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I want every child to be in school; free SHS won’t be cancelled – Akufo-Addo

President Nana Addo Dankwa Akufo-Addo has said the Free Senior High School programme will not be cancelled despite the economic challenges. He said he wants every child to be in school. “Government will continue to intervene and remain responsible for the provision of free, quality basic and secondary education for all. Education should be a right for all of Ghana’s youth. “Education is the equalizer for opportunities. I want every child to be in school not only for what they learn in the books but also the life experiences that they will gain,” he said at the University of Health and Allied Sciences (UHAS), in Ho, on Friday July 15 when he attended the 10th anniversary of the establishment of the University. UHAS is pursuing aggressively the realisation of its agenda of becoming our nation’s pre-eminent health learning and teaching institution, dedicated to research and community service. Mr Akufo-Addo said the evidence is in the great strides it has chalked in health research, in being ranked amongst the top three (3) Universities in Ghana, and, also, being named number one in the Times Higher Education (THE) Impact Rankings 2022 in the SDG-3 category in Ghana. The President in a Facebook post after the event said “I also inspected ongoing work on $60 million Phase Two Expansion Project of the University, whose sod I cut in September last year. “As a demonstration of our commitment to this project, Government has made available GH¢6.2 million of counterpart funding for the preliminary works, which covers extension of electricity, municipal water supply, construction of storm and waste drains, and all ancillary services required for the project implementation. “Eight months on, I am happy to note that the Phase II Project, which will accommodate the Central Administration of the University and the School of Nursing and Midwifery, is progressing steadily according to schedule. “Some thirty six percent (36.3%) of work has been completed, and, at this rate, I am convinced that work will be completed on time.” Read the full article

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<p><strong> THe role of glucocorticoids</strong><br /><br />The GnRH gene contains a glucocorticoid response element (1), which suggest that glucocorticoids have a direct regulatory function on GnRH expression in the hypothalamus. Chandran et al (2) demonstrated that dexamethasone had a direct supressive effect in GnRH release.<br /><br /><a href="https://www.1steroids.net/injectable-steroids-1162/aquatest-100-mg-21844.html">Testosterone</a> and DHT are known to inhibit HPTA by slowing GnRH pulse in the hypothalamus. In a rat study (3) castrated and adrenolectomized rats saw a huge increase in LH and FSH secretion. Simply adding testosterone however did not stop the rise in gonadotrophins. only when corticosterone was added did testosterone resume its inhibitory functions. However testosterone had no effect on glucocorticoid mediated GnRH supression (4), which suggest that corticosteroids are inhibitory at the pituitary level as well, quite possibly by reducing pituitary sensitivity to GnRH.<br /><br />This was confirmed by Kubajak and Kamel (5) who found that corticosterone had no effect with maximal concentrations of testosterone, but augmented the inhibitory effect on LH release in the presence of lower levels of testosterone. This would also warn those against jumping to conclusions that testosterone might not be supressive if no glucocorticoids are present, since maximal levels of T supressed LH maximally as well.<br /><br />This all taken together suggest the need for glucocorticoid control in the PCT if we want to achieve maximal recovery. In the first place we can do this by avoiding the use of 17AA steroids near the end of a cycle. It has been shown that several 17AA steroids including <a href="https://www.anabolic-steroids.biz/dragon-pharma-orals-1283/winstrol-25297.html">Stanozolol</a>, danazol and methyltestosterone, but not fluoxymesterone or metribolone, can upregulate GR expression (6). Potent short-acting androgens however may be the best way to finish a cycle. Short-acting, to avoid lingering supression from androgens that won't clear the body fast enough, and potent because it has been demonstrated that AR activation in the adrenocortical cells inhibits their growth and steroidogenisis. (7). Lastly I may have finally found a reason to use those pesky arginine supplements the market was swarmed with just a short while ago, (8,9), since there is evidence that nitric oxide can inhibit glucocorticoid action by reducing binding to the GR. This may actually be a wiser choice than searching for a competitive GR inhibitor, since such inhibitors invariably show some affinity for androgen and progesterone receptors as well.<br /><br />The conclusion is that some form of glucocorticoid control is necessary during PCT, and that there is some evidence that even Glucocorticoid managemen on-cycle can reduce problems post-cycle, likely the reason oxandrolone for instance tends to allow people to bounce back faster than for example stanozolol or <a href="https://www.buytestosterone.net/methandienone-1506/dianobol-lab-31849">Dbol</a>.<br /><br /><strong>The role of IGF-1</strong><br /><br />More evidence seems to suggest that there is plausible evidence for cycling between androgens and GH/IGF-1. At Least one study (10) demonstrates that IGF-1 plays a key role in regulating GnRH release via a Ras/Raf-1/Mapk induced pathway and an increase in the c-fos factor.<br /><br />This makes a great case for starting IGF-1 after finishing androgens, both in aiding recovery, as well as keeping gains going. I'm not a big fan of IGF-1 due to the high cost and low returns, but no one can deny its use for athletes that need to maintain mass and keep gaining it while continuous steroid use is not an option.<br /><br /><strong>The role of progesterone</strong><br /><br />Calogero et al (4) also found a modulating effect of progesterone on corticosterone-related GnRH-inhibition. Though the results of studies cited show differing roles for progesterone, on the one hand protective, on the other hand inhibitory. It was even suggested that progesterone may inhibit corticosterone-related inhibition, but not when higher doses of corticosterone were used. This suggests that we may be able to take the edge off of some really supressive estrogenic drugs, nandrolone and more notably MENT and trenbolone, by reducing glucocorticoid action even a little, as suggested above.<br /><br />Although it was also suggested that this could be mediated by a progesterone metabolite (progesterone is the base for many neurologically important steroids), which would of course not be plausible with androgenic progestins. So this remains PURE speculation until futher elucidation of the mechanism of progesterone in this regard becomes available, and should not be carried into conversation as saying "hey Big Cat said that progesterone is good for you post-cycle if you lower cortisol". <br /><br /><strong> Role of estrogen</strong><br /><br />Another study (11) suggests that, at least at the hypothalamic level, estrogen may actually stimulate the HPTA. This data may be consistent with some reports that suggest tamoxifen is estrogenic and not anti-estrogenic at this level. This data does not suggest any different approach, merely explains how it could be possible that <a href="https://www.buy-steroids.biz/dragon-pharma-1277/nolvadex-27612.html">Nolvadex</a> seems to work better than <a href="https://www.roids-shop.biz/ancillaries-320/clomed-8653.html">clomid</a>, since it acts as an estrogen at the hypothalamus and as an anti-estrogen at the pituitary.<br /><br /><br /><strong> References </strong><br /><em><br /><br />(1) Radovick S, Wondisford FE, Nakayama Y, Yamada M, Cutler GB Jr, Weintraub BD.Isolation and characterization of the human gonadotropin-releasing hormone gene in the hypothalamus and placenta.Mol Endocrinol. 1990 Mar;4(3):476-80.<br /><br />(2)Chandran UR, Attardi B, Friedman R, Zheng Z, Roberts JL, DeFranco DB.Glucocorticoid repression of the mouse gonadotropin-releasing hormone gene is mediated by promoter elements that are recognized by heteromeric complexes containing glucocorticoid receptor.J Biol Chem. 1996 Aug 23;271(34):20412-20.<br /><br />(3) Vreeburg JT, de Greef WJ, Ooms MP, van Wouw P, Weber RF.<br />Effects of adrenocorticotropin and corticosterone on the negative feedback action of testosterone in the adult male rat.Endocrinology. 1984 Sep;115(3):977-83.<br /><br />(4) Calogero AE, Burrello N, Bosboom AM, Garofalo MR, Weber RF, D'Agata R.Glucocorticoids inhibit gonadotropin-releasing hormone by acting directly at the hypothalamic level.J Endocrinol Invest. 1999 Oct;22(9):666-70.<br /><br />(5)Kamel F, Kubajak CL.Modulation of gonadotropin secretion by corticosterone: interaction with gonadal steroids and mechanism of action.Endocrinology. 1987 Aug;121(2):561-8.<br /><br />(6)Fernandez L, Boada LD, Luzardo OP, Zumbado M, Lopez A, Diaz-Chico BN, Chirino R.dexamethasone binding activity in liver microsomes is modulated differently by 17 alpha-alkylated androgens and testosterone in vivo.Pharmacol Toxicol. 1995 Oct;77(4):264-9.<br /><br />(7)Rossi R, Zatelli MC, Valentini A, Cavazzini P, Fallo F, del Senno L, degli Uberti EC.Evidence for androgen receptor gene expression and growth inhibitory effect of dihydrotestosterone on human adrenocortical cells.J Endocrinol. 1998 Dec;159(3):373-80.<br /><br />(8) Duma D, Silva-Santos JE, Assreuy J.Inhibition of glucocorticoid receptor binding by nitric oxide in endotoxemic rats.Crit Care Med. 2004 Nov;32(11):2304-10.<br /><br />(9)Pennisi P, D'Alcamo MA, Leonetti C, Clementi A, Cutuli VM, Riccobene S, Parisi N, Fiore CE.Supplementation of L-arginine prevents glucocorticoid-induced reduction of bone growth and bone turnover abnormalities in a growing rat model.J Bone Miner Metab. 2005;23(2):134-9.<br /><br />(10)Zhen S, Zakaria M, Wolfe A, Radovick S.Regulation of gonadotropin-releasing hormone (GnRH) gene expression by insulin-like growth factor I in a cultured GnRH-expressing neuronal cell line.Mol Endocrinol. 1997 Jul;11(8):1145-55.<br /><br />(11)Radovick S, Ticknor CM, Nakayama Y, Notides AC, Rahman A, Weintraub BD, Cutler GB Jr, Wondisford FE.Evidence for direct estrogen regulation of the human gonadotropin-releasing hormone gene.J Clin Invest. 1991 Nov;88(5):1649-55.</em></p>

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UHAS has chalked great strides in health research – Akufo-Addo

President Nana Addo Dankwa Akufo-Addo was at the University of Health and Allied Sciences (UHAS), in Ho, on Friday July 15 to attend the 10th anniversary of the establishment of the University. UHAS is pursuing aggressively the realisation of its agenda of becoming our nation’s pre-eminent health learning and teaching institution, dedicated to research and community service. Mr Akufo-Addos aid the evidence is in the great strides it has chalked in health research, in being ranked amongst the top three (3) Universities in Ghana, and, also, being named number one in the Times Higher Education (THE) Impact Rankings 2022 in the SDG-3 category in Ghana. The President in a Facebook post after the event said “I also inspected ongoing work on $60 million Phase Two Expansion Project of the University, whose sod I cut in September last year. “As a demonstration of our commitment to this project, Government has made available GH¢6.2 million of counterpart funding for the preliminary works, which covers extension of electricity, municipal water supply, construction of storm and waste drains, and all ancillary services required for the project implementation. “Eight months on, I am happy to note that the Phase II Project, which will accommodate the Central Administration of the University and the School of Nursing and Midwifery, is progressing steadily according to schedule. “Some thirty six percent (36.3%) of work has been completed, and, at this rate, I am convinced that work will be completed on time.” Read the full article