ELF5 drives angiogenesis suppression though stabilizing WDTC1 in renal cell carcinoma.

BACKGROUND: Renal cell carcinoma (RCC) is a common malignant tumor of the urinary system. Angiogenesis is a main contributing factor for tumorigenesis. E74-like transcription factor 5 (ELF5) has been verified to participate in the progression of different cancers and can regulate angiogenesis. This study was aimed to explore the functions of ELF5 in RCC. METHODS: Bioinformatics tools were used to predict the expression of ELF5 in RCC. RT-qPCR was applied for testing ELF5 expression in RCC cells. Cell behaviors were evaluated by colony formation, CCK-8, and transwell assays. The tube formation assay was used for determining angiogenesis. Methylation-specific PCR (MSP) was utilized for measuring the methylation level of ELF5 in RCC cells. ChIP and luciferase reporter assays were applied for assessing the binding of ELF5 and ubiquitin-specific protease 3 (USP3). Co-IP and GST pull-down were utilized for detecting the interaction of WD40 and tetratricopeptide repeats 1 (WDTC1) and USP3. Ubiquitination level of WDTC1 was determined by ubiquitination assay. RESULTS: ELF5 was lowly expressed in RCC cells and tissues. High expression of ELF5 expression notably suppressed RCC cell proliferative, migratory, and invasive capabilities, and inhibited angiogenesis. The tumor growth in mice was inhibited by ELF5 overexpression. ELF5 was highly methylated in RCC samples, and DNA methyltransferases (DNMTs) can promote hypermethylation level of ELF5 in RCC cells. ELF5 was further proved to transcriptionally activate USP3 in RCC. Moreover, USP3 inhibited WDTC1 ubiquitination. ELF5 can promote USP3-mediated WDTC1 stabilization. Additionally, WDTC1 silencing reversed the functions of ELF5 overexpression on RCC progression. CONCLUSION: Downregulation of ELF5 due to DNA hypermethylation inhibits RCC development though the USP3/WDTC1axis in RCC.

Rationally Designed CdS-Based Ternary Heterojunctions: A Case of 1T-MoS2 in CdS/TiO2 Photocatalyst.

As promising heterojunction photocatalysts, the binary CdS-based heterojunctions were investigated extensively. In most of the reported CdS-based heterojunctions, however, electrons come from the semiconductor with wide band gap (e.g., TiO2) would limit the visible-light absorption of CdS and hence lower the performance. In this work, we introduced 1T-MoS2 to form a novel ternary heterojunction, namely CdS/1T-MoS2/TiO2, in which 1T-MoS2 has more positive conduction band than CdS and TiO2. The hydrogen evolution rate of CdS/1T-MoS2/TiO2 reaches 3.15 mmol g-1 h-1, which is approximately 12 and 35 times higher than that of pure CdS and CdS/TiO2 binary heterojunction under the same conditions, respectively. This performance enhancement could be attributed to the presence of 1T-MoS2 and a plausible mechanism is proposed based on photoelectrochemical characterizations. Our results illustrate that the performance of CdS-based heterojunctions for solar hydrogen evolution can be greatly improved by appropriate materials selection.

Comparative proteomics illustrates the complexity of Fe, Mn and Zn deficiency-responsive mechanisms of potato (Solanum tuberosum L.) plants in vitro.

MAIN CONCLUSION: The present study is the first to integrate physiological and proteomic data providing information on Fe, Mn and Zn deficiency-responsive mechanisms of potato plants in vitro. Micronutrient deficiency is an important limiting factor for potato production that causes substantial tuber yield and quality losses. To under the underlying molecular mechanisms of potato in response to Fe, Mn and Zn deficiency, a comparative proteomic approach was applied. Leaf proteome change of in vitro-propagated potato plantlets subjected to a range of Fe-deficiency treatments (20, 10 and 0 µM Na-Fe-EDTA), Mn-deficiency treatments (1 and 0 µM MnCl2·4H2O) and Zn-deficiency treatment (0 µM ZnCl2) using two-dimensional gel electrophoresis was analyzed. Quantitative image analysis showed a total of 146, 55 and 42 protein spots under Fe, Mn and Zn deficiency with their abundance significantly altered (P < 0.05) more than twofold, respectively. By MALDI-TOF/TOF MS analyses, the differentially abundant proteins were found mainly involved in bioenergy and metabolism, photosynthesis, defence, redox homeostasis and protein biosynthesis/degradation under the metal deficiencies. Signaling, transport, cellular structure and transcription-related proteins were also identified. The hierarchical clustering results revealed that these proteins were involved in a dynamic network in response to Fe, Mn and Zn deficiency. All these metal deficiencies caused cellular metabolic remodeling to improve metal acquisition and distribution in potato plants. The reduced photosynthetic efficiency occurred under each metal deficiency, yet Fe-deficient plants showed a more severe damage of photosynthesis. More defence mechanisms were induced by Fe deficiency than Mn and Zn deficiency, and the antioxidant systems showed different responses to each metal deficiency. Reprogramming of protein biosynthesis/degradation and assembly was more strongly required for acclimation to Fe deficiency. The signaling cascades involving auxin and NDPKs might also play roles in micronutrient stress signaling and pinpoint interesting candidates for future studies. Our results first provide an insight into the complex functional and regulatory networks in potato plants under Fe, Mn and Zn deficiency.

Syntheses, crystal structures and biological evaluation of two new Cu(II) and Co(II) complexes based on (E)-2-(((4H-1,2,4-triazol-4-yl)imino)methyl)-6-methoxyphenol.

Two transition metal complexes of [M(TMP)2(H2O)2] (TMP-Cu, M = Cu; TMP-Co, M = Co) with (E)-2-(((4H-1,2,4-triazol-4-yl)imino)methyl)-6-methoxyphenol (H-TMP) were first synthesized and characterized by infrared analysis, elemental analysis and single crystal X-ray diffraction analysis. Notably, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay showed that TMP-Cu displayed relatively high cytotoxic activity against Hep-G2 cancer cells, and high selectivity between human hepatocellular carcinoma cells and normal HL-7702 cells, in comparison to TMP-Co and cisplatin. Further studies showed that TMP-Cu and TMP-Co caused cell cycle arrest at S phase through regulation of S phase related protein expressions and induced Hep-G2 cell apoptosis via the mitochondrial pathway.

Cadmium-Based Coordination Polymers from 1D to 3D: Synthesis, Structures, and Photoluminescent and Electrochemiluminescent Properties.

Cadmium-based coordination polymers, namely, {[Cd(HL)(L)] ⋅ HN(Et)3 }n (1), [Cd2 (L)2 (H2 O)5 ]n (2), [Cd(L)(phen)]n (3), [Cd(L)(2,2'-bpy)]n (4), [Cd(L)(4,4'-bpy)]n (5), [Cd(L)(bpp)]n (6), [Cd(L)(dpa)]n (7), {[Cd(L)(dpa)] ⋅ H2 O}n (8) (H2 L=4,4'-((p-tolylazanediyl)bis(methylene))dibenzoic acid, phen=1,10-phenanthroline, 2,2'-bpy=2,2'-bipyridine, 4,4'-bpy=4,4'-bipyridine, bpp=1,3-bis(4-pyridyl)propane, dpa=bis(4-pyridyl)amine) have been synthesized in hydro/solvothermal reactions. 1 is a 4-connect 3D network with an eightfold interpenetrating diamond topology. The 1D ladder chain structure of 2 was composed of the dinuclear [Cd2 (CO2 )4 ] subunit bridged with two L2- ligands. 3 shows a 1D double-chain with a channel formed by edging out the coordination water with the rigid co-ligand phen. Polymer 4 displays a 2D lamellar structure based on superseding the coordination water molecules by the rigid chelating auxiliary ligands 2,2'-bpy. By substituting the small molecules with a rigid bridging ligand 4,4'-bpy, a 2D undulating structure of 5 was built. Compounds 6 and 7 exhibit a 2D layer structure with a 4-connect (44 ⋅ 62 ) sql-net. Compound 8 presents a 3D architecture with a sixfold interpenetrating diamond topology. Through our construction strategy, versatile structures from 1D-3D have been rationally designed by controlling the process condition and rigid/flexible of N-donor spacers. Additionally, the photoluminescence, charge transfer, and electrochemical luminescence (ECL) properties of 1-8 have been demonstrated.

Effects of aspirin combined with cilostazol on thromboangiitis obliterans in diabetic patients.

The present study explored the effects of aspirin combined with cilostazolin in the treatment of diabetic patients with thromboangiitis obliterans and the effects on the related inflammatory factors. A total of 90 diabetic patients with thromboangiitis obliterans admitted to Weifang People's Hospital from August 2015 to June 2017 were selected and divided into the control group (n=45) and the combination group (n=45). Patients in the control group were given aspirin, and those in the combination group were given aspirin combined with cilostazol. Before treatment and 6 weeks after treatment, the clinical data including ankle-brachial index (ABI), 6-min walk test (6MWT) and test data including serum inflammatory factors interleukin (IL)-8, IL-6 and matrix metalloprotease (MMP)-2 and MMP-9 of the two groups were collected for quantitative and statistical analysis. Compared with those in the control group, the ABI and 6MWT in the combination group could be effectively reduced, and the differences were statistically significant (P<0.05). At the same time, cilostazol combined with aspirin could effectively reduce the levels of serum inflammatory factors MMP-2 and MMP-9 in patients, except for nitric oxide (NO), and the differences were statistically significant (P<0.05). Compared with that before treatment, the control and the combination group can significantly improve the clinical symptoms of the patients, and aspirin combined with cilostazol can effectively improve the clinical curative effect of diabetic patients with thromboangitis obliterans and delay the progression of the disease.

Photonic crystal slab fabricated on the platform of lithium niobate-on-insulator.

We report on a photonic crystal slab patterned on a 690 nm thick LiNbO3 thin film bonded to SiO2 on lithium niobate substrate. The transmission spectrum is measured and a broad and clear photonic bandgap ranging from 1335 to 1535 nm with a maximum extinction ratio of more than 20 dB is observed. The bandgap is simulated by plane wave expansion and 3D finite-difference time-domain methods. Such a deep and broad bandgap structure can be used to form high-performance photonic devices and circuits on the platform of lithium niobate-on-insulator.

Optical waveguides in TiO2 formed by He ion implantation.

We report on the formation and the optical properties of the planar and ridge optical waveguides in rutile TiO2 crystal by He+ ion implantation combined with micro-fabrication technologies. Planar optical waveguides in TiO2 are fabricated by high-energy (2.8 MeV) He+-ion implantation with a dose of 3 × 10¹6 ions/cm² and triple low energies (450, 500, 550) keV He+-ion implantation with all fluences of 2 × 10¹6 ions/cm² at room temperature. The guided modes were measured by a modal 2010 prism coupler at wavelength of 1539 nm. There are damage profiles in ion-implanted waveguides by Rutherford backscattering (RBS)/channeling measurements. The refractive-index profile of the 2.8 MeV He+-implanted waveguide was analyzed based on RCM (Reflected Calculation Method). Also ridge waveguides were fabricated by femtosecond laser ablation on 2.8 MeV ion implanted planar waveguide and Ar ion beam etching on the basis of triple keV ion implanted planar waveguide, separately. The loss of the ridge waveguide was estimated. The measured near-field intensity distributions of the planar and ridge modes are all shown.

Optical properties of a single mode planar waveguide in Nd:YVO4 fabricated by multienergy He ion implantation.

We fabricated a single-mode planar waveguide in z-cut Nd:YVO(4) by multienergy He ion implantation in total fluence of 4.5×10(16) ions/cm(2) at room temperature and investigated optical properties of Nd:YVO(4) before and after He ion implantation by measuring transmission, confocal microluminescence, and confocal Raman spectra. Absorption bands and the photoluminescence features of the bulk Nd:YVO(4) crystal have been preserved after He ion implantation. In Raman spectra, most of the peak positions and peak widths had no obvious change before and after He ion implantation. The guiding mode and near-field image in the waveguide were measured by the prism coupling method and end-face coupling method, respectively. We investigated the damage behavior of a Nd:YVO(4) waveguide after implantation, annealing treatment by the Rutherford backscattering/channeling technique. The minimum yield of the virgin z-cut Nd:YVO(4) was 1.98%, which increased to 4.73% after He ion implantation and decreased to 3.20% after annealing at 600 K for 30 minutes.

Optical confinement achieved in ZnO crystal by O+ ions implantation: analysis of waveguide formation and properties.

Optical confinement in ZnO crystal was observed by O(+) implantation with different MeV energies and doses. Planar optical waveguides were formed in the as-implanted ZnO samples. The optical properties of the planar waveguide were investigated by the prism-coupling and the end-face coupling methods at the wavelength of 633 nm. The crystal lattice damage in the guiding region caused by the O(+) ions implantation was analyzed by the Rutherford backscattering/Channeling technique, results show that even high dose at 2 × 10(15) ions/cm(2) can hardly produce defect in near surface of ZnO. A theoretical model is developed to explain the principle of waveguide formation in ZnO crystal and the refractive index profile in the implanted waveguide was reconstructed accordingly. The experimental result and analysis are significant for application of ZnO crystal, especially for the design of ZnO light emitter devices.

Planar and ridge waveguides formed in LiNbO3 by proton exchange combined with oxygen ion implantation.

We report on the fabrication of planar and ridge waveguides in lithium niobate by proton exchange combined with oxygen ion implantation. The implanted energy ranges from 600 to 1400 keV with a dose of 1 x 10(15) ions/cm(2). The modes in proton exchanged waveguide can be modulated by O ion implantation. There are different damage profiles in proton-exchanged and ion-implanted waveguides in Rutherford backscattering/channeling spectra. The refractive index profile in single-mode waveguide in lithium niobate has been obtained based on Intensity Calculation Method. Also ridge waveguide was fabricated on the basis of planar waveguide by Ar ion beam etching. The measured near-field intensity distributions of the ridge waveguide modes show a reasonable agreement with the simulated ones. The estimated propagation loss was approximately 2.2 dB/cm.

[Effect of Shenmai injection on expression of hypoxia-inducible factor-1alpha in hypoxic-ischemic brain damage: experiment with rats].

OBJECTIVE: To investigate the effects of Shenmai injection containing active principles of Ginseng and ophiopogon root on the expression of hypoxia-inducible factor 1-alpha (HIF-1alpha) in brain after hypoxic-ischemic brain damage (HIBD). METHODS: 108 neonatal SD rats were randomly divided into 2 equal groups: (1) Shenmai group (Group SM), undergoing ligation of the right common carotid artery to establish HIBD models, breathing immediately a mixed gas with 8% oxygen and 92% nitrogen for 2 hours to cause HI insult, and then injected intraperitoneally with Shenmai injection 10 mg/kg once a day for 7 days, and (2) normal saline (NS) group (Group NS) undergoing ligation of the right common carotid artery to establish HIBD models, breathing immediately a mixed gas with 8% oxygen and 92% nitrogen for 2 h, and then injected intraperitoneally with NS 10 mg/kg once a day for 7 days. Another 54 neonatal rats underwent sham operation but did not undergo hypoxia as control group (Group C), 2, 12, and 24 hours, and 3, 7, and 14 days after HI insult 9 rats from each group were killed with their right hippocampal tissues taken out. Flow cytometry was used to examine the apoptotic rate of the hippocampal neurons. RT-PCR was used to detect the mRNA expression of HIF-1alpha. RESULTS: (1) The apoptosis rate of the right hippocampal tissues began increase 2 h after Hi insult, peaked 24 h after HI, then gradually decreased, and almost returned to the original levels 14 d after HI. There was no significant differences in apoptosis rates 14d after HI among the 3 groups (all P > 0.05). The neuron apoptosis rates 12 h, 24 h, 3 d, and 7 d after HI of Group SM were all significantly lower than those of Group NS (e.g 24 h: (11.95 +/- 1.13)% vs (16.80 +/- 1.44)%, all P < 0.05). (2) The HIF-1alpha mRNA expression level in right brain began to increase 2 h after HI, peaked 24 h after HI, then gradually decreases, and returned to the original level 14 d after Hi in both Group SM and Group NS; The HIF-1alpha mRNA expression in right brain 12 h, 24 h, 3 d, and 7 d after HI of Group SM were all significantly higher than those of Group NS (e.g 24 h: (44.32 +/- 4.03)% vs (35.63 +/- 3.73)%, all P < 0.05). CONCLUSION: The HIF-1alpha mRNA expression in brain tissue is up-regulated after HI insult. Shenmai injection helps increase the mRNA expression of HIF-1alpha in brain and reduces the apoptosis of hippocampus neurons after HI insult.

[Effects of Shenfu injection on hypoxic-ischemic brain damage: experiment with neonatal rats].

OBJECTIVE: To investigate the effect of Shenfu (ginseng and aconite root) injection on hypoxic-ischemic brain damage (HIBD). METHODS: Sixty 7-day-old Sprague-Dawley rats undergoing ligation of left common carotid artery and then put into a container with 8% O2 and 92% N(2) for 2 h so as to establish HIBD models, were randomly divided into 3 groups: Shenfu injection pretreatment group (since 4 days before the experiment Shenfu injection 10 ml/kg was injected intraperitoneally once a day for 4 days), Shenfu injection treatment group [Shenfu injection 10 ml/kg was injected intraperitoneally immediately after hypoxic-ischemia (HI) insult once a day for 7 days], and control group (normal saline 10 ml/mg was injected intraperitoneally immediately after HI insult once a day for 7 days). Twenty neonatal rats underwent sham operation as control group. The 4 groups were further divided into subgroups of 6 rats according to the time points: 2 hours before and 2 hours, 12 hours, 24 hours, 3 days, 7 days, 14 days, and 28 days after HI insult. 3, 7, 14, and 28 days after the HI insult the body weight was observed and the survival rate was observed 28 d after the HI insult. At different time points the rats of different subgroups were killed and their brains were taken out. Flow cytometry was used to calculate the neuron apoptosis rate in the hippocampal CA1 region. RESULTS: The body weight increase levels 3, 7, 14 and 28 days after HI insult of the control group were all significantly less than those of the sham operation group (e.g 7 days: 8.8 g +/- 2.1 g vs 14.0 g +/- 2.9 g, all P < 0.01) and the body weight increase levels 3, 7, 14, and 28 days after HI insult of the control group were all significantly less than those of the Shenfu injection pretreatment group (e.g 7 d: 11.7 g +/- 3.3 g) and Shenfu injection treatment group (e.g 7 d: 10.9 g +/- 2.7 g, P < 0.01 or P < 0.05). The survival rate 28 d after HI insult of the control group was 60%, significantly less than those of other groups (all P < 0.05), and there was no significant difference in the survival rate among the other groups (all P > 0.05). Compared with the sham operation group the neuron apoptosis rates of the hippocampal CA1 region of the Shenfu injection treatment group and Shenfu injection pretreatment group began to increase 2 hours after HI insult, peaked 24 hours after, then gradually decreased, and recovered to normal 14 days after. The neuron apoptosis rates 2, 12, 24, 72 hours, and 7 days after HI insult of the Shenfu injection pretreatment group were all significantly lower than those of the control group (e.g 24 hours: 16.0% +/- 4.2% vs 11.9% +/- 2.3% vs 18.1%, P < 0.01 or P < 0.05), and the neuron apoptosis rates 72 hours and 7 days after HI insult of the Shenfu injection treatment group were significantly lower than those of the control group. CONCLUSION: Shenfu injection can enhance the physical development and elevate the survival rate of neonatal rats with HI insult, and significantly prevents apoptosis of the hippocampus neurons from HI insult.