Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Artigo em Inglês | MEDLINE | ID: mdl-38466055

RESUMO

Objective: To investigate the risk factors for cancer malnutrition after radical tumor resection. Methods: A total of 110 cancer patients who used parenteral nutrition from January 2022 to June 2023 were selected for retrospective analysis and 50 patients who did not need parenteral nutrition support after radical tumor resection were selected as the control group to analyze the general data of the two groups. Univariate and multivariate logistic analyses were used to determine the factors influencing malnutrition in patients supported by parenteral nutrition after radical tumor resection. Results: The age(P = .032), body mass index(P = .012), education level(P = .025), per capita monthly household income(P = .029), concurrent chemotherapy ratio(P = .035), phobia disease progression(P = .037), and depression(P = .038) of patients who underwent parenteral nutrition after radical tumor resection were all influencing factors, and the differences were statistically significant (P < .034). After undergoing a radical tumor resection, patients with dysphagia grade 2-3, loss of appetite grade 2-3, and nausea and vomiting grade 2-3, as well as diarrhea grade 2-3, require parenteral nutrition support. The risk factors for malnutrition in patients who require such support include age, education, per capita household income, fear of disease progression, depression, pain, and diarrhea. Conclusion: Patients may suffer from malnutrition after radical tumor resection and need parenteral nutrition support, including age, education level, per capita monthly household income, fear of disease progression, depression, pain, diarrhea, etc., so in clinical nursing, nursing staff should pay more attention to such high-risk factors, so as to carry out personalized nursing programs for patients undergoing radical tumor resection and improve the effectiveness of disease treatment.

2.
Exp Mol Pathol ; 118: 104570, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33166496

RESUMO

BACKGROUND: Intervertebral disc degeneration (IDD) causes lower back pain, and is often accompanied with robust inflammation. However, whether inflammation plays a role in IDD remains controversial, and the mechanism is ill-elucidated. METHODS: Cartilage specimens from patients with scoliosis (control) and IDD were examined for IL-6 and its receptor expression by qPCR and western blot. Primary human articular chondrocyte was employed as a model for in vitro assessment of IL-6 effects in cell viability, cellular oxidative stress and iron homeostasis by MTT, MDA, ROS and Iron Colorimetric assays. The underlying mechanism was explored by qPCR, western blot, RIP in combination with bioinformatics analysis. RESULTS: We found in this study that IL-6 and its receptor were aberrantly expressed in cartilage tissues of IDD patients. IL-6 down-regulated miR-10a-5p, which subsequently derepressed IL-6R expression. IL-6 exposure caused cartilage cell ferroptosis by inducing cellular oxidative stress and disturbing iron homeostasis. Overexpressing miR-10a-5p suppressed IL-6R expression, and partially abolished IL-6-induced ferroptosis. CONCLUSION: Results from current study suggests that inflammatory cytokine IL-6 appeared in IVD aggravates its degeneration by inducing cartilage cell ferroptosis. This is caused partially by inhibiting miR-10a-5p and subsequently derepressing IL-6R signaling pathway. Our study provides a novel mechanism explaining inflammatory cytokine-caused cartilage cell death in degenerative IVD, and makes IL-6/miR-10a-5p/IL-6R axis a potential therapeutic target for intervention of IDD.


Assuntos
Condrócitos/patologia , Regulação da Expressão Gênica/efeitos dos fármacos , MicroRNAs/genética , Receptores de Interleucina-6/metabolismo , Escoliose/patologia , Apoptose , Estudos de Casos e Controles , Proliferação de Células , Células Cultivadas , Condrócitos/efeitos dos fármacos , Condrócitos/metabolismo , Ferroptose , Humanos , Interleucina-6/farmacologia , Receptores de Interleucina-6/genética , Escoliose/tratamento farmacológico , Escoliose/metabolismo , Transdução de Sinais
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA