Most landfi lled plastic waste is a mixture or is in the form of composites with incombustible wastes such as glass, metals, and ceramics. After hydrothermal treatment, including a steam-explosion process, the separation of mixed waste (MW) into organic and inorganic substances becomes easy. However, the effect of hydrothermal pretreatment on the subsequent liquefaction of organic substances from MW is not obvious. In this study, the effects on the liquefaction of polystyrene and high-density polyethylene are discussed. Moreover, optimum conditions for the liquefaction of organic substances from hydrothermally treated MW are identifi ed. By means of this hydrothermal pretreatment, including the steam-explosion process, polystyrene and high-density polyethylene can be signifi cantly converted to oil by liquefaction at 300°-400°C. In comparison with liquefaction of hydrothermally pretreated mixed waste (HMW) at 300°-400°C with a batch type reactor, the yield of oil increases signifi cantly on liquefaction using a semi-batch type reactor. It is considered that the radical chain and termination reactions among the radicals from HMW were inhibited in the semi-batch type reactor. On liquefaction of HMW in a semi-batch reactor, the conversion of HMW to oil was enhanced on increasing the liquefaction temperature to 350°C and the holding time to 60 min.
Galectin-9 is an eosinophil chemoattractant produced by activated T lymphocytes. We have addressed expression of galectin-9 in normal human astrocytes in culture. Expression of galectin-9 mRNA and protein were examined by reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, and immunofluorescent staining. Interleukin-1beta (IL-1beta) was found to enhance the galectin-9 expression in time- and concentration-dependent manners. Galectin-9 protein was detected in the membrane fraction, 105 000 x g precipitate, and immunofluorescent staining revealed diffuse cellular and perinuclear distributions. Dexamethasone pretreatment almost completely suppressed the production. We conclude that astrocytes produce galectin-9 in response to the stimulation with IL-1beta, and this may contribute to inflammatory reactions in the CNS.
We developed a method to quantify galectin-7 extracted from adult mouse tissues by Western blot analysis. More than 0.5 ng of galectin-7 per mg of tissue was detectable by this method. The amounts of galectin-7 in tissues were determined as follows: skin, 62 +/- 3 ng/mg; esophagus, 23 +/- 8 ng/mg; stomach, 18 +/- 6 ng/mg; anus, 13 +/- 1 ng/mg; and tongue, 12 +/- 2 ng/mg. This indicates that galectin-7 production coincides with the degree of stratification of the epithelia. Interestingly, we also detected significant amounts of galectin-7, 5.9 plus minus 1.4 and 2.7 +/- 0.6 ng/mg, in the trachea and ovaries, respectively. Moreover, we found that galectin-7 is localized in the pseudostratified epithelium of the trachea and stromal epithelium of the ovaries by immunohistochemistry. Thus, galectin-7 protein might be produced primarily in stratified epithelia, but also in some wet epithelia, and plays a unique role in cell-mucus contact, or the growth of ovarian follicles.
Intestinal microflora has been associated with obesity. While visceral fat is more strongly associated with cardiovascular disorder, a complication linked to obesity, than the body mass index (BMI), the association between intestinal microflora and obesity (as defined in terms of BMI) has been studied widely. However, the link between visceral fat area (VFA) and intestinal microflora has been little studied. In this study, we investigate the association between intestinal microflora and VFA and BMI using a longitudinal study on Japanese subjects with different VFA statuses (N = 767). Principal component analysis of the changes in intestinal microflora composition over the one-year study period revealed the different associations between intestinal microflora and VFA and BMI. As determined by 16S rRNA amplicon sequencing, changes in the abundance ratio of two microbial genera—Blautia and Flavonifractor—were significantly associated with VFA changes and changes in the abundance ratio of four different microbial genera were significantly associated with BMI changes, suggesting that the associated intestinal microbes are different. Furthermore, as determined by metagenomic shotgun sequences, changes in the abundance ratios of two Blautia species—Blautia hansenii and Blautia producta—were significantly and negatively associated with VFA changes. Our findings might be used to develop a new treatment for visceral fat.
CX3CL1/fractalkine is a chemokine with a unique CX3C motif. Hypoxia mediates the expression of various genes, such as vascular endothelial growth factor (VEGF), cyclooxygenase-2, and plasminogen-activator inhibitor-1, in vascular endothelial cells. We studied the effect of hypoxia on the expression of fractalkine induced by interferon-gamma (IFN-gamma) in endothelial cells. Human umbilical vein endothelial cells were cultured, and the stimulation of the cells with IFN-gamma was found to induce the expression of fractalkine. Hypoxia inhibited the expression of fractalkine mRNA and protein by IFN-gamma, and this effect was observed with concomitant increase in VEGF expression. Desferrioxamine, an iron chelator that mimics hypoxia in vitro, also inhibited the fractalkine production induced by IFN-gamma. Hypoxia did not affect the degradation of fractalkine mRNA. The inhibition of fractalkine expression by hypoxia was reversed on returning the cultures to reoxygenation condition. Inhibition of IFN-induced fractalkine expression by hypoxia was not affected by the presence of a radical scavenger, N-acetyl-L-cysteine, and the involvement of reactive oxygen species may be excluded. Inhibition of fractalkine expression by hypoxia may be involved in the pathophysiology of ischemic diseases.
Objective To clarify the clinical significance of vascular endothelial growth factor (VEGF) in Japanese patients with small cell lung cancer (SCLC).Materials and Methods We measured serum VEGF levels using an enzyme-linked immunosorbent assay in 45 patients with SCLC before treatment and in 38 patients with benign pulmonary disease and in 32 healthy subjects (71 non-malignant subjects). VEGF immunostaining was performed in tissue biopsies obtained from 23 SCLC patients during bronchoscopic examination.Results Median serum VEGF level was 332 pg/ml in patients with SCLC and 160 pg/ml in non-malignant subjects, respectively. The 95% cut-off level to exclude nonmalignant subjects was 500 pg/ml. An elevated VEGF level (>500 pg/ml) was found more frequently in patients with extensive disease of SCLC than in those with the limited disease (p<0.01). A significant positive correlation was found between the serum VEGF level and platelet count in SCLC patients (r=0.389; p=0.0083). Serum VEGF level also correlated with serum lactate dehydrogenase in SCLC patients (r=0.381; p=0.0098). However, it did not correlate with serum neuron-specific enolase and pro-gastrin-releasing peptide level. Patients with the elevated VEGF levels had significantly shorter progressionfree time than those with the normal VEGF levels (p<0.05). Patients with the elevated VEGF levels had a significantly shorter overall survival time than those with the normal VEGF levels in univariate survival analysis (p<0.05). Further, the elevated VEGF level remained as a significant determinant of poor survival in multivariate analysis (p<0.01). Serum VEGF level was significantly higher in patients with positive VEGF protein immunoreactivity in tumor tissue in SCLC. Conclusion
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.