Unveiling the nexus between rural population aging, technical efficiency, and carbon emissions in Chinese agriculture.

INTRODUCTION: According to the seventh national population census in China, the proportion of people aged 65 and above in the population reached 13.5%. The aging trend is more pronounced in rural areas, indicating that China has entered an aging society. This article focuses on agricultural carbon emissions in the context of aging, studying the impact of rural population aging on agricultural carbon emissions. STUDY OBJECTIVES: Under the background of deepening population aging, let us discuss how to maintain the green and sustainable development of agriculture in China. METHODOLOGY: Fixed effects and mediating effects models are used. Technical efficiency is used as a mediating variable to discuss the relationship between rural population ageing, technical efficiency and agricultural carbon emissions. RESULTS: This paper adopts the classical carbon emission calculation theory of IPCC to measure agricultural carbon emissions from 2010 to 2019, and China's plantation carbon emissions show an "inverted U-shaped" trend, reaching a high level in 2015 and then starting to decline. In addition, the fixed-effects benchmark regression found that the aging of the rural population promotes agricultural carbon emissions, and the technical efficiency of agriculture suppresses agricultural carbon emissions. Finally, the mediating effect model is applied to explore the relationship between the three. Using technical efficiency as the mediating variable, it is found that under the masking effect, rural population aging will weaken agricultural carbon emissions through technical efficiency, thus achieving the suppression of agricultural carbon emissions. POLICY RECOMMENDATION: The formulation and modification of agricultural carbon-reducing policy row policies should take full account of the broader context of rural population ageing; increase the interconnectedness and interaction between rural population ageing and agricultural production technology, and actively play a positive role in promoting the efficiency of agricultural technology as a result of rural population ageing; and, in accordance with the actual situation of agricultural research, appropriately increase the strength of financial support for agriculture to improve agricultural technology and promote low-carbon development in agriculture.

Knocking Down lncRNA HOXA-AS2 Mitigates the Progression of Epilepsy via Regulation of the miR-372-3p/STAT3 Axis.

AIM: To explore the potential activity of HOXA cluster antisense RNA 2 (HOXA-AS2), a long non-coding RNA (lncRNA), in epilepsy progression, as well as the mechanisms behind its activity. MATERIAL AND METHODS: Kainic acid (KA) was used to treat rat astroglial CTX-TNA2 cells to establish a cellular model of epilepsy. Reverse transcription-quantitative PCR was conducted to examine the expression levels of HOXA-AS2, microRNA (miR)-372-3p and STAT3. Cell Counting Kit-8, flow cytometry and western blot assays were performed to analyze cell viability and apoptosis. The secretion levels of various inflammatory factors (IL-6, IL-1? and TNF-?) were identified by ELISA. To validate the functional interaction between HOXA-AS2/STAT3 and miR?372-3p, dual-luciferase reporter assay was performed. RESULTS: The HOXA-AS2 and STAT3 expression levels were notably upregulated, whereas miR?372-3p was downregulated in KAtreated CTX-TNA2 cells. Silencing HOXA-AS2 or overexpressing miR-372-3p inhibited the secretion of inflammatory factors and apoptosis in KA-treated CTX-TNA2 cells. HOXA-AS2 negatively regulated miR?372-3p, and miR?372-3p targeted STAT3 mRNA. Suppression of miR-372-3p or overexpression of STAT3 abrogated the rescue effect of small interfering HOXA-AS2 in KA-treated CTX-TNA2 cells. CONCLUSION: The current study suggested that targeting HOXA-AS2 could alleviate cellular damages in the epileptic model by regulating the miR-372-3p/STAT3 axis. Therefore, HOXA-AS2 may serve as a potential anti-epilepsy therapeutic target.

LncRNA SNHG15 mediates 1-methyl-4-phenylpyridinium (MPP+)-induced neuronal damage through targeting miR-29c-3p/SNCA axis.

BACKGROUND: Parkinson's disease (PD) is the most prevalent neurodegenerative disease in the elderly people. Long non-coding ribose nucleic acids (LncRNAs) can serve as molecular sponges for micro RNA (miRNA) and regulate gene expression, which is implicated in the occurrence and progression of PD. In this work, we investigated the functional role of lncRNA SNHG15 in a neuronal damage cell model and its potential mechanism. METHODS: SK-N-SH cells treated with 1-methyl-4-phenylpyridinium (MPP+) were employed as the in vitro cellular model to mimic neuronal degeneration. The expression levels of SNHG15, miR-29c-3p, and SNCA were determined by qRT-PCR. ELISA, CCK-8 proliferation assay, and flow cytometry were conducted to explore the effects of SNHG15 and miR-29c-3p on the production of inflammatory factors, cell proliferation, and apoptosis, respectively. Dual-luciferase reporter assay was utilized to validate the functional interactions among SNHG15, miR-29c-3p, and SNCA. SNCA protein levels were examined by Western blot. RESULTS: SNHG15 was highly induced in the cell model of MPP+-induced neuronal damage. SNHG15 knockdown significantly mitigated MPP+-induced damages in SK-N-SH cells. SNHG15 served as a sponge to down-regulate miR-29c-3p, thereby releasing the inhibition of miR-29c-3p on SNCA expression, which promoted neuronal damages upon MPP+ challenge. CONCLUSION: The upregulation of SNHG15 upon MPP+ challenge mediates neuronal damages in SK-N-SH cells by regulating miR-29c-3p/SNCA axis. Future work is required to validate these findings in PD patients and animal models, which could provide insights into the diagnosis and therapy of PD.

Knockdown of small nucleolar RNA host gene 10 (SNHG10) alleviates the injury of human neuroblastoma cells via the miR-1277-5p/insulin substrate receptor 2 axis.

Parkinson's disease is a common neurodegenerative disease with a complex physio-pathology. So far, there is no effective medical strategies to prevent the progression of Parkinson's disease. Understanding the mechanisms underlying the progression of Parkinson's disease could provide insights into the formulation of novel preventative or treatment strategies. Small nucleolar RNA host gene 10 (SNHG10) is a lncRNA which has been implicated in the development of many cancers. However, its potential role in Parkinson's disease remains unknown. In this study, we found that SNHG10 was upregulated while miR-1277-5p was downregulated in the Parkinson's disease cell model of 1-Methyl-4-phenyl-pyridine ion (MPP+) induced SH-SY5Y cells. We further revealed that SNHG10 sponged miR-1277-5p to negatively regulate its expression, and miR-1277-5p could bind to the 3'UTR of insulin substrate receptor 2 (IRS2) mRNA to suppress its expression. These data suggest that SNHG10 regulates IRS2 through interacting with miR-1277-5p in the cell model of Parkinson's disease. Through a series of molecular experiments and functional assays, we demonstrated that downregulating SNHG10 in the cell model of Parkinson's disease attenuated the cell injury by reducing the expression of IRS2. Meanwhile, inhibiting miR-1277-5p or overexpressing IRS2 could partially reverse the effect of SNHG10 knockdown. In summary, our data indicate that knockdown of SNHG10 mitigates MPP+ induced damage in SH-SY5Y cells via the miR-1277-5p/IRS2 axis.

Enhancing Cell Performance of Lithium-Rich Manganese-Based Materials via Tailoring Crystalline States of a Coating Layer.

Li-rich Mn-based-layered oxides are considered to be the most felicitous cathode material candidates for commercial application of lithium-ion batteries on account of high energy density. Nevertheless, defects containing an unsatisfactory initial Coulombic efficiency and rapid voltage decay seriously impede their practical utilization. Herein, a coating layer with three distinct crystalline states are employed as a coating layer to modify Li[Li0.2Mn0.54Ni0.13Co0.13]O2, respectively, and the effects of coating layers with distinct crystalline states on the crystal structure, diffusion kinetics, and cell performance of host materials are further explored. A coating layer with high crystallinity enables mitigatory voltage decay and better cyclic stability of materials, while a coating layer with planar defects facilitates Li+ transfer and enhances the rate performance of materials. Consequently, optimizing the crystalline state of coating substances is critical for preferable surface modification.

Characteristics of poly-silicate aluminum sulfate prepared by sol method and its application in Congo red dye wastewater treatment.

A novel method for synthesizing poly-silicate aluminum sulfate coagulant (PSAS) using a silica-alumina sol was reported. Herein, two modalities (nSiO2/nNa2O: 1.11 and 3.27) of self-made water glasses were used as the silica source for synthesizing the sol precursor. Then, the PSAS1.11 and PSAS3.27 with different basicity were obtained by controlling the Al molar ratio of precursor to aluminum sulfate. The results showed that the PSAS1.11 coagulant prepared with low modulus water glass (LMWS, 1.11) has low turbidity and good stability. Using low modulus water glass, the effect of the Al molar ratio of precursor to aluminum sulfate on the basicity and stability of PSAS1.11 with Al/Si of 20 and the effect of the molar ratio of aluminum to silicon on the basicity and stability of PSAS1.11 were studied, respectively. Based on XRD and Fourier infrared (FTIR) characterization of the sol precursor and PSAS1.11, the synthesis mechanism of PSAS by the silica-alumina sol method was discussed. Al species distribution of PSAS1.11 was determined using the Al-Ferron timed spectrophotometric method. Moreover, the performance of PSAS1.11 coagulant was examined, regarding its efficiency towards color removal of Congo red. The results showed that PSAS1.11 coagulant with Al/Si of 20 and Al molar ratio of 1/12 exhibits excellent performance, and the color removal rate reached 98.6% at an initial pH of 11 and coagulant dosage of 40 mg L-1 (Al mg L-1). Finally, the PSAS coagulant mechanism was discussed in detail through infrared characterization, 27Al NMR, Raman, morphology and mapping of the flocs.

Brain-derived neurotrophic factor-modified umbilical cord mesenchymal stem cell transplantation improves neurological deficits in rats with traumatic brain injury.

This study explored the effect of brain-derived neurotrophic factor (BDNF) gene-modified umbilical cord mesenchymal stem cell (UCMSC) transplantation on neurological functional improvement in rats after brain trauma. A rat model of cerebral contusion in the motor-sensory cortex was established by the weight hammer-falling method. UCMSCs were cultured and transferred with BDNF gene. After determining BDNF expression and activity, the BDNF gene-modified UCMSCs were implanted into brains of rats receiving the brain injury. The neurological function was evaluated 1 and 2 weeks after brain injury. BDNF expression was then determined by immunohistochemistry. Severe neurological dysfunction was observed in animals subjected to contusion brain injury (10.50 ± 0.53). A significant improvement in neurological function was found in the UCMSC transplantation animals (7.75 ± 0.71) compared with the brain injury only group (p < 0.01). Rats with BDNF gene-modified UCMSCs showed the highest improvement in behavior (5.50 ± 0.76; p < 0.01). BDNF gene-modified UCMSCs can survive and migrate in rat cerebral tissues. The transplantation of these UCMSCs can improve the neurological functions of rats with traumatic brain injury.

[Expression vector for the inhibitor of growth-1 gene is constructed and the NLS-GFP fusion protein expresses in MRC-5 cells].

OBJECTIVE: To construct the NLS(ING1)-GFP vector, transfer it into MRC-5 cells and establish a cell model expressing NLS (ING1)-GFP fusion protein. METHODS: Firstly, cDNA fragment of nuclear locating sequence (NLS) of inhibitor of growth-1 gene (ING1) was gained by RT-PCR and inserted into multi-clone site of pEGFP-C1 to construct the NLS (ING1)-GFP expression vector. Then the vector was used to transfect the MRC-5 cells to observe the subcellular signal localization of green fluorescence protein (GFP). RESULTS: We successfully constructed the expressing vector of NLS (ING1)-GFP fusion protein. After transferring the fusion expressing vector into MRC-5 cells, we observed that green fluorescence signal located in the cell nucleus. However, the green fluorescence signal located in the cytoplasm in MRC-5 cells transfected with pEGFP-C1 control only expressing GFP. CONCLUSION: In living cells, physiologically p33 ING1b locates absolutely in nucleus. The p33(ING1b) NLS plays a decisive role in the transporting process of subcellular localization.