Footnotes, June/July 2001, Vol.25, no.6/7

Monthly newsletter for the State Libary of Iowa

Footnotes July 2000, Vol.24, no.7

Monthly newsletter of the State Library of Iowa

Smart News, Issue 7, Fall, 2001

Newsletter for Economic Development

Enfermedad neumococica invasiva en pacientes con neoplasias hematológicas. La influencia de la introducción de la vacuna neumocócica conjugada 7-valente (VNC-7V) en la población infantil

La enfermedad neumocócia invasora (ENI)es una infección grave en los pacientes con neoplasias hematológicas, especialmente en los pacientes con mieloma múltiple y leucemia linfática crónica con altas tasas de mortalidad. Tras la introducción la vacuna VCN-7V, las ENI causadas por serotipos vacunales han disminuido mientras que las ENI causadas por serotipos no vacunales han aumentado. El cambio de serotipos no se ha traducido en importantes cambios clínicos, excepto por un aumento de tendencia al desarrollo de neumonías y shock séptico. Además destaca que la susceptibilidad a la penicilina y eritromicina ha aumentado en el periodo postvacunal

[Costante] Girardengo [coureur cycliste italien disputant une course au vélodrome d'hiver le 7-12-19] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57116

Inflammasome activators induce interleukin-1α secretion via distinct pathways with differential requirement for the protease function of caspase-1.

Through their capacity to sense danger signals and to generate active interleukin-1β (IL-1β), inflammasomes occupy a central role in the inflammatory response. In contrast to IL-1β, little is known about how IL-1α is regulated. We found that all inflammasome activators also induced the secretion of IL-1α, leading to the cosecretion of both IL-1 cytokines. Depending on the type of inflammasome activator, release of IL-1α was inflammasome dependent or independent. Calcium influx induced by the opening of cation channels was sufficient for the inflammasome-independent IL-1α secretion. In both cases, IL-1α was released primarily in a processed form, resulting from intracellular cleavage by calpain-like proteases. Inflammasome-caspase-1-dependent release of IL-1α and IL-1β was independent of caspase-1 catalytic activity, defining a mode of action for caspase-1. Because inflammasomes contribute to the pathology of numerous chronic inflammatory diseases such as gout and diabetes, IL-1α antagonists may be beneficial in the treatment of these disorders.

Lottery Action, October 7-20, 2002 Vol. 9 no. 19

Newsletter for Iowa Lottery

Lottery Action, August 25-September 7, 2003, Vol. 10, no. 17

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, April 7-20, 2003, Vol. 10, no. 7

Iowa Lottery Authority Retailer Information Newsletter

7-1-19 [i.e. 7-1-20], intérieur de la salle de la Maison des syndicats [rue de la Grange-aux-Belles, Paris] : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57542

Managing IT, December 2001, Vol.7, no.1

Newsletter for Information Tecnology Department

Missing Persons Summary, July 7, 2003

Missing persons summary

Missing Persons Summary, April 7, 2003

Missing persons summary

The orphan receptor CRF2-4 is an essential subunit of the interleukin 10 receptor.

The orphan receptor CRF2-4 is a member of the class II cytokine receptor family (CRF2), which includes the interferon receptors, the interleukin (IL) 10 receptor, and tissue factor. CRFB4, the gene encoding CRF2-4, is located within a gene cluster on human chromosome 21 that comprises three interferon receptor subunits. To elucidate the role of CRF2-4, we disrupted the CRFB4 gene in mice by means of homologous recombination. Mice lacking CRF2-4 show no overt abnormalities, grow normally, and are fertile. CRF2-4 deficient cells are normally responsive to type I and type II interferons, but lack responsiveness to IL-10. By approximately 12 wk of age, the majority of mutant mice raised in a conventional facility developed a chronic colitis and splenomegaly. Thus, CRFB4 mutant mice recapitulate the phenotype of IL-10-deficient mice. These findings suggest that CRF2-4 is essential for IL-10-mediated effects and is a subunit of the IL-10 receptor.