Pembangunan Database Destinasi Pariwisata Indonesia dan Implementasinya pada Sistem Berbasis Web

Regarding to: (1) the increasing region\u27s need in developing tourism destinations; (2) the needs of tourists in selecting appropriate attractions according to specified criteria; (3) the need of travel businesses to offer sights of interest in accordance with the needs of potential tourists, (4) the need to deepen and continue our previous research titled "Development of Tourism Destination Media Potential and Utilizing Local Resources in the Era of Autonomy and Regional Expansion ", we need to develop a complete database of tourism destinations in Indonesia that can facilitate those needs. We build a web-based database that is capable of storing complete information about Indonesian tourism destinations in thorough, systematic, and structured way. It is also able to classify a variety of attractions based on attributes such as: location (the name of the island, province, district), type/ tourism products, how to achieve the object, cost, and a variety of informal information, such as the ins and outs of the attraction area incorporated by the local or tourist experiences. The research will focus on deepening and refinement of the model and database structure design and implementation with the collection, processing, and data entry of primary and secondary data which amounts to approximately 140 tourism destinations in Indonesia. The research is arranged in stages as follows: (1) designing models and the database structure, (2) making a web-based program, (3) installation and hosting ; (4) data collection, (5) data processing and data entry, (6) evaluation and improvement/ refinement. Once developed, the database can be used as a starting point in the development of Data Warehouse, Decision Support System, and Expert System for Indonesian tourism industry

MOESM1 of Infectious bursal disease virus inoculation infection modifies Campylobacter jejuni–host interaction in broilers

Additional file 1: Figure S1. Flow cytometric analysis of Bu1+ B cells in peripheral blood lymphocytes (PBL) of broiler chickens at different days pvi from Exp. A (A) and Exp. B (B). *indicates significant differences between non-inoculated control and vvIBDV inoculated birds (P < 0.05). Error bars indicate standard deviation. Control = virus-free control, vvIBDV = vvIBDV-inoculated group, pvi = post IBDV inoculation

MOESM1 of Infectious bursal disease virus inoculation infection modifies Campylobacter jejuni–host interaction in broilers

Additional file 1: Figure S1. Flow cytometric analysis of Bu1+ B cells in peripheral blood lymphocytes (PBL) of broiler chickens at different days pvi from Exp. A (A) and Exp. B (B). *indicates significant differences between non-inoculated control and vvIBDV inoculated birds (P < 0.05). Error bars indicate standard deviation. Control = virus-free control, vvIBDV = vvIBDV-inoculated group, pvi = post IBDV inoculation

image_1_Characterization of Chicken Tumor Necrosis Factor-α, a Long Missed Cytokine in Birds.jpeg

<p>Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine playing critical roles in host defense and acute and chronic inflammation. It has been described in fish, amphibians, and mammals but was considered to be absent in the avian genomes. Here, we report on the identification and functional characterization of the avian ortholog. The chicken TNF-α (chTNF-α) is encoded by a highly GC-rich gene, whose product shares with its mammalian counterpart 45% homology in the extracellular part displaying the characteristic TNF homology domain. Orthologs of chTNF-α were identified in the genomes of 12 additional avian species including Palaeognathae and Neognathae, and the synteny of the closely adjacent loci with mammalian TNF-α orthologs was demonstrated in the crow (Corvus cornix) genome. In addition to chTNF-α, we obtained full sequences for homologs of TNF-α receptors 1 and 2 (TNFR1, TNFR2). chTNF-α mRNA is strongly induced by lipopolysaccharide (LPS) stimulation of monocyte derived, splenic and bone marrow macrophages, and significantly upregulated in splenic tissue in response to i.v. LPS treatment. Activation of T-lymphocytes by TCR crosslinking induces chTNF-α expression in CD4⁺ but not in CD8⁺ cells. To gain insights into its biological activity, we generated recombinant chTNF-α in eukaryotic and prokaryotic expression systems. Both, the full-length cytokine and the extracellular domain rapidly induced an NFκB-luciferase reporter in stably transfected CEC-32 reporter cells. Collectively, these data provide strong evidence for the existence of a fully functional TNF-α/TNF-α receptor system in birds thus filling a gap in our understanding of the evolution of cytokine systems.</p

Lungs from chickens infected intratracheally with IMT5155 (10⁹ CFU).

<p>Lungs were fixed 24 h p.i.; sections were stained with (A) HE or (B) anti-O2 antibody and counter-stained with hematoxylin, and examined with a light microscope. Inflamed parabronchi coincide with the presence of bacteria, labeled with anti-O2. Scale bars 400 µm. BV, blood vessel.</p

TUNEL-positive cells in the lungs of APEC-infected chickens.

<p>Lungs were fixed at 12 h p.i. (A) Clogged parabronchus of MT78-infected chicken, stained with HE; the boxed region is amplified and was stained with anti-O2 antibody in (D), and by TUNEL in (G). (B) Clogged parabronchus of IMT5155-infected chicken, stained with HE; the boxed region is amplified and was stained with anti-O2 antibody in (E), and by TUNEL in (H). (C) Lung section from PBS-inoculated chicken, showing intact parabronchi, open and aerated atria and air capillaries, and absence of TUNEL-positive cells. (F) Parabronchus of UEL17-infected chicken, stained by TUNEL. (I) Parabronchus of IMT5104-infected chicken, stained by TUNEL. All <i>E. coli</i>-infected chickens had TUNEL-positive cells in inflamed lung areas. Scale bars, A, B and C, 200 µm; D–I, 50 µm. PL, parabronchial lumen; A, atria; AC, air capillary; S, interparabronchial septa; BV, blood vessel.</p

Association of APEC with HD11 chicken macrophages.

<p>Cells were infected at a MOI of 150 CFU/cell as described in Section 2.4. (A) At 6 h p.i., the association of bacteria with macrophages was visualized by Giemsa staining. Magnification is 1000×. (B) Graph shows percentage of infected cells (grey bars) and number of associated bacteria per cell (black bars) for each strain. Data are mean ± standard deviation of three experiments performed in triplicate. 100–200 cells were counted in each sample.</p

Virulence-associated gene fingerprint of <i>E. coli</i> strains.

<p>Positive (+) and negative signs (−) indicate the presence and absence, respectively, of the indicated genes.</p>a<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0041031#pone.0041031-Matter1" target="_blank">[19]</a>;</p>b<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0041031#pone.0041031-Anto1" target="_blank">[2]</a>;</p>c<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0041031#pone.0041031-Ewers1" target="_blank">[14]</a>.</p