Preservasi, Konservasi dan Renovasi Kawasan Kota Tua Jakarta

“Great nation is a nation who\u27s always appreciates their own history,” that was a statement from Bung Karno. This paper is trying to lift a heritage district in Kota Tua Jakarta. A legacy that full of arts, cultures, stories, romance and tragedy that happened, and how the origin of the city formed. It\u27s very unfortunate if you see the condition right now. When all of the nations soo proud of their culture and history, everyone is competing to maintain and conserve their heritage and run the management very well. What happened with our heritage? Nowadays, Kota Tua district has been revitalized, but sadly, the process didn\u27t maintained well. So the results looks neglected and not in the good shape

Genomic Comparison between <em>Salmonella</em> Gallinarum and Pullorum: Differential Pseudogene Formation under Common Host Restriction

<div><p>Background</p><p><i>Salmonella</i> serovars Enteritidis and Gallinarum are closely related, but their host ranges are very different: the former is host-promiscuous and the latter can infect poultry only. Comparison of their genomic sequences reveals that Gallinarum has undergone much more extensive degradation than Enteritidis. This phenomenon has also been observed in other host restricted <i>Salmonella</i> serovars, such as Typhi and Paratyphi A. The serovar Gallinarum can be further split into two biovars: Gallinarum and Pullorum, which take poultry as their common host but cause distinct diseases, with the former eliciting typhoid and the latter being a dysentery agent. Genomic comparison of the two pathogens, with a focus on pseudogenes, would provide insights into the evolutionary processes that might have facilitated the formation of host-restricted <i>Salmonella</i> pathogens.</p> <p>Methodologies/Principal Findings</p><p>We sequenced the complete genome of Pullorum strains and made comparison with Gallinarum and other <i>Salmonella</i> lineages. The gene contents of Gallinarum and Pullorum were highly similar, but their pseudogene compositions differed considerably. About one fourth of pseudogenes had the same inactivation mutations in Gallinarum and Pullorum but these genes remained intact in Enteritidis, suggesting that the ancestral Gallinarum may have already been restricted to poultry. On the other hand, the remaining pseudogenes were either in the same genes but with different inactivation sites or unique to Gallinarum or Pullorum, reflecting unnecessary functions in infecting poultry.</p> <p>Conclusions</p><p>Our results support the hypothesis that the divergence between Gallinarum and Pullorum was initiated and facilitated by host restriction. Formation of pseudogenes instead of gene deletion is the major form of genomic degradation. Given the short divergence history of Gallinarum and Pullorum, the effect of host restriction on genomic degradation is huge and rapid, and such effect seems to be continuing to work. The pseudogenes may reflect the unnecessary functions for <i>Salmonella</i> within the poultry host.</p> </div

Circular Map of Pullorum str. CDC1983-67 genome.

<p>Circles range from 1 (inner circle) to 8 (outer circle): 1, coordinates of the genome; 2, GC content; 3, GC skew; 4–8, comparison of gene content with bvPu strain RKS5078, bvGA, Enteritidis, Dublin and Typhimurium, respectively. The locations of seven rRNA operons are indicated by the small outer orange blocks. The outmost arcs represent the chromosomal rearrangements between bvGa and bvPu (the larger one) and between bvGa and Enteritidis (the smaller one).</p

Relationship between bvPu str. CDC1983-67 and other <i>Salmonella</i> strains.

<p>(A) Association between dN/dS (y axis) and dS (x axis). dS represents synonymous substitution rate and dN represents non-synonymous substitution rate. (B) Association between indel/dS (y axis) and dS (x axis). The points in the plot are: bvPu, bvPu str. RKS5078; bvGa, bvGa str. 287/91; SEN, Enteritidis str. P125109; SDU, Dublin str. CT_02021853; SAR, <i>S. arizonae</i> str. RSK2980; other points represent the <i>S. enterica</i> subspecies I strains used for comparison in this study.</p

Maximum Likelihood Tree for <i>Salmonella enterica</i> strains.

<p>Genes that are conserved in all strains were aligned and concatenated for tree construction. In the brackets are the accession numbers of these genomes downloaded from NCBI database. A scale bar for the genetic distance is shown at the bottom.</p

Identification of Genes to Differentiate Closely Related <em>Salmonella</em> Lineages

<div><p>Background</p><p><i>Salmonella</i> are important human and animal pathogens. Though highly related, the <i>Salmonella</i> lineages may be strictly adapted to different hosts or cause different diseases, from mild local illness like gastroenteritis to fatal systemic infections like typhoid. Therefore, rapid and accurate identification of <i>Salmonella</i> is essential for timely and correct diagnosis of <i>Salmonella</i> infections. The current identification methods such as 16S rRNA sequencing and multilocus sequence typing are expensive and time consuming. Additionally, these methods often do not have sufficient distinguishing resolution among the <i>Salmonella</i> lineages.</p> <p>Methodologies/Principal Findings</p><p>We compared 27 completely sequenced <i>Salmonella</i> genomes to identify possible genomic features that could be used for differentiation of individual lineages. We concatenated 2372 core genes in each of the 27 genomes and constructed a neighbor-joining tree. On the tree, strains of each serotype were clustered tightly together and different serotypes were unambiguously separated with clear genetic distances, demonstrating systematic genomic divergence among the <i>Salmonella</i> lineages. We made detailed comparisons among the 27 genomes and identified distinct sets of genomic differences, including nucleotide variations and genomic islands (GIs), among the <i>Salmonella</i> lineages. Two core genes STM4261 and <i>entF</i> together could unambiguously distinguish all <i>Salmonella</i> lineages compared in this study. Additionally, strains of a lineage have a common set of GIs and closely related lineages have similar sets of GIs.</p> <p>Conclusions</p><p><i>Salmonella</i> lineages have accumulated distinct sets of mutations and laterally acquired DNA (e.g., GIs) in evolution. Two genes <i>entF</i> and STM4261 have diverged sufficiently among the <i>Salmonella</i> lineages to be used for their differentiation. Further investigation of the distinct sets of mutations and GIs will lead to novel insights into genomic evolution of <i>Salmonella</i> and greatly facilitate the elucidation of pathogeneses of <i>Salmonella</i> infections.</p> </div

Phylogenetic trees of the 27 <i>Salmonella</i> strains based on the core genome.

<p>Accession numbers are used for the bacterial strains (See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055988#pone-0055988-t001" target="_blank">Table 1</a>).</p

Numbers of lineage-specific nucleotides within the core gene sets.

<p>A, <i>S. bongori</i>; B, <i>S. arizonae</i>; C, <i>S.</i> Paratyphi A; D, <i>S.</i> Typhi; E, <i>S.</i> Agona; F, <i>S.</i> Schwarzengrund; G, <i>S.</i> Newport; H, <i>S.</i> Gallinarum; I, <i>S.</i> Enteritidis; J, <i>S.</i> Dublin; K, <i>S.</i> Choleraesuis; L, <i>S.</i> Paratyphi C; M, <i>S.</i> Paratyphi B; N, <i>S.</i> Heidelberg; O, <i>S.</i> Typhimurium.</p

Genomes analyzed in this study.

<p>Genomes analyzed in this study.</p

Apolipoprotein E3 Inhibits Rho to Regulate the Mechanosensitive Expression of Cox2

<div><p>Apolipoprotein E3 (apoE3) is thought to protect against atherosclerosis by enhancing reverse cholesterol transport. However, apoE3 also has cholesterol-independent effects that contribute to its anti-atherogenic properties. These include altering extracellular matrix protein synthesis and inhibiting vascular smooth muscle cell proliferation. Both of these cholesterol-independent effects result from an apoE3-mediated induction of cyclooxygenase-2 (Cox2). Nevertheless, how apoE3 regulates Cox2 remains unknown. Here, we show that apoE3 inhibits the activation of Rho, which reduces the formation of actin stress fibers and focal adhesions and results in cellular softening. Inhibition of Rho-Rho kinase signaling or direct cellular softening recapitulates the effect of apoE3 on Cox2 expression while a constitutively active Rho mutant overrides the apoE3 effect on both intracellular stiffness and Cox2. Thus, our results describe a previously unidentified mechanism by which an atheroprotective apolipoprotein uses Rho to control cellular mechanics and Cox2.</p></div