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1.
J Chromatogr A ; 1729: 465035, 2024 Aug 16.
Artículo en Inglés | MEDLINE | ID: mdl-38851029

RESUMEN

This work presents the development, synthesis, and application of a layered double hydroxide (LDH) coupled to magnetic particles for the removal of antibiotics as tetracyclines (TC´s): tetracycline (TC), chlortetracycline (CT), oxytetracycline (OT), and doxycycline (DT) from milk samples. The LDH synthesis conditions, reaction time (30-90 min), molar ratios Mg2+/Al3+ (7:1-1:7), interlayer anion (NO3-, Cl-, CO32-, and dodecyl sulphate (DS-)) were evaluated. Under synthesis conditions (reaction time of 30 min, Mg2+/Al3+ molar ratio of 7:1, and DS- as interlayer anion), the LDH was coupled in a magnetic solid phase microextraction (MSPµE) methodology. At the optimal extraction conditions (pH 6, 5 min of contact time, 10 mg of adsorbent), a removal percentage of 99.0 % was obtained for each tetracycline. FTIR, TGA, SEM, and adsorption isotherms were employed to characterize the optimal adsorbent. Each experiment was corroborated by large-volume sample stacking capillary electrophoresis (LVSS-CE). The adsorbent was applied directly to positive milk samples (previously tested) for TC´s removal.


Asunto(s)
Hidróxidos , Leche , Tetraciclinas , Leche/química , Animales , Tetraciclinas/aislamiento & purificación , Tetraciclinas/análisis , Tetraciclinas/química , Hidróxidos/química , Adsorción , Microextracción en Fase Sólida/métodos , Antibacterianos/aislamiento & purificación , Antibacterianos/química , Antibacterianos/análisis , Dióxido de Silicio/química
2.
Mol Genet Metab ; 66(1): 16-23, 1999 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-9973543

RESUMEN

Although the role of vitamins as prosthetic groups of enzymes is well known, their participation in the regulation of their genetic expression has been much less explored. We studied the effect of biotin on the genetic expression of rat liver mitochondrial carboxylases: pyruvate carboxylase (PC), propionyl-CoA carboxylase (PCC), and 3-methylcrotonyl-CoA carboxylase (MCC). Rats were made biotin-deficient and were sacrificed after 8 to 10 weeks, when deficiency manifestations began to appear. At this time, hepatic PCC activity was 20% of the control values or lower, and there was an abnormally high urinary excretion of 3-hydroxyisovaleric acid, a marker of biotin deficiency. Biotin was added to deficient primary cultured hepatocytes. It took at least 24 h after the addition of biotin for PCC to achieve control activity and biotinylation levels, whereas PC became active and fully biotinylated in the first hour. The enzyme's mass was assessed in liver homogenates from biotin-deficient rats and incubated with biotin to convert the apocarboxylases into holocarboylases, which were detected by streptavidin blots. The amount of PC was minimally affected by biotin deficiency, whereas that of the alpha subunits of PCC and of MCC decreased substantially in deficient livers, which likely explains the reactivation and rebiotinylation results. The expression of PC and alphaPCC was studied at the mRNA level by Northern blots and RT/PCR; no significant changes were observed in the deficient livers. These results suggest that biotin regulates the expression of the catabolic carboxylases (PCC and MCC), that this regulation occurs after the posttranscriptional level, and that pyruvate carboxylase, a key enzyme for gluconeogenesis, Krebs cycle anaplerosis, and fatty acid synthesis, is spared of this control.


Asunto(s)
Biotina/farmacología , Carboxiliasas/efectos de los fármacos , Hígado/efectos de los fármacos , Piruvato Carboxilasa/efectos de los fármacos , ARN Mensajero/efectos de los fármacos , Animales , Biotina/deficiencia , Biotinilación , Ligasas de Carbono-Carbono/efectos de los fármacos , Ligasas de Carbono-Carbono/metabolismo , Carboxiliasas/genética , Carboxiliasas/metabolismo , Electroforesis en Gel de Poliacrilamida , Hígado/citología , Hígado/enzimología , Masculino , Metilmalonil-CoA Descarboxilasa , Piruvato Carboxilasa/genética , Piruvato Carboxilasa/metabolismo , ARN Mensajero/genética , Ratas , Ratas Wistar , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Estreptavidina
3.
Salud Publica Mex ; 31(1): 91-9, 1989.
Artículo en Español | MEDLINE | ID: mdl-2711260

RESUMEN

This article describes the stages in the building of the general hospitals of 144 beds included in the Health Services Reconstruction and Reordering Program. The Program is being carried out by the Health Ministry in the metropolitan area of Mexico City, emphasizing the reordering sense of the activities developed to cope with the observed unbalances in the distribution of health services among the various zones in the area. The article examines also the coordination among the internal units of the Health Ministry and other agencies in the Health Sector. Finally, the lessons of the experience derived from those processes are discussed.


Asunto(s)
Administración de los Servicios de Salud , Administración Hospitalaria , Planificación Hospitalaria/organización & administración , Hospitales Urbanos/organización & administración , Servicios de Salud/provisión & distribución , Capacidad de Camas en Hospitales , Arquitectura y Construcción de Hospitales/economía , Planificación Hospitalaria/economía , Humanos , México
5.
Rev. invest. clín ; Rev. invest. clín;33(3): 299-301, 1981.
Artículo en Español | LILACS | ID: lil-7027

RESUMEN

La deficiencia congenita de F XIII es un padecimiento raro que se manifiesta por sangrado anormal caracteristicamente de aparicion tardia y cicatrices quirurgicas defectuosas.Ambas manifestaciones son el resultado de la estabilizacion inadecuada de los polimeros de fibrina. Se describe una familia con 2 miembros afectados; la proposita ha presentado 3 episodios severos de sangrado. El comportamiento clinico semejo a las hemofilias. El diagnostico se confirmo con la prueba de la urea 5M. La transfusion de sangre fresca y plasma ha resuelto los episodios de sangrado.Un hermano de la proposita, portador de deficiencia de F XIII fallecio por insuficiencia respiratoria de causa no identificada


Asunto(s)
Deficiencia del Factor XIII
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