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Exceptionally High FECO Yields


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Good Afternoon 420,
As anticipated, the trike inspections on both cultivars CFD 3 & 4 indicated the time for harvest as established by gardener protocols, resulting in them hanging upside down in the drying area now. Was different taking them down so unceremoniously compared to the song and dance we have harvesting one beautiful branch at a time. With these little ones one snip and off she goes. Dang

The remaining cousin clones are making us a bit nervous in a good way. The buds are giant, and very near where intervention will be required in deploying structural support methods. Aside from that, they are both very happy and look forward to joining our data bank stored in mason jars.

In traveling thru some denser vegetation visiting our gorilla site we encountered a snake that was around 4 foot long. On the same trip in, the pooch detected folks in the woods behind a tree line on a trail that may have had a small opportunity to observe us first. The bird watching began and soon we withdrew without visiting our objective. Be safe my friends.


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Good Evening 420

The dust is settling and we have a picture of what is coming up for our analysis. The rosters are as follows;

Control cultivars fertigated normally (not stressed).

FD #1 82 grams curing jarred

FD #2` 44 grams curing jarred

Total 126 grams

Drought stressed cultivars.

FD #3 50 grams curing jarred

FD #4 74 grams curing jarred

Total 124 grams

Currently evaluating the best way to proceed , possibly concentrate results into two teams instead of four. Not sure, and any opinions are welcome food for thought my friends. :peace:

Lab testing not yet available.


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Since you're processing 100 gram batches, do you have any choice except to combine the plants?
Thinking (because of what I ended up with after playing Santa) I could run four smaller identical batches and expect statistical extrapolations of 100 gram batches could reasonably be presented. Maybe 28 or 30 grams extractions.


Member of the Month: July 2019
Are you having any thoughts to solve the oil out of the flower and measure it when the solvent is evaporated? Just what is the method of telling ? Checking for terps?


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Straw Hat notes,
Just reading how seeds are rich in ABA. Is this why clones are such snowflakes? Think. What if we add ABA to our rooting powder? If the advantage seeds enjoy over cuttings rests with a starter dose of hormones, how can we level the playing field. hm
p.s. can the hormone package given seed be silenced for ABA ?

I have access to this guys e-mail, little nervous about reaching out though.
Peter J. Davies
Department of Plant Biology, Cornell University, Ithaca, New York
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Member of the Month: July 2019
Rosin press and dabs. Nothing shows the terps better then the taste in a dab from the rosen press at 170f.:circle-of-love::peace:
Shows I believe yes. Don't we want to be able to make this measurable? Oh we can still measure the rosin at same time, heat, pressure. I get it. Thanks.


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Rosin press and dabs. Nothing shows the terps better then the taste in a dab from the rosen press at 170f.:circle-of-love::peace:
Hi DG,
I think this might be another must have, (rosin press) dang. can you make a recommendation for personal pressing?
TBH I have zero experience pressing dabs to date.
I have not even borrowed the hair straightener always in my way.
Like I told Otter, I am afraid of all these things until somehow I get froggy.
Santa has some tips in the gratuity jar... she need not know? coward.
Please tell how the BB99 is doing when you get a chance.
Maybe I will bug Otter for a Strawberry update...pls.


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Straw Hat Notes;​

A few thoughts written down while memory serves me. This is a living study of the girls, so it is evolving and I gotta take notes. Anyhow, some musings copied tonight follow.

Back in 1937 hormones had been busted being something a plant can actually transfer from one part to another (Went/Thimann Phytohormones1937). From there, biological understandings have quantum leaped.

It is now known plant hormones differ from our human (mammalian) hormones in that plants synthesize hormones both locally (like us) and in a wide range of tissues, or cells within tissues.

It is interesting to note that, of all the original established group of plant

hormones, only the chemical identification of abscisic acid was made from

higher plant tissue
Davies re;

Over the last few years there has been

active progress in elucidating the biosynthesis, signal transduction and action

of almost every hormone. Thus whereas previously the progress in

understanding the action of one hormone was much better than that of

another we now find increased understanding of hormone action across the

board. yu betcha.

It should, however, be emphasized that

hormones do not act alone but in conjunction, or in opposition, to each other

such that the final condition of growth or development represents the net

effect of a hormonal balance
(Chapter A2) (5) uh huh

Abscisic acid (ABA)


Abscisic acid is a single compound with the following formula:

Its name is rather unfortunate. The first name given was "abscisin II"

because it was thought to control the abscission of cotton bolls. At almost

the same time another group named it "dormin" for a purported role in bud

dormancy. By a compromise the name abscisic acid was coined (1). It now

appears to have little role in either abscission (which is regulated by

ethylene; 2E: G2) or bud dormancy, but we are stuck with this name. As a

result of the original association with abscission and dormancy, ABA has

become thought of as an inhibitor. While exogenous applications can inhibit

growth in the plant, ABA appears to act as much as a promoter, such as in

the promotion of storage protein synthesis in seeds (Chapter E4), as an

inhibitor, and a more open attitude towards its overall role in plant

development is warranted. One of the main functions is the regulation of

stomatal closure
(Chapters D6 and E3)

Sites of synthesis

ABA is synthesized from glyceraldehyde-3-phosphate via isopentenyl

diphosphate and carotenoids (Chapter B5) in roots and mature leaves,

particularly in response to water stress
(Chapters B5 and E3). Seeds are also

rich in ABA which may be imported from the leaves or synthesized in situ.


ABA is exported from roots in the xylem and from leaves in the phloem.

There is some evidence that ABA may circulate to the roots in the phloem

and then return to the shoots in the xylem (Chapters A2 and E4).

This is how we get in I'm thinking.


! Stomatal closure - water shortage brings about an increase in ABA

which leads to stomatal closure (Chapters D6 and E3).

! ABA inhibits shoot growth (but has less effect on, or may promote, root

growth). This may represent a response to water stress (Chapter E3; 2E:


! ABA induces storage protein synthesis in seeds (Chapter E4).

! ABA counteracts the effect of gibberellin on α-amylase synthesis in

germinating cereal grains (Chapter C2).

! ABA affects the induction and maintenance of some aspects of

dormancy in seeds (Chapters B5 and E4). It does not, however, appear

to be the controlling factor in ‘true dormancy’ or ‘rest,’ which is

dormancy that needs to be broken by low temperature or light.

! Increase in ABA in response to wounding induces gene transcription,

notably for proteinase inhibitors, so it may be involved in defense

against insect attack (2E: E5


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ABA is exported from roots in the xylem and from leaves in the phloem. There is some evidence that ABA may circulate to the roots in the phloem and then return to the shoots in the xylem (Chapters A2 and E4).
So then maybe, when a cutting is taken access to the xylem becomes far less complicated. Import mechanism need looked in to.


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Got some pics of our outdoor experiment and a couple of the two clones remaining in flower.



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The first two clone specimens CFD1unstressed and CFD2stressed are laying on the drying screens. I will probably manicure them tomorrow down to buds (stem and sugar removed). Again, the focus will be to isolate the cured buds and produce equal batches of what I call FECO. I used to call it RSO but was corrected (I think) into calling it something else besides RSO because I use grain alcohol. Im good with CCO. I dont want to talk much about how I make it until after all the batches have been extracted using exact same methods. I can improve my recipe later if need be, but I want to make it the way I did when we got the 16% return.

The four seed cultivars in our consideration are jarred and nearing end of normal cure. Longer is always better my Canadian cook tells us. Anyhow, we will be performing extractions soon judging by my refrigerator only having food in my special spot.

in one pic i said day 59 should say 49 , nevermind I learned another new trick editing pictures. :)

Hope that made sense. :peace:
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Next Experimental Study Planning

Thoughts, Ideas and problematic controls.​

  • We would like two seed strains to begin the study. This may not be the statistically superior method compared to a single strain/phenotype study? With a single mother we have four identical cultivars to play with. The two-strain idea will probably get tossed.
  • Both seed strain Mother’s to be kept in vegetative mode until clone specimens are ready for the photoperiod adjustments.
  • Clone specimens to be clearly labeled with Mother’s name.
  • Mother plants will mature in 3.5 gal containers.
  • Clone specimens will mature in 5 gal containers.
  • Clone specimens in HID will be under a scrog.
  • Mother plants will have F.S. LED illumination.
  • All required medium to be prepared in advance as a large well mixed lot prior to distribution to the pots.
  • The strategy of less is more approach to flower fertigation’s in terms of quantity of nutrients will be observed. The frequency of fertigation other than during intentional withholdings will be as needed by individual cultivar presentations.
  • Considering the presentation of low grade solutions of locally gathered ABA during different stages of Mother’s life cycle after we strip her of a few branches.
  • :peace:


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More straw-hat notes

Phenotypic plasticity is one of those themes that continues to fascinate biologists from diverse backgrounds from ecologists and geneticists to developmental and evolutionary biologists. It is often a subject that students have difficulty grasping, for phenotypic plasticity is the result of the interplay between two distinct but interacting identities – the genetics of an organism and its environment.

The role of the environment in inducing the observed variation in phenotypic expression is critical to an assessment of phenotypic plasticity; variable phenotypic expression that is solely a consequence of genetics is not considered plasticity.

Phenotypic traits for which plastic expression has been documented in plants include morphological (e.g., leaf shape, branching patterns), allocational (e.g., root to shoot mass ratios, leaf area ratios, reproductive effort), anatomical (e.g., cuticle thickness, palisade mesophyll depth, stomatal density), physiological (e.g., light saturated photosynthetic rates, basal metabolic rates), and biochemical (e.g., defensive chemical production, Rubisco contents) traits.

Phenotypic variation that does not correlate with a specific genotype or specific environmental cue, but is the result of stochasticity in the biochemical processes involved in gene and protein expression and other cellular noise that occurs throughout development, is referred to as “developmental noise ” (Bradshaw 1965). If developmental noise generates sufficient variation in phenotypic expression, genetically identical individuals grown in the same environment will exhibit different phenotypes. The resulting phenotype could be adaptive, maladaptive, or neutral depending on the environmental conditions (DeWitt and Scheiner 2004).

Comparing plant phenotypes at a common age versus a common developmental stage may result in incorrect conclusions regarding the nature of the observed phenotypic variation.


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Coronary Artery Calcification project notes;
CAC notes;

The discovery of endocannabinoids and their functional roles in the brain and other parts of the body has had tremendous implications in medical science. Cannabinoid receptors are widely present all over the cardiovascular system and that’s the reason researchers believe the endocannabinoid system might play a key role in the regulation of blood circulation and cardiac functions.

Expression of CB2 receptors in the cardiovascular system, such as myocardial cells, blood vessels and smooth muscle cells, are now confirmed.

Studies have reported variations in the expression of CB2 receptors in carotid artery plaques among stroke and asymptomatic patients. Therefore, CB2 receptor expression and signaling appears to be a protective response against acute and chronic pathological events. Additionally, the protective role of CB2 receptors has been documented in various events of atherosclerosis, including restenosis, myocardial ischemia and cerebral ischemiaor reperfusion injury.

Studies are now zeroing in on biologically active molecules that influence the cannabinoid system, particularly phytocannabinoids. These studies preferentially employed cannabidiol (CBD) as it lacks psychoactive effects. Due to ongoing research studies, the therapeutic role of cannabinoids in the treatment of cardiovascular diseases, including atherosclerosis, is now recognized. Studies have shown that selective activation of CB2 receptors by cannabidiol could be helpful in maintaining the integrity of coronary arteries by mitigating the endothelial dysfunctions, such as the accumulation of oxidized LDL and the narrowing of blood vessels.

So, the role of endocannabinoids and cannabinoid receptors are now evident. Altogether, we can assume that modulation of these receptors may have therapeutic implications on atherosclerosis. Another study has concluded that low dose oral THC has decreased inflammatory response in atherosclerotic plaques by attenuating lymphocyte proliferation and macrophage chemotaxis within atherosclerotic lesions, which are the crucial steps in the pathogenesis of atherosclerosis. This study clearly demonstrates the presence of CB2-receptors in the inflammatory cells, atherosclerotic plaques and the target organs.
About CAC
Despite a significant amount of research addressing CAC, our understanding of the pathogenesis, clinical implication and management of CAC remains limited. In terms of pathophysiology of CAC, the governing factors are not fully understood regarding formation of intimal versus medial calcification, and the clinical significance of these two types of CAC remains to be elucidated. On the other hand, CAC carries prognostic importance. Coronary CTA is an established tool to assess CAC, and a score > 400 is associated with worse clinical outcomes in patients with an intermediate risk of developing CHD and in those with established CHD. Currently, there is no specific medical therapy targeting the reduction of CAC, and whether the treatment strategy limits the progression or enhances the regression of CAC or has prognostic impact needs further clinical studies. On the other hand, in patients with CHD and significant coronary stenosis which necessitate revascularization therapy, the presence of moderate to severe CAC pose a clinical challenge. Specifically, developed PCI strategies have contributed to significantly higher procedure success, though morbidities are usually higher than in those patients without CAC as a result of the increased complexity of the procedures and higher cardiovascular risk profiles. Future studies should focus on the understanding of pathophysiologic mechanisms of CAC, identify targets of potential therapy, and improve interventional strategies.


Well-Known Member
CAC notes;
Cannabinoid receptors in atherosclerosis.

Recent findings suggesting that cannabinoid receptors are potential targets for the treatment of atherosclerosis are reviewed.
Cannabinoids, such as Delta9-tetrahydrocannabinol, the major psychoactive compound of marijuana, their synthetic analogs and endogenous cannabinoid ligands, produce their biological effects by interacting with specific receptors. In the apolipoprotein E knockout mouse model of atherosclerosis, Delta9-tetrahydrocannabinol was shown to inhibit disease progression through pleiotropic effects on inflammatory cells. Blocking of cannabinoid receptor CB2, the main cannabinoid receptor expressed on immune cells, abolished the observed effects. The development of novel cannabinoid receptor ligands that selectively target CB2 receptors or pharmacological modulation of the endocannabinoid system might offer novel therapeutic strategies in the treatment of atherosclerosis. Several reports demonstrating an implication of the endocannabinoid system in different inflammatory conditions support this hypothesis.
The immunomodulatory capacity of cannabinoids is now well established and suggests a broad therapeutic potential of cannabinoids for a variety of conditions, including atherosclerosis. New strategies based on nonpsychotropic cannabinoid receptor ligands or compounds modulating endocannabinoid synthesis or stability might solve the problem of the unwanted side effects associated with cannabinoid administration.


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We have received encouraging initial correspondence from a Professor of Biology Emeritus from Cornell who had published a study on Phytohormones. It is with fingers crossed I wait for further correspondence. The first message related to biology and he responded favorably. Now I have loosed the cat from the bag, and mentioned specifically what we are up to with regard to cannabis glandular production through hormonal stimulation..

Let's hope the scientist in him helps assuage the hurdles of prohibition and compels him to explore with us..


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@Graytail, @neikodog, @Amy Gardner, @InTheShed , @MagicJim, @Ganjagrowergu , @beez0404 , @Happy Hemper, @Amadeus Forzin, @Oldbear, @Bode, @Buck5050, @BrixNewb, @overlord.

That’s all I could think of off the top of my head.

This is important for us to catch. Maritimer serendipitously stumbled onto the timing for increased glandular production. We’ve been tossing this idea around casually for a couple years, and it may be time to focus and fine tune. Neiko shared that he’s seen this happen in his garden, and shares my belief that this is worth our attention.

I’d like to find out if it’s strain-dependent, and find out which ones don’t respond, as well as which ones do best. I think we’re capable of that, in the very least.

Let’s spread the word, and see how much we can learn. :circle-of-love:
I’m in!


Member of the Year: 2015 & 2016 - Member of the Month: Mar 2015, Sept 2016 - Nug of the Month: Oct 2017 - Creme de la Creme Photos: Dec 2016
We have received encouraging initial correspondence from a Professor of Biology Emeritus from Cornell who had published a study on Phytohormones. It is with fingers crossed I wait for further correspondence. The first message related to biology and he responded favorably. Now I have loosed the cat from the bag, and mentioned specifically what we are up to with regard to cannabis glandular production through hormonal stimulation..

Let's hope the scientist in him helps assuage the hurdles of prohibition and compels him to explore with us..
Took my breath away. I have goosebumps, and I’m feeling a little stunned at the power of curiosity. :5::5::5:

And welcome @medmanmike. I’m glad your brilliantly curious mind found us. :5:
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