Supplementary document for Eigendecomposition-Free Inverse Design of Meta-Optics Devices - 6923153.pdf

supplementary documen

Table_1_Association between blood chromium and hepatic steatosis assessed by liver ultrasound transient elastography: National Health and Nutrition Examination Survey 2017–2020.docx

BackgroundHepatic steatosis is a significant pathological feature of fatty liver disease (FLD) which is widely spread with no effective treatment available. Previous studies suggest that chromium (Cr) intake reduces lipid deposition in the liver in animals. However, the connection between blood Cr and hepatic steatosis among humans remains inconclusive.MethodsUsing the data from the National Health and Nutrition Examination Survey (NHANES) 2017–2020, we performed a cross-sectional analysis, including 4,926 participants. The controlled attenuation parameter (CAP) measured by the vibration controlled transient elastography (VCTE) was used to evaluate the degree of liver steatosis. Weighted univariate regression, multivariate linear regression, smooth fitting curves and subgroup analysis were used. In addition, we carried out trend tests, multiple interpolations, and interaction analyses to conduct sensitivity analyses.ResultsAfter adjusting with various covariables, multivariate linear regression analysis demonstrated a significant negative correlation between blood Cr and CAP [β (95% CI) = −5.62 (−11.02, −0.21)]. The negative correlation between blood Cr and CAP was more significant in the males, 50–59 years, overweight, hypercholesterolemia, HDL-C ≥ 65 mg/dL, HbA1c (5.70–6.10 %), HOMA-IR (0.12–2.76), total bilirubin (0.30–0.40 mg/dL), ever alcohol consumption subjects. Of note, the relationships between blood Cr and CAP followed a U-shaped curve in the smokers and non-smokers, with blood Cr thresholds of 0.48, 0.69 μg/L, respectively.ConclusionsThere is an independently negative correlation between blood Cr and hepatic steatosis in American. Our study provides clinical researchers with a new insight into the prospective prevention of hepatic steatosis.</p

The validation in in vivo xenograft model.

<p>(A) Representative images of tumor size in different groups of nude mice on the 60th day after treatment. (B) Growth curves in different groups of nude mice. *<i>P</i><0.05 vs control group, ^#<i>P</i><0.05 vs HGF group.</p

Immunofluorescent analysis of the MET/PI3K/AKT activation and GRP78 expression on the microfluidic chip.

<p>A549 cells were cultured in triplicate in the maintenance medium alone, mixed with the CAF matrix in the presence or absence of anti-HGF or containing 40 ng/ml of human HGF in the 3D chambers for 48h. The cells were stained with the indicated FITC-conjugated antibodies, and examined under a fluorescent microscope. Furthermore, the cells were cultured in the mixture of maintenance medium and CAF matrix in the presence or absence of an inhibitor for c-Met, PI3K or GRP78 for 48h and stained as described above. Data are representative images (magnification x 200) from three separate experiments. (A)The CAF matrix or HGF enhances the c-Met/PI3K/AKT activation and GRP78 expression in A549 cells. (B)The effect of an inhibitor of c-Met, PI3K or GRP78 on the CAF-enhanced c-Met/PI3K/AKT activation and GRP78 expression in A549 cells.</p

The design and validation of a 3D culture microfluidic chip.

<p>(a)The schematic design of the microfluidic chip with CGG and downstream cell chambers (the upper panel) and the fabricated chip with pumping machine (the lower panel). (b)The diffused Rh-123 in the 3D chamber within 30 min and >95% cells were viable (green). Magnification ×100. (c) The morphological features of A549 cells in the 3D chamber without or with CAF matrix. The white arrows indicate apoptotic cells. (d)The α-SMA immunofluorescence assay of HFL1 cells. HFL1 cells induced by A549 medium showed a positive α-SMA staining (right) compared to the untreated HFL1 (left). Magnification ×400. (e) Immunohistochemistry assay for lung cancer tissues. The expression of α-SMA protein in the lung cancer tissues is higher than that in adjacent tissues. Magnification ×200.</p

Western blot analysis of the c-Met/PI3K/AKT activation and GRP78 expression in A549 cells.

<p>A549 cells were cultured in the condition as described above and the relative levels of phosphorylated Met, PI3Kp85, AKT and GRP78 expression in the different groups of cells were characterized by Western blot assays and quantified. Data are representative images and expressed as the means ± SD of each protein in individual groups of cells from three separate experiments. *<i>P</i><0.05; **<i>P</i><0.01 vs. the controls.</p

Additional file 1 of Association of immune cell composition with the risk factors and incidence of acute coronary syndrome

Additional file 1. Figure S1. Histograms of immune cell proportions after arcsine square root transformation. Immune cell composition observed from routine blood tests (A) and estimated from DNA methylation profiles (B). Lym, lymphocyte proportion; Mono, monocyte proportion; Neu, neutrophil proportion; CD8T, CD8+ T cell proportion; CD4T, CD4+ T cell proportion; B, B cell proportion; and NK, natural killer cell proportion

Additional file 2 of Association of immune cell composition with the risk factors and incidence of acute coronary syndrome

Additional file 2. Table S3. Association between immune cell composition and risk factors of ACS