Background: Serum lipids are highly inheritable and play a major role in bone health. However, the relationship between low-density lipoprotein cholesterol (LDL-C) and bone mineral density (BMD) remains uncertain. The goal of this study was to see if there was a link between LDL-C levels and BMD in persons aged 20 to 59. Methods: Using data from the National Health and Nutrition Examination Survey (NHANES) 2011-2018, multivariate logistic regression models were utilized to investigate the association between LDL-C and lumbar BMD. Fitted smoothing curves and generalized additive models were also used.
Results:The analysis included a total of 4909 adults. After controlling for various variables, we discovered that LDL-C was negatively linked with lumbar BMD. The favorable connection of LDL-C with lumbar BMD was maintained in subgroup analyses stratified by gender and race in both males and females, Whites and Mexican Americans, but not in Blacks and other races. The relationship between LDL-C and lumbar BMD in other races was an inverted U-shaped curve with the inflection point: 2.327 (mmol/L).
Conclusion:In people aged 20 to 59, our research discovered a negative relationship among LDL-C and lumbar BMD. Among races other than Whites, Blacks, Mexican Americans, this relationship followed an inverted U-shaped curve (inflection point: 2.327mmol/L). LDL-C measurement might be used as a responsive biomarker for detecting osteoporosis early and guiding therapy.
Background
Thyroid dysfunction is a common thyroid disorder in our life and its symptoms are non‐specific, therefore the diagnosis of thyroid dysfunction is important for patients. Albumin (ALB) can carry thyroid hormones to their sites of action as a way to achieve rapid delivery of thyroid hormones to the tissues. The purpose of this study was to investigate the relationship between serum ALB levels and total triiodothyronine (TT3) in adults.
Methods
Data from the 2007–2012 National Health and Nutrition Examination Survey (NHANES) were used to examine the association between ALB and TT3 using multivariate logistic regression models. Fitting smoothed curves and generalized weighted models were also used.
Results
The analysis included a total of 7933 participants that we found an independent positive relationship between ALB and TT3 among participants [0.006 (0.003, 0.009)]. In men, there was a significant positive correlation between ALB and TT3, whereas in women ALB and TT3 suggested a significant negative correlation. Moreover, our study revealed that the independent association between the levels of ALB and TT3 was significant in Non‐Hispanic White, but not in Non‐Hispanic Black. Notably, we found a U‐shaped association between ALB and serum TT3 in total participants (inflection point for ALB: 41 g/L) and females after adjusted covariates (inflection point for ALB: 46 g/L).
Conclusions
We found a U‐shaped relationship between serum ALB and TT3 with infection point at 41 g/L for ALB, which may provide a reference for future screening in adults with thyroid dysfunction.
BackgroundHepatocellular carcinoma (HCC) is one of the most aggressive malignancies. Increasing evidence revealed that long noncoding RNAs (lncRNAs) were frequently involved in various malignancies. Here, we explored the clinical significances, roles, and mechanisms of lncRNA ADORA2A antisense RNA 1 (ADORA2A-AS1) in HCC.MethodsThe clinical significances of ADORA2A-AS1 in HCC were analyzed using RNA sequencing (RNA-seq) data from The Cancer Genome Atlas (TCGA) project. The expressions of ADORA2A-AS1, Fascin Actin-Bundling Protein 1 (FSCN1), Matrix Metallopeptidase 2 (MMP2), and Baculoviral IAP Repeat Containing 7 (BIRC7) in HCC tissues and cells were measured by qRT-PCR. Cell Counting Kit-8 (CCK-8), 5-ethynyl-2’-deoxyuridine (EdU), caspase-3 activity assay, transwell migration and invasion assays, and xenograft growth and metastasis experiments were performed to evaluate the roles of ADORA2A-AS1 in HCC. RNA pull-down, RNA immunoprecipitation, qRT-PCR, Western blot, and RNA stability assay were performed to elucidate the mechanisms of ADORA2A-AS1 in HCC.ResultsADORA2A-AS1 was identified as an HCC-related lncRNA, whose low expression was correlated with advanced stage and poor outcome in HCC. Gain- and loss-of functional experiments demonstrated that ADORA2A-AS1 inhibited HCC cell proliferation, induced cell apoptosis, repressed cell migration and invasion, and repressed xenograft growth and metastasis in vivo. Mechanistically, ADORA2A-AS1 competitively bound HuR (Hu Antigen R), repressed the binding of HuR to FSCN1 transcript, decreased FSCN1 transcript stability, and downregulated FSCN1 expression. The expression of FSCN1 was negatively correlated with ADORA2A-AS1 in HCC tissues. Through downregulating FSCN1, ADORA2A-AS1 repressed AKT pathway activation. Functional rescue assays showed that blocking of FSCN1/AKT axis abrogated the roles of ADORA2A-AS1 in HCC.ConclusionLow-expression ADORA2A-AS1 is correlated with poor survival of HCC patients. ADORA2A-AS1 exerts tumor-suppressive roles in HCC via binding HuR and repressing FSCN1/AKT axis.
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