sorry,i didn't had any DNA test.
i think i have it (ankylosing spondylitis), because of the way my back feels and the absent of motions/posters/flexability ranges. it get much better while on the diet+b12. only b12 and it dosen't work, i have to eat accordingly. the diet thing is for the suspected Klebsiella pneumoniae reaction(some say it is the cause and not the gene. maybe both)
thanks for the study violeta.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912611/
''In transgenic rats, HLA-B27 misfolding generates ER stress and leads to activation of the unfolded protein response (UPR),''
HLA proteins. i went to read the open post and it does mention patogens as a possible cause misfolded protein/ER stress
i googled ''Klebsiella pneumoniae ER stress''
for now i have found this:
http://intimmabs.oxfordjournals.org/content/22/Suppl_1_Pt_1/i131.abstract
''Our previous results demonstrated that decapsulated
Klebsiella pneumoniae (KP) cause ER stress of immune cells but not colonrectum adenocarcinoma cells.''
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0079961
Activation of IFN-γ/STAT/IRF-1 in Hepatic Responses to Klebsiella pneumoniae Infection
''IFN-γ induces apoptosis of various cell types, including hepatocytes; however, its mechanism is divergent and involves multiple downstream pathways [
22,
23]. Generation of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress were also demonstrated to promote apoptosis of cultured hepatocytes [
24].''
''IFN-γ elicits apoptosis in a number of normal cells, including hepatocytes. Among the multiple pathways involved, ER stress has been shown to play a critical role in the signaling of IFN-γ induced apoptosis of primary hepatocytes [
36]. Given that several apoptotic characteristics were noted in the
K. pneumoniae-infected diabetic mice (
Figure 3G and H), the involvement of ER stress was investigated. The level of phosphorylated eukaryotic initiation factor 2-alpha (peIF2α) (
Figure 5A, G, and H), induced by PKR-like ER-localized eIF2α kinase (PERK) due to the ER protein load, was elevated exclusively in the diabetic mice upon
K. pneumoniae infection. Moreover, protein level of p20 subunit of the activated caspase 3 that was proteolytically generated during apoptosis (
Figure 5A; indicated by an arrow) was significantly increased in the
K. pneumoniae-infected naïve and diabetic mice in comparison with the uninfected control''
''the comparable levels of phospho-eIF2α exhibited in the PBS-control group of diabetic and naïve mice suggested that the diabetes-related ER stress was mainly provoked by
K. pneumoniae infection (
Figure 5H). Besides induction of ER stress,
K. pneumoniae also caused 2-fold enhancement of hepatic apoptosis in mice with diabetes. These findings suggested that induction of ER stress by the liver-invading
K. pneumoniae, probably through IFN-γ signaling, elevated the level of phospho-eIF2α to attenuate protein translation, and the failure to rescue ER stress led to augmented apoptosis in mice with diabetes.''