EFEK PERKUATAN GLASS FIBER REINFORCE POLYMER-SHEET PADA BALOK BETON BERTULANG DENGAN TULANGAN KOROSI

Abstrak Artikel ini menyajikan tentang balok beton bertulang yang tulangannya telah korosi kemudian diberi perkuatan ekternal berupa serat glass tipe lembaran atau Glass Fiber reinforced Polymer-Sheet (GFRP-S). Pada studi ini variabel berdasarkan variasi tingkat korosi pada tulangan. Lima macam benda uji yang digunakan berbentuk balok dengan dimensi 15x20 cm panjang 160 cm. Tulangan utama yang digunakan besi f12 dan tulangan sengkang f8-100. Mutu beton digunakan 25 MPa. Balok beton bertulangan normal tanpa perkuatan sebagai balok kontrol (BN), balok beton bertulangan normal dengan perkuatan GFRP-S (BP), balok beton bertulangan korosi dengan perkuatan GFRP-S (BPK), variasi waktu pengkorosian tulangan selama 2 minggu (BPK2), 4 minggu (BPK4) dan 6 minggu (BPK6) dengan metode perendaman pada larutan asam sulfat 2,0%. Balok diperkuat GFRP-S pada daerah Tarik di bagian bawah balok. Pengujian lentur dengan twopoint load. Hasil penelitian menunjukkan bahwa balok beton bertulang yang diperkuat dengan GFRP-S mempunyai kapasitas lebih besar dibandingkan dengan balok normal sebesar 12,07%. Balok beton bertulang dengan tulangan tingkat korosi lebih besar (pengkorosian 6 minggu) cenderung menurunkan kapasitas balok namun kapasitasnya masih lebih besar dari balok normal sebesar 1,38%. Kata kunci: balok beton, tulangan korosi, asam sulfat, GFRP-S  Abstract This article presents about reinforced concrete beams whose reinforcement has been corroded and then externally reinforced in the form of sheet type glass fiber or Glass Fiber Reinfroced Polymer-Sheet (GFRP-S). In this study, the variables are based on variations in the level of corrosion on the reinforcement. Five kinds of test objects used in the form of blocks with dimensions of 15x20 cm and length of 160 cm. The main reinforcement used is f12 and f8-100 stirrup reinforcement. The quality of the concrete used is 25 MPa. Normal reinforced concrete beams without reinforcement as control beams (BN), normal reinforced concrete beams with GFRP-S reinforcement (BP), corrosion reinforced concrete beams with GFRP-S reinforcement (BPK), variations in reinforcement corrosion time for 2 weeks (BPK2), 4 weeks (BPK4)and 6 weeks (BPK6) by immersion method in 2.0% sulfuric acid solution. The beam is reinforced with GFRP-S in the Tensile region at the bottom of the beam. Flexural test with two point load. The results showed that reinforced concrete beams reinforced with GFRP-S had a larger capacity than normal beams by 12.70%. Reinforced concrete beams with reinforcement with a higher corrosion rate (6 weeks corrosion) tend to reduce the capacity of the beam but its capacity is still larger than normal beams by 1.38%. Keywords: concrete beam, corrosion reinforcement, sulfuric acid, GFRP-S

XIAP Regulates Cytosol-Specific Innate Immunity to Listeria Infection

The inhibitor of apoptosis protein (IAP) family has been implicated in immune regulation, but the mechanisms by which IAP proteins contribute to immunity are incompletely understood. We show here that X-linked IAP (XIAP) is required for innate immune control of Listeria monocytogenes infection. Mice deficient in XIAP had a higher bacterial burden 48 h after infection than wild-type littermates, and exhibited substantially decreased survival. XIAP enhanced NF-κB activation upon L. monocytogenes infection of activated macrophages, and prolonged phosphorylation of Jun N-terminal kinase (JNK) specifically in response to cytosolic bacteria. Additionally, XIAP promoted maximal production of pro-inflammatory cytokines upon bacterial infection in vitro or in vivo, or in response to combined treatment with NOD2 and TLR2 ligands. Together, our data suggest that XIAP regulates innate immune responses to L. monocytogenes infection by potentiating synergy between Toll-like receptors (TLRs) and Nod-like receptors (NLRs) through activation of JNK- and NF-κB–dependent signaling

Management of obstetric anal sphincter injury: a systematic review & national practice survey

BACKGROUND: We aim to establish the evidence base for the recognition and management of obstetric anal sphincter injury (OASI) and to compare this with current practice amongst UK obstetricians and coloproctologists. METHODS: A systematic review of the literature and a postal questionnaire survey of consultant obstetricians, trainee obstetricians and consultant coloproctologists was carried out. RESULTS: We found a wide variation in experience of repairing acute anal sphincter injury. The group with largest experience were consultant obstetricians (46.5% undertaking ≥ 5 repairs/year), whilst only 10% of responding colorectal surgeons had similar levels of experience (p < 0.001). There was extensive misunderstanding in terms of the definition of obstetric anal sphincter injuries. Overall, trainees had a greater knowledge of the correct classification (p < 0.01). Observational studies suggest that a new 'overlap' repair using PDS sutures with antibiotic cover gives better functional results. However, our literature search found only one randomised controlled trial (RCT) on the technique of repair of OASI, which showed no difference in incidence of anal incontinence at three months. Despite this, there was a wide variation in practice, with 337(50%) consultants, 82 (55%) trainees and 80 (89%) coloproctologists already using the 'overlap' method for repair of a torn EAS (p < 0.001). Although over 50% of colorectal surgeons would undertake long-term follow-up of their patients, this was the practice of less than 10% of obstetricians (p < 0.001). Whilst over 70% of coloproctologists would recommend an elective caesarean section in a subsequent pregnancy, only 22% of obstetric consultants and 14% of trainees (p < 0.001). CONCLUSION: An agreed classification of OASI, development of national guidelines, formalised training, multidisciplinary management and further definitive research is strongly recommended

Canine models of copper toxicosis for understanding mammalian copper metabolism

Hereditary forms of copper toxicosis exist in man and dogs. In man, Wilson’s disease is the best studied disorder of copper overload, resulting from mutations in the gene coding for the copper transporter ATP7B. Forms of copper toxicosis for which no causal gene is known yet are recognized as well, often in young children. Although advances have been made in unraveling the genetic background of disorders of copper metabolism in man, many questions regarding disease mechanisms and copper homeostasis remain unanswered. Genetic studies in the Bedlington terrier, a dog breed affected with copper toxicosis, identified COMMD1, a gene that was previously unknown to be involved in copper metabolism. Besides the Bedlington terrier, a number of other dog breeds suffer from hereditary copper toxicosis and show similar phenotypes to humans with copper storage disorders. Unlike the heterogeneity of most human populations, the genetic structure within a purebred dog population is homogeneous, which is advantageous for unraveling the molecular genetics of complex diseases. This article reviews the work that has been done on the Bedlington terrier, summarizes what was learned from studies into COMMD1 function, describes hereditary copper toxicosis phenotypes in other dog breeds, and discusses the opportunities for genome-wide association studies on copper toxicosis in the dog to contribute to the understanding of mammalian copper metabolism and copper metabolism disorders in man