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Laizhou Bay, a major breeding ground for economic marine organisms in the northern waters of China, is facing rapid environmental degradation. In this study, field surveys in this area were conducted in the spring, summer, and autumn of 2020. Microscopic observation and RuBisCO large subunit (rbcL) gene analysis were employed to understand the community structure and temporal dynamics of phytoplankton. The phytoplankton community structures detected by the two methods showed significant differences. Microscopic observation revealed the dominance of dinoflagellates in spring that shifted to the dominance of diatoms in summer and autumn. However, rbcL gene sequencing consistently identified diatoms as dominant throughout all three seasons, with their relative abundance showing an increasing trend. Conversely, the relative abundance of the second- and third-most abundant taxa, namely, haptophytes and ochrophytes, decreased as the seasons transitioned. rbcL gene sequencing annotated more species than microscopy. It could detect haptophytes and cryptophytes, which were overlooked by microscopy. In addition, rbcL gene sequencing detected a remarkable amount of Thalassiosira profunda, which was previously unidentified in this sea area. However, it appeared to underestimate the contribution of dinoflagellates considerably, with most taxa being only identified through microscopic identification. The two methods jointly identified 28 harmful algal bloom taxa with similar detection quantities but substantial differences in species composition. Phytoplankton communities were influenced by temperature, salinity, and nutrients. The results of this work suggest that a combination of multiple techniques is necessary for a comprehensive understanding of phytoplankton.
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The volatile profiles of wheat flour during maturation were examined through headspace solid-phase micro-extraction gas chromatography-mass spectrometry (HS-SPME-GC/MS) combined with electronic nose (E-nose) and electronic tongue (E-tongue) analyses. The wheat flour underwent maturation under three distinct conditions for predetermined durations. While GC/MS coupled with E-tongue exhibited discernment capability among wheat flour samples subjected to varying maturation conditions, E-nose analysis solely relying on principal component analysis failed to achieve discrimination. 83 volatile compounds were identified in wheat flour, with the highest abundance observed in samples matured for 50 d at 25 °C. Notably, trans-2-Nonenal, decanal, and nonanal were the main contributors to the characteristic flavor profile of wheat flour. Integration of HS-SPME-GC/MS with E-tongue indicated superior flavor development and practical viability in wheat flour matured for 50 d at 25 °C. This study furnishes a theoretical groundwork for enhancing the flavor profiles of wheat flour and its derivative products.
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Nariz Electrónica , Harina , Cromatografía de Gases y Espectrometría de Masas , Microextracción en Fase Sólida , Gusto , Triticum , Compuestos Orgánicos Volátiles , Harina/análisis , Compuestos Orgánicos Volátiles/análisis , Triticum/química , Manipulación de Alimentos/métodos , Análisis de Componente Principal , Odorantes/análisisRESUMEN
Improper management of diabetic wound effusion and disruption of the endogenous electric field can lead to passive healing of damaged tissue, affecting the process of tissue cascade repair. This study developed an extracellular matrix sponge scaffold (K1P6@Mxene) by incorporating Mxene into an acellular dermal stroma-hydroxypropyl chitosan interpenetrating network structure. This scaffold is designed to couple with the endogenous electric field and promote precise tissue remodelling in diabetic wounds. The fibrous structure of the sponge closely resembles that of a natural extracellular matrix, providing a conducive microenvironment for cells to adhere grow, and exchange oxygen. Additionally, the inclusion of Mxene enhances antibacterial activity(98.89%) and electrical conductivity within the scaffold. Simultaneously, K1P6@Mxene exhibits excellent water absorption (39 times) and porosity (91%). It actively interacts with the endogenous electric field to guide cell migration and growth on the wound surface upon absorbing wound exudate. In in vivo experiments, the K1P6@Mxene sponge reduced the inflammatory response in diabetic wounds, increased collagen deposition and arrangement, promoted microvascular regeneration, Facilitate expedited re-epithelialization of wounds, minimize scar formation, and accelerate the healing process of diabetic wounds by 7 days. Therefore, this extracellular matrix sponge scaffold, combined with an endogenous electric field, presents an appealing approach for the comprehensive repair of diabetic wounds.
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Antibacterianos , Cicatrización de Heridas , Cicatrización de Heridas/efectos de los fármacos , Animales , Antibacterianos/farmacología , Antibacterianos/química , Masculino , Matriz Extracelular/química , Hemostáticos/farmacología , Hemostáticos/química , Andamios del Tejido/química , Diabetes Mellitus Experimental/complicaciones , Ratones , Quitosano/química , Ratas , Humanos , Conductividad Eléctrica , Ratas Sprague-DawleyRESUMEN
Solution blowing process was used to prepare cellulose nonwovens, by using N-methyl morpholine-N-oxide (NMMO) as solvent, and salicylic acid (SA) microcapsules as antibacterial additives. The structure and properties of cellulose nonwovens modified with different SA microcapsules contents were compared and evaluated. The results showed that more uniform and denser web structure was formed with the increase of SA microcapsules content, the average fiber diameter of cellulose nonwoven increased from 1.99 µm to 2.65 µm. The air flow resistance and filtration efficiency of cellulose nonwovens increased with addition of SA microcapsules, whereas the mechanical properties, and wearing comfort including air permeability, moisture vapor transfer rate, and softness of cellulose nonwovens decreased slightly, under the same basis weight. SA microcapsules modified cellulose nonwovens exhibited good sustained-release behavior and antimicrobial activity against Escherichia coli. The higher SA microcapsules content in cellulose nonwovens, the faster release rate and the higher antimicrobial activity. The cellulose solution-blown nonwovens modified with SA microcapsules are expected to find applications in medical and healthcare fields due to its antibacterial activity and biodegradability.
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Antibacterianos , Cápsulas , Celulosa , Escherichia coli , Ácido Salicílico , Solventes , Celulosa/química , Ácido Salicílico/química , Ácido Salicílico/farmacología , Antibacterianos/farmacología , Antibacterianos/química , Escherichia coli/efectos de los fármacos , Solventes/química , Liberación de Fármacos , Óxidos N-Cíclicos/química , Soluciones , Pruebas de Sensibilidad MicrobianaRESUMEN
Nitenpyram, taking the place of imidacloprid, is a widely used neonicotinoid insecticide to control Nilaparvata lugens in Asia. Two P450s, CYP4CE1 and CYP6ER1, are key factors in the metabolic resistance against nitenpyram and imidacloprid. In this study, we found that CYP4CE1 expression was strongly associated with nitenpyram resistance in 8 field-collected populations, whereas CYP6ER1 expression correlated with imidacloprid resistance. Hence, we focused on nitenpyram metabolism by CYP4CE1, due to that imidacloprid metabolism by CYP6ER1 has intensively investigated. Mass spectrometry analysis revealed that recombinant CYP4CE1 metabolized nitenpyram into three products, N-desmethyl nitenpyram, hydroxy-nitenpyram, and N-desmethyl hydroxy-nitenpyram, with a preference for hydroxylation. In contrast, CYP6ER1 metabolized nitenpyram into a single product, N-desmethyl nitenpyram. These results provide new insights into the specific catalytic mechanisms of P450 enzymes in neonicotinoid metabolism and underscore the importance of different catalytic reactions in neonicotinoid insecticide resistance.
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Proteínas de Insectos , Insecticidas , Neonicotinoides , Oxidación-Reducción , Neonicotinoides/metabolismo , Neonicotinoides/química , Insecticidas/metabolismo , Insecticidas/química , Hidroxilación , Animales , Proteínas de Insectos/metabolismo , Proteínas de Insectos/genética , Proteínas de Insectos/química , Desmetilación , Hemípteros/metabolismo , Hemípteros/genética , Hemípteros/enzimología , Nitrocompuestos/metabolismo , Nitrocompuestos/química , Sistema Enzimático del Citocromo P-450/metabolismo , Sistema Enzimático del Citocromo P-450/genética , Resistencia a los Insecticidas/genéticaRESUMEN
BACKGROUND: The endocycle can generate cells referred to as 'polyploid'. Fizzy-related protein (Fzr) plays an important role in driving the mitosis-to-endocycle transition. The brown planthopper (BPH), Nilaparvata lugens (Stål), a serious insect pest, feeds exclusively on rice. However, polyploidy and its regulatory mechanisms are poorly understood in BPH. RESULTS: Here, we found that the ploidy levels of follicles H (FH) and accessory gland (AG) significantly increased with BPH age when examining the polyploidy of FH and AG of salivary glands. Fzr was identified as an important regulator for polyploidy in BPH salivary gland. Knockdown of Fzr resulted in a decrease in cell size and DNA content in nymph salivary glands. Fzr knockdown transcriptionally upregulated cyclin-dependent kinase 1 (CDK1), CDK2, cyclin A (CycA) and CycB, and downregulated CycD, CycE, Myc and mini-chromosome maintenance protein 2-7 (MCM2-7). Phenotypically, Fzr knockdown significantly suppressed salivary protein production, feeding and survival in BPH nymphs. CONCLUSION: Our results show that BPH salivary glands exhibit obvious polyploidy, and Fzr positively regulates the endocycle in nymph salivary gland. These findings provide clues for the study of the regulatory mechanisms of insect polyploidy. © 2024 Society of Chemical Industry.
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ABSTRACT: A 49-year-old woman patient with thyroid cancer accepted thyroidectomy and parathyroid transplantation. One month later, localized 131 I uptake in the deltoid muscle bilaterally was detected by 131 I whole-body imaging performed in 2 days after 131 I administration.
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Músculo Deltoides , Radioisótopos de Yodo , Glándulas Paratiroides , Humanos , Femenino , Persona de Mediana Edad , Glándulas Paratiroides/diagnóstico por imagen , Glándulas Paratiroides/metabolismo , Músculo Deltoides/diagnóstico por imagen , Músculo Deltoides/metabolismo , Radioisótopos de Yodo/metabolismo , Imagen de Cuerpo Entero , Transporte BiológicoRESUMEN
Osteoarthritis (OA) is a common degenerative disease that affects millions of individuals worldwide. OBJECTIVE: There is no conclusive epidemiological evidence regarding the relationship between OA, depression, and whole-body fat mass. In this study, we conducted a two-step Mendelian randomization analysis to determine the causal relationships between them. DESIGN: The published summary-level data are from genome-wide association studies (GWAS). Our study included 357,957 samples and 10,828,862 SNPs. Finally, the outcome GWAS data for OA came from a GWAS on the genetic architecture of OA using UK Biobank data. This study included 50,508 samples and 15,845,511 SNPs. We used five different modes of analysis, including inverse variance weighted meta-analysis (IVW), MR-Egger regression, weighted median, simple mode, and weighted mode, to explore causal relationships. RESULTS: We found a positive correlation between depression and body fat mass, with depression leading to body fat mass an increase in (IVW result: p = 3.39E-07, OR (95 % CI) =2.16 (1.61, 2.90)). We also found a positive correlation between body fat mass and OA, with body fat mass increasing the risk of OA (IVW result: p = 1.65E-33, OR (95 % CI) = 1.98 (1.77, 2.21). Body fat mass played an important role as a mediator in the causal relationship between depression and OA, with approximately 14 % of the risk of OA caused by depression being mediated by body fat mass. CONCLUSIONS: Our study offers reliable evidence that depression has a detrimental impact on the risk of OA. Future research can support these associations from improving depressed effect, including social, biological, and behavioral factors, to reduce the risk of chronic diseases such as osteoarthritis. And we identified high-risk variation of alleles which associated with OA and depression can be used to predict disease and provide a basis for clinical intervention and treatment of OA.
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Depresión , Estudio de Asociación del Genoma Completo , Análisis de la Aleatorización Mendeliana , Osteoartritis , Polimorfismo de Nucleótido Simple , Humanos , Osteoartritis/genética , Osteoartritis/epidemiología , Depresión/genética , Depresión/epidemiología , Tejido Adiposo , Predisposición Genética a la Enfermedad/genéticaRESUMEN
Influenza virus infection poses a continual menace to public health. Here, we developed soluble trimeric HA ectodomain vaccines by establishing interprotomer disulfide bonds in the stem region, which effectively preserve the native antigenicity of stem epitopes. The stable trimeric H1 ectodomain proteins exhibited higher thermal stabilities in comparison with unmodified HAs and showed strong binding activities towards a panel of anti-stem cross-reactive antibodies that recognize either interprotomer or intraprotomer epitopes. Negative stain transmission electron microscopy (TEM) analysis revealed the stable trimer architecture of the interprotomer disulfide-stapled WA11#5, NC99#2, and FLD#1 proteins as well as the irregular aggregation of unmodified HA molecules. Immunizations of mice with those trimeric HA ectodomain vaccines formulated with incomplete Freund's adjuvant elicited significantly more potent cross-neutralizing antibody responses and offered broader immuno-protection against lethal infections with heterologous influenza strains compared to unmodified HA proteins. Additionally, the findings of our study indicate that elevated levels of HA stem-specific antibody responses correlate with strengthened cross-protections. Our design strategy has proven effective in trimerizing HA ectodomains derived from both influenza A and B viruses, thereby providing a valuable reference for designing future influenza HA immunogens.
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Anticuerpos Neutralizantes , Anticuerpos Antivirales , Disulfuros , Glicoproteínas Hemaglutininas del Virus de la Influenza , Vacunas contra la Influenza , Ratones Endogámicos BALB C , Infecciones por Orthomyxoviridae , Animales , Vacunas contra la Influenza/inmunología , Vacunas contra la Influenza/genética , Glicoproteínas Hemaglutininas del Virus de la Influenza/inmunología , Glicoproteínas Hemaglutininas del Virus de la Influenza/genética , Glicoproteínas Hemaglutininas del Virus de la Influenza/química , Anticuerpos Antivirales/inmunología , Ratones , Disulfuros/química , Infecciones por Orthomyxoviridae/prevención & control , Infecciones por Orthomyxoviridae/inmunología , Infecciones por Orthomyxoviridae/virología , Anticuerpos Neutralizantes/inmunología , Femenino , Protección Cruzada/inmunología , Reacciones Cruzadas , Humanos , Gripe Humana/prevención & control , Gripe Humana/inmunología , Gripe Humana/virología , Epítopos/inmunología , Epítopos/genética , Epítopos/química , Multimerización de Proteína , Virus de la Influenza B/inmunología , Virus de la Influenza B/genética , Virus de la Influenza B/químicaRESUMEN
BACKGROUND: The effectiveness of laparoscopic nephroureterectomy (LNU) vs open nephroureterectomy (ONU) for upper tract urothelial carcinoma (UTUC) is unclear. METHODS: We conducted a meta-analysis of studies based on propensity score-matched cohorts to compare the surgical and oncological outcomes of LNU and ONU in UTUC patients. A literature search was conducted on PubMed, Embase, and Cochrane Library until July 12, 2023. The Newcastle-Ottawa Scale was utilized to assess the quality of eligible studies. Measurements of surgical and oncological outcomes were extracted and pooled including mean difference (MD), risk ratio (RR), hazard ratios (HR), and 95% confidence intervals (CI). RESULTS: Five high-quality retrospective studies were included, totaling 6422 patients; 2080 (32.4%) underwent LNU, and 4342 (67.6%) underwent ONU. With respect to surgical outcomes, patients in the LNU group experienced less estimated blood loss and had shorter hospital stay than those in the ONU group, but there was no significant difference in complication rates and operation time. In regard to oncological outcomes, there were no significant differences between the LNU and ONU groups in 3-year overall survival (OS) and cancer-specific survival (CSS). However, 3-year intravesical recurrence free survival (IVRFS) was worse in the LNU group compared to the ONU group. CONCLUSION: LNU was associated with less estimated blood loss and shorter hospital stays than ONU, but there were no differences in OS and CSS between the surgical modalities. Nonetheless, LNU might result in poorer IVRFS than ONU.
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Laparoscopía , Nefroureterectomía , Puntaje de Propensión , Humanos , Nefroureterectomía/métodos , Laparoscopía/métodos , Laparoscopía/estadística & datos numéricos , Carcinoma de Células Transicionales/cirugía , Carcinoma de Células Transicionales/mortalidad , Neoplasias Ureterales/cirugía , Neoplasias Ureterales/mortalidad , Neoplasias Urológicas/cirugía , Neoplasias Urológicas/mortalidad , Neoplasias Renales/cirugía , Neoplasias Renales/mortalidad , MasculinoRESUMEN
PURPOSE: The abnormal growth factors-induced epithelial-mesenchymal transition (EMT) in retinal pigment epithelial (RPE) cells was known as a vital pathogenesis of proliferative vitreoretinopathy (PVR). This study aims to explore how survivin inhibition affects EMT induced by epidermal growth factor (EGF) in RPE cells. METHODS: Human primary RPE cells were identified in vitro. EMT in RPE cells was induced by EGF. Inhibition of survivin in RPE cells was accomplished through the use of a survivin inhibitor (YM155) and survivin siRNA. The viability, proliferation and migration of RPE cells was detected by methylthiazol tetrazolium assay, bromodeoxyuridine labeling assay, and wound healing assay, respectively. The EGF receptor /mitogen-activated protein kinase (EGFR/MAPK) proteins and EMT-related proteins were measured by western blot and immunofluorescence assay. RESULTS: EGF induced significant EMT in RPE cells, activated the phosphorylation of EGFR/MAPK signaling proteins, and caused changes to EMT-related proteins. YM155 suppressed RPE cells' viability, proliferation, and migration; induced the phosphorylation of EGFR, JNK, and P38MAPK; and down regulated EGFR and phosphorylated ERK. YM155 also increased expression of E-cadherin and ZO-1 proteins and reduced expression of N-cadherin, Vimentin, and α-SMA proteins. The EGF-induced increase of RPE cell proliferation and migration was constrained by survivin inhibition. Moreover, survivin inhibition in RPE cells suppressed the EGF-caused phosphorylation of EGFR/MAPK proteins and attenuated the EGF-induced reduction of E-cadherin and ZO-1 proteins and increase of N-cadherin, Vimentin, and α-SMA proteins. CONCLUSIONS: Survivin inhibition attenuates EGF-induced EMT of RPE cells by affecting the EGFR/MAPK signaling pathway. Survivin might be a promising target for preventing PVR.
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Cadherinas , Movimiento Celular , Proliferación Celular , Factor de Crecimiento Epidérmico , Transición Epitelial-Mesenquimal , Receptores ErbB , Imidazoles , Sistema de Señalización de MAP Quinasas , Naftoquinonas , Epitelio Pigmentado de la Retina , Survivin , Humanos , Transición Epitelial-Mesenquimal/efectos de los fármacos , Survivin/metabolismo , Survivin/antagonistas & inhibidores , Receptores ErbB/metabolismo , Receptores ErbB/antagonistas & inhibidores , Epitelio Pigmentado de la Retina/metabolismo , Epitelio Pigmentado de la Retina/citología , Epitelio Pigmentado de la Retina/efectos de los fármacos , Factor de Crecimiento Epidérmico/farmacología , Naftoquinonas/farmacología , Proliferación Celular/efectos de los fármacos , Movimiento Celular/efectos de los fármacos , Imidazoles/farmacología , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Cadherinas/metabolismo , Supervivencia Celular/efectos de los fármacos , Proteínas Inhibidoras de la Apoptosis/metabolismo , Fosforilación/efectos de los fármacos , Vimentina/metabolismo , Proteína de la Zonula Occludens-1/metabolismo , Células Cultivadas , Actinas/metabolismo , ARN Interferente Pequeño/genéticaRESUMEN
The maturation of wheat flour is a transformative process that elevates its processing and culinary attributes to their peak performance levels. Despite extensive research on starch and gluten protein modifications, the impact of lipid changes has been largely unexplored. This study addresses this gap by examining the maturation of freshly milled wheat flour at 15 °C, 25 °C, and 40 °C over 60 days, focusing on enzymatic activities-lipase, lipoxidase, and catalase-and lipid metabolites, including free fatty acids, conjugated trienes, p-anisidine value, and total oxidation value. The results of this study showed that free fatty acids continued to increase at all temperatures, with the most significant increase of 50% at 15 °C. The p-anisidine value followed a pattern of initial increase followed by a decline, while conjugated trienes were markedly higher at 40 °C, suggesting temperature's significant influence on lipid peroxidation. Notably, total oxidation values became erratic post 30 days, indicating a shift in oxidative dynamics. This study underscores the correlation between lipid metabolites and enzymatic activities, revealing the enzymes' pivotal role in lipid oxidation. The interplay of temperature and time offers valuable insights for optimizing wheat flour maturation, ensuring superior quality for various applications.
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Aristolochic acids (AAs) have been identified as a significant risk factor for hepatocellular carcinoma (HCC). Ferroptosis is a type of regulated cell death involved in the tumor development. In this study, we investigated the molecular mechanisms by which AAs enhanced the growth of HCC. By conducting bioinformatics and RNA-Seq analyses, we found that AAs were closely correlated with ferroptosis. The physical interaction between p53 and AAs in HepG2 cells was validated by bioinformatics analysis and SPR assays with the binding pocket sites containing Pro92, Arg174, Asp207, Phe212, and His214 of p53. Based on the binding pocket that interacts with AAs, we designed a mutant and performed RNA-Seq profiling. Interestingly, we found that the binding pocket was responsible for ferroptosis, GADD45A, NRF2, and SLC7A11. Functionally, the interaction disturbed the binding of p53 to the promoter of GADD45A or NRF2, attenuating the role of p53 in enhancing GADD45A and suppressing NRF2; the mutant did not exhibit the same effects. Consequently, this event down-regulated GADD45A and up-regulated NRF2, ultimately inhibiting ferroptosis, suggesting that AAs hijacked p53 to down-regulate GADD45A and up-regulate NRF2 in HepG2 cells. Thus, AAs treatment resulted in the inhibition of ferroptosis via the p53/GADD45A/NRF2/SLC7A11 axis, which led to the enhancement of tumor growth. In conclusion, AAs-hijacked p53 restrains ferroptosis through the GADD45A/NRF2/SLC7A11 axis to enhance tumor growth. Our findings provide an underlying mechanism by which AAs enhance HCC and new insights into p53 in liver cancer. Therapeutically, the oncogene NRF2 is a promising target for liver cancer.
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This study aimed to elucidate the effects of coastal environmental stress on the composition of sediment bacterial communities and their cooccurrence patterns in fishing harbors around the Bohai Economic Circle, China. Compared with the natural sea area, fishing harbors contained higher levels of organic pollution (organic pollution index = 0.12 ± 0.026) and considerably reduced bacterial richness and evenness. The distributions of sediment microbial communities clustered along the pollutant concentration gradients across fishing harbors. Betaproteobacteria dominated (76%) organically polluted fishing harbors, which were mostly disturbed by anthropogenic activities. However, the harbors also revealed the absence of numerous pathogenic (Coxiella and Legionella) and photosynthetic (Synechococcus and Leptolyngbya) bacteria. Abundant genera, including Thiobacillus and Arenimonas, exhibited a positive correlation with total phosphorus and a negative correlation with total nitrogen in sediments. Meanwhile, Sulfurovum, Psychrobacter, and Woeseia showed the opposite trend. Pollutant accumulation and anthropogenic activities caused the decrease in the sediment microbial diversity and dispersal ability and promoted convergent evolution. Severely polluted harbors with simplified cooccurrence networks revealed the presence of destabilized microbial communities. In addition, the modularity of bacterial networks decreased with organic pollution. Our results provide important insights into the adjustment mechanism of microbial communities to community organization and functions under environmental pollution stress. Overall, this study enhanced our understanding of how microbial communities in coastal sediments adapted and survived amidst anthropogenic activities like oily effluent discharges from large ships, wash water, domestic sewage, garbage, and fisheries wastes. It also examined their resilience to future contamination.
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Bacterias , Sedimentos Geológicos , Microbiota , China , Bacterias/clasificación , Sedimentos Geológicos/microbiología , Monitoreo del Ambiente , Explotaciones PesquerasRESUMEN
Objective: To explore the risk factors contributing to the development of premature coronary artery disease (PCAD) in patients with ankylosing spondylitis (AS) and assess the clinical implications of this association. Methods: The study used a retrospective analysis design to investigate the risk factors and clinical significance of ankylosing spondylitis (AS) combined with early-onset coronary heart disease (AS-PCAD). A total of 80 patients diagnosed with AS and coronary heart disease who were admitted to the hospital between February 2019 and February 2022 were included in the analysis. The patients were divided into two groups based on the age of onset of coronary heart disease - the PCAD group (n=42, mean age 41.48±2.69 years) and the non-early-onset coronary heart disease (NPCAD) group (n=38, mean age 69.13±4.50 years). Relevant clinical data, including demographics, medical history, laboratory results, and imaging findings, were extracted from electronic health records. Binary logistic regression analysis was employed to identify risk factors influencing the incidence of AS-PCAD. The study aimed to uncover the distinctive clinical features and risk factors associated with AS patients who experience early-onset coronary heart disease, in order to guide diagnosis and treatment strategies for this patient population. Results: The results of the study revealed several notable findings. Significant differences were observed between the PCAD and NPCAD groups in terms of age and age at AS onset (P < .05). Specifically, patients in the PCAD group had a younger mean age at AS onset compared to the NPCAD group (41.48±2.69 years vs 69.13±4.50 years, respectively). Additionally, the two groups exhibited statistically significant differences in several laboratory parameters. Levels of C-reactive protein (CRP) were found to be markedly higher in the PCAD group compared to the NPCAD group (P < .05). Hemoglobin levels and the prevalence of anemia also showed significant variations between the two cohorts (both P < .05). Importantly, the binary logistic regression analysis identified two key risk factors that independently influenced the incidence of PCAD in AS patients: younger age at AS onset and elevated levels of C-reactive protein. Conclusions: The key findings of this study underscore the heightened risk of premature coronary artery disease in patients with ankylosing spondylitis, particularly those with a younger age of AS onset and elevated levels of systemic inflammation as marked by C-reactive protein. These results have important clinical implications. Identifying AS patients at increased risk for PCAD, based on factors such as younger disease onset and higher inflammatory burden, enables targeted screening and early intervention strategies. Comprehensive cardiovascular risk assessment and management should be an integral part of the care approach for this patient population. Early recognition of PCAD risk, followed by aggressive management of modifiable risk factors and implementation of appropriate therapeutic measures, can help mitigate the burden of premature cardiovascular complications in individuals with ankylosing spondylitis.
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The aim of this study was to investigate the effects of miR-424-5p on biological behaviors and angiogenesis of the HTR-8/SVneo Cells. Our study included 60 parturient women, which were divided into an PA group (placenta accreta, n = 30) and a normal group (normal placenta, n = 30). QPCR was used to measure the expression of miR-424-5p in placental tissues. The effects of the miR-424-5p mimic on proliferation, migration, and invasion of human HTR-8/SVneo cells and angiogenesis were analyzed. The potential modulated relationship between miR-424-5p and low-density lipoprotein receptor-related protein-6 (LRP6) was demonstrated by luciferase assay. The expression of LRP6, ß-catenin, matrix metalloproteinase-2 (MMP-2), placental growth factor (PGF) and vascular endothelial growth factor (VEGF) were measured by qPCR and Western blot assays. The expression of miR-424-5p in the PA group was significantly decreased than that in the normal group. The expression of miR-424-5p has negative correlation with blood loss. Upregulation of miR-424-5p significantly suppressed the cell proliferation, migration, and invasion of HTR-8/SVneo cells in vitro, as well as the tube formation of human umbilical vein endothelial cells (HUVECs). The luciferase assay demonstrated that LRP6 was a target of miR-424-5p. The expression of LRP6, ß-catenin, MMP-2, PGF and VEGF were also decreased with upregulation of miR-424-5p (p < 0.05). The inhibitory effects of miR-424-5p on HTR-8/SVneo cells and angiogenesis were enhanced by downregulation of LRP6, but were reversed by upregulation of LRP6. The present study suggests that downregulation of miR-424-5p is related to the occurrence of PA. Enhancing miR-424-5p inhibits proliferation, migration, invasion and angiogenesis of the HTR-8/SVneo cells through targeting LRP6 mediated ß-catenin, providing more insights about PA.
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Carbapenem-resistant organism (CRO) are defined as gram-negative bacteria. The lack of safe and effective antibiotics has led to an increase in incidence rate. The purpose of this study is to establish and determine a risk nomogram to predict CRO infection in hospitalized patients. Hospitalized patients' information were collected from the electronic medical record system of hospital between January 2019 and December 2022. Based on the inclusion and exclusion criteria, we identified 131390 inpatients who met the criteria for this study. For the training cohort, the area under the curves (AUC) for predicting the CRO infection was 0.935. For the validation cohort, the AUC for predicting the CRO infection was 0.937. We have developed the first novel nomogram to predict CRO infection in hospitalized patients, which is reliable and high-performance. The nomogram performs well among hospitalized patients and has good predictive ability.
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Antibacterianos , Carbapenémicos , Infecciones por Bacterias Gramnegativas , Nomogramas , Humanos , Carbapenémicos/farmacología , Masculino , Femenino , Persona de Mediana Edad , Infecciones por Bacterias Gramnegativas/microbiología , Infecciones por Bacterias Gramnegativas/tratamiento farmacológico , Antibacterianos/farmacología , Antibacterianos/uso terapéutico , Anciano , Hospitalización , Bacterias Gramnegativas/efectos de los fármacos , Bacterias Gramnegativas/aislamiento & purificación , Adulto , Estudios Retrospectivos , Anciano de 80 o más Años , Registros Electrónicos de SaludRESUMEN
PURPOSE: Lung adenocarcinoma (LUAD) is a prevalent malignant tumor worldwide, with high incidence and mortality rates. However, there is still a lack of specific and sensitive biomarkers for its early diagnosis and targeted treatment. Disulfidptosis is a newly identified mode of cell death that is characteristic of disulfide stress. Therefore, exploring the correlation between disulfidptosis-related long non-coding RNAs (DRGs-lncRNAs) and patient prognosis can provide new molecular targets for LUAD patients. METHODS: The study analysed the transcriptome data and clinical data of LUAD patients in The Cancer Genome Atlas (TCGA) database, gene co-expression, and univariate Cox regression methods were used to screen for DRGs-lncRNAs related to prognosis. The risk score model of lncRNA was established by univariate and multivariate Cox regression models. TIMER, CIBERSORT, CIBERSORT-ABS, and other methods were used to analyze immune infiltration and further evaluate immune function analysis, immune checkpoints, and drug sensitivity. Real-time polymerase chain reaction (RT-PCR) was performed to detect the expression of DRGs-lncRNAs in LUAD cell lines. RESULTS: A total of 108 lncRNAs significantly associated with disulfidptosis were identified. A prognostic model was constructed by screening 10 lncRNAs with independent prognostic significance through single-factor Cox regression analysis, LASSO regression analysis, and multiple-factor Cox regression analysis. Survival analysis of patients through the prognostic model showed that there were obvious survival differences between the high- and low-risk groups. The risk score of the prognostic model can be used as an independent prognostic factor independent of other clinical traits, and the risk score increases with stage. Further analysis showed that the prognostic model was also different from tumor immune cell infiltration, immune function, and immune checkpoint genes in the high- and low-risk groups. Chemotherapy drug susceptibility analysis showed that high-risk patients were more sensitive to Paclitaxel, 5-Fluorouracil, Gefitinib, Docetaxel, Cytarabine, and Cisplatin. Additionally, RT-PCR analysis demonstrated differential expression of DRGs-lncRNAs between LUAD cell lines and the human bronchial epithelial cell line. CONCLUSIONS: The prognostic model of DRGs-lncRNAs constructed in this study has certain accuracy and reliability in predicting the survival prognosis of LUAD patients, and provides clues for the interaction between disulfidptosis and LUAD immunotherapy.
Asunto(s)
Adenocarcinoma del Pulmón , Biomarcadores de Tumor , Regulación Neoplásica de la Expresión Génica , Inmunoterapia , Neoplasias Pulmonares , ARN Largo no Codificante , Humanos , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Adenocarcinoma del Pulmón/genética , Adenocarcinoma del Pulmón/inmunología , Adenocarcinoma del Pulmón/mortalidad , Adenocarcinoma del Pulmón/tratamiento farmacológico , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/inmunología , Neoplasias Pulmonares/mortalidad , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/patología , Pronóstico , Biomarcadores de Tumor/genética , Inmunoterapia/métodos , Masculino , Femenino , Línea Celular Tumoral , Transcriptoma , Persona de Mediana EdadRESUMEN
Efficient management of hemorrhage is vital for preventing hemorrhagic shock and safeguarding wounds against infection. Inspired by the traditional Chinese steamed bread-making process, which involves kneading, foaming, and steaming, we devised a hemostatic sponge by amalgamating an acellular dermal matrix gel, hydroxyethyl starch, and rice hydrolyzed protein. The integration of hydroxyethyl starch bolstered the sponge's mechanical and hemostatic attributes, while the inclusion of rice hydrolyzed protein, acting as a natural foaming agent, enhanced its porosity This augmentation facilitated rapid blood absorption, accelerated clot formation, and stimulated the clotting cascade. Experimental findings underscore the exceptional biocompatibility and physicochemical characteristics of the hemostatic sponge, positioning it on par with commercially available collagen hemostatic sponges for hemorrhage control. Mechanistically, the sponge fosters aggregation and activation of red blood cells and platelets, expediting coagulation kinetics both in vivo and in vitro. Notably, this hemostatic sponge activates the clotting cascade sans crosslinking agents, offering a premium yet cost-effective biomaterial with promising clinical applicability.
Asunto(s)
Dermis Acelular , Hemostasis , Hemostáticos , Polisacáridos , Animales , Hemostasis/efectos de los fármacos , Hemostáticos/farmacología , Hemostáticos/química , Polisacáridos/química , Polisacáridos/farmacología , Coagulación Sanguínea/efectos de los fármacos , Materiales Biocompatibles/química , Materiales Biocompatibles/farmacología , Humanos , Proteínas/química , Oryza/química , MasculinoRESUMEN
AIM: To explore the effect of epidermal growth factor receptor (EGFR) inhibition by erlotinib and EGFR siRNA on epidermal growth factor (EGF)-induced activation of retinal pigment epithelium (RPE) cells. METHODS: Human RPE cell line (ARPE-19 cells) was activated by 100 ng/mL EGF. Erlotinib and EGFR siRNA were used to intervene EGF treatment. Cellular viability, proliferation, and migration were detected by methyl thiazolyl tetrazolium (MTT) assay, bromodeoxyuridine (BrdU) staining assay and wound healing assay, respectively. EGFR/protein kinase B (AKT) pathway proteins and N-cadherin, α-smooth muscle actin (α-SMA), and vimentin were tested by Western blot assay. EGFR was also determined by immunofluorescence staining. RESULTS: EGF treatment for 24h induced a significant increase of ARPE-19 cells' viability, proliferation and migration, phosphorylation of EGFR/AKT proteins, and decreased total EGFR expression. Erlotinib suppressed ARPE-19 cells' viability, proliferation and migration through down regulating total EGFR and AKT protein expressions. Erlotinib also inhibited EGF-induced an increase of proliferative and migrative ability in ARPE-19 cells and clearly suppressed EGF-induced EGFR/AKT proteins phosphorylation and decreased expression of N-cadherin, α-SMA, and vimentin proteins. Similarly, EGFR inhibition by EGFR siRNA significantly affected EGF-induced an increase of cell proliferation, viability, and migration, phosphorylation of EGFR/AKT proteins, and up-regulation of N-cadherin, α-SMA, and vimentin proteins. CONCLUSION: Erlotinib and EGFR-knockdown suppress EGF-induced cell viability, proliferation, and migration via EGFR/AKT pathway in RPE cells. EGFR inhibition may be a possible therapeutic approach for proliferative vitreoretinopathy (PVR).