l. The effect of drinking red wine on the MeOH balance is difficult to calculate. On one hand, drinking wine introduces exogenous MeOH; on the other hand, wine EtOH can increase the pool of endogenous MeOH. Our calculations show that the MeOH contribution from wine was an essential part of its increase in the blood. However, we allowed for the contribution of endogenous MeOH sources because the EtOH in wine can “block” ADH and reduce the “flow” of endogenous MeOH. The accelerated increase in FA levels during the second hour after taking red wine also suggests 3 Dietary Methanol Regulates Human Gene Activity the involvement of an endogenous pool of MeOH. Endogenous sources of MeOH are not known, but we can assume a high level of production because the MeOH content in the blood is determined primarily by its transformation to FA and also through MeOH removal from the blood by renal and pulmonary excretion. Evaluating the impact of endogenous sources in the MeOH production is possible when the oxidation of MeOH is reduced during ADH competitive inhibition with EtOH. Experiments with volunteers after EtOH intake can assess lower-level MeOH production by endogenous sources because it is difficult to imagine the complete removal of ADH molecules from MeOH metabolism. To conduct this experiment, we selected a group of volunteers weighing 47 to 90 kg and aged 21 to 67 years. Each volunteer was drinking alcohol on an empty stomach at a volume of 1 ml of 40% EtOH per 1 kg of weight. The alcohol was free of MeOH, as evidenced by GC. Verifying microarray data with qRT-PCR Microarray data verification was conducted by using WBCs from volunteers after administering pectin or red wine. Oligonucleotide primers for the 7 genes related to oxygen transport, cell signaling, AD and the earlier identified MRGs were used to validate the microarray data by qRTPCR. The brain genome-wide analysis of mice after inhalation of vapors of injured plants and of MeOH The reduced mRNA synthesis of hemoglobin genes in WBCs may be a common reaction of cells to an 22408714 increase in the plasma levels of MeOH. To test this hypothesis, we conducted a genomewide analysis of the brain in mice after exposure to methanol vapor under 
conditions that were close to natural: the mice breathed the vapors from injured plants known to contain methanol . RNA samples collected from the mouse brain after inhalation of the wounded plant leaf vapors or MeOH were used to generate cDNA. The brain RNA samples after the inhalation of methanol served as a positive control. The cDNA were analyzed using Illumina Whole-Genome 8 microarrays with probes for approximately 25,600 transcripts. We identified those transcripts that were expressed with P-values of,0.05. A genome-wide analysis of human WBCs after the ingestion of citrus pectin To understand the role of endogenous and dietary MeOH in AG-221 web humans, we conducted a full-genome analysis of WBCs in volunteers after administering pectin as a MeOH-generating substance. The WBC transcripts of 18 volunteers who received citrus pectin were analyzed on the Human HT-12 v.4. Expression BeadChip arrays by targeting more than 25,000 annotated genes with more than 48,000 probes. Significant gene expression differences between the samples after pectin intake and the 17628524 controls were visualized in a cluster diagram. We identified transcripts that were expressed with detection q-values, 0.05 as follows: 106 were up-regulated and 17 were down-regulated. Among these results, we
