Correction to: Meningomyeloradiculitis following yellow fever 17D vaccination: a case report.

There was an error in the original article. In the last paragraph of the Case Report section, the sentence "One month later, two plasma exchanges were followed by only slight improvements in upper-limb motor function (Fig. 1)." should have been "One month later, four plasma exchanges were followed.

Meningomyeloradiculitis following yellow fever 17D vaccination: a case report.

The yellow fever 17D vaccine contains live-attenuated virus. Initial efficacy and safety reports were favorable. Recently, however, neurologic and viscerotropic adverse events (AE) were described. We managed a 61-year-old man who experienced meningomyeloradiculitis 18 days after receiving the yellow fever 17D vaccine. The manifestations were atypical. The cerebrospinal fluid contained high titers of anti-yellow fever immunoglobulins M and G and of anti-flavivirus immunoglobulins G. After methylprednisolone (1 g/day for 3 days), intravenous human immunoglobulins (140 g over 5 days), and two plasma exchanges, the symptoms improved only slightly. Neurological adverse events after yellow fever vaccination are rare or underestimated. To our knowledge, this is the first reported case of meningomyeloradiculitis after yellow fever vaccination. A remarkable feature is the intrathecal production of yellow fever antibodies, which probably played a pathogenic role and may have been related to a recent episode of influenza.

Hypoxia-inducible factor 1 controls the expression of the uncoordinated-5-B receptor, but not of netrin-1, in first trimester human placenta.

Uncoordinated-5 homologs 1-4 (UNC5H1-4) transmembrane netrin receptors are reported to control a number of cellular processes, including axonal guidance, angiogenesis and cell proliferation. These receptors are known as "dependence receptors" because they are able to induce apoptosis in the absence of their ligand, netrin. We have recently reported the localization of netrin-1 and its uncoordinated-5-B (UNC5B) receptor in both villous and extravillous cytotrophoblasts in the human placenta. However, the roles that netrin-1 and UNC5B play in the development of the placenta, as well as the regulation of their expression during the early stages of placental development, remain unexplored. Placental explants were used to demonstrate a proliferative effect of netrin-1 on cytotrophoblasts, as assessed by Ki67 staining. Primary cytotrophoblasts collected at different gestational ages during the first trimester of pregnancy indicated that netrin-1 mRNA expression decreased after 6 weeks of gestation (wg), whereas UNC5B expression increased gradually up to 13-14 wg. The BeWo cell line was used to evaluate the effect of hypoxia on the expression of netrin-1 and UNC5B. Primary cytotrophoblast and BeWo cells cultured under hypoxic conditions exhibited a decrease in the expression of UNC5B both at the mRNA and protein levels; in contrast, hypoxia induced no change in the levels of netrin-1. When hypoxia-inducible factor 1α (HIF-1α) was knocked down by siRNA, we found a significant increase in UNC5B expression, indicating that the HIF-1 pathway is involved in hypoxia-induced UNC5B transcriptional down-regulation. Altogether, these results demonstrate the role of netrin-1 as a new mitogenic factor for cytotrophoblastic cells, report the pattern of expression of netrin-1 and its receptor, UNC5B, in the human placenta during the first trimester of pregnancy, and bring insights into the direct control of the expression of UNC5B by HIF-1.