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【Objective】 The study was conducted to build an evaluation system of modern urban agriculture, measure urban agriculture development level and differences in different areas in Guangdong-Hong Kong-Macao Greater Bay Area(GBA), analyse the driving factors, and put forward the optimization path of the development of urban agriculture in the GBA, providing theoretical support for the high-quality development of urban agriculture in developed urban agglomerations such as the GBA. 【Method】 The entropy method was used to evaluate the development of modern urban agriculture in the GBA from 2013 to 2020. The Dagum Gini coefficient decomposition was used to analyse the regional differences, and the geographical detector method was used to study the driving factors of urban agriculture development in the GBA. 【Result】 The average annual growth rate of modern urban agriculture development level in the GBA is 5.3%, and Guangzhou is the city with the highest development level. The vegetable-basket product support capability in the GBA develops stably, agricultural ecology and sustainable development level rises in volatility, and level of integrated development of three industries develops quickly, with the average annual growth rate of 12.1%. Agglomeration level of advanced agricultural production factors increases slightly, with an average annual growth rate of 0.45%, and modern agricultural management level increases rapidly, with an average annual growth rate of 17.2%. The overall Gini coefficient of the area decline in the volatility, and the differences mainly come from the gap among areas. Currently, proportion of cultivated land area, proportion of three industries and percapita GDP are important driving factors for the development of urban agriculture. The driving factors differ in areas, and the interaction of all factors is "double factor enhancement", and any two driving factors acting together will enhance the intensity of their effects on urban agriculture differentiation. 【Conclusion】 During sample observation period, there is a growing trend of the modern urban agriculture in Guangdong-Hong Kong-Macao Greater Bay Area generally, but there are declining trends between the gap of regional development of urban agriculture and the gaps among cities are still large. It is recommended to improve the overall planning and regional shortcomings, the development factors of modern urban agriculture and policy supply.

Abstract Background Accumulating evidence suggests tRNA-derived fragments (tRFs) play important roles in cellular homeostasis. Here we aimed to explore aberrant expression of tRFs in CD4+ T cells from patients with systemic lupus erythematosus (SLE) and their potential function in the SLE pathogenesis. Methods First, small RNA sequencing was performed on CD4+ T cells from four SLE patients and three healthy controls (HCs). Candidate tRFs were then validated in CD4+ T cells from 97 SLE patients and their relevant disease controls using qRT-PCR. Then sequencing was used to investigate the profiles of HC-derived CD4+ T cells transfected with tRF-3009. Lastly, tRF-3009 siRNA or tRF-3009 mimics were transfected into CD4+ T cells with/without IFN-α. Changes in oxygen consumption rate (OCR), ATP, and ROS production were analyzed. Results We identified 482 differentially expressed tRFs from SLE CD4+ T cells and chose tRF-3009 for further analysis due to its upregulation and the positive correlations between its expression and SLEDAI, active lupus nephritis and serum IFN-α levels. In vitro, tRF-3009 over-expressing CD4+ T cell profiling and putative analysis linked this product to the type I IFN and oxidative phosphorylation (OXPHOS) pathways. Interestingly, IFN-α is capable of inducing ROS and ATP production in CD4+ T cells, while knockdown of tRF-3009 reversed this process. Overexpression of tRF-3009 in CD4+ T cells alone was sufficient to upregulate OCR, ROS, and ATP production. Conclusions Our study is the first to link aberrant tRF expression and SLE. tRF-3009 may participate in metabolic modulation of IFN-α-induced CD4+ T cell OXPHOS in lupus.

The SPRY domain-containing SOCS box proteins SPSB1, SPSB2, and SPSB4 utilize their SPRY/B30.2 domain to interact with a short region in the N-terminus of inducible nitric oxide synthase (iNOS), and recruit an E3 ubiquitin ligase complex to polyubiquitinate iNOS, resulting in the proteasomal degradation of iNOS. Inhibitors that can disrupt the endogenous SPSB-iNOS interactions could be used to augment cellular NO production, and may have antimicrobial and anticancer activities. We previously reported the rational design of a cyclic peptide inhibitor, cR8, cyclo(RGDINNNV), which bound to SPSB2 with moderate affinity. We, therefore, sought to develop SPSB inhibitors with higher affinity. Here, we show that cyclic peptides cR7, cyclo(RGDINNN), and cR9, cyclo(RGDINNNVE), have ~6.5-fold and ~2-fold, respectively, higher SPSB2-bindng affinities than cR8. We determined high-resolution crystal structures of the SPSB2-cR7 and SPSB2-cR9 complexes, which enabled a good understanding of the structure–activity relationships for these cyclic peptide inhibitors. Moreover, we show that these cyclic peptides displace full-length iNOS from SPSB2, SPSB1, and SPSB4, and that their inhibitory potencies correlate well with their SPSB2-binding affinities. The strongest inhibition was observed for cR7 against all three iNOS-binding SPSB proteins. [ABSTRACT FROM AUTHOR]

China has limited arable land area, and its output value is increased with enhanced agricultural inputs such as machinery, irrigation, fertilizers, and pesticides. However, this mode is accompanied by an increase in agricultural carbon emissions. With the aim to further examine the driving effect of scientific and technological innovation on economic growth and green agriculture, this study uses the Solow growth model coupled with the Cobb–Douglas production function and vector autoregressive models. Then, the agricultural scientific and technological innovation capacity in Guangdong Province during 2006–2020 is evaluated by using the contribution rate of agricultural scientific and technological progress (ASTP) as the assessment index. In addition, the carbon footprints of green agricultural indexes such as machinery, irrigation, fertilizers, and pesticides are measured to analyze the relationship between green agriculture and agricultural scientific and technological innovation capacity. Results demonstrate the gradual increase in the contribution rate of ASTP in Guangdong Province. During the 11th, 12th, and 13th Five-Year Plan periods, the rates were 65.09%, 65.94%, and 70.40%, respectively, indicating that the agricultural scientific and technological innovation ability constantly improved. Among the indexes of green agriculture, the carbon footprints of machinery have a significant impact on agricultural scientific and technological innovation, which is quickly transformed into machinery. Such innovation requires the driving force of science and technology itself, which have relatively significant and rapid effects. On the basis of the results, corresponding policy suggestions are proposed: increasing investments in scientific and technological innovation in the agricultural field, vigorously developing new energy-saving and emission reduction products and processes for fertilizers, and increasing the research and promotion of agricultural machinery. The proposed method provides good prospects for the development of agricultural production towards mechanization, intelligence, efficiency, and greenness. [ABSTRACT FROM AUTHOR]

The plasticity of Schwann cells (SCs) following nerve injury is a critical feature in the regeneration of peripheral nerves as well as surrounding tissues. Here, we show a pivotal role of Schwann cell‐derived cells in alveolar bone regeneration through the specific ablation of proteolipid protein 1 (Plp)‐expressing cells and the transplantation of teased nerve fibers and associated cells. With inducible Plp specific genetic tracing, we observe that Plp+ cells migrate into wounded alveolar defect and dedifferentiate into repair SCs. Notably, these cells barely transdifferentiate into osteogenic cell lineage in both SCs tracing model and transplant model, but secret factors to enhance the proliferation of alveolar skeletal stem cells (aSSCs). As to the mechanism, this effect is associated with the upregulation of extracellular matrix (ECM) receptors and receptor tyrosine kinases (RTKs) signaling and the downstream extracellular signal‐regulated kinase (ERK)/mitogen‐activated protein kinase (MAPK) pathway and the phosphoinositide 3‐kinase–protein kinase B (PI3K‐Akt) pathway. Collectively, our data demonstrate that SCs dedifferentiate after neighboring alveolar bone injury and contribute to bone regeneration mainly by a paracrine function. © 2022 American Society for Bone and Mineral Research (ASBMR). [ABSTRACT FROM AUTHOR]

Objective To develop a short-term renal outcome prediction model for acute kidney injury (AKI) in patients with LN. Methods Two lupus AKI cohorts from two independent centres during 2013–2019 were included: a derivation cohort from a rheumatology centre and a validation cohort from a nephrology centre. Clinical characteristics and renal histologic features were obtained. The outcome measurement was the recovery of kidney function within 12 months. Lasso regression was used for feature selection. Prediction models with or without pathology were built and a nomogram was plotted. Model evaluation including calibration curve and decision curve analysis was performed. Results A total of 130 patients were included in the derivation cohort and 96 patients in the validation cohort, of which 82 and 73 patients received a renal biopsy, respectively. The prognostic nomogram model without pathology included determinants of SLE duration, days from AKI onset to treatment and baseline creatinine level [C-index 0.85 (95% CI 0.78, 0.91) and 0.79 (95% CI 0.70, 0.88) for the two cohorts]. A combination of histologic tubulointerstitial (TI) fibrosis in the nomogram gave an incremental predictive performance (C-index 0.93 vs 0.85; P  = 0.039) in the derivation cohort but failed to improve the performance in the validation cohort (C-index 0.81 vs 0.79; P  = 0.78). Decision curve analysis suggested clinical benefit of the prediction models. Conclusion The predictive nomogram models might facilitate more accurate management for lupus patients with AKI. [ABSTRACT FROM AUTHOR]

Objectives Anti-melanoma differentiation-associated gene 5 (MDA5) positive DM is a life-threatening disease often complicated with rapidly progressive interstitial lung disease (ILD). This study aimed to establish and validate a clinical prediction model for 6-month all-cause mortality in Chinese patients with anti-MDA5 positive DM-ILD. Methods We conducted a retrospective observational study using a single-centre derivation cohort and a multicentre validation cohort. Hospitalized DM patients with positive anti-MDA5 antibody and ILD course ≤3 months on admission were included. Patients' baseline characteristics were described and compared between the deceased and survivors by univariable Cox regression. Optimal cut-off values were defined by the 'survminer' R package for significant continuous variables. Independent prognostic factors were determined by the final multivariable Cox regression model chosen by backward stepwise algorithm, which could be reproduced in both cohorts. The Kaplan–Meier survival analyses based on the derived predictor were conducted. Results A total of 184 and 81 eligible patients were included with a cumulative 40.8 and 40.7% 6-month mortality in the derivation and validation cohorts, respectively. Based on multivariable Cox regression, the prognostic factor at baseline was identified and validated as three-category forced vital capacity (FVC)%: FVC% ≥50%, FVC% <50%, unable to perform. This significantly distinguishes three risk stages with mortalities of 15.3, 46.8, 97.4% in the derivation cohort, and 14.9, 58.3, 86.4 in the validation cohort, respectively (all P  <0.05). Conclusion The validated FVC%-based categorical predictor in anti-MDA5 positive DM-ILD is helpful for risk stratification in clinical practice and might facilitate cohort enrichment for future trials. [ABSTRACT FROM AUTHOR]

N6‐methyladenosine (m6A), as a eukaryotic mRNA modification catalyzed by methyltransferase METTL3, is involved in various processes of development or diseases via regulating RNA metabolism. However, the effect of METTL3‐mediated m6A modification in tooth development has remained elusive. Here we show that METTL3 is prevalently expressed in odontoblasts, dental pulp cells, dental follicle cells, and epithelial cells in Hertwig's epithelial root sheath during tooth root formation. Depletion of METTL3 in human dental pulp cells (hDPCs) impairs proliferation, migration, and odontogenic differentiation. Furthermore, conditional knockout of Mettl3 in Osterix‐expressing cells leads to short molar roots and thinner root dentin featured by decreased secretion of pre‐dentin matrix and formation of the odontoblast process. Mechanistically, loss of METTL3 cripples the translational efficiency of the key root‐forming regulator nuclear factor I‐C (NFIC). The odontogenic capacity of METTL3‐silenced hDPCs is partially rescued via overexpressing NFIC. Our findings suggest that m6A methyltransferase METTL3 is crucial for tooth root development, uncovering a novel epigenetic mechanism in tooth root formation. © 2020 American Society for Bone and Mineral Research (ASBMR). [ABSTRACT FROM AUTHOR]

Trauma rapidly mobilizes the immune response of surrounding tissues and activates regeneration program. Manipulating immune response to promote tissue regeneration shows a broad application prospect. However, the understanding of bone healing dynamics at cellular level remains limited. Here, we characterize the landscape of immune cells after alveolar bone injury and reveal a pivotal role of infiltrating natural killer T (NKT) cells. We observe a rapid increase in NKT cells after injury, which inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and impair alveolar bone healing. Cxcl2 is up-regulated in NKT cells after injury. Systemic administration of CXCL2-neutralizing antibody or genetic deletion of Cxcl2 improves the bone healing process. In addition, we fabricate a gelatin-based porous hydrogel to deliver NK1.1 depletion antibody, which successfully promotes alveolar bone healing. In summary, our study highlights the importance of NKT cells in the early stage of bone healing and provides a potential therapeutic strategy for accelerating bone regeneration.

Introduction: It remains unclear how the presence of renal involvement will affect the cardiovascular (CV) risk factors and complications in patients with SLE., Methods: We conducted a systematic review and meta-analysis using PubMed, EMBASE, MEDLINE and Scopus to identify studies published between 1947 and 2022 that evaluate the CV risk factors and complications in patients with SLE with or without lupus nephritis (LN)., Results: 58 studies were evaluated, with 22 two-arm studies (n=8675) included in two-arm meta-analysis and 45 studies (n=385 315) included in proportional meta-analysis. Patients with SLE with LN showed significantly higher risk of hypertension (HT) (OR=4.93, 95% CI=3.17 to 7.65, p<0.00001, I 2 =56%), hyperlipidaemia (OR=11.03, 95% CI=4.20 to 28.95, p<0.00001, I 2 =0%) and diabetes mellitus (DM) (OR=1.88, 95% CI=1.09 to 3.25, p=0.02, I 2 =32%) compared with those without LN. Patients with LN showed numerically higher prevalence of myocardial infarction (OR=1.35, 95% CI=0.53 to 3.45, p=0.52, I 2 =78%) and cerebrovascular accident (OR=1.64, 95% CI=0.79 to 3.39, p=0.27, I 2 =23%) than general patients with SLE. The incidence rates of CV mortality are also increased in patients with SLE with LN compared with those without LN (11.7/1000 patient-years vs 3.6/1000 patient-years)., Conclusion: Patients with SLE with LN show increased risk of CV risk factors including DM, HT and hyperlipidaemia. Early identification and optimal control of these CV risk factors may reduce the risk of CV disease and other non-CV complications., Prospero Registration Number: CRD42022314682., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

N6-methyladenosine (m 6 A), as a eukaryotic mRNA modification catalyzed by methyltransferase METTL3, is involved in various processes of development or diseases via regulating RNA metabolism. However, the effect of METTL3-mediated m 6 A modification in tooth development has remained elusive. Here we show that METTL3 is prevalently expressed in odontoblasts, dental pulp cells, dental follicle cells, and epithelial cells in Hertwig's epithelial root sheath during tooth root formation. Depletion of METTL3 in human dental pulp cells (hDPCs) impairs proliferation, migration, and odontogenic differentiation. Furthermore, conditional knockout of Mettl3 in Osterix-expressing cells leads to short molar roots and thinner root dentin featured by decreased secretion of pre-dentin matrix and formation of the odontoblast process. Mechanistically, loss of METTL3 cripples the translational efficiency of the key root-forming regulator nuclear factor I-C (NFIC). The odontogenic capacity of METTL3-silenced hDPCs is partially rescued via overexpressing NFIC. Our findings suggest that m 6 A methyltransferase METTL3 is crucial for tooth root development, uncovering a novel epigenetic mechanism in tooth root formation. © 2020 American Society for Bone and Mineral Research (ASBMR)., (© 2020 American Society for Bone and Mineral Research (ASBMR).)