To avoid the irregularities during the level set evolution, a fractional distance regularized variational model is proposed for image segmentation. We first define a fractional distance regularization term which punishes the deviation of the level set function (LSF) and the signed distance function. Since the fractional derivative of the constant value function outside the starting point is nonzero, the fractional gradient modular of the LSF does not approach infinity where the integer order gradient modular is close to 0. This prevents the sharp reverse diffusion of LSF in flat areas and ensures the smooth evolution of LSF. Then, we use the Grünwald-Letnikov (G-L) fractional derivative to derive the discrete forms of the conjugate of fractional derivatives and fractional divergence. To facilitate the calculation of fractional derivatives and their conjugates, we designed their covering templates. Finally, a numerical solution to the minimization of the energy functional is obtained from these discrete forms and covering templates. Numerical experiments of medical images with different modalities show that the model in this paper can well segment weak images and intensity inhomogeneity images.
A series of quinoline oligoamide foldamers bearing a β-pinene-derived pyridyl group at the N-terminus or the C-terminus were synthesized, and the efficiencies of chiral inductions have been evaluated by H NMR and CD spectra. The chiral inductions were quantitative when chiral pyridyl acid was appended at the N-terminus, but were inferior when chiral pyridyl amine was appended at the C-terminus. Unexpectedly, N-oxidation on the pyridine ring at the C-terminus does not notably enhance the chiral induction efficiency in spite of the presence of three-center hydrogen bonds.
Background/Aims: Osteoarthritis (OA) is the prevalent degenerative disease caused by various factors. MicroRNAs are important regulators in the inflammation and immune response. The aim of this study was to investigate the effect of microRNA-34a (MiR-34a) on the death of chondrocytes, senescence, as well as its role in OA progression. Methods: A series of experiments involving CCK-8, flow cytometry, β-galactosidase staining and wound healing assays were conducted to determine the cellular capabilities of proliferation, cell apoptosis, senescence and the ability of cells to recover from injury, respectively. Binding sites between miR-34a and delta-like protein 1 (DLL1) were identified using a luciferase reporter system, whereas mRNA and protein expression of target genes was determined by RT-PCR and immunoblot, respectively. OA model was generated via surgery. Results: We found that miR-34a expression was increased in the cartilage of OA patients. In rat chondrocytes and chondrosarcoma cells, miR-34a transfections noticeably inhibited the expression of DLL1, triggered cell death and senescence, suppressed proliferation, and prevented scratch assay wound closure. However, transfection of a miR-34a inhibitor displayed adverse effects. Additionally, secretion and expression of factors associated with cartilage degeneration were altered via miR-34a. Moreover, miR-34a directly inhibits DLL1 mRNA. Furthermore, concentrations of DLL1, total PI3K, and p-AKT declined in chondrocytes that overexpress miR-34a. DLL1 overexpression elevated PI3K and p-AKT levels, and eliminated cell death triggered by a miR-34a mimic. In vivo, miR-34a remarkably inhibited miR-34a up-regulation, while enhanced the level of DLL1 expression. In the knee joints of surgery-induced OA rats, articular chondrocyte death and loss of cartilage were attenuated via miR-34a antagomir injection. Conclusions: These findings indicate that miR-34a contributes to chondrocyte death, causing OA progression through DLL1 and modulation of the PI3K/AKT pathway.
When S- or R- oxazolylaniline
enantiomers were attached to achiral quinoline oligoamide foldamers
(QOFs), a single diastereomerically pure P- or M-handed foldamer was
observed and exhibits negative or positive circularly polarized luminescence
with the emission dissymmetry factors |g
lum| up to 0.038, which is significantly larger than that of QOF with
incomplete chiral induction. More importantly, the CPL dissymmetry
factors, together with the absorption dissymmetry factors, are enhanced
with increases in the lengths of QOFs.
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