Mekanisme Reaksi Asam Borat Dengan Produk Radiolisis Akibat Radiasi Sinar- Pada Temperatur 25oc

MEKANISME REAKSI ASAM BORAT DENGAN PRODUK RADIOLISIS AKIBAT RADIASI SINAR- PADA TEMPERATUR 25OC. Telah dilakukan simulasi yang bertujuan untuk memahami mekanisme reaksi antara asam borat (H3BO3) yang ditambahkan kedalam air pendingin primer PWR dengan produk radiolisis akibat radiasi dengan sinar- pada temperatur 25oC. Simulasi dilakukan dengan menggunakan perangkat lunak ‘Facsimile\u27 yang berbasis kinetika reaksi yang berkelanjutan. Sebagai masukan adalah set reaksi kimia yang terdiri dari 61 jenis reaksi dengan konstanta kecepatan reaksinya, nilai-G spesi radiolisis akibat radiasi sinar-, laju dosis 10 dan 104 Gy/s, konsentrasi awal oksigen yang berhubungan dengan sistem aerasi (0,25M), deaerasi dan konsentrasi asam borat hingga konsentrasi 1M. Luaran di program berupa seri Perubahan konsentrasi vs waktu iradiasi. Data luaran kemudian diolah menggunakan perangkat pembuat grafik ‘Origin\u27. Validasi dilakukan dengan membandingkannya dengan hasil simulasi sebelumnya. Hasil validasi menunjukkan perbedaan yang tidak signifikan, sehingga diputuskan bahwa set reaksi sekarang adalah valid. Penambahan asam borat menekan konsentrasi oksigen secara signifikan. Hubungan kenaikan logaritmik penambahan konsentrasi H3BO3 vs produk oksigen menunjukkan hubungan linear yang menurun. Dari hasil simulasi dapat dipahami bahwa penambahan H3BO3 tidak hanya mengatur reaktivitas neutron pada temperatur 25oC tetapi juga memberikan imbas positif didalam menekan konsentrasi produk oksigen yang memegang peran penting di dalam proses korosi

Periodicity Manifestations in the Turbulent Regime of Globally Coupled Map Lattice

We revisit the globally coupled map lattice (GCML). We show that in the so called turbulent regime various periodic cluster attractor states are formed even though the coupling between the maps are very small relative to the non-linearity in the element maps. Most outstanding is a maximally symmetric three cluster attractor in period three motion (MSCA) due to the foliation of the period three window of the element logistic maps. An analytic approach is proposed which explains successfully the systematics of various periodicity manifestations in the turbulent regime. The linear stability of the period three cluster attractors is investigated.Comment: 34 pages, 8 Postscript figures, all in GCML-MSCA.Zi

Role of the podocyte in proteinuria

In recent years, the podocyte, with its elaborate cytoarchitecture and slit diaphragm, has been the focus of extensive research, yet its precise role in the glomerular filtration barrier is still debated. There are puzzling observations indicating that a comprehensive mechanistic model for glomerular filtration is still necessary. There is no doubt that podocytes are essential for glomerular filtration barrier integrity. However, most albumin never reaches the podocyte because it is prevented from entering the glomerular filter at the endothelium level. Another puzzling observation is that the glomerular filter never clogs despite its high load of several kilograms of plasma proteins per day. Recently, we proposed a novel model in which an electrical potential difference is generated across the glomerular filtration barrier by filtration. The model offers novel potential solutions to some of the riddles regarding the glomerular filter

Interferon-driven alterations of the host’s amino acid metabolism in the pathogenesis of typhoid fever

Enteric fever, caused by Salmonella enterica serovar Typhi, is an important public health problem in resource-limited settings and, despite decades of research, human responses to the infection are poorly understood. In 41 healthy adults experimentally infected with wild-type S. Typhi, we detected significant cytokine responses within 12 h of bacterial ingestion. These early responses did not correlate with subsequent clinical disease outcomes and likely indicate initial host–pathogen interactions in the gut mucosa. In participants developing enteric fever after oral infection, marked transcriptional and cytokine responses during acute disease reflected dominant type I/II interferon signatures, which were significantly associated with bacteremia. Using a murine and macrophage infection model, we validated the pivotal role of this response in the expression of proteins of the host tryptophan metabolism during Salmonella infection. Corresponding alterations in tryptophan catabolites with immunomodulatory properties in serum of participants with typhoid fever confirmed the activity of this pathway, and implicate a central role of host tryptophan metabolism in the pathogenesis of typhoid fever

The renal cortical interstitium: morphological and functional aspects

The renal interstitial compartment, situated between basement membranes of epithelia and vessels, contains two contiguous cellular networks. One network is formed by interstitial fibroblasts, the second one by dendritic cells. Both are in intimate contact with each other. Fibroblasts are interconnected by junctions and connected to basement membranes of vessels and tubules by focal adhesions. Fibroblasts constitute the “skeleton” of the kidney. In the renal cortex, fibroblasts produce erythropoietin and are distinguished from other interstitial cells by their prominent F-actin cytoskeleton, abundance of rough endoplasmic reticulum, and by ecto-5′-nucleotidase expression in their plasma membrane. The resident dendritic cells belong to the mononuclear phagocyte system and fulfil a sentinel function. They are characterized by their expression of MHC class II and CD11c. The central situation of fibroblasts suggests that signals from tubules, vessels, and inflammatory cells converge in fibroblasts and elicit an integrated response. Following tubular damage and inflammatory signals fibroblasts proliferate, change to the myofibroblast phenotype and increase their collagen production, potentially resulting in renal fibrosis. The acquisition of a profibrotic phenotype by fibroblasts in renal diseases is generally considered a main causal event in the progression of chronic renal failure. However, it might also be seen as a repair process

Megalin/LRP2 Expression Is Induced by Peroxisome Proliferator-Activated Receptor -Alpha and -Gamma: Implications for PPARs' Roles in Renal Function

BACKGROUND: Megalin is a large endocytic receptor with relevant functions during development and adult life. It is expressed at the apical surface of several epithelial cell types, including proximal tubule cells (PTCs) in the kidney, where it internalizes apolipoproteins, vitamins and hormones with their corresponding carrier proteins and signaling molecules. Despite the important physiological roles of megalin little is known about the regulation of its expression. By analyzing the human megalin promoter, we found three response elements for the peroxisomal proliferator-activated receptor (PPAR). The objective of this study was to test whether megalin expression is regulated by the PPARs. METHODOLOGY/PRINCIPAL FINDINGS: Treatment of epithelial cell lines with PPARα or PPARγ ligands increased megalin mRNA and protein expression. The stimulation of megalin mRNA expression was blocked by the addition of specific PPARα or PPARγ antagonists. Furthermore, PPAR bound to three PPAR response elements located in the megalin promoter, as shown by EMSA, and PPARα and its agonist activated a luciferase construct containing a portion of the megalin promoter and the first response element. Accordingly, the activation of PPARα and PPARγ enhanced megalin expression in mouse kidney. As previously observed, high concentrations of bovine serum albumin (BSA) decreased megalin in PTCs in vitro; however, PTCs pretreated with PPARα and PPARγ agonists avoided this BSA-mediated reduction of megalin expression. Finally, we found that megalin expression was significantly inhibited in the PTCs of rats that were injected with BSA to induce tubulointerstitial damage and proteinuria. Treatment of these rats with PPARγ agonists counteracted the reduction in megalin expression and the proteinuria induced by BSA. CONCLUSIONS: PPARα/γ and their agonists positively control megalin expression. This regulation could have an important impact on several megalin-mediated physiological processes and on pathophysiologies such as chronic kidney disease associated with diabetes and hypertension, in which megalin expression is impaired