In situ X-ray absorption spectroscopic studies of TiO2 photocatalytic active sites for degradation of trace CHCl3 in drinking water.

Toxic disinfection byproducts such as trihalomethanes (e.g. CHCl3) are often found after chlorination of drinking water. It has been found that photocatalytic degradation of trace CHCl3 in drinking water generally lacks an expected relationship with the crystalline phase, band-gap energy or the particle sizes of the TiO2-based photocatalysts used such as nano TiO2 on SBA-15 (Santa Barbara amorphous-15), TiO2 clusters (TiO2-SiO2) and atomic dispersed Ti [Ti-MCM-41 (Mobil Composition of Matter)]. To engineer capable TiO2 photocatalysts, a better understanding of their photoactive sites is of great importance and interest. Using in situ X-ray absorption near-edge structure (XANES) spectroscopy, the A1 (4969 eV), A2 (4971 eV) and A3 (4972 eV) sites in TiO2 can be distinguished as four-, five- and six- coordinated Ti species, respectively. Notably, the A2 Ti sites that are the main photocatalytic species of TiO2 are shown to be accountable for about 95% of the photocatalytic degradation of trace CHCl3 in drinking water (7.2 p.p.m. CHCl3 gTiO2-1 h-1). This work reveals that the A2 Ti species of a TiO2-based photocatalyst are mainly responsible for the photocatalytic reactivity, especially in photocatalytic degradation of CHCl3 in drinking water.

In situ X-ray absorption spectroscopic studies of photocatalytic oxidation of As(III) to less toxic As(V) by TiO2 nanotubes.

Arsenic in groundwater caused the black-foot disease (BFD) in many countries in the 1950-1960s. It is of great importance to develop a feasible method for removal of arsenic from contaminated groundwater in BFD endemic areas. Photocatalytic oxidation of As(III) to less toxic As(V) is, therefore, of significance for preventing any arsenic-related disease that may occur. By in situ synchrotron X-ray absorption spectroscopy, the formation of As(V) is related to the expense of As(III) disappearance during photocatalysis by TiO2 nanotubes (TNTs). Under UV/Vis light irradiation, the apparent first-order rate constant for the photocatalytic oxidation of As(III) to As(V) is 0.0148 min-1. It seems that As(III) can be oxidized with photo-excited holes while the not-recombined electrons may be scavenged with O2 in the channels of the well defined TNTs (an opening of 7 nm in diameter). In the absence of O2, on the contrary, As(III) can be reduced to As(0), to some extent. Cu(II) (CuO), as an electron acceptor, was impregnated on the TNTs surfaces in order to gain a better understanding of electron transfer during photocatalysis. It appears that As(III) can be oxidized to As(V) while Cu(II) is reduced to Cu(I) and Cu(0). The molecular-scale data are very useful in revealing the oxidation states and interconversions of arsenic during the photocatalytic reactions. This work has implications in that the toxicity of arsenic in contaminated groundwater or wastewater can be effectively decreased via solar-driven photocatalysis, which may facilitate further treatments by coagulation.

[Relationships between decreased LAMC3 and poor prognosis in ovarian cancer].

Objective: To investigate the correlations of laminin subunit gamma 3 (LAMC3) expression with prognosis of ovarian cancer (OC). Methods: LAMC3 protein expression was measured using immunohistochemical streptavidin-peroxidase-biotin connection method (IHC). Gene expression and related clinical data in the cancer genome atlas (TCGA) cohort and clinical proteomic tumor analysis consortium (CPTAC) were applied to analyse the correlation between gene and protein expressions and clinical outcomes. Correlations between LAMC3 and clinicopathological factors were evaluated using the Pearson χ2 test (2-sided). The probability of survival and significance was calculated using the Kaplan-Meier plot. The functional clustering of biological pathways enriched from co-expressed genes of LAMC3 was used to explore the possible mechanisms that LAMC3 might contribute to poor prognosis. Results: Based on the IHC results of 216 OC tissues or ovaries (including 208 tumors and 8 normal tissues) and 51 OC tissues (including 24 chemotherapy-resistant and 27 sensitive tissues), and the protein expression data from CPTAC (including 100 primary tumors and 25 normal tissues), the results showed that the protein expression of LAMC3 was significantly decreased in OC tissues compared with normal, decreased in advanced-stage tissues compared with early-stage tissues, and decreased in drug-resistant tissues compared with sensitive tissues (all P<0.05). Furthermore, low expression of LAMC3 protein was significantly associated with poor disease-free survival (DFS) and overall survival (OS) in 51 OC tissues (P<0.01), consistent with the results that the low levels of LAMC3 mRNA predicted short DFS and OS in 489 OC tissues of the TCGA cohort (P<0.05). The results suggested that low expression of LAMC3 might be the adverse factors for OC development, such as drug resistance and advanced tumors, and might be a risk indicator for prognosis. Moreover, functional clustering of biological pathways enriched from the co-expressed genes of LAMC3 in TCGA ovarian cohort indicated that LAMC3 potentially involved in regulation of OC via oncogene-pathways such as Ras associated protein 1 (Rap1), mitogen-activated protein kinase (MAPK), Ras and cell adhesion-related pathways such as extra cellular matrix (ECM)-receptor interaction and focal adhesion. It indicated that LAMC3 might contribute to short survival and tumor progression by regulation of the above pathways. Conclusion: Low expression of LAMC3 is related to poor prognosis and malignant progression in OC, and thus it is expected to be a new prognostic marker and therapeutic target for clinical treatment.

Inhibition of Cannabinoid Receptor 1 Can Influence the Lipid Metabolism in Mice with Diet-Induced Obesity.

A growing number of evidences accumulated about critical metabolic role of cannabinoid type 1 receptor (CB1), carnitine palmitoyltransferase-1 (CPT1) and peroxisome proliferator-activated receptors (PPARs) in some peripheral tissues, including adipose tissue, liver, skeletal muscle and heart. To better understand the interactions of CB1, CPT1 and PPARs in these tissues, 30 diet-induced obese (DIO) C57BL/6J male mice were obtained, weight-matched and divided into two groups (15 in each group): (i) DIO/vehicle mice (D-Veh) and (ii) DIO/SR141716 mice (D-SR) treated with SR141716 (or rimonabant, a selective CB1 receptor blocker) administered orally (10 mg/kg daily). Another 15 mice fed standard diet (STD) formed the STD/vehicle group (S-Veh). At the end of 3-week treatment, mean body weight was 28.4 ± 0.5, 36.5 ± 0.8, and 30.3 ± 1.2 g for the S-Veh, D-Veh, and D-SR group, respectively (p < 0.05; D-Veh vs. D-SR). Liver weight in the D-SR group was also decreased significantly compared to the D-Veh group (p < 0.05). Serum levels of total cholesterol, high-density lipoprotein cholesterol, leptin and adiponectin in the D-SR group were ameliorated compared to the D-Veh group (p < 0.05). Both qRT-PCR and Western blot assay revealed that CB1 expression levels were efficiently blocked by SR141716 in subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), skeletal muscles and liver (D-SR vs. D-Veh; p < 0.05), whereas there was no significant difference between S-Veh and D-Veh mice (p > 0.05). Simultaneously with the reduction of CB1 expression in the D-SR group, the expression levels of CPT1A isoform (protein) in the liver and heart and CPT1B isoform (protein) in the SAT, VAT, liver and skeletal muscles were significantly increased (p < 0.05; D-SR vs. D-Veh). Interestingly, the CPT1A and CPT1B expression levels in heart were detected slightly. The expression levels of PPARα in the SAT, VAT, liver and skeletal muscles and PPARγ in the SAT and skeletal muscles in the D-SR group were significantly increased compared to the D-Veh mice (p < 0.05). However, the PPARß expression level differed from that of PPARα and PPARγ. Taken together, these data indicate that the inhibition of CB1 could ameliorate lipid metabolism via the stimulation of the CPT1A and CPT1B expression in vivo. Simultaneously, the PPARα and PPARγ expression levels significantly differed compared to that of PPARß in obesity and lipid metabolism-related disorders under blockade of CB1. Both the mechanism of the influence of CB1 inhibition on lipid metabolism in the examined tissues and the specific mechanism of PPARα, PPARγ and PPARß involvement in lipid exchange under these conditions remain to be further elucidated.

Investigation of JAKs/STAT-3 in lipopolysaccharide-induced intestinal epithelial cells.

Janus-activated kinase (JAKs)-signal transducer and activator of transcription 3 (STAT-3) signalling play critical roles in immunoregulation and immunopathology, which involve inflammatory responses and enteritis. JAK phosphorylates STAT-3 in response to stimulation by cytokines or growth factors, and then activates or represses the gene expression. STAT-3 is activated persistently in cancer cells and contributes to the malignant progression of various types of cancer and inflammation. To elucidate the different roles of JAKs in the activation of STAT-3, the lipopolysaccharide-induced primary intestinal epithelial cell (IEC) acute inflammatory model was established. Small interference RNAs (siRNAs) were then employed to attenuate the expression levels of JAKs. Real-time quantitative reverse transcription-polymerase chain reaction (PCR) (qRT-PCR) revealed that JAK mRNA levels were reduced efficiently by JAK-specific siRNAs. Under the IEC inflammatory model transfected with si-JAK, which equates to effective silencing, qRT-PCR and Western blot assays, suggested that knockdowns of JAK attenuated the JAK-induced down-regulation of STAT-3 at the mRNA or protein levels. In particular, JAK1 played a key role, which was consistent with the RNA-Seq results. Subsequently, the expression levels of proinflammatory cytokines interleukin (IL)-1ß and tumour necrosis factor (TNF)-α were down-regulated in the IEC inflammatory model transfected with si-JAK1. JAK1 appears as a direct activator for STAT-3, whereas treatments targeting JAK1 repressed STAT-3 sufficiently pathways in the IEC inflammatory model. Therefore, the control of JAK1 using siRNAs has the potential to be an effective strategy against enteritis.