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1.
Int J Neurosci ; : 1-6, 2024 Mar 21.
Artículo en Inglés | MEDLINE | ID: mdl-38497414

RESUMEN

OBJECTIVE: To evaluate the efficacy of graded nutrition intervention strategy in improving patients with different degrees of impaired swallowing function after stroke. METHODS: According to the way of nursing, the patients were divided into two group. The main outcome measure was Kota swallowing index (WSI) score, and the secondary outcome was complications during the intervention. SF-36 scale was used to evaluate the improvement of quality of life before and intervention. RESULTS: The WSI score in the control group was 62.34 ± 10.23 at 1 week after treatment, 70.52 ± 13.45 at 6 weeks after treatment, and 80.48 ± 9.87 at 12 weeks after treatment, while that in the intervention group was 71.45 ± 9.68 at 1 week after treatment, 75.81 ± 11.78 at 6 weeks after treatment, and 84.12 ± 14.32 at 12 weeks after treatment. The WSI scores of the intervention group were significantly higher than those of the control group (t = 5.634, p < 0.001), suggesting better swallowing function of the patients The incidence of pulmonary infection, malnutrition and gastroesophageal reflux in the intervention group was significantly lower than that in the control group (p < 0.05). There was no significant difference in throat inflammation and dehydration between the two groups (p > 0.05). In addition, graded nutrition interventions significantly improved patients' quality of life, including dimensions of physical functioning, role physics, physical pain, and social functioning. CONCLUSION: Compared with conventional treatment, personalized graded nutrition intervention can significantly improve the swallowing function and reduce the pulmonary infection rate in patients with swallowing disorders after stroke.

2.
Clin Hemorheol Microcirc ; 85(4): 355-370, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37927249

RESUMEN

BACKGROUND: circRNAs (circRNAs) are involved in the process of cerebral ischemia-reperfusion injury (CI/RI). Our study aims to explore circRBM33 in the endothelial function of the blood-brain barrier (BBB). METHODS: The mouse middle cerebral artery occlusion model (MCAO) was established and restored to perfusion, and OGD/R-induced endothelial cells were used to simulate CI/RI. circRBM33, miR-6838-5p and PDCD4, as well as Occludin, ZO-1 and Claudin-5 TJs were evaluated by quantitative PCR and Western blot. The ring structure of circRBM33 was verified by RNAse R and actinomycin D experiments. MTT and LDH Cytotoxicity assay determined viability and toxicity, and flow cytometry determined apoptosis rate. Inflammatory cytokines and the number of microglia in brain tissue were measured by ELISA and IHC. The interaction between genes was verified by RIP and dual luciferase reporter assay. RESULTS: circRBM33 was a circrRNA present in the cytoplasm and up-regulated in the brain tissue of MCAO mice and OGD/R-induced endothelial cells. Silenced circRBM33 promoted Occludin, ZO-1, and Claudin-5 expression and cell proliferation, and inhibited cytotoxicity, inflammatory response, and apoptosis. Functionally, circRBM33-absorbed miR-6838-5p was involved in regulating PDCD4, leading to endothelial cell dysfunction, and thus affecting the function of the BBB. CONCLUSIONS: circRBM33 by mediating miR-6838-5p/PDCD4 axis induces endothelial dysfunction, thereby affecting the BBB in mice with CI/RI.


Asunto(s)
MicroARNs , ARN Circular , Daño por Reperfusión , Animales , Ratones , Apoptosis , Barrera Hematoencefálica/metabolismo , Claudina-5/metabolismo , Células Endoteliales/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Ocludina/genética , Ocludina/metabolismo , Daño por Reperfusión/genética , Daño por Reperfusión/metabolismo , ARN Circular/genética
3.
Front Endocrinol (Lausanne) ; 14: 1093991, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-36950677

RESUMEN

Background: Insulin resistance (IR) is a normal feature of pregnancy and plays a crucial role in the pathophysiology of hypertensive disorder of pregnancy (HDP). The triglyceride-glucose index (TyG index) has been shown as a simple and reliable alternative IR marker. This work aimed to investigate the association between the TyG index and the incidence of HDP and adverse pregnancy outcomes. Methods: From January 2016 to December 2018, 289 women with HDP and 861 women without HDP were recruited at Shanghai Fifth People's Hospital, Fudan University to determine the relationship between the TyG index and the incidence of HDP and adverse pregnancy outcomes. Results: In the case-control study, the incidence of HDP was found to be significantly associated with the TyG index. Moreover, logistic regression indicated that the TyG index is an independent risk factor for HDP development and incidence of low birth weight (LBW) and fetal distress. In the cohort study, the results showed that the TyG index increased, there was a stepwise increase in HDP incidence, SBP, and DBP levels one week before delivery as well as in LBW and fetal distress incidence. The early trimester TyG index was positively associated with pre-pregnancy BMI, systolic blood pressure (SBP), and diastolic blood pressure (DBP) one week before delivery. Spline regression showed that there was a significant linear association between HDP incidence and early trimester TyG index when it was >8.5. Conclusions: This work suggested that the early trimester TyG index was closely associated with the development of HDP and adverse pregnancy outcomes.


Asunto(s)
Hipertensión Inducida en el Embarazo , Resistencia a la Insulina , Embarazo , Humanos , Femenino , Resultado del Embarazo/epidemiología , Estudios de Cohortes , Glucosa , Incidencia , Triglicéridos , Estudios de Casos y Controles , Sufrimiento Fetal , China/epidemiología , Hipertensión Inducida en el Embarazo/epidemiología
4.
Oncotarget ; 7(35): 57145-57159, 2016 Aug 30.
Artículo en Inglés | MEDLINE | ID: mdl-27494891

RESUMEN

Epithelial ovarian cancer is most lethal in female reproductive carcinomas owing to the high chemoresistance and metastasis, so more efficient therapeutic agents are terribly needed. A propadiene compound: 1-phenylpropadienyl phosphine oxide (PHPO), was employed to test the chemotherapeutic efficacy against ovarian cancer cell lines. MTT assay showed that PHPO displayed a much lower IC50 than cisplatin and paclitaxel, while combination treatment of cells with PHPO + cisplatin induced more apoptosis than with PHPO + paclitaxel or with cisplatin + paclitaxel (p < 0.05). Animal assays demonstrated that subcutaneous tumor growth was highly inhibited by PHPO + cisplatin, compared with that inhibited by PHPO or by cisplatin treatment alone, indicating PHPO and cisplatin may have synergistic effects against ovarian cancer growth. We also found that PHPO induced few side effects on animals, compared with cisplatin. Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP. Taken together, PHPO may induce cell apoptosis through multiple signal pathways, especially when used along with cisplatin. Therefore, PHPO may be explored as a prospective agent to effectively treat ovarian cancer.


Asunto(s)
Alcadienos/administración & dosificación , Antineoplásicos/administración & dosificación , Ensayos de Selección de Medicamentos Antitumorales , Neoplasias Ováricas/tratamiento farmacológico , Animales , Apoptosis , Proteínas de la Ataxia Telangiectasia Mutada/metabolismo , Línea Celular Tumoral , Proliferación Celular , Quinasa de Punto de Control 2/metabolismo , Cisplatino/administración & dosificación , Resistencia a Antineoplásicos/efectos de los fármacos , Sinergismo Farmacológico , Femenino , Humanos , Concentración 50 Inhibidora , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Trasplante de Neoplasias , Paclitaxel/administración & dosificación , Fosfatidilinositol 3-Quinasas/metabolismo
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