bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of candesartan and lisinopril alone and in combination on blood pressure and microalbuminuria
Authors: Morgan Trefor , Anderson Adrianne , Bertram Denise , MacInnis Robert Jeffrey 
Published: May 2007

Background Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blocking drugs (ARB) block the effect of angiotensin II by different mechanisms. It has been suggested that combined therapy may be more effective at reducing blood pressure (BP) than higher doses of either drug. Methods Twenty-three elderly patients with systolic hypertension completed a double-blind crossover study comparing placebo, candesartan (C) 16 mg, C32 mg, lisinopril (L) 20 mg, L40 mg and C16 mg + L20 mg. Treatment periods were one month and ambulatory BP measurements were performed at the end of each period. The effects on albumin excretion in eight patients with microalbuminuria were determined. Results All treatments lowered BP. The falls in systolic and diastolic BP with C16, C32, L20 and L40 were similar. Plasma renin rose to a similar extent. A plateau effect was reached with C16 and L20. Systolic BP on the combination of C16 + L20 was lower than on each monotherapy (C16, 3.8 mmHg [p=0.002]; C32, 6.4 [0.0003]; L20, 2.9 [0.05]; L40, 3.3 [0.003]). The additional fall in BP with the combination appeared to be due to recruitment of non-responders, rather than to an additive effect in most patients. All treatments reduced microalbuminuria to a similar extent. The combination was well tolerated and there was no deterioration in renal function. Conclusion When patients are on a plateau dose of an ACE inhibitor or an ARB, addition of the other drug class has a small but significant incremental effect on BP in the overall group. However, some patients respond better to one drug class than to the other and this may explain the results. This study lends no support to the use of these two drugs in combination to treat hypertension.
Comparative study of the inhibitory effects of adrenomedullin on angiotensin II contraction in rat conductance and resistance arteries
Authors: Haulica Ion , Bild Walther , Mihaila Christian , Serban Dragomir N , Serban Lacramioara , Boisteanu Daniela , Ionita Teodor , Radasanu Oana 
Published: May 2007

Adrenomedullin (ADM), a ubiquitous vasoactive peptide, has been the target of a multitude of studies concerning its effect on the vascular tone. The present work aims at clarifying a series of its interactions with the renin-angiotensin system.The study uses the rat aorta ring as a model of conductance vessels, with or without vascular endothelium, and the second order branch of rat mesenteric arteries as a model of resistance arteries. Interactions between various concentrations of ADM and angiotensin II (Ang II) were studied, in the presence of L-NAME (a nitric oxide [NO] synthase inhibitor) and methylene blue (MB; a soluble guanylate cyclase inhibitor).Results point out differences in the mechanism of the inhibitory action of ADM upon Ang II effects in the two vessel types studied. Inhibition of Ang II contraction by ADM involves guanylate cyclase in both cases. However, NO is involved in ADM-induced inhibition of angiotensinergic not in the resistance ones. vasoconstriction only in the conductance arteries, not in the resistance ones.
The epidemiology of heart failure
Authors: Tendera Michal 
Published: May 2007

Heart failure is becoming increasingly common. More than 20 million people worldwide are estimated to have heart failure. Prevalence is rising because the population is ageing: in both men and women, the prevalence of heart failure in those aged 80–89 years is roughly 10 times the prevalence in those aged 50–59 years. Coronary artery disease is now the most common cause of heart failure. Better treatment of myocardial infarction means that more people survive with impaired myocardial function, and some of these will develop heart failure in time. Hypertension is also an important contributing factor. Valvular disease, once a major cause of heart failure, has become less prevalent. The median survival after diagnosis of heart failure was only 1.7 years for men and 3.2 years for women, according to Framingham data for the years 1948 to 1988. After five years, only 25% of men and 38% of women were still alive. Preventive and treatment measures have improved this picture somewhat: deaths from heart failure have decreased by about 12% per decade. However, heart failure continues to carry a grave prognosis.
Review: The revised role of ACE-inhibition after myocardial infarction in the thrombolytic/primary PCI era
Authors: de Kam Pieter J , Voors Adriaan A , Fici Francesco , van Veldhuisen Dirk J , van Gilst Wiek H 
Published: May 2007

Many studies have investigated the process of left ventricular (LV) dilatation and the effects of angiotensin-converting enzyme (ACE) inhibitors after myocardial infarction (MI). It has been generally accepted that progression of LV dilatation is a major predictor of heart failure and death after MI. Also, attenuation of LV dilatation is thought to be one of the main mechanisms by which ACE inhibitors (ACE-Is) produce their beneficial effects. However, evidence for this hypothesis came from studies that were performed before thrombolytic therapy and primary percutaneous coronary intervention (PCI) were routinely used after acute MI. Nowadays, reperfusion is obtained much more frequently and LV dilatation after MI has become less prevalent. Nevertheless, ACE-Is proved effective in reducing cardiac morbidity and mortality. Therefore, mechanisms other than attenuation of LV dilatation, such as anti-atherosclerotic effects or plaque stabilisation, may explain the long-term beneficial effects of ACE-Is after MI. In the present overview, we evaluate the role of LV dilatation and the effects of ACE-Is after MI in the thrombolytic/primary PCI era and provide recommendations on ACE-I use in clinical practice.
Elevated dietary sodium intake exacerbates myocardial hypertrophy associated with cardiac-specific overproduction of angiotensin II
Authors: Porrello Enzo R , Huggins Catherine E , Curl Claire L , Domenighetti Andrea A , Pedrazzini Thierry , Delbridge Leanne MD , Morgan Trefor O 
Published: May 2007

Introduction/hypothesis Cardiac hypertrophy is an independent risk factor predictive of cardiovascular disease and is significantly associated with morbidity and mortality. The mechanism by which angiotensin II (Ang II) and dietary sodium exert additive effects on the development of cardiac hypertrophy is unclear. The goal of this study was to evaluate the hypothesis that, where there is a genetic predisposition to Ang II-dependent hypertrophy, there is also an increased susceptibility to sodium-induced hypertrophy mediated by AT1-receptor expression. Methods Diets of low sodium (LS, 0.3% w:w) and high sodium (HS, 4.0% w:w) content were fed to adult (age 25 weeks) control wild-type mice (WT) and to weeks) control wild-type mice (WT) and to transgenic mice exhibiting cardiac specific overexpression of angiotensinogen (TG). At the conclusion of a 40-day dietary treatment period, cardiac tissue weights were compared and the relative expression levels of Ang II receptor subtypes (AT1A and AT2) were evaluated using RT-PCR. Results WT and TG mice fed HS and LS diets maintained comparable weight gains during the treatment period. The normalised heart weights of TG mice were elevated compared to WT, and the extent of the increase was greater for mice maintained on the HS diet treatments (WT 12% vs. TG 41% increase in cardiac weight index). While a similar pattern of growth was observed for ventricular tissues, the atrial weight parameters demonstrated an additional significant effect of dietary sodium intake on tissue weight, independent of animal genetic type. No differences in the relative (GAPDH normalised) expression levels of AT1A- and AT2-receptor mRNA were observed between diet or animal genetic groups. Conclusion This study demonstrates that, where there is a pre-existing genetic condition of Ang II-dependent cardiac hypertrophy, the pro-growth effect of elevated dietary sodium intake is selectively augmented. In TG and WT mice, this effect was evident with a relatively short dietary treatment intervention (40 days). Evaluation of the levels of Ang II receptor mRNA further demonstrated that this differential growth response was not associated with an altered relative expression of either AT1A- or AT2-receptor subtypes. The cellular mechanistic bases for this specific Ang II-dietary sodium interaction remain to be elucidated.
Angiotensin (1-7) re-establishes impulse conduction in cardiac muscle during ischaemia-reperfusion. The role of the sodium pump
Authors: De Mello Walmor C 
Published: May 2007

Introduction The effect of angiotensin (1-7) (Ang 1-7) on membrane potential and excitability of rat heart muscle under ischaemia/reperfusion was investigated. Materials and methods The hearts of adult rats were removed under deep anaesthesia and perfused using the Langendorff method. After 40 minutes of global no-flow ischaemia, the heart was reperfused for five minutes and the right ventricle was dissected out and transferred to a transparent chamber, through which normal oxygenated Krebs solution flowed continuously (37°C). Measurements of membrane potential were performed using an intracellular microelectrode connected to a high impedance preamplifier. The muscle was stimulated with rectangular current pulses (3 ms duration; 0.6 Hz) generated by an electronic stimulator and isolation unit. To study the influence of Ang (1-7) on sodium pump current, isolated myocytes were voltageclamped at -40 mV and the current generated by the pump was recorded before and after the administration of Ang (1-7) (10 M)to the bath. Results Results Ang (1-7) (10-8 M) hyperpolarised the ischaemic heart fibre and re-established impulse propagation. The increment of resting potential was related to the activation of the sodium pump. Indeed, Ang (1-7) (10-8 M) enhanced the transient outward current generated by an electrogenic sodium pump. Both effects of Ang (1-7) on membrane potential and pump current were abolished by ouabain (10-7 M). The cardiac refractoriness was also increased by Ang (1-7) (10-8 M). Conclusions Ang (1-7) activates the sodium pump, hyperpolarises the heart cell and re-establishes the impulse conduction during ischaemia/reperfusion. These effects of Ang (1-7), and the increment of cardiac refractoriness, provide an explanation for the reduced incidence of arrhythmias during ischaemia/reperfusion in the presence of Ang (1-7).
Effects of Intravenous PD 123319 on Haemodynamic and Arterial Stiffness Indices in Healthy Volunteers
Authors: Brillante Divina G , Johnstone Martina T , Howes Laurence G 
Published: May 2007

Relatively little is known about the functional expression of cardiovascular angiotensin type 2 (AT2)-receptors in healthy young adult humans. We performed a randomised, placebo-controlled crossover study of the effects of intravenous administration of the selective AT2-receptor antagonist PD 123319 on haemodynamics and arterial stiffness in normal volunteers.Sixteen normal subjects aged 29.9 ± 13.8 years (range 18—30 years) received an intravenous infusion of PD 123319 (10 mcg/minute for 5 minutes) and placebo, separated by one week. Haemodynamics (cardiac index, stroke index and systemic vascular resistance) were measured non-invasively using a BioZ.com thoracic impedance detection system. Blood pressure was measured from an arm cuff using oscillometry. Stiffness index, a measure of arterial stiffness, was measured using a PulseTrace recorder.No significant changes in blood pressure (p=0.92), cardiac index (p=0.52), stroke index (p=0.61), systemic vascular resistance index (p=0.32) or stiffness index (p=0.57) was demonstrated following PD 123319 infusion, compared with placebo.The results of this study do not support the functional presence of cardiovascular AT2receptors that mediate acute haemodynamic effects in healthy young adults. It remains possible that higher doses of PD 123319 may be required to demonstrate functional cardiovascular AT2-receptors in this population, if they are present.
Angiotensin Receptor Blockers: Cardiovascular Protection in the Metabolic Syndrome
Authors: Deedwania Prakash C , Schmieder Roland 
Published: May 2007

It is well recognised that the metabolic syndrome, a constellation of risk factors including obesity, hypertension, insulin resistance and dyslipidaemia, is associated with an increased risk of cardiovascular complications and the development of Type 2 diabetes. Consequently, timely identification and management of all components of the metabolic syndrome is warranted. In particular, guidelines have emphasised the importance of targeting elevated blood pressure (BP) and dyslipidaemia as a method of reducing global cardiovascular risk. Findings from the Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial show that the angiotensin receptor blocker, valsartan, reduces cardiovascular events and the development of Type 2 diabetes in high-risk individuals. This profile is being further explored in the ongoing Nateglinide And Valsartan in Impaired Glucose Tolerance Outcomes Research (NAVIGATOR) trial. Given the potential advantages to patients and physicians of tackling more than one of the components of the metabolic syndrome, antihypertensive agents such as valsartan would appear to be an important addition to the management of vulnerable patients at high risk of cardiovascular events.
Vasopeptidase Inhibition Prevents Target Organ Damage and Improves Survival in Spontaneously Hypertensive Rats
Authors: Linz Wolfgang , Schäfer Stefan , Afkham Freni , Gerl Martin , Schmidts Hans-Ludwig , Rütten Hartmut 
Published: May 2007

Background. Vasopeptidase inhibition has been shown to be an effective antihypertensive principle but its long-term effects on hypertensive target organ damage are not known. We investigated the myocardial, vascular and renal effects of chronic vasopeptidase inhibition in arterial hypertension. Methods and Results. One hundred and thirty-nine male spontaneously hypertensive rats aged 15 months were treated chronically with either the pure angiotensin-converting enzyme (ACE) inhibitor, ramipril (1 mg/kg/d in drinking water, n=46), or the vasopeptidase inhibitor AVE7688 (30 mg/kg/d in chow, n=46), or placebo (n=47) and followed up until they died. After six months, both ramipril and AVE7688 had markedly reduced plasma ACE activity, normalised blood pressure (BP), reduced left ventricular mass and improved systolic function to similar extents. Acetylcholine mediated relaxation of aortic rings was improved by both ramipril and AVE7688. There was substantial albuminuria in the placebo group (albumin-to-creatinine ratio 107±54 µg/mg), which was significantly reduced by ramipril to 57±34 µg/mg, and practically abolished in the AVE7688 group (22±12 µg/mg, p<0.05 vs. placebo and ramipril).Tubulointerstitial damage (semi-quantitative score) was significantly reduced by AVE7688 and ramipril. significantly reduced byAVE7688 and ramipril. Overall mortality was markedly reduced in the ramipril and AVE7688 groups (13% and 16% at six months, respectively), both p<0.05 vs. placebo (71%). Conclusions. Vasopeptidase inhibition effectively controls BP and reduces myocardial, vascular and renal target organ damage, resulting in a markedly prolonged survival.At similar degrees of plasma ACE inhibition, AVE7688 compared to ramipril offers superior protection against hypertensive kidney damage.
Early, but not late therapy with a vasopressin V1a-antagonist ameliorates the development of renal damage after 5/6 nephrectomy
Authors: Windt Willemijn AKM , Tahara Atsua , Kluppel Alex CA , de Zeeuw Dick , Henning Robert H , van Dokkum Richard PE 
Published: May 2007

Introduction. Vasopressin, mainly through the V1a-receptor, is thought to be a major player in the maintenance of hyperfiltration. Its inhibition could therefore lead to a decrease in progression of chronic renal failure.To this end, the effect of the vasopressin V1a-receptor-selective antagonist, YM218, was studied on proteinuria and focal glomerulosclerosis in early and late intervention after 5/6 nephrectomy in rats, and compared with an angiotensin-converting enzyme inhibitor (ACE-I). Materials and methods. After 5/6 nephrectomy, early intervention was performed between week 2 and 10 thereafter with the V1a-receptor-selective antagonist (VRA, 10 mg/kg/day, n=10), enalapril (ACE-I, 10 mg/kg/day, n=9), or vehicle (n=8). Late intervention was performed in another group between week 6 and 12 with VRA (10 mg/kg/day, n=7), lisinopril (ACE-I, 5 mg/kg/day, n=7), or vehicle (n=7). Results. In early intervention, proteinuria and focal glomerulosclerosis were significantly decreased by VRA compared to vehicle (44 7% and 59+8% respectively). ACE-I significantly decreased proteinuria (67 7%) and a trend towards a decrease in focal glomerulosclerosis was observed (30 18%). In late intervention, VRA did not decrease proteinuria and focal glomerulosclerosis compared to vehicle (21 20% and 0%, respectively),ACE-I significantly lowered proteinuria (92 2%) and a focal glomerulosclerosis (69+1%) lowering trend was observed. Conclusion. These results indicate that VRA may protect against early progression of renal injury after 5/6 nephrectomy, whereas its effectiveness seems limited in established renal damage.
Citations of microRNA Biomarker Articles That Were Retracted
Authors: Zhu Hongmei , Jia Yongliang , Leung Siu-wai 
Published: March 2024

ImportanceRetraction is a tool that journals can use to deter research misconduct and alert their audience to erroneous content published in the journals. However, retracted articles may continue to damage science if they are still cited as legitimate articles.ObjectiveTo characterize patterns of postretraction citations, particularly in microRNA biomarker research, a field with one of the highest rates of retraction.Evidence ReviewRetracted scientific articles on microRNAs were retrieved from PubMed, Web of Science, and Retraction Watch between database inception and July 17, 2021, according to preestablished search strategies. Control articles with characteristics in common with retracted articles (ie, published in the same journals in the same years and months and with the same number of authors) were matched and retrieved from PubMed. Citation metrics of retractions and control articles were collected from Web of Science. PubPeer was referenced to examine the public response or comments on included retractions. Data were analyzed from September 2021 through March 2023.FindingsA total of 10 461 articles were analyzed, with 887 retractions and 9574 articles as controls. Among retracted articles, which were published from 1999 to 2021, there were 756 articles (85.23%) written by researchers affiliated with Chinese institutions. Retracted articles were cited 6327 times after retraction. Of 792 retracted articles that were cited, 621 articles (78.41%) were cited at least once after retraction and 238 articles (30.05%) were cited more often after retraction than before retraction. Overall citations (comprising citations before and after retraction) and postretraction citations accumulated over time (eg, the median [IQR] number of postretraction citations was 1 [1-2] and 23 [9-44] citations at the first 6 and 66 months, respectively, between retraction and citation retrieval). A random sample of 87 retracted articles (9.81%) recorded 478 citations after retraction, with 208 citations (43.51%) in articles published 12 months or longer after retraction. Of these citing articles, 19 articles (3.97%) mentioned the retractions. Compared with the control group of 1620 nonretracted articles, no significant differences were found in overall number of citations or citations after retraction. Among 478 articles citing retracted articles, 414 articles were found on PubMed and had matched control articles; these articles had higher odds of being subsequently retracted than 7954 matched control articles (odds ratio, 6.57; 95% CI, 3.39-12.72).Conclusions and RelevanceIn this study, retraction was not associated with a reduction in citations of retracted articles, but articles that cited retracted publications had higher odds of later retraction. These findings suggest that journals may need to implement mechanisms for detection of postretraction citations.
Molecular analysis of the extracellular microenvironment: from form to function
Authors: Macdonald Jade K. , Mehta Anand S. , Drake Richard R. , Angel Peggi M. 
Published: March 2024

The extracellular matrix (ECM) proteome represents an important component of the tissue microenvironment that controls chemical flux and induces cell signaling through encoded structure. The analysis of the ECM represents an analytical challenge through high levels of post‐translational modifications, protease‐resistant structures, and crosslinked, insoluble proteins. This review provides a comprehensive overview of the analytical challenges involved in addressing the complexities of spatially profiling the extracellular matrix proteome. A synopsis of the process of synthesizing the ECM structure, detailing inherent chemical complexity, is included to present the scope of the analytical challenge. Current chromatographic and spatial techniques addressing these challenges are detailed. Capabilities for multimodal multiplexing with cellular populations are discussed with a perspective on developing a holistic view of disease processes that includes both the cellular and extracellular microenvironment.
Folded Well‐Defined 3D Architecture from Synthetic Helical and Sheet‐Like Polymers
Authors: Wang Chengyuan , Mann Arielle , Hannigan Matthew D. , Garvey Regina H. , Dumlao Bianca L. , Weck Marcus 
Published: March 2024

AbstractThe fabrication of truly hierarchically folded single‐chain polymeric nanoparticles with primary, secondary, and defined 3D architecture is still an unfulfilled goal. In this contribution, a polymer is reported that folds into a well‐defined 3D structure from a synthetic sheet‐helix block copolymer. The sheet‐like poly(p‐phenylene vinylene) (PPV) block is synthesized via the ring‐opening metathesis polymerization of a thymine‐bearing dialkoxy‐substituted [2.2]paracyclophane‐1,9‐diene. The PPV block is terminated with a Pd complex using a Pd‐containing chain‐terminating agent. The terminal Pd complex catalyzes the polymerization of isocyanide monomers with side‐chains containing either a chiral menthol or an achiral diaminopyridine resulting in the formation of a helical poly(isocyanide) (PIC) random copolymer. The PIC side‐chains are capable of engaging in complementary hydrogen‐bonding with thymine units along the PPV block resulting in the folding of the two secondary structural domains into a well‐defined 3D structure. The folding and unfolding of the polymer in both chloroform and THF are monitored using dynamic light scattering and NMR spectroscopy. This work is the first example of a hierarchically folded synthetic polymer featuring a defined 3D structure achieved by using two different polymer backbones with two distinct secondary structures.