Objective To determine the image feature and clinical value of first-trimester ultrasonographic diagnosis of fetal holoprosencephaly.Methods A total 35 580 fetuses at gestational age between 11 + 6 and 13 + 6 weeks were scanned in our hospital by color Doppler ultrasound according to the prenatal ultrasound from Jan 2009 to Jan 2017.Fetal craniocerebral and faceprestige were checked carefully.Cases of fetal holoprosencephaly diagnosed in first-trimester were followed sonographically,and the clinical outcomes were recorded.Results Totally five cases of fetal holoprosencephaly were detected.Four fetuses with other associated malformations were detected by first trimester ultrasound,including one case with beak nosetril,eyes too close,one case with beak nosetril,fetal cleft lip and palate,fetal hydrops,congenital heart disease and mid gut herniation,one case with thickened nucha.One translucency (NT),one case with mandibular micrognathia,one case with trisomy 13 syndrome,the other four cases were not checked.Terminal of pregnancy was performed in four cases during early pregnancy,one case was loss to follow-up.Autopsy was refused in these cases.Fetal appearance revealed one case of cleft lip,single nostril,mandibular micrognathia,one case of hydrops,polyphalangia,microtia,one case of beak nosetril,fetal cleft lip and palate,mid gut herniation,hydrops,one case of beak nosetril,eyes too close.Conclusion Fetal holoprosencephaly can be effectively detected and diagnosed during early pregnancy with standardized prenatal ultrasound.

Objective To determine the imaging features and clinical value of first-trimester ultrasonographic screening of fetal megacystis in multifetal pregnancy.Methods Retrospective analysis was undertaken in 2159 cases of multifetal pregnancy screened in our hospital at gestational age from 11th to 13 + 6th weeks by color Doppler ultrasound between Jan 2011 and April 2016.Fetal bladder was defined by showing two umbilical arteries and the longitudinal length of the bladder was measured in mid-sagittalplane.Clinical progression of fetal megacystis diagnosed in first-trimester were followed and the outcomes were recorded.Results Totally six cases of fetal megacystis in multifetal pregnancy were detected,in which five cases were detected in one fetus of twin pregnancy and the other case was detected in one fetus of triplet pregnancy.In all cases of fetal megacystis,longitudinal length of the fetal bladder was more than 7 mm and double umbilical arteries were detected.In two cases of naturally-occurring twin pregnancy,abortion was performed and postnatal autopsy revealed prune belly syndrome.In the rest four cases of multifetal pregnancy through in vitro fertilization-embryo transfer (IVF-ET),two cases of twin pregnancies underwent selective feticide.The other two cases of twin and triplet pregnancies refused intervention,among which still birth happened in the megacystis fetus and spontaneous fetal death at gestational age of 13 + 2 weeks happened in the monochorionic monoamniotic twins of the triplet pregnancy.Totally,four live babies were born,among which three were healthy.The other baby was found to have 1.5 Mb deletion in chromosome 17q12 by microarray at gestational age of 32 weeks due to increased renal echogenicity.Conclusions First-trimester ultrasonography can effectively detect and diagnose megacystis in multifetal pregnancy.Early diagnosis and timely intervention are helpful for improving the outcome of fetal megacystis in multifetal pregnancy.

Objective:To investigate different regulatory effects of S100A8/A9 expressed by keratinocytes in 3 common inflammatory skin injury modes: UVB-induced skin injury, allergic contact dermatitis, and psoriasis.Methods:Wild-type C57BL/6JGpt mice aged 6 to 8 weeks were selected for the following experiments: (1) mouse models of UVB-induced skin injury were established by single exposure to ultraviolet B (UVB) radiation on the shaved dorsal skin of mice (UVB group, n = 4), with the mice receiving no UVB radiation serving as a control group ( n = 4) ; (2) mouse models of allergic contact dermatitis were established by application of 2,4-dinitrochlorobenzene (DNCB) to the right ears of mice (DNCB group, n = 4), with the left ears of mice treated with a vehicle control serving as a control group ( n = 4) ; (3) mouse models of psoriasis-like skin inflammation were established by topical application of imiquimod cream to the depilated dorsal skin of mice (imiquimod group, n = 4), with the mice treated with vaseline serving as a control group ( n = 4). Hematoxylin-eosin (HE) staining was performed to assess histopathological changes in mouse skin tissues obtained from each group, and immunohistochemical study and Western blot analysis were performed to determine the expression of S100A8 and S100A9 in the mouse dorsal epidermis or ear skin lesions. In vitro cultured HaCaT cells were subjected to the following experiments: (1) cells in the UVB group were treated with a single UVB irradiation at a dose of 50 mJ/cm 2, and cells in the control group received no irradiation; (2) some cells were treated with tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) (collectively referred to as TI), and named as the TI group, which simulated the inflammatory environment in allergic contact dermatitis, while cells treated with corresponding solvents served as the control group; (3) cells were treated with 5 cytokines (interleukin 17A [IL-17A], IL-22, IL-1α, oncostatin M, and TNF-α, collectively referred to as M5), and named as the M5 group, which simulated the inflammatory environment in psoriasis, while cells treated with corresponding solvents served as the control group. Real-time fluorescence-based quantitative PCR, Western blot analysis, and enzyme-linked immunosorbent assay were performed to determine the mRNA and protein expression of S100A8 and S100A9, and to detect the extracellular secretion level of S100A8/A9, respectively. Results:Immunohistochemical study and Western blot analysis revealed that S100A8 and S100A9 expression levels were significantly higher in the skin lesions of mouse models of UVB-induced skin injury, allergic contact dermatitis, and psoriasis-like skin inflammation than in their corresponding control groups; immunohistochemical study further demonstrated that the increase in the expression of the two proteins was more pronounced in the mouse models of psoriasis-like skin inflammation. In the in vitro cell experiments, the mRNA expression of S100A8 and S100A9 in HaCaT cells at 12 and 24 hours were markedly higher in the UVB group (e.g., at 24 hours, 6.14 ± 0.60 vs. 1.00 ± 0.08, 2.58 ± 0.06 vs. 1.02 ± 0.22, respectively, both P < 0.01), TI group (e.g., at 24 hours, 3.90 ± 0.75 vs. 1.00 ± 0.02, 2.42 ± 0.30 vs. 1.01 ± 0.13, respectively, both P < 0.05), and M5 group (e.g., at 24 hours, 157.59 ± 9.30 vs. 1.00 ± 0.11, 251.37 ± 6.63 vs. 1.00 ± 0.03, both P < 0.001) than in the corresponding control groups, so were the extracellular secretion levels of S100A8/A9 at 24 and 48 hours (all P < 0.001), with some differences observed in their response patterns; notably, the response was more pronounced in the mouse model of psoriasis-like skin inflammation. Additionally, the protein expression levels of S100A8 and S100A9 in HaCaT cells were significantly higher in the M5 group than in the control group ( t = 4.66, 4.63, respectively, both P < 0.01), but were significantly lower in the UVB group ( t = -3.75, -3.34, P = 0.020, 0.029, respectively) and TI group ( t = -3.30, -4.50, P = 0.030, 0.011, respectively) than in the control groups. Conclusion:Keratinocytes exhibited active responses following 3 common inflammatory skin injuries, with their effector molecules S100A8 and S100A9, as damage-associated molecular patterns, playing crucial roles in UVB-induced skin injury, allergic contact dermatitis, and psoriasis, and the response seemed to be more pronounced in psoriasis-like dermatitis.