Pilot-scale study of esterification of waste oil for biodiesel production

<p>Biodiesel, one of the alternative energy supplies from sustainable sources, is attracting great attention to replace conventional fossil fuels. Waste oil, including oil from ditches, waste cooking oil, and leftover oil in the oil factory, is considered as raw materials for biodiesel production. A pilot plant with a capacity of 30 metric tonnes of crude biodiesel per day has been built to optimize process conditions for esterification of the waste oil using polyferric sulphate catalysts in a stirred tank. The optimized process conditions are: 1.5–2.0 wt% catalyst, methanol vapor at a molar ratio of 1.5 to the waste oil, and reaction temperature at 100–110°C. The conversion of waste oil to fatty acid methyl esters was above 98% for most batches. Refined biodiesel was obtained in a yield of 93%, and the main properties of biodiesel from waste oil in this process are comparable to the international standards.</p

G-protein-coupled receptor 30 mediates the effects of estrogen on endothelial cell tube formation in vitro

The placenta is the exchange organ between the mother and the fetus. The inadequate function of this organ is associated with a number of pregnancy disorders. Hypoxia and oxidative stress during placental development may induce endothelial dysfunction, resulting in the reduction in the perfusion of the placenta. During pregnancy, the levels of estrogen are increased. Decreased estrogen levels have been reported in women with preeclampsia. However, whether estrogen is involved in placental angiogenesis remains unclear. In this study, we aimed to investigate the effects of estrogen on endothelial cell tube formation and to elucidate the underlying mechanisms. For this purpose, human umbilical vein endothelial cells (HUVECs) were cultured with 17‑β‑estradiol under conditions of hypoxia/reoxygenation (H/R). The total pipe length of the tube‑like structure on endothelial cells was measured. The expression levels of G‑protein‑coupled receptor 30 (GPR30) and endothelial nitric oxide synthase (eNOS) and Akt were also measured in the endothelial cells following treatment with 17‑β‑estradiol under H/R conditions by western blot analysis and immunostaining. We found that the total pipe length of the tube‑like structure on endothelial cells was significantly reduced. This reduction was reversed by treatment with 17‑β‑estradiol. The expression of GPR30 in endothelial cells was significantly increased following treatment with 17‑β‑estradiol under H/R conditions. Furthermore, the levels of eNOS and Akt in endothelial cells were also significantly increased following treatment with 17-β-estradiol under H/R conditions. The activation of eNOS was inhibited by wortmannin, an inhibitor of PI3K/Akt. Our data thus demonstrate that estrogen prevents the failure of endothelial cell tube formation induced by H/R. GPR30 plays an important role in these protective effects through the activation of eNOS and Akt in endothelial cells. Our data suggest that increased levels of estrogen are important for placental angiogenesis

Decreased IL-33 Production Contributes to Trophoblast Cell Dysfunction in Pregnancies with Preeclampsia

Preeclampsia (PE) is a life-threatening pregnancy complication which is related to aggradation of risk regarding fetal and maternal morbidity and mortality. Dysregulation of systemic inflammatory response and dysfunction of trophoblast cells have been proposed to be involved in the development and progression of PE. Some studies have demonstrated that interleukin-33 (IL-33) is an immunomodulatory cytokine that is associated with the immune regulation of tumor cells. However, little is known whether IL-33 and its receptor ST2/IL-1 R4 could regulate trophoblast cells, which are associated with the pathogenesis of PE. In this study, our target is to explore the impact of IL-33 on trophoblast cells and elucidate its underlying pathophysiological mechanisms. Placental tissues from the severe PE group () and the normotensive pregnant women’s group () were collected for the protein expression and distribution of IL-33 along with its receptor ST2/IL-1 R4 via Western blot analysis and immunohistochemistry, respectively. We discovered that the level of IL-33 was decreased in placental tissues of pregnant women with PE, while no distinction was observed in the expression of ST2/IL-1 R4. These results were further verified in villous explants which were treated with sodium nitroprusside with different concentrations, to simulate the pathological environment of PE. To investigate IL-33 effects on trophoblast cells separately, IL-33 shRNA was introduced into HTR8/SVneo cells and villi. IL-33 shRNA weakened the proliferation, migration, and invasion capacity of HTR8/SVneo cells. The migration distance of villous explants was also markedly decreased. The reduced invasion of trophoblast cells is a result of IL-33 knockdown which could be related to the decline of MMP2/9 activity and the increased utterance of TIMP1/2. Overall, our findings demonstrated that the reduction of IL-33 production was connected with the reduced functional capability of trophoblast cells, thus inducing placental insufficiency that has been linked to the development of PE

Kinetic Studies of Ni Organic Complexes Using Diffusive Gradients in Thin Films (DGT) with Double Binding Layers and a Dynamic Numerical Model

In situ deployments of diffusive gradients in thin films (DGT) can provide direct information on complex dissociation rates in natural waters. Recent advances in understanding the dynamics of the interactions of metal complexes within DGT devices have highlighted the characteristics of the binding layer, but there are few data to complement these theoretical developments. In this work the penetration into the Chelex binding layer of complexes of Ni with nitrilotriacetic (NTA) and Suwannee River fulvic and humic acids (FA and HA) in solution at pH 7 was investigated by deployment of DGT devices with two sequential binding layers, a “front” and a “back” layer. In Ni–NTA experiments, the masses of Ni bound by the front and back binding layers were similar, as predicted for slowly dissociating complexes. For Ni–FA/HA solutions, a higher mass of Ni was taken up by the front binding layer, consistent with fast dissociation from a high proportion of the binding sites. The ratio of Ni in the front to back binding layers was significantly lower (<i>p</i> < 0.05) for solutions of Ni–HA compared to those of Ni–FA, indicating that Ni–HA complexes are less labile than Ni–FA complexes in similar solutions (FA = 10 mg L^–1 and HA = 8 mg L^–1). A dynamic numerical model of the complexes in a DGT system was used to estimate the dissociation rate constants that provided the best agreement with the experimental data. Values obtained of 2 ± 0.5 × 10^–4 s^–1 for Ni–NTA and 2.5 × 10^–3 s^–1 for Ni–FA when FA = 20 mg L^–1 and 3.42 × 10^–4 s^–1 for Ni–HA when HA = 8 mg L^–1, could be rationalized with current knowledge of the dynamics of these systems. This approach can improve kinetic information obtainable using DGT and widen the range of considered complex labilities

Impaired mitochondrial fusion, autophagy, biogenesis and dysregulated lipid metabolism is associated with preeclampsia.

Preeclampsia(PE) is a pregnancy complication that is diagnosed by the new onset of hypertension and proteinuria. The etiology of PE remains unclear; however, growing evidence indicates that mitochondrial impairment contributes to the pathogenesis. Therefore, we aim to investigate the function of mitochondria in the development of PE. The mitochondrial metabolome in preeclamptic (n = 11) and normal (n = 11) placentas were analyzed using Gas chromatography-mass spectrometry (GC-MS). Student's t-tests and receiver operating characteristic (ROC) curves were conducted to determine which mitochondrial metabolites differed significantly between the two groups. The Pathway Activity Profiling (PAPi) R package was used to predict which metabolic pathways were affected by PE. Western blot analysis was performed to identify the candidate proteins which were associated with mitochondrial repair regulation. GC-MS analysis demonstrated that higher levels of 38 metabolites and lower levels of 2 metabolites were observed in the placenta of patients with severe PE (sPE). Five fatty acids had an area under the ROC curve above 90%. Furthermore, we revealed abnormal regulation of mitochondrial dynamics, autophagy, and biogenesis in sPE. Our discoveries indicate that the compromised lipid metabolism in sPE may result from dysfunctional mitochondria, thus revealing new insights into the etiology of the disease

Effect of Opening Geometry on the Heat Transfer Characteristics for External Flames Impinging on an Exterior Wall

<div><p>The heat transfer characteristics of external flames impinging on an exterior vertical wall have been investigated experimentally. The external flame was produced by the combustion of liquid fuel n-heptane in a compartment and then ejected from the compartment opening. The effect of opening geometry on the heat flux distribution is studied. Results indicate that the opening aspect ratio, which is defined as the ratio of opening height to width, has great influence on the heat flux distribution on the exterior wall. With increasing the opening width, the external flame inclines to the wall side and becomes shallower, which improves the heat transfer to the wall. A correlation is developed for correlating the heat flux to the flame height.</p> </div

Imbalance between proliferation and apoptosis-related impaired GPR30 expression is involved in preeclampsia.

The proliferation and apoptosis of cells in the placenta play a critical role in preeclampsia (PE) in which estrogen has been implicated via estrogen receptors (ERs). A novel ER, G-protein-coupled receptor 30 (GPR30), has recently been shown to be involved in PE. We investigated the basic levels of proliferation and apoptosis in normal placentae and placentae with PE and compared GPR30 expression levels between the two groups. We demonstrated that low GPR30 expression levels, more apoptosis, and less proliferation were associated with PE. Moreover, our in vitro study showed that both the selective GPR30 agonist G1 and the general ER agonist 17-β-estradiol were able to protect the placenta from hypoxia-reoxygenation injuries, resulting in decreased apoptosis and increased proliferation. Furthermore, this protective effect was abolished by the addition of the selective GPR30 inhibitor G15. These results provide evidence that (1) GPR30 is involved in regulating cell proliferation and apoptosis; (2) pharmacologic upregulation of GPR30 is beneficial for PE management; (3) GPR30 may therefore be an interventional target for pregnancies complicated by PE

Visualization 1: Coexistence and interaction of vector and bound vector solitons in a dispersion-managed fiber laser mode locked by graphene

Visualization 1 Originally published in Optics Express on 25 January 2016 (oe-24-2-1814

Additional file 1: Table S1. of A retrospective paired study: efficacy and toxicity of nimotuzumab versus cisplatin concurrent with radiotherapy in nasopharyngeal carcinoma

Prognostic factors for overall survival (Univariate) (N = 104). Table S2. Prognostic factors for overall survival (multivariable) (N = 104). Table S3. Toxicities in stage III and IV patients with h-R3/RT and CDDP/RT (N = 78). Table S4. Assignment expressions for factors in the table of patients’ characteristics. Table S5. Patients’ compliance (104 cases). Table S6. Neoadjuvant chemotherapy was recommended by NCCN guidelines of Head and Neck Cancer. Table S7. General information for all 302 patients of CDDP/RT and h-R3/RT group. Table S8. Prognostic factors for Overall Survival of all 302 patients (Univariate). Table S9. Prognostic factors for Overall Survival of all 302 patients (Multivariable). (ZIP 437 kb

Expression of cyclooxygenase-1 and cyclooxygenase-2, syndecan-1 and connective tissue growth factor in benign and malignant breast tissue from premenopausal women

<p>Stromal factors have been identified as important for tumorigenesis and metastases of breast cancer. From 49 premenopausal women, samples were collected from benign or malignant tumors and the seemingly normal tissue adjacent to the tumor. The factors studied, with real-time polymerase chain reaction (PCR) and immunohistochemistry, were cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2), syndecan-1 (S-1) and connective tissue growth factor (CTGF).</p> <p>COX-1 and S-1 mRNA levels were higher in the malignant tumors than in normal and benign tissues. The COX-2 mRNA level was lower in the malignant tumor than in the normal tissue, while CTGF mRNA did not differ between the groups.</p> <p>COX-1 immunostaining was higher in stroma from malignant tumors than in benign tissues, whereas COX-2 immunostaining was higher in the malignant tissue. Glandular S-1 immunostaining was lower in malignant tumors compared to benign and normal tissues, and the opposite was found in stroma.</p> <p>Conclusively, mRNA levels of COX-1 and COX-2 were oppositely regulated, with COX-1 being increased in the malignant tumor while COX-2 was decreased. S-1 protein localization switched from glandular to stromal cells in malignant tissues. Thus, these markers are, in premenopausal women, localized and regulated differently in normal/benign breast tissue as compared to the malignant tumor.</p