(1) Background: With the aging demographic shift in society, there is a growing number of middle-aged and elderly individuals affected by metabolic syndrome (MetS), a risk factor contributing to all causes of mortality. Inflammation plays a crucial role in the development of MetS. This study aims to examine the correlation between MetS and pro-inflammatory diets in middle-aged and elderly individuals, utilizing the Dietary Inflammation Index (DII) as a measure. (2) Methods: Data were extracted from the 2007–2016 National Health and Nutrition Examination Survey (NHANES) database for individuals who were 45 years of age or older. The DII was determined for each participant through 24-h dietary recall interviews. The relationship between DII and MetS was assessed using binary logistic regression analysis, and the association between DII and MetS-related indicators was further explored through generalized linear model (GLM) and quantile regression analysis. (3) Results: A total of 3843 middle-aged and elderly individuals were included in the study. After controlling for confounding factors, the highest quartile of DII was associated with a higher risk of MetS (OR${}_{Q4:Q1}$ = 1.339; 95% CI: 1.013, 1.769; p for trend = 0.018). The top DII quartile also increased the risk of reduced HDL-C (OR${}_{Q4:Q1}$ = 1.499; 95% CI: 1.005, 2.234; p for trend = 0.048) and raised FG (OR${}_{Q4:Q1}$ = 1.432; 95% CI: 1.095, 1.873; p for trend = 0.010) compared to the lowest DII quartile. The levels of DII were found to be positively correlated with BMI ($\beta$ = 0.258, p = 0.001), FPG ($\beta$ = 0.019, p = 0.049), TG ($\beta$ = 2.043, p = 0.013), waistline ($\beta$ = 0.580, p = 0.002), and negatively correlated with HDL-C ($\beta$ = −0.672, p = 0.003). (4) Conclusions: In middle-aged and elderly individuals in the United States, a high DII score has been linked to the presence of MetS, low HDL-C, and hyperglycemia. Therefore, dietary recommendations for the middle-aged and elderly should focus on reducing the DII by choosing foods rich in antioxidants, dietary fiber, and unsaturated fatty acids.

Zinc deficiency could lead to a dynamic variation in gut microbial composition and function in animals. However, how zinc deficiency affects the gut microbiome in school-age children remains unclear. The purpose of this study was to profile the dynamic shifts in the gut microbiome of school-age children with zinc deficiency, and to determine whether such shifts are associated with dietary intake. A dietary survey, anthropometric measurements, and serum tests were performed on 177 school-age children, and 67 children were selected to explore the gut microbial community using amplicon sequencing. School-age children suffered from poor dietary diversity and insufficient food and nutrient intake, and 32% of them were zinc deficient. The inflammatory cytokines significantly increased in the zinc deficiency (ZD) group compared to that in the control (CK) group (p < 0.05). There was no difference in beta diversity, while the Shannon index was much higher in the ZD group (p < 0.05). At the genus level, Coprobacter, Acetivibrio, Paraprevotella, and Clostridium_XI were more abundant in the ZD group (p < 0.05). A functional predictive analysis showed that the metabolism of xenobiotics by cytochrome P450 was significantly depleted in the ZD group (p < 0.05). In conclusion, gut microbial diversity was affected by zinc deficiency with some specific bacteria highlighted in the ZD group, which may be used as biomarkers for further clinical diagnosis of zinc deficiency.

Nickel (Ni) is a common environmental pollutant, which has toxic effects on reproductive system. Nowadays, nano-selenium (Nano-Se) has aroused great attention due to its unique antioxidant effect, excellent biological activities and low toxicity. The aim of this study was to explore the protective effects of Nano-Se on NiSO₄-induced testicular injury and apoptosis in rat testes. Nickel sulfate (NiSO₄) (5 mg/kg b.w.) was administered intraperitoneally and Nano-Se (0.5, 1, 2 mg Se/kg b.w., respectively) was given by oral gavage in male Sprague-Dawley rats. Histological changes in the testes were determined by H&E staining. The terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay and immunohistochemistry were performed to evaluate the apoptosis in testes. Expression levels of mitochondrial apoptosis-related genes and proteins were analyzed by RT-qPCR and Western blot. The results showed that Nano-Se improved lesions of testicular tissue induced by NiSO₄. Nano-Se significantly alleviated NiSO₄-induced apoptosis in rat testes, as well as significantly downregulated the Bak, cytochrome c, caspase-9 and caspase-3 and upregulated Bcl-2 expression levels, all of which were involved in mitochondria-mediated apoptosis. Altogether, we concluded that Nano-Se may potentially exert protective effects on NiSO₄-induced testicular injury and attenuate apoptosis, at least partly, via regulating mitochondrial apoptosis pathways in rat testes.

Paclitaxel (PTX) is one of the most efficient drugs for late-stage non-small cell lung cancer (NSCLC) patients. However, most patients gradually develop resistance to PTX with long-term treatments. The identification of new strategies to reverse PTX resistance in NSCLC is crucially important for the treatment. PTX is an agonist for the pregnane X receptor (PXR) which regulates PTX metabolism. Antagonizing PXR, therefore, may render the NSCLC more sensitive to the PTX treatment. In this study, we investigated the PXR antagonist SPA70 and its role in PTX treatment of NSCLC. In vitro, SPA70 and PTX synergistically inhibited cell growth, migration and invasion in both paclitaxel-sensitive and paclitaxel-resistant A549 and H460 lung cancer cells. Mechanistically, we found PTX and SPA70 cotreatment disassociated PXR from ABCB1 (MDR1, P-gp) promoter, thus inhibiting P-gp expression. Furthermore, the combination regimen synergistically enhanced the interaction between PXR and Tip60, which abrogated Tip60-mediated α-tubulin acetylation, leading to mitosis defect, S-phase arrest and necroptosis/apoptosis. Combination of PXT and SPA70 dramatically inhibited tumor growth in a paclitaxel-resistant A549/TR xenograft tumor model. Taken together, we showed that SPA70 reduced the paclitaxel resistance of NSCLC. The combination regimen of PTX and SPA70 could be potential novel candidates for the treatment of taxane-resistant lung cancer.