This study compared the levels of signal transducer and activator of transcription 3 (STAT3) and cyclin D1 protein in paired primary and recurrent astrocytic tumours, and analysed their correlation with clinicopathological and treatment factors. A total of 48 samples from 24 patients who had undergone surgical removal of primary and recurrent astrocytic tumours were analysed. Levels of STAT3 and cyclin D1 protein were detected using immunohistochemistry. Increased STAT3 and decreased cyclin D1 levels were observed in recurrent astrocytic tumours compared with their paired primary tumours. There was a significant correlation between higher levels of STAT3 protein and shorter progression-free survival in primary tumours after surgery (r = 0.417), and a significant correlation between decreased cyclin D1 protein levels and radiotherapy in recurrent tumours (r = 0.468). It was concluded that increased STAT3 and decreased cyclin D1 protein levels may contribute to the recurrence of astrocytic tumours. Detection of STAT3 may be useful in predicting progressionfree survival in primary astrocytic tumours after surgery. In addition, radiotherapy may decrease cyclin D1 levels in astrocytic tumours, but the nature of this association requires further investigation.
Erectile dysfunction (ED) is a worldwide problem threatens men's health. The incidence of ED in diabetic patients is higher than that in the healthy population. The incidence of peripheral and autonomic neuropathy is significantly higher in diabetic patients than in normal men. Vasomotor nerves play an important role in the regulation of erectile function. Degeneration of autonomic and sensory nerves is a common type of diabetic neuropathy (DNP) and is closely related to erectile function. Brain-derived neurotrophic factor (BDNF) has been demonstrated to improve diabetic erectile dysfunction in rat models and in humans. However, this process has not yet been fully elucidated yet. In this article, we summarise the mechanisms by which BDNF improves diabetic erectile dysfunction.
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