kim

Myrose, It's bad enough for children and parents to deal with the tics and some of the issues that go along with it. It's horrible when things escalate. I think all of us have been through the quite times and the panic times. I pray you get some answers quickly. Thoughts and prayers are with you. Kim

A few things to share here. I'm finding it harder and harder to pray for this man's soul (Offit.... vaccine safety mouth piece and patent holder) and everyone who continues to shove what I consider to be misleading facts down the throats of unsuspecting young parents about the "safety studies" and such. This cat is out of the bag. Gerber is either woefully uninformed or is being outright misleading, IMO as there are numerous studies that DO support the theory that toxins from the environment play a role. I do not have an autistic child, but I do believe I have children that were harmed by vaccines. Edit...to remove some harsh language Don't miss the dental amalgam article near the bottom http://ca.news.yahoo.com/s/capress/080511/...tism_court_case and http://www.ageofautism.com/2008/03/paul-offit-the.html The bio below his Op-Ed piece reads: "Paul A. Offit, chief of the infectious diseases division of the Children’s Hospital of Philadelphia, is the author of “Vaccinated: One Man’s Quest to Defeat the World’s Deadliest Diseases.” We thought you should understand the implications of the rest of Dr. Offit's bio (including his disclaimer line in the piece.) Just to be clear. If he's going to speak out in a national publication about the safety of vaccines, you should know that he has a financial interest in vaccinations. And that he has served on the CDC Advisory Committee on Immunization Practices (ACIP.) Perhaps The Times just didn't have enough column inches to spare for that part? Paul Offit makes money every time your child has her 2 month, 4 month and 6 month well visit and receives the Rotateq vaccine, which is now safely ensconced on the AAP vaccine schedule. *Aluminum and Vaccine Ingredients: What Do We Know? What Don't We Know?* by Lawrence B. Palevsky, MD, FAAP http://www.northportwellnessexpo.com/article-nvic.html - - - - *Is Aluminum the New Thimerosal?* By Robert W. Sears Issue 146, January/February 2008 http://www.mothering.com/articles/growing_...thimerosal.html http://content.karger.com/ProdukteDB/produkte.asp?Doi=107546 *Aluminum-induced mitochondrial dysfunction leads to lipid accumulation in human hepatocytes: a link to obesity* Mailloux R, Lemire J, Appanna V. Cell Physiol Biochem. 2007;20(5):627- 38. Mitochondrial dysfunction is the cause of a variety of pathologies associated with high energy-requiring tissues like the brain and muscles. Here we show that aluminum (Al) perturbs oxidative-ATP production in human hepatocytes (HepG2 cells). This Al-induced mitochondrial dysfunction promotes enhanced lipogenesis and the accumulation of the very low density lipoprotein (VLDL). Al-stressed HepG2 cells secreted more cholesterol, lipids and proteins than control cells. The level of apolipoprotein B-100 (ApoB-100) was markedly increased in the culture medium of the cells exposed to Al. (13)C-NMR and HPLC studies revealed a metabolic profile favouring lipid production and lowered ATP synthesis in Al-treated cells. Electrophoretic and immunoblot analyses pointed to increased activities and expression of lipogenic enzymes such as glycerol 3-phosphate dehydrogenase (G3PDH), acetyl CoA carboxylase (ACC) and ATP-citrate lyase (CL) in the hepatocytes exposed to Al, and a sharp diminution of enzymes mediating oxidative phosphorylation. D-Fructose elicited the maximal secretion of VLDL in the Al-challenged cells. These results suggest that the Al-evoked metabolic shift favours the accumulation of lipids at the expense of oxidative energy production in hepatocytes. Copyright © 2007 S. Karger AG, Basel. PMID: 17762189 *Microarray Analysis of GI Tissue in a Macaque Model of the Effects of Infant Vaccination* Saturday, May 17, 2008 IMFAR / S. J. Walker , Institute for Regenerative Medicine, Wake Forest University Health Sciences, E. K. Lobenhofer , Cogenics, a Division of Clinical Data E. Klein , Division of Laboratory Animal Resources, University of Pittsburgh, A. Wakefield , Thoughtful House Center for Children, Austin, TX L. Hewitson , Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA/ Background: There has been considerable debate regarding the question of an interaction between childhood vaccinations and adverse sequelae in the gastrointestinal tract, immune system, and central nervous system of some recipients. These systems, either singly or in combination, appear to be adversely affected in many ASD children. Although pre-clinical tests of individual vaccines routinely find the risk/benefit ratio to be low, previously there has not been a study to examine the effects of the comprehensive vaccination regime currently in use for infants. Objectives: This study was designed to evaluate potential alterations in normal growth and development resulting from the vaccine regimen that was in use from 1994-1999. Specifically, this portion of the study was to compare the gene expression profiles obtained from gastrointestinal tissue from vaccinated and unvaccinated infants. Methods: Infant male macaques were vaccinated (or given saline placebo) using the human vaccination schedule. Dosages and times of administration were adjusted for differences between macaques and humans. Biopsy tissue was collected from the animals at three time points: (1) 10 weeks [pre-MMR1], (2) 14 weeks [post-MMR1] and, (3) 12-15 months [at necropsy]. Whole genome microarray analysis was performed on RNA extracted from the GI tissue from 7 vaccinated and 2 unvaccinated animals at each of these 3 time points (27 samples total). Results: Histopathological examination revealed that vaccinated animals exhibited progressively severe chronic active inflammation, whereas unexposed animals did not. Gene expression comparisons between the groups (vaccinated versus unvaccinated) revealed only 120 genes differentially expressed (fc >1.5; log ratio p<0.001) at 10 weeks, whereas there were 450 genes differentially expressed at 14 weeks, and 324 differentially expressed genes between the 2 groups at necropsy. Conclusions: We have found many significant differences in the GI tissue gene expression profiles between vaccinated and unvaccinated animals. These differences will be presented and discussed. - - - - /The authors and organizations are withholding comment or elaboration until the full articles are published. / * The material in this post is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.For more information go to: http://www4. law.cornell. edu/uscode/ 17/107.html http://oregon. uoregon.edu/ ~csundt/document s.htm If you wish to use copyrighted material from this email for purposes that go beyond 'fair use', you must obtain permission from the copyright owner*.* // [Non-text portions of this message have been removed] Is the proliferation of vaccinations really in your child's best interest?* May 15, 2008 By Barbara Jamison, R.N. For the News-Sentinel http://www.news-sentinel.com/apps/pbcs.dll...ORIAL/805150318 All parents should review the list of routinely recommended vaccinations for babies, toddlers and young children prior to giving consent. Read the available information about each vaccine. Go online or to the public library. Ask a friend, co-worker, nurse or doctor for in-depth information regarding each vaccine. Ask questions such as: How dangerous is the illness? Is my child likely to contract the illness? What are the risks of the vaccine? Vaccination against disease has been an ongoing process since the smallpox inoculations in the late 1700s. At that time, the etiology of common infectious diseases was unknown. Today in America, most people have an excellent quality of food, water and proper sanitation. We understand how disease is spread and have access to treatment. It is time to take a new look at the need for specific vaccinations. Vaccination is designed to benefit the public health. It is a one-size-fits- all approach. Thus, the rural Midwestern baby receives the same treatment as the crowded inner-city baby. Surely, the needs of these babies are not the same. Hepatitis B vaccine is recommended for men who have sex with men, IV drug users and babies prior to hospital discharge after birth. This is because the government wishes to avoid future cases of Hepatitis B. Thus, all babies, regardless of the likelihood of exposure, are given this injection. Does that seem appropriate to you? This same theory is the reason for the recent push to vaccinate all 11- to 12-year-old females against HPV (human papilloma virus), which is spread by sexual contact. Another example: Hepatitis A is a contagious liver disease spread through contaminated food and water. Children are not among the high-risk group. Does your infant really need this shot? A prudent approach would be to target a specific vaccine to specific patient populations. The minimal recommended vaccination schedule includes 60 doses --- some different strains of the same illness --- for 14 diseases by age 18 months. It is common for the shots to be bunched in one day. If the baby is "off" schedule, your 15-month-old may receive all the 12-18 monthly doses on the same office or clinic visit. Surely, this must have some adverse effect on the immature immune system. Some scientists correlate the proliferation of autoimmune disorders in our society to multiple vaccinations at that very early age --- illnesses such as asthma, diabetes, lupus, inflammatory bowel, rheumatoid arthritis, allergies and certain cancers. Some medical researchers and parents believe components of vaccine products cause or did cause autism and other neurological disorders. All vaccines carry risk and can be fatal. Indeed, a reaction is the expected outcome necessary to provide immunity. Scientists are continually making new vaccines and more trivalent-polyvalen t forms. These are combinations of vaccines in one dose. The more combinations, the less likely science will be able to determine which vaccine causes a possible severe reaction in your child. And the likelihood of severe reaction increases. Even today, we do not know the true extent of problems post injection. The FDA estimates that parents or physicians do not report 90 percent of adverse vaccine reactions. Reactions such as seizures, high-pitched screaming, fever, severe diarrhea, vomiting and shallow breathing are not reported. SIDS will not be reported as a vaccine reaction unless it happens within 48 hours of the shot. Yet many vaccine responses occur within one to four weeks. The medical establishment equates refusal to vaccinate or choosing partial vaccination as tantamount to child neglect. These parents are often treated with contempt. Perhaps these parents are better parents. Maybe it is best to allow viral contact between children. It is impossible to prevent the spread of most viruses anyway. This would encourage young immune systems to respond normally. This letter is meant to increase parental awareness about childhood vaccination and to encourage a more individual approach. Otherwise, the price we pay is the loss of natural immunity to many diseases. /Barbara Jamison is a registered nurse. * /The material in this post is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.For more information go to: http://www4. law.cornell. edu/uscode/ 17/107.html http://oregon. uoregon.edu/ ~csundt/document s.htm If you wish to use copyrighted material from this email for purposes that go beyond 'fair use', you must obtain permission from the copyright owner*.* [Non-text portions of this message have been removed] *Philly First In The Nation To Require Mercury Disclosures* > > By: JENNY DeHUFF, The Bulletin > 05/14/2008 > http://www.thebulletin.us/site/index.cfm?n...576361&rfi= > > Philadelphia - Freya Koss said she developed multiple sclerosis, lupus > and other health problems from a silver dental filling containing > mercury. She and several other consumer advocates and health > professionals were at City Hall yesterday to tell their stories of > cavity fillings gone wrong. > > The Pennsylvania Coalition for Mercury-Free Dentistry and Consumers for > Dental Choice (CDC) stood in front of large signs warning of the dangers > of silver amalgam fillings - most notable for their high levels of the > neurotoxin mercury. > > In December, Philadelphia City Council unanimously passed legislation > backed by Councilwoman Blondell Reynolds Brown that requires dentists to > distribute patient brochures disclosing the dangers of silver amalgam > fillings. > > "The textbooks don't tell us this," said Charlie Brown, spokesman for > the CDC. "It is absurd to think nothing is damaged when a neurotoxin is > placed an inch from someone's brain." > > "I quickly learned of the harrowing effects of mercury when an old > filling was removed and a silver filling replaced it," said Ms. Koss, > director of the Pennsylvania Coalition for Mercury-Free Dentistry. > "Seven days later, I got sick." > > Don Robbins operates a mercury-free dentist practice out of Exton. He > called himself one of the few dentists committed to informing patients > of the risk of silver amalgam fillings. Holding a jar of dental mercury > filling, Mr. Robbins pointed out the skull and crossbones icon on the > label, warning that the substance is hazardous to children and to handle > the container with gloves and protective gear. > > "It's deeply disturbing what's going on in our profession," Mr. Robbins > said. "Less than 60 percent of dentists in the U.S. belong to the > American Dental Association (ADA). Silver fillings are 50 percent > mercury. If you have two, three or more silver fillings, you are above > the Environmental Protection Agency's (EPA) limit for mercury intake." > > Earlier in the day, consumers protested statements made by the president > of the Pennsylvania Dental Association. "No dentist places mercury in a > patient's mouth," he was reported to have said. > > The alternatives to these types of fillings are typically white > composite resin fillings, which are more commonly used today but don't > last as long as silver fillings. > > Jenny DeHuff can be reached at jdehuff@... > > ©The Evening Bulletin 2008 > > The material in this post is distributed without > profit to those who have expressed a prior interest > in receiving the included information for research > and educational purposes.For more information go to: > http://www4. law.cornell. edu/uscode/ 17/107.html > http://oregon. uoregon.edu/ ~csundt/document s.htm > If you wish to use copyrighted material from this > email for purposes that go beyond 'fair use', you > must obtain permission from the copyright owner*.* > Our results indicate the genotoxic and cytotoxic effect of TH in cultured human peripheral blood lymphocytes at tested doses in cultures with/without S9 fraction 1: Toxicol In Vitro. 2008 Jun;22(4):927- 34. Epub 2008 Feb 1.Click here to read Links Genotoxicity of thimerosal in cultured human lymphocytes with and without metabolic activation sister chromatid exchange analysis proliferation index and mitotic index. Eke D, Celik A. Mersin University, Faculty of Science and Letters, Department of Biology, 33343 Mersin, Turkey. Thimerosal is an antiseptic containing 49.5% of ethyl mercury that has been used for years as a preservative in many infant vaccines and in flu vaccines. Thimerosal is an organic mercurial compound used as a preservative in biomedical preparations. In this study, we evaluated the genotoxic effect of thimerosal in cultured human peripheral blood lymphocytes using sister chromatid exchange analysis in culture conditions with and without S9 metabolic activation. This study is the first report investigating the genotoxic effects of thimerosal in cultured human peripheral blood lymphocyte cells using sister chromatid exchange analysis. An analysis of variance test (ANOVA) was performed to evaluate the results. Significant induction of sister chromatid exchanges was seen at concentrations between 0.2 and 0.6mug/ml of thimerosal compared with negative control. A significant decrease (p<0.001) in mitotic index (MI) and proliferation index (PRI) as well as an increase in SCE frequency (p<0.001) was observed compared with control cultures. Our results indicate the genotoxic and cytotoxic effect of TH in cultured human peripheral blood lymphocytes at tested doses in cultures with/without S9 fraction

Faith, When trying to figure out how to answer that question, it occured to me that I needed to go back and look at people that had the multiple hereditary syndrome. I was making an assumption that my boys sort of developed this, not necessarly born with it. I was perfectly willing to accept that it was just an inherited condition, but I was mostly looking at current research. When I did that (went back and looked at the hereditary symdrome), it hit me that my boys most likely DO NOT have that disorder. I should have been focusing on Sunshine's info. The CBS mutation. Sunshine, if you're reading, could you PM your Dr.s phone #. I would very much like to speak with her and make arrangements for testing for at least one of the boys. I can probably find it, but if you have it handy, I would really appreciate it. I left this thread hang, as I was trying to digest how foolish it was to jump to what was very likely the wrong conclusion. Sunshine, I think for now we can forget the problem that occurs in the golgi. I do think the study that I have been referring to provides very useful info though. I'm typing on the way out the door, but I appreciate SO much the discussion on this thread. I'll be back and will try to give more info to some of the remarks here. Thank you all again!

Cheri, Since I had posted this article a few times already I was going to see if I could find anything new, but I can't find anything that explains MTHFR or CBS mutations any better than this. I know you haven't had time to read every post here, so here it is again. I sure hope things are looking up for your husband. http://www.med.uiuc.edu/hematology/PtHomocysteinemia.htm

Caryn, I bet with all of your knowledge regarding Celiac, that you weren't even surprised. Caryn, can you share which genes those are? You know how I'm looking for genes or mostly areas of different chromosomes, that might be part of this complex. I'm also curious as heck to see if either of these genes are located near any of the EXT genes. Thanks tons for all of your very valuable posts/info.

myrose, I just saw a heading like this. Again, probably not a significant amt. just caught my eye. [PDF] SULFONAMIDE CROSS-REACTIONS EXPLAINED File Format: PDF/Adobe Acrobat - View as HTML Many medications contain sulfur but are not sulfonamides, e.g., amoxicillin,. captopril, omeprazole, spironolactone, sulfates and sulfites. ... Don't mean to a pain regarding the petachias, but it can occur anywhere i believe. Most of the google image pics look like extreme cases. I didn't realize the one I posted was the result of chemo. Her is a pic of an individual dot from wiki I have seen those dots on the throat. I still don't know if there is any real significance. I don't think it's real uncommon (especially in throat?) but wondering if it is a sign of something else with our kids? http://en.wikipedia.org/wiki/Petechia from list here Childhood protein-energy malnutrition ?????

Cheri, You didn't sound one bit unthankful. THANK YOU for hanging in here with me on this! I want you to scan this study. It just seems I'm seeing a reoccuring theme here. Something to do with clotting abilities and how the Gags are sulfated. Remember when we were talking about connective tissue and conditions your son was born with? http://www.ncbi.nlm.nih.gov/pubmed/8095623 We have studied the distribution and nature of sulphated glycosaminoglycans (GAGs) within normal and inflamed intestine. There is increasing evidence that these negatively charged polysaccharides, which both regulate the ability of albumin to leave the vasculature and inhibit thrombosis, may be affected by inflammatory cells and their products. We obtained samples of freshly resected intestinal tissue from eight controls, eleven patients with Crohn's disease, and six with ulcerative colitis. Sulphated GAGs were detected by means of a gold-conjugated poly-L-lysine probe, and the tissue density of anionic sites was assessed semiquantitatively by means of a Lennox graticule. In normal intestine there was staining in the vascular endothelium and the subepithelial basal lamina and throughout the extracellular matrix of the lamina propria and submucosa. Tissue from the patients with inflammatory bowel disease showed inflammation macroscopically and on histology. There were profound abnormalities of extracellular matrix GAGs, limited to the mucosa in ulcerative colitis and greatest in the submucosa in Crohn's disease. There was also substantial loss of GAGs from the subepithelial basal lamina in both disorders and from the vascular endothelium in submucosa in Crohn's disease. The extent of local GAG disruption was associated with the distribution of macrophages immunoreactive for tumour necrosis factor alpha and the activation marker RM 3/1. We suggest that inflammatory disruption of vascular and connective tissue GAGs may be an important pathogenetic mechanism, contributing to the leakage of protein and fluid, thrombosis, and tissue remodelling seen in inflammatory bowel disease. These were the two things that really grab my attention but I'm wondering if it's the other way around, the GAGs have a problem FIRST only in a different area...bolding mine and

Oh CP you totally made me cry. Thank you too! I know how I must frustrate people, but honestly I'm doing the best I can. I need a signature line that says something like "How can I explain to others concepts that I don't fully understand" Hugs to you too. If there is anything that I can help anyone here with, even at the risk of making a complete fool of myself, well, I guess i'll risk it. Cheri, I understand about your son not wanting blood work. I wonder if a urine test would work? Your son appears to be doing so well, it seems obvious that whatever you're doing is working well. Supplementing methionine, wouldn't have anything to do with the interplay of the genetics that may be involved here. Let's say that the MTHFR mutation is one of the important mutations involved in this syndrome. Folic acid and B12 are important in getting this pathway to function right, if you have it. I'll try to find you a good link. IF you carry this mutation, you don't have what's needed to get to methionine and utimately to glutathione (major antioxidant). You can supplement methionine and get glutathione production increase, but you may also have homocysteine levels that are rising, if the form of B12 isn't being utilized correctly or not at all, and your folate, folanic acid (may be necessary instead of folate...i never got that straight) isn't where it should be. I'm going to go back and check this info. These mutations, CBS and MTHFR (there are others...COMP is one, which is a defect in sythesizing neurotransmittlers but having that mutation would just be too easy wouldn't it!) are part of the Yasko genetic testing. Other DAN's are testing these too. Sunshine's son who has the same type of bony tumor that my son has, showed a CBS hetro mutation (one copy that's not working) I believe these two mutations have quite a bit in common, with problems that result from different origins. If your husbands mom had glaucoma it may just be an indication of part of the genetics involved, again, supplementing methionine might be beneficial in one way, but harmful in another. That's what you would want to watch out for. Does that help? If not, ask anything. I might edit, if I find where I explained something wrong here. As always, this is only for discussion purposes! I'm not capable of getting all of this right, only giving others a place to look for there own answers. I'm really starting to wonder how much mom AND dad contribute to all of this. It may appear to be so clear cut, but the more I learn, the more I wonder, in our case at least.

Cheri, I forgot to include the links, Sorry! I'm posting in the middle of "multitasking" too http://www.molvis.org/molvis/v14/a79/ C677T polymorphism in the methylenetetrahydrofolate reductase gene is associated with primary closed angle glaucoma The MTHFR C677T polymorphism was found to be associated with PCAG but not POAG in patients of Pakistani origin. http://www.ncbi.nlm.nih.gov/pubmed/1248649...Pubmed_RVDocSum Bleich S, Jünemann A, von Ahsen N, Lausen B, Ritter K, Beck G, Naumann GO, Kornhuber J. Department of Psychiatry and Psychotherapy, Friedrich-Alexander-University, Schwabachanlage 6-10, D-91054 Erlangen-Nuremberg, Federal Republic of Germany. stefan.bleich@psych.imed.uni-erlangen.de Homocysteine levels and the frequency of heterozygous methylenetetrahydrofolate reductase (MTHFR) C677T mutation are increased in open-angle glaucoma. Since homocysteine can induce vascular injury, alterations in extracellular matrix remodelling, and neuronal cell death, these findings may have important implications for understanding glaucomatous optic neuropathy.

Cheri, I have had a bottle of SamE sitting on my cupboard for a couple of months. I have no doubt about it's ability to help. The possible problem I see, is where eleveated levels of homocysteine come in. You could get the benefits because you are supplementing something that is lacking at the top, but have an underlying problem worsening that wouldn't be apparent. I think a simple blood test to check homosysteine levels would be all that might be necessary.

Cheri again! I'm going to take this one step further and I hesitate to do this because this info may not be accurate and certainly not complete. This is just my very limited understanding and what I was looking for to begin with. My understanding....... If you have a homozygous (two copies --) mutation in either of these genes it will result in more serious consequences. If you have only one (-) copy or a heterozyguos mutation, the evidence is lighter on a problem with converting homocysein to cystein (from mainstream artilces, it doesn't look like a problem at all). I wasn't aware that MTHFR caused this same problem (as CBS) of converting homocystein to cystein, but ran across something this weekend, that looked like it did. I don't know if they were talking about -- or +- though. Anyway, if you have a problem with homo, to cystein, it looked to me like you didn't want to supplement with methionine or SamE because it could cause homocystein levels to rise, which apears to have an effect on vessel health. Cheri, this is why I hesitate to post this. I don't want to scare anyone away from something that could be very beneficial, but if there is any possibility that I have this right , then it is something that people need to be aware of too (maybe more important in long term use?). I guess it wouldn't apply at all if there is no mutation, or if it relates to people with a homozygous mutation only, I just don't know. I guess that's why I keep hoping someone else will do some research on some of this and clarify. My time is getting so limited. I have about worn out my families tolerance.

Cheri, In addition to above post..... Again, I wasn't looking for this (was looking for something else). Thought I would post it, so you can take a look when you get a chance. If there is anyway this mutation could be important to your family, i wouldn't want to let it slip by. I didn't read this article throughly at all but Faith made me realize that we didn't have a hereditary disorder regarding heperan sulfate. I'm suspecting the CBS or MTHFR mutation may be more likely involved (the hereditary component) which may have been triggered by "events" that manifested in a similar end results. As always, I totally reserve the right to say I was wrong!

N-acetylglucosamine (GlcNAc) bolding mine http://today.uci.edu/news/release_detail.asp?key=1666 and http://www.msrc.co.uk/index.cfm?fuseaction...CFTOKEN=5729539 The research suggests that individuals with MS have a higher body burden of aluminium and that their urinary excretion of aluminium is linked to changes taking place during the relapsing-remitting stage of the disease. edit...sorry about the link, corrected now

Just wanted to drop this here. Bottom 2/3's of page mentions glaucoma/Chondroitin sulfate quite a bit http://209.85.165.104/search?q=cache:X_JXX...;cd=9&gl=us Eye drop vaccination for acute and chronic glaucoma: Morphological and functional evidence of neuroprotection. Journal of molecular medicine 2005 Aug 12;83(11):904-16. 6. Rolls A,. Bakalash S., Schwartz M. A sulfated disaccharide derived from chondroitin sulfate proteoglycan protects against inflammation-associated neurodegeneration. FASEB J Mar;20(3):547-9 Oct. 2005 7. Bakalash S*., Rolls A*., Lider O., Schwartz M. Chondroitin sulfate proteoglycan-derived disaccharides as a therapeutic compound for Glaucoma. Accepted IOVS Oct 2005.* equal contribution 8. Ben Simon, G.*,Bakalash, S.*, Aloni, E., Rosner, M., Wheeler, L., Schwartz, M. 2004. (*equal contribution) A rat model for acute glaucoma: Immune modulation as a therapeutic strategy. American Journal Ophthalmology 2006 Jun; 141(6):1105-11. 9. Bakalash S, Rolls A, Lider O, Schwartz M. 2007 Mar. Chondroitin sulfate-derived disaccharide protects retinal cells from elevated intraocular pressure in aged and immunocompromised rats. Invest Ophthalmol Vis Sci.;48(3):1181-90.

myrose, Can you determine from these links if those dots were Petechiaes? I don't know how long that condition takes to clear up. Did it start to get better when you discontinued the amox? I'm wondering what kind of Dr. this is. I'm sure it's in one of your posts, but I was told a new Dr. "really only needs their vax records." by old office when transferring to a new one. Like that was all in their medical history that was really important. I hope your new Dr. is looking for something else there. This may be totally outta left field, but when reading sulfur info, I came across something that said that amox contains sulfur. Not sure if that means anything or not, but thought I would mention it. Image http://images.google.com/imgres?imgurl=htt...I7DMUS%26sa%3DN Petechiae http://www.google.com/search?hl=en&saf...iae&spell=1 Petechiae on soft palate............I thought those red dots were just part of the strep. Now I'm wondering if others see those dots when their kids have strep? http://images.google.com/imgres?imgurl=htt...I7DMUS%26sa%3DN

Peglem/All, Faith's question on another thread caused me to re evaluate a hypothesis of sorts, based on the research that is being done on people with multiple ostero tumors (which I have been trying to figure out how much relates to our situtation ). Anyway, it led me to this article. Is any of this familiar to you. Do you have any knowledge of the Cog's mentioned here? http://hmg.oxfordjournals.org/cgi/reprint/ddl476v1.pdf Because of her occasional coagulation problems, bleeding or thrombosis, and the fluctuation of the coagulation parameters through out development (protein C and protein S deficiency, decreased prothrombin time and coagulation factors), a wide study for “increased risk of thrombosis” was performed. While homocysteine, vitamin B12 and folic acid levels were normal, a heterozygous C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene was found. The factor V Leiden and factor II mutations were absent. Her father also has a very high level of plasma homocysteine, undetectable vitamin B12 levels, antibodies against intrinsic factor and incipient macrocitic anemia. He was diagnosed with a pernicious anemia. The mother is heterozygous for the C677T mutation in the MTHFR gene. Other basal laboratory analyses, coagulation studies, creatin kinase, lipids, thyroid hormones and levels of CDT in serum were normal in both parents. A summary of the clinical features is presented in table 1.

response to others posted above CP, Seems we have something in common here. Why such exteme low values. Did your Dr. comment on that? I think they commonly look at that as a marker for "bad" bacteria but I think something else might be up with this. I was actually looking at lactic acid and it got me thinking about a dysbiosis profile that youngest had quite a while ago. Here are a couple of things that made me wonder. Remember, I'm looking for things that indicate low gluconic acid. don't know how the phenyl part plays in. Lot's of reading to do on this. Our hippurate was way low too, but I think that is because he eats so little protein. Did your son have anything to indicate high ammonia? http://jn.nutrition.org/cgi/content/abstract/132/8/2229 Gluconic acid reaches the large intestine to stimulate lactic acid bacteria. However, the fermentation pattern of gluconic acid has yet to be elucidated. Accordingly, we examined the fermentation properties induced by gluconic acid in the pig cecal digesta in vitro. We also tested sorbitol and glucose, substrates for which the fermentation rate and patterns are known. The gluconic acid–utilizing bacteria were further isolated from pig cecal digesta and identified to examine the effect of gluconic acid on hind gut fermentation. Gluconic acid was fermented more slowly than were the other two substrates. Gluconic acid stimulated butyrate production; the butyrate molar percentage reached 26%, which is considered a high butyrate production. The majority of gluconic acid fermenters were identified as lactic acid bacteria, such as Lactobacillus reuteri and L. mucosae, and acid-utilizing bacteria, such as Megasphaera elsdenii and Mitsuokella multiacida. The gluconic acid fermented by lactic acid bacteria, and the lactate and acetate that were produced were used to form butyrate by acid-utilizing bacteria, such as M. elsdenii. Gluconic acid may be useful as a prebiotic to stimulate butyrate production in the large intestine. http://en.wikipedia.org/wiki/Butyric_acid Butyric acid has been associated with the ability to inhibit the function of histone deacetylase enzymes, thereby favouring an acetylated state of histones in the cell. Acetylated histones have a lower affinity for DNA than non-acetylated histones, due to the neutralisation of electrostatic charge interactions. In general, it is thought that transcription factors will be unable to access regions where histones are tightly associated with DNA (ie non-acetylated, e.g., heterochromatin). Therefore, it is thought that butyric acid enhances the transcriptional activity at promoters, which are typically silenced/downregulated due to histone deacetylase activity.

nursepatty If you read the articles about supplementing sulfur in the form of MSM, it says people that that have problems with sulfa drugs don't have problems with MSM, but I sure wouldn't buy that until I really did some digging. Are these drug allergies the liver's inability to detox a certain substance in the drug, what is the difference btwn sulfa sulfur sulfate? I guess once again, if you ask the "why" questions, you might find answers to other questions as well. I haven't looked at it, but if you do please let us know what you find. Faith, Without going back and looking at MTHFR (so always confirm on your own), I think the idea is that you are not making it to methionine. If you don't have methionine you don't make gluathione properly because of the problem with B12. Glutathione is about the most important antioxidant in our bodies. Not enough glut, improper detox. The CBS mutation is the one where homocystein is not converting to cystein. If you're looking at sulfur deficiency, Waring's article says you need methionine and cystein to get sulfur. Well, we (my boys) may have enough of all of these, but maybe not the enzyme that gets it out of the cell in the glucosaminoglycan chains. So, as Peglem said, you can have different problems along a pathway, with the same end result. You have to figure out where the problem is. Faith, I don't think one "bad" copy of the MTHFR gene is the whole answer either but I sure respect what I have read on the Yasko forum. It's all just such a big picture with different pieces for everyone, so it's really impossible for me to answer what your asking. I'm just doing the best I can to try connect some dots. It may not apply to anyone on this forum, or there could be peices that are important to many but the bottom line, you either have to pay one of the best, or spend hours and hours using every clue in your particular situation and READING some tough stuff. Boy Faith, posting this to you, just turned on a big old light bulb for me. Thanks Faith, you're a genious!!!!!!!! Keep asking those questions of yours! Sunshine, I will get back to you! One thing thou, when you said osteo in spades I'm assuming that you meant osteoarthritis? Michelle and Myrose If you're reading, I hope you guys will contribute to anything that rings a bell for you too.

oceanperiwinkle, Thank you for posting. I know you're new to the forum, and I hope that I don't confuse the heck out of you, but within 5 minutes of reading about fifth disease, I was sitting here shaking my head, thinking "here it is again." I certainly don't have all of this figured out, but I think there is some important stuff here. I don't know what all of this means, by a long shot. There are only a few words here that I was really looking at. It appears that my boys have an problem with something that catalyses GlcNAc to the cell surface. There is another substance too, but we'll skip that, until you see if you can digest some of this. Boy, I'm afraid people are going to start hating to see my name pop up on their thread, but I can't help but get the feeling that we have work to do here (on this forum) and I need help! First read this article 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) Ok, I googled fifth disease and saw where it is human parvo virus. This is just a heading from the search, didn't open the article Human Parvovirus B19 Infection: Autoimmune Disease Trigger Human Parvovirus B19 has been linked to a number of different autoimmune diseases, including vasculitis and connective tissue disorders. Then I saw this one http://www.wadsworth.org/databank/b19virus.htm The most common manifestation of human parvovirus B19 infections is erythema infectiosm ("Fifth Disease"). This is characterized by mild symptoms, fever (in some patients) and a red rash on the face ("slapped cheek"). and Erythema is redness of the skin caused by capillary congestion. Then this http://www.jtrauma.com/pt/re/jtrauma/abstr...#33;8091!-1 Results: Thromboelastogram data show that poly-N-acetyl glucosamine fibers (p-GlcNAc) significantly reduced the R time in platelet-poor plasma, PRP, and PRP supplemented with red blood cells. Poly-N-acetyl glucosamine fibers increased, but not significantly, Annexin V and factor X binding to platelets, platelet microparticles, and red blood cell Annexin V binding. Poly-N-acetyl glucosamine fibers increased the production of thromboxane B2 by PRP. Conclusion: Poly-N-acetyl glucosamine slurry activates platelets. and this http://glycob.oxfordjournals.org/cgi/conte...ract/15/11/1067 The bisecting N-acetylglucosamine (GlcNAc) structure, formed through catalysis by UDP-N-acetylglucosamine : ß-D-mannoside ß-1,4-N-acetylglucosaminyltansferase III (GnT-III), is responsible for a variety of biological functions. Can you (or anyone) spend some time figuring out what the role of GlcNac is that is talked about in the last two articles? It may take you week or a day, it may take an hour of googling words, don't know, but it could be important, not only to your daughter but other's as well. Again, I'm sorry for throwing this at you periwinkle. I know you are probably upset by what's happening with your daughter anyway and the last thing you need is to look at all these words that make no sense to you, but if you stick with it and read other posts here, it just might start to.

Cp/anyone, Does anyone have testing that shows Phenylacetate or Phenylpropionate? If so, can you comment on high or low values?

CP, Now remember, I don't know what I'm talking about 1/2 of the time so take this as such, ok? You know what I've been looking at, so I'm just looking for any common ground. Doesn't mean there is any although, some things that I read sound quite striking with other situations here. Just wish I could understand/explain better. Anyway in the 2nd article that HSPG is "heparan sulfate protoglycans." First this http://www.wecare4lungs.com/pe.htm What is Pectus Excavatum? and Now this Here more of that copy http://www.pubmedcentral.nih.gov/articlere...i?artid=1387052

Sunshine, I was hoping you would take a look at this. Geeeez Louise! Again, this is from the osteo study. The two things that are supposed to be stuck in the Golgi (instead of making it to the cell surface and the extra cellular matrix) were GlcNAc and GlcA. I've been kind of ignoring the GlcA, trying to understand heparan sulfate and I still don't know where GlcNAc comes from. Does your body make it, or does it come from diet? Anyway, look at what wiki says about GlcA http://en.wikipedia.org/wiki/Gluconic_acid Gluconic acid occurs naturally in fruit, honey, kombucha tea, and wine. As a food additive (E574[1]), it is an acidity regulator and The gluconate anion chelates Ca2+, Fe2+, Al3+, and other heavy metals. I'm wondering if this means that all the boys need for a long healthy life is nicotine and wine. Ok, just trying to keep it light, this all get a bit intense at times.

Peglem, Once again, we are looking at similar issues. From the reseach that I'm assuming is likely to be part of our issue (althou, I think we have a less severe problem with lack of transferase than what they are studying which is a multiple hereditary thing) the lack of heperan sulfate, would be due to lack of an enzyme which catalyzes it to the cell surface too, missing components. http://www.researchcrossroads.com/index.ph...rant_id=3210354 Now the really interesting thing is that the GluR1 subunit of AMPA-type glutamate receptors, that they say is drastically reduced, is stimulated, if I'm understanding what I'm reading by (edit. I thought acetylcholine was implicated here too, but when I went back to cite the article that I took it from, looks like I better do some more reading) nicotine. It looks like the GluR1's of AMPA glutamate receptors, play an inhibitory role. So, I'm wondering the same thing. By supplementing sulfur, there is no evidence that it is going to link up with heparan and change the situation, however, I do think there would be benefit. They may have found a lack of surface heparan sulfate when studying this disorder, but what about the other GAGS that need sulfation? chondroitin sulfate (cartilage), keratin sulfate (cartilage, bone, and cornea), dermatan sulfate (skin, tendons, lungs, blood vessels). I copied that last part from this site, which I didn't even read, just looking for something that spelled out the GAGS. The "hyaluronic" they reference there, is a GAG also, but it isn't sulfated. I think that is one of the things that they look for cross reactivity in an autoimmune situation with PANDAS. It is found in the host and in the strep bacteria as is N acetylglucosime. Again, if anyone follows up on any of this, and finds where i'm interpreting something dead wrong, PLEASE correct me. Some of this info is found on the Anti Basil Ganglia testing thread. http://www.wellnessresources.com/products/...uronic_acid.php http://www.ihop-net.org/UniPub/iHOP/pm/124...p;pmid=17898222 The same nicotine treatment increased the levels of the AMPA glutamate receptor subunit GluR1

Heather I don't know how closely you have been following some of the threads here, but I wanted to post this as I think it may be important to your son. These are the same family of genes that are implicated in the benign tumor that my son has on his ankle. Would love to hear how your little guy is doing! http://www.genome.org/cgi/content/abstract/7/1/10 We have localized this gene by fluorescence in situ hybridization to metaphase chromosomes and by whole genome radiation hybrid mapping to chromosome 1p36.1 between DIS458 and DIS511, region that frequently shows loss of heterozygosity in a variety of tumor types. This gene, EXTL (for EXT-like), is therefore a new member of the EXT gene family and is a potential candidate for several disease phenotypes. A Region of Consistent Deletion in Neuroblastoma Maps within Human ...Allelic Losses at 1p36 and 19q13 in Gliomas: Correlation with Histologic .... Identification and localization of the gene for EXTL, a third member of the http://www.pnas.org/cgi/content/abstract/92/12/5520 A Region of Consistent Deletion in Neuroblastoma Maps within Human Chromosome 1p36.2-36.3 Allelic losses at 1p36 and 19q13 in gliomas: correlation with ...Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic ... Because most 1p deletions in gliomas involve almost the entire chromosome arm, ... www.ncbi.nlm.nih.gov/pubmed/15709179

bmom, more and more my vote is the Yasko approach. I'm not saying ALL of the answers are there, but I think she sure is on the right track. Quickly, I was looking for something that I came across for CP. It seems I had read about a mutation on 1p36 that had to do with potassium and chloride (?). That area of that chromosome seems to come up quite a bit. I know there is an EXTL (the L stands for "like") gene, located on 1p36. The EXT genes are what are implicated in my son's bony growth and what shows a problem with heparan sulfate sythesis. I think the MTHFR gene is there, can't remember what else, but I listed some of them on the genetics thread. You can probably see by the highlights in this article what i searched. This was interesting. Peglem, I'm not interested in debating vaccines anymore either. I carefully reseached all I needed to know, awhile back. I think the current vax schedule is recklessly dangerous PERIOD. There may be a case for some vaccines, but they need to be given with a GREAT DEAL MORE CARE than they are now, IMO, with careful consideration to family history, the overall health of the child etc. Anyway this popped up. Sorry CP, i just don't have anymore time right now. One other thing, I was search pub med regarding Crohn's today. Some of the current research seems to be looking at vessel involvement and coagulation factors. http://64.233.167.104/search?q=cache:qjxuR...cd=11&gl=us Peglem have you ever used Pant. acid? http://www.raysahelian.com/bvitamin.html Pantothenic acid (B5) is essential for biological reactions involving acetylation and energy production. This vitamin helps in the formation of acetylcholine, the metabolism of fatty acids, and the incorporation of fatty acids into cell membrane phospholipids. Pantothenic acid is also involved in making steroid hormones, vitamin A, vitamin D, and cholesterol. Good sources are egg yolk and fresh vegetables. The recommended daily intake is about 5 mg. Pantothenic acid is sold over the counter in dosages ranging from 5 to 250 mg. My patients report that pantothenic acid helps improve their mood and energy. Personally, I notice an improvement in alertness, concentration, energy, and visual clarity with dosages ranging from 100 to 250 mg. I do experience insomnia, though, when I take more than 250 mg, even if I take it in the morning. Benita von Klingspor, a nutritionist in Marina Del Rey, California, says, "Pantothenic acid is one of my favorite nutrients. I know the effects of this nutrient extremely well since I’ve been taking 100 to 250 mg most mornings for more than thirty years. I often recommend it to many clients with low energy. Pantothenic acid increases their alertness and focus, improves their mood, and enhances their joy in life. They begin to have more interest in whatever they’re doing. However, if people take too much pantothenic acid, they can become overstimulated, wired, and easily aggravated." Pantothenic acid is available in its activated form known as pantethine. Pantethine, itself, is part of coenzyme A, a very important substance that participates in the metabolism of carbohydrates, amino acids, fatty acids and dozens of other important chemical reactions. Cognitive effects of oral pantethine administration to humans have not been published. Pantethene is sold over the counter in dosages ranging from 5 to 50 mg. In my experience, a lower dosage of pantethine provides similar effects as a higher dosage of pantothenic acid.