The present study was a part of a larger research project that aimed to investigate the effects of Met-Met supplementation on fish growth and intestinal health. This study mainly focused on the relationship between dietary Met-Met and intestinal physical barrier function in fish. Seven iso-nitrogenous diets supplemented with 2.50 g/kg DL-methionine (DL-Met) and six graded levels of Met-Met (0.00, 0.79, 1.44, 1.84, 2.22, and 2.85 g/kg) were used to feed juvenile grass carp for 10 weeks, after which a 14-day Aeromonas hydrophila challenge test was performed. The results indicated that optimum levels of Met-Met decreased intestinal oxidative damage, probably by increasing total antioxidant capacity, and the activity and gene expression levels of several antioxidant enzymes, which were closely related to the changed Nrf2/Keap1 signaling. Meanwhile, optimum levels of Met-Met decreased intestinal apoptosis and improved the intestinal tight junction, as evident by the downregulated mRNA levels of initiator and executioner caspases; the pro-apoptotic-related proteins FasL, Apaf-1, and Bax; and upregulated mRNA levels of the anti-apoptotic proteins Bcl-2, Mcl-1b, and IAP and the TJ proteins claudins, occludin, and ZOs. Furthermore, the positive effects of Met-Met on improving intestinal physical barrier function were superior to those of DL-Met in fish. These findings showed that optimal Met-Met supplementation improved intestinal physical barrier function, probably by changing antioxidant capacity, apoptosis, and tight junction proteins in fish.
Alzheimer's disease (AD) is currently a major global health issue that could induce several cognitive and mental problems in early-stage patients, and dementia in varying degrees, even death, in middle and late-stage patients. The formation of beta-amyloid (A-beta) plaque in neurons and the pathological accumulation of tau protein are the two well-known ideas that explain the process of AD. This essay has concluded some research achievements in the past decade, including some important mechanisms (regarding some specific molecules like APOE4 and PyK2) of tau pathologies in AD, several influences on animal and cell models, as well as methods for detection of neuronal tau accumulation in physical and biological fields. The possible therapies with mirodenafil and melatonin were also introduced. In the future, the creation and combination of more new technology, such as real-time monitoring and imaging technology, as well as the clinical discovery of new effects of some drugs on AD patients would help the research and remedies of AD make a progress.
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