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Background: Protein-tyrosine phosphatase MEG2 (MEG2) is a classic tyrosine-specific protein tyrosine phosphatase (PTP). It has been reported that MEG2 participates in the carcinogenesis of the breast and liver. However, functions of MEG2 in gastric cancer remain poorly understood. Methods: We examined the expression of MEG2 protein by western blotting and that of miR-181a-5p by qRT-PCR. We used bioinformatic analyses to search for miRNAs that potentially target MEG2. We performed a luciferase reporter assay to investigate the interaction between miR-181a-5p and MEG2. In addition, we assessed the effects of MEG2 and miR-181a-5p on gastric cancer cells in vitro and in vivo. Results: We found that MEG2 is downregulated in human gastric cancer and that miR-181a-5p is predicted to be a potential regulator of MEG2. We also observed that expression of MEG2 is reversely correlated with that of miR-181a-5p in gastric cancer. Moreover, we observed that MEG2 regulation by miR-181a-5p significantly suppresses the proliferation and migration of gastric cancer cells in vitro and decelerates tumour growth in vivo. Conclusions: Our results revealed that MEG2 is a tumour suppressor gene and negatively regulated by miR-181a-5p in gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Directed cell migration can be driven by a range of external stimuli, such as spatial gradients of: chemical signals (chemotaxis); adhesion sites (haptotaxis); or temperature (thermotaxis). Continuum models of cell migration typically include a diffusion term to capture the undirected component of cell motility and an advection term to capture the directed component of cell motility. However, there is no consensus in the literature about the form that the advection term takes. Some theoretical studies suggest that the advection term ought to include receptor saturation effects. However, others adopt a much simpler constant coefficient. One of the limitations of including receptor saturation effects is that it introduces several additional unknown parameters into the model. Therefore, a relevant research question is to investigate whether directed cell migration is best described by a simple constant tactic coefficient or a more complicated model incorporating saturation effects. Results: We study directed cell migration using an experimental device in which the directed component of the cell motility is driven by a spatial gradient of electric potential, which is known as electrotaxis. The electric field (EF) is proportional to the spatial gradient of the electric potential. The spatial variation of electric potential across the experimental device varies in such a way that there are several subregions on the device in which the EF takes on different values that are approximately constant within those subregions. We use cell trajectory data to quantify the motion of 3T3 fibroblast cells at different locations on the device to examine how different values of the EF influences cell motility. The undirected (random) motility of the cells is quantified in terms of the cell diffusivity, D, and the directed motility is quantified in terms of a cell drift velocity, v. Estimates D and v are obtained under a range of four different EF conditions, which correspond to normal physiological conditions. Our results suggest that there is no anisotropy in D, and that D appears to be approximately independent of the EF and the electric potential. The drift velocity increases approximately linearly with the EF, suggesting that the simplest linear advection term, with no additional saturation parameters, provides a good explanation of these physiologically relevant data. Conclusions: We find that the simplest linear advection term in a continuum model of directed cell motility is sufficient to describe a range of different electrotaxis experiments for 3T3 fibroblast cells subject to normal physiological values of the electric field. This is useful information because alternative models that include saturation effects involve additional parameters that need to be estimated before a partial differential equation model can be applied to interpret or predict a cell migration experiment. [ABSTRACT FROM AUTHOR]

Background: Accumulating evidence suggests the pro-inflammatory cytokine interleukin-6 (IL-6) in tumor microenvironment may promote the development of hepatocellular carcinoma (HCC). However, the underlying mechanism remains largely unknown. Methods: The expression and promoter activity of lncTCF7 were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and luciferase reporter assay. The function of the STAT3 binding site in the lncTCF7 promoter region was tested by luciferase reporter assay with nucleotide substitutions. The binding of STAT3 to the lncTCF7 promoter was confirmed by chromatin immunoprecipitation assay (CHIP) in vivo. The effects of decreasing STAT3 with small interference RNA and inhibiting STAT3 activation by small molecular inhibitor on lncTCF7 expression were also determined. Results: We demonstrate that IL-6 could induce lncTCF7 expression in a time- and dose-dependent manner, and we showed that IL-6 transcriptionally activated the expression of lncTCF7 in HCC cells by activating STAT3, a transcription activator which binds to promoter regions of lncTCF7. Furthermore, knocking-down STAT3 and inhibiting STAT3 activation reduced lncTCF7 expression. Importantly, RNA interference-based attenuation of lncTCF7 prevented IL-6-induced EMT and cell invasion. Conclusion: Thus, these data provides evidence to the existence of an aberrant IL-6/STAT3/ lncTCF7 signaling axis that leads to HCC aggressiveness through EMT induction, which could be novel therapeutic targets in malignancies. [ABSTRACT FROM AUTHOR]

Background: Amphiphilic poly(N-isopropylacrylamide)-block-poly(ε-caprolactone) (PNiPAAm-b-PCL) copolymers were synthesized by ring-opening polymerization to form thermosensitive micelles as nanocarriers for bioimaging and carboplatin delivery. Results: The critical micelle concentration increased from 1.8 to 3.5 mg/l following the decrease of the PNiPAAm chain length. The copolymers revealed a lower critical solution temperature (LCST) between 33 and 40°C. The copolymers self-assembled to form spherical particles of 146-199 nm in diameter. Carboplatin in micelles exhibited a slower release at 37°C relative to that at 25°C due to the gel layer formation on the micellar shell above the LCST. The micelles containing dye or carboplatin were intravenously injected into the rats for in vivo bioimaging and drug biodistribution. The bioimaging proiles showed a signiicant accumulation of micelles in the lungs. The micelles could minimize the reticuloendothelial system (RES) recognition of the dye. In vivo biodistribution demonstrated an improved pulmonary accumulation of carboplatin from 2.5 to 3.4 μg/mg by the micelles as compared to the control solution. Carboplatin accumulation in the heart and kidneys was reduced after encapsulation by the micelles. Conclusion: This study supports the potential of PNiPAAm-b-PCL micelles to passively target the lungs and attenuate RES uptake and possible side efects. [ABSTRACT FROM AUTHOR]

Background Type 2 diabetes is one of the most common causes of cardiovascular disease as it causes arterial stiffness changes. The purpose of this study is to characterize, in vivo, carotid arterial structural and functional changes by applying radio frequency and X-strain ultrasound techniques. Methods Ninety-one subjects were assigned into two groups; a diabetes group and a control group. Structural and functional changes in the common carotid arterial wall were investigated by quality intima-media thickness (QIMT), quality arterial stiffness (QAS), and X-strain analysis with a Mylab Twice ultrasound instrument. The relationships among variables between the two groups were analyzed in this study. Results There was no significant difference in carotid IMT (626.5 ± 169.1 μm vs. 568.5 ± 122.6 μm, P = 0.1506) between two groups. Pulse wave velocity (PWV) and stiffness index (β) were remarkably greater (8.388 ± 3.254 m/s vs. 7.269 ± 1.332 m/s; 12.51 ± 14.16 vs.9.279 ± 2.871), while compliance coefficient (CC) decreased significantly in the diabetes group (0.802 ± 0.3094 mm2/Kpa vs. 0.968 ± 0.3992 mm2/Kpa) (P < 0.05). The displacement difference of radial (RD-D), longitudinal (LD-D) and rotation (ROT-D) directions were significantly different between two groups' comparison (P = 0.0212, P = 0.0235 and P = 0.0072, respectively). The time of circumferential peak strain difference (CS-DT) and the time of radial peak strain rate (RSR-T) were found to be significantly different between the two groups (341.9 ± 77.56 ms vs. 369.0 ± 78.26 ms, P = 0.0494; 142.7 ± 22.43 ms vs. 136.2 ± 30.70 ms, P = 0.0474). CS-TD and RSR-T were also found to be positively correlated with CC value (r = 0.3908, P < 0.005 and r = 0.3027, P = 0.0326, respectively). Finally, PWV was negatively correlated with CC with (r = -0.6177, P < 0.001). Conclusions In type 2 diabetes, the functional changes in CCA can be identified using the methods presented in this article earlier than the structural changes. Arterial stiffness values provided by QAS and X-strain analysis can be used as indicators of CCA functional lesions in patients with type 2 diabetes. [ABSTRACT FROM AUTHOR]

Reverse cholesterol transport (RCT) has been characterized as a crucial step for antiatherosclerosis, which is initiated by ATPbinding cassette A1 (ABCA1) to mediate the efflux of cellular phospholipids and cholesterol to lipid-free apolipoprotein A-I (apoA-I). However, the mechanisms underlying apoA-I/ABCA1 interaction to lead to the lipidation of apoA-I are poorly understood. There are several models proposed for the interaction of apoA-I with ABCA1 as well as the lipidation of apoA-I mediated by ABCA1. ApoA-I increases the levels of ABCA1 protein markedly. In turn, ABCA1 can stabilize apoA-I. The interaction of apoA-I with ABCA1 could activate signaling molecules that modulate posttranslational ABCA1 activity or lipid transport activity. The key signaling molecules in these processes include protein kinase A (PKA), protein kinase C (PKC), Janus kinase 2 (JAK2), Rho GTPases and Ca2+, and many factors also could influence the interaction of apoA-I with ABCA1. This review will summarize these mechanisms for the apoA-I interaction with ABCA1 as well as the signal transduction pathways involved in these processes. [ABSTRACT FROM AUTHOR]

Atherosclerosis is characterized by a chronic inflammatory condition that involves numerous cellular and molecular inflammatory components. A wide array of inflammatory mediators, such as cytokines and proteins produced by macrophages and other cells, play a critical role in the development and progression of the disease. ATP-binding membrane cassette transporter A1 (ABCA1) is crucial for cellular cholesterol efflux and reverse cholesterol transport (RCT) and is also identified as an important target in antiatherosclerosis treatment. Evidence from several recent studies indicates that inflammation, along with other atherogenic- related mediators, plays distinct regulating roles in ABCA1 expression. Proatherogenic cytokines such as interferon (IFN)-γ and interleukin (IL)-1β have been shown to inhibit the expression of ABCA1, while antiatherogenic cytokines, including IL-10 and transforming growth factor (TGF)-β1, have been shown to promote the expression of ABCA1. Moreover, some cytokines such as tumor necrosis factor (TNF)-α seem to regulate ABCA1 expression in species-specific and dose-dependent manners. Inflammatory proteins such as C-reactive protein (CRP) and cyclooxygenase (COX)-2 are likely to inhibit ABCA1 expression during inflammation, and inflammation induced by lipopolysaccharide (LPS) was also found to block the expression of ABCA1. Interestingly, recent experiments revealed ABCA1 can function as an antiinflammatory receptor to suppress the expression of inflammatory factors, suggesting that ABCA1 may be the molecular basis for the interaction between inflammation and RCT. This review aims to summarize recent findings on the role of inflammatory cytokines, inflammatory proteins, inflammatory lipids, and the endotoxin-mediated inflammatory process in expression of ABCA1. Also covered is the current understanding of the function of ABCA1 in modulating the immune response and inflammation through its direct and indirect antiinflammatory mechanisms including lipid transport, high-density lipoprotein (HDL) formation and apoptosis. [ABSTRACT FROM AUTHOR]

Three Chinese patients suffered from severe lumbar spinal stenosis with debilitating symptoms due to a rare condition of ligamentum flavum cysts in the midline of the lumbar spine. This disease is distinct from synovial cyst of the facet joints or ganglion cysts, both intraoperatively and histopathologically. Magnetic Resonance imaging features of the ligamentum flavum cyst are also demonstrated. We share our surgical experiences of identification of the ligamentum flavum cysts, decompression and excision for two of the patients with demonstrably good recovery. This disease should be considered in the differential diagnosis of an extradural instraspinal mass in patients with lumbar spinal stenosis. [ABSTRACT FROM AUTHOR]

Paediatric supracondylar fractures of the femur are not common. The treatment options depend on the age of child, the site of the fracture, the pattern of injury and the surgeon's preference. We report a case of an 11-year old boy who sustained a comminuted displaced supracondylar fracture of the femur and was treated with indirect reduction and internal fixation with the Less Invasive Stabilization System (LISS) tibial plate. [ABSTRACT FROM AUTHOR]

Background: Amphiphilic poly(N-isopropylacrylamide)-block-poly(ε-caprolactone) (PNiPAAm-b-PCL) copolymers were synthesized by ring-opening polymerization to form thermosensitive micelles as nanocarriers for bioimaging and carboplatin delivery., Results: The critical micelle concentration increased from 1.8 to 3.5 mg/l following the decrease of the PNiPAAm chain length. The copolymers revealed a lower critical solution temperature (LCST) between 33 and 40°C. The copolymers self-assembled to form spherical particles of 146-199 nm in diameter. Carboplatin in micelles exhibited a slower release at 37°C relative to that at 25°C due to the gel layer formation on the micellar shell above the LCST. The micelles containing dye or carboplatin were intravenously injected into the rats for in vivo bioimaging and drug biodistribution. The bioimaging profiles showed a significant accumulation of micelles in the lungs. The micelles could minimize the reticuloendothelial system (RES) recognition of the dye. In vivo biodistribution demonstrated an improved pulmonary accumulation of carboplatin from 2.5 to 3.4 μg/mg by the micelles as compared to the control solution. Carboplatin accumulation in the heart and kidneys was reduced after encapsulation by the micelles., Conclusion: This study supports the potential of PNiPAAm-b-PCL micelles to passively target the lungs and attenuate RES uptake and possible side effects.

Three Chinese patients suffered from severe lumbar spinal stenosis with debilitating symptoms due to a rare condition of ligamentum flavum cysts in the midline of the lumbar spine. This disease is distinct from synovial cyst of the facet joints or ganglion cysts, both intraoperatively and histopathologically. Magnetic Resonance imaging features of the ligamentum flavum cyst are also demonstrated. We share our surgical experiences of identification of the ligamentum flavum cysts, decompression and excision for two of the patients with demonstrably good recovery. This disease should be considered in the differential diagnosis of an extradural instraspinal mass in patients with lumbar spinal stenosis.

Paediatric supracondylar fractures of the femur are not common. The treatment options depend on the age of child, the site of the fracture, the pattern of injury and the surgeon's preference. We report a case of an 11-year old boy who sustained a comminuted displaced supracondylar fracture of the femur and was treated with indirect reduction and internal fixation with the Less Invasive Stabilization System (LISS) tibial plate.

Background and Objective: Multinodular hepatocellular carcinoma(HCC) might originate from multicentric occurrence (MO) or intrahepatic metastasis(IM). This study was to find out proteins which play important roles in clonal origin of multinodular hepatocellular carcinoma bt screening the differentially expressed proteins between the MO and IM tissues using comparative proteomic analysis., Methods: Total protein extracted was separated by two-dimensional gel electrophoresis. Comparative analyses of the 2-DE protein patterns between the two groups were carried out using computerized imaging techniques. Proteins exhibiting significant alternations were subsequently isolated and identified by mass spectrometry., Results: A total 1025+/-52 and 900+/-98 spots were detected in the protein profile in IM and MO, respectively. Twenty-five protein spots were statistically different at expression levels between the two groups. Twenty of them were identified by MALDI-TOF-MS and bioinformatics., Conclusions: The protein profile of MO HCC tissues is different from that in IM HCC tissues. The twenty differentially expressed proteins might play a key role in the carcinogenesis and progression of multinodular HCC. These newly identified proteins might be potential and valuable biomarkers for identifying the multinodular HCC of clonal origin.

Study Design: A retrospective study was conducted to study the post operative upper limb palsy after laminoplasty for cervical myelopathy., Objective: To identify a reliable and simple preoperative radiological parameter in predicting the risk of post operative upper limb palsy., Background: Post operative upper limb palsy is one of the causes of patient dissatisfaction after surgery. There had been no simple, standard preoperative radiological parameters reliably predict the occurrence of this problem., Materials and Methods: Seventy-four patients received posterior cervical decompression from 1998 to 2008. Medical record and preoperative radiological information were evaluated. Clinical presentations of the palsy were described. The relationship between the occurrence of palsy and different preoperative radiological information is analyzed., Results: Eighteen patients (24.3%) presented with post operative upper limb palsy. Majority of patients presented with dysesthesia (17/18) and with deficit of the C5 segment (17/18). Ten patients presented with pure dysesthesia and 8 patients presented with mixed motor-sensory deficit and dysesthesia. Multilevel involvement was exclusively presented in patients with motor weakness. A longer duration of symptom (16.7 Vs 57.2 days) was noticed in patients in the motor deficit group. Average Pavlov ratio less then 0.65 (P = 0.027, Odds Ratio = 3.68) and compression at the C3/4 in preoperative MRI image (P = 0.025, Odds Ratio = 6) were significant risk factors for development of this problem., Conclusion: Post operative upper limb palsy is not uncommon and thorough preoperative explanation is important. There is a spectrum of clinical presentation and patients with multi-level involvement and motor deficit are associated with poorer prognosis. Average Pavlov ratio < 0.65 and compression at C3/4 segment on preoperative MRI image are simple and reliable preoperative predictor for the development of this problem.