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1.
Curr Med Sci ; 43(2): 417-420, 2023 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-37037972

RESUMEN

Donor-derived infection (DDI) associated with Scedosporium spp is extremely rare, and results in a very poor prognosis. The present study reports a probable DDI due to Scedosporium boydii (S. boydii) from a donor with neuropsychiatric systemic lupus erythematosus. Two recipients developed Scedosporiosis after kidney transplantation from the same donor. Recipient 1 died of central nervous system infection due to S. boydii based on the clinical presentations, and the positive metagenomic next-generation sequencing (mNGS) and culture results for the cerebrospinal fluid. The other recipient with urinary tract obstruction due to S. boydii, which was identified through the positive culture and mNGS results of the removed stents, was successfully treated by stent replacement and voriconazole administration. Undiagnosed disseminated donor infection and the transmission of S. boydii should be given attention, particularly when the donor and recipients have primary immunodeficiency disease. The screening of donors and recipients for S. boydii using mNGS may be helpful in guiding antifungal prophylaxis and treatment recipients, due to its higher sensitivity and shorter diagnostic time relative to other traditional techniques.


Asunto(s)
Infecciones Fúngicas Invasoras , Trasplante de Riñón , Lupus Eritematoso Sistémico , Humanos , Trasplante de Riñón/efectos adversos , Voriconazol/uso terapéutico , Lupus Eritematoso Sistémico/tratamiento farmacológico
2.
Sci Rep ; 6: 26954, 2016 06 01.
Artículo en Inglés | MEDLINE | ID: mdl-27246399

RESUMEN

The activation of innate immunity via myeloid differentiation factor 88 (MyD88) contributes to ischemia reperfusion (I/R) induced acute kidney injury (AKI) and chronic kidney injury. However, since there have not yet been any effective therapy, the exact pharmacological role of MyD88 in the prevention and treatment of renal ischemia reperfusion injury (IRI) is not known. We designed a small molecular compound, TJ-M2010-2, which inhibited MyD88 homodimerization. We used an established unilateral I/R mouse model. All mice undergoing 80 min ischemia through uninephrectomy died within five days without intervention. However, treatment with TJ-M2010-2 alone significantly improved the survival rate to 58.3%. Co-treatment of TJ-M2010-2 with the CD154 antagonist increased survival rates up to 100%. Twenty-eight days post-I/R of 60 min ischemia without nephrectomy, TJ-M2010-2 markedly attenuated renal interstitial and inhibited TGF-ß1-induced epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Furthermore, TJ-M2010-2 remarkably inhibited TLR/MyD88 signaling in vivo and in vitro. In conclusion, our findings highlight the promising clinical potential of MyD88 inhibitor in preventing and treating acute or chronic renal I/R injuries, and the therapeutic functionality of dual-system inhibition strategy in IRI-induced AKI. Moreover, MyD88 inhibition ameliorates renal I/R injury-induced tubular interstitial fibrosis by suppressing EMT.


Asunto(s)
Anticuerpos Monoclonales/farmacología , Ligando de CD40/antagonistas & inhibidores , Factor 88 de Diferenciación Mieloide/antagonistas & inhibidores , Piperazinas/farmacología , Daño por Reperfusión/prevención & control , Tiazoles/farmacología , Animales , Sitios de Unión , Ligando de CD40/genética , Ligando de CD40/inmunología , Diseño de Fármacos , Quimioterapia Combinada , Células Epiteliales/efectos de los fármacos , Células Epiteliales/inmunología , Células Epiteliales/patología , Transición Epitelial-Mesenquimal/efectos de los fármacos , Expresión Génica , Inmunidad Innata/efectos de los fármacos , Riñón/efectos de los fármacos , Riñón/inmunología , Riñón/patología , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Endogámicos C57BL , Simulación del Acoplamiento Molecular , Factor 88 de Diferenciación Mieloide/genética , Factor 88 de Diferenciación Mieloide/inmunología , Unión Proteica , Conformación Proteica en Hélice alfa , Conformación Proteica en Lámina beta , Dominios y Motivos de Interacción de Proteínas , Multimerización de Proteína/efectos de los fármacos , Daño por Reperfusión/genética , Daño por Reperfusión/inmunología , Daño por Reperfusión/mortalidad , Análisis de Supervivencia
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