Additional file 1 of Joint association of physical activity and diet quality with dyslipidemia: a cross-sectional study in Western China

Additional file 1: Additional table 1. Frequency of each dietary term in dyslipidemia and normal groups. Additional table 2. Lipid levels based on different subpopulation. Additional Fig. 1. Kernel density plots for lipid subtypes based on age, sex, and physical activity. Additional table 3. Prevalence of different types of dyslipidemia. Additional Fig. 2. The prevalence of borderline high and high of lipid subtypes based on sex. Additional Fig. 3. Dose-response association between moderate-to-vigorous physical activity, diet quality with dyslipidemia. Additional table 4. Joint associations of physical activity and diet quality with dyslipidemia. Additional table 5. Joint associations of physical activity and age with dyslipidemia. Additional table 6. Joint associations of diet quality and age with dyslipidemia

Caspase-3 was inhibited by XIAP and XIAP was downregulated by binding of Smac after radiation.

<p>CNE-1 cells (lane C) were treated with NK-92 cells for 4 h (lane C/N) before combined treatment with 800 cGy of radiation. (A) Cell lysates were immunoprecipitated with anti-XIAP antibody and immunoblotted with anti-Smac, anti-caspase-3 or anti-XIAP antibody. (B) CNE-1 cells were transfected with 80 nM of XIAP siRNA for 16 h and co-cultured with NK-92 cells for 4 h before NK-92 cells were washed away. The cells were assayed using Annexin-V to determine the percentage of apoptotic cells (AnnexinV⁺). (C) Cell lysates were immunoprecipitated by anti-Smac antibody and detected with anti-XIAP antibody by Western blot. (D) CNE-1 cells were treated with NK-92 cells for 4 h (C/N) before combined treatment with 800 cGy of radiation (C/N+RT) or CNE-1 treated with 800 cGy of radiation alone (C+RT). After treatment, cells were further incubated for 0 min, 15 min, 2 h, or 24 h, then harvested and fractionated into cytosolic (Cyto) and mitochondrial (Mito) fractions for assay by western blot. β-actin was used as the loading control for each fraction. Density of the XIAP normalized with β-actin was assayed by Image J. The bar chart was average of three independent experiments.</p

The caspase signaling pathway was induced after co-culture.

<p>CNE-1 cells were co-cultured with 2.5 fold of NK-92 cells for 4 h, then NK-92 cells were washed away, and CNE-1 cells were exposed to 800 cGy of radiation. Control cells of CNE-1 alone or CNE-1 cells that had been co-cultured were not irradiated. After 24 h of incubation, cells were harvested for western blot analysis of procaspase/caspase-3, procaspase-8, and procaspase-9 protein in lysates of CNE-1 alone (lane C), CNE-1 cells cultures with NK-92 cells (lane C/N). The arrows indicate cleaved (activated) caspase 3 at about 17 kDa and its precursor, pro-caspase 3, at about 43 kDa; precaspase 8, at about 55kDa; procaspase 9, at about 45kDa. β-actin was used as the internal control.</p

Effect of NK-92-treated CNE-1 cells on Fas blockage.

<p>CNE-1 cells were co-cultured with 2.5 fold NK-92 cells for 4 h in presence of anti-FasL blocking antibody (10 µg/ml). The percentage of apoptotic cells after irradiation 48 h under various co-culture conditions was analyzed by Annexin-V assay (AnnexinV⁺, D). Results from 3 independent experiments are shown; bars indicate mean ± SD.</p

Mechanism of reciprocal interaction between NK cells and radiation in target cells.

<p>NK cells damage target cell through perforin/granzyme B and death receptor/caspase mediated pathway. The radiosensitisation effect through NK cell depends more on the perforin/granzyme B pathway. Without radiation, the suboptimal activation of NK cells cause up-regulation of XIAP. With radiation, the mitochondria releases Smac to neutralize XIAP and enhances NK cell-mediated cytotoxicity.</p

pNK and NK-92 cells sensitized tumor cells.

<p>1×10⁵ of various tumor cells were seeded in 96-well tissue-culture plates, co-cultured with 2.5×10⁵ pNK cells for 4 h, washed and then exposed to 800 cGy of irradiation and evaluated 48 h late for cell proliferation by the MTS (A). C, cancer cell alone; C/NK, cancer cell and NK coculture; C+RT, cancer cell treated with 800 cGy radiation; C/NK+RT, cancer cell and pNK coculture followed by radiation. The apoptosis of CNE-1 cells after irradiation 48 h under various co-culture conditions that described previously was analyzed by (B) Annexin-V assay and (C) cell cycle analysis. (D) CNE-1 cells were incubated with NK-92 cells in 1∶2.5 ratios for 2, 4, and 8 h and irradiated at indicated doses. (E) 1×10⁵ CNE-1 cells were cultured in the lower chambers of transwells, and 2.5×10⁵ NK-92 cells were cultured in the upper chambers for 4 and 8 h. Both of (D) and (E) were assayed using Annexin-V to detect apoptotic cells (AnnexinV⁺). (*, <i>p</i><0.05).</p

Primary NK cells sensitized tumor cells with same pathway.

<p>CNE-1 cells were transfected with 80 nM of XIAP siRNA for 16 h and co-cultured with pNK cells for 4 h before pNK cells were washed away. The cells were assayed using Annexin-V to determine the percentage of apoptotic cells.</p

Inflammation’s Association with Metabolic Profiles before and after a Twelve-Week Clinical Trial in Drug-Naïve Patients with Bipolar II Disorder

<div><p></p><p>Inflammation is thought to be involved in the pathophysiology of bipolar disorder (BP) and metabolic syndrome. Prior studies evaluated the association between metabolic profiles and cytokines only during certain mood states instead of their changes during treatment. We enrolled drug-naïve patients with BP-II and investigated the correlation between changes in mood symptoms and metabolic indices with changes in plasma cytokine levels after 12 weeks of pharmacological treatment. Drug-naïve patients (n = 117) diagnosed with BP-II according to DSM-IV criteria were recruited. Metabolic profiles (cholesterol, triglyceride, HbA1C, fasting serum glucose, body mass index (BMI) and plasma cytokines (TNF-α, CRP, IL-6, and TGF-β) were measured at baseline and 2, 8, and 12 weeks post-treatment. To adjust within-subject dependence over repeated assessments, multiple linear regressions with generalized estimating equation methods were used. Seventy-six (65.0%) patients completed the intervention. Changes in plasma CRP were significantly associated with changes in BMI (<i>P</i> = 1.7E-7) and triglyceride (<i>P</i> = 0.005) levels. Changes in plasma TGF-β1 were significantly associated with changes in BMI (<i>P</i> = 8.2E-6), cholesterol (<i>P</i> = 0.004), and triglyceride (<i>P</i> = 0.006) levels. However, changes in plasma TNF-α and IL-6 were not associated with changes in any of the metabolic indices. Changes in Hamilton Depression Rating Scale scores were significantly associated with changes in IL-6 (<i>P</i> = 0.003) levels; changes in Young Mania Rating Scale scores were significantly associated with changes in CRP (<i>P</i> = 0.006) and TNF-α (<i>P</i> = 0.039) levels. Plasma CRP and TGF-β1 levels were positively correlated with several metabolic indices in BP-II after 12 weeks of pharmacological intervention. We also hypothesize that clinical symptoms are correlated with certain cytokines. These new findings might be important evidence that inflammation is the pathophysiology of clinical symptoms and metabolic disturbance in BP-II.</p><p>Trial Registration</p><p>ClinicalTrials.gov <a href="http://clinicaltrials.gov/ct2/show/NCT01188148" target="_blank">NCT01188148</a>.</p></div

Additional file 1: Figure A. of Improving immunological tumor microenvironment using electro-hyperthermia followed by dendritic cell immunotherapy

(a) Representative flow cytometric analysis on immature and mature DCs. The purple histograms represent the isotype-matched control, and the red line histograms represent staining with specific antibodies. *MFI represents the mean fluorescence intensity, which are expressed on the right upper corner of each histogram. Error bars represent standard errors. (b) Histogram plot of MFI. (*) P < 0.05, (**) P < 0.01 (t-test) compared with the immature DC. Figure B. Endocytotic activity was measured by flow cytometry in DCs generated from bone marrow cultured for 9 d with 20 ng/ml of GM-CSF; mDCs obtained from iDCs were incubated with 10 g/mL of AH1 and 50 g/mL of Hsp70 for 24 h and reacted with 100 mg/mL of FITC-Dextran at 4°C (purple) or 37 °C (green line) for 2 h before analysis. This result was represented from one of three independent experiments. (DOCX 608 kb

Correlation of changes in metabolic profiles and cytokines before and after 12 weeks of pharmacological treatment.

<p>CRP: C-reactive protein; TGF-β1: transforming growth factor β1; TNF-α: tumor necrosis factor α; IL-6: interleukin 6.</p>**<p><b><i>P</i></b><0.001.</p