Success rate of external cephalic version in relation to the woman's body mass index and other factors-a population-based cohort study.

Introduction: The aim of this study was to evaluate the impact of women's body mass index (BMI) on the probability of a successful external cephalic version (ECV).

Material And Methods: A retrospective population-based observational study including all women that underwent an ECV in the southeast region of Sweden from January 2014 to December 2019. Data were collected from electronic medical records, Obstetrix, Cerner.

Immunoglobulin domain interface exchange as a platform technology for the generation of Fc heterodimers and bispecific antibodies.

Bispecific antibodies (bsAbs) are of significant importance to the development of novel antibody-based therapies, and heavy chain (Hc) heterodimers represent a major class of bispecific drug candidates. Current technologies for the generation of Hc heterodimers are suboptimal and often suffer from contamination by homodimers posing purification challenges. Here, we introduce a new technology based on biomimicry wherein the protein-protein interfaces of two different immunoglobulin (Ig) constant domain pairs are exchanged in part or fully to design new heterodimeric domains.

The Wilms' tumor gene 1 (WT1) induces expression of the N-myc downstream regulated gene 2 (NDRG2).

The Wilms' tumor gene 1 (WT1) protein is a transcriptional regulator that is highly expressed in immature hematopoietic progenitor cells and in the majority of patients with acute and chronic myeloid leukemia. However, it is still unclear how WT1 exerts its function(s) in hematopoietic cells. The aim of this work was to investigate the function of WT1 as a transcription factor in human hematopoietic progenitor cells.

DNA-binding dependent and independent functions of WT1 protein during human hematopoiesis.

The Wilms tumor gene 1 (WT1) encodes a zinc-finger-containing transcription factor highly expressed in immature hematopoietic progenitor cells. Overexpression and presence of somatic mutations in acute leukemia indicate a role for WT1 in the pathogenesis of leukemia. CD34+ progenitor cells were transduced with one splice variant of human WT1 without the KTS insert in the zinc-finger domain, WT1(+/-), and with a deleted mutant of WT1 lacking the entire zinc-finger region, WT1(delZ), thus incapable of binding DNA.