Decomposition and Mineralization of Dimethyl Phthalate in an Aqueous Solution by Wet Oxidation

Dimethyl phthalate (DMP) was treated via wet oxygen oxidation process (WOP). The decomposition efficiency ηDMP of DMP and mineralization efficiency ηTOC of total organic carbons were measured to evaluate the effects of operation parameters on the performance of WOP. The results revealed that reaction temperature T is the most affecting factor, with a higher T offering higher ηDMP and ηTOC as expected. The ηDMP increases as rotating speed increases from 300 to 500 rpm with stirring enhancement of gas liquid mass transfer. However, it exhibits reduction effect at 700 rpm due to purging of dissolved oxygen by overstirring. Regarding the effects of pressure PT, a higher PT provides more oxygen for the forward reaction with DMP, while overhigh PT increases the absorption of gaseous products such as CO2 and decomposes short-chain hydrocarbon fragments back into the solution thus hindering the forward reaction. For the tested PT of 2.41 to 3.45 MPa, the results indicated that 2.41 MPa is appropriate. A longer reaction time of course gives better performance. At 500 rpm, 483 K, 2.41 MPa, and 180 min, the ηDMP and ηTOC are 93 and 36%, respectively

Modified mallampati classification as a clinical predictor of peroral esophagogastroduodenoscopy tolerance

<p>Abstract</p> <p>Background</p> <p>Unsedated esophagogastroduodenoscopy (EGD) is simpler and safer than sedated EGD; however, approximately 40% of patients cannot tolerate it. Early identification of patients likely to poorly tolerate unsedated EGD is valuable for improving compliance. The modified Mallampati classification (MMC) has been used to evaluate difficult tracheal intubation and laryngoscope insertion. We tried to assess the efficacy of MMC to predict the tolerance of EGD in unsedated patients.</p> <p>Methods</p> <p>Two hundred patients who underwent an unsedated diagnostic EGD were recruited. They were stratified according to the view of the oropharynx as either MMC class I + II (good view) or class III + IV (poor view). EGD tolerance was assessed in three ways: gag reflex by endoscopist assessment, patient satisfaction by interview, and the degree of change in vital signs.</p> <p>Results</p> <p>MMC was significantly correlated to gag reflex (<it>P </it>< 0.001), patient satisfaction (<it>P </it>= 0.028), and a change of vital signs (<it>P </it>= 0.024). Patients in the poor view group had a 3.87-fold increased risk of gag reflex (<it>P </it>< 0.001), a 1.78-fold increased risk of unsatisfaction (<it>P </it>= 0.067), and a 1.96-fold increased risk of a change in vital signs (<it>P </it>= 0.025) compared to those in the good view group.</p> <p>Conclusions</p> <p>MMC appears to be a clinically useful predictor of EGD tolerance. Patients with poor view of oropharynx by MMC criteria may be candidates for sedated or transnasal EGD.</p

A fatal case of drug reaction with eosinophilia and systemic symptom syndrome associated with cytomegalovirus reactivation

Drug reaction with eosinophilia and systemic symptom (DRESS) syndrome is a severe adverse drug-induced reaction. Diagnosing DRESS syndrome is also challenging due to the diversity of cutaneous eruption and the organs involved. Here, we described an 88-year-old Chinese woman who developed DRESS syndrome under combined therapy of nonsteroidal anti-inflammatory drugs (NSAIDs) and chlormezanone (CM) accompanied with cytomegalovirus reactivation. DRESS syndrome should be highly suspected in patients with symptoms, including skin rash, fever, liver involvement, hypereosinophilia, and lymphadenopathy, especially coexisted with reactivation of the cytomegalovirus. Early withdrawal of the culprit drug is necessary once the diagnosis is established

YC-1 Antagonizes Wnt/β-Catenin Signaling Through the EBP1 p42 Isoform in Hepatocellular Carcinoma

Novel drugs targeting Wnt signaling are gradually being developed for hepatocellular carcinoma (HCC) treatment. In this study, we used a Wnt-responsive Super-TOPflash (STF) luciferase reporter assay to screen a new compound targeting Wnt signaling. 3-(5&#8242;-Hydroxymethyl-2&#8242;-furyl)-1-benzylindazole (YC-1) was identified as a small molecule inhibitor of the Wnt/&#946;-catenin pathway. Our coimmunoprecipitation (co-IP) data showed that YC-1 did not affect the &#946;-catenin/TCF interaction. Then, by mass spectrometry, we identified the ErbB3 receptor-binding protein 1 (EBP1) interaction with the &#946;-catenin/TCF complex upon YC-1 treatment. EBP1 encodes two splice isoforms, p42 and p48. We further demonstrated that YC-1 enhances p42 isoform binding to the &#946;-catenin/TCF complex and reduces the transcriptional activity of the complex. The suppression of colony formation by YC-1 was significantly reversed after knockdown of both isoforms (p48 and p42); however, the inhibition of colony formation was maintained when only EBP1 p48 was silenced. Taken together, these results suggest that YC-1 treatment results in a reduction in Wnt-regulated transcription through EBP1 p42 and leads to the inhibition of tumor cell proliferation. These data imply that YC-1 is a drug that antagonizes Wnt/&#946;-catenin signaling in HCC

Promoter Methylation of SFRP3 Is Frequent in Hepatocellular Carcinoma

Oncogenic activation of the Wnt/β-catenin signaling pathway is common in human cancers. The secreted frizzled-related proteins (SFRPs) function as negative regulators of Wnt signaling and have important implications in carcinogenesis. Because there have been no reports about the role of SFRP3 in hepatocellular carcinoma (HCC), we investigated the level of methylation and transcription of SFRP3. Four HCC cell lines, 60 HCCs, 23 cirrhosis livers, 37 chronic hepatitis livers, and 30 control livers were prescreened for SFRP3 promoter methylation by methylation-specific polymerase chain reaction (MS-PCR) and bisulfite sequencing. SFRP3 promoter methylation was observed in 100%, 60%, 39.1%, 16.2%, and 0% in HCC cell lines, primary HCCs, cirrhosis livers, chronic hepatitis livers, and control livers, respectively. Demethylation treatment with 5-aza-2′-deoxycytidine in HCC cells restored or increased the SFRP3 mRNA expression. We next used quantitative MS-PCR (QMSP) to analyze the methylation level of SFRP3 in 60 HCCs and their corresponding nontumor tissues. Methylation of SFRP3 promoter region in HCCs increased significantly compared with control tissues. There is a positive correlation between promoter hypermethylation and SFRP3 mRNA downregulation. Our data suggest that promoter hypermethylation of SFRP3 is a common event in HCCs and plays an important role in regulation of SFRP3 mRNA expression

Correction: Hepatitis C Virus Core Protein Down-Regulates p21Waf1/Cip1 and Inhibits Curcumin-Induced Apoptosis through MicroRNA-345 Targeting in Human Hepatoma Cells.

[This corrects the article DOI: 10.1371/journal.pone.0061089.]

NKX6.1 Represses Tumorigenesis, Metastasis, and Chemoresistance in Colorectal Cancer

Accumulating evidence suggests that NKX6.1 (NK homeobox 1) plays a role in various types of cancer. In our previous studies, we identified NKX6.1 hypermethylation as a promising marker and demonstrated that the NKX6.1 gene functions as a metastasis suppressor through the epigenetic regulation of the epithelial-to-mesenchymal transition (EMT) in cervical cancer. More recently, we have demonstrated that NKX6.1 methylation is related to the chemotherapy response in colorectal cancer (CRC). Nevertheless, the biological function of NKX6.1 in the tumorigenesis of CRC remains unclear. In this study, we showed that NKX6.1 suppresses tumorigenic and metastatic ability both in vitro and in vivo. NKX6.1 represses cell invasion partly through the modulation of EMT. The overexpression of NKX6.1 enhances chemosensitivity in CRC cells. To further explore how NKX6.1 exerts its tumor-suppressive function, we used RNA sequencing technology for comprehensive analysis. The results showed that differentially expressed genes (DEGs) were mainly related to cell migration, response to drug, transcription factor activity, and growth factor activity, suggesting that these DEGs are involved in the function of NKX6.1 suppressing cancer invasion and metastasis. Our results demonstrated that NKX6.1 functions as a tumor suppressor partly by repressing EMT and enhancing chemosensitivity in CRC, making it a potential therapeutic target