Research Status and Progress of Nutritional Support Therapy for Ovarian Cancer.

Ovarian cancer is one of the most fatal gynecological cancers. For most ovarian cancer patients, nutritional risk or malnutrition may accompany them for life. Regular nutritional risk screening, timely nutritional assessment and necessary nutritional treatment play an extremely important role in the process of comprehensive treatment of ovarian cancer. The nutritional status and influence of ovarian cancer patients, preoperative screening and assessment of nutritional risk, preoperative and postoperative nutritional treatment indicate that nutritional treatment of ovarian cancer is one of the key factors in the treatment of cancer. We have summarized the status and progress of nutritional support therapy for ovarian cancer. We are aimed to improve the understanding of the impact of nutritional support therapy for ovarian cancer and to guide the clinical work.

Neuroprotective effect of transcorneal electrical stimulation on ischemic damage in the rat retina.

Some previous studies have showed that transcorneal electrical stimulation (TES) could protect retinal neurons in certain rodent models. However, it is not yet clear whether TES could also definitely protect retinal neurons against ischemic insults. In the present study, we hypothesized that TES had such a neuroprotective effect and further investigated its underlying mechanism. Adult female Sprague-Dawley (SD) rats received TES treatment every other day after ocular ischemia was induced by elevating the intraocular pressure to 120 mm Hg for 60 min. Retinal ganglion cells (RGCs) were labeled retrogradely 7 days before ischemia and were counted 7 and 14 days later. At the same time points, retinal function was assessed by scotopic electroretinography (ERG), combined with retinal histological analysis. The glutamine synthetase (GS) immunoreactivity was compared between ischemic retinas with TES and those with sham stimulation under identical confocal laser microscope conditions. The immunohistochemical indications were confirmed by Western blot analysis. Higher mean density of RGCs was quantified in TES treated retinas compared to retinas with sham stimulation on days 7 and 14 after ischemia. Similarly, histological analysis showed that TES better preserved the mean thickness of separate retinal layers. ERG studies indicated that by undergoing TES treatment, the b-wave amplitude was also significantly preserved on day 7 after ischemia and recovered robustly on day 14. Immunohistochemical and Western blot analysis both revealed that GS levels remarkably increased after TES and lasted for at least 7 days. Our results indicate that TES can protect retinal neurons against ischemic insults, probably related to increasing levels of GS localized in Müller cells. These findings suggest a new approach for potential clinical application to ocular ischemic diseases.