scholarly journals Tropical forest soil carbon stocks do not increase despite 15 years of doubled litter inputs

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Emma J. Sayer ◽  
Luis Lopez-Sangil ◽  
John A. Crawford ◽  
Laëtitia M. Bréchet ◽  
Ali J. Birkett ◽  
...  

AbstractSoil organic carbon (SOC) dynamics represent a persisting uncertainty in our understanding of the global carbon cycle. SOC storage is strongly linked to plant inputs via the formation of soil organic matter, but soil geochemistry also plays a critical role. In tropical soils with rapid SOC turnover, the association of organic matter with soil minerals is particularly important for stabilising SOC but projected increases in tropical forest productivity could trigger feedbacks that stimulate the release of stored SOC. Here, we demonstrate limited additional SOC storage after 13–15 years of experimentally doubled aboveground litter inputs in a lowland tropical forest. We combined biological, physical, and chemical methods to characterise SOC along a gradient of bioavailability. After 13 years of monthly litter addition treatments, most of the additional SOC was readily bioavailable and we observed no increase in mineral-associated SOC. Importantly, SOC with weak association to soil minerals declined in response to long-term litter addition, suggesting that increased plant inputs could modify the formation of organo-mineral complexes in tropical soils. Hence, we demonstrate the limited capacity of tropical soils to sequester additional C inputs and provide insights into potential underlying mechanisms.

2020 ◽  
Author(s):  
Emma J. Sayer ◽  
Catherine Baxendale ◽  
Ali J. Birkett ◽  
Laëtitia M. Bréchet ◽  
Biancolini Castro ◽  
...  

AbstractSoil organic matter (SOM) in tropical forests is an important store of carbon (C) and nutrients. Although SOM storage could be affected by global changes via altered plant productivity, we know relatively little about SOM stabilisation and turnover in tropical forests compared to temperate systems. Here, we investigated changes in soil C and N within particle size fractions representing particulate organic matter (POM) and mineral-associated organic matter (MAOM) after 13 years of experimental litter removal (L−) and litter addition (L+) treatments in a  lowland tropical forest. We hypothesized that reduced nitrogen (N) availability in L− plots would result in N-mining of MAOM, whereas long-term litter addition would increase POM, without altering the C:N ratio of SOM fractions. Overall, SOM-N declined more than SOM-C with litter removal, providing evidence of N-mining in the L− plots, which increased the soil C:N ratio. However, contrary to expectations, the C:N ratio increased most in the largest POM fraction, whereas the C:N ratio of MAOM remained unchanged. We did not observe the expected increases in POM with litter addition, which we attribute to rapid turnover of unprotected SOM. Measurements of ion exchange rates to assess changes in N availability and soil chemistry revealed that litter removal increased the mobility of ammonium-N and aluminium, whereas litter addition increased the mobility of nitrate-N and iron, which could indicate SOM priming in both treatments. Our study suggests that altered litter inputs affect multiple processes contributing to SOM storage and we propose potential mechanisms to inform future work.


2015 ◽  
Vol 123 (1-2) ◽  
pp. 221-235 ◽  
Author(s):  
Benjamin L. Turner ◽  
Joseph B. Yavitt ◽  
Kyle E. Harms ◽  
Milton N. Garcia ◽  
S. Joseph Wright

2020 ◽  
Vol 27 (6) ◽  
pp. 955-982 ◽  
Author(s):  
Kyoung Sang Cho ◽  
Jang Ho Lee ◽  
Jeiwon Cho ◽  
Guang-Ho Cha ◽  
Gyun Jee Song

Background: Neuroinflammation plays a critical role in the development and progression of various neurological disorders. Therefore, various studies have focused on the development of neuroinflammation inhibitors as potential therapeutic tools. Recently, the involvement of autophagy in the regulation of neuroinflammation has drawn substantial scientific interest, and a growing number of studies support the role of impaired autophagy in the pathogenesis of common neurodegenerative disorders. Objective: The purpose of this article is to review recent research on the role of autophagy in controlling neuroinflammation. We focus on studies employing both mammalian cells and animal models to evaluate the ability of different autophagic modulators to regulate neuroinflammation. Methods: We have mostly reviewed recent studies reporting anti-neuroinflammatory properties of autophagy. We also briefly discussed a few studies showing that autophagy modulators activate neuroinflammation in certain conditions. Results: Recent studies report neuroprotective as well as anti-neuroinflammatory effects of autophagic modulators. We discuss the possible underlying mechanisms of action of these drugs and their potential limitations as therapeutic agents against neurological disorders. Conclusion: Autophagy activators are promising compounds for the treatment of neurological disorders involving neuroinflammation.


Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 253
Author(s):  
Xi Guo ◽  
Hong Yi ◽  
Tin Chiu Li ◽  
Yu Wang ◽  
Huilin Wang ◽  
...  

Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the developing embryo and the endometrium. There is a correlation between the alteration of VEGF expression and reproductive failure, including recurrent implantation failure (RIF) and recurrent miscarriage (RM). In order to clarify the role of VEGF in embryo implantation, we reviewed recent literature concerning the expression and function of VEGF in the reproductive system around the time of embryo implantation and we provide a summary of the findings reported so far. We also explored the effects and the possible underlying mechanisms of action of VEGF in embryo implantation.


2018 ◽  
Vol 123 (9) ◽  
pp. 3016-3027 ◽  
Author(s):  
Yang Lin ◽  
Amrita Bhattacharyya ◽  
Ashley N. Campbell ◽  
Peter S. Nico ◽  
Jennifer Pett-Ridge ◽  
...  

2018 ◽  
Vol 19 (11) ◽  
pp. 3390 ◽  
Author(s):  
Sudip Paudel ◽  
Regan Sindelar ◽  
Margaret Saha

Accumulating evidence over the past three decades suggests that altered calcium signaling during development may be a major driving force for adult pathophysiological events. Well over a hundred human genes encode proteins that are specifically dedicated to calcium homeostasis and calcium signaling, and the majority of these are expressed during embryonic development. Recent advances in molecular techniques have identified impaired calcium signaling during development due to either mutations or dysregulation of these proteins. This impaired signaling has been implicated in various human diseases ranging from cardiac malformations to epilepsy. Although the molecular basis of these and other diseases have been well studied in adult systems, the potential developmental origins of such diseases are less well characterized. In this review, we will discuss the recent evidence that examines different patterns of calcium activity during early development, as well as potential medical conditions associated with its dysregulation. Studies performed using various model organisms, including zebrafish, Xenopus, and mouse, have underscored the critical role of calcium activity in infertility, abortive pregnancy, developmental defects, and a range of diseases which manifest later in life. Understanding the underlying mechanisms by which calcium regulates these diverse developmental processes remains a challenge; however, this knowledge will potentially enable calcium signaling to be used as a therapeutic target in regenerative and personalized medicine.


1998 ◽  
Vol 30 (10-11) ◽  
pp. 1309-1315 ◽  
Author(s):  
B. Grisi ◽  
C. Grace ◽  
P.C. Brookes ◽  
A. Benedetti ◽  
M.T. Dell'abate

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