Erratum: SLP-2 interacts with Parkin in mitochondria and prevents mitochondrial dysfunction in Parkin-deficient human iPSC-derived neurons and Drosophila (Human Molecular Genetics (2017) 26:13 (2412-2425) DOI: 10.1093/hmg/ddx132)

The authors of the article "SLP-2 interacts with Parkin in mitochondria and prevents mitochondrial dysfunction in Parkin-deficient human iPSC-derived neurons and Drosophila" would like to report the incorrect description of an iPSC line in the paper. Authentication analysis at Coriell Institute for Medical Research (Camden, New Jersey) revealed that the cell line named iPS-HFF in the article was not derived from newborn foreskin fibroblasts (as reported in Table S2) but from cells of a female patient with osteogenesis imperfecta (GM17602/GM17604), carrier of a heterozygous missense mutation (p.G700C; NM_000089) in the COL1A2 gene. Repeated karyotype analysis performed for the line named iPS-HFF showed a normal female karyotype, which means that the male karyotype displayed in Figure S4B is mislabeled and was not derived from iPS-HFF. Differentiated dopaminergic neurons from the line named iPS-HFF were examined for mitochondrial complex I activity (Figure 4A) and mitochondrial morphology (Figure 4B) as one of in total three analyzed control iPSC lines compared to Parkin mutant lines. Importantly, both experiments display robust phenotypes and are replicative analysis of results shown in Parkin knockdown SH-SY5Y cells: Loss-of-Parkin leads to decreased complex I activity (Figure 2B) and an increased amount of fragmented mitochondria (Figure 2D), while overexpression of SLP-2 rescues both phenotypes. This confirms that the analyzed data in Figure 4 are not influenced by the COL1A2 mutation. Furthermore, mutations in the COL1A2 gene have not been associated with neurodegenerative diseases and the symptoms of neurological movement disorders have not been described for osteogenesis imperfecta. Therefore, the fact that this particular cell line is from a diseased individual with osteogenesis imperfecta rather than a healthy control does not alter the interpretation of our results as pertaining to rescue of mitochondrial phenotypes as described in the manuscript. The authors would like to apologize for this mistake

Specificity of late-night salivary cortisol measured by automated electrochemiluminescence immunoassay for Cushing’s disease in an obese population

Purpose Data about the specificity of late-night salivary cortisol (LNSC) in obese subjects are still conflicting. Therefore, with this study, we aimed to evaluate the specificity of LNSC measurement in an obese cohort with or without type 2 diabetes mellitus (T2DM) using an automated electrochemiluminescence immunoassay (ECLIA). Methods A total number of 157 patients involving 40 healthy subjects (HS) with BMI?<?25 kg/m2, 83 obese subjects (OS) with BMI???35 kg/m2, and 34 histopathologically proven Cushing’s disease (CD) were included. All patients underwent LNSC testing. Salivary cortisol was measured at 11 p.m. for all groups using an ECLIA. Reference range was established using values of LNSCs of HS and ROC curves were used to determine diagnostic cutoffs. Results In the HS group, mean LNSC was 4.7 nmol/l (SD?±?3.1), while the OS group had a mean value of 10.9 nmol/l (SD?±?7.5) and the CD group of 19.9 nmol/l (SD?±?15.4). All groups differed significantly (p?<?0.001). The ROC analysis of CD against HS alone showed a sensitivity of 85.3% and a specificity of 87.5% with a cut-off value of 8.3 nmol/l. The ROC analysis between OS and CD showed a maximum sensitivity of 67.6% and specificity of 78.3% for a cut-off value of 12.3 nmol/l. Taken both (HS and OS) groups together against the CD group, ROC analysis showed a maximum sensitivity of 67.6% and specificity of 85.4% for a cut-off value of 12.3 nmol/l. No correlation was found between BMI, T2DM, and LNSC for all groups. Conclusions In our obese cohort, we found that LNSC assayed by ECLIA had a low specificity in the diagnosis of CD.PeerReviewe