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dbol question

  1. offsides25's Avatar
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    dbol question


    hey, i know your supposed to split up dbol as evenly as you can over the day because of the short half life, but i have a question. When people have like 50 mg pills, and there about the size of like -- O -- how are you expected to cut that up?

    I know some of the newer UG labs are putting out like 50 mg and 55 mg pills, but how do you split them up, afraid it will shatter everywhere. Would it really be that much less effective to take it in the morning?

    Also, what about swallowing or chewing. I know ive read people say to chew IPs but are all UG labs supposed to be chewed, or swallowed?

  2. Beelzebub's Avatar
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    I used a boxcutter to split mine and they were pretty damn big. Do you plan to take anything with the dbol or is it going to be a solo cycle?
  3. Matthew D's Avatar
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    Pill cutter from walmart..
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  4. Jergo's Avatar
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    From all that I've read about user reports, users that dose them all at once seem to get better gains than the users who spread throughout the day due to a higher spike in blood levels. But they also say that the sides get worse along with it of course.

    Some even argue that they work rather by gene transcription. I haven't had the chance to read anymore into that, but does sound interesting.

    I have 55mg caps, even tried to see if I could get them in smaller mg's/cap. But was told that the 55mg caps are what most prefer nowadays....

    Bump for more response...
  5. Beelzebub's Avatar
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    Quote Originally Posted by Jergo
    I have 55mg caps, even tried to see if I could get them in smaller mg's/cap. But was told that the 55mg caps are what most prefer nowadays....
    I was told the same thing about the 50's being more available. Might not need to talk price Matt D
  6. jweave23's Avatar
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    I'm also a fan of taking any methylated AS in the morning (once daily that is), I don't really feel that 17aa compunds necessarily need to be taken throughout the day to acheieve the same results. But if you wish, go to Walmart like Matt said, pill cutters are like $5
  7. jminis's Avatar
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    I've taken it both ways and didn't see a bit of difference.
  8. Dwight Schrute's Avatar
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    Quote Originally Posted by Jergo
    Some even argue that they work rather by gene transcription. I haven't had the chance to read anymore into that, but does sound interesting.

    ...

    Its not an arguemnt, its a fact. In a very basic explanation, steroids bind to receptors which cause a dimer to enter the nucleus of a cell and binds to DNA which in turn promotes gene transcription and translation. This causes increased production of proteins (protein synthesis).

    The increased rate is not dependent on the level of hormone present.
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  9. canadian champ's Avatar
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    Quote Originally Posted by Bobo
    Its not an arguemnt, its a fact. In a very basic explanation, steroids bind to receptors which cause a dimer to enter the nucleus of a cell and binds to DNA which in turn promotes gene transcription and translation. This causes increased production of proteins (protein synthesis).

    The increased rate is not dependent on the level of hormone present.
    Dimer formation is 1 of 4 ways in which hormones can increase gene transcription rate. Hormones have other function than solely increasing transcription rate.
    cc
  10. Dwight Schrute's Avatar
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    Quote Originally Posted by canadian champ
    Dimer formation is 1 of 4 ways in which hormones can increase gene transcription rate. Hormones have other function than solely increasing transcription rate.
    cc
    But the dimerization of the steroid receptor complex is the main source of increased gene transcription. Also the protein formed is often a regulatory protein which is also responsible for activating and deactiviating other genes.
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    Quote Originally Posted by canadian champ
    Dimer formation is 1 of 4 ways in which hormones can increase gene transcription rate. Hormones have other function than solely increasing transcription rate.
    cc
    And nobody said it was the only way. Its an example of how the effects are not dependent on the amount circulating.
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  12. canadian champ's Avatar
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    Quote Originally Posted by Bobo
    But the dimerization of the steroid receptor complex is the main source of increased gene transcription. Also the protein formed is often a regulatory protein which is also responsible for activating and deactiviating other genes.
    In your original comment I thought you were talking about a hormone which facilitates the binding of two monomers which, alone, lack sufficient DNA binding affinity. The picture you posted is a simply one way in which hormones affect transcription factors and gene transcription.
    cc
  13. canadian champ's Avatar
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    Quote Originally Posted by Bobo
    And nobody said it was the only way. Its an example of how the effects are not dependent on the amount circulating.
    I never said that you made the comment that it was the ONLY way, i was simply letting others know that there are other effects of hormones.
    cc
  14. Dwight Schrute's Avatar
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    Yes but as I said, its the most significant.
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  15. Dwight Schrute's Avatar
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    Quote Originally Posted by canadian champ
    I never said that you made the comment that it was the ONLY way, i was simply letting others know that there are other effects of hormones.
    cc
    Of course there are but the discussion was whether the effects are better when doses are taken all at once or spread out. And my point was that there are many factors that are involved (such as gene trascription in whic Jergo brought up) that are not dependent on when the dose is taken. Increased hepatic IGF-1 is another.
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  16. canadian champ's Avatar
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    Quote Originally Posted by Bobo
    Of course there are but the discussion was whether the effects are better when doses are taken all at once or spread out. And my point was that there are many factors that are involved (such as gene trascription in whic Jergo brought up) that are not dependent on when the dose is taken. Increased hepatic IGF-1 is another.
    Perhaps this is a discussion for another thread then.
  17. Dwight Schrute's Avatar
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    I hope you don't want to discuss the superfamily. I don't think I have the capacity to think about this right now. Thats why I tried to make it as general as possible.
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  18. canadian champ's Avatar
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    Quote Originally Posted by Bobo
    I hope you don't want to discuss the superfamily. I don't think I have the capacity to think about this right now. Thats why I tried to make it as general as possible.
    haha fair enough. im tired too... got an exam quasi related to this stuff that i should be studying for anyways.
    cc
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    I don't envy you. Good luck.
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  20. lvtrojan's Avatar
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    Quote Originally Posted by Bobo
    And nobody said it was the only way. Its an example of how the effects are not dependent on the amount circulating.
    Wouldnt a greater amount of circulating hormone though cause protein synthesis in a greater number of cells?
  21. Dwight Schrute's Avatar
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    Without writing a 5 page explanation and going into receptor binding times, no it won't. (Remember we are comparing the same amount of hormone over a 24 hour peroid). Your questions can easily be misinterpretted if that is not emphasized.
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  22. lvtrojan's Avatar
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    Quote Originally Posted by Bobo
    Without writing a 5 page explanation and going into receptor binding times, no it won't. (Remember we are comparing the same amount of hormone over a 24 hour peroid). Your questions can easily be misinterpretted if that is not emphasized.
    Fair enough. Thanks.
  23. Jergo's Avatar
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    Bobo, I would definately like to hear more about that....that is whenever you have the time...

    One more thing though. How long does/can it take gene transcription take effect? Does this happen almost instantaneously, or is it an actual process that takes a bit of time in order to happen?

    I was just wondering because if it did maybe the half-life would (in reality) be much longer than only the estimated 3-4 hours for d-bol...maybe I'm confusing you now, dunno..
  24. canadian champ's Avatar
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    Quote Originally Posted by lvtrojan
    Wouldnt a greater amount of circulating hormone though cause protein synthesis in a greater number of cells?
    Hormone receptors are not found in all cells or in the same concentration.
    cc
  25. Dwight Schrute's Avatar
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    Quote Originally Posted by Jergo
    Bobo, I would definately like to hear more about that....that is whenever you have the time...

    One more thing though. How long does/can it take gene transcription take effect? Does this happen almost instantaneously, or is it an actual process that takes a bit of time in order to happen?

    I was just wondering because if it did maybe the half-life would (in reality) be much longer than only the estimated 3-4 hours for d-bol...maybe I'm confusing you now, dunno..

    Well here is a little tidbit.




    R. Juliano 2004


    STEROIDS AND THEIR RECEPTORS


    I. Overview


    The steroid hormones are a class of lipid-like mediators produced in the adrenal cortex or in the gonads under the influence of polypeptide hormones secreted by the pituitary; there are feedback loops between the steroid producing tissues and the pituitary. The receptors for steroids are ligand-activated transcription factors that regulate expression of certain genes and thus levels of their protein products; this results in changes in cell function. The steroid receptors are part of a protein superfamily that includes receptors for retinoids, thyroid hormone, vitamin D3, and other ligands. The physiological actions of adrenal steroids include effects on salt/water balance and on carbohydrate, lipid, and protein metabolism. Sex steroids affect secondary sexual characteristics and reproduction. The major pharmacological use of agents related to adrenal cortical steroids is regulation of immune system function; the corticosteroids are profoundly immunosuppressive. Pharmacological agents related to sex steroids are used in contraception, in post-menopausal maintenance therapy, and in gynecological cancer.



    II. Regulation of Steroid Hormone Production


    1. Releasing hormones of the hypothalmus (eg corticotropin releasing hormone (CTH), gonadotropin releasing hormone (GnRH), others)



    2. Anterior pituitary hormones (ACTH, Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH), others). These act on target organs by binding to GPCRs and stimulate cAMP.



    3. Feedback control of pituitary hormone production by circulating steroid hormones



    III. Biosynthesis of Steroid Hormones


    A. Adrenocortical Steroids


    1. Definitions: glucocorticoids—primarily affect metabolism; mineralocorticoids—primarily affect salt/water balance.



    2. Corticosteroid synthesis takes place within the mitochondria of cells of the adrenal cortex. A series of cytochrome p450-type enzymes mediate the various steps in the pathway. The rate limiting steps are (a) the provision of cholesterol (stimulated by ACTH via increased uptake & biosynthesis) and (b) conversion of cholesterol to pregnenolone. In humans the most important glucocorticoid is cortisol, while the most important mineralocorticoid is aldosterone. Corticosteroids circulate in plasma bound to CBG, an a-globulin.



    B. Sex Steroids


    1. Definitions: estrogens (primarily 17 beta estradiol) regulate secondary sex characteristics and reproductive cycles in females; androgens (primarily testosterone and dihydrotestosterone) regulate male fetal development and secondary sex characteristics; progestins (progesterone) are responsible for maintenance of the endometrium and act with estrogens to promote breast development in pregnancy.



    2. Sex steroids are made in the gonads under the influence of LH and FSH. As with corticosteroids, a series of p450 type enzymes convert cholesterol to estrogens, progestins, or androgens.




    IV. The Mechanism of Action of Steroid Hormones


    A Review of Transcriptional Regulation


    1. RNA polymerase II transcribes genes that code for proteins. Pol II functions as part of a multiprotein complex that includes the so-called basal or general transcription factors. One of these factors, TFIID, recognizes a TATAA sequence in the gene promoter region just upstream (5’) of the transcription start site. Recruitment of TFIID helps triggers the formation the multiprotein initiation complex (pol II +TFIID, B, F, H, etc). As transcription proceeds the 5’ nascent mRNA is “capped’ with a methyl G in a 5’-5’ linkage and the 3’ end acquires a polyA tail. Pre-mRNA is spliced to remove introns prior to export from the nucleus. This is done by specialized RNA/Protein complexes called SNRPs or splicesosomes.



    2. Enhancers are sites that are recognized by transcription factors—enhancers may be near or far from the TATAA sequence. TFs have a DNA binding domain (eg helix-turn-helix, zinc finger, leucine zipper etc) and a “transactivating“ domain. Binding of a TF to an enhancer site helps to trigger recruitment and activation of the general PolII transcription machinery. One way in which this happens is by direct interaction between the TF transactivating domain and components of the PolII complex. Some types of TFs have “repressor” domains rather than transactivating domains.


    3. Much mammalian chromatin is inactive in terns of gene expression because it is highly condensed into histone-rich nucleosomes and other structures. The Pol II complex can’t access DNA in nucleosomes. However some TFs can, and they can further recruit protein complexes that dis-assemble nucleosomes. Important among these are histone acetyl transferases (HATs) such as p300/CBP & SRC-1(human) and SAGA (yeast). HAT aceylate histone lysines and weaken histone-DNA association. Conversely transcriptional repressors can directly or indirectly (via a co-repressor complex called Sin3) recruit histone deacetylases (HDACs) such as HDCA1. Finally, there are groups of chromatin remodeling ATPases such as SWI/SNF and NURD that alter nucleosome structure in poorly understood fashion.



    B. Structure and Function of Steroid Superfamily Receptors


    1. Steroid receptors are ligand (hormone) activated TFs. They are comprised of several domains including a DNA binding domain and a ligand binding+transactivation domain. The DNA binding domain is a “zinc finger’ with 4 cysteine residues chelating Zn to pack the protein into 2 helices one of which “reads” the DNA and the other is involved in dimerization.



    2. Steroid receptors recognize “HREs” short palindromic sequences in DNA. The recptors bind as dimers. In some cases the specificity is determined by the spacing between the 2 half sites (eg 3,4,5 rule for VitDR, TR, RAR).



    3. Ligand binding dissociates heat shock proteins (hsp90,70) normally associated with the receptor increasing DNA binding and allowing function of the transactivating domain. One mechanism of gene regulation entails direct interaction of the steroid receptor with the Pol II complex. (possibly TFIB).



    4. Some steroid family receptors bind DNA in the absence of ligand and can “silence’ basal transcription. Some of this may be due to direct interactions with the Pol II complex, but some is also mediated by chromatin remodeling due to recruitment of co-repressors and HDACs. Likewise the presence of hormone can affect chromatin by allowing the receptor to recruit co-activators such as p300/CBP and HATs.SL11



    V. Physiological Actions of Steroids


    A. Adrenal Steroids


    Corticosteroids are involved in multiple aspects of metabolism, salt/water balance, and responses to stress.


    1) Metabolism--"protects” glucose utilization by brain & heart--thus induces protein breakdown and lipolysis in periphery, glucose production by liver, increased blood glucose levels

    2) Salt & water balance--induces NaK ATPase, also other actions on Na K channels, works to increase sodium retention (aldosterone)

    3) Complex effects in CNS--too much or too little both lead to CNS disorders

    4). Complex effects on bone metabolism-too much leads to osteoporosis

    5) Permissive effects for adrenergic agonists--thus importance in stress situations--in maintaining blood pressure.

    6) Cushings Syndrome-adrenal cortical hyperplasia



    B. Sex Steroids


    Sex steroids are involved in the maintenance of secondary sex characteristics and in the menstrual cycle in females. Estrogens also contribute to bone maintenance and to a positive cardiovascular scenario (low LDL high HDL). These effects are lost after menopause.…...



    VI. Aspects of the Pharmacology of Steroids


    A. Corticosteroids and Immune Regulation


    1. Effects on the Immune System

    Corticosteroids suppress immune system function at several points and are thus very effective but potentially hazardous agents.


    2. Therapeutic Uses

    SYSTEMIC (with extreme caution!) TOPICAL (with considerable safety)

    Rheumatoid arthritis Contact & atopic dermatitis, urticaria, insect stings

    Rheumatoid arthritis

    Systemic lupus

    Asthma Asthma

    Inflammatory bowel disease

    (Crohns & ulcer. colitis)



    3. Toxicity


    Infections; Metabolic imbalance (Cushingoid); Salt/water balance (hypertension);Osteoporosis; Disruption of adrenal-pituitary axis (stress)(problems when coming off therapy).


    4. Examples of Corticosteroid Drugs

    Cortisol, prednisone, dexamethasone, beclomethasone



    B. Therapeutic Uses of Sex Steroids


    1. Estrogen replacement therapy. Used post menopause. Progestin is often included to prevent hyperstimulation of the uterine lining.



    2. Tamoxifen—an anti-estrogen-actually a weak partial agonist--(a) used in therapy of ER+ breast cancer, (b) being tested for chemoprevention of breast cancer.



    3. Oral contraceptives--usually an estrogen/progestin combination (eg Ortho-Tricyclen-ethinyl estradiol/norgestimate). About 98% effective in practice. These agents block ovulation by acting on the hypothalmus/pituitary to block GnRH pulses and LH and FSH release. Side effects include increased risk of thromboembolic events and lingering (but unproven) concerns about stimulating breast cancer.





    VII. Other Drugs used for Immune System Regulation



    Selective immunosuppression: cyclosporine and related drugs.



    1. Perspective.

    There have been revolutionary advances in heterologous organ transplantation over the last decade. Much of this progress has been due to the development of cyclosporine, a cyclic peptide that is a selective immunosuppressive agent. More recently, a number of other selective immunosuppressive agents have been developed; two of these, tacrolimus (“FK506”) and mycophenolate mofetil, are now in widespread clinical use, while sirolimus (rapamycin) entered the clinic in 1999.



    2. Mechanism.

    In contrast to corticosteroids or the cytotoxic immunosuppressive agents, cyclosporine and functionally related compounds such as FK506 can suppress the immune system functions that are most closely associated with graft rejection, without producing generalized immunodebilitation. Cyclosporine blocks early responses to antigen and to cytokines in populations of helper T cells. The cellular binding sites of cyclosporine and FK506 (tacrolimus) are a class of low molecular weight cytosolic proteins, the cyclophilins.

    The discovery that the cyclophilins were ubiquitous peptidyl-prolyl isomerase enzymes involved in the correct folding of newly synthesized proteins initially made little sense in terms of the unique T cell specificity of cyclosporine and related compounds. However, more recent research has elucidated a special role for the cyclophilin-cyclosporine complex in signaling initiated by the T cell receptor (TCR). Engagement of this receptor by antigen leads to increases in intracellular calcium, which in turn activate a calcium-responsive phosphatase termed “calcineurin.” This phosphatase then acts on transcription factors that regulate expression of IL-2 in activated T cells.

    The cyclosporine/cyclophilin complex binds to and inhibits calcineurin, thus disrupting the path between the T cell receptor and IL-2 production. This suppresses the clonal expansion of antigen-activated T cell clones



    3. Absorption, pharmacokinetics, excretion.

    Cyclosporine is readily taken up from the GI tract (20-50%), although intravenous infusion is also sometimes used. Much of the drug in the blood is bound to cells or lipoproteins; the blood t1/2 is about 6 hr. Cyclosporine is widely distributed in tissues and binds to cell lipids and proteins. The drug is metabolized in the liver via cytochrome P450 system-mediated oxidation of its side chains, and parent compound and metabolites are excreted in the bile. Thus hepatic dysfunction can markedly affect the pharmacokinetic parameters of this drug.



    4. Adverse effects.

    The primary adverse effect of cyclosporine is nephrotoxicity, occurring in 25-75% of patients. This is usually dose related and reversible. Drug interactions with other nephrotoxic agents such as aminoglycosides can occur. Neurological toxicity including tremor and seizures is also relatively common. Hirsuitism and gingival hyperplasia are common cosmetic side effects. Although cyclosporine use is associated with an increased risk of infection, this is less than with nonselective immunosuppressives.



    5. Clinical use.

    The primary current use of cyclosporine is to sustain renal, hepatic, and cardiac transplants. Cyclosporine is often used in combination with prednisone and less often with azathioprine (the later combination has been suspected of giving rise to lymphomas). One-year graft survival rates with cadaveric kidneys are now 70-85% with cyclosporine, and 1-year survivals of heart and liver transplants are approaching 75%. This agent is also being used experimentally to treat a variety of inflammatory and autoimmune diseases including rheumatoid arthritis, glomerulonephritis, and psoriasis.
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  26. canadian champ's Avatar
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    Just a little more detail for those interested
    Quote Originally Posted by Bobo


    One of these factors, TFIID, recognizes a TATAA sequence in the gene promoter region just upstream (5’) of the transcription start site.
    .
    The actual consensus sequence is TATANT.
    TBP (TATA binding protein) is a componenet of TFIID that binds TATA BOX, if TATA BOX is present. Promoters lacking TATA BOX bind via Transcription Factors to Initiator element. Another TATA-less binding method involves binding to a GC BOX via SP1 (zinc finger protein) and Transcription Factors.
    Upon binding, TBP distorts DNA to allow for recruitment for other transcription factors and RNA polymerase II.

    Quote Originally Posted by Bobo
    Recruitment of TFIID helps triggers the formation the multiprotein initiation complex (pol II +TFIID, B, F, H, etc).
    .
    The order of the joining of transcription factors are correct EXCEPT RNA poly. II binds with TFIIF, not first (TFIID, TFIIB, TFIIF + poly II, TFIIH). Then the promoter is melted with ATP and mediated by TFIIH --helicase like activity.

    The general design for the superfamily receptors is well conserved. They have (in the following order) Variable Region (100-400aa's) which works as a TRANS-activator of gene expression, region for protein interaction, and as a nuclear localization signal. DNA binding region (68 aa's) which is rich in basic amino acids, cysteine rich + zinc finger rich.

    cc
  27. canadian champ's Avatar
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    Quote Originally Posted by Bobo



    2. Enhancers are sites that are recognized by transcription factors—enhancers may be near or far from the TATAA sequence.
    Enhancers may be upstream or downstream of the start site. They can be located in an intron or gene regions.


    In addition, a mediator protein is present in vivo which associates with the CTD (C-terminus domain) tail of RNA poly II and interacts with many activators and repressors. *This can affect transcription rates by a large amount.

    cc
  28. Dwight Schrute's Avatar
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    Quote Originally Posted by canadian champ
    Hormone receptors are not found in all cells or in the same concentration.
    cc
    There is a reason for "no neck syndrome"


    Here's something else for you Jergo. Its a .pdf by Dr. Kroetz.
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  29. Jergo's Avatar
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    Holy **** that was a lot of good info. Thanks Bobo, I appreciatte it. Man, if you end up leaving afterall, we won't have things like this anymore....
  

  
 

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