BACKGROUND: Complications caused by female genital mutilation (FGM), such as clitoral pain, reduced sensation, and diminished sexual function, can be alleviated by clitoral reconstruction, which can also improve the aesthetics and restore the anatomy of the genitalia.

OBJECTIVES: The aim of this study was to create sensate labial flaps to cover the neoclitoris and assess the outcome of the procedure.

METHODS: Between December 2018 and July 2020, 40 patients with FGM underwent clitoral reconstruction and coverage with sensate labial flaps donated by the remnant of the labia minora and were followed prospectively. Flaps were mapped on the less-mutilated labia minora according to recent descriptions of arterial anatomy and innervation. Before the surgery, the patients' clitoral sensation was assessed on a 6-point scale and they were also given the Female Sexual Functional Index (FSFI) questionnaire to complete. Eight and 24 weeks postoperatively, the same assessment was repeated and the data compared.

RESULTS: The mean Female Sexual Functional Index score increased significantly from 11.64 (range, 2.8-25.6) preoperatively to 29.14 (range, 12.8-35.4) postoperatively. Similarly, clitoral sensation increased significantly from 2.35 (range, 1-4) before the surgery to 4.9 (range, 2-6) after the surgery. In total, 95% of patients benefited from the surgery.

CONCLUSIONS: Clitoral reconstruction with sensate labial flaps after FGM resulted in significant improvements in sexual function, clitoral sensation, genital aesthetics, and self-esteem.

LEVEL OF EVIDENCE: 4:

The addition of polyoxyethylene sorbitan monooleate (Tween 80) to a culture of mycobacteria greatly influences cell permeability and sensitivity to antibiotics but very little is known regarding the underlying mechanism. Here we show that Corynebacterium matruchotii (surrogate of mycobacteria) converts Tween 80 to a structural series of polyoxyethylenic acids which are then used to form novel series-2A and series-2B glycolipids. Minor series-3 glycolipids were also synthesized. The polyoxyethylenic acids replaced corynomycolic acids in the cell wall. Correspondingly the trehalose dicorynomycolate content was reduced. MALDI mass spectrometry, MS-MS, (1)H-NMR, and (13)C-NMR were used to characterize the series-2 glycolipids. Series-2A glycolipid is trehalose 6-C(36:2)-corynomycolate-6'-polyoxyethylenate and series-2B glycolipid is trehalose 6-C(36:2)-corynomycolate-6'-furan ring-containing polyoxyethylenate. Mycobacterium smegmatis grown in the presence of Tween 80 also synthesizes series-2 type glycolipids. The synthesis of these novel glycolipids in corynebacteria and mycobacteria should result in gross changes in the cell wall permeability and drug sensitivity.

The various malformations of the aerodigestive tract collectively known as esophageal atresia/tracheoesophageal fistula (EA/TEF) constitute a rare group of birth defects of largely unknown etiology. Previous studies have identified a small number of rare genetic variants causing syndromes associated with EA/TEF. We performed a pilot exome sequencing study of 45 unrelated simplex trios (probands and parents) with EA/TEF. Thirteen had isolated and 32 had nonisolated EA/TEF; none had a family history of EA/TEF. We identified de novo variants in protein-coding regions, including 19 missense variants predicted to be deleterious (D-mis) and 3 likely gene-disrupting (LGD) variants. Consistent with previous studies of structural birth defects, there is a trend of increased burden of de novo D-mis in cases (1.57-fold increase over the background mutation rate), and the burden is greater in constrained genes (2.55-fold, p = 0.003). There is a frameshift de novo variant in EFTUD2, a known EA/TEF risk gene involved in mRNA splicing. Strikingly, 15 out of 19 de novo D-mis variants are located in genes that are putative target genes of EFTUD2 or SOX2 (another known EA/TEF gene), much greater than expected by chance (3.34-fold, p value = 7.20e−5). We estimated that 33% of patients can be attributed to de novo deleterious variants in known and novel genes. We identified APC2, AMER3, PCDH1, GTF3C1, POLR2B, RAB3GAP2, and ITSN1 as plausible candidate genes in the etiology of EA/TEF. We conclude that further genomic analysis to identify de novo variants will likely identify previously undescribed genetic causes of EA/TEF.

In this paper, we propose a new attribute reduction strat-
egy based on rough sets and grey wolf optimization (GWO). Rough sets
have been used as an attribute reduction technique with much success,
but current hill-climbing rough set approaches to attribute reduction are
inconvenient at nding optimal reductions as no perfect heuristic can
guarantee optimality. Otherwise, complete searches are not feasible for
even medium sized datasets. So, stochastic approaches provide a promis-
ing attribute reduction technique. Like Genetic Algorithms, GWO is a
new evolutionary computation technique, mimics the leadership hierar-
chy and hunting mechanism of grey wolves in nature. The grey wolf
optimization nd optimal regions of the complex search space through
the interaction of individuals in the population. Compared with GAs,
GWO does not need complex operators such as crossover and mutation,
it requires only primitive and easy mathematical operators, and is com-
putationally inexpensive in terms of both memory and runtime. Experi-
mentation is carried out, using UCI data, which compares the proposed
algorithm with a GA-based approach and other deterministic rough set
reduction algorithms. The results show that GWO is ecient for rough
set-based attribute reduction.