The root architecture is crucial for the robust growth and nutrient absorption in cereals. However, it is urgent to identify the factors that simultaneously optimize root architecture and nutrient utilization in wheat. In this study, a beneficial role of the class II AP2/ERF transcription factor WHEAT FRIZZY PANICLE (WFZP) on lateral root number (LRN), root length (RL), and nitrogen utilization is revealed. In addition, interactors of WFZP including TaSYD are identified, as a subunit of the chromatin remodeling complex. The Tasyd mutants show a significant reduction in LRN, RL, and nitrogen uptake efficiency, resembling the phenotype of wfzp mutants. Furthermore, it is revealed that the WFZP-TaSYD module promotes the expression of root development and nitrate uptake-related genes by modulating chromatin accessibility and histone modifications. Finally, an elite allele (WFZP-A-I) associated with improved LRN and thousand-grain weight (TGW) is identified. Hence, these findings not only unveil the mechanisms underlying the coordination of root development and nitrogen uptake efficiency, but also provide valuable targets for breeding high-yield crops.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
Abstract The association between psoriasis and cardiovascular disease (CVD) has long been discussed and continually refined. However, there is currently a lack of prospective studies on the cardiovascular risk attributed to psoriasis in the United States general population. Representative adult participants were selected from the National Health and Nutrition Examination Survey (NHANES). Risks of cardiovascular symptoms and diseases prevalence were evaluated between participants with and without psoriasis. The hazards for all‐cause mortality and CVD mortality were stratified by psoriasis status. Mediation analysis was then conducted to identify potential mediators between psoriasis and cardiac death. Overall, 19 741 participants were included in the current study, 542 (2.7%) had psoriasis and 19 199 (97.3%) did not have psoriasis. After adjusting for known CVD risk factors, odds for hypertension (OR = 1.37, 95% CI: 1.13–1.66, p = 0.001), hypercholesterolemia (OR = 1.37, 95% CI: 1.13–1.64, p < 0.001) and angina pectoris (OR = 1.74, 95% CI: 1.11–2.60, p = 0.011) were higher in psoriasis patients. Compared with participants without psoriasis, moderate/severe but not mild patients showed significantly higher CVD mortality (HR = 2.55, 95% CI: 1.27–5.15, p = 0.009). This result was supported by subgroup analyses. Mediation analysis further suggested that the direct effect of moderate/severe psoriasis on CVD mortality accounted for 81.4% (65.8%–97.1%). Besides, the indirect effect might derive from disturbance of serum albumin, urea nitrogen and uric acid. Moderate‐to‐severe psoriasis is an independent risk factor for cardiovascular disease, making it necessary to regularly conduct cardiovascular disease‐related examinations for patients with higher severity of psoriasis in clinical settings.
Highlights•This study refines a model for limb reimplantation, improving blood flow obstruction and perfusion methods.•Hydrogen-rich infusion pre-perfusion demonstrates protective effects on the skeletal muscle of amputated limbs.•Hydrogen significantly mitigates oxidative stress injuries in the skeletal muscles of severed limbs.•Hydrogen activates the Nrf2/HO-1 signaling pathway in skeletal muscles within a limb reimplantation model.•The activation of the Nrf2/HO-1 pathway has an impact on Bax-mediated apoptosis.AbstractBackgroundIschaemia–reperfusion injury (IRI) is a critical complication post-limb replantation. The oxidative stress and cellular apoptosis due to IRI considerably hinder the healing process. This study aimed to investigate the modulatory effects of pre-perfusion with hydrogen-rich heparin sodium on the nuclear factor erythroid 2–related factor 2 (NRF2)/haeme oxygenase-1 (HO-1) pathway and its potential mechanisms in mitigating skeletal muscle IRI post-limb replantation.MethodsForty healthy Sprague–Dawley rats (250–300 g) were classified into five groups (n = 8 each): normal control, IRI + heparin sodium pre-perfusion (heparin group), IRI + hydrogen-rich heparin sodium pre-perfusion (hydrogen-rich heparin group), IRI + hydrogen-rich heparin sodium pre-perfusion + NRF2 inhibitor (hydrogen-rich heparin + all-trans retinoic acid [ATRA] group), and IRI + heparin sodium pre-perfusion + NRF2 inhibitor (heparin + ATRA group). The activation of the NRF2/HO-1 pathway in skeletal muscle IRI was evaluated based on HO-1 expression using western blotting and immunofluorescence. Furthermore, haematoxylin and eosin staining and transmission electron microscopy were employed to determine the histopathological characteristics. Additionally, superoxide dismutase and malondialdehyde levels in skeletal muscle tissue were measured to assess antioxidant capacity and the degree of oxidative stress damage. Tissue hypoxia was assessed based on hypoxia-inducible factor 1-alpha expression, whereas apoptosis markers BCL-2-associated X protein (BAX) and Caspase-3 in skeletal muscle tissues were analysed using western blotting with terminal deoxynucleotidyl transferase dUTP nick end labelling staining to quantify cell apoptosis.ResultsCompared with the control group, the heparin group exhibited significant pathological changes, including inflammatory infiltration and cellular hypertrophy, with increased apoptosis and oxidative stress. Notably, NRF2 suppression aggravated these effects. However, hydrogen-rich heparin sodium prominently activated the NRF2/HO-1 pathway, enhancing antioxidant defence and reducing BAX/Caspase-3-mediated apoptosis, thereby mitigating IRI-induced damage. The use of an NRF2 inhibitor to inhibit NRF2 excitation by hydrogen-rich heparin sodium notably weakened NRF2 activation and the antioxidant response, resulting in a substantial increase in cellular apoptosis.ConclusionPre-perfusion with hydrogen-rich heparin sodium markedly diminishes the BAX/Caspase-3-mediated apoptotic pathway in skeletal muscle tissues with IRI through the excitation of the NRF2/HO-1 pathway.Graphical abstractMechanism underlying the molecular action of hydrogen.
Background: People do experience stress throughout their lifetime, and it is associated with chronic diseases. However, it remains unclear whether life stress is associated with uric acid metabolism and related gout.Methods: In UK Biobank, 361481 participants that reported stressful life events in the past 2 years, completed serum urate test, and passed genotype quality control were included in the cross-sectional study. 353928 participants without gout at baseline were included in the prospective cohort. A urate-related polygenic risk score based on 114 single-nucleotide polymorphisms was calculated for abnormal serum uric acid metabolism and gout. Binary logistic regression and cox proportional hazards models were separately used for the cross-sectional study and the prospective cohort to investigate the association between life stress and abnormal serum uric acid metabolism and gout.Findings: Compared with those who did not experience any stressful life events, people who experienced single (1), dual (2), and multiple (3-6) stressful life events were 1.05(95%CI, 1.03-1.07), 1.08(95%CI, 1.04-1.12), and 1.25(95%CI, 1.17-1.33) higher in abnormal serum uric acid levels odds, respectively. And those experienced single (1), dual (2), and multiple (3-6) stressful life events were 1.07(95%CI, 1.01-1.13), 1.17(95%CI, 1.07-1.28), and 1.34(95%CI, 1.15-1.57) higher risk in gout onset during the median follow-up of 13.0 years. Specifically, people who experienced serious illness, injury or assault, death of a spouse or partner, and financial difficulties were more able to get abnormal serum uric acid levels (OR, 1.21; 95%CI, 1.17-1.25; OR, 1.10; 95%CI, 1.01-1.19; OR, 1.13; 95%CI, 1.09-1.17) and develop into gout (HR, 1.29; 95%CI, 1.20-1.39; HR, 1.10; 95%CI, 1.01-1.20; HR, 1.13; 95%CI, 1.05-1.23) in the future. Urate-related genetic risk did not modify the association between life stress and abnormal serum uric acid levels and gout.Interpretation: Life stress was associated with uric acid metabolism and would increase the risk of future gout onset.Funding: The Key Project of National Natural Science Foundation of China (81830117), the Joint Funds of National Natural Science Foundation of China (U22A20365), the Scientific Research Fund of Yangjiang People's Hospital, China (2021002, 2021003, G2021004).Declaration of Interest: The authors declare that the research does not have any commercial or financial conflicts of interest related to the publication of this paper and have signed their consent for publishing the article.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
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