kim

mack5mom, I'm sorry if I missed something in your posts, but I'm wondering why your daughter see's a cardiologist? I hope all was well at the appointment. kim

My husband had an episode of alopecia arieta (sp?) and my sister in law has Hashimoto's. I believe their aunt (husband and sister in law's...which would be my boys great aunt) was supposed to have lupus antibodies. I think one other aunt on that side of the family was supposed to have had the alopecia problem too. My boys don't have classic PANDAS symptoms. I dismissed PANDAS as we never saw an explosive onset. I'm starting to look at this whole syndrome a little differently right now though.

mack5mom, I'm wondering if you meant thyroid disease or all 3 conditions? I'm so sorry your daughter is going thru all of this and wanted to say welcome to the forum. kim

http://www.md-journal.com/pt/re/medicine/a...#33;8091!-1 Chorea in the Antiphospholipid Syndrome: Clinical, Radiologic, and Immunologic Characteristics of 50 Patients from Our Clinics and the Recent Literature. http://lup.sagepub.com/cgi/content/abstract/8/2/127 (bolding mine) Y Shoenfeld Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel Hashomer, Israel A D Korczyn Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv 69978, Tel Hashomer, Israel http://www.annalsnyas.org/cgi/content/abstract/1109/1/473 and more articles on this subject http://www.google.com/search?hl=en&rls...ion&spell=1

http://www.jneurosci.org/cgi/content/full/20/21/7932 Regulation of AMPA Receptor GluR1 Subunit Surface Expression by a 4.1N-Linked Actin Cytoskeletal Association (bolding mine) and

If you google UK antibasal ganglia test, I felt it was pretty apparent that they were not talking about ASO/antiDnase levels (in regards to original posters question) This one helps explain some of the questions about the study that Panda's Denmark posted. Autoimmunity Streptococcal mimicry and antibody-mediated cell signaling in the pathogenesis of Sydenham's chorea http://intramural.nimh.nih.gov/pdn/pubs/pub-15.pdf Recent Publications http://intramural.nimh.nih.gov/pdn/recent_publications.htm http://www.ncbi.nlm.nih.gov/pubmed/16158191 Gangliosides, a heterogeneous family of glycosphingolipids abundant in the brain, have been shown to affect neuronal plasticity during development, adulthood and aging. This review will examine old and recent evidence that exogenous gangliosides and in particular GM1, the prototype member of this family, exhibit multimodal neurotrophic effects.

ad ccl has mentioned that her sons vocals have improved with carnitine use (right Alison?) thought this was interesting http://www.translational-medicine.com/content/4/1/34

HeatherB. I'm wondering if you caught my 2 posts to you, right above myrose's welcome message?

Tami, I missed the response from you and Cheri above Pmom's. Let me ask you this (it's way premature...as usual I have this wicked tendency to move above concepts when I'm not even sure of the basics) Did you get from the anti basil ganglia thread, that GlcNAc was what was being attached in brain tissue and in the strep capsule? Was GlcNAC one of the cross reactive glycans? I sure do agree about the inflammation aspect, but I'm still looking at these genetic issues.

P Mom YES! I'm so glad you read the studies to the right. Those adhesion molecules are what is taking up every minute that I can spare. I didn't think there was any point mentioning it, because I don't understand it enough to explain anything, but like I said, I'm trying! this is just a starting point http://en.wikipedia.org/wiki/Intercellular_adhesion_molecule

http://www.sciencedirect.com/science?_ob=A...89cd000043cecff Case study Anti-basal ganglia antibodies and acute movement disorder following herpes zoster and streptococcal infections Received 29 September 2006; revised 3 November 2006; accepted 3 November 2006. Available online 11 December 2006. Abstract Anti-basal ganglia antibodies (ABGA) have been associated with poststreptococcal encephalitis similar to encephalitis lethargica (EL). We report two children with parainfectious encephalitis of similar phenotype and IgG ABGA. However, the associated pathogens in the two cases differed; β-hemolytic streptococcus and herpes zoster. ABGA may not be specific to poststreptococcal encephalitis, but rather a surrogate marker of an inflammatory mediated movement disorder, which may respond to immunotherapy.

Cheri, Interesting on NPY http://lib.bioinfo.pl/auth:Sallee,FR If anyone can make anything of that neuropeptide Y stuff and pertussis, I sure would like to know!

HeatherB In addition to last post, I wanted to share this with you. You may want to ask your Neuro about this. http://www.ncbi.nlm.nih.gov/pubmed/11893522 New clues about vitamin D functions in the nervous system Vitamin D looks interesting in regards to what I'm looking at with my boys. I'll be posting some other Vit D studies too.

HeatherB, As I was looking for gut info (youngest son's limited diet) regarding the Heparan synthesis and GlcNAc that I have recently become aware may play a role in my sons tics, I ran across an article that talked about disordered HS in gliomas. I knew that I had heard that word before and did a search of the forum, and up you popped. Just wanted to tell you that you might want to read some of the studies from the link that I just posted on this thread (mentions 10,000,000. grant) http://www.latitudes.org/forums/index.php?showtopic=3255 I don't know if there is info there that could be beneficial to your son or not, but possibly worth looking at. If you see or make any connections, I hope you'll let us know.

Diagram GlcNAC discussed in article PANDAS Denmark posted and the condition I'm looking at, AND http://www.newscientist.com/data/images/ar...07/26074501.jpg These guys are working on this ($10,000,000 grant) The studies are clickable on the left http://www.researchcrossroads.com/index.ph...amp;user=640119 autosomal dominant bone disorder that is caused by defective HS synthesis due to mutations of the GlcNAc/GIcA co-polymerase EXT1. Interestingly, there have been clinical reports indicating that HME patients associate autistic traits.

Cheri, I feel almost comatose today. I stayed up waaaay too late last nite. I just had to take a minute though to send a hug to Cheri...Our Glial Cell Notwithstanding, glial cells are imperative for the proper function of neurons since it is through them that support, insulation and nutrition are adequately provided. Perhaps the most familiar example of a glial cell is the myelin sheath, a fatty substance that wraps around neuron axons to facilitate signal transduction. Other types of glia include astrocytes, Schwann cells, satellite cells and radial glia. Glial cells provide support and protection for neurons, the other main type of cell in the nervous system. They are thus known as the "glue" of the nervous system. The four main functions of glial cells are to surround neurons and hold them in place, to supply nutrients and oxygen to neurons, to insulate one neuron from another, and to destroy pathogens and remove dead neurons. from one of the neurons

In addition to last post, I wanted to leave this here too. The interactions btwn bacteria and host, and what were talking about here (extends to other pathogen too...trying to piece together varicella in this mess) seems the way GAGS (glucosaminoglycans) interact with each is be important. I know Carolyn N. just hit on some of this info in regards to hormones, it's not always illness. http://www.blackwell-synergy.com/doi/full/...33.2003.03600.x 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.

? http://en.wikipedia.org/wiki/N-Acetylglucosamine GlcNAc is the monomeric unit of the polymer chitin, which forms the outer coverings of insects and crustaceans. GlcNAc is also of note in neurotransmission, where it is thought to be an atypical neurotransmitter functioning in nocioceptive (pain) pathways. It has been proposed as a treatment for autoimmune diseases.[1 From the PANDAS study (bolding mine) http://www.csus.edu/bios/faculty/Kirvan/Ki...JNI_article.pdf Most importantly, PANDAS CSF showed highly elevated levels of CaM kinase II induction similar to that of positive control SC CSF (Fig. 4a). Non-PANDAS CSF showed no activation of CaM kinase II. PANDAS CSF-induced CaM kinase II activity was blocked by the streptococcal associated GlcNAc epitope, but not by group A streptococcal serotype 5 M protein, suggesting that antibodies directed against an epitope of the group A carbohydrate of Streptococcus pyogenes may be important in mediating cell signaling (Fig. 4b). Therefore, signaling activity found in behavior and movement disorders during the symptomatic phase of disease suggests that antibodies present in the sera and CSF were associated with and may contribute to the clinic symptoms in acute phases of disease. I don't have a clue what this is saying, but looks important http://www.jneurosci.org/cgi/content/abstract/13/2/559 Overexpression of Ca2+/calmodulin-dependent protein kinase II in Neuro2a and NG108-15 neuroblastoma cell lines promotes neurite outgrowth and growth cone motility

http://www.newscientist.com/channel/health...=mg19426074.500 Previous studies suggested that glucosamine, a dietary supplement commonly taken by people with osteoarthritis, has some immunosuppressive effects. This led Michael Demetriou and colleagues at the University of California, Irvine, to investigate a similar but more potent compound called N-acetylglucosamine (GlcNAc)

Excellent Carolyn! Now think about this. We have two posters here that have each had testing done that has shown a mutation in either MTHFR and one with a CBS mutation. From one of your links Now check out this page http://www.med.uiuc.edu/hematology/PtHomocysteinemia.htm * my note MS=methionine synthesis......you can supplement methionine, but you may not avoid the problem of increased homocysteine by going that route. and and This one makes me wonder if a high fever or an increase in problems during hot months could factor in?

Mom2a, Did your state exemption form have language in it about acknowledging that you are putting others at risk by excercising your choice not to vaccinate? My kids vax records were only checked in 6th grade. We were current. I thought my youngest son was due for that 6th Tdap, but we were just under the wire. My oldest son's record was not checked in 9th grade. As soon as they make the 2nd varicella manditory (or HPV or whatever is next), they will be flagged and I'll be dealing with the exemption issue. I am not happy with the language in the form that can be printed from the state web site. One suggestion. If you sign a waiver at the Ped/reg. Dr. office, scratch out that language (about putting others at risk) initial and have someone in the office initial too. This is not for the state, it's for the Dr.s records for proof that they made you aware of which vaccines your child is due for. I doubt that they will give you a problem, if they don't throw you out of the practice for declining a vax in the first place, that is. I do want to add here too, that I am not suggesting that anyone get or not get any particular vaccination. Just urging everyone to make the best choice you can with all of the info that you can gather.

bmom, Not sure what you mean here Are you talking about filing an exemption?

ilovedogs, I think the hope was/is that they can vax to the point where the titers will stay elevated for long enough to attain about the same level of protection that the wild caught would have afforded (boy do I sound stuffy!) Some people will get shingles with the wild caught too, but this way, it almost has to be way more if you ask me. The whole program DOES NOT MAKE SENSE to me either, unless I'm one of the people who will profit hugely if I can make people think that this is a good thing. We could walk through almost each vax and look at similar issues that make you go "WHAT?"

Crohn's Gene http://www.blackwell-synergy.com/doi/abs/1...41.2007.01661.x The American Journal of Gastroenterology Volume 103 Issue 3 Page 615-620, March 2008 CONCLUSIONS: Our findings confirm recently reported genome-wide associations between the IL-23R gene and CD. They suggest that the gene is also associated with pediatric-onset CD among Canadian children. A genome-wide association study identifies IL 23 R as an ...We found a highly significant association between Crohn's disease and the IL 23 R gene on chromosome 1 p 31, which encodes a subunit of the receptor for the ... Enovin, a member of the glial cell-line-derived neurotrophic ...chromosome 1, region p31.3-p32. In vitro, enovin stimulates neurite outgrowth and content.febsjournal.org/cgi/reprint/266/3/892.pdf From above post 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 MTHFR is also found in this area

Cheri, If there is one thing I can say with clarity after bumbling through growth facters, cell to cell communication, words I recognize, but can't pronounce. They are getting close. I really really believe that. Technology has advanced to the point where there will be new info soon. It's sad to say, but with the explosion in autism, there is a lot of motivation.