RESUMEN
Integrating complementary information from multiple magnetic resonance imaging (MRI) modalities is often necessary to make accurate and reliable diagnostic decisions. However, the different acquisition speeds of these modalities mean that obtaining information can be time consuming and require significant effort. Reference-based MRI reconstruction aims to accelerate slower, under-sampled imaging modalities, such as T2-modality, by utilizing redundant information from faster, fully sampled modalities, such as T1-modality. Unfortunately, spatial misalignment between different modalities often negatively impacts the final results. To address this issue, we propose FEFA, which consists of cascading FEFA blocks. The FEFA block first aligns and fuses the two modalities at the feature level. The combined features are then filtered in the frequency domain to enhance the important features while simultaneously suppressing the less essential ones, thereby ensuring accurate reconstruction. Furthermore, we emphasize the advantages of combining the reconstruction results from multiple cascaded blocks, which also contributes to stabilizing the training process. Compared to existing registration-then-reconstruction and cross-attention-based approaches, our method is end-to-end trainable without requiring additional supervision, extensive parameters, or heavy computation. Experiments on the public fastMRI, IXI and in-house datasets demonstrate that our approach is effective across various under-sampling patterns and ratios. Our code will be available at: https://github.com/chenxm12394/FEFA.
RESUMEN
AIM: To investigate the quality of life in patients with endometrial carcinoma and provide theoretical basis for nursing care. DESIGN: In this study, 69 patients diagnosed with endometrial carcinoma from 2016-2018 were included in the cohort. METHODS: Sixty-nine patients from our hospital who underwent endometrial cancer surgeries were selected. The SF-36 was used to investigate and analyse the patients' quality of life in the first, second and third months after their operations. Questionnaires were administered to analyse the factors affecting postoperative quality of life. RESULTS: Quality of life for the second and third months was obviously better than that for the first month after the operation (p < .05). Based on multivariate regression analysis, we found that patients with higher family income had better quality of life after surgery(p < .05). These results can provide some guidance for daily nursing work after endometrial cancer operation.
Asunto(s)
Neoplasias Endometriales , Calidad de Vida , Estudios de Cohortes , Neoplasias Endometriales/patología , Neoplasias Endometriales/cirugía , Femenino , Humanos , Estudios Longitudinales , Encuestas y CuestionariosRESUMEN
BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory disease with increasing prevalence worldwide. Barrier defect in intestinal epithelial cells (IECs) is one of the main pathogeneses in UC. Pyroptosis is a programmed lytic cell death and is triggered by inflammatory caspases, while little is known about its role in UC. METHODS: Differentially expressed genes (DEGs) were identified by comparing UC patients with healthy controls from the GEO datasets. The candidate genes involved in pyroptosis were obtained, and the underlying molecular mechanism in the progression of UC was explored in vivo and in vitro. RESULTS: Pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2), a protein phosphatase, was downregulated and involved in regulating inflammation-induced IEC pyroptosis by modulating the NF-κB signaling in UC through bioinformatics analysis. Moreover, we demonstrated that PHLPP2 was downregulated in UC patients and UC mice. Besides, we found that PHLPP2 depletion activated the NF-κB signaling and increased the expressions of caspase-1 P20, Gasdermin N, IL-18, and IL-1ß contributing to IEC pyroptosis and inflammation in UC mice. Furthermore, we found that PHLPP2-/- mice developed hypersensitivity to dextran sulfate sodium (DSS) treatment toward colitis showing activated NF-κB signaling and dramatically induced expressions of caspase-1 P20, Gasdermin N, IL-18, and IL-1ß. Mechanically, this inflammation-induced downregulation of PHLPP2 was alleviated by an NF-κB signaling inhibitor in intestinal organoids of PHLPP2-/- mice and fetal colonic cells. CONCLUSIONS: PHLPP2 downexpression activated the NF-κB signaling and promoted the IEC pyroptosis, leading to UC progression. Therefore, PHLPP2 might be an attractive candidate therapeutic target for UC.
Asunto(s)
Colitis Ulcerosa/patología , Fosfoproteínas Fosfatasas/genética , Piroptosis , Transducción de Señal , Animales , Colitis Ulcerosa/inducido químicamente , Sulfato de Dextran/toxicidad , Modelos Animales de Enfermedad , Regulación hacia Abajo , Humanos , Interleucina-18/metabolismo , Interleucina-1beta/metabolismo , Mucosa Intestinal/citología , Mucosa Intestinal/metabolismo , Intestinos/citología , Intestinos/metabolismo , Ratones , Ratones Endogámicos C57BL , FN-kappa B/metabolismo , Fosfoproteínas Fosfatasas/antagonistas & inhibidores , Fosfoproteínas Fosfatasas/metabolismo , Interferencia de ARN , ARN Interferente Pequeño/metabolismoRESUMEN
PURPOSE: The purpose of this research was to assess whether the efficacy of the seminar-case learning model is superior to the traditional lecture-based learning model in the gastroenterology curriculum for first-year graduate students. MATERIALS & METHODS: This research was a prospective randomized controlled trial that enrolled 92 first-year postgraduate students with a rotation internship in the gastroenterology department. The students were randomly divided into 2 groups and then subjected to an identical version of the curriculum for 8 weeks. The experimental group (n = 50) used the seminar-case learning model, while the control group (n = 42) used the traditional lecture-based learning model. Examinations consisted of a theoretical test and a case analysis test, and anonymous questionnaires were used to assess teaching quality. RESULTS: All participants completed the examinations and questionnaires. The average theoretical test score of the experimental group was no statistical significance with that of the control group (P = 0.17). The average case analysis test score of the experimental group was significantly higher than that of the control group (P < 0.05). The indicators of the experimental group's feedback were better than those of the control group, such that there were significantly higher learning interest and motivation, a better understanding of diseases and knowledge, improvements in clinical thinking and summary ability, and an active classroom atmosphere in the experimental group (P < 0.05). However, students in the experimental group felt more burdensome. CONCLUSION: Compared to the traditional method, the seminar-case learning model showed a higher efficacy. The seminar-case learning model effectively improved students' outcomes and satisfaction, which helped students narrow the gap between theoretical knowledge and clinical practical application.
RESUMEN
[This corrects the article DOI: 10.1186/s12986-020-0434-8.].
RESUMEN
Background: Pyroptosis is a novel programmed cell death. It is identified as caspase-1 dependent and characterized by plasma-membrane rupture and release of proinflammatory intracellular contents inculuding IL-1 beta and IL-18. Pyroptosis is distinct from other forms of cell death, especially apoptosis that is characterized by nuclear and cytoplasmic condensation and is elicited via activation of a caspase cascade. In pyroptosis, gasdermin D (GSDMD) acts as a major executor, while NLRP3 related inflammasome is closely linked to caspase-1 activation. Given that pyroptosis has played a critical role in the progression of non-alcoholic steatohepatitis (NASH), here, we investigated whether the regulation of pyroptosis activation is responsible for the protective role of monounsaturated oleic acids in the context of hepatocellular lipotoxicity. Methods: Human hepatoma cell line HepG2 cells were exposed to palmitic acid (PA) with or without oleic acids (OA) or/and endoplasmic reticulum (ER) stress inhibitor tauroursodeoxycholic acid (TUDCA) for 24 h. Besides, the cells were treated with the chemical ER stressor tunicamycin (TM) with or without OA for 24 h as well. The expressions of pyroptosis and ER stress related genes or proteins were determined by real-time PCR, Western blot or immunofluorescence. The morphology of pyroptosis was detected by acridine orange and ethidium bromide (AO/EB) staining. The release of IL-1 beta and tumor necrosis factor alpha (TNF-α) was determined by ELISA. Sprague-Dawley (SD) rats were fed with high fat diet (HFD) for 16 w, then, HFD was half replaced by olive oil to observe the protective effects of olive oil. The blood chemistry were analyzed, and the liver histology and the expressions of related genes and proteins were determined in the liver tissues. Results: We demonstrated that PA impaired the cell viability and disturbed the lipid metabolism of HepG2 cells (P < 0.01), but OA robustly rescued cells from cell death (P < 0.001). More importantly, we found that instead of cell apoptosis, PA induced significant pyroptosis, evidenced by remarkably increased mRNA and protein expressions of inflammasome marker NLRP3, Caspase-1 and IL-1beta, as well as cell membrane perforation driving protein GSDMD (P < 0.05). Furthermore, we demonstrated that the PA stimulated ER stress was causally related to pyroptosis. The enhanced expressions of ER stress markers CHOP and BIP were found subcellular co-located to pyroptosis markers NLRP3 and ASC. Additionally,TM was able to induce pyroptosis like PA did, and ER stress inhibitor TUDCA was able to inhibit both PA and TM induced ER stress as well as pyroptosis. Furthermore, we demonstrated that OA substantially alleviated either PA or TM induced ER stress and pyroptosis in HepG2 cells (P < 0.01). In vivo, only olive oil supplementation did not cause significant toxicity, while HFD for 32 w obviously induced liver steatosis and inflammation in SD rats (P < 0.05). Half replacement of HFD with olive oil (a mixed diet) has remarkably ameliorated liver abnormalities, and particularly inhibited the protein expressions of either ER stress and pyroptosis markers (P < 0.05). Conclusion: Palmitic acid induced predominant pyroptosis in HepG2 cells, and ER stress may be responsible for the induction of pyroptosis and subsequent cell death. Monounsaturated oleic acids were able to ameliorate hepatocellular lipotoxicity both in vitro and in vivo, and OA mediated inhibition of ER stress and pyroptosis may be the underlying mechanisms.
RESUMEN
This study mainly investigated the effect of matrine on TNBS-induced intestinal inflammation in mice. TNBS treatment caused colonic injury and gut inflammation. Matrine (1, 5, and 10 mg/kg) treatment alleviated colonic injury and gut inflammation via reducing bleeding and diarrhea and downregulating cytokines expression (IL-1ß and TNF-α). Meanwhile, serum immunoglobulin G (IgG) was markedly reduced in TNBS treated mice, while 5 and 10 mg/kg matrine alleviated IgG reduction. Fecal microbiota was tested using 16S sequencing and the results showed that TNBS caused gut microbiota dysbiosis, while matrine treatment markedly improved gut microbiota communities (i.e., Bacilli and Mollicutes). Functional analysis showed that cell motility, nucleotide metabolism, and replication and repair were markedly altered in the TNBS group, while matrine treatment significantly affected cell growth and death, membrane transport, nucleotide metabolism, and replication and repair. In conclusion, matrine may serve as a protective mechanism in TNBS-induced colonic inflammation and the beneficial effect may be associated with gut microbiota.
RESUMEN
Gastric cancer (GC) is one of the most common malignancies that threatens human health. As the molecular mechanisms unerlying GC are not completely understood, identification of genes related to GC could provide new insights into gene function as well as potential treatment targets. We discovered that UGT2B15 may contribute to the pathogenesis and progression of GC using GEO data and bioinformatic analysis. Using TCGA data, UGT2B15 mRNA was found to be significantly overexpressed in GC tissues; patients with higher UGT2B15 had a poorer prognosis. It was further discovered that UGT2B15 and FOXA1 were both upregulated, and UGT2B15 and Foxa1 were positively correlated in GC. It is known that Foxa1 is a vital threshold to activate the HippoYAP signaling pathway. In addition, we suggest that a potential molecular mechanisms includes UGT2B15 which may upregulate Foxa1, activate the HippoYAP signaling pathway and contribute to the development of GC. Taken together, our findings demonstrate that UGT2B15 may be an oncogene in GC and is a promising therapeutic target for cancer treatment.
Asunto(s)
Proteínas Adaptadoras Transductoras de Señales/metabolismo , Biomarcadores de Tumor/metabolismo , Biología Computacional/métodos , Glucuronosiltransferasa/metabolismo , Factor Nuclear 3-alfa del Hepatocito/metabolismo , Fosfoproteínas/metabolismo , Proteínas Serina-Treonina Quinasas/metabolismo , Neoplasias Gástricas/patología , Proteínas Adaptadoras Transductoras de Señales/genética , Apoptosis , Biomarcadores de Tumor/genética , Estudios de Casos y Controles , Proliferación Celular , Femenino , Estudios de Seguimiento , Regulación Neoplásica de la Expresión Génica , Glucuronosiltransferasa/genética , Factor Nuclear 3-alfa del Hepatocito/genética , Vía de Señalización Hippo , Humanos , Masculino , Persona de Mediana Edad , Fosfoproteínas/genética , Pronóstico , Mapas de Interacción de Proteínas , Proteínas Serina-Treonina Quinasas/genética , Transducción de Señal , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismo , Tasa de Supervivencia , Factores de Transcripción , Células Tumorales Cultivadas , Proteínas Señalizadoras YAPRESUMEN
Long non-coding RNAs (lncRNAs) are important regulators of many cellular processes, and their aberrant expression and/or function is associated with many different diseases, including cancer. However, the identification of functional lncRNAs in gastric cancer is still a challenge. In this study, we describe a novel functional lncRNA, linc00483, that is upregulated and associated with tumorigenesis, tumour size, metastasis and poor prognosis in gastric cancer. In our study, linc00483 promoted gastric cancer cell proliferation, invasiveness and metastasis in vitro and in vivo. Mechanistically, upregulated expression of linc00483 in gastric cancer acts as a sponge to absorb endogenous tumour suppressor miR-30a-3p. Furthermore, it restores SPAG9 expression, which is negatively regulated by miR-30a-3p, and actives MAPK signaling pathway in gastric cancer cells. Thus, linc00483 is an oncogenic lncRNA in gastric cancer and targeting linc00483 or its pathway can potentially be useful in development of targeted therapies for patients with gastric cancer. Our results show that linc00483 is an important regulator in carcinogenesis and may be a useful biomarker to predict prognosis of gastric cancer patients. We believe our findings are novel and will be of interest to scientists working in many areas related to biomarkers in cancer.
RESUMEN
Clinical trials of suicide gene therapy have achieved limited success, which suggests a need for improvement. Angiogenesis plays a crucial role in the progression of cancers, which is greatly regulated by vascular endothelial growth factor (VEGF).The current study was designed to evaluate the anti-tumor effects of VEGF siRNA in combination with fusion suicide gene yCDglyTK. Introduction of a VEGF-targeted small hairpin RNA (shVEGF) to CDTK/5-FC system could induce cell apoptosis more effectively and decrease micro vessel density in xenograft tissue, thus resulted in a significant tumor growth delay in SGC7901 xenografts. These findings for the first time suggest the potential of combination gene therapy using suicide gene therapy and anti-angiogenesis gene therapy.