3,806 research outputs found
Valsalva maneuver, uncontrolled hypertension, asymmetric septal hypertrophy and dynamic outflow obstruction: a case report
A 83-year-old woman presented with a 25-year history of hypertension which was long-standing, uncontrolled, severe hypertension because of irregular oral administration of antihypertensive drug underwent an echocardiographic examination as part of an evaluation of hypertension. She described chest distress associated with activity, syncope for three times in the past one year. On physical examination, she was in no acute distress, with a regular pulse rate and blood pressure of 185/115 mmHg. On auscultation, her lung fields were clear. There was a III/VI late peaking crescendo/decrescendo systolic murmur along the left sternal border radiating to the apex, which increased with standing and Valsalva's maneuver and decreased with squatting. There was no report of provocative maneuvers performed during auscultation. There was no edema. Transthoracic echocardiography showed a hyperdynamic left ventricle with markedly increased left ventricular wall thicknesses and asymmetrical septal hypertrophy. M-mode echocardiography showed systolic anterior motion of the mitral valve apparatus and midsystolic closure of the aortic valve. A dynamic left ventricular outflow tract obstruction was present, with a resting maximal instantaneous gradient of 55 mmHg. With the Valsalva maneuver, the gradient increased to 114 mmHg. No any factors that could cause hypertension were found at kidney, adrenal gland and renal artery etc. by ultrasound and multislice compute tomography
Highly heterogeneous Late Mesozoic lithospheric mantle beneath the North China Craton: evidence from SrāNdāPb isotopic systematics of mafic igneous rocks
The lithospheric mantle beneath the North China Craton changed dramatically in its geophysical and geochemical characteristics from Palaeozoic to Cenozoic times. This study uses samples of Mesozoic basalts and mafic intrusions from the North China Craton to investigate the nature of this mantle in Mesozoic times. Sr-Nd-Pb isotopic data demonstrate that the Late Mesozoic lithospheric mantle was extremely heterogeneous. In the central craton or the Luzhong region, it is slightly Sr-Nd isotopically enriched, beneath the Taihangshan region it has an EMI character (87Sr/86Sri = 0.7050-0.7066; ĪµNd = -17--10), and beneath the Luxi-Jiaodong region, it possesses EM2-like characteristics (87Sr/86Sri up to 0.7114). Compositional variation with time is also apparent in the Mesozoic lithospheric mantle. Our data suggest that the old lithospheric mantle was modified during Mesozoic times by a silicic melt, where beneath the Luxi-Jiaodong region it was severely modified, but in the Luzhong and Taihangshan regions the effects were much less marked. The silicic melt may have been the product of partial melting of crustal materials brought into the mantle by the subducted slab during the formation of circum-cratonic orogenic belts. This Mesozoic mantle did not survive for a long time, and was replaced by a Cenozoic mantle with depleted geochemical characteristics. Ā© 2004 Cambridge University Press.published_or_final_versio
Effect of initial conditions on interaction between a boundary layer and a wall-mounted finite-length-cylinder wake
Author name used in this publication: Y. ZhouAuthor name used in this publication: C. K. ChanAuthor name used in this publication: K. S. Lam2006-2007 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe
The finite-length square cylinder near wake
2009-2010 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe
Coiled-coil motif as a structural basis for the interaction of HTLV type 1 Tax with cellular cofactors
Human T lymphotropic virus type 1 (HTLV-1) Tax is a multifunctional protein centrally involved in transcriptional regulation, cell cycle control, and viral transformation. The regulatory functions of Tax are thought to be mediated through protein-protein interaction with cellular cofactors. Previously we have identified several novel binding partners for Tax, including human mitotic checkpoint protein MAD1 (TXBP181), G-protein pathway suppressor GPS2 (TXBP31), and IĪŗB kinase regulatory subunit IKK-Ī³. Here we described two additional Tax partners, TXBP151 and TXBP121. A closer examination of the sequences of eight independent cellular Tax-binding proteins identified by us and others revealed that all of them share a single characteristic, a highly structured coiled-coil domain. We also noted that Tax and the Tax-binding coiled-coil proteins can homodimerize. Additionally, the same domain in Tax is responsible for interaction with different coiled-coil proteins. Taken together, our findings point to a particular coiled-coil structure as one of the Tax-recognition motifs. The interaction of Tax with a particular subgroup of cellular coiled-coil proteins represents one mechanism by which Tax dysregulates cell growth and proliferation.published_or_final_versio
Soil organic carbon storage changes in coastal wetlands of the modern Yellow River Delta from 2000 to 2009.
Understanding the Epidemiology of Heart Failure to Improve Management Practices: An Asia-Pacific Perspective
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Developing a voltage-stability-constrained security assessment system part I: Determination of power system voltage security operation limits
The method for determining the voltage security operation limits in a practical voltage security analysis (VSA) system based on VSAT software for large power systems is introduced in this paper. These operation limits include bus voltage limits, branch/corridor transfer power limits and P-load limit of the whole system. The voltage security operation limits are determined by the most critical contingency among the studied contingency set. The most critical contingency determines the P-load limit of the whole system, and all kinds of operation parameter limits are operation parameter values corresponding to this P-load limit under pre-contingency. An operation parameter limit is upper limit if the function relationship between this operation parameter and load power is an increasing curve, or lower limit if the function relationship between this operation parameter and load power is an decreasing curve. These operation parameter limits are helpful for operators to monitor the system operation state. Ā© 2005 IEEE.published_or_final_versio
Characterization of human and mouse peroxiredoxin IV: Evidence for inhibition by Prx-IV of epidermal growth factor- and p53-induced reactive oxygen species
The aim of this study was to identify and characterize human and mouse Prx-IV. We identified mouse peroxiredoxin IV (Prx-IV) by virtue of sequence homology to its human ortholog previously called AOE372. Mouse Prx-IV conserves an amino-terminal presequence coding for signal peptide. The amino acid sequences of mature mouse and human Prx-IV share 97.5% identity. Phylogenetic analysis demonstrates that Prx-IV is more closely related to Prx-I/-II/-III than to Prx-V/-VI. Previously, we mapped the mouse Prx-IV gene to chromosome X by analyzing two sets of multiloci genetic crosses. Here we performed further comparative analysis of mouse and human Prx-IV genomic loci. Consistent with the mouse results, human Prx-IV gene localized to chromosome Xp22.135-136, in close proximity to SAT and DXS7178. A bacterial artificial chromosome (BAC) clone containing the complete human Prx-IV locus was identified. The size of 7 exons and the sequences of the splice junctions were confirmed by PCR analysis. We conclude that mouse Prx-IV is abundantly expressed in many tissues. However, we could not detect Prx-IV in the conditioned media of NIH-3T3 and Jurkat cells. Mouse Prx-IV was specifically found in the nucleus-excluded region of cultured mouse cells. Intracellularly, overexpression of mouse Prx-IV prevented the production of reactive oxygen species induced by epidermal growth factor or p53. Taken together, mouse Prx-IV is likely a cytoplasmic or organellar peroxiredoxin involved in intracellular redox signaling.published_or_final_versio
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