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Abstract. Background. Electrical stimulation has been recommended as an effective therapy to prevent muscle atrophy after nerve injury. However, the effect of electrical stimulation on the proliferation of satellite cells in denervated muscles has not yet been fully elucidated. This study was aimed to evaluate the changes in satellite cell proliferation after electrical stimulation in nerve injury and to determine whether these changes are related to the restoration of myofiber cross-section area (CSA). Methods. Sciatic nerve crush injury was performed in 48 male Sprague-Dawley rats. In half (24/48) of the rats, the gastrocnemius was electrically stimulated transcutaneously on a daily basis after injury, while the other half were not stimulated. Another group of 24 male Sprague-Dawley rats were used as sham operation controls without injury or stimulation. The rats were euthanized 2, 4, and 6 weeks later. After 5-bromo-2’-deoxyuridine (BrdU) labeling, the gastrocnemia were harvested for the detection of paired box protein 7 (Pax7), BrdU, myofiber CSA, and myonuclei number per fiber. All data were analyzed using two-way analysis of variance and Bonferroni post-hoc test. Results. The percentages of Pax7-positive nuclei (10.81 ± 0.56%) and BrdU-positive nuclei (34.29 ± 3.87%) in stimulated muscles were significantly higher compared to those in non-stimulated muscles (2.58 ± 0.33% and 1.30 ± 0.09%, respectively, Bonferroni t = 15.91 and 18.14, P

Changes of total nitrogen (TN), organic matter, microbial metabolic activity, aerobic denitrifying bacteria and aerobic denitrifying genes (nirS and nirK) in water and surface sediments under mixing aeration were studied in Heihe Jinpen Reservoir. Results showed that compared with the control area, the total nitrogen concentration of water and surface sediments in the enhanced area decreased by 29.7%~49.2% and 17.9%. Metabolic activity of microorganisms increased by more than 14%, the utilization rate of carbon source increased by 30% and the McIntosh diversity index of microorganisms increased by 20%. The number of aerobic denitrifiers and genes of aerobic denitrifiers was also increased by 20%. Illumina high-throughput DNA sequencing results showed that the proportion of aerobic denitrifiers such as Acidovorax increased from 0.01% to 0.15%, showing an increase of 15 times. The production practice showed that mixed aeration can improve the metabolic activity and denitrification characteristics of indigenous aerobic denitrifiers, providing theoretical support and technical guarantee for denitrification and carbon removal of slightly polluted source water.

Abstract Background The prognosis of spinal cord injury (SCI) is closely related to secondary injury, which is dominated by neuroinflammation. There is evidence that α-synuclein aggregates after SCI and that inhibition of α-synuclein aggregation can improve the survival of neurons after SCI, but the mechanism is still unclear. This study was designed to investigate the effects of α-synuclein on neuroinflammation after SCI and to determine the underlying mechanisms. Method A T3 spinal cord contusion model was established in adult male Sprague-Dawley rats. An SNCA-shRNA-carrying lentivirus (LV-SNCA-shRNA) was injected into the injury site to block the expression of α-synuclein (forming the SCI+KD group), and the SCI and sham groups were injected with an empty vector. Basso-Beattie-Bresnahan (BBB) behavioural scores and footprint analysis were used to detect motor function. Inflammatory infiltration and myelin loss were measured in the spinal cord tissues of each group by haematoxylin-eosin (HE) and Luxol Fast Blue (LFB) staining, respectively. Immunohistochemistry, Western blot analysis, and RT-qPCR were used to analyse protein expression and transcription levels in the tissues. Immunofluorescence was used to determine the morphology and function of glial cells and the expression of matrix metalloproteinase-9 in the central canal of the spinal cord. Finally, peripheral serum cytokine levels were determined by enzyme-linked immunosorbent assay. Results Compared with the SCI group, the SCI+KD group exhibited reduced inflammatory infiltration, preserved myelin, and functional recovery. Specifically, the early arrest of α-synuclein inhibited the pro-inflammatory factors IL-1β, TNF-α, and IL-2 and increased the expression of the anti-inflammatory factors IL-10, TGF-β, and IL-4. The neuroinflammatory response was regulated by reduced proliferation of Iba1+ microglia/macrophages and promotion of the shift of M1-polarized Iba1+/iNOS+ microglia/macrophages to M2-polarized Iba1+/Arg1+ microglia/macrophages after injury. In addition, compared with the SCI group, the SCI+KD group also exhibited a smaller microglia/astrocyte (Iba1/GFAP) immunostaining area in the central canal, lower MMP-9 expression, and improved cerebrospinal barrier function. Conclusion Lentivirus-mediated downregulation of α-synuclein reduces neuroinflammation, improves blood-cerebrospinal barrier function, promotes functional recovery, reduces microglial activation, and promotes the polarization of M1 microglia/macrophages to an M2 phenotype to confer a neuroprotective immune microenvironment in rats with SCI.

Abstract Background Endogenous α-synuclein (α-Syn) is involved in many pathophysiological processes in the secondary injury stage after acute spinal cord injury (SCI), and the mechanism governing these functions has not been thoroughly elucidated to date. This research aims to characterize the effect of α-Syn knockdown on transcriptional levels after SCI and to determine the mechanisms underlying α-Syn activity based on RNA-seq. Result The establishment of a rat model of lentiviral vector-mediated knockdown of α-Syn in Sprague-Dawley rats with T3 spinal cord contusion (LV_SCI group). The results of the RNA-seq analysis showed that there were 337 differentially expressed genes (DEGs) between the SCI group and the LV_SCI group, and 153 DEGs specific to LV_SCI between the (SCI vs LV_SCI) and (SCI vs CON) comparisons. The top 20 biological transition terms were identified by Gene ontology (GO) analysis. The Kyoto Gene and Genomic Encyclopedia (KEGG) analysis showed that the LV_SCI group significantly upregulated the cholinergic synaptic & nicotine addiction and the neuroactive ligand receptor interaction signaling pathway. Enriched chord analysis analyzes key genes. Further cluster analysis, gene and protein interaction network analysis and RT-qPCR results showed that Chrm2 and Chrnb2 together significantly in both pathways. The proliferation of muscarinic cholinergic receptor subtype 2 (Chrm2) and nicotinic cholinergic receptor subtype β2 (Chrnb2), and the neurogenesis were elevated in the injury site of LV_SCI group by immunofluorescence. Further by subcellular localization, the LV_SCI group enhanced the expression of Chrnb2 at the cell membrane. Conclusion Knockdown of α-Syn after SCI enhance motor function and promote neurogenesis probably through enhancing cholinergic signaling pathways and neuroreceptor interactions. This study not only further clarifies the understanding of the mechanism of knockdown of α-Syn on SCI but also helps to guide the treatment strategy for SCI.

Fluctuations in temperature and precipitation are expected to increase with global climate change, with more frequent, more intense and longer-lasting extreme events, posing greater challenges for the security of global food production. Here we proposed a generic framework to assess the impact of climate-induced crop yield risk under both current and future scenarios by combining a stochastic model for synthetic climate generation with a well-validated statistical crop yield model. The synthetic climate patterns were generated using the extended Empirical Orthogonal Function method based on historically observed and projected climate conditions. We applied our framework to assess the corn and soybean yield risk in the U.S. Midwest for historical and future climate conditions. We found that: (1) in the U.S. Midwest, about 45% and 40% of the interannual variability in corn and soybean yield, respectively, can be explained by the climate; (2) the risk level is higher in the southwest and northwest regions of the U.S. Midwest corresponding to 25% yield reduction for both corn and soybean compared to other regions; (3) the severity for the 1988 and 2012 major droughts quantified by our method represent 21-year and 30-year events for corn, and 7-year and 12-year events for soybean, respectively; (4) the crop yield risk will increase under a future climate scenario (i.e., Representative Concentration Pathway 8.5 or RCP 8.5 at 2050) compared with the current climate condition, with averaged yield decreases and yield variability increases for both corn and soybean. The framework and the results of this study enable applications for risk management policies and practices for the agriculture sectors.