Pcgl steroids

Pneumocystis carinii pneumonia remains a prevalent opportunistic disease among immunocompromised individuals. Although aggressive prophylaxis has decreased the number of acute P. carinii pneumonia cases, many patients cannot tolerate the available drugs, and experience recurrence of the infection, which can be fatal. It is now generally agreed that the organism should be placed with the fungi, but the idfection, which can be fatal. It is now generally agreed that the organism should be placed with the fungi, but the identification of extant fungal species representing its closest kins, remains debated. Most recent data indicate that P. carinii represents a diverse group of organisms. Since the lack of methods for the continuous subcultivation of this organism hampered P. carinii research, molecular cloning and nucleotide sequencing approaches led the way for understanding the biochemical nature of this pathogen. However, within the last 5 years, the development of improved protocols for isolating and purifying viable organisms from infected mammalian host lungs has enabled direct biochemical and metabolism studies on the organism. The protein moiety of the major high mol. wt surface antigen, represented by numerous isoforms, is encoded by different genes. These proteins are post-transcriptionally modified by carbohydrates and lipids. The organism has the shikimic acid pathway that leads to the formation of compounds which mammals cannot synthesise (., folic acid), hence drugs that inhibit these pathways are effective against the pathogen. Ornithine decarboxylase has now been detected; rapid and complete depletion of polyamines occurs in response to difluoromethylornithine (DFMO). Instead of ergosterol (the major sterol of higher fungi), P. carinii synthesises distinct Δ 7 , C-24-alkylated sterols. An unusual C 32 sterol, pneumocysterol, has been indentified in human-derived P. carinii . Another signature lipid discovered is cis -9,10-epoxy stearic acid. CoQ 10 , identified as the major ubiquinone homologue, is synthesised de novo by P. carinii . Atovaquone and other hydroxynaphthoquinone drugs with anti- P. carinii activity probably inhibit pathogen respiration as CoQ analogues. Unlike its effects on Plasmodium , atovaquone does not inhibit the P. carinii dihydroorotate dehydrogenase and pyrimidine metabolism.

if the problem is joint pain the deca durabolin (Nandrolone) steroid could help – but alot of times in the shoulder it is muscle related, or tendons. BUT…
Deca increases the synovial fluid in the bursas between our joints. So the relief from joint pain is actually more cushion. As far as healing properties versus masking symptoms? I think that if you use deca during a cycle and have bad joints, and during cycle joint pain is alleviated, then it is like buying some time for your joints, and wont necessarily make them any worse, but when you come off of deca, synovial fluids decrease, and your back to where you were except with a little more gains in strength and size. So when you do your next cycle that does NOT include deca, your joints will suffer a little more because you are adding more stress to them via new strength gains.

Pcgl steroids

pcgl steroids