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Modern lightweight woven fabric composite structures play an important role in industrial field. The occurrence and accumulation of structure damages can threaten the integrity of in-service structures. With the high damage sensitivity, guided wave-based structural health monitoring has been regarded as the effective tool for damage detection. In this study, a damage shape recognition algorithm has been developed to continuously identify the damage extent in composite woven fabric structures, which is necessary for further analysis of remaining life estimation. The proposed algorithm is established relying on the accurate guided wave propagation information and precise damage scattered wave sources identification, and consists of the following stages: guided wave velocity calculation, guided wave signals collection, damage location identification, extraction of time of flight (TOF), damage boundary estimation, noise points filtering and damage shape and size recognition. The semi-analytical finite element method is presented to model guided wave propagation in multi-ply woven fabric panels. The numerical predictions are experimentally validated using the novel omnidirectional wave velocity measurement of guided wave collected by mobile PZT transducer. The precise TOF extraction and noise point elimination method are first proposed for improving effectiveness of damage identification. The approach was validated by several cases of damage at arbitrary positions. The estimated numerical and experimental results show the potential of the proposed algorithm in identifying various damage features in anisotropic composite plates, such as its location, shape and size, and achieve good agreement with the actual damage. [ABSTRACT FROM AUTHOR]

Trastuzumab is currently used for patients with Her2+ advanced gastric cancer. However, the response rate to trastuzumab among the patients is low. The molecular mechanisms underlying trastuzumab resistance in gastric cancer are unknown. Our in vitro data show that activation of β2-adrenergic receptor (β2-AR) triggered by catecholamine caused "targeting failure" of trastuzumab in gastric cancer cells. The antitumor activities of trastuzumab were significantly impeded by chronic catecholamine stimulation in gastric cancer cells and in the mice bearing human gastric cancer xenografts. Mechanistically, catecholamine induced upregulation of the MUC4 expression at both transcription and protein levels via activating STAT3 and ERK. The effects of catecholamine could be effectively blocked by β2-AR antagonist ICI-118,551, indicating that β2-AR-mediated signaling pathway plays a key role in upregulation of MUC4, which was previously demonstrated to interfere with the recognition and physical binding of trastuzumab to Her2 molecules. Moreover, a significant elevation of the MUC4 level was observed in the xenograft tissues in nude mice chronically treated with isoproterenol. Knockdown of MUC4 restored the binding activities of trastuzumab to Her2-overexpressing gastric cancer cells. In addition, coexpression of β2-AR and MUC4 were observed in gastric cancer tissues. Our data indicated a novel trastuzumab resistance mechanism, by which catecholamine-induced β2-AR activation mediates desensitization of gastric cancer cells to trastuzumab through upregulating the MUC4 expression. [ABSTRACT FROM AUTHOR]

Objective(s): This study aimed to investigate the function of transient receptor potential vanilloid 1 (TRPV1) in regulating periodontal lesions. In addition, we explored the underlying mechanism of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway. Materials and Methods: Lipopolysaccharide (LPS) stimulation of human periodontal ligament cells (HPDLCs) was used to construct a periodontitis cell model, and experimental periodontitis (EP) rats were established by ligation. The mechanism by which TRPV1 regulates periodontitis was further verified by injecting the TRPV1 agonist capsaicin (CPS) and antagonist capsazepine (CPZ) into the gingiva of rats; the alveolar bone losses in each group were measured by stereomicroscopy. Realtime quantitative polymerase chain reaction (qRT-PCR) and Western blotting (WB) were used to research the expression of TRPV1 and proinflammatory cytokines, and WB was performed to test the phosphorylation of PI3K and AKT. Results: In vitro experiments showed that LPS induced the upregulation of TRPV1 and proinflammatory cytokines and promoted the phosphorylation of PI3K and AKT proteins in HPDLCs, which was consistent with their expression in the rat periodontitis model. Moreover, in vivo studies indicated that CPZ had anti-inflammatory effects through the PI3K/AKT pathway and inhibited bone loss induced by periodontal ligation in rats, while CPS had the opposite effect. Conclusion: TRPV1 was involved in the process of alveolar bone defects and the inflammatory response in rats with periodontitis induced by ligation. Its mechanism might be related to the phosphorylation of related proteins in the PI3K/AKT signaling pathway. [ABSTRACT FROM AUTHOR]

• Premise of the study: Tetracentron sinense (Trochodendraceae) is a Tertiary relict endemic to East Asia. Microsatellite markers were developed and characterized to investigate the population genetics of the species. • Methods and Results: Microsatellite markers were isolated from the genome of T. sinense using the protocol of Fast Isolation by AFLP of Sequences COntaining repeats (FIASCO). Eight polymorphic microsatellite markers were assessed in 44 samples collected from three wild populations. The number of alleles observed for each locus ranged from two to five. The observed and expected heterozygosities ranged from 0.0000 to 0.9375 and 0.0000 to 0.7681, respectively. • Conclusions: The microsatellite markers will be helpful in further studies of the population genetics and phylogeography of T. sinense. [ABSTRACT FROM AUTHOR]

Angiogenesis is an important factor in invasive tumor growth, progression, and metastasis. Multiple proangiogenic mechanisms are involved in tumor angiogenesis. In this study, we showed that the neurotransmitter norepinephrine upregulated VEGF (VEGFA) expression in breast cancer cells and that the culture supernatant from norepinephrine-treated breast cancer cells promoted the formation of the capillary-like network of endothelial cells. However, the effects of norepinephrine were further enhanced when the endothelial cells were cocultured with breast cancer cells, indicating a critical role of tumor cell-endothelial cell contacts in norepinephrine-induced tumor angiogenesis. Interestingly, norepinephrine dramatically induced the activation of the Notch pathway, which is a cell-contact-mediated intercellular signaling pathway and tightly linked to tumor cell-stromal cell interaction and angiogenesis, in the endothelial cells that had been cocultured with breast cancer cells. Furthermore, the expression of the Notch ligand Jagged 1 was significantly upregulated by norepinephrine at both mRNA and protein levels in breast cancer cells. Inhibitors of β2-adrenergic receptor (β2-AR), protein kinase A (PKA), and mTOR could reverse norepinephrine-induced Jagged 1 upregulation, indicating that the β2-AR-PKA-mTOR pathway participates in this process. Knockdown of Jagged 1 expression in breast cancer cells not only repressed norepinephrine- induced activation of the Notch pathway in cocultured endothelial cells but also evidently impaired the effects of norepinephrine on capillary-like sprout formation. These data demonstrate that tumor angiogenesis mediated by the Jagged 1/Notch intercellular signaling is governed by the norepinephrine-activated β2-AR-PKA-mTOR pathway. [ABSTRACT FROM AUTHOR]

Objective: To investigate the root and canal morphology of permanent mandibular anterior teeth in a Chongqing population using cone-beam computed tomography (CBCT).Methods: CBCT images of 1,725 patients in a Chongqing population were selected, and a total of 9,646 mandibular anterior teeth were analyzed. The number of root canals and the canal configurations were investigated.Results: In total, 0.3% (11/3,257) of lateral incisors and 0.8% (26/3,014) of canines had double roots, and 3.8% (127/3,375) of central incisors, 10.6% (345/3,257) of lateral incisors, and 4.2% (127/3,014) of canines had multi-root canals. The difference in the incidence of multi-canals in lateral incisors between female and male was statistically significant. The frequency of multi-canals in the different age groups was 5.0% for central incisors for ages 21-30 years, 14.7% for lateral incisors for ages 41-50 years, and 8.1% for canines for ages 41-50 years.Conclusion: With the limitations of the current study, we found that a high percentage of mandibular anterior teeth had multiple canals in the studied Chinese Chongqing population. The current data may provide clinicians practicing in Chongqing with a more thorough understanding of root canal morphology. [ABSTRACT FROM AUTHOR]

Background: Our previous studies show that β2-adrenergic receptor (β2-AR) is highly expressed in most Her2-overexpressing breast cancers. However, the mechanisms underlying upregulation of the β2-AR expression in Her2-overexpressing breast cancer cells are not fully understood. The clinical significance of the β2-AR overexpression in breast cancer is unclear.Methods: Human breast cancer cells MCF-7 and MCF-7/Her2 were transfected with the let-7 mimics or inhibitors. The expression of β2-AR was analyzed by Western blot. The β2-AR status in primary and metastatic sites of breast cancer and the human breast cancer tissue microarrays containing 49 primary tumors and 50 metastatic lymph node tissues was analyzed by immunohistochemistry. The correlation of lymph node metastasis with the β2-AR level was determined in 59 primary tumor tissues from the patients with Her2-positive breast cancer. The clinical prognostic significance of the β2-AR overexpression in the patients with Her2-positive breast cancers was evaluated by a retrospective study.Results: The let-7f level in Her2-overexpressing breast cancer cells SKBR3 and BT474 was significantly lower than that in MCF-7 cells, which express low level of Her2. Ectopic expression of Her2 in MCF-7 cells (MCF-7/Her2) represses the expression of microRNA let-7f, which is previously identified to regulate baseline β2-AR expression. The treatment with MEK1/2 inhibitors PD98059 or PD184352 effectively restored the let-7f level, suggesting that Her2-overexpression-mediated ERK constitutive activation inhibited let-7f, leading to the upregulation of the β2-AR expression. The transfection with the let-7f mimics markedly downregulated the β2-AR level, whereas the let-7 inhibitor significantly upregulated the β2-AR expression in both parental MCF-7 and MCF-7/Her2 cells. In addition, treatment of MCF-7/Her2 cells with isoproterenol resulted in a concentration-dependent reduction of the let-7f expression, demonstrating that the inhibitory effect of Her2 overexpression on let-7f can be reinforced by agonist-triggered β2-AR activation. We further demonstrate that high level of β2-AR associates with lymph node metastasis and poor outcome in the patients with Her2-positive breast cancer.Conclusions: The mutual and reciprocal interaction between Her2, β2-AR, and let-7f may maintain a high level of β2-AR in breast cancer cells. Our data suggest that β2-AR may be a new useful biomarker for predicting prognosis in Her2-positive breast cancer and may also be a promising selective therapeutic target for the aggressive subtype of breast cancer. [ABSTRACT FROM AUTHOR]

Background: Proteins overexpressed on the surface of tumor cells can be selectively targeted. Epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) are among the most often targeted proteins. The level and stability of expression in both primary tumors and corresponding metastases is crucial in the assessment of a receptor as target for imaging in nuclear medicine and for various forms of therapy. So far, the expression of EGFR and HER2 has only been determined in primary cervical cancers, and we have not found published data regarding the receptor status in corresponding metastatic lesions. The goal of this study was to evaluate whether any of these receptors are suitable as target for clinical diagnosis and therapy. Methods: Expression of EGFR and HER2 was investigated immunohistochemically in both lymph node metastases and corresponding primary cervical cancers (n = 53). HER2 and EGFR expression was scored using HercepTest criteria (0, 1+, 2+ or 3+). Results: EGFR overexpression (2+ or 3+) was found in 64% (35/53) of the primary cervical tumors and 60% (32/53) of the corresponding lymph node metastases. There was a good concordance between the primary tumors and the paired metastases regarding EGFR expression. Only four patients who had 2+ or 3+ in the primary tumors changed to 0 or 1+ in lymph node metastases, and another two cases changed the other way around. None of the primary tumors or the lymph node metastases expressed HER2 protein. Conclusion: The EGFR expression seems to be common and stable during cervical cancer metastasis, which is encouraging for testing of EGFR targeted radiotherapy. HER2 appears to be of poor interest as a potential target in the treatment of cervical cancer. [ABSTRACT FROM AUTHOR]