U-shaped association of serum uric acid with all-cause mortality in patients with hyperlipidemia in the United States: a cohort study.

Background: Serum uric acid (SUA) interferes with lipid metabolism and is considered an independent risk factor for atherosclerosis, a major complication in patients with hyperlipidemia. However, the effects of uric acid levels on mortality in hyperlipidemic patients has yet to be sufficiently determined. In this study, we aimed to assess the association between all-cause mortality and SUA in a hyperlipidemic population. Methods: To determine mortality rates, we obtained data for 20,038 hyperlipidemia patients from the U.S. National Health and Nutrition Examination Surveys (NHANES) 2001-2018 and National Death Index. To examine the all-cause mortality effect of SUA, multivariable Cox regression models, restricted cubic spline models, and two pairwise Cox regression models were used. Results: Over a median follow-up of 9.4 years, a total of 2079 deaths occurred. Mortality was examined according to SUA level quintiles: <4.2, 4.3-4.9, 5.0-5.7, 5.8-6.5, and >6.6 mg/dl. In multivariable analysis using 5.8-6.5 mg/dl SUA as a reference, the hazard ratios (95% confidence interval) of all-cause mortality across the five groups were 1.24 (1.06-1.45), 1.19 (1.03-1.38), 1.07 (0.94-1.23), 1.00 (reference), and 1.29 (1.13-1.48), respectively. According to a restricted cubic spline, we noted a U-shaped relationship between SUA and all-cause mortality. The inflection point was approximately 6.30 mg/dl, with hazard ratios of 0.91 (0.85-0.97) and 1.22 (1.10-1.35) to the left and right of the inflection point, respectively. In both sexes, SUA was characterized by a U-shaped association, with inflection points at 6.5 and 6.0 mg/dl for males and females, respectively. Conclusion: Using nationally representative NHANES data, we identified a U-shaped association between SUA and all-cause mortality in participants with hyperlipidemia.

U-Shaped Relationship Between Serum Lactate Dehydrogenase with All-Cause Mortality in Patients with Chronic Obstructive Pulmonary Disease.

Purpose: In the anaerobic metabolic pathway, lactate dehydrogenase (LDH) plays an important role in hypoxia, inflammation, and cell damage, making it a potential biomarker for the progression of chronic obstructive pulmonary disease (COPD). We aimed to examine the relationship between LDH levels and all-cause mortality in participants with COPD. Patients and Methods: Data of participants in the US National Health and Nutrition Examination Surveys (NHANES) 2007-2012 aged ≥20 years who underwent spirometry tests were examined, and follow-up mortality data were obtained. According to serum LDH levels, participants with COPD were divided into five groups (59-111, 112-123, 124-135, 136-150, and 151-344 U/L). To evaluate whether LDH levels were independently associated with COPD mortality, we used multivariate Cox regression analysis and smooth curve fitting. Results: We included 1320 subjects, 64 with stage III or IV COPD and 541 with stage II COPD. Over a median follow-up of 9.7 years (IQR: 7.8, 11.2), 252 of the 1320 subjects died. The mean LDH level was 132.5 U/L (standard deviation [SD], 27.0). A U-shaped relationship was observed between LDH levels and all-cause mortality. Below and above the inflection point, which was approximately 110 U/L, we found different slopes for the correlation between LDH and all-cause mortality of patients with COPD. Below the threshold, per 1-standard deviation (1SD) increase in LDH resulted in a 68% reduced risk of all-cause mortality (hazard ratio [HR] 0.32, 95% confidence interval [CI] 0.13-0.81, P=0.016); conversely, above the threshold, per 1SD increase in LDH accelerated the risk of all-cause mortality (HR 1.23, 95% CI: 1.08-1.41, P= 0.002). Conclusion: Using the nationally representative NHANES data, we found a U-shaped association between LDH level and all-cause mortality in participants with COPD. An optimal LDH level of approximately 110 U/L was associated with the lowest risk of all-cause mortality.

Recent advances in nanomaterial-based electrochemical and optical sensing platforms for microRNA assays.

MicroRNA (MiRNA) plays a crucial role in biological cells to enable assessment of a cancer's development stage. Increasing evidence has shown that the accurate and sensitive detection of miRNA holds the key toward correct disease diagnosis. However, some characteristics of miRNAs, such as their short chains, low concentration, and similar sequences, make it difficult to detect miRNA in biological samples. Nanomaterials usually have good optical, electronic, and mechanical properties and therefore provide new possibilities for improving the performance of miRNA assays. Many different sorts of nanomaterials, including metal nanomaterials, carbon nanomaterials, quantum dots, and transition-metal dichalcogenides, have been used to construct optical and electrochemical assays for miRNA and have shown attractive results. This review describes recent efforts in the application of nanomaterials as sensing elements in electrochemical and optical miRNA assays. The analytical figures of merit of various methods for the detection of miRNA are compared in the present article. The current capabilities, limitations, and future challenges in miRNA detection and analysis based on nanomaterials are also addressed.

Tetrahedral DNA probe coupling with hybridization chain reaction for competitive thrombin aptasensor.

A novel competitive aptasensor for thrombin detection is developed by using a tetrahedral DNA (T-DNA) probe and hybridization chain reaction (HCR) signal amplification. Sulfur and nitrogen co-doped reduced graphene oxide (SN-rGO) is firstly prepared by a simple reflux method and used for supporting substrate of biosensor. Then, T-DNA probe is modified on the electrode by Au-S bond and a competition is happened between target thrombin and the complementary DNA (cDNA) of aptamer. The aptamer binding to thrombin forms an aptamer-target conjugate and make the cDNA remained, and subsequently hybridizes with the vertical domain of T-DNA. Finally, the cDNAs trigger HCR, which results in a great current response by the catalysis of horseradish peroxidase to the hydrogen peroxide + hydroquinone system. For thrombin detection, the proposed biosensor shows a wide linearity range of 10-13-10-8M and a low detection limit of 11.6fM (S/N = 3), which is hopeful to apply in biotechnology and clinical diagnosis.