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1.
Immunohematology ; 25(4): 152-9, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-20406022

RESUMEN

The Lutheran blood group system consists of 19 antigens: four pairs of antithetical antigens--Lu(a)/Lu(b), Lu6/Lu9, Lu8/Lu14, and Au(a)/Au(b)--and 11 antigens of very high frequency. These antigens are located on four of the five immunoglobulin-like domains of both isoforms of the Lutheran glycoprotein. The LU gene is on chromosome 19 and comprises 15 exons. The two glycoprotein isoforms differ in the length of their cytoplasmic tails as a result of alternative splicing of intron 13. Lu(null) phenotype arises from homozygosity for inactivating mutations in the LU gene.The dominantly inherited Lu(mod) phenotype, In(Lu), results from heterozygosity for inactivating mutations in KLF1, the gene for the erythroid transcription binding factor EKLF. Clinically, antibodies of the Lutheran system are relatively benign. When hemolytic, they generally cause only mild, delayed hemolytic transfusion reactions or hemolytic disease of the fetus and newborn that can be treated by phototherapy. The Lutheran glycoproteins, which are members of the immunoglobulin superfamily of adhesion molecules and receptors, bind isoforms of laminin with alpha5 chains,components of the extracellular matrix abundant in vascular endothelia. The primary function of the Lutheran glycoproteins on RBCs could involve the transfer of maturing RBCs from the bone marrow to the peripheral circulation. They could also be involved in vascular occlusion and thrombotic events as complications of sickle cell disease and polycythemia vera, respectively.


Asunto(s)
Anemia de Células Falciformes/metabolismo , Moléculas de Adhesión Celular/metabolismo , Eritroblastosis Fetal/metabolismo , Eritrocitos/metabolismo , Sistema del Grupo Sanguíneo Lutheran/metabolismo , Policitemia Vera/metabolismo , Anemia de Células Falciformes/genética , Anemia de Células Falciformes/patología , Anemia de Células Falciformes/fisiopatología , Moléculas de Adhesión Celular/genética , Eritroblastosis Fetal/genética , Eritroblastosis Fetal/patología , Eritroblastosis Fetal/fisiopatología , Eritrocitos/patología , Eritropoyesis , Regulación de la Expresión Génica , Predisposición Genética a la Enfermedad , Humanos , Factores de Transcripción de Tipo Kruppel/genética , Factores de Transcripción de Tipo Kruppel/metabolismo , Sistema del Grupo Sanguíneo Lutheran/genética , Mutación/genética , Policitemia Vera/genética , Policitemia Vera/patología , Policitemia Vera/fisiopatología , Polimorfismo Genético , Isoformas de Proteínas/genética , Trombocitosis
2.
Eur J Immunol ; 30(8): 2268-80, 2000 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-10940918

RESUMEN

In this study we show that the retinal autoantigen, S-antigen, contains a functional TNF-alpha homologous domain which stimulates maturation and differentiation of cultured dendritic cells (DC) or tissue DC via the p55 TNF-alpha receptor. Tissue DC became more dendritiform in shape, and migrated into culture supernatant. S-antigen also stimulated accumulation of cell surface MHC class II antigen with a corresponding loss of acidic intracellular vesicles, and induced IL-1beta and IL-12 mRNA expression in cultured bone marrow-derived DC. In addition, cultured splenic DC primed immune responses to S-antigen in vivo in the absence of other, exogenous cytokine sources. DC pulsed with either retinal S-antigen or another retinal autoantigen, interphotoreceptor retinoid binding protein (IRBP), were able to stimulate naive T cell proliferation in vitro, but only S-antigen-pulsed DC were able to induce an immune response in vivo and initiate antibody class switching. In contrast, IRBP-pulsed DC had no detectable in vivo priming effect and IgG antibody levels remained suppressed even after immunization with IRBP in complete Freund's adjuvant. These results indicate that DC from the same precursor population can either induce or suppress a B cell-specific response to self antigen in vivo, the outcome being dependent upon DC activation at the time of antigen uptake and presentation.


Asunto(s)
Antígenos CD/fisiología , Arrestina/inmunología , Linfocitos B/inmunología , Células Dendríticas/fisiología , Proteínas del Ojo , Receptores del Factor de Necrosis Tumoral/fisiología , Animales , Células Cultivadas , Femenino , Inmunización , Inmunoglobulina G/biosíntesis , Inmunoglobulina G/clasificación , FN-kappa B/fisiología , Ratas , Ratas Endogámicas Lew , Receptores Tipo I de Factores de Necrosis Tumoral , Proteínas de Unión al Retinol/inmunología , Linfocitos T/inmunología
3.
Recept Channels ; 6(1): 51-64, 1998.
Artículo en Inglés | MEDLINE | ID: mdl-9664622

RESUMEN

Sodium-dependent glutamate transporters influence neurotransmission in the central nervous system by removing synaptically released glutamate from the extracellular space and by maintaining extracellular glutamate concentrations below neurotoxic levels. In insects, glutamate also serves as the neurotransmitter at the neuromuscular junction, but the mechanism for neurotransmitter clearance at this synapse has not well-established. Here we report that cloning and characterization of a sodium-dependent glutamate transporter, dEAAT, from Drosophila melanogaster. The 479 amino acid dEAAT gene product is 40-50% homologous to mammalian members of this carrier family. A 3.3 kilobase (kb) transcript for dEAAT was detected in adult fly heads and to a lesser extent in bodies by Northern-blot analysis and was also localized to neurons in the central nervous system by in situ hybridization. The transport activity observed following express of dEAAT in Xenopus oocytes or COS-7 cells shows a high affinity for L-glutamate, L-aspartate and D-aspartate, an absolute dependence on external sodium ions, and considerable stereoselectivity for the transport of L-glutamate over D-glutamate. As has been observed for the human carriers, EAAT 4 and EAAT 5, a significant component of the current activated by L-glutamate application to dEAAT-expressing oocytes appears to arise from the activation of a chloride channel associated with the carrier.


Asunto(s)
Transportadoras de Casetes de Unión a ATP/genética , ADN Complementario/genética , Drosophila melanogaster/genética , Transportadoras de Casetes de Unión a ATP/metabolismo , Secuencia de Aminoácidos , Sistema de Transporte de Aminoácidos X-AG , Animales , Secuencia de Bases , Células COS , Canales de Cloruro/metabolismo , Cartilla de ADN/genética , ADN Complementario/aislamiento & purificación , Drosophila melanogaster/metabolismo , Femenino , Expresión Génica , Genes de Insecto , Humanos , Hibridación in Situ , Técnicas In Vitro , Datos de Secuencia Molecular , Neuronas/metabolismo , Oocitos/metabolismo , ARN Mensajero/genética , ARN Mensajero/metabolismo , Homología de Secuencia de Aminoácido , Xenopus
4.
J Holist Nurs ; 12(2): 184-92, 1994 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-8195575

RESUMEN

Work with nursing diagnosis has provided a classification system for what nursing does and has helped to focus nursing interventions to include more independent nursing care. Natural therapies (an umbrella term covering the many healing and health promotion modalities, traditional and modern, that do not use prescription pharmaceuticals or surgery) are among the more independent care modalities available to nursing. Accepted nursing interventions cover a growing number of practices, such as progressive relaxation, guided imagery, yoga, therapeutic touch, music therapy, active listening, aromatherapy, reflexology, advocacy, and centered presence. Most of these nursing interventions would seem to fit comfortably within the realm of natural therapies. As the illness-healing paradigms shift and converge, and the concept of holism rises more and more to the fore, the role of the nurse is shifting from caregiver to healer. Nursing diagnosis, as a classification system for nursing phenomena, can serve as a mechanism to enhance visibility of this healing role of the nurse.


Asunto(s)
Terapias Complementarias , Salud Holística , Diagnóstico de Enfermería , Humanos , Naturopatía
5.
Beginnings ; 12(9): 1, 4-5, 1992 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-1392353
6.
J Am Vet Med Assoc ; 186(10): 1084-5, 1985 May 15.
Artículo en Inglés | MEDLINE | ID: mdl-3997622

RESUMEN

Selenium toxicosis was diagnosed as the cause of fatal paralytic disease in a group of feeder pigs. Lumbar poliomyelomalacia and coronary band necrosis were the principal lesions. High selenium concentrations were detected in liver and kidney. Excessive selenium was traced to the premix added to the complete ration.


Asunto(s)
Alimentación Animal/envenenamiento , Parálisis/veterinaria , Selenio/envenenamiento , Enfermedades de los Porcinos/inducido químicamente , Animales , Hígado/patología , Parálisis/inducido químicamente , Parálisis/patología , Médula Espinal/patología , Porcinos , Enfermedades de los Porcinos/patología
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