First report about a successful ECLS implantation and subsequent helicopter transfer of a super obese patient with a BMI of 78 kg/m2

Our tertiary center provides 24/7 ECMO implantation and transport service nationwide. In 2018, 150 ECLS/ECMO were implanted, and 40 patients were transported on ECLS/ECMO. In this report, we describe a successful veno-arterial ECLS implantation in a super obese (BMI 78 kg/m2) 50-year-old female patient at a primary care hospital with subsequent helicopter transfer to our tertiary center

Data from: Hybrid sterility locus on Chromosome X controls meiotic recombination rate in mouse

Meiotic recombination safeguards proper segregation of homologous chromosomes into gametes, affects genetic variation within species, and contributes to meiotic chromosome recognition, pairing and synapsis. The Prdm9 gene has a dual role, it controls meiotic recombination by determining the genomic position of crossover hotspots and, in infertile hybrids of house mouse subspecies Mus m. musculus (Mmm) and Mus m. domesticus (Mmd), it further functions as the major hybrid sterility gene. In the latter role Prdm9 interacts with the hybrid sterility X 2 (Hstx2) genomic locus on Chromosome X (Chr X) by a still unknown mechanism. Here we investigated the meiotic recombination rate at the genome-wide level and its possible relation to hybrid sterility. Using immunofluorescence microscopy we quantified the foci of MLH1 DNA mismatch repair protein, the cytological counterparts of reciprocal crossovers, in a panel of inter-subspecific chromosome substitution strains. Two autosomes, Chr 7 and Chr 11, significantly modified the meiotic recombination rate, yet the strongest modifier, designated meiotic recombination 1, Meir1, emerged in the 4.7 Mb Hstx2 genomic locus on Chr X. The male-limited transgressive effect of Meir1 on recombination rate parallels the male-limited transgressive role of Hstx2 in hybrid male sterility. Thus, both genetic factors, the Prdm9 gene and the Hstx2/Meir1 genomic locus, indicate a link between meiotic recombination and hybrid sterility. A strong female-specific modifier of meiotic recombination rate with the effect opposite to Meir1 was localized on Chr X, distally to Meir1. Mapping Meir1 to a narrow candidate interval on Chr X is an important first step towards positional cloning of the respective gene(s) responsible for variation in the global recombination rate between closely related mouse subspecies

Data from: Hybrid sterility locus on Chromosome X controls meiotic recombination rate in mouse

Meiotic recombination safeguards proper segregation of homologous chromosomes into gametes, affects genetic variation within species, and contributes to meiotic chromosome recognition, pairing and synapsis. The Prdm9 gene has a dual role, it controls meiotic recombination by determining the genomic position of crossover hotspots and, in infertile hybrids of house mouse subspecies Mus m. musculus (Mmm) and Mus m. domesticus (Mmd), it further functions as the major hybrid sterility gene. In the latter role Prdm9 interacts with the hybrid sterility X 2 (Hstx2) genomic locus on Chromosome X (Chr X) by a still unknown mechanism. Here we investigated the meiotic recombination rate at the genome-wide level and its possible relation to hybrid sterility. Using immunofluorescence microscopy we quantified the foci of MLH1 DNA mismatch repair protein, the cytological counterparts of reciprocal crossovers, in a panel of inter-subspecific chromosome substitution strains. Two autosomes, Chr 7 and Chr 11, significantly modified the meiotic recombination rate, yet the strongest modifier, designated meiotic recombination 1, Meir1, emerged in the 4.7 Mb Hstx2 genomic locus on Chr X. The male-limited transgressive effect of Meir1 on recombination rate parallels the male-limited transgressive role of Hstx2 in hybrid male sterility. Thus, both genetic factors, the Prdm9 gene and the Hstx2/Meir1 genomic locus, indicate a link between meiotic recombination and hybrid sterility. A strong female-specific modifier of meiotic recombination rate with the effect opposite to Meir1 was localized on Chr X, distally to Meir1. Mapping Meir1 to a narrow candidate interval on Chr X is an important first step towards positional cloning of the respective gene(s) responsible for variation in the global recombination rate between closely related mouse subspecies

Balcova - raw data

The file structure is the same for all of .csv files. Each column represents one individiual mouse of the genotype stated in the header. Each cell of the column represents MLH1 or RAD51/DMC1 (according to the file name) count of analyzed cell of the given mouse. Strain abbreviation: D# is B6.PWD-Chr#; D7F1 is B6.PWD-Chr7 x B6 F1 The data were analyzed in R 3.2.2 and using its packages as is declared in Materials and Methods of the published paper

Fine mapping of meiotic recombination 1, <i>Meir1</i>, on Chr X^PWD using subconsomic strains.

<p>(<b>A</b>) The 4.7 Mb interval of the proximal part of Chr X shared by B6.PWD-Chr X.1s and B6.PWD-Chr X.2, but absent in B6.PWD-Chr X.1 and B6.PWD-Chr X.3, harbors a transgressive modifier of meiotic recombination rate <i>Meir1</i>. The Y axis shows the distance from the centromere in megabases (GRCm38). Chromosome intervals carrying the B6 DNA sequence are depicted in orange, the PWD sequence in blue. (<b>B</b>) The B6.PWD-Chr X.# subconsomics are abbreviated DX.# in column scatters. The significance of differences between strains (excluding PWD) is marked only when p<0.05. See <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005906#pgen.1005906.g002" target="_blank">Fig 2</a> for legend.</p