Trial of labour versus elective caesarean delivery for estimated large for gestational age foetuses after prior caesarean delivery: a multicenter retrospective study.

BACKGROUND: Lower rates of successful trial of labor after cesarean (TOLAC) in association with fetal macrosomia were previously reported. This study aimed to compare TOLAC to elective caesarean delivery (CD) in women with estimated fetal weight large for gestational age (eLGA) and a prior CD. Primary outcome was to analyse the mode of delivery in case of TOLAC. Secondary outcome was to compare maternal and foetal morbidity. METHODS: We conducted a retrospective, descriptive, multicentric, cohort study in five maternity units between January and December 2020. Inclusion criteria were: women with a single prior CD and eLGA or neonatal weight > 90th percentile with singleton pregnancy and gestational age ≥ 37 weeks. MAIN OUTCOME MEASURES: rate of vaginal delivery, maternal and fetal morbidity including: shoulder dystocia, neonatal hospitalization, fetal trauma, neonatal acidosis, uterine rupture, 3rd and 4th perineal tears, post-partum hemorrhage, and a need for blood transfusion. RESULTS: Four hundred forty women met inclusion criteria, including 235 (53.4%) eLGA. 170 (72.3%) had a TOLAC (study group) and 65 (27.7%) an elective CD (control). 117 (68.82%) TOLAC had a vaginal delivery. No significant differences were found between the two groups in the rates of: postpartum haemorrhage, transfusion, Apgar score, neonatal hospitalization, and foetal trauma. Cord lactate was higher in the case of TOLAC (3.2 vs 2.2, p < 0.001). Median fetal weight was 3815 g (3597-4085) vs. 3865 g (3659-4168): p = 0.068 in the study vs. controls group respectively. CONCLUSION: TOLAC for eLGA fetuses is legitimate because there is no difference in maternal-fetal morbidity, and the CD rate is acceptable.

Inherited human IFN-γ deficiency underlies mycobacterial disease.

Mendelian susceptibility to mycobacterial disease (MSMD) is characterized by a selective predisposition to clinical disease caused by the Bacille Calmette-Guérin (BCG) vaccine and environmental mycobacteria. The known genetic etiologies of MSMD are inborn errors of IFN-γ immunity due to mutations of 15 genes controlling the production of or response to IFN-γ. Since the first MSMD-causing mutations were reported in 1996, biallelic mutations in the genes encoding IFN-γ receptor 1 (IFN-γR1) and IFN-γR2 have been reported in many patients of diverse ancestries. Surprisingly, mutations of the gene encoding the IFN-γ cytokine itself have not been reported, raising the remote possibility that there might be other agonists of the IFN-γ receptor. We describe 2 Lebanese cousins with MSMD, living in Kuwait, who are both homozygous for a small deletion within the IFNG gene (c.354_357del), causing a frameshift that generates a premature stop codon (p.T119Ifs4*). The mutant allele is loss of expression and loss of function. We also show that the patients' herpesvirus Saimiri-immortalized T lymphocytes did not produce IFN-γ, a phenotype that can be rescued by retrotransduction with WT IFNG cDNA. The blood T and NK lymphocytes from these patients also failed to produce and secrete detectable amounts of IFN-γ. Finally, we show that human IFNG has evolved under stronger negative selection than IFNGR1 or IFNGR2, suggesting that it is less tolerant to heterozygous deleterious mutations than IFNGR1 or IFNGR2. This may account for the rarity of patients with autosomal-recessive, complete IFN-γ deficiency relative to patients with complete IFN-γR1 and IFN-γR2 deficiencies.

In the privacy of their own homes: using the internet to assess racial bias.

Recent studies suggest that research participants show reduced distortion of their taboo attitudes and behaviors when they take part in Internet-based procedures from outside the laboratory. We explored whether such procedures would reduce distortion in the assessment of racial bias. In Study 1, White participants who completed the study in the laboratory evaluated Black targets more favorably than White targets. This unexpected "outgroup-favoring" pattern occurred in both pencil-and-paper and Internet versions of the study, showing that modality did not produce it; but when participants worked outside the laboratory via the Internet, this pattern disappeared. Study 2 replicated the above findings and further indicated that the reduced distortion in Internet-based studies was due to the removal of the experimenter rather than removing the participants from the laboratory environment. The implications of these findings for the study of controlled processes of prejudice and the nature of Internet-based social communication are discussed.