Objectives:To determine and compare the repeatability and reproducibility of anterior scleral parameters measured by the corneoscleral profile (CSP) module of Pentacam in keratoconus (KC) and control eyes.Methods:This is a prospective observational study. Thirty KC participants (30 eyes) and 24 control participants (24 eyes) were examined three times using the CSP. Sagittal height mean (SHM), sagittal height astigmatism (SHA), and mean bulbar slope (BSM) were measured in 12 mm and 16 mm chord lengths. The repeatability and reproducibility of these measurements were also assessed. Coefficients of variation (CoV), intraclass correlation coefficient (ICC), coefficient of repeatability (CoR1), and coefficient of reproducibility (CoR2) were adopted to assess the reliability.Results:In the KC and control groups, SHM showed high repeatability and reproducibility (coefficients of variation [CoVs]≤0.96%, intraclass correlation coefficient [ICCs]≥0.97), and SHM of control eyes showed higher repeatability and reproducibility than that of KC eyes at 12 mm chord length (KC group, CoRs ranged from 35.56 μm to 43.52 μm, control group, ranged from 23.50 μm to 30.31 μm) and 16 mm chord length (KC group, CoRs ranged from 79.54 μm to 81.58 μm, control group, ranged from 48.25 μm to 66.10 μm). Mean bulbar slope also showed high repeatability and reproducibility (CoVs≤3.65%, CoRs≤2.64). Furthermore, the SHA of control eyes showed higher repeatability and reproducibility when compared with KC eyes (control group: CoVs≤29.95%, KC group: CoVs≥32.67%).Conclusions:Keratoconus and control eyes demonstrated high repeatability and reproducibility when using CSP measurements, which may prove helpful in fitting contact lenses.

Objective: Our study aims to evaluate the association between heart rate variability (HRV) and short and long-term prognosis in patients admitted to intensive care unit (ICU). Methods and Results: Adult patients continuously monitored for over 24h in ICUs from the MIMIC-IV Waveform Database were recruited in our study. Twenty HRV-related variables (8 time-domain, 6 frequency-domain; and 6 nonlinear variables) were calculated based on RR intervals. The association between HRV and 30-day all-cause mortality was assessed. Ninety-three patients met the inclusion criteria and were classified into 30-day survivor group and non-survivor groups based on their survival status. The 30-day all-cause mortality rate was 17.2%. NN50 and pNN50 were both significantly higher in non-survivors compared to survivors, whereas the rest of the time-domain, frequency domain and non-linear HRV parameters did not differ significantly between the two groups (all P >0.05). In addition, at 180 days after admission, non-survivors had significantly higher levels of NN50 and rMSSD than the survivors. However, NN50 was not an independent predictor of 30-day all-cause mortality in patients by multivariate COX regression analysis (HR, 1.0; 95% CI, 1.000 - 1.001; P =0.594). The Area Under the Curve (AUC), cut-off value, sensitivity and specificity of NN50 for predicting 30-day all-cause mortality using ROC were 0.67, 799, 0.813 and 0.584, respectively. Plotting Kaplan-Meier analysis using this cut-off value showed that patients with high NN50 had considerably greater 30-day all-cause mortality than those with low NN50 (P < 0.001). Conclusion: NN50 and pNN50 are associated with elevated 30-day all-cause mortality in ICU patients but are not independent predictors of all-cause mortality using multivariate COX regression analysis.

Our study aims to evaluate the association between heart rate variability (HRV) and short-and long-term prognosis in patients admitted to intensive care unit (ICU). Methods and Results: Adult patients continuously monitored for over 24 h in ICUs from the the American Medical Information Mart for Intensive Care (MIMIC)-IV Waveform Database were recruited in our study. Twenty HRV-related variables (8 time domain, 6 frequency domain, and 6 nonlinear variables) were calculated based on RR intervals. The association between HRV and all-cause mortality was assessed. Ninety-three patients met the inclusion criteria and were classified into atrial fibrillation (AF) and sinus rhythm (SR) groups, which were further divided into 30-day survivor group and nonsurvivor\groups based on their survival status. The 30-day all-cause mortality rates in AF and SR groups were 36.3% and 14.6%, respectively. All the time domain, frequency domain, and nonlinear HRV parameters did not differ significantly between survivors and nonsurvivors with or without AF (all P > 0.05). Presence of renal failure, malignancy, and elevated blood urea nitrogen level were associated with increased 30-day all-cause mortality in SR patients, while presence of sepsis, infection, higher platelet count, and magnesium level were associated with increased 30-day all-cause mortality in AF patients. Conclusions: Heart rate variability variables were not associated with increased 30-day all-cause mortality in ICU patients with or without AF.

Background: Previous studies have demonstrated that hypoxia preconditioning (HP) can promote mesenchymal stem cells (MSCs) survival and vascularization. Long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a newly discovered regulator of MSCs viability and differentiation. Evidences have indicated that MALAT1 can be strongly induced by hypoxia. This study aimed to investigate the role of MALAT1 in HP mediated MSCs survival and vascularization as well as the relevant underlying mechanism in vitro.Methods: MSCs were obtained from C57BL/6 mice and cultured in vitro. Cells at the third passage were divided into the following groups: normoxia (N), hypoxia preconditioning (HP), HP + MALAT1, HP + MALAT1 NC, HP+si-MALAT1 and HP +si-MALAT1 NC. The normoxia group was cultured in 20% O2 for 24 h. All the other groups were exposed to hypoxia (1% O2) for 24 hours. MALAT1 and relevant scramble RNA were transfected in the HP+MALAT1 and HP+MALAT1 NC groups respectively. HP+si-MALAT1 and HP +si-MALAT1 NC groups were transfected with MALAT1 siRNA and relevant siRNA scramble respectively. MSCs proliferation, apoptosis and vascular densities were evaluated. Bioinformatics and dual luciferase reporter assay were performed. Relevant biomarkers were examined in different experimental groups.Results: MSCs survival and vascularization were significantly enhanced in the HP group. Transfection of MALAT1 further strengthened the viability and angiogenic potential of MSCs in the condition of HP, whereas its knockdown attenuated cells survival and vascularization. MALAT1 and vascular endothelial growth factor A (VEGFA) were obviously increased after hypoxia exposure, while miR-195 was decreased. miR-195 targeted and downregulated VEGFA. miR-195 was a target of MALAT1. Overexpression of MALAT1 led to a decreased level of miR-195, accompanied with an augmented expression of VEGFA. However, both miR-195 and VEGFA exhibited contrary alterations after MALAT1 blockage. Conclusion: HP enhanced MSCs survival and vascularization potential in vitro, and the activation of MALAT1/miR-195/VEGFA axis might be involved in this procedure. This study reveals a new molecular mechanism of HP mediated MSCs survival and vascularization. It will be conducive for the development of novel strategies to improve the therapeutic efficiency of MSCs based on HP.