Steroid Forum: This is a discussion on Questions For Anthony Roberts within the Anabolic Steroids forums, part of the extensive steroid information at MESO-Rx; Here are a few of your published ideas, taken directly from your posts and papers. Can you explain them to ...
This COULD get interesting, but SWALE scared off Anthony "Bill" Roberts.
He won't respond to this post b/c they already spent 14 pages on the same subject two weeks ago. Sill funny, though. MANWHORE--you always crack me up........"what about Aromasin"..........just egging them on, LOL.
What happened to the sexy angel; I can't get my dick up with out looking at it.......now what am I supposed to do??
"what about Aromasin"..........just egging them on, LOL
Yes i could see myself doing something like that but i was being serious. I didn't know Hooker was Bill R. shit i didn't even know .. put 2 and 2 together and even knew Bill was back. Bill is short for Anthony? Yes i am in my own world and basically just see what i want to .. anyway,i was reading Mr. Roberts article about Aromasin on another board i go to which is basically all Vets and is very private. What ever Swale and Bill have going on is up to them,but i did like Bills article and has me thinking about other PCT options. .. There is even a source that has mixed up a PCT with Aromasin in it and guys (not newbees either) are really into it
The "Bill" Roberts I respect has been around for years. I met him when I considered T-Mag home. He has a background in the sciences, and was working on his PhD in Biochem or Pharm or some related topic at the time. An extremely knowledgeable individual, he is also quite a gentleman.
This "Anthony" Roberts has no training whatsoever in any of the related topics. He obviously has never even read about any of them, nor does he know how to act.
Let's not insult Bill Roberts by confusing him with this character.
O OK .. was that the BILL Roberts i use to talk to way back on Meso? .. the one you know? .. I didn't really talk to him,i would just ask questions about some PCt products and he would answer ... Now who is the guy mentioned in Anabolics 2002 as the steriod researcher (something like that)? that isn't this guy? It's the Bill you know?
Here are a few of your published ideas, taken directly from your posts and papers. Can you explain them to us, please:
1. SERM'S lower estrogens.
2. "take baths in spironolactone",
3. Use of finasteride for PCT.
4. HCG stimulates thyroid hormone production.
We are hoping for logical, reasonable discussion of the above topics. If you require financial compensation for same, please let us know.
Please find the exact article where I said the comments in blue, link us to them (by post) and re-post it, highlighted. Just so I know the context you are referring to....
Also...you're under the mistaken assumption that I read this board regularly, I see. I can't imagine why you think that. I participate on boards where I get a direct benefit from said interaction. This isn't one of them.
I said to switch to Prop at the end of a cycle, and use finasteride, becase in this study (animal), finasteride prevented LH-suppression caused by testosterone propionate...here's a chart from the study:
that chart shows the baseline level of LH in male sheep given a 5-Alpha-Reductase inhibitor (Finasteride), then a chart showing the LH levels in sheep given testosterone propionate, and finally a chart showing LH levels of sheep given testosterone propionate + the inhibitor (graph 3 in the series). You’ll note that although using the inhibitor alone produced no remarkable effects on LH at all, when administered with testosterone, it seems to have allowed LH pulsality to continue very much unaffected (slightly affected, but still very close to baseline) even though exogenous testosterone propionate was administered...all three are from reference...
Reference:Effect of inhibiting 5 alpha-reductase activity on the ability of testosterone to inhibit luteinizing hormone release in male sheep.
Biol Reprod. 1994 Jun;50(6):1244-50
Previous studies have indicated that hCG has a weak intrinsic thyroid-stimulating activity. Differences in the molecular composition and biological activity of hCG in patients with trophoblastic diseases and pregnant women occur, but are not well defined. Therefore, we have studied the effect of serum samples and purified hCG preparations from patients with trophoblastic diseases on T3 release from human and porcine thyroid slices in vitro. We examined 30 serum samples from 13 patients with nonseminomatous testicular germ cell tumors, 3 from women with choriocarcinoma, and 5 from patients with hydatidiform moles. In all but 1 serum sample from the tumor patients, but in none of 11 serum samples of pregnant women, T3-releasing activity was found. Two patients with testicular cancer and 1 patient with molar pregnancy experienced episodes of frank hyperthyroidism. Isoelectric focusing on polyacrylamide gels of tumor sera (n = 15) revealed substantial amounts of acidic isoelectric variants, pI 3.3-3.9, which were only barely detectable in pregnancy sera. The percentage of acidic hCG variants with pI 3.3-4.0 to total hCG with pI 3.3-5.2, as determined by hCG (+hCG beta) RIA of the eluted fractions of polyacrylamide gel isoelectric focussing, varied from 12-45% in sera of tumor patients and from 0-4% in pregnant sera. We purified the acidic variants of hCG with pI 3.6-3.8 (hCGav) from the urine of our patients. The beta-subunit of purified hCGav had a slightly higher mol wt (35,750) than that of hCG CR 119 (34,190) on polyacrylamide gel electrophoresis. The hCGav showed a dose-dependant stimulation of T3 release and cAMP generation from human thyroid slices, whereas the other hCG fractions on isoelectric focussing had no thyrotropic effect in similar dose levels. The TSH-like activity of hCGav could be roughly estimated as 10 mIU TSH/IU hCGav. Anti-hCG (+hCG beta) antiserum, but not anti-hTSH antiserum, neutralized the biological activity of hCGav. These findings strongly suggest that acidic hCG variants act as functional stimulators of the human thyroid in vitro. Since these molecular variants of hCG can exist in patients with trophoblastic diseases in significant amounts, they could be responsible for some cases of hyperthyroidism in trophoblastic diseases.
PMID: 3004921 [PubMed - indexed for MEDLINE] Hyperthyroidism due to secretion of human chorionic gonadotropin in a patient with metastatic choriocarcinoma.
Servico de Endocrinologia e Metabologia, Hospital de Clinicas da UFPR, 80060-240 Curitiba, PR. ludimylameister@yahoo.com.br
A 26-year-old pregnant woman presenting with repeated episodes of vaginal bleeding, weight loss, and shortness of breath was diagnosed with choriocarcinoma with metastases to both lungs. Chorionic gonadotropin levels (hCG) were >2.5 x 10(6)mU/mL. Consistent with hCG-induced subclinical hyperthyroidism, she had a suppressed TSH of 0.037 mU/L (0.49 - 4.67), a T4 of 18.1 microg/dL (4.9 - 10.7), and T3 of 136 ng/dL (45 - 137). Chemotherapy with a combined regimen with etoposide, methotrexate, and dactinomycine was started. The initial course was complicated by urosepsis with respiratory distress requiring endotracheal intubation for 3 days. She then improved rapidly, and her thyroid function tests were within normal limits by day 12. Six months later, after ten cycles of chemotherapy, the patient was in remission without signs of residual tumor or hCG-induced paraneoplastic activity.
: Gynecol Endocrinol. 2004 May;18(5):269-77.Related Articles,Links The human chorionic gonadotropin molecule from patients with trophoblastic diseases has a high thyrotropic activity but is less active in the ovary.
Department of Obstetrics and Gynecology, University of Essen, Essen, Germany.
To examine the pathogenesis of hyperthyroidism in women with trophoblastic diseases, the biological activity of human chorionic gonadotropin (hCG) molecules in women with normal pregnancy (n = 85) and in women with trophoblastic diseases (vesicular mole, n = 30; and choriocarcinoma, n = 12) was compared. Hyperthyroidism (thyroid stimulating hormone (TSH) < 0.3 mIU/l) was observed more frequently in women with trophoblastic diseases. All the sera were then subjected to Chinese hamster ovary cells transfected with the human TSH receptor (CHO-hTSHr cells) and cAMP production was compared. Sera from the women with choriocarcinoma showed the highest cAMP production. Interestingly, significant correlation between serum hCG level and cAMP production in CHO-hTSHr cells was observed only in women with trophoblastic disease. All the sera were then applied to CHO cells transfected with hCG/luteinizing hormone (LH) receptor (CHO-hCG/LHr cells). In contrast to the findings with the TSH receptor, sera from the women with normal pregnancy showed the highest cAMP production in these cells. Correlation between serum hCG level and cAMP production in CHO-hCG/LHr cells was significant only in normal pregnancy. These results indicate that the hCG molecule from women with trophoblastic diseases displays enhanced thyrotropic activity.
Medical Department II, Klinikum Grosshadern, University of Munich, Germany.
hCG is a putative thyroid stimulator. The present studies were undertaken to examine its interaction and that of its desialylated variant asialo-hCG with recombinant human TSH (hTSH) receptor (hTSHr). To this end, we transfected a human thyroid carcinoma cell line (HTC) lacking endogenous TSHr with the full-length cDNA of the hTSHr. Unlike the wild type, the transfected cells, termed HTC-TSHr cells, were able to bind bovine TSH (bTSH) with high affinity and increase cAMP production in response to bTSH stimulation. Of the hCG forms, intact hCG displayed a weak activity to inhibit [125I] bTSH binding to HTC-TSHr cells, with 100 mg/L (2.6 x 10(-6) mol/L) producing maximally a 20% inhibition, whereas asialo-hCG achieved half-maximum binding inhibition at a concentration of 8 mg/L (2.3 x 10(-7) mol/L). The inhibitory constant (Ki) of asialo-hCG for recombinant hTSHr was calculated from saturation experiments in the presence of variable doses of bTSH and a fixed concentration of asialo-hCG to be approximately 8 x 10(-8) mol/L. The interaction of asialo-hCG with TSHr was further assessed by studies of the direct binding of the radioactively labeled hormone to both HTC and HTC-TSHr cells. [125I]Asialo-hCG binding to HTC-TSHr cells was 4.7%, compared to 1.5% in the wild-type cells lacking TSHr and was displaceable by bTSH (0.1-100 IU/L), indicating specific binding of the tracer to TSHr. Functionally, hCG (up to 100 mg/L; 2.6 x 10(-6) mol/L) proved unable to evoke any significant cAMP response over basal values in HTC-TSHr cells, as did asialo-hCG. Asialo-hCG, but not hCG, inhibited bTSH-stimulated adenylate cyclase activity in the cells in a dose-dependent manner. In conclusion, the present data show that intact hCG binds only weakly to HTC-TSHr cells and produces no significant cAMP stimulation, which is at variance with data obtained in FRTL-5 and Chinese hamster ovary-TSHr cells, but in good accord with previous findings in human thyroid membranes. Asialo-hCG, on the other hand, strongly binds to recombinant TSHr and inhibits the cAMP response to bTSH in HTC-TSHr cells, indicating that the desialylated hCG variant directly interacts with the receptor and truly is an antagonist of the hTSHr.
PMID: 8157724 [PubMed - indexed for MEDLINE] Making you look stupid is almost too easy. But I'll take my usual per-article fee for it. Contact the board owner for payment details.
Questions For Anthony Roberts 
Yes i could see myself doing something like that but i was being serious. I didn't know Hooker was Bill R. shit i didn't even know .. put 2 and 2 together and even knew Bill was back. Bill is short for Anthony? 
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