Strategic tillage achieves lower carbon footprints with higher carbon accumulation and grain yield in a wheat-maize cropping system.

Continuous single tillage has the potential to increase greenhouse gas (GHG) emissions and decrease the accumulation of soil organic carbon (SOC), thus increasing carbon footprints (CFs). However, in a wheat-maize cropping system, limited information was available about the effects of strategic tillage on CFs. Thus, a four-year field experiment was conducted, including continuous rotary tillage (RT), continuous no-till (NT), RT + subsoiling (RS), and NT + subsoiling (NS), to investigate the effects of NS (strategic tillage) on the unit area and unit yield. The results showed that CO2 emission was the highest contributor to CFs (73.92%) in a winter wheat-summer maize cropping system, following the order of NS < NT < RS < RT. The direct N2O emissions from fertilizers and residues were 4.43-4.51 t CO2-eq ha-1 yr-1 during the wheat and maize seasons, and indirect N2O emissions from irrigation and fertilizer inputs had a proportion of >80% from total agricultural inputs. The differences in SOC storage significantly affected the CFs. Although the NS treatment increased the amount of GHG emissions from the residues returned and consumption of diesel, the enhancement of SOC storage by deeper SOC increased. Thus, lower area-scaled CFs were observed in the NS treatment. Furthermore, a higher grain yield and an annual change of SOC storage compared with other treatments were observed under the NS system, which helped to reduce the CFs. The yield-scaled CFs followed the order of RT > RS > NT > NS when considering the changes in SOC storage. Therefore, the NS treatment resulted in a higher grain yield and SOC sequestration with lower CFs, and thus, it could be recommended as the best tillage method to achieve sustainable production and environmental balance in a wheat-maize cropping system.

[Effect of Fuzheng Kang'ai Recipe Combined Gefitinib on Lung Cancer A549 Cells and Its Mecha- nism Research].

Objective To observe the effect of Fuzheng Kang'ai Recipe (FKR) combined ge- fitinib on the proliferation and apoptosis of lung cancer A549 cells , and to study its potential synergistic mechanish with gefitinib. Methods The effects of FKR (0. 211, 0. 316, 0. 474, 0. 711, 1. 067, 1. 600, 2. 400, 3. 600 mg/mL) combined gefitinib (3. 95, 5. 92, 8. 18, 13. 33, 20. 00, 30. 00, 45. 00, 67. 50 µmol/ L) on the proliferation of A549 cells were detected by MTT assay. The apoptosis of A549 cells in the control group (complete culture medium) , FKR (1. 6 mg/mL) , gefitinib (45 µmol/L) , and FKR plus gefitinib (1. 6 mg/mL +45 µmol/L) were detected by flow cytometry (FCM). Their expressions of epidermal growth factor receptor (EGFR) , phosphorylating epidermal growth factor receptor ( p-EGFR) , enhancer of zeste homolog 2 (EZH2), peroxisome proliferator-activated receptor-γ ( PPAR-γ) , and P53 protein in A549 cells were detected by Western blot. Results Both FKR and gefitinib could inhibit the proliferation of A549 cells. The apoptotic rate was 12. 6% ±4. 5% in the FKR combined gefitinib group, obviously higher than that of the FKR group (4. 6% ± 0. 7%) and the gefitinib group (7. 8% ± 2. 7%) , showing statistical difference (P <0. 05). Compared with the control group, the expressions of p-EGFR and EZH2 were sig- nificantly down-regulated (P <0. 05) , the expressions of PPAR-γ and P53 protein were up-regulated in the FKR combined gefitinib group (P <0. 05); the expression of EZH2 was down-regulated in the gefitinib group and the FKR group (P <0. 05) ; the expression of PPAR-y was up-regulated in the FKR group (P < 0. 05). Compared with the gefitinib group, the expression of p-EGFR was down-regulated, and the expression of PPAR-γ was up-regulated in the FKR combined gefitinib group (both P <0. 05). Compared with the FKR group, the expression of p-EGFR was down-regulated in the FKR combined gefitinib group (P < 0. 05). Conclusions Combination of FKR and gefitinib could significantly inhibit the proliferation and growth of A549 cells,and induce cell apoptosis. Its potential synergistic mechanism of anti-tumor activities might be associated with down-regulating mRNA expressions of p-EGFR and EZH2, and up-regulating protein expressions of PPAR-y and P53.

Anticancer actions of PPARγ ligands: Current state and future perspectives in human lung cancer.

Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent nuclear transcription factors and members of the nuclear receptor superfamily. Of the three PPARs identified to date (PPARγ, PPARß/δ, and PPARα), PPARγ has been studied the most, in part because of the availability of PPARγ agonists (also known as PPARγ ligands) and its significant effects on the management of several human diseases including type 2 diabetes, metabolic syndrome, cardiovascular disease and cancers. PPARγ is expressed in many tumors including lung cancer, and its function has been linked to the process of lung cancer development, progression and metastasis. Studies performed in gynogenic and xenograft models of lung cancer showed decreased tumor growth and metastasis in animals treated with PPARγ ligands. Furthermore, data are emerging from retrospective clinical studies that suggest a protective role for PPARγ ligands on the incidence of lung cancer. This review summarizes the research being conducted in this area and focuses on the mechanisms and potential therapeutic effects of PPARγ ligands as a novel anti-lung cancer treatment strategy.

Activated PPARgamma Targets Surface and Intracellular Signals That Inhibit the Proliferation of Lung Carcinoma Cells.

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily. Their discovery in the 1990s provided insights into the cellular mechanisms involved in the control of energy homeostasis, the regulation of cell differentiation, proliferation, and apoptosis, and the modulation of important biological and pathological processes related to inflammation and cancer biology, among others. Since then, PPARs have become an exciting target for the development of therapies directed at many disorders including cancer. PPARs are expressed in many tumors including lung cancer, and their function has been linked to the process of carcinogenesis. Consequently, intense research is being conducted in this area with the hope of discovering new PPAR-related therapeutic targets for the treatment of lung cancer. This review summarizes the research being conducted in this area, and focuses on the mechanisms by which a member of this family (PPARgamma) is believed to affect lung tumor cell biology.

Regulation and modulation of abnormal immune responses in endometriosis.

There is ample evidence demonstrating that endometriosis is accompanied by inflammatory reactions in the peritoneum, resulting in abnormal levels of a variety of cytokines and chemokines in the peritoneal fluid. Among the immunological parameters that have been shown to be altered in the peritoneal cavity of women with endometriosis, an increase in the number of activated nonadherent macrophages that show reduced surface expression of scavenger receptors has been observed. The cause-and-effect relationship between aberrant peritoneal macrophage activity and endometriosis is still unknown. We have demonstrated that steroid hormone receptor agonists and antagonists [e.g., retinoids, antiglucocorticoids, ligands to peroxisome proliferator activated receptors (PPARs)] can regulate macrophage functions in ways that could either suppress or stimulate the growth of ectopic endometrial lesions. Our studies include a number of relevant findings: (1) RU486, acting as an antioxidant, can suppress activation of NFkappaB, a nuclear transcription factor that affects the expression of several inflammatory genes such as those for MCP-1, GM-CSF, CSF-1, and various adhesion molecules; (2) IL-6 secretion from a variety of cell types including endometrial cells is inhibited by retinoic acid; and (3) retinoids and PPARgamma ligands can upregulate the expression of scavenger receptors in cells of the monocyte/macrophage lineage. These observations, combined with the possibility that macrophage activity may play a fundamental role in endometriosis, suggest that pharmacologic manipulation of macrophage function may provide a novel mechanism for treating this disease.