or anyone in group

[Guest guest]

Can anyone tell me if sleeping problems is linked to tapering of prednisone. My husband is almost 2 years post-transplant in April and they are tapering his prednisone down and he has about two weeks left before he can stop taking it. Just wondering if there is any side effects to this. Thanks Tina

Re: PSC - The arteriosclerosis of the bile duct (LONG reply to Nina)

Dear Nina;Sorry to hear that Sam's ALP is not improving with the fish oils. As an aside I'd like to mention that I found this patent from Dr. D. Freedman relating to PPARalpha, fibrates, PSC and CFTR. In a nutshell, it looks like he's "patented" the use of fibrates, EPA and DHA (i.e. fish oils) in the treatment of PSC! And he's claiming that the cystic fibrosis gene is a "cause of PSC".____________ _________ _____Applicaton #: 20060160867 07/20/06Methods for modulating ppar biological activity for the treatment of diseases caused by mutations in the cftr geneSome of the relevant sections of the patent are reproduced below:[0004] Approximately one in 2000 Caucasians have cystic fibrosis (CF), a genetic disorder caused by inactivating mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR protein, a member of the ABC transporter family,

forms a chloride channel localized to the plasma membrane. The protein consists of five domains: two membrane-spanning domains that form the chloride ion channel, two nucleotide-binding domains that hydrolyze ATP, and a regulatory domain. Expression of the CFTR gene is highest in cells that line passageways of the lungs, pancreas, colon, ileum, and genitourinary tract. [0005] In addition to CF, defects in the CFTR gene are associated with diseases including, for example, pancreatitis, chronic obstructive pulmonary disease (COPD), asthma, chronic sinusitis, primary sclerosing cholangitis, and congenital bilateral absence of the vas deferens (CBAVD). .....[0007] The invention features a method for treating a disease in a human patient that has a mutation in the CFTR gene by administering to the patient a therapeutically effective amount of a peroxisome proliferator- activated receptor (PPAR) inducer,

a PPAR agonist, an AP-1 inhibitor, a STAT inhibitor, an NFkB inhibitor, or an LXR agonist. PPARs generally include PPAR.alpha., PPAR.delta., and PPAR.gamma.. Diseases caused by mutations in a CFTR gene include, for example, cystic fibrosis, pancreatitis, chronic obstructive pulmonary disease (COPD), asthma, chronic sinusitis, primary sclerosing cholangitis, liver disease, bile duct injury, and congenital bilateral absence of the vas deferens. The diseases that are treatable by the therapeutic methods of the invention include any disease caused by any of the 1,300 or more mutations in the CFTR protein. See for example, J. Zielenski, Canadian CF registry database; Cutting et al., Nature 346:366-369, 1990; Dean et al., Cell 61:863-870, 1990; Kerem et al., Science 245:1073-1080, 1989; Kerem et al., Proc. Natl. Acad. Sci. USA 87:8447-8451, 1990; and Welsh et al., "Cystic Fibrosis," Metabolic and Molecular Basis of

Inherited Disease (8.sup.th Ed. 2001), pp. 5121-88. Particularly amenable to treatment are diseases caused by a deletion of the phenylalanine normally present at amino acid residue 508 of the CFTR protein (.DELTA.F508) . The patients being treated according to the methods of this invention may be heterozygous or homozygous for a CFTR mutation. [0008] Useful PPAR inducers and agonists affect any PPAR, but particularly PPAR.gamma., (e.g., PPAR.gamma.1 and PPAR.gamma.2) , PPAR.alpha., and PPAR.delta.. Examples include eicosapentaenoic acid; any of the thiazolidinediones, but particularly pioglitazone (ACtos.TM., Takeda Pharmaceuticals) , rosiglitazone (Avandia.TM. , GlaxoKline) , thioglitazone and analogs thereof; L-tyrosine derivatives such as fluoromethyloxycarb onyl; non-steroidal anti-inflammatory drugs such as indomethacin, ibuprofen, naprosyn, and fenoprofen; and anti-oxidants such as vitamin E, vitamin C,

S-adenosyl methionine, selenium, idebenone, cysteine, dithioerythritol, dithionite, dithiothreitol, and pyrosulfate. Additional examples of PPAR.alpha. agonists and inducers include DHA, WY14643, and any of the fibrates, particularly, fenofibrate, bezafibrate, gemfibrozil, and analogs thereof. ____________ _________ _____Best regards,Dave (father of (21); PSC 07/03; UC 08/03)

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