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Molecular Diagnosis of <i>Taenia saginata</i> Tapeworm Infection in 2 Schoolchildren, Myanmar
Won, Eun Jeong,Jung, Bong-Kwang,Song, Hyemi,Kim, Mi-Seon,Kim, Hyun-Seung,Lee, Keon Hoon,Kim, Min-Jae,Shin, Myung Geun,Shin, Jong Hee,Suh, Soon-Pal,Hong, Sung-Jong,Sohn, Woon-Mok,Htoon, Thi Thi,Tin, Ht Centers for Disease Control and Prevention 2018 Emerging infectious diseases Vol.24 No.6
<P><I>Taenia saginata</I> is the most common human tapeworm worldwide but has been unknown in Myanmar. In 2017, fecal examination in Yangon, Myanmar, revealed eggs of <I>Taenia</I> species in 2 children from a monastic school. Several proglottids expelled after medication with praziquantel were morphologically and molecularly confirmed to be <I>T. saginata</I> tapeworms.</P>
Prevention of Acute/Severe Hypoglycemia-Induced Neuron Death by Lactate Administration
Won, Seok Joon,Jang, Bong Geom,Yoo, Byung Hoon,Sohn, Min,Lee, Min Woo,Choi, Bo Young,Kim, Jin Hee,Song, Hong Ki,Suh, Sang Won SAGE Publications 2012 Journal of cerebral blood flow and metabolism Vol.32 No.6
<P> Hypoglycemia-induced cerebral neuropathy can occur in patients with diabetes who attempt tight control of blood glucose and may lead to cognitive dysfunction. Accumulating evidence from animal models suggests that hypoglycemia-induced neuronal death is not a simple result of glucose deprivation, but is instead the end result of a multifactorial process. In particular, the excessive activation of poly (ADP-ribose) polymerase-1 (PARP-1) consumes cytosolic nicotinamide adenine dinucleotide (NAD<SUP>+</SUP>), resulting in energy failure. In this study, we investigate whether lactate administration in the absence of cytosolic NAD<SUP>+</SUP> affords neuroprotection against hypoglycemia-induced neuronal death. Intraperitoneal injection of sodium L-lactate corrected arterial blood pH and blood lactate concentration after hypoglycemia. Lactate administered without glucose was not sufficient to promote electroencephalogram recovery from an isoelectric state during hypoglycemia. However, supplementation of glucose with lactate reduced neuronal death by ∼80% in the hippocampus. Hypoglycemia-induced superoxide production and microglia activation was also substantially reduced by administration of lactate. Taken together, these results suggest an intriguing possibility: that increasing brain lactate following hypoglycemia offsets the decrease in NAD<SUP>+</SUP> due to overactivation of PARP-1 by acting as an alternative energy substrate that can effectively bypass glycolysis and be fed directly to the citric acid cycle to maintain cellular ATP levels. </P>