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In the version of this article initially published, the following statement was missing from the Acknowledgements: “We are grateful to the GenoBiRD core facility (Biogenouest), the Clinical Investigation Center (INSERM CIC1413) and the Center of Biological Resources in Nantes (BB-0033-00040; CHU Nantes, France) for their assistance in managing and genotyping the ICAN and PREGO biobanks. R.R. was supported by the French Regional Council of Pays-de-la-Loire (VaCaRMe program) and the Agence Nationale de la Recherche (ANR-15-CE17-0008-01 to G.L). H.D. and R.B. were supported by the French Ministry of Health (clinical trial NCT02848495 to H.D.), the Genavie Foundation, the Société Française de Radiologie and the Société Française de Neuroradiologie.” The error has been corrected in the HTML and PDF versions of the article. *Lists of authors and their affiliations appear online. Korrektur zu 10.1038/s41588-020-00725-7

It has been proposed that the stalling of the replication forks can induce homologous recombination in several organisms, and that arrested replication forks may offer nuclease targets, thereby providing a substrate for proteins involved in double-strand repair. In this article, we constructed a plasmid with the potential for transcription-replication collision (TRC), in which DNA replication and RNA transcription occur on the same DNA template simultaneously. Theoretically, transcription will impede DNA replication and increase homologous recombination. To validate this hypothesis, another plasmid was constructed that contained a homologous sequence with the exception of some mutated sites. Co-transfection of these two plasmids into 293T cells resulted in increased recombination frequency. The ratio of these two plasmids also affected the recombination frequency. Moreover, we found high expression levels of RAD51, which indicated that the increase in the recombination rate was probably via the homologous recombination pathway. These results indicate that mutant genes in plasmids can be repaired by TRC-induced recombination.

We previously reported that myleran, a cell cycle nonspecific drug, can stimulate gamma-globin gene expression in anemic adult rhesus monkeys. This finding prompted us to treat two patients with severe beta-thalassemia with myleran. Both patients received an initial course of therapy, constantly of myleran at a dosage of 0.2 mg/kg/d for 9 days followed by 0.15 mg/kg/d for the next 11 days. One patient received an additional 20-day course of myleran at a dosage of 0.2 mg/kg/d beginning 44 days after completion of the first course. No severe ill effects related to the drug were observed during or after drug administration. After 20 days of myleran treatment, levels of HbF and reticulocytes increased in both patients and level of F cells increased in patient 1. In patient 1, Hb concentration rose from 42g/L (9 days after transfusion) before treatment to a maximum of 65g/L afterward; in patient 2, it rose from 74g/L to a maximum of 106g/L. A value of 15g/L above baseline lasted for about 5 months in both patients. Hypomethylation of bone marrow DNA near the gamma-globin gene was demonstrated in patient 1.

Through the research on the assignment of leisure time of Chinese city dwellers in 1987, the following findings have been worked out: 1. The increase in the standard of living and in leisure time has resulted in new and varied patterns of leisure. 2. Watching TV, as a newly-born pattern of leisure, has entered most dwellers' leisure time. Like a catalyst, it has also promoted the establishment of another leisure pattern, i.e. the development of sports in China. 3. As time goes by, the position of sports will become more and more important in the city dwellers' leisure time. This tendency will probably speed up the development of more recreative and entertaining sports items in China.