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A comprehensive understanding of the regional vegetation responses to long-term climate change will help to forecast Earth system dynamics. Based on a new well-dated pollen data set from Kanas Lake and a review on the published pollen records in and around the Altai Mountains, the regional vegetation dynamics and forcing mechanisms are discussed. In the Altai Mountains, the forest optimum occurred during 10-7ka for the upper forest zone and the tree line decline and/or ecological shifts were caused by climatic cooling from around 7ka. In the lower forest zone, the forest reached an optimum in the middle Holocene, and then increased openness of the forest, possibly caused by both climate cooling and human activities, took place in the late Holocene. In the lower basins or plains around the Altai Mountains, the development of protograssland or forest benefited from increasing humidity in the middle to late Holocene. Plain Language Summary In the Altai Mountains and surrounding area of central Asia, the previous studies of the Holocene paleovegetation and paleoclimate studies did not discuss the different ecological limiting factors for the vegetation in high mountains and low-elevation areas due to limited data. With accumulating fossil pollen data and surface pollen data, it is possible to understand better the geomorphological effect on the vegetation and discrepancies of vegetation/forest responses to large-scale climate forcing, and it is also possible to get reliable quantitative reconstructions of climate. Here our new pollen data and review on the published fossil pollen data will help us to look into the past climate change and vertical evolution of vegetation in this important area of the Northern Hemisphere. Based on our study, it can be concluded that the growth of taiga forest in the wetter areas may be promoted under a future warmer climate, while the forest in the relatively dry areas is liable to decline, and the different vegetation dynamics will contribute to future high-resolution coupled vegetation-climate model for Earth system modelling.
Manganese (Mn) is an essential nutrient for intracellular activities; it functions as a cofactor for a variety of enzymes, including arginase, glutamine synthetase (GS), pyruvate carboxylase and Mn superoxide dismutase (Mn-SOD). Through these metalloproteins, Mn plays critically important roles in development, digestion, reproduction, antioxidant defense, energy production, immune response and regulation of neuronal activities. Mn deficiency is rare. In contrast Mn poisoning may be encountered upon overexposure to this metal. Excessive Mn tends to accumulate in the liver, pancreas, bone, kidney and brain, with the latter being the major target of Mn intoxication. Hepatic cirrhosis, polycythemia, hypermanganesemia, dystonia and Parkinsonism-like symptoms have been reported in patients with Mn poisoning. In recent years, Mn has come to the forefront of environmental concerns due to its neurotoxicity. Molecular mechanisms of Mn toxicity include oxidative stress, mitochondrial dysfunction, protein misfolding, endoplasmic reticulum (ER) stress, autophagy dysregulation, apoptosis, and disruption of other metal homeostasis. The mechanisms of Mn homeostasis are not fully understood. Here, we will address recent progress in Mn absorption, distribution and elimination across different tissues, as well as the intracellular regulation of Mn homeostasis in cells. We will conclude with recommendations for future research areas on Mn metabolism.
Manganese (Mn) is an essential nutrient for intracellular activities; it functions as a cofactor for a variety of enzymes, including arginase, glutamine synthetase (GS), pyruvate carboxylase and Mn superoxide dismutase (Mn-SOD). Through these metalloproteins, Mn plays critically important roles in development, digestion, reproduction, antioxidant defense, energy production, immune response and regulation of neuronal activities. Mn deficiency is rare. In contrast Mn poisoning may be encountered upon overexposure to this metal. Excessive Mn tends to accumulate in the liver, pancreas, bone, kidney and brain, with the latter being the major target of Mn intoxication. Hepatic cirrhosis, polycythemia, hypermanganesemia, dystonia and Parkinsonism-like symptoms have been reported in patients with Mn poisoning. In recent years, Mn has come to the forefront of environmental concerns due to its neurotoxicity. Molecular mechanisms of Mn toxicity include oxidative stress, mitochondrial dysfunction, protein misfolding, endoplasmic reticulum (ER) stress, autophagy dysregulation, apoptosis, and disruption of other metal homeostasis. The mechanisms of Mn homeostasis are not fully understood. Here, we will address recent progress in Mn absorption, distribution and elimination across different tissues, as well as the intracellular regulation of Mn homeostasis in cells. We will conclude with recommendations for future research areas on Mn metabolism.
Loss of pdr-1/parkin influences Mn homeostasis through altered ferroportin expression in C-elegans
(2015)
Advanced catalysis triggered by photothermal conversion effects has aroused increasing interest due to its huge potential in environmental purification.
In this work, we developed a novel approach to the fast degradation of 4-nitrophenol (4-Nip) using porous MoS2 nanoparticles as catalysts, which integrate the intrinsic catalytic property of MoS2 with its photothermal conversion capability.
Using assembled polystyrene-b-poly(2-vinylpyridine) block copolymers as soft templates, various MoS 2 particles were prepared, which exhibited tailored morphologies (e.g., pomegranate-like, hollow, and open porous structures).
The photothermal conversion performance of these featured particles was compared under near-infrared (NIR) light irradiation.
Intriguingly, when these porous MoS2 particles were further employed as catalysts for the reduction of 4-Nip, the reaction rate constant was increased by a factor of 1.5 under NIR illumination.
We attribute this catalytic enhancement to the open porous architecture and light-to-heat conversion performance of the MoS2 particles. This contribution offers new opportunities for efficient photothermal-assisted catalysis.
Loss of pdr-1/parkin influences Mn homeostasis through altered ferroportin expression in C. elegans
(2015)
Overexposure to the essential metal manganese (Mn) can result in an irreversible condition known as manganism that shares similar pathophysiology with Parkinson's disease (PD), including dopaminergic (DAergic) cell loss that leads to motor and cognitive impairments. However, the mechanisms behind this neurotoxicity and its relationship with PD remain unclear. Many genes confer risk for autosomal recessive, early-onset PD, including the parkin/PARK2 gene that encodes for the E3 ubiquitin ligase Parkin. Using Caenorhabditis elegans (C. elegans) as an invertebrate model that conserves the DAergic system, we previously reported significantly increased Mn accumulation in pdr-1/parkin mutants compared to wildtype (WT) animals. For the current study, we hypothesize that this enhanced accumulation is due to alterations in Mn transport in the pdr-1 mutants. While no change in mRNA expression of the major Mn importer proteins (smf-1-3) was found in pdr-1 mutants, significant downregulation in mRNA levels of the putative Mn exporter ferroportin (fpn-1.1) was observed. Using a strain overexpressing fpn-1.1 in worms lacking pdr-1, we show evidence for attenuation of several endpoints of Mn-induced toxicity, including survival, metal accumulation, mitochondrial copy number and DAergic integrity, compared to pdr-1 mutants alone. These changes suggest a novel role of pdr-1 in modulating Mn export through altered transporter expression, and provides further support of metal dyshomeostasis as a component of Parkinsonism pathophysiology.