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1.
Nano Lett ; 24(25): 7741-7747, 2024 Jun 26.
Artigo em Inglês | MEDLINE | ID: mdl-38870320

RESUMO

The existence of fractionally quantized topological corner charge serves as a key indicator for two-dimensional (2D) second-order topological insulators (SOTIs), yet it has not been experimentally observed in realistic materials. Here, based on effective model analysis and symmetry arguments, we propose a strategy for achieving SOTI phases with in-gap corner states in 2D systems with antiferromagnetic (AFM) order. We discover that the band topology originates from the interplay between intrinsic spin-orbital coupling and interlayer AFM exchange interactions. Using first-principles calculations, we show that the 2D AFM SOTI phase can be realized in (MnBi2Te4)(Bi2Te3)m films. Moreover, we demonstrate that the SOTI states are linked to rotation topological invariants under 3-fold rotation symmetry C3, resulting in fractionally quantized corner charge, i.e., n3|e| (mod e). Due to the great achievements in (MnBi2Te4)(Bi2Te3)m systems, our results providing reliable material candidates for experimentally accessible AFM SOTIs should draw intense attention.

2.
Theranostics ; 14(7): 2993-3013, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38773972

RESUMO

The sirtuin (SIRT) family is well-known as a group of deacetylase enzymes that rely on nicotinamide adenine dinucleotide (NAD+). Among them, mitochondrial SIRTs (SIRT3, SIRT4, and SIRT5) are deacetylases located in mitochondria that regulate the acetylation levels of several key proteins to maintain mitochondrial function and redox homeostasis. Mitochondrial SIRTs are reported to have the Janus role in tumorigenesis, either tumor suppressive or oncogenic functions. Although the multi-faceted roles of mitochondrial SIRTs with tumor-type specificity in tumorigenesis, their critical functions have aroused a rising interest in discovering some small-molecule compounds, including inhibitors and activators for cancer therapy. Herein, we describe the molecular structures of mitochondrial SIRTs, focusing on elucidating their regulatory mechanisms in carcinogenesis, and further discuss the recent advances in developing their targeted small-molecule compounds for cancer therapy. Together, these findings provide a comprehensive understanding of the crucial roles of mitochondrial SIRTs in cancer and potential new therapeutic strategies.


Assuntos
Mitocôndrias , Neoplasias , Sirtuínas , Sirtuínas/metabolismo , Humanos , Neoplasias/tratamento farmacológico , Neoplasias/metabolismo , Mitocôndrias/metabolismo , Mitocôndrias/efeitos dos fármacos , Animais , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Carcinogênese/metabolismo , Carcinogênese/efeitos dos fármacos
3.
FEBS Open Bio ; 14(7): 1101-1115, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38710658

RESUMO

Heart failure with preserved ejection fraction (HFpEF) is one of the major subtypes of heart failure (HF) and no effective treatments for this common disease exist to date. Cardiac fibrosis is central to the pathology of HF and a potential avenue for the treatment of HFpEF. To explore key fibrosis-related genes and pathways in the pathophysiological process of HFpEF, a mouse model of HFpEF was constructed. The relevant gene expression profiles were downloaded from the Gene Expression Omnibus database, and single-sample Gene Set Enrichment Analysis (ssGSEA) was performed targeting fibrosis-related pathways to explore differentially expressed genes (DEGs) in healthy control and HFpEF heart tissues with cross-tabulation analysis of fibrosis-related genes. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the identified fibrosis-related genes. The two most significant DEGs were selected, and further validation was conducted in HFpEF mice. The results indicated that myocardial fibrosis was significantly upregulated in HFpEF mice compared to healthy controls, while the ssGSEA results revealed significant differences in the enrichment of nine fibrosis-related pathways in HFpEF myocardial tissue, with 112 out of 798 DEGs being related to fibrosis. The in vivo results demonstrated that expression levels of resistin-like molecule gamma (Relmg) and adenylate cyclase 1 (Adcy1) in the heart tissues of HFpEF mice were significantly higher and lower, respectively, compared to healthy controls. Taken together, these results suggest that Relmg and Acdy1 as well as the fibrosis process may be potential targets for HFpEF treatment.


Assuntos
Adenilil Ciclases , Fibrose , Insuficiência Cardíaca , Animais , Camundongos , Fibrose/genética , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/genética , Insuficiência Cardíaca/patologia , Adenilil Ciclases/metabolismo , Adenilil Ciclases/genética , Miocárdio/metabolismo , Miocárdio/patologia , Masculino , Modelos Animais de Doenças , Perfilação da Expressão Gênica , Camundongos Endogâmicos C57BL
4.
Biomed Pharmacother ; 175: 116689, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38703508

RESUMO

Ischemic heart disease invariably leads to devastating damage to human health. Nicotinamide ribose (NR), as one of the precursors of NAD+ synthesis, has been discovered to exert a protective role in various neurological and cardiovascular disorders. Our findings demonstrated that pretreatment with 200 mg/kg NR for 3 h significantly reduced myocardial infarct area, decreased levels of CK-MB and LDH in serum, and improved cardiac function in the rats during myocardial ischemia-reperfusion (I/R) injury. Meanwhile, 0.5 mM NR also effectively increased the viability and decreased the LDH release of H9c2 cells during OGD/R. We had provided evidence that NR pretreatment could decrease mitochondrial reactive oxygen species (mtROS) production and MDA content, and enhance SOD activity, thereby mitigating mitochondrial damage and inhibiting apoptosis during myocardial I/R injury. Further investigations revealed that NR increased NAD+ content and upregulated SIRT3 protein expression in myocardium. Through using of SIRT3 small interfering RNA and the SIRT3 deacetylase activity inhibitor 3-TYP, we had confirmed that the cardioprotective effect of NR on cardiomyocytes was largely dependent on the inhibition of mitochondrial oxidative stress via SIRT3-SOD2 axis. Overall, our study suggested that exogenous supplementation with NR mitigated mitochondrial damage and inhibited apoptosis during myocardial I/R injury by reducing mitochondrial oxidative stress via SIRT3-SOD2-mtROS pathway.


Assuntos
Apoptose , Traumatismo por Reperfusão Miocárdica , Niacinamida , Estresse Oxidativo , Compostos de Piridínio , Ratos Sprague-Dawley , Transdução de Sinais , Sirtuína 3 , Superóxido Dismutase , Animais , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Traumatismo por Reperfusão Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/patologia , Sirtuína 3/metabolismo , Transdução de Sinais/efeitos dos fármacos , Masculino , Niacinamida/farmacologia , Niacinamida/análogos & derivados , Superóxido Dismutase/metabolismo , Ratos , Apoptose/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Compostos de Piridínio/farmacologia , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Espécies Reativas de Oxigênio/metabolismo , Linhagem Celular , Cardiotônicos/farmacologia , Sirtuínas
5.
Redox Biol ; 73: 103176, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38705094

RESUMO

Excitotoxicity is a prevalent pathological event in neurodegenerative diseases. The involvement of ferroptosis in the pathogenesis of excitotoxicity remains elusive. Transcriptome analysis has revealed that cytoplasmic reduced nicotinamide adenine dinucleotide phosphate (NADPH) levels are associated with susceptibility to ferroptosis-inducing compounds. Here we show that exogenous NADPH, besides being reductant, interacts with N-myristoyltransferase 2 (NMT2) and upregulates the N-myristoylated ferroptosis suppressor protein 1 (FSP1). NADPH increases membrane-localized FSP1 and strengthens resistance to ferroptosis. Arg-291 of NMT2 is critical for the NADPH-NMT2-FSP1 axis-mediated suppression of ferroptosis. This study suggests that NMT2 plays a pivotal role by bridging NADPH levels and neuronal susceptibility to ferroptosis. We propose a mechanism by which the NADPH regulates N-myristoylation, which has important implications for ferroptosis and disease treatment.


Assuntos
Ferroptose , NADP , Humanos , NADP/metabolismo , Animais , Aciltransferases/metabolismo , Aciltransferases/genética , Camundongos , Processamento de Proteína Pós-Traducional
6.
Lipids Health Dis ; 23(1): 157, 2024 May 25.
Artigo em Inglês | MEDLINE | ID: mdl-38796440

RESUMO

AIMS: About 20-40% patients with type 2 diabetes mellitus (T2DM) had an increased risk of developing diabetic nephropathy (DN). Dipeptidyl peptidase-4 inhibitors (DPP-4i) were recommended for treatment of T2DM, while the impact of DPP-4i on renal function remained unclear. This study aimed to explore the effect of DPP-4i on renal parameter of estimated glomerular filtration rate (eGFR) and albumin-to-creatinine ratio (ACR) in T2DM. METHODS: A systematic search was performed across PubMed, Embase and Cochrane Library. A fixed or random-effects model was used for quantitative synthesis according to the heterogeneity, which was assessed with I2 index. Sensitivity analysis and publication bias were performed with standard methods, respectively. RESULTS: A total of 17 randomized controlled trials were identified. Administration of DPP-4i produced no significant effect on eGFR (WMD, -0.92 mL/min/1.73m2, 95% CI, -2.04 to 0.19) in diabetic condition. DPP-4i produced a favorable effect on attenuating ACR (WMD, -2.76 mg/g, 95% CI, -5.23 to -0.29) in patients with T2DM. The pooled estimate was stable based on the sensitivity test. No publication bias was observed according to Begg's and Egger's tests. CONCLUSIONS: Treatment with DPP-4i preserved the renal parameter of eGFR in diabetic condition. Available evidences suggested that administration of DPP-4i produced a favorable effect on attenuating ACR in patients with T2DM. INTERNATIONAL PROSPECTIVE REGISTER FOR SYSTEMATIC REVIEW (PROSPERO) NUMBER: CRD.42020144642.


Assuntos
Diabetes Mellitus Tipo 2 , Nefropatias Diabéticas , Inibidores da Dipeptidil Peptidase IV , Taxa de Filtração Glomerular , Rim , Ensaios Clínicos Controlados Aleatórios como Assunto , Humanos , Diabetes Mellitus Tipo 2/tratamento farmacológico , Diabetes Mellitus Tipo 2/complicações , Inibidores da Dipeptidil Peptidase IV/uso terapêutico , Taxa de Filtração Glomerular/efeitos dos fármacos , Nefropatias Diabéticas/tratamento farmacológico , Rim/efeitos dos fármacos , Rim/fisiopatologia , Creatinina/urina , Creatinina/sangue
7.
Acta Pharmacol Sin ; 2024 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-38750074

RESUMO

Hypoxia-ischemia (HI) is one of the main causes of neonatal brain injury. Mitophagy has been implicated in the degradation of damaged mitochondria and cell survival following neonatal brain HI injury. Pleckstrin homology-like domain family A member 1 (PHLDA1) plays vital roles in the progression of various disorders including the regulation of oxidative stress, the immune responses and apoptosis. In the present study we investigated the role of PHLDA1 in HI-induced neuronal injury and further explored the mechanisms underlying PHLDA1-regulated mitophagy in vivo and in vitro. HI model was established in newborn rats by ligation of the left common carotid artery plus exposure to an oxygen-deficient chamber with 8% O2 and 92% N2. In vitro studies were conducted in primary hippocampal neurons subjected to oxygen and glucose deprivation/-reoxygenation (OGD/R). We showed that the expression of PHLDA1 was significantly upregulated in the hippocampus of HI newborn rats and in OGD/R-treated primary neurons. Knockdown of PHLDA1 in neonatal rats via lentiviral vector not only significantly ameliorated HI-induced hippocampal neuronal injury but also markedly improved long-term cognitive function outcomes, whereas overexpression of PHLDA1 in neonatal rats via lentiviral vector aggravated these outcomes. PHLDA1 knockdown in primary neurons significantly reversed the reduction of cell viability and increase in intracellular reactive oxygen species (ROS) levels, and attenuated OGD-induced mitochondrial dysfunction, whereas overexpression of PHLDA1 decreased these parameters. In OGD/R-treated primary hippocampal neurons, we revealed that PHLDA1 knockdown enhanced mitophagy by activating FUNDC1, which was abolished by FUNDC1 knockdown or pretreatment with mitophagy inhibitor Mdivi-1 (25 µM). Notably, pretreatment with Mdivi-1 or the knockdown of FUNDC1 not only increased brain infarct volume, but also abolished the neuroprotective effect of PHLDA1 knockdown in HI newborn rats. Together, these results demonstrate that PHLDA1 contributes to neonatal HI-induced brain injury via inhibition of FUNDC1-mediated neuronal mitophagy.

8.
Front Immunol ; 15: 1342658, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38680495

RESUMO

Objectives: Inflammatory cytokines (ICs) play an important role in erectile dysfunction (ED). Previous studies have demonstrated that most ED patients have high levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8). The causality between 41 ICs and ED is investigated using the Mendelian randomization (MR) approach. Methods: Single nucleotide polymorphisms (SNPs) exposure data of 41 ICs came from a genome-wide association study (GWAS) of 8293 subjects. At the same time, the FINNGEN R9 database provided the ED outcome data containing 2205 ED patients and 164104 controls. MR-Egger (ME), inverse variance weighting (IVW), and weighted median (WM) were applied to conduct the MR study and IVW was taken as the main criterion. Results: From a genetic perspective, the increase of interferon-inducible protein-10 (IP-10) level significantly increased the risk of ED (P=0.043, odds ratio (OR)=1.269, 95% confidence interval (95%CI): 1.007-1.600), while the increase of interleukin-1 receptor antagonist (IL-1RA) markedly decreased the risk of ED (P=0.037, OR=0.768, 95%CI: 0.600-0.984). Meanwhile, IP-10 (p=0.099) and IL-1RA (p=0.135) failed to demonstrate causality in reverse MR analysis. Conclusions: Changes in ICs levels will significantly affect the risk of ED, especially IP-10 as a risk component for ED and IL-1RA as a protective component for ED. In the future, we can achieve targeted treatment and prevention of ED by intervening with specific inflammatory factors.


Assuntos
Citocinas , Disfunção Erétil , Estudo de Associação Genômica Ampla , Análise da Randomização Mendeliana , Polimorfismo de Nucleotídeo Único , Humanos , Masculino , Disfunção Erétil/genética , Citocinas/genética , Predisposição Genética para Doença , Mediadores da Inflamação/metabolismo , Quimiocina CXCL10/genética
9.
Ecotoxicol Environ Saf ; 277: 116361, 2024 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-38663189

RESUMO

Soil heavy metal contamination has become a global environmental issue, which threaten soil quality, food security and human health. Symphytum officinale L. have exhibited high tolerance and restoration capacity to heavy metals (HMs) stress. However, little is known about the mechanisms of HMs in S. officinale. In this study, transcriptomic and physiological changes of S. officinale response to different HMs (Pb, Cd and Zn) were analyzed and investigated the key genes and pathways involved in HMs uptake patterns. The results showed that phenotypic effects are not significant, and antioxidant enzyme activities were all upregulated. Transcriptome analysis indicated that 1247 differential genes were up-regulated, and 1963 differential genes were down-regulated under Cd stress, while 3752 differential genes were up-regulated, and 7197 differential genes were down-regulated under Pb stress; and 527 differential genes were up-regulated; and 722 differential genes were down-regulated under Zn stress. Based on their expression, we preliminarily speculate that different HMs resistance of S. officinale may be regulated by the differential expression of key genes. These results provide a theoretical basis for determining the exact expression of genes in plants under different heavy metal stress, the processes involved molecular pathways, and how they can be efficiently utilized to improve plant tolerance to toxic metals and improve phytoremediation efficiency.


Assuntos
Metais Pesados , Poluentes do Solo , Transcriptoma , Metais Pesados/toxicidade , Poluentes do Solo/toxicidade , Transcriptoma/efeitos dos fármacos , Estresse Fisiológico/efeitos dos fármacos , Estresse Fisiológico/genética , Chumbo/toxicidade , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Cádmio/toxicidade , Perfilação da Expressão Gênica , Biodegradação Ambiental , Zinco/toxicidade
10.
Sensors (Basel) ; 24(7)2024 Mar 24.
Artigo em Inglês | MEDLINE | ID: mdl-38610287

RESUMO

Fringe projection profilometry (FPP), with benefits such as high precision and a large depth of field, is a popular 3D optical measurement method widely used in precision reconstruction scenarios. However, the pixel brightness at reflective edges does not satisfy the conditions of the ideal pixel-wise phase-shifting model due to the influence of scene texture and system defocus, resulting in severe phase errors. To address this problem, we theoretically analyze the non-pixel-wise phase propagation model for texture edges and propose a reprojection strategy based on scene texture modulation. The strategy first obtains the reprojection weight mask by projecting typical FPP patterns and calculating the scene texture reflection ratio, then reprojects stripe patterns modulated by the weight mask to eliminate texture edge effects, and finally fuses coarse and refined phase maps to generate an accurate phase map. We validated the proposed method on various texture scenes, including a smooth plane, depth surface, and curved surface. Experimental results show that the root mean square error (RMSE) of the phase at the texture edge decreased by 53.32%, proving the effectiveness of the reprojection strategy in eliminating depth errors at texture edges.

11.
Autophagy ; : 1-21, 2024 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-38686804

RESUMO

Obesity is one of the most common metabolic diseases around the world, which is distinguished by the abnormal buildup of triglycerides within adipose cells. Recent research has revealed that autophagy regulates lipid mobilization to maintain energy balance. TIGAR (Trp53 induced glycolysis regulatory phosphatase) has been identified as a glycolysis inhibitor, whether it plays a role in the metabolism of lipids is unknown. Here, we found that TIGAR transgenic (TIGAR+/+) mice exhibited increased fat mass and trended to obesity phenotype. Non-target metabolomics showed that TIGAR caused the dysregulation of the metabolism profile. The quantitative transcriptome sequencing identified an increased levels of LRRK2 and RAB7B in the adipose tissue of TIGAR+/+ mice. It was confirmed in vitro that TIGAR overexpression increased the levels of LRRK2 by inhibiting polyubiquitination degradation, thereby suppressing macroautophagy and chaperone-mediated autophagy (CMA) while increasing lipid accumulation which were reversed by the LRRK2 inhibitor DNL201. Furthermore, TIGAR drove LRRK2 to interact with RAB7B for suppressing lysosomal degradation of lipid droplets, while the increased lipid droplets in adipocytes were blocked by the RAB7B inhibitor ML282. Additionally, fat-specific TIGAR knockdown of TIGAR+/+ mice alleviated the symptoms of obesity, and adipose tissues-targeting superiority DNL201 nano-emulsion counteracted the obesity phenotype in TIGAR+/+ mice. In summary, the current results indicated that TIGAR performed a vital function in the lipid metabolism through LRRK2-mediated negative regulation of macroautophagy and CMA in adipocyte. The findings suggest that TIGAR has the potential to serve as a viable therapeutic target for treating obesity and its associated metabolic dysfunction.

13.
J Plant Res ; 137(4): 605-617, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38506958

RESUMO

The intervention of nectar robbers in plant pollination systems will cause some pollinators to modify their foraging behavior to act as secondary robbers, consequently adopting a mixed foraging strategy. The influence of nectar robbing on pollinator behavior may be affected by spatio-temporal difference of robbing intensity, and consequently, may have different effects on the pollination of host plants. However, whether and how the nectar robbing might influence pollinators under different robbing intensity still needs further investigation. In this study, Symphytum officinale was used to detect the effect of nectar robbers on pollinators under different robbing intensity as well as their effects on plant reproductive success. Six robbing levels and three bumblebees with mixed foraging behaviors were used to evaluate the effect of different robbing intensity on pollinator behavior, visitation rate, flower longevity and pollen deposition. Our results indicated that the robbing rate increased gradually with the proportion of robbed flowers, but which did not affect the frequency of legitimate visits. The increase of robbing rate promoted the corolla abscission, and then enhanced the self-pollen deposition, but which had no significant effect on cross-pollen deposition. These results indicate that the overall fitness of S. officinale was improved by combined self and cross-pollination modes when visited by both pollinators and nectar robbers simultaneously. Although nectar robbing is not uncommon, its consequences for pollination in the interaction web have not been well studied. Our results emphasize the significance of indirect impacts in mediating the adaptive outcomes of species interactions.


Assuntos
Boraginaceae , Flores , Néctar de Plantas , Polinização , Reprodução , Polinização/fisiologia , Flores/fisiologia , Animais , Abelhas/fisiologia , Reprodução/fisiologia , Néctar de Plantas/fisiologia , Boraginaceae/fisiologia , Pólen/fisiologia
14.
J Cancer Res Clin Oncol ; 150(3): 132, 2024 Mar 16.
Artigo em Inglês | MEDLINE | ID: mdl-38492096

RESUMO

OBJECTIVES: To develop a radiomics model based on diffusion-weighted imaging (DWI) utilizing automated machine learning method to differentiate cerebral cystic metastases from brain abscesses. MATERIALS AND METHODS: A total of 186 patients with cerebral cystic metastases (n = 98) and brain abscesses (n = 88) from two clinical institutions were retrospectively included. The datasets (129 from institution A) were randomly portioned into separate 75% training and 25% internal testing sets. Radiomics features were extracted from DWI images using two subregions of the lesion (cystic core and solid wall). A thorough image preprocessing method was applied to DWI images to ensure the robustness of radiomics features before feature extraction. Then the Tree-based Pipeline Optimization Tool (TPOT) was utilized to search for the best optimized machine learning pipeline, using a fivefold cross-validation in the training set. The external test set (57 from institution B) was used to evaluate the model's performance. RESULTS: Seven distinct TPOT models were optimized to distinguish between cerebral cystic metastases and abscesses either based on different features combination or using wavelet transform. The optimal model demonstrated an AUC of 1.00, an accuracy of 0.97, sensitivity of 1.00, and specificity of 0.93 in the internal test set, based on the combination of cystic core and solid wall radiomics signature using wavelet transform. In the external test set, this model reached 1.00 AUC, 0.96 accuracy, 1.00 sensitivity, and 0.93 specificity. CONCLUSION: The DWI-based radiomics model established by TPOT exhibits a promising predictive capacity in distinguishing cerebral cystic metastases from abscesses.


Assuntos
Abscesso Encefálico , Neoplasias Supratentoriais , Humanos , Radiômica , Estudos Retrospectivos , Abscesso Encefálico/diagnóstico por imagem , Imagem de Difusão por Ressonância Magnética , Aprendizado de Máquina
15.
Aging (Albany NY) ; 16(6): 5676-5702, 2024 03 20.
Artigo em Inglês | MEDLINE | ID: mdl-38517387

RESUMO

Macrophages are found in a variety of tumors and play a critical role in shaping the tumor microenvironment, affecting tumor progression, metastasis, and drug resistance. However, the clinical relevance of marker genes associated with macrophage in kidney renal clear cell carcinoma (KIRC) has yet to be documented. In this study, we initiated a thorough examination of single-cell RNA sequencing (scRNA-seq) data for KIRC retrieved from the Gene Expression Omnibus (GEO) database and determined 244 macrophage marker genes (MMGs). Univariate analysis, LASSO regression, and multivariate regression analysis were performed to develop a five-gene prognostic signature in The Cancer Genome Atlas (TCGA) database, which could divide KIRC patients into low-risk (L-R) and high-risk (H-R) groups. Then, a nomogram was constructed to predict the survival rate of KIRC patients at 1, 3, and 5 years, which was well assessed by receiver operating characteristic curve (ROC), calibration curve, and decision curve analyses (DCA). Functional enrichment analysis showed that immune-related pathways (such as immunoglobulin complex, immunoglobulin receptor binding, and cytokine-cytokine receptor interaction) were mainly enriched in the H-R group. Additionally, in comparison to the L-R cohort, patients belonging to the H-R cohort exhibited increased immune cell infiltration, elevated expression of immune checkpoint genes (ICGs), and a higher tumor immune dysfunction and exclusion (TIDE) score. This means that patients in the H-R group may be less sensitive to immunotherapy than those in the L-R group. Finally, IFI30 was validated to increase the ability of KIRC cells to proliferate, invade and migrate in vitro. In summary, our team has for the first time developed and validated a predictive model based on macrophage marker genes to accurately predict overall survival (OS), immune characteristics, and treatment benefit in KIRC patients.


Assuntos
Carcinoma de Células Renais , Neoplasias Renais , Humanos , Carcinoma de Células Renais/genética , Prognóstico , Análise de Sequência de RNA , Neoplasias Renais/genética , Imunoglobulinas , Rim , Microambiente Tumoral/genética
16.
Nanoscale ; 16(13): 6662-6668, 2024 Mar 28.
Artigo em Inglês | MEDLINE | ID: mdl-38487896

RESUMO

Developing high-performance bifunctional electrocatalysts towards the hydrogen evolution reaction/oxygen evolution reaction (HER/OER) holds great significance for efficient water splitting. This work presents a two-stage metal-organic thermal evaporation strategy for the fabrication of Ru-based catalysts (Ru/NF) through growing ruthenium (Ru)/ruthenium dioxide (RuO2) nanoparticles (NPs) on nickel foam (NF). The optimal Ru/NF shows remarkable performance in both the HER (26.1 mV) and the OER (235.4 mV) at 10 mA cm-2 in an alkaline medium. The superior OER performance can be attributed to the synergistic interaction between Ru and RuO2, facilitating fast alkaline water splitting. Density functional theory studies reveal that the resulting Ru/RuO2 with the (110) crystal surface reinforces the adsorption of oxygen on RuO2, while metallic Ru improves water dissociation in alkaline electrolytes. Besides, Ru/NF requires only 1.50 V at 10 mA cm-2 for overall water splitting, surpassing 20 wt% Pt/C/NF||RuO2/NF. This work demonstrates the promising potential of a thermal evaporation approach for designing stable Ru-based nanomaterials loaded onto conductive substrates for high performance overall water splitting.

17.
Plant J ; 118(3): 717-730, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38213282

RESUMO

Cryptotaenia japonica, a traditional medicinal and edible vegetable crops, is well-known for its attractive flavors and health care functions. As a member of the Apiaceae family, the evolutionary trajectory and biological properties of C. japonica are not clearly understood. Here, we first reported a high-quality genome of C. japonica with a total length of 427 Mb and N50 length 50.76 Mb, was anchored into 10 chromosomes, which confirmed by chromosome (cytogenetic) analysis. Comparative genomic analysis revealed C. japonica exhibited low genetic redundancy, contained a higher percentage of single-cope gene families. The homoeologous blocks, Ks, and collinearity were analyzed among Apiaceae species contributed to the evidence that C. japonica lacked recent species-specific WGD. Through comparative genomic and transcriptomic analyses of Apiaceae species, we revealed the genetic basis of the production of anthocyanins. Several structural genes encoding enzymes and transcription factor genes of the anthocyanin biosynthesis pathway in different species were also identified. The CjANSa, CjDFRb, and CjF3H gene might be the target of Cjaponica_2.2062 (bHLH) and Cjaponica_1.3743 (MYB). Our findings provided a high-quality reference genome of C. japonica and offered new insights into Apiaceae evolution and biology.


Assuntos
Antocianinas , Apiaceae , Genoma de Planta , Genômica , Antocianinas/biossíntese , Antocianinas/genética , Antocianinas/metabolismo , Genoma de Planta/genética , Apiaceae/genética , Apiaceae/metabolismo , Filogenia , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Regulação da Expressão Gênica de Plantas , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Cromossomos de Plantas/genética
18.
IEEE Trans Pattern Anal Mach Intell ; 46(5): 3796-3812, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38170661

RESUMO

Successful point cloud registration relies on accurate correspondences established upon powerful descriptors. However, existing neural descriptors either leverage a rotation-variant backbone whose performance declines under large rotations, or encode local geometry that is less distinctive. To address this issue, we introduce RIGA to learn descriptors that are Rotation-Invariant by design and Globally-Aware. From the Point Pair Features (PPFs) of sparse local regions, rotation-invariant local geometry is encoded into geometric descriptors. Global awareness of 3D structures and geometric context is subsequently incorporated, both in a rotation-invariant fashion. More specifically, 3D structures of the whole frame are first represented by our global PPF signatures, from which structural descriptors are learned to help geometric descriptors sense the 3D world beyond local regions. Geometric context from the whole scene is then globally aggregated into descriptors. Finally, the description of sparse regions is interpolated to dense point descriptors, from which correspondences are extracted for registration. To validate our approach, we conduct extensive experiments on both object- and scene-level data. With large rotations, RIGA surpasses the state-of-the-art methods by a margin of 8 ° in terms of the Relative Rotation Error on ModelNet40 and improves the Feature Matching Recall by at least 5 percentage points on 3DLoMatch.

19.
Ann Thorac Cardiovasc Surg ; 30(1)2024 Jan 26.
Artigo em Inglês | MEDLINE | ID: mdl-37730311

RESUMO

PURPOSE: Functional preserving sublobectomy (FPSL), a novel balancing strategy for segmentectomy and wedge resection, allows rapid and accurate removal of invisible nodules without the use of any preoperative localization markers. This study aimed to share single-center experience of lateral dorsal basal lung resection based on FPSL, so as to provide new surgical options for thoracic surgeons. METHODS: A retrospective analysis was performed on 13 patients who underwent thoracoscopic basal lung resection after FPSL at XX hospital from January 2021 to August 2022. RESULTS: The operation was successfully performed in 13 patients by using FPSL, including 12 patients with malignant tumors. The mean operating time was 107.5 ± 25.6 min. The mean postoperative hospital stay was 3.7 ± 2.4 days. None of the patients needed extended excision, such as an entire basal or inferior lobectomy. CONCLUSION: Our single-center experience showed that the FPSL method only dealt with the target vessels, which greatly reduced the technical difficulty of surgery. In addition, both arteries and veins could be used as target vessels, and in particular cases such as undeveloped interlobar fissure, the operation could still be completed successfully. Lateral dorsal basal lung resection based on FPSL may be a new surgical option for surgeons.


Assuntos
Neoplasias Pulmonares , Humanos , Neoplasias Pulmonares/diagnóstico por imagem , Neoplasias Pulmonares/cirurgia , Neoplasias Pulmonares/patologia , Estudos Retrospectivos , Resultado do Tratamento , Pneumonectomia/efeitos adversos , Pneumonectomia/métodos , Pulmão/cirurgia , Cirurgia Torácica Vídeoassistida/efeitos adversos , Cirurgia Torácica Vídeoassistida/métodos
20.
Neurosci Bull ; 40(3): 363-382, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-37856037

RESUMO

Autophagy involves the sequestration and delivery of cytoplasmic materials to lysosomes, where proteins, lipids, and organelles are degraded and recycled. According to the way the cytoplasmic components are engulfed, autophagy can be divided into macroautophagy, microautophagy, and chaperone-mediated autophagy. Recently, many studies have found that autophagy plays an important role in neurological diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, neuronal excitotoxicity, and cerebral ischemia. Autophagy maintains cell homeostasis in the nervous system via degradation of misfolded proteins, elimination of damaged organelles, and regulation of apoptosis and inflammation. AMPK-mTOR, Beclin 1, TP53, endoplasmic reticulum stress, and other signal pathways are involved in the regulation of autophagy and can be used as potential therapeutic targets for neurological diseases. Here, we discuss the role, functions, and signal pathways of autophagy in neurological diseases, which will shed light on the pathogenic mechanisms of neurological diseases and suggest novel targets for therapies.


Assuntos
Doença de Alzheimer , Doença de Huntington , Doenças do Sistema Nervoso , Doença de Parkinson , Humanos , Autofagia/fisiologia , Doença de Parkinson/metabolismo
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