Safety assessment of the prophylactic use of silicone gel sheets (Lady Care®) for the prevention of hypertrophic scars following caesarean section.

This study aimed to investigate the side effects of silicone gel sheet (Lady Care®) and evaluate its prophylactic efficacy in preventing abnormal scarring. Sixty women who underwent caesarean section were recruited from September 2016 to September 2017 in this prospective study. Lady Care® was applied from the 2nd to the 6th postoperative months. Side effects of Lady Care® were evaluated through medical examinations and questionnaires. A plastic surgeon diagnosed abnormal scarring. Pruritus was diagnosed in 25 (47.2%) patients; folliculitis, four (7.5%); dry skin, four (7.5%); contact dermatitis, three (5.7%); wound infection, two (3.8%); and epidermolysis, one (1.9%), albeit with mild severity. Following Lady Care® application, no abnormal scarring and mild hypertrophic scarring was observed in 32 (64.0%) and 18 (36.0%) patients respectively. Of seven patients with pre-existing hypertrophic scars, only two showed hypertrophic scarring after Lady Care® application. Our findings support the safety and prophylactic efficacy of Lady Care®.Impact StatementWhat is already known on this subject? The incidence of abnormal scarring, i.e. keloid or hypertrophic scar formation after caesarean section (CS) is reported to be ∼41%. Abnormal or excessive scar formation can lead to functional limitations, pruritus, pain and cosmetic issues. Studies have also shown a prophylactic effect of the application of silicone materials against the development of hypertrophic and keloid scars, though prohibitive cost and lack of adhesiveness of such gel sheets are known factors limiting their usage.What the results of this study add? The new silicone gel sheet 'Lady Care®' has strong adhesive properties and is consequently not easily peeled off. Furthermore, it is easy to use and economically efficient.What the implications are of these findings for clinical practice and/or further research? This is the first clinical trial on the application of Lady Care® silicone gel sheet for the prevention of CS scarring. Our findings support the safety and prophylactic efficacy of Lady Care®.

Inhibitory effect of all-trans retinoic acid on ferroptosis in BeWo cells mediated by the upregulation of heme Oxygenase-1.

INTRODUCTION: This study aimed to explore the association between ferroptosis, a newly identified type of cell death, and the role of retinoic acid in developing pregnancy complications. Therefore, the effects of all-trans retinoic acid (ATRA) on ferroptosis susceptibility in BeWo cells were assessed to understand abnormal placental development. METHODS: BeWo cells were used as surrogates for cytotrophoblasts. The effect of ATRA on ferroptosis sensitivity was assessed on BeWo cells pretreated with ATRA or dimethyl sulfoxide (DMSO; control), following which the LDH-releasing assay was performed. The effects of ATRA pretreatment on the antioxidant defense system (including glutathione [GSH], mitochondrial membrane potential, and heme oxygenase-1 [HMOX1]) in BeWo cells were assessed using assay kits, RT-qPCR, and HMOX1 immunostaining. To evaluate the effect of ATRA on BeWo cells, HMOX1 was silenced in BeWo cells using shRNA. RESULTS: ATRA pretreatment increased ferroptosis resistance in BeWo cells. Although with pretreatment, qPCR indicated upregulation of HMOX1, no significant change was observed in the GSH levels or mitochondrial membrane potential. This was corroborated by intensified immunostaining for heme oxygenase-1 protein (HO-1). Notably, the protective effect of ATRA against ferroptosis was negated when HO-1 was inhibited. Although HMOX1-silenced BeWo cells exhibited heightened ferroptosis sensitivity compared with controls, ATRA pretreatment counteracted ferroptosis in these cells. DISCUSSION: ATRA pretreatment promotes BeWo cell viability by suppressing ferroptosis and upregulating HMOX1 and this can be used as a potential therapeutic strategy for addressing placental complications associated with ferroptosis.

Molecular genetic analysis reveals atypical confined placental mosaicism with a small supernumerary marker chromosome derived from chromosome 18: A clinical report of discordant results from three prenatal tests.

We present a case with discordant results in three prenatal screening methods, with additional genetic analyses. Non-invasive prenatal testing (NIPT) was performed on a 41-year-old Japanese woman at 10 weeks of gestation, and the result was positive for trisomy 18 with high accuracy. Amniocentesis was performed at 16 weeks of gestation. However, the result showed 47,XX,+mar[16]/47,XX,+18[2]. Fetal examination by ultrasound revealed no malformations. After termination of the pregnancy, we performed additional genetic analyses, and confirmed the presence of confined placental mosaicism (CPM). Furthermore, a small supernumerary marker chromosome (sSMC) was detected in fetal cells, which was derived de novo from the centromere of chromosome 18. Single nucleotide polymorphism array analysis revealed that fetal chromosome 18 was inherited with maternal uniparental disomy, with a relatively large copy-neutral loss of heterozygosity, including its centromere. Our genetic analyses strongly indicated the cause of result discrepancy in prenatal testing as incomplete trisomy 18 rescue leading to atypical CPM with a sSMC. These findings also offer insight into the mechanisms by which chromosomal aberrations form during human oogenesis and embryogenesis.

Characterization of a Small Supernumerary Marker Chromosome Derived from Xq28 and 14q11.2 Detected Prenatally.

We present the characterization of a case with a small supernumerary marker chromosome (sSMC) detected prenatally derived from Xq28 and 14q11.2 maternal translocation. A 33-year-old Japanese woman, primigravida, underwent amniocentesis because of fetal growth restriction and fetal structural abnormality at 30 weeks of gestation. The fetal karyotype was identified as 47,XY,+mar. Additionally, the single nucleotide polymorphism array analysis revealed copy number gains at Xq28 and 14q11.2. A male infant, weighing 1,391 g, was delivered at term by cesarean section. Maternal and paternal karyotypes were 46,X,t(X; 14)(q28; q11) and 46,XY, respectively. These findings indicated that the sSMC might have originated from chromosome disjunction at a ratio of three to one. Here we describe a case with an sSMC derived from Xq28 and 14q11.2. Our findings suggest that this sSMC is most likely pathogenic. The collection of additional cases may be required.