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Dat's - CJC-1295 & GHRP-6 (Basic Guides)

I have tried a bunch of GDA supps and have found (IMO) that Corosolic Acid (contained in Banaba Leaf aka Lagerstoemia Speciosa) is by far the best of any products alone and works great in the stack I take. If you try it make sure you get at least 1% Banaba which is common for 3mg of CA (300mg banaba). I usually take 900mg of 1% Banaba (9mg Corosolic Acid) to have a decent effect. I have knocked off about 20-30 points (average) 15min after my PWO shake if I take it 30min before the shake. I do get much better results with higher dosages or when combined with na-rala, VS, Gymnema Sylvestre, and Bitter Melon...

Banaba Powder 1% is $1.50 per gram at bulknutrition which seem pricey to me.

Banaba Extract Powder 1% Corosolic Acid is only $8.75 per 50grams which is 18 cents per gram at Beyond A Century.

Gymnema Sylvestre (25% Gymnemic Acid) is $4.50 per 50 grams (9 cents per gram) at Beyond A Century.

As you can see this is a very inexpensive way to control blood glucose release post-meal.

I'm sure there are plenty of cheap places to buy these items in bulk. Just be careful of that ridiculous bulknutrition price.
 
Also i regards to fourthgen's post with me running 2x 4iu everyday do you feel it would be better to run it 6 days with 1 whole day off a week ?

Yes it would make sense for you. The reason is simply that you want a break from insulin and during that break you want your tissue to overcome any insulin resistance it was dealing with during GH usage.

So on an insulin day off also take a GH day off.
 
Yes it would make sense for you. The reason is simply that you want a break from insulin and during that break you want your tissue to overcome any insulin resistance it was dealing with during GH usage.

So on an insulin day off also take a GH day off.


Dat
i don't use insulin everyday my insulin GH use is

Mon: Train- Insulin AM and PWO/GH 4iux 2
Tue: Train- Insulin AM and PWO/GH 4iux 2
Wed: No training- GH 4iux 2
Thur: Train- Insulin AM and PWO/GH 4iux 2
Fri: Train- Insulin AM and PWO/GH 4iux 2
Sat: No training- GH 4iux 2
Sun: No training- GH 4iux 2

So was considering dropping GH on sunday making that a complete day off insulin and GH

PB
 
Bobaslaw if you dont mind:

1.) What dose of Gymnema Sylvestre do you recommened.

2.) Do you take Gymnema Sylv,Corosolic,vanadyl,etc.. before you have the carb meal or with the meal? If before, how long before?

3.) At the doses you recommened is there a specific carb amount they relate to. For ex, havent heard your anwser to the Gymnema dosing yet but lets say you recommened xxgrams so would you take xxgrams Gymn and 9g corosolic with say an average carb meal, like 50carbs, and double the dosing with 100carbs,etc..?? Thank You

Hey Bro, thought I'd chim in on this one.

I have tried a bunch of GDA supps and have found (IMO) that Corosolic Acid (contained in Banaba Leaf aka Lagerstoemia Speciosa) is by far the best of any products alone and works great in the stack I take. If you try it make sure you get at least 1% Banaba which is common for 3mg of CA (300mg banaba). I usually take 900mg of 1% Banaba (9mg Corosolic Acid) to have a decent effect. I have knocked off about 20-30 points (average) 15min after my PWO shake if I take it 30min before the shake. I do get much better results with higher dosages or when combined with na-rala, VS, Gymnema Sylvestre, and Bitter Melon...

There are numerous studies on CA and its plasma glucose lowering effects. Here are a couple of abstracts:
 
Bobaslaw if you dont mind:

1.) What dose of Gymnema Sylvestre do you recommened.

2.) Do you take Gymnema Sylv,Corosolic,vanadyl,etc.. before you have the carb meal or with the meal? If before, how long before?

3.) At the doses you recommened is there a specific carb amount they relate to. For ex, havent heard your anwser to the Gymnema dosing yet but lets say you recommened xxgrams so would you take xxgrams Gymn and 9g corosolic with say an average carb meal, like 50carbs, and double the dosing with 100carbs,etc..?? Thank You


Hey fourthgen,

NP, glad to share what I have experienced and point out some additional thoughts ;)

1) Gymnemic Acids are a very interesting GDA agent and differs in some of its mediated action from other GDAs. I will post some study abstracts below. Basically, the antihyperglycemic effect that GA invokes is at least partially do to its ability to increase actual plasma insulin most likely thru stimulatory mechanisms directly on the pancreatic beta cells.
This is one reason I have avoided Gymnema if I am strictly looking to solely aid BF loss period. Not enough is known about these herbs especially long term studies, but what is known helps me make decisions for my current goals. Due to the lack of control over the time period insulin may be raised throughout the day. One study shows an Intraperitoneal dose can increase plasma insulin for 2-4hrs after dosage. Not sure about how much longer the oral curve may be as well as dosage dependancies.
So far I have only used it PWO in my stack, and will continue to use it accordingly most likely when not on a strict Fat Burning regimen. I use 1 520mg dose (25% GA = 130mg of GA).
Now, when Bulking, I may consider looking into changing my approach but would like to get a bit more info on this compound.

2) I dose about 30min prior to injesting carbs. The thing with most these herbs and studies show that they reach peak action after a certain period of time. For CA it is approx 90min as per the previous study so it could be tailored better to the type of carb source you will be using, I guess... I'm not getting that anal about it though and just do it half hour before and am happy with my readings ;)

3) I totally think this area needs some good BG monitoring to know how it will affect you for sure and whether higher doses will be beneficial. not to mention the longer term dosing of such compounds... Not enough studies have been done.
I just typically use 300-600mg 1% Banaba (CA at 3-6mg) before carb meals, 9mg CA PWO, 3 times per day maximum. I use 1 Na-Rala (143mg) and 10mg VS along with it. Also 520mg of Gymnema (130mg GA) along with the PWO dose.
I did add Bitter Melon for a while, but dropped it as the stack was getting out of hand, lol. Plus I like to know how each compound acts on its own along with some more info from research. BM contains glycosides such as charantin that shows effects of lowering BG, although a combination of compounds is speculated to produce that result (via some research).
BTW, my use of these compouds may be far from ideal. I'm just tailoring according to what I have learned about their actions and pay attention to my body while using them. I also plan to stop them completely and monitor my body after an off period of use...
If anyone has anything to add or observations and/or experiences, please let me know. I'm learning here just like the rest of us ;)

Here are some of the study abstracts on Gymnema (Gymnemic Acids):

Antihyperglycemic effects of gymnemic acid IV, a compound derived from Gymnema sylvestre leaves in streptozotocin-diabetic mice.
Sugihara Y, Nojima H, Matsuda H, Murakami T, Yoshikawa M, Kimura I.
Department of Chemical Pharmacology, Toyama Medical and Pharmaceutical University, Sugitani, Japan.

We investigated the antihyperglycemic action of a crude saponin fraction and five triterpene glycosides (gymnemic acids I-IV and gymnemasaponin V) derived from the methanol extract of leaves of Gymnema sylvestre R. BR. (Asclepiadaceae) in streptozotocin (STZ)-diabetic mice. The saponin fraction (60mg/kg) reduced blood glucose levels 2 4h after the intraperitoneal administration. Gymnemic acid IV, not the other 4 glycosides at doses of 3.4-13.4mg/kg reduced the blood glucose levels by 13.5-60.0% 6h after the administration comparable to the potency of glibenclamide, and did not change the blood glucose levels of normal mice. Gymnemic acid IV at 13.4 mg/kg increased plasma insulin levels in STZ-diabetic mice. Gymnemic acid IV (1 mg/mL) did not inhibit alpha-glycosidase activity in the brush border membrane vesicles of normal rat small intestines. These results indicate that insulin-releasing action of gymnemic acid IV may contribute to the antihyperglycemic effect by the leaves of G. sylvestre. Gymnemic acid IV may be an anti-obese and antihyperglycemic pro-drug.

Antidiabetic effect of a leaf extract from Gymnema sylvestre in non-insulin-dependent diabetes mellitus patients.
Postgraduate Institute of Basic Medical Sciences Madras, India
J Ethnopharmacol 1990 Oct;30(3):295-300

The effectiveness of GS4, an extract from the leaves of Gymnema sylvestre, in controlling hyperglycaemia was investigated in 22 Type 2 diabetic patients on conventional oral anti-hyperglycaemic agents. Gymnema (400 mg/day) was administered for 18-20 months as a supplement to the conventional oral drugs. During Gymnema supplementation, the patients showed a significant reduction in blood glucose, glycosylated haemoglobin and glycosylated plasma proteins, and conventional drug dosage could be decreased. Five of the 22 diabetic patients were able to discontinue their conventional drug and maintain their blood glucose homeostasis with Gymnema alone. These data suggest that the beta cells may be regenerated/repaired in Type 2 diabetic patients on Gymnema sylvestre supplementation. This is supported by the appearance of raised insulin levels in the serum of patients after Gymnema sylvestre supplementation.
 
Excellent. I think im just gonna stick with r-ala and VS at first and check my bsl readings and if they are appropriate i'll be cool, if not I will add CS next to see how that helps. I will probably hold off on the Gymnema since im dieting.
 
Further Note on GH & Insulin

In plain language, GH in certain circumstances increases glucose uptake identical to that of insulin into both muscle and adipose tissue. This involves translocations of glut 4 and to a lesser extent glut 1 from an intracellular pool to the plasma membrane. BUT in order for this to happen there must be an absence of GH for prolonged periods of time. It appears that this rarely occurs because the base level of GH is still too high to create this effect. *

Of more importance is the "likely" effect of GH on glucose transport into adipose tissue. GH, dose dependently reduces glucose transport (diabetogenic effect). The addition of GH to adipocytes in vitro and dose dependently in vivo reduces the rate of glucose uptake in a way that we could characterize as the opposite of the insulin effect.

"The data reported here not only confirm the earlier findings but also further demonstrate the importance of GH in vivo for the restriction of basal glucose transport in adipocytes.
...
The data give evidence for the importance of GH in vivo, in balance with insulin, for the control of the activity of the glucose carrier in adipose tissue." - Glucose transport in adipocytes and its control by growth hormone in vivo, Schoenle et al. 242 (6): E368. (1982)

So there is a good possibility that although GH in the presence of insulin will not lead to substantial fat loss via lipolysis, it will inhibit the uptake of glucose into adipose tissue. This leads us to the generalization that concurrent administration of GH & insulin will skew nutrient partitioning in favor of muscle tissue and away from adipose tissue.

One further note of interest though is this glucose uptake inhibiting effect of GH leads to a restoration of sensitivity to insulin in that tissue.

* - Cellular mechanism of the insulin-like effect' of growth hormone in adipocytes Rapid translocation of the HepG2-type and adipocyte/muscle glucose transporters, Tanner, J. W. et al, Biochem. J. (1992) 282, 99-106
 
If you have no choice but to store the un-reconstituted vials at room temperature, would they lose potency within say 3 months?

I know you mentioned elsewhere they'll last one year in the freezer

I guess saying "Here go read my post here:" http://www.professionalmuscle.com/fo...&postcount=209

...failed to take...so I suppose if I said it again it still wouldn't work.

So let me go read what you should have....okay...that was a very informative post Dat...thank you.

Now that I have read that post I see that GHRP-6 in acetate is very stable and it should still be very potent after 3 months in a room-temperature environment after all it was 90% potent after almost 5 years.

Now that I have read that post I see that GRF(1-29) is not as stable. But that it should still be fully potent after one month at 77 degrees Fahrenheit and then it will likely lose potency.
 
Spreadsheet demonstrating how DNP builds up in the body. This is posted in response to a private message. PMs do not allow attachments.

Posted for xxxxx but a good thing for everyone to understand because DNP can be deadly.

Spreadsheet demonstrates how the following doses build up substantially. NOTE: I DO NOT RECOMMEND DNP USE.

250mg per day 1-3
250mg 2x per day (500mg total) for 10 days​


Clipboard02.jpg
 
Spreadsheet demonstrating how DNP builds up in the body. This is posted in response to a private message. PMs do not allow attachments.

Posted for xxxxx but a good thing for everyone to understand because DNP can be deadly.

Spreadsheet demonstrates how the following doses build up substantially. NOTE: I DO NOT RECOMMEND DNP USE.

250mg per day 1-3
250mg 2x per day (500mg total) for 10 days​


View attachment 23333
.
 
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A quick question for jesterthefester my tumor biology guy.

Glucose starvation as described below results in P53 activation and cellular apotosis. But many tumors "deactivate" P53. How they do this is a black box for me simply because I haven't taken the time to study it. So my question to you is whether glucose starvation can reactivate the full P53 response in the presence of cancer that deactivates p53?

The phosphorylation of ser-15 on the p53 protein by itself does not activate or stabilize p53. Rather it is an early step in activation of p53 that requires further phosphorylation events, at ser-20, ser-33, and ser-46, and thr-18, which then appear to favor a p53 apoptotic response. Thus glucose starvation that results in ser-15 phosphorylation in a transient manner in normal MEFs does not result in apoptosis. However, if those cells contain an activated oncogene, such as E1A, which binds the Rb protein and liberates E2F-1 to activate p19 ARF, then glucose starvation results in a full p53 response and cellular apoptosis (S. Lowe, pers. comm. *). Thus glucose starvation sensitizes the p53 protein (ser- 15 transiently by AMPK) and, if other signal transduction pathways are engaged, the second steps (MDM2 is degraded and other serines and threonines on p53 are phosphorylated by the ATM, ATR, p38 mitogenactivated protein kinase [MAPK], casein kinase) result in an activated p53, and consequently cell cycle arrest or apoptosis. - Coordination and communication between the p53 and IGF-1-AKT-TOR signal transduction pathways, Arnold J. Levine, Zhaohui Feng, Tak W. Mak, et al., Genes & Dev. 2006 20: 267-275

* Lowe, S.W., Ruley, H.E., Jacks, T., and Housman, D.E. 1993, p53-dependent apoptosis modulates the cytotoxicity of anticancer agents, Cell 74: 957–967.

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Loading a pin with ghrp6 and modified grf for a few hours...

I know it's been said in this thread that you shouldn't mix ghrp6 and cjc(or modified grf) for storage. My question was if it's ok to load a syringe with them mixed to be used about ~4 hours later? Kind of hard to bring vials and load a pin at work.

Also, I've seen this thread change it's course a little with somewhat related topics. One topic discussed was insulin and glycemic levels in the blood. I can't seem to understand a couple points...maybe someone can clear it up.

1. If insulin is produced to pull glucose out of the blood and store it as fat, then why do people/bodybuilders use it? I thought I also read it shuttles nutrients to the muscle, but now I'm not sure after reading some posts.

2. Are there any bad side effects to changing to a low glycemic diet and keeping your blood sugar levels low? Is it possible to gain mass with a low glycemic diet? Finally, what is more important to losing fat...low calories or low blood sugar?

Thanks.
 
kutch said:
My question was if it's ok to load a syringe with them mixed to be used about ~4 hours later? Kind of hard to bring vials and load a pin at work.

Yes. And it has been done by many for that very reason.

kutch said:
1. If insulin is produced to pull glucose out of the blood and store it as fat, then why do people/bodybuilders use it? I thought I also read it shuttles nutrients to the muscle, but now I'm not sure after reading some posts.

It is an indiscriminate storage hormone. It will do both. There are times when preferential treatment is evoked.

Primarily it prevents protein degradation & when coupled with GH which promotes protein synthesis, tissue can accrue.

Concerning the post-meal blood glucose wave it will take on different shapes and amplitudes based on the amount of "work"/glucose it needs to dispose and how resistant/sensitive tissue (both muscle & fat) is to insulin.

The blood glucose wave can have different amplitudes. For example 140ng/ml, 160ng/ml, 200ng/ml, etc.

The wave can have different durations. For example it can last for 45 minutes or an hour and 15 minutes or 2 hours.

The shape of the curve does not have to be bell shaped. Often activity can change the initial shape of the curve such as going for a post meal walk.

After exercise or following a meal when you are in a caloric deficit insulin is more apt to store nutrients in muscle then adipose tissue.

There is a subjective threshold above which insulin will have a "spill over" effect and store nutrients in adipose tissue. This threshold is comprised of both a blood glucose amplitude number and a duration number w/ the possibility for the shape of the curve to influence the outcome.

So for example if you have a blood glucose wave of 50 minutes duration that peaks at say 140ng/ml it maybe that most of those nutrients will be stored in muscle and not adipose tissue. If instead your dietary consumption drives blood glucose to 180ng/ml for an hour and a half you may have a lot of those nutrients stored in adipose tissue.

These numbers are very subjective. For me 140ng/ml is too high if I want to lose fat.

When we talked about glucose disposal agents we were in a way attempting to increase muscle sensitivity to insulin. In addition we are influencing the wave characteristics of blood glucose. These are probably two different ways to look at the same concept - Tissue sensitivity/resistance & glucose wave characteristics/spillover.

In caloric surpluses in a non-post work out environment you can not count on preferential disposal to muscle or use the specific wave numbers you determined when you dieted. But you can do things in an anabloic environment that skew things toward disposal in muscle and not adipose tissue. Steroid administration is one such thing which will influence nutrient disposal in favor of muscle.


kutch said:
2. Are there any bad side effects to changing to a low glycemic diet and keeping your blood sugar levels low? Is it possible to gain mass with a low glycemic diet? Finally, what is more important to losing fat...low calories or low blood sugar?

Have you ever had your bodyfat in the single digits...I mean true single digits measured in a water tank?

Bad side effects? Actually the bad side effects concerning insulin resistance, pre-diabetes, fat gain and poor cardiovascular health come from not controling you blood sugar levels.

Gain mass on a low glycemic diet? Sure. How much of an insulin spike do you think you need IF you are not using GH & steroids? The answer is the sugar you consume in your post-work out shake results in spill-over. Taking in oatmeal as your post work out carb would be just as effective with less fat gain.

The supplement industry has done a number on peoples heads. You don't need sugar & you don't need whey protein PWO. In fact they may even get in your way.

Having said all of that you are either losing bodyfat or gaining muscle. It is not possible to both at the same time.

Now some that are seriously in tune with their body might be able to do both within a small time frame by oscillating ...but they aren't doing it concurrently.

Take in the majority of your calories pre & post workout. Take in carbs (higher GI carbs even) during those times. Spend the rest of the day either eating to lose fat if you are on a diet or eating to gain mass if you are attempting to gain muscle.

Finally, what is more important to losing fat...low calories or low blood sugar? - Come on bro. The answer is glucagon. How are you going to make sure that is present and insulin is absent?
ERRATUM: The answer is really keep insulin from rising rather then driving into a deep glucagon response which will just end up dumping glucose into the bloodstream.
 
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Hey with all this talk of using GH on a diet in an on/off fashion, you know what might be a beneficial addition?

GH Fragment (176-191) used during the trough or GH off times. That might actually work real well.

Too bad my 4th generation lab rat has the attention span of a gnat. :a:tion-sm
 
Finally, what is more important to losing fat...low calories or low blood sugar?[/COLOR] - Come on bro. The answer is glucagon. How are you going to make sure that is present and insulin is absent?


It's all about proper balance.

I agree that for the most optimum lipolytic environment, glucagon levels need to surpass insulin levels to a certain degree.
This is because mole for mole, insulin has more anti lipolytic activity, than glucagon has in lipolytic action.

So, the lower you can keep you BG, the better this is to keep the ratio of G/I (Glucagon/Insulin) at its highest. What can increase this ratio? Keeping BG in the lower range, exercise, beta agonist drugs all stimulate glucagon release from the pancreas. Coupled with a caloric deficit, makes for an efficient fat burning regimen.

Dat, feel free to poke holes in anything or expand on it if you have the desire. I just put out what I vaguely remeber for research here and there ;)

Take Care.

EDIT: I just read post 381 as I have missed quite a bit of this thread here vs the other thread on AM ;) Yep, ain't I just regurgitating pretty much what was already spoken of, sorry...
 
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Would taking Melatonin before bed as a sleep aid negatively or positively effect administration of GRF(1-29) and GHRP-6? Does it affect GH/IGF-1 levels at all?
 
Would taking Melatonin before bed as a sleep aid negatively or positively effect administration of GRF(1-29) and GHRP-6? Does it affect GH/IGF-1 levels at all?

From: Pathophysiology of the Neuroregulation of Growth Hormone Secretion in Experimental Animals and the Human, Andrea Giustina and Johannes D. Veldhuis, Endocrine Reviews 19 (6): 717-797 1998

J. Melatonin

The pineal gland, via melatonin, may also modulate GH secretion. Oral administration of melatonin to normal subjects increases basal GH levels and the GH response to GHRH (516), but marginally affects GH responses to hypoglycemia or apomorphine (517, 518). This suggests that melatonin might play a minimal (stimulatory) role in baseline GH secretion, possibly acting at the hypothalamic level via inhibition of somatostatin. The GH response to L-dopa is reduced in blind human subjects (519), who presumptively lack both light-mediated inhibition of melatonin release and the normal slow wave sleep-associated rise in plasma GH concentrations (520). Thus, it is possible, but entirely unproven, that variations in the release of endogenous melatonin could modulate GH secretion in humans


516 - Valcavi R, Dieguez C, Azzarito C, Edwards CA, Dotti C, Page MD, Portioli I, Scanlon MF 1987 Effect of oral administration of melatonin on GH response to GRF 1–44 in normal subjects. Clin Endocrinol (Oxf) 26:453–458

517 - Smythe GA, Lazarus L 1974 Suppression of human growth hormone secretion by melatonin and cyproheptadine. J Clin Invest 54:116–121

518 - Koulu M, Lammintausta R 1979 Effect of melatonin on L-tryptophan and aphomorphine stimulated growth hormone secretion in man. J Clin Endocrinol Metab 49:70–72

519 - Bellastella A, Colucci C, D’Alessandro B, Cicero ML 1977 L-Dopa stimulated growth hormone release in the blind. J Clin Endocrinol Metab 44:194–195

520 - Krieger DT, Glick S 1971 Absent sleep peak of growth hormone release in blind subjects: correlation with sleep EEG stages. J Clin Endocrinol Metab 3:847–850

While we are on the the topic of neuromodulators here is a pretty good figure from the aforementioned study.

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Would taking Melatonin before bed as a sleep aid negatively or positively effect administration of GRF(1-29) and GHRP-6? Does it affect GH/IGF-1 levels at all?


From: Effects of a single dose of N-Acetyl-5-methoxytryptamine (Melatonin) and resistance exercise on the growth hormone/IGF-1 axis in young males and females,E Nassar,et al., J Int Soc Sports Nutr, January 1, 2007; 4: 14.

ABSTRACT: Melatonin and resistance exercise alone have been shown to increase the levels of growth hormone (GH). The purpose of this study was to determine the effects of ingestion of a single dose of melatonin and heavy resistance exercise on serum GH, somatostatin (SST), and other hormones of the GH/insulin-like growth factor 1 (IGF-1) axis.

Physically active males (n = 30) and females (n = 30) were randomly assigned to ingest either a melatonin supplement at 0.5 mg or 5.0 mg, or 1.0 mg of dextrose placebo. After a baseline blood sample, participants ingested the supplement and underwent blood sampling every 15 min for 60 min, at which point they underwent a single bout of resistance exercise with the leg press for 7 sets of 7 reps at 85% 1-RM. After exercise, participants provided additional blood samples every 15 min for a total of 120 min.

Serum free GH, SST, IGF-1, IGFBP-1, and IGFBP-3 were determined with ELISA. Data were evaluated as the peak pre- and post-exercise values subtracted from baseline and the delta values analyzed with separate three-way ANOVA (p < 0.05). In males, when compared to placebo, 5.0 mg melatonin caused GH to increase (p = 0.017) and SST to decrease prior to exercise (p = 0.031), whereas both 0.5 and 5.0 mg melatonin were greater than placebo after exercise (p = 0.045) and less than placebo for SST. No significant differences occurred for IGF-1; however, males were shown to have higher levels of IGFBP-1 independent of supplementation (p = 0.004). The 5.0 mg melatonin dose resulted in higher IGFBP-3 in males (p = 0.017).

In conclusion, for males 5.0 mg melatonin appears to increase serum GH while concomitantly lowering SST levels; however, when combined with resistance exercise both melatonin doses positively impacts GH levels in a manner not entirely dependent on SST.
 

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