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OBJECTIVE: Several observational studies have revealed a possible association between asthma and miscarriage. However, inferring causal relationships from observational studies may be fraught with problems like bias, reverse causation, and residual confounding. Therefore, to assess the possible causal effect of asthma on miscarriage, we performed a two-sample Mendelian randomization (MR) analysis. MATERIALS AND METHODS: Asthma (56,167 cases and 352,255 controls) and miscarriage (9,113 cases and 89,340 controls) data from two GWAS of European ancestry were evaluated. Single nucleotide polymorphisms (SNPs) were used as instrumental variables (IVs). The random effect inverse-variance weighted (IVW) Mendelian randomization approach was used as the primary method, and MR-Egger, weighted-median, and MR-PRESSO approaches were replenished as sensitivity analysis to test the robustness of the results. RESULTS: In total, 70 SNPs were obtained using the SNP criteria. Additionally, the MR study found substantial evidence of the causality between asthma and miscarriage [IVW, OR=1.092; 95% CI=1.017-1.174; p<0.05]. The sensitivity analysis demonstrated the reliability of the MR findings [horizontal pleiotropy (MR-Egger, intercept=-0.0002; Standard error of mean, se=0.006; p=0.975)]. CONCLUSIONS: Asthma is a causal risk factor for miscarriage in European populations, according to MR evidence. Our results emphasize the significance of asthma management in reducing the risk of miscarriage in individuals with asthma. [ABSTRACT FROM AUTHOR]

To explore the function of curcumin on the cartilage cells, the cell proliferation and apoptosis by transforming growth factor-beta/suppressor of mothers against decapentaplegic/a disintegrin and metalloproteinase with thrombospondin motifs-7 axis was the objective of the study. The cell viability was detected by cell counting kit-8. The expression of transforming growth factor-beta, suppressor of mothers against decapentaplegic protein, a disintegrin and metalloproteinase with thrombospondin motifs-7, caspase-9, B-cell lymphoma 2, Bcl-2-associated X protein was determined by Western blot. The cartilage cells were treated with 1 mmol/l sodium nitroprusside for 24 h. Then, the cells were treated with different concentration of curcumin for 24 h. We found that 1 μmol/l curcumin could recover the cartilage cells proliferation. The transforming growth factor-beta and suppressor of mothers against decapentaplegic protein show high expression and a disintegrin and metalloproteinase with thrombospondin motifs-7 was low in the curcumin treatment group. Meanwhile, the apoptosis pathway was also detected. The caspase-9 and B-cell lymphoma 2 was higher in the curcumin treatment group than without curcumin group. However, the Bcl-2-associated X protein was lower. The cell viability, a disintegrin and metalloproteinase with thrombospondin motifs-7, caspase-9, B-cell lymphoma 2 and Bcl-2-associated X proteins also show no changes with or without curcumin when the transforming growth factor-beta was inhibited. We found that a disintegrin and metalloproteinase with thrombospondin motifs-7 show over expression, the transforming growth factor-beta and suppressor of mothers against decapentaplegic protein show high expression in the curcumin treatment group, the cell viability, caspase-9, B-cell lymphoma 2 and Bcl-2-associated X proteins show no changes with or without curcumin. Curcumin can promote the cartilage cells proliferation via transforming growth factor-beta/suppressor of mothers against decapentaplegic/a disintegrin and metalloproteinase with thrombospondin motifs-7 axis and inhibit the cell apoptosis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of the study was to quantify the macular vascular density and retinal thickness in the eyes of young myopic people with myopia without pathological changes using optical coherence tomography angiography (OCTA). PATIENTS AND METHODS: In this cross-sectional study, 160 eyes of 80 myopia subjects without pathological changes were classified into three groups: mild myopia (N=40 eyes), moderate myopia (N=66 eyes), and high myopia (N=54 eyes). Macular vascular density (VD), retinal thickness, area of the foveal avascular zone, the flow area of the outer retina and choriocapillaris (CC) were measured using OCTA. The effects of other confounding factors including axial length, the spherical equivalent, and some systemic factors (blood pressure, height, weight, etc.) were also considered. RESULTS: As the severity of myopia increases, the CC flow area decreased (p=0.029). The superficial VD in the temporal, superior, nasal, and inferior regions was significantly lower in high myopia group compared to moderate and low myopia groups (all p<0.001). With increasing myopia, a significant reduction of deep VD was found in the superior region of the macula (p=0.007). In the fovea, there was no difference in the superficial or deep VD across groups (p=0.268 and p=0.413, respectively). Parafoveal retinal thickness was thinnest in the high myopia group and thickest in the mild myopia group (all p<0.05). The fovea was thickest in the high myopia group and thinnest in the mild myopia group (p=0.030). CONCLUSIONS: In young myopic people without pathological changes, superficial VD and retinal thickness decreased with myopia progression, except in the fovea. The CC flow area decreased with increasing myopia. [ABSTRACT FROM AUTHOR]

Autophagy is a main metabolic process in which eukaryotic cells use lysosomes to eliminate abnormal proteins and damaged organelles to maintain cell homeostasis. Studies have revealed that neurodegenerative diseases, tumor, hepatic diseases, etc. are related to abnormal autophagy processes in recent years. Recent studies have shown that TFEB is a major transcription regulator of autophagy-lysosomal pathway (ALP) transcriptional regulation, which positively regulates the expression of autophagy and lysosomal biogenesis-related genes, thereby promoting autophagosome formation, autophagosome-lysosome fusion, and degradation of autophagy substrates. It has also been found that TFEB promotes clearance of intracellular substrates through lysosomal exocytosis. Therefore, the study of biological functions and related regulatory mechanisms of TFEB will provide important clues and theoretical basis for further explaining its physiological pathogenesis and the treatment of related diseases. [ABSTRACT FROM AUTHOR]