Surface structure tuning of BiOCl nanosheets by the sequential introduction of oxygen vacancies, PO43- and Ag+ for boosting photodegradation of tetracycline hydrochloride.

The surface structure significantly impacts the physicochemical properties of semiconductors. Constructing heterojunction is a universal approach to tune surface structure, which can effectively accelerate the charge transfer at the interface. Here, BiOCl nanosheets which occupy high ratio of surface atoms to entire atoms were used as a model photocatalyst, and a strategy was proposed to tune its surface structure by sequential introduction of oxygen vacancies, PO43- and Ag+ on surface of BiOCl nanosheets. In order to inhibit the overgrowth of heterogeneous component, the excess PO43- was timely removed by centrifugation before adding Ag+. As a result, the as-obtained optimal sample which was confirmed to be a composite composed of BiOCl, BiPO4 and AgCl showed superior photocatalytic activity for tetracycline hydrochloride degradation with the rate of 38 times higher than that of pristine BiOCl, which was mainly attributed to the quick migration of photongenerated carrier. The active species h+ and •O2- played a vital role in this degradation process. Our strategy not only greatly saved investment of noble metal Ag, but also provide superior stability. On the basis of experimental results and density functional theory calculation, the visible-light driven catalytic mechanism was revealed.

Photocatalytic reduction of Cr(VI) over cinder-based nanoneedle in presence of tartaric acid: Synergistic performance and mechanism.

Cr(VI) is a common heavy metal ion, which will seriously harm human body and environment. Therefore, the removal of Cr(VI) has become an attractive topic. In this work, cinder was used as a raw material to synthesize a nanoneedle material: γ-(AlOOH@FeOOH) (γ-Al@Fe). The physicochemical properties of γ-Al@Fe were thoroughly characterized, and its effectiveness as a catalyst for photocatalytic reduction of Cr(VI) was evaluated. The results showed that Cr(VI) could be efficiently reduced by γ-Al@Fe in the presence of tartaric acid (TA) under visible light. The variable factors on the reaction were investigated in detail, and the results showed that under optimal conditions (γ-Al@Fe 0.4 g/L, TA 0.6 g/L, pH 2), Cr(VI) was completely reduced within 7 min. Besides, scavenger experiments and EPR proved that O2• - and CO2• - played a significant role in the photocatalytic reduction of Cr(VI). TA acts as a sacrificial agent to trap the holes and generate strong reducing free radicals: CO2• -. Dissolving O2 could react with electrons to generate O2• -. This work discussed the performance and mechanism of photocatalytic reduction of Cr(VI) in detail, which provided a new idea for the resource utilization of solid waste and the treatment of heavy metal sewage.

Cytotoxic effects, inflammatory response and apoptosis induction of cyclophosphamide in the peripheral blood leukocyte of blunt snout bream (Megalobrama amblycephala).

The present study was aimed to evaluate the effects of the cyclophosphamide (CY) exposure (Control, 0.032, 0.32, 1.0, 1.6 and 3.2 mg/mL) on the damage in the peripheral blood leukocytes of blunt snout bream for 24 h, which including cell viability, apoptosis, lactate dehydrogenase (LDH) release, mitochondrial membrane potential (Δѱm), ROS, antioxidant enzyme activity and the relative mRNA levels of apoptosis. Results showed that cell viability and Δѱm effects of CY were greatly reduced, and occurred in a dose-dependent manner. CY exposure (0.32-3.2 mg/mL) significantly increased the LDH release and induced apoptosis accompanied by ΔΨm disruption and ROS generation compared to the control. The cellular ROS was significantly increased with increase of CY level from 0.032 mg/mL to 1 mg/mL and the plateau occurred at 0.32 mg/mL. Additionally CY exposure led to oxidative stress as evidenced by significantly the decrease of SOD and CAT and increase of MDA concentration after treating cells with 3.2 mg/mL of CY. Besides, the relative mRNA levels of caspase-3 in the dose of 0.032, 0.32 mg/mL CY, caspase-9 and interleukins-1ß (IL-1ß) in the dose of 0.32 mg/mL CY, tumor necrosis factor-alpha (TNF-α) in the dose of 0.032 mg/mL CY significantly higher than that of the control. In conclusion, 0.32-3.2 mg/mL CY could lead to cytotoxic effect, inflammatory response and induce the apoptosis of the peripheral blood leukocyte of Megalobrama amblycephala.

Unraveling the highest oxidation states of actinides in solid-state compounds with a particular focus on plutonium.

The nature and extent of the highest oxidation state (HOS) in solid-state actinide compounds are still unexplored compared with those of small molecules, and there is burgeoning interest in studying the actinide-ligand bonding nature in the condensed state. A comprehensive understanding of the electronic structure and unraveling the possibility of a HOS are of paramount importance in solid-state actinide chemistry. Here, we report the physical OS of the early to middle actinides (Th → Cm) in solid-state compounds via a more rigorous quantum mechanical definition of OS under the DFT+U theoretical frameworks for the first time. This work implies that the highest physical OS of the Pu solid ion is PuV in PuO2F and PuOF4, which can be achieved via tuning the ligand, thus improving our knowledge of oxidation states and chemical bonding in high OS solid-state compounds. We highlight the importance of ligand design in terms of the actinide HOS, employing a highly electronegative ligand and showing the capacity to form multiple bonds.

The effects of crowding stress on the growth, physiological response, and gene expression of the Nrf2-Keap1 signaling pathway in blunt snout bream (Megalobrama amblycephala) reared under in-pond raceway conditions.

We evaluated the effects of high density stress on growth performance, antioxidant parameters, and Nrf2 pathway signaling molecules after different lengths of exposure (30, 60, or 90 days) of Megalobrama amblycephala to in-pond raceway aquaculture systems (IPRS). M. amblycephala (average initial weight 2.33 ±â€¯0.15 g) were reared at two different initial densities (low density group [LD] had 534 fish/m3 and high density group [HD] had 1073 fish/m3) for 90 days. The growth performance was adversely influenced by the high stocking density. The HD group had elevated white blood cell counts, hemoglobin content, and hematocrit on days 60 and 90. The mRNA levels of NOX2 on days 60 and 90, Nrf2 on days 30, 60, and 90, Keap1 on day 30, Bach1 on days 30 and 60, SOD on day 30, and CAT on day 30 were significantly higher in the HD group than in the LD group. Similarly, higher trends were observed in the enzymatic activities of SOD on day 60, CAT on days 60 and 90, and GPx on day 60 in the HD group, compared to the LD group. Furthermore, HD bream showed an increased MDA content on days 60 and 90 compared to that of the LD group. This study demonstrates that high density-induced antioxidant defenses were involved in modifications to the enzymatic and transcriptional regulation of Nrf2-Keap1 signaling molecules and that M. amblycephala growth was reduced in a crowded IPRS.

Comparative proteomic analysis of hepatic mechanisms of Megalobrama amblycephala infected by Aeromonas hydrophila.

Hemorrhage syndrome is one of the most prevalent and epidemic diseases that is mainly caused by Aeromonas hydrophila invasion in Megalobrama amblycephala. Recent studies have uncovered a number of immune enzymes and transcripts that are differently expressed in this disease, but the molecular mechanism elicited still remain largely unknown. Here, we constructed an in vivo A. hydrophila infection to investigate the immune mechanism in M. amblycephala using comparative proteomic approach at the one day after infection. 30 altered protein spots were found to undergo differential expression against A. hydrophila infection in the hepatopancreas of M. amblycephala based on 2-DE and were all successfully identified using MALDI-TOF/TOF, representing 18 unique proteins. These proteins were functionally classified into metabolism, antioxidant, cofactors and vitamins, chaperone and signal transduction. Network interaction and Gene Ontology annotation indicated 13 unique proteins were closely related to immune response and directly regulated by each other. Compared with the control group, A. hydrophila infection significantly decreased the metabolism-related mRNA expressions of ENO3, APOA1, CAT and FASN, but increased the mRNA expressions of MDH, ALDOB and RSP12, which was consistent with the protein expression. Nevertheless, FAH was down-regulated at both levels but had no significant difference in mRNA level, ALDH8a1 was down-regulated at protein level but non-significantly up-regulated at the mRNA level. GSTm was up-regulated at protein level but down-regulated at the mRNA level. Consequently, these results revealed that A. hydrophila infection altered the related antioxidative proteins via complex regulatory mechanisms and reduced the immune ability of M. amblycephala at the one day after infection.

Oxidized fish oil injury stress in Megalobrama amblycephala: Evaluated by growth, intestinal physiology, and transcriptome-based PI3K-Akt/NF-κB/TCR inflammatory signaling.

Lipids are essential nutrients for animal. Oxidized lipid might induce injury stress for fish. Here we conducted a 12-week rearing experiment with diets containing 0, 2, 4, and 6% oxidized fish oil (6F, 4F2OF, 2F4OF, and 6OF) to describe the oxidative impairment mechanism on teleost fish blunt snout bream, Megalobrama amblycephala. Results were evaluated by growth performance, intestinal physiology, and transcriptome-based PI3K-Akt/NF-κB/TCR inflammatory signaling. From the results, 6OF reduced growth performance with increased FCR and reduced FBW, WGR and SGR compare with 6 F. Meanwhile, oxidized fish oil treatments also increased antioxidant enzyme activity, suggesting an impaired physiological condition. The plasmatic antioxidant enzyme activity of T-SOD, GSH-Px, ASAFR, concentration of MDA and cortisol were significantly increased in 6OF, while GSH concentration was decreased. Histological ultrastructure revealed the integrity of mid-intestinal cells and villus were destroyed in 6OF. Moreover, transcriptomic analysis revealed PI3K-Akt/NF-κB/TCR inflammatory signaling were active to oxidized fish oil stress. We verified the expression of twelve key genes related to this signaling by RT-PCR, which revealed TLR2, PI3K, Akt, NF-κB, MHCII-ß, TCR-α, TGF-ß, TNF-α, IL-6, IL-1ß, GPx1 and GSTm were all activated under 6OF stimulation. We found that oxidized fish oil may induce oxidative stress, destroy intestinal integrity, produce free radical, dysregulate lipid metabolism and oxidative balance, reversely affect the physiological adaptation, and eventually lead to growth inhibition. This study revealed the mechanism of PI3K-Akt/NF-κB/TCR inflammatory signaling in M. amblycephala under oxidized fish oil stress, which may help to understand the complex regulation involved in lipid oxidative stress resistance.

The effects of emodin on cell viability, respiratory burst and gene expression of Nrf2-Keap1 signaling molecules in the peripheral blood leukocytes of blunt snout bream (Megalobrama amblycephala).

We determined the effects of emodin on the cell viability, respiratory burst activity, mRNA levels of antioxidative enzymes (Cu-Zn SOD, CAT and NOX2), and gene expressions of the Nrf2-Keap1 signaling molecules in the peripheral blood leukocytes of blunt snout bream. Triplicate groups of cultured cells were treated with different concentrations of emodin (0.04-25 µg/ml) for 24 h. Results showed that the emodin caused a dramatic loss in cell viability, and occurred in a dose-dependent manner. Emodin exposure (1-25 µg/ml) were significantly induced the ROS generation compared to the control. The respiratory burst and NADPH oxidase activities were significantly induced at a concentration of 0.20 µg/ml, and inhibited at 25 µg/ml. Besides, mRNA levels of antioxidant enzyme genes were dramatically regulated by emodin exposure for 24 h. During low concentrations of exposure, mRNA levels of Cu-Zn SOD in the cells treated with 0.04, 0.20 µg/ml, CAT, NOX2 and Nrf2 in the cells treated with 1 µg/ml were sharply increased, respectively. Whereas, high concentrations were dramatically down-regulated the gene expressions of CAT in the cells treated with 5, 25 µg/ml and NOX2 in the cells treated with 25 µg/ml. Furthermore, sharp increase in Keap1and Bach1 expression levels were observed a dose-dependent manner. In conclusion, this study demonstrated that emodin could induce antioxidant defenses which were involved in cytotoxic activities, respiratory burst and the transcriptional regulation levels of antioxidant enzymes and Nrf2-Keap1 signaling molecules.

[Recent progress of weightlessness impact on the eye].

The impact of weightlessness on the eye becomes more and more important with the increase of human space exploration. There is significant elevation in cephalad fluid and ophthalmic vein when individuals are in the state of weightlessness. In this paper, we review adverse effects in weightlessness station, including: retina damage (disc edema, choroidal folds, cotton wool spots, nerve fiber layer thickening), visual function decrease (decreased near vision, decreased ability of acquire and fixate on the target), and intraocular pressure increase.

A novel T→G splice site mutation of CRYBA1/A3 associated with autosomal dominant nuclear cataracts in a Chinese family.

PURPOSE: The purpose of this study was to identify the disease-causing mutation and the molecular phenotype that are responsible for the presence of an autosomal dominant congenital nuclear cataract disease in a Chinese family. METHODS: The family history and clinical data were recorded. The patients were given a physical examination and their blood samples were collected for DNA extraction. Direct sequencing was used to detect the mutation. Transcription analysis of the mutant crystallin, beta A1 (CRYBA1/A3) gene was performed to verify whether the defective mutation had influenced the splice of the mature mRNA. RESULTS: The phenotype of the congenital cataract in the family was identified as a nuclear cataract type, by using slit-lamp photography. Direct sequencing revealed a novel mutation IVS3+2 T→G in CRYBA1/A3. This mutation co-segregated with all affected individuals in the family, but was not found in unaffected family members nor in the 100 unrelated controls. Transcription analysis of the mutant CRYBA1/A3 gene indicated that this mutation had influenced the splice of the mature mRNA. CONCLUSIONS: Our study identified a novel splice site mutation in CRYBA1/A3. This mutation was responsible for aberrant splicing of the mature mRNA and had caused the congenital nuclear cataracts in the family. This is the first report relating an IVS3+2 T→G mutation of CRYBA1/A3 to congenital cataracts.

A nonsense mutation of CRYGC associated with autosomal dominant congenital nuclear cataracts and microcornea in a Chinese pedigree.

PURPOSE: To report the identification of a nonsense mutation in γC-crystallin (CRYGC) associated with autosomal dominant congenital nuclear cataracts and microcornea in a Chinese family. METHODS: We investigated four generations of a Chinese family six of whose members were affected by nuclear cataracts and microcornea. The genomic DNA was extracted from peripheral blood leukocytes. All reported nuclear cataract-related candidate genes were screened for causative mutations by direct DNA sequencing. The effects of amino acid changes on the structure and function of proteins were predicted by bioinformatics analysis. RESULTS: All affected individuals in this family exhibited nuclear cataracts and microcornea. Direct sequencing of the candidate gene cluster showed a c.471G>A transition in exon 3 of CRYGC, which co-segregated according to family members with cataracts, and was not observed in 100 normal controls. This single nucleotide change was predicted to introduce a translation stop codon at tryptophan 157 (W157X). Bioinformatics analysis showed that the mutation was predicted to affect the function and secondary structure of the CRYGC protein. CONCLUSIONS: This study identified a disease-causing mutation c.471G>A in CRYGC in a Chinese family with cataracts, expanding the mutation spectrum of CRYGC causing congenital cataracts.

A G→T splice site mutation of CRYBA1/A3 associated with autosomal dominant suture cataracts in a Chinese family.

PURPOSE: To identify the genetic defect in a five-generation Chinese family with congenital Y-suture cataracts. METHODS: A five-generation Chinese family with inherited Y-suture cataract phenotype was recruited. Detailed family history and clinical data of the family were recorded. Candidate genes sequencing was performed to screen out the disease-causing mutation. RESULTS: The congenital cataract phenotype of the family was identified as Y-suture cataract type by using slit-lamp photography. Direct sequencing revealed a G→T splice site mutation in crystallin, beta A1 (CRYBA1/A3).This mutation co-segregated with all affected individuals in the family and was not found in unaffected family members or 100 unrelated controls. CONCLUSIONS: Our study identified a novel type of a splice site mutation in CRYBA1/A3 .The mutation was responsible for the congenital Y-suture cataracts in the family. This is the first report relating a G→T mutation of CRYBA1/A3 to congenital Y-suture cataract.

Crystallinity-dependent photodegradation of metallic Bi in situ grown on perovskite Bi3TiNbO9 nanosheets toward antibiotic.

Owing to its wide band gap of ~3.2 eV, perovskite Bi3TiNbO9 only absorbs the solar spectrum in the ultraviolet range, which restricts its use as an effective photocatalyst. Here, a controllable and facile reduction strategy was adopted to promote the in-situ growth of metallic Bi in perovskite Bi3TiNbO9 nanosheets. The in-situ growth of metallic Bi extended photoresponse to cover the whole visible region. Adsorption of tetracycline hydrochloride (TC-H) on the surface of Bi3TiNbO9 with in-situ growth of metallic Bi (BTNOOV-Bi0) was dramatically enhanced, while BTNOOV-Bi0 exhibited a superior photocatalytic performance for tetracycline hydrochloride (TC-H) degradation under visible light irradiation with the degradation rate of 5 times higher than that of pristine Bi3TiNbO9. Moreover, the degradation activity was strongly dependent on the crystallinity of metallic Bi phase in BTNOOV-Bi0 samples. On the basis of experiment results, the visible-light driven catalytic mechanism of BTNOOV-Bi0 was elucidated. Besides, the in-situ growth of metallic Bi was also introduced in perovskite Bi5FeTi3O15, resulting in an enhanced photocatalytic activity, which indicated an enormous potential of this strategy in semiconductor structure tuning. Our study provides an effective approach to boost the performance of photocatalysts for solar-energy conversion.

The curcumin derivative WZ35 activates ROS-dependent JNK to suppress hepatocellular carcinoma metastasis.

Tumor metastasis is the leading cause of cancer death; due to the progress made in the elucidation of the mechanism of cancer cell metastasis, there is hope for patients with severe stages of cancer. Curcumin, as a novel anti-cancer drug, has been applied in cancer therapy; however, the toxicity of curcumin hinders its application. Herein, we constructed a novel derivative, WZ35, and evaluated its metastatic inhibition properties in vitro and in vivo. CCK-8 assay was performed to evaluate the tumor suppressive activity of WZ35. Cell apoptosis was detected by flow cytometry analysis. Transwell cell migration assay and RTCA were used to detect cell migration in mock and WZ35-treated cells. Western blotting was performed to analyze molecular alteration with different treatments. In this study, we found that curcumin and its derivative WZ35 could dramatically suppress proliferation, invasion, and migration of the hepatocellular HCCLM3, HepG2, and Huh7 cancer cells. Moreover, the cancer cell metastatic markers MMP-2, MMP-9, and N-cadherin were decreased, and E-cadherin was up-regulated. In addition, our data show that WZ35 promotes ROS-dependent JNK activation that is essential for WZ35-caused cell metastasis suppression. Moreover, the NAC and JNK inhibitor SP600125 could dramatically reverse WZ35-caused MMP-2, MMP-9, and N-cadherin reduction and E-cadherin up-regulation. We have also found that WZ35 exhibits powerful anti-metastasis activity of HCCLM3 in vivo. In conclusion, our data indicated that WZ35 could be a candidate for the treatment of metastatic liver cancer patients.

Mutation analysis in Chinese families with autosomal dominant hereditary cataracts.

PURPOSE: To identify the molecular basis and clinical phenotype in three Chinese families with hereditary cataracts. METHODS: Detailed family history and clinical data were recorded. The phenotypes were documented using slit-lamp photography. Candidate genes sequencing was performed to screen out the disease causing mutation. Bioinformatics analysis was performed to predict the function of mutant genes. RESULTS: The phenotypes of the families were identified as nuclear cataract in Family 1, pulverulent cataract in Family 2, and nuclear cataract in Family 3. Direct sequencing revealed transversions of C > T at c.218 (p. S73F) in GJA8 in Family 1, A > C at c.125 (p. E42A) in GJA3 in Family 2, and C > T at c.268 (p. L90F) in GJA3 in Family 3. These mutations co-segregated with all affected individuals in the family and were not found in unaffected family members nor in the 100 unrelated controls. Bioinformatics analysis indicated that S73F in GJA8, E42A and L90F in GJA3 are highly conserved. S73F in GJA8, E42A and L90F in GJA3 could possibly be damaging predicted by PolyPhen-2, with score of 0.858, 1.000, 1.000, respectively. CONCLUSIONS: This study identified three mutations in three Chinese families with hereditary cataracts. Of the three mutations, two were novel (c.125 A > C in GJA3 and c.268 C > T in GJA3), one was previously reported (c.218 C > T in GJA8).

A R54L mutation of CRYAA associated with autosomal dominant nuclear cataracts in a Chinese family.

PURPOSE: To identify the genetic defect in a three-generation Chinese family with congenital cataracts. METHODS: The phenotype of a three-generation Chinese family with congenital cataract was recruited. Detailed family history and clinical data of the family were recorded. Candidate genes sequencing was performed to screen out the disease-causing mutation. Bioinformatics analysis was performed to predict the function of mutant gene. RESULTS: The phenotype of the family was identified as nuclear cataract. Direct sequencing revealed a c.161 G > T transversion in exon 1 of crystallin alpha-A (CRYAA). This mutation co-segregated with all affected individuals in the family and was not found in unaffected family members nor in the 100 unrelated controls. Bioinformatics analysis indicated that the 54th amino acid position was highly conserved and the mutation R54L caused an increase of local hydrophobicity around the substitution site. CONCLUSIONS: This study identified a novel disease-causing mutation c.161 G > T (p.R54L) in CRYAA in a Chinese family with autosomal dominant nuclear cataracts, this is the first report relating a G > T mutation in CRYAA leading to congenital nuclear cataract.

Identification and functional analysis of GJA8 mutation in a Chinese family with autosomal dominant perinuclear cataracts.

Congenital cataract is a clinically and genetically heterogeneous group of eye disorders that causes visual impairment and childhood blindness. The purpose of this study was to identify the genetic defect associated with autosomal dominant congenital perinuclear cataract in a Chinese family. A detailed family history and clinical data of the family were recorded, and candidate gene sequencing was performed to screen for mutation-causing disease in our study. Direct sequencing revealed a c.601G>A (p.E201K) transversion in exon 2 of GJA8. This mutation co-segregated with all affected individuals in the family and was not found in unaffected family members or 100 unrelated controls. The function and mechanism of novel GJA8 point mutation E201K in Chinese patients were then investigated in this study. We found E201K aberrantly located in cytoplasm and prevented its location in the plasma membrane. Induction of E201K expression led to a decrease in cell growth and viability by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. Our study provides important evidence that GJA8 is a disease-causing gene for congenital cataract and that mutation of GJA8 has a potential causative effect.