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Bangkok, Thailand

Mahidol University is a public research university in Bangkok, Thailand. Established in 1888 as School of Medical Practitioners, Siriraj Hospital and reorganized in 1943 as University of Medical science . The university originally focused on Health science but also expanded to other fields in recent decades. MU hosted the first medical school of Thailand, the Siriraj Medical School, from which the university traced its origin. Today, MU offers a wide range of graduate and undergraduate programs from natural science to liberal arts with remote campuses in Kanchanaburi, Nakhon Sawan, and Amnat Charoen provinces. In terms of fiscal budget and portion of budget spent on research programs, MU receives the highest budget of any public university; about $147 million each year, most of which is granted for graduate research programs. Mahidol University has been ranked Thailand's No. 1 university in 2011 by QS Asian University Rankings. Wikipedia.

Jitrapakdee S.,Mahidol University
International Journal of Biochemistry and Cell Biology | Year: 2012

Hepatic gluconeogenesis is a major pathway that maintains normal plasma glucose levels during prolonged starvation. The aim of this review is to provide insights into the integration of transcriptional regulation of gluconeogenic enzyme genes in response to nutritional and hormonal changes. The roles of transcription factors/co-regulators in response to those factors will be discussed. Overall, glucagon and glucocorticoids are positive regulators of gluconeogenesis. Glucagon, via cAMP, promotes the interaction of cAMP-responsive binding protein with CREB-regulated transcription coactivator 2 which facilitates its binding to cAMP-responsive elements (CREs). The response to glucocorticoids is mediated by the glucocorticoid receptor that binds to glucocorticoid responsive elements (GREs) in the promoters of gluconeogenic genes. These CREs and GREs may be arranged as distinct elements or combined to form a "unit" to ensure the maximal transcriptional response to these hormones. The hepatocyte nuclear factors, forkhead O box, and the peroxisome proliferator-activated receptor-γ coactivator 1α can also synergistically increase transcription of gluconeogenic genes. Surtuin 1, an energy sensor can also modify the transcriptional activity of some of these transcription factors. In contrast, insulin secreted during fed conditions acts to repress transcription of gluconeogenic enzymes. This is achieved via activation of Akt/PKB and the consequent disruption of interactions between certain transcription factors/coactivators and their positive response elements in the promoters of those genes. Hypothalamic signaling via the insulin/leptin axis also regulates hepatic gluconeogenesis. Mice lacking the above transcription factors/coactivators show impaired gluconeogenesis, indicating their essential roles in the control of this vital metabolic process. © 2011 Elsevier Ltd. All rights reserved. Source

Siripunvaraporn W.,Mahidol University
Surveys in Geophysics | Year: 2012

In the last few decades, the demand for three-dimensional (3-D) inversions for magnetotelluric data has significantly driven the progress of 3-D codes. There are currently a lot of new 3-D inversion and forward modeling codes. Some, such as the WSINV3DMT code of the author, are available to the academic community. The goal of this paper is to summarize all the important issues involving 3-D inversions. It aims to show how inversion works and how to use it properly. In this paper, I start by describing several good reasons for doing 3-D inversion instead of 2-D inversion. The main algorithms for 3-D inversion are reviewed along with some comparisons of their advantages and disadvantages. These algorithms are the classical Occam's inversion, the data space Occam's inversion, the Gauss-Newton method, the Gauss-Newton with the conjugate gradient method, the non-linear conjugate gradient method, and the quasi-Newton method. Other variants are based on these main algorithms. Forward modeling, sensitivity calculations, model covariance and its parallel implementation are all necessary components of inversions and are reviewed here. Rules of thumb for performing 3-D inversion are proposed for the benefit of the 3-D inversion novice. Problems regarding 3-D inversions are discussed along with suggested topics for future research for the developers of the next decades. © 2011 Springer Science+Business Media B.V. Source

White N.J.,Mahidol University
Malaria Journal | Year: 2011

Plasmodium vivax is a major cause of febrile illness in endemic areas of Asia, Central and South America, and the horn of Africa. Plasmodium vivax infections are characterized by relapses of malaria arising from persistent liver stages of the parasite (hypnozoites) which can be prevented only by 8-aminoquinoline anti-malarials. Tropical P. vivax relapses at three week intervals if rapidly eliminated anti-malarials are given for treatment, whereas in temperate regions and parts of the sub-tropics P. vivax infections are characterized either by a long incubation or a long-latency period between illness and relapse - in both cases approximating 8-10 months. The epidemiology of the different relapse phenotypes has not been defined adequately despite obvious relevance to malaria control and elimination. The number of sporozoites inoculated by the anopheline mosquito is an important determinant of both the timing and the number of relapses. The intervals between relapses display a remarkable periodicity which has not been explained. Evidence is presented that the proportion of patients who have successive relapses is relatively constant and that the factor which activates hypnozoites and leads to regular interval relapse in vivax malaria is the systemic febrile illness itself. It is proposed that in endemic areas a large proportion of the population harbours latent hypnozoites which can be activated by a systemic illness such as vivax or falciparum malaria. This explains the high rates of vivax following falciparum malaria, the high proportion of heterologous genotypes in relapses, the higher rates of relapse in people living in endemic areas compared with artificial infection studies, and, by facilitating recombination between different genotypes, contributes to P. vivax genetic diversity particularly in low transmission settings. Long-latency P. vivax phenotypes may be more widespread and more prevalent than currently thought. These observations have important implications for the assessment of radical treatment efficacy and for malaria control and elimination. © 2011 White; licensee BioMed Central Ltd. Source

White N.J.,Mahidol University
The Lancet infectious diseases | Year: 2013

Falciparum malaria is transmitted by anopheline mosquitoes that have fed on blood containing gametocytes of Plasmodium falciparum. In areas of low malaria transmission, where symptomatic infections contribute substantially to malaria transmission, the use of gametocytocidal drugs reduces the incidence of malaria. Artemisinin-based combination therapies provide high cure rates and substantially reduce gametocyte carriage. Artemisinin resistance in P falciparum lessens overall gametocytocidal activity, which provides a selective pressure to the spread of these resistant parasites. The 8-aminoquinoline compounds possess unique gametocytocidal properties and rapidly sterilise the mature transmissible stages of P falciparum. The addition of one dose of primaquine to artemisinin-based combination regimens could help to counter the spread of artemisinin resistance. Although primaquine is commonly recommended for falciparum and vivax malaria, concerns about drug-related haemolysis frequently prevent its administration. The limited available evidence on transmission-blocking effects of primaquine and its forerunner plasmoquine suggests that doses lower than currently recommended (0.50-0.75 mg base per kg), which would be safer, might still be very effective. Copyright © 2013 Elsevier Ltd. All rights reserved. Source

Angchaisuksiri P.,Mahidol University
Thrombosis Research | Year: 2014

Blood coagulation activation is frequently found in patients with malaria. Clinically apparent bleeding or disseminated intravascular coagulation (DIC) is associated with very severe disease and a high mortality. Protein C, protein S, and antithrombin levels were found to be low in P. falciparum, but were normal in P. vivax infection. Plasma levels of plasminogen activator inhibitor-1 were high in cases of P. falciparum infection whereas tissue plasminogen activator levels were low. Elevated plasma levels of von Willebrand factor (vWF) and vWF propeptide, thrombomodulin, endothelial microparticles have been reported in P. falciparum-infected patients. It has been demonstrated that severe P. falciparum infection is associated with acute endothelial cell (EC) activation, abnormal circulating ultralarge vWF multimers, and a significant reduction in plasma ADAMTS13 function. These changes may result in intravascular platelet aggregation, thrombocytopenia, and microvascular disease. It has also been shown that P. falciparum-parasitized red blood cells (pRBCs) induce tissue factor (TF) expression in microvascular ECs in vitro. Recently, loss of endothelial protein C receptor (EPCR) localized to sites of cytoadherent pRBCs in cerebral malaria has been demonstrated. Severe malaria is associated with parasite binding to EPCR. The cornerstone of the treatment of coagulopathy in malaria is the use of effective anti-malarial agents. DIC with spontaneous systemic bleeding should be treated with screened blood products. Study in Thailand has shown that for patients who presented with parasitemia > 30% and severe systemic complications such as acute renal failure and ARDS, survival was superior in the group who received exchange transfusion. The use of heparin is generally restricted to patients with DIC and extensive deposition of fibrin, as occurs with purpura fulminans or acral ischemia. Antiplatelet agents interfere with the protective effect of platelets against malaria and should be avoided. © 2013 Elsevier Ltd. All rights reserved. Source

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