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Tree establishment following severe or stand-replacing disturbance is critical for achieving U.S. climate change mitigation goals and for maintaining the co-benefits of intact forest ecosystems. In many contexts, natural post-fire tree regeneration is sufficient to maintain forest cover and associated ecosystem services, but increasingly the pattern and scale of disturbance exceeds ecological thresholds and active reforestation may be warranted. Our capacity to plant trees, however, is not keeping pace with reforestation needs. This shortfall is uniquely apparent in the western U.S., where wildfire size and severity have increased in recent decades and long-term divestment in the reforestation supply chain has limited our ability to respond to existing needs. Here we present an analysis of key facets of both the supply and demand side of reforestation in the western U.S. and address six questions: (1) What is the current backlog of potential reforestation needs driven by high-severity wildfire?; (2) How will increasing wildfire activity through the end of the century affect potential reforestation needs?; (3) What is our capacity to meet current and future reforestation needs?; (4) How can we scale the reforestation supply chain to meet current and future demands?; (5) What approaches to reforestation can promote forest resilience to climate change and wildfire?; and (6) Where are opportunities emerging from recent policy initiatives, innovative public-private partnerships, and natural capital markets for scaling reforestation? Between 1984 and 2000, annual tree planting capacity met post-fire needs but cumulatively over the last two decades (2000 to 2021) it has fallen short of fire-driven needs by an estimated 1.5 million ha (ca. 3.8 million ac). We anticipate this gap will increase 2 to 3 fold by 2050. Scaling up reforestation efforts to close this gap will require increased investment across all facets of the reforestation supply chain, public-private partnerships, and novel approaches to reforestation that increase the resilience of western forests to drought and wildfire. We highlight emerging opportunities from recent policy initiatives and conservation finance for expanding reforestation efforts.

A rapid method for measurement of assimilable organic carbon (AOC) is proposed. The time needed to perform the assay is reduced by increasing the incubation temperature and increasing the inoculum density. The ATP luciferin-luciferase method quickly enumerates the test organisms without the need for plate count media or dilution bottles. There was no significant difference between AOC values determined with strain P17 for the ATP and plate count procedures. For strain NOX, the plate count procedure underestimated bacterial levels in some samples. Comparison of AOC values obtained by the Belleville laboratory (by the ATP technique) and the Stroud Water Research Center (by plate counts) showed that values were significantly correlated and not significantly different. The study concludes that the rapid AOC method can quickly determine the bacterial growth potential of water within 2 to 4 days.

1. The modification of the vasodilator effect of calcitonin gene-related peptide (CGRP) by a panel of monoclonal antibodies (MAbs), which map to discrete epitopes on the CGRP molecule, was investigated in pig coronary artery rings (PCA). The preparations were pre-constricted with acetylcholine (3 x 10(-7) M) and concentration-response curves to CGRP (2 x 10(-10)-2.56 x 10(-8) M) were obtained in the presence or absence of each MAb. 2. CGRP caused a concentration-dependent relaxation of PCAs which reached a maximum (98.2 +/- 4.8%, n = 25) at 1.28 x 10(-8) M and gave an EC50 of 3.8 +/- 0.8 x 10(-9) M. 3. Two MAbs which map to the N-terminal, CN1 and CRA3, did not affect the CGRP response whilst a third, CRA5, significantly inhibited its effect. 4. The C-terminal MAb, CRA2, did not modify the CGRP response whilst, in contrast, CB3 (C-terminal) potentiated its effect. A similar augmentation of the CGRP-induced vasodilatation was seen in the presence of the middle-region MAb, CRA8. 5. These results suggest that regional specific MAbs can modify the vasodilator effect of CGRP causing either inhibition (CRA5, N-terminal) or potentiation (CB3, C-terminal; CRA8, middle region).

Children undergoing continuous corticosteroid therapy become stunted in height. The mechanism of this inhibition of natural growth has been investigated in the lower femoral epiphysial growth plate of young rabbits on daily corticosteroid. The growth plate became narrow: fewer cells in the germinative zone gave rise to short widely-spaced chondrocyte columns, each with a reduced number of mature and hypertrophic cells; the pattern of trabecular bone in the metaphysis was also disturbed. After even small doses these changes develop very rapidly, and therefore impose a threat to the growth of children receiving treatment with corticosteroids.