Impact of policy change on late-term abortion: a two-decade analysis.

OBJECTIVE: Advances in ultrasound and molecular genetics have changed the field of late termination of pregnancy (LTOP), sparking ethical debates worldwide. In 2007, Israel updated its LTOP policies, requiring a 30% or higher probability of severe handicap for approval of LTOP after 24 weeks' gestation. PURPOSE: In this retrospective study, we compared LTOP indications and approval rates before (Group 1: 1998-2007) and after (Group 2: 2008-2021) this policy change. METHODS: Shamir medical records from January 1, 1998 to December 31, 2021 were examined and yielded 4047 abortions, of which 248 were identified as LTOP preformed after 24 weeks' gestation. These cases were then categorized into two groups. Data including maternal age, obstetric history, indications for abortion, diagnosis, week of termination, and genetic/sonographic findings were analyzed. The approval rates and indications pre- and post-policy change were compared. RESULTS: Group 1 (LTOP 1998-2007) comprised 95 cases (10.6%), and Group 2 (LTOP 2008-2021) was composed of 153 cases (4.9%). Fetal structural anomalies remained the dominant indication for both groups (67.4 and 65.3%, respectively), with a slight increase in confirmed genetic anomalies from 26.3% (Group 1) to 28% (Group 2). CONCLUSION: Our findings indicate a decrees in the proportion per year from 10.6 to 4.9% LTOP. Technological advances in genetic evaluation and sonography may have contributed to the early increased detection and decrees in cases reaching LTOP. These results highlight the importance of ongoing ethical reviews and adherence to strict protocols for early detection and termination before 24 weeks' gestation.

The Significance of Fetal Brain Ventricular Asymmetry Without Dilation.

OBJECTIVES: Fetal brain non-dilated ventricular asymmetry (NDVA) is a common finding on prenatal ultrasound exams. However, the optimal prenatal management in these cases remains unknown. We aimed to evaluate the benefit of prenatal genetic and magnetic resonance imaging (MRI) exams performed in cases of fetal NDVA detected on ultrasound. METHODS: A historical cohort study from a tertiary medical center. Singleton pregnancies with fetal brain NDVA diagnosed on ultrasound were included. We defined ventricular asymmetry as a difference of ≥2.0 mm between the lateral ventricles and ventricular dilation as ventricular width of >10.0 mm. Outcomes were evaluated with genetic exams (karyotype and chromosomal microarray analysis [CMA]) and fetal brain MRI. RESULTS: During the study period, there were 145 cases diagnosed with NDVA on ultrasound that comprised the cohort study. The rate of abnormal karyotype was 1.8% (1/56) and of abnormal CMA was 10% (3/30). The rate of minor additional CNS findings did not differ between ultrasound and MRI (3.4 versus 2.8%, respectively, p = .74). No major additional fetal brain findings were detected on MRI performed after ultrasound. CONCLUSIONS: In cases diagnosed with NDVA on ultrasound, no significant additional anomalies were detected on fetal brain MRI. The rate of abnormal genetic tests was relatively high and warrants further studies.

ATP binding to synaspsin IIa regulates usage and clustering of vesicles in terminals of hippocampal neurons.

Synaptic transmission is expensive in terms of its energy demands and was recently shown to decrease the ATP concentration within presynaptic terminals transiently, an observation that we confirm. We hypothesized that, in addition to being an energy source, ATP may modulate the synapsins directly. Synapsins are abundant neuronal proteins that associate with the surface of synaptic vesicles and possess a well defined ATP-binding site of undetermined function. To examine our hypothesis, we produced a mutation (K270Q) in synapsin IIa that prevents ATP binding and reintroduced the mutant into cultured mouse hippocampal neurons devoid of all synapsins. Remarkably, staining for synaptic vesicle markers was enhanced in these neurons compared with neurons expressing wild-type synapsin IIa, suggesting overly efficient clustering of vesicles. In contrast, the mutation completely disrupted the capability of synapsin IIa to slow synaptic depression during sustained 10 Hz stimulation, indicating that it interfered with synapsin-dependent vesicle recruitment. Finally, we found that the K270Q mutation attenuated the phosphorylation of synapsin IIa on a distant PKA/CaMKI consensus site known to be essential for vesicle recruitment. We conclude that ATP binding to synapsin IIa plays a key role in modulating its function and in defining its contribution to hippocampal short-term synaptic plasticity.