What Strain is it? NIRVANA BLACK JACK
Is it Indica, Sativa or Hybrid? What percentages?
How Many Plants? 8 BUT ONLY 1 IS AFFECTED
Is it in Vegetative or Flowering Stage? VEG
If in Vegetative Stage… How Long? 2WEEKS
If in Flowering Stage… How Long?
Indoor or Outdoor? INDOOR
Soil or Hydro?SOIL
If Hydro, Reservoir size?
If Hydro, Reservoir Temperature?
If Hydro, what type of Medium?
If Hydro, what type of Setup?
If Soil… What is in your Mix? FFOF,40% PERLITE
If Soil… What Size Pot? 1GAL
Size (Wattage) of Light? How Many? 400 WATT MH
Is it Air Cooled? YES
Temperature of Room/Cabinet? 78.2 F
RH of Room/Cabinet?46%
PH of Medium or Reservoir? 6.3
Any Pests? NOT THAT IM AWARE OF
How Often are you Watering? WHEN POTS ARE LIGHT, ONCE A WEEK AT THIS PIONT
Type and Strength of Fertilizers used? HUMBOLTS OWN (I HAVE COMPLETE LINE OF PRODUCTS), HAVENT REALLY USED ANY NUTES, OTHER THAN SOME ST, SOME DARK ENERGY, SUPER NOVA. ABOUT 1/2 STREGTH OF RECOMMENDED DOSAGE
Size or Square Footage of Room? 2X4

HERES SOME PICS OF THE ISSUE IM HAVING, IT APPEARS ATLEAST TO ME (FIRST GROW) THAT IS A Mg ISSUE?

TOMORROW I WAS GONNA PIC UP SOME EPSOM SALT AND ALSO DO A FLUSH.?? ANYHOW HERES SPOME PICS OF ISSUE. ANY AND ALL HELP IS GREATLY APPRECIATED

Via possible Mg issue? help needed asap!

Apart from their effects on mood and reward, cannabinoids exert beneficial actions such as neuroprotection and attenuation of inflammation. The immunosuppressive activity of cannabinoids has been well established. However, the underlying mechanisms are largely unknown. We previously showed that the psychoactive cannabinoid Δ(9) -tetrahydrocannabinol (THC) and the non-psychoactive cannabidiol (CBD) differ in their anti-inflammatory signalling pathways.To characterize the transcriptional effects of CBD and THC, we treated BV-2 microglial cells with these compounds and performed comparative microarray analysis using the Illumina MouseRef-8 BeadChip platform. Ingenuity Pathway Analysis was performed to identify functional subsets of genes and networks regulated by CBD and/or THC.Overall, CBD altered the expression of many more genes; from the 1298 transcripts found to be differentially regulated by the treatments, 680 gene probe sets were up-regulated by CBD and 58 by THC, and 524 gene products were down-regulated by CBD and only 36 by THC. CBD-specific gene expression profile showed changes associated with oxidative stress and glutathione depletion, normally occurring under nutrient limiting conditions or proteasome inhibition and involving the GCN2/eIF2α/p8/ATF4/CHOP-TRIB3 pathway. Furthermore, CBD-stimulated genes were shown to be controlled by nuclear factors known to be involved in the regulation of stress response and inflammation, mainly via the (EpRE/ARE)-Nrf2/ATF4 system and the Nrf2/Hmox1 axis.These observations indicated that CBD, but much less than THC, induced a cellular stress response in microglial cells and suggested that this effect could underlie its anti-inflammatory activity. LINKED ARTICLES: This article is part of a themed section on Cannabinoids in Biology and Medicine. To view the other articles in this section visit British Journal of Pharmacology – Volume 165, Issue 8 – Themed Section: Cannabinoids in Biology and Medicine, Part II. Guest Editors: Itai Bab and Steve Alexander – Wiley Online Library. To view Part I of Cannabinoids in Biology and Medicine visit British Journal of Pharmacology – Volume 163, Issue 7 – Cannabinoids in Biology and Medicine, Part I. Guest Editors: Itai Bab and Steve Alexander – Wiley Online Library.

Source: unboundmedicine.com
Via Differential Transcriptional Profiles Mediated By Exposure To The Cannabinoids

We and others have reported that simultaneous targeted deletion of CB(1) and CB(2) resulted in exacerbation of immune reactivity, suggesting a role of endocannabinoids in down-regulating immune function. In this study, we demonstrate that APC function is enhanced specifically in the absence of CB(1) and CB(2) signaling, resulting in an exacerbated immune response phenotype. After influenza infection, CB(1)(-/-)CB(2)(-/-) mice showed more pronounced pulmonary damage, increased inflammatory cell infiltrate, inflammation, and a greater cellular immune responses compared with WT mice, as evidenced by transcriptome analysis, more robust T cell activation, and effector cell cytokine production. After direct activation in vitro, there were no differences in the percentages of cytokine-producing CD4(+) T cells between CB(1)(-/-)CB(2)(-/-) and WT mice. However, untreated CB(1)(-/-)CB(2)(-/-) mice routinely had fewer nave T cells compared with WT, suggesting dysregulation of APC immune homeostasis. Moreover, bmDCs and AM isolated from CB(1)(-/-)CB(2)(-/-) mice exhibited a more mature phenotype, with and without TLR stimulation, and bmDCs elicited T cells more robustly than WT mice. Collectively, these findings implicate a role for CB(1) and CB(2) on APCs in regulating immune responses and immune homeostasis.

Source: pubmed.gov
Via Deletion Of Cannabinoid Receptors 1 And 2 Exacerbates APC Function

The inflammatory response plays an important role in the pathogenesis of many diseases in the central nervous system. Cannabinoids exhibit diverse pharmacological actions including anti-inflammatory activity. In this study, we tried to elucidate possible effects of cannabinoids on lipopolysaccharide (LPS)-induced expression of inflammatory cytokine mRNAs in rat cerebellar granule cells.Inhibitory effects of cannabinoids on cytokine induction in cerebellar granule cells were determined by RT-PCR method.In these cells, both mRNA and protein of cannabinoid receptor 1 (CB(1) ), but not CB(2) , were expressed. LPS (1 g/ml) produced a marked increase in the induction of inflammatory cytokines, including interleukin-1β, interleukin-6 and tumour necrosis factor-α. CP55940, a synthetic cannabinoid analogue, concentration-dependently inhibited inflammatory cytokine expression induced by LPS. On the other hand, the endocannabinoids 2-arachidonoylglycerol and anandamide were not able to inhibit this inflammatory response. Notably, a CB(1) /CB(2) antagonist NESS0327 (3 m) did not reverse the inhibition of cytokine mRNA expression induced by CP55940. GPR55, a putative novel cannabinoid receptor, mRNA was also expressed in cerebellar granule cells. Although it has been suggested that G(q) associates with GPR55, cannabinoids including CP55940 did not promote phosphoinositide hydrolysis and consequent elevation of intracellular Ca([2+]) concentration. Furthermore, a putative GPR55 antagonist, cannabidiol, also showed a similar inhibitory effect to that of CP55940.These results suggest that the synthetic cannabinoid CP55940 negatively modulates cytokine mRNA expression in cerebellar granule cells by a CB and GPR55 receptor-independent mechanism.

Source: unboundmedicine.com
Via A Synthetic Cannabinoid, CP55940, Inhibits Lipopolysaccharide-Induced Cytokine mRNA