kim

tlk, moved response to the bony tumor thread. Should have named that something different

Jewels/Chemar, Thank you guys for making me feel a little less foolish for undertaking something I probably have no business doing! Jules, please, please, never confuse me for someone who has any medical knowledge. I have absolutely none. I hold two state licenses, and they don't require the skills of a rocket scientist, believe me! Jewels any commonalities that you can kick up, would be great. I wanted to drop this on this thread. This Eph2/syndecan thing is something that I have done no reading on, but it is part of the research that I posted on another thread, and I thought it was interesting that the gene appears to be in the same region as the MTHFR. http://www.burnham.org/print.asp?contentID=196 EphB2/syndecan-2 signaling in dendritic spine development Dendritic spines are small protrusions on the surface of dendrites that receive the vast majority of excitatory synapses. and In a subsequent study, we demonstrated that syndecan-2 is phosphorylated on two tyrosine residues by EphB2, a receptor tyrosine kinase that is also concentrated in dendritic spines. Syndecan-2 and EphB2 associate to form a complex in neurons and in the brain. Phosphorylation by EphB2 is necessary for syndecan-2 to associate with EphB2 and to induce dendritic spine formation in cultured neurons. http://genome-www.stanford.edu/cgi-bin/gen...p.pl?gene=EPHB2 Entrez Gene cytogenetic band: 1p36.1-p35 Ensembl cytogenetic band: 1p36.12 HGNC cytogenetic band: 1p36.1-p35 http://www.nanosphere.us/VerigeneMTHFRNucl...stIVD_4468.aspx The MTHFR gene, located on human chromosome 1p36.3, encodes an enzyme that catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methylenetetrahydrofolate, the primary circulating form of folate. This substrate is vital for both DNA synthesis1 and the methionione synthase-catalyzed conversion of homocysteine to methionine.

PROTEOGLYCANS IN THE DEVELOPING NERVOUS SYSTEM http://www.burnham.org/print.asp?contentID=196 excerpts http://www.burnham.org/print.asp?contentID=196 PROTEOGLYCANS IN THE DEVELOPING NERVOUS SYSTEM Proteoglycans are a family of glycoproteins that carry sulfated polysaccharides (glycosaminoglycans). There are four classes of glycosaminoglycans, namely heparan sulfate, chondroitin sulfate, keratan sulfate, and hyaluronan. Proteoglycans have been implicated in various biological processes, such as the modulation of growth factor/morphogen signaling during development and tissue remodeling, regulation of cell proliferation, adhesion, and migration. Our laboratory has been studying the role of proteoglycans in neural development and physiology. and Analysis of the role of heparan sulfate in development using a conditional knockout system To understand the role of heparan sulfate in mammalian nervous system, we created loxP-modified Ext1 allele by homologous recombination. Ext1 encodes an enzyme essential for heparan sulfate synthesis. As the first conditional knockout study using this system, we performed a developing brain-targeted Ext1 knockout using the nestin-Cre driver transgene. All the nestinCre-Ext1 conditional knockout mice died at birth, presumably due to respiratory failure. The brain of conditional knockout mice exhibited various patterning defects that are composites of those caused by mutations of multiple heparan sulfate-binding morphogens. Furthermore, these brains displayed severe guidance errors in major commissural tracts, revealing a pivotal role of heparan sulfate in midline axon guidance (5). [This paper was featured in Signal Transduction Knowledge Environment (STKE): Sci. STKE, November 11, 2003.] http://www.ncbi.nlm.nih.gov/pubmed/1637821...ed_Discovery_RA 1: Med Microbiol Immunol. 2006 Sep;195(3):133-41. Epub 2005 Dec 24. Links Heparan sulfate proteoglycans mediate Staphylococcus aureus interactions with intestinal epithelium.Hess DJ, Henry-Stanley MJ, Erlandsen SL, Wells CL. Department of Surgery, University of Minnesota, Minneapolis, MN 55455, USA. Staphylococcus aureus can be internalized by non-professional phagocytes, and may colonize the intestine in normal and antibiotic-treated individuals. Intestinal colonization may depend on the interactions of S. aureus with the intestinal epithelium. The best described mechanism of S. aureus binding to eukaryotic cells involves S. aureus fibronectin binding proteins (FnBPs), using fibronectin as a bridging molecule to beta1 integrins on the eukaryotic cell surface. Because S. aureus can be internalized by enterocytes, and because S. aureus is known to bind heparan sulfate (HS), we hypothesized that heparan sulfate proteoglycans (HSPGs) widely expressed on epithelia may mediate S. aureus interactions with intestinal epithelial cells. Internalization of S. aureus RN6390 by cultured intestinal epithelial cells was inhibited in a dose-dependent fashion by the HS mimic heparin, and by HS itself. Internalization of S. aureus DU5883, which lacks expression of staphylococcal FnBPs, was also inhibited by heparin. S. aureus adherence to ARH-77 cells, transfected to express the HSPG syndecan-1, was greatly increased when compared to adherence to plasmid control ARH-77 cells which have little detergent extractable HS. In addition, compared to wild-type HS-expressing Chinese hamster ovary (CHO) cells, internalization of S. aureus was decreased using mutant CHO cells with decreased HS expression. These findings are consistent with a model wherein S. aureus internalization by intestinal epithelial cells (and perhaps other epithelia) is mediated by S. aureus binding to the HS moiety of cell-surface HSPGs, and this interaction appears independent of fibronectin binding. http://www.ncbi.nlm.nih.gov/pubmed/1631738...ed_Discovery_RA Ability of the heparan sulfate proteoglycan syndecan-1 to participate in bacterial translocation across the intestinal epithelial barrier.Henry-Stanley MJ, Hess DJ, Erlandsen SL, Wells CL. Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455-0374, USA. Although hundreds of microbial species reside in the human intestinal tract, comparatively few (e.g., Escherichia coli and other enterobacteria, Enterococcus faecalis, etc.) are typically associated with systemic infection in postsurgical, shock, and trauma patients. Syndecan-1 is the predominant cell surface heparan sulfate proteoglycan expressed on epithelia, and there is substantial evidence that heparan sulfate participates in interactions of a variety of frankly pathogenic microbes with mammalian cells. To investigate the role of syndecan-1 in interactions of enteric flora with intestinal epithelium, bacteria that might use the enterocyte as a portal of entry for systemic infection (including E. faecalis, E. coli, and other enterobacteria, and several species of staphylococci and streptococci) were studied for their abilities to interact with syndecan-1. Streptococcus bovis, S. agalactiae, S. pyogenes, Staphylococcus aureus, and S. epidermidis showed increased adherence to ARH-77 cells transfected to express syndecan-1. Heparin, a heparan sulfate analog, inhibited internalization of S. bovis, S. agalactiae, S. pyogenes, and S. aureus by HT-29 enterocytes (prominent syndecan-1 expression), but not Caco-2 enterocytes (relatively low syndecan-1 expression). Data from experiments with Chinese hamster ovary cells with altered glycosaminoglycan expression indicated that heparan sulfate and chondroitin sulfate (glycosaminoglycans on the syndecan-1 ectodomain) participated in bacterial interactions with mammalian cells. Thus, although E. faecalis, E. coli, and other gram-negative enterobacteria did not appear to interact with syndecan-1, this heparan sulfate proteoglycan may mediate enterocyte interactions with some staphylococci and streptococci that are known to cause systemic infections in specific populations of high-risk, immunosuppressed, postsurgical, and trauma patientsNOT ONLINE YET 2008 study This Article: Craig N. Morrell, Henry Sun, Masahiro Ikeda, Jean-Claude Beique, Anne Marie Swaim, Emily Mason, Tanika V. Martin, Laura E. Thompson, Oguz Gozen, David Ampagoomian, Rolf Sprengel, Jeffrey Rothstein, Nauder Faraday, Richard Huganir, and Charles J. Lowenstein http://www.ncbi.nlm.nih.gov/pubmed/3290104...ed_Discovery_RA Heparin-inhibitable basement membrane-binding protein of Streptococcus pyogenes.Bergey EJ, Stinson MW. Department of Microbiology, School of Medicine and Biomedical Sciences, State University of New York, Buffalo 14214. Solubilized surface proteins of Streptococcus pyogenes serotype M6 were found by indirect immunofluorescence assays to bind selectively to proteoglycan-containing regions of basement membranes of kidney and cardiac muscle in vitro. Epithelial, endothelial, and interstitial cells were unstained. Binding of streptococcal protein to basement membranes was competitively inhibited by heparin and, to a lesser extent, by heparan sulfate. Weak inhibition was also observed with other glycosaminoglycans, including dermatan sulfate, chondroitin sulfate, and hyaluronic acid. Type IV collagen, gelatin, serum fibronectin, glucuronic acid, and a selection of monosaccharides had no significant effects on binding. The heparin-inhibitable basement membrane-binding protein was purified by affinity chromatography on heparin-Sepharose 6-B. Polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and urea dissociated the affinity-purified protein into two polypeptides of 9,000 and 15,000 mrs. Chemical analyses revealed that the purified protein was devoid of cysteine, amino and neutral sugars, and phosphate. Thus, the polypeptides are not glycosylated or complexed with trace amounts of lipoteichoic acid or polysaccharide. Binding of purified protein to tissue was determined by direct radioassay and indirect immunofluorescence and was inhibitable by heparin. Although the in vivo effects of this streptococcal component remain to be determined, its deposition on basement membranes in vitro supports the hypothesis that it contributes to the pathogenesis of poststreptococcal glomerulonephritis or acute rheumatic fever. Glutamate mediates platelet activation through the AMPA receptor J. Cell Biol. 2008 180: i13 Similiar articles http://www.jcb.org/cgi/search?qbe=jcb;JCB1...p;minscore=5000 http://cat.inist.fr/?aModele=afficheN&cpsidt=17332123 Heparin, a heparan sulfate analog, inhibited internalization of S. bovis, S. agalactiae, S. pyogenes, and S. aureus by HT-29 enterocytes (prominent syndecan-1 expression), but not Caco-2 enterocytes (relatively low syndecan-1 expression). Data from experiments with Chinese hamster ovary cells with altered glycosaminoglycan expression indicated that heparan sulfate and chondroitin sulfate (glycosaminoglycans on the syndecan-1 ectodomain) participated in bacterial interactions with mammalian cells. http://www.nature.com/nature/journal/v414/...bs/414648a.html Streptococcus pyogenes (also known as group A Streptococcus, GAS), the agent of streptococcal sore throat and invasive soft-tissue infections, attaches to human pharyngeal or skin epithelial cells through specific recognition of its hyaluronic acid capsular polysaccharide by the hyaluronic-acid-binding protein CD44 (refs 1, 2). Because ligation of CD44 by hyaluronic acid can induce epithelial cell movement on extracellular matrix3, 4, 5, we investigated whether molecular mimicry by the GAS hyaluronic acid capsule might induce similar cellular responses. Here we show that CD44-dependent GAS binding to polarized monolayers of human keratinocytes induced marked cytoskeletal rearrangements manifested by membrane ruffling and disruption of intercellular junctions. Transduction of the signal induced by GAS binding to CD44 on the keratinocyte surface involved Rac1 and the cytoskeleton linker protein ezrin, as well as tyrosine phosphorylation of cellular proteins. Studies of bacterial translocation in two models of human skin indicated that cell signalling triggered by interaction of the GAS capsule with CD44 opened intercellular junctions and promoted tissue penetration by GAS through a paracellular route. These results support a model of host cytoskeleton manipulation and tissue invasion by an extracellular bacterial pathogen. http://ajp.amjpathol.org/cgi/content/abstract/161/6/2219 CD44 is a major cell-surface receptor for hyaluronic acid (HA), a glycosaminoglycan component of extracellular matrix. HA-CD44 interactions have been implicated in leukocyte extravasation into an inflammatory site SEARCH TITLE....LOSS O SULFATED GAGS STREP A INFECTION http://lib.bioinfo.pl/meid:13671 Infect Immun. 1980 Feb ;27 (2):444-8 6991416 (P,S,E, Cited:58 Growth characteristics of group A streptococci in a new chemically defined medium. I van de Rijn, R E Kessler A new chemically defined medium for the growth of group A streptococci has been formulated. The advantages of this new medium over previously described defined media are: (i) rates of growth (i.e., doubling times) of 20 strains were comparable to the rates of growth in complex media; (ii) each strain grew to a higher culture density in the new defined medium than in complex media; (iii) transfer from complex media with small inocula was possible without any prior adaptation regimen; and (iv) the production of virulence factors (i.e., M protein and hyaluronic acid) and extracellular enzymes during growth in this new medium was comparable to that in complex media. Mesh-terms: Bacterial Proteins :: biosynthesis; Culture Media; Deoxyribonucleases :: biosynthesis; Hyaluronic Acid :: biosynthesis; Kinetics; Streptococcus pyogenes :: growth & development; Streptococcus pyogenes :: metabolism; Streptolysins :: biosynthesis; Support, U.S. Gov't, P.H.S.; http://lib.bioinfo.pl/auth:Sj%C3%B6bring,U Eur J Biochem. 2003 May ;270 (10):2303-11 12752450 (P,S,E, Cited:1 Interactions between M proteins of Streptococcus pyogenes and glycosaminoglycans promote bacterial adhesion to host cells. Inga-Maria Frick, Artur Schmidtchen, Ulf Sjöbring Department of Cell and Molecular Biology, Section for Molecular Pathogenesis, Lund University, Sweden. Inga-Maria.Frick@medkem.lu.se Several microbial pathogens have been reported to interact with glycosaminoglycans (GAGs) on cell surfaces and in the extracellular matrix. Here we demonstrate that M protein, a major surface-expressed virulence factor of the human bacterial pathogen, Streptococcus pyogenes, mediates binding to various forms of GAGs. Hence, S. pyogenes strains expressing a large number of different types of M proteins bound to dermatan sulfate (DS), highly sulfated fractions of heparan sulfate (HS) and heparin, whereas strains deficient in M protein surface expression failed to interact with these GAGs. Soluble M protein bound DS directly and could also inhibit the interaction between DS and S. pyogenes. Experiments with M protein fragments and with streptococci expressing deletion constructs of M protein, showed that determinants located in the NH2-terminal part as well as in the C-repeat region of the streptococcal proteins are required for full binding to GAGs. Treatment with ABC-chondroitinase and HS lyase that specifically remove DS and HS chains from cell surfaces, resulted in significantly reduced adhesion of S. pyogenes bacteria to human epithelial cells and skin fibroblasts. Together with the finding that exogenous DS and HS could inhibit streptococcal adhesion, these data suggest that GAGs function as receptors in M protein-mediated adhesion of S. pyogenes. Mesh-terms: Bacterial Adhesion; Bacterial Proteins :: chemistry; Bacterial Proteins :: metabolism; Cell Adhesion; Dermatan Sulfate :: chemistry; Dermatan Sulfate :: metabolism; Dose-Response Relationship, Drug; Electrophoresis, Polyacrylamide Gel; Epithelial Cells :: cytology; Gene Deletion; Glycosaminoglycans :: chemistry; Glycosaminoglycans :: metabolism; Human; Protein Binding; Streptococcus pyogenes :: metabolism; Support, Non-U.S. Gov't; Tumor Cells, Cultured; Virulence Factors :: chemistry; http://www.blackwell-synergy.com/doi/pdf/1...0.x?cookieSet=1 Interactions between M proteins of Streptococcus pyogenes and glycosaminoglycans promote bacterial adhesion to host cells http://www3.interscience.wiley.com/cgi-bin...017607/ABSTRACT Keywords glycosaminoglycan • hyaluronan • chondroitin • heparin or heparan • synthase • polysaccharide • glycosyltransferase • extracellular matrix Abstract Glycosaminoglycans (linear polysaccharides with a repeating disaccharide backbone containing an amino sugar) are essential components of extracellular matrices of animals. These complex molecules play important structural, adhesion, and signaling roles in mammals. Direct detection of glycosaminoglycans has been reported in a variety of organisms, but perhaps more definitive tests for the glycosyltransferase genes should be utilized to clarify the distribution of glycosaminoglycans in metazoans. Recently, glycosyltransferases that form the hyaluronan, heparin/heparan, or chondroitin backbone were identified at the molecular level. The three types of glycosyltransferases appear to have evolved independently based on sequence comparisons and other characteristics. All metazoans appear to possess heparin/heparan. Chondroitin is found in some worms, arthropods, and higher animals. Hyaluronan is found only in two of the three main branches of chordates. The presence of several types of glycosaminoglycans in the body allows multiple communication channels and adhesion systems to operate simultaneously. Certain pathogenic bacteria produce extracellular coatings, called capsules, which are composed of glycosaminoglycans that increase their virulence during infection. The capsule helps shield the microbe from the host defenses and/or modulates host physiology. The bacterial and animal polysaccharides are chemically identical or at least very similar. Therefore, no immune response is generated, in contrast to the vast majority of capsular polymers from other bacteria. In microbial systems, it appears that in most cases functional convergent evolution of glycosaminoglycan glycosyltransferases occurred, rather than direct horizontal gene transfer from their vertebrate hosts. Anat Rec 268:317-326, 2002. © 2002 Wiley-Liss, Inc.

Sunshine mentioned that her son has a CBS mutation. Faith mentions MTHFR mutation. I remember bits and pieces about the CBS mutation from reading the Yasko forum. Look at the 2nd cite that I clicked on, when searching it. http://www.med.uiuc.edu/hematology/PtHomocysteinemia.htm Carolyn N just mentioned NAC that she became interested in from her sulfur research. Seems were onto something here!

Great post regarding heparin/hepran sulfate and Petechiae/purpura http://onibasu.com/archives/am/140593.html .

http://www.researchcrossroads.com/index.ph...amp;user=640119

Ruby, I was looking for something on the forum and read this thread, must have missed it before. Just wanted to say WAY TO GO on requesting the VAERS report! Did he do it? This is not about eczema but thought you might want to read it. The 2nd article is from a Merck website . Go figure. bolding mine http://www.ingentaconnect.com/content/mksg...70h90.henrietta In the unvaccinated group, there were no significant associations between pertussis infection and atopic disorders. In the vaccinated group, all associations between pertussis infection and atopic disorders were positive, the associations with asthma [odds ratio (OR) = 2.24, 95% confidence interval (CI95%): 1.36-3.70], hay fever (OR = 2.35, CI95%: 1.46-3.77) and food allergy (OR = 2.68, CI95%: 1.48-4.85) being significant. There was a positive association between pertussis infection and atopic disorders in the pertussis vaccinated group only. From the present study, it cannot be concluded whether this association is causal or due to reverse causation. Does reverse causation suggest that these kids may have developed these allergies because they didn't get the vaccination? Yep, I bet that's it. I bet my boys wouldn't have had allergies if I would have dosed them with MORE alum, mercury and antigens. http://www.merck.com/mmpe/sec13/ch165/ch165c.html But trends in developed countries toward smaller families with fewer children, cleaner indoor environments, and early use of vaccinations and antibiotics may deprive children of these exposures and inhibit TH2-cell suppression; such behavioral changes may explain the increased prevalence of some allergic disorders. Other factors thought to contribute to allergy development include chronic allergen exposure and sensitization, diet, and physical activity.

http://brain.oxfordjournals.org/cgi/conten...30/9/2302?rss=1 Novel locus for benign hereditary chorea with adult onset maps to chromosome 8q21.3–q23.3 Also, i have read a few posts here regarding seizures. I wanted to post this as there are quite a few area's of this chromosome that look to be seizure related in that 8q region. http://www.genecards.org/cgi-bin/listdisea...om&search=8 (oops edit to include link to page) In light of the info in the PANDAS study on the other thread about the "suspected pyruvate autoantigen" I thought it was interesting to see 8q22.1 Pyruvate dehydrogenase phosphatase deficiency [MIM:608782]

CP, I'm almost positive that this Dr. wouldn't have recognised the word thimerosal if he would have looked at flu vax insert. Then if he google it, he would see numrous studies disproving a connection to neuro problems. If he bothered to find the 3 separate studies showing increased incidence in tics in boys (which the CDC acknowledges) he would say the tiny amt in the flu shot far outweigh the risk. Hence my inability to trust that these people are really qualified to advise me in this area Kelly, We have a huge history with strep, however, in my guys case i think that any assoc problems are yes connected to strep but more to the functioning of the overall immune system, not a full blown auto immune attack resulting in the kind of symptoms that many report here. I wouldn't say that I have ever seen either of the boys "wake up a different child." Our illness related symptoms are usually in the way of tics, sometime after they were largely recovered. Neither ever tic while in the throws of illness. This is the first time since I have really gotten into this whole thing, that i can say that i clearly saw any type of psyc. assoc problems. My oldest son used to wake up (not really awake) and say he was sorry..over and over. At the time, i didn't know enough to look for those episodes in relationship to illness. Since looking at this heparan sulfate issue, I have been trying to see what i could come up with, regarding illness. If you get bored during this blessed holiday weekend, you might want to relax with this little study I totally expected to find that the inability to synthesize (whoa how do you spell that?) heparan sulfate would leave them more vulnerable to strep. This almost looks like they would be less vunerable????? Now I have to look at the dermation sulfate stuff. I will grow old (er) and die before i really know enough to make a difference here (big sigh with a smile). I hope there are no tics in heaven, or i'm afraid ill be right back at it. http://www.blackwell-synergy.com/doi/pdf/1...33.2003.03600.x Has anyone ever been told exactly what reactive antibodies appear to be causing a problem? Searching the things mentioned here, was quite enlighteneing. http://www.pubmedcentral.nih.gov/articlere...i?artid=1853370 A number of proteins of varying size have been identified as possible antigenic target proteins in the sera of tic disorder and early-onset OCD patients. Two studies have identified a protein of 60 kDa as a possible target (Church et al., 2003; Hoekstra et al., 2003), while a third study showed numerous proteins with different molecular weights as contributing to changes in TS antibody repertoires (Wendlandt et al., 2001). Most recently three neuronal glycolytic proteins, pyruvate kinase, aldolase and enolase have been suggested to be potential autoantigens in a group of patients with post-streptococcal movement and psychiatric disorders (Dale et al., 2006).

I wanted to add that we have had a terrible 8 days around here. 3:00 am last Sat morning youngest son wakes up moaning. He says his stomach feel horribly acidy. He is afraid if he throws up it will burn his throat out. I gave him some aloe water. Eventually woke hubby up to go get some rollaids. I was almost panicking. He vomits 3 or 4 times, then diarrhea starts. By Sun he's complaining of pain in his right side. He's sick, really sick acting, but his stomach does seem better. I decide to take him to a "med express" to let a Dr. make sure he doesn't see anything that would indicated appendix. I have been fairly happy with this place on other occasions. As the nurse is weighing him, she asks if he's up to date on his immunizations. I answer "unfortunatley yes." We get in the exam room and she asks me if my kids had vax reactions and tells me she has an autistic son. Dr. enters. Big guy with dreadlocks. Have never seen him in there before. I'm anticiating someone with a good sense of humor. WRONG! This guy is totally stuck on repeating that my son would not be there if he would have gotten the flu shot. Why oh why was this happening (i'm asking myself). I took it as long as i could, then ask him if he was really willing to be injected with mercury to avoid a case of the flu. I told him that it was all over the place that the flu vax was not even a good match this year. He says "worked for me" I said, no you must have a good immune system. He argues over and over that "there ain't no mercury in the flu shot" mercury is illegal, can't even get a mercury thermometer. I told him to go get the package insert. He kept repeating that he didn't know why i would be talking about mercury in the flu shot. Impossible, illegal, on and on. I backed all the way out of the exam room past the desk (where another Dr. was sitting) nurses, receptionists, repeating "go get an insert." A different nurse has to let us out, as they had closed, and the doors were locked. She asks me if i would mind telling her what that was all about and informs me that the Dr.s don't know, or don't want to talk about it. She tells me that they almost lost there 4 year old so to autism after his last round of shots. Started lining up his toys and starring at lights. She is no longer vaxing her 3 yr old daughter or her son. I told her "I WANT TO TALK ABOUT IT" why doesn't she tell those Dr.s in there, instead of hushed voice talking to me. These are our kids. I also told her, I was paying that guy (dr.) TO KNOW. I was furious. Monday the diarrhea starts again. Totally explosive. Did i mention that his fever was running 104? He says his throat is sore. This child is now crying inconsolably and telling me that there are some things that he has to tell me about and that it's all so terrible. Nothing makes sense. He is feeling guilty and insists that he just can't tell me. Over and over (this child is afraid he will die if he breaks a glow stick and some gets on his skin...i KNEw there was nothing here to really know). I take him to family Dr. who saw him only one time previously. It was for strep, which he had no increase in neuro problems with a few months ago. I requested and this dr. prescribed zith last time. He tells me that he some some very enlarged lymph nodes (nothing new there, they used to get the size of a golf ball) a horrible looking throat (although no white spots) and the stomach sounds are there, but not horrible, so he hopes the viral intestinal part is mostly behind us. Does a swab, says to go get amox filled in case it's strep. If no strep it's viral that is affecting his whole system. We get home, my baby comes out of his room telling me that the bad thoughts won't stop. He's crying. He tells me it has been going on for over and hour and he can't make it stop. With all of my wisdom and research, I do what any informed mom would do. I send my husband to Target to get him an air hero guitar (something that was planned for Easter instead of candy). The Dr. calls that same evening (God bless him) he's says strep is positive. We started amox that nite. Two horrible episodes of guilt/fear/anxiety in the same day...nothing since. These episodes were NOT normal "child not feeling well" acts out of sorts, type of thing. I still don't know if it was the strep or viral illness that caused this as it looks like he had two things at once. This started to be about sleep issues. Both boys do this weird thing where they will sort of wake up and act like they are picking at some tiny thing. Both of them. Got off topic sorry, but I guess i'll resist the temptation to delete.

Carolyn N. Have to ask you if your son was given the birth dose of Hep B during this time also. Wanted to say that I missed you! As I have been doing tons and tons of research on this gene thing (oldest sons bony growth) and sulfur or heparan sulfate to be more precise, i have thought of you. I had an awesome article bookmarked that explained GAGs. Now when i click on it, it doesn't work. Anyway, since I have WAY raised the bar on this research...spending hours learning about words like endoplasmic reticulum (sp?), cellular matrix, endothelium, etc. I'm wondering if you could scan this search and see if there is more info here, that can be useful. I will be posting much of what I'm trying to piece together on the bony tumor thread, as soon as I can. Since we have genetic evidence of a problem with sulfur metabolism (the sulfur appears to get stuck just outside of the nucleaus of the cell instead of being transported to the cell surface where it is used in further signaling or stored in the extracellular matrix, where it can be picked up and used in other functions), i'm very hopeful that this could prove to be a least part of the picture that could be helpful for at least a subset, if not many people dealing with TS/tics (wouldn't THAT just be too much to hope for!). Since you have an interest and a great knack for picking out useful info and posting in a way others can understand, I thought you would be just the person to help me out here the first is the entire search, the 2nd two are articles that I read thru http://www.google.com/search?q=susan+owens...amp;rlz=1I7DMUS Have to scroll down to the part written in english Susan Owens http://www.genitoricontroautismo.org/index...7&Itemid=46 symptoms of sulfur met http://64.233.167.104/search?q=cache:DK4aM...;cd=6&gl=us

Jules, This site will give you numerous links to autism groups. www.treatment4autism.com/resources.html This is a particular site that has been extremely helpful. These parents tend to get into the nitty gritty of why certain supplements help. I have to know the "whys," so parents who are dealing with much more challenging issues than we are have provided a lot of insight. health.groups.yahoo.com/group/autisminfo/ I'm sorry things didn't go well. It seems sometimes getting some support in place prior to yeast treatment is helpful. I hope you will keep us posted on any advice that you get that helps!

It might be in here, bmom I didn't wait for the whole thing to load. I have 13 tabs open and my computer is running pretty slow http://books.google.com/books?hl=en&id...JDElOfU#PPA5,M1

bmom, do you see it anywhere on this page. It may be the first one. When I clicked on it, it said no page found. If it's online, you won't have to go thru scanning it. http://www.google.com/search?q=Clinical+Ma...amp;rlz=1I7DMUS

Hey all, Caryn, from what i remember, you could see almost immediate reactions when your son ingested gluten containing products? I know you responded to a question that i asked, and i thought "wow." Don't remember all of the details though. It would probably be helpful for people investigating this route to search Caryn's posts. She has provided a wealth of info on this subject. Just click on her name anywhere on the forum, and you will get an option on the left hand side of a new screen that says "search members posts." For others, it may be a different issue. I have such a limited eater, with one son, the other eats normally, that even a rotation diet has not been doable. Neither have autism/asperger's or such. Youngest (11) did test reactive for cow's milk and interestingly...not grains, which i wonder if that's accurate? Anyway, a couple of articles on the low cholesterol. Again, autism research, but i have heard of negative behaviors when reducing food groups in low cholesterol children and cholesterol is important in overall health, which i'm certainly no expert on. Pamela Kay, I would fully investigate ANY condition that seems to run in your family. I'm finding some of the associated disease stuff, may provide a lot of clues about which pathways are the most problematic. Learn everything you can about cholesterol, lipids, what supplements help with utilizing fats etc. It's surprising what you can kick up! http://www.docguide.com/news/content.nsf/n...52571E2006F2657 Study Discovers Statistically Significant Link Between Abnormally Low Cholesterol Levels and Autism Spectrum Disorders You might want to search "low cholesterol+autism" there are quite a few articles.

Another thing to consider http://www.fda.gov/bbs/topics/consumer/CON00115.html and Look what's happening with Prevnar. They are changing it to include more strains, because ones that were lesser seen are becoming more prevalent. what "twist" might we see after widespread use of this new vaccine?

Calicat, I was glad to see that someone else found that article easy to understand. I learned much of that piece by piece. An article like that would have saved A LOT of time. Emma, I wonder if there will be any warnings in regards to people who have had unusual reactions to strep in the past. I wonder who, that has a family history of Rheumatic fever or abrupt onset of tics/ocd, is going to volunteer for the clinical trials. Once approved, the peds are probably going to say that a family with strep related problems are exactly the ones who should get the vaccine.

Betty, Be sure to get concise guidance on that low cholestrol level from the DAN! If you are considering eliminating milk and egg, you want to be careful there. Does your child eat meat?

Nicola, Welcome. By all means don't jump to a worse case scenerio. I'm wondering if you used any cold medicines during your son's cold last week. Did you give him tylenol? Any family history of tic disorders? hate to overwhelm you with questions, but if you have been reading thru the threads here, you probably know there are a lot of parents that are really determined to find the best way to keep our kids safe and healthy. Sharing info has been such a huge part of this forum, we don't want you to feel left out! Many of us have seen neurologist. The majority (with a few exceptions) have not found it to be very helpful. I guess my personal feeling is that it's not a bad idea in regards to ruling out other conditions. However, if they determine "it's just a tic," you will probably leave with a wait and see approach and not really any other useful information.

Very adverse drug reactions have been discussed here. One remark was regarding a poster's mom, who is dealing with Parkinson's. I wanted to mention that thimerosal has been mentioned as screwing up sulfur pathways in many articles. Anytime you see the word thiol or mercaptan, you know they are talking about a pathway that detoxing mercury would be important/associated with. http://en.wikipedia.org/wiki/Thiol In organic chemistry, a thiol is a compound that contains the functional group composed of a sulfur atom and a hydrogen atom (-SH). Being the sulfur analogue of an alcohol group (-OH), this functional group is referred to either as a thiol group or a sulfhydryl group. More traditionally, thiols are often referred to as mercaptans. The term mercaptan comes from the Latin mercurius captans, meaning 'laying hold of mercury,' because the –SH group binds tightly to the element mercury. http://gut.bmj.com/cgi/content/abstract/52/4/547 Conclusions: Microsomal epoxide hydrolase may play a role in the pathophysiology of Crohn’s disease. Furthermore, the epoxide hydrolase gene is located on chromosome 1q, close to a region previously linked to Crohn’s disease. http://en.wikipedia.org/wiki/Epoxide_hydrolase Epoxide hydrolase (also known as Epoxide hydratase) functions in detoxication during drug metabolism. It converts epoxides from the degradation of aromatic compounds to trans-dihydrodiols which can be conjugated and excreted from the body. Epoxides are significant as cytochrome P450 oxidase metabolites of unsaturated carbon-carbon bonds, but are also mutagenic. Epoxide hydrolase is present in large quantity on endoplasmic reticulum. http://gut.bmj.com/cgi/content/abstract/47/2/206?ck=nck BACKGROUND Luminal anionic sulphide may contribute to epithelial damage in ulcerative colitis. Thiol methyltransferase (TMT) governs sulphide detoxification by the colonic mucosa and circulating erythrocytes. AIMSTo measure levels of TMT activity in erythrocytes of surgically treated cases of colitis or in rectal biopsies of defined groups of colitis. PATIENTSVenepuncture blood was obtained from 37 blood donors and 27 subjects who had previously undergone a proctocolectomy for colitis: 18 for ulcerative colitis and nine for Crohn's colitis. Rectal biopsies from 122 cases were obtained: 47 without mucosal disease, 33 post-colon resection for cancer, 14 with moderate to severe ulcerative colitis, 15 with quiescent ulcerative colitis, seven with acute Crohn's colitis, and six with radiation proctitis. METHODSTMT activity was measured by high performance liquid chromatography with radioactive detection to measure 14C methylmercaptoethanol formation, the reaction product of cell extracts incubated with mercaptoethanol and 14C S-adenosylmethionine. RESULTS Erythrocyte TMT activity of surgically treated cases of colitis was significantly elevated (p<0.001) compared with control cases. TMT activity of rectal biopsies was significantly decreased (p<0.02) in acute but not quiescent ulcerative colitis, Crohn's colitis, or radiation colitis. CONCLUSIONS Erythrocyte TMT activity was persistently elevated after proctocolectomy for Crohn's disease and ulcerative colitis. No primary defect of TMT activity was found in any case of unoperated colitis but mucosal activity was diminished with disease progression of ulcerative colitis. Studies of genetic control of TMT activity of erythrocytes in inflammatory bowel disease appear worthwhile. Keywords: thiol methyltransferase; hydrogen sulphide; methylation; ulcerative colitis; Crohn's disease

This article is not about strep, but contains so many really important concepts thought I'd include it here anyway. Rare to get so much all in one article. This is written by Russel Baylock, the MSG awareness guy http://web.mac.com/rblaylock/Russell_Blayl..._Disorders.html

I realised that I forgot to include the links for the articles about the strep and AIDS hanging out intercellularly, on the first page of this thread. Opps. Notice the words cysteine protease in the pubmed article. http://www.pubmedcentral.nih.gov/articlere...i?artid=1326258 Background Group A streptococcal severe soft tissue infections, such as necrotizing fasciitis, are rapidly progressive infections associated with high mortality. Group A streptococcus is typically considered an extracellular pathogen, but has been shown to reside intracellularly in host cells. Methods and Findings We characterized in vivo interactions between group A streptococci (GAS) and cells involved in innate immune responses, using human biopsies (n = 70) collected from 17 patients with soft tissue infections. Immunostaining and in situ image analysis revealed high amounts of bacteria in the biopsies, even in those collected after prolonged antibiotic therapy. Viability of the streptococci was assessed by use of a bacterial viability stain, which demonstrated viable bacteria in 74% of the biopsies. GAS were present both extracellularly and intracellularly within phagocytic cells, primarily within macrophages. Intracellular GAS were predominantly noted in biopsies from newly involved tissue characterized by lower inflammation and bacterial load, whereas purely extracellular GAS or a combination of intra- and extracellular GAS dominated in severely inflamed tissue. The latter tissue was also associated with a significantly increased amount of the cysteine protease streptococcal pyrogenic exotoxin SpeB. In vitro studies confirmed that macrophages serve as reservoirs for viable GAS, and infection with a speB-deletion mutant produced significantly lower frequencies of cells with viable GAS following infection as compared to the wild-type bacteria. http://www.rochestercitynewspaper.com/news...here+it+lives+/ Eventually the virus's ability to hide in the body, and replicate itself, allows it to overcome the immune system. Researchers have long understood that HIV has the unusual ability to infect two different types of cells critical to the immune defense arsenal in humans - T-cells and macrophages. T-cells can sense that foreign organisms have invaded the body, and quickly multiply and grow into small armies designed specifically to counterattack the invaders. Macrophages perform a different, but equally important role. They roam the body independently, a bit like scavengers, seeking dead cells and bacteria to engulf and digest. They don't undergo cell division and rapidly multiply like T-cells. HIV's ability to infect both of these dividing and non-dividing cells is the reason scientists often refer to it as an "intelligent" virus. It's also the reason HIV is so deadly. HIV attacks T-cells because every time these cells divide, they create another opportunity for the invading virus to replicate itself. T-cells try to defend the body by committing suicide, and they self-destruct so quickly that HIV would be eliminated if it didn't have the macrophages as a fallback. "The purpose of every living organism is to survive, and HIV has brilliantly learned how to hide in macrophage cells over many years," http://www.rochestercitynewspaper.com/news...here+it+lives+/

No Tx, I don't think it's still in her system, but I don't know if the effects that could have been induced, would reverse quickly if there was a propensity for it in the first place. If you look at the half life, the longest I see is on the wiki site. It sounds from your post like it was well beyond the period that the actual drug might still be in effect. I'm not sure about Tamiflu. I don't know if it would have a 1/2 life like a drug? I guess btwn the illness, stress, and the two drugs, it's kind of hard to say what was the trigger. I sure hope it just passes without further incident. Just learn as much as you can about the possible "triggers" like anitcholergenics and such, so you can be on the lookout in the future. Also, you may want to google something like "drugs that induce movement disorders" I know I have read through those several times. http://en.wikipedia.org/wiki/Promethazine 1/2 life info is on the chart on the right http://www.migraines.org/treatment/prophnrg.htm The elimination half-life is 10-14 hours, with excretion of metabolites in the urine and the feces.

I'm so relieved to read that CP. I will add to the brag thread as soon as I have a chance. I'm staying signed on, but am away from the ole laptop most of the time. Little one has that stomach flu that Tx was talking about, I'm afraid. Was up most of the nite (nothing new there!) but was pretty worried as he kept complaining about his stomach feeling so acidy and burning. I thought he was having a major acid reflux thing going on, but as time goes on it looks more like a flu. Aching, fever, and both ends are very active. Aghhh.

In addition to last post, thought you might want to search "Tamiflu+dangers." You may be aware of some of the adverse reports with this drug? Boy, I feel more and more like the grim reaper here lecithin promotes choline. Is your daughter taking a multi vit? Egg yolks provide it too. This is something i ran across in my "saved files" i didn't go back over it, but thought there might be something helpful http://www.pslgroup.com/dg/10472a.htm Tacrine is a cholinergic agent that promotes acetylcholine transmission in the brain. It is currently approved for the management of selected memory disorders but not for Tourette syndrome. In contrast to Tacrine, drugs that block acetylcholine transmission can aggravate tic and need to be used cautiously in Tourette syndrome, Dr. Juncos said