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1.
World J Clin Cases ; 9(22): 6457-6463, 2021 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-34435012

RESUMO

BACKGROUND: Malignant peripheral nerve sheath tumor (MPNST) is a type of spindle cell sarcoma originating from the peripheral nerve, which usually results in the corresponding nerve sign on magnetic resonance imaging (MRI). Patients with MPNST may also have neurofibromatosis type 1. CASE SUMMARY: A 78-year-old male was admitted to the hospital due to a tumor in his left knee. He had a previous history of superficial spreading melanoma on the left thigh. Color Doppler ultrasonography showed a hypoechoic mass in the subcutaneous soft tissues of the medial left knee with an abundant rich blood flow. Computed tomography scanning did not show obvious signs of bone destruction, but the skin adjacent to the tumor was slightly thickened. MRI examination revealed that the hypervascular lesion was well-circumscribed, lobulated, invaded the surrounding soft tissues and demonstrated heterogeneous enhancement but lacked an entering and exiting nerve sign. The MRI result indicated the invasiveness of the tumor. The patient underwent a left knee joint mass expanded resection and the first histopathological examination showed a MPNST with positive surgical margins. Therefore, the second extended resection was performed, and the patient had a good outcome in the short term. CONCLUSION: MRI is a useful technique for revealing the biological characteristics of MPNST and provides clinical support for evaluation of the surgical area before operation.

2.
Nan Fang Yi Ke Da Xue Xue Bao ; 37(4): 505-511, 2016 Apr 20.
Artigo em Chinês | MEDLINE | ID: mdl-28446404

RESUMO

OBJECTIVE: To investigate the protective effects of irbesartan against cardiac inflammation associated with diabetes and obesity in the db/db mouse model of type 2 diabetes and explore the underlying mechanisms. METHODS: Twenty- four 10-week-old diabetic db/db mice were equally randomized into irbesartan treatment (50 mg/kg per day) group and model group, using 12 nondiabetic littermates (db/+) as the controls, The mice were treated with irbesartan or saline vehicle for 16 consecutive weeks, after which the heart pathology was observed and the heart weight, body weight, and serum levels of fasting blood glucose (FBG), total cholesterol(TC), and triglycerides(TG) were measured. The expression of nuclear factor-kappaB (NF-κB) p65 in the myocardium was assessed with immunohistochemistry, the protein levels of P-IκBα ,IκBα and ß-actin were analyzed with Western blotting, and the pro-inflammatory cytokines IL-6 and TNF-α mRNA were detected using quantitative real-time PCR (qPCR). RESULTS: Compared with db/+ mice, the saline-treated db/db mice developed obesity, hyperglycemia and hyperlipidemia (P<0.01). Histopathological examination of the heart tissue revealed inflammatory cell infiltration, increased myocardial interstitium and disorders of myocardial fiber arrangement. The diabetic mice showed increased P-IαBα and decreased IκBα protein levels, enhanced activity and expression of NF-κB in the hearts, and increased mRNA expression of IL-6 and TNF-α in the myocardium. These abnormalities were all associated with increased inflammatory response. Treatment with irbesartan improved the heart architecture and attenuated high glucose-induced inflammation in the diabetic mice. CONCLUSION: Treatment with irbesartan attenuates cardiac inflammation in type 2 diabetic db/db mice, and this effect was probably associated with the suppression of cardiac angiotensin II and NF-κB signaling pathway.


Assuntos
Compostos de Bifenilo/farmacologia , Doenças Cardiovasculares/tratamento farmacológico , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Tipo 2/complicações , Inflamação/tratamento farmacológico , Tetrazóis/farmacologia , Actinas/metabolismo , Angiotensina II/metabolismo , Animais , Interleucina-6/metabolismo , Irbesartana , Camundongos , Obesidade/complicações , Distribuição Aleatória , Reação em Cadeia da Polimerase em Tempo Real , Transdução de Sinais , Fator de Transcrição RelA/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
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