Occlusion-aware light field depth estimation using side window angular coherence.

Depth estimation is crucial in many light field applications. However, the accuracy of light field depth estimation is prone to be affected by occlusions. In this paper, a method of side window angular coherence is proposed to handle different types of occlusions, and the ability of the proposed method to resist occlusions is theoretically analyzed. The angular patch is divided into several discrete side window subsets. These subsets are a pure occluder-type subset, a pure object point-type subset, and a hybrid-type subset. The photo-consistency of the pure object point-type subset can reflect the true depth. Meanwhile, the occlusion edges can be detected to identify occluded points and nonoccluded points so the robustness of the algorithm can be further enhanced by processing the two types of points. Moreover, fast guided filtering is applied to cost volume for improving the accuracy of depth estimation. Experimental results demonstrate that our method outperforms the state-of-the-art depth estimation methods on both synthetic and real scenes, especially near occlusion boundaries.

Dysmorphic Neurofilament-Positive Ganglion Cells in the Myenteric Plexus at the Proximal Resection Margin Indicate Worse Postoperative Prognosis in Hirschsprung's Disease.

BACKGROUND: Hirschsprung's disease (HD) is a congenital disorder affecting neonates that presents with distal intestinal obstruction. It is the most common type of anorectal malformation. Treatment of HD consists of surgical removal of the distal colon including the most distal aganglionic segment, the transitional zone, and a prudent length of proximal colon that is determined during the surgical procedure to be normally ganglionated by intraoperative demonstration of normal ganglion cells up to and including the surgical resection margin. METHODS: In a retrospective study of formalin-fixed paraffin-embedded colon tissue from the proximal resection margin (PRM) of 209 HD patients, we made morphometric measures and detected immature ganglion cells defined as dysmorphic by immunohistochemical demonstration of cytoplasmic neurofilament (NF). RESULTS: The majority of NF-positive ganglion cells in HD patients appeared immature, with less cytoplasm. Occasional positive ganglion cells in the same patients appeared mature with abundant eosinophilic cytoplasm, Nissl bodies, prominent nucleoli, and adjacent glial cells. Patients with NF-positive ganglion cells in the myenteric plexuses at the PRM may have poor postoperative recovery. CONCLUSION: We propose that NF expression in dysmorphic ganglion cells at the PRM may predict poor outcome after pull-through surgery for HD.

(Methanol-κO)(methano-lato-κO)oxido[N-(2-oxidobenzyl-idene)isoleucinato-κ(3)O,N,O']vanadium(V).

In the title complex, [V(C(13)H(15)NO(3))O(CH(3)O)(CH(3)OH)], the V(V) atom is six-coordinated by a tridentate O,N,O'-donor ligand, derived from the condensation of salicyl-aldehyde and l-isoleucine, a vanadyl O atom, a methano-late O atom and a methanol O atom in a distorted octa-hedral geometry. The asymmetric unit contains two complex mol-ecules. In the crystal, inter-molecular O-H⋯O and C-H⋯O hydrogen bonds connect the mol-ecules into a one-dimensional chain along [100].

Bis[µ-N-(3-meth-oxy-2-oxidobenzyl-idene-1:2κ(2)O(2):O(2))-l-isoleucinato-2κ(2)N,O]bis-(1,10-phenanthroline-1κ(2)N,N')dinickel(II) methanol tetra-solvate trihydrate.

In the title complex, [Ni(2)(C(14)H(17)NO(4))(2)(C(12)H(8)N(2))(2)]·4CH(3)OH·3H(2)O, the two Ni(II) ions are bridged by two Schiff base anions, leading to a dinuclear complex. One Ni(II) ion is six-coordinated by four O atoms and two N atoms of two tridentate Schiff base ligands derived from the condensation of l-isoleucine and o-vanillin. The other Ni(II) ion is six-coordinated by four N atoms of two 1,10-phenanthroline ligands and two O atoms of the Schiff base ligands. In the crystal, inter-molecular O-H⋯O and C-H⋯O hydrogen bonds lead to a three-dimensional structure. Intra-molecular C-H⋯O hydrogen bonds are also present. One of the methyl groups of the l-isoleucinate moieties is disordered over two sets of sites with an occupancy ratio of 0.687 (19):0.313 (19) and two methanol mol-ecules are half-occupied.

{N-[(2-Oxido-1-naphth-yl)methyl-idene]-serinato-κO,N,O'}(1,10-phenanthroline-κN,N')copper(II).

In the title complex, [Cu(C(14)H(11)NO(4))(C(12)H(8)N(2))], the tridentate Schiff base ligand is derived from the condensation of 2-hydr-oxy-1-naphthaldehyde and l-serine. The Cu(II) atom is five-coordinated by one N atom and two O atoms from the Schiff base ligand and by two N atoms from a 1,10-phenanthroline ligand in a distorted square-pyramidal geometry. In the crystal structure, the combination of inter-molecular O-H⋯O and C-H⋯O hydrogen bonds results in a two-dimensional network structure parallel to (001).

Bis[1-(2-naphthyl-imino-meth-yl)-2-naphtholato-κN,O]copper(II).

In the title complex, [Cu(C(21)H(14)NO)(2)], the Cu(II) atom, lying on an inversion center, is coordinated by two bidentate 1-(2-naphthyl-imino-meth-yl)-2-naphtholate ligands in a trans arrangement, forming a slightly distorted square-planar coordination geometry. The mean planes of two naphthyl systems of the ligand make a dihedral angle of 40.32 (11)°.

(Methoxo-κO)oxidobis(quinolin-8-olato-κN,O)vanadium(V).

In the title complex, [V(C(9)H(6)NO)(2)(CH(3)O)O], the central V(V) atom is coordinated by the O atoms from the oxido and methoxo ligands and the N and O atoms of two bis-chelating quinolin-8-olate ligands, forming a distorted octa-hedral environment. In the crystal structure, weak inter-molecular C-H⋯O hydrogen bonds connect mol-ecules into centrosymmetric dimers which are, in turn, linked by weak C-H⋯π inter-actions into chains along the b axis.

Di-µ-oxido-bis-[(4-formyl-2-methoxy-phenolato-κO)oxido(1,10-phenan-throline-κN,N')vanadium(V)].

The title complex, [V(2)(C(8)H(7)O(3))(2)O(4)(C(12)H(8)N(2))(2)], is a centrosymmetric dimer formed by two V(V) complex units bridged by two µ(2)-oxido groups. The V(V) atom is six-coordinated by three oxide O atoms, one O atom from a vanillinate ligand and two N atoms from a 1,10-phenanthroline ligand in a significantly distorted octa-hedral geometry. In the crystal structure, weak inter-molecular C-H⋯O hydrogen bonds connect the mol-ecules into a three-dimensional network.

Aqua-{6,6'-dimeth-oxy-2,2'-[ethane-1,2-diylbis(nitrilo-methyl-idyne)]diphenolato}nickel(II).

The title complex, [Ni(C(18)H(18)N(2)O(4))(H(2)O)], lies on a mirror plane with the Ni(II) ion coordinated by two N and two O atoms of a tetra-dentate Schiff base ligand and one water O atom in a distorted square-pyramidal enviroment. The -CH(2)-CH(2)- group of the ligand is disordered equally over two sites about the mirror plane. The dihedral angle between the mean planes of the two symmetry-related chelate rings is 37.16 (6)°. In the crystal structure, inter-molecular O-H⋯O hydrogen bonds link complex mol-ecules into one-dimensional chains along [100] and these chains are linked, in turn, by very weak inter-molecular C-H⋯O hydrogen bonds into a two-dimensional network.

Aplnra/b Sequentially Regulate Organ Left-Right Patterning via Distinct Mechanisms.

The G protein-coupled receptor APJ/Aplnr has been widely reported to be involved in heart and vascular development and disease, but whether it contributes to organ left-right patterning is largely unknown. Here, we show that in zebrafish, aplnra/b coordinates organ LR patterning in an apela/apln ligand-dependent manner using distinct mechanisms at different stages. During gastrulation and early somitogenesis, aplnra/b loss of function results in heart and liver LR asymmetry defects, accompanied by disturbed KV/cilia morphogenesis and disrupted left-sided Nodal/spaw expression in the LPM. In this process, only aplnra loss of function results in KV/cilia morphogenesis defect. In addition, only apela works as the early endogenous ligand to regulate KV morphogenesis, which then contributes to left-sided Nodal/spaw expression and subsequent organ LR patterning. The aplnra-apela cascade regulates KV morphogenesis by enhancing the expression of foxj1a, but not fgf8 or dnh9, during KV development. At the late somite stage, both aplnra and aplnrb contribute to the expression of lft1 in the trunk midline but do not regulate KV formation, and this role is possibly mediated by both endogenous ligands, apela and apln. In conclusion, our study is the first to identify a role for aplnra/b and their endogenous ligands apela/apln in LR patterning, and it clarifies the distinct roles of aplnra-apela and aplnra/b-apela/apln in orchestrating organ LR patterning.

1-(Hydroxy-imino-meth-yl)-2-naphthol.

The title compound, C(11)H(9)NO(2), was prepared by a condens-ation reaction of 2-hydr-oxy-1-naphthaldehyde with hydroxyl-ammonium chloride in refluxing ethanol. An intra-molecular O-H⋯N hydrogen bond is observed. In the crystal structure, inter-molecular O-H⋯O and C-H⋯O hydrogen-bond inter-actions result in a two-dimensional network.

BMP4 knockdown of NCSCs leads to aganglionosis in the middle embryonic stage.

Transplacental bone morphogenetic protein (BMP)4 RNA interference (RNAi) is a technique used to knockdown genes in embryos. BMP4 are essential for the development of nervous system in the differentiation of neural crest stem cells (NCSCs). The failure of differentiation and migration of NCSCs may lead to aganglionosis. In the present study, pregnant mice were divided into three groups: Ringer's group, pSES group and RNAi­BMP4 group. In order to silence the BMP4 gene in the first generation (F1), 11.5 day pregnant mice were injected with the small interfering RNA BMP4 plasmid, pSES or Ringer's solution via the tail vein. Semi­quantitative reverse transcriptase­polymerase chain reaction (RT­PCR)and western blotting were employed to ensure the downregulation of BMP4. Finally, X­rays were performed following a barium enema. Aganglionosis was diagnosed by general anatomy and immunohistochemistry. Compared with the control group, transplacental RNAi was able to downregulate the BMP4­Smad4 of 11.5 day embryos, as determined by semi­quantitative RT­PCR and western blotting. The megacolons of the mice were demonstrated by X­ray and confirmed by general anatomy. Aganglionosis of colonic mucosa and submucosa were diagnosed by pathology, and immunohistochemistry. Knockdown of BMP4 in pregnant mice at the middle embryonic stage led to aganglionosis. It was therefore demonstrated that BMP­Smad was essential to the NCSCs of middle stage embryos. BMP­Smad served important roles in the generation of aganglionosis. This technique of knockdown BMP4 gene may be used to establish an aganglionosis mouse model.

Heterogeneous nuclear-transferred-embryos reconstructed with camel (Camelus bactrianus) skin fibroblasts and enucleated ovine oocytes and their development H-M.

This study reconstructed heterogeneous embryos using camel skin fibroblast cells as donor karyoplasts and ovine oocytes as recipient cytoplasts for investigating the developmental potential of the reconstructed embryos. Serum-starved adult camel skin fibroblast cells were used as donor somatic cells. Ovine oocytes matured in vitro were employed as recipient cytoplasts. The fusion of fibroblast cells into recipient cytoplasm was induced by electrofusion. The fused oocytes were activated by 5mM/ml inomycin with 2mM/ml 6-dimethylaminopurine (6-DMAP). The activated reconstructed embryos were co-cultured with ovine cumulus cells in synthetic oviduct fluid supplemented with amino acid (SOFaa) and 10% fetal calf serum (FCS) for 168h. A total of 300 enucleated ovine oocytes were available for xenonuclear embryo reconstruction. The results showed that 71% of the nuclear transfer couplets were successfully fused, 55% of the fused oocytes cleaved within 48h after activation, 82% of the cleaved oocytes developed to 2-16-cell embryo stages and 18% of the cleaved nuclear transfer zygotes developed to the morula stage. This study demonstrated that the xenonuclear transfer camel embryos can undergo the first embryonic division and subsequent development to morula stage in vitro.

Colorectal polyp model established by transplacental BMP4 RNAi.

Previous studies have shown that disruption of the bone morphogenetic protein (BMP) signaling pathway is an important cause of intestinal cancer in human and animal models. Thus, the purpose of this study was to construct a Balb/C model of colorectal polyps. Pregnant mice at 9.5 days gestation were injected via the tail vein with the pSES-Si BMP4 plasmid bearing a fluorochrome (DsRed) reporter, in order to silence the BMP4 gene in the first generation (F1); this group of mice was named the pSES-BMP4 group Intestinal fluorescence was detected at 1-, 4- and 8-week­old F1 mice, and reverse transcription-polymerase chain reaction (RT-PCR) and western-blotting assays were used to determine changes in the expression of BMP4. A dissecting microscope and hematoxylin and eosin (H&E) staining were used to observe the cell morphology and appearance of the polyps. DsRed fluorescence was observed in the intestines of 1-week-old F1 mice of the pSES-BMP4 group. BMP4 expression at the mRNA and protein level was reduced in 1-, 4- and 8-week-old F1 mice (P<0.05). However, the level of Smad4 mRNA was only reduced in 8-week-old F1 mice (P<0.05). Multiple hyperplasic polyps emerged in the colon and rectum of the intestines of 4-week-old F1 mice in the pSES-BMP4 group. The size of colorectal polyps increased at 8 weeks, when vessels and polyp pedicles became apparent. In conclusion, silencing of the BMP4 gene using transplacental RNAi injection can induce formation of colorectal polyps in mice.

Foveolar cell hyperplasia at the pyloric canal: an unusual cause of gastric outlet obstruction in 3 young children.

Foveolar cell hyperplasia (FCH) in the pylorus is rare in children. Between January 1993 and December 2008, 3 children with pyloric canal FCH presented with gastric outlet obstruction and/or anemia and underwent operation because a clear diagnosis could not be established with conservative management. The median age of the children was 18 months. The onset of FCH at the pyloric canal is problematic, and its diagnosis is difficult to make in pediatric patients. Exploratory laparotomy is a reasonable method of establishing the diagnosis and managing the condition.