Risk factors for subsidence in anterior cervical fusion with stand-alone polyetheretherketone (PEEK) cages: a review of 82 cases and 182 levels

INTRODUCTION: To determine risk factors for subsidence in patients treated with anterior cervical discectomy and fusion (ACDF) and stand-alone polyetheretherketone (PEEK) cages. MATERIALS AND METHODS: Records of patients with degenerative spondylosis or traumatic disc herniation resulting in radiculopathy or myelopathy between C2 and C7 who underwent ACDF with stand-alone PEEK cages were retrospectively reviewed. Cages were filled with autogenous cancellous bone harvested from iliac crest or hydroxyapatite. Subsidence was defined as a decrease of 3 mm or more of anterior or posterior disc height from that measured on the postoperative radiograph. Eighty-two patients (32 males, 50 females; 182 treatment levels) were included in the analysis. RESULTS: Most patients had 1–2 treatment levels (62.2 %), and 37.8 % had 3–4 treatment levels. Treatment levels were from C2–7. Of the 82 patients, cage subsidence occurred in 31 patients, and at 39 treatment levels. Multivariable analysis showed that subsidence was more likely to occur in patients with more than two treatment levels, and more likely to occur at treatment levels C5–7 than at levels C2–5. Subsidence was not associated with postoperative alignment change but associated with more disc height change (relatively oversized cage). CONCLUSION: Subsidence is associated with a greater number of treatment levels, treatment at C5–7 and relatively oversized cage use

The Research of Online Service Recovery Based on Kano’s Model

To identify customer requirements regarding e-retailing service failures, this study applied Kano’s model to sort the e-retailing compensation elements into various categories for identifying the key elements, maximizing customer satisfaction and minimizing customer dissatisfaction based on investigation of the sample of 167 e-retailing customers. The result indicates that a psychological compensation is the basic requirement of e-retailing customer and a refund can improve customer satisfaction when any service failure is occurred. Moreover, an economic compensation is indifferent for a dissatisfied customer. The result can help the e-retailer to understand what different compensations would have diverse effects on customers and provide effective guidelines to reduce customer’s dissatisfaction caused by the service failure

Tackling MARCKS-PIP3 circuit attenuates fibroblast activation and fibrosis progression.

Targeting activated fibroblasts, including myofibroblast differentiation, has emerged as a key therapeutic strategy in patients with idiopathic pulmonary fibrosis (IPF). However, there is no available therapy capable of selectively eradicating myofibroblasts or limiting their genesis. Through an integrative analysis of the regulator genes that are responsible for the activation of IPF fibroblasts, we noticed the phosphatidylinositol 4,5-bisphosphate (PIP2)-binding protein, myristoylated alanine-rich C-kinase substrate (MARCKS), as a potential target molecule for IPF. Herein, we have employed a 25-mer novel peptide, MARCKS phosphorylation site domain sequence (MPS), to determine if MARCKS inhibition reduces pulmonary fibrosis through the inactivation of PI3K/protein kinase B (AKT) signaling in fibroblast cells. We first observed that higher levels of MARCKS phosphorylation and the myofibroblast marker α-smooth muscle actin (α-SMA) were notably overexpressed in all tested IPF lung tissues and fibroblast cells. Treatment with the MPS peptide suppressed levels of MARCKS phosphorylation in primary IPF fibroblasts. A kinetic assay confirmed that this peptide binds to phospholipids, particularly PIP2, with a dissociation constant of 17.64 nM. As expected, a decrease of phosphatidylinositol (3,4,5)-trisphosphate pools and AKT activity occurred in MPS-treated IPF fibroblast cells. MPS peptide was demonstrated to impair cell proliferation, invasion, and migration in multiple IPF fibroblast cells in vitro as well as to reduce pulmonary fibrosis in bleomycin-treated mice in vivo. Surprisingly, we found that MPS peptide decreases α-SMA expression and synergistically interacts with nintedanib treatment in IPF fibroblasts. Our data suggest MARCKS as a druggable target in pulmonary fibrosis and also provide a promising antifibrotic agent that may lead to effective IPF treatments.-Yang, D. C., Li, J.-M., Xu, J., Oldham, J., Phan, S. H., Last, J. A., Wu, R., Chen, C.-H. Tackling MARCKS-PIP3 circuit attenuates fibroblast activation and fibrosis progression

An UML-XML-RDB Model Mapping Solution for Facilitating Information Standardization and Sharing

Abstract: To facilitate information standardization and sharing in Construction Industry, this paper presents a simple but effective approach that maps the UML (Unified Modeling Language) object-oriented information model related to a construction project to an XML schema, then to a Relational DataBase (RDB) schema. First of all, the mapping between UML model and XML schema is discussed since UML has been a popular tool to model the static structure and dynamic behaviors of the information and processes in a construction project, while XML has become a de-facto standard for information sharing and exchange. Then, a set of consistent rules for mapping from XML schema to RDB's Entity-Relational (E-R) model are studied and established since RDB has been the most popular choice for information management. The present study focuses on making the set of rules simple and easy-to-implement for most applications in construction industry. Finally, a mapping tool for automatically generating RDB schemas from XML Schemas is developed

Novel variant Pro143Ala in HTRA2 contributes to Parkinson’s disease by inducing hyperphosphorylation of HTRA2 protein in mitochondria

Mutations in the gene encoding the mitochondrial protein high temperature requirement A2 (HTRA2) are inconsistently associated with a risk of Parkinson’s disease (PD). We assessed the presence of HTRA2 mutations among patients with PD and performed functional assay of identified mutations or variants. Among the total 1,373 subjects, the entire HTRA2 coding region was sequenced in 113 early-onset PD (EOPD), 20 familial PD patients and 150 control subjects. An additional 390 sporadic late-onset PD patients and 700 controls were subsequently screened to validate possible mutations found in the first set. We identified two novel heterozygous variants, c.427C > G (Pro143Ala) and c.906 +3 G > A, in 2 (1.5%) EOPD patients. The missense variant, Pro143Ala, was also observed in one late-onset PD patient but was absent in total 850 control subjects (relative risk 2.3, 95% CI 1.5–2.8, P = 0.04). Expressing Pro143Ala variant of HTRA2 in primary dopaminergic neurons causes neurite degeneration. Following exposure to rotenone, the ultra-structural mitochondrial abnormality, the percentage of mitochondrial dysfunction and apoptosis in cells carrying the HTRA2 Pro143Ala variant was significantly higher than wild-type cells. Mechanistically, protein level of phosphorylated HTRA2 was increased in cells carrying the Pro143Ala variant, suggesting Pro143Ala variant promotes HTRA2 phosphorylation with resultant mitochondrial dysfunction. Our results support a biologically relevant role of HTRA2 in PD susceptibility in Taiwanese. Further large-scale association studies are warranted to confirm the role of HTRA2 Pro143Ala variant in the risk of PD