Effects of plastic contamination on carbon fluxes in a subtropical coastal wetland of East China.

Coastal wetlands are recognized as carbon sinks that play an important role in mitigating global climate change because of the strong carbon uptake by vegetation and high carbon sequestration in the soil. Over the last few decades, plastic waste pollution in coastal zones has become increasingly serious owing to high-intensity anthropogenic activities. However, the influence of plastic waste (including foam waste) accumulation in coastal wetlands on carbon flux remains unclear. In the Yangtze Estuary, we investigated the variabilities of vegetation growth, carbon dioxide (CO2) and methane (CH4) fluxes, and soil properties in a clean Phragmites australis marsh and mudflat and a plastic-polluted marsh during summer and autumn. The clean marsh showed a strong CO2 uptake capacity (a carbon sink), and the clean mudflat showed a weak CO2 sink during the measurement period. However, polluted marshes are a significant source of CO2 emissions. Regardless of the season, the gross primary production and vegetation biomass of the polluted marshes were on average 9.5 and 1.1 times lower than those in the clean marshes, respectively. Ecosystem respiration and CH4 emissions in polluted marshes were significantly higher than those in clean marshes and mudflats. Generally, the soil bulk density and salinity in polluted marshes were lower, whereas the median particle size was higher at the polluted sites than at the clean sites. Increased soil porosity and decreased salinity may favor CO2 and CH4 emissions through gas diffusion pathways and microbiological behavior. Moreover, the concentrations of heavy metals in the soil of plastic-polluted marshes were 1.24-1.49 times higher than those in the clean marshes, which probably limited vegetation growth and CO2 uptake. Our study highlights the adverse effects of plastic pollution on the carbon sink functions of coastal ecosystems, which should receive global attention in coastal environmental management.

Impacts of plastic pollution on soil-plant properties and greenhouse gas emissions in wetlands: A meta-analysis.

Plastic pollution in wetlands has recently emerged as an urgent environmental problem. However, the impacts of plastic contamination on soil-plant properties and greenhouse gas (GHG) emissions in wetlands remain unclear. Thus, this study conducted a meta-analysis based on 44 study sites to explore the influence of plastic pollution on soil physicochemical variables, soil microorganisms, enzyme activity, functional genes, plant characteristics, and GHG emissions (CO2, CH4, and N2O) in different wetland types. Based on the collected dataset, the plastic pollution significantly increased soil organic matter and organic carbon by on average 28.9 % and 34.2 %, respectively, while decreased inorganic nutrient elements, bacteria alpha diversity and enzyme activities by an average of 5.9 -14.2 %. The response of bacterial abundance to plastic pollution varied depending on phylum classes. Plant biomass and photosynthetic efficiency were decreased by an average of 12.8 % and 18.4 % due to plastic pollution. The concentration and exposure time of plastics play a key role in influencing the soil and plant properties in wetlands. Furthermore, plastic exposure notably increased the abundance of the functional genes related to C degradation and the ammonia oxidizing microorganisms, and the consequent CO2 and N2O emissions (with effect sizes of 2.10 and 1.94, respectively). We also found that plastic concentrations and exposure duration affected the wetland soil-plant system. Our results might be helpful to design further investigations on plastic effects and develop appropriate measures for mitigating plastic pollution in wetlands.

A novel reaction-based fluorescent probe with a nanomolar sensitivity for detection of Hg(II) and its multiple application.

An easily synthesized reaction-based probe for the fluorescence detection of Hg2+ ions using was reported. The designed probe exhibited "turn-on" fluorescence response towards Hg2+ ions via deprotection of the thiocarbonate-protecting group to alcohol in the HEPES/EtOH=8:2 (v/v, 5 mM, pH 7.4). The investigation results of probe Bzp-1 properties for Hg2+ detection indicated that probe Bzp-1 has satisfactory high selectivity and sensitivity. The detection limit of Bzp-1 for Hg2+ was found to be 4.2 nM. The recognition mechanism of Bzp-1 for Hg2+ was confirmed by ESI-MS. Moreover, the probe Bzp-1 has been successfully used to rapidly detect trace amounts of hazardous Hg2+ ions in real samples such as tap water, seafood and soil with good recoveries and less the relative standard deviations. Moreover, the Bzp-1 can also be used for fluorescence imagining of Hg2+ in living cells.

Projections from anteromedial thalamus nucleus to the midcingulate cortex mediate pain and anxiety-like behaviors in mice.

Prior research has demonstrated the involvement of the midcingulate cortex (MCC) and its downstream pathway in pain regulation. However, the mechanism via which pain information is conveyed to the MCC remains unclear. The present study utilized immunohistochemistry, chemogenetics, optogenetics, and behavior detection methods to explore the involvement of MCC, anteromedial thalamus nucleus (AM), and AM-MCC pathway in pain and emotional regulation. Chemogenetics or optogenetics methods were employed to activate/inhibit MCCCaMKIIα, AMCaMKIIα, AMCaMKIIα-MCC pathway. This manipulation evokes/relieves mechanical and partial heat hyperalgesia, as well as anxiety-like behaviors. In the complete Freund,s adjuvant (CFA) inflammatory pain model, chemogenetic inhibition of the AMCaMKIIα-MCCCaMKIIα pathway contributed to pain relief. Notably, this study presented the first evidence implicating the AM in the regulation of nociception and negative emotions. Additionally, it was observed that the MCC primarily receives projections from the AM, highlighting the crucial role of this pathway in the transmission of pain and emotional information.

Projections from the Rostral Zona Incerta to the Thalamic Paraventricular Nucleus Mediate Nociceptive Neurotransmission in Mice.

Zona incerta (ZI) is an integrative subthalamic region in nociceptive neurotransmission. Previous studies demonstrated that the rostral ZI (ZIR) is an important gamma-aminobutyric acid-ergic (GABAergic) source to the thalamic paraventricular nucleus (PVT), but whether the ZIR-PVT pathway participates in nociceptive modulation is still unclear. Therefore, our investigation utilized anatomical tracing, fiber photometry, chemogenetic, optogenetic and local pharmacological approaches to investigate the roles of the ZIRGABA+-PVT pathway in nociceptive neurotransmission in mice. We found that projections from the GABAergic neurons in ZIR to PVT were involved in nociceptive neurotransmission. Furthermore, chemogenetic and optogenetic activation of the ZIRGABA+-PVT pathway alleviates pain, whereas inhibiting the activities of the ZIRGABA+-PVT circuit induces mechanical hypersensitivity and partial heat hyperalgesia. Importantly, in vivo pharmacology combined with optogenetics revealed that the GABA-A receptor (GABAAR) is crucial for GABAergic inhibition from ZIR to PVT. Our data suggest that the ZIRGABA+-PVT pathway acts through GABAAR-expressing glutamatergic neurons in PVT mediates nociceptive neurotransmission.

Dkk1-mediated inhibition of Wnt signaling in bone results in osteopenia.

Mutations affecting the activity of the Wnt co-receptors LRP5 and LRP6 that cause alterations in skeletal biology confirmed the involvement of Wnt signaling in bone formation. We evaluated the potential role of Dkk1, an inhibitor of LRP5/6 activity, in bone formation by examining the normal expression pattern of Dkk1 in normal young mice and by assessing the consequences of osteoblast overexpression of Dkk1 in transgenic mice. Endogenous Dkk1 expression was detected primarily in osteoblasts and osteocytes. Transgenic over-expression of Dkk1 using two different rat collagen 1A1 promoters resulted in distinct bone phenotypes. More widespread Dkk1 expression (driven by the Col1A1 3.6 kb promoter) yielded osteopenia with forelimb deformities and hairlessness, while expression restricted to osteoblasts (driven by the Col1A1 2.3 kb promoter) induced severe osteopenia without limb defects or alopecia. The decrease in bone mass in vivo resulted from a significant 49% reduction in osteoblast numbers and was reflected in a 45% reduction in serum osteocalcin concentration; an in vitro study revealed that Dkk1 caused a dose-dependent suppression of osteoblast matrix mineralization. These data indicate that Dkk1 may directly influence bone formation and suggest that osteopenia develops in mice over-expressing Dkk1 at least in part due to diminished bone formation resulting from reduced osteoblast numbers.