Retinal blood vessel segmentation based on Densely Connected U-Net.

The segmentation of blood vessels from retinal images is an important and challenging task in medical analysis and diagnosis. This paper proposes a new architecture of the U-Net network for retinal blood vessel segmentation. Adding dense block to U-Net network makes each layer's input come from the all previous layer's output which improves the segmentation accuracy of small blood vessels. The effectiveness of the proposed method has been evaluated on two public datasets (DRIVE and CHASE_DB1). The obtained results (DRIVE： Acc = 0.9559， AUC = 0.9793， CHASE_DB1： Acc = 0.9488， AUC = 0.9785) demonstrate the better performance of the proposed method compared to the state-of-the-art methods. Also, the results show that our method achieves better results for the segmentation of small blood vessels and can be helpful to evaluate related ophthalmic diseases.

Knockdown of Angiopoietin-Like Protein 2 Inhibits Proliferation and Invasion in Glioma Cells via Suppressing the ERK/MAPK Signaling Pathway.

Angiopoietin-like protein 2 (ANGPTL2), a member of the glycoprotein family, is mainly secreted by adipose tissues under normal conditions. Recently, ANGPTL2 has been found to be upregulated in some types of cancers and is considered to be a tumor promoter. However, the functional significance of ANGPTL2 in glioma has not yet been elucidated. In this study, we investigated the specific role of ANGPTL2 in glioma. The results showed that ANGPTL2 was highly expressed in glioma tissues and cell lines. Knockdown of ANGPTL2 reduced the proliferative and invasive abilities of glioma cells. Moreover, the tumorigenesis assay showed that ANGPTL2 knockdown inhibited glioma tumor growth in vivo. We also found that ANGPTL2 knockdown decreased the protein levels of p-ERK1/2 in glioma cells and thus blocked the activity of the ERK/MAPK signaling pathway. Taken together, our study provided the first evidence that ANGPTL2 played an oncogenic role in glioma development and might be considered as a new therapeutic target for glioma treatment.

Interleukin-18 Down-Regulates Multidrug Resistance-Associated Protein 2 Expression through Farnesoid X Receptor Associated with Nuclear Factor Kappa B and Yin Yang 1 in Human Hepatoma HepG2 Cells.

Multidrug resistance-associated protein 2 (MRP2) plays an important role in bile acid metabolism by transporting toxic organic anion conjugates, including conjugated bilirubin, glutathione, sulfate, and multifarious drugs. MRP2 expression is reduced in cholestatic patients and rodents. However, the molecular mechanism of MRP2 down-regulation remains elusive. In this report, we treated human hepatoma HepG2 cells with interleukin-18 (IL-18) and measured the expression of MRP2, nuclear factor kappa B (NF-κB), farnesoid X receptor (FXR), and the transcription factor Yin Yang 1 (YY1) by quantitative real-time quantitative polymerase chain reaction (PCR) and western blotting. We found that expression of MRP2 was repressed by IL-18 at both the mRNA and protein levels in a dose- and time-dependent manner. Furthermore, the activated NF-κB pathway increased YY1 and reduced FXR. These changes were all attenuated in HepG2 cells with knockdown of the NF-κB subunit, p65. The reduced expression of FXR and MRP2 in HepG2 cells that had been caused by IL-18 treatment was also attenuated by YY1 knockdown. We further observed significantly elevated IL-18, NF-κB, and YY1 expression and decreased FXR and MRP2 expression in bile duct-ligated Sprague Dawley rat livers. Chromatin immunoprecipitation assays also showed that FXR bound to the promoter region in MRP2 was less abundant in liver extracts from bile duct-ligated rats than sham-operated rats. Our findings indicate that IL-18 down-regulates MRP2 expression through the nuclear receptor FXR in HepG2 cells, and may be mediated by NF-κB and YY1.

[Genetic Polymorphisms in Wnt Signaling Pathway and Acute Leukemia].

OBJECTIVE: To determine the impacts of Wnt signaling pathway products-polymorphisms of rs4135385, rs11079571 and rs7832767 located in ß-catenin gene (CTNNB1), Axin gene (AXIN2), and secreted frizzled-related protein gene (SFRP1) on the risk and treatment outcomes of acute leukemia. METHODS: Bone marrows (volume 1-1. 5 mL) were collected from 372 untreated patients with acute myeloid leukemia (AML) or acute lymphoblastic leukemia (ALL), and peripheral blood samples (2. 0 mL) were obtained from 401 healthy controls for the purpose of total DNA extraction. Polymorphisms of rs4135385, rs11079571 and rs7832767 located in CTNNB1, AXIN2 and SFRP1 were genotyped with high-resolution melting method (HRM). Chi-square analyses were performed to compare the genotype and allele distributions of the three single nucleotides (SNPs) between the leukemia patients and healthy controls. Single factor variance tests were performed to compare the differences in clinical features among different genotype groups. Complete remission (CR) rates after induction chemotherapy were also compared between different genotype groups using Chi-square tests. RESULTS: No significant differences were found beiween the leukemia patients and healthy controls in the frequencies of alleles and genotypes of CTNNB1 rs4135385, SFRP1 rs7832767 polymorphisms. Those with A allele in AXIN2 rs11079571 polymorphism was less likely to have acute myelomonocytic/monocytic leukemia than those with G allele (P = 0. 016, OR=0. 677, 95%CI:0. 439-0. 930). Acute bead monocyte/mononuclear cell leukemia (AML-M4/5)patients with AA genotype presented higher platelet count (P = 0. 040), and higher complete remission rate after chemotherapy (P = 0. 040), compared with the patients with AG and GG genotypes. CONCLUSION: AML-M4/5 patients have less frequency of A allele in AXIN2 rs11079571 polymorphism than healthy controls. Patients carrying A allele have higher platelet counts and higher sensitivity to chemotherapy.

Tetra-aqua-(2,2'-diamino-4,4'-bi-1,3-thia-zole-κN,N)nickel(II) bis-(pyridine-2,6-dicarboxyl-ato-κO,N,O)nickel(II) trihydrate.

The crystal structure of the title compound, [Ni(C(6)H(6)N(4)S(2))(H(2)O)(4)][Ni(C(7)H(3)NO(4))(2)]·3H(2)O, consists of Ni(II) complex cations, Ni(II) complex anions and lattice water mol-ecules. The Ni(II) ions in both the complex cation and anion assume a distorted octa-hedral coordination geometry. O-H⋯O, N-H⋯O and C-H⋯S hydrogen bonds occur in the crystal structure.

Bis(3,5-dimethyl-1H-pyrazole-κN)(pyridine-2,6-dicarboxyl-ato-κO,N,O)copper(II).

In the crystal structure of the title compound, [Cu(C(7)H(3)NO(4))(C(5)H(8)N(2))(2)], the Cu(II) cation assumes a distorted trigonal-bipyramidal coordination geometry formed by a pyridine-2,6-dicarboxyl-ate dianion and two 3,5-dimethyl-1H-pyrazole mol-ecules. N-H⋯O hydrogen bonding is present in the crystal structure.