bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrocardiogram and clinical characteristics of patients referred for cardiac transplantation: Implications for pacing in heart failure
Authors: Freudenberger Ronald , Sikora Jo Ann , Fisher Michael , Wilson Alan , Gold Michael 
Published: June 2007

AbstractBackground: Permanent pacing for the treatment of heart failure (HF) has been the subject of intense research over the past decade. Those with conduction abnormalities may benefit most from pacing. The incidence of these conduction abnormalities in patients referred for cardiac transplantation and its relationship to outcome has not been well described.Hypothesis: This study sought to determine the incidence of these abnormalities and to correlate these findings to outcome in this patient population.Methods: A review of 100 patients referred for transplantation was performed. Data were analyzed in two groups: those with QRS duration < 120 ms and those with a QRS duration > 120 ms. Times to transplantation or death were analyzed in these two groups.Results: Of these patients, 34% had QRS duration ≥ 120 ms and survival was inversely associated with QRS duration. Of those with QRS duration < 120 ms, 24% (16) went on to cardiac transplantation or died. Of those with a QRS duration ≥ 120 ms, 55% (17) went on to transplantation or died (p = 0.0134).Conclusions: This suggests that in addition to a multi‐drug regimen for heart failure, 34% of patients referred for transplantation may benefit from additional therapy with biventricular pacing.
The effect of st resolution on QT dispersion after interventional treatment in acute myocardial infarction
Authors: Ilkay Erdoǧan , Yavuzkir Mustafa , Karaca Ilgin , Akbulut Mehmet , Pekdemir Murat , Aslan Nadi 
Published: June 2007

AbstractBackground: It has been reported that reperfusion treatment reduces QT dispersion (QTD) in cases of acute myocardial infarction (AMI). Successful myocardial perfusion is not synonymous with Thrombolysis in Myocardial Infarction (TIMI) III flow. It has been demonstrated that in AMI, the grade of ST‐resolution correlates strongly with left ventricular (LV) function, enzyme elevation, and mortality after primary angioplasty.Hypothesis: This study investigated the relation between ST‐resolution grade and QTD and the feasibility of using QTD as a determinant of successful myocardial tissue perfusion in patients in whom TIMI III flow in the infarct‐related artery (IRA) is restored by interventional treatment for AMI.Methods: The study included 57 patients (38 men, 19 women, average age 54.4 ± 11.6 years), whose IRA was perfused by primary angioplasty after the diagnosis of anterior AMI with ST elevation. Electrocardiograms of patients were taken 45 ± 12 min post procedure, and patients were divided into three groups depending on the grade of ST resolution: Group 1, full ST resolution; Group 2, partial ST resolution; and Group 3, unsuccessful ST resolution.Results: Full ST resolution was seen in 19 cases (33%), partial resolution in 26 cases (47%), and unsuccessful resolution in 12 cases (20%). There were no differences among groups in terms of risk factors, stent diameters, symptom onset–balloon time, LV function, and preprocedure corrected QTD (QTcD) (p = 0.274). After the procedure, a signiFICAnt reduction in QTcD was found within the groups (p = 0.0001 in Group 1, p = 0.004 in Group 2, and p = 0.011 in Group 3). Reductions in QTcD post procedure were 24.21 ± 14.27, 11.85 ± 16.18, and 12.50 ± 11.58 ms in Groups 1, 2, and 3, respectively. There was a statistically signiFICAnt difference of p = 0.015 between Groups 1 and 2 and a difference of p = 0.028 between Groups 1 and 3. There was no statistically signiFICAnt difference between Groups 2 and 3 (p = 0.916).Conclusion: In acute MI, TIMI III flow led to a reduction in QTcD, and full myocardial perfusion made an additional contribution to the electrical stability of the myocardium.
A case of paradoxical embolism “in situ” associated with massive pulmonary embolism: Role of echocardiography
Authors: Sumner Andrew D. , Henderson Rick , Martin Deena , Sorrell Vincent L. 
Published: June 2007

AbstractA 49‐year‐old man was admitted in transfer for further management of a pulmonary embolism (PE) and possible mitral valve vegetation. Transthoracic echocardiography performed at our institution showed evidence of right ventricular (RV) enlargement and dysfunction. Within the right atrium was a serpentine mobile thrombus which traversed the interatrial septum at the level of the fossa ovalis and extended into the left atrium to the level of the anterior mitral valve leaflet. Because of the patient's dyspnea, RV dysfunction, and large clot burden, thrombolytic therapy was considered and would have been administered had the thrombus in situ not been identified. In light of the thrombus in situ and the concern about possible systemic embolization with thrombolytic therapy, the patient underwent successful surgical thrombectomy. This case highlights the importance of echocardiography in the management of patients with PE. We believe that all patients should undergo echocardiography prior to receiving thrombolytic therapy for pulmonary emboli. Careful interrogation of the interatrial septum for the presence of a thrombus in situ is warranted. Thrombectomy should be considered in individuals with PE who have a thrombus in situ.
Role of noninvasive studies in risk stratification for sudden cardiac death
Authors: Kunavarapu Chandra , Bloomfield Daniel M. 
Published: June 2007

AbstractSudden cardiac death (SCD) is one of the leading causes of mortality in developing countries. To prevent SCD, it is crucial to have effective tools for identifying patients at risk, given that there are now effective devices and medications that can prevent SCD. Two noninvasive electrocardio‐graphic tools have been approved by the Food and Drug Administration and are being used clinically for identifying patients at risk for SCD: the signal‐averaged electrocardiogram (SAECG) and T‐wave alternans (TWA). This article reviews each of these approaches and includes a discussion of the mechanisms and a summary of the clinical studies published to date.
Reduced quality of life after myocardial infarction in women compared with men
Authors: Agewall Stefan , Berglund Margareta , Henareh Loghman 
Published: June 2007

AbstractBackground: Psychosocial factors have been suggested as risk factors for atherosclerotic disease.Hypothesis: The purpose of the present study was to examine whether there is a gender difference in quality of life after a myocardial infarction with modern treatment of acute ischemic heart disease.Methods: In all, 123 men and women aged between 31 and 80 years, and with a hospital‐diagnosed myocardial infarction occurring 1‐‐12 months prior to inclusion, were studied. Minor symptoms evaluation profile (MSEP) was used to estimate quality of life at entry.Results: Age, hemodynamic data, smoking habits, as well as laboratory data, concomitant cardiovascular disease, and revascularization rate did not differ between men and women. Women had significantly more negative feelings regarding all the estimated dimensions of quality of life (Contentment, Vitality, and Sleep) than did men.Conclusion: Self‐assessed quality of life after a myocardial infarction was significantly lower among women than among men despite similar age, treatment, and hemodynamic and laboratory data. The causal relationship is however, not known. Further studies are needed to evaluate the underlying mechanism of this observation. This may lead to the development of novel treatment strategies in female patients after a myocardial infarction.
Gender‐specific association between preproendothelin‐1 genotype and reduction of systolic blood pressure during antihypertensive treatment‐‐‐results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA)
Authors: Hallberg P. , Karlsson J. , Lind L. , Michaëlsson K. , Kurland L. , Kahan T. , Malmqvist K. , Öhman K. P. , Nyström F. , Liljedahl U. , Syvänen A. C. , Melhus H. 
Published: June 2007

AbstractBackground: Studies suggest that endothelin‐1 contributes to the pathogenesis of hypertension. A G5665T gene polymorphism of preproendothelin‐1 has been shown to be associated with higher blood pressure in overweight patients. No study has yet determined the effect of this polymorphism on the change in blood pressure during antihypertensive treatment.Hypothesis: This study aimed to determine this effect in hypertensive patients with left ventricular (LV) hypertrophy during antihypertensive treatment with either irbesartan or atenolol.Methods: We determined the preproendothelin‐1 genotype using minisequencing in 102 patients with essential hypertension and LV hypertrophy verified by echocardiography, randomized in a double‐blind fashion to treatment with either the AT1‐receptor antagonist irbesartan or the beta1‐adrenoceptor antagonist atenolol.Results: The change in systolic blood pressure (SBP) after 12 weeks of treatment was related to the preproendothelin‐1 genotype in men; after adjustment for potential covariates (age, blood pressure, and LV mass index at study entry, dose of irbesartan/atenolol, and type of treatment), those carrying the T‐allele responded on average with a more than two‐fold greater reduction than those with the G/G genotype (‐21.9 mmHg [3.9] vs. ‐8.9 [2.3], p = 0.007). No significant differences in blood pressure change between G/G and carriers of the T‐allele were seen among women.Conclusions: Our finding suggests a gender‐specific relationship between the G5665T preproendothelin‐1 polymorphism and change in SBP in response to antihypertensive treatment with irbesartan or atenolol, suggesting the endothelin pathway to be a common mechanism included in the hypertensive action of the drugs.
Prospective validation of a quantitative method for differentiating ischemic versus nonischemic cardiomyopathy by technetium‐99m sestamibi myocardial perfusion single‐photon emission computed tomography
Authors: Yao Siu‐Sun , Qureshi Ehtasham , Nichols Kenneth , Diamond George A. , Depuey E. Gordon , Rozanski Alan 
Published: June 2007

AbstractBackground: Myocardial perfusion single‐photon emission computed tomography (SPECT) permits assessment of stress perfusion and resting left ventricular (LV) function. Quantitative analysis of perfusion patterns among patients with LV dysfunction offers an opportunity for developing criteria to differentiate ischemic from nonischemic cardiomyopathy.Hypothesis: Quantitative assessment of SPECT may allow differentiation between ischemic and nonischemic cardiomyopathy.Methods: We evaluated 144 patients with LV ejection fraction ≤40%, divided into 63 patients with nonischemic and 81 with ischemic cardiomyopathy. Mean relative myocardial counts were obtained for regions drawn over defect and normal zones on rest and stress polar perfusion maps.Results: Multivariate logistic regression analysis of significant univariate SPECT predictors of ischemic cardiomyopathy revealed that the stress defect severity ratio (SDSR) was the best predictor of ischemic cardiomyopathy (p < 0.0001). By receiver operator characteristic (ROC) curve analysis, an SDSR of ≤ 45% optimized prediction of ischemic cardiomyopathy (sensitivity 81%, specificity 96%). An SDSR of ≤ 45% occurred in 65 of 81 (80%) patients with ischemic cardiomyopathy, but in only 3 of the 63 (4%) patients with nonischemic cardiomyopathy (p < 0.0001). Applying the ≤45% SDSR threshold to a prospective group of 89 patients yielded a somewhat lower sensitivity (60%), but retained high specificity (91%) for identifying ischemic cardiomyopathy (p = NS vs. retrospective group).Conclusions: Presence of a severe and extensive stress perfusion defect is a hallmark of ischemic cardiomyopathy. By contrast, a mild stress perfusion defect (SDSR of > 45%) is commonly present among patients with ischemic and non‐ischemic cardiomyopathy. An SDSR of ≤45% is a reproducible specific marker for identifying the presence of ischemic cardiomyopathy.
Effort/gains dynamics in heterogeneous networks
Authors: Mamatas L. , Tsaoussidis V. 
Published: June 2007

AbstractWe investigate the behaviour of TCP(α, β) protocols in the presence of wireless networks. We seek an answer to strategic issues of maximizing energy and bandwidth exploitation, without damaging the dynamics of multiple‐flow equilibrium. We take a fresh perspective on protocol design: What is the return of the effort that a protocol expends? Can we achieve more gains with less effort? We study first the design assumptions of TCP(α, β) protocols and discuss the impact of equation‐based modulation of α and β on protocol efficiency. We introduce two new measures to capture protocol behaviour: the ‘Extra Energy Expenditure’ and the ‘Unexploited Available Resource Index’. We confirm experimentally that, in general, smoothness and responsiveness constitute a tradeoff; however, we show that this tradeoff does not graft its dynamics into a conservative/aggressive behaviour, as it is traditionally believed. We uncover patterns of unjustified tactics; our results suggest that an adaptive congestion control algorithm is needed to integrate the dynamics of heterogeneous networks into
protocol behaviour. Copyright © 2007 John Wiley & Sons, Ltd.
Homeostatic proliferation of intestinal intraepithelial lymphocytes precedes their migration to extra‐intestinal sites
Authors: Stankovic Sanda , Zhan Yifan , Harrison Leonard C. 
Published: June 2007

AbstractCells with the phenotype of intraepithelial lymphocytes (IEL) are present systemically and have been implicated in immune regulation. To determine whether IEL undergo homeostatic proliferation and migrate from the small intestine, we analysed the fate of congenic IEL transferred into lymphopenic mice. Donor IEL homed to the small intestinal epithelium, where they expanded in an IL‐15‐dependent manner and expressed CD69, CD44 and CD103; proliferation did not occur in the spleen, the main other site of IEL detection early after transfer. By 12 days after transfer, a small proportion of intestinal IEL had up‐regulated the trafficking molecule CD62L. Four weeks after transfer, donor IEL with a CD69–CD44hiCD103– phenotype similar to memory T cells were present in spleen and other extra‐intestinal sites. Treatment of mice with blocking antibody to CD62L reduced appearance of cells in mesenteric lymph nodes; treatment with FTY720, a sphingosine 1‐phosphate receptor agonist that blocks egress of T cells from lymph nodes, reduced appearance of cells in spleen. The distribution of TCR αβ and γδ IEL varied between organs, αβ IEL being predominant. IEL proliferation and emigration under lymphopenic conditions suggests similar IEL turnover, albeit at a lower level, under physiological conditions.
Two‐chiral component microemulsion EKC – chiral surfactant and chiral oil. Part 2: Diethyl tartrate
Authors: Kahle Kimberly A. , Foley Joe P. 
Published: June 2007

AbstractIn this second study on dual‐chirality microemulsions containing a chiral surfactant and a chiral oil, a less hydrophobic and lower interfacial tension chiral oil, diethyl tartrate, is employed (Part 1, Foley, J. P. et al.., Electrophoresis, DOI: 10.1002/elps.200600551). Six stereochemical combinations of dodecoxycarbonylvaline (DDCV: R, S, or racemic, 2.00% w/v), racemic 2‐hexanol (1.65% v/v), and diethyl tartrate (D, L, or racemic, 0.88% v/v) were examined as pseudostationary phases (PSPs) for the enantioseparation of six chiral pharmaceutical compounds: pseudoephedrine, ephedrine, N‐methyl ephedrine, metoprolol, synephrine, and atenolol. Average efficiencies increased with the addition of a chiral oil to R‐DDCV PSP formulations. Modest improvements in resolution and enantioselectivity (αenant) were achieved with two‐chiral‐component systems over the one‐chiral‐component microemulsion. Slight enantioselective synergies were confirmed using a thermodynamic model. Results obtained in this study are compared to those obtained in Part 1 as well as those obtained with chiral MEEKC using an achiral, low‐interfacial‐tension oil (ethyl acetate). Dual‐chirality microemulsions with the more hydrophobic oil dibutyl tartrate yielded, relative to diethyl tartrate, higher efficiencies (100 000–134 000 vs. 80 800–94 300), but lower resolution (1.64–1.91 vs. 2.08–2.21) due to lower enantioselectivities (1.060–1.067 vs. 1.078–1.081). Atenolol enantiomers could not be separated with the dibutyl tartrate‐based microemulsions but were partially resolved using diethyl tartrate microemulsions. A comparable single‐chirality microemulsion based on the achiral oil ethyl acetate yielded, relative to diethyl tartrate, lower efficiency (78 300 vs. 91 600), higher resolution (1.99 vs. 1.83), and similar enantioselectivities.
Holocene climatic change and human settlement between the central Sahara and the Nile Valley: Archaeological and geomorphological results
Authors: Bubenzer Olaf , Riemer Heiko 
Published: June 2007

AbstractSupraregional investigations of the Holocene occupational history of the eastern Sahara west of the Nile combined with the study of climatic, environmental, and geomorphological archives were carried out in contrasting desert regions from the Mediterranean coast strip to Wadi Howar in Sudan. The research areas are located far away from groundwater influence and are therefore capable of indicating environmental changes. Climatic development in accordance with nearly 500 14C dates from archaeological sites indicates a Holocene optimum lasting from approximately 9500 B.P. till the beginning of the drying trend that set in about 6300 B.P. (9000–5300 cal. B.C.). Although the faunal and floral remains are arid types, they indicate slightly wetter conditions than today. Surface water was the key factor that influenced the adaptation strategies of the mobile hunter‐gatherers (and in some parts, the pastoralists) in the desert regions. Large episodic camp sites agglomerated at favorable drainage systems and water pools, and settlement patterns strongly correlate with the paleohydrological factors examined with remote sensing cartography, geomorphological work, and the analysis of digital elevation models. © 2007 Wiley Periodicals, Inc.
Impaired liver regeneration and increased oval cell numbers following T cell–mediated hepatitis
Authors: Hines Ian N. , Kremer Michael , Isayama Fuyumi , Perry Ashley W. , Milton Richard J. , Black April L. , Byrd Christy L. , Wheeler Michael D. 
Published: June 2007

Abstract

The regeneration of liver tissue following transplantation is often complicated by inflammation and tissue damage induced by a number of factors, including ischemia and reperfusion injury and immune reactions to the donor tissue. The purpose of the current study is to characterize the effects of T cell–mediated hepatitis induced by concanavalin A (ConA) on the regenerative response in vivo. Liver regeneration following a partial (70%) hepatectomy (pHx) was associated with elevations in serum enzymes and the induction of key cell cycle proteins (cyclin D, cyclin E, and Stat3) and hepatocyte proliferation. The induction of T cell–mediated hepatitis 4 days before pHx increased serum enzymes 48 hours after pHx, reduced early cyclin D expression and Stat3 activation, and suppressed hepatocyte proliferation. This inhibition of proliferation was also associated with increased expression of p21, the activation of Smad2, the induction of transforming growth factor beta and interferon gamma expression, and reduced hepatic interleukin 6 production. Moreover, the ConA pretreatment increased the numbers of separate oval cell-like CD117+ cells and hematopoietic-like Sca-1+ cell populations 48 hours following pHx. The depletion of natural killer (NK) cells, an important component of the innate immune response, did not affect liver injury or ConA-induced impairment of hepatocyte proliferation but did increase the numbers of both CD117-positive and Sca-1–positive cell populations. Finally, splenocytes isolated from ConA-pretreated mice exerted cytotoxicity toward autologous bone marrow cells in an NK cell–dependent manner.

Conclusion:

T cell–mediated hepatitis alters early cytokine responses, reduces hepatocellular regeneration, and induces NK cell–sensitive oval cell and hematopoietic-like cell expansion following pHx. (HEPATOLOGY 2007;46:229–241.)
Sodium retention and ascites formation in a cholestatic mice model
Authors: Ackermann Daniel , Mordasini David , Cheval Lydie , Imbert-Teboul Martine , Vogt Bruno , Doucet Alain 
Published: June 2007

Abstract

Renal sodium retention in experimental liver cirrhosis originates from the distal nephron sensitive to aldosterone. The aims of this study were to (1) determine the exact site of sodium retention along the aldosterone-sensitive distal nephron, and (2) to evaluate the role of aldosterone and mineralocorticoid receptor activation in this process. Liver cirrhosis was induced by bile duct ligation in either adrenal-intact or corticosteroid-clamped mice. Corticosteroid-clamp was achieved through adrenalectomy and corticosteroid supplementation with aldosterone and dexamethasone via osmotic minipumps. 24-hours renal sodium balance was evaluated in metabolic cages. Activity and expression of sodium- and potassium-dependent adenosine triphosphatase were determined in microdissected segments of nephron. Within 4-5 weeks, cirrhosis induced sodium retention in adrenal-intact mice and formation of ascites in 50% of mice. At that time, sodium- and potassium-dependent adenosine triphosphatase activity increased specifically in cortical collecting ducts. Hyperaldosteronemia was indicated by increases in urinary aldosterone excretion and in sgk1 (serum- and glucocorticoid-regulated kinase 1) mRNA expression in collecting ducts. Corticosteroid-clamp prevented induction of sgk1 but not cirrhosis-induced sodium retention, formation of ascites and stimulation of sodium- and potassium-dependent adenosine triphosphatase activity and expression (mRNA and protein) in collecting duct. These findings demonstrate that sodium retention in cirrhosis is independent of hyperaldosteronemia and of the activation of mineralocorticoid receptor.

Conclusion:

Bile duct ligation in mice induces cirrhosis which, within 4-5 weeks, leads to the induction of sodium- and potassium-dependent adenosine triphosphatase in cortical collecting ducts, to renal sodium retention and to the formation of ascites. Sodium retention, ascites formation and induction of sodium- and potassium-dependent adenosine triphosphatase are independent of the activation of mineralocorticoid receptors by either aldosterone or glucocorticoids. (HEPATOLOGY 2007;46:173–179.)