The CHY-type zinc finger protein MoChy1 is involved in polarized growth, conidiation, autophagy and pathogenicity of Magnaporthe oryzae.

Polarized growth is critical for the development of filamentous phytopathogens, and the CHY-type zinc finger protein Chy1 regulates microtubule assembly to influence polarized growth and thereby affect plant infections. However, the biological role of a Chy1 homolog MoChy1 remains unknown in Magnaporthe oryzae. We found here that the MoChy1-GFP was distributed in the cytoplasm outside the vacuole in hyphae and localized mainly to the vacuole compartments as the appressorium matured. The Mochy1 mutants showed an extremely slow growth rate, curved and branched mycelium, reduced conidiation, and a smaller size in the appressorium. Meanwhile, the Mochy1 mutants showed increased sensitivity to benomyl, damaged microtubule cytoskeleton, and mislocalized polarisome protein MoSpa2 and chitin synthase MoChs6 in hyphae. Compared to Guy11, the Mochy1 mutants exhibited increased sensitivity to H2O2, impaired ability to eliminate host-derived ROS and reduced penetration into host plants, resulting in a strong reduction in pathogenicity of Mochy1 mutants. Furthermore, the Mochy1 mutants also exhibited defects in chitin distribution, osmotic stress tolerance, and septin ring organization during appressorium differentiation and fungal development. Nonselective autophagy was negatively regulated in Mochy1 mutants compared to Guy11. In summary, MoChy1 plays multiple roles in fungal polar growth and full virulence of M. oryzae.

Enzymatic modular synthesis of asymmetrically branched human milk oligosaccharides.

Human milk oligosaccharides (HMOs) are intricate glycans that promote healthy growth of infants and have been incorporated into infant formula as food additives. Despite their importance, the limited availability of asymmetrically branched HMOs hinders the exploration of their structure and function relationships. Herein, we report an enzymatic modular strategy for the efficient synthesis of these HMOs. The key branching enzyme for the assembly of branched HMOs, human ß1,6-N-acetylglucosaminyltransferase 2 (GCNT2), was successfully expressed in Pichia pastoris for the first time. Then, it was integrated with six other bacterial glycosyltransferases to establish seven glycosylation modules. Each module comprises a one-pot multi-enzyme (OPME) system for in-situ generation of costly sugar nucleotide donors, combined with a glycosyltransferase for specific glycosylation. This approach enabled the synthesis of 31 branched HMOs and 13 linear HMOs in a stepwise manner with well-programmed synthetic routes. The binding details of these HMOs with related glycan-binding proteins were subsequently elucidated using glycan microarray assays to provide insights into their biological functions. This comprehensive collection of synthetic HMOs not only serves as standards for HMOs structure identification in complex biological samples but also significantly enhances the fields of HMOs glycomics, opening new avenues for biomedical applications.

Overexpression of transcription factor FaMYB63 enhances salt tolerance by directly binding to the SOS1 promoter in Arabidopsis thaliana.

Salinity is a pivotal abiotic stress factor with far-reaching consequences on global crop growth, yield, and quality and which includes strawberries. R2R3-MYB transcription factors encompass a range of roles in plant development and responses to abiotic stress. In this study, we identified that strawberry transcription factor FaMYB63 exhibited a significant upregulation in its expression under salt stress conditions. An analysis using yeast assay demonstrated that FaMYB63 exhibited the ability to activate transcriptional activity. Compared with those in the wild-type (WT) plants, the seed germination rate, root length, contents of chlorophyll and proline, and antioxidant activities (SOD, CAT, and POD) were significantly higher in FaMYB63-overexpressing Arabidopsis plants exposed to salt stress. Conversely, the levels of malondialdehyde (MDA) were considerably lower. Additionally, the FaMYB63-overexpressed Arabidopsis plants displayed a substantially improved capacity to scavenge active oxygen. Furthermore, the activation of stress-related genes by FaMYB63 bolstered the tolerance of transgenic Arabidopsis to salt stress. It was also established that FaMYB63 binds directly to the promoter of the salt overly sensitive gene SOS1, thereby activating its expression. These findings identified FaMYB63 as a possible and important regulator of salt stress tolerance in strawberries.

Relationship between hemoglobin and lung cancer: evidence from Mendelian randomization and National Health and Nutrition Examination Survey

Background Lung cancer is the primary cause of cancer-related mortality worldwide. Hemoglobin (Hb) represents the most widely utilized test parameter in clinical settings. However, few articles have examined the causal relationship between Hb concentration and lung cancer incidence. Methods Mendelian randomization (MR) was first conducted to investigate the potential causality between Hb and lung cancer. Sensitivity analyses were applied to validate the reliability of MR results. Then, the National Health and Nutrition Examination Survey (NHANES) database was used to verify the effect of Hb on the prognosis of lung cancer. Results The MR analysis demonstrated that Hb was casually associated with the decreased risk of lung cancer in the European population (ORIVW 0.84, 95% CI 0.75–0.95, p = 0.006; ORWeighted-median 0.78, 95% CI 0.65–0.94, p = 0.008; ORMR-Egger 0.82, 95% CI 0.64–1.04, p = 0.11). The results from the NHANES database showed that a high value of Hb was associated with better outcomes for patients with lung cancer (HR 0.45, 95% CI 0.26–0.79, p = 1.6E−03). Conclusions Our study provides further evidence for the relationship between Hb levels and lung cancer, highlighting the potential significance of Hb as a biomarker for predicting the risk and prognosis of lung cancer (AU)

Midterm Outcomes of Multicenter Castor Single-Branch Stent Graft Use in the Treatment of Thoracic Aortic Diseases.

PURPOSE: The aim of this study was to evaluate the midterm efficacy and safety of a single-branch Castor stent graft in the treatment of thoracic aortic disease. MATERIALS AND METHODS: Clinical data of 106 patients with thoracic aortic disease treated with Castor single-branch stent graft at 3 centers were collected between May 2018 and June 2023. The indicators included technical success, stent-related complication, reintervention, retrograde dissection, endoleak, distal stent graft-induced entry (dSINE), branch patency, and mortality. The outcomes of the Castor stent graft for multibranch reconstruction above the arch was also analyzed. RESULTS: The technical success was 98.1% (104/106), while the surgical success was 93.4% (99/106). The reintervention was 2.8% (3/106), consisting of a case of retrograde type A dissection, an endoleak, and a dSINE. The retrograde dissection was 1.9% (2/106), while type I endoleak was 1.9% (2/106). The new dSINE was 2.8% (3/106), and the branch patency rate was 100%. The mortality was 1.9% (2/106). The mean follow-up time was 29.1±17.7 months. The 2-year post-surgery cumulative survival rate was 91.0%±3.1%, while the cumulative branch patency rate was 96.2%±2.2%. In addition, the cumulative freedom from stent-related reintervention rate was 93.2%±2.8%. A comparison showed no significant difference in the stent-related complication, branch patency, endoleak, reintervention, and mortality when the proximal end of the Castor stent graft was anchored to zones 1 or 2 of the aorta. CONCLUSION: Castor single-branch stent graft showed favorable early and midterm outcomes in the treatment of thoracic aortic disease. In addition, it was feasible to combine Castor stent graft with other advanced techniques for multibranch aortic arch reconstruction. CLINICAL IMPACT: The Castor single-branch stent graft was approval by the Chinese Food and Drug Administration in 2017. However, there were few studies on the mid-term outcomes for thoracic aortic disease after launching, which mainly focused on small single-center retrospective study. In the study, we assessed the mid-term outcomes of Castor stent graft through multi-center cases, Castor stent graft combined with other advanced techniques (such as fenestration and hybrid) for multi-branch reconstruction of aortic arch were also conducted. We found Castor single-branch stent graft showed favorable early and mid-term outcomes in the treatment of thoracic aortic disease. Additionally, it was feasible to combine Castor stent graft with other advanced technique for multi-branch aortic arch reconstruction. As an off-the-shelf branched stent graft with a wide range of models, it could be also used in most emergent situation. The Castor stent graft was expected to become more widely used in the future.

FHL2 promotes the aggressiveness of lung adenocarcinoma by inhibiting autophagy via activation of the PI3K/AKT/mTOR pathway.

BACKGROUND: Increasing evidence indicates that four and a half LIM domains 2 (FHL2) plays a crucial role in the progression of various cancers. However, the biological functions and molecular mechanism of FHL2 in lung adenocarcinoma (LUAD) remain unclear. METHODS: We evaluated the prognostic value of FHL2 in LUAD using public datasets and further confirmed its prognostic value with our clinical data. The biological functions of FHL2 in LUAD were evaluated by in vitro and in vivo experiments. Pathway analysis and rescue experiments were subsequently performed to explore the molecular mechanism by which FHL2 promoted the progression of LUAD. RESULTS: FHL2 was upregulated in LUAD tissues compared to adjacent normal lung tissues, and FHL2 overexpression was correlated with unfavorable outcomes in patients with LUAD. FHL2 knockdown significantly suppressed the proliferation, migration and invasion of LUAD cells, while FHL2 overexpression had the opposite effect. Mechanistically, FHL2 upregulated the PI3K/AKT/mTOR pathway and subsequently inhibited autophagy in LUAD cells. The effects FHL2 on the proliferation, migration and invasion of LUAD cells are dependent on the inhibition of autophagy, as of induction autophagy attenuated the aggressive phenotype induced by FHL2 overexpression. CONCLUSIONS: FHL2 promotes the progression of LUAD by activating the PI3K/AKT/mTOR pathway and subsequently inhibiting autophagy, which can be exploited as a potential therapeutic target for LUAD.

IKBKE promotes the ZEB2-mediated EMT process by phosphorylating HMGA1a in glioblastoma.

IKBKE (Inhibitor of Nuclear Factor Kappa-B Kinase Subunit Epsilon) is an important oncogenic protein in a variety of tumors, which can promote tumor growth, proliferation, invasion and drug resistance, and plays a critical regulatory role in the occurrence and progression of malignant tumors. HMGA1a (High Mobility Group AT-hook 1a) functions as a cofactor for proper transcriptional regulation and is highly expressed in multiple types of tumors. ZEB2 (Zinc finger E-box Binding homeobox 2) exerts active functions in epithelial mesenchymal transformation (EMT). In our current study, we confirmed that IKBKE can increase the proliferation, invasion and migration of glioblastoma cells. We then found that IKBKE can phosphorylate HMGA1a at Ser 36 and/or Ser 44 sites and inhibit the degradation process of HMGA1a, and regulate the nuclear translocation of HMGA1a. Crucially, we observed that HMGA1a can regulate ZEB2 gene expression by interacting with ZEB2 promoter region. Hence, HMGA1a was found to promote the ZEB2-related metastasis. Consequently, we demonstrated that IKBKE can exert its oncogenic functions via the IKBKE/HMGA1a/ZEB2 signalling axis, and IKBKE may be a prominent biomarker for the treatment of glioblastoma in the future.

Neu5Gc binding loss of subtype H7 influenza A virus facilitates adaptation to gallinaceous poultry following transmission from waterbirds but restricts spillback.

Migratory waterfowl, gulls, and shorebirds serve as natural reservoirs for influenza A viruses, with potential spillovers to domestic poultry and humans. The intricacies of interspecies adaptation among avian species, particularly from wild birds to domestic poultry, are not fully elucidated. In this study, we investigated the molecular mechanisms underlying avian species barriers in H7 transmission, particularly the factors responsible for the disproportionate distribution of poultry infected with A/Anhui/1/2013 (AH/13)-lineage H7N9 viruses. We hypothesized that the differential expression of N-glycolylneuraminic acid (Neu5Gc) among avian species exerts selective pressure on H7 viruses, shaping their evolution and enabling them to replicate and transmit efficiently among gallinaceous poultry, particularly chickens. Our glycan microarray and biolayer interferometry experiments showed that AH/13-lineage H7N9 viruses exclusively bind to Neu5Ac, in contrast to wild waterbird H7 viruses that bind both Neu5Ac and Neu5Gc. Significantly, reverting the V179 amino acid in AH/13-lineage back to the I179, predominantly found in wild waterbirds, expanded the binding affinity of AH/13-lineage H7 viruses from exclusively Neu5Ac to both Neu5Ac and Neu5Gc. When cultivating H7 viruses in cell lines with varied Neu5Gc levels, we observed that Neu5Gc expression impairs the replication of Neu5Ac-specific H7 viruses and facilitates adaptive mutations. Conversely, Neu5Gc deficiency triggers adaptive changes in H7 viruses capable of binding to both Neu5Ac and Neu5Gc. Additionally, we assessed Neu5Gc expression in the respiratory and gastrointestinal tissues of seven avian species, including chickens, Canada geese, and various dabbling ducks. Neu5Gc was absent in chicken and Canada goose, but its expression varied in the duck species. In summary, our findings reveal the crucial role of Neu5Gc in shaping the host range and interspecies transmission of H7 viruses. This understanding of virus-host interactions is crucial for developing strategies to manage and prevent influenza virus outbreaks in diverse avian populations.

Relationship between hemoglobin and lung cancer: evidence from Mendelian randomization and National Health and Nutrition Examination Survey.

BACKGROUND: Lung cancer is the primary cause of cancer-related mortality worldwide. Hemoglobin (Hb) represents the most widely utilized test parameter in clinical settings. However, few articles have examined the causal relationship between Hb concentration and lung cancer incidence. METHODS: Mendelian randomization (MR) was first conducted to investigate the potential causality between Hb and lung cancer. Sensitivity analyses were applied to validate the reliability of MR results. Then, the National Health and Nutrition Examination Survey (NHANES) database was used to verify the effect of Hb on the prognosis of lung cancer. RESULTS: The MR analysis demonstrated that Hb was casually associated with the decreased risk of lung cancer in the European population (ORIVW 0.84, 95% CI 0.75-0.95, p = 0.006; ORWeighted-median 0.78, 95% CI 0.65-0.94, p = 0.008; ORMR-Egger 0.82, 95% CI 0.64-1.04, p = 0.11). The results from the NHANES database showed that a high value of Hb was associated with better outcomes for patients with lung cancer (HR 0.45, 95% CI 0.26-0.79, p = 1.6E-03). CONCLUSIONS: Our study provides further evidence for the relationship between Hb levels and lung cancer, highlighting the potential significance of Hb as a biomarker for predicting the risk and prognosis of lung cancer.

SeMet alleviates AFB1-induced oxidative stress and apoptosis in rabbit kidney by regulating Nrf2//Keap1/NQO1 and PI3K/AKT signaling pathways.

The purpose of this study was to explore the protective effect of SeMet on renal injury induced by AFB1 in rabbits and its molecular mechanism. Forty rabbits of 35 days old were randomly divided into control group, AFB1 group (0.3 mg AFB1/kg b.w), 0.2 mg/kg Se + AFB1 group (0.3 mg AFB1/kg b.w + 0.2 mg SeMet/kg feed) and 0.4 mg/kg Se + AFB1 group (0.3 mg AFB1/kg b.w + 0.4 mg SeMet/kg feed). The SeMet treatment group was fed different doses of SeMet diets every day for 21 days. On the 17-21 day, the AFB1 treatment group, the 0.2 mg/kg Se + AFB1 group and the 0.4 mg/kg Se + AFB1 group were administered 0.3 mg AFB1 /kg b.w by gavage (dissolved in 0.5 ml olive oil) respectively. The results showed that AFB1 poisoning resulted in the changes of renal structure, the increase of renal coefficient and serum biochemical indexes, the ascent of ROS and MDA levels, the descent of antioxidant enzyme activity, and the significant down-regulation of Nrf2, HO-1 and NQO1. Besides, AFB1 poisoning increased the number of renal apoptotic cells, rised the levels of PTEN, Bax, Caspase-3 and Caspase-9, and decreased the levels of PI3K, AKT, p-AKT and Bcl-2. In summary, SeMet was added to alleviate the oxidative stress injury and apoptosis of kidney induced by AFB1, and the effect of 0.2 mg/kg Se + AFB1 is better than 0.4 mg/kg Se + AFB1.

Systematic Review and Meta-analysis of Short-term and Mid-term Outcomes After Use of t-Branch Off-the-shelf Multibranched Endograft for Elective and Urgent Treatment of Thoracoabdominal Aortic Aneurysms.

OBJECTIVE: To conduct a meta-analysis to assess the safety and efficacy of t-Branch off-the-shelf multibranched endograft for the treatment of thoracoabdominal aortic aneurysm (TAAA). DATA SOURCES: PubMed, Embase, and Web of Science. REVIEW METHODS: Online databases were searched from June 2012 to March 2023. The data were pooled together using a random-effects model of proportions. The outcomes overall included technical success, spinal cord ischemia, target vessel occlusion, type I or III endoleak, reintervention, early mortality (30-day), and mid-term outcomes. Subgroup meta-analyses and meta-regression were performed to explore variation among studies. RESULTS: A total of 15 studies containing 1238 patients were included in the meta-analysis. The overall study quality assessment was found to be moderate to good. The pooled technical success was 97.0% (95% confidence interval [CI]=95.5-98.6, I2=53.01%, 1185/1238 cases, 15 studies). Overall, early mortality was 7.3% (95% CI=4.4-10.1, I2=74.48%, 124/1238 cases, 15 studies). Early spinal cord ischemia was 13.4% (95% CI=9.6-17.2, I2=67.24%, 160/1238 cases, 15 studies), and early type I or III endoleak was 6.0% (95% CI=3.4-8.5, I2=53.71%, 68/1032 cases, 9 studies). Mid-term outcomes showed target vessel occlusion was 4% (95% CI=1.4-6.5, I2=65.18%, 28/528 cases, 10 studies, 5-21.2 months), type I or III endoleak was 4.7% (95% CI=2-7.5, I2=49.74%, 38/512 cases, 10 studies, 5-21.2 months), reintervention was 11.2% (95% CI=8.1-14.3, I2=31.06%, 85/650 cases, 10 studies, 5-21.2 months), and pooled mortality was 13.9% (95% CI=7.2-20.7, I2=76.32%, 84/550 cases, 11 studies, 5-21.2 months). Meta-regression found a significant linear association between higher technical success and earlier publication year (p=0.014) and studies with anatomic inclusion criteria (p=0.037). Urgent patients (p=0.021) and later publication year (p=0.048) were significantly associated with higher early mortality. CONCLUSION: The use of the off-the-shelf t-Branch multibranched endograft for elective or urgent endovascular TAAA repair is associated with high technical success rates and proved to be safe and effective at early and mid-term follow-up. However, the heterogeneity between the included studies is high, and prospective, randomized studies along with future larger studies with long-term follow-up are needed. CLINICAL IMPACT: The Zenith t-Branch (Cook Medical, Bloomington, Ind) was approved as a commercially available device in Europe in June 2012. Although a decade has past, the outcomes of t-Branch have rarely been synthesized at the global level. This meta-analysis included 15 studies containing 1238 patients. The meta-analyses included technical success, major adverse events, reintervention, early mortality, and mid-term outcomes. The outcome was very meaningful and representative for the use of t-Branch. It is helpful for endovascular surgeons to make decisions on the treatment of TAAA patients.

Layer-Structured Multitransition-Metal Oxide Cathode Materials for Potassium-Ion Batteries with Long Cycling Lifespan and Superior Rate Capability.

Manganese (Mn)-based layer-structured transition metal oxides are considered as excellent cathode materials for potassium ion batteries (KIBs) owing to their low theoretical cost and high voltage plateau. The energy density and cycling lifetime, however, cannot simultaneously satisfy the basic requirements of the market for energy storage systems. One of the primary causes results from the complex structural transformation and transition metal migration during the ion intercalation and deintercalation process. The orbital and electronic structure of the octahedral center metal element plays an important role for maintaining the octahedral structural integrity and improving the K+ diffusivity by the introduced heterogeneous [Me-O] chemical bonding. A multitransition metal oxide, P3-type K0.5Mn0.85Co0.05Fe0.05Al0.05O2 (KMCFAO), was synthesized and employed as a cathode material for KIBs. Beneficial from the larger layer spacing for K+ to better accommodate and effectively preventing the irreversible structural transformation in the insertion/extraction process, it can reach a superior capacity retention up to 96.8% after 300 cycles at a current density of 500 mA g-1. The full cell of KMCFAO//hard carbon exhibits an encouraging promising energy density of 113.8 W h kg-1 at 100 mA g-1 and a capacity retention of 72.6% for 500 cycles.

Therapeutic targeting of vimentin by ALD-R491 impacts multiple pathogenic processes to attenuate acute and chronic colitis in mice.

BACKGROUND: Vimentin, an intermediate filament protein, crucially contributes to the pathogenesis of inflammatory bowel disease (IBD) by interacting with genetic risk factors, facilitating pathogen infection, and modulating both innate and adaptive immune responses. This study aimed to demonstrate preclinical proof-of-concept for targeting vimentin therapeutically in IBD across diverse etiologies. METHODS: The small molecule compound ALD-R491 was assessed for vimentin binding using microscale thermophoresis, off-target effects via Eurofins screening, and therapeutic effects in mice with dextran sulfate sodium (DSS)-induced acute colitis and in IL-10 KO with spontaneous colitis. Parameters measured included body weight, survival, disease activity, colon length, and histology. The study analyzed intestinal proinflammatory cytokines, Th17/Treg cells, and epithelial barrier molecules, along with gut microbiota profiling. RESULTS: ALD-R491 specifically bound vimentin with a dissociation constant (KD) of 328 ± 12.66 nM and no off-target effects. In the DSS model, orally administered ALD-R491 exhibited dose-dependent therapeutic effects, superior to 5-ASA and Tofacitinib. In the IL-10 KO model, ALD-R491 significantly delayed colitis onset and progression, with near-zero disease activity index scores over a 15-week treatment. ALD-R491 consistently showed in both models a reduced proinflammatory cytokine expression, including TNF-α, IL-1ß, IL-6, IL-17, IL-22, a rebalanced Th17/Treg axis by reducing RORγt while enhancing FoxP3 expression, and an improved epithelial barrier integrity by increasing intestinal expressions of Mucin-2, ZO-1 and Claudin5. The intestinal dysbiosis was restored with enriched presence of probiotics. CONCLUSIONS: Targeting vimentin exhibits significant therapeutic effects on various facets of IBD pathogenesis, representing a compelling approach for the development of highly effective treatments in IBD.

FreqSense: Adaptive Sampling Rates for Sensor-Based Human Activity Recognition Under Tunable Computational Budgets.

Recent years have witnessed great success of deep convolutional networks in sensor-based human activity recognition (HAR), yet their practical deployment remains a challenge due to the varying computational budgets required to obtain a reliable prediction. This article focuses on adaptive inference from a novel perspective of signal frequency, which is motivated by an intuition that low-frequency features are enough for recognizing "easy" activity samples, while only "hard" activity samples need temporally detailed information. We propose an adaptive resolution network by combining a simple subsampling strategy with conditional early-exit. Specifically, it is comprised of multiple subnetworks with different resolutions, where "easy" activity samples are first classified by lightweight subnetwork using the lowest sampling rate, while the subsequent subnetworks in higher resolution would be sequentially applied once the former one fails to reach a confidence threshold. Such dynamical decision process could adaptively select a proper sampling rate for each activity sample conditioned on an input if the budget varies, which will be terminated until enough confidence is obtained, hence avoiding excessive computations. Comprehensive experiments on four diverse HAR benchmark datasets demonstrate the effectiveness of our method in terms of accuracy-cost tradeoff. We benchmark the average latency on a real hardware.

Road-Network-Map-Assisted Vehicle Positioning Based on Pose Graph Optimization.

Satellite signals are easily lost in urban areas, which causes difficulty in vehicles being located with high precision. Visual odometry has been increasingly applied in navigation systems to solve this problem. However, visual odometry relies on dead-reckoning technology, where a slight positioning error can accumulate over time, resulting in a catastrophic positioning error. Thus, this paper proposes a road-network-map-assisted vehicle positioning method based on the theory of pose graph optimization. This method takes the dead-reckoning result of visual odometry as the input and introduces constraints from the point-line form road network map to suppress the accumulated error and improve vehicle positioning accuracy. We design an optimization and prediction model, and the original trajectory of visual odometry is optimized to obtain the corrected trajectory by introducing constraints from map correction points. The vehicle positioning result at the next moment is predicted based on the latest output of the visual odometry and corrected trajectory. The experiments carried out on the KITTI and campus datasets demonstrate the superiority of the proposed method, which can provide stable and accurate vehicle position estimation in real-time, and has higher positioning accuracy than similar map-assisted methods.

lnc-HC ameliorates steatosis by promoting miR-130b-3p biogenesis and the assembly of an RNA-induced silencing complex.

Hepatic lipid deposition is the main cause of non-alcoholic fatty liver disease (NAFLD). Our previous study identified that lnc-HC prevents NAFLD by increasing the expression of miR-130b-3p. In the present study, we show that lnc-HC, an lncRNA derived from hepatocytes, positively controls miR-130b-3p maturation at multiple levels and contributes to its action by enhancing the assembly of an RNA-induced silencing complex (RISC). lnc-HC negatively regulates the downstream target genes of miR-130b-3p, including peroxisome proliferator-activated receptor gamma (PPARγ) and acyl-CoA synthetase long-chain family member 1 and 4 (Acsl1 and Acsl4, respectively), thus suppressing hepatic lipid droplet accumulation. Mechanistically, lnc-HC enhanced the promoter activity of miR-130b-3p by positively regulating the expression of transcription factors MAF bZIP transcription factor B (Mafb) and Jun proto-oncogene (Jun). Then, lnc-HC contributed the processing step of primary (pri-) miR-130b and strengthened the interaction between Drosha enzyme and the 5'-flanking sequence of pri-miR-130b to produce more precursor transcripts. Through direct binding with the chaperone heat shock protein 90 alpha family class A member 1 (HSP90AA1), lnc-HC contributed to RISC assembly, which was composed of HSP90AA1, argonaute RISC catalytic component 2 (AGO2) and miR-130b-3p. In a high-fat, high-cholesterol-induced hepatic lipid disorder E3 model, we confirmed that the hepatic expression of lnc-HC/miR-130b-3p negatively correlated with that of the target genes and was closely associated with liver triglycerides concentration. These findings provide a deeper understanding of the regulatory roles of lnc-HC in hepatic lipid metabolism and NAFLD development.

Genomic analysis of a new heterotic maize group reveals key loci for pedigree breeding.

Genome-wide analyses of maize populations have clarified the genetic basis of crop domestication and improvement. However, limited information is available on how breeding improvement reshaped the genome in the process of the formation of heterotic groups. In this study, we identified a new heterotic group (X group) based on an examination of 512 Chinese maize inbred lines. The X group was clearly distinct from the other non-H&L groups, implying that X × HIL is a new heterotic pattern. We selected the core inbred lines for an analysis of yield-related traits. Almost all yield-related traits were better in the X lines than those in the parental lines, indicating that the primary genetic improvement in the X group during breeding was yield-related traits. We generated whole-genome sequences of these lines with an average coverage of 17.35× to explore genome changes further. We analyzed the identity-by-descent (IBD) segments transferred from the two parents to the X lines and identified 29 and 28 IBD conserved regions (ICRs) from the parents PH4CV and PH6WC, respectively, accounting for 28.8% and 12.8% of the genome. We also identified 103, 89, and 131 selective sweeps (SSWs) using methods that involved the π, Tajima's D, and CLR values, respectively. Notably, 96.13% of the ICRs co-localized with SSWs, indicating that SSW signals concentrated in ICRs. We identified 171 annotated genes associated with yield-related traits in maize both in ICRs and SSWs. To identify the genetic factors associated with yield improvement, we conducted QTL mapping for 240 lines from a DH population (PH4CV × PH6WC, which are the parents of X1132X) for ten key yield-related traits and identified a total of 55 QTLs. Furthermore, we detected three QTL clusters both in ICRs and SSWs. Based on the genetic evidence, we finally identified three key genes contributing to yield improvement in breeding the X group. These findings reveal key loci and genes targeted during pedigree breeding and provide new insights for future genomic breeding.

Antiadhesion Superhydrophobic Bipolar Electrocoagulation Tweezers with High Conductivity and Stability.

Irregularly shaped electrosurgical devices face significant challenges in electrosurgery due to serious blood and tissue adhesion. Superhydrophobic surfaces inspired by lotus leaves have attracted great attention for their promising antiadhesion properties. However, there are few methods for efficiently preparing superhydrophobic irregularly shaped bipolar electrocoagulation tweezers (BETs). Herein, we propose a simple and environmentally friendly method to fabricate antiadhesion superhydrophobic surfaces on BETs. The superhydrophobicity is obtained by combining laser texturing to form rough structures and low surface energy modification via stearic acid. The formation mechanism of superhydrophobicity is investigated through analyzing microstructures and chemical compositions by scanning electron microscopy, white-light interferometry, and X-ray photoelectron spectroscopy. The functionalized BET surfaces exhibit excellent water repellency with a contact angle of 159.6°, a roll-off angle of 1°, and a surface energy of 14.3 mJ/m2, possessing excellent antiadhesion properties against blood, chicken breast tissue, and pork tissue. Compared with ordinary BETs, the mass of blood, pork tissue, and chicken breast tissue adhered to the superhydrophobic BET is reduced by 97.70, 70.34, and 75.35%, respectively. Moreover, the superhydrophobic BETs have excellent conductivity and maintain good antiadhesion properties after low-temperature storage for 2 weeks, after being impacted by sand and blood and 30 cycles of tape peeling tests. With outstanding antiadhesion performance, the superhydrophobic BET may have promising application prospects in the electrosurgery field.