Abrupt loss and uncertain recovery from fires of Amazon forests under low climate mitigation scenarios.

Tropical forests contribute a major sink for anthropogenic carbon emissions essential to slowing down the buildup of atmospheric CO2 and buffering climate change impacts. However, the response of tropical forests to more frequent weather extremes and long-recovery disturbances like fires remains uncertain. Analyses of field data and ecological theory raise concerns about the possibility of the Amazon crossing a tipping point leading to catastrophic tropical forest loss. In contrast, climate models consistently project an enhanced tropical sink. Here, we show a heterogeneous response of Amazonian carbon stocks in GFDL-ESM4.1, an Earth System Model (ESM) featuring dynamic disturbances and height-structured tree-grass competition. Enhanced productivity due to CO2 fertilization promotes increases in forest biomass that, under low emission scenarios, last until the end of the century. Under high emissions, positive trends reverse after 2060, when simulated fires prompt forest loss that results in a 40% decline in tropical forest biomass by 2100. Projected fires occur under dry conditions associated with El Niño Southern Oscillation and the Atlantic Multidecadal Oscillation, a response observed under current climate conditions, but exacerbated by an overall decline in precipitation. Following the initial disturbance, grassland dominance promotes recurrent fires and tree competitive exclusion, which prevents forest recovery. EC-Earth3-Veg, an ESM with a dynamic vegetation model of similar complexity, projected comparable wildfire forest loss under high emissions but faster postfire recovery rates. Our results reveal the importance of complex nonlinear responses to assessing climate change impacts and the urgent need to research postfire recovery and its representation in ESMs.

Voluntary Age Regression Entering "Headspace" in a Child With Post-traumatic Stress Disorder.

In patients with post-traumatic stress disorder (PTSD), the use of coping mechanisms seems to correlate with higher levels of resiliency; however, in the age of the internet, patients may find it easier to discover new unhealthy skills that can hinder their treatment and further progress their symptoms. This report describes the case of a 12-year-old female with PTSD who was admitted for suicidal ideation and who presented with age regression that was voluntary in nature, characterized by reverting to the age of a six-year-old girl while her boyfriend took on a parental role for her. These behaviors were learned through her use of social media. This case demonstrates the use of maladaptive behaviors to cope with their trauma and the need for parental supervision on the use of the internet and social media by the younger population.

Next-generation ensemble projections reveal higher climate risks for marine ecosystems.

Projections of climate change impacts on marine ecosystems have revealed long-term declines in global marine animal biomass and unevenly distributed impacts on fisheries. Here we apply an enhanced suite of global marine ecosystem models from the Fisheries and Marine Ecosystem Model Intercomparison Project (Fish-MIP), forced by new-generation Earth system model outputs from Phase 6 of the Coupled Model Intercomparison Project (CMIP6), to provide insights into how projected climate change will affect future ocean ecosystems. Compared with the previous generation CMIP5-forced Fish-MIP ensemble, the new ensemble ecosystem simulations show a greater decline in mean global ocean animal biomass under both strong-mitigation and high-emissions scenarios due to elevated warming, despite greater uncertainty in net primary production in the high-emissions scenario. Regional shifts in the direction of biomass changes highlight the continued and urgent need to reduce uncertainty in the projected responses of marine ecosystems to climate change to help support adaptation planning.

Tracking Improvement in Simulated Marine Biogeochemistry Between CMIP5 and CMIP6.

Purpose of Review: The changes or updates in ocean biogeochemistry component have been mapped between CMIP5 and CMIP6 model versions, and an assessment made of how far these have led to improvements in the simulated mean state of marine biogeochemical models within the current generation of Earth system models (ESMs). Recent Findings: The representation of marine biogeochemistry has progressed within the current generation of Earth system models. However, it remains difficult to identify which model updates are responsible for a given improvement. In addition, the full potential of marine biogeochemistry in terms of Earth system interactions and climate feedback remains poorly examined in the current generation of Earth system models. Summary: Increasing availability of ocean biogeochemical data, as well as an improved understanding of the underlying processes, allows advances in the marine biogeochemical components of the current generation of ESMs. The present study scrutinizes the extent to which marine biogeochemistry components of ESMs have progressed between the 5th and the 6th phases of the Coupled Model Intercomparison Project (CMIP).

A novel ex-situ bio-remediation process for perchlorate contaminated soil.

A novel, ex-situ remediation process for perchlorate contaminated soil is reported in this study. This approach comprises washing the contaminated soil with water, followed by treatment of the wash water in a bioreactor. The treated water reused for the next batch of soil, and the cycle continued. The pilot-scale treatment unit comprising of a soil washing unit (0.75 m3) and a fixed-film bioreactor (140 L), both connected in series for continuous operation for a period of three months. The bioreactor was inoculated with a novel perchlorate reducing microbial consortium comprising Serratia marcescens (Gen bank no. HM751096), Bacillus pumilus (Gen bank no. JQ820452) and Micrococcus sp. (Gen bank no. KJ410671). The microbial activity was supported by glucose (glucose/perchlorate ratio = 5), and trace mineral solution. In a typical washing cycle, 2.5 g perchlorate (KClO4) spiked in 670 kg soil was completely removed in three washing cycles, that completed in 6.3 h consuming ∼360 L water. The pooled wash water containing perchlorate at 8.5 mg/L was treated completely in the bioreactor operated at 4.5 h HRT and -200 mV ORP. Compared with both in-situ and ex-situ remediation methods reported, the present approach has many advantages for treating perchlorate contaminated soil.

Lack of Resources for Aftercare for Children With Psychosis: A System's Failure.

Very early-onset schizophrenia (VEOS) is a rare disorder that is associated with poor outcomes, especially with securing aftercare plans that will lead to stabilization of illness and prevent recidivism. There is a scarcity of resources available to patients with VEOS and their families once they leave inpatient treatment to achieve long-term success. Here we report a case of a 12-year-old-female who was diagnosed with VEOS at age 11 and since that diagnosis has struggled with finding appropriate resources to meet her needs, requiring frequent hospitalizations and displaying a continued decline in functioning.

Rhodiola rosea Improves Lifespan, Locomotion, and Neurodegeneration in a Drosophila melanogaster Model of Huntington's Disease.

Huntington's disease (HD) is a dominant, late-onset disease characterized by choreiform movements, cognitive decline, and personality disturbance. It is caused by a polyglutamine repeat expansion in the Huntington's disease gene encoding for the Huntingtin protein (Htt) which functions as a scaffold for selective macroautophagy. Mutant Htt (mHtt) disrupts vesicle trafficking and prevents autophagosome fusion with lysosomes, thus deregulating autophagy in neuronal cells, leading to cell death. Autophagy has been described as a therapeutic target for HD, owing to the key role Htt plays in the cellular process. Rhodiola rosea, a plant extract used in traditional medicine in Europe and Asia, has been shown to attenuate aging in the fly and other model species. It has also been shown to inhibit the mTOR pathway and induce autophagy in bladder cancer cell lines. We hypothesized that R. rosea, by inducing autophagy, may improve the phenotype of a Huntington's disease model of the fly. Flies expressing HttQ93 which exhibit decreased lifespan, impaired locomotion, and increased neurodegeneration were supplemented with R. rosea extract, and assays testing lifespan, locomotion, and pseudopupil degeneration provided quantitative measures of improvement. Based on our observations, R. rosea may be further evaluated as a potential therapy for Huntington's disease.

Rapid emergence of climate change in environmental drivers of marine ecosystems.

Climate change is expected to modify ecological responses in the ocean, with the potential for important effects on the ecosystem services provided to humankind. Here we address the question of how rapidly multiple drivers of marine ecosystem change develop in the future ocean. By analysing an ensemble of models we find that, within the next 15 years, the climate change-driven trends in multiple ecosystem drivers emerge from the background of natural variability in 55% of the ocean and propagate rapidly to encompass 86% of the ocean by 2050 under a 'business-as-usual' scenario. However, we also demonstrate that the exposure of marine ecosystems to climate change-induced stress can be drastically reduced via climate mitigation measures; with mitigation, the proportion of ocean susceptible to multiple drivers within the next 15 years is reduced to 34%. Mitigation slows the pace at which multiple drivers emerge, allowing an additional 20 years for adaptation in marine ecological and socio-economic systems alike.

Reconciling fisheries catch and ocean productivity.

Photosynthesis fuels marine food webs, yet differences in fish catch across globally distributed marine ecosystems far exceed differences in net primary production (NPP). We consider the hypothesis that ecosystem-level variations in pelagic and benthic energy flows from phytoplankton to fish, trophic transfer efficiencies, and fishing effort can quantitatively reconcile this contrast in an energetically consistent manner. To test this hypothesis, we enlist global fish catch data that include previously neglected contributions from small-scale fisheries, a synthesis of global fishing effort, and plankton food web energy flux estimates from a prototype high-resolution global earth system model (ESM). After removing a small number of lightly fished ecosystems, stark interregional differences in fish catch per unit area can be explained (r = 0.79) with an energy-based model that (i) considers dynamic interregional differences in benthic and pelagic energy pathways connecting phytoplankton and fish, (ii) depresses trophic transfer efficiencies in the tropics and, less critically, (iii) associates elevated trophic transfer efficiencies with benthic-predominant systems. Model catch estimates are generally within a factor of 2 of values spanning two orders of magnitude. Climate change projections show that the same macroecological patterns explaining dramatic regional catch differences in the contemporary ocean amplify catch trends, producing changes that may exceed 50% in some regions by the end of the 21st century under high-emissions scenarios. Models failing to resolve these trophodynamic patterns may significantly underestimate regional fisheries catch trends and hinder adaptation to climate change.

Comparative Population Genetic Structure of the Endangered Southern Brown Bandicoot, Isoodon obesulus, in Fragmented Landscapes of Southern Australia.

Genetic connectivity is a key factor for maintaining the persistence of populations in fragmented landscapes. In highly modified landscapes such us peri-urban areas, organisms' dispersal among fragmented habitat patches can be reduced due to the surrounding matrix, leading to subsequent decreased gene flow and increased potential extinction risk in isolated sub-populations. However, few studies have compared within species how dispersal/gene flow varies between regions and among different forms of matrix that might be encountered. In the current study, we investigated gene flow and dispersal in an endangered marsupial, the southern brown bandicoot (Isoodon obesulus) in a heavily modified peri-urban landscape in South Australia, Australia. We used 14 microsatellite markers to genotype 254 individuals which were sampled from 15 sites. Analyses revealed significant genetic structure. Our analyses also indicated that dispersal was mostly limited to neighbouring sites. Comparisons of these results with analyses of a different population of the same species revealed that gene flow/dispersal was more limited in this peri-urban landscape than in a pine plantation landscape approximately 400 km to the south-east. These findings increase our understanding of how the nature of fragmentation can lead to profound differences in levels of genetic connectivity among populations of the same species.

Net primary productivity estimates and environmental variables in the Arctic Ocean: An assessment of coupled physical-biogeochemical models.

The relative skill of 21 regional and global biogeochemical models was assessed in terms of how well the models reproduced observed net primary productivity (NPP) and environmental variables such as nitrate concentration (NO3), mixed layer depth (MLD), euphotic layer depth (Zeu), and sea ice concentration, by comparing results against a newly updated, quality-controlled in situ NPP database for the Arctic Ocean (1959-2011). The models broadly captured the spatial features of integrated NPP (iNPP) on a pan-Arctic scale. Most models underestimated iNPP by varying degrees in spite of overestimating surface NO3, MLD, and Zeu throughout the regions. Among the models, iNPP exhibited little difference over sea ice condition (ice-free versus ice-influenced) and bottom depth (shelf versus deep ocean). The models performed relatively well for the most recent decade and toward the end of Arctic summer. In the Barents and Greenland Seas, regional model skill of surface NO3 was best associated with how well MLD was reproduced. Regionally, iNPP was relatively well simulated in the Beaufort Sea and the central Arctic Basin, where in situ NPP is low and nutrients are mostly depleted. Models performed less well at simulating iNPP in the Greenland and Chukchi Seas, despite the higher model skill in MLD and sea ice concentration, respectively. iNPP model skill was constrained by different factors in different Arctic Ocean regions. Our study suggests that better parameterization of biological and ecological microbial rates (phytoplankton growth and zooplankton grazing) are needed for improved Arctic Ocean biogeochemical modeling.

Effects of mibefradil, a T- and L-type calcium channel blocker, on cardiac remodeling in the UM-X7.1 cardiomyopathic hamster.

Abnormalities of T-type calcium channel function reported to occur in the transition phase to heart failure in the hamster cardiomyopathy may contribute to progression of the disease. We tested the hypothesis that chronic exposure to mibefradil, a selective T-type calcium channel blocker, improves the deleterious cardiac remodeling observed in this condition. In the present study, 40 normal (N) and 40 UM-X7.1 cardiomyopathic hamsters (CMH), aged 180 days, were treated daily by gavage for 21 days with mibefradil (30 mg/Kg). Eight to 10 animals from each group were sacrificed at the end of the treatment period while the remainder were followed for an additional 30 days without treatment (washout period). Hearts were harvested, fixed with 10%-buffered paraformaldehyde and then cut in half down the middle. Several slices were dehydrated, embedded in paraffin and stained with Masson Trichrome. Wall thickness and dilatation index of the left ventricle were estimated by planimetry. Myocardial capillary density was also computed. The greater heart weight/body weight ratio seen in untreated CMH (7.7 +/- 0.4 vs 5.5 +/- 0.2 in N, p < 0.05) was improved with mibefradil. The dilatation index averaged 0.504 +/- 0.04 in N was increased in untreated CMH (0.566 +/- 0.03) and ameliorated in mibefradil-treated CMH. The 1-month washout period led to further deterioration of the dilatation index in untreated and mibefradil-treated CMH. Capillary density averaged 10,000 +/- 781 per mm2 in hearts from untreated N hamsters and 8,830 +/- 795 per mm2 in untreated CMH (p = NS). Chronic exposure to mibefradil resulted in a significant reduction of capillary density in both N and CMH hearts. Following the 1-month washout period, the change in myocardial capillary density associated with mibefradil was no longer detectable. In conclusion, chronic exposure to mibefradil, a T- and L-type calcium channel blocker, exerts opposite effects during the transition phase to heart failure in CMH, improving the deleterious left ventricular remodeling in UM-X7.1 hamsters and reducting myocardial capillary density independently of the disease process.

Age-related serum levels of insulin-like growth factor-I, -II and IGF-binding protein-3 following myocardial infarction.

Aging retards the repair process by decreasing hormone secretion from the somatotrophic axis, which plays a major role in tissue reconstruction after injury. The aim of this study was to determine the effect of aging on serum insulin-like growth factor-I (IGF-I), IGF-II and IGF-binding protein-3 (IGFBP-3) levels following myocardial infarction (MI). For four consecutive days, we monitored the variation of serum IGF-I, IGF-II and IGFBP-3 concentrations in 26 patients aged 19-71 years who were diagnosed with MI. Serum IGF-I, IGF-II and IGFBP-3 were measured daily by double antibody radioimmunoassay. Daily serum IGF-I concentrations showed a significant negative correlation with age (r = -0.528, P< 0.001). Total serum IGF-I was significantly (P = 0.002) higher in the younger age group (patients under 50 years) compared to the older group (50 years and over); 206 +/- 16 ng/ml vs 136 +/- 12 ng/ml. During this investigation, younger patients (under 50 years) showed no significant daily variations in IGF-I levels compared to older patients (50 years and over) who presented a significant decline (P = 0.012). Total serum IGF-II in both groups decreased significantly with time. Total serum IGFBP-3 in the younger age group was significantly higher (P = 0.046) than in the older age group (3.42 +/- 0.18 microgram/ml vs 2.95 +/- 0.13 microgram/ml). MI patients in both groups showed significantly lower IGF-I and IGF-II (IGFs) with higher IGFBP-3 compared to age- and sex-adjusted levels of normal adults (controls). The present results confirm that age and cardiac condition affect IGFs and IGFBP-3 levels. We are inclined to believe that older patients with a cardiac condition are less able to maintain their blood IGF-I levels during the recovery period compared to younger patients. Given the biological impact of IGF-I on regeneration, this could explain why older patients take longer to recover and heal poorly in comparison to younger patients.

Cardioprotective efficacy of verapamil and mibefradil in young UM-X7.1 cardiomyopathic hamsters.

Since calcium overload and increased in T-type calcium channel activity have been observed in the cardiomyopathic (CM) hamster, we hypothesized that mibefradil (Ro 40-5967), a new T- and L-type calcium channel blocker, may exert significant cardioprotection in the early phase of the disease. Young (30-day-old) CM hamsters of the UM-X7.1 subline were treated with mibefradil or verapamil for 4 to 6 weeks. Mibefradil doses were in the range of 0.5 to 8 mg/kg/day while verapamil was given at a dose of 5-10 mg/kg/day, both drugs being injected twice daily (s.c. and i.p. alternatively). At the end of the treatment period, myocardial and skeletal muscle (tongue) were harvested and processed for assessment of necrotic changes and calcification. In hearts from control CM hamsters, numerous necrotic and calcified foci were observed. These myocardial necrosis markers were not attenuated by mibefradil in the dose range studied whereas verapamil significantly reduced their severity. The dystrophic process in skeletal muscle (tongue) was not inhibited by mibefradil or verapamil. These results suggest that mechanisms other than inhibition of T- and L-type calcium channels are related to the cardioprotection observed in the presence of verapamil. A specific action on the sarcoplasmic reticulum (ryanodine-sensitive calcium channel) or the mitochondria may explain the efficacy of phenylalkylamines (verapamil) in this condition.

Effect of orotic acid and magnesium orotate on the development and progression of the UM-X7.1 hamster hereditary cardiomyopathy.

This study deals with the potential therapeutic effect of orotic acid (OA) and Mg Orotate (MgO) on myocardial degeneration and the development of congestive heart failure in cardiomyopathic (CM) hamsters of the UM-X7.1 line. Two major age groups (group I, < 30 days and group II, > 180 days old) were used in these experiments, which lasted 30 and 50 days, respectively; the orotic salts were incorporated (10%) into Purina Lab Chow given ad libitum. Macroscopic and microscopic assessment of pathologic changes together with ECG recordings revealed that MgO treatment significantly reduces myocardial damage, especially the severity of calcific changes. ECG recordings clearly demonstrated a significant shortening of QTc and PR intervals, resulting in partial electrical stabilization of failing hearts, with a significant delay in systemic congestive changes. The prevention of heart lesions was less evident in animals receiving OA, but both preparations proved to be equally efficient in prolonging survival of the CM hamsters.

Effects of phosphoramidon, BQ 788, and BQ 123 on coronary and cardiac dysfunctions of the failing hamster heart.

Coronary dysfunctions identified in the presence of chronic heart failure are an important pathophysiologic abnormality that influences the prognosis of the disease. Because the endothelin pathway plays a significant role in the increased peripheral vascular tone associated with heart failure, we hypothesized that the endothelin pathway may be involved in the abnormal coronary vasomotion associated with this pathologic condition. Experiments were carried out in failing hearts (UM-X7.1 cardiomyopathic hamsters, aged 225-250 days) and normal hearts (Syrian LVG hamsters, also aged 225-250 days). Isolated hearts were perfused at constant flow and exposed to the blocker of the generation of endothelin-1 (ET-1), phosphoramidon (10 microM infusion), as well as to the selective ET(A)-receptor antagonist BQ 123 (10 microM infusion) and to a selective ET(B)-receptor antagonist BQ 788 (1 microM infusion). Coronary and cardiac effects of exogenous ET-1 (0.01-100 pmol) were also studied. Phosphoramidon, BQ 788, and BQ 123 did not altered coronary perfusion pressure either in normal or in failing hearts, whereas cardiac contractility was significantly impaired in the presence of phosphoramidon and BQ 123. Coronary sensitivity to exogenous ET-1 did not demonstrate a significant difference between normal and failing hearts [median effective concentration (EC50), 7 pmol in failing hearts vs. 12 pmol in normal hearts; p = NS]. In the presence of exogenous ET-1, cardiac contractility was significantly increased in both groups. In normal hearts, the exogenous ET-1-induced increase in coronary perfusion pressure was completely antagonized by BQ 123, whereas combined administration of BQ 788 and BQ 123 was necessary to induce complete inhibition in failing hearts. The positive inotropic effect elicited by exogenous ET-1 (EC50) was completely abolished in the presence of BQ 123, whereas BQ 788 had no significant effect. Results indicate that the endothelin pathway does not play a significant role in the altered coronary vasomotion observed in this model of chronic heart failure. On the contrary, the endothelin pathway appears to participate in the maintenance of myocardial contractility. According to these observations, administration of an inhibitor of ET-1 synthesis, as well as the use of an ET(A)-receptor antagonist, may be contraindicated in the presence of poor left ventricular function because the endothelin pathway contributes significantly to the maintenance of cardiac contractility.

Increases of T-type Ca2+ current in heart cells of the cardiomyopathic hamster.

In the present study, the whole-cell voltage clamp technique was used in order to record the T- and L-type Ca2+ currents in single heart cells of newborn and young normal and hereditary cardiomyopathic hamsters. Our results showed that the I/V relationship curve as well as the kinetics of the L-type Ca2+ currents (ICa(L)) in both normal and cardiomyopathic heart cells were the same. However, the proportion of myocytes from normal heart hamster that showed L-type ICa was less than that of heart cells from cardiomyopathic hamster. The I/V relationship curve of the T-type ICa (ICa(T)) was the same in myocytes of both normal and cardiomyopathic hamsters. The main differences between ICa(T) of cardiomyopathic and normal hamster are a larger window current and the proportion of ventricular myocytes that showed this type of current in cardiomyopathic hamster. The high density of ICa(T) as well as the large window current and proportion of myocytes showing ICa(T) may explain in part Ca2+ overload observed in cardiomyopathic heart cells of the hamster.

Early fetal like slow Na+ current in heart cells of cardiomyopathic hamster.

Using the whole-cell voltage-clamp technique, early embryonic tetrodotoxin (TTX) and Mn(2+)-insensitive slow Na+ current was detected in 10-22 week old fetal human heart cells as well as in 1 day old and young cardiomyopathic hamster myocytes. This slow Na+ current in both heart cell preparations has the same kinetics and pharmacology. This type of slow Na+ current was absent in heart cells of newborn and young normal hamsters and became less present in myocytes of 19 and 22 week old human heart myocytes. Our results demonstrate that the slow Na+ channel does exist in early fetal human life and this type of channel continues to be functional after birth in myocytes of the hereditary cardiomyopathic hamster.

Myocardial reactive hyperemia in experimental chronic heart failure: evidence for the role of K+ adenosine triphosphate-dependent channels and cyclooxygenase activity.

BACKGROUND: Several studies suggest that coronary perfusion is abnormal in heart failure. The fact that these deficits may results in an altered coronary reserve remains controversial. Therefore, coronary adaptability to short-duration ischemia and the resultant myocardial reactive hyperemia were investigated in a model of chronic heart failure. METHODS AND RESULTS: Experiments were performed in normal and failing hamster hearts (UM-X7.1, aged > 225 days). Heart rate, left ventricular developed pressure, and coronary flow were recorded continuously before and after each 30-second ischemia in isolated perfused heart preparations. Studies were conducted under control conditions and in the presence of four inhibitors of potential mediators of the reactive hyperemia response: the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (30 microM), the adenosine antagonist 8-(p-sulfophenyl)theophylline (50 microM), the K+ cyclic adenosine triphosphate-dependent channel antagonist glibenclamide (10 microM), and the cyclooxygenase inhibitor indomethacin (10 microM). Baseline hemodynamic parameters were all significantly impaired in failing hearts. Under control conditions, failing hearts were able to respond adequately to a 30-second ischemia: repayment-to-debt ratio averaged 1.02 +/- 0.09 as compared with 1.10 +/- 0.09 in normal hearts (P = NS). All inhibitors significantly reduced basal coronary perfusion except for indomethacin. Of the four inhibitors of potential mediators of the myocardial reactive hyperemic response, only glibenclamide and indomethacin impaired the repayment-to-debt ratio. In their presence, repayment-to-debt ratio was reduced by 40% of the baseline response (P < .01) without significant difference between normal and failing hearts. On the contrary, NG-nitro-L-arginine methyl ester and 8-(p-sulfophenyl)theophylline did not alter the repayment-to-debt ratio. CONCLUSIONS: These observations demonstrate the capacity of the failing heart to tolerate short-duration ischemia despite the presence of significant alterations in its basal coronary perfusion. In addition, results suggest that activation of K+ adenosine triphosphate-dependent channels and the presence of cyclooxygenase by-products are important determinants of coronary adaptation to short-duration ischemia in this model of chronic heart failure.