Pseudohyperchloremia caused by the long-term use of phenobarbital and sodium bromide compound tablets: a case report.

Background: Serum chloride (Cl-), which is an important analyte that reflects the electrolyte and acid-base balance in humans, is affected by several specific agents or substances. It has been reported that the abuse of bromine-containing drugs, such as bromvalerylurea may lead to pseudohyperchloremia, which is very rare yet, caused by the treatment dose of bromine-containing drugs. In this case report, we describe an epilepsy patient whose serum Cl- was falsely elevated due to the long-term use of phenobarbital and sodium bromide compound tablets. We also discuss the anti-interference capacity of different analyzers and the disturbance of bromide-containing drugs in Cl- determination. Case Description: A 34-year-old woman diagnosed with epilepsy for 11 years was admitted to our hospital for further treatment. She had increasingly frequent loss of consciousness and seizures. Her medication history included carbamazepine, levetiracetam, phenobarbital and sodium bromide compound tablets. The video electroencephalogram (VEEG) was moderately abnormal. No obvious abnormality was found in blood routine test, liver and kidney function, except an aberrantly elevated serum Cl- level of 130 mmol/L; however, the patient did not present with the relevant signs and symptoms of hyperchloremia, such as thirst, fatigue, nausea and vomiting. Subsequently, we used three different analyzers to determine her Cl- level and obtained the following results: an arterial blood Cl- level of 107 mmol/L; a serum Cl- level of 112 mmol/L; and no result. Reviewing her medical history, we discovered that the patient had been taking phenobarbital and sodium bromide compound tablets for 6 months to treat her seizures. Her serum bromide was 4.89 mmol/L, which may cause pseudohyperchloremia. After changing her treatment to phenobarbital tablets, her serum Cl- returned to the normal range (106 mmol/L). Conclusions: Bromide-containing drugs can cause a falsely elevated Cl- level. When pseudohyperchloremia is suspected, different methods or instruments should be used to measure Cl- levels.

Capabilities of hepatitis B surface antigen are divergent from hepatitis B virus DNA in delimiting natural history phases of chronic hepatitis B virus infection.

Objective: Quantitative hepatitis B surface antigen (HBsAg) and hepatitis B virus (HBV) DNA in the natural history of chronic HBV infection have not been rationally evaluated. This study aimed to re-characterize quantitative HBsAg and HBV DNA in the natural history phases. Methods: A total of 595 and 651 hepatitis B e antigen (HBeAg)-positive patients and 485 and 705 HBeAg-negative patients were assigned to the early and late cohorts, respectively. Based on the 'S-shape' receiver operating characteristic (ROC) curves, the HBeAg-positive sub-cohorts with possibly high HBV replication (PHVR) and possibly low HBV replication (PLVR) and the HBeAg-negative sub-cohorts with possibly high HBsAg expression (PHSE) and possibly low HBsAg expression (PLSE) were designated. Results: The areas under the ROC curve (AUCs) of HBsAg and HBV DNA in predicting HBeAg-positive significant hepatitis activity (SHA) in the early cohort, sub-cohort with PHVR, and sub-cohort with PLVR were 0.655 and 0.541, 0.720 and 0.606, and 0.553 and 0.725, respectively; those in the late cohort, sub-cohort with PHVR, and sub-cohort with PLVR were 0.646 and 0.501, 0.798 and 0.622, and 0.603 and 0.674, respectively. The AUCs of HBsAg and HBV DNA in predicting HBeAg-negative SHA in the early cohort, sub-cohort with PHSE, and sub-cohort with PLSE were 0.508 and 0.745, 0.573 and 0.780, and 0.577 and 0.729, respectively; those in the late cohort, sub-cohort with PHSE, and sub-cohort with PLSE were 0.503 and 0.761, 0.560 and 0.814, and 0.544 and 0.722, respectively. The sensitivity and specificity of HBsAg ≤4.602 log10 IU/ml in predicting HBeAg-positive SHA in the early cohort were 82.6% and 45.8%, respectively; those in the late cohort were 87.0% and 44.1%, respectively. The sensitivity and specificity of HBV DNA >3.301 log10 IU/ml in predicting HBeAg-negative SHA in the early cohort were 73.4% and 60.8%, respectively; those in the late cohort were 73.6% and 64.1%, respectively. Conclusion: Quantitative HBsAg and HBV DNA are valuable, but their capabilities are divergent in delimiting the natural history phases.

Hereditary nonspherocytic hemolytic anemia caused by glucose-6-phosphate isomerase (GPI) deficiency in a Chinese patient: a case report.

BACKGROUND: Glucose phosphate isomerase (GPI) deficiency is a rare autosomal recessive disorder that causes hereditary nonspherocytic hemolytic anemia (HNSHA). Homozygous or compound heterozygous mutation of the GPI gene on chromosome 19q13 is the cause of GPI deficiency. Fifty-seven GPI mutations have been reported at the molecular level. CASE PRESENTATION: A 5-month-old boy was presented with repeated episodes of jaundice after birth. He suffered from moderate hemolytic anemia (hemoglobin levels ranging from 62 to 91 g/L) associated with macrocytosis, reticulocytosis, neutropenia, and hyperbilirubinemia. Whole-exome sequencing showed that he has a missense mutation c.301G > A (p.Val101Met) in exon 4 and a frameshift mutation c.812delG (p.Gly271Glufs*131) in exon 10. Mutation p.Gly271Glufs*131 is a novel frameshift null mutation in GPI deficiency. CONCLUSION: In a patient with recurrent jaundice since birth, mutations in the GPI gene associated with HNSHA should be evaluated. The c.812delG (p.Gly271Glufs*131) variant may be a novel mutation of the GPI gene. Compound heterozygous mutations c.301G > A (p.Val101Met) and c.812delG (p.Gly271Glufs*131) are not relevant to neurological impairment.

Quantitative HBsAg versus HBV DNA in Predicting Significant Hepatitis Activity of HBeAg-Positive Chronic HBV Infection.

(1) Background: As specialparameters in predicting significant hepatitis activity of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B virus (HBV) infection, the quantitative standard of HBV DNA has not been agreed and that of hepatitis B surface antigen(HBsAg) has not been formed. Our objective is to evaluate the validity of HBsAg and HBV DNA in predicting the significant hepatitis activity of HBeAg-positive patients. (2) Methods: A population of 516 patients with HBeAg-positive chronic HBV infection was enrolled. Serum ALT was measured using an Abbott Architect c16000 autoanalyzer; diagnoses of liver pathological grade and stage referred to the Scheuer standard. Three levels of significant hepatitis activity were preset, which were successively "ALT ≥ 20 IU/L or Grade > G1 or Stage > S1", "ALT ≥ 30 IU/L or Grade > G1 or Stage > S1" and "ALT ≥ 40 IU/L or Grade > G1 or Stage > S1". (3) Results: A subpopulation of 288 patients with possible high HBV replication was selected based on locally weighted scatterplot smoothing regression curves between ALT and HBsAg, HBeAg and HBV DNA. In the subpopulation with possible high HBV replication, areas under receiver operating characteristic curves of HBsAg for predicting the three levels of significant hepatitis activity were successively 0.868, 0.839 and 0.789, which were all significantly greater than those of HBV DNA, as those were successively 0.553, 0.550 and 0.574 (p = 0.0002, p < 0.0001 and p < 0.0001). With the standard of HBsAg ≤ 4.699 log10 IU/mL, the sensitivity and specificity of HBsAg for predicting the three levels of significant hepatitis activity were successively 75.81% and 81.82%, 79.23% and 78.57% and 80.82% and 67.44%. (4) Conclusion: Quantitative HBsAg instead of HBV DNA is valuable in predicting significant hepatitis activity of HBeAg-positive chronic HBV infection.

A Novel Non-invasive Model Based on GPR for the Prediction of Liver Fibrosis in Patients With Chronic Hepatitis B.

Background: Some controversy remains regarding conventional serum indices for the evaluation of liver fibrosis. Therefore, we aimed to combine the existing index with other serum parameters to discriminate liver fibrosis stages in patients with chronic hepatitis B (CHB). Methods: A total of 1,622 treatment-naïve CHB patients were divided into training (n = 1,211) and validation (n = 451) cohorts. Liver histology was assessed according to the Scheuer scoring scheme. All common demographic and clinical parameters were analyzed. Results: By utilizing the results of the logistic regression analysis, we developed a novel index, the product of GPR, international normalized ratio (INR), and type IV collagen (GIVPR), to discriminate liver fibrosis. In the training group, the areas under the ROCs (AUROCs) of GIVPR, APRI, FIB-4, and GPR for significant fibrosis were 0.81, 0.75, 0.72, and 0.77, respectively; the AUROCs of GIVPR, APRI, FIB-4, and GPR for advanced fibrosis were 0.82, 0.74, 0.74, and 0.78, respectively; and the AUROCs of GIVPR, APRI, FIB-4, and GPR for cirrhosis were 0.87, 0.78, 0.78, and 0.83, respectively. Similar results were also obtained in the validation group. Furthermore, the decision curve analysis suggested that GIVPR represented superior clinical benefits in both independent cohorts. Conclusion: The GIVPR constructed on GPR represents a superior predictive model for discriminating liver fibrosis in CHB patients.

LncRNA XIST knockdown alleviates LPS-induced acute lung injury by inactivation of XIST/miR-132-3p/MAPK14 pathway : XIST promotes ALI via miR-132-3p/MAPK14 axis.

Acute lung injury (ALI) is a fatal inflammatory response syndrome. LncRNA XIST (XIST) is a lung cancer-related gene and participates in pneumonia. However, whether XIST participates in lipopolysaccharides (LPS)-induced ALI remains unclear. LPS-induced inflammation model was constructed in vitro, then cell viability, cytokines, cell apoptosis, protein, and mRNA expressions were individually detected by cell counting kit-8, enzyme-linked immunosorbent assay and flow cytometry, Western blot, and qRT-PCR. A dual-luciferase reporter assay confirmed the relationships among XIST, miR-132-3p, and MAPK14. Furthermore, inflammation and conditions after knockdown of XIST were assessed by hematoxylin and eosin staining, lung wet-to-dry weight ratio, PaO2/FiO2 ratio, and malondialdehyde (MDA) contents using LPS-induced in vivo model. Our findings indicated that the LPS challenge decreased cell viability, increased cell apoptosis, and caused secretions of pro-inflammatory cytokines. Noticeably, LPS significantly upregulated XIST, MAPK14, and downregulated miR-132-3p. Mechanistically, XIST acted as a molecular sponge to suppress miR-132-3p, and MAPK14 was identified as a target of miR-132-3p. Functional analyses demonstrated that XIST silencing remarkably increased cell survival and alleviated cell death and lung injury through decreasing TNF-α, IL-1ß, IL-6, accumulation of inflammatory cells, alveolar hemorrhage, MDA release, and increased PaO2/FiO2 ratio, as well as upregulating Bcl-2, and downregulating Bax, MAPK14, and p-extracellular signal-regulated kinases ½. In contrast, inhibition of the miR-132-3p antagonized the effects of XIST silencing. In conclusion, inhibition of XIST exhibited a protective role in LPS-induced ALI through modulating the miR-132-3p/MAPK14 axis.

Design, synthesis, and evaluation of mono-carbonyl analogues of curcumin (MCACs) as potential antioxidants against periodontitis.

BACKGROUND AND OBJECTIVE: The application of curcumin is limited by its instability. Mono-carbonyl analogues of curcumin (MCACs) are structurally stable, yet the intermediate bridging ketones in their skeletons account for increased toxicity. This study aimed to synthesize and screen MCACs that exhibit low cytotoxicity and high antioxidant ability, and the effects of MCACs on experimental periodontitis were also investigated. MATERIALS AND METHODS: The cytotoxicity of MCACs on MC3 T3-E1 was determined by MTT assay. The antioxidant capacity was investigated by the cell viability against H2 O2 -induced damage and the level of reactive oxygen species (ROS) and malondialdehyde (MDA). The localization and protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was detected by immunofluorescence and western blot, respectively. In addition, MCAC was intragastrically administrated in rats with ligature-induced experimental periodontitis. The effects were assessed by bone resorption, as well as the immunohistology staining of inflammatory and oxidative stress markers. RESULTS: MCACs with cyclopentanone and containing pyrone showed lower toxicity than natural curcumin were synthesized (1A-10A, 1H-10H), among which, 1A exhibited the most potent cytoprotective effect against H2 O2 -induced damage. Such effects could be explained by the reduced MDA and ROS level, possibly through the nucleus translocation of Nrf2 and the induction of HO-1. Micro-CT results further indicated that 1A significantly reduced bone loss, along with an increased level of Nrf2 and HO-1, and decreased TNF-α and IL-1ß. CONCLUSION: The present study has synthesized a novel antioxidant MCAC 1A with good biosafety and stability. MCAC 1A could serve as a host response modulator with preventive and protective effects on periodontitis.

Adipose triglyceride lipase promotes the proliferation of colorectal cancer cells via enhancing the lipolytic pathway.

Abnormal lipid metabolism is the sign of tumour cells. Previous researches have revealed that the lipolytic pathway may contribute to the progression of colorectal cancer (CRC). However, adipose triglyceride lipase (ATGL) role in CRC cells remains unclear. Here, we find that elevated ATGL positively correlates with CRC clinical stages and negatively associates with overall survival. Overexpression of ATGL significantly promotes CRC cell proliferation, while knockdown of ATGL inhibits the proliferation and promotes the apoptosis of CRC cells in vitro. Moreover, in vivo experiments, ATGL promotes the growth of CRC cells. Mechanistically, ATGL enhances the carcinogenic function of CRC cells via promoting sphingolipid metabolism and CoA biosynthesis pathway-related gene levels by degrading triglycerides, which provides adequate nutrition for the progression of CRC. Our researches clarify for the first time that ATGL is a novel oncogene in CRC and may provide an important prognostic factor and therapeutic target for CRC.

circ_0072088 promotes the malignant biological behaviors of non-small cell lung cancer cells by regulating miR-545-3p/STAT3 axis / 中国肿瘤生物治疗杂志

@#目的：探究环状 RNA(circular RNA, circRNA）0072088 在非小细胞肺癌（non-small cell lung cancer，NSCLC）细胞中 的生物学功能及其作用机制。方法：在公共基因芯片数据库 Gene Expression Omnibus（GEO）中下载 GSE101684 数据集，通过 GEO2R 分析得到差异基因。通过 qPCR 检测 NSCLC 细胞 H165、H358、H460、H226 和 A549 细胞中 circ_0072088 的表达水平， 随后采用 CCK-8 法和 Transwell 小室法分别检测 circ_0072088 对 NSCLC 细胞增殖、迁移和侵袭的作用。通过 CircInteractome 和 TargetScan 数据库预测 circ_0072088 与 miR-545-3p、miR-545-3p 与 STAT3 之间的靶向关系，并通过双荧光素酶报告基因实 验和 RNA 结合蛋白免疫沉淀（RNA binding protein immunoprecipitation，RIP）实验验证 circ_0072088、miR-545-3p 与 STAT3 之 间的靶向关系。结果：circ_0072088 在 NSCLC 细胞系中的表达均显著上调（均 P<0.05）。过表达 circ_0072088 促进了 NSCLC 细胞的增殖、侵袭和迁移（均 P<0.05）；敲低 circ_0072088 抑制了 NSCLC 细胞的增殖、侵袭和迁移（均 P<0.05）。miR-545-3p 是 circ_0072088 的下游靶点，可以被 circ_0072088 吸附；STAT3 是 miR-545-3p 的靶基因，可以被 circ_0072088 间接正向调控。 结论：Circ_0072088 通过调节 miR-545-3p /STAT3 轴促进 NSCLC 细胞的增殖和转移。

Identification of prognostic significance of BIRC5 in breast cancer using integrative bioinformatics analysis.

AIMS: Baculoviral inhibitor of apoptosis repeat containing 5 (BIRC5) plays vital roles in carcinogenesis by influencing cell division and proliferation and by inhibiting apoptosis. However, the prognostic significance of BIRC5 remains unclear in breast cancer. METHODS: BIRC5 expression and methylation status were evaluated using the Oncomine and The Cancer Genome Atlas (TCGA) databases. The relevance between BIRC5 and different clinicopathological features as well as survival information was analyzed using the bc-GenExMiner database and Kaplan-Meier Plotter. BIRC5-drug interaction network was obtained using the Comparative Toxicogenomics Database. RESULTS: Based on the results from databases and own hospital data, BIRC5 was higher expressed in different breast cancer subtypes compared with the matched normal individuals. Hormone receptors were negatively correlated with BIRC5 expression, whereas the Scarff-Bloom-Richardson (SBR) grade, Nottingham Prognostic Index (NPI), human epidermal growth factor receptor-2 (HER-2) status, basal-like status, and triple-negative status were positively related to BIRC5 level in breast cancer samples with respect to normal tissues. High BIRC5 expression was responsible for shorter relapse-free survival, worse overall survival, reduced distant metastasis free survival, and increased risk of metastatic relapse event. BIRC5-drug interaction network indicated that several common drugs could modulate BIRC5 expression. Furthermore, a positive correlation between BIRC5 andcell-division cycle protein 20 (CDC20) gene was confirmed. CONCLUSION: BIRC5 may be adopted as a promising predictive marker and potential therapeutic target in breast cancer. Further large-scale studies are needed to more precisely confirm the value of BIRC5 in treatment of breast cancer.

The Association Between AXIN2 Gene Polymorphisms and the Risk of Breast Cancer in Chinese Women.

Background: The protein AXIN2 is involved in the negative feedback regulation of the Wnt/ß-catenin signaling pathway; it functions by promoting ß-catenin degradation. AXIN2 mutations have been studied in various cancers. In this study, we genotyped three single nucleotide polymorphisms in the AXIN2 gene and investigated their association with the risk of breast cancer (BC) in the Chinese Han population. Methods: In a population of 415 BC patients and 528 controls the expression of AXIN2 was measured using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and compared with the overall survival (OS) of BC patients analyzed through Oncomine and Kaplan-Meier plotter databases. Bioinformatic analyses demonstrated that AXIN2 mRNA levels were downregulated in BC patients; this in turn correlated with a poorer survival rate for BC patients. Results: The polymorphisms rs11079571 and rs3923087, but not rs3923086, were associated with an increased risk of BC. The minor allele containing genotypes of polymorphism rs3923087 were positively associated with lymph node metastases. A haplotype analysis demonstrated that the ATA haplotype was correlated with an increased risk of BC. Conclusion: In conclusion, the downregulation of AXIN2 is related to poorer OS for BC patients. Its polymorphisms rs11079571 and rs3923087 confer susceptibility to BC. These findings should be confirmed with larger studies that include more diverse ethnic populations.

Biosurfactant rhamnolipid enhanced modification of corn stalk and its application for sorption of phenanthrene.

The application of modified agricultural wastes for removing polycyclic aromatic hydrocarbons (PAHs) from water is gaining a growing interest. However, most modified methods using synthetic chemicals may cause secondary pollution. To overcome this limitation, in this study, a rhamnolipid modified corn stalk (RL-CS) for the removal of phenanthrene (PHE) from aqueous solution was prepared using a rhamnolipid-enhanced acid modification method. RL-CS with higher surface area and lower polarity exhibited higher PHE removal efficiency than that of raw corn stalk (RCS). The adsorption kinetics of RL-CS fitted well with pseudo-second-order kinetics (R2 > 0.999). Sorption coefficients and carbon-normalized sorption coefficient of RL-CS were 4.68 and 2.86 times higher than that of RCS. Sorption process of RL-CS was nonlinear. Meanwhile, the sorption was an exothermic process and could occur spontaneously. The present study demonstrated that biosurfactant-modified biosorbent RL-CS may be of great potential for the removal of low concentrations of PAHs from the contaminated waters.

Comparative transcriptomic evidence for Tween80-enhanced biodegradation of phenanthrene by Sphingomonas sp. GY2B.

Previous study of the effects of surfactants on the biodegradation of phenanthrene focused on investigating alterations of the cell characteristics of Sphingomonas sp. GY2B. However, genes regulation associated with biodegradation and biological processes in response to the presence of surfactants, remains unclear. In this study, comparative transcriptome analysis was conducted to observe the gene expression of GY2B during phenanthrene biodegradation in the presence and absence of Tween80. A diverse set of genes was regulated by Tween80, leading to increased biodegradation of phenanthrene by GY2B: (i) Tween80 increased expression of genes related to H+ transport in the plasma membrane to provide a driving force (i.e., ATP) for accelerating transmembrane transport of phenanthrene with increasing Tween80 concentrations, thereby enhancing the uptake and degradation of phenanthrene by GY2B; (ii) Tween80 (1 and 8 CMC) promoted intracellular biodegradation of phenanthrene by stimulating expression of genes encoding dioxygenases and monooxygenase, increasing expression of genes involved in intracellular metabolic processes (e.g., TCA cycle); and (iii) Tween80 likely increased GY2B vitality and growth by inducing expression of genes associated with ABC transporters and protein transport, regulating genes involved in other biological processes (e.g., transcription, translation).

Direct Asymmetric Aza-Vinylogous-Type Michael Additions of Nitrones from Isatins to Nitroalkenes.

Nitrones commonly act as 1,3-dipoles and electrophiles to furnish valuable isoxazolidine and N-hydroxyl products, respectively. They also can be converted to nitrone ylide species and undergo [3+2] formal cycloadditions to access N-hydroxyl pyrrolidines. Here, asymmetric direct aza-vinylogous-type additions of nitrones from isatins to nitroalkenes are presented, catalyzed by a bifunctional thiourea-tertiary amine, affording highly functionalized nitrones with extended carbon skeletons in excellent stereoselectivity. Notably, the nitrone moiety can be easily removed, thus furnishing the formal asymmetric α-functionalization of alkylamine-type substances. Moreover, the remaining electrophilic nitrone motif enables the subsequent annulations to construct spirocyclic products in high molecular complexity and diversity, which might have potential applications for drug discovery.

Catalyst-Controlled Switch in Chemo- and Diastereoselectivities: Annulations of Morita-Baylis-Hillman Carbonates from Isatins.

Regulating both the chemo- and diastereoselectivity, divergently, of a reaction is highly attractive but extremely challenging. Presented herein is a catalyst-controlled switch in the chemo- and diastereodivergent annulation reactions of Morita-Baylis-Hillman carbonates, derived from isatins and 2-alkylidene-1H-indene-1,3(2H)-diones, in exclusive α-regioselectivity. α-Isocupreine efficiently catalyzed [2+1] reactions to access cyclopropane derivatives, and the diastereodivergent [3+2] annulations were accomplished by employing either a chiral phosphine or a DMAP-type molecule. All reactions exhibited excellent chemoselectivities, and good to remarkable stereoselectivities were furnished, thus leading to a collection of compounds with skeletal and stereogenic diversity. Moreover, DFT computational calculations elucidated the catalyst-based switch in mechanism.

Cosolubilization synergism occurrence in codesorption of PAH mixtures during surfactant-enhanced remediation of contaminated soil.

Surfactant-enhanced remediation (SER) has been widely applied in decontaminating PAH-polluted soil. Most researches focus on evaluating washing efficiency without considering pollutants' mutual interaction. This study aims to investigate cosolubilization effect between phenanthrene (Phe) and pyrene (Pyr) in nonionic surfactant Triton X-100 (TX100) solution on their codesorption performance from soil. Cosolubilization experiment showed that, when cosolubilized, solubility of Phe and Pyr in TX100 increased by 15.38% and 18.19%, respectively, as quantified by the deviation ratio of molar solubilization ratio in single and binary solute solubilization systems. The synergism may be due to the enlarged micelle volume caused by PAHs solubilized in the shell region of the micelle. The cosolubilization effect was further observed in the soil washing process. The strengthened TX100 solubilization capacity towards Phe and Pyr could increase the two PAHs' codesorption efficiency from soil, accompanied by synergistic extent of 6-15%. However, synergism in codesorption was weaker than that observed in the cosolubilization system, which may be related to surfactant loss to soil and PAH partition into soil organic matter and the sorbed surfactants. The improved remediation performance during codesorption of mixed PAHs implies the significance of combining PAHs' mutual interaction into evaluating SER, which may reduce the surfactant washing concentration and save remediation cost.

Electrokinetic-Enhanced Remediation of Phenanthrene-Contaminated Soil Combined with Sphingomonas sp. GY2B and Biosurfactant.

Electrokinetic-microbial remediation (EMR) has emerged as a promising option for the removal of polycyclic aromatic hydrocarbons (PAHs) from contaminated soils. The aim of this study was to enhance degradation of phenanthrene (Phe)-contaminated soils using EMR combined with biosurfactants. The electrokinetic (EK) remediation, combined with Phe-degrading Sphingomonas sp. GY2B, and biosurfactant obtained by fermentation of Pseudomonas sp. MZ01, degraded Phe in the soil with an efficiency of up to 65.1 % at the anode, 49.9 % at the cathode after 5 days of the treatment. The presence of biosurfactants, electricity, and a neutral electrolyte stimulated the growth of the degrading bacteria as shown by a rapid increase in microbial biomass with time. The electrical conductivity and pH changed little during the course of the treatment, which benefitted the growth of microorganisms and the remediation of Phe-contaminated soil. The EMR system with the addition of biosurfactant had the highest Phe removal, demonstrating the biosurfactant may enhance the bioavailability of Phe and the interaction with the microorganism. This study suggests that the EMR combined with biosurfactants can be used to enhance in situ bioremediation of PAH-contaminated soils.

[Effect of RNA interference of CD59 gene on proliferation of non-small cell lung cancer cell line GLC-P in vitro].

OBJECTIVE: To investigate the effect of CD59 gene inhibition mediated by RNA interference on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) GLC-P cells in vitro. METHODS: Recombinant plasmids for RNA interference of CD59 gene were constructed and transfected into GLC-P cells via lipofectamine 2000. The stably transfected cells were examined with real-time RT-PCR, MTT assay and enzyme-linked immunosorbent assay to investigate the changes in cell proliferation and apoptosis. RESULTS: Compared with the control cells, the cells transfected with CD59-siRNA showed significantly decreased expression levels of CD59 mRNA (P<0.05) and significantly inhibited cell proliferation. CONCLUSION: CD59 gene is highly expressed in NSCLC and RNA interference-mediated CD59 silencing can strongly inhibit the proliferation and induce apoptosis in GLC-P cells, which shed light on a potentially new target for targeted gene therapy of NSCLC.

[miRNA-144 in the saliva is a genetic marker for early diagnosis of esophageal cancer].

OBJECTIVE: To investigate the presence of miRNA-144 in the saliva of patients with esophageal cancer and its value for early diagnosis of esophageal cancer. METHODS: Saliva samples were collected form patients with esophageal cancer admitted in the Fourth Affiliated Hospital of Jinan University and the First Affiliated Hospital of Guangzhou Medical College between January, 2011 and May, 2013, with saliva samples from 50 middle-aged healthy volunteers matched for age and gender ratio as the control group. The contents of miRNA-144 in the samples were detected with RT-PCR. RESULTS: The levels of miRNA-144 in both the whole saliva and saliva supernatant were significantly higher in esophageal cancer group than in the control group (P<0.05). In the whole saliva, the cut-off point of miRNA-144 was ≥100, with a sensitivity of 74.6% and a specificity of 92.0% for esophageal cancer diagnosis (Az=0.865); in saliva supernatant, the cut-off point was ≥20 with a sensitivity of 53.7% and a specificity of 94.0% (Az=0.754), suggesting a moderate diagnostic value of miRNA-144 in whole saliva and saliva supernatant. CONCLUSION: miRNA-144 is highly expressed in the saliva of patients with esophageal cancer and can be used as a genetic marker for early diagnosis of esophageal cancer.

Ln[N(SiMe3)2]3-catalyzed cycloaddition of terminal alkynes to azides leading to 1,5-disubstituted 1,2,3-triazoles: new mechanistic features.

The first example of rare earth metal-catalyzed cycloaddition of terminal alkynes to azides resulting in the formation of 1,5-disubstituted 1,2,3-triazoles is described. Preliminary studies revealed that the present cycloaddition shows unprecedented mechanistic features involving a tandem anionic cascade cyclization and anti-addition across the C≡C triple bond.