Selenium supplementation enhanced the expression of selenoproteins in hippocampus and played a neuroprotective role in LPS-induced neuroinflammation.

Selenium (Se) is obtained from organic and inorganic selenium food content, which mainly depends on the regional soil selenium content. Selenium deficiency and decreased selenoprotein functions have been shown to associate with the progression of cognitive decline and neurodegenerations including Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Selenoproteins are well recognized for their anti-oxidative activities. Given the high oxygen consumption, mammalian brains preferent@ially supplied with Se. Here, we propose a beneficiary role for dietary supplementation of sodium selenite (300 ng per gram of body weight) in ameliorating neuroinflammation induced by bilateral intracerebroventricular injection of 1 µL LPS (1 µg/µL), evidenced by the significantly reduced oxidative stress, downregulated pro-inflammatory cytokines expression, improved integrity of blood-brain barrier, as well as suppressed glial activation and shifted microglial MI/M2 polarization in Se-sup mouse brain. Se intake also reduced neural cell death and significantly improved the cognition in Se-sup mice following LPS challenge. The neuroprotective role for supplementary Se is likely to be ascribed to the overall elevated expression of selenoproteins, especially Selenoprotein P (SELENOP) and Glutathione peroxidase 4 (GPX4), ranking on top of the change in selenoprotein expression hierarchy. The regional hierarchy of Se induced elevation of SELENOP expression was further characterized. The SELENOP expression in the mediodorsal thalamic nucleus, dendric gyrus (DG) and cornu ammonis 3 (CA3) of hippocampus and lateral habenular nucleus was highly sensitive to dietary Se intake.

The oncological outcome and influence of neoadjuvant chemotherapy on the surgery in the resectable and locally advanced oral squamous cell carcinoma.

AIM: The role of neoadjuvant chemotherapy (NCT) in the treatment of advanced oral squamous cell carcinoma (OSCC) is still controversial. Especially, there are still few studies investigating the influence of NCT on the following surgery. In this retrospective single-center attended cohort study, we investigated the oncological effect of NCT and its influence on the following surgery in patients with resectable locally advanced OSCC. METHOD: The clinical data of 88 patients with locally advanced but resectable OSCC (T3/4) were reviewed retrospectively. NCT plus conservative surgery and radical surgery were compared. Five-year disease-specific survival (DSS) was observed as the main endpoint. RESULTS: Among 88 patients enrolled in this study, 56 patients received upfront radical surgery (non-NCT group) and 32 patients received NCT followed by surgery (NCT group). The patients in the non-NCT group had a statistically better DSS than the patients in the NCT group (P=0.041). Twenty-one out of 32 (65.6%) patients who received NCT were good responders including two patients (6.2%) had a complete response and 19 patients (59.4%) had a partial response. There was no statistical difference between good and poor responders in 5-year DSS (P=0.823). Eleven patients (34.4%) had conservative surgery without flap reconstruction and 21 patients had radical surgery with flap reconstruction after NCT. No statistical difference in surgical margins was found between the two types of surgery (P=0.519). There was also no statistical difference in 5-year DSS between the two types of surgery (P=0.652). CONCLUSION: NCT plus surgery could not improve survival compared with upfront surgery. NCT could modify the surgical extent but would not affect the surgical margins. This conclusion should be explained cautiously, and randomized clinical trials with large sample size were needed to further answer the question.