Atomic spectrometry and the determination of metals in polymeric materials

Polymeric materials are widely used in the chemical industry and are part of our daily lives. Inorganic species may be added to them as additives, anti-oxidizing agents, stabilizers, plasticizers, colorants and catalysts and may be present in a wide range of concentrations. Their determination demands the development of analytical methods considering different kinds of polymeric materials, their composition and the final use of the material. Although many different analytical techniques may be used, this review emphasizes those based on atomic absorption and emission spectrometry. Solid sampling techniques and digestion methods are described and discussed and compared considering published results.1533154

A espectrometria atômica e a determinação de elementos metálicos em material polimérico

Polymeric materials are widely used in the chemical industry and are part of our daily lives. Inorganic species may be added to them as additives, anti-oxidizing agents, stabilizers, plasticizers, colorants and catalysts and may be present in a wide range of concentrations. Their determination demands the development of analytical methods considering different kinds of polymeric materials, their composition and the final use of the material. Although many different analytical techniques may be used, this review emphasizes those based on atomic absorption and emission spectrometry. Solid sampling techniques and digestion methods are described and discussed and compared considering published results

Relationship of Ventricular Function and Morphometry in Patients with Symptomatic Severe Aortic Stenosis

Objectives To evaluate systolic and diastolic ventricular function in patientswith symptomatic severe aortic stenosis with preservedejection fraction and its correlation with collagen volumefraction and myocyte cross-sectional area.Material and MethodsA total of 12 patients with symptomatic severe aortic stenosiswere evaluated and compared with 6 patients withoutvalvular heart disease; mean age was 65±13 years and 58%were men. All patients underwent tissue Doppler imagingand cardiac catheterization. Endomyocardial biopsies wereobtained to determine collagen volume fraction and myocytecross-sectional area (mm2).ResultsMean collagen volume was 6.1±0.7%; mean myocyte crosssectionalarea was 388.4±15.8mm2 and median strain in thebasal septum was 14% (IIC 6.9-19). There was a significantcorrelation between septal strain measured by tissue Dopplerimaging and collagen volume fraction (correlation coefficient–0.79; p = 0.03). We found no correlation between septalstrain and myocyte cross-sectional area (R2 = 0.15; p = 0.8).The max positive dP/dt normalized for left ventricular enddiastolicpressure obtained during cardiac catheterizationhad a negative correlation with the myocyte cross-sectionalarea (R –0.94; p = 0.005).The time constant of pressure decay(tau) increased by 55%±3,5% (p <0,05) and had a positivecorrelation with the myocyte cross-sectional area (R = 0.81;p = 0.04).ConclusionThis study demonstrates the presence of anomalies in diastolicand systolic function in patients with symptomatic severeaortic stenosis and preserved ejection fraction that correlatewith structural changes in the left ventricle, represented byincreased interstitial collagen volume fraction and myocytecross-sectional area.Objetivos Evaluar la función ventricular sistólica y diastólica en pacientes con estenosis aórtica gravesintomática con fracción de eyección conservada y correlacionarla con el volumen de colágenoy el área miocitaria.Material y métodosSe estudiaron 12 pacientes, edad 65 ± 13 años, sexo masculino 58%, con estenosis aórticagrave sintomática y 6 pacientes sin patología valvular. En todos se realizaron Doppler tisulary cateterismo cardíaco; asimismo, se efectuaron biopsias intraoperatorias para determinar elvolumen de colágeno y el área miocitaria (mm2).ResultadosLa media ± error estándar del volumen de colágeno fue del 6,1% ± 0,7%, la del área miocitariafue de 388,4 ± 15,8 mm2 y la mediana del strain tisular del septum basal fue del 14% (IIC 6,9-19). Se observó una correlación significativa entre el strain tisular del septum y el volumende colágeno (coeficiente de correlación de -0,79; p = 0,03). No se observó correlación entre elstrain tisular del septum y el área miocitaria (R2 = 0,15; p = 0,8). La +dP/dtmáx normalizadapor presión de fin de diástole del ventrículo izquierdo obtenida en estudio hemodinámico secorrelacionó en forma negativa con el área miocitaria (R –0,94; p = 0,005). La constante decaída de la presión (tau) se incrementó el 55% ± 3,5% (p < 0,05) y se correlacionó positivamentecon el área miocitaria (R = 0,81; p = 0,04)

Loss of dystrophin is associated with increased myocardial stiffness in a model of left ventricular hypertrophy

Transition from compensated to decompensated left ventricular hypertrophy (LVH) is accompanied by functional and structural changes. Here, the aim was to evaluate dystrophin expression in murine models and human subjects with LVH by transverse aortic constriction (TAC) and aortic stenosis (AS), respectively. We determined whether doxycycline (Doxy) prevented dystrophin expression and myocardial stiffness in mice. Additionally, ventricular function recovery was evaluated in patients 1 year after surgery. Mice were subjected to TAC and monitored for 3 weeks. A second group received Doxy treatment after TAC. Patients with AS were stratified by normal left ventricular end-diastolic wall stress (LVEDWS) and high LVEDWS, and groups were compared. In mice, LVH decreased inotropism and increased myocardial stiffness associated with a dystrophin breakdown and a decreased mitochondrial O2 uptake (MitoMVO2). These alterations were attenuated by Doxy. Patients with high LVEDWS showed similar results to those observed in mice. A correlation between dystrophin and myocardial stiffness was observed in both mice and humans. Systolic function at 1 year post-surgery was only recovered in the normal-LVEDWS group. In summary, mice and humans present diastolic dysfunction associated with dystrophin degradation. The recovery of ventricular function was observed only in patients with normal LVEDWS and without dystrophin degradation. In mice, Doxy improved MitoMVO2. Based on our results it is concluded that the LVH with high LVEDWS is associated to a degradation of dystrophin and increase of myocardial stiffness. At least in a murine model these alterations were attenuated after the administration of a matrix metalloprotease inhibitor.Fil: Donato, Pablo Martín. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Buchholz, Bruno. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Morales, Celina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Valdez, Laura Batriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Zaobornyj, Tamara. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Baratta, Sergio. Hospital Austral; ArgentinaFil: Paez, Diamela T.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Matoso, Mirian. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Vaccarino, Guillermo. Hospital Austral; ArgentinaFil: Chejtman, Demian. Hospital Austral; ArgentinaFil: Agüero, Oscar. Hospital Austral; ArgentinaFil: Telayna, Juan. Hospital Austral; ArgentinaFil: Navia, José. Hospital Austral; ArgentinaFil: Hita, Alejandro. Hospital Austral; ArgentinaFil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Gelpi, Ricardo Jorge. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Galectin-1 controls cardiac inflammation and ventricular remodeling during acute myocardial infarction

Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, plays essential roles in the control of inflammation and neovascularization. Although identified as a major component of the contractile apparatus of cardiomyocytes, the potential role of Gal-1 in modulating heart pathophysiology is uncertain. Here, we aimed to characterize Gal-1 expression and function in the infarcted heart. Expression of Gal-1 was substantially increased in the mouse heart 7 days after acute myocardial infarction (AMI) and in hearts from patients with end-stage chronic heart failure. This lectin was localized mainly in cardiomyocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas. Both simulated hypoxia and proinflammatory cytokines selectively up-regulated Gal-1 expression in mouse cardiomyocytes, whereas anti-inflammatory cytokines inhibited expression of this lectin or had no considerable effect. Compared with their wild-type counterpart, Gal-1-deficient (Lgals1-/-) mice showed enhanced cardiac inflammation, characterized by increased numbers of macrophages, natural killer cells, and total T cells, but reduced frequency of regulatory T cells, leading to impaired cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI. Treatment of mice with recombinant Gal-1 attenuated cardiac damage in reperfused AMI. Taken together, our results indicate a protective role for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflammation. Thus, Gal-1 treatment represents a potential novel strategy to attenuate heart failure in AMI. © 2013 American Society for Investigative Pathology.Fil: Seropian, Ignacio Miguel. Virginia Commonwealth University; Estados UnidosFil: Cerliani, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Toldo, Stefano. Virginia Commonwealth University; Estados UnidosFil: Van Tassell, Benjamín W.. Virginia Commonwealth University; Estados UnidosFil: Ilarregui, Juan Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: González, Germán Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Matoso, Mirian. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Salloum, Fadi N.. Virginia Commonwealth University; Estados UnidosFil: Melchior, Ryan. Virginia Commonwealth University; Estados UnidosFil: Gelpi, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Stupirski, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Benatar, Alejandro Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Morales, Maria Celina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Abbate, Horacio Antonio. Virginia Commonwealth University; Estados UnidosFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentin