Anthropogenic carbon dioxide origin tracing study in Anmyeon-do, South Korea: Based on STILT-footprint and emissions data.

Tracking the origin of greenhouse gases (GHGs) is critical for understanding regional GHG concentration variation and developing effective policies to reduce GHG emissions. This study provides quantitative information about the surface contribution to enhancement of carbon dioxide (CO2) concentration at Anmyeon-do (AMY), South Korea, using Stochastic Time-Inverted Lagrangian Transport (STILT) model and anthropogenic CO2 emission data. CO2 enhancement simulated by the STILT and emission data was positively correlated with measured CO2 anomalies at AMY with a correlation coefficient above 0.5. High and low CO2 days were selected using ground measurements of the CO2 mixing ratio at AMY during the winter season of 2018-2019. The surface contributions for the high and low CO2 days at AMY were compared quantitatively. When the high concentration was observed in AMY, the CO2 enhancements were dominated by domestic regions, especially from the metropolitan area in South Korea, due to the high footprint and large CO2 emissions. From the perspective of foreign regions, the surface contribution of eastern China regions (Shandong, Jiangsu-Shanghai) increased during high CO2 days compared to low CO2 days at AMY. During the high CO2 days, the ratio between CO2 and carbon monoxide, a co-emitted species, is large when the surface contribution of eastern China regions is relatively strong due to different regional combustion efficiency (i.e., high combustion efficiency in South Korea compared to that in China). The surface contribution based on STILT and emission data is useful for understanding the cause of high GHG concentration at the receptor (AMY in this study).

Effects of Novel Probiotics in a Murine Model of Irritable Bowel Syndrome.

Background/Aims: Dysbiosis is an important factor in the pathogenesis of irritable bowel syndrome (IBS). Several studies have reported promising results using probiotics for the treatment of IBS. This study evaluated the efficacy of novel probiotics isolated from Kimchi, a Korean fermented food, and the feces of healthy Vietnamese people in a murine model of IBS. Methods: Lactobacillus paracasei DK121 was isolated from Kimchi, and L. salivarius V4 and L. plantarum V7 were isolated from the feces of healthy Vietnamese people residing in Korea. Forty rats were allocated to receive one of the study strains, a mixture of the strains, or the vehicle. After 5 days of administration, the rats were restrained in a cage to induce IBS. The effects of the probiotics on IBS were analyzed by evaluating the stool weights and stool consistency scores. Results: The primary outcome was analyzed upon the completion of a three-week experiment. The rats in the V7 group showed lower stool weights than those in the control group at week 2 (median: 1.10 [V7] vs. 2.35 [control], p=0.04, Mann-Whitney U-test) and week 3 (median: 1.10 [V7] vs. 2.80 [control], p=0.017). The rats in the DK121 (median: 2.00, p=0.007), V7 (median: 2.00, p=0.004), and mixture (median: 1.50, p=0.001) groups showed better stool consistency scores at week 2 than the control group (median: 3.00). Conclusions: The novel probiotics have beneficial effects on defecation in a murine model of IBS. Human studies confirming the efficacy are warranted.

MicroRNA 486 is a potentially novel target for the treatment of spinal cord injury.

MicroRNAs have been shown to effectively regulate gene expression at the translational level. Recently, we identified novel microRNAs that were upregulated in a mouse model of spinal cord injury. Among those, we have focused on microRNA 486, which directly represses NeuroD6 expression through a conserved sequence in its untranslated region. We correlated the overexpression of microRNA 486 in motor neurons with a poor outcome due to progressive neurodegeneration and a pathophysiology that is mediated by reactive oxygen species. The expression of microRNA 486 was induced by reactive oxygen species that were produced by inflammatory factors, and reactive oxygen species were accumulated in response to the knockdown of NeuroD6, which enhances the downregulation of glutathione peroxidase 3 and thioredoxin-like 1 after traumatic spinal cord injury. NeuroD6 directly bound to regulatory regions of thioredoxin-like 1 and glutathione peroxidase 3 in motor neurons and activated their expression, which promoted reactive oxygen species scavenging. Moreover, knocking down microRNA 486 induced the expression of NeuroD6, which effectively ameliorated the spinal cord injury and allowed the mice to recover motor function. The infusion of exogenic NeuroD6 in spinal cord injury lesions effectively blocked apoptosis by reactivating thioredoxin-like 1 and glutathione peroxidase 3, which was accompanied by a recovery of motor function. Collectively, these findings have identified a novel microRNA in spinal cord injury lesions called microRNA 486, demonstrating a new role for NeuroD6 in neuroprotection, and suggest a potential therapeutic target for spinal cord injuries.