RFID-enabled real-time manufacturing execution system for discrete manufacturing: Software design and implementation

Discrete manufacturing (DM) refers to produce products in non-sequential processes so as to respond to market and customer requirements quickly under limited lead-time. However, in shop-floor management, DM companies usually confront challenges such as information gaps between different manufacturing units, slow responsiveness to customer changes, and poor visualization. The main reasons are lacking of efficient manufacturing data collection manners and software to support shop-floor management. This paper introduces an RFID-enabled real-time manufacturing execution system (RT-MES) for improving DM shop-floor management level in the perspective of illustrating the RT-MES software design and implementation. Several contributions from this paper are significant. First, a framework of RFID-enabled RT-MES is proposed, which is generic and helpful for enterprise information system (EIS) construction. Second, a plug-universal database-aided design (PUDAD) concept and its realization are elaborated, which could reduce RT-MES development and implementation cycle. Third, an interface middleware is reported to enable RT-MES real-time intercommunication with other EISs such as SAP ERP. Fourth, a real-life case study describes how RT-MES to enhance a typical DM firm's shop-floor management, which can be referenced by other DM companies when they initiate and implement RFID-enabled solutions. © 2011 IEEE.published_or_final_versionThe 2011 IEEE International Conference on Networking, Sensing and Control (ICNSC 2011), Delft, the Netherlands, 11-13 April 2011. In Proceedings of ICNSC, 2011, p. 311-31

Cardiac tissue regeneration: A preliminary study on carbon-based nanotubes gelatin scaffold

The aim of this study was set-up and test of gelatin and carbon nanotubes scaffolds. Gelatin-based (5%) genipin cross-linked (0.2%) scaffolds embedding single-walled carbon nanotubes (SWCNTs, 0.3, 0.5, 0.7, 0.9, and 1.3% w/w) were prepared and mechanically/electrically characterized. For biological evaluation, H9c2 cell line was cultured for 10 days. Cytotoxicity, cell growth and differentiation, immunohistochemistry, and real-time PCR analysis were performed. Myoblast and cardiac differentiation were obtained by serum reduction to 1% (C1%) and stimulation with 50 nM all trans-retinoic acid (CRA), respectively. Immunohistochemistry showed elongated myotubes in C1%while round and multinucleated cells in CRAwith also a significantly increased expression of natriuretic peptides (NP) and ET-1 receptors in parallel with a decreased ET-1. On scaffolds, cell viability was similar for Gel-SWCNT0.3%/0.9%; NP and ET systems expression decreased in both concentrations with respect to control and CX-43, mainly due to a lacking of complete differentiation in cardiac phenotype during that time. Although further analyses on novel biomaterials are necessary, these results represent a useful starting point to develop new biomaterial-based scaffolds

Skeletal Adaptation to Intramedullary Pressure-Induced Interstitial Fluid Flow Is Enhanced in Mice Subjected to Targeted Osteocyte Ablation

Interstitial fluid flow (IFF) is a potent regulatory signal in bone. During mechanical loading, IFF is generated through two distinct mechanisms that result in spatially distinct flow profiles: poroelastic interactions within the lacunar-canalicular system, and intramedullary pressurization. While the former generates IFF primarily within the lacunar-canalicular network, the latter generates significant flow at the endosteal surface as well as within the tissue. This gives rise to the intriguing possibility that loading-induced IFF may differentially activate osteocytes or surface-residing cells depending on the generating mechanism, and that sensation of IFF generated via intramedullary pressurization may be mediated by a non-osteocytic bone cell population. To begin to explore this possibility, we used the Dmp1-HBEGF inducible osteocyte ablation mouse model and a microfluidic system for modulating intramedullary pressure (ImP) to assess whether structural adaptation to ImP-driven IFF is altered by partial osteocyte depletion. Canalicular convective velocities during pressurization were estimated through the use of fluorescence recovery after photobleaching and computational modeling. Following osteocyte ablation, transgenic mice exhibited severe losses in bone structure and altered responses to hindlimb suspension in a compartment-specific manner. In pressure-loaded limbs, transgenic mice displayed similar or significantly enhanced structural adaptation to Imp-driven IFF, particularly in the trabecular compartment, despite up to ∼50% of trabecular lacunae being uninhabited following ablation. Interestingly, regression analysis revealed relative gains in bone structure in pressure-loaded limbs were correlated with reductions in bone structure in unpressurized control limbs, suggesting that adaptation to ImP-driven IFF was potentiated by increases in osteoclastic activity and/or reductions in osteoblastic activity incurred independently of pressure loading. Collectively, these studies indicate that structural adaptation to ImP-driven IFF can proceed unimpeded following a significant depletion in osteocytes, consistent with the potential existence of a non-osteocytic bone cell population that senses ImP-driven IFF independently and potentially parallel to osteocytic sensation of poroelasticity-derived IFF

The Global Reciprocal Reprogramming between Mycobacteriophage SWU1 and Mycobacterium Reveals the Molecular Strategy of Subversion and Promotion of Phage Infection

Bacteriophages are the viruses of bacteria, which have contributed extensively to our understanding of life and modern biology. The phage-mediated bacterial growth inhibition represents immense untapped source for novel antimicrobials. Insights into the interaction between mycobacteriophage and Mycobacterium host will inform better utilizing of mycobacteriophage. In this study, RNA sequencing technology (RNA-seq) was used to explore the global response of Mycobacterium smegmatis mc2 155 at an early phase of infection with mycobacteriophage SWU1, key host metabolic processes of M. smegmatis mc2 155 shut off by SWU1, and the responsible phage proteins. The results of RNA-seq were confirmed by Real-time PCR and functional assay. 1174 genes of M. smegmatis mc2 155 (16.9% of the entire encoding capacity) were differentially regulated by phage infection. These genes belong to six functional categories: (i) signal transduction, (ii) cell energetics, (iii) cell wall biosynthesis, (iv) DNA, RNA, and protein biosynthesis, (v) iron uptake, (vi) central metabolism. The transcription patterns of phage SWU1 were also characterized. This study provided the first global glimpse of the reciprocal reprogramming between the mycobacteriophage and Mycobacterium host

Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression

T helper cells that produce IL-17 (Th17 cells) have recently been identified as the third distinct subset of effector T cells. Emerging data suggests that Th17 cells play an important role in the pathogenesis of many liver diseases by regulating innate immunity, adaptive immunity, and autoimmunity. In this study, we examine the role and mechanism of Th17 cells in the pathogenesis of autoimmune hepatitis (AIH). The serum levels of IL-17 and IL-23, as well as the frequency of IL-17+ cells in the liver, were significantly elevated in patients with AIH, compared to other chronic hepatitis and healthy controls. The hepatic expressions of IL-17, IL-23, ROR-γt, IL-6 and IL-1β in patients with AIH were also significantly increased and were associated with increased inflammation and fibrosis. IL-17 induces IL-6 expression via the MAPK signaling pathway in hepatocytes, which, in turn, may further stimulate Th17 cells and forms a positive feedback loop. In conclusion, Th17 cells are key effector T cells that regulate the pathogenesis of AIH, via induction of MAPK dependent hepatic IL-6 expression. Blocking the signaling pathway and interrupting the positive feedback loop are potential therapeutic targets for autoimmune hepatitis

Specification and guideline for technical aspects and scanning parameter settings of neonatal lung ultrasound examination

Lung ultrasound (LUS) is now widely used in the diagnosis and monitor of neonatal lung diseases.Nevertheless, in the published literatures,the LUS images may display a significant variation in technical execution,while scanning parameters may influence diagnostic accuracy.The inter- and intra-observer reliabilities of ultrasound exam have been extensively studied in general and in LUS.As expected,the reliability declines in the hands of novices when they perform the point-of-care ultrasound (POC US).Consequently,having appropriate guidelines regarding to technical aspects of neonatal LUS exam is very important especially because diagnosis is mainly based on interpretation of artifacts produced by the pleural line and the lungs.The present work aimed to create an instrument operation specification and parameter setting guidelines for neonatal LUS.Technical aspects and scanning parameter settings that allow for standardization in obtaining LUS images include (1)select a high-end equipment with high-frequency linear array transducer (12-14 MHz).(2)Choose preset suitable for lung examination or small organs.(3)Keep the probe perpendicular to the ribs or parallel to the intercostal space.(4)Set the scanning depth at 4-5 cm.(5)Set 1-2 focal zones and adjust them close to the pleural line.(6)Use fundamental frequency with speckle reduction 2-3 or similar techniques.(7)Turn off spatial compounding imaging.(8)Adjust the time-gain compensation to get uniform image from the near-to far-field

Prokineticin 2 Regulates the Electrical Activity of Rat Suprachiasmatic Nuclei Neurons

Neuropeptide signaling plays roles in coordinating cellular activities and maintaining robust oscillations within the mammalian suprachiasmatic nucleus (SCN). Prokineticin2 (PK2) is a signaling molecule from the SCN and involves in the generation of circadian locomotor activity. Prokineticin receptor 2 (PKR2), a receptor for PK2, has been shown to be expressed in the SCN. However, very little is known about the cellular action of PK2 within the SCN. In the present study, we investigated the effect of PK2 on spontaneous firing and miniature inhibitory postsynaptic currents (mIPSCs) using whole cell patch-clamp recording in the SCN slices. PK2 dose-dependently increased spontaneous firing rates in most neurons from the dorsal SCN. PK2 acted postsynaptically to reduce γ-aminobutyric acid (GABA)-ergic function within the SCN, and PK2 reduced the amplitude but not frequency of mIPSCs. Furthermore, PK2 also suppressed exogenous GABA-induced currents. And the inhibitory effect of PK2 required PKC activation in the postsynaptic cells. Our data suggest that PK2 could alter cellular activities within the SCN and may influence behavioral and physiological rhythms

Lymphocytes Accelerate Epithelial Tight Junction Assembly: Role of AMP-Activated Protein Kinase (AMPK)

The tight junctions (TJs), characteristically located at the apicolateral borders of adjacent epithelial cells, are required for the proper formation of epithelial cell polarity as well as for sustaining the mucosal barrier to the external environment. The observation that lymphocytes are recruited by epithelial cells to the sites of infection [1] suggests that they may play a role in the modulation of epithelial barrier function and thus contribute to host defense. To test the ability of lymphocytes to modulate tight junction assembly in epithelial cells, we set up a lymphocyte-epithelial cell co-culture system, in which Madin-Darby canine kidney (MDCK) cells, a well-established model cell line for studying epithelial TJ assembly [2], were co-cultured with mouse lymphocytes to mimic an infection state. In a typical calcium switch experiment, the TJ assembly in co-culture was found to be accelerated compared to that in MDCK cells alone. This accelaration was found to be mediated by AMP-activated protein kinase (AMPK). AMPK activation was independent of changes in cellular ATP levels but it was found to be activated by the pro-inflammatory cytokine TNF-α. Forced suppression of AMPK, either with a chemical inhibitor or by knockdown, abrogated the accelerating effect of lymphocytes on TJ formation. Similar results were also observed in a co-culture with lymphocytes and Calu-3 human airway epithelial cells, suggesting that the activation of AMPK may be a general mechanism underlying lymphocyte-accelerated TJ assembly in different epithelia. These results suggest that signals from lymphocytes, such as cytokines, facilitate TJ assembly in epithelial cells via the activation of AMPK