17 research outputs found
Effective detrending methodology for harmonic transient pressure response
No full textHarmonic Pulse Testing (HPT) is an unconventional well testing methodology in which the injection or production rate is varied in a periodic way following, in common practice, a square pulsing scheme. HPT was developed with the aim of characterizing and monitoring well performance and reservoir behavior without interrupting ongoing field production activities and without resorting to dedicated well testing surface equipment. Interpretation of HPT requires pressure response and associated rate history to be analyzed in the frequency domain through the application of Fourier transform. However, detrending of pressure pulsing data is necessary because signal decomposition into multiple frequency components is affected by the upward trend of the first transient and possibly by other phenomena associated to reservoir operation. In this paper a detrending methodology is considered as an algorithm aimed at isolating the pure periodic component of a pressure signal generated by harmonic rate history, from any other effect. An interesting heuristic algorithm for pressure data detrending was proposed by Ahn and Horne in 2011 but it's reliable application is limited to particular cases associated to simple production/injection schemes. Based on Ahn and Horne's previous work, a new heuristic algorithm is proposed by the author with the goal of overcoming the limitation of the previous one
Telepathology as a Service Support for Pap Test Diagnosis in Zambia: The Experience of Pathology Beyond Borders
No full textAuthor Correction: A genetically encoded sensor for in vivo imaging of orexin neuropeptides.
No full textPapillary thyroid carcinoma presenting as a solitary soft tissue arm metastasis in an elderly hyperthyroid patient. Case report and review of the literature
No full textBladder tumor antigen assay as compared to voided urine cytology in the diagnosis of bladder cancer
No full textCorrection: A Simplified Ultrasonographic Score for the Prediction of Cytologically Suspicious Thyroid Nodules
No full textThe development of recommendations for the implementation of nutrition therapy for coloured women with a type 2 diabetes attending CHC's in the Cape Metropole
No full text
Dual renin-angiotensin system inhibition for prevention of renal and cardiovascular events: do the latest trials challenge existing evidence?
No full textCirculatory and tissue renin-angiotensin systems (RAS) play a central role in cardiovascular (CV) and renal pathophysiology, making RAS inhibition a logical therapeutic approach in the prevention of CV and renal disease in patients with hypertension. The cardio- and renoprotective effects observed with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) monotherapy, together with the availability of a direct renin inhibitor (DRI), led to the investigation of the potential benefits of dual RAS inhibition. In small studies, ARB and ACE inhibitor combinations were shown to be beneficial in patients with CV or renal disease, with improvement in surrogate markers. However, in larger outcome trials, involving combinations of ACE inhibitors, ARBs or DRIs, dual RAS inhibition did not show reduction in mortality in patients with diabetes, heart failure, coronary heart disease or after myocardial infarction, and was in fact, associated with increased harm. A recent meta-analysis of all major trials conducted over the past 22 years involving dual RAS inhibition has clearly shown that the risk-benefit ratio argues against the use of dual RAS inhibition. Hence, the recent evidence clearly advocates against the use of dual RAS inhibition, and single RAS inhibition appears to be the most suitable approach to controlling blood pressure and improving patient outcomes. © 2013 Mallat; licensee BioMed Central Ltd.Abe M, 2012, HYPERTENS RES, V35, P874, DOI 10.1038-hr.2012.45; [Anonymous], 1997, LANCET, V349, P1857; BALL SG, 1993, LANCET, V342, P821; YUSUF S, 1991, NEW ENGL J MED, V325, P293; Baker WL, 2009, ANN INTERN MED, V151, P861, DOI [10.7326-0003-4819-151-12-200912150-00162, 10.7326-0000605-200912150-00162]; Bakris GL, 2007, KIDNEY INT, V72, P879, DOI 10.1038-sj.ki.5002455; Bakris GL, 2013, J CLIN HYPERTENS, V15, P92, DOI 10.1111-jch.12032; Basevi V, 2011, DIABETES CARE S1, V34, pS11, DOI DOI 10.2337-DC11-0174; Basi S, 2008, DIABETES CARE, V31, pS194, DOI 10.2337-dc08-s249; Bilic M, 2011, COLLEGIUM ANTROPOL, V35, P1061; Braunwald E, 2004, NEW ENGL J MED, V351, P2058; Brenner BM, 2001, NEW ENGL J MED, V345, P861, DOI 10.1056-NEJMoa011161; Brewster UC, 2004, AM J MED, V116, P263, DOI 10.1016-j.amjmed.2003.09.034; Catala-Lopez F, 2013, REV ESP CARDIOL, V66, P412, DOI [10.1016-j.recesp.2012.11.010, 10.1016-j.rec.2012.11.010]; Catapano F, 2008, AM J KIDNEY DIS, V52, P475, DOI 10.1053-j.ajkd.2008.03.008; Chan C, 2011, J HYPERTENS SA, V29, pe17; Cheng J, 2012, INT J CLIN PRACT, V66, P917, DOI 10.1111-j.1742-1241.2012.02970.x; CHEP, 2012, CAN REC MAN HYP; Cherney DZI, 2012, DIABETES CARE, V35, P2324, DOI 10.2337-dc12-0773; Cice G, 2010, J AM COLL CARDIOL, V56, P1701, DOI 10.1016-j.jacc.2010.03.105; COHN JN, 1991, NEW ENGL J MED, V325, P303, DOI 10.1056-NEJM199108013250502; Dickstein K, 2002, LANCET, V360, P752, DOI 10.1016-S0140-6736(02)09895-1; Doulton TWR, 2005, HYPERTENSION, V45, P880, DOI 10.1161-01.HYP.0000161880.59963.da; DZAU V, 1991, AM HEART J, V121, P1244, DOI 10.1016-0002-8703(91)90694-D; SWEDBERG K, 1987, NEW ENGL J MED, V316, P1429; EMA, 2013, REV STAND COMB US RE; Epstein M, 2009, NAT CLIN PRACT NEPHR, V5, P12, DOI 10.1038-ncpneph0980; Farsang Csaba, 2011, Vasc Health Risk Manag, V7, P605, DOI 10.2147-VHRM.S23468; Fliser D, 2010, J NEPHROL, V23, P369; Fox KM, 2003, LANCET, V362, P782; Fried LF, 2009, CLIN J AM SOC NEPHRO, V4, P361, DOI 10.2215-CJN.03350708; Frimodt-Moller M, 2010, NEPHROL DIAL TRANSPL, V25, P842, DOI 10.1093-ndt-gfp547; Frimodt-Moller M, 2012, PLOS ONE, V7, DOI 10.1371-journal.pone.0041757; Gaede P, 2008, NEW ENGL J MED, V358, P580, DOI 10.1056-NEJMoa0706245; Gheorghiade M, 2013, JAMA-J AM MED ASSOC, V309, P1125, DOI 10.1001-jama.2013.1954; Grandi AM, 2008, AM J HYPERTENS, V21, P231, DOI 10.1038-ajh.2007.47; Granger CB, 2003, LANCET, V362, P772, DOI 10.1016-S0140-6736(03)14284-5; Halabi Carmen M, 2005, Am J Cardiovasc Drugs, V5, P389, DOI 10.2165-00129784-200505060-00006; Harel Z, 2012, BMJ, V9, p[344, e42]; Heart Outcomes Prevention Evaluation (HOPE) Study investigators, 2000, LANCET, V355, P253; Hollenberg NK, 2003, KIDNEY INT, V63, P172, DOI 10.1046-j.1523-1755.2003.00701.x; Hunyady L, 2006, MOL ENDOCRINOL, V20, P953, DOI 10.1210-me.2004-0536; Ishibashi K, 2013, HEART VESSELS, V28, P7, DOI 10.1007-s00380-011-0204-7; Kelly DJ, 2007, DIABETOLOGIA, V50, P2398, DOI 10.1007-s00125-007-0795-9; Kintscher U, 2005, ACTA DIABETOL, V42, pS26, DOI 10.1007-s00592-005-0178-y; KOBER L, 1995, NEW ENGL J MED, V333, P1670, DOI 10.1056-NEJM199512213332503; Krause MW, 2011, KIDNEY INT, V80, P245, DOI 10.1038-ki.2011.142; Kuenzli A, 2010, PLOS ONE, V5, DOI 10.1371-journal.pone.0009946; Kunz R, 2008, ANN INTERN MED, V148, P30; Kurnik D, 2011, CLIN THER, V33, P456, DOI 10.1016-j.clinthera.2011.04.011; Laakso M, 1998, ATHEROSCLEROSIS, V137, pS65, DOI 10.1016-S0021-9150(97)00314-6; Lakhdar R, 2008, J CARD FAIL, V14, P181, DOI [10.1016-j.cardfail.2007.11.008, 10.1016-j.cardfail.2607.11.008]; LEWIS EJ, 1993, NEW ENGL J MED, V329, P1456, DOI 10.1056-NEJM199311113292004; Lewis EJ, 2001, NEW ENGL J MED, V345, P851, DOI 10.1056-NEJMoa011303; Lizakowski S, 2013, POL ARCH MED WEWN, V123, P221; Maggioni AP, 1999, EUR HEART J, V20, P634; Maione A, 2011, NEPHROL DIAL TRANSPL, V26, P2827, DOI 10.1093-ndt-gfq792; Makani H, 2013, BMJ-BRIT MED J, V346, DOI 10.1136-bmj.f360; Makino H, 2007, DIABETES CARE, V30, P1577, DOI 10.2337-dc06-1998; Mallat SG, 2012, CARDIOVASC DIABETOL, V11, DOI 10.1186-1475-2840-11-32; Mancia G, 2009, BLOOD PRESSURE, V18, P308, DOI 10.3109-08037050903450468; Mancia G, 2007, J HYPERTENS, V25, P1105, DOI 10.1097-HJH.0b013e3281fc975a; Mann JFE, 2013, J HYPERTENS, V31, P414, DOI 10.1097-HJH.0b013e32835bf7b0; Mann JFE, 2009, ANN INTERN MED, V151, P1; Mann JFE, 2008, LANCET, V372, P547, DOI 10.1016-S0140-6736(08)61236-2; Viberti G, 2002, CIRCULATION, V106, P672, DOI 10.1161-01.CIR.0000024416.33113.0A; McAlister FA, 2011, CAN MED ASSOC J, V183, P655, DOI 10.1503-cmaj.101333; McMurray JJV, 2003, LANCET, V362, P767, DOI 10.1016-S0140-6736(03)14283-3; McMurray JJV, 2012, EUR J HEART FAIL, V14, P341, DOI 10.1093-eurjhf-hfs033; McMurray JJV, 2008, CIRC-HEART FAIL, V1, P17, DOI 10.1161-CIRCHEARTFAILURE.107.740704; Messerli FH, 2013, AM J MED, V126, pE1, DOI 10.1016-j.amjmed.2012.07.006; Messerli FH, 2010, EUR HEART J, V31, P2205, DOI 10.1093-eurheartj-ehq255; Messerli FH, 2009, J AM COLL CARDIOL, V53, P468, DOI 10.1016-j.jacc.2008.10.036; Miyazaki S, 2010, CIRC J, V74, P1158, DOI 10.1253-circj.CJ-09-0412; Mogensen CE, 2000, BRIT MED J, V321, P1440, DOI 10.1136-bmj.321.7274.1440; Morrish NJ, 2001, DIABETOLOGIA, V44, pS14, DOI 10.1007-PL00002934; Munger Mark A, 2011, P T, V36, P22; National PBM Bulletin, 2013, NAT PBM B; Ninomiya T, 2009, J AM SOC NEPHROL, V20, P1813, DOI 10.1681-ASN.2008121270; Parving HH, 2012, NEW ENGL J MED, V367, P2204, DOI 10.1056-NEJMoa1208799; Parving HH, 2008, NEW ENGL J MED, V358, P2433, DOI 10.1056-NEJMoa0708379; Parving HH, 2001, NEW ENGL J MED, V345, P870, DOI 10.1056-NEJMoa011489; Parving HH, 2002, CURR HYPERTENS REP, V4, P387, DOI 10.1007-s11906-002-0069-3; Persson F, 2009, DIABETES CARE, V32, P1873, DOI 10.2337-dc09-0168; Pfeffer MA, 2003, LANCET, V362, P759, DOI 10.1016-S0140-6736(03)14282-1; PFEFFER MA, 1992, NEW ENGL J MED, V327, P669, DOI 10.1056-NEJM199209033271001; Pfeffer MA, 2003, NEW ENGL J MED, V349, P1893, DOI 10.1056-NEJMoa032292; Pilz B, 2005, HYPERTENSION, V46, P569, DOI 10.1161-01.HYP.0000179573.91016.3f; Pitt B, 2011, EUR J HEART FAIL, V13, P755, DOI 10.1093-eurjhf-hfr034; Pitt B, 1997, LANCET, V349, P747, DOI 10.1016-S0140-6736(97)01187-2; Pitt B, 2000, LANCET, V355, P1582, DOI 10.1016-S0140-6736(00)02213-3; Pouleur AC, 2011, J RENIN-ANGIO-ALDO S, V12, P483, DOI 10.1177-1470320311414453; Ravid M, 2009, DIABETES CARE, V32, pS410, DOI 10.2337-dc09-S349; RAVID M, 1993, ANN INTERN MED, V118, P577; Ruggenenti P, 2011, J NEPHROL, V24, P274, DOI 10.5301-JN.2011.7763; Robles NR, 2009, EUR J INTERN MED, V20, P186, DOI 10.1016-j.ejim.2008.06.002; Sata Masataka, 2010, J Med Invest, V57, P12; Schmieder RE, 2007, DIABETES CARE, V30, P1351, DOI 10.2337-dc06-1551; Scirica BM, 2010, EUR HEART J, V31, P1993, DOI 10.1093-eurheartj-ehq190; Siragy HM, 2010, AM J NEPHROL, V31, P541, DOI 10.1159-000313363; Solomon SD, 2011, EUR HEART J, V32, P1227, DOI 10.1093-eurheartj-ehq522; Solomon SD, 2009, CIRCULATION, V119, P530, DOI 10.1161-CIRCULATIONAHA.108.826214; Staessen JA, 2006, LANCET, V368, P1449, DOI 10.1016-S0140-6736(06)69442-7; St Peter WL, 2013, PHARMACOTHERAPY, V33, P496, DOI 10.1002-phar.1232; Strippoli GFM, 2006, J AM SOC NEPHROL, V17, pS153, DOI 10.1681-ASN.2005121337; Szeto CC, 2013, PLOS ONE, V8, DOI 10.1371-journal.pone.0062736; Taal MW, 2000, KIDNEY INT, V57, P1803, DOI 10.1046-j.1523-1755.2000.00031.x; Taniwaki H, 2003, DIABETES CARE, V26, P132, DOI 10.2337-diacare.26.1.132; Ginsberg HN, 2010, NEW ENGL J MED, V362, P1563, DOI 10.1056-NEJMoa1001282; NICKLAS JM, 1992, NEW ENGL J MED, V327, P685; Tobe SW, 2011, CIRCULATION, V123, P1098, DOI 10.1161-CIRCULATIONAHA.110.964171; Trimarchi Hernán, 2011, Int J Nephrol Renovasc Dis, V4, P41, DOI 10.2147-IJNRD.S6653; UK Medicines Information, 2012, WHAT IS RAT EV COMB; Veglio F, 2012, CURR PHARM DESIGN, V18, P952; Verges B, 2004, DIABETES METAB, V30, P7, DOI 10.1016-S1262-3636(07)70083-6; Volpe M, 2012, J HYPERTENS, V30, P647, DOI 10.1097-HJH.0b013e32834f6e00; Wong J, 2013, DIABETES VASC DIS RE, V10, P193, DOI 10.1177-1479164112463710; Yusuf S, 2003, LANCET, V362, P777, DOI 10.1016-S0140-6736(03)14285-7; Yusuf S, 2000, NEW ENGL J MED, V342, P145; Yusuf S, 2008, LANCET, V372, P1174, DOI 10.1016-S0140-6736(08)61242-8; Yusuf S, 2008, NEW ENGL J MED, V358, P154732
Adipose tissue derived factors in obesity, inflammation & energy homeostasis
No full textObesity is the foremost contributory factor in the progression to type 2 diabetes
mellitus (T2DM). Moreover, chronic inflammation, through activation of innate
immunity is proposed to link obesity, insulin resistance and T2DM. Adipose tissue,
traditionally considered a storage compartment for triglycerides, also functions as an
active endocrine organ. Adipocyte-secreted products, termed adipokines, may link
obesity-associated inflammation and insulin resistance. Adipokines exert multiple
effects on insulin sensitisation, glucose homeostasis, inflammatory processes or
central systems mediating energy expenditure. This thesis principally examined two
adipokines; resistin and adiponectin. Resistin and components of innate immunity
were assessed in human obesity. In-vitro analysis established that resistin was
expressed and secreted by human adipocytes. Furthermore, key factors in the innate
immune pathway were highly expressed in obese and T2DM adipose tissue. This
thesis further explored the pro-inflammatory actions of resistin in adipocytes. Resistin
stimulated the secretion of inflammatory cytokines from adipocytes and, the
expression of key intermediates of the innate immune and insulin signalling pathways.
Clinical studies entailed examination of resistin as a marker of inflammation in
childhood obesity. Serum analysis revealed gender-differences in resistin levels in
obese children. Furthermore, bacterial endotoxin correlated with several markers of
inflammation and cardiovascular disease; suggesting endotoxin as a contributor to
inflammation in childhood obesity. This thesis subsequently examined another
adipokine, adiponectin; considered to have a `ying-and-yang' relationship with
resistin. Studies explored a central role for adiponectin in energy homeostasis. Gelfiltration
liquid chromatography established that the adiponectin trimer was
predominant in human cerebrospinal fluid. Such identification of trimeric adiponectin
in vivo implicates the pharmacologically generated globular adiponectin in central
regulation of energy expenditure. In conclusion, resistin may serve as a pathogenic
pro-inflammatory factor, exacerbating inflammation within adipose tissue; potentially
contributing to the progression of obesity-driven T2DM. Alternatively, adiponectin
may have favourable central actions, influencing energy expenditure through its basic
trimeric form. Collectively, this thesis suggests that resistin and adiponectin, with a
range of opposing properties, may substantially affect whole-body metabolism
