Atenolol oral en el manejo del hemangioma infantil: serie de casos de 46 pacientes / Oral Atenolol for Infantile Hemangioma: Case Series of 46 Infants

El propranolol, un betabloqueante no selectivo, sigue siendo la primera línea de tratamiento para el hemangioma infantil problemático. Sin embargo, aunque poco frecuente, un subgrupo de pacientes experimenta efectos secundarios indeseables, lo que despierta el interés sobre otros betabloqueantes selectivos. Presentamos una amplia serie de casos de 46 lactantes tratados con éxito con atenolol, un bloqueante selectivo beta-1

Propranolol, a non-selective beta-blocker, remains the first line of treatment for problematic infantile hemangioma. However, although rarely, a subset of patients experience undesirable side effects, raising interest in other selective beta-blockers. We present a large case series of 46 infants treated successfully with oral atenolol, a selective beta-1 blocker

Oral Atenolol for Infantile Hemangioma: Case Series of 46 Infants. / Atenolol oral en el manejo del hemangioma infantil: serie de casos de 46 pacientes.

Propranolol, a non-selective beta-blocker, remains the first line of treatment for problematic infantile hemangioma. However, although rarely, a subset of patients experience undesirable side effects, raising interest in other selective beta-blockers. We present a large case series of 46 infants treated successfully with oral atenolol, a selective beta-1 blocker.

Papulosis de células claras: una serie de casos / Clear Cell Papulosis: A Case Series

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Hemangioma infantil de crecimiento mínimo o detenido segmentario en un síndrome LUMBAR / Segmental Infantile Hemangioma With Minimal or Arrested Growth in LUMBAR Syndrome

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Purification and characterization of saxitoxin from Mytilus chilensis of southern Chile.

In the current communication we describe an innovative method to purify saxitoxin (STX), a toxin presents in contaminated muscle of Mylitus chilensis extracted in the southern part of Chile, using a liquid chromatographic methodology based on ionic pairs. The STX was extracted using HCl and treated with ammonium sulfate following a treatment with trichloroacetic acid and hexane/diethyl ether (97/3). The samples were analyzed by a semi-preparative HPLC in order to collect pure fractions of STX and these fractions were eluted in solid-phase cationic interchange SCX extraction columns. The purified STX was stable and homogeneous and its identity was confirmed by LC-MS-MS, which demonstrated a high quality purification of STX, without presence of analogs such as neosaxitoxin (Neo) and decarbamoyl saxitoxin (dcSTX). The STX biological activity was analyzed in a bioassay in mice model and compared to the standard STX produced by the FDA and no significant differences were observed.

Subgrupos de Lupus Eritematoso Sistémico: influencia de la edad de inicio, la raza, el sexo y el perfil de anticuerpos en las manifestaciones clínicas de la enfermedad / No presenta

El Lupus Eritematoso Sistémico (LES) es una enfermedad heterogénea en su presentación clínica y serológica, pero factores raciales, etarios e inmunológicos determinan subgrupos más homogéneos tanto en sus manifestaciones como en su pronóstico. El LES en los hombres cursa con mayor actividad y daño acumulado y mayor frecuencia y gravedad del compromiso renal; los hombres afroamericanos tienen un rápido desarrollo de LES después del primer síntoma y manifestaciones graves renales, neurológicas, hematológicas y compromiso de las serosas desde el inicio de la enfermedad. El grupo de inicio antes de los 18 años cursa con mayor actividad, adenopatías, visceromegalias, citopenias y nefritis mientras que los que inician después de los 50 años tienen menos actividad lúpica y nefritis pero más daño acumulado, comorbilidades y compromiso cardiovascular. Los diferentes autoanticuerpos se asocian a ciertos subgrupos. Los anti-DNA predicen nefropatía y LES activo, los anti-Ro se asocian a fotosensibilidad, lupus neonatal y LES de inicio tardío y los anti-fosfolípidos (AFL) se asocian a daño orgánico trombótico.

Systemic Lupus Erythematosus (SLE) is a heterogeneus disease; clinical, serologic and epidemiologic subsets are determinated by age, race and genetic factors. Male lupus patiens have a worst prognosis with more lupus nephritis and disease activity; African-American male have an early severe compromise with lupus nephritis (LN) pleuritis and cytopenias. In children SLE has more lupus nephritis, lymph node enlargement and splenomegaly. In older than 50 years at diagnosis SLE has accrual damage and cardiovascular disease. Antibodies are predictive of clinical subsets; anti-DNA is associated with LN and SLE activity; Anti-Ro is asociated with neonatal lupus syndrome, fotosensitivity and late onset SLE; Antiphospholipid antibodies are predictive of organ damage in SLE.

Direct inhibition of the hexose transporter GLUT1 by tyrosine kinase inhibitors.

The facilitative hexose transporter GLUT1 is a multifunctional protein that transports hexoses and dehydroascorbic acid, the oxidized form of vitamin C, and interacts with several molecules structurally unrelated to the transported substrates. Here we analyzed in detail the interaction of GLUT1 with a group of tyrosine kinase inhibitors that include natural products of the family of flavones and isoflavones and synthetic compounds such as the tyrphostins. These compounds inhibited, in a dose-dependent manner, the transport of hexoses and dehydroascorbic acid in human myeloid HL-60 cells, in transfected Chinese hamster ovary cells overexpressing GLUT1, and in normal human erythrocytes, and blocked the glucose-displaceable binding of cytochalasin B to GLUT1 in erythrocyte ghosts. Kinetic analysis of transport data indicated that only tyrosine kinase inhibitors with specificity for ATP binding sites inhibited the transport activity of GLUT1 in a competitive manner. In contrast, those inhibitors that are competitive with tyrosine but not with ATP failed to inhibit hexose uptake or did so in a noncompetitive manner. These results, together with recent evidence demonstrating that GLUT1 is a nucleotide binding protein, support the concept that the inhibitory effect on transport is related to the direct interaction of the inhibitors with GLUT1. We conclude that predicted nucleotide-binding motifs present in GLUT1 are important for the interaction of the tyrosine kinase inhibitors with the transporter and may participate directly in the binding transport of substrates by GLUT1.

An outbreak of hantavirus pulmonary syndrome in western Paraguay.

During an investigation of hantavirus pulmonary syndrome (HPS) in Paraguay in 1995, sera from persons with HPS-like illness, houshold contacts of confirmed HPS case-patients, and a sample of the area residents were analyzed by ELISA for antibodies to Sin Nombre virus (SNV). Rodent serosurveys and analysis of precipitation records were also conducted. Twenty-three of 24 available probable cases were SNV antibody-positive, 17 of whom were ill between July 1995 and January 1996. Four (14.8%) of 27 case-contacts and 44 (12.8%) of 345 community residents were also seropositive. Calomys laucha (vesper mouse) was the most common rodent species captured and the most frequently SNV-seropositive. Rainfall in May 1995 was 10-fold greater than that seen in May over the preceding 11 years. This 17 case-cluster represents the largest documented outbreak since HPS was first recognized in 1993. Calomys laucha is the likely primary rodent reservoir for a SNV-like hantavirus in western Paraguay. Fluctuations in monthly precipitation rates may have contributed to increased risk for HPS in this region.

Human erythrocytes express GLUT5 and transport fructose.

Although erythrocytes readily metabolize fructose, it has not been known how this sugar gains entry to the red blood cell. We present evidence indicating that human erythrocytes express the fructose transporter GLUT5, which is the major means for transporting fructose into the cell. Immunoblotting and immunolocalization experiments identified the presence of GLUT1 and GLUT5 as the main facilitative hexose transporters expressed in human erythrocytes, with GLUT2 present in lower amounts. Functional studies allowed the identification of two transporters with different kinetic properties involved in the transport of fructose in human erythrocytes. The predominant transporter (GLUT5) showed an apparent Km for fructose of approximately 10 mmol/L. Transport of low concentrations of fructose was not affected by 2-deoxy-D-glucose, a glucose analog that is transported by GLUT1 and GLUT2. Similarly, cytochalasin B, a potent inhibitor of the functional activity of GLUT1 and GLUT2, did not affect the transport of fructose in human erythrocytes. The functional properties of the fructose transporter present in human erythrocytes are consistent with a central role for GLUT5 as the physiological transporter of fructose in these cells.

Increased uptake and accumulation of vitamin C in human immunodeficiency virus 1-infected hematopoietic cell lines.

Vitamin C (ascorbic acid) is required for normal host defense and functions importantly in cellular redox systems. To define the interrelationship between human immunodeficiency virus (HIV) infection and vitamin C flux at the cellular level, we analyzed vitamin C uptake and its effects on virus production and cellular proliferation in HIV-infected and uninfected human lymphoid, myeloid, and mononuclear phagocyte cell lines. Chronic or acute infection of these cell lines by HIV-1 led to increased expression of glucose transporter 1, associated with increased transport and accumulation of vitamin C. Infected cells also showed increased transport of glucose analogs. Exposure to vitamin C had a complex effect on cell proliferation and viral production. Low concentrations of vitamin C increased or decreased cell proliferation depending on the cell line and either had no effect or caused increased viral production. Exposure to high concentrations of vitamin C preferentially decreased the proliferation and survival of the HIV-infected cells and caused decreased viral production. These findings indicate that HIV infection in lymphocytic, monocytic, and myeloid cell lines leads to increased expression of glucose transporter 1 and consequent increased cellular vitamin C uptake. High concentrations of vitamin C were preferentially toxic to HIV-infected host defense cell lines in vitro.

Genistein is a natural inhibitor of hexose and dehydroascorbic acid transport through the glucose transporter, GLUT1.

Genistein is a dietary-derived plant product that inhibits the activity of protein-tyrosine kinases. We show here that it is a potent inhibitor of the mammalian facilitative hexose transporter GLUT1. In human HL-60 cells, which express GLUT1, genistein inhibited the transport of dehydroascorbic acid, deoxyglucose, and methylglucose in a dose-dependent manner. Transport was not affected by daidzein, an inactive genistein analog that does not inhibit protein-tyrosine kinase activity, or by the general protein kinase inhibitor staurosporine. Genistein inhibited the uptake of deoxyglucose and dehydroascorbic acid in Chinese hamster ovary (CHO) cells overexpressing GLUT1 in a similar dose-dependent manner. Genistein also inhibited the uptake of deoxyglucose in human erythrocytes indicating that its effect on glucose transporter function is cell-independent. The inhibitory action of genistein on transport was instantaneous, with no additional effect observed in cells preincubated with it for various periods of time. Genistein did not alter the uptake of leucine by HL-60 cells, indicating that its inhibitory effect was specific for the glucose transporters. The inhibitory effect of genistein was of the competitive type, with a Ki of approximately 12 microM for inhibition of the transport of both methylglucose and deoxyglucose. Binding studies showed that genistein inhibited glucose-displaceable binding of cytochalasin B to GLUT1 in erythrocyte ghosts in a competitive manner, with a Ki of 7 microM. These data indicate that genistein inhibits the transport of dehydroascorbic acid and hexoses by directly interacting with the hexose transporter GLUT1 and interfering with its transport activity, rather than as a consequence of its known ability to inhibit protein-tyrosine kinases. These observations indicate that some of the many effects of genistein on cellular physiology may be related to its ability to disrupt the normal cellular flux of substrates through GLUT1, a hexose transporter universally expressed in cells, and is responsible for the basal uptake of glucose.

Resolution of the facilitated transport of dehydroascorbic acid from its intracellular accumulation as ascorbic acid.

We performed a detailed kinetic analysis of the uptake of dehydroascorbic acid by HL-60 cells under experimental conditions that enabled the differentiation of dehydroascorbic acid transport from the intracellular reduction/accumulation of ascorbic acid. Immunoblotting and immunolocalization experiments identified GLUT1 as the main glucose transporter expressed in the HL-60 cells. Kinetic analysis allowed the identification of a single functional activity involved in the transport of dehydroascorbic acid in the HL-60 cells. Transport was inhibited in a competitive manner by both 3-O-methyl-D-glucose and 2-deoxy-D-glucose. In turn, dehydroascorbic acid competitively inhibited the transport of both sugars. A second functional component identified in experiments measuring the accumulation of ascorbic acid appears to be associated with the intracellular reduction of dehydroascorbic acid to ascorbic acid and is not directly involved in the transport of dehydroascorbic acid via GLUT1. Transport of dehydroascorbic acid by HL-60 cells was independent of the presence of external Na+, whereas the intracellular accumulation of ascorbic acid was found to be a Na(+)-sensitive process. Thus, the transport of dehydroascorbic acid via glucose transporters is a Na(+)-independent process which is kinetically and biologically separable from the reduction of dehydroascorbic acid to ascorbic acid and its subsequent intracellular accumulation.