Molecular cloning and sequence analysis of the cat myostatin gene 5´ regulatory region

Cat is an important experimental and pet animal and plays a key role in keeping ecological balance. Myostatin is a negative regulator of skeletal muscle growth and development in mammals, but the gene sequence of it keeps unknown in cat. To better understand the structure and function of the myostatin promoter in cat, a 1409 bp fragment containing the 5'-regulatory region of the cat myostatin gene was cloned and sequenced (GenBank accession number is GU938462). Many potential transcription factor binding sites have been found by the bioinformatics analysis, such as TATA boxes, CAAT box, E-boxes, MEF2, MEF3, MTBF, PAX3, SMAD, HBOX, HOMF and TEAF motifs. Comparative analysis for some motifs showed both conservations and differences among cat, horse, porcine and human.Key words: Cat, myostatin 5'-regulatory region, molecular cloning, sequence analysis and comparison, transcription factor binding sites

Nasopharyngeal Carcinoma Metastatic to the Mandible

Nasopharyngeal carcinoma (NPC) is one of the most common malignancies in the head and neck region, especially among those of Chinese origin. NPC has multifactorial aetiologies including genetic susceptibility, consumption of food with high salt content, and the Epstein–Barr virus. The primary tumour usually arises from the lateral walls of the nasopharynx and is characterized by a rich sub-mucosal lymphatic structure, often leading to cervical lymph node metastasis. Distant metastasis has been recognized to be a major cause of treatment failure in patients with nasopharyngeal carcinoma. Bone, liver and lung are the most frequent sites of NPC metastases

Vav3 oncogene activates estrogen receptor and its overexpression may be involved in human breast cancer

<p>Abstract</p> <p>Background</p> <p>Our previous study revealed that Vav3 oncogene is overexpressed in human prostate cancer, activates androgen receptor, and stimulates growth in prostate cancer cells. The current study is to determine a potential role of Vav3 oncogene in human breast cancer and impact on estrogen receptor a (ERα)-mediated signaling axis.</p> <p>Methods</p> <p>Immunohistochemistry analysis was performed in 43 breast cancer specimens and western blot analysis was used for human breast cancer cell lines to determine the expression level of Vav3 protein. The impact of Vav3 on breast cancer cell growth was determined by siRNA knockdown of Vav3 expression. The role of Vav3 in ERα activation was examined in luciferase reporter assays. Deletion mutation analysis of Vav3 protein was performed to localize the functional domain involved in ERα activation. Finally, the interaction of Vav3 and ERα was assessed by GST pull-down analysis.</p> <p>Results</p> <p>We found that Vav3 was overexpressed in 81% of human breast cancer specimens, particularly in poorly differentiated lesions. Vav3 activated ERα partially via PI3K-Akt signaling and stimulated growth of breast cancer cells. Vav3 also potentiated EGF activity for cell growth and ERα activation in breast cancer cells. More interestingly, we found that Vav3 complexed with ERα. Consistent with its function for AR, the DH domain of Vav3 was essential for ERα activation.</p> <p>Conclusion</p> <p>Vav3 oncogene is overexpressed in human breast cancer. Vav3 complexes with ERα and enhances ERα activity. These findings suggest that Vav3 overexpression may aberrantly enhance ERα-mediated signaling axis and play a role in breast cancer development and/or progression.</p

What's wrong with the murals at the Mogao Grottoes : a near-infrared hyperspectral imaging method

Although a significant amount of work has been performed to preserve the ancient murals in the Mogao Grottoes by Dunhuang Cultural Research, non-contact methods need to be developed to effectively evaluate the degree of flaking of the murals. In this study, we propose to evaluate the flaking by automatically analyzing hyperspectral images that were scanned at the site. Murals with various degrees of flaking were scanned in the 126th cave using a near-infrared (NIR) hyperspectral camera with a spectral range of approximately 900 to 1700 nm. The regions of interest (ROIs) of the murals were manually labeled and grouped into four levels: normal, slight, moderate, and severe. The average spectral data from each ROI and its group label were used to train our classification model. To predict the degree of flaking, we adopted four algorithms: deep belief networks (DBNs), partial least squares regression (PLSR), principal component analysis with a support vector machine (PCA + SVM) and principal component analysis with an artificial neural network (PCA + ANN). The experimental results show the effectiveness of our method. In particular, better results are obtained using DBNs when the training data contain a significant amount of striping noise

Decreased Autocrine EGFR Signaling in Metastatic Breast Cancer Cells Inhibits Tumor Growth in Bone and Mammary Fat Pad

Breast cancer metastasis to bone triggers a vicious cycle of tumor growth linked to osteolysis. Breast cancer cells and osteoblasts express the epidermal growth factor receptor (EGFR) and produce ErbB family ligands, suggesting participation of these growth factors in autocrine and paracrine signaling within the bone microenvironment. EGFR ligand expression was profiled in the bone metastatic MDA-MB-231 cells (MDA-231), and agonist-induced signaling was examined in both breast cancer and osteoblast-like cells. Both paracrine and autocrine EGFR signaling were inhibited with a neutralizing amphiregulin antibody, PAR34, whereas shRNA to the EGFR was used to specifically block autocrine signaling in MDA-231 cells. The impact of these was evaluated with proliferation, migration and gene expression assays. Breast cancer metastasis to bone was modeled in female athymic nude mice with intratibial inoculation of MDA-231 cells, and cancer cell-bone marrow co-cultures. EGFR knockdown, but not PAR34 treatment, decreased osteoclasts formed in vitro (p<0.01), reduced osteolytic lesion tumor volume (p<0.01), increased survivorship in vivo (p<0.001), and resulted in decreased MDA-231 growth in the fat pad (p<0.01). Fat pad shEGFR-MDA-231 tumors produced in nude mice had increased necrotic areas and decreased CD31-positive vasculature. shEGFR-MDA-231 cells also produced decreased levels of the proangiogenic molecules macrophage colony stimulating factor-1 (MCSF-1) and matrix metalloproteinase 9 (MMP9), both of which were decreased by EGFR inhibitors in a panel of EGFR-positive breast cancer cells. Thus, inhibiting autocrine EGFR signaling in breast cancer cells may provide a means for reducing paracrine factor production that facilitates microenvironment support in the bone and mammary gland

Cathepsin S Deficiency Results in Abnormal Accumulation of Autophagosomes in Macrophages and Enhances Ang II–Induced Cardiac Inflammation

BACKGROUND: Cathepsin S (Cat S) is overexpressed in human atherosclerotic and aneurysmal tissues and may contributes to degradation of extracellular matrix, especially elastin, in inflammatory diseases. We aimed to define the role of Cat S in cardiac inflammation and fibrosis induced by angiotensin II (Ang II) in mice. METHODS AND RESULTS: Cat S-knockout (Cat S(-/-)) and littermate wild-type (WT) C57BL/6J mice were infused continuously with Ang II (750 ng/kg/min) or saline for 7 days. Cat S(-/-) mice showed severe cardiac fibrosis, including elevated expression of collagen I and α-smooth muscle actin (α-SMA), as compared with WT mice. Moreover, macrophage infiltration and expression of inflammatory cytokines (tumor necrosis factor α, transforming growth factor β and interleukin 1β) were significantly greater in Cat S(-/-) than WT hearts. These Ang II-induced effects in Cat S(-/-) mouse hearts was associated with abnormal accumulation of autophagosomes and reduced clearance of damaged mitochondria, which led to increased levels of reactive oxygen species (ROS) and activation of nuclear factor-kappa B (NF-κB) in macrophages. CONCLUSION: Cat S in lysosomes is essential for mitophagy processing in macrophages, deficiency in Cat S can increase damaged mitochondria and elevate ROS levels and NF-κB activity in hypertensive mice, so it regulates cardiac inflammation and fibrosis

Co-Inoculation with Rhizobia and AMF Inhibited Soybean Red Crown Rot: From Field Study to Plant Defense-Related Gene Expression Analysis

Background: Soybean red crown rot is a major soil-borne disease all over the world, which severely affects soybean production. Efficient and sustainable methods are strongly desired to control the soil-borne diseases. Principal Findings: We firstly investigated the disease incidence and index of soybean red crown rot under different phosphorus (P) additions in field and found that the natural inoculation of rhizobia and arbuscular mycorrhizal fungi (AMF) could affect soybean red crown rot, particularly without P addition. Further studies in sand culture experiments showed that inoculation with rhizobia or AMF significantly decreased severity and incidence of soybean red crown rot, especially for coinoculation with rhizobia and AMF at low P. The root colony forming unit (CFU) decreased over 50 % when inoculated by rhizobia and/or AMF at low P. However, P addition only enhanced CFU when inoculated with AMF. Furthermore, root exudates of soybean inoculated with rhizobia and/or AMF significantly inhibited pathogen growth and reproduction. Quantitative RT-PCR results indicated that the transcripts of the most tested pathogen defense-related (PR) genes in roots were significantly increased by rhizobium and/or AMF inoculation. Among them, PR2, PR3, PR4 and PR10 reached the highest level with co-inoculation of rhizobium and AMF. Conclusions: Our results indicated that inoculation with rhizobia and AMF could directly inhibit pathogen growth and reproduction, and activate the plant overall defense system through increasing PR gene expressions. Combined wit

Determination of the number of J/ψ events with J/ψ → inclusive decays

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