BackgroundThis meta-analysis aimed to assess the correlation between the high-intensity zone (HIZ) of a lumbar MRI and discography.MethodsWe conducted an electronic search of the PubMed, MEDLINE, Embase, and ScienceDirect databases from their respective inceptions to October 2016 using the following search terms: “low back pain,” “discogenic low back pain,” “HIZ or high-intensity zone,” and “discography”. Relevant journals and conference proceedings were manually searched. Two reviewers independently assessed the quality of the studies, extracted data from the included studies, and analyzed the data.ResultsEleven studies were included. The results of the meta-analysis indicated that outstanding relativity and statistically significant correlations were observed between the HIZ and abnormal disc morphology (OR = 47.79; 95% CI: 17.07 to 133.77; P < 0.00001), HIZ and pain reproduction (OR = 8.65, 95% CI: 6.01 to 15.23, P < 0.00001), and HIZ and abnormal morphology pain reproduction (OR = 11.74, 95% CI: 1.99 to 69.36, P = 0.007).ConclusionsThe presence of an HIZ on a lumbar MRI T2-weighted image indicates abnormal disc morphology. There is a strong relationship between the HIZ and pain reproduction. The HIZ can be an effective index for prediction of discogenic low back pain.

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Tryptophan has drawn wide attention due to its involvement in improving intestinal immune defense directly and indirectly by regulating metabolic pathways. The study aims to elucidate the potential modulating roles of tryptophan to protect against intestinal inflammation and elucidate the underlying molecular mechanisms. The protective effects of tryptophan against intestinal inflammation are examined in the lipopolysaccharide (LPS)-induced inflammatory model. We first found that tryptophan markedly (p < 0.01) inhibited proinflammatory cytokines production and nuclear factor κB (NF-κB) pathway activation upon LPS challenge. Next, we demonstrated that tryptophan (p < 0.05) attenuated LPS-caused intestinal mucosal barrier damage by increasing the number of goblet cells, mucins, and antimicrobial peptides (AMPs) in the ileum of mice. In addition, tryptophan (p < 0.05) inhibited LPS-induced autophagic flux through the AMP-activated protein kinase (AMPK)-sirtuin 1 (SIRT1) pathway in the intestinal systems to maintain autophagy homeostasis. Meanwhile, tryptophan also reshaped the gut microbiota composition in LPSchallenge mice by increasing the abundance of short-chain fatty acid (SCFA)-producing bacteria such as Acetivibrio (0.053 ± 0.017 to 0.21 ± 0.0041%). Notably, dietary tryptophan resulted in the activation of metabolic pathways during the inflammatory response. Furthermore, exogenous treatment of tryptophan metabolites kynurenine (Kyn) and 5-HT in porcine intestinal epithelial cells (IPEC-J2 cells) reproduced similar protective effects as tryptophan to attenuate LPS-induced intestinal inflammation through regulating the AMPK-SIRT1-autophagy. Taken together, the present study indicates that tryptophan exhibits intestinal protective and immunoregulatory effects resulting from the activation of metabolic pathways, maintenance of gut mucosal barrier integrity, microbiota composition, and AMPK-SIRT1-autophagy level.