<p>Supplemental Tables S1-S7. Table S1. Response to Reporting Recommendations for Tumor Marker Prognostic Studies (REMARK). Table S2. High expression of all three genes of OCT4, NANOG and IGF-IR was significantly associated with a higher proportion of subjects with hepatitis B, TNM stage, microvascular invasion and satellite nodules as well as a lower proportion of subjects with hepatitis C (N = 191). Table S3. Variables associated with early tumor recurrence after hepatectomy for HCC (N = 120). Table S4. Comparison of tumor formation incidence following the implantation of Hep3B HCC cells with PBS and IL-6 treatments of the implantation sites. Table S5. Associations of tumor formation with cell number and IL-6 treatment. Table S6. Real-time PCR primers and product size. Table S7. List of antibodies.</p>
Different parts of the rice (Oryza sativa L.) plant at different growth stages were analyzed for sucrose synthase (SS) by enzyme activity assay and enzyme-linked immunosorbent assay directly on the extracts or on the eluates from a gel filtration column. On a dry matter basis, the amount of soluble protein and SS activity decreased significantly, but the amount of enzyme protein changed little in growing leaves. In the grain, the SS activity was the highest at the early ripening stage and decreased later, but the amount of SS protein increased with the increase in maturity. In the root, a low activity of SS was detectable only in the tillering but not in other stages. Immunoblotting of SS protein extracted from different parts of rice showed two bands. Elution patterns of crude extracts from a gel filtration column showed the presence of several types of SS protein. Among them, two to three types with larger elution volumes had the SS activity but others with smaller elution volumes (considered as the aggregated forms) had no activity. The SS purified from different parts of the plant showed similar but distinctly different electrophoretic mobilities in a native gel. It has been concluded that different isozymes are expressed in different tissues at different growth stages.
Abstract Background Human placenta-derived multipotent cells (hPDMCs) are isolated from a source uncomplicated by ethical issues and are ideal for therapeutic applications because of their capacity for multilineage differentiation and proven immunosuppressive properties. It is known that heat-shock preconditioning induces the upregulation of heat-shock proteins (HSPs), which enhance survival and engraftment of embryonic stem cells (ESCs) during transplantation in live animal models, although whether heat-shock preconditioning has the same effects in hPDMCs is unclear. Methods The hPDMCs were isolated from placenta of healthy donors. The cells were treated with heat shock (43°C, 15 min), followed by evaluation of cell viability. Furthermore, the HSPs expression were assessed by Western blot, qPCR. The reactive oxygen species (ROS) production and signal pathway activation were determined by flow cytometry and Western blot, respectively. The regulatory pathways involved in HSPs expression were examined by pretreatment with chemical inhibitors, and siRNAs, and then investigating HSPs expression. Results This study demonstrates that subjecting hPDMCs to heat shock treatment induced ROS generation and upregulated HSPs in hPDMCs. Heat shock stimulation also increased p38 MAPK and Akt phosphorylation. These effects were reduced by inhibitors of ROS, p38 MAPK and Akt. Moreover, we found that heat stress reduced levels of the transcription factor heat shock factor 1 (HSF1) in the cytosol, but that heat shock enhanced HSF1 translocation from the cytosol to the cell nucleus. Pretreatment of hPDMCs with ROS scavengers, SB203580 and Akt inhibitors also reduced the translocation of HSF1 induced by heat shock. Conclusions Our data indicate that heat shock acts via ROS to activate p38 MAPK and Akt signaling, which subsequently activates HSF1, leading to HSP activation and contributing to the protective role of hPDMCs.
<p>Supplementary Table S1. Primer sequences. Supplementary Table S2. Antibody list. Supplementary Table S3. Mean values of the half maximal inhibitory concentration (IC50; {plus minus} standard deviation; SD) of NCCIT cells under normoxic or hypoxic conditions for 24 h.</p>
BackgroundPrevious animal studies have shown that certain respiratory oncoviruses can lead to tumorigenesis, especially influenza virus. However, no clinical studies other than animal studies have been conducted to test this hypothesis.ObjectiveTo investigate the association between influenza and the risk of lung cancer using the Taiwan Cancer Registry Database (TCRD) and Taiwan's National Health Insurance Research Database (NHIRD).MethodsWe identified a study cohort consisting of patients aged 40 years or above who were enrolled in the NHIRD between 1 January 2012 and 31 December 2014. Among them, we identified patients with lung cancer (cases) and their matched controls (matched by age, sex, and disease risk score (DRS) at a ratio of 1:10). Multivariate conditional logistic regression models were used to evaluate the association between exposure to influenza (timing and cumulative number) and risk of lung cancer.ResultsWe identified 32,063 cases and 320,627 matched controls. Influenza was associated with a 1.09-fold increased risk of lung cancer (aOR 1.09, 95% CI 1.04–1.14, p < 0.0001). The risk of lung cancer increased slightly with cumulative exposure to influenza (1–2 exposures: aOR 1.05, 95% CI 1.00–1.11; 3-4 exposures: aOR 1.12, 95% CI 1.00–1.25; 5+ exposures: aOR 1.25, 95% CI 1.13–1.39).ConclusionExposure to influenza was associated with an increased risk of lung cancer and the risk increased with cumulative exposure to influenza. However, the lack of valid information on smoking could lead to confounding, and future studies collecting patients' smoking histories are warranted to validate the association between influenza and lung cancer.
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