1,721,399 research outputs found
Sistem Informasi Pemesanan Rangkaian Bunga Pada Wan-Wan Florist
No full textBusiness of stick werk and hand bouquet for all occasions is one of the growing business in Medan. Customers of that business can be individuals, companies and foundations, both in the seminar, custom , birthday , wedding , until the funeral ceremony. To attract customers, the florist must always innovate, create models of attractive flower arrangements. Wan- Wan Florist is a flower shop in Medan who constantly provide various kinds of shapes and attractive flower arrangements for all occasions. The number of booking transactions from customers and many types of circuits that do also contribute to increase the density of business operations . The system used for recording transactions Wan - Wan Florist still manual so it is still less efficient in terms of time and also in terms of the accuracy of the data is still not guaranteed.The purpose of the research is to design an information system for recording and processing transaction data terkomputersasi so as to facilitate the operations of the company.To design a computerized information system , used Visual Basic 6.0 and Microsoft Access 2000 and in preparing reports use Crystal Report 8.5T
Identifying Author Fingerprints in Texts via Graph Neural Networks
No full textThe world is generating more and more network data in many different areas (e.g., sensor networks, social networks and even text). A unique characteristic of these data is the coupling between data values and underlying irregular structure on which these values are defined. Thus, researchers developed Graph Neural Networks (GNNs) to use deep learning approaches on these irregular network data. GNNs developers tried to replicate the recent success of Convolutional Neural Networks (CNNs) and developed its graph counterpart Graph Convolutional Neural Network (GCNN) and more different variations of GNNs (e.g. EdgeNet). However, all these architectures are relatively young, and the impact of different parameters to classification result is not well researched compared to regular neural network architectures. To address this issue, we propose to use authorship attribution problem to research the impact of different architectures and their variations to classification accuracy and how GNNs can be used to improve on authorship attribution task compared to the baseline architectures. Explicitly, we define the dataset which is going to be used throughout the experiments and the method to convert text excerpts of authors into the network that can be classified with GNNs (called WAN). WAN is as a network that captures unique author fingerprint. We also define the set of GNN architectures (and different combinations and variations of them), baseline architecture (SVM) and experiments that are used with those architectures. This experiment setting allows us to compare different GNN architectures among themselves and the baseline architecture. Also, we define a method to reduce the dimensions of author fingerprints (WANs) and use these sparse author fingerprints for the same experiments with the same architectures. Numerical results show the improvement over the baseline architectures in nearly all defined experiments. Also, we found that more complex GNN architectures (e.g. EdgeNets) are superior to shallower architectures with more laborious experiments (e.g. classification by gender). More complex architectures also require hyperparameter re-tuning in order to achieve optimal results. Furthermore, experiments with sparse author fingerprints showed that we could achieve comparable results to standard fingerprints with faster training times and significantly reduced dimensions. GNN architectures used with sparse author fingerprints were usually superior to baseline architectures
Modulation of Inos Induction by Pge2 in Macrophages: Distinct Susceptability in Murine J774 and Raw 264.7 Macrophages
No full textComparative finite element analysis of stress distribution of different implant- supported crown and abutment materials / Chan Wan Wan
No full textThis study aimed to evaluate the stress distribution of three-dimensional (3D) printed ceramic filled hybrid materials and zirconia as abutments and implant-supported crowns using a finite element study model. Five groups of materials were: computer-aided design and computer-aided manufacturing (CAD/CAM) zirconia implant-supported crown with CAD/CAM zirconia custom abutment (ZR-ZR); 3D printed VarseoSmile® Crown Plus implant-supported crown with CAD/CAM zirconia custom abutment (VSC-ZR); CAD/CAM zirconia implant-supported crown with 3D printed VarseoSmile® Crown Plus custom abutment (ZR-VSC); 3D printed VarseoSmile® TriniQ® implant-supported crown with CAD/CAM zirconia custom abutment (VST-ZR); and CAD/CAM zirconia implant-supported crown with 3D printed VarseoSmile® TriniQ® (ZR-VST) custom abutment. The implant-supported crown of a mandibular first molar was designed and modelled in computer-aided design (CAD) software, and analysed using finite element analysis (FEA) ANSYS Workbench 2021 R1 software. All the materials were considered homogenous, isotropic, and linearly elastic. A 600N vertical load (Load Case 1) was applied to the central axis of implant onto the crown, while a 225N oblique load (Load Case 2) was applied 45° to the central axis of implant onto the crown. The von Mises stress was recorded at crown, cement between crown and CAD/CAM custom abutment, CAD/CAM custom abutment, cement between CAD/CAM custom abutment and titanium base (Ti-base) abutment, abutment screw, titanium base abutment, fixture, cortical, and cancellous bone. The von Mises stress percentage difference was compared to the control group ZR-ZR. The stress concentration areas were indicated by colorimetric map. At the crown, Group ZR-VST had the highest von Mises stress (214.39 MPa; 112.72 MPa), while Group VST-ZR had the lowest (173.66 MPa; 101.58 MPa) in Load Case 1 and 2, respectively. The stress concentration areas were the crown's occlusal area, the cement layer of the neck and top region of the abutment, top region of titanium base abutment, the internal connection to the abutment screw, the collar area at gingival level, first thread of abutment screw, and cervical area of titanium base abutment. At the CAD/CAM custom abutments, Groups ZR-VSC and ZR-VST demonstrated the lowest stress in Load Case 1 and 2, which were 46.66 MPa and 44.62 MPa; 45.34 MPa and 41.95 MPa, respectively. The cement between the crown and the CAD/CAM custom abutment showed the lowest stress in Group ZR-VSC (28.19 MPa) and Group ZR-VST (28.92 MPa) in Load Case 1. In Load Case 1, the cement between the CAD/CAM custom abutment and the Ti-base abutment demonstrated the greatest stress in Groups ZR-VSC (70.14 MPa) and ZR-VST (72.52 MPa), similarly observed in Load Case 2 (Group ZR-VSC:54.72 MPa; Group ZR-VST: 57.76 MPa). The stress at the fixture in the cortical and cancellous bones was comparable across all groups under both loads. In conclusion, the combination of implant-supported crown and abutment with different moduli of elasticity positively influences stress distribution at the crown, cement between crown and CAD/CAM custom abutment, CAD/CAM custom abutment, abutment screw, cement between CAD/CAM custom abutment and Ti-base abutment, Ti-base abutment and fixture, but no effect on stress distribution in the peri-implant bone structure
Effects of Cannabinoids on Lps-Stimulated Inflammatory Mediator Release from Macrophages: Involvement of Eicosanoids
No full textDelta (9)-Tetrahydrocannabinol (Delta (9)-THC) is the major psychoactive component of marijuana and elicits pharmacological actions via cannabinoid receptors. Anandamide (AEA) and 2-arachidonoyl-glycerol (2-AG) are endogenous ligands for cannabinoid receptors, which because of their structural similarities to arachidonic acid (AA), AEA, and 2-AG could serve as substrates for lipoxygenases and cyclooxygenases (COXs) that metabolize polyunsaturated fatty acids to potent bioactive molecules. In this study, we have compared the effects of Delta (9)-THC, AEA, 2-AG, and another cannabinoid agonist, indomethacin morpholinylamide ( IMMA), on lipopolysaccharide (LPS)induced NO, IL-6, and PGE ( 2) release from J774 macrophages. Delta (9)-THC, IMMA, and AEA diminish LPS-induced NO and IL-6 production in a concentration-dependent manner. 2-AG inhibits the production of IL-6 but slightly increases iNOS-dependent NO production . Delta (9)-THC and IMMA also inhibit LPS-induced PGE(2) production and COX- 2 induction, while AEA and 2-AG have no effects. These discrepant results of 2-AG on iNOS and COX-2 induction might be due to its bioactive metabolites, AA and PGE(2), whose incubation cause the potentiation of both iNOS and COX-2 induction. On the contrary, the AEA metabolite, PGE(2) -ethanolamide, influences neither the LPS-induced NO nor IL-6 production. Taken together, direct cannabinoid receptor activation leads to anti- inflammatory action via inhibition of macrophage function. The endogenous cannabinoid, 2-AG, also serves as a substrate for COX- catalyzing PGE(2) production, which in turn modulates the action of CB2. J. Cell. Biochem. 81:715-723, 2001. (C) 2001 Wiley-Liss, Inc
Proteasome Inhibitors Stimulate Interleukin-8 Expression Via Ras and Apoptosis Signal-Regulating Kinase-Dependent Extracellular Signal-Related Kinase and C-Jun N-Terminal Kinase Activation
No full textIn this study, we investigated the effects of proteasome inhibibors (MG 132 and lactacystin) on interleukin (IL)-8 induction. In human epithelial A549 cells, MG132 and lactacystin induced IL-8 release within the range of 0.1-30 muM. The effect of MG132 resulted from IL-8 gene transcription and was blocked by PD 98059, but was unaffected by GF109203X, Ro 31-8220, or SB 203580. Mutational analysis of the 5' flanking region of the IL-8 gene revealed that activator protein (AP)-1-binding element, but not that element responsive to nuclear factor (NF)-IL-6 or NF-kappaB, was necessary for MG132 stimulation. Consistent with this, MG132 and lactacystin increased the DNA-binding and reporter activities of AP-1, but reduced cytokine-elicited kappaB activation. Moreover, AP-1 stimulation was associated with increased extracellular signal-related kinase (ERK), mitogen-activated protein/ERK kinase (MEK), and c-Jun N-terminal kinase ( JNK) phosphorylation, whereas IL-8 activity was sensitive to the dominant- negative mutants of JNK1, JNK2, SEK, ASK, ERK2, and Ras, but not those of MEKK1, TAK, and p38 mitogen-activated protein kinase. In addition, activations of the IL-8 gene and AP-1 by MG132 and lactacystin were inhibited by GSH and NAC. Herein we present a novel action of proteasome inhibitors, possibly through ROS production, of targeting the upstream signaling molecules, ERK and JNK, which leads to AP-1 activation and IL-8 gene expression
Ceramide Inhibits Lipopolysaccharide-Mediated Nitric Oxide Synthase and Cyclooxygenase-2 Induction in Macrophages: Effects on Protein Kinases and Transcription Factors
No full textThe goal of this study was to elucidate whether triggering the sphingomyelin pathway modulates LPS-initiated responses. For this purpose we investigated the effects of N- acetylsphingosine (C-2-ceramide) on LPS- induced production of NO and PGE(2) in murine RAW 264.7 macrophages and explored the signaling pathways involved. We found that within a range of 10-50 muM, C-2-ceramide inhibited LPS- elicited NO synthase and cyclooxygenase-2 induction accompanied by a reduction in NO and PGE, formation. By contrast, a structural analog of C-2-ceramide that does not elicit functional activity, C-2-dihydroceramide, did not affect the LPS response. The nuclear translocation and DNA binding study revealed that ceramide can inhibit LPS-induced NF-kappaB and AP-I activation. The immunocomplex kinase assay indicated that I kappaB kinase activity stimulated by LPS was inhibited by ceramide, which concomitantly reduced the I kappaB alpha degradation caused by LPS within 1-6 h. In concert with the decreased cytosolic p65 protein level, LPS treatment resulted in rapid nuclear accumulation of NF- kappaB subunit p65 and its association with the cAMP- responsive element binding protein. Ceramide coaddition inhibited all the LPS responses. In addition, LPS-induced PKC and p38 mitogen-activated protein kinase activation were overcome by ceramide. In conclusion, we suggest that ceramide inhibition of LPS-mediated induction of inducible NO synthase and cyclooxygenase-2 is due to reduction of the activation of NF-kappaB and AP-1, which might result from ceramide's inhibition of LPS-stimulated I kappaB kinase, p38 mitogen-activated protein kinase, and protein kinase C
Signaling Mechanisms of Enhanced Neutrophil Phagocytosis and Chemotaxis by the Polysaccharide Purified from Ganoderma Lucidum
No full text1 The polysaccharide from Ganoderma lucidum (PS-G) has been reported to enhance immune responses and to elicit antitumor effects. In our previous study, we found that PS-G efficiently inhibited spontaneously and Fas- enhanced neutrophil apoptosis when cultured in vitro. Since phagocytosis and chemotaxis play essential roles in host defense mediated by neutrophils, it is of great interest to know the effect of PS-G on these two cell functions, and the molecular events leading to these actions. 2 Using latex beads and heat-inactive Escherichia coli serving as particles for neutrophil engulfment, we found that PS-G is able to enhance phagocytic activity of human primary neutrophils and neutrophilic- phenotype cells differentiated from all trans retinoic acid-treated HL-60 cells. 3 Chemotactic assay using Boyden chamber also revealed the ability of PS-G to increase neutrophil migration. 4 Exposure of neutrophils to PS- G time dependently caused increases in protein kinase C (PKC), p38 mitogen -activated protein kinase (MAPK), Hck, and Lyn activities. 5 Results with specific kinase inhibitors indicate that phagocytic action of PS-G was reduced by the presence of wortmannin ( Phosphatidylinositol 3-kinase, PI3 K inhibitor), pyrazolpyrimidine 2 (Src-family tyrosine kinase inhibitor), Ro318220 (PKC inhibitor), and SB203580 (p38 MAPK inhibitor), but not by PD 98059 (mitogen-activated protein/ERK kinase inhibitor). Moreover, chemotactic action of PS-G requires the activities of PI3K, p38 MAPK, Src tyrosine kinases and PKC. 6 All these results demonstrate the abilities of PS-G to enhance neutrophil function in phagocytosis and chemotaxis, and further provide evidence to strengthen the beneficial remedy of G. lucidum in human to enhance defense system
Inhibition of Ifn-Gamma-Mediated Inducible Nitric Oxide Synthase Induction by the Peroxisome Proliferator-Activated Receptor Gamma Agonist, 15-Deoxy-Delta(12,14)-Prostaglandin J(2), Involves Inhibition of the Upstream Janus Kinase/Stat1 Signaling Pathway
No full textPeroxisome proliferator-activated receptor gamma (PPAR-gamma ) ligands have been reported to exert anti-inflammatory activities in macrophages by competition for transcriptional coactivators with some transcriptional factors, including NF-kappaB. In the present study the influence of PPARgamma activators on IFN-gamma-elicited macrophage stimulation and signaling cascades was investigated. The results show that IFN-gamma- induced inducible NO synthase (iNOS) gene transcription, iNOS protein induction, and NO production are more sensitive to inhibition by 15-deoxy- Delta(12,14)- prostaglandin J(2) (15dPGJ(2)) than by the other two PPARgamma agonists, GW1929 and ciglitazone. Delayed addition of 15dPGJ(2) for 2 h resulted in reduced inhibition, suggesting action by 15dPGJ(2) on the upstream signaling cascades. Immunoblotting, DNA binding, and reporter gene assays consistently revealed the inhibitory ability of 15 dPGJ(2), but not GW1929 or ciglitazone, on IFN-gamma- elicited signaling cascades, including tyrosine phosphorylation of Janus tyrosine protein kinase 2 and STAT1 , DNA binding, and IFN regulatory factor-1 trans-activation of STAT1 . These effects of 15dPGJ(2) were not abrogated by the PPARgamma antagonist, bisphenol A diglycidyl ether, indicating the PPARgamma- independent actions. 15dPGJ(2) also attenuated IL-6-induced tyrosine phosphorylation of STAT1 and STAT3 in Hep3B hepatoma cells. Consistent with the inhibitory effect of reactive oxygen species on STAT1 signaling, STAT1, inhibition by 15dPGJ(2) was abrogated by N -acetylcysteine, glutathione, superoxide dismutase, and catalase. Furthermore, 15dPGJ(2)- induced inhibition of STAT1 phosphorylation and NO production still occurred in the presence of peroxovanadate, ruling out the action mechanism of 15dPGJ(2) on tyrosine phosphatase. Taken together, for the first time in this study we demonstrate that 15dPGJ(2) can inhibit cytokine-stimulated Janus kinase 2-STAT signaling through a PPARgamma- independent, reactive oxygen species-dependent mechanism. These data provide a novel molecular mechanism of iNOS inhibition by 15dPGJ(2) and confirm its physiological role in anti-inflammation
Silymarin Protects Dopaminergic Neurons against Lipopolysaccharide- Induced Neurotoxicity by Inhibiting Microglia Activation
No full textAn inflammatory response in the central nervous system mediated by activation of microglia is a key event in the early stages of the development of neurodegenerative diseases. Silymarin is a polyphenolic flavanoid derived from milk thistle that has anti-inflammatory, cytoprotective and anticarcinogenic effects. In this study, we first investigated the neuroprotective effect of silymarin against lipopolysaccharide (LPS)-induced neurotoxicity in mesencephalic mixed neuron-glia cultures. The results showed that silymarin significantly inhibited the LPS-induced activation of microglia and the production of inflammatory mediators, such as tumour necrosis factor-alpha and nitric oxide (NO), and reduced the damage to dopaminergic neurons. Therefore, the inhibitory mechanisms of silymarin on microglia activation were studied further. The production of inducible nitric oxide synthase (iNOS) was studied in LPS- stimulated BV-2 cells as a model of microglia activation. Silymarin significantly reduced the LPS-induced nitrite, iNOS mRNA and protein levels in a dose-dependent manner. Moreover, LPS could induce the activation of p38 mitogen- activated protein kinase (MAPK) and c-jun N- terminal kinase but not extracellular signal-regulated kinase. The LPS- induced production of NO was inhibited by the selective p38 MAPK inhibitor SB203580. These results indicated that the p 38 MAPK signalling pathway was involved in the LPS-induced NO production. However, the activation of p38 MAPK was not inhibited by silymarin. Nevertheless, silymarin could effectively reduce LPS-induced superoxide generation and nuclear factor kappaB (NF-kappaB) activation. It suggests that the inhibitory effect of silymarin on microglia activation is mediated through the inhibition of NF -kappaB activation
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