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Laura Villarreal‐Martínez Jaime García‐Chvez Berenice Snchez‐Jara Aida Mashenka Moreno‐Gonzlez Janet Soto‐Padilla Efraín Aquino‐Fernndez Rogelio Paredes‐Aguilera Karla Maldonado‐Silva Cecilia Rodríguez‐Castillejos Ana Itamar Gonzlez‐vila María Mora‐Torres Hector Manuel Tiznado‐García Natalia Elizabeth Padilla‐Durn Nuria Citlali Luna‐Silva Eric Israel Gutirrez‐Jurez Jorge Nemi‐Cueto Claudia Sofia Gmez‐Gonzlez Ricardo De Len‐Figueroa Adela Lpez‐Miranda Mirna Guadalupe Ríos‐Osuna Edna Liliana Tamez‐Gmez Elio Aarn Reyes‐Espinoza Irving Armando Domínguez‐Varela Gerardo Gonzlez‐Martínez Elias Adn Godoy‐Salinas 《Haemophilia》2020,26(2):290-297
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Andrew M. Lippa Karen E. Ocwieja Julie Iglesias Rima Fawaz Scott Elisofon Christine Lee Tanvi S. Sharma 《Transplant infectious disease》2020,22(4)
A 20‐year‐old male presented 3.5 years after intestinal transplantation with rapidly progressive sensorineural hearing loss. Initial brain imaging was consistent with inflammation and/or demyelination. Lumbar puncture was initially non‐diagnostic and a broad infectious workup was unrevealing. Three months after presentation, a repeat LP detected JC virus for which tests had not earlier been conducted. He continued to deteriorate despite withdrawal of prior immunosuppression and addition of mirtazapine, maraviroc, and steroids. He died of progressive neurologic decompensation 5 months after his initial presentation. This case highlights progressive multifocal leukoencephalopathy (PML) as a rare complication after solid organ transplantation and acute sensorineural hearing loss as an unusual first presenting symptom of PML. JC virus should be considered in the differential diagnosis of acute sensorineural hearing loss in any immunocompromised patient. 相似文献
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Stewart JD Marchan R Lesjak MS Lambert J Hergenroeder R Ellis JK Lau CH Keun HC Schmitz G Schiller J Eibisch M Hedberg C Waldmann H Lausch E Tanner B Sehouli J Sagemueller J Staude H Steiner E Hengstler JG 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(21):8155-8160
Metastasis from primary tumors remains a major problem for tumor therapy. In the search for markers of metastasis and more effective therapies, the tumor metabolome is relevant because of its importance to the malignant phenotype and metastatic capacity of tumor cells. Altered choline metabolism is a hallmark of cancer. More specifically, a decreased glycerophosphocholine (GPC) to phosphocholine (PC) ratio was reported in breast, ovarian, and prostate cancers. Improved strategies to exploit this altered choline metabolism are therefore required. However, the critical enzyme cleaving GPC to produce choline, the initial step in the pathway controlling the GPC/PC ratio, remained unknown. In the present work, we have identified the enzyme, here named EDI3 (endometrial differential 3). Purified recombinant EDI3 protein cleaves GPC to form glycerol-3-phosphate and choline. Silencing EDI3 in MCF-7 cells decreased this enzymatic activity, increased the intracellular GPC/PC ratio, and decreased downstream lipid metabolites. Downregulating EDI3 activity inhibited cell migration via disruption of the PKCα signaling pathway, with stable overexpression of EDI3 showing the opposite effect. EDI3 was originally identified in our screening study comparing mRNA levels in metastasizing and nonmetastasizing endometrial carcinomas. Both Kaplan-Meier and multivariate analyses revealed a negative association between high EDI3 expression and relapse-free survival time in both endometrial (P < 0.001) and ovarian (P = 0.029) cancers. Overall, we have identified EDI3, a key enzyme controlling GPC and choline metabolism. Because inhibition of EDI3 activity corrects the GPC/PC ratio and decreases the migration capacity of tumor cells, it represents a possible target for therapeutic intervention. 相似文献
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