NH3 Plasma Functionalization of UiO-66-NH2 for Highly Enhanced Selective Fluorescence Detection of U(VI) in Water.

Radioactive U(VI) in nuclear wastewater is a global environmental pollutant that poses a great threat to human health. Therefore, it is of great significance to develop a U(VI) sensor with desirable sensitivity and selectivity. Inspired by electron-donating group modification for enhancement of binding affinity toward U(VI), we report an amine group functionalization of UiO-66-NH2, using a low-cost, environmentally friendly, and low-temperature NH3 plasma technique as a fluorescence switching nanoprobe for highly sensitive and selective detection of U(VI). The resulting amine-functionalized UiO-66-NH2 (LTP@UiO-66-NH2) shows dramatically enhanced fluorescence emission and selective sensitivity for U(VI) on the basis of the quenching effect. The quenching efficiency increases from 58 to 80% with the same U(VI) concentration (17.63 µM) after NH3 plasma functionalization. As a result, the LTP@UiO-66-NH2 has the best Ksv (1.81 × 105 M-1, 298 K) and among the lowest LODs (0.08 µM, 19.04 ppb) compared with those reported in the literature. Intraday and interday precision and application in real environment experiments indicate stable and accurate U(VI) detection performance. Fluorescence lifetime and temperature-dependent detection experiments reveal that the quenching mechanism belongs to the static quenching interaction. The highly selective fluorescence detection is attributed to the selective binding of U(VI) by the rich functionalized amine groups of LTP@UiO-66-NH2. This work provides an efficient fluorescence probe for highly sensitive U(VI) detection in water, and a new strategy of tailored plasma functionalization for developing a practical MOF sensor platform for enhanced fluorescence emission, sensitivity, and selectivity for detecting trace amounts of radioactive species in the environment.

Long Non-Coding RNA HOXA11-AS Modulates Proliferation, Apoptosis, Metastasis and EMT in Cutaneous Melanoma Cells Partly via miR-152-3p/ITGA9 Axis.

BACKGROUND: Long non-coding RNA homeobox A11 antisense RNA (HOXA11-AS) was showed to participate in the progression of different kinds of tumors, but the specific role of HOXA11-AS in cutaneous melanoma is not entirely unambiguous. METHODS: The levels of HOXA11-AS, microRNA-152-3p (miR-152-3p) and integrin alpha9 (ITGA9) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was detected via 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), and apoptosis was measured by flow cytometry. The assessment of cell metastasis was performed by transwell migration and invasion assays. The protein levels were detected through Western blot. Dual-luciferase reporter assay was utilized to explore the target relationship among HOXA11-AS, miR-152-3p and ITGA9. The effect of HOXA11-AS on melanoma in vivo was investigated via xenograft experiment. RESULTS: HOXA11-AS and ITGA9 were up-regulated while miR-152-3p was down-regulated in melanoma. Knockdown of HOXA11-AS refrained cell proliferation, metastasis and epithelial-mesenchymal transition (EMT) but induced apoptosis in melanoma cells. HOXA11-AS targeted miR-152-3p and overexpression of HOXA11-AS mitigated the miR-152-3p-induced effects on melanoma cellular behaviors. ITGA9 was a target of miR-152-3p and miR-152-3p inhibitor relieved the repression on proliferation, metastasis and EMT while elevation on apoptosis caused by si-ITGA9 via elevating ITGA9. HOXA11-AS knockdown restrained ITGA9 expression via up-regulating miR-152-3p. Suppression of HOXA11-AS inhibited melanoma progression in part through increasing miR-152-3p and decreasing ITGA9 expression in vivo. CONCLUSION: HOXA11-AS modulated proliferation, apoptosis, metastasis and EMT in melanoma cells by regulating miR-152-3p/ITGA9 axis in part. HOXA11-AS could promote melanoma development and be used as a promising biomarker in the diagnosis and treatment for cutaneous melanoma.

Hydrothermal preparation of hierarchical ZIF-L nanostructures for enhanced CO2 capture.

A zeolitic imidazolate framework (ZIF-L) with hierarchical morphology was synthesized through hydrothermal method. The hierarchical product consists of ZIF-L leaves with length of several micrometers, width of 1 ∼ 2 µm and thickness of ∼300 nm cross connected symmetrically. It was found that the hydrothermal temperature is crucial for the formation of such hierarchical nanostructure. The formation mechanism was investigated to be a secondary crystal growth process. The hierarchical ZIF-L has larger surface area compared with the two-dimensional (2D) ZIF-L leaves. Subsequently, the hierarchical ZIF-L exhibited enhanced CO2 adsorption capacity (1.56 mmol·g-1) as compared with that of the reported two-dimensional ZIF-L leaves (0.94 mmol·g-1). This work not only reveals a new strategy for the formation of hierarchical ZIF-L nanostructures, but also supplies a potential material for CO2 capture.

Rapid Construction of ZnO@ZIF-8 Heterostructures with Size-Selective Photocatalysis Properties.

To selectively remove heavy metal from dye solution, inspired by the unique pore structure of ZIF-8, we developed a synthetic strategy for rapid construction of ZnO@ZIF-8 heterostructure photocatalyst for selective reduction of Cr(VI) between Cr(VI) and methylene blue (MB). In particular, ZnO@ZIF-8 core-shell heterostructures were prepared by in situ ZIF-8 crystal growth using ZnO colloidal spheres as template and zinc source within 8-60 min. The shell of the resulting ZnO@ZIF-8 core-shell heterostructure with a uniform thickness of around 30 nm is composed of ZIF-8 crystal polyhedrons. The concentration of organic ligand 2-methylimidazole (Hmim) was found to be crucial for the formation of ZnO@ZIF-8 core-shell heterostructures. Different structures, ZnO@ZIF-8 core-shell spheres and separate ZIF-8 polyhedrons could be formed by altering Hmim concentration, which significantly influences the balance between rate of Zn(2+) release from ZnO and coordinate rate. Importantly, such ZnO@ZIF-8 core-shell heterostructures exhibit size-selective photocatalysis properties due to selective adsorption and permeation effect of ZIF-8 shell. The as-synthesized ZnO@ZIF-8 heterostructures exhibited enhanced selective reduction of Cr(VI) between Cr(VI) and MB, which may find application in the dye industry. This work not only provides a general route for rapid fabrication of such core-shell heterostructures but also illustrates a strategy for selectively enhanced photocatalysis performance by utilizing adsorption and size selectivity of ZIF-8 shell.

Morphological control of multihollow polymer latex particles through a controlled phase separation in the seeded emulsion polymerization.

In this work, we first reported that the phase separation can take place both inside and outside of a multihollow-structured cross-linked seed microspheres swollen by styrene monomers in water during the radiation-induced seeded emulsion polymerization. The phase separation process in these two opposite directions will determine the morphology of final latex particles. First, sulfonated cross-linked polystyrene (SCPS) seed microspheres were swollen by styrene in water. Water will permeate into the SCPS seed microspheres during the swelling process, forced by the osmotic pressure produced by the strong hydrophilicity of the sulfonic acid groups. New aqueous phases are created and stabilized by the hydrophilic -SO3H groups, resulting in a multihollow structure of swollen SCPS seed microspheres. When the polymerization of styrene is induced by (60)Co γ-ray radiation, the phase separation of newly formed polystyrene phase will occur at the seed microsphere-water interface inside and/or outside of the SCPS seed microspheres through adjusting the diameter of seed microsphere, the content of cross-link agent, and the sulfonation degree of SCPS seed microspheres. As a result, SCPS latex particles with a variety of special morphologies, such as spherical multihollow, plum-like, and walnut-like latex particles were obtained. The results of this study provide not only a simple and interesting way to design and synthesize multihollow polymer latex particles with controllable surface morphologies but also a better understanding on phase separation mechanism during the swelling and polymerization of monomers in cross-linked amphiphilic polymer networks.

[Discovery and genetic analysis of blue-eyed mutant in the white rex rabbits].

Using cross, backcross, and full-sib mating experiments, allelism test was conducted to study the genetic mechanism of blue-eyed mutant of the white rex rabbits originated from the F1 generation from the cross American White rex rabbits(♂) × Chinchilla meat rabbits(♀). The study showed that the reason for the blue-eyed mutant of the white rex rabbits was a recessive mutation in Vienna locus. When the V locus was homozygous for the recessive v gene, it was recessive epistatic to other loci (including A, B, C, D, and E), which also controlled the coat color. Regardless of the genotypes in other gene loci, the rabbits appeared blue eyes and white coat color as long as the genotype vv occurred at the Vienna locus. Thus, the combination of genotype vv and genotype rr will produce the blue-eyed and the white rex rabbits. As the blue-eyed mutant of the white rex rabbits is a new finding in China's rabbit breeding program, it is significant to explain the genetic mechanism of the blue-eyed mutant for the breeding and production of rex rabbits.

Genetic variation in the promoter of DNMT3B is associated with the risk of colorectal cancer.

PURPOSE: DNA methyltransferase-3B (DNMT3B) plays an important role in the generation of aberrant methylation in carcinogenesis. Polymorphisms of the DNMT3B gene may influence DNMT3B enzyme activity on DNA methylation, thereby modulating the susceptibility to colorectal cancer (CRC). METHODS: The polymorphisms in the promoter region of the DNMT3B gene [-149C>T (rs2424913) and -579G>T (rs1569686)] were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), and a total of 544 CRC patients and 533 age- and sex-matched healthy controls were enrolled in the case-control study. RESULTS: The results showed that the -579G allele was associated with a significantly decreased risk of CRC (adjusted OR, 0.50; 95%CI, 0.35-0.72; P = 0.0002) when compared with the -579TT genotype. However, the DNMT3B-149CT genotype was not associated with the risk of CRC (adjusted OR, 0.48; 95%CI, 0.18-1.30; P = 0.151). In addition, stratification analysis revealed that the increased risk was predominant in both colon cancer and rectal cancer showing no effect of primary occurrence site. CONCLUSION: Our research demonstrated the -579G allele was a potential protective factor for the occurrence of CRC.

Polymorphisms in interleukin-1B (IL-1B) and interleukin 1 receptor antagonist (IL-1RN) genes associate with gastric cancer risk in the Chinese population.

BACKGROUND: Gastric cancer is one of the most common malignancies afflicting the Chinese population. Polymorphisms in interleukin-1B (IL-1B) and interleukin-1 receptor antagonist (IL-1RN) genes have been associated with increased gastric cancer risk. AIMS: A case-control study enrolled 392 gastric cancer patients and 508 healthy were carried out to investigate the association between polymorphisms in IL-1B and IL-1RN and gastric cancer risk. METHODS: Polymerase chain reaction (PCR)-restriction fragment length polymorphism was used for detection of two potentially functional polymorphisms (IL-1B-31 and IL-1B-511) in the IL-1B gene promoter and PCR was used for detection of the variable tandem repeat in the second intron of IL-1RN. RESULTS: The data showed that the IL-1B-31CC genotype increased gastric cancer risk to an adjusted odd of 2.27 (95% CI, 1.49-3.46), IL-1B-31CT to 1.48 (95% CI, 1.01-2.16) and IL-1B-31CT/CC to 1.68 (95% CI, 1.17-2.40), while IL-1B-51TT genotype associated with increased gastric cancer risk to an adjusted odd of 2.53 (95% CI, 1.67-3.84), IL-1B-511TC to 1.45 (95% CI, 1.02-2.06), and IL-1B-511TC TT/TC to 1.72 (95% CI, 1.23, 2.39). Furthermore, IL-1RN heterogeneity genotype (IL-1RN2L) was associated with gastric cancer risk to an adjusted odd of 1.70 (95% CI, 1.05-2.74) compared to the wild-type homozygote (IL-1RNLL). In addition, H. pylori infection enhanced gastric cancer risk through these SNPs. CONCLUSIONS: The data from the current study demonstrated that the genotype CC or CT of IL-1B-31, TT or CT of IL-1B-511, and 2L of IL-1RN increased risk of gastric cancer in this Chinese population and the risk was further enhanced by H. pylori.

Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.

Type 2 diabetes is a common complex disorder with environmental and genetic components. The aim of the present study was to investigate the association between the polymorphisms of RAPGEF1, TP53 and NRF1 and the risk of type 2 diabetes in the Chinese Han population. We genotyped rs11243444 (RAPGEF1), rs1042522 (TP53) and rs1882095 (NRF1) in a case-control study, including 273 type 2 diabetes and 247 healthy controls. A significant association was found in a variant of TP53 (rs1042522, odd ratio (OR)=1.28, 95% confidence interval (CI)=1.00-1.64; P=0.046), whereas polymorphisms in RAPGEF1, NRF1 were not associated with the risk of type 2 diabetes. Furthermore, a potential gene-gene interaction showed the odds of being affected with type 2 diabetes was 2.54 times greater in subjects with the TP53 (rs1042522) and RAPGEF1 (rs11243444) risk alleles than those without either (95% CI=1.34-4.81; P=0.004) and the NRF1 gene polymorphism reached significance when paired with TP53:(OR=3.87, 95% CI=1.87-8.40; P=0.0006). We demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.

Inhibition of CD147 gene expression via RNA interference reduces tumor cell invasion, tumorigenicity and increases chemosensitivity to cisplatin in laryngeal carcinoma Hep2 cells.

CD147, also named extracelluar matrix metalloproteinase inducer (EMMPRIN), is a member of the immunoglobulin family and a glycoprotein enriched on the surface of tumor cells, which promotes invasion, metastasis, growth and survival of malignant cells, and is known to confer resistance to some chemotherapeutic drugs. To determine the possible role of CD147 in the invasive properties of laryngeal carcinoma, we used an RNA interference approach to silence CD147 expression in the Hep2 cell line at high levels of CD147 expression. Our results showed that CD147 expression was significantly impeded at both mRNA and protein levels, which resulted in a decrease of the Hep2 invasion activity in vitro and tumorigenicity in nude mice. The suppression of CD147 expression also sensitized cells to cisplatin. Our current results indicated that CD147 was a laryngeal carcinoma-related gene and CD147 might be a potential target for therapeutic anti-cancer drugs.

Targeted tumor gene therapy based on loss of IGF2 imprinting.

Loss of imprinting (LOI) of the insulin-like growth factor 2 gene (IGF2) is one of the most common epigenetic abnormalities seen in human neoplasms. LOI may be associated with the lack of Zinc-finger DNA binding protein CTCF-mediated enhancer insulation, presumably due to the gain of methylation on the maternal allele of the differentially methylated domain (DMD) of the imprinting control region. This results in an interaction between the IGF2 promoters and enhancers; and IGF2 is produced from both alleles. In this study we investigated the feasibility of a novel anti-cancer adenovirus (AdDC312-DT-A) driven by H19 enhancer DMD-H19 promoter complex. Cell lines with IGF2 LOI (HCT-8, HT-29 and H-522) that were infected with AdDC312-EGFP produced the EGFP protein. However, in cells in which imprinting was maintained (MOI) (MCF-7 and GES-1), no EGFP protein was produced. The AdDC312-DT-A significantly decreased cell viability and induced apoptosis only in LOI cells in vitro, and suppressed tumour development in HCT-8 xenografts in nude mice. In conclusion, the toxin gene therapy proves effective in inhibiting LOI cell growth in vitro and in vivo and provides a novel option for targeted gene therapy based on loss of IGF2 imprinting.

RNAi-mediated silencing of CD147 inhibits tumor cell proliferation, invasion and increases chemosensitivity to cisplatin in SGC7901 cells in vitro.

BACKGROUND: CD147 is a widely distributed cell surface glycoprotein that belongs to the Ig superfamily. CD147 has been implicated in numerous physiological and pathological activities. Enriched on the surface of many tumor cells, CD147 promotes tumor growth, invasion, metastasis and angiogenesis and confers resistance to some chemotherapeutic drugs. In this study, we investigated the possible role of CD147 in the progression of gastric cancer. METHODS: Short hairpin RNA (shRNA) expressing vectors targeting CD147 were constructed and transfected into human gastric cancer cells SGC7901 and CD147 expression was monitored by quantitative realtime RT-PCR and Western blot. Cell proliferation, the activities of MMP-2 and MMP-9, the invasive potential and chemosensitivity to cisplatin of SGC7901 cells were determined by MTT, gelatin zymography, Transwell invasion assay and MTT, respectively. RESULTS: Down-regulation of CD147 by RNAi approach led to decreased cell proliferation, MMP-2 and MMP-9 activities and invasive potential of SGC7901 cells as well as increased chemosensitivity to cisplatin. CONCLUSION: CD147 involves in proliferation, invasion and chemosensitivity of human gastric cancer cell line SGC7901, indicating that CD147 may be a promising therapeutic target for gastric cancer.