Strategi Pembangunan Pariwisata melalui Sinergitas Dinas Pariwisata dengan Desa Adat ( Studi Kasus pada Pengelolaan Obyek Wisata Pantai Labuan Sait dalam Meningkatkan Retribusi Daerah di Kabupaten Badung)

A gradual Tourism development is very important to improve the quality of tourism each year to compete with other tourist attraction. The synergy between the Central Government with local government plays an important role to the development of tourism. The background to this research is the development of tourism which is still insufficient in Labuan Sait both in terms of means and infrastructure, promotion, as well as structuring tourism. This study measures how does tourism development strategy through the synergy with the customary village tourism office on the management of Beach Tourism Labuan Sait in increasing the levy County in Badung Regency with the theory of development that uses the concept of planning development by Sjahrizal in the regional development planning in the era of autonomy. The indicator consists of planning, implementation, monitoring and evaluation. In addition also use the concept of synergy from Najiyati and Rahmat which consists of indicators communication and coordination as well as indicators of the SWOT by Freddy Rangkuti. Method used in this study is a qualitative method with descriptive approach with data collection techniques in the form of in-depth interviews to several informants associated with this research. The results of the research showed that the development strategy of tourism through the synergy with the customary village Tourism Office on the management of Beach Tourism Labuan Sait in improving regional levies in Badung Regency are still insufficient. That is because the is still lacking from the indicator monitoring and implementation and evaluation of the impact against the decline of levy of admission attractions Labuan Sait in the 2017.     Keywords: Development, Tourism, Synergy, and Strateg

Antibiotic resistance, phage susceptibility and geographic/ecological metadata of <i>Achromobacter</i> strains.

<p>(A) Quantitative display of susceptibility of 62 strains (rows on the y-axis) to 35 antibiotics (columns on the x-axis) shown as heatmap of antibiotic susceptibility values using Euclidian distance and Ward clustering for both rows and columns as implemented in the heatmap.2() function of the R gplots package <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086935#pone.0086935-Capparelli2" target="_blank">[77]</a>. The colour code of the heatmap is given in the upper left corner of the heatmap. The more red the colour, the more resistant is the strain to the antibiotic (for fields covered by the legend, all strains are fully resistant to the respective antibiotic). Only the row dendrogram is shown, which depicts clusters of strains with similar antibiotic resistance patterns (see main text). Antimicrobial agents are grouped according to their clusters of susceptibility patterns of the strains (column dendrogram is not shown). The names of the antibiotics are colored according to their chemical classification. The respective color legend is shown at the bottom of A. (B) Horizontal bar plot which depicts the sum of phages to which a given strain is susceptible (for details see section C). (C) Host range analysis of isolated phages (columns in C). The detailed results of susceptibility of strains per phage are shown as level plot with rows being ordered according to Fig. 2A. A grey color indicates resistance or immunity, blue color indicates plaque formation of a given phage (see the labeling of the x-axis of C) on a given strain (y-axis). The respective legend is shown in the upper right corner of C (for fields covered by the legend, phages do not propagate on the indicated strains). The order of phages (columns of levelplot in C) is based on the number of strains on which a given phage is able to propagate (indicative for the width of the host range). This number of strains is given in the vertical bar plot below the level plot. (D) Names of the <i>Achromobacter</i> strains and respective geographic and ecological metadata. Strain names were marked in colors according to clusters from MLSA (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086935#pone-0086935-g001" target="_blank">Figure 1</a>), metadata values are differently colored in order to facilitate readability (a colour legend is not separately given).</p

Determination of the frequency of bacteriophage-insensitive mutants or lysogens after phage treatment.

<p>Putative life cycles of the isolated phages were assumed after determination of plaque morphology and reinduction experiments.</p><p>Mean numbers of viable counts in one ml of culture after phage treatment were divided by mean numbers viable counts without phage treatment. “0” describes the total elimination of all cells, “1” stands for no significant elimination.</p

Electron micrographs of several <i>Achromobacter</i> phages with different morphotypes.

<p>Negative staining (4% (w/v) uranyl acetate, pH 5.0). Bars represent 100 nm.</p

Molecular and phenotypic characterization of the <i>Achromobacter</i> isolates.

<p>The tree with the highest log likelihood is shown. The percentage of trees in which the associated taxa clustered together, as determined by 500 bootstrap replicates, is shown next to the branches. Only values above 90% are shown. The tree is drawn to scale, with branch lengths measured in the number of substitutions per site. Vertical colored bars indicate robust clades with bootstrap support >90%. Brackets indicate strains that are identical throughout the four partially sequenced genes. Strains that are marked by squared rectangles of the same color belong to the same eBURST group, i.e., share at least one identical locus (gene). Red circles indicate so-called singletons which do not share an identical locus with any of the other strains.</p

Southern blot hybridization analysis of hydrolyzed genomic DNA of <i>Achromobacter</i> phages.

<p>Phage DNAs were hydrolyzed with endonuclease NdeI, after agarose gel electrophoresis and Southern blotting, the DNAs were hybridized with DNA from phage 83–24 as a probe. λ DNA hydrolyzed with EcoRI and HindIII was used as marker (M). 1% agarose gel.</p

Overview and metadata of isolated environmental phages.

<p>Overview and metadata of isolated environmental phages.</p

Characterization of epithelial barrier function.

<p>(<b>A</b>) IEC-Mx2Luc-10 cells were seeded on porous cell culture inserts with a 0.4 µm pore size. Transepithelial electrical resistance (TEER) was monitored over time in triplicates and is expressed as resistance in ohms multiplied by the area of the cell culture insert (Ω*cm² ± SD). (<b>B</b>) Electron microscopy of apical microvillus formation 10 days after seeding and (<b>C</b>) junctional complex formation (arrowheads) at lateral cell-cell borders 12 days after seeding of IEC-1 and IEC-Mx2Luc-10 cell lines on transwell cell culture inserts.</p

Interferon response of intestinal epithelial interferon reporter cell line.

<p>(<b>A</b>) Stimulation of IEC-Mx2Luc-10 cells with indicated amounts of IFN-β or IFN-λ3 for 24 h. Fold induction represents relative luminescence units (RLU) of treated compared to untreated cells. All values are depicted as mean ± SD (n=3). (<b>B</b>) Antiviral protection of IEC-Mx2Luc-10 cells upon treatment with IFN-β and IFN-λ3. Cells were pre-treated with 1000 U/ml IFN-β or 50 ng/ml IFN-λ3 for 24 h and infected with 80 HAU/ml Newcastle disease virus (NDV) for 24 h. Cells were stained for expression of NDV hemagglutinin-neuraminidase (HN) and analyzed by flow cytometry.</p

Intracellular <i>Staphylococcus aureus</i> eludes selective autophagy by activating a host cell kinase

<p>Autophagy, a catabolic pathway of lysosomal degradation, acts not only as an efficient recycle and survival mechanism during cellular stress, but also as an anti-infective machinery. The human pathogen <i>Staphylococcus aureus</i> (<i>S. aureus</i>) was originally considered solely as an extracellular bacterium, but is now recognized additionally to invade host cells, which might be crucial for persistence. However, the intracellular fate of <i>S. aureus</i> is incompletely understood. Here, we show for the first time induction of selective autophagy by <i>S. aureus</i> infection, its escape from autophagosomes and proliferation in the cytoplasm using live cell imaging. After invasion, <i>S. aureus</i> becomes ubiquitinated and recognized by receptor proteins such as SQSTM1/p62 leading to phagophore recruitment. Yet, <i>S. aureus</i> evades phagophores and prevents further degradation by a MAPK14/p38α MAP kinase-mediated blockade of autophagy. Our study demonstrates a novel bacterial strategy to block autophagy and secure survival inside the host cell.</p