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Purpose: To determine the efficacy of probiotics in the treatment of rheumatoid arthritis (RA). Methods: Clinical trials were searched from online medicine databases. Outcomes such as changes in inflammatory cytokines and disability parameters such as American College of Rheumatology 20 % (ACR20) response, were analyzed. Results: Nine trials were eligible, and 385 patients were included. Meta-analysis showed that probiotic consumption significantly improved 28-joint disease activity (DAS28) score and decreased levels of high-sensitivity CRP (95 % CI = -3.23, -0.80; p = 0.001), tumor necrosis factor-α (95 % CI = -1.40, -0.67; p < 0.00001), interleukin (IL)-1β (95 % CI = -11.37, -0.84; p = 0.02) and IL-12 (95 % CI = -94.91, -53.58; p < 0.00001) in RA patients when compared with placebo. However, probiotics did not affect ACR20 response, erythrocyte sedimentation rate, IL-6, and IL-10, when compared with placebo. Conclusion: The effects of probiotic consumption on RA are very beneficial and have some reference significance for formulating treatment guidelines for RA. However, more trials are needed to confirm the influence of probiotics on RA patients. Furthermore, more clinical trials with larger sample sizes are needed to affirm the effectiveness of probiotics in mitigating disability and inflammatory status in RA patients. [ABSTRACT FROM AUTHOR]

An enhanced failure mode effect analysis (FMEA) based risk assessment for subsea compressor systems was proposed in this study. The enhanced model was established using a combination of fuzzy analytic hierarchy process (FAHP), fuzzy comprehensive evaluation, and FMEA. Different from the traditional FMEA model, the model improved the capability to identify system faults and to further measure the risk of a subsea compressor system through effective qualitative and quantitative analyses. A case study was then conducted to demonstrate the capability of the developed method in a complete risk assessment for a subsea compressor system and the subsystems and subcomponents with low reliabilities were identified. Comparing the enhanced model with previous models, it is found that the potential risks of some components are changed, and the components with higher potential risks in the system are identified. Sensitivity analysis to investigate the impact of parameters of subcomponents on system reliability was also performed. [ABSTRACT FROM AUTHOR]

Unmanned surface vehicles (USVs) are vessels that operate without any crew onboard. There is an increased demand for USVs in recent years, particularly for the use of water quality monitoring and ocean data mapping. In China, USVs are widely used as a luring fish boat which acts as the assisting boat of light luring seine vessel. One of the main problems of such boat is that the traditional propulsion system is poorly matched with the high energy consumption that is required during certain specific operation, which results in poor vessel performance. A hybrid electric propulsion systemconfiguration solution is proposed to increase the overall propulsion efficiency of such USVs. The typical operating profile was identified and a comprehensive simulation was conducted to demonstrate the compatibility during vessel operations. An intelligent equipment selection analysis was also carried out to recommend the optimal equipment selection by considering a multiobjective problem. The result shows that the configuration solution proposed can reduce fuel consumption and the optimal intelligent selection method can provide a suitable selection solution for decision makers. This article highlights an energy management strategy focusing on the threshold method based on support vector machine pattern recognition. A multiobjective particle swarm optimization algorithm based on the dynamic inertia weight and chaotic motion was used to optimize the equipment selection by considering fuel consumption and emissions. The proposed propulsion system configuration and equipment selection solution can be implemented for the design of USVs, which has a routine fixed operating pattern. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM), one of the most aggressive human malignant brain tumors, is induced by multiple complex pathological mechanisms. The main cause of mortality in patients with GBM is the invasion-metastasis cascade of tumor cells. The dysfunction of Parkinson protein 2 E3 ubiquitin protein ligase (PARK2) is closely linked with the development of certain human cancers. However, whether PARK2 is associated with metastasis in GBM remains unknown. The present study demonstrated that the metastasis and invasion of U87 cells were significantly repressed by PARK2 overexpression. Conversely, knockdown of PARK2 facilitated the metastasis and invasion of A172 cells. Furthermore, PARK2 downregulated zinc finger E-box-binding homeobox 1 (ZEB1) expression and mitigated epithelial-mesenchymal transition (EMT). Promoter effects of PARK2 knockdown on cell metastasis and EMT were antagonized by silencing ZEB1 expression. These results indicated that PARK2 participated in regulating the invasion-metastasis cascade of cancer cells by depressing ZEB1 expression and acting as a metastasis suppressor in GBM progression, providing a potential therapeutic approach for GBM treatment. [ABSTRACT FROM AUTHOR]

Hsp70 regulates α-Synuclein (α-Syn) degeneration in Parkinson's disease (PD), indicating that Hsp70 promotion may be able to prevent or reverse α-Syn-induced toxicity in PD. Additionally, it has been demonstrated that glutamine (Gln) enhances Hsp70 expression. In the present study, Gln-induced Hsp70 promotion in pheochromocytoma was investigated with reverse transcription-quantitative polymerase chain reaction and western blotting methods. Then it was observed whether heat shock factor (HSF)-1 was required for this phenomenon with an RNA interference strategy. The regulatory role of Gln on α-Syn degeneration was also determined in the α-Syn-overexpressed PC12 [PC12 (α-Syn+)] cells, which were treated with or without the proteasomal inhibitor lactacystin (Lac). The results demonstrated that treatment with =10 mM Gln significantly increased Hsp70 mRNA and protein levels (P<0.05) and that this promotion was HSF-1-dependent, as HSF-1 knockout with HSF-1-specific small interfering RNA abrogated Hsp70 promotion in PC12 (α-Syn+) cells. Furthermore, Gln treatment markedly upregulated α-Syn degeneration in PC12 (α-Syn+) cells, which was significantly reduced (P<0.05) in the presence of Lac. Therefore, the present study suggests that Gln is able to induce the promotion of Hsp70 expression in PC12 cells in an HSF-1-dependent manner and that Gln-mediated Hsp70 promotion may increase α-Syn degradation even in the presence of proteasomal inhibitor. Thus, glutamine may be a potential therapeutic agent to prevent α-Syn aggregation in PD. [ABSTRACT FROM AUTHOR]

N-myc downstream-regulated gene 1 (NDRG1) was previously shown to exhibit low expression in glioma tissue as compared with that in normal brain tissue; however, the role of NDRG1 in human glioma cells has remained to be elucidated. The present study used the U87 MG and SHG-44 human glioma cell lines as well as the normal human astrocyte cell line 1800, which are known to have differential NDRG1 expression. Small interfering (si)RNA targeting NDRG1, and NDRG1 overexpression vectors were transfected into the SHG-44 and U87 MG glioma cells, respectively. Cell proliferation, invasion, apoptosis and cell cycle arrest were subsequently examined by MTT assay, transwell chamber assay, flow cytometry and western blot analysis, respectively. Furthermore, a subcutaneous tumor mouse model was used to investigate the effects of NDRG1 on the growth of glioma cells in vivo. Overexpression of NDRG1 was shown to inhibit cell proliferation and invasion, and induce apoptosis in the U87 MG glioma cells, whereas NDRG1 downregulation increased proliferation, suppressed apoptosis and promoted invasion of the SHG-44 glioma cells. In addition, in the subcutaneous tumor mouse model, overexpression of NDRG1 in U-87 MG cells suppressed tumorigenicity in vivo. The findings of the present study indicated that NDRG1 is required for the inhibition of gliomagenesis; therefore, targeting NDRG1 and its downstream targets may represent novel therapies for the treatment of glioma. [ABSTRACT FROM AUTHOR]

Purpose Hippocampal sclerosis (HS), the most common feature of mesial temporal lobe epilepsy (MTLE), is widely accepted as surgical indication for refractory epilepsy. Pathological hallmarks in hippocampal dentate gyrus (DG), including granule cell loss (GCL) and granule cell dispersion (GCD), are known to be closely related to the status epilepticus and spontaneous seizure. Our aim was to assess the association between volumetric changes in the hippocampal CA4/DG determined with 3-Tesla (3 T) magnetic resonance imaging (MRI) and the postoperative seizure outcomes in MTLE patients with or without dentate gyrus pathology (DGP). Methods High-resolution T2- and T1-weighted three-dimensional (3D) MRI scans were performed on 39 MTLE patients before surgery with a 3 T Philips scanner. ITK-SNAP software was used for segmentation and volumetry of the CA4/DG segment, and NASP software was used for 3D reconstructions of the CA4/DG region. Immunostaining for Neuronal Nuclei (NeuN) was performed on resected hippocampal specimens after surgery to verify the accuracy of CA4/DG segmentation and histopathological changes in DG. Results The CA4/DG subfield could be precisely segmented with high-resolution 3 T MRI and confirmed by comparison of NeuN-immunoreactive slices with MRI results. MTLE patients with DGP showed smaller CA4/DG volume and favorable postoperative seizure outcomes. Conclusion The volumetry of CA4/DG was associated with the pathological changes in DG in MTLE patients. The volumetry of CA4/DG with preoperative 3 T MRI could predict the postoperative seizure outcomes in those patients. [ABSTRACT FROM AUTHOR]

In this study, we examined the effect of chronic administration of simvastatin immediately after status epilepticus (SE) on rat brain with temporal lobe epilepsy (TLE). First, we evaluated cytokines expression at 3 days post KA-lesion in hippocampus and found that simvastatin-treatment suppressed lesion-induced expression of interleukin (IL)-1b and tumor necrosis factora (TNF-a). Further, we quantified reactive astrocytosis using glial fibrillary acidic protein (GFAP) staining and neuron loss using Nissl staining in hippocampus at 4-6 months after KA-lesion. We found that simvastatin suppressed reactive astrocytosis demonstrated by a significant decrease in GFAP-positive cells, and attenuated loss of pyramidal neurons in CA3 and interneurons in dentate hilar (DH). We next assessed aberrant mossy fiber sprouting (MFS) that is known to contribute to recurrence of spontaneous seizure in epileptic brain. In contrast to the robust MFS observed in saline-treated animals, the extent of MFS was restrained by simvastatin in epileptic rats. Attenuated MFS was related to decreased neuronal loss in CA3 and DH, which is possibly a mechanism underlying decreased hippocampal susceptibility in animal treated with simvastatin. Electronic encephalography (EEG) was recorded during 4 to 6 months after KA-lesion. The frequency of abnormal spikes in rats with simvastatin-treatment decreased significantly compared to the saline group. In summary, simvastatin treatment suppressed cytokines expression and reactive astrocytosis and decreased the frequency of discharges of epileptic brain, which might be due to the inhibition of MFS in DH. Our study suggests that simvastatin administration might be a possible intervention and promising strategy for preventing SE exacerbating to chronic epilepsy. [ABSTRACT FROM AUTHOR]