Human Growth Hormone - Efficacy of recombinant hGH therapy in cured acromegaly patien

New Exercise and Fitness Review

Human Growth Hormone – Efficacy of recombinant hGH therapy in cured acromegaly patien

Related Articles Efficacy of recombinant hGH therapy in cured acromegaly patients with GH deficiency: a single centre experience.

Endocr Connect. 2015 Jan 19;

Authors: Dutta P, Mahendran B, Reddy KS, Ahluwalia J, Vaiphei K, Kochhar RK, Gupta P, Srinivasan A, Kumar M, Mukherjee KK, Shah VN, Parthan G, Bhansali A

Abstract
Introduction: The effectiveness and short-term safety of recombinant human growth hormone (r-hGH) in patients with acromegaly who develop growth hormone deficiency (GHD) after treatment, is not well established. Subjects and Methods: Ten subjects with acromegaly who had GHD were treated with r-hGH for six months. Control groups consisted of ten age, gender and body mass index matched healthy subjects and ten active acromegaly patients who were treatment naïve. Body composition, quality of life, muscle strength, lipid profile and cardiovascular risk factors were assessed in all subjects at baseline, and the same parameters were reassessed after 6 months of therapy with r-hGH in acromegaly with GHD. Repeat MRI of the sella was performed in treated subjects. Optical colonoscopy was done and biopsies were taken from multiple sites for proliferation indices (Ki-67). Result: The median duration of GHD was 17.8 months and dose of r-hGH administered was 5.7±1.5 µg/kg/d. There was improvement in bone mineral content (p 0.01), bone mineral density (p 0.04), muscle strength (p

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Human Growth Hormone - Efficacy of recombinant hGH therapy in cured acromegaly patien

Cytotoxic Effect of S-Petasin and Iso-S-Petasin on the Proliferation of Human Prostat

New Exercise and Fitness Review

Cytotoxic Effect of S-Petasin and Iso-S-Petasin on the Proliferation of Human Prostat

Cytotoxic Effect of S-Petasin and Iso-S-Petasin on the Proliferation of Human Prostate Cancer Cells.

Anticancer Res. 2015 Jan;35(1):191-199

Authors: Wang Z, Hsu H, Chou J, Yu C, Bau D, Wang G, Huang C, Wang PS, Wang S

Abstract
Background: Petasin (Petasides hybridus) is a perennial shrub that is found in Europe as well as parts of Asia and North America and is being used to treat hypertension, tumors and asthma. In a previous study, we reported that petasin possesses biological effects including inhibition of testosterone production and the release of corticosterone from rat zona fasciculata-reticularis cells, and anti-proliferative effect on human T24 bladder carcinoma cells. Materials and Methods: In the present study, we assessed the effects of S-petasin and iso-S-petasin on the growth and proliferation of two hormone-independent DU145 and PC3 and one hormone-dependent LNCaP prostate cancer cell line at concentrations of 10(-7)-10(-5) mol/l. The cell proliferation index, cell number index, expression of caspases and apoptosis-associated proteins and cell morphology were measured. Results: S-Petasin and iso-S-petasin reduced the viable cell number and increased the numbers of apoptotic cells in the tested cell lines in a dose-dependent manner. Western blot analysis revealed that S-petasin and iso-S-petasin reduced the protein levels of procaspase 3, 8, and 9 and cleaved poly(ADP-ribose) polymerase (PARP) in all tested prostate cancer cell lines, and reduced that of procaspase 7 in LNCaP and PC3 cells. At the same time, S-petasin and iso-S-petasin increased mitochondrial membrane permeability and cytochrome c release from mitochondria to the cytosol via reducing the ratio of BCL2/BAX in DU145 and PC3 cells, and up-regulating the levels of p53 in DU145 cells but down-regulating it in PC3 cells. Conclusion: These results indicate that S-petasin and iso-S-petasin induce apoptosis via the activation of mitochondria-related pathways in prostate cancer cells, suggesting S-petasin and iso-S-petasin could be potential anticancer agents.

PMID: 25550551 [PubMed - as supplied by publisher]

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Cytotoxic Effect of S-Petasin and Iso-S-Petasin on the Proliferation of Human Prostat

Human Growth Hormone - [Effects of r-hGH replacement therapy on glucose and lipid met

New Exercise and Fitness Review

Human Growth Hormone – [Effects of r-hGH replacement therapy on glucose and lipid met

[Effects of r-hGH replacement therapy on glucose and lipid metabolism and thyroid function in children with idiopathic short stature.]

Zhongguo Dang Dai Er Ke Za Zhi. 2014 Dec;16(12):1236-1240

Authors: Zheng F, Wang X, Wang X

Abstract
OBJECTIVE: To study the effects of recombinant human growth hormone (r-hGH) replacement therapy on glucose and lipid metabolism and thyroid function in children with idiopathic short stature (ISS).
METHODS: Forty-seven ISS children with a mean age of 10±3 years treated between January 2009 and January 2013 were enrolled. All children underwent r-hGH replacement therapy for 3-24 months and were followed up once every 3 months. Fasting blood glucose (FBG), insulin (INS), blood lipids and thyroid function were measured before treatment and after 0-1 and 1-2 years of treatment.
RESULTS: After treatment with r-hGH, there were no significant changes in FBG, INS, insulin sensitivity index (ISI), and FBG/INS ratio (FGIR), but the FGIR showed a declining trend. The percentage of patients with FGIR

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Human Growth Hormone - [Effects of r-hGH replacement therapy on glucose and lipid met

Monsanto’s Bt-Toxins Found to Kill Human Embryo Cells

New Exercise and Fitness Review

Monsanto’s Bt-Toxins Found to Kill Human Embryo Cells
by Christina Sarich
Posted on January 24, 2014

Many individuals have heard it a million times, but for the uninformed, or those just looking to fuel their 2014 fire to finally defeat Monsanto and their cronies, you’ll be interested to know that Monsanto’s Bt-toxin is far from ‘safe’ as the chemical company claimed it would be when filing their papers with the FDA. New research from Canada show that BT toxins are showing up in pregnant women, and low and behold – they are killing human embryo cells. 2014 is the year of the horse, but we’re not through beating this one to death.

It’s called reproductive toxicology, and just like their suicide seeds, these Bt toxins are starting to kill our own unborn children. This is no exaggeration. Hopefully reading further will compel you to take action. It is time to put Monsanto to rest, bankrupt them, and let the world know their ‘secrets’ near and far.

Bt toxins are prominent in genetically altered crops such as corn, soy, wheat, and others, called Cry1Ab – and they can be lethal. Not only do these cry-toxins target the kidney cells of developing human fetuses, but when Cry1Ab and Cry1Ac are combined with RoundUp, they can delay apoptosis of human cancer cells. What’s worse, glyphosate, the main ingredient in RoundUp, also causes necrosis – i.e. the death of human tissue, and this happens even when the substance is found in much smaller amounts than what is currently being used on our agricultural crops. The stuff is still carcinogenic in the parts per trillion range.

In its rush to remain the ‘agricultural leader’ of the world, the US government erected defunct regulatory bodies that have no means to truly examine the ramifications of biotechnology on our food. The National Institute of Health (NIH) is a joke and the FDA gave Monsanto an indefinite hall pass to cause mayhem on the food supply.

More people need to file lawsuits against this company until they are without one red cent to continue poisoning the planet and killing our unborn babies. The Organic Seed Grower’s Association sued Monsanto in 2011, and Idaho wheat growers are suing Monsanto for cross-contamination, but what about parental groups? Mother’s Against Drunk Driving was formed when a mom lost her baby to a drunk driver. Perhaps the mothers who face reproductive failure due to Monsanto’s hand can sue them collectively.

The FDA’s internal memos about their concerns surrounding GMO seed crops recently surfaced in one lawsuit, though the public was never meant to see them. GMO foods are not the foods we have always eaten. This is an outright lie.

Any lawyers out there willing to go against the monopoly? I’d sign a class action suit today. Would you? In the meantime, utilize these 5 tips for avoiding GMOs while you write your local senator, state representatives, congressman, and president.

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Monsanto’s Bt-Toxins Found to Kill Human Embryo Cells

stk "s information about human growth hormone

New Exercise and Fitness Review

stk ‘s information about human growth hormone

here you go bros..

USUALLY with a SERO kit , (like Sturge said) you add 1cc of water to the powder in ONE vial to get 18iu. This means 1cc of mixed water = 18iu.

This also means 1/2cc of mixed water = 9iu, and 1/4cc of water = 4.5iu of GH.

if you have a slin pin that goes from 10-100, this really means it goes from 10% -100% of 1cc. Still with me?

So if you only wanted 1/4cc of water to get your daily dose of 4.5iu of gh, just fill the insulin syringe up to the 25 mark. (actually since there is probably NO 25 mark, pull it to half way between the 20 and the 30)

If you want 9iu per day (in one shot) fill it to the 50 mark. (50% of 1cc)

easy isnt it??

Here ya go..you have 6mg (approx 18iu) of gh per bottle (I’m assuming you’re talking about Sero or one of the knockoffs). Okey dokey…now, you also have approx 1ml of dilutent..if you have a REAL Sero kit, there will be slightly more than 1ml of aqueous solution.

Okay…so if you dump a full ml of water into the 6mg of powder, then the equation will look like this: 1ml = 18iu. Very simple. You can adjust that depending on what dose you’re going to use.

Say you want to do 6iu/day. That means that each 6mg (18iu) bottle will give you 3 doses (or pretty damn close anyway). Now…it’s not real easy to get 3 doses out of 1ml, so let’s make it a number that’s easier to divide into thirds. How about .9ml? That works nicely. So…instead of putting the full ml into the bottle, just use .9ml or the 90 mark on an insulin syringe. Keep in mind that insulin syringes are marked for use with INSULIN, nothing else, so even though it says ‘iu’ on the syringe, that’s not how many ius you’re getting. Okay..so now you have .9ml in your gh powder…perfect. So to get your dose of 6iu (2mg), you would fill an insulin syringe to the 30 mark (which indicates 30iu of insulin…but we’re not using insulin), which is one THIRD of .9ml. Got it?

INSULIN AND GROWTH HORMONE
Growth hormone (GH) is one of the most sought after bodybuilding drugs due to its’ legendary abilities to strip off body fat and increase muscle mass. The former is accomplished through direct lipolysis (fat release from adipocytes), which GH does to an incredible degree.

Muscle mass acquisition is accomplished through: the direct stimulation of protein synthesis, increasing amino acid uptake by muscle cells, and by greatly stimulating IGF-1 synthesis in the liver. It is this last point that is of interest to us because it is the main anabolic mechanism for GH, and it is also where insulin comes in to play.

More than half of GHs’ anabolic effect is due to IGF-1 production, but unfortunately this is quite often wasted. This is because IGF-1 has an extremely short half life in the bloodstream, so it usually doesn’t reach many target tissues (muscles for our interest) to exert maximum anabolic effect. To rectify this situation, insulin can be used to increase the amount of an IGF-1 binding protein (specifically IGF1-BP3) that actually helps IGF-1 to reach the muscles and exert its’ extreme anabolism.

Insulin also reduces the amount of “bad” IGF1 BP’s, (BP’s 2 and 4) that would normally interfere with IGF-1 uptake and use by muscle. To say that there is a synergistic effect between insulin and GH doesn’t do the combination justice.

It makes me shudder to think of the hundreds of thousands of dollars spent on GH, without using it to the maximum anabolic potential. From a fat loss perspective, GH is incredible. It should directly negate the lipogenic effect of insulin, leaving you with one KICK ASS combination.

SouthernTrendKiller *SULTAN OF SIZE*

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stk "s information about human growth hormone

Human Growth Hormone - Utility of Extended FAST in Blunt Chest Trauma: Is it the Time

New Exercise and Fitness Review

Human Growth Hormone – Utility of Extended FAST in Blunt Chest Trauma: Is it the Time

Related Articles Utility of Extended FAST in Blunt Chest Trauma: Is it the Time to be Used in the ATLS Algorithm?

World J Surg. 2014 Sep 10;

Authors: Abdulrahman Y, Musthafa S, Hakim SY, Nabir S, Qanbar A, Mahmood I, Siddiqui T, Hussein WA, Ali HH, Afifi I, El-Menyar A, Al-Thani H

Abstract
INTRODUCTION: The clinical significance of extended Focused Assessment with Sonography for Trauma (EFAST) for diagnosis of pneumothorax is not well defined.
OBJECTIVES: To investigate the utility of EFAST in blunt chest trauma (BCT) patients.
STUDY DESIGN: A single blinded, prospective study. Participants: All patients admitted with BCT (2011-2013).
SETTINGS: Level 1 trauma center in Qatar.
PROCEDURES AND OUTCOME MEASURES: Patients were screened by EFAST and results were compared to the clinical examination (CE) and chest X-ray (CXR). Chest-computed tomography (CT) scoring system was used to confirm and measure the pneumothorax. Diagnostic accuracy of diagnostic modalities of pneumothorax was measured using sensitivity, specificity, predictive values (PVs), and likelihood ratio.
RESULTS: A total of 305 BCT patients were included with median age of 34 (18-75). Chest CT was positive for pneumothorax in 75 (24.6.%) cases; of which 11.% had bilateral pneumothorax. Chest CT confirmed the diagnosis of pneumothorax in 43, 41, and 11.% of those who were initially diagnosed by EFAST, CE, and CXR, respectively. EFAST was positive in 42 hemithoraces and its sensitivity (43.%) was higher in comparison to CXR (11.%). Positive and negative PVs of EFAST were 76 and 92.%, respectively. The frequency of missed cases by CXR was higher in comparison to EFAST and CE. The lowest median score of missed pneumothorax was observed by EFAST.
CONCLUSION: EFAST can be used as an efficient triaging tool in BCT patients to rule out pneumothorax. Based on our analysis, we would recommend EFAST as an adjunct in ATLS algorithm.

PMID: 25205343 [PubMed - as supplied by publisher]

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Human Growth Hormone - Utility of Extended FAST in Blunt Chest Trauma: Is it the Time

Human Growth Hormone - hGH isoform differential immunoassays applied to blood samples

New Exercise and Fitness Review

Human Growth Hormone – hGH isoform differential immunoassays applied to blood samples

Related Articles hGH isoform differential immunoassays applied to blood samples from athletes: Decision limits for anti-doping testing.

Growth Horm IGF Res. 2014 Jun 11;

Authors: Hanley JA, Saarela O, Stephens DA, Thalabard JC

Abstract
OBJECTIVE: To detect hGH doping in sport, the World Anti-Doping Agency (WADA)-accredited laboratories use the ratio of the concentrations of recombinant hGH (‘rec’) versus other ‘natural’ pituitary-derived isoforms of hGH (‘pit’), measured with two different kits developed specifically to detect the administration of exogenous hGH. The current joint compliance decision limits (DLs) for ratios derived from these kits, designed so that they would both be exceeded in fewer than 1 in 10,000 samples from non-doping athletes, are based on data accrued in anti-doping labs up to March 2010, and later confirmed with data up to February-March 2011. In April 2013, WADA asked the authors to analyze the now much larger set of ratios collected in routine hGH testing of athletes, and to document in the peer-reviewed literature a statistical procedure for establishing DLs, so that it be re-applied as more data become available.
DESIGN: We examined the variation in the rec/pit ratios obtained for 21,943 screened blood (serum) samples submitted to the WADA accredited laboratories over the period 2009-2013. To fit the relevant sex- and kit-specific centiles of the logs of the ratios, we classified ‘rec/pit’ ratios based on low ‘rec’ and ‘pit’ values as ‘negative’ and fitted statistical distributions to the remaining log-ratios. The flexible data-driven quantile regression approach allowed us to deal with the fact that the location, scale and shape of the distribution of the modeled ‘rec/pit’ ratios varied with the concentrations of the ‘rec’ and ‘pit’ values. The between-kit correlation of the ratios was included in the fitting of the DLs, and bootstrap samples were used to quantify the estimation error in these limits. We examined the performance of these limits by applying them to the data obtained from investigator-initiated hGH administration studies, and in athletes in a simulated cycling stage race.
RESULTS: The mean and spread of the distribution of the modeled log-ratios depended in different ways on the magnitude of the rec and pit concentrations. Ultimately, however, the estimated limits were almost invariant to the concentrations, and similar to those obtained by fitting simpler (marginal) log-normal and Box-Cox transformed distributions. The estimated limits were similar to the (currently-used) limits fitted to the smaller datasets analyzed previously. In investigator-initiated instances, the limits distinguished recent use of rec-hGH from non-use.
CONCLUSIONS: The distributions of the rec/pit ratios varied as a function of the rec and pit concentrations, but the patterns in their medians and spreads largely canceled each other. Thus, ultimately, the kit- and sex-specific ratio DL obtained from the simpler model was very close to the ‘curve of DLs’ obtained from the more complex one. Both were close to previously established limits.

PMID: 24973245 [PubMed - as supplied by publisher]

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Human Growth Hormone - hGH isoform differential immunoassays applied to blood samples