Investigation of jetting piping system in the spudcan of wind turbine installation jack-up vessel

The offshore wind turbine in shallow water is installed by a self-elevated mobile unit which is usually\ud referred to as jack-up barge or jack-up vessel. The jack-up vessel consists of a buoyant platform together with\ud independent legs that can position the vessel above the water reducing external loadings for safe operation condition.\ud The retrieval process of jack-up legs could be very difficult due to the high extraction resistance caused by soft soil. In\ud soft clay, since the high suction force can be developed around the spudcan attached at the end of jack-up legs, a jetting\ud system is required to break the suction to pull out the legs. It is important to design the jetting system with optimized\ud piping arrangement to allow the easy operation. There are various factors to be considered in the design of jetting piping\ud system since the level of embedment and the type of soil and pipe size and locations, etc. can affect the performance of\ud the system. In this paper, the design of 500m^3/hr jetting system is introduced with PIPENET program analysis. Also\ud the various consideration factors in the analysis are discussed

Intermittent fasting increases adult hippocampal neurogenesis

10.1002/brb3.1444Brain and Behavior101e0144

Nano-scale observation of charge transport and potential distribution of photovoltaic Cu(In,Ga)Se 2 thin-films

Understanding of grain boundary (GB) is critical for photovoltaic applications since electron-hole recombination at GBs determines the conversion efficiency. However, our local electrical and optical analysis shows positive potential at GBs in Cu(In,Ga)Se 2 (CIGS), which suppresses the recombination at GBs. We report on a direct measurement of potential distribution and local electrical transport on the surface of photovoltaic CIGS using a nano-scale electrical characterization of Kelvin probe microscopy and conductive atomic force microscopy. This reveals that the positively charged surface potential at GB is expected to increase the minority carrier collection and the enhanced current at GB leads to large carrier mobility and electron-hole separation at the GBs. Micro-Raman scattering results helps to analyze electrical behavior from defect analysis. © 2011 IEEE

Supplementary Material for: Increased Carotid Intima-Media Thickness and Plasma Homocysteine Levels Predict Cardiovascular and All-Cause Death: A Population-Based Cohort Study

<b><i>Background:</i></b> There is still debate over the utility of carotid intima-media thickness (C-IMT) or carotid plaque in predicting future cardiovascular events and death. Additionally, the importance of plasma homocysteine levels was raised as a predictor of cardiovascular events and death. <b><i>Methods:</i></b> 1,391 subjects were recruited from the Ansan Geriatric cohort. We used B-mode carotid ultrasonography to assess C-IMT and plaque, measuring average maximal IMT and average mean IMT through 6-8 measurements of far-wall IMT in both common carotid arteries. We evaluated the presence of plaque in carotid segments. Multivariable Cox regression analysis was used to predict both cardiovascular and all-cause mortality. <b><i>Results:</i></b> During a mean follow-up of 62.4 ± 12.4 months, 71 subjects (5.12%) died and 23 (1.66%) died of cardiovascular causes. Multivariable Cox regression analysis found the predictors of cardiovascular mortality to be average maximal IMT (HR = 3.709; 95% CI: 1.202-11.446) and plasma homocysteine (HR = 1.057; 95% CI: 1.012-1.103). All-cause mortality was independently associated with C-IMT (average maximal and average mean IMT) and plasma homocysteine. <b><i>Conclusions:</i></b> C-IMT and plasma homocysteine levels were found to predict cardiovascular and all-cause mortality independently of the presence of carotid plaque and other cardiovascular risk factors

Genome-Wide Transcriptome Analysis Reveals Intermittent Fasting-Induced Metabolic Rewiring in the Liver

10.1177/1559325819876780Dose-Response17

Similar levels of complement activation in both patients with thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome: The report from the Korean TTP registry

Background: Uncontrolled complement activation has a major role in the pathogenesis of atypical HUS (aHUS) and the restraint of this process by eculizumab is life saving. However, the evidence of complement dysregulation in the pathogenesis of Thrombotic Thrombocytopenic Purpura (TTP) is still unclear. In this study we examined the presence of complement activation biomarkers in patients with aHUS and TTP and the levels were compared to normal healthy controls . Patients and Methods: Patients with thrombotic microangiopathic thrombocytopenia diagnosed either as TTP with low ADAMTS13 activity less than 10% or aHUS with impaired renal function, Cr> 2mg/dL and normal ADAMTS13 activity were chosen from the Korean TTP registry from February 2012 to June 2014. Prospective plasma and serum samples prior to intervention were collected from newly diagnosed patients with TTP (n=20), aHUS (n=20), and 20 healthy controls and frozen at -700C. Complement activation products (C3a, Bb as alternative pathway; C4d as classic pathway; C5a, C5b-9; terminal pathway) were measured by ELISA. Results: Significantly increased levels of Bb and C5b-9 were observed in TTP (median [range], ng/mL; Bb, 1220 [540.0 – 16560], p=0.048; C5b - 9, 390.1 [238.5 - 938.7], p<0.0001) when compared with controls (Bb, 870.0 [630.0 - 2070]; C5b - 9, 190.8 [77.96 - 458.9]). Increased levels of C3a, C5a, C5b - 9, and Factor Bb were observed in HUS (C3a, 231.3 [80.70 - 791.8], p<0.0001; C5a, 21.38 [5.590 - 34.96], p= 0.006; C5b - 9, 0.49 [0.21 - 1.41], p<0.0001; Bb, 1490 [540.0 – 11800], p= 0.0003) as compared with controls (C3a, 108.7 [30.98 - 425.1]; C5a, 8.620 [2.660 - 26.93]; C5b - 9, 0.49 [0.21 - 1.41]; Bb, 870.0 [630.0 - 2070]). These suggested alternative and terminal complement pathways were activated in initial episodes of TTP or HUS. However levels of C4d were not different in HUS and TTP as compared with controls which suggested classic complement pathways were not important in this process. There were no significant differences in complement levels between TTP and HUS although levels of C3a, C4d, C5b - 9 in HUS (C3a, 231.3 [80.70 - 791.8]; C4d, 2140 [10.00 - 960.0]; C5b - 9, 488.4 [212.7 – 1414]) tended to be increased as compared with TTP (C3a, 134.5 [61.97 - 378.4]; C4d, 1330 [2.000 - 699.0]; C5b - 9, 390.1 [238.5 - 938.7]). Conclusion: Complement biomarkers are activated to a similar level in both newly diagnosed cases of TTP and aHUS. Complement activation product levels did not differentiate aHUS from TTP