The adsorption of biogenetic odorants onto activated carbon: Adsorption characteristics and impacts of algal organic matter.

Powdered activated carbon (PAC) adsorption is regarded as an efficient method for removing odorants from drinking water. However, in eutrophic aquatic environments, the presence of algal organic matter (AOM) produced by cyanobacteria considerably impedes the adsorption of odorous compounds by activated carbon. This study focused on investigating the adsorption characteristics of three representative odorants: 2-methylisoborneol (2-MIB), ß-cyclocitral (ß-cyclo), and butyl sulfide (BS) by PAC and the effects of AOM on the PAC adsorption of odorants. The removal of the three odorants reached 83.5-97.5% at a PAC dosage of 10 mg/L after 12 h of exposure in a competition-free scenario. The adsorption kinetics demonstrated higher conformity (R2 > 0.9) with the pseudo-second-order model, whereas the adsorption capacity exhibited stronger conformity (R2 > 0.9) with the Freundlich model. The presence of AOM resulted in varying levels of competition for PAC for the adsorption of the three odorants. As the concentration of AOM increased from 0 to 5 mg C/L, the removal of 2-MIB was the most affected (from 83.5% to 10.0%), followed by ß-cyclo (from 86.6% to 55.0%), and BS (from 97.5% to 92.0%). The competitive adsorption of AOM at the molecular level was studied using density functional theory (DFT). The DFT results suggested that odorants with higher and more uniformly distributed electrostatic potentials exhibited a heightened affinity for PAC adsorption and a diminished susceptibility to disruption caused by AOM. This study provides valuable insights into the mitigation of odorous compounds during drinking water purification.

A systematic analysis of molecular mechanisms in non-metastatic renal cancer delineates affected regulatory pathways and genes in tumor growth.

In the recent century, Kidney cancer has emerged as one of the critical renal diseases. Therefore, we analyzed gene expression profiles of non-metastatic kidney cancer to find mechanisms associated with the early-stage pathogenesis of the disease. We concentrated on the most dysregulated genes in expression to discover possible unknown proliferative molecular mechanisms and oncogenic pathways promoting kidney renal cancer growth. Survival analysis, expression profiling, and gene set over-representation analysis were conducted on the most upregulated and most down-regulated genes alongside the hub genes. Our results demonstrated that pathways engaged in the metabolism of amino acids and carbohydrates and those involved in peroxisome organization were shown to be important in developing benign tumors. Furthermore, upregulation of genes such as CXCL9 and 10 genes and CXCR4 in chemokine response pathways would bolster differentiation and engagement of immune cells in the tumor microenvironment. C3, one of the essential members of the complement system, with a high degree and betweenness centrality in the PPI network, upregulated significantly not only in our analysis but also in the validation expression profiling results and survival analysis. We also identified genes such as TYROBP, ITGB2, and EGFR to be engaged in both immunological pathways and superoxide pathways. Furthermore, we found that downregulation of Aldolase B engaged in Glycolysis and Gluconeogenesis pathways would help develop benign tumors. Finally, many top hub genes, including TYMS, PTPRC, AURKA, FN1, UBE2C, and CD53 were proposed to be engaged in the progression of non-metastatic renal tumors. This holistic interrogation calls attention to investigate further and experimentally validate the proposed molecular mechanisms.

Long non-coding RNA H19 acts as a microRNA-194 sponge to inhibit the apoptosis and promote the proliferation of hypertrophic scar fibroblasts.

The effects of long non-coding RNAs (lncRNAs) on the proliferation of hypertrophic scars have been described, however, the underlying mechanisms are not well characterized. The present study aimed to investigate the mechanisms of lncRNA H19 in hypertrophic scars. The effects of the lncRNA H19 on the proliferation and apoptosis of hypertrophic scar fibroblasts (HSFs) were analyzed using 5'-ethynyl-2'-deoxyuridine staining, flow cytometry, and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT). The results revealed H19 promoted the proliferation and inhibited the apoptosis in HSF. In addition, the binding associations between H19 and microRNA-194 (miR-194), and miR-194 and insulin-like growth factor I receptor (IGF1R) were identified using bioinformatics screening and verified using dual-luciferase assays. Furthermore, the effects of the IGF1R knockdown on H19-induced HSF phenotypes and regulation over the p38 MAPK pathway were determined. Mechanistically, miR-194 was identified as the downstream effector of the H19-mediated phenotypes of HSFs through its ability to directly target IGF1R, thus modulating the p38 MAPK signaling pathway. In conclusion, the findings suggested that H19 may inhibit the apoptosis and promote the proliferation of HSFs through the miR-194/IGF1R/p38 MAPK signaling axis, thereby contributing to the progression of hypertrophic scars. These findings may provide novel targets for the treatment of hypertrophic scars.

Heparanase-1-induced shedding of heparan sulfate from syndecan-1 in hepatocarcinoma cell facilitates lymphatic endothelial cell proliferation via VEGF-C/ERK pathway.

Heparanase-1/syndecan-1 axis plays critical roles in tumorigenesis and development. The main mechanism includes heparanase-1 (HPA-1) degrades the heparan sulfate chain of syndecan-1 (SDC-1), and the following shedding of heparan sulfate from tumor cell releases and activates SDC-1 sequestered growth factors. However, the significance of Heparanase-1/syndecan-1 axis and its effects on the microenvironment of lymphatic metastasis in hepatocellular carcinogenesis (HCC) procession have not been reported. Herein, we found that HPA-1 could degrade the heparan sulfate on hepatocarcinoma cell surface. Importantly, HPA-1-induced shedding of heparan sulfate chain from SDC-1 facilitated the release of vascular endothelial growth factor C (VEGF-C) from SDC-1/VEGF-C complex into the medium of hepatocarcinoma cell. Further studies indicated that VEGF-C secretion from hepatocarcinoma cell promoted lymphatic endothelial cell growth through activating extracellular signal-regulated kinase (ERK) signaling. Taken together, this study reveals a novel existence of Heparanase-1/syndecan-1 axis in hepatocarcinoma cell and its roles in the cross-talking with the microenvironment of lymphatic metastasis.

Overexpression of DEK is an indicator of poor prognosis in patients with gastric adenocarcinoma.

Increased expression of the human DEK proto-oncogene (DEK) gene has been associated with numerous human malignancies. The DEK protein is associated with chromatin reconstruction and gene transcription, and is important in cell apoptosis. The present study aimed to elucidate the role of DEK with regard to gastric adenocarcinoma tumor progression and patient prognosis. DEK protein expression was analyzed using immunohistochemistry in 192 tumors paired with adjacent non-cancerous gastric mucosa that had been surgically resected from patients with primary gastric adenocarcinoma. The association between DEK expression and the clinicopathological characteristics of the patients was evaluated using the χ2 test and Fisher's exact test. The survival rates of the patients were calculated using the Kaplan-Meier method. Cox analysis evaluated the association between the expression of DEK and the survival rate of the patients. The DEK protein was expressed in 84 patients with gastric adenocarcinoma (43.8%) and in 20 of the paired normal gastric mucosa tissues (11.5%). The DEK expression rate was found to be associated with tumor size (P=0.006), tumor grade (P=0.023), lymph node metastasis (P=0.018), serous invasion (P=0.026), tumor stage (P=0.001) and Ki-67 expression (P=0.003). Furthermore, patients with gastric adenocarcinoma that expressed DEK had decreased disease-free (log-rank, 16.785; P<0.0001) and overall (log-rank, 15.759; P<0.0001) survival rates compared with patients without DEK expression. Patients with late-stage gastric adenocarcinoma that expressed DEK exhibited a lower overall survival rate compared with patients without DEK expression (P=0.002). Additional analysis revealed that DEK expression was an independent prognostic factor for the prognosis of gastric adenocarcinoma (hazard ratio, 0.556; 95% confidence interval, 0.337-0.918; P=0.022). From the results of the present study, it can be concluded that the detection of DEK protein expression in gastric adenocarcinoma tissues may be important for the diagnosis and prognosis of patients, and may be a targeted therapy for the treatment of gastric adenocarcinoma.

Clinical implications of insulin-like growth factor II mRNA-binding protein 3 expression in non-small cell lung carcinoma.

In order to examine the role of insulin-like growth factor II mRNA-binding protein 3 (IMP3) expression for the prognostic evaluation of non-small cell lung carcinoma (NSCLC), a total of 186 breast cancer patients, with adjacent non-tumor lung tissues, were selected for immunohistochemical staining of IMP3 protein. The NSCLC tissues and paired adjacent non-tumor tissues of six patients were quantified using reverse transcription quantitative polymerase chain reaction. The correlations between IMP3 overexpression and the clinical features of NSCLC were evaluated using the χ2 test and Fisher's exact test. The survival rate was calculated using the Kaplan-Meier method, and the association between prognostic factors and patient survival was also analyzed by Cox's proportional hazards models. The results showed that IMP3 protein exhibited a mainly cytoplasmic staining pattern in the NSCLC tissues. The positive rate of IMP3 protein expression was 74.7% (139/186) in the NSCLC tissues and was significantly higher than the rate of 19.9% (37/186) in the adjacent non-tumor tissues. The expression rate of the NQO1 protein was correlated with a large tumor size, poor differentiation, lymph node metastasis, late clinical stage, and disease-free and overall survival rates in the NSCLC patients. In the early- and late-stage NSCLC groups, the disease-free and overall survival rates of the patients with IMP3 expression were significantly lower than those of the patients without IMP3 expression. Further analysis using Cox's proportional hazard regression model revealed that IMP3 expression was a significant independent hazard factor for the overall survival rate of patients with NSCLC. In conclusion, the present study found that IMP3 plays a significant role in the progression of NSCLC, and that it may potentially be used as an independent biomarker for prognostic evaluation of the cancer.

Twelve novel Atm mutations identified in Chinese ataxia telangiectasia patients.

Ataxia telangiectasia (A-T) is an autosomal recessive disease characterized mainly by progressive cerebellar ataxia, oculocutaneous telangiectasia, and immunodeficiency. This disease is caused by mutations of the ataxia telangiectasia mutated (Atm) gene. More than 500 Atm mutations that are responsible for A-T have been identified so far. However, there have been very few A-T cases reported in China, and only two Chinese A-T patients have undergone Atm gene analysis. In order to systemically investigate A-T in China and map their Atm mutation spectrum, we recruited eight Chinese A-T patients from six unrelated families nationwide. Using direct sequencing of genomic DNA and the multiplex ligation-dependent probe amplification, we identified twelve pathogenic Atm mutations, including one missense, four nonsense, five frameshift, one splicing, and one large genomic deletion. All the Atm mutations we identified were novel, and no homozygous mutation and founder-effect mutation were found. These results suggest that Atm mutations in Chinese populations are diverse and distinct largely from those in other ethnic areas.