Introduction: contains Cover, Table of Contents, Letter from the Editor, and Masthead

The Richmond Journal of Law and Technology is proud to present the third issue of the 2008–2009 academic school year, which also is our Annual Survey on E-Discovery

KAJIAN KUAT LENTUR BALOK BETON BERTULANG PASCA PEMBAKARAN BERDASARKAN VARIASI MUTU DAN SUHU

Kebakaran merupakan salah satu bencana yang harus diwaspadai karena banyak menimbulkan kerugian bagi pemilik maupun orang yang berada di sekitar bangunan. Penurunan kapasitas lentur diakibatkan oleh pemanasan terhadap beton yang berfungsi membungkus tulangan baja mengalami kerusakan dan temperatur panas itu masuk melalui pori-pori beton sehingga baja mendapat perlakuan panas yang dapat menyebabkan penurunan kekuatan struktur tersebut. Tujuan dalam penelitian ini adalah mengetahui perubahan kuat lentur balok beton bertulang dengan pembakaran 500oC dan 750oC, dengan variasi mutu c’= 25 MPa, c’= 30 MPa, dan c’= 35 Mpa. Hasil dari penelitian menunjukkan bahwa Kuat lentur balok beton bertulang pasca pembakaran pada suhu 500oC dan 750oC untuk c ’= 25 MPa mengalami penurunan dari 105,73 MPa menjadi 70,84 MPa dan 49,63 MPa, sehingga persentase penurunannya sebesar 33,00% dan 79,18%. Untuk balok beton bertulang c ’= 30 MPa pada pembakaran suhu 500oC dan 750oC mengalami penurunan dari 138,32 MPa menjadi 94,85 MPa dan 66,02 MPa, sehingga persentase penurunannya sebesar 31,43% dan 76,23%. Untuk balok beton bertulang c ’= 35 MPa pada pembakaran suhu 500oC dan 750oC mengalami penurunan dari 144,40 MPa menjadi 120,98 MPa dan 69,67 MPa, sehingga persentase penurunannya sebesar 16,22% dan 61,77%. Kata kunci: Beton bertulang; Kebakaran; Kuat lentur; Mutu; Suh

Genome wide transcriptome profiling of a murine acute melioidosis model reveals new insights into how Burkholderia pseudomallei overcomes host innate immunity

Abstract Background At present, very little is known about how Burkholderia pseudomallei (B. pseudomallei) interacts with its host to elicit melioidosis symptoms. We established a murine acute-phase melioidosis model and used DNA microarray technology to investigate the global host/pathogen interaction. We compared the transcriptome of infected liver and spleen with uninfected tissues over an infection period of 42 hr to identify genes whose expression is altered in response to an acute infection. Results Viable B. pseudomallei cells were consistently detected in the blood, liver and spleen during the 42 hr course of infection. Microarray analysis of the liver and spleen over this time course demonstrated that genes involved in immune response, stress response, cell cycle regulation, proteasomal degradation, cellular metabolism and signal transduction pathways were differentially regulated. Up regulation of toll-like receptor 2 (TLR2) gene expression suggested that a TLR2-mediated signalling pathway is responsible for recognition and initiation of an inflammatory response to the acute B. pseudomallei infection. Most of the highly elevated inflammatory genes are a cohort of "core host immune response" genes commonly seen in general inflammation infections. Concomitant to this initial inflammatory response, we observed an increase in transcripts associated with cell-death, caspase activation and peptidoglysis that ultimately promote tissue injury in the host. The complement system responsible for restoring host cellular homeostasis and eliminating intracellular bacteria was activated only after 24 hr post-infection. However, at this time point, diverse host nutrient metabolic and cellular pathways including glycolysis, fatty acid metabolism and tricarboxylic acid (TCA) cycle were repressed. Conclusions This detailed picture of the host transcriptional response during acute melioidosis highlights a broad range of innate immune mechanisms that are activated in the host within 24 hrs, including the core immune response commonly seen in general inflammatory infections. Nevertheless, this activation is suppressed at 42 hr post-infection and in addition, suboptimal activation and function of the downstream complement system promotes uncontrolled spread of the bacteria.</p