Amazon forest response to repeated droughts Feldpausch, T. R.; Phillips, O. L.; Brienen, R. J. W. ...
Global biogeochemical cycles,
July 2016, Letnik:
30, Številka:
7
Journal Article
Recenzirano
Odprti dostop
The Amazon Basin has experienced more variable climate over the last decade, with a severe and widespread drought in 2005 causing large basin‐wide losses of biomass. A drought of similar ...climatological magnitude occurred again in 2010; however, there has been no basin‐wide ground‐based evaluation of effects on vegetation. We examine to what extent the 2010 drought affected forest dynamics using ground‐based observations of mortality and growth from an extensive forest plot network. We find that during the 2010 drought interval, forests did not gain biomass (net change: −0.43 Mg ha−1, confidence interval (CI): −1.11, 0.19, n = 97), regardless of whether forests experienced precipitation deficit anomalies. This contrasted with a long‐term biomass sink during the baseline pre‐2010 drought period (1998 to pre‐2010) of 1.33 Mg ha−1 yr−1 (CI: 0.90, 1.74, p < 0.01). The resulting net impact of the 2010 drought (i.e., reversal of the baseline net sink) was −1.95 Mg ha−1 yr−1 (CI:−2.77, −1.18; p < 0.001). This net biomass impact was driven by an increase in biomass mortality (1.45 Mg ha−1 yr−1 CI: 0.66, 2.25, p < 0.001) and a decline in biomass productivity (−0.50 Mg ha−1 yr−1, CI:−0.78, −0.31; p < 0.001). Surprisingly, the magnitude of the losses through tree mortality was unrelated to estimated local precipitation anomalies and was independent of estimated local pre‐2010 drought history. Thus, there was no evidence that pre‐2010 droughts compounded the effects of the 2010 drought. We detected a systematic basin‐wide impact of the 2010 drought on tree growth rates across Amazonia, which was related to the strength of the moisture deficit. This impact differed from the drought event in 2005 which did not affect productivity. Based on these ground data, live biomass in trees and corresponding estimates of live biomass in lianas and roots, we estimate that intact forests in Amazonia were carbon neutral in 2010 (−0.07 Pg C yr−1 CI:−0.42, 0.23), consistent with results from an independent analysis of airborne estimates of land‐atmospheric fluxes during 2010. Relative to the long‐term mean, the 2010 drought resulted in a reduction in biomass carbon uptake of 1.1 Pg C, compared to 1.6 Pg C for the 2005 event.
Key Points
During the 2010 drought interval, Amazon forests did not gain biomass, regardless of whether forests experienced precipitation deficit anomalies
Biomass losses were partially driven by a decline in productivity related to precipitation anomalies
Pre‐2010 droughts did not compound the effects of the 2010 drought
Depot-dependent differences in adipose tissue physiology may reflect specialized functions and local interactions between adipocytes and surrounding tissues. We combined time-resolved microarray ...analyses of mesenteric- (MWAT), subcutaneous- (SWAT) and epididymal adipose tissue (EWAT) during high-fat feeding of male transgenic ApoE3Leiden mice with histology, targeted lipidomics and biochemical analyses of metabolic pathways to identify differentially regulated processes and site-specific functions. EWAT was found to exhibit physiological zonation. De novo lipogenesis in fat proximal to epididymis was stably low, whereas de novo lipogenesis distal to epididymis and at other locations was down-regulated in response to high-fat diet. The contents of linoleic acid and alpha-linolenic acid in EWAT were increased compared to other depots. Expression of the androgen receptor (Ar) was higher in EWAT than in MWAT and SWAT. We suggest that Ar may mediate depot-dependent differences in de novo lipogenesis rate and propose that accumulation of linoleic acid and alpha-linolenic acid in EWAT is favored by testosterone-mediated inhibition of de novo lipogenesis and may promote further elongation and desaturation of these polyunsaturated fatty acids during spermatogenesis.
We conducted a combined genome-wide association study (GWAS) of 7,481 individuals with bipolar disorder (cases) and 9,250 controls as part of the Psychiatric GWAS Consortium. Our replication study ...tested 34 SNPs in 4,496 independent cases with bipolar disorder and 42,422 independent controls and found that 18 of 34 SNPs had P < 0.05, with 31 of 34 SNPs having signals with the same direction of effect (P = 3.8 × 10−7). An analysis of all 11,974 bipolar disorder cases and 51,792 controls confirmed genome-wide significant evidence of association for CACNA1C and identified a new intronic variant in ODZ4. We identified a pathway comprised of subunits of calcium channels enriched in bipolar disorder association intervals. Finally, a combined GWAS analysis of schizophrenia and bipolar disorder yielded strong association evidence for SNPs in CACNA1C and in the region of NEK4-ITIH1-ITIH3-ITIH4. Our replication results imply that increasing sample sizes in bipolar disorder will confirm many additional loci.
Aims/hypothesis
Individuals with type 2 diabetes have aberrant intestinal microbiota. However, recent studies suggest that metformin alters the composition and functional potential of gut microbiota, ...thereby interfering with the diabetes-related microbial signatures. We tested whether specific gut microbiota profiles are associated with prediabetes (defined as fasting plasma glucose of 6.1–7.0 mmol/l or HbA
1c
of 42–48 mmol/mol 6.0–6.5%) and a range of clinical biomarkers of poor metabolic health.
Methods
In the present case–control study, we analysed the gut microbiota of 134 Danish adults with prediabetes, overweight, insulin resistance, dyslipidaemia and low-grade inflammation and 134 age- and sex-matched individuals with normal glucose regulation.
Results
We found that five bacterial genera and 36 operational taxonomic units (OTUs) were differentially abundant between individuals with prediabetes and those with normal glucose regulation. At the genus level, the abundance of
Clostridium
was decreased (mean log
2
fold change −0.64 (SEM 0.23),
p
adj
= 0.0497), whereas the abundances of
Dorea
,
Ruminococcus
,
Sutterella
and
Streptococcus
were increased (mean log
2
fold change 0.51 (SEM 0.12),
p
adj
= 5 × 10
−4
; 0.51 (SEM 0.11),
p
adj
= 1 × 10
−4
; 0.60 (SEM 0.21),
p
adj
= 0.0497; and 0.92 (SEM 0.21),
p
adj
= 4 × 10
−4
, respectively). The two OTUs that differed the most were a member of the order Clostridiales (OTU 146564) and
Akkermansia muciniphila
, which both displayed lower abundance among individuals with prediabetes (mean log
2
fold change −1.74 (SEM 0.41),
p
adj
= 2 × 10
−3
and −1.65 (SEM 0.34),
p
adj
= 4 × 10
−4
, respectively). Faecal transfer from donors with prediabetes or screen-detected, drug-naive type 2 diabetes to germfree Swiss Webster or conventional C57BL/6 J mice did not induce impaired glucose regulation in recipient mice.
Conclusions/interpretation
Collectively, our data show that individuals with prediabetes have aberrant intestinal microbiota characterised by a decreased abundance of the genus
Clostridium
and the mucin-degrading bacterium
A. muciniphila
. Our findings are comparable to observations in overt chronic diseases characterised by low-grade inflammation.
Genetic risk prediction has several potential applications in medical research and clinical practice and could be used, for example, to stratify a heterogeneous population of patients by their ...predicted genetic risk. However, for polygenic traits, such as psychiatric disorders, the accuracy of risk prediction is low. Here we use a multivariate linear mixed model and apply multi-trait genomic best linear unbiased prediction for genetic risk prediction. This method exploits correlations between disorders and simultaneously evaluates individual risk for each disorder. We show that the multivariate approach significantly increases the prediction accuracy for schizophrenia, bipolar disorder, and major depressive disorder in the discovery as well as in independent validation datasets. By grouping SNPs based on genome annotation and fitting multiple random effects, we show that the prediction accuracy could be further improved. The gain in prediction accuracy of the multivariate approach is equivalent to an increase in sample size of 34% for schizophrenia, 68% for bipolar disorder, and 76% for major depressive disorders using single trait models. Because our approach can be readily applied to any number of GWAS datasets of correlated traits, it is a flexible and powerful tool to maximize prediction accuracy. With current sample size, risk predictors are not useful in a clinical setting but already are a valuable research tool, for example in experimental designs comparing cases with high and low polygenic risk.
Abstract
Neuroscience has a rich history of studies focusing on neurobiology of aging. However, much of the aging studies in neuroscience occur outside of the gerosciences. The goal of this primer is ...2-fold: first, to briefly highlight some of the history of aging neurobiology and second, to introduce to geroscientists the broad spectrum of methodological approaches neuroscientists use to study the neurobiology of aging. This primer is accompanied by a corresponding geroscience primer, as well as a perspective on the current challenges and triumphs of the current divide across these 2 fields. This series of manuscripts is intended to foster enhanced collaborations between neuroscientists and geroscientists with the intent of strengthening the field of cognitive aging through inclusion of parameters from both areas of expertise.
Abstract
While neurodegenerative diseases can strike at any age, the majority of afflicted individuals are diagnosed at older ages. Due to the important impact of age in disease diagnosis, the field ...of neuroscience could greatly benefit from the many of the theories and ideas from the biology of aging—now commonly referred as geroscience. As discussed in our complementary perspective on the topic, there is often a “silo-ing” between geroscientists who work on understanding the mechanisms underlying aging and neuroscientists who are studying neurodegenerative diseases. While there have been some strong collaborations between the biology of aging and neuroscientists, there is still great potential for enhanced collaborative effort between the 2 fields. To this end, here, we review the state of the geroscience field, discuss how neuroscience could benefit from thinking from a geroscience perspective, and close with a brief discussion on some of the “missing links” between geroscience and neuroscience and how to remedy them. Notably, we have a corresponding, concurrent review from the neuroscience perspective. Our overall goal is to “bridge the gap” between geroscience and neuroscience such that more efficient, reproducible research with translational potential can be conducted.
Hernandez et al aim to propose a new, collaborative paradigm to study cognitive aging. The field of cognitive aging from the neuroscience perspective has focused on studying cognition over the life ...span from the "neck up," while fields studying the biology of aging/age-related diseases, known collectively as geroscience, have focused from the "neck down." However, it is abundantly clear that there is no discrete boundary at which the body ages independently of the brain, and the existing division between neuroscience and geroscience has led to an incomplete picture of the aging process.
Most psychiatric disorders are moderately to highly heritable. The degree to which genetic variation is unique to individual disorders or shared across disorders is unclear. To examine shared genetic ...etiology, we use genome-wide genotype data from the Psychiatric Genomics Consortium (PGC) for cases and controls in schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD). We apply univariate and bivariate methods for the estimation of genetic variation within and covariation between disorders. SNPs explained 17-29% of the variance in liability. The genetic correlation calculated using common SNPs was high between schizophrenia and bipolar disorder (0.68 ± 0.04 s.e.), moderate between schizophrenia and major depressive disorder (0.43 ± 0.06 s.e.), bipolar disorder and major depressive disorder (0.47 ± 0.06 s.e.), and ADHD and major depressive disorder (0.32 ± 0.07 s.e.), low between schizophrenia and ASD (0.16 ± 0.06 s.e.) and non-significant for other pairs of disorders as well as between psychiatric disorders and the negative control of Crohn's disease. This empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.
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