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Chlorophyll a fluorescence induction kinetics (CFI) is an important tool that reflects the photosynthetic function of leaves, but it remains unclear whether it is affected by leaf structure. Therefore, in this study, the leaf structure and CFI curves of sunflower and sorghum seedlings were analyzed. Results revealed that there was a significant difference between the structures of palisade and spongy tissues in sunflower leaves. Their CFI curves, measured on both the adaxial and abaxial sides, also differed significantly. However, the differences in the leaf structures and CFI curves between both sides of sorghum leaves were not significant. Further analysis revealed that the differences in the CFI curves between the adaxial and abaxial sides of sunflower leaves almost disappeared due to reduced incident light scattering and refraction in the leaf tissues; more importantly, changes in the CFI curves of the abaxial side were greater than the adaxial side. Compared to leaves grown under full sunlight, weak light led to decreased differences in the CFI curves between the adaxial and abaxial sides of sunflower leaves; of these, changes in the CFI curves and palisade tissue structure on the adaxial side were more obvious than on the abaxial side. Therefore, it appears that large differences in sunflower leaf structures may affect the shape of CFI curves. These findings lay a foundation for enhancing our understanding of CFI from a new perspective.

Background Central post-stroke pain (CPSP) is an intractable and disabling central neuropathic pain that severely affects patients’ lives, well-being, and socialization abilities. However, CPSP has been poorly studied mechanistically and its treatment remains challenging. Here, we used a rat model of CPSP induced by thalamic hemorrhage to investigate its underlying mechanisms and the effect of stellate ganglion block (SGB) on CPSP and emotional comorbidities. Methods Thalamic hemorrhage was produced by injecting collagenase IV into the ventral-posterolateral nucleus (VPL) of the right thalamus. The up-and-down method with von Frey hairs was used to measure the mechanical allodynia. Behavioral tests were carried out to examine depressive and anxiety-like behaviors including the open field test (OFT), elevated plus maze test (EPMT), novelty-suppressed feeding test (NSFT), and forced swim test (FST). The peri-thalamic lesion tissues were collected for immunofluorescence, western blotting, and enzyme-linked immunosorbent assay (ELISA). Genetic knockdown of thalamic hypoxia-inducible factor-1α (HIF-1α) and NOD-like receptor thermal protein domain associated protein 3 (NLRP3) with microinjection of HIF-1α siRNA and NLRP3 siRNA into the VPL of thalamus were performed 3 days before collagenase injection into the same regions. Microinjection of lificiguat (YC-1) and MCC950 into the VPL of thalamus were administrated 30 min before the collagenase injection in order to inhibited HIF-1α and NLRP3 pharmacologically. Repetitive right SGB was performed daily for 5 days and laser speckle contrast imaging (LSCI) was conducted to examine cerebral blood flow. Results Thalamic hemorrhage caused persistent mechanical allodynia and anxiety- and depression-like behaviors. Accompanying the persistent mechanical allodynia, the expression of HIF-1α and NLRP3, as well as the activities of microglia and astrocytes in the peri-thalamic lesion sites, were significantly increased. Genetic knockdown of thalamic HIF-1α and NLRP3 significantly attenuated mechanical allodynia and anxiety- and depression-like behaviors following thalamic hemorrhage. Further studies revealed that intra-thalamic injection of YC-1, or MCC950 significantly suppressed the activation of microglia and astrocytes, the release of pro-inflammatory cytokines, the upregulation of malondialdehyde (MDA), and the downregulation of superoxide dismutase (SOD), as well as mechanical allodynia and anxiety- and depression-like behaviors following thalamic hemorrhage. In addition, repetitive ipsilateral SGB significantly restored the upregulated HIF-1α/NLRP3 signaling and the hyperactivated microglia and astrocytes following thalamic hemorrhage. The enhanced expression of pro-inflammatory cytokines and the oxidative stress in the peri-thalamic lesion sites were also reversed by SGB. Moreover, LSCI showed that repetitive SGB significantly increased cerebral blood flow following thalamic hemorrhage. Most strikingly, SGB not only prevented, but also reversed the development of mechanical allodynia and anxiety- and depression-like behaviors induced by thalamic hemorrhage. However, pharmacological activation of thalamic HIF-1α and NLRP3 with specific agonists significantly eliminated the therapeutic effects of SGB on mechanical allodynia and anxiety- and depression-like behaviors following thalamic hemorrhage. Conclusion This study demonstrated for the first time that SGB could improve CPSP with comorbid anxiety and depression by increasing cerebral blood flow and inhibiting HIF-1α/NLRP3 inflammatory signaling.

Mesenchymal stem/stromal cells (MSCs) derived from placental tissue show great therapeutic potential and have been used in medical treatment, but the similarity and differences between the MSCs derived from various parts of the placenta remain unclear. In this study, we compared MSCs derived from different perinatal tissues, including the umbilical cord (UC), amniotic membrane (AM), chorionic plate (CP) and decidua parietalis (DP). Using human leukocyte antigen (HLA) typing and karyotype analysis, we found that the first three cell types were derived from the foetus, while the MSCs from the decidua parietalis were derived from the maternal portion of the placental tissue. Our results indicate that both foetal and maternal MSCs share a similar phenotype and multi-lineage differentiation potential, but foetal MSCs show a significantly higher expansion capacity than do maternal MSCs. Furthermore, MSCs from all sources showed significant differences in the levels of several paracrine factors.

To reveal the global regulation of photosynthetic electron transport (PET) in shade plants, the changes in chlorophyll a fluorescence induction kinetics (CFI) curves and proteomics were investigated using Hosta varieties. There was a significant difference in CFI curves between Hosta ‘Fire Island’ and other varieties (such as Hosta ‘Sum and Substance’) grown under weak light. Weak light induced the appearance of the W phase of CFI curves in the two varieties, which was consistent with a clear decrease in the oxygen-evolving complex and a large upregulation of photosystem (PS) II proteins. In Hosta ‘Fire Island’, the O-J rise of the CFI curves increased faster under weak light than under appropriate light, and this was not only accompanied by a large upregulation of the PS II protein but also a great downregulation in cytochrome b6/f, plastocyanin, and PS I. Moreover, weak light resulted in a considerable increase in photosynthetic rate and Rubisco abundance in Hosta ‘Fire Island’, yet the non-photochemical quenching and abundance of CP24 declined significantly. By contrast, weak light had fewer effects on these parameters in Hosta ‘Sum and Substance’. Therefore, we suggest that the PET is mainly affected by the abundance of PS II, oxygen-evolving complex, cytochrome b6/f, plastocyanin, and PS I in Hosta plants grown under weak light; meanwhile, the improved photosynthetic capacity under weak light was mainly related to the enhancement of light energy absorption and capture of PS II as well as the increase in the abundance of Rubisco.

Balanced steady-state free processing (bSSFP) MR sequence has long been considered the gold standard method for ventricular function assessment (VFA), and normal values are based on this acquisition. However, bSSFP sequence suffers from susceptibility artifacts due to scenarios such as cardiac implants. The T1-TFE sequence, also known as ultrafast spoiled gradient sequence, is less affected by such susceptibility artifacts. While it is unclear if T1-TFE sequence yields similar VFA results as the bSSFP sequence. To validate if the T1-TFE sequence, with an intravascular blood pool contrast agent, yields similar results for VFA as the gold-standard non-contrast bSSFP approach, so that the T1-TFE sequence can be used for VFA when bSSFP approach fails. Two sets of images from two different sequences were utilized in this study. T1-TFE (with contrast) scans were used as one while bSSFP-derived images were used as the other. 37 pediatric patients were recruited into this study. Semi-automated software (cvi42) was used to segment and derive ventricular volumes. Image quality was objectively assessed by comparing signal-to-noise (SNR) and contrast-to-noise ratio (CNR) scores. Last, two expert readers provided a subjective analysis of image quality. Paired t-tests were used to assess significant differences in volumetric values (end-diastolic and end-systolic) between T1-TFE and bSSFP sequences. A Bland-Altman analysis evaluated potential bias and agreement between these sequences. Ventricular function assessment via volumetric data analysis resulted in no statistically significant differences (P > 0.05), and high R2 values. SNR and CNR scores also presented with no statistically significant differences (P > 0.05), and nearly identical scores (SNR T1-TFE mean: 29.5 ± 3.1, SNR bSSFP mean: 28.8 ± 3.7, CNR T1-TFE mean: 28.8 ± 3.3, CNR bSSFP mean: 28.1 ± 4.0). Image quality assessment via expert subjective image analysis scores is consistent with the data. All Bland-Altman plots show good agreement and reveal no systematic bias or random error. T1-TFE sequences in combination with Ferumoxytol allow reliable ventricular function assessment and overcome the limitations of traditional bSSFP MR sequences in this context.

Rheumatoid arthritis (RA) is a chronic autoimmune disease of complex aetiology in which adaptive immune responses mediated by T cells play a major role in driving synovial inflammation and joint damage.1 Before developing effector functions, naïve T cells are conventionally understood to require an initial antigen-specific stimulus transduced through their T cell receptor (TCR). TCR-mediated recognition is also required for targeted cell lysis by cytotoxic T cells. Previous studies have sought to characterise the functional roles of various T cell populations in RA, and have demonstrated patterns of oligoclonal expansion among them.2 It has also been shown that some T cell clones may be shared among multiple patients as a public repertoire.3 However, the antigen specificities of synovial T cells remain poorly studied outside of a few epitopes, and open resources of TCRs and repertoires associated with RA are lacking.

ContextPreeclampsia is a leading cause of fetal and maternal morbidity and mortality during pregnancy. Although the etiology of preeclampsia is unknown, preeclampsia offspring have increased risks of developing cardiovascular disorders in adulthood, implicating that preeclampsia programs fetal vasculature in utero.ObjectiveWe hypothesize that preeclampsia alters expression profiles of endothelial microRNAs (miRNAs) in fetal endothelial cells and disturbs the vascular endothelial growth factor A (VEGFA)- and fibroblast growth factor 2 (FGF2)-induced endothelial function.Design and SettingUnpassaged (P0) human umbilical vein endothelial cells (HUVECs) were isolated immediately after cesarean-section delivery from normotensive (NT) and preeclamptic (PE) pregnancies. Differentially expressed miRNAs between P0-HUVECs from NT and PE pregnancies were identified using a miRNA polymerase chain reaction (PCR) array and confirmed using reverse transcription quantitative PCR. To determine the function of these differentially expressed miRNAs, miRNAs of interest were knocked down in NT-HUVECs following by cell functional assays.ResultsSixteen miRNAs, including miR-29a/c-3p, were downregulated in P0-HUVECs from the PE group compared with the NT group. Bioinformatics analysis predicted the PI3K–v-akt murine thymoma viral oncogene homolog 1 (AKT) signaling pathway was dysregulated in P0-HUVECs from the PE group, which was associated with the miR-29a/c-3p downregulation. We further demonstrated that miR-29a/c-3p knockdown inhibited the VEGFA- and FGF2-induced endothelial migration as well as FGF2-induced AKT1 phosphorylation in HUVECs. However, miR-29a/c-3p knockdown did not alter the extracellular signal-regulated kinase 1/2 phosphorylation, cell proliferation, and endothelial monolayer integrity in response to VEGFA and FGF2 in HUVECs.ConclusionsPreeclampsia-downregulated miR-29a/c-3p may impair fetal endothelial function by disturbing the FGF2-activated PI3K-AKT signaling pathway, hence inhibiting endothelial cell migration.Preeclampsia downregulates 16 miRNAs, including miR-29a/c-3p, in fetal endothelial cells, which may impair fetal endothelial cell migration by disturbing the FGF2-stimulated PI3K-AKT1 pathway.

Myocardial infarction (MI) is a coronary artery-related disease and ranks as the leading cause of sudden death globally. Resveratrol (Res) is a bioactive component and has presented antioxidant, anti-inflammatory and anti-microbial properties. However, the effect of Res on ferroptosis during MI progression remains elusive. Here, we aimed to explore the function of Res in the regulation of ferroptosis and myocardial injury in MI. We observed that the treatment of Res attenuated the MI-related myocardium injury and fibrosis in the rats. The expression of collagen 1 and α-SMA was induced in MI rats, in which the treatment of Res could decrease the expression. Treatment of Res suppressed the levels of IL-6 and IL-1β in MI rats. The GSH levels were inhibited and MDA, lipid ROS, and Fe 2+ levels were induced in MI rats, in which the treatment of Res could reverse the phenotypes. Meanwhile, the expression of GPX4 and SLC7A11 was reduced in MI rats, while the treatment of Res could rescue the expression in the model. Meanwhile, Res relieved oxygen-glucose deprivation (OGD)-induced cardiomyocyte injury. Importantly, Res repressed OGD-induced cardiomyocyte ferroptosis in vitro . Mechanically, we identified that Res was able to enhance GPX4 expression by inducing KAT5 expression. We confirmed that KAT5 alleviated OGD-induced cardiomyocyte injury and ferroptosis. The depletion of KAT5 or GPX4 could reverse the effect of Res on OGD-induced cardiomyocyte injury. Thus, we concluded that Res attenuated myocardial injury by inhibiting ferroptosis via inducing KAT5/GPX4 in myocardial infarction. Our finding provides new evidence of the potential therapeutic effect of Res on MI by targeting ferroptosis.

[Display omitted] •Combining α-C-GC with aluminum hydroxide boosts T-cell responses to SARS-CoV-2 RBD-Fc protein.•αGC-CPOEt and aluminum hydroxide synergistically enhance neutralizing antibody responses.•Structural modifications of αGC for better interaction with aluminum hydroxide do not improve adjuvant efficacy over natural αGC. Protein-based subunit vaccines like RBD-Fc are promising tools to fight COVID-19. RBD-Fc fuses the receptor-binding domain (RBD) of the SARS-CoV-2 virus spike protein with the Fc region of human IgG1, making it more immunogenic than RBD alone. Earlier work showed that combining RBD-Fc with iNKT cell agonists as adjuvants improved neutralizing antibodies but did not sufficiently enhance T cell responses, a limitation RBD-Fc vaccines share with common adjuvants. Here we demonstrate that aluminum hydroxide combined with α-C-GC, a C-glycoside iNKT cell agonist, significantly improved the RBD-Fc vaccine’s induction of RBD-specific T-cell responses. Additionally, aluminum hydroxide with α-GC-CPOEt, a phosphonate diester derivative, synergistically elicited more robust neutralizing antibodies. Remarkably, modifying αGC with phosphate (OPO3H2) or phosphonate (CPO3H2) to potentially enhance aluminum hydroxide interaction did not improve efficacy over unmodified αGC with aluminum hydroxide. These findings underscore the straightforward yet potent potential of this approach in advancing COVID-19 vaccine development and provide insights for iNKT cell-based immunotherapy.