Does anyone have any idea if and when fallon is going to start publishing?
Posted by pq (Member # 6886) on :
my question too!
thanx aligondo
Posted by lou (Member # 81) on :
When he finds a journal that the steerites don't have in a hammerlock. Good luck to him.
Posted by uma (Member # 7064) on :
i spoke to a dr. at columbia,who works with dr.fallon.they will be publishing reslts of the lates study soon.
Posted by trails (Member # 1620) on :
When When When?? Gosh we can't hardly wait can we? Looks like some folks on the board REALLY need his study to prove their need for Longer term IV.
Posted by Aligondo Bruce (Member # 6219) on :
well...I suspect there are some very interesting reasons why the study hasn't yet been published..among them are probably evaluation of patient DNA to compare with results of a recent german study...and sneakier reasons also...
Posted by hm (Member # 3333) on :
Aligondo Bruce,
would you be so kind to clarify what "recent german study" you are talking about and where I can find more informations about it.
I am a member of the german lyme association (Borreliose Bund Deutschland e.V.) and the moderator of the german internet discussion forum. I have not heard of any recent study here that could be comparable to the work of Brian Fallon.
I just heard from Dr. F today that the study has not yet been published, it is under review.
Posted by Aligondo Bruce (Member # 6219) on :
quote:Originally posted by hm: Aligondo Bruce,
would you be so kind to clarify what "recent german study" you are talking about and where I can find more informations about it.
I am a member of the german lyme association (Borreliose Bund Deutschland e.V.) and the moderator of the german internet discussion forum. I have not heard of any recent study here that could be comparable to the work of Brian Fallon.
sure...I'm guessing that anyone who has studied these phenomena, ie klempner and fallon, would want to go back and check the patients for this:
J Immunol. 2005 Aug 15;175(4):2534-40. Related Articles, Links
Heterozygous Arg753Gln polymorphism of human TLR-2 impairs immune activation by Borrelia burgdorferi and protects from late stage Lyme disease.
Schroder NW, Diterich I, Zinke A, Eckert J, Draing C, von Baehr V, Hassler D, Priem S, Hahn K, Michelsen KS, Hartung T, Burmester GR, Gobel UB, Hermann C, Schumann RR.
Institut fur Mikrobiologie und Hygiene, Charite University Medical Center, Berlin, Germany.
Lyme disease (LD) is caused by Borrelia burgdorferi and displays different stages, including localized, early disseminated, and persistent infection, all of which are associated with profound inflammatory reactions in the host. Induction of proinflammatory cytokines by B. burgdorferi is mainly mediated by outer surface proteins interacting with TLR-2/TLR-1 heterodimers. In this study, we show that TNF-alpha induction by Borrelia lysate was impaired in heterozygous TLR-2 knockout mice, while reactivity to lipoteichoic acid, another TLR-2 ligand signaling via TLR-2/TLR-6 heterodimers, was unaffected. Blood from individuals heterozygous for the TLR-2 polymorphism Arg753Gln was tested for cytokine release upon stimulation with Borrelia lysate, and induction of TNF-alpha and IFN-gamma was significantly lower as compared with individuals not exhibiting this variation. Overexpression of TLR-2 carrying the Arg753Gln polymorphism in HEK 293 cells led to a significantly stronger impairment of activation by TLR-2/TLR-1 ligands as compared with TLR-2/TLR-6 ligands. To study whether heterozygosity for the Arg753Gln variant of TLR-2 influenced susceptibility for LD, we analyzed 155 patients for this polymorphism. The Arg753Gln variant occurs at a significantly lower frequency in LD patients as compared with matched controls (5.8 vs 13.5%, odds ratio 0.393, 95% confidence interval 0.17-0.89, p = 0.033), with an even more pronounced difference when late stage disease was observed (2.3 vs 12.5%, odds ratio 0.163, 95% confidence interval 0.04-0.76, p = 0.018). These data suggest that Arg753Gln may protect from the development of late stage LD due to a reduced signaling via TLR-2/TLR-1.