A 3.3-Ma impact in argentina and possible consequences

Enigmatic glassy materials (escorias) and red bricklike materials (tierras cocidas) occur at a restricted stratigraphic level (the top of the Chapadmalal Formation). Materials from one locality near Mar del Plata are attributed to a mid-Pliocene impact event with a radiometric and magnetostratigraphic age of 3.3 million years ago (Ma). An extinction of endemic fauna (including the glyptodonts and flightless cariamid birds) correlates with the unit containing the impact glasses. Moreover, the age of the glasses is coincident within dating uncertainties with a pulselike change in the oxygen isotope marine record in the Atlantic and Pacific Oceans just before the late Pliocene deterioration of the climate.

[Helicobacter pylori: 14C urea breath test in clinical practice at a general hospital]. / Helicobacter pylori: prueba de la respiración con 14C urea en la práctica clinica de un hospital general.

Using isotope methods we studied in 125 patients the absence or presence of gastric urease. Carbon 14 urea was given orally, breath samples were collected over a 30 min period, and the amount of 14CO2 excreted every 10 min was determined. The patients were divided in two groups: 1) uninfected with Helicobacter pylori (HP) (n = 64), 2) infected (n = 41), depending on whether the excretion of the 14CO2 in the breath was greater o lower that 1% of the administered dose. Compared with the infected patients the uninfected patients have shown a mean values of 14CO2 in the breath significantly lower at 10-20-30 min. Among 38 patients who underwent both the 14C urea breath test and endoscopy biopsy of the antral mucosa for histological examination, 22 (58%) and 16 (42%) showed positive or negative HP on biopsy respectively. Among these HP-positive patients, 16 (73%) had chronic gastritis, 3 (14%) gastritis acute and 3 (14%) had duodenal ulcer. Excretion of 14CO2 in breath, lower than 1% and higher than 1% has a specificity of 81% and sensitivity accuracy, positive predictive power of 86%, 84% and 86% respectively. In conclusion 14C urea breath test is a simple noninvasive and easy way to detect with high degree of confidence the presence or absence of gastric urease.

Laser 40Ar/39Ar Evaluation of Slow Cooling and Episodic Loss of 40Ar from a Sample of Polymetamorphic Muscovite.

Volume diffusion models predict that crystals with large diffusion dimensions can record a wide range of thermal conditions in the Earth's crust. Direct measurements of the zoning of radiogenic argon-40 in single muscovite porphyroblasts, from a complex terrain in the Vermont Appalachians, record multiple crustal events that span 150 million years. The crystal radius was the effective dimension for argon diffusion (approximately 1000 micrometers). Late deformation features inside the crystals locally decreased the diffusion dimension and promoted loss of argon-40. Zoning patterns of radiogenic isotopes, as observed in this study, are an increasingly important diagnostic tool for studying the thermal record of tectonic processes.

[Extracellular fluid, plasma and interstitial volume in cirrhotic patients without clinical edema or ascites]. / Determinación del volumen extracelular, plasmático, e intersticial en pacientes cirróticos sin ascitis ni edema clínico.

Extracellular fluid volume (E.C.F.) and plasma volume (P.V.), were measured with sodium sulfate labeled with 35I and 131I human serum albumin, respectively, by the dilution technique in control subjects and in cirrhotic patients without clinical ascites or edema, renal or hepatic failure, gastrointestinal bleeding or diuretics. Results are expressed as mean +/- DS in both ml/m2 and ml/kg. In normal subjects E.C.F. (n = 8) was 7,533 +/- 817 ml/m2 (201.3 +/- 182 ml/kg), P.V. (n = 11) 1,767 +/- 337 ml/m2 (47.2 +/- 9.3 ml/kg), and interstitial fluid (I.S.F.) (n = 7) 5,758 +/- 851 ml/m2 (Table 2). In cirrhotic patients E.C.F. (n = 11) was 10,318 +/- 2,980 ml/m2 (261.7 +/- 76.8 ml/kg), P.V. (n = 12) 2,649 +/- 558 ml/m2 (67.7 +/- 15.6 ml/kg) and I.S.F. (n = 11) 7,866 +/- 2,987 ml/m2 (Table 3). Cirrhotic patients compared with normal subjects have hypervolemia due to a significant E.C.F. and P.V. expansion (p less than 0.02 and less than 0.001 respectively) (Fig. 1). Reasons for E.C.F. and P.V. abnormalities in cirrhotic patients may reflect urinary sodium retention related to portal hipertension which stimulates aldosterone release or enhanced renal tubular sensitivity to the hormone. However, it is also possible that these patients, in the presence of hypoalbuminemia (Table 1), have no clinical edema or ascites due to increased glomerular filtration, suppressed release of vasopressin, increased natriuretic factor, and urinary prostaglandin excretion, in response to the intravascular expansion, all of which increased solute and water delivery to the distal nephron and improved renal water excretion. We conclude that in our clinical experience cirrhotic patients without ascites or edema have hypervolemia because of a disturbance in E.C.F.

Determinacion del volumen extracelular, plasmatico, e intersticial en pacientes cirroticos sin ascitis ni edema clinico / Extracellular fluid, plasma and interstitial volume in cirrhotic patients without clinical edema or ascitis

En el presente trabajo se estudió con técnicas de dilución isotópica los volumenes intravbasculares y extravasculares, en 2 grupos: Grupo I: controles sanos, Grupo II: pacientes cirróticos, sin evidencia clínica de edema o ascitis, insuficiencia renal, hepática, hemorragia gastrointestinal o tratamiento diurético. El volumen del líquido extracelular (V.L.E.) se determinó con sulfato de sodio (355 Na**2), y el volumen plasmático (V.P.) con albúmina marcada con I 131 (Risah), calculándose posteriormente el volumen de líquido intersticial (V.L.I.). En el Grupo I, los valores fueron: Vd.L.E. (n = 8) 7 533 ñ 817 ml/m**2 (201 ñ 182 ml/kg(), V.P. (n = 11), l 767 ñ 337 ml/m**2 *(47,2 ñ 9,3 ml/kg), V.K.I. (n = 7) 5 758 ñ 851 ml/ml**2. En el Grupo II el V.L.E. (n = 11) fue de 10318 ñ 2980 ml/m2 (261,7 ñ 76,8 ml/kg), el V.P. (n = 12) fue de 2649 ñ 558 ml/m**2 (67,7 ñ l5,6 ml/kg(), y el V.L.I. (n = 11) de 7866 ñ 2987 ml/m[[2. Comparados con los controles, los pacientes cirróticos tienen significativa expansión de los volúmenes extracelular e intravascular (p<0,l02 y <0,001 respecitivamente). El V.L.I. no mostró cambios significativos. Concluimos que los pacientes cirróticos sin ascitis o edema clínico, tienen hipervolemia por alteración del V.L.E

Determinación del volumen extracelular, plasmático, e intersticial en pacientes cirróticos sin ascitis ni edema clínico. / [Extracellular fluid, plasma and interstitial volume in cirrhotic patients without clinical edema or ascites]

Extracellular fluid volume (E.C.F.) and plasma volume (P.V.), were measured with sodium sulfate labeled with 35I and 131I human serum albumin, respectively, by the dilution technique in control subjects and in cirrhotic patients without clinical ascites or edema, renal or hepatic failure, gastrointestinal bleeding or diuretics. Results are expressed as mean +/- DS in both ml/m2 and ml/kg. In normal subjects E.C.F. (n = 8) was 7,533 +/- 817 ml/m2 (201.3 +/- 182 ml/kg), P.V. (n = 11) 1,767 +/- 337 ml/m2 (47.2 +/- 9.3 ml/kg), and interstitial fluid (I.S.F.) (n = 7) 5,758 +/- 851 ml/m2 (Table 2). In cirrhotic patients E.C.F. (n = 11) was 10,318 +/- 2,980 ml/m2 (261.7 +/- 76.8 ml/kg), P.V. (n = 12) 2,649 +/- 558 ml/m2 (67.7 +/- 15.6 ml/kg) and I.S.F. (n = 11) 7,866 +/- 2,987 ml/m2 (Table 3). Cirrhotic patients compared with normal subjects have hypervolemia due to a significant E.C.F. and P.V. expansion (p less than 0.02 and less than 0.001 respectively) (Fig. 1). Reasons for E.C.F. and P.V. abnormalities in cirrhotic patients may reflect urinary sodium retention related to portal hipertension which stimulates aldosterone release or enhanced renal tubular sensitivity to the hormone. However, it is also possible that these patients, in the presence of hypoalbuminemia (Table 1), have no clinical edema or ascites due to increased glomerular filtration, suppressed release of vasopressin, increased natriuretic factor, and urinary prostaglandin excretion, in response to the intravascular expansion, all of which increased solute and water delivery to the distal nephron and improved renal water excretion. We conclude that in our clinical experience cirrhotic patients without ascites or edema have hypervolemia because of a disturbance in E.C.F.

Determinacion del volumen extracelular, plasmatico, e intersticial en pacientes cirroticos sin ascitis ni edema clinico / Extracellular fluid, plasma and interstitial volume in cirrhotic patients without clinical edema or ascitis

En el presente trabajo se estudió con técnicas de dilución isotópica los volumenes intravbasculares y extravasculares, en 2 grupos: Grupo I: controles sanos, Grupo II: pacientes cirróticos, sin evidencia clínica de edema o ascitis, insuficiencia renal, hepática, hemorragia gastrointestinal o tratamiento diurético. El volumen del líquido extracelular (V.L.E.) se determinó con sulfato de sodio (355 Na**2), y el volumen plasmático (V.P.) con albúmina marcada con I 131 (Risah), calculándose posteriormente el volumen de líquido intersticial (V.L.I.). En el Grupo I, los valores fueron: Vd.L.E. (n = 8) 7 533 ñ 817 ml/m**2 (201 ñ 182 ml/kg(), V.P. (n = 11), l 767 ñ 337 ml/m**2 *(47,2 ñ 9,3 ml/kg), V.K.I. (n = 7) 5 758 ñ 851 ml/ml**2. En el Grupo II el V.L.E. (n = 11) fue de 10318 ñ 2980 ml/m2 (261,7 ñ 76,8 ml/kg), el V.P. (n = 12) fue de 2649 ñ 558 ml/m**2 (67,7 ñ l5,6 ml/kg(), y el V.L.I. (n = 11) de 7866 ñ 2987 ml/m[[2. Comparados con los controles, los pacientes cirróticos tienen significativa expansión de los volúmenes extracelular e intravascular (p<0,l02 y <0,001 respecitivamente). El V.L.I. no mostró cambios significativos. Concluimos que los pacientes cirróticos sin ascitis o edema clínico, tienen hipervolemia por alteración del V.L.E (AU)