A case report of type VI dual left anterior descending coronary artery anomaly presenting with non-ST-segment elevation myocardial infarction

BACKGROUND: Type VI dual left anterior descending artery (LAD) is a rare coronary anomaly, the first case of which has recently been described. This is the first report of type VI dual LAD anomaly in which the patient presented with non-ST-segment elevation myocardial infarction and percutaneous coronary intervention was performed in the anomalously originating LAD. CASE PRESENTATION: A 52-year-old man with diabetes, hypertension and hyperlipidemia presented with chest pain without ST elevation on EKG, although the patient’s troponin I level was elevated. Coronary angiography revealed a short LAD originating from the left main coronary artery and a long LAD originating from the proximal portion of the right coronary artery (RCA). Three-dimensional reconstruction of computed tomography of images revealed that the long LAD originated from the proximal RCA and coursed between the right ventricular outflow tract (RVOT) and the aortic root before entering the mid anterior interventricular groove. The high take-off RCA originated underneath the RVOT, pointing downwards and forming an acute angle with the proximal portion of the long LAD. The anomalous long LAD displayed significant stenosis. We performed successful percutaneous coronary intervention (PCI) in the anomalous artery. CONCLUSION: With accurate understanding of the coronary anatomy and appropriate hardware selection, successful PCI can be performed in the in the long LAD in patients with type VI dual LAD anomaly

There are arbitrary large minimal 2-pinning configurations

International audienceWe characterize minimal configurations that pin a line in every $2$-plane

Fatty acid desaturase (FADS) gene polymorphisms and insulin resistance in association with serum phospholipid polyunsaturated fatty acid composition in healthy Korean men: cross-sectional study

<p>Abstract</p> <p>Background</p> <p>We investigated the relationship between fatty acid desaturase (<it>FADS</it>) gene polymorphisms and insulin resistance (IR) in association with serum phospholipid polyunsaturated fatty acid (FA) composition in healthy Korean men.</p> <p>Methods</p> <p>Healthy men (n = 576, 30 ~ 79 years old) were genotyped for rs174537 near <it>FADS1 </it>(<it>FEN1</it>-10154G>T), <it>FADS2 </it>(rs174575C>G, rs2727270C>T), and <it>FADS3 </it>(rs1000778C>T) SNPs. Dietary intake, serum phospholipid FA composition and HOMA-IR were measured.</p> <p>Results</p> <p>Fasting insulin and HOMA-IR were significantly higher in the rs174575G allele carriers than the CC homozygotes, but lower in the rs2727270T allele carriers than the CC homozygotes. The proportion of linoleic acid (18:2ω-6, LA) was higher in the minor allele carriers of <it>FEN1</it>-10154G>T, rs174575C>G and rs2727270C>T than the major homozygotes, respectively. On the other hand, the proportions of dihomo-γ-linolenic acid (20:3ω-6, DGLA) and arachidonic acid (20:4ω-6, AA) in serum phospholipids were significantly lower in the minor allele carriers of <it>FEN1</it>-10154 G>T carriers and rs2727270C>T than the major homozygotes respectively. AA was also significantly lower in the rs1000778T allele carriers than the CC homozygotes. HOMA-IR positively correlated with LA and DGLA and negatively with AA/DGLA in total subjects. Interestingly, rs174575G allele carriers showed remarkably higher HOMA-IR than the CC homozygotes when subjects had higher proportions of DLGA (≥1.412% in total serum phospholipid FA composition) (<it>P </it>for interaction = 0.009) or of AA (≥4.573%) (<it>P </it>for interaction = 0.047).</p> <p>Conclusion</p> <p>HOMA-IR is associated with <it>FADS </it>gene cluster as well as with FA composition in serum phospholipids. Additionally, HOMA-IR may be modulated by the interaction between rs174575C>G and the proportion of DGLA or AA in serum phospholipids.</p

Leisure sedentary time is differentially associated with hypertension, diabetes mellitus, and hyperlipidemia depending on occupation

Abstract Background Sedentary behavior is considered an independent cause of cardio-metabolic diseases, regardless of physical activity level and obesity. Few studies have reported the association between leisure sedentary time and cardio-vascular diseases in terms of occupation. Methods We performed a cross-sectional study using data from the Korean Community Health Survey (KCHS) for 240,086 participants assessed in 2011 and 2013. Occupation was categorized into four groups: farmer or fisherman, laborer, and soldier (Group I); service worker, salesperson, technician, mechanic, production worker, and engineer (Group II); manager, expert, specialist, and clerk (Group III); and unemployed (Group IV). Leisure sedentary time was divided into five groups: 0 h, 1 h, 2 h, 3 h, and 4+ h. The association between leisure sedentary time on weekdays and hypertension/diabetes mellitus/hyperlipidemia for different occupations was analyzed using simple and multiple logistic regression analyses with complex sampling. Results In Groups I, II and III, no length of sedentary time was associated with hypertension, and only 3 h or 4+ h of sedentary time was associated with diabetes mellitus and hyperlipidemia. Group IV showed a significant association with hypertension and diabetes mellitus for the 2 h, 3 h, and 4+ h sedentary times. Conclusions The unemployed are more susceptible than other occupation groups to cardio-metabolic diseases when leisure time is sedentary

Auxin response factor 2 (ARF2) plays a major role in regulating auxin-mediated leaf longevity

Auxin regulates a variety of physiological and developmental processes in plants. Although auxin acts as a suppressor of leaf senescence, its exact role in this respect has not been clearly defined, aside from circumstantial evidence. It was found here that ARF2 functions in the auxin-mediated control of Arabidopsis leaf longevity, as discovered by screening EMS mutant pools for a delayed leaf senescence phenotype. Two allelic mutations, ore14-1 and 14-2, caused a highly significant delay in all senescence parameters examined, including chlorophyll content, the photochemical efficiency of photosystem II, membrane ion leakage, and the expression of senescence-associated genes. A delay of senescence symptoms was also observed under various senescence-accelerating conditions, where detached leaves were treated with darkness, phytohormones, or oxidative stress. These results indicate that the gene defined by these mutations might be a key regulatory genetic component controlling functional leaf senescence. Map-based cloning of ORE14 revealed that it encodes ARF2, a member of the auxin response factor (ARF) protein family, which modulates early auxin-induced gene expression in plants. The ore14/arf2 mutation also conferred an increased sensitivity to exogenous auxin in hypocotyl growth inhibition, thereby demonstrating that ARF2 is a repressor of auxin signalling. Therefore, the ore14/arf2 lesion appears to cause reduced repression of auxin signalling with increased auxin sensitivity, leading to delayed senescence. Altogether, our data suggest that ARF2 positively regulates leaf senescence in Arabidopsis