Associations between mixed urinary phenols and parabens metabolites and bone mineral density: Four statistical models.

Phenols and parabens widely exist in personal care and consumer products and have been proved to be endocrine disrupting chemicals that could disturb bone metabolism. The current studies focusing on the associations between phenols and parabens with bone mineral density (BMD) drew contradictory conclusions. Considering the bias might be due to not considering the effects of mixed exposure, we conducted the first cross-sectional study to investigate the associations of both single and mixed metabolites of phenols and parabens with BMD in three populations by setting up four models: generalized linear regression model (GLM), weighted quantile sum (WQS) regression model, quantile g-computation (qgcomp) model and Bayesian kernel machine regression (BKMR) model, based on the US National Health and Nutrition Examination Survey (NHANES) database. We found that the association between the mixtures and total femur BMD in men was significantly negative. Bisphenol A (BPA) was shown to play the most important role in this negative association in the BKMR model, and this negative association was also confirmed in the GLM model with ß coefficient (95% CI) being -0.02 (-0.04, -0.01). The relationships between the mixtures and femoral neck and trochanter BMD in postmenopausal women were significantly positive. Benzophenone-3 (BP-3) played the most significant role in the positive association with trochanter BMD, as confirmed by the WQS, qgcomp and BKMR models, and this positive association was also verified by the GLM model with ß coefficient (95% CI) being 0.01 (0.00, 0.02). In conclusion, the association between the mixed phenols and parabens and BMD was negative in men while was positive in postmenopausal women, which was gender-specific. This study might provide new ideas for the prevention and treatment of osteoporosis and the control of personal care and consumer products containing phenols and parabens in the future.

Negative correlations between bile reflux gastritis and Helicobacter pylori infection.

OBJECTIVE: There are a few articles to study the relationship between bile reflux gastritis (BRG) and H. pylori infection, and the results are debatable. This study set out to determine the relationship between BRG and Helicobacter pylori (H. pylori) infection. METHODS: In this retrospective study, patients from January, 1st 2013 to January, 1st, 2021 were divided into two groups based on whether they had BRG. The control group was got by 1:1 propensity-score matching (PSM) based on age and sex. Then, the relationship between BRG and H. pylori in patients was analyzed via Chi-squared test and Phi (φ) detection. RESULTS: 26449 patients were included in this study, and there were 1918 patients in each group after age and sex matching. patients with HP were responsible for 35% (9345/26449) and patients with BRG were 7% (1918/26449). Further relationship exploration, there is a negative, but weak, the relationship between BRG and HP infection (X2 = 45.62, p < .001, Phi (φ)= -0.109). CONCLUSION: Patients with bile reflux may have less likely to get HP infection. HP eradication is an important thing for the prevention of gastric cancer and this study serves as a foundation and may provide directions for future research.

Role of Mitophagy in the Pathogenesis of Stroke: From Mechanism to Therapy.

Mitochondria can supply adenosine triphosphate (ATP) to the tissue, which can regulate metabolism during the pathologic process and is also involved in the pathophysiology of neuronal injury after stroke. Recent studies have suggested that selective autophagy could play important roles in the pathophysiological process of stroke, especially mitophagy. It is usually mediated by the PINK1/Parkin-independent pathway or PINK1/Parkin-dependent pathway. Moreover, mitophagy may be a potential target in the therapy of stroke because the control of mitophagy is neuroprotective in stroke in vitro and in vivo. In this review, we briefly summarize recent researches in mitophagy, introduce the role of mitophagy in the pathogenesis of stroke, then highlight the strategies targeting mitophagy in the treatment of stroke, and finally propose several issues in the treatment of stroke by targeting mitophagy.

Comparison of gene mutation spectra in younger and older Chinese acute myeloid leukemia patients and its prognostic value.

Differences in the gene mutation spectra of younger and older Chinese adult AML patients and the prognostic significance of these differentially presented gene mutations are rarely reported. One hundred and thirteen newly diagnosed Chinese adults with AML, divided into groups of younger and older patients, were enrolled in this study. Bone marrow samples from the patients were analyzed using targeted next-generation sequencing with a panel of 141 genes. Ninety-eight mutated genes were detected and the top 10 mutated genes were KMT2D, FLT3, FAT1, ASXL1, NRAS, DNMT3A, RELN, TET2, JAK2, and KRAS. The top five functional groups were the tyrosine kinase pathway, transcription factors, DNA methylation, chromatin modifiers, and the JAK-STAT signaling pathway. Younger patients exhibited higher incidences of KMT2D (33.8% vs 10.4%, P = 0.004) and KRAS (15.4% vs 2.1%, P = 0.042) mutations than older patients; whereas, older patients harbored more SRSF2 (20.8% vs 0%, P = 0.002), transcription factor (85.4% vs 67.7%, P = 0.031), DNA methylation (58.3% vs 36.9%, P = 0.024), and RNA splicing (31.3% vs 12.3%, P = 0.013) mutations than younger patients. Moreover, patients with SRSF2 mutations exhibited a lower rate of overall survival (P < 0.001) and relapse-free survival (P < 0.001) than patients carrying wild-type SRSF2. In conclusion, rarely reported KMT2D, FAT1, and RELN mutations were detected at high frequencies in our cohort. The gene mutation spectrum of older patients was different to that of younger patients. Moreover, older patients harbored more SRSF2 mutations, which predicted lower rates of overall and relapse-free survival.

[Effects of dicyandiamide on cadmium accumulation in pakchoi under instant soluble nitrogen fertilizers]. / é€Ÿæ•ˆæ°®è‚¥é æ–½åŒæ°°èƒºå¯¹å‡æŽ§å°ç™½èœé•‰ç§¯ç´¯çš„ä½œç”¨.

We investigated the effects of dicyandiamide (DCD) on the growth and Cd concentrations in pakchoi cultivated under different instant soluble N fertilizers [ammonium sulfate, ammonium sulfate and sodium nitrate (1:1, ammonium/nitrate), and urea] in Cd-contaminated soils. The results showed that the fresh weight of the edible parts of Cd-stressed pakchoi were increased by 583.3%, 41.5%, and 206.8% under ammonium, ammonium/nitrate, and urea treatments in the presence of DCD, respectively compared with control, and the tolerance index and photosynthetic rate significantly increased, whereas no significant changes were observed under nitrate supply. Under all N treatments with DCD, the MDA and H2O2 contents and the superoxide radical production rate in the leaves of pakchoi were decreased, with the highest reduction occurred in ammonium and urea treatments. Cd concentrations in the leaves of pakchoi fertilized with ammonium, ammonium/nitrate, and urea were lowered by 58.3%, 34.0%, and 44.5% and those in the petioles were lowered by 61.8%, 29.4%, and 55.6%, respectively. Cd concentration in the leaves and petioles of pakchoi in the nitrate treatment did not differ significantly from control. These changes could be attributable to the reduction in the acidification of rhizosphere soil in response to the combined application of N fertilizer and DCD. Accordingly, in Cd-contaminated soils with a low buffering capacity, the application of DCD combined with ammonium, ammonium/nitrate, or urea N fertili-zers could alleviate Cd-induced growth stress and inhibit photosynthesis in pakchoi plants and effectively minimize the Cd accumulation.

A signal-amplification circuit between miR-218 and Wnt/ß-catenin signal promotes human adipose tissue-derived stem cells osteogenic differentiation.

Human adipose-derived stem cells (hASCs) have become a highly attractive source of seed cells in bone regenerative. It has become a key issue how to effectively improve osteogenic differentiation of hASCs in the bone tissue engineering. Numerous regulatory pathways dominate osteogenic differentiation of hASCs involve transcriptional factors and signaling molecules. However, how these factors combine with each other to regulate hASCs osteogenic differentiation still remain to be illustrated. The identification of microRNAs will illuminate this and might permit finely tuning the osteogenic differentiation process. Here, we present evidence that miR-218 acts as a positive regulator of hASCs osteogenesis. Real-time PCR shows that miR-218 was up-regulated during osteogenic differentiation. Overexpression of exogenous miR-218 enhanced osteogenic differentiation in vitro, whereas inhibition of miR-218 would suppress osteogenic differentiation. Furthermore, miR-218 directly targeted SFRP2 and DKK2, which is a WNT signaling pathway antagonist, and enhanced Wnt/ß-catenin signaling activity. Finally, we found that mimicking Wnt/ß-catenin signal strengthened the expression level of miR-218, while blocking the signal attenuated the expression level of miR-218. This feed-forward regulatory circuit provides additional insight into how miRNAs acting as a signal amplifier interact with signal molecules during hASCs osteogenic differentiation. Taken together, we have established a regulatory network with a central role for the miR-218 in hASCs osteogenic differentiation.