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1.
Chinese Journal of Practical Nursing ; (36): 2133-2138, 2022.
Artigo em Chinês | WPRIM | ID: wpr-954983

RESUMO

Objective:To summarize the characteristics and nursing experience of patients of transthyretin amyloid polyneuropathy.Methods:A retrospective study was performed in 9 patients with transthyretin amyloid polyneuropathy from different area in china from February 2018 to October 2021 in the Second Affiliated Hospital Zhejiang University School of Medical, summarized nursing points:used list to popularize disease knowledge, improved the nursing skills of rare diseases; did a good job in the safety nursing of sensory motor disorders to prevent pressure sores, scalds, fall, thrombosis and other complications, paid attention to the nursing of autonomic nerve dysfunction, prevented postural hypotension. Observe and prevent heart failure, manage diarrhea and constipation, and applied the guide to personalized urinary tract management;provided genetic counseling services, personalized continuing care and psychological care.Results:During hospitalization, the clinical symptoms of 9 patients were improved to varying degrees, after 3 months of telephone follow-up after discharge, 9 patients had no adverse events such as pressure ulcer and fall.Conclusions:By improving specialized skills, predictive risk management and symptom care, the symptoms of postural hypotension, urinary retention, constipation, diarrhea and other symptoms of transthyretin amyloid polyneuropathy patients can be prevented and improved, and adverse events such as falls and pressure sores can be avoided.

2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 17-23, 2012.
Artigo em Inglês | WPRIM | ID: wpr-635481

RESUMO

Pim kinases contribute to tumor formation and development of lymphoma, which shows enhanced DNA replication, DNA recombination and repair. Endothelial cells

3.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 704-708, 2010.
Artigo em Inglês | WPRIM | ID: wpr-349757

RESUMO

This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.


Assuntos
Animais , Masculino , Ratos , Animais Recém-Nascidos , Isquemia Miocárdica , Metabolismo , Traumatismo por Reperfusão Miocárdica , Metabolismo , Miocárdio , Metabolismo , Estresse Oxidativo , Fisiologia , Proteínas Serina-Treonina Quinases , Genética , Metabolismo , Ratos Sprague-Dawley , Transdução de Sinais , Regulação para Cima
4.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 704-8, 2010.
Artigo em Inglês | WPRIM | ID: wpr-634950

RESUMO

This study examined the effect of ischemia-reperfusion injury on the expression of Pim-3 gene in myocardial tissues and their underlying mechanism. Rat models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery of the rats. A total of 30 SD male adult rats were randomly divided into 5 groups: group A (sham operation, n=6); group B (in which the rats were subjected to 15 min of ischemia by ligation of the left anterior descending coronary artery, n=6); group C (in which the rats received 30 min of ischemia, n=6), group D and group E (in which the left anterior descending coronary artery of the rats were ligated for 30 min and then reperfused for 30 min or 120 min, n=6 in each). The left ventricular tissues were removed immediately after the ischemia-reperfusion injury. Neonatal cardiomyocytes were cultured and treated with different concentrations of H(2)O(2) (0, 5, 10, 20 μmol/L) or tumor necrosis factor-α (TNF-α, 0, 1, 5, 10 ng/mL). The mRNA and protein expression of Pim-3 gene was determined by using RT-PCR, western blotting and immunohistochemistry. Additionally, neonatal cardiomyocytes were transfected with Pim-3 siRNA, and induced to develop apoptosis by using H(2)O(2). The results showed that normal myocardial tissues expressed a quantity of Pim-3 gene mRNA and protein. Ischemia-reperfusion injury could up-regulate the mRNA and protein expression of Pim-3 gene in myocardial tissues. Furthermore, H(2)O(2) but not TNF-α up-regulated the Pim-3 gene expression in cultured cardiomyocytes. And Pim-3 silencing failed to strengthen the H(2)O(2)-inducing apoptosis in cardiomyocytes. It was concluded that ischemia-reperfusion injury up-regulated the Pim-3 gene expression through oxidative stress signaling pathway in myocardial tissues.

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