[Short-term nitrogen deposition changes chemical composition of litter and soil organic matter in a Moso bamboo forest]. / 短期氮沉降改变毛竹林凋落物和土壤有机质化学组成.

To investigate the effects of short-term nitrogen (N) deposition on organic matter composition of litter and soil in Moso bamboo (Phyllostachys edulis) forests, we established a N-addition treatments (50 kg N·hm-2·a-1) to simulate the ambient and N deposition in a subtropical Moso bamboo forest from July 2020 to January 2022. We analyzed the organic matter composition of Moso bamboo leaf/root litter and soil by using pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS) technique. The results showed that short-term N deposition significantly increased the relative content of soil phenols by 50.9%, while significantly decreased fatty acids by 26.3%. The rela-tive content of alkanes & alkenes and lignin in leaf litter was significantly increased by 51.9% and 33.5%, respectively, while that of phenols and polysaccharides significantly decreased by 52.2% and 56.3%. In root litter, eleva-ted N significantly decreased the relative content of polycyclic aromatic hydrocarbons by 16.6%. Moreover, the relative content of fatty acids in soil organic matter was significantly positively correlated with the relative content of poly-saccharides in leaf litter. The relative content of phenols in soil organic matter was significantly positively correlated with the relative content of lignin, and negatively correlated with the relative content of polysaccharides in leaf litter. Our results demonstrated that short-term N deposition did not change the concentration of total organic carbon, total nitrogen, and C/N of the soil, leaf litter, and root litter, but significantly altered the chemical composition of organic matter. In addition, the changes in chemical composition of organic matter in soil under short-term N deposition were affected by the composition of organic matter in leaf litter.

Effects of plant residues on C:N:P of soil, microbial biomass, and extracellular enzyme in an alpine mea-dow on the Qinghai-Tibetan Plateau, China.

Plant residues can affect C:N:P of soil, microbial biomass, and extracellular enzyme, but the effects are still unclear. We conducted a field experiment in an alpine meadow on the eastern part of the Qinghai-Tibetan Plateau to explore the effects of removing aboveground plant or roots and adding plant residues on the C:N:P of soil, microbial biomass, and extracellular enzyme. The results showed that removing aboveground plant biomass significantly decreased soil C:N (the change was -23.7%, the same below) and C:P (-14.7%), microbial biomass C:P and N:P, while significantly increased microbial biomass C:N, and enzyme C:N:P compared with meadow without human disturbance. Removing all plant biomass (aboveground and roots) significantly reduced soil C:N (-11.6%), C:P (-24.0%), N:P (-23.3%) and microbial biomass C:N in comparison to removing aboveground plant, while significantly improved microbial biomass N:P and enzyme N:P. Adding plant residues after removing aboveground plant significantly increased microbial biomass C:N and C:P, enzyme C:N compared with removing aboveground plant, while significantly decreased enzyme N:P. Compared with removing all the plant, adding plant residues after removing whole plant significantly reduced soil C:N (-16.4%), microbial biomass C:P, N:P and enzyme N:P, while significantly increased enzyme C:N. Our results suggest that removal of plants could have a strong effect on C:N:P of soil, microbial biomass, and extracellular enzyme, and C:N:P of microbial biomass and that extracellular enzyme woule be more sensitive to plant residues. Roots could play a key role in stabilizing C:N:P of soil, microbial biomass, and extracellular enzyme under plant residues addition. Adding plant residues could be a suitable solution for restoring alpine meadows under the circumstance of intact roots, which was conducive to soil C storage, but might not be suitable for alpine meadows with serious root damage, which would increase soil CO2 emission.

Antagonism of histamine H3 receptor promotes angiogenesis following focal cerebral ischemia.

Our previous study showed that H3 receptor antagonists reduced neuronal apoptosis and cerebral infarction in the acute stage after cerebral ischemia, but through an action independent of activation of histaminergic neurons. Because enhanced angiogenesis facilitates neurogenesis and neurological recovery after ischemic stroke, we herein investigated whether antagonism of H3R promoted angiogenesis after brain ischemia. Photothrombotic stroke was induced in mice. We showed that administration of H3R antagonist thioperamide (THIO, 10 mg·kg-1·d-1, i.p., from D1 after cerebral ischemia) significantly improved angiogenesis assessed on D14, and attenuated neurological defects on D28 after cerebral ischemia. Compared with wild-type mice, Hrh3-/- mice displayed more blood vessels in the ischemic boundary zone on D14, and THIO administration did not promote angiogenesis in these knockout mice. THIO-promoted angiogenesis in mice was reversed by i.c.v. injection of H3R agonist immepip, but not by H1 and H2 receptor antagonists, histidine decarboxylase inhibitor α-fluoromethylhistidine, or histidine decarboxylase gene knockout (HDC-/-), suggesting that THIO-promoted angiogenesis was independent of activation of histaminergic neurons. In vascular endothelial cells (bEnd.3), THIO (10-9-10-7 M) dose-dependently facilitated cell migration and tube formation after oxygen glucose deprivation (OGD), and H3R knockdown caused similar effects. We further revealed that H3R antagonism reduced the interaction between H3R and Annexin A2, while knockdown of Annexin A2 abrogated THIO-promoted angiogenesis in bEnd.3 cells after OGD. Annexin A2-overexpressing mice displayed more blood vessels in the ischemic boundary zone, which was reversed by i.c.v. injection of immepip. In conclusion, this study demonstrates that H3R antagonism promotes angiogenesis after cerebral ischemia, which is independent of activation of histaminergic neurons, but related to the H3R on vascular endothelial cells and its interaction with Annexin A2. Thus, H3R antagonists might be promising drug candidates to improve angiogenesis and neurological recovery after ischemic stroke.