Publications by authors named "Perich R"

Large epidemiologic and clinical estimates of spondyloarthritis (SpA) in Latin America are not available. In this narrative review, our goal was to descriptively summarize the prevalence and features of SpA in Latin America, based on available small studies. A review of peer-reviewed literature identified 41 relevant publications.

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Introduction: Non-compaction of the ventricular myocardium (NCVM) is a rare congenital heart disease. Heightened awareness has resulted in increased detection of the morphological features of NCVM in routine clinical practice.

Patients And Methods: Multicentre study including paediatric patients affected by NCVM according to the echocardiographic criteria of Chin and Jenni.

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Background: Type 3 long-QT syndrome (LQT-3) is caused by gain-of-function mutations in the SCN5A encoding the cardiac sodium channel. Familial atrial fibrillation (AF), previously considered a potassium channelopathy, has recently been related to sodium genetic variants, both in isolated forms and in patients with underlying heart disease.

Objective: The purpose of this study was to describe the first family associating LQT-3 and AF due to a gain-of-function mutation in SCN5A and assess the usefulness of the sodium blocker flecainide in individuals with both phenotypes.

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Objective: Tuberculosis (TB) in patients with rheumatoid arthritis (RA) undergoing treatment with anti-tumor necrosis factor (TNF) agents is commonly the result of reactivation of latent TB infection (LTBI); detection and treatment of LTBI is essential before treatment with anti-TNF agents. We reported previously that the tuberculin skin test (TST) is inaccurate for diagnosis of LTBI in patients with RA. Here, we compare the prevalence of LTBI in RA patients and matched controls according to positive TST and QuantiFeron-TB Gold In-Tube version (QFT) results and determine their agreement.

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The 22q11.2 region is susceptible to chromosomal rearrangements, leading to various types of congenital malformation and mental retardation. The most common anomaly is 22q11.

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Background: The purified protein derivative (PPD) skin test is the only widely used method which detects latent tuberculosis infection (LTBI) and is dependent on a normal T cell function. In rheumatoid arthritis (RA) the T cell function is altered, which may result in an inability to develop an adequate PPD reaction.

Objectives: To evaluate the response to PPD in patients with RA and to compare it with that of control subjects.

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Objective: To examine the effect of ZD7155, an angiotensin II receptor antagonist, on blood pressure, heart rate and occupancy of tissue angiotensin II receptor in two-kidney, one-clip Goldblatt hypertensive rats.

Methods: Goldblatt hypertension was produced in Sprague-Dawley rats. ZD7155 was administered orally at 3 mg/kg and blood pressure and heart rate were monitored for up to 48 h.

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Review and pooled analysis of the relevant worldwide literature was investigated from 1975 to 1996. Eighteen surveys out of 54 were suitable for analysis according to the selection criteria. This represents a total of 60494 observations from 26 countries all over the world.

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The potent bradykinin B2 receptor antagonist analogue, [125I]HPP-HOE140, ([125I]-3-4-hydroxyphenyl-propionyl-D-Arg0-[Hyp3, Thi5,D-Tic7, Oic8]bradykinin), was used to localize and characterize guinea-pig tissue bradykinin B2 receptors. Analysis of competition for the radioligand binding, using membrane preparations of lung, ileum and uterus, revealed the presence of a high- and low-affinity binding site: at the high-affinity site, the apparent Ki for the various bradykinin B2 receptor ligands ranged from 0.26 to 2.

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The localization and characterization of bradykinin B2 receptors in sheep uterus was carried out using a radiolabelled B2 receptor ligand, 3,4-hydroxyphenypropionyl-D-Arg0-[Hyp3,Thi5,D-++ +Tic7,D-Oic8] bradykinin (HPP-HOE140). Competition of the radioligand, [125I]HPP-HOE140, from membrane preparations of anoestrus sheep uterus by bradykinin agonists and antagonists revealed the presence of high- and low-affinity binding sites with ligand specificity typical of the bradykinin B2 receptor. Using in vitro autoradiography on tissue sections, intense binding was visible over the superficial epithelial layer of the endometrium and inner third of the myometrium of anoestrus sheep uterus.

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The tissue renin angiotensin system may play a role in cardiovascular pathophysiology. Angiotensin converting enzyme in tissues is now a target for pharmacological inhibition. It is therefore important to determine whether ACE is evenly distributed throughout the vascular tree and whether the enzyme has the same characteristics in different vascular beds.

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1. We investigated the role of angiotensin converting enzyme (ACE) in the cardiovascular effects of N-[1-(R,S)-carboxy-3-phenylpropyl]-Ala-Ala-Tyr-p-aminobenzoate (cFP), a peptidase inhibitor selective for metalloendopeptidase (EP) E.C.

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1. Plasma dipeptidyl carboxypeptidase-1 (DCP1; angiotensin I-converting enzyme, kininase II; EC 3.4.

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Angiotensin converting enzyme active sites from rat plasma, lung, kidney and testis were assessed by comparative radioligand binding studies under physiological chloride conditions. Displacement of [125I]Ro 31-8472 from somatic and plasma angiotensin converting enzyme by angiotensin converting enzyme inhibitors of different structure indicated two binding sites (perindoprilat: high affinity carboxyl site, KDC 18 +/- 6 pM), and a single high affinity binding site on testis angiotensin converting enzyme (KDC 20 +/- 1 pM). Displacement of [125I]351A from plasma, somatic and testis angiotensin converting enzyme occurred at a single high affinity binding site.

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1. The haemodynamic and hormonal responses of four patients with acute post-surgical oliguria (urine output < 0.5 mL/kg per h) were measured in response to the renin inhibitor enalkiren.

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Purified angiotensin-converting enzyme (ACE) from rat lung and testis, membrane preparations of ACE from lung, kidney, and testis, and ACE from plasma were used in radioligand binding studies, to seek evidence for two binding sites in ACE of somatic origin, as predicted by molecular biology studies. 125I-Ro 31-8472, a radioiodinated hydroxy derivative of cilazaprilat, and 125I-351A, a radioiodinated p-hydroxybenzamidine analogue of lisinopril, were used as radioligands. Autoradiographic study of renal ACE using 125I-Ro 31-8472 or 125I-351A showed the same distribution of radioligand binding across kidney sections and identical radioligand binding for purified lung and testis ACE by Western blot, confirming that the same protein bound both radioligands.

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1. ACE from rat lung and testis was characterized by radioligand binding studies using [125I]-Ro 31-8472, the radioiodinated hydroxy derivative of the potent ACE inhibitor cilazaprilat. 2.

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1. Angiotensin-converting enzyme (ACE) concentration was measured in mesenteric and brain microvessels from spontaneously hypertensive rats (SHR) and compared with normotensive controls using a specific radioligand binding assay. 2.

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Objective: Abnormalities in the vascular renin-angiotensin system have been hypothesized to contribute to the pathogenesis and complications of hypertension. In animal models of hypertension, there is wide variation in reported vascular angiotensin converting activity, particularly in cerebral microvessels. In this study, we sought to characterize, quantitate and compare cerebral microvessel angiotensin converting enzyme (ACE) in genetically hypertensive rats and normotensive rats.

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1. The effects of angiotensin-converting enzyme (ACE) inhibitors on the tissue ACE were assessed by quantitative in vitro autoradiography after acute and chronic administrations of the drugs. 2.

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1. The components of the renin-angiotensin system exist in many cardiovascular tissues (heart vessels, kidneys, adrenal glands). 2.

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Angiotensin converting enzyme (ACE) inhibitors lead to induction of ACE in animals and humans. This complicates the use of ACE enzymatic activity as an index of inhibition in plasma or tissues after chronic administration of ACE inhibitors. We have, therefore, developed a method for ACE measurement by in vitro autoradiography using an 125I-labelled inhibitor to quantitate total ACE and the concentration of free (not inhibited) ACE in tissues after prolonged administration of ACE inhibitors to rats.

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1. Angiotensin-converting enzyme (ACE) was measured in the aorta, cerebral and mesenteric microvessels of Wistar-Kyoto rats using a specific radioligand assay. 2.

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1. Chronic heart failure was induced in rats by ligation of the left coronary artery to produce a left ventricular myocardial infarct. 2.

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Inhibition of angiotensin-converting enzyme (ACE) in rat plasma and tissue was studied after administration of quinapril, a new orally active ACE inhibitor with an intermediate duration of action. Tissue and plasma ACE was assessed by a radioinhibitor-binding assay and by in vitro autoradiography using [125I]351A as the radioligand. Individual tissues in rats were differentially inhibited in time and degree.

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