Additional file 2: of Effects of mindfulness-based stress reduction for adults with sleep disturbance: a protocol for an update of a systematic review and meta-analysis

Sample search strategy for ovidMEDLINE. (DOC 28 kb

MOESM1 of Ataxia telangiectasia mutated (ATM) interacts with p400 ATPase for an efficient DNA damage response

Additional file 1: Figure S1. Sf9 cells were infected with the baculovirus expressing indicated heterologous transgenes and cultured for 24, 36 or 48 h before processing. (A) Flag-ATM (red) is found in the nucleus (identified by DAPI staining; blue) as well as in the cytosplasm (cell boundaries are visible in the DIC image) at all-time points. (B) HA-p400 (green) is also distributed in all cellular compartments 24 h after infection. As time advances (36, 48 h), the protein exits from the nucleus (delineated by DAPI; blue) until it is exclusively cytoplasmic. (C) cells co-expressing Flag-ATM (red) and HA-p400 (green) exhibit dynamic protein relocalisation. 24 h post-infection a common pool of ATM and p400 is observed in the nucleus (DAPI; blue). The nuclear localisation of both proteins decreases with a concomitant enrichment of the cytoplasmic fraction (36, 48 h). All scale bars are 5 µm

Additional file 1: of Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition

The effect of SFN in cell viability of TGF-β1-stimulated cells for 24, 48, and 72 h. In A549 cells, TGF-β1 did not induce significant proliferation (A). TGF-β1-induced proliferation of MRC-5 cells showed inhibition by treatment of SFN for 1 h (B). (PDF 315 kb

Additional file 2: of Sulforaphane attenuates pulmonary fibrosis by inhibiting the epithelial-mesenchymal transition

Time response in the phosphorylation of SMAD2/3 by TGF-β1 and SFN treatment. In Western blotting of both A549 cells (A) and MRC-5 cells (B) showed phosphorylation of SMAD2/3 in early time within 1 h by TGF-β1. (PDF 113 kb

Additional file 2: of Expression patterns of STAT3, ERK and estrogen-receptor Îą are associated with development and histologic severity of hepatic steatosis: a retrospective study

Immunohistochemical staining for leptin (A-20, 1:50; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and leptin-receptor (B-3, 1:25; Santa Cruz Biotechnology) in hepatic steatosis cases, and non-neoplastic hepatocytes and carcinoma cells from hepatocellular carcinomas. (a-b) Hepatic steatosis with nuclear and/or cytoplasmic staining of leptin (a), and diffuse granular staining of leptin-receptor (b). (c-e) Leptin in hepatocellular carcinomas. Nuclear and cytoplasmic staining of leptin in non-neoplastic hepatocytes (left side of each picture), and negative (c), weak (d) or strong (e) leptin staining in hepatocellular carcinoma cells (right side of each picture). (f-g) Leptin-receptor in hepatocellular carcinomas. Diffuse granular cytoplasmic expression of leptin-receptor in non-neoplastic hepatocytes (left), and weak focal (f) or strong diffuse (g) staining of leptin-receptor in hepatocellular carcinoma cells (right). (JPEG 4962 kb

Additional file 1: of Expression patterns of STAT3, ERK and estrogen-receptor Îą are associated with development and histologic severity of hepatic steatosis: a retrospective study

Differential features between non-alcoholic fatty liver disease (NAFLD) subgroups stratified by NAS and SAF. (DOCX 47 kb

Additional file 1: Figure S1. of Sac-1004, a vascular leakage blocker, reduces cerebral ischemia—reperfusion injury by suppressing blood–brain barrier disruption and inflammation

Sac-1004 increases HBMEC survival. HBMECs were starved and treated with various concentrations of Sac-1004. Chemical structure of Sac-1004 (A). Cell survival was detected using an MTT assay (B). Under the same experimental conditions, cell viability was also determined by microscopy after incubation for 48 h (C). All data are presented the means ± SEM. ***P < 0.001. (JPG 82 kb

MOESM1 of Association between brachial-ankle pulse wave velocity and progression of coronary artery calcium: a prospective cohort study

Additional file 1: Table 1. The Risk of Progression of Coronary Calcium Score According to Baseline Brachial-Ankle Pulse Wave Velocity: Odds Ratio (95 % Confidence Interval) of Difference [√CAC(follow-up) − √CAC(baseline)] >2.5 by Pulse Wave Velocity quartiles—The SQRT Analysis. Table 2. The Risk of Progression of Coronary Calcium Score According to Pulse Pressure and Brachial-ankle Pulse Wave Velocity: Odds ratio (95 % Confidence Interval) of Difference [√CAC(follow-up) − √CAC(baseline)] >2.5 by Pulse Wave Velocity 50 % and pulse pressure 50 %—The SQRT Analysis. Table 3. The Risk of Progression of Coronary Calcium Score According to Baseline Brachial-Ankle Pulse Wave Velocity: Odds ratio (95 % Confidence Interval) of Coronary Calcium Score Change change >=10 by Pulse Wave Velocity Quartiles