Climate warming increases extreme daily wildfire growth risk in California.

California has experienced enhanced extreme wildfire behaviour in recent years1-3, leading to substantial loss of life and property4,5. Some portion of the change in wildfire behaviour is attributable to anthropogenic climate warming, but formally quantifying this contribution is difficult because of numerous confounding factors6,7 and because wildfires are below the grid scale of global climate models. Here we use machine learning to quantify empirical relationships between temperature (as well as the influence of temperature on aridity) and the risk of extreme daily wildfire growth (>10,000 acres) in California and find that the influence of temperature on the risk is primarily mediated through its influence on fuel moisture. We use the uncovered relationships to estimate the changes in extreme daily wildfire growth risk under anthropogenic warming by subjecting historical fires from 2003 to 2020 to differing background climatological temperatures and aridity conditions. We find that the influence of anthropogenic warming on the risk of extreme daily wildfire growth varies appreciably on a fire-by-fire and day-by-day basis, depending on whether or not climate warming pushes conditions over certain thresholds of aridity, such as 1.5 kPa of vapour-pressure deficit and 10% dead fuel moisture. So far, anthropogenic warming has enhanced the aggregate expected frequency of extreme daily wildfire growth by 25% (5-95 range of 14-36%), on average, relative to preindustrial conditions. But for some fires, there was approximately no change, and for other fires, the enhancement has been as much as 461%. When historical fires are subjected to a range of projected end-of-century conditions, the aggregate expected frequency of extreme daily wildfire growth events increases by 59% (5-95 range of 47-71%) under a low SSP1-2.6 emissions scenario compared with an increase of 172% (5-95 range of 156-188%) under a very high SSP5-8.5 emissions scenario, relative to preindustrial conditions.

Approximate calculations of the net economic impact of global warming mitigation targets under heightened damage estimates.

Efforts to mitigate global warming are often justified through calculations of the economic damages that may occur absent mitigation. The earliest such damage estimates were speculative mathematical representations, but some more recent studies provide empirical estimates of damages on economic growth that accumulate over time and result in larger damages than those estimated previously. These heightened damage estimates have been used to suggest that limiting global warming this century to 1.5 °C avoids tens of trillions of 2010 US$ in damage to gross world product relative to limiting global warming to 2.0 °C. However, in order to estimate the net effect on gross world product, mitigation costs associated with decarbonizing the world's energy systems must be subtracted from the benefits of avoided damages. Here, we follow previous work to parameterize the aforementioned heightened damage estimates into a schematic global climate-economy model (DICE) so that they can be weighed against mainstream estimates of mitigation costs in a unified framework. We investigate the net effect of mitigation on gross world product through finite time horizons under a spectrum of exogenously defined levels of mitigation stringency. We find that even under heightened damage estimates, the additional mitigation costs of limiting global warming to 1.5 °C (relative to 2.0 °C) are higher than the additional avoided damages this century under most parameter combinations considered. Specifically, using our central parameter values, limiting global warming to 1.5 °C results in a net loss of gross world product of roughly forty trillion US$ relative to 2 °C and achieving either 1.5 °C or 2.0 °C require a net sacrifice of gross world product, relative to a no-mitigation case, though 2100 with a 3%/year discount rate. However, the benefits of more stringent mitigation accumulate over time and our calculations indicate that stabilizing warming at 1.5 °C or 2.0 °C by 2100 would eventually confer net benefits of thousands of trillions of US$ in gross world product by 2300. The results emphasize the temporal asymmetry between the costs of mitigation and benefits of avoided damages from climate change and thus the long timeframe for which climate change mitigation investment pays off.

Greater future global warming inferred from Earth's recent energy budget.

Climate models provide the principal means of projecting global warming over the remainder of the twenty-first century but modelled estimates of warming vary by a factor of approximately two even under the same radiative forcing scenarios. Across-model relationships between currently observable attributes of the climate system and the simulated magnitude of future warming have the potential to inform projections. Here we show that robust across-model relationships exist between the global spatial patterns of several fundamental attributes of Earth's top-of-atmosphere energy budget and the magnitude of projected global warming. When we constrain the model projections with observations, we obtain greater means and narrower ranges of future global warming across the major radiative forcing scenarios, in general. In particular, we find that the observationally informed warming projection for the end of the twenty-first century for the steepest radiative forcing scenario is about 15 per cent warmer (+0.5 degrees Celsius) with a reduction of about a third in the two-standard-deviation spread (-1.2 degrees Celsius) relative to the raw model projections reported by the Intergovernmental Panel on Climate Change. Our results suggest that achieving any given global temperature stabilization target will require steeper greenhouse gas emissions reductions than previously calculated.

Change in the magnitude and mechanisms of global temperature variability with warming.

Natural unforced variability in global mean surface air temperature (GMST) can mask or exaggerate human-caused global warming, and thus a complete understanding of this variability is highly desirable. Significant progress has been made in elucidating the magnitude and physical origins of present-day unforced GMST variability, but it has remained unclear how such variability may change as the climate warms. Here we present modeling evidence that indicates that the magnitude of low-frequency GMST variability is likely to decline in a warmer climate and that its generating mechanisms may be fundamentally altered. In particular, a warmer climate results in lower albedo at high latitudes, which yields a weaker albedo feedback on unforced GMST variability. These results imply that unforced GMST variability is dependent on the background climatological conditions, and thus climate model control simulations run under perpetual preindustrial conditions may have only limited relevance for understanding the unforced GMST variability of the future.

Photochromic switching behaviour of donor-acceptor Stenhouse adducts in organic solvents.

We report photochromic donor-acceptor Stenhouse adducts (DASAs) capable of fully reversible photoisomerization with visible light in organic solvents including chloroform, acetonitrile and benzene. The rates of photoisomerization and thermal reversion can be tuned by altering the electronics of the donor adduct. X-Ray crystallography and photo-NMR experiments unambiguously establish molecular structures.

Spread in the magnitude of climate model interdecadal global temperature variability traced to disagreements over high-latitude oceans.

Unforced variability in global mean surface air temperature can obscure or exaggerate global warming on interdecadal timescales, thus understanding both the magnitude and generating mechanisms of such variability is of critical importance for both attribution studies as well as decadal climate prediction. Coupled atmosphere-ocean general circulation models (climate models) simulate a wide range of magnitudes of unforced interdecadal variability in global mean surface air temperature (UITglobal), hampering efforts to quantify the influence of UITglobal on contemporary global temperature trends. Recently, a preliminary consensus has emerged that unforced interdecadal variability in local surface temperatures (UITlocal) over the tropical Pacific Ocean are particularly influential on UITglobal. Therefore, a reasonable hypothesis might be that the large spread in the magnitude of UITglobal across climate models can be explained by the spread in the magnitude of simulated tropical Pacific UITlocal. Here we show that this hypothesis is mostly false. Instead, the spread in the magnitude of UITglobal is linked much more strongly to the spread in the magnitude of UITlocal over high-latitude regions characterized by significant variability in oceanic convection, sea ice concentration, and energy flux at both the surface and the top of the atmosphere (TOA). Thus, efforts to constrain the climate model produced range of UITglobal magnitude would be best served by focusing on the simulation of air-sea interaction at high latitudes.

Comparing the model-simulated global warming signal to observations using empirical estimates of unforced noise.

The comparison of observed global mean surface air temperature (GMT) change to the mean change simulated by climate models has received much public and scientific attention. For a given global warming signal produced by a climate model ensemble, there exists an envelope of GMT values representing the range of possible unforced states of the climate system (the Envelope of Unforced Noise; EUN). Typically, the EUN is derived from climate models themselves, but climate models might not accurately simulate the correct characteristics of unforced GMT variability. Here, we simulate a new, empirical, EUN that is based on instrumental and reconstructed surface temperature records. We compare the forced GMT signal produced by climate models to observations while noting the range of GMT values provided by the empirical EUN. We find that the empirical EUN is wide enough so that the interdecadal variability in the rate of global warming over the 20(th) century does not necessarily require corresponding variability in the rate-of-increase of the forced signal. The empirical EUN also indicates that the reduced GMT warming over the past decade or so is still consistent with a middle emission scenario's forced signal, but is likely inconsistent with the steepest emission scenario's forced signal.

Characterization and evaluation of mesenchymal stem cells derived from human embryonic stem cells and bone marrow.

Embryonic stem cells (ESCs) and mesenchymal stem cells (MSCs) have been studied for years as primary cell sources for regenerative biology and medicine. MSCs have been derived from cell and tissue sources, such as bone marrow (BM), and more recently from ESCs. This study investigated MSCs derived from BM, H1- and H9-ESC lines in terms of morphology, surface marker and growth factor receptor expression, proliferative capability, modulation of immune cell growth and multipotency, in order to evaluate ESC-MSCs as a cell source for potential regenerative applications. The results showed that ESC-MSCs exhibited spindle-shaped morphology similar to BM-MSCs but of various sizes, and flow cytometric immunophenotyping revealed expression of characteristic MSC surface markers on all tested cell lines except H9-derived MSCs. Differences in growth factor receptor expression were also shown between cell lines. In addition, ESC-MSCs showed greater capabilities for cell proliferation, and suppression of leukocyte growth compared to BM-MSCs. Using standard protocols, induction of ESC-MSC differentiation along the adipogenic, osteogenic, or chondrogenic lineages was less effective compared to that of BM-MSCs. By adding bone morphogenetic protein 7 (BMP7) into transforming growth factor beta 1 (TGFß1)-supplemented induction medium, chondrogenesis of ESC-MSCs was significantly enhanced. Our findings suggest that ESC-MSCs and BM-MSCs show differences in their surface marker profiles and the capacities of proliferation, immunomodulation, and most importantly multi-lineage differentiation. Using modified chondrogenic medium with BMP7 and TGFß1, H1-MSCs can be effectively induced as BM-MSCs for chondrogenesis.

Stem cell-based tissue engineering approaches for musculoskeletal regeneration.

The field of regenerative medicine and tissue engineering is an ever evolving field that holds promise in treating numerous musculoskeletal diseases and injuries. An important impetus in the development of the field was the discovery and implementation of stem cells. The utilization of mesenchymal stem cells, and later embryonic and induced pluripotent stem cells, opens new arenas for tissue engineering and presents the potential of developing stem cell-based therapies for disease treatment. Multipotent and pluripotent stem cells can produce various lineage tissues, and allow for derivation of a tissue that may be comprised of multiple cell types. As the field grows, the combination of biomaterial scaffolds and bioreactors provides methods to create an environment for stem cells that better represent their microenvironment for new tissue formation. As technologies for the fabrication of biomaterial scaffolds advance, the ability of scaffolds to modulate stem cell behavior advances as well. The composition of scaffolds could be of natural or synthetic materials and could be tailored to enhance cell self-renewal and/or direct cell fates. In addition to biomaterial scaffolds, studies of tissue development and cellular microenvironments have determined other factors, such as growth factors and oxygen tension, that are crucial to the regulation of stem cell activity. The overarching goal of stem cell-based tissue engineering research is to precisely control differentiation of stem cells in culture. In this article, we review current developments in tissue engineering, focusing on several stem cell sources, induction factors including growth factors, oxygen tension, biomaterials, and mechanical stimulation, and the internal and external regulatory mechanisms that govern proliferation and differentiation.

Combinatorial screening of chemically defined human mesenchymal stem cell culture substrates.

Self-assembled monolayers (SAMs) of alkanethiolates on gold are chemically defined substrates that can be used to evaluate the effects of an immobilized biomolecule. However, the types of biomolecules that can influence stem cell behavior are numerous and inter-related, and efficient experimental formats are a critical need. Here we employed a SAM array technology to investigate the effects of multiple, distinct peptides and peptide combinations on human mesenchymal stem cell (hMSC) behavior. Specifically, we characterized the conjugation of peptide mixtures to SAM arrays and then investigated the combined effects of a bone morphogenic protein receptor-binding peptide (BR-BP), a heparin proteoglycan-binding peptide (HPG-BP), and varied densities of the integrin-binding ligand Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP) on hMSC surface coverage and alkaline phosphatase activity. Results indicate that an amine reactive fluorescent probe can be used to characterize peptide composition after immobilization in SAM array spots. Furthermore, hMSC response to BR-BP and HPG-BP is dependent on GRGDSP density and at day 7, hMSC alkaline phosphatase expression is highly dependent on GRGDSP density. Taken together, we demonstrate how a SAM array approach can be used to probe the combinatorial effects of multiple peptides and motivate further investigations into potential synergies between cell adhesion and other bioactive peptides.

Vitellogenesis in Oncopeltus fasciatus: PLC/IP(3), DAG/PK-C pathway triggered by CaM.

In Oncopeltus fasciatus, evidence shown here indicates it is calmodulin (CaM) that activates phospholipase-C (PLC), beginning a signalling pathway necessary for endocytic uptake of yolk precursor molecules. Epithelial cell-produced CaM, transported to oocytes via gap junctions, has been shown to be required for receptor-mediated endocytic uptake of vitellogenins (Vgs, the protein precursors of yolk). To determine if CaM was directly or indirectly stimulating the phospholipase-C (PLC) signalling cascade and thus controlling Vg endocytosis we used a series of molecules known to inactivate various elements of the pathway. W-7 prevents CaM from interacting with other molecules. Neomycin isolates PIP(2) from PLC. U-73122 directly inactivates PLC. 2-APB blocks IP(3) receptors which would otherwise cause release of Ca(2+). Verapamil and CdCl(2) block Ca(2+) release channels. Staurosporin and calphostin are inhibitors of PK-C. 1-Hexadecyl-2-acetyl glycerol (HAG) binds to diacylglycerol (DAG). Through the use of these antagonists we show here that: (1) the activation of phospholipase-C in this system requires CaM. (2) Stimulated phospholipase-C converts PIP(2) into IP(3) and DAG. (3) IP(3) causes increase in cytosolic Ca(2+). (4) DAG and Ca(2+) each stimulate phosphokinase-C, resulting in endocytosis of Vgs.