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The technique of molecular-beam, mass spectrometric (MBMS) sampling is applied to the elucidation of the molecular pathways in the fast pyrolysis of wood and its principal isolated constituents. The goal is the optimization of high-value fuel products by thermal and catalytic means. The positive-ion mass spectra shown are obtained from real-time, direct sampling of light gases, reactive intermediates, and condensible vapors simultaneously. The cellulose, lignin, and hemicellulose (e.g., xylan) components of wood pyrolyze largely to monomer and monomer-related fragments and give characteristic mass spectral signatures. Whole wood appears to behave as the sum of its constituents, with few if any vapor species derived from interaction of the main polymer constituents. An important interaction, however, is the influence of mineral matter in the wood on the carbohydrate pyrolysis pathways. Vapor phase cracking of the primary products proceeds through a stage of light hydrocarbons and oxygenates to the ultimate formation of aromatic tars and H2, CO, C02, and H20. These steps are illustrated and discussed. Consistent with these observations, a relatively simple pyrolysis reaction scheme is proposed.

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B-lymphoid transcription factors (e.g. PAX5, IKZF1) are critical for early B-cell development1–2, yet genetic lesions occur in >80% of cases of B-cell acute lymphoblastic leukemia (ALL)3–4. The significance of these lesions in ALL remained unclear. Combining ChIP-seq and RNA-seq studies, we identified a novel B-lymphoid program for transcriptional repression of glucose and energy supply. Our metabolic analyses revealed that PAX5 and IKZF1 enforce a state of chronic energy deprivation, resulting in constitutive activation of the energy-stress sensor AMPK5–7. Dominant-negative mutants of PAX5 and IKZF1 relieved glucose and energy restriction. Studying a transgenic pre-B ALL mouse model, heterozygous deletion of Pax5 increased glucose uptake and ATP-levels by >25-fold. Reconstitution of PAX5 and IKZF1 in pre-B ALL patient samples restored a non-permissive state and induced energy crisis and cell death. A CRISPR/Cas9-based screen of PAX5- and IKZF1- transcriptional targets identified NR3C1 (glucocorticoid receptor)8, TXNIP (glucose feedback sensor)9 and CNR2 (cannabinoid receptor)10 as central effectors of B-lymphoid restriction of glucose and energy supply. Interestingly, transport-independent lipophilic methyl-conjugates of pyruvate and TCA cycle metabolites bypassed the gatekeeper function of PAX5 and IKZF1 and readily enabled leukemic transformation. Conversely, pharmacological TXNIP- and CNR2-agonists and a small molecule AMPK-inhibitor strongly synergized with glucocorticoids, identifying TXNIP, CNR2 and AMPK as potential therapy-targets. Furthermore, our results provide a mechanistic explanation for the empiric finding that glucocorticoids are effective in the treatment of B-lymphoid but not myeloid malignancies. We conclude that B-lymphoid transcription factors function as metabolic gatekeepers by limiting the amount of cellular ATP to levels that are insufficient for malignant transformation.