Publications by authors named "B Batchuluun"

Article Synopsis
  • * Prion-infected cells showed disruptions in the nuclear translocation of NF-κB, leading to increased mitochondrial reactive oxygen species (mtROS) and activation of NLRP3 inflammasomes, which suppressed cell death (necroptosis) due to IAV.
  • * The findings suggest that cytosolic PrP may play a protective role against viral infections by interfering with NF-κB functioning and stimulating an antiviral immune response via NLRP3 inflammasome activation.
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Atherosclerotic cardiovascular disease is characterized by both chronic low-grade inflammation and dyslipidemia. The AMP-activated protein kinase (AMPK) inhibits cholesterol synthesis and dampens inflammation but whether pharmacological activation reduces atherosclerosis is equivocal. In the current study, we found that the orally bioavailable and highly selective activator of AMPKβ1 complexes, PF-06409577, reduced atherosclerosis in two mouse models in a myeloid-derived AMPKβ1 dependent manner, suggesting a critical role for macrophages.

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Midwives are professionals who fulfill maternal and child health needs. In Mongolia, midwives were unable to transfer their knowledge and skills to the next generation midwives last few decades. The details of their experiences and the comprehensive aspects of continuing professional development (CPD) are still unclear.

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Unlabelled: In contrast to the well-defined biological feedback loops controlling glucose, the mechanisms by which the body responds to changes in fatty acid availability are less clearly defined. Growth differentiating factor 15 (GDF15) suppresses the consumption of diets high in fat but is paradoxically increased in obese mice fed a high-fat diet. Given this interrelationship, we investigated whether diets high in fat could directly increase GDF15 independently of obesity.

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Increased liver de novo lipogenesis (DNL) is a hallmark of nonalcoholic steatohepatitis (NASH). A key enzyme controlling DNL upregulated in NASH is ATP citrate lyase (ACLY). In mice, inhibition of ACLY reduces liver steatosis, ballooning, and fibrosis and inhibits activation of hepatic stellate cells.

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