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1.
Eur J Surg Oncol ; 50(10): 108565, 2024 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-39059192

RESUMEN

BACKGROUND: Gastrointestinal tumors, as one of the most common cancers worldwide, pose a significant threat to human health. In this context, the advent of fluorescence probe technology has offered new perspectives and methods for the diagnosis and surgical treatment of gastrointestinal tumors. However, there is currently a lack of systematic bibliometric analysis on the research concerning gastrointestinal cancer and fluorescence probes. METHOD: This study retrieved and comprehensively analyzed 1816 documents from the Web of Science database using the Cite Space tool, exploring the spatiotemporal distribution, author and subject category distribution, research themes, and keywords in this field. RESULTS: As of February 3, 2024, a total of 1816 records were retrieved, encompassing nine document types. Original research papers dominated the dataset, accounting for 89.922 %, followed by review articles at 6.773 %. We conducted a comprehensive analysis from various perspectives including countries, authors, institutions, keywords, journals, and references. Our findings reveal a strengthening trend in research on gastrointestinal cancer and fluorescent probes since 2010, with primary focus on drug delivery, endoscopy techniques, and genomic hybridization. CONCLUSION: In recent years, there has been a growing interest in the design, application, and quantitative analysis techniques of fluorescent probes, marking a notable frontier in this field. Our research findings offer fundamental insights and aid in identifying potential collaborators for future endeavors in this area.


Asunto(s)
Bibliometría , Colorantes Fluorescentes , Neoplasias Gastrointestinales , Humanos , Neoplasias Gastrointestinales/diagnóstico
2.
J Inflamm Res ; 17: 4993-5004, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-39070128

RESUMEN

Introduction: Recombinant humanized collagen, as a novel biomaterial, exhibits multiple excellent biological functions, such as inhibition of inflammation, promotion of cell proliferation and vascular proliferation, and promotion of tissue healing. However, there is a lack of conclusive evidence regarding the specific role of recombinant humanized collagen type 17 (rhCol 17) in oral ulcer healing. This study explored whether rhCol 17 could promote the proliferation of human gingival fibroblasts (HGFs) and inhibit its inflammation, and whether it could promote the healing of oral ulcers in rats by inhibiting inflammation and accelerating tissue healing. Methods: At the cellular level, we investigated the effect of rhCol 17 on the proliferation of (HGFs) by CCK8; HGFs were mixed with lipopolysaccharide (LPS) to investigate the effect of rhCol 17 on HGFs in an inflammatory state. Eighteen adult male Sprague-Dawley rats were randomly distributed into three groups: blank control group, carbomer group (carbomer sprayed only), and rhCol 17 group (carbomer containing rhCol 17 sprayed), 1 time/day. The samples were collected at D3 and D5. At completion, histological staining and PCR were carried out to study its effect on the healing of oral ulcers in rats. Results: Through cellular experiments, we found that rhCol 17 possesses good biocompatibility and anti-inflammatory properties, and can effectively promote the proliferation and migration of HGFs, as well as significantly reduce the inflammation level of the cells. The animal experimental results showed that rhCol 17 could significantly reduce the inflammation level, promote collagen deposition and angiogenesis at the ulcer site, thus effectively accelerating the healing of oral ulcers in rats. Conclusion: In summary, the collagen sprays containing rhCol 17 have excellent anti-inflammatory effects and could accelerate tissue healing and are expected to provide a new effective treatment for patients with recurrent oral ulcers.

3.
BMC Pulm Med ; 24(1): 220, 2024 May 03.
Artículo en Inglés | MEDLINE | ID: mdl-38702679

RESUMEN

BACKGROUND: Recent research suggests that periodontitis can increase the risk of chronic obstructive pulmonary disease (COPD). In this study, we performed two-sample Mendelian randomization (MR) and investigated the causal effect of periodontitis (PD) on the genetic prediction of COPD. The study aimed to estimate how exposures affected outcomes. METHODS: Published data from the Gene-Lifestyle Interaction in the Dental Endpoints (GLIDE) Consortium's genome-wide association studies (GWAS) for periodontitis (17,353 cases and 28,210 controls) and COPD (16,488 cases and 169,688 controls) from European ancestry were utilized. This study employed a two-sample MR analysis approach and applied several complementary methods, including weighted median, inverse variance weighted (IVW), and MR-Egger regression. Multivariable Mendelian randomization (MVMR) analysis was further conducted to mitigate the influence of smoking on COPD. RESULTS: We chose five single-nucleotide polymorphisms (SNPs) as instrumental variables for periodontitis. A strong genetically predicted causal link between periodontitis and COPD, that is, periodontitis as an independent risk factor for COPD was detected. PD (OR = 1.102951, 95% CI: 1.005-1.211, p = 0.039) MR-Egger regression and weighted median analysis results were coincident with those of the IVW method. According to the sensitivity analysis, horizontal pleiotropy's effect on causal estimations seemed unlikely. However, reverse MR analysis revealed no significant genetic causal association between COPD and periodontitis. IVW (OR = 1.048 > 1, 95%CI: 0.973-1.128, p = 0.2082) MR Egger (OR = 0.826, 95%CI:0.658-1.037, p = 0.1104) and weighted median (OR = 1.043, 95%CI: 0.941-1.156, p = 0.4239). The results of multivariable Mendelian randomization (MVMR) analysis, after adjusting for the confounding effect of smoking, suggest a potential causal relationship between periodontitis and COPD (P = 0.035). CONCLUSION: In this study, periodontitis was found to be independent of COPD and a significant risk factor, providing new insights into periodontitis-mediated mechanisms underlying COPD development.


Asunto(s)
Estudio de Asociación del Genoma Completo , Análisis de la Aleatorización Mendeliana , Polimorfismo de Nucleótido Simple , Enfermedad Pulmonar Obstructiva Crónica , Fumar , Humanos , Enfermedad Pulmonar Obstructiva Crónica/genética , Enfermedad Pulmonar Obstructiva Crónica/epidemiología , Factores de Riesgo , Fumar/epidemiología , Fumar/efectos adversos , Periodontitis/genética , Periodontitis/epidemiología , Índice de Severidad de la Enfermedad , Predisposición Genética a la Enfermedad , Enfermedades Periodontales/genética , Enfermedades Periodontales/epidemiología
4.
Clin Oral Investig ; 27(10): 5895-5903, 2023 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-37581767

RESUMEN

BACKGROUND: The association between periodontal disease (PD) and erectile dysfunction (ED) has been well-documented in observational studies. However, observational studies are vulnerable to reverse causality and confounding factors, making the inference of causal-effect relationships challenging. Contrary to the current belief, Mendelian randomization (MR) can be applied to comprehensively assess the bi-directional causal effects between PD and ED. METHODS: A two-sample MR analysis was performed using pooled statistics from genome-wide association studies involving European populations with PD (12,289 patients with PD and 22,326 controls) and ED (6,175 patients with clinically diagnosed ED and 217,630 controls). In this MR analysis, three methods--the inverse-variance weighted (IVW) average, weighted median, and MR-Egger regression methods--were used to evaluate the causal relationships between PD and ED. RESULTS: According to the IVW analysis results, genetically predicted PD did not have a causal effect on ED (odds ratio 1.07, 95% confidence interval 0.96-1.20, p = 0.22). Furthermore, there was no clear indication of a significant causal effect of ED on PD in the reverse MR analysis (odds ratio 0.98, 95% confidence interval 0.90-1.08, p = 0.74). The results of the MR-Egger regression and weighted median methods were consistent with those of the IVW method. Based on the sensitivity analysis results, a major bias from genetic pleiotropy was unlikely to distort the causal estimates. CONCLUSION: The present study does not support a causal effect between PD and ED. CLINICAL RELEVANCE: From the perspective of genetics, PD does not appear to be a risk factor for the development of ED.

5.
Neurol Ther ; 12(4): 1159-1169, 2023 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-37184737

RESUMEN

INTRODUCTION: Previous observational studies have associated periodontitis (PD) with migraine; however, the results are inconclusive and the causality of the association between PD and migraine remains unclear. This two-sample Mendelian randomization (MR) study was performed to explore the bi-directional causal relationship between PD and migraine. METHODS: To investigate the relationship between PD (17,353 cases; 28,210 controls) and migraine (1072 cases; 360,122 controls), we used genetic tools from the largest available genome-wide association study of European descent. Inverse variance-weighted (IVW) and a series of sensitivity analyses were used to explore the association between migraine and PD. We performed an MR study using seven SNPs (single nucleotide polymorphisms) as instrumental variables for PD to investigate the causal relationship between migraine and PD. RESULTS: We found no significant causal relationship between PD and migraine (odds ratio, OR = 1.000; 95% confidence interval, CI = 0.99-1.00; p = 0.65). Similarly, no evidence supported a causal relationship between migraine and PD (OR = 0.07; CI = 2.04 × 10-9-2.65 × 106; p = 0.77). A sensitivity analysis revealed that no potential polymorphic effect (p = 0.356) and heterogeneity (p = 0.652) exists for the variants used in constructing the genetic instrument. CONCLUSIONS: Based on the results of our MR study, there is no causal relationship between PD and migraines or migraines and PD.

6.
Front Immunol ; 13: 881914, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35844488

RESUMEN

Background: Early diagnosis of sepsis in children was essential to reducing mortality. This study aimed to explore the value of ferroptosis-related genes in children with sepsis. Methods: We screened the septic children microarray dataset from the GEO database and analyzed the ferroptosis-related differentially expressed genes (DEGs). A functional analysis of ferroptosis-related DEGs was performed. The protein-protein interaction network was used to identify hub genes. We explored the immune landscape of sepsis and controls. The value of hub genes in diagnosing sepsis was tested in the training (GSE26440) and validation sets (GSE13904), and ELISA was used to verify their diagnostic value in children with sepsis in our hospital. Results: A total of 2,103 DEGs in GSE26440 were obtained, of which ferroptosis-related DEGs were 34. Enrichment analysis showed significant enrichment in the ferroptosis and hypoxia pathways (i.e., HIF-1 pathway). The top three genes (HMOX1, MAPK14, TLR4) were selected as hub genes. Immunological analysis suggested that 10 cell types (i.e., CD8/CD4 T cells) were lower in sepsis. Immune checkpoint-related genes CD274 (PD-L1), HAVCR2 (TIM3), and SIGLEC15 were overexpressed in sepsis. The AUROC for the diagnosis of sepsis for HMOX1 and TLR4 ranged from 0.77 to 0.81, while the AUROC of MAPK14 reached 0.935 and 0.941 in the training and validation sets. Serum ELISA results of HMOX1 and TLR4 showed no significant difference in differentiating sepsis. The AUROC of MAPK14 was 0.877. When the diagnostic threshold was 74.852 ng/ml, the sensitivity and specificity were 0.906 and 0.719, respectively. Conclusion: Ferroptosis-related gene MAPK14 is of considerable value in the early diagnosis of sepsis in children.


Asunto(s)
Ferroptosis , Proteína Quinasa 14 Activada por Mitógenos , Sepsis , Niño , Biología Computacional/métodos , Ferroptosis/genética , Ontología de Genes , Humanos , Sepsis/diagnóstico , Sepsis/genética , Receptor Toll-Like 4
7.
Front Genet ; 13: 936051, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35873471

RESUMEN

Pea (Pisum sativum L.) is one of the most important legume crops in the world, and it has attracted great attention for its high nutritive values. Recently, the crop breeding program has been focused on the crop metabolic engineering (i.e., color, flavor, nutrition) to improve the quality of crop. As a major group of transcription factors forming the ternary MYB-bHLH-WD repeat protein (MBW) complex to regulate the anthocyanin biosynthesis pathway, members of R2R3-MYB gene family have always been the focus of research targets to improve the valuable metabolic product of crops. Until now, few report about the R2R3-MYB gene family of pea has been released. In this study, we identified 119 R2R3-MYB genes in the assembled pea genome (Version 1a), of which 111 were distributed across 14 chromosomes. Combining with the 126 R2R3-MYB protein sequences of Arabidopsis, we categorized 245 R2R3-MYB proteins into 36 subgroups according to sequence similarity and phylogenetic relationships. There was no member from subgroup 12, 15 and 29 existing in pea genome, whereas three novel subgroups were found in pea and named as N1-N3. Further analyses of conserved domains and Motifs, gene structures, and chromosomal locations showed that the typical R2 and R3 domains were present across all R2R3-MYB proteins, and Motif 1, 2, and 3 were identified in most members. Most of them had no more than two introns. Additionally, 119 pea R2R3-MYB genes did not experience large-scale duplication events. Finally, we concluded that several candidate genes may be responsible for the spatiotemporal accumulation of anthocyanins in pea petals. PsMYB116 was predominantly expressed in the dorsal petals to presumably activate the anthocyanin biosynthesis pathway, while PsMYB37 and PsMYB32 may positively regulates the anthocyanin accumulation in the lateral petals. This study not only provides a good reference to further characterize the diverse functions of R2R3-MYB genes but also helps researchers to understand the color formation of pea flowers.

8.
Mikrochim Acta ; 187(10): 556, 2020 09 10.
Artículo en Inglés | MEDLINE | ID: mdl-32910220

RESUMEN

Based on the etching of gold nanorods (GNRs) and enzyme-linked immunosorbent assay (ELISA), a multicolor immunosensor for visual detection of enterovirus 71 infection is proposed. Once the immunocomplex is formed, the horseradish peroxidase bound to the ELISA plate oxidizes 3,3',5,5'-tetramethylbenzidine (TMB) into TMB2+ in the presence of hydrogen peroxide. Subsequently, TMB2+ quantitatively etches GNRs to the short GNRs, leading to a blue shift of longitudinal localized surface plasmon resonance and corresponding color responses. This change is used to develop two types of cut-off standards, which respond to the human anti-enterovirus at a concentration of 71 IgM antibody. The method has been validated with clinical serum samples and showed high sensitivity and specificity . This visual immunosensor has an important application value for point-of-care detection of EV71, especially in areas lacking detection equipment. Graphical abstract.


Asunto(s)
Técnicas Biosensibles/métodos , Enterovirus Humano A/patogenicidad , Oro/química , Humanos
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