Unitarity and the color confinement

We discuss how confinement property of QCD results in the rational unitarization scheme and how unitarity saturation leads to appearance of a hadron liquid phase at very high temperatures.Comment: 10 pages, no figire

Determination of 13 Free Fatty Acids in Pheretima Using Ultra-Performance LC-ESI-MS

Abstract: A simple and rapid ultra-performance liquid chromatography-electrospray ionization mass spectrometry method for the simultaneous determination of thirteen free fatty acids (FFAs) in Pheretima has been developed and validated. Measurements for each FFA were linear over a wide range (0.05-3.95 μg mL −1 ) with good correlation coefficients (>0.99). The limit of detection and limit of quantification for all the fatty acids were below 26 and 78 ng mL −1 , respectively. The intra-and inter-assay precision and accuracy for the thirteen FFAs fell well within the predefined limits of acceptability. Satisfactory recoveries were in the range of 96-103%. Article: INTROCUDTION Pheretima has been well known for its wide therapeutic properties such as anti-inflammatory, anti-oxidative [1], anti-asthmatic, thrombolytic, reducing symptoms of the central nervous system decline including memory loss in traditional Chinese medicine (TCM) for over 2,000 years Although fatty acids have measurable absorbance in the range of 190-215 nm, the interference of most solvents is a limiting factor for sensitive detection when analyzed directly by liqui

Proceedings of the 38th International Symposium on Multiparticle Dynamics (ISMD08)

Proceedings of ISMD08Comment: Edited by: J. Bartels, K. Borras, G. Gustafson, H. Jung, K. Kutak, S. Levonian, and J. Mnic

Heterozygous Tropomodulin 3 mice have improved lung vascularization after chronic hypoxia.

The molecular mechanisms leading to high-altitude pulmonary hypertension (HAPH) remains poorly understood. We previously analyzed the whole genome sequence of Kyrgyz highland population and identified eight genomic intervals having a potential role in HAPH. Tropomodulin 3 gene (TMOD3), which encodes a protein that binds and caps the pointed ends of actin filaments and inhibits cell migration, was one of the top candidates. Here we systematically sought additional evidence to validate the functional role of TMOD3. In-silico analysis reveals that some of the SNPs in HAPH associated genomic intervals were positioned in a regulatory region that could result in alternative splicing of TMOD3. In order to functionally validate the role of TMOD3 in HAPH, we exposed Tmod3-/+ mice to 4 weeks of constant hypoxia, i.e. 10% O2 and analyzed both functional (hemodynamic measurements) and structural (angiography) parameters related to HAPH. The hemodynamic measurements, such as right ventricular systolic pressure, a surrogate measure for pulmonary arterial systolic pressure, and right ventricular contractility (RV- ± dP/dt), increases with hypoxia did not separate between Tmod3-/+ and control mice. Remarkably, there was a significant increase in the number of lung vascular branches and total length of pulmonary vascular branches (P < 0.001) in Tmod3-/+ after 4 weeks of constant hypoxia as compared with controls. Notably, the Tmod3-/+ endothelial cells migration was also significantly higher than that from the wild-type littermates. Our results indicate that, under chronic hypoxia, lower levels of Tmod3 play an important role in the maintenance or neo-vascularization of pulmonary arteries

Hypoxia‐induced pulmonary hypertension – utilising experiments of nature

An increase in pulmonary artery pressure is a common observation in adult mammals exposed to global alveolar hypoxia. It is considered a maladaptive response that places an increased workload on the right ventricle. The mechanisms initiating and maintaining the elevated pressure are of considerable interest to understanding pulmonary vascular homeostasis. There is an expectation that identifying the key molecules in the integrated vascular response to hypoxia will inform potential drug targets. One strategy is to take advantage of experiments of nature; specifically, to understand the genetic basis for the inter-individual variation in the pulmonary vascular response to acute and chronic hypoxia. To date, detailed phenotyping of highlanders has focused on haematocrit and oxygen saturation rather that cardiovascular phenotypes. This review explores what we can learn from those studies with respect to the pulmonary circulation

Simultaneous determination of 17 ginsenosides in rat urine by ultra performance liquid chromatography-mass spectrometry with solid-phase extraction. Anal Chim Acta

Abstract: A rapid analytical method for quantifying 17 ginsenosides in rat urine by ultra performance liquid chromatography (UPLC) coupled to electrospray ionization mass spectrometry (ESI-MS) is described. All analytes were extracted by solid-phase extraction optimized to obtain good recovery and quantified using digoxin as an internal standard. ESI-MS was optimized for different cone voltages at positive ionization mode to allow simultaneous analysis of all analytes in a relatively short time. Qualitative methodological considerations, including the linear range, precision, limit of quantification, limit of detection, recovery and sensitivity are also provided

Hypoxia‐induced pulmonary hypertension—Utilizing experiments of nature

An increase in pulmonary artery pressure is a common observation in adult mammals exposed to global alveolar hypoxia. It is considered a maladaptive response that places an increased workload on the right ventricle. The mechanisms initiating and maintaining the elevated pressure are of considerable interest to understanding pulmonary vascular homeostasis. There is an expectation that identifying the key molecules in the integrated vascular response to hypoxia will inform potential drug targets. One strategy is to take advantage of experiments of nature; specifically, to understand the genetic basis for the inter-individual variation in the pulmonary vascular response to acute and chronic hypoxia. To date, detailed phenotyping of highlanders has focused on haematocrit and oxygen saturation rather that cardiovascular phenotypes. This review explores what we can learn from those studies with respect to the pulmonary circulation