Determination of anthracnose (Colletotrichum fructicola) resistance mechanism using transcriptome analysis of resistant and susceptible pear (Pyrus pyrifolia).

BACKGROUND: Anthracnose, mainly caused by Colletotrichum fructicola, leads to severe losses in pear production. However, there is limited information available regarding the molecular response to anthracnose in pears. RESULTS: In this study, the anthracnose-resistant variety 'Seli' and susceptible pear cultivar 'Cuiguan' were subjected to transcriptome analysis following C. fructicola inoculation at 6 and 24 h using RNA sequencing. A total of 3186 differentially expressed genes were detected in 'Seli' and 'Cuiguan' using Illumina sequencing technology. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses indicated that the transcriptional response of pears to C. fructicola infection included responses to reactive oxygen species, phytohormone signaling, phenylpropanoid biosynthesis, and secondary metabolite biosynthetic processes. Moreover, the mitogen-activated protein kinase (MAPK) signaling pathway and phenylpropanoid biosynthesis were involved in the defense of 'Seli'. Furthermore, the gene coexpression network data showed that genes related to plant-pathogen interactions were associated with C. fructicola resistance in 'Seli' at the early stage. CONCLUSION: Our results showed that the activation of specific genes in MAPK, calcium signaling pathways and phenylpropanoid biosynthesis was highly related to C. fructicola resistance in 'Seli' and providing several potential candidate genes for breeding anthracnose-resistant pear varieties.

PbbHLH155 enhances iron deficiency tolerance in pear by directly activating PbFRO2 and PbbHLH38.

Iron (Fe) deficiency is a general stress for many horticulture crops, causing leaf chlorosis and stunted growth. The basic-helix-loop-helix (bHLH) transcription factor (TF) was reported to function in Fe absorption; however, the regulatory mechanism of bHLH genes on iron absorption remains largely unclear in pear. In this study, we found that PbbHLH155 was significantly induced by Fe deficiency. Overexpression of PbbHLH155 in Arabidopsis thaliana and pear calli significantly increases resistance to Fe deficiency. The PbbHLH155-overexpressed Arabidopsis lines exhibited greener leaf color, higher Fe content, stronger Fe chelate reductase (FCR) and root acidification activity. The PbbHLH155 knockout pear calli showed lower Fe content and weaker FCR activity. Interestingly, PbbHLH155 inhibited the expressions of PbFRO2 and PbbHLH38, which were positive regulators in Fe-deficiency responses (FDR). Furthermore, yeast one-hybrid (Y1H) and Dual-Luciferase Reporter (DLR) assays revealed that PbbHLH155 directly binds to the promoters of PbFRO2 and PbbHLH38, thus activating their expression. Overall, our results showed that PbbHLH155 directly promote the expression of PbFRO2 and PbbHLH38 to activate FCR activity for iron absorption. This study provided valuable information for pear breeding.

Application of 3D­printed porous titanium interbody fusion cage vs. polyether ether ketone interbody fusion cage in anterior cervical discectomy and fusion: A systematic review and meta­analysis update.

The present study aimed to compare the differences between 3D-printed porous titanium and polyether ether ketone (PEEK) interbody fusion cages for anterior cervical discectomy and fusion (ACDF). Literature on the application of 3D-printed porous titanium and PEEK interbody fusion cages for ACDF was searched in the PubMed, Web of Science, Embase, China National Knowledge Infrastructure, Wanfang and VIP databases. A total of 1,181 articles were retrieved and 12 were finally included. The Cochrane bias risk assessment criteria and Newcastle-Ottawa scale were used for quality evaluation and Review Manager 5.4 was used for data analysis. The 3D cage group was superior to the PEEK cage group in terms of operative time [mean difference (MD): -7.68; 95% confidence interval (CI): -11.08, -4.29; P<0.00001], intraoperative blood loss (MD: -6.17; 95%CI: -10.56, -1.78; P=0.006), hospitalization time (MD: -0.57; 95%CI: -0.86, -0.28: P=0.0001), postoperative complications [odds ratio (OR): 0.35; 95%CI: 0.15, 0.80; P=0.01], C2-7 Cobb angle (MD: 2.85; 95%CI: 1.45, 4.24; P<0.0001), intervertebral space height (MD: 1.20; 95%CI: 0.54, 1.87; P=0.0004), Japanese Orthopaedic Association Assessment of Treatment (MD: 0.69; 95%CI: 0.24, 1.15; P=0.003) and visual analogue scale score (MD: -0.43; 95%CI: -0.78, -0.07; P=0.02). The difference was statistically significant, while there was no significant difference between the two groups in terms of fusion rate (OR: 1.74; 95%CI: 0.71, 4.27; P=0.23). The use of 3D-printed porous titanium interbody fusion cage in ACDF has the advantages of short operation time, less bleeding loss, shorter hospitalization time and fewer postoperative complications. It can better maintain the cervical curvature and intervertebral height, relieve pain and accelerate postoperative functional recovery.

Sporotrichosis Mimicking Rosacea Lesions: A Case Report.

Sporotrichosis is a subacute or chronic infectious disease caused by sporothrix. It is mainly caused by Sporothrix inoculation after accidental skin injury during human labor. The clinical manifestations of sporotrichosis are variable, ranging from nodules, plaques, ulcers, verrucous lesions, and subcutaneous masses. Some reports indicate that sporotrichosis can mimic psoriasis-like lesions. We herein report a case of sporotrichosis mimicking rosacea lesions. In addition, the patient had a history of nasal trauma, and we believe that the patient was inoculated with Sporothrix after the nasal skin was damaged during labor activities. The patient was given itraconazole 200 mg orally daily for 3 months, which effectively resolved the rash.

Cardiolipin oxidized by ROS from complex II acts as a target of gasdermin D to drive mitochondrial pore and heart dysfunction in endotoxemia.

Cardiac dysfunction, an early complication of endotoxemia, is the major cause of death in intensive care units. No specific therapy is available at present for this cardiac dysfunction. Here, we show that the N-terminal gasdermin D (GSDMD-N) initiates mitochondrial apoptotic pore and cardiac dysfunction by directly interacting with cardiolipin oxidized by complex II-generated reactive oxygen species (ROS) during endotoxemia. Caspase-4/11 initiates GSDMD-N pores that are subsequently amplified by the upregulation and activation of NLRP3 inflammation through further generation of ROS. GSDMD-N pores form prior to BAX and VDAC1 apoptotic pores and further incorporate into BAX and VDAC1 oligomers within mitochondria membranes to exacerbate the apoptotic process. Our findings identify oxidized cardiolipin as the definitive target of GSDMD-N in mitochondria of cardiomyocytes during endotoxin-induced myocardial dysfunction (EIMD), and modulation of cardiolipin oxidation could be a therapeutic target early in the disease process to prevent EIMD.

Evaluation of genetic polymorphisms in TNF­α­308G/A rs1800629 associated with susceptibility and severity of rheumatoid arthritis: A systematic review and meta­analysis.

To investigate the association of gene polymorphisms of TNF-α-308G/A rs1800629 with the susceptibility and severity of rheumatoid arthritis (RA), literature from PubMed, EMBASE, Web of Science and CNKI databases was searched. Two authors screened the literature independently, extracted data and evaluated the risk of bias of the included studies. According to the inclusion and exclusion criteria, five genetic models were established: The allelic model (A vs. G), dominant model (GA + AA vs. GG), recessive model (AA vs. GG + GA), co-dominant model (AA vs. GG) and super-dominant model (GG + AA vs. GA). Stata 17.0 software was used for the meta-analysis. A total of 34 eligible studies with 12,611 subjects were included, including 6,030 cases in the RA group and 6,581 controls. Meta-analysis calculations revealed that the genetic polymorphisms of TNF-α-308G/A rs1800629 were not significantly associated with susceptibility to RA, with an odds ratio and 95% confidence interval (CI) for each genetic model [A vs. G: 0.937 (0.762-1.152); GA + AA vs. GG: 0.918 (0.733-1.148); AA vs. GG + GA: 1.131 (0.709-1.802); AA vs. GG: 1.097 (0.664-1.813); and GG + AA vs. GA: 1.108 (0.894-1.373)]. For the association between TNF-α-308G/A rs1800629 gene polymorphisms and the severity of RA, the results of subgroup analysis calculations showed that TNF-α-308G/A rs1800629 gene polymorphisms were associated with the severity of RA in European populations, with the gene model and 95% CI [GA + AA vs. GG: 0.503 (0.297-0.853); and GG + AA vs. GA: 2.268 (1.434-3.590)]. When assessing the confidence in the positive results of the present study through the false-positive report probability, the positive results were observed to be reliable. No significant association was observed between genetic polymorphisms in TNF-α-308G/A rs1800629 and susceptibility to RA. However, a significant association exists with the severity of RA in European populations.

The dysregulated autophagy in osteoarthritis: Revisiting molecular profile.

The risk factors of osteoarthritis (OA) are different and obesity, lifestyle, inflammation, cell death mechanisms and diabetes mellitus are among them. The changes in the biological mechanisms are considered as main regulators of OA pathogenesis. The dysregulation of autophagy is observed in different human diseases. During the pathogenesis of OA, the autophagy levels (induction or inhibition) change. The supportive and pro-survival function of autophagy can retard the progression of OA. The protective autophagy prevents the cartilage degeneration. Moreover, autophagy demonstrates interactions with cell death mechanisms and through inhibition of apoptosis and necroptosis, it improves OA. The non-coding RNA molecules can regulate autophagy and through direct and indirect control of autophagy, they dually delay/increase OA pathogenesis. The mitochondrial integrity can be regulated by autophagy to alleviate OA. Furthermore, therapeutic compounds, especially phytochemicals, stimulate protective autophagy in chondrocytes to prevent cell death. The protective autophagy has ability of reducing inflammation and oxidative damage, as two key players in the pathogenesis of OA.

SlMYC2 promotes SlLBD40-mediated cell expansion in tomato fruit development.

As a plant-specific transcription factor, lateral organ boundaries domain (LBD) protein was reported to regulate plant growth and stress response, but the functional research of subfamily II genes is limited. SlMYC2, a master regulator of Jasmonic acid response, has been found to exhibit high expression levels in fruit and has been implicated in the regulation of fruit ripening and resistance to Botrytis. However, its role in fruit expansion remains unknown. In this study, we present evidence that a subfamily II member of LBD, namely SlLBD40, collaborates with SlMYC2 in the regulation of fruit expansion. Overexpression of SlLBD40 significantly promoted fruit growth by promoting mesocarp cell expansion, while knockout of SlLBD40 showed the opposite result. Similarly, SlMYC2 knockout resulted in a significant decrease in cell expansion within the fruit. Genetic analysis indicated that SlLBD40-mediated cell expansion depends on the expression of SlMYC2. SlLBD40 bound to the promoter of SlEXPA5, an expansin gene, but did not activate its expression directly. While, the co-expression of SlMYC2 and SlLBD40 significantly stimulated the activation of SlEXPA5, leading to an increase in fruit size. SlLBD40 interacted with SlMYC2 and enhanced the stability and abundance of SlMYC2. Furthermore, SlMYC2 directly targeted and activated the expression of SlLBD40, which is essential for SlLBD40-mediated fruit expansion. In summary, our research elucidates the role of the interaction between SlLBD40 and SlMYC2 in promoting cell expansion in tomato fruits, thus providing novel insights into the molecular genetics underlying fruit growth.

Genome-wide identification of GA2ox genes family and analysis of PbrGA2ox1-mediated enhanced chlorophyll accumulation by promoting chloroplast development in pear.

BACKGROUND: Chlorophyll (Chl) is an agronomic trait associated with photosynthesis and yield. Gibberellin 2-oxidases (GA2oxs) have previously been shown to be involved in Chl accumulation. However, whether and how the PbrGA2ox proteins (PbrGA2oxs) mediate Chl accumulation in pear (Pyrus spp.) is scarce. RESULTS: Here, we aimed to elucidate the role of the pear GA2ox gene family in Chl accumulation and the related underlying mechanisms. We isolated 13 PbrGA2ox genes (PbrGA2oxs) from the pear database and identified PbrGA2ox1 as a potential regulator of Chl accumulation. We found that transiently overexpressing PbrGA2ox1 in chlorotic pear leaves led to Chl accumulation, and PbrGA2ox1 silencing in normal pear leaves led to Chl degradation, as evident by the regreening and chlorosis phenomenon, respectively. Meanwhile, PbrGA2ox1-overexpressing (OE) tobacco plants discernably exhibited Chl built-up, as evidenced by significantly higher Pn and Fv/Fm. In addition, RNA sequencing (RNA-seq), physiological and biochemical investigations revealed an increase in abscisic acid (ABA), methyl jasmonate (MeJA), and salicylic acid (SA) concentrations and signaling pathways; a marked elevation in reducing and soluble sugar contents; and a marginal decline in the starch and sucrose levels in OE plants. Interestingly, PbrGA2ox1 overexpression did not prominently affect Chl synthesis. However, it indeed facilitated chloroplast development by increasing chloroplast number per cell and compacting the thylakoid granum stacks. These findings might jointly contribute to Chl accumulation in OE plants. CONCLUSION: Overall, our results suggested that GA2oxs accelerate Chl accumulation by stimulating chloroplast development and proved the potential of PbrGA2ox1 as a candidate gene for genetically breeding biofortified pear plants with a higher yield.

Assessing inter-intraspecific variability of leaf vulnerability to embolism for 10 alpine Rhododendron species growing in Southwestern China.

Alpine Rhododendron species are prominent constituents and renowned ornamental plants in alpine ecosystems. Consequently, evaluating the genetic variation in embolism resistance within the genus Rhododendron and predicting their adaptability to future climate change is important. Nevertheless, the assessment of embolism resistance in Rhododendron species remains limited. This investigation aimed to examine leaf vulnerability to embolism across ten alpine Rhododendron species, which are frequently employed as ornamental species in Rhododendron forests in Southwest China. The study analyzed the correlation between embolism resistance and various morphological traits, while also conducting water control experiments to evaluate the relationship between embolism resistance and drought resistance. The outcomes indicated pronounced variations in leaf vulnerability to embolism among species, as reflected by the water potential at 50% of embolized pixels (P50 ). Furthermore, the leaf P50 exhibited a significant positive correlation with vessel diameter (D) (R2 = 0.44, P = 0.03) and vessel wall span (b) (R2 = 0.64, P = 0.005), while displaying a significant negative correlation with vessel reinforcement ((t/b)2 ) (R2 = 0.67, P = 0.004). These findings underscore the reliability of selecting species based on embolism vulnerability to preserve the diversity of alpine ecosystems and foster resilience to climate change.

Transcriptome Analysis Reveals Key Genes Involved in the Response of Pyrus betuleafolia to Drought and High-Temperature Stress.

Drought and high-temperature stress are the main abiotic stresses that alone or simultaneously affect the yield and quality of pears worldwide. However, studies on the mechanisms of drought or high-temperature resistance in pears remain elusive. Therefore, the molecular responses of Pyrus betuleafolia, the widely used rootstock in pear production, to drought and high temperatures require further study. Here, drought- or high-temperature-resistant seedlings were selected from many Pyrus betuleafolia seedlings. The leaf samples collected before and after drought or high-temperature treatment were used to perform RNA sequencing analysis. For drought treatment, a total of 11,731 differentially expressed genes (DEGs) were identified, including 4444 drought-induced genes and 7287 drought-inhibited genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that these DEGs were more significantly enriched in plant hormone signal transduction, flavonoid biosynthesis, and glutathione metabolism. For high-temperature treatment, 9639 DEGs were identified, including 5493 significantly upregulated genes and 4146 significantly downregulated genes due to high-temperature stress. KEGG analysis showed that brassinosteroid biosynthesis, arginine metabolism, and proline metabolism were the most enriched pathways for high-temperature response. Meanwhile, the common genes that respond to both drought and high-temperature stress were subsequently identified, with a focus on responsive transcription factors, such as MYB, HSF, bZIP, and WRKY. These results reveal potential genes that function in drought or high-temperature resistance. This study provides a theoretical basis and gene resources for the genetic improvement and molecular breeding of pears.

Different modalities of patellar management in primary total knee arthroplasty: a Bayesian network meta-analysis of randomized controlled trials.

BACKGROUND: The primary management modalities for the patella in TKA include patellar resurfacing, patellar non-resurfacing, patellar resurfacing with denervation, and patellar non-resurfacing with denervation. Traditionally, meta-analyses have predominantly focused on examining comparisons between two management modalities. However, this study performed a network meta-analysis to compare all four patellar management interventions to identify the most optimal approach for patellar management in TKA. METHODS: A computer-based search of PubMed, China National Knowledge Infrastructure (CNKI), The Cochrane Library, Web of science, Embase, and MEDLINE databases was performed to identify randomized controlled trials focusing on the four management interventions for the patella in TKA. Comparisons included two-by-two comparisons as well as those involving more than two concurrent comparisons. The search timeframe spanned from inception to June 30, 2023. Two independent authors extracted the data and evaluated the quality of the literature. The Cochrane Collaboration Risk of Bias (ROB) tool was used to evaluate the overall quality of the literature. Subsequently, a network meta-analysis was conducted using the "gemtc" package of the R-4.2.3 software. Outcome measures such as anterior knee pain (AKP), reoperation rate, and patient satisfaction rate were evaluated using odd ratio (OR) and 95% confidence intervals (CI). Additionally, the knee society score (KSS), function score (FS), and range of motion (ROM) were evaluated using mean differences (MD) with associated 95% CI. The different treatment measures were ranked using the surfaces under the cumulative ranking curves (SUCRA). RESULTS: A total of 50 randomized controlled trials involving 9,283 patients were included in the analysis. The findings from this network meta-analysis revealed that patellar resurfacing exhibited significantly lower postoperative reoperation rate (OR 0.44, 95% CI 0.24-0.63) and AKP (OR 0.58, 95% CI 0.32-1) compared to non-resurfacing. Additionally, patellar resurfacing exhibited higher postoperative KSS clinical scores in comparison with non-resurfacing (MD: 1.13, 95% CI 0.18-2.11). However, for postoperative FS, ROM, and patient satisfaction, no significant differences were observed among the four management interventions. CONCLUSION: Patellar resurfacing emerges as the optimal management modality in primary TKA. However, future studies should aim to reduce sources of heterogeneity and minimize the influence of confounding factors on outcomes. SYSTEMATIC REVIEW REGISTRATION: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023434418 identifier: CRD42023434418.

Serine 31 Phosphorylation-Driven Regulation of AGPase Activity: Potential Implications for Enhanced Starch Yields in Crops.

ADP-Glc pyrophosphorylase (AGPase), which catalyzes the transformation of ATP and glucose-1-phosphate (Glc-1-P) into adenosine diphosphate glucose (ADP-Glc), acts as a rate-limiting enzyme in crop starch biosynthesis. Prior research has hinted at the regulation of AGPase by phosphorylation in maize. However, the identification and functional implications of these sites remain to be elucidated. In this study, we identified the phosphorylation site (serine at the 31st position of the linear amino acid sequence) of the AGPase large subunit (Sh2) using iTRAQTM. Subsequently, to ascertain the impact of Sh2 phosphorylation on AGPase, we carried out site-directed mutations creating Sh2-S31A (serine residue replaced with alanine) to mimic dephosphorylation and Sh2-S31D (serine residue replaced with aspartic acid) or Sh2-S31E (serine residue replaced with glutamic acid) to mimic phosphorylation. Preliminary investigations were performed to determine Sh2 subcellular localization, its interaction with Bt2, and the resultant AGPase enzymatic activity. Our findings indicate that phosphorylation exerts no impact on the stability or localization of Sh2. Furthermore, none of these mutations at the S31 site of Sh2 seem to affect its interaction with Bt2 (smaller subunit). Intriguingly, all S31 mutations in Sh2 appear to enhance AGPase activity when co-transfected with Bt2, with Sh2-S31E demonstrating a substantial five-fold increase in AGPase activity compared to Sh2. These novel insights lay a foundational groundwork for targeted improvements in AGPase activity, thus potentially accelerating the production of ADP-Glc (the primary substrate for starch synthesis), promising implications for improved starch biosynthesis, and holding the potential to significantly impact agricultural practices.

Site-Directed Mutations at Phosphorylation Sites in Zea mays PHO1 Reveal Modulation of Enzymatic Activity by Phosphorylation at S566 in the L80 Region.

Starch phosphorylase (PHO) is a pivotal enzyme within the GT35-glycogen-phosphorylase (GT; glycosyltransferases) superfamily. Despite the ongoing debate surrounding the precise role of PHO1, evidence points to its substantial influence on starch biosynthesis, supported by its gene expression profile and subcellular localization. Key to PHO1 function is the enzymatic regulation via phosphorylation; a myriad of such modification sites has been unveiled in model crops. However, the functional implications of these sites remain to be elucidated. In this study, we utilized site-directed mutagenesis on the phosphorylation sites of Zea mays PHO1, replacing serine residues with alanine, glutamic acid, and aspartic acid, to discern the effects of phosphorylation. Our findings indicate that phosphorylation exerts no impact on the stability or localization of PHO1. Nonetheless, our enzymatic assays unveiled a crucial role for phosphorylation at the S566 residue within the L80 region of the PHO1 structure, suggesting a potential modulation or enhancement of PHO1 activity. These data advance our understanding of starch biosynthesis regulation and present potential targets for crop yield optimization.

Meta-Analysis of Single-Cell RNA-Seq Data Reveals the Mechanism of Formation and Heterogeneity of Tertiary Lymphoid Organ in Vascular Disease.

BACKGROUND: Tertiary lymphoid organs (TLOs) are ectopic lymphoid organs developed in nonlymphoid tissues with chronic inflammation, but little is known about their existence in different types of vascular diseases and the mechanism that mediated their development. METHODS: To take advantage of single-cell RNA sequencing techniques, we integrated 28 single-cell RNA sequencing data sets containing 5 vascular disease models (atherosclerosis, abdominal aortic aneurysm, intimal hyperplasia, isograft, and allograft) to explore TLOs existence and environment supporting its growth systematically. We also searched Medline, Embase, PubMed, and Web of Science from inception to January 2022 for published histological images of vascular remodeling for histological evidence to support TLO genesis. RESULTS: Accumulation and infiltration of innate and adaptive immune cells have been observed in various remodeling vessels. Interestingly, the proportion of such immune cells incrementally increases from atherosclerosis to intimal hyperplasia, abdominal aortic aneurysm, isograft, and allograft. Importantly, we uncovered that TLO structure cells, such as follicular helper T cells and germinal center B cells, present in all remodeled vessels. Among myeloid cells and lymphocytes, inflammatory macrophages, and T helper 17 cells are the major lymphoid tissue inducer cells which were found to be positively associated with the numbers of TLO structural cells in remodeled vessels. Vascular stromal cells also actively participate in vascular TLO genesis by communicating with myeloid cells and lymphocytes via CCLs (C-C motif chemokine ligands), CXCL (C-X-C motif ligand), lymphotoxin, BMP (bone morphogenetic protein) chemotactic, FGF-2 (fibroblast growth factor-2), and IGF (insulin growth factor) proliferation mechanisms, particularly for lymphoid tissue inducer cell aggregation. Additionally, the interaction between stromal cells and immune cells modulates extracellular matrix remodeling. Among TLO structure cells, follicular helper T, and germinal center B cells have strong interactions via TCR (T-cell receptor), CD40 (cluster of differentiation 40), and CXCL signaling, to promote the development and maturation of the germinal center in TLO. Consistently, by reviewing the histological images from the literature, TLO genesis was found in those vascular remodeling models. CONCLUSIONS: Our analysis showed the existence of TLOs across 5 models of vascular diseases. The mechanisms that support TLOs formation in different models are heterogeneous. This study could be a valuable resource for understanding and discovering new therapeutic targets for various forms of vascular disease.

Transcriptomic, Physiological, and Metabolomic Response of an Alpine Plant, Rhododendron delavayi, to Waterlogging Stress and Post-Waterlogging Recovery.

Climate change has resulted in frequent heavy and prolonged rainfall events that exacerbate waterlogging stress, leading to the death of certain alpine Rhododendron trees. To shed light on the physiological and molecular mechanisms behind waterlogging stress in woody Rhododendron trees, we conducted a study of Rhododendron delavayi, a well-known alpine flower species. Specifically, we investigated the physiological and molecular changes that occurred in leaves of R. delavayi subjected to 30 days of waterlogging stress (WS30d), as well as subsequent post-waterlogging recovery period of 10 days (WS30d-R10d). Our findings reveal that waterlogging stress causes a significant reduction in CO2 assimilation rate, stomatal conductance, transpiration rate, and maximum photochemical efficiency of PSII (Fv/Fm) in the WS30d leaves, by 91.2%, 95.3%, 93.3%, and 8.4%, respectively, when compared to the control leaves. Furthermore, the chlorophyll a and total chlorophyll content in the WS30d leaves decreased by 13.5% and 16.6%, respectively. Both WS30d and WS30d-R10d leaves exhibited excessive H2O2 accumulation, with a corresponding decrease in lignin content in the WS30d-R10d leaves. At the molecular level, purine metabolism, glutathione metabolism, photosynthesis, and photosynthesis-antenna protein pathways were found to be primarily involved in WS30d leaves, whereas phenylpropanoid biosynthesis, fatty acid metabolism, fatty acid biosynthesis, fatty acid elongation, and cutin, suberin, and wax biosynthesis pathways were significantly enriched in WS30d-R10d leaves. Additionally, both WS30d and WS30d-R10d leaves displayed a build-up of sugars. Overall, our integrated transcriptomic, physiological, and metabolomic analysis demonstrated that R. delavayi is susceptible to waterlogging stress, which causes irreversible detrimental effects on both its physiological and molecular aspects, hence compromising the tree's ability to fully recover, even under normal growth conditions.

Virtual screening-molecular docking-activity evaluation of Ailanthus altissima (Mill.) swingle bark in the treatment of ulcerative colitis.

BACKGROUND: The dried bark of Ailanthus altissima (Mill.) Swingle is widely used in traditional Chinese medicine for the treatment of ulcerative colitis. The objective of this study was to explore the therapeutic basis of the dried bark of Ailanthus altissima (Mill.) Swingle for the treatment of ulcerative colitis based on Virtual Screening-Molecular Docking-Activity Evaluation technology. METHODS: By searching the Traditional Chinese Medicine Systems Pharmacology TCMSP Database and Analysis Platform, 89 compounds were obtained from the chemical components of the dried bark of Ailanthus altissima (Mill.) Swingle. Then, after preliminarily screening the compounds based on Lipinski's rule of five and other relevant conditions, the AutoDock Vina molecular docking software was used to evaluate the affinity of the compounds to ulcerative colitis-related target proteins and their binding modes through use of the scoring function to identify the best candidate compounds. Further verification of the compound's properties was achieved through in vitro experiments. RESULTS: Twenty-two compounds obtained from the secondary screening were molecularly docked with ulcerative colitis-related target proteins (IL-1R, TLR, EGFR, TGFR, and Wnt) using AutoDock Vina. The free energies of the highest scoring compounds binding to the active cavity of human IL-1R, TLR, EGFR, TGFR, and Wnt proteins were - 8.7, - 8.0, - 9.2, - 7.7, and - 8.5 kcal/mol, respectively. The potential compounds, dehydrocrebanine, ailanthone, and kaempferol, were obtained through scoring function and docking mode analysis. Furthermore, the potential compound ailanthone (1, 3, and 10 µM) was found to have no significant effect on cell proliferation, though at 10 µM it reduced the level of pro-inflammatory factors caused by lipopolysaccharide. CONCLUSION: Among the active components of the dried bark of Ailanthus altissima (Mill.) Swingle, ailanthone plays a major role in its anti-inflammatory properties. The present study shows that ailanthone has advantages in cell proliferation and in inhibiting of inflammation, but further animal research is needed to confirm its pharmaceutical potential.

Evidence That PbrSAUR72 Contributes to Iron Deficiency Tolerance in Pears by Facilitating Iron Absorption.

Iron is an essential trace element for plants; however, low bioactive Fe in soil continuously places plants in an Fe-deficient environment, triggering oxidative damage. To cope with this, plants make a series of alterations to increase Fe acquisition; however, this regulatory network needs further investigation. In this study, we found notably decreased indoleacetic acid (IAA) content in chlorotic pear (Pyrus bretschneideri Rehd.) leaves caused by Fe deficiency. Furthermore, IAA treatment slightly induced regreening by increasing chlorophyll synthesis and Fe2+ accumulation. At that point, we identified PbrSAUR72 as a key negative effector output of auxin signaling and established its close relationship to Fe deficiency. Furthermore, the transient PbrSAUR72 overexpression could form regreening spots with increased IAA and Fe2+ content in chlorotic pear leaves, whereas its transient silencing does the opposite in normal pear leaves. In addition, cytoplasm-localized PbrSAUR72 exhibits root expression preferences and displays high homology to AtSAUR40/72. This promotes salt tolerance in plants, indicating a putative role for PbrSAUR72 in abiotic stress responses. Indeed, transgenic plants of Solanum lycopersicum and Arabidopsis thaliana overexpressing PbrSAUR72 displayed less sensitivity to Fe deficiency, accompanied by substantially elevated expression of Fe-induced genes, such as FER/FIT, HA, and bHLH39/100. These result in higher ferric chelate reductase and root pH acidification activities, thereby hastening Fe absorption in transgenic plants under an Fe-deficient condition. Moreover, the ectopic overexpression of PbrSAUR72 inhibited reactive oxygen species production in response to Fe deficiency. These findings contribute to a new understanding of PbrSAURs and its involvement in Fe deficiency, providing new insights for the further study of the regulatory mechanisms underlying the Fe deficiency response.

Oblique lumbar interbody fusion versus minimally invasive transforaminal lumbar interbody fusion for the treatment of degenerative disease of the lumbar spine: a systematic review and meta-analysis.

This meta-analysis compared the efficacy of oblique lumbar interbody fusion (OLIF) and minimally invasive transforaminal lumbar interbody fusion (MIS-TLIF) in the treatment of lumbar degenerative diseases. A computer search for the published literature on OLIF and MIS-TLIF for the treatment of lumbar degenerative diseases in the PubMed, Web of Science, Embase, CINAHL, MEDLINE, Cochrane Library, and other databases was performed, from which 522 related articles were retrieved and 13 were finally included. Two reviewers independently extracted data from the included studies and analyzed them using RevMan 5.4. The quality of the studies was assessed using the Cochrane systematic analysis and the Newcastle-Ottawa scale. Meta-analysis showed that the blood loss [95% confidence intervals (CI) (- 121.01, - 54.56), [Formula: see text]], hospital stay [95% CI (- 1.98, - 0.85), [Formula: see text]], postoperative fusion rate [95%CI (1.04, 3.60), [Formula: see text]], postoperative disc height [95% CI (0.50, 3.63), [Formula: see text]], and postoperative foraminal height [95% CI (0.96, 4.13), [Formula: see text]] were all better in the OLIF group; however, the complication rates were significantly lower in the MIS-TLIF group [95% CI (1.01, 2.06), [Formula: see text]]. However, there were no significant differences between the two in terms of surgery time, patient satisfaction, or postoperative functional scores. The OLIF group had the advantages of lower blood loss, a shorter hospital stay, a higher postoperative fusion rate, and better recovery of the disc and foraminal heights, whereas MIS-TLIF had a relatively lower complication rate.

Comparing modelling approaches for the estimation of government intervention effects in COVID-19: Impact of voluntary behavior changes.

The efficacy of government interventions in epidemic has become a hot subject since the onset of COVID-19. There is however much variation in the results quantifying the effects of interventions, which is partly related to the varying modelling approaches employed by existing studies. Among the many factors affecting the modelling results, people's voluntary behavior change is less examined yet likely to be widespread. This paper therefore aims to analyze how the choice of modelling approach, in particular how voluntary behavior change is accounted for, would affect the intervention effect estimation. We conduct the analysis by experimenting different modelling methods on a same data set composed of the 500 most infected U.S. counties. We compare the most frequently used methods from the two classes of modelling approaches, which are Bayesian hierarchical model from the class of computational approach and difference-in-difference from the class of natural experimental approach. We find that computational methods that do not account for voluntary behavior changes are likely to produce larger estimates of intervention effects as assumed. In contrast, natural experimental methods are more likely to extract the true effect of interventions by ruling out simultaneous behavior change. Among different difference-in-difference estimators, the two-way fixed effect estimator seems to be an efficient one. Our work can inform the methodological choice of future research on this topic, as well as more robust re-interpretation of existing works, to facilitate both future epidemic response plans and the science of public health.