The academic thinking based on the perspective of fashion design

With the contemporary socio-economic, political, and cultural diversity, Fashion Design leads us toward a broader field rapidly. Under the "people-oriented" principle, Fashion design which integrating the design concept of multi-angle, multi-paradigm and multi-aspect should be on the stand of severing people so as to meet people\u27s physiological and mental needs and to enrich people\u27s spiritual and material life for the purpose. It further opens up a new vision for Modern fashion frontier and will be bound to the clothing design practice

Incorporating a Local Binary Fitting Model into a Maximum Regional Difference Model for Extracting Microscopic Information under Complex Conditions

This paper presents a novel region-based method for extracting useful information from microscopic images under complex conditions. It is especially used for blood cell segmentation and statistical analysis. The active model detects several inner and outer contours of an object from its background. The method incorporates a local binary fitting model into a maximum regional difference model. It utilizes both local and global intensity information as the driving forces of the contour model on the principle of the largest regional difference. The local and global fitting forces ensure that local dissimilarities can be captured and globally different areas can be segmented, respectively. By combining the advantages of local and global information, the motion of the contour is driven by the mixed fitting force, which is composed of the local and global fitting term in the energy function. Experiments are carried out in the laboratory, and results show that the novel model can yield good performances for microscopic image analysis

Bis[2,4-dibromo-6-(n-propyl­imino­methyl)phenolato-κ2 N,O]cobalt(II)

In the title complex, [Co(C10H10Br2NO)2], the CoII atom lies on a twofold rotation axis, the N2O2 units having distorted tetra­hedral coordination environments comprising two bidentate chelate 2,4-dibromo-6-(n-propyl­imino­meth­yl)phenolate Schiff base ligands [Co—N = 1.989 (3) Å, Co—O = 1.924 (2) Å and O/N—Co—O/N = 94.53 (10)–125.40 (15)°]. In the crystal structure, the mol­ecules are linked via weak inter­molecular C—H⋯O hydrogen bonds [3.334 (5) Å] and there are also short inversion-related intermolecular Br⋯Br contacts [3.4263 (6) Å

Bis[2,4-dibromo-6-(ethyl­imino­methyl)phenolato-κ2 N,O]cobalt(II)

In the title compound, [Co(C9H8Br2NO)2], the CoII atom, located on a twofold axis, is in a pseudo-tetra­hedral environment, with two bidentate 2,4-dibromo-6-(ethyl­imino­meth­yl)phenolate Schiff base ligands acting as chelates through their phenolate O and azomethine N atoms. C—H⋯O hydrogen bonds link the complex mol­ecules to form a chain parallel to the b axis

Suppression of MyD88-dependent signaling alleviates neuropathic pain induced by peripheral nerve injury in the rat

Abstract Background MyD88 is the adaptor protein of MyD88-dependent signaling pathway of TLRs and IL-1 receptor and regulates innate immune response. However, it was not clear whether and how MyD88 and related signaling pathways in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH) are involved in neuropathic pain. Methods Chronic constriction injury (CCI) was used to induce neuropathic pain in the rat. The expression of MyD88, TRIF, IBA1, and GFAP was detected with immunofluorescent staining and Western blot. The expression of interleukin-1 beta (IL-1β), high mobility group box 1 (HMGB1), NF-κB-p65, phosphorylated NF-κB-p65, ERK, phosphorylated ERK, and tumor necrosis factor-alpha (TNF-α) was detected with Western blot. Pain-related behavioral effects of MyD88 homodimerization inhibitory peptide (MIP) were accessed up to 3 weeks after intrathecal administration. Results Peripheral nerve injury significantly increased the protein level of MyD88 in the DRG and SDH, but had no effect on TRIF. MyD88 was found partly distributed in the nociceptive neurons in the DRGs and the astrocytes and microglia in the SDH. HMGB1 and IL-1β were also found upregulated in nociceptive pathways of CCI rats. Intrathecal application of MIP significantly alleviated mechanical and thermal hyperalgesia in the CCI rats and also reversed CCI-induced upregulation of MyD88 in both DRG and SDH. Further investigation revealed that suppression of MyD88 protein reduced the release of TNF-α and glial activation in the SDH in the CCI rats. Conclusions MyD88-dependent TIR pathway in the DRG and SDH may play a role in CCI-induced neuropathic pain. MyD88 might serve as a potential therapeutic target for neuropathic pain

Maslinic acid potentiates the anti-tumor activity of tumor necrosis factor α by inhibiting NF-κB signaling pathway

<p>Abstract</p> <p>Background</p> <p>Tumor necrosis factor alpha (TNFα) has been used to treat certain tumors in clinic trials. However, the curative effect of TNFα has been undermined by the induced-NF-κB activation in many types of tumor. Maslinic acid (MA), a pharmacological safe natural product, has been known for its important effects as anti-oxidant, anti-inflammatory, and anti-viral activities. The aim of this study was to determine whether MA potentiates the anti-tumor activity of TNFα though the regulation of NF-κB activation.</p> <p>Results</p> <p>In this study, we demonstrate that MA significantly enhanced TNFα-induced inhibition of pancreatic cancer cell proliferation, invasion, and potentiated TNFα-induced cell apoptosis by suppressing TNFα-induced NF-κB activation in a dose- and time-dependent manner. Addition of MA inhibited TNFα-induced IκBα degradation, p65 phosphorylation, and nuclear translocation. Furthermore, MA decreased the expression levels of NF-κB-regulated genes, including genes involved in tumor cell proliferation (Cyclin D1, COX-2 and c-Myc), apoptosis (Survivin, Bcl-2, Bcl-xl, XIAP, IAP-1), invasion (MMP-9 and ICAM-1), and angiogenesis (VEGF). In athymic nu/nu mouse model, we further demonstrated that MA significantly suppressed pancreatic tumor growth, induced tumor apoptosis, and inhibited NF-κB-regulated anti-apoptotic gene expression, such as Survivin and Bcl-xl.</p> <p>Conclusions</p> <p>Our data demonstrate that MA can potentiate the anti-tumor activities of TNFα and inhibit pancreatic tumor growth and invasion by activating caspase-dependent apoptotic pathway and by suppressing NF-κB activation and its downstream gene expression. Therefore, MA together with TNFα could be new promising agents in the treatment of pancreatic cancer.</p

Celecoxib ameliorates diabetic sarcopenia by inhibiting inflammation, stress response, mitochondrial dysfunction, and subsequent activation of the protein degradation systems

Aim: Diabetic sarcopenia leads to disability and seriously affects the quality of life. Currently, there are no effective therapeutic strategies for diabetic sarcopenia. Our previous studies have shown that inflammation plays a critical role in skeletal muscle atrophy. Interestingly, the connection between chronic inflammation and diabetic complications has been revealed. However, the effects of non-steroidal anti-inflammatory drug celecoxib on diabetic sarcopenia remains unclear.Materials and Methods: The streptozotocin (streptozotocin)-induced diabetic sarcopenia model was established. Rotarod test and grip strength test were used to assess skeletal muscle function. Hematoxylin and eosin and immunofluorescence staining were performed to evaluate inflammatory infiltration and the morphology of motor endplates in skeletal muscles. Succinate dehydrogenase (SDH) staining was used to determine the number of succinate dehydrogenase-positive muscle fibers. Dihydroethidium staining was performed to assess the levels of reactive oxygen species (ROS). Western blot was used to measure the levels of proteins involved in inflammation, oxidative stress, endoplasmic reticulum stress, ubiquitination, and autophagic-lysosomal pathway. Transmission electron microscopy was used to evaluate mitophagy.Results: Celecoxib significantly ameliorated skeletal muscle atrophy, improving skeletal muscle function and preserving motor endplates in diabetic mice. Celecoxib also decreased infiltration of inflammatory cell, reduced the levels of IL-6 and TNF-α, and suppressed the activation of NF-κB, Stat3, and NLRP3 inflammasome pathways in diabetic skeletal muscles. Celecoxib decreased reactive oxygen species levels, downregulated the levels of Nox2 and Nox4, upregulated the levels of GPX1 and Nrf2, and further suppressed endoplasmic reticulum stress by inhibiting the activation of the Perk-EIF-2α-ATF4-Chop in diabetic skeletal muscles. Celecoxib also inhibited the levels of Foxo3a, Fbx32 and MuRF1 in the ubiquitin-proteasome system, as well as the levels of BNIP3, Beclin1, ATG7, and LC3Ⅱ in the autophagic-lysosomal system, and celecoxib protected mitochondria and promoted mitochondrial biogenesis by elevating the levels of SIRT1 and PGC1-α, increased the number of SDH-positive fibers in diabetic skeletal muscles.Conclusion: Celecoxib improved diabetic sarcopenia by inhibiting inflammation, oxidative stress, endoplasmic reticulum stress, and protecting mitochondria, and subsequently suppressing proteolytic systems. Our study provides evidences for the molecular mechanism and treatment of diabetic sarcopenia, and broaden the way for the new use of celecoxib in diabetic sarcopenia

Myocardial Motion Analysis for Determination of Tei-Index of Human Heart

The Tei index, an important indicator of heart function, lacks a direct method to compute because it is difficult to directly evaluate the isovolumic contraction time (ICT) and isovolumic relaxation time (IRT) from which the Tei index can be obtained. In this paper, based on the proposed method of accurately measuring the cardiac cycle physical phase, a direct method of calculating the Tei index is presented. The experiments based on real heart medical images show the effectiveness of this method. Moreover, a new method of calculating left ventricular wall motion amplitude is proposed and the experiments show its satisfactory performance