Environmental impacts on algal-bacterial-based aquaponics system by different types of carbon source addition: water quality and greenhouse gas emission.

Carbon source addition is an important way improving the carbon and nitrogen transformation in aquaculture system; however, its effectiveness of algal-bacterial-based aquaponics (AA) through carbon source addition is still vague. In this study, the influences of organic carbon (OC-AA system) and inorganic carbon (IC-AA system) addition and without carbon source addition (C-AA system) on the operational performance of AA system were investigated. Results showed that 10.1-19.5% increase of algal-bacterial biomass enhanced the purifying effect of ammonia nitrogen in OC-AA system and IC-AA system relative to C-AA system. Moreover, extra electron donor supply in the OC-AA system obtained the lowest NO3--N concentration. However, that was at the cost of aggravated N2O conversion ratio, which increased by more than 2.0-folds than other systems, attributing to 2.9-folds increase of nirS gene abundance. In addition, carbon source addition increased the pH and then decreased the fish biomass production of AA system. The results of this study would provide theoretical supports of carbon source addition on the performance of nutrient transformation and greenhouse gas effect in AA system.

New insights for simultaneous nutrient removal enhancement and greenhouse gas emissions reduction of constructed wetland by optimizing its redox environment through manganese oxide addition.

Manganese oxide (MnOx) is receiving increased interest in the nutrient removal of constructed wetlands (CWs); however, its service effectiveness for simultaneous greenhouse gas (GHG) emissions reduction is still vague. In this study, three vertical flow CWs, i.e., volcanics (CCW), manganese sand uniformly mixing with volcanics (Mn-CW) and MnOx doped volcanics (MnV-CW), were constructed to investigate the underlying mechanisms of MnOx on nutrient removal enhancement and greenhouse gas (GHG) emissions reduction. The results showed that the MnOx doped volcanics optimized the oxidation-reduction potential surrounding the substrate (-164.0 ∼ +141.1 mv), and resulted in the lowest GHG emissions (CO2-equivalent) from MnV-CW, 16.8-36.5 % lower than that of Mn-CW and CCW. This was mainly ascribed to mitigation of N2O produced during the NO3--N reduction process, according to results of 15N stable isotope labeling. Analysis of the microbial community structure revealed that due to the optimized redox conditions through chemical doping of MnOx on volcanics, the abundance of microbe involved in denitrification and Mn-oxidizing process in the MnV-CW was significantly increased at genus level, which led to a higher Mn cycling efficiency between biogenic MnOx and Mn2+, and enhanced denitrification efficiency and N2O emission reduction. This study would help to understand and provide a preferable reference for future applications for manganese-based CW.

Water-energy-greenhouse gas nexus of a novel high-rate activated sludge-two-stage vertical up-flow constructed wetland system for low-carbon wastewater treatment.

Municipal wastewater treatment which is associated with high energy consumption and excessive greenhouse gas (GHG) emissions, has been facing severe challenges toward carbon emissions. In this study, a high-rate activated sludge-two-stage vertical up-flow constructed wetland (HRAS-TVUCW) system was developed to reduce carbon emissions during municipal wastewater treatment. Through carbon management, optimized mass and energy flows were achieved, resulting in high treatment efficiency and low operational energy consumption. The carbon emission of the HRAS-TVUCW system (i.e., 0.21 kg carbon dioxide equivalent/m3 wastewater) was 4.1-folds lower than that of the conventional anaerobic/anoxic/aerobic (A2O) process. Meanwhile, the recovered energy from the HRAS-TVUCW system increased its contribution to carbon neutrality to 40.2%, 4.6-folds higher than that of the A2O process. Results of functional microbial community analysis at the genus level revealed that the controlled dissolved oxygen allocation led to distinctive microbial communities in each unit of HRAS-TVUCW system, which facilitated denitrification efficiency increase and carbon emissions reduction. Overall, the HRAS-TVUCW system could be considered as a cost-effective and sustainable low-carbon technology for municipal wastewater treatment.

Oroxylin A inhibits Kaposi's sarcoma-associated herpes virus (KSHV) vIL-6-mediated lymphatic reprogramming of vascular endothelial cells through modulating PPARγ/Prox1 axis.

BACKGROUND AND PURPOSE: Kaposi's sarcoma-associated herpes virus (KSHV) vIL-6 is sufficient to induce lymphatic reprogramming of vascular endothelial cells, which is a key event in Kaposi's sarcoma (KS) development. This study was aimed to investigate the effect of Chinese herb oroxylin A on lymphatic reprogramming and neovascularization by KSHV vIL-6 in vitro and in vivo. METHODS: The lymphatic-phenotype endothelial cell line was generated by lentiviral KSHV vIL-6 infection. Cell viability and apoptosis were determined by MTT assay or flow cytometry with annexin V/propidium iodide staining. Migration, invasion, and neovascularization of the vIL-6-expressing lymphatic-phenotype endothelial cells were determined by wound healing assay, transwell chamber assay, microtubule formation assay, and chick chorioallantoic membrane assay, respectively. Quantitative polymerase chain reaction and Western blot analysis were used to test the expression of Prox1, VEGFR3, podoplanin, LYVE-1, and PPARγ in cells. Co-localization of Prox1 and PPARγ was determined by immunofluorescence. Ubiquitination of Prox1 was detected by in vivo ubiquitination assay. RESULTS: The lymphatic-phenotype endothelial cell line expressing KSHV vIL-6 was successfully generated. Oroxylin A induced cellular invasion abrogation, apoptosis induction, and neovascularization inhibition of the vIL-6-expressing endothelial cells. Mechanically, oroxylin A elevated PPARγ expression, which in turn interacted with and facilitated Prox1 to undergo ubiquitinational degradation, and subsequently leads to VEGFR3, LYVE-1, and podoplanin reduction. CONCLUSION: Through modulating PPARγ/Prox1 axis, oroxylin A inhibits lymphatic reprogramming and neovascularization of KSHV vIL-6. Thus, oroxylin A may serve as a candidate for the treatment of KS as well as other aggressive angiomas.

Combination of procalcitonin, C-reaction protein and carcinoembryonic antigens for discriminating between benign and malignant pleural effusions.

Pleural effusion (PE) is a common manifestation associated with certain chest diseases. However, there is no effective diagnostic marker with high sensitivity and specificity. The aim of the present study was to evaluate the diagnostic performance of several biomarkers in the use of detecting malignant pleural disorder. One hundred and fifty patients with a specific diagnosis of exudative PE were enrolled in this study and were divided into the benign PE group (n=93) and the malignant PE group (n=57). Thoracoscopy was conducted to identify the reasons for the PE. Biomarkers in pleural fluid and in sera were determined either by microparticle enzyme immunoassay [carcinoembryonic antigen (CEA)], fluorescence immunoassay [procalcitonin (PCT)] or light-scattering turbidimetric immunoassay [C-reaction protein (CRP)]. Then, correlation analysis and receiver-operating characteristic (ROC) curve analysis individually or in combination were performed. The CRP and PCT levels were higher in benign PE than they were in malignant PE (PCT: P=0.017, P=0.032; CRP: P=0.001, P<0.001, respectively), while CEA levels were lower in benign PE than in malignant PE (CEA: P=0.001, P=0.001, respectively). During the ROC curve analysis, an optimal discrimination was identified by combining pleural CRP, pleural CEA and serum (s)PCT with an area under the curve of 0.973 (sensitivity, 98.9%; specificity, 89.5%). In the diagnosis of PE, there was no single biomarker that appeared to be adequately accurate. The combination of pleural CRP, pleural CEA and sPCT may represent an efficient diagnostic procedure for guiding the patient towards follow-up clinical treatment.

PGRMC1-dependent autophagy by hyperoside induces apoptosis and sensitizes ovarian cancer cells to cisplatin treatment.

Cisplatin treatment some times leads to chemoresistance, which is now acknowledged partially due to the inductive expression of progesterone receptor membrane component (PGRMC)1 in ovarian cancer cells. PGRMC1 enhances autophagy, activates cytochrome p450, and inveigles signaling pathways to promote cell survival and reduce the effect of drug treatments. In this study, we give first line evidence that hyperoside inhibits cell viability, triggers autophagy and apoptosis in ovarian cancer cell lines. Mechanistically, PGRMC1-dependent autophagy was utilized by hyperoside to induce apoptotic cell death. Hyperoside induced the conversion of LC3B-I to LC3B-II and the formation of autophagosomes in ovarian cancer cells. Notably, PGRMC1 colocolized with LC3B­II, and PGRMC1 overexpression enhanced hyperoside-induced autophagy and apoptosis, while PGRMC1 knockdown abrogated the action. Additionally, AKT signaling and Bcl-2 family were also involved in the hyperoside-induced autophagy and apoptosis. Importantly, in cisplatin-resistant ovarian cancer cells where PGRMC1 was overexpressed, hyperoside sensitized the cells to cisplatin treatment. Together these findings indicate hyperoside functions as a complementary therapy for ovarian cancer patients receiving platinum-based therapy.

C5a Induces the Synthesis of IL-6 and TNF-α in Rat Glomerular Mesangial Cells through MAPK Signaling Pathways.

Inflammatory response has been reported to contribute to the renal lesions in rat Thy-1 nephritis (Thy-1N) as an animal model of human mesangioproliferative glomerulonephritis (MsPGN). Besides C5b-9 complex, C5a is also a potent pro-inflammatory mediator and correlated to severity of various nephritic diseases. However, the role of C5a in mediating pro-inflammatory cytokine production in rats with Thy-1N is poorly defined. In the present studies, the levels of C5a, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were first determined in the renal tissues of rats with Thy-1N. Then, the expression of IL-6 and TNF-α was detected in rat glomerular mesangial cells (GMC) stimulated with our recombinant rat C5a in vitro. Subsequently, the activation of mitogen-activated protein kinase (MAPK) signaling pathways (p38 MAPK, ERK1/2 and JNK) and their roles in the regulation of IL-6 and TNF-α production were examined in the GMC induced by C5a. The results showed that the levels of C5a, IL-6 and TNF-α were markedly increased in the renal tissues of Thy-1N rats. Rat C5a stimulation in vitro could up-regulate the expression of IL-6 and TNF-α in rat GMC, and the activation of MAPK signaling pathways was involved in the induction of IL-6 and TNF-α. Mechanically, p38 MAPK activation promoted IL-6 production, while either ERK1/2 or JNK activation promoted TNF-α production in the GMC with exposure to C5a. Taken together, these data implicate that C5a induces the synthesis of IL-6 and TNF-α in rat GMC through the activation of MAPK signaling pathways.

Progesterone protects ovarian cancer cells from cisplatin-induced inhibitory effects through progesterone receptor membrane component 1/2 as well as AKT signaling.

Progesterone, also known as P4 (pregn-4-ene-3, 20-dione), is a C-21 steroid hormone involved in the female menstrual cycle, pregnancy (supports gestation) and embryogenesis of humans and other species. Despite the physiological effects, P4 is also effective for the treatment of numerous pathological states, such as multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus as well as cancer. Considering the hormone microenvironment of gynecological cancers, P4 should be particularly noted in ovarian cancer. The present study demonstrated that P4 protected the ovarian cancer cell line HO-8910 from cisplatin (CDDP)-induced cell cycle arrest and restored the cell migratory capability following treatment of CDDP. Mechanistically, both progesterone receptor membrane component 1 (PGRMC1) and the progesterone receptor (PGR) were decreased in the cells treated with CDDP plus P4, while the level of progesterone receptor membrane component 2 (PGRMC2) was significantly elevated. Reversely, in the HO-8910 cells treated with CDDP alone, levels of both PGRMC1 and PGR were increased while the level of PGRMC2 was decreased. In addition to the receptor expression profile, the PI3K/AKT signaling pathway was also involved in the action of P4 in the CDDP-resistant HO-8910 cells, and a chemical inhibitor for PI3K, LY294002, significantly abolished the anti-apoptotic effect of P4. Consequently, the addition of a PI3K inhibitor to CDDP-based chemotherapy may have a more beneficial application for ovarian cancer therapy.