underconnectivity” in certain regions of the brain.
    (7) http://www.bmj.com/rapid-response/20...y-cause-autism

    According to World Health Organization, in 2007, nearly 2 billion individuals had insufficient iodine intake, a third being of school age. ... Thus iodine deficiency, as the single greatest preventable cause of mental retardation, is an important public-health problem."

    Melatonin for sleep in children with autism: a controlled trial examining dose, tolerability, and outcomes. Malow B, Adkins KW, McGrew SG, Wang L, Goldman SE, Fawkes D, Burnette C.
    Source
    Sleep Disorders Division, Department of Neurology and Kennedy Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. beth.malow@vanderbilt.edu Supplemental melatonin has shown promise in treating sleep onset insomnia in children with autism spectrum disorders (ASD). Twenty-four children, free of psychotropic medications, completed an open-label dose-escalation study to assess dose-response, tolerability, safety, feasibility of collecting actigraphy data, and ability of outcome measures to detect change during a 14-week intervention. Supplemental melatonin improved sleep latency, as measured by actigraphy, in most children at 1 or 3 mg dosages. It was effective in week 1 of treatment, maintained effects over several months, was well tolerated and safe, and showed improvement in sleep, behavior, and parenting stress. Our findings contribute to the growing literature on supplemental melatonin for insomnia in ASD.
    Last edited by sheme; 19th October 2013 at 18:01.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    http://www.autismspeaks.org/science/...thology-autism

    Glia Pathology in Autism

    Status: Completed

    Investigator: Ordway, Gregory

    Institution: East Tennessee State University

    Grant Amount: $119,663.00

    Grant Term: 2 years

    Award Type: Pilot

    City: Johnson City

    State: TN

    Country: United States

    Year: 2010

    Website: http://www.etsu.edu

    Description
    It is inherently difficult to devise targeted treatment for autism when little is known about how the brain is different in individuals with autism versus neurotypical individuals. The development of better treatments for autism will be facilitated greatly by the identification of precise molecular pathology of the human brain in individuals with autism. Several previous studies of individuals with autism have shown that there is reduced activity in a specific brain region called the anterior cingulate cortex, an area of the brain that regulates social interaction. This area of the brain has a complex circuitry that involves among others, two principal cellular players, glial cells and pyramidal neurons. Glial cells are often considered to be helper cells to neurons. However, many recent advances have shown that several brain disorders are characterized by pathology of glia, and numerous studies demonstrate that glia play a major role in the transmission of information between neurons in the brain. This study will examine a specific type of glia, astrocytes, in the anterior cingulate cortex. The investigators believe that circuitry dysfunction in the anterior cingulate cortex may underlie disruption of social interactions, a core feature of autism. Since astrocytes play a major role in regulating neurotransmission in the cortex, and because there is evidence of deficits in astrocyte markers in autism, the specific hypothesis of this proposal is that glial dysfunction in autism directly contributes to altered neurotransmission in anterior cingulate cortex. This pilot study measures the levels of expression several genes that will provide an index of neurotransmission in the anterior cortex. Gene expression in two distinct cell types in the brain will be studied using a high technology method of laser capture microdissection along with traditional molecular biological techniques. The research represents a novel exploration of non-neuronal elements (i.e., astrocytes) of neural transmission in autism, and has the potential to facilitate the identification of new specific molecular pathologies. Knowledge of these pathologies will contribute directly or indirectly to the development of novel and improved treatments for autism.


    http://sfari.org/news-and-opinion/co...ytes-to-autism

    Video: Connecting astrocytes to autism
    E-mail Print Share This Virginia Hughes
    13 October 2012
    The great majority of researchers studying the neuroscience of autism focus on neurons, brain cells that pass messages to each other via chemical and electrical signals. That makes sense, as many genes linked to the disorder function at the synapse, or junction between neurons.

    But neurons make up just ten percent of cells in the human brain. The rest, called glia — from the Greek word for glue — were for decades thought of simply as support cells for neurons.

    In the past few years, however, researchers have discovered that glia play a direct role in cell communication and are involved in many brain disorders, including autism-related syndromes.

    Take, for example, the star-shaped glia called astrocytes, which wrap themselves around synapses. In 2005, Ben Barres’s team at Stanford University showed that developing neurons must be in the presence of astrocytes (or the chemicals they secrete) in order to form synapses. “Glia are literally acting as an on/off switch for synapse formation,” Barres says.

    SFARI.org sat down with Barres on Saturday morning at the 2012 Society for Neuroscience annual meeting in New Orleans. Barres talked about a new project in which he and colleague Ricardo Dolmetsch are studying astrocytes in culture by reprogramming stem cells from children with autism.




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

    There are various explanations why liver dysfunction or portosystemic shunting might lead to encephalopathy. In healthy subjects, nitrogen-containing compounds from the intestine, generated by gut bacteria from food, are transported by the portal vein to the liver, where 80–90% is metabolised through the urea cycle and/or excreted immediately. This process is impaired in all subtypes of hepatic encephalopathy, either because the hepatocytes (liver cells) are incapable of metabolising the waste products or because portal venous blood bypasses the liver through collateral circulation or a medically constructed shunt. Nitrogenous waste products accumulate in the systemic circulation (hence the older term "portosystemic encephalopathy"). The most important waste product is ammonia (NH3). This small molecule crosses the blood–brain barrier and is absorbed and metabolised by the astrocytes, a population of cells in the brain that constitutes 30% of the cerebral cortex. Astrocytes use ammonia when synthesising glutamine from glutamate. The increased levels of glutamine lead to an increase in osmotic pressure in the astrocytes, which become swollen. There is increased activity of the inhibitory γ-aminobutyric acid (GABA) system, and the energy supply to other brain cells is decreased. This can be thought of as an example of brain oedema of the "cytotoxic" type.[11]

    Despite numerous studies demonstrating the central role of ammonia, ammonia levels don't always correlate with the severity of the encephalopathy; it is suspected that this means that more ammonia has already been absorbed into the brain in those with severe symptoms whose serum levels are relatively low.[1][2] Other waste products implicated in hepatic encephalopathy include mercaptans (substances containing a thiol group), short-chain fatty acids and phenol.[2]

    Numerous other abnormalities have been described in hepatic encephalopathy, although their relative contribution to the disease state is uncertain. Benzodiazepine-like compounds have been detected at increased levels as well as abnormalities in the GABA neurotransmission system. An imbalance between aromatic amino acids (phenylalanine, tryptophan and tyrosine) and branched-chain amino acids (leucine, isoleucine and valine) has been described; this would lead to the generation of false neurotransmitters (such octopamine and 2-hydroxyphenethylamine). Dysregulation of the serotonin system, too, has been reported. Depletion of zinc and accumulation of manganese may play a role.[1][2] Inflammation elsewhere in the body may precipitate encephalopathy through the action of cytokines and bacterial lipopolysaccharide on astrocytes.[4]

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    http://questioning-answers.blogspot....mmonia-in.html

    Views on autism research and other musings.

    Friday, 27 April 2012

    Short chain fatty acids and ammonia in autism
    It is perhaps apt that Jon Brock over at Cracking the Enigma recently posted about the Australasian Society for Autism Research highlighting the various links being forged regarding autism research in that part of the world. Apt because there are several very good autism research groups producing findings which have some potential real-world application to autism, in that part of the World. I speak in particular of the team based at the Sansom Institute for Health Research based at the University of South Australia. Members of UNISA recently publishing a fine review of how glutathione and relations show quite a consistent relationship to cases of autism. Autism research movers and shakers please take note.

    Indeed another paper published by Wang and colleagues* adds to the repertoire, suggesting that levels of fecal short chain fatty acids (SCFAs) and ammonia were higher in their cohort of children with autism compared to asymptomatic controls and hence showing alteration in the fermentation process.

    As a sort of introduction to SCFAs and fermentation, readers might find this article by Topping & Clifton** (full-text) and this article by Macfarlane & Macfarlane*** (full-text) to be of interest. Basically, think carbohydrates and gut bacteria and eventually you head the direction of SCFAs. If you happen to brew your own beer, fermentation might not necessarily be a strange concept alongside memories of 'auto-brewery syndrome' (not personal memories I might add).

    Unfortunately I can't post a link to the full-text but here are a few details:

    Based on the collective studies of Dr Wang's PhD (scroll down to see her thesis details), this study looked at fecal specimens from a relatively small group: 23 children (mean age ~ 10 years) diagnosed with ASD compared with 31 age-matched controls.
    Although not everyone's choice of biological medium to work with, fecal samples - as in poo samples - were analysed via various methods including colorimetry (ammonia) and gas chromatography (SCFAs). Other compounds such as p-cresol were analysed via liquid chromatography.
    Results: fecal concentrations of total SCFAs were elevated in autism samples (p=0.012) as were levels of ammonia (p=0.007). Interestingly no elevation was observed in levels of p-cresol in autism samples as has previously been described.
    More specifically with individual SCFAs, some interesting compounds cropped up as being elevated in autism samples including: propionic acid, butyric and isobutyric acids and valeric and isovaleric acids. Indeed out of the battery of SCFAs analysed, only caproic acid showed no significant difference between the groups.
    The authors conclude that fecal levels of these large bowel fermentation products might tie into the accompanying gastrointestinal (GI) findings observed in some children with autism and differences in the bacteria inhabiting the darkest recesses.

    There are some obvious caveats to accompany this latest study. Aside from participant numbers being relatively small and covering quite a lot of chronological age in childhood, and the slight discrepancy in controlling for gender, there was quite a bit of 'overlap' when it came to individual results from the autism and control groups. Indeed if I were to criticise at all, I perhaps would have like to have seen some plotted information on the dispersion of values obtained from individuals just to visualise and ensure that results were not skewed by a few outlier results. As has however been discussed recently, outliers in a heterogeneous condition like autism are very often a source of great interest.

    This is not the first time that the words 'autism' and 'fermentation' have come to my attention. Quite a few years back I remember some interesting work being done at Cranfield University by Maria Pilar Bilbao Montoya as part of her higher studies. Working with gastroenterologist, John Hunter, Maria presented some initial work suggesting similar things in their cohort I believe. I might be wrong but I also remember that Dr Sophie Rosseneu might have had some unpublished work in this area also as a tie up with her findings on yeasts and autism?

    Memories aside, there are some interesting points to take from this research. SCFAs such as propionic acid (PA) have recently been seen in the autism research arena as per this paper (full-text) by El-Ansary and colleagues looking at what happens when you inject rats with PA in sizeable quantities. For those of you who are unimpressed with the proposed PA-gut-brain link, maybe a few other choice papers might be useful, here and here. And perhaps some evidence for the presence of PA in other biological fluids from cases of autism?

    I've talked ammonia before on this blog with reference to some mitochondrial findings. Wang and colleagues look more to the GI effects of ammonia given that it was detected in stool samples and how this might tie into issues with gut permeability so commonly discussed. Indeed ammonia - the whole nitrogen balance - takes us back to some old friends, glutamine and glutamate, one of which has been making quite a bit of news lately (here's the paper abstract).

    The big question has to be why the reported differences in this latest study? I can't give a specific answer to this question but given the interest in carbohydrate metabolism and autism, the suggestion of things like lactose intolerance, added to the growing research base on gut bacteria and autism, one has to suspect that the answer might lie, partially at least, somewhere in these regions.

    * Wang L. et al. Elevated fecal short chain fatty acids and ammonia concentrations in children with autism spectrum disorder. Digestive Diseases and Sciences. April 2012
    DOI: 10.1007/s10620-01202167-7

    ** Topping DL. & Clifton PM. Short-Chain Fatty Acids and Human Colonic Function: Roles of Resistant Starch and Nonstarch Polysaccharides. Physiological Reviews. 2001; 81: 1031-1064

    *** Macfarlane S. & Macfarlane GT. Regulation of short chain fatty acid production. Proceedings of the Nutrition Society. 2003; 62: 67-72
    Posted by Paul Whiteley at 12:53












    http://articles.mercola.com/sites/ar...nutrition.aspx



    Autism and Malnutrition: The Milk Connection
    June 26, 2004 | 17,327 views


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    By Linda Carlton
    To understand autism we can begin this journey from what we have learned about how seemingly insignificant dietary changes can affect newborn primates. In October 1975, three Japanese scientists raised a group of infant primates. By artificial nursing, these primates were fed a casein powdered milk formula. When they modified the infant formula to reduce the content of protein and increased the lactose to supplement the appropriate number of calories, the primate infants developed abnormal behaviors such as stereotype rocking, fear, aggression, head banging and other autistic-like behaviors. Completely unaware of what they had discovered, the scientists had induced autism in a clinical setting.

    Now, they were aware that by reducing the protein content they caused the infants to become malnourished. They also observed that without human contact some infants were much more impaired. They learned that the infants that received the standard solution were reared successfully. At that time they concluded that a protein deficiency had caused a decline in physical and mental growth. Subsequent studies have supported this, whereby protein deficiency does cause developmental delay.

    Autism Versus Developmental Delay

    But it is important to know which symptoms are truly autistic and which are that of developmental delay. These disorders are often used interchangeably, but they are very different. For example, hand flapping is an autistic symptom, but it is not a common characteristic of developmental delay. In developmental delay children are often slow to learn, and will quickly fall behind their peers. The symptoms of these primates were more than just symptoms of developmental delay--they were symptoms of autism.

    The most important information we have about these infant primates is that the researchers had also increased the lactose content in their diet. If the quantity of protein matched that of the quantity of lactose, this might not have occurred, or it might also have occurred if they had been fed too much protein. The standard formula given to the infant primates that were reared successfully were given the same amount of lactose, and what would have been the normal amount of protein for these size mammals.

    Lactose and Autism

    Lactose is the key to unraveling what happened to these infants. Bacteria use lactose, or milk sugar, as a nutrient base. Bifidobacteria and clostridia use lactose, and they often describe these strains of bacteria as lactose-fermenting bacteria. One difference in Bifidobacteria and Clostridia is that only one can produce significant amounts of ammonia, only one can damage the intestines. Milk oligosaccharides contain lactose; they are fermented in the infant colon where they selectively stimulate the growth of Bifidobacteria. Clostridia are competitors of Bifidobacteria, and Clostridia produce ammonia. Ammonia and only ammonia produced from bacteria could have caused the aberrant behaviors.

    The infant primates had developed symptoms of autism because there was protein restriction, milk proteins needed for ammonia detoxification, and not necessarily just casein. They were fed lactose and lactose ferments ammonia, producing bacteria. They were unable to detoxify on a protein-deficient diet. It is a simple formula:

    Protein + Lactose = Normal Development
    Low protein + High Lactose = Autism

    But protein malnutrition does not equal autism nor does lactose feeding equal autism. However,

    Protein malnutrition + high-lactose feeding + (the unknown factor) = Autism

    There has to be an unknown factor for this to occur, a combination of things that all relate to one another. The unknown factor can be found by testing these three variables. We have to review other information that we have on children with autism to give us the correct answer to the unknown factor.

    A low-protein diet offsets a nitrogen balance to detoxify ammonia, whereas lactose feeding ferments bacteria. The only variable that could account for the unknown factor is ammonia. In autism, there are signs of ammonia detoxification, for example when GABA and nitric oxide are increased. So instead of developing overt ammonia toxicity, they are able to detoxify this excess ammonia. As encouraging as this sounds it still depletes cellular energy. Many parents can recall 'staring spells' as the first behavioral change in a child prior to autistic regression. This can be the first sign of increased blood ammonia.

    Other symptoms found in children with only minimal increases in blood ammonia were:

    Developmental regression
    Loss of acquired speech
    Stereotype hand movements
    Myoclonic seizures
    Generalized epileptic discharges
    Repetitive behaviors
    Sensory dysfunction
    Auditory and visual hallucinations
    Finegold and his colleagues have published three studies on children with autism. The first study was with the use of antibiotics. The second study of stool specimens indicated a vast overpopulation of Clostridia in children with autism. Many physicians use antibiotics for treatment of elevated blood ammonia to kill the ammonia-producing bacteria. Antibiotics have produced dramatic effects in children with autism, however this treatment did inevitably fail. Experiments with fermented foods after antibiotic treatments have been somewhat successful in preventing relapsing Clostridial infections.

    Quote Chris Rock: Never Scared (2004)
    00:49:32 I'm talking about the white family that owns all the Similac. Those rich mother****ers.

    Time - Phrase
    00:49:24 "Bling-bling!"

    00:49:28 I'm not talking 'bout rich, I'm talking 'bout wealth, OK?

    00:49:32 I'm talking about the white family that owns all the Similac. Those rich mother****ers.

    00:49:38 I'm talking about the white family that owns the colour blue. Those rich bastards.

    00:49:45 I ain't talking 'bout Oprah, I'm talking 'bout Bill Gates, OK?
    Last edited by Tesla_WTC_Solution; 23rd October 2013 at 04:09.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    A thread on this topic exists at : https://projectavalon.net/forum4/show...909#post752909

    but I wanted to link it here because it's key to autism research.

    http://www.ncbi.nlm.nih.gov/pubmed/9881820

    Med Hypotheses. 1998 Aug;51(2):133-44.
    Autism and Clostridium tetani.
    Bolte ER.
    Abstract
    Autism is a severe developmental disability believed to have multiple etiologies. This paper outlines the possibility of a subacute, chronic tetanus infection of the intestinal tract as the underlying cause for symptoms of autism observed in some individuals. A significant percentage of individuals with autism have a history of extensive antibiotic use. Oral antibiotics significantly disrupt protective intestinal microbiota, creating a favorable environment for colonization by opportunistic pathogens. Clostridium tetani is an ubiquitous anaerobic bacillus that produces a potent neurotoxin. Intestinal colonization by C. tetani, and subsequent neurotoxin release, have been demonstrated in laboratory animals which were fed vegetative cells. The vagus nerve is capable of transporting tetanus neurotoxin (TeNT) and provides a route of ascent from the intestinal tract to the CNS. This route bypasses TeNT's normal preferential binding sites in the spinal cord, and therefore the symptoms of a typical tetanus infection are not evident. Once in the brain, TeNT disrupts the release of neurotransmitters by the proteolytic cleavage of synaptobrevin, a synaptic vesicle membrane protein. This inhibition of neurotransmitter release would explain a wide variety of behavioral deficits apparent in autism. Lab animals injected in the brain with TeNT have exhibited many of these behaviors. Some children with autism have also shown a significant reduction in stereotyped behaviors when treated with antimicrobials effective against intestinal clostridia. When viewed as sequelae to a subacute, chronic tetanus infection, many of the puzzling abnormalities of autism have a logical basis. A review of atypical tetanus cases, and strategies to test the validity of this paper's hypothesis, are included.
    PMID: 9881820 [PubMed - indexed for MEDLINE]

    _____________________________________________

    I told a fellow in my autism support group that Clostridia is behind some cases of autism, without knowing why, and now I know exactly why -- the infection is sub-acute and gradually poisons the brain without the typical symptom of paralysis.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    http://sfari.org/news-and-opinion/vi...role-in-autism

    Maternal anti-brain antibodies may play a role in autism
    E-mail Print Share This Betty Diamond, Lior Brimberg, Peter Gregersen
    21 February 2012


    Self destruction: Antibodies carried in the blood of mothers of children with autism (top), but not those of mothers of typically developing children (bottom) attack proteins in mouse brains.

    The possibility that autoimmune mechanisms are a contributing factor in autism spectrum disorders has been entertained for decades, ever since early studies suggested that individuals with autism have a family history of autoimmune disease1,2.

    Much of the early data were acquired from a fairly small number of individuals with autism. However, a 2009 Danish study examined autoimmune disorders in more than 600,000 children born between 1993 and 2004, and found an association between autism and both rheumatoid arthritis and celiac disease1. In fact, the study concluded that the risk of autism more than doubles for children who have a mother with one of these disorders.

    The presence of autoantibodies, which are immune proteins that mistakenly attack the body’s own cells, in both diseases raises the possibility of a relationship between maternal autoantibodies and autism. In this model, maternal autoantibodies cross the placenta and enter the fetal brain, leading to alterations in its development. A variety of data published in the past few years provide evidence that such a model is biologically plausible.

    The passage of maternal antibodies across the placenta is a well-known mechanism for fetal immune protection. Maternal antibodies reach all fetal tissues, even the brain. In adults, the entry of circulating soluble molecules and cells into brain tissue is limited by the blood-brain barrier, but in recent years it has become increasingly clear that the brain is less of an immune-privileged organ than it was previously considered to be.

    In the fetus, the blood-brain barrier is not fully formed, making the developing brain vulnerable to blood-borne substances. In fact, acquired changes or genetic impairments in cognition and behavior have been shown to be a consequence of circulating brain-specific antibodies that can alter function if they gain access to brain tissue3.

    Case studies:

    The children of individuals with systemic lupus erythematosus (SLE) provide compelling data supporting this hypothesis. Congenital heart block, a type of arrhythmia, and skin rash are clearly transmissible to children by autoantibodies that are commonly present in women who have SLE.

    The children of women with SLE also have a high incidence of learning disorders4. This effect has been linked to autoantibodies in mice, but not in humans, however. Intriguingly, many anti-DNA antibodies that are characteristic of SLE cross-react with the N-methyl-D-aspartate receptor (NMDAR), which is involved in learning and memory5.

    We have shown that pregnant female mice harboring DNA- and NMDAR-specific antibodies have pups with abnormal fetal brain development. When the pups are born, their reflexes don’t develop as quickly as those of controls and, as adults, they have selected impairments in cognitive tasks6.

    Several investigators have identified the presence of antibodies that bind to human fetal brain tissue in a subset of women who have children with autism7,8. When researchers gave these antibodies to pregnant mice and monkeys, they caused abnormal behavior in their offspring9.

    In a 2003 study, researchers gave serum with anti-brain antibodies from mothers of children with autism to pregnant mice. The offspring had deficits in social behavior and motor skills, as well as cerebellar abnormalities10.

    In a subsequent study, pregnant mice were given immunoglobulin antibodies isolated from the blood of mothers of children with autism. In this case, the offspring were more anxious during adolescence, had alterations in sociability and were more sensitive to noise than controls were11.

    Researchers have also administered similar antibodies to pregnant rhesus monkeys. The offspring have more social deficits, motor activity and repetitive behaviors compared with offspring born to monkeys given immunoglobulin from mothers of typically developing children12.

    The results from these studies suggest that maternal antibodies targeting the brain can affect brain development in their offspring, resulting in altered cognition, behavior and motor skills.

    Risk rate:

    By studying families in the Simons Simplex Collection (SSC), we have confirmed that mothers of children with autism are five times more likely to have anti-brain antibodies than are members of a control group consisting of healthy women of childbearing age. The SSC is a database of genetic and clinical information from families that have one child with autism, and unaffected parents and siblings, funded by SFARI.org’s parent organization.

    Anti-nuclear antibodies, which are directed against the cell’s nucleus, are characteristic of many autoimmune diseases. We found that they are elevated in the blood of mothers of children with autism who also carry anti-brain antibodies compared with those who do not have anti-brain antibodies. This is consistent with the theory that autoimmunity predisposes mothers to having brain-reactive antibodies and giving birth to children with autism.

    Interestingly, women with rheumatoid arthritis are as likely to have anti-brain antibodies as are mothers of children with autism. We are investigating whether genetic variants that have been linked to rheumatic arthritis and celiac disease are present in women who have both anti-brain antibodies and a child with autism.

    Confirming an immune mechanism for some proportion of autism cases may help identify at-risk pregnancies, by allowing pregnant women or women planning to become pregnant to be screened for harmful anti-brain antibodies. It could eventually lead to the development of drugs that block these antibodies, thereby preventing autism from developing in vulnerable children.

    These observations suggest that genetic studies in autism should be integrated with investigations into environmental exposures, including the maternal immune repertoire, in order to fully understand the genetic susceptibility of autism. Studying the targets of harmful anti-brain antibodies may also provide insights into disease mechanisms and pathways — which is a top priority for our future studies.

    Betty Diamond is head of the Center for Autoimmune and Musculoskeletal Disorders at The Feinstein Institute for Medical Research in Long Island, New York. Lior Brimberg is a postdoctoral fellow in her laboratory. Peter Gregersen is head of the Robert S. Boas Center for Genomics and Human Genetics at the Feinstein Institute.

    References:

    1: Atladóttir H.O. et al. Pediatrics 124, 687-694 (2009) PubMed

    2: Keil A. et al. Epidemiology 21, 805-808 (2010) PubMed

    3: Diamond B. et al. Nat. Rev. Immunol. 9, 449-456 (2009) PubMed

    4: Lahita R.G. Psychoneuroendocrinology 13, 385-396 (1988) PubMed

    5: DeGiorgio L.A. et al. Nat. Med. 7, 1189-1193 (2001) PubMed

    6: Lee J.Y. et al. Nat. Med. 15, 91-96 (2009) PubMed

    7: Croen L.A. et al.. Biol. Psychiatry 64, 583-588 (2008) PubMed

    8: Singer H.S. et al. J. Neuroimmunol. 194, 165-172 (2008) PubMed

    9: Enstrom A.M. et al. Curr. Opin. Investig. Drugs 10, 463-473 (2009) PubMed

    10: Dalton P. et al. Ann. Neurol. 53, 533-537 (2003) PubMed

    11: Singer H.S. et al. J. Neuroimmunol. 211, 39-48 (2009) PubMed

    12: Martin L.A. et al. Brain Behav. Immun. 22, 806-816 (2008) PubMed

    Related Content:

    http://www.ageofautism.com/2013/07/m...nd-autism.html

    Maternal Antibodies and Autism and Flu Shots Oh Why?

    Vax PregnantBy Teresa Conrick

    The research on maternal antibodies as a cause of some cases of autism continues to grow. From TIME this week: "Mother’s Antibodies May Explain a Quarter of Autism Cases"

    In a study published in Translational Psychiatry, researchers report that 23% of all cases of autism may result from the presence of maternal antibodies that interfere with fetal brain development during pregnancy. The work builds on a 2008 study from the same scientists that first described the group of antibodies in mothers-to-be.

    This is interesting and important work as we continue to see autism as a disorder with roots to the immune system. It did make me wonder if it was possible that the maternal immune activation discussed here as a cause in 23% of the cases could correlate to immune activation created artifically by influenza vaccination. It seemed a valid point and one worth investigating especially when I saw this, also in that TIME article:

    The antibodies belong to a class of compounds called autoantibodies, which are immune cells that the body makes to target — often mistakenly — its own cells. Scientists do not know why or when the mothers produce these antibodies, which appear to monkey with normal nerve development in the fetal brain by interfering with their growth, migration and genetic replication. It is possible that infections during pregnancy — a known risk factor for autism —can prompt the immune system to produce them. Exposure to toxic chemicals can also cause immune defenders to mistake healthy cells for invaders, Van de Water notes.


    Note the last two sentences - the first related to infection in pregnancy and the second to toxic chemicals.

    Can infection in pregnancy cause autism? I wondered about that and did some background reading and wrote this article in January, "Can Influenza Vaccines Cause Maternal Immune Activation Linked To Autism?

    Mothers who get the flu while pregnant could risk affecting their baby's brain, which might lead to 'infantile autism' in their child.

    A Danish study shows that children were slightly more likely to be diagnosed with the condition before the age of three if their mother had the flu.

    Researchers claim that when the mother's immune system is triggered - for example, when they have an influenza virus - it is possible that the foetus' developing brain could be affected.
    But they have clarified that pregnant women and mothers should not be concerned by the findings, as only a tiny portion of those who had influenza gave birth to children with 'infantile autism' and that the research was so limited and early that no concrete findings had been discovered."

    Interesting. So why is it then that in 1918, the Great Influenza Epidemic swept the world, but yet autism was not identified nor described until Dr. Leo Kanner diagnosed it with those first eleven children born in the 1930's?:

    “Since 1938 , there have come to our attention a number of children whose condition differs so markedly and uniquely from anything reported so far that each case merits—and, I hope will eventually receive—a detailed consideration of its fascinating peculiarities...."

    So let's look at the mechanism described:

    "..the pro-inflammatory cytokine interleukin 6, which is known to induce placental inflammatory processes46 and has been shown to mediate the neurodevelopmental effects of gestational inflammation.47 It is possible that such inflammatory processes could be related to the production of maternal antibodies that recognize fetal antigens through maternal-fetal cross talk48 or that maternal antibody to antigen interactions may precipitate inflammation-induced neurodevelopmental alterations similarly to bacterial or viral challenge."



    That is interesting and similar to what I found in my reading, which brings me to the second method identified as a causative factor in producing these maternal antibodies -- toxic chemicals. What else can cause Interleukin 6 (IL-6) a pro-inflammatory cytokine, to be produced?
    "Effect of influenza vaccine on markers of inflammation and lipid profile"

    Despite wide use of the influenza vaccine, relatively little is known about its effect on the measurement of inflammatory markers....We drew blood from 22 healthy individuals 1 to 6 hours before they were given an influenza vaccination and 1, 3, and 7 days after the vaccination...Our findings show that the influenza vaccination causes transient changes in select markers of inflammation and lipids. Consequently, clinical and epidemiologic interpretation of the biomarkers affected should take into account the possible effects of influenza vaccination.

    Inflammatory responses to trivalent influenza virus vaccine among pregnant women
    In the U.S., seasonal trivalent influenza virus vaccine (TIV) is currently universally recommended for all pregnant women. However, data on the maternal inflammatory response to vaccination is lacking and would better delineate the safety and clinical utility of immunization.......Significant increases in CRP were seen at one and two days post-vaccination (ps<05). A similar effect was seen for TNF-α, for which an increase at two days post-vaccination approached statistical significance (p=.06). There was considerable variability in magnitude of response; coefficients of variation for change at two days post-vaccination ranged from 122% to 728%, with the greatest variability in IL-6 responses at this timepoint.......Trivalent influenza virus vaccination elicits a measurable inflammatory response among pregnant women. ......further research is needed to confirm that the mild inflammatory response elicited by vaccination is benign in pregnancy.

    Can Thimerosal, the mercury used in vaccines as a preservative, be part of this picture? This past year, it was reported by the CDC about the total number of flu shots and then the Thimerosal-free flu shots:

    "145 million doses of influenza vaccine .... 62 million doses of thimerosal-free or preservative-free (trace thimerosal) influenza vaccine."

    Could any of these women, who were part of this study, have had a flu shot? It looks as if Thimerosal in any of those flu vaccines could possibly cause an increase in IL-6, the same IL-6 described above in the study -- "the pro-inflammatory cytokine interleukin 6, which is known to induce placental inflammatory processes46 and has been shown to mediate the neurodevelopmental effects of gestational inflammation...."

    Thimerosal is shown to have profound effects on the immune system and is in many of the influenza vaccines:

    "When thimerosal, at a concentration as low as 20 parts per billion, alters the fidelity of normal calcium signals, dendritic cells show abnormal secretion of IL-6 cytokine - a potent chemical signal that initiates inflammatory responses."

    It appears very possible that influenza vaccination, especially with Thimerosal, could start off this inflammatory process in a pregnancy. I need to mention too, that the percent in this study, the 23% who went on and had a child diagnosed with autism -- is in the ballpark of the percent of pregnant women who reportedly get a flu shot -" between 10 percent and one-quarter of women"
    Another imperative reason we need this research and precautions is that I met one of the women in this study. She had a flu shot when pregnant.

    Teresa Conrick is Contributing Editor to Age of Autism.


    Posted by Age of Autism at July 22, 2013 at 5:45 AM in Teresa Conrick | Permalink | Comments (28)
    Last edited by Tesla_WTC_Solution; 24th November 2013 at 17:12.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    Wanted to point out: I received a flu shot in 2007, mere months before my son was born on Jan 1.
    Some days afterwards, I ended up in the hospital because my fetus had stopped moving.
    Years later, in 2013, doctors are starting to realize that maternal antibodies play a role in the brain protein loss typical of autism.
    What we are wondering now, of course, is whether maternal exposure to influenza vaccine during pregnancy may have caused autoimmunity against fetal tissue.

    It was almost as if my son had the flu himself after I got the vaccine.
    What could make a healthy fetus stop moving for a week?

    He was diagnosed with autism at age 1, shortly before second birthday.
    We've always wondered if his babyhood shot regimen worsened his autism.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    http://www.medicinenet.com/flu_vacci...mments-859.htm

    Patient Comments: Flu Vaccination - Side Effects

    Quote Comment from: skategirl, 65-74 Female (Patient)Published: March 07
    I have gotten a yearly flu shot for years and had no problems. However, this year I was given the flu shot for seniors (I'm 68). I had a number of side effects with this one, including nausea, severe neck and shoulder pain on my left side. The neck and shoulder pain lasted for about a couple of weeks. I began to do some gentle exercise again after that, and the shoulder pain came back. It was severe and I was only able to sleep 4 or 5 hours at a time after taking Ibuprofen. I couldn't eat much because of the nausea and pain and lost weight. The second episode of shoulder pain also lasted two weeks. I also had tingling in my left arm and hand. I was given the shot in my right arm. I haven't had any pain in three weeks, and the tingling is almost gone now, so hope I'm over this. I'm not aware of anything I did to cause the pain, so believe it was the flu shot. It was scary as I'm not a sickly person & had never had anything like this. I'll never get another flu shot!
    Related Medications: Ibuprofen


    Comment from: Bev, 55-64 Female (Patient)Published: March 07
    I received a flu shot in 09 just about killed me. I was passing out on leaving the exam room. I was wheeled back in the exam room where I felt extremely hot, a burning back up my back as if I was on fire. I was in terrible pain to the point of crying. I have a high tolerance for pain but this was something horrific. My heart was racing extremely fast my blood pressure dropped to almost nothing. I was given an injection to counter act the adverse reaction. Within 20 minutes I was feeling better. Months after this I was diagnosed with Rheumatoid Arthritis though no one in my family has had this. Now I read it could be linked to the flu shot. I am need of surgeries for knee replacements, I have pain in every joint in my body from the R/A. I have not taken a flu shot since but will regret doing so for the rest of my life
    .
    http://www.hindawi.com/crim/rheumatology/2012/785028/

    Quote Case Reports in Rheumatology
    Volume 2012 (2012), Article ID 785028, 3 pages
    http://dx.doi.org/10.1155/2012/785028
    Case Report
    Rheumatoid Arthritis and Swine Influenza Vaccine: A Case Report


    Gurjot Basra,1 Praveen Jajoria,2 and Emilio Gonzalez2
    1Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555, USA
    2Division of Rheumatology, University of Texas Medical Branch, Galveston, TX 77555, USA

    Received 3 April 2012; Accepted 15 June 2012

    Academic Editors: D. Aeberli, J. V. Dunne, and F. Schiavon

    Copyright © 2012 Gurjot Basra et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

    Abstract

    Rheumatoid arthritis (RA) is the most common chronic inflammatory joint disease. Multiple scientific articles have documented that vaccinations for influenza, MMR, and HBV, to name a few, could be triggers of RA in genetically predisposed individuals. However, there is limited data regarding the association of swine flu vaccine (H1N1) and RA. We report the case of a Mexican American female who developed RA right after vaccination with H1N1 vaccine. Genetically, RA has consistently been associated with an epitope in the third hypervariable region of the HLA-DR chains, known as the “shared epitope”, which is found primarily in DR4 and DR1 regions. The presence of HLA-DRB1 alleles is associated with susceptibility to RA in Mexican Americans. Hence, certain individuals with the presence of the “shared epitope” may develop RA following specific vaccinations. To our knowledge, this is the first reported case of RA following vaccination with the swine flu vaccine.

    1. Introduction

    Rheumatoid arthritis (RA) is the most frequent of all chronic inflammatory joint diseases characterized by pain, swelling, stiffness, and destruction of joints due to synovial inflammation and effusion resulting in disability. It affects 0.5–1% of population in industrialized world with annual incidence reported to be around 12–1200 per 100,000 [1]. Women are affected two to three times as often as men and peak age of onset is between the ages 30 and 55 but can occur at any age. The etiology of RA is multifactorial and includes hormonal, environmental, genetic, infectious, and other variables. RA is associated with the presence of an epitope in the third hypervariable region of the HLA-DR β chains, known as the “shared epitope." Individuals with the sequence leu-glu-lys-arg-ala in residues 67–74 have a much higher incidence of developing RA [2]. This sequence is found in DR4, DR14, and DR1 β chains. HLA-DRB1 allele is associated with susceptibility to RA in Mexican Americans while HLA-DRB1*08 appears to have a protective influence on RA susceptibility and disease severity in Mexican Americans.

    It has been shown that the onset of rheumatic disease after vaccination signifies that the vaccine may trigger persistent autoimmune response in genetically predisposed individuals. Vaccinations that are suspected to cause RA include influenza, MMR, HBV, tetanus toxoid, typhoid, paratyphoid A and B (TAB), polio, diphtheria, and small pox [3]. HLA DR-4 was frequently present in the above-described patients, suggesting that genetically susceptible individuals are at increased risk for RA after vaccinations. However, there is no causal association between swine flu vaccination and RA onset that has been documented so far. We report a case of Mexican American female who develops RA after vaccination (H1N1) exposure which could possibly be due to her genetic susceptibly explained by above factors.

    2. Case Report

    A 33-year-old Hispanic female with no significant past medical history was referred to the rheumatology clinic in May 2010 by her primary care physician for having pain and swelling in multiple joints since November 2009. Patient received a seasonal flu shot in October and a week later, she noted some joint pain and aches in hands, wrists, and knees, which resolved within a few days and patient became asymptomatic. A month later, she received H1N1 (swine influenza) vaccine and a week after started experiencing joint pain, swelling, and stiffness in hand, wrist, elbow, shoulder, and knee joints. She also complained of significant morning stiffness that last for more than one hour. On physical examination she had bilateral synovitis in fourth and fifth metacarpophalangeal (MCP), second, and third proximal interphalangeal (PIP) joints, with prominent left ulnar styloid. She fulfilled most of the criteria for classification of RA based on American College of Rheumatology (ACR) guidelines.
    Last edited by Tesla_WTC_Solution; 24th November 2013 at 21:09.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    SUPER IMPORTANT:

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    Forced Flu Vaccine's planned for New York schoolchildren
    « on: Today at 07:41:31 PM »
    http://politicker.com/2013/12/protes...-flu-vaccines/

    Autism advocates are set to protest tomorrow against a quiet effort by Mayor Michael Bloomberg’s administration to require annual flu vaccinations for all New York City schoolchildren.

    On Wednesday, with just three weeks to go until he leaves office, Mr. Bloomberg’s controversial Board of Health is set to vote on new rules that would force children as young as six months old to be immunized each year before December 31 if they attend licensed day care or pre-school programs.

    “Young children have a high risk of developing severe complications from influenza. One-third of children under five in New York City do not receive an annual influenza vaccination, even though the vaccine safely and effectively protects them against influenza illness,” the Health Department said in a statement. “This mandate will help protect the health of young children, while reducing the spread of influenza in New York City.”

    The Board is stocked with mayoral appointees and controversial initiatives–from smoking bans to regulations on soda cup sizes–have sailed through with little opposition, angering a small, but passionate group of advocates who claim the vaccinations are potentially dangerous.

    “The Bloomberg administration is wildly exaggerating the benefit of the flu shot and we think they are wildly underestimating the risks involved with it,” said John Gilmore, the executive director of the Autism Action Network, speaking more broadly than the controversial claim that links vaccines to autism.

    “There are risks associated with every medical procedure,” he said, citing allergic reactions, toxic mercury used as a preservative and questions as to whether the Board’s move is legal given state government jurisdictions.

    Mr. Gilmore’s organization is helping organize tomorrow’s protest. And though he doesn’t expect the Board’s vote to go his way, he hopes the rally will get Mayor-elect Bill de Blasio’s attention, potentially opening the door for a reversal once he takes office in January.

    “This is basically to put the mayor-elect [on alert], make him aware that this is an issue that he’s going to have to deal with it. It’s not going to go away,” said Mr. Gilmore said, criticizing the way the Bloomberg administration has pushed the rules through. “He is kind of doing this in a stealth fashion. He just proposed this about 6 weeks ago. I don’t think there was any announcement.”

    According to a Board of Health notice made public in September, influenza results in 20,000 hospitalizations and 30 to 150 deaths in children under 5 nation-wide each year.

    Under the proposed rule, which had a public hearing in October, the vaccinations would be required “unless the vaccine may be detrimental to the child’s health, as certified by a physician licensed to practice medicine in this state, or the parent, parents, or guardian of a child hold genuine and sincere religious beliefs which are contrary to the practices herein required.”

    ________________________________________________________

    http://www.freeinews.com/health/auti...ics-study-says

    Researchers developed mice with autism-like symptoms by referring to a previous finding that severe viral infection during pregnancy seems to increase the risk the child will have autism. So, the researchers triggered an infection-like immune response in pregnant mice, which led to offspring with autism-like symptoms.

    http://www.ncbi.nlm.nih.gov/pubmed/22235050

    Lupus. 2012 Feb;21(2):175-83. doi: 10.1177/0961203311429817.
    Autoimmune response following influenza vaccination in patients with autoimmune inflammatory rheumatic disease.

    Perdan-Pirkmajer K, Thallinger GG, Snoj N, Čučnik S, Žigon P, Kveder T, Logar D, Praprotnik S, Tomšič M, Sodin-Semrl S, Ambrožič A.
    Source

    University Medical Centre Ljubljana, Department of Rheumatology, Ljubljana, Slovenia.

    Abstract

    Vaccines have undoubtedly brought overwhelming benefits to mankind and are considered safe and effective. Nevertheless, they can occasionally stimulate autoantibody production or even a recently defined syndrome known as autoimmune/inflammatory syndrome induced by adjuvants (ASIA). There is scarce data regarding autoimmune response after seasonal/influenza A (H1N1) vaccine in patients with autoimmune inflammatory rheumatic disease (AIRD). The objective of our study was therefore to determine autoimmune response in a large group of AIRD patients vaccinated against seasonal and/or H1N1 influenza. We conducted a prospective cohort study with a 6-month follow-up. Two-hundred and eighteen patients with AIRD (50 vaccinated against seasonal influenza, six against H1N1, 104 against both, 58 non-vaccinated controls) and 41 apparently healthy controls (nine vaccinated against seasonal influenza, three against H1N1, 18 against both, 11 non-vaccinated controls) were included. Blood samples were taken and screened for autoantibodies [antinuclear antibody (ANA), anti-extractable nuclear antigen (anti-ENA), anticardiolipin (aCL) IgG/IgM antibodies, anti-beta 2-glycoprotein I (anti-β2GPI)] at inclusion in the study, before each vaccination, 1 month after the last vaccination and 6 months after inclusion. For non-vaccinated participants (patients and healthy controls) blood samples were taken at the time of inclusion in the study and 6 months later. We report that after the administration of seasonal/H1N1 vaccine there were mostly transient changes in autoantibody production in AIRD patients and in healthy participants. However, a small subset of patients, especially ANA-positive patients, had a tendency towards anti-ENA development. Although no convincing differences between the seasonal and H1N1 vaccines were observed, our results imply that there might be a slight tendency of the H1N1 vaccine towards aCL induction. Although seasonal and H1N1 vaccines are safe and effective, they also have the potential to induce autoantibodies in selected AIRD patients and healthy adults. Follow-up of such individuals is proposed and further research is needed.
    PMID: 22235050 [PubMed - indexed for MEDLINE]

    _______________________________________________________

    Adjuvants are experimental immune system irritants that without exception result in autoimmunity and misery in some portion of the vaccinated population.

    If vaccines were crucial to human life, there would be no surviving Amish people left.
    Last edited by Tesla_WTC_Solution; 10th December 2013 at 03:09.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    all it takes is one bad jab and life as you know it can end in an instant.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    Here is a good one from a week or so ago!

    J Autism Dev Disord. 2013 Nov 29. [Epub ahead of print]
    Rigid-Compulsive Behaviors are Associated with Mixed Bowel Symptoms in Autism Spectrum Disorder.
    Peters B, Williams KC, Gorrindo P, Rosenberg D, Lee EB, Levitt P, Veenstra-Vanderweele J.

    Source
    Vanderbilt University, 1601 23rd Avenue South, Suite 300, Nashville, TN, 37212, USA, brittany.peters@vanderbilt.edu.

    Abstract

    Based on clinical experience, we hypothesized that rigid-compulsive behaviors are associated with severe constipation and co-occurring diarrhea or underwear staining in children with autism spectrum disorder. Using data from the Autism Treatment Network, we evaluated the association between these gastrointestinal symptoms and measures of rigid compulsive behavior in children ages 2-17. Following statistical correction, four of five primary measures were significantly associated with constipation and diarrhea or underwear staining, including parental report of repetitive behavior, parental report of compulsive behavior, clinician diagnosis of obsessive-compulsive disorder, and report of rituals observed on the autism diagnostic observation schedule. This association could point to a causal connection between these symptoms or to a common biological pathway that impacts both gut and brain.

    PMID: 24293040 [PubMed - as supplied by publisher]

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    Heparan Sulfate Link to Autism and Leaky Gut, link to Hep B vaccine, pathogenicity of altered gut flora

    http://coolinginflammation.blogspot.com/

    Antibiotics Select for E. coli that Stick to Rectal Surface of Cattle
    Pathogenic E. coli are not found throughout cattle fecal material, but rather they are only in the outermost surface layer. This outer layer of material contains bacteria from the surface of the rectum just as the cow pies are deposited. E. coli does not normally stick to this surface, because it lacks a protein, such as a hemagglutinin capable of binding to the surface polysaccharides, heparan sulfate. Antibiotics kill off the bacteria normally residing on the surface. As a member of the intestinal biofilm community, E. coli continually exchanges DNA/genes with other bacteria in the gut and picks up three useful genes, to become a pathogen:
    Antibiotic resistance

    Hemagglutinin for sticking to surfaces
    Toxin to release nutrients from the intestinal walls.



    ________________________________________________________________

    When your kid gets the Hep B vaccine, it can trade dangerous genes for surface proteins with other germs living in your child already.
    E coli that would otherwise be harmless assumes genes that allow it to bind directly to the intestinal wall, leading to leaky gut, damaged vili, and chronic infection.

    Constirrhea in a nutshell. autism too.

    Heparan sulfate is found in the intestine, and also in the brain.

    Depletion of heparan sulfate in mice is known to cause autism-like symptoms.

    this is directly linked to the health of the gut.

    Apparently BS is a pretty big deal when it has the wrong germs in it, lol

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    http://healthyprotocols.com/2_vac_hep%20B.htm

    __________________________________________________

    I blogged about Heparan Sulfate on my website nuclearnuttery about two years ago,
    saying that the binding mechanism of hepatitis B strips the human body of necessary proteins.
    this is much more severe in infants, for obvious reasons (size)



    according to google there are some recent research results in the area of linking autism to heparan sulfate.
    i am hoping they go the extra mile and realize hep B could be directly involved in this unfortunate process of elimination of healthy children.

    Autism, Sulphate, Sunshine, and Nutrition | Musings from the Chiefio
    chiefio.wordpress.com/2013/02/.../autism-sulphate-sunshine-and-nutritio...‎

    Feb 20, 2013 - Of special interest is a recent discovery that a postnatally induced heparan sulfate deficiency in the brain is capable of causing autistic behavior ...
    Trends in Autism Research - Page 207 - Google Books Result
    books.google.com/books?isbn=159454042X
    O. T. Ryaskin - 2004 - ‎Medical
    The glomerular basement membrane (GBM) of the kidneys contains heparan sulfate and chondroitin sulfate proteoglycans (Ehara et al., 1994). They are ...

    Autism Link found in Children with Bone Disorders | Medical News ...
    http://www.ivanhoe.com/channels/p_ch...d=29101‎
    Mar 13, 2012 - "There is growing evidence that many autistic people have related genetic ... who are autistic might have similar defects in heparan sulfate.






    http://chiefio.wordpress.com/2013/02...and-nutrition/

    Quote Entropy 2012, 14(10), 1953-1977; doi:10.3390/e14101953
    Review

    Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?

    Samantha Hartzell and Stephanie Seneff* email

    Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge 02139, MA, USA
    * Author to whom correspondence should be addressed.
    Received: 28 September 2012; in revised form: 16 October 2012 / Accepted: 16 October 2012 / Published: 18 October 2012
    (This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)

    Abstract: Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the alarming rise in the incidence of autism in the last three decades suggests that environmental factors play a key role as well. This dichotomy can be easily explained if we invoke a heritable epigenetic effect as the primary factor. Researchers are just beginning to realize the huge significance of epigenetic effects taking place during gestation in influencing the phenotypical expression. Here, we propose the novel hypothesis that sulfates deficiency in both the mother and the child, brought on mainly by excess exposure to environmental toxins and inadequate sunlight exposure to the skin, leads to widespread hypomethylation in the fetal brain with devastating consequences. We show that many seemingly disparate observations regarding serum markers, neuronal pathologies, and nutritional deficiencies associated with autism can be integrated to support our hypothesis.

    Keywords: autism; epigenetics; cholesterol sulfate; DNA methylation; sulfotransferases; heparan sulfate; folate; cobalamin; zinc

    http://www.ivanhoe.com/channels/p_ch...?storyid=29101

    Quote Reported March 13, 2012
    Autism Link found in Children with Bone Disorders

    (Ivanhoe Newswire)-- Children with multiple hereditary exostoses (MHE), suffer from multiple growths in their bones that cause pain and disfigurement. However aside from the physical impairments, parents also notice that their children with MHE also experience autism-like social problems.

    With the encouragement of parents, researchers at Sanford-Burnham Medical Research Institute are able to uncover the link between autism and MHE by using a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism.

    "There is growing evidence that many autistic people have related genetic defects, or defects that are exacerbated by this one," Yu Yamaguchi, M.D., Ph.D., professor in the Sanford Children's Health Research Center at Sanford-Burnham." Yamaguchi led this study, along with colleagues Fumitoshi Irie, Ph.D. and Hedieh Badie-Mahdavi, Ph.D., was quoted as saying.

    In humans, MHE is caused by a mutation in one of two genes, Ext1 or Ext2. Together, these genes encode an enzyme necessary to produce heparan sulfate—a long sugar chain that helps bone cells grow and proliferate. In this study, Yamaguchi and his team used mice that lack the Ext1 gene in just a certain type of neuron to understand the mechanism of social problems in MHE patients.

    The mice were tested for the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior. The team found that the mutant mice were less social than normal mice. They also exhibited language deficiencies, as determined using ultrasound vocalization measurements, a well-characterized substitute for mouse language. Lastly, Yamaguchi's team took at look at repetitive behaviors in these mice. Using a board covered with holes, they observed that normal mice will poke their noses in many holes at random, while the mutant mice poke their noses in the same hole again and again.

    This information clearly demonstrates what the parents of children with MHE have always suspected—the disease affects more than just bones. The genetic defect that causes skeletal deformities also causes social and cognitive problems.

    Not all autistic children have MHE, nor are all MHE children autistic. But, according to Yamaguchi, there is evidence that some people who are autistic might have similar defects in heparan sulfate. This is the sugar chain that's defective in MHE, where it causes bone deformities and social deficits.

    "There are a few studies that compared the genomes of healthy and autistic people and they revealed differences in some heparan sulfate-related genes," Yamaguchi was quoted as saying.

    There are most likely many different genetic abnormalities that can lead to autism in the general population. This study and others now indicate that for some, the condition could be caused by mutations in genes encoding enzymes and proteins involved in making heparan sulfate.

    Yamaguchi's team is now comparing DNA from autistic and non-autistic volunteers to look for mutations in heparan sulfate genes. So far the initial results have been encouraging.

    "I can't emphasize enough how much it helped that the parents of kids with MHE got involved and supported this research," Yamaguchi said. "As parents, they noticed their kids had social problems that gave them challenges at school. School officials and other people didn't take these observations seriously—they usually just waved off the problems, assuming that the kids' bone deformities just make them shy. This latest research doesn't solve any bone issues for MHE patients, but it does help support what the parents always knew—these children need special care."

    SOURCE: Proceedings of the National Academy of Sciences, March 2012.

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    Default Re: File It Away Right Here Before You Forget! A Thread for Autism Research Paper Links

    http://www.hightimes.com/read/mariju...d-treat-autism

    Marijuana May Be Used to Treat Autism
    BY MIKE ADAMS · THU OCT 31, 2013


    Recent studies indicate that compounds found in marijuana may be used to successfully treat autism.

    Researchers at Stanford University say that the debilitating effects of autism are primarily caused by a gene mutation that blocks the body’s natural production of cannabinoids, called endocannabinoids, and hinders the way those molecules communicate with the brain.

    In the study, researchers found that the mutation of the neurologin-3 gene, which is responsible for creating and sustaining normal communication between brain cells, appears to have a direct correlation to autism -- introducing derivatives of cannabis to the brain could ease symptoms associated with the disease.

    Although the exact science revolving around how a disturbance in endocannabinoid signaling contributes to autism symptoms, researchers say there is significant evidence that suggest medical marijuana may be a viable treatment option for this condition.

    Researchers from the University of Irvine in California believe the folks at Stanford may be on to something: because they, too, have discovered a link between endocannabinoids and autism.

    In a study of mice with fragile X syndrome, it “showed dramatic behavioral improvements in maze tests measuring anxiety and open-space acceptance.” And because THC, the active compound in marijuana, stimulates the same receptors as the endocannabinoids, researchers concluded, “increasing natural marijuana-like chemicals in the brain can help correct behavioral issues related to fragile X syndrome, the most common known genetic cause of autism.”

    A recent article published in the Autism Daily Newscast indicates that many families are already experimenting with marijuana as a treatment for their children’s autism -- as an alternative to other drugs with major side effects and questionable results.

    Researchers add that while they do not advocate giving medical marijuana to children with autism, they believe their findings will lead to the development of important treatments for this devastating disease.

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