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Increasing wildfire activity at high northern latitudes has the potential to mobilize large amounts of terrestrial mercury (Hg). However, understanding implications for Hg cycling and ecosystems is hindered by sparse research on peatland wildfire Hg emissions. In this study, we used measurements of soil organic carbon (SOC) and Hg, burn depth, and environmental indices derived from satellite remote sensing to develop machine learning models for predicting Hg emissions from major wildfires in the permafrost peatland of the Yukon-Kuskokwim Delta (YKD) in southwestern Alaska. Wildfire Hg emissions during summer 2015─estimated as the product of Hg:SOC (0.38 ± 0.17 ng Hg g C 1- ), predicted SOC stores (mean [5th-95th] = 9.1 [5.3-11.2] kg C m -2 ), and burn depth (11.3 [8.2-13.9] cm)─were 556 [164-1138] kg Hg or approximately 6% of Hg emissions from wildfire activity >60°N. Modeling estimates suggest that wildfire nearly doubled summertime Hg deposition within 10 km, despite advection of more than 75% of total emissions beyond Alaska. YKD areal emissions combined with remote sensing estimates of burned area suggest that wildfire Hg emissions from northern peatlands (25.4 [14.9-33.6] Mg y -1 ) are an important component of the northern Hg budget. Additional research is needed to refine these estimates and understand the implications for Arctic and global Hg cycling.

Plant biomass is a fundamental ecosystem attribute that is sensitive to rapid climatic changes occurring in the Arctic. Nevertheless, measuring plant biomass in the Arctic is logistically challenging and resource intensive. Lack of accessible field data hinders efforts to understand the amount, composition, distribution, and changes in plant biomass in these northern ecosystems. Here, we present The Arctic plant aboveground biomass synthesis dataset, which includes field measurements of lichen, bryophyte, herb, shrub, and/or tree aboveground biomass (g m -2 ) on 2,327 sample plots from 636 field sites in seven countries. We created the synthesis dataset by assembling and harmonizing 32 individual datasets. Aboveground biomass was primarily quantified by harvesting sample plots during mid- to late-summer, though tree and often tall shrub biomass were quantified using surveys and allometric models. Each biomass measurement is associated with metadata including sample date, location, method, data source, and other information. This unique dataset can be leveraged to monitor, map, and model plant biomass across the rapidly warming Arctic., (© 2024. The Author(s).)

The hydroxyl radical (OH) fuels atmospheric chemical cycling as the main sink for methane and a driver of the formation and loss of many air pollutants, but direct OH observations are sparse. We develop and evaluate an observation-based proxy for short-term, spatial variations in OH (Proxy OH ) in the remote marine troposphere using comprehensive measurements from the NASA Atmospheric Tomography (ATom) airborne campaign. Proxy OH is a reduced form of the OH steady-state equation representing the dominant OH production and loss pathways in the remote marine troposphere, according to box model simulations of OH constrained with ATom observations. Proxy OH comprises only eight variables that are generally observed by routine ground- or satellite-based instruments. Proxy OH scales linearly with in situ [OH] spatial variations along the ATom flight tracks (median r 2 = 0.90, interquartile range = 0.80 to 0.94 across 2-km altitude by 20° latitudinal regions). We deconstruct spatial variations in Proxy OH as a first-order approximation of the sensitivity of OH variations to individual terms. Two terms modulate within-region Proxy OH variations-water vapor (H 2 O) and, to a lesser extent, nitric oxide (NO). This implies that a limited set of observations could offer an avenue for observation-based mapping of OH spatial variations over much of the remote marine troposphere. Both H 2 O and NO are expected to change with climate, while NO also varies strongly with human activities. We also illustrate the utility of Proxy OH as a process-based approach for evaluating intermodel differences in remote marine tropospheric OH.

Climate change is creating widespread ecosystem disturbance across the permafrost zone, including a rapid increase in the extent and severity of tundra wildfire. The expansion of this previously rare disturbance has unknown consequences for lateral nutrient flux from terrestrial to aquatic environments. Lateral loss of nutrients could reduce carbon uptake and slow recovery of already nutrient-limited tundra ecosystems. To investigate the effects of tundra wildfire on lateral nutrient export, we analyzed water chemistry in and around the 10-year-old  Anaktuvuk River fire scar in northern Alaska. We collected water samples from 21 burned and 21 unburned watersheds during snowmelt, at peak growing season, and after plant senescence in 2017 and 2018. After a decade of ecosystem recovery, aboveground biomass had recovered in burned watersheds, but overall carbon and nitrogen remained ~20% lower, and the active layer remained ~10% deeper. Despite lower organic matter stocks, dissolved organic nutrients were substantially elevated in burned watersheds, with higher flow-weighted concentrations of organic carbon (25% higher), organic nitrogen (59% higher), organic phosphorus (65% higher), and organic sulfur (47% higher). Geochemical proxies indicated greater interaction with mineral soils in watersheds with surface subsidence, but optical analysis and isotopes suggested that recent plant growth, not mineral soil, was the main source of organic nutrients in burned watersheds. Burned and unburned watersheds had similar δ 15 N-NO 3 - , indicating that exported nitrogen was of preburn origin (i.e., not recently fixed). Lateral nitrogen flux from burned watersheds was 2- to 10-fold higher than rates of background nitrogen fixation and atmospheric deposition estimated in this area. These findings indicate that wildfire in Arctic tundra can destabilize nitrogen, phosphorus, and sulfur previously stored in permafrost via plant uptake and leaching. This plant-mediated nutrient loss could exacerbate terrestrial nutrient limitation after disturbance or serve as an important nutrient release mechanism during succession., (© 2021 John Wiley & Sons Ltd.)

Recent warming in the Arctic, which has been amplified during the winter 1-3 , greatly enhances microbial decomposition of soil organic matter and subsequent release of carbon dioxide (CO 2 ) 4 . However, the amount of CO 2 released in winter is highly uncertain and has not been well represented by ecosystem models or by empirically-based estimates 5,6 . Here we synthesize regional in situ observations of CO 2 flux from arctic and boreal soils to assess current and future winter carbon losses from the northern permafrost domain. We estimate a contemporary loss of 1662 Tg C yr -1 from the permafrost region during the winter season (October through April). This loss is greater than the average growing season carbon uptake for this region estimated from process models (-1032 Tg C yr -1 ). Extending model predictions to warmer conditions in 2100 indicates that winter CO 2 emissions will increase 17% under a moderate mitigation scenario-Representative Concentration Pathway (RCP) 4.5-and 41% under business-as-usual emissions scenario-RCP 8.5. Our results provide a new baseline for winter CO 2 emissions from northern terrestrial regions and indicate that enhanced soil CO 2 loss due to winter warming may offset growing season carbon uptake under future climatic conditions.

Fire frequency and severity are increasing in tundra and boreal regions as climate warms, which can directly affect climate feedbacks by increasing carbon (C) emissions from combustion of the large soil C pool and indirectly via changes in vegetation, permafrost thaw, hydrology, and nutrient availability. To better understand the direct and indirect effects of changing fire regimes in northern ecosystems, we examined how differences in soil burn severity (i.e., extent of soil organic matter combustion) affect soil C, nitrogen (N), and phosphorus (P) availability and microbial processes over time. We created experimental burns of three fire severities (low, moderate, and high) in a larch forest in the northeastern Siberian Arctic and analyzed soils at 1, 8 days, and 1 year postfire. Labile dissolved C and N increased with increasing soil burn severity immediately (1 day) postfire by up to an order of magnitude, but declined significantly 1 week later; both variables were comparable or lower than unburned soils by 1 year postfire. Soil burn severity had no effect on P in the organic layer, but P increased with increasing severity in mineral soil horizons. Most extracellular enzyme activities decreased by up to 70% with increasing soil burn severity. Increasing soil burn severity reduced soil respiration 1 year postfire by 50%. However, increasing soil burn severity increased net N mineralization rates 1 year postfire, which were 10-fold higher in the highest burn severity. While fires of high severity consumed approximately five times more soil C than those of low severity, soil C pools will also be driven by indirect effects of fire on soil processes. Our data suggest that despite an initial increase in labile C and nutrients with soil burn severity, soil respiration and extracellular activities related to the turnover of organic matter were greatly reduced, which may mitigate future C losses following fire., (© 2018 John Wiley & Sons Ltd.)

The treatment of fluorosurfactant-containing wastewater is still challenging nowadays. Here, a method is presented to remove fluorosurfactants from water, amongst others from electroplating wastewater. This elimination technique is based on the generation of gas bubbles in solution, enrichment and scavenging of fluorosurfactants by transport of the gas bubbles to the water surface. Finally the bubbles collapse and release an aerosol which is enriched with fluorosurfactants. By sampling of the released aerosols a mass balance was established for 6:2 fluorotelomer sulfonic acid (6:2 FTSA). Thereby 99.8% of the initial amount was revocered in the collected aerosols. Fluorosurfactant concentration in solution decreased exponentially with half-lives ranging from 2 to 6 min for 6:2 FTSA as well as perfluorooctane carboxylate (PFOA) and perfluorooctane sulfonate (PFOS). Elimination rate in defined matrix (0.2 M H2SO4) within 60 min was 99.6, 99.9 and 99.8% for 6:2 FTSA, PFOA and PFOS, respectively. The removal rate of 6:2 FTSA increased in solutions with higher ionic strength. Different wastewater from an electroplating industry containing 6:2 FTSA was treated with the described method without any sample pre-treatment and elimination of 6:2 FTSA took place with the same effectiveness as in synthetic matrices., (Copyright © 2016. Published by Elsevier Ltd.)

The parasite Toxoplasma gondii controls tissue-specific nitric oxide (NO), thereby augmenting virulence and immunopathology through poorly-understood mechanisms. We now identify TgMAPK1, a Toxoplasma mitogen-activated protein kinase (MAPK), as a virulence factor regulating tissue-specific parasite burden by manipulating host interferon (IFN)-γ-mediated inducible nitric oxide synthase (iNOS). Toxoplasma with reduced TgMAPK1 expression (TgMAPK1(lo)) demonstrated that TgMAPK1 facilitates IFN-γ-driven p38 MAPK activation, reducing IFN-γ-generated NO in an MKK3-dependent manner, blunting IFN-γ-mediated parasite control. TgMAPK1(lo) infection in wild type mice produced ≥ten-fold lower parasite burden versus control parasites with normal TgMAPK1 expression (TgMAPK1(con)). Reduced parasite burdens persisted in IFN-γ KO mice, but equalized in normally iNOS-replete organs from iNOS KO mice. Parasite MAPKs are far less studied than other parasite kinases, but deserve additional attention as targets for immunotherapy and drug discovery., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Acidosis, a critical aspect of central nervous system (CNS) pathophysiology and a metabolic corollary of the hypoxic stem cell niche, could be an expedient trigger for hippocampal neurogenesis and brain repair. We recently tracked the function of our isoxazole stem cell-modulator small molecules (Isx) through a chemical biology-target discovery strategy to GPR68, a proton (pH) sensing G protein-coupled receptor with no known function in brain. Isx and GPR68 coregulated neuronal target genes such as Bex1 (brain-enriched X-linked protein-1) in hippocampal neural progenitors (HCN cells), which further amplified GPR68 signaling by producing metabolic acid in response to Isx. To evaluate this proneurogenic small molecule/proton signaling circuit in vivo, we explored GPR68 and BEX1 expression in brain and probed brain function with Isx. We localized proton-sensing GPR68 to radial processes of hippocampal type 1 neural stem cells (NSCs) and, conversely, localized BEX1 to neurons. At the transcriptome level, Isx demonstrated unrivaled proneurogenic activity in primary hippocampal NSC cultures. In vivo, Isx pharmacologically targeted type 1 NSCs, promoting neurogenesis in young mice, depleting the progenitor pool without adversely affecting hippocampal learning and memory function. After traumatic brain injury, cerebral cortical astrocytes abundantly expressed GPR68, suggesting an additional role for proton-GPCR signaling in reactive astrogliosis. Thus, probing a novel proneurogenic synthetic small molecule's mechanism-of-action, candidate target, and pharmacological activity, we identified a new GPR68 regulatory pathway for integrating neural stem and astroglial cell functions with brain pH.

Although cancer tends to affect the elderly, most preclinical studies are carried out in young subjects. In this study, we developed a melanoma-specific cancer immunotherapy that shows efficacy in aged but not young hosts by mitigating age-specific tumor-associated immune dysfunction. Both young and aged CD4(+)CD25(hi) regulatory T cells (Treg) exhibited equivalent in vitro T-cell suppression and tumor-associated augmentation in numbers. However, denileukin diftitox (DT)-mediated Treg depletion improved tumor-specific immunity and was clinically effective only in young mice. DT-mediated Treg depletion significantly increased myeloid-derived suppressor cell (MDSC) numbers in aged but not young mice, and MDSC depletion improved tumor-specific immunity and reduced tumor growth in aged mice. Combining Treg depletion with anti-Gr-1 antibody was immunologically and clinically more efficacious than anti-Gr-1 antibody alone in aged B16-bearing mice, similar to Treg depletion alone in young mice. In contrast, DT increased MDSCs in young and aged mice following MC-38 tumor challenge, although effects were greater in aged mice. Anti-Gr-1 boosted DT effects in young but not aged mice. Aged antitumor immune effector cells are therefore competent to combat tumor when underlying tumor-associated immune dysfunction is appropriately mitigated, but this dysfunction varies with tumor, thus also varying responses to immunotherapy. By tailoring immunotherapy to account for age-related tumor-associated immune dysfunctions, cancer immunotherapy for aged patients with specific tumors can be remarkably improved.

Protozoan pathogens are a highly diverse group of unicellular organisms, several of which are significant human pathogens. One group of protozoan pathogens includes obligate intracellular parasites such as agents of malaria, leishmaniasis, babesiosis, and toxoplasmosis. The other group includes extracellular pathogens such as agents of giardiasis and amebiasis. An unfortunate unifying theme for most human protozoan pathogens is that highly effective treatments for them are generally lacking. We will review targeting protozoan mitogen-activated protein kinases (MAPKs) as a novel drug discovery approach towards developing better therapies, focusing on Plasmodia, Leishmania, and Toxoplasma, about which the most is known.

CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) are immunopathogenic in cancers by impeding tumor-specific immunity. B7-homologue 1 (B7-H1) (CD274) is a cosignaling molecule with pleiotropic effects, including hindering antitumor immunity. In this study, we demonstrate sex-dependent, B7-H1-dependent differences in tumor immunity and response to immunotherapy in a hormone-independent cancer, murine B16 melanoma. Antitumor immunity was better in B7-H1(-/-) females versus males as a result of reduced regulatory T cell function in the B7-H1(-/-) females, and clinical response following B7-H1 blockade as tumor immunotherapy was significantly better in wild-type females than in males, owing to greater B7-H1 blockade-mediated reduction of Treg function in females. Wild-type female Tregs expressed significantly lower B7-H1 versus males but were insensitive to estrogen in vitro. Female B7-H1(-/-) Tregs were exquisitely sensitive to estrogen-mediated functional reduction in vitro, suggesting that B7-H1 effects occur before terminal Treg differentiation. Immune differences were independent of known B7-H1 ligands. Sex-dependent immune differences are seldom considered in designing immune therapy or interpreting immunotherapy treatment results. Our data demonstrate that sex is an important variable in tumor immunopathogenesis and immunotherapy responses through differential Treg function and B7-H1 signaling.

Context: Abdominal obesity is a major risk factor for diabetes. Dual-energy x-ray absorptiometry (DXA) of the lumbar spine provides an index of abdominal fat., Objective: Our objective was to examine the hypothesis that DXA-derived abdominal fat measurement in women undergoing osteoporosis investigation predicts risk for subsequent diagnosis of diabetes., Design: This historical cohort study was derived from the Manitoba Bone Density Program Database for the Province of Manitoba, Canada., Setting and Patients: 30,252 nondiabetic women aged 40 yr and older were referred for baseline osteoporosis assessment with DXA between January 1990 and March 2007., Main Outcome Measures: Each woman's longitudinal provincial health service record was assessed for the presence of diabetes diagnosis codes after DXA testing., Results: During 5.2 + or - 2.6 yr of observation, 1252 (4.1%) women met the case definition for diabetes. A greater proportion of abdominal fat from spine DXA was strongly related to subsequent diabetes diagnosis in models adjusted for age, body mass index, and other comorbidities. Those in the highest quintile had 3.56 (95% confidence interval = 2.67-4.75) times the risk for subsequent diabetes diagnosis compared with those in the lowest (reference) quintile. Fat from hip DXA was not predictive of subsequent diabetes after adjustment for the same variables (1.00, 95% confidence interval = 0.79-1.26)., Conclusions: Predictive information about diabetes risk can be obtained from spine DXA scans performed for osteoporosis risk assessment. This is consistent with evidence linking abdominal fat with insulin resistance and the metabolic syndrome.

Both innate and adaptive immune systems are considered important for cancer prevention, immunosurveillance, and control of cancer progression. It is known that, although both systems initially eliminate emerging tumor cells efficiently, tumors eventually escape immune attack by a variety of mechanisms, including differentiation and recruitment of immunosuppressive CD11b(+)Gr-1(+) myeloid suppressor cells into the tumor microenvironment. However, we show that CD11b(+)Gr-1(+) cells found in ascites of epithelial ovarian cancer-bearing mice at advanced stages of disease are immunostimulatory rather than being immunosuppressive. These cells consist of a homogenous population of cells that morphologically resemble neutrophils. Moreover, like dendritic cells, immunostimulatory CD11b(+)Gr-1(+) cells can strongly cross-prime, augmenting the proliferation of functional CTLs via signaling through the expression of costimulatory molecule CD80. Adoptive transfer of these immunostimulatory CD11b(+)Gr-1(+) cells from ascites of ovarian cancer-bearing mice results in the significant regression of s.c. tumors even without being pulsed with exogenous tumor Ag prior to adoptive transfer. We now show for the first time that adaptive immune responses against cancer can be augmented by these cancer-induced granulocyte-like immunostimulatory myeloid (CD11b(+)Gr-1(+)) cells, thereby mediating highly effective antitumor immunity in an adoptive transfer model of immunity.

Cytotoxic T cells (CTLs) are an important component of adaptive immunity. The study of antigen-specific CTLs in vivo is desirable yet difficult. Identification of the class I-restricted peptide used by CTLs for target recognition is often required for detailed studies, but is generally not known for most antigens. Toxoplasma gondii is a medically important, obligate intracellular parasite and is often used as a model for studies of parasite immunology. No class I-restricted peptides for CTLs are known. We show here a new and convenient method to detect T. gondii-specific CTLs in vivo. We engineered T. gondii tachyzoites to express the model antigen ovalbumin, for which many useful reagents and transgenic mice are available. Using ovalbumin-transgenic T. gondii tachyzoites, antigen-specific CTLs were detected in vivo, and at much earlier time points post-infection than previously reported. This new method has several additional advantages over current methods to detect T. gondii-specific CTLs., (Copyright 2010 Elsevier B.V. All rights reserved.)

The functions of molecular chaperones have been extensively investigated biochemically in vitro and genetically in bacteria and yeast. We have embarked on a functional genomic analysis of the Hsp90 chaperone machine in the mouse by disrupting the p23 gene using a gene trap approach. p23 is an Hsp90 cochaperone that is thought to stabilize Hsp90-substrate complexes and, independently, to act as the cytosolic prostaglandin E2 synthase. Gene deletions in budding and fission yeasts and knock-down experiments with the worm have not revealed any clear in vivo requirements for p23. We find that p23 is not essential for overall prenatal development and morphogenesis of the mouse, which parallels the observation that it is dispensable for proliferation in yeast. In contrast, p23 is absolutely necessary for perinatal survival. Apart from an incompletely formed skin barrier, the lungs of p23 null embryos display underdeveloped airspaces and substantially reduced expression of surfactant genes. Correlating with the known function of glucocorticoids in promoting lung maturation and the role of p23 in the assembly of a hormone-responsive glucocorticoid receptor-Hsp90 complex, p23 null fibroblast cells have a defective glucocorticoid response. Thus, p23 contributes a nonredundant, temporally restricted, and tissue-specific function during mouse development.

Studies have suggested that 17beta estradiol (E2) can modify apolipoprotein E (apoE) expression. The current study determined if apoE protein varied in different regions of the mouse brain as a function of the estrous cycle and if E2 could increase apoE protein expression. In this study apoE concentration was lowest on estrus in the hippocampus, cingulate cortex and frontal cortex. In contrast, apoE concentration was highest on estrus in the olfactory bulb and cerebellum. There were no differences in the striatal apoE expression throughout the estrous cycle. Exogenous E2 significantly raised tissue levels of apoE in the olfactory bulb and cerebellum at 5 days after treatment. There was a slight, but nonsignificant increase in cortical expression of apoE and no change in striatum. Immunocytochemical localization studies found estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) in cortical neurons and glia. In the cerebellum and olfactory bulb, ERbeta was seen primarily in glia. ERalpha was not observed in the cerebellum and was rare in the olfactory bulb. Neither ERalpha nor ERbeta was seen in the striatum. Our data show regional differences in the production of apoE throughout the estrous cycle. In addition, exogenous E2 has regionally specific effects on apoE expression. Regional variability in apoE production appears to vary as a function of the estrogen receptor subtype.

We present an unusual case of a 41-year-old woman with a known glomus tumor, an adrenal mass, hypertension, and elevated catecholamines. The glomus tumor was shown to be the site of excessive catecholamine production in what we believe to be one of the few descriptions of 123I-metaiodobenzylguanidine (MIBG) scanning for this uncommon tumor. The diagnostic difficulties of such a case are discussed. A literature review of catecholamine-secreting glomus tumors and a systematic approach to catecholamine-secreting tumor localization in such patients is presented. Therapeutic options of surgery, radiation therapy, and embolization are reviewed. We conclude that the management of patients with functioning glomus tumors needs to be individualized. A careful, systematic approach is required if needless surgery is to be avoided. Further, the use of 123I-MIBG scanning deserves consideration to help localize catecholamine production in such patients.

A potentially lethal chlorpropamide overdose in a patient with chronic renal failure on long-term hemodialysis was treated by two courses of charcoal hemoperfusion. Hemoperfusion shortened the half-life clearance of the drug from a mean value of 93.6 to 3.4 hours. Calculation of the fractional extraction indicated that hemoperfusion reduced the body burden of the drug by 24% and 19% (mean values) during the first and second hours of treatment, respectively. We conclude that charcoal hemoperfusion should be considered a definitive therapeutic option in such cases.

Twenty-nine children, aged 1-15 yr, with newly diagnosed insulin-dependent diabetes mellitus (IDDM) had sera taken before insulin therapy to be examined for the presence of insulin-receptor antibodies by measuring the inhibition of binding of radiolabeled insulin to IM-9 lymphocytes in both whole serum and purified IgG fractions. Groups of children with long-standing IDDM and autoimmune endocrine disease as well as a normal control group were studied. A positive result, defined as binding greater than or equal to 2 SD below the mean zero standard, was found in 3 (10.3%) of the 29 newly diagnosed diabetic patients. As a group, they showed significantly greater binding inhibition than the normal control group for both whole serum and purified IgG (one-tailed t test, P less than .05 and P less than .002, respectively). Insulin autoantibodies were also measured by a sensitive radioimmunoassay technique. A positive result, defined as binding greater than 3 SD above the normal control pooled sera, was found in 9 (37.5%) of 24 of the newly diagnosed IDDM group tested. All 3 subjects positive for insulin-receptor antibodies were also positive for insulin autoantibodies, whereas 6 of the 21 receptor-antibody-negative subjects were positive for insulin autoantibodies (Fisher's exact test, P = .0415). This suggests the possibility that the presence of insulin autoantibodies is a prerequisite for the development of insulin-receptor antibodies, i.e., as an anti-idiotypic response. Insulin-receptor antibodies and insulin autoantibodies may play a currently undefined pathophysiologic role in the development of IDDM.(ABSTRACT TRUNCATED AT 250 WORDS)