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Wollastonite application in cadmium-contaminated soils can reduce cadmium concentrations in plant, while the side effect is the synchronous immobilization of micronutrients, which reduces micronutrient uptake in plant, inducing micronutrient deficient symptoms. Accordingly, we investigated whether the supplement of Zn and Mn fertilizers after the wollastonite addition could promote the growth and photosynthesis in amaranth ( Amaranthus tricolor L.). In this study, plants were cultivated in cadmium-contaminated soil under micronutrient fertilization alone, wollastonite addition, and combination of wollastonite and micronutrient fertilization treatments. Then, plant biomass; photosynthesis parameters; and total Cd, Zn, and Mn concentrations were investigated. Moreover, chemical extractions were performed on soil samples. The results show that application of wollastonite decreased Cd, Zn, and Mn concentrations in plant and availability in soil and it increased the gas exchange ability of plants. But, it reduced the chlorophyll content in leaves and had no positive influence on plant biomass. In comparison, Zn and Mn fertilization after wollastonite application greatly increased plant biomass and photosynthetic ability. It also reduced Cd phytoavailability more efficiently. Therefore, synergistic improvement of physiological status of farmland crop by sequential treatment with first wollastonite for cadmium immobilization, and then micronutrient fertilization to avoid micronutrient deficiency, was demonstrated. [ABSTRACT FROM AUTHOR]

Aim and scope: To address the role of interferon-induced protein of 10 kDa (IP-10) in the course of corneal neovascularization (CrNV) in a mouse model of experimental corneal neovascularization. Material and method: BALB/c mice that were 7- to 8-week-old male were included in the study. Corneal injury was induced by NaOH. Mice were randomly divided into 2 groups of IP-10 and vehicle. The alkali-treated eyes received 5 μl of 5 μg/ml IP-10 dissolved in 0.2% sodium hyaluronate for IP-10-treated group, or 5 μl of 0.2% sodium hyaluronate for vehicle-treated group twice a day for 7 days immediately after the alkali injury. 2 weeks after alkali injury, corneas were removed and used for whole mount CD31 staining. The percentages of neovascularization on corneal photographs were examined with digital image analysis. In other experiments, at indicated time intervals, the corneas were removed. Angiogenic factor expression in the early phase after injury was quantified by real-time PCR and western blot. The VEGF expression in macrophages infiltrating into burned corneas was examined by Flow cytometry (FCM) and immunofluorescence. Tube formation and cell proliferation of human retinal endothelial cells (HRECs) were detected after being stimulated with IP-10in vitro. Results: The mRNA and protein expression of IP-10 and C-X-C motif chemokine receptor 3 (CXCR3) was augmented after the alkali injury (p < 0.05). Compared with vehicle-treated mice, IP-10-treated mice exhibited reduced CrNV 2 weeks after injury, as evidenced by diminished CD31-positive areas (p < 0.05). Concomitantly, the intracorneal mRNA and protein expression enhancement of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) was lower in IP-10-treated mice than in vehicle-treated mice after injury (p < 0.05). Moreover, IP-10 inhibited HREC tube formation and proliferationin vitro. Conclusion: IP-10-treated mice exhibited reduced alkali-induced CrNV through decreasing intracorneal VEGF and bFGF expression, and inhibiting endothelial cell proliferation and tube formation. [ABSTRACT FROM PUBLISHER]

Nonnegative matrix factorization (NMF) is a useful technique to explore a parts-based representation by decomposing the original data matrix into a few parts-based basis vectors and encodings with nonnegative constraints. It has been widely used in image processing and pattern recognition tasks due to its psychological and physiological interpretation of natural data whose representation may be parts-based in human brain. However, the nonnegative constraint for matrix factorization is generally not sufficient to produce representations that are robust to local transformations. To overcome this problem, in this paper, we proposed a topographic NMF (TNMF), which imposes a topographic constraint on the encoding factor as a regularizer during matrix factorization. In essence, the topographic constraint is a two-layered network, which contains the square nonlinearity in the first layer and the square-root nonlinearity in the second layer. By pooling together the structure-correlated features belonging to the same hidden topic, the TNMF will force the encodings to be organized in a topographical map. Thus, the feature invariance can be promoted. Some experiments carried out on three standard datasets validate the effectiveness of our method in comparison to the state-of-the-art approaches. [ABSTRACT FROM PUBLISHER]

Objective: To explore the effect of CCR3 antagonist on the development of experimental corneal neovascularization., Methods: Mouse corneas were burned by NaOH to induce corneal neovascularization.Fifty four clean male BABL/c mice aged 7-8 weeks were divided into control group, CCR3 antagonist group and VEGF antibody positive group according to randomized number table. The gene expression of CCR3 and its ligand eotaxin in burned corneas was examined by Real-time PCR. CCR3 antagonist was locally administrated after alkali injury and the formation of corneal neovascular 2 weeks after injury was examined using a digital camera linked to a slit lamp microscope and corneal whole mount staining with CD31. The mRNA and protein expression of chemokines in burned corneas was detected by Real-time PCR and western blot., Results: Compared to control group, CCR3 antagonist treated mice resulted in significantly decreased corneal neovascularization. The related CNV area was 0.51 ± 0.03 in the CCR3 antagonist group, and that in the control group was 0.77 ± 0.15, with significant difference between them (t = 12.91, P = 0.00).Western blot detection did not show significant difference of VEGF protein expression between two groups.Expression level of VEGF in the CCR3 antagonist group was 0.91 ± 0.24, and that in the control group was 1.15 ± 0.30, showing no significant difference (t = 1.08, P = 0.34)., Conclusions: Alkali-induced corneal neovascularization was inhibited by CCR3 antagonist. The mechanism that CCR3 pathway plays an important role in corneal neovascularization needs further exploration.

Purpose: To investigate the roles of an adrenomedullin receptor antagonist (adrenomedullin(22-52)) on high-glucose-induced human retinal endothelial cell (HREC) in vitro cell biology., Methods: HRECs were cultured with different concentrations of glucose and adrenomedullin(22-52). The proliferation of HRECs was evaluated by a cell counting kit-8 assay. Cell migration was assessed by scratch wound assay, and cell sprouting was detected by tube formation assay. The mRNA levels of adrenomedullin (ADM), vascular endothelial growth factor (VEGF), ADAMTS-1, and TSP-1 were measured by reverse-transcription polymerase chain reaction (RT-PCR). The VEGF and phosphatidylinositol 3' kinase (PI3K) pathway protein expression levels were assessed by western blot analysis., Results: Compared with 5 mM normal glucose treatment, 30 mM glucose significantly promoted the migration of HRECs, which was attenuated by 1 μg/ml adrenomedullin(22-52). The proliferation of HRECs was also suppressed by 1 μg/ml adrenomedullin(22-52). Furthermore, compared with other groups, 5 μg/ml of adrenomedullin(22-52) was shown to suppress high-glucose-induced tube formation of HRECs. With adrenomedullin(22-52) treatment, the mRNA level of ADAMTS-1 was significantly increased. Moreover, western blot and RT-PCR analyses showed that HRECs treated with 30 mM glucose exhibited increased VEGF and PI3K pathway protein levels, while the expression levels were suppressed by 5 μg/ml of adrenomedullin(22-52)., Conclusions: Our study indicated that adrenomedullin(22-52) mediated the migration, proliferation and tube formation after HRECs were exposed to high levels of glucose, which may be related to its ability to affect the expression of VEGF through the PI3K pathway.