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1.
Front Neurol ; 15: 1243597, 2024.
Article in English | MEDLINE | ID: mdl-38994494

ABSTRACT

Aim: To evaluate the comparative efficacy and safety of various doses of oral cannabidiol (CBD) in treating refractory epilepsy indications, thus providing more informative evidence for clinical decision-making. Methods: A literature search of PubMed, Embase, the Cochrane library, and Web of Science (WoS) was performed to retrieve relevant randomized controlled trials (RCTs) that compared different doses of oral CBD with placebo or each other in refractory epilepsy indications. The search was limited from the inception of each database to January 3, 2023. Relative risk [RR] with a 95% confidence interval [CI] was used to express results. STATA/SE 14 was employed for network meta-analysis. Results: Six RCTs involving 972 patients were included in the final data analysis. Network meta-analysis showed that, CBD10 (10 mg/kg/day) (RR: 1.77, 95%CI: 1.28 to 2.44), CBD20 (20 mg/kg/day) (RR: 1.91, 95%CI: 1.49 to 2.46), CBD25 (25 mg/kg/day) (RR: 1.61, 95%CI: 0.96 to 2.70), and CBD50 (50 mg/kg/day) (RR: 1.78, 95%CI: 1.07 to 2.94) were associated with higher antiseizure efficacy although the pooled result for CBD25 was only close to significant. In addition, in terms of the risk of treatment-emergent adverse events (TEAEs), the difference between different doses is not significant. However, CBD20 ranked first in terms of antiseizure efficacy, followed by CBD50, CBD10, and CBD25. For TEAEs, CBD25 ranked first, followed by CBD10, CBD50, CBD5, and CBD20. Conclusion: For refractory indications, CBD20 may be optimal option for antiseizure efficacy; however, CBD25 may be best for TEAEs. Therefore, an appropriate dose of oral CBD should be selected based on the actual situation. Due to the limitations of eligible studies and the limited sample size, more studies are needed in the future to validate our findings.

2.
Sci Rep ; 14(1): 13914, 2024 Jun 17.
Article in English | MEDLINE | ID: mdl-38886386

ABSTRACT

This research paper presents a comprehensive investigation into the utilization of color image processing technologies and deep learning algorithms in the development of a robot vision system specifically designed for 8-ball billiards. The sport of billiards, with its various games and ball arrangements, presents unique challenges for robotic vision systems. The proposed methodology addresses these challenges through two main components: object detection and ball pattern recognition. Initially, a robust algorithm is employed to detect the billiard balls using color space transformation and thresholding techniques. This is followed by determining the position of the billiard table through strategic cropping and isolation of the primary table area. The crucial phase involves the intricate task of recognizing ball patterns to differentiate between solid and striped balls. To achieve this, a modified convolutional neural network is utilized, leveraging the Xception network optimized by an innovative algorithm known as the Improved Chaos African Vulture Optimization (ICAVO) algorithm. The ICAVO algorithm enhances the Xception network's performance by efficiently exploring the solution space and avoiding local optima. The results of this study demonstrate a significant enhancement in recognition accuracy, with the Xception/ICAVO model achieving remarkable recognition rates for both solid and striped balls. This paves the way for the development of more sophisticated and efficient billiards robots. The implications of this research extend beyond 8-ball billiards, highlighting the potential for advanced robotic vision systems in various applications. The successful integration of color image processing, deep learning, and optimization algorithms shows the effectiveness of the proposed methodology. This research has far-reaching implications that go beyond just billiards. The cutting-edge robotic vision technology can be utilized for detecting and tracking objects in different sectors, transforming industrial automation and surveillance setups. By combining color image processing, deep learning, and optimization algorithms, the system proves its effectiveness and flexibility. The innovative approach sets the stage for creating advanced and productive robotic vision systems in various industries.

3.
Oncol Rep ; 52(2)2024 08.
Article in English | MEDLINE | ID: mdl-38940337

ABSTRACT

The incidence of tumors in the human digestive system is relatively high, including esophageal cancer, liver cancer, pancreatic cancer, gastric cancer and colorectal cancer. These malignancies arise from a complex interplay of environmental and genetic factors. Among them, long non­coding RNAs (lncRNAs), which cannot be translated into proteins, serve an important role in the development, progression, migration and prognosis of tumors. Small nucleolar RNA host gene 16 (SNHG16) is a typical lncRNA, and its relationship with digestive system tumors has been widely explored. The prevailing hypothesis suggests that the principal molecular mechanism of SNHG16 in digestive system tumors involves it functioning as a competitive endogenous RNA that interacts with other proteins, regulates various genes and influences a downstream target molecule. The present review summarizes recent research on the relationship between SNHG16 and numerous types of digestive system cancer, encompassing its biological functions, underlying mechanisms and potential clinical implications. Furthermore, it outlines the association between SNHG16 expression and pertinent risk factors, such as smoking, infection and diet. The present review indicated the promise of SNHG16 as a potential biomarker and therapeutic target in human digestive system cancer.


Subject(s)
Biomarkers, Tumor , Digestive System Neoplasms , Gene Expression Regulation, Neoplastic , RNA, Long Noncoding , Humans , RNA, Long Noncoding/genetics , Digestive System Neoplasms/genetics , Digestive System Neoplasms/pathology , Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Prognosis
4.
Biosensors (Basel) ; 14(6)2024 Jun 01.
Article in English | MEDLINE | ID: mdl-38920589

ABSTRACT

The ratiometric detection method has a strong attraction for photoelectrochemical bioanalysis due to its high reliability and real-time calibration. However, its implementation typically depends on the spatial resolution of equipment and the pairing of wavelength/potential with photoactive materials. In this paper, a novel ratiometric photoelectrochemical biosensor based on front and back illumination was prepared for the detection of glutathione (GSH). Unlike traditional ratio methods, this ratiometric biosensor does not require voltage and wavelength modulation, thereby avoiding potential crosstalk caused by voltage and wavelength modulation. Additionally, the formation of a heterojunction between mTiO2 and Ag2S is conducive to enhancing light absorption and promoting charge separation, thereby boosting the photocurrent signal. Apart from forming a heterojunction with TiO2, Ag2S also shows a specific affinity towards GSH, thus enhancing the selectivity of the mTiO2/Ag2S ratiometric photoelectrochemical biosensor. The results demonstrate that the ratiometric photoelectrochemical biosensor exhibits a good detection range and a low detection limit for GSH, while also possessing significant interference elimination capability. The GSH detection range is 0.01-10 mmol L-1 with a detection limit of 6.39 × 10-3 mmol·L-1. The relative standard deviation of 20 repeated detections is 0.664%. Impressively, the proposed novel ratiometric PEC biosensor demonstrates enviable universality, providing new insights for the design and construction of PEC ratiometric sensing platforms.


Subject(s)
Biosensing Techniques , Electrochemical Techniques , Glutathione , Titanium , Glutathione/analysis , Titanium/chemistry , Limit of Detection
5.
BMC Ophthalmol ; 24(1): 228, 2024 May 31.
Article in English | MEDLINE | ID: mdl-38822340

ABSTRACT

BACKGROUND: Several autoimmune disorders have been linked to polymorphisms in IL10 and IL6R genes. This research aimed to study whether single nucleotide polymorphisms (SNPs) in the genes of IL10 and IL6R were associated with acute anterior uveitis (AAU) in Han Chinese. METHODS: Genotyping was carried out by the iPLEX Gold Genotyping Assay. Our study comprised 420 patients with AAU and 918 healthy subjects from Han Chinese. Using the chi-square (χ2) test, alleles and genotypes were analyzed between AAU subjects and healthy controls. RESULTS: All ten SNPs were successfully genotyped and four SNPs (IL10/rs1800871, IL10/rs3021094, IL10/rs2222202, IL6R/rs4845618) exhibited weak associations with AAU, as indicated by their Puncorr values. However, upon applying the Bonferroni correction, there was no significant association between AAU and the control subjects. Additionally, the haplotype analysis of the ten SNPs revealed no association with AAU. CONCLUSION: Our findings suggested that polymorphisms of the tested ten SNPs on the IL10 and IL6R genes did not show any association with the risk of developing AAU among the Han Chinese population.


Subject(s)
Asian People , Genetic Predisposition to Disease , Genotype , Interleukin-10 , Polymorphism, Single Nucleotide , Receptors, Interleukin-6 , Uveitis, Anterior , Humans , Uveitis, Anterior/genetics , Male , Interleukin-10/genetics , Female , Receptors, Interleukin-6/genetics , Adult , China/epidemiology , Acute Disease , Middle Aged , Asian People/genetics , Case-Control Studies , Gene Frequency , Young Adult , Alleles , Haplotypes , Aged , East Asian People
6.
Nat Commun ; 15(1): 3437, 2024 Apr 23.
Article in English | MEDLINE | ID: mdl-38653755

ABSTRACT

Phytoalexin sakuranetin functions in resistance against rice blast. However, the mechanisms underlying the effects of sakuranetin remains elusive. Here, we report that rice lines expressing resistance (R) genes were found to contain high levels of sakuranetin, which correlates with attenuated endocytic trafficking of plasma membrane (PM) proteins. Exogenous and endogenous sakuranetin attenuates the endocytosis of various PM proteins and the fungal effector PWL2. Moreover, accumulation of the avirulence protein AvrCO39, resulting from uptake into rice cells by Magnaporthe oryzae, was reduced following treatment with sakuranetin. Pharmacological manipulation of clathrin-mediated endocytic (CME) suggests that this pathway is targeted by sakuranetin. Indeed, attenuation of CME by sakuranetin is sufficient to convey resistance against rice blast. Our data reveals a mechanism of rice against M. oryzae by increasing sakuranetin levels and repressing the CME of pathogen effectors, which is distinct from the action of many R genes that mainly function by modulating transcription.


Subject(s)
Ascomycota , Disease Resistance , Endocytosis , Flavonoids , Oryza , Phytoalexins , Plant Diseases , Plant Proteins , Oryza/microbiology , Oryza/metabolism , Oryza/drug effects , Oryza/genetics , Plant Diseases/microbiology , Endocytosis/drug effects , Disease Resistance/genetics , Disease Resistance/drug effects , Plant Proteins/metabolism , Plant Proteins/genetics , Sesquiterpenes/pharmacology , Sesquiterpenes/metabolism , Gene Expression Regulation, Plant/drug effects , Cell Membrane/metabolism , Cell Membrane/drug effects , Plants, Genetically Modified , Fungal Proteins/metabolism , Fungal Proteins/genetics
8.
Cell Death Differ ; 31(6): 697-710, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38589495

ABSTRACT

Hematopoietic stem and progenitor cells (HSPCs) that have impaired differentiation can transform into leukemic blasts. However, the mechanism that controls differentiation remains elusive. Here, we show that the genetic elimination of Proteinase 3 (PRTN3) in mice led to spontaneous myeloid differentiation. Mechanistically, our findings indicate that PRTN3 interacts with the N-terminal of STAT3, serving as a negative regulator of STAT3-dependent myeloid differentiation. Specifically, PRTN3 promotes STAT3 ubiquitination and degradation, while simultaneously reducing STAT3 phosphorylation and nuclear translocation during G-CSF-stimulated myeloid differentiation. Strikingly, pharmacological inhibition of STAT3 (Stattic) partially counteracted the effects of PRTN3 deficiency on myeloid differentiation. Moreover, the deficiency of PRTN3 in primary AML blasts promotes the differentiation of those cells into functional neutrophils capable of chemotaxis and phagocytosis, ultimately resulting in improved overall survival rates for recipients. These findings indicate PRTN3 exerts an inhibitory effect on STAT3-dependent myeloid differentiation and could be a promising therapeutic target for the treatment of acute myeloid leukemia.


Subject(s)
Cell Differentiation , Leukemia, Myeloid, Acute , Myeloblastin , STAT3 Transcription Factor , Animals , Humans , Mice , Leukemia, Myeloid, Acute/pathology , Leukemia, Myeloid, Acute/metabolism , Mice, Inbred C57BL , Mice, Knockout , Myeloblastin/metabolism , Myeloblastin/genetics , Myeloid Cells/metabolism , Myeloid Cells/pathology , Phosphorylation , STAT3 Transcription Factor/metabolism , Ubiquitination
9.
Exp Gerontol ; 190: 112422, 2024 Jun 01.
Article in English | MEDLINE | ID: mdl-38599502

ABSTRACT

The onset of Alzheimer's disease is related to neuron damage caused by massive deposition of Aß in the brain. Recent studies suggest that excessive Aß in the brain mainly comes from peripheral blood, and BBB is the key to regulate Aß in and out of the brain. In this study, we explored the pathogenesis of AD from the perspective of Aß transport through the BBB and the effect of QKL injection in AD mice. The results showed that QKL could improve the cognitive dysfunction of AD mice, decrease the level of Aß and Aß transporter-RAGE, which was supported by the results of network pharmacology, molecular docking and molecular dynamics simulation. In conclusion, RAGE is a potential target for QKL's therapeutic effect on AD.


Subject(s)
Alzheimer Disease , Amyloid beta-Peptides , Disease Models, Animal , Receptor for Advanced Glycation End Products , Alzheimer Disease/drug therapy , Alzheimer Disease/metabolism , Animals , Receptor for Advanced Glycation End Products/metabolism , Mice , Amyloid beta-Peptides/metabolism , Blood-Brain Barrier/metabolism , Blood-Brain Barrier/drug effects , Male , Molecular Docking Simulation , Mice, Transgenic , Molecular Dynamics Simulation , Brain/metabolism , Brain/drug effects , Brain/pathology , Cognitive Dysfunction/drug therapy , Cognitive Dysfunction/metabolism
10.
Article in English | MEDLINE | ID: mdl-38536076

ABSTRACT

Three yeast strains belonging to the ascomycetous yeast genus Pichia were isolated from two soil samples from Yunnan and Guizhou provinces and a marine water sample from Liaoning province, PR China. Phylogenetic analyses based on the sequences of the D1/D2 domains of the large subunit(LSU) rRNA gene and the internal transcribed spacer (ITS) region indicate that these three strains, together with 12 additional strains isolated from various substrates collected in different regions or countries of the world, represent a novel species of the genus Pichia, for which the name Pichia kurtzmaniana sp. nov. (holotype: strain CGMCC 2.7213) is proposed. The novel species differs from its close relatives Candida californica by eight (1.5 %) and 26 (11.1 %) mismatches in the D1/D2 domains and the ITS region, respectively; and from Pichia chibodasensis by 11 (2.1 %) and 20 (8.7 %) mismatches in the D1/D2 domains and the ITS region, respectively. In addition, eight Candida species which belong to the Pichia clade are transferred to the genus Pichia, resulting in the proposal of the following new combinations: Pichia cabralensis comb. nov., Pichia californica comb. nov., Pichia ethanolica comb. nov., Pichia inconspicua comb. nov., Pichia phayaonensis comb. nov., Pichia pseudolambica comb. nov., Pichia rugopelliculosa comb. nov., and Pichia thaimueangensis comb. nov.


Subject(s)
Candida , Pichia , Bacterial Typing Techniques , Base Composition , China , DNA, Bacterial/genetics , Fatty Acids/chemistry , Phylogeny , RNA, Ribosomal, 16S/genetics , Sequence Analysis, DNA
11.
Int J Immunogenet ; 51(3): 143-148, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38468428

ABSTRACT

Genome-wide association studies analysis has revealed associations between ankylosing spondylitis (AS) and loci on the TBX21 gene across various populations. This study aimed to investigate if there is a connection between a higher risk of AS in a Chinese population and two polymorphism loci on the TBX21 gene. To achieve this, we performed a case-control investigation involving 363 patients with AS and 907 healthy individuals. Genotyping was carried out using the iPLEX Gold genotyping assay. The analysis of genotypes and haplotypes was performed using SPSS 23.0 and SHEsis software. The results revealed no statistically significant correlation between the two specified single-nucleotide polymorphisms of TBX21 (rs11657479 C/T and rs4794067 C/T) and susceptibility to AS. However, upon conducting stratification analysis, our findings demonstrated a significant association between rs11657479 and susceptibility to human leucocyte antigen (HLA)-B27+ AS in allelic (C vs. T: odds ratio [OR] = 1.52, 95%CI = 1.09-2.11, corrected p [pc] = .028), heterozygous (CT vs. TT: OR = 1.63, 95%CI = 1.13-2.34, pc = .016) and dominant (CT + CC vs. TT: OR = 1.60, 95%CI = 1.12-2.28, pc = .018) models. Furthermore, the haplotype rs4794067/C-rs11657479/C of TBX21 was found to increase the risk of HLA-B27+ AS cases. In conclusion, our findings indicate a correlation between TBX21 gene polymorphism and HLA-B27+ AS patients within the Chinese population.


Subject(s)
Asian People , Genetic Predisposition to Disease , Haplotypes , Polymorphism, Single Nucleotide , Spondylitis, Ankylosing , T-Box Domain Proteins , Adult , Female , Humans , Male , Middle Aged , Alleles , Asian People/genetics , Case-Control Studies , China , East Asian People , Gene Frequency , Genome-Wide Association Study , Genotype , HLA-B27 Antigen/genetics , Spondylitis, Ankylosing/genetics , T-Box Domain Proteins/genetics
12.
Front Pediatr ; 12: 1362104, 2024.
Article in English | MEDLINE | ID: mdl-38529050

ABSTRACT

Introduction: To explore the factors affecting the success of testicular torsion manual reduction and the safety of subsequent conservative treatment after successful reduction. Methods: Clinical data of 66 patients with testicular torsion treated in our emergency department from February 2017 to February 2022 were retrospectively collected. Manual reduction without anesthesia was performed in 19 patients. Patients with successful manual reduction chose different subsequent treatments according to the wishes of themselves and their guardians, including continuing conservative treatment and surgical exploration. Relevant clinical data were collected and analyzed. Results: Manual reduction was successful in 11 patients (11/19). Seven of them chose to continue conservative treatment, and four underwent surgical exploration immediately. Among the 7 patients who were treated conservatively, 3 underwent surgical treatment due to scrotal discomfort or testicular torsion at different stages, and the remaining 4 patients showed no recurrence of torsion during follow-up. Compared with other patients, patients with successful manual reduction had the shorter duration of pain (p < 0.05). The time from visiting our hospital to surgery in patients who attempted manual reduction was slightly shorter than those who underwent surgery directly (p > 0.05). The testes of these 11 patients were all successfully preserved. Conclusions: The short duration of pain may contribute to the success of manual reduction, and manual reduction did not increase the preparation time before surgery. Due to the unpredictable risk of recurrence, immediate surgical treatment is still recommended, or postponed elective surgical treatment should be offered in the next days or weeks.

13.
Front Immunol ; 15: 1326354, 2024.
Article in English | MEDLINE | ID: mdl-38433839

ABSTRACT

Introduction: Disulfidptosis is a recently identified form of cell death that contributes to maintaining the internal environment balance of an organism. However, the molecular basis of disulfidptosis in ulcerative colitis (UC), ankylosing spondylitis (AS), and Crohn's disease (CD) has not been thoroughly explored. Methods: Firstly, the differentially expressed genes (DEGs) and disulfidptosis-associated genes (DAGs) were obtained through differential analysis between diseases (AS, CD, and UC) and control groups. After the disulfidptosis score was acquired using the single-sample gene set enrichment analysis (ssGSEA) algorithm, the DE-DAGs were screened by overlapping DAGs and DEGs of the three diseases. Next, the feature genes were selected through a combination of machine learning algorithms, receiver operating characteristic (ROC) curves, and expression analysis. Based on these feature genes, nomograms were created for AS, CD and UC. The co-feature genes were then identified by taking the intersections of the genes featured in all three diseases. Meanwhile, single-gene set enrichment analysis (GSEA) and the TF-mRNA-miRNA network were utilized to investigate the molecular mechanisms of the co-feature genes. To validate the expression differences of the co-feature genes between healthy controls and patients (AS and IBD), RT-PCR was performed. Lastly, mendelian randomization (MR) analysis was utilized to explore the causality between genetic variants of S100A12 with AS, UC and CD. Results: In this study, 11 DE-DAGs were obtained. Functional enrichment analysis revealed their involvement in cytokine production and fatty acid biosynthesis. Latterly, AS/CD/UC -feature genes were derived, and they all had decent diagnostic performance. Through evaluation, the performance of the nomogram was decent for three diseases. Then, 2 co-feature genes (S100A12 and LILRA5) were obtained. The GSEA enrichment results indicated that the co-feature genes were mainly enriched in the cytokine-cytokine receptor interaction and drug metabolism cytochrome P450. As shown by functional experiments, there was a correlation between the mRNA expression of S100A12 with AS, UC and CD. Additionally, a causal connection between S100A12 and IBD was detected through MR analysis. Discussion: In this study, 2 co-feature genes (S100A12 and LILRA5) were screened, and their functions were investigated in AS, CD and UC, providing a basis for further research into diagnosis and treatment.


Subject(s)
Colitis, Ulcerative , Crohn Disease , Inflammatory Bowel Diseases , Spondylitis, Ankylosing , Humans , S100A12 Protein , Spondylitis, Ankylosing/genetics , Inflammatory Bowel Diseases/genetics , Crohn Disease/genetics , Cytokines , RNA, Messenger
14.
Chem Biol Interact ; 391: 110892, 2024 Mar 01.
Article in English | MEDLINE | ID: mdl-38364601

ABSTRACT

Sodium aescinate (SA) is extracted from Aesculus wilsonii Rehd seeds and was first marketed as a medicament in German. With the wide application of SA in clinical practice, reports of adverse drug reactions and adverse events have gradually increased, including renal impairment. However, the pathogenic mechanisms of SA have not yet been fully elucidated. The toxic effects and underlying mechanisms of SA were explored in this study. Our data showed that SA significantly elevated the levels of blood urea nitrogen (BUN), serum creatinine (Scr) and Kidney injury molecule 1 (Kim-1), accompanied by pathologically significant changes in renal tissue. SA induced NRK-52E cell death and disrupted the integrity of the cell membrane. Moreover, SA caused significant reductions in FTH, Nrf2, xCT, GPX4, and FSP1 levels, but increased TFR1 and ACSL4 levels. SA decreased glutathione peroxidase (GPx), glutathione (GSH) and cysteine (Cys) levels, but improved Fe2+, malondialdehyde (MDA), reactive oxygen species (ROS) and lipid peroxidation levels, ultimately leading to the induction of ferroptosis. Importantly, inhibition of ferroptosis or activation of the Nrf2/GPX4 pathway prevented SA-induced nephrotoxicity. These findings indicated that SA induced oxidative damage and ferroptosis-mediated kidney injury by suppressing the Nrf2/GPX4 axis activity.


Subject(s)
Drug-Related Side Effects and Adverse Reactions , Ferroptosis , Saponins , Triterpenes , Humans , NF-E2-Related Factor 2 , Glutathione
16.
Discov Med ; 36(181): 248-255, 2024 Feb.
Article in English | MEDLINE | ID: mdl-38409830

ABSTRACT

Macrophage polarization is a critical determinant of disease progression and regression. Studies on macrophage plasticity and polarization can provide a theoretical basis for the tactics of diagnosis and treatment for macrophage-related diseases. These include inflammation-related diseases, such as sepsis, tumors, and metabolic disorders. Growth differentiation factor-15 (GDF-15) or macrophage inhibitory cytokine-1, a 25 kDa secreted homodimeric protein, is a member of the transforming growth factor-ß (TGF-ß) superfamily that is released in response to external stressors. GDF-15 regulates biological effects such as tumor occurrence, inflammatory response, tissue damage, angiogenesis, and bone metabolism. It has been shown to exert anti-inflammatory and pro-inflammatory effects in inflammation-related diseases. Moreover, inflammatory stimuli can induce GDF-15 expression in immune and parenchymal cells. GDF-15 exhibits a feedback inhibitory effect by inhibiting tumor necrosis factor-α secretion during the macrophage activation anaphase, suggesting that there may be a close association between the two. GDF-15 directly induces CD14+ monocytes to produce the M2-like macrophage phenotype, inhibits monocyte-derived macrophage for M1-like polarization, and induces monocyte-derived Mφ for M2-like polarization. This review summarizes the macrophage polarization mechanism of GDF-15 under the conditions of sepsis, colon cancer, atherosclerosis, and obesity. An improved understanding of the role and molecular mechanisms of action of GDF-15 could greatly elucidate the mechanism of disease occurrence and development and provide new ideas for targeted disease prevention and treatment. An advanced understanding of the function and molecular mechanisms of action of GDF-15 may be helpful in the assessment of its potential value as a therapeutic and diagnostic target.


Subject(s)
Growth Differentiation Factor 15 , Sepsis , Humans , Growth Differentiation Factor 15/metabolism , Growth Differentiation Factor 15/pharmacology , Macrophage Activation , Macrophages , Transforming Growth Factor beta/metabolism , Inflammation/metabolism
17.
Medicine (Baltimore) ; 103(7): e36932, 2024 Feb 16.
Article in English | MEDLINE | ID: mdl-38363947

ABSTRACT

Pancreatic cancer (PC) is a malignant tumor of the digestive system with a poor prognosis. PC patients with pancreatitis have a worse prognosis. But nobody reported the relationship between inflammation and prognosis in PC. Based on this, we are going to explore inflammation-related prognostic signature to predict patients' survival and potential therapeutic target. We screened gene expression profile and corresponding clinical information of patients from The Cancer Genome Atlas (TCGA) database. Gene set enrichment analysis (GSEA) was performed to identify differentially expressed genes (DEGs) between tumor and normal tissues with P value < .05. Univariate and multivariate Cox regression analysis was applied to identify possible prognostic inflammation genes and establish an inflammation-related risk score system, which was validated by Kaplan-Meier and Receiver operating characteristic (ROC) curves. Finally, we used the TISIDB database to predict targeted drugs for up-regulated gene hepatocyte growth factor receptor (MET) and used AUTODOCK software for molecular docking. We built a prognostic model consisted of 3 inflammation-related genes (tumor necrosis factor receptor associated factor 1/TFAR1, tyrosine kinase 2/TYK2, MET). According to the median value of those genes' risk score, PC patients were ranked into high- (88) and low-risk (89) groups. Then, the results of the Kaplan-Meier curves and the area under the curve (AUC) of the ROC curves showed this model had a good predictive power (P < .001, AUC = 0.806). The result of human protein atlas (HPA) database showed the expression of TRAF1 and TYK2 were low in pancreatic cancer, the expression of MET was high. TISIDB database founded brigatinib could target to MET. And AUTODOCK showed brigatinib had a nice docking with MET. Taken together, our study suggested that inflammation-associated prognostic signature might be used as novel biomarkers for predicting prognosis in PC patients and potential therapeutic target of the disease.


Subject(s)
Organophosphorus Compounds , Pancreatic Neoplasms , Pyrimidines , Humans , Prognosis , Molecular Docking Simulation , Pancreatic Neoplasms/genetics , Inflammation/genetics
18.
Small ; : e2312019, 2024 Feb 22.
Article in English | MEDLINE | ID: mdl-38389179

ABSTRACT

The growing interest in so-called interface coupling strategies arises from their potential to enhance the performance of active electrode materials. Nevertheless, designing a robust coupled interface in nanocomposites for stable electrochemical processes remains a challenge. In this study, an epitaxial growth strategy is proposed by synthesizing sulfide rhenium (ReS2 ) on exfoliated black phosphorus (E-BP) nanosheets, creating an abundance of robust interfacial linkages. Through spectroscopic analysis using X-ray photoelectron spectroscopy and X-ray absorption spectroscopy, the authors investigate the interfacial environment. The well-developed coupled interface and structural stability contribute to the impressive performance of the 3D-printed E-BP@ReS2 -based micro-supercapacitor, achieving a specific capacitance of 47.3 mF cm-2 at 0.1 mA cm-2 and demonstrating excellent long-term cyclability (89.2% over 2000 cycles). Furthermore, density functional theory calculations unveil the positive impact of the strongly coupled interface in the E-BP@ReS2 nanocomposite on the adsorption of H+ ions, showcasing a significantly reduced adsorption energy of -2.17 eV. The strong coupling effect facilitates directional charge delocalization at the interface, enhancing the electrochemical performance of electrodes and resulting in the successful construction of advanced micro-supercapacitors.

19.
Biochem Genet ; 2024 Feb 23.
Article in English | MEDLINE | ID: mdl-38393623

ABSTRACT

N6-methyladenosine (m6A) regulates gene expression and governs many important biological processes. However, the function of m6A in the development of bronchopulmonary dysplasia (BPD) remains poorly characterized. Thus, the purpose of this investigation was to evaluate the effects of m6A RNA methylation regulators on the development of BPD. BPD-related transcriptome data were downloaded from the GEO database. Differentially expressed m6A methylation regulators between BPD and control group were identified. Consensus clustering was conducted for the classification of BPD and association between clusters and BPD phenotypes were explored. Analysis of differentially expressed genes (DEGs) and immune-related DEGs was performed. The GSEA, GO and KEGG analyses were used to interpret the functional enrichments. The composition of immune cell subtypes in BPD subsets was predicted by CIBERSORT analysis. Compared with the control group, expression of most m6A regulators showed significant alteration, especially for IGF2BP1/2/3. BPD was classified into 2 subsets, and cluster 1 was correlated with severe BPD. Furthermore, the results of functional enrichment analyses showed a disturbed immune-related signaling pathway. Based on CIBERSORT analysis, we found that the proportion of immune cell subsets changed between cluster 1 and cluster 2. Our study revealed the implication of m6A methylation regulators in the development of BPD, which might provide a novel insight for the diagnosis and treatment of BPD.

20.
J Pediatr Orthop B ; 2024 Feb 27.
Article in English | MEDLINE | ID: mdl-38373109

ABSTRACT

The effect on acetabular management in developmental dysplasia of the hip (DDH) patients aged 7 or older with modified low Dega osteotomy procedure was evaluated. Patients between 7 and 14 years old were managed with modified low Dega osteotomy and open reduction and concomitant procedures to evaluate whether low level osteotomy improved the clinical and radiologic outcomes after treatment. Clinical status was assessed using the modified McKay's criteria; radiologic evaluations were assessed for the modified Severin classification, the mean acetabular index (AI), Sharp angle and center-edge (CE) angle. And occurrence of triradiate cartilage injury and complications was recorded. Forty-two DDH patients (57 hips) between 7 and 14 years old were managed with modified low Dega osteotomy. The results demonstrated the latest follow-up 43 hips (75.4%) were rated excellent and 10 hips (17.5%) rated good according to the modified McKay criteria and 41 hips (71.9%) were rated excellent and 11 hips (19.3%) rated good according to Modified Severin classification, respectively. The mean Hip Score improved from 69.53 ±â€…7.14 before the operation to 93.17 ±â€…8.43 at the final follow-up. The mean AI changed from 31.9° to 20.2°, mean Sharp angle decreased from 59.3° to 38.8° and mean CE angle increased from -10.9° to 35.2°, preoperatively and at latest follow-up, respectively. The modified low Dega osteotomy combined with open reduction and concomitant procedures were found to be adequate in improving instant and sustained clinical and radiographic outcomes for the late detected pediatric walking DDH patients.

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