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Background: Endometrial fibrosis may cause infertility. Accurate evaluation of endometrial fibrosis helps clinicians to schedule timely therapy. Purpose: To explore T2 mapping for assessing endometrial fibrosis. Study Type: Prospective. Population: Ninety‐seven women with severe endometrial fibrosis (SEF) and 21 patients with mild to moderate endometrial fibrosis (MMEF), diagnosed by hysteroscopy, and 37 healthy women. Field Strength/Sequence: 3T, T2‐weighted turbo spin echo (T2‐weighted imaging) and multi‐echo turbo spin echo (T2 mapping) sequences. Assessment: Endometrial MRI parameters (T2, thickness [ET], area [EA], and volume [EV]) were measured by N.Z. and Q.H. (9‐ and 4‐years' experience in pelvic MRI) and compared between the three subgroups. A multivariable model including MRI parameters and clinical variables (including age and body mass index [BMI]) was developed to predict endometrial fibrosis assessed by hysteroscopy. Statistical Tests: Kruskal–Wallis; ANOVA; Spearman's correlation coefficient (rho); area under the receiver operating characteristic curve (AUC); binary logistic regression; intraclass correlation coefficient (ICC). P value <0.05 for statistical significance. Results: Endometrial T2, ET, EA, and EV of MMEF patients (185 msec, 8.2 mm, 168 mm2, and 2181 mm3) and SEF patients (164 msec, 6.7 mm, 120 mm2, and 1762 mm3) were significantly lower than those of healthy women (222 msec, 11.7 mm, 316 mm2, and 3960 mm3). Endometrial T2 and ET of SEF patients were significantly lower than those of MMEF patients. Endometrial T2, ET, EA, and EV were significantly correlated to the degree of endometrial fibrosis (rho = −0.623, −0.695, −0.694, −0.595). There were significant strong correlations between ET, EA, and EV in healthy women and MMEF patients (rho = 0.850–0.908). Endometrial MRI parameters and the multivariable model accurately distinguished MMEF or SEF from normal endometrium (AUCs >0.800). Age, BMI, and MRI parameters in univariable analysis and age and T2 in multivariable analysis significantly predicted endometrial fibrosis. The reproducibility of MRI parameters was excellent (ICC, 0.859–0.980). Data Conclusion: T2 mapping has potential to noninvasively and quantitatively evaluate the degree of endometrial fibrosis. Evidence Level: 2 Technical Efficacy: Stage 2 [ABSTRACT FROM AUTHOR]

Background: Noninvasive fetal RHD genotyping has been provided to nonimmunized RhD‐negative pregnant women to guide anti‐D prophylaxis. Among the Chinese, more than 30% of the RhD‐negative phenotype is associated with variant RHD alleles, which would limit the accuracy of fetal RHD status prediction; thus, more targeting and proper programs need to be developed. Study Design and Methods: Fluorescence quantitative polymerase chain reaction PCR (qPCR) or Sanger sequencing on all RHD exons was used to detect maternal RHD genotypes. For pregnant women with RHD*01N.01 or RHD*01N.03 alleles, the presence of RHD exons 5 and 10 in cell‐free DNA was determined by qPCR. For pregnant women with the RHD(1227G>A) allele, high‐throughput sequencing on exon 9 of the RHD gene and RHCE gene was used to predict fetal RhD phenotype. Results: Among 65 cases of Chinese pregnant women with the serologic RhD‐negative phenotype, three major genotypes were identified: RHD*01N.01/RHD*01N.01 (61.5%), RHD*01N.01/RHD(1227G>A) or RHD*01N.03/RHD(1227G>A) (20%), and RHD*01N.01/RHD*01N.03 (13.8%), along with three cases of minor genotypes (4.6%). For 43 pregnant women with the RHD*01N.01 or RHD*01N.03 alleles, qPCR on maternal cell‐free DNA yielded a 98.5% (42/43) accuracy rate and 100% successful prediction rate. High‐throughput sequencing was successfully used to predict fetal RhD phenotypes for 13 pregnant women with RHD(1227G>A). Conclusion: On the basis of maternal RHD genotyping, fetal genotyping through qPCR or high‐throughput sequencing can improve the accuracy and success rate of prenatal fetal RhD phenotype prediction among Chinese pregnant women. It plays a potential role in guiding anti‐D prophylaxis and pregnancy management in Chinese pregnant women. [ABSTRACT FROM AUTHOR]

Macrophages are a key and heterogeneous cell population involved in endometrial repair and regeneration during the menstrual cycle, but their role in the development of intrauterine adhesion (IUA) and sequential endometrial fibrosis remains unclear. Here, we reported that CD301+ macrophages were significantly increased and showed their most active interaction with profibrotic cells in the endometria of IUA patients compared with the normal endometria by single‐cell RNA sequencing, bulk RNA sequencing, and experimental verification. Increasing CD301+ macrophages promoted the differentiation of endometrial stromal cells into myofibroblasts and resulted in extracellular matrix accumulation, which destroyed the physiological architecture of endometrial tissue, drove endometrial fibrosis, and ultimately led to female infertility or adverse pregnancy outcomes. Mechanistically, CD301+ macrophages secreted GAS6 to activate the AXL/NF‐κB pathway, upregulating the profibrotic protein synthesis. Targeted deletion of CD301+ macrophages or inhibition of AXL by Bemcentinib blunted the pathology and improved the outcomes of pregnancy in mice, supporting the therapeutic potential of targeting CD301+ macrophages for treating endometrial fibrosis. Synopsis: This study highlights the role of CD301+ macrophages in facilitating endometrial fibrosis in intrauterine adhesion (IUA) through the GAS6/AXL/NF‐κB pathway. By depleting CD301+ macrophages or employing the pharmacological inhibitor Bemcentinib to target AXL, the progression of fibrosis can be suppressed, ultimately improving pregnancy outcomes in mice. CD301+ macrophages exhibit elevated levels in the endometrial fibrosis of IUA patients.CD301+ macrophages secrete GAS6, activating the AXL/NF‐κB pathway and promoting fibrosis.Depletion of CD301+ macrophages or treatment with the AXL inhibitor Bemcentinib shows promising potential for treating endometrial fibrosis and enhancing pregnancy outcomes. [ABSTRACT FROM AUTHOR]

The bonding state of the pile-soil interaction is complex. Traditional monitoring methods and tools have not been fully applied to monitor and evaluate it although it affects the lifecycle safety of the pile. In this study, a health monitoring method is proposed to evaluate the bonding state of the pile-soil contact area; it is a transient impact response method based on piezoelectric ceramic sensors to monitor the pile-soil bonding state. During the test, different damage degrees of the pile-soil bonding state were simulated by considering the working conditions of different soil densities and different crack depths as examples. A horizontal transient impact stress was applied to the pile top, and a piezoelectric ceramic sensor embedded in the pile detected the stress wave. As the stress wave response differs in different damage conditions, an energy index was established to quantitatively monitor the degree of damage. [ABSTRACT FROM AUTHOR]

Neural progenitor cell (NPC) transplantation is a promising approach for repairing spinal cord injury (SCI). However, cell survival, maturation and integration after transplantation are still major challenges. Here, we produced a novel centimeter‐scale human spinal cord neural tissue (hscNT) construct with human spinal cord neural progenitor cells (hscNPCs) and human spinal cord astrocytes (hscAS) on a linearly ordered collagen scaffold (LOCS). The hscAS promoted hscNPC adhesion, survival and neurite outgrowth on the LOCS, to form a linearly ordered spinal cord‐like structure consisting of mature neurons and glia cells. When transplanted into rats with SCI, the hscNT created a favorable microenvironment by inhibiting inflammation and glial scar formation, and promoted neural and vascular regeneration. Notably, the hscNT promoted neural circuit reconstruction and motor functional recovery. Engineered human spinal cord implants containing astrocytes and neurons assembled on axon guidance scaffolds may therefore have potential in the treatment of SCI. [ABSTRACT FROM AUTHOR]

During central nervous system development, neurogenesis and gliogenesis occur in an orderly manner to create precise neural circuitry. However, no systematic dataset of neural lineage development that covers both neurogenesis and gliogenesis for the human spinal cord is available. We here perform single‐cell RNA sequencing of human spinal cord cells during embryonic and fetal stages that cover neuron generation as well as astrocytes and oligodendrocyte differentiation. We also map the timeline of sensory neurogenesis and gliogenesis in the spinal cord. We further identify a group of EGFR‐expressing transitional glial cells with radial morphology at the onset of gliogenesis, which progressively acquires differentiated glial cell characteristics. These EGFR‐expressing transitional glial cells exhibited a unique position‐specific feature during spinal cord development. Cell crosstalk analysis using CellPhoneDB indicated that EGFR glial cells can persistently interact with other neural cells during development through Delta‐Notch and EGFR signaling. Together, our results reveal stage‐specific profiles and dynamics of neural cells during human spinal cord development. Synopsis: Using single‐cell nuclei and single‐cell RNA‐seq, this study reveals a developmental timeline and uncovers genetic heterogeneity in neural cells during embryonic and fetal stages of human spinal cord development. Single‐cell RNA‐seq of human spinal cord cells during embryonic and fetal stages.Timeline of sensory neurogenesis and gliogenesis in the human spinal cordEGFR‐expressing transitional glial cells exhibit a unique regional‐specific feature during spinal cord development. [ABSTRACT FROM AUTHOR]

Aim: The aim of the study was to develop and validate a magnetic resonance imaging (MRI)‐based nomogram for predicting invasive forms of placental accreta spectrum (PAS) disorders (placenta increta and percreta) with "uncertain ultrasound diagnosis." Methods: This was a retrospective cohort study of a primary cohort of 118 patients and a validation cohort of 65 patients with "uncertain ultrasound diagnosis," who were further evaluated by MRI. MRI signs associated with PAS disorders were analyzed between invasive and noninvasive groups by both univariate and logistic regression to construct the nomogram. The accuracy and discriminative ability of the nomogram were measured by concordance index (C‐index) and calibration curve internally and externally. Results: The history of previous cesarean deliveries (odds ratio [OR], 3.27; 95% confidence interval [CI], 1.16–9.27), loss of double‐line sign (OR, 9.49; 95% CI, 3.06–29.48), abnormal uterine bulging (OR, 4.05; 95% CI, 1.53–10.69), and disorganized abnormal placenta vascularity (OR, 3.38; 95% CI, 1.09–10.50) were imputed for the nomogram. The C‐index of the nomogram was 0.85 for internal validation and 0.84 for external validation. Calibration curve showed good agreement with predicted risk and actual observation for both primary and validation cohort. Conclusions: MRI can be a useful adjunct for clinical staging of patients with "uncertain ultrasound diagnosis." [ABSTRACT FROM AUTHOR]

The single crystal of a silver complex bis (imidazole) silver(I) nitrate (Ag(C3H4N2)2(NO3), BISN) has been obtained and characterized by X‐ray single‐crystal diffraction. Its crystal thin film was prepared using direct growth on quartz substrates. The surface morphology of the thin film was studied by atomic force microscopy (AFM). The nonlinear optical (NLO) properties of the thin film were investigated by using closed‐aperture Z‐scan technique with 20 picosecond (ps) pulses at wavelength 532 nm. Using time‐dependent density‐functional theory (TDDFT) with the basis set LanL2DZ, its linear and NLO properties were calculated. [ABSTRACT FROM AUTHOR]

The single crystals of a new coordination polymer catena‐poly[aqua‐dichlorido‐bis(1H‐imidazole)‐manganese(ii)] ([Mn(C3H4N2)2Cl2(H2O)]n) (CPADBIM) are obtained and characterized by X‐ray single crystal diffraction. It's second hyperpolarizability γ value is investigated by using a closed aperture Z‐scan technique with 20 ps pulses at wavelength 532 nm. Time‐dependent density‐functional theory with basis sets 6‐311++G(3d,3p) is used in computing the linear and non‐linear optical properties. The theoretical calculated γ value is in agreement with the experimental results. [ABSTRACT FROM AUTHOR]

Severe uterine injuries may lead to infertility or pregnancy complications. There is a lack of effective methods to restore the structure and function of seriously injured uteri. Leukemia inhibitory factor (LIF), which plays a crucial role in blastocyst implantation, promotes the process of regeneration after injury in several different tissues. In this study, we explored the effect of LIF on the regeneration of rat uterine horns following full‐thickness injury. One hundred and twenty four female Sprague–Dawley rats were assigned to three groups, including a sham‐operated group (n = 34 uterine horns), a PBS/collagen group (n = 90 uterine horns), and a LIF/collagen group (n = 124 uterine horns). The regenerated uterine horns were collected at 1, 2, 4, 8, or 12 weeks after the surgery. The results showed that LIF/collagen scaffolds increased the number of endometrial cells and neovascularization 2 weeks after uterine full‐thickness defect in excision sites (p < 0.001 vs PBS/collagen). Eight weeks after the surgery, the number of endometrial glands was dramatically higher in the LIF/collagen scaffolds group (35.2 ± 4.1/field) than in the PBS/collagen scaffolds (15.1 ± 1.4/field). The percentage of a‐smooth muscle actin (a‐SMA)‐positive areas in the LIF/collagen scaffolds (88.8% ± 9.8%) was also significantly higher than that in the PBS/collagen group (52.9% ± 3.7%). Moreover, LIF improved the pregnancy rate and fetus number. We also found that LIF inhibited the infiltration of inflammatory cells and down‐regulated the pro‐inflammatory cytokine IL‐12 expression while up‐regulating the anti‐inflammatory cytokine IL‐10 expression in the injured part of the uterine horns. Our results indicate that LIF promotes regeneration of the uterus after injury, and this is at least partially due to its immunomodulatory properties. In addition, it is worth to explore further the possibility for LIF/collagen to be an alternative therapeutic approach for uterine damage in the clinic in near future. [ABSTRACT FROM AUTHOR]

In this study, we aimed to investigate the effects of water temperature and stocking density on the survival, feeding and growth of the juveniles of the hybrid yellow catfish from Pelteobagrus fulvidraco (♀) × Pelteobagrus vachelli (♂) using the parameters as follows: survival rate (%), feeding rate (% day−1), feed conversion ratio, specific growth rate (% day−1), coefficient of variation (%), productivity (P, g m−3 day−1) and condition factor. We reared the juvenile fish (3.25 ± 0.21 g) at 12 water temperature levels and six stocking density levels (each level included three aquaria in two batches of experiments). The results showed that all groups survived at a temperature range of ≤35°C during a 46-day experimental period, and they could achieve a high growth at a water temperature range of 26-32°C. The optimal temperature for growth was 29.8°C. Productivity peaked at a stocking density of 1.9 kg m−3. Our results indicated that the hybrid is very suitable for commercial aquaculture. [ABSTRACT FROM AUTHOR]

Objective: To assess the clinical implication of chromosomal microarray analysis (CMA) in prenatal diagnosis of MCDK.Methods: Thirty-seven cases with MCDKs detected by prenatal ultrasound were enrolled in the study; 33 cases were isolated MCDKs and four cases were non-isolated MCDKs. CMA was performed on the Affymetrix CytoScan HD platform. The frequencies of the detected CNVs were compared with 461 cases that underwent CMA for anomalies unrelated to congenital anomalies of kidney and urinary tract (CAKUT) or 124 healthy newborns as controls. All of the annotated CNVs were validated by MLPA or qPCR.Results: Pathogenic CNVs were detected in 13.5% (5/37) of MCDKs. Two 17q12 deletions, one untypical 22q11.2 deletion, and one 22q11.2 duplication were detected in four isolated MCDK cases. Duplication of 1q31.3q44 was identified in a non-isolated MCDK case. Three of the five pathogenic CNVs were inherited. We also validated eight CNVs of uncertain significance only detected in MCDKs and five CNVs with higher frequency in MCDKs.Conclusion: A substantial proportion of MCDKs were associated with pathogenic CNVs. Family members with the same CNV were asymptomatic or of different kind of renal malformations. It may be reasonable to perform CMA when MCDKs are identified prenatally. © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Objective: To determine the type and frequency of pathogenic chromosomal abnormalities in fetuses diagnosed with congenital heart disease (CHD) using chromosomal microarray analysis (CMA) and validate next-generation sequencing as an alternative diagnostic method.Method: Chromosomal aneuploidies and submicroscopic copy number variations (CNVs) were identified in amniocytes DNA samples from CHD fetuses using high-resolution CMA and copy number variation sequencing (CNV-Seq).Result: Overall, 21 of 115 CHD fetuses (18.3%) referred for CMA had a pathogenic chromosomal anomaly. In six of 73 fetuses (8.2%) with an isolated CHD, CMA identified two cases of DiGeorge syndrome, and one case each of 1q21.1 microdeletion, 16p11.2 microdeletion and Angelman/Prader Willi syndromes, and 22q11.21 microduplication syndrome. In 12 of 42 fetuses (28.6%) with CHD and additional structural abnormalities, CMA identified eight whole or partial trisomies (19.0%), five CNVs (11.9%) associated with DiGeorge, Wolf-Hirschhorn, Miller-Dieker, Cri du Chat and Blepharophimosis, Ptosis, and Epicanthus Inversus syndromes and four other rare pathogenic CNVs (9.5%). Overall, there was a 100% diagnostic concordance between CMA and CNV-Seq for detecting all 21 pathogenic chromosomal abnormalities associated with CHD.Conclusion: CMA and CNV-Seq are reliable and accurate prenatal techniques for identifying pathogenic fetal chromosomal abnormalities associated with cardiac defects. © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSCs) play an important role in the pathology of preeclampsia (PE). Our previous microarray analysis found that microRNA-494 (miR-494) is highly expressed in decidua-derived MSCs (dMSCs) from PE. We hypothesized that aberrant expression of miR-494 in dMSCs is involved in PE development. In the present study, we found that miR-494 arrests G1/S transition in dMSCs by targeting CDK6 and CCND1. We also found that supernatant from miR-494-overexpressing dMSCs reduces HTR-8/SVneo migration and impairs HUVEC capillary formation by suppressing VEGF. Taken together, we report an unrecognized mechanism of miR-494 affecting dMSC proliferation and function in the pathology of PE. [ABSTRACT FROM AUTHOR]

Highlights: [•] miR-133b promotes estrogen production in human and mouse granulosa cells. [•] The Forkhead L2 (Foxl2) gene is a novel miR-133b target. [•] miR-133b attenuates the Foxl2-induced transcriptional repression of StAR and CYP19A1. [Copyright &y& Elsevier]

Highlights: [•] miR-145 protects against cardiomyocyte hypertrophy induced by the βAR agonist ISO. [•] GATA6 is a direct functional target gene of miR-145. [•] miR-145 attenuates GATA6 nuclear translocation through inhibition of GSK3β phosphorylation. [ABSTRACT FROM AUTHOR]

Although many patients with duplication 3q syndrome have been described reports on duplication derivatives from an insertion are rare in the previous literature. Here we describe the genotype and phenotype of a 32-month-old boy with a partial trisomy of 3q24-q28. We carefully mapped the aberration with SNP-array analysis, and found a duplication region of 44 Mb. By conventional cytogenetic techniques including fluorescence in situ hybridization (FISH) and spectral karyotyping (SKY) analysis, the patient was found to have inherited a derivative chromosome 6 from his father, which was contained a direct insertion from 3q24-28. The main clinical features of the patient included severe mental retardation, postnatal developmental delay, ventricular septal defect (VSD), and craniofacial anomalies including cleft palate, frontal bossing, hypertelorism, and a broad nasal bridge. The symptoms partially overlap with previously reported patients with duplication in the same region. Prenatal diagnosis for the fetus of this family was performed based on the results of genetic tests and ultrasonic evaluation. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Pre-eclampsia is thought to be a systemic disease of maternal endothelial cell dysfunctions. mi RNAs regulate various basic biological functions in cells, including stem cells. Mesenchymal stem cells exist in almost all tissues and are the key cellular source for tissue repair and regeneration. Our aims are to investigate whether mi RNAs regulate MSCs in fetal-maternal interfaces to influence the pathogenesis of pre-eclampsia. The differential expression of mi RNAs in decidua-derived mesenchymal stem cells of all patients with severe pre-eclampsia ( n = 20) and normal groups ( n = 20) was first screened by microarray analysis and validated by quantitative real-time PCR analysis. The integrated bioinformatics analysis showed that miR-16 showed the highest number of connections in the mi RNA GO network and the mi RNA gene network. Moreover, over-expressed miR-16 inhibited the proliferation and migration of decidua-derived mesenchymal stem cells and induced cell-cycle arrest by targeting cyclin E1. Interestingly, over-expression of miR-16 by decidua-derived mesenchymal stem cells reduced the ability of human umbilical vein endothelial cells to form blood vessels and reduced the migration of trophoblast cells. Furthermore, decidua-derived mesenchymal stem cell-expressed endothelial growth factor VEGF-A was involved in migration of trophoblast cells and human umbilical vein endothelial cells as well as tube and network formation. Importantly, the levels of cyclin E1 and VEGF-A were negatively correlated with the level of miR-16 expression in decidua-derived mesenchymal stem cells from the patients with severe pre-eclampsia. Together, these data suggest that the alteration of miR-16 expression in decidua-derived mesenchymal stem cells may be involved in the development of pre-eclampsia. [ABSTRACT FROM AUTHOR]

Problem Progesterone ( P4) plays a central role in the establishment and maintenance of pregnancy. It also has profound effects on the regulation of immune responses. Mesenchymal stem cells ( MSCs), which are thought to have the ability to modulate immunocyte activation, are present in human endometrium and deciduas and highly express progesterone receptor ( PR). Especially, during pregnancy, both P4 and MSCs are present and regulatively changed at the fetal-maternal interface, but the effect of P4 on the MSCs remains unknown. Therefore, in this study, we investigated the effects of P4 on the immunomodulatory ability of MSCs and the underlying mechanisms. Method of study Mesenchymal stem cells were obtained from human umbilical cords. The effects of P4 on the cell morphology, phenotype, proliferation, apoptosis, and expression levels of cytokine and protein were examined. Results Progesterone did not affect the phenotype, morphology, proliferation, and apoptosis of MSCs, but promoted the production of PGE2 and IL-6 in MSCs. Furthermore, the up-regulation of PGE2 and IL-6 was related to the activation of p38 and NF-κB. Conclusions Progesterone enhances immunomodulatory function of MSCs through up-regulation of PGE2 and IL-6. The data suggest that P4-regulated MSCs may play a crucial role in modulating the local immune balance of fetal-maternal interface. [ABSTRACT FROM AUTHOR]

Abstract: MicroRNAs (miRNAs) are a class of 21- to 25-nucleotide non-coding RNAs, some of which are important gene regulators involved in folliculogenesis. In this study, we used CCK-8, real-time PCR and Western blot assays to demonstrate that miR-145 inhibits mouse granulosa cell (mGC) proliferation. Combined with the results of luciferase reporter assays that studied the 3′-untranslated region of ACVRIB mRNA, these assays identified ACVRIB as a direct target of miR-145. The ectopic expression of miR-145 reduced the levels of both ACVRIB mRNA and protein and also interfered with activin-induced Smad2 phosphorylation. Altogether, this study revealed that miR-145 suppresses mGC proliferation by targeting ACVRIB. [Copyright &y& Elsevier]

Problem The objective of this study was to determine whether there was any association between the peripheral blood CD4+ CD25+ Foxp3+ regulatory T cells ( Treg cells) and implantation success in patients undergoing in vitro fertilization ( IVF) treatment. Method of study Prospective observational study of 101 randomly selected women who underwent IVF treatment for tubal factor from May 2011 to June 2011. The percentage of peripheral blood Treg cells and the expression levels of Foxp3 and CTLA4 mRNA in peripheral blood mononuclear cells ( PBMCs) were recorded and their relations to IVF treatment outcomes were analyzed. Results Treg cells were significantly elevated in the pregnant group ( P = 0.03). The expression level of Foxp3 mRNA in PBMCs from pregnant group also significantly increased ( P = 0.02). A receiver operating characteristic analysis (area under curve = 0.631) found that those women with Treg cells >0.6%, the pregnancy rate and live birth rate were much higher as compared to women with Treg cells below this level ( P < 0.05). An increase of Treg cells in the peripheral blood was associated with a better IVF treatment outcome ( OR 4.3, 95% CI = 1.76-10.48), with a sensitivity of 64%, specificity of 71%. Conclusion An elevated level of circulating Treg cells was associated with increased rates of pregnancy and live birth in IVF treatment. [ABSTRACT FROM AUTHOR]

Problem Uterine natural killer cells (u NK) do not express progesterone receptor, but express glucocorticoid receptor ( GR). So, we speculate that progesterone may regulate u NK cells through a GR-mediated process. Method of Study After mouse NK cells were stimulated with Cp G with or without IL-12 in the presence or absence pre-treatment of progesterone, the effects of progesterone on NK via GR were investigated by using RU486 (progesterone receptor and GR antagonist) and CDB-2914 (progesterone receptor antagonist). The expressions of CD69 and IFN-γ were determined by flow cytometry and q PCR. Phosphorylation of Iκ B and STAT4 was determined by Western blot. Furthermore, we purified u NK cells from human decidual tissues using anti- CD56 microbeads to verify the effect of progesterone on u NK via GR. Results Progesterone suppressed CD69 and IFN-γ expression of mouse spleen NK cells and human u NK cells induced by Cp G combined with IL-12. CDB-2914 had no effect on IFN-γ expression suppressed by progesterone, while RU486 could abolish the inhibitory effect of progesterone. In addition, progesterone could decrease the phosphorylation of both STAT4 and Iκ B. Conclusions In the present study, we first prove that progesterone can regulate NK cells via GR. It is valuable for further understanding the role of u NK in progesterone regulated gestation process. [ABSTRACT FROM AUTHOR]

Citation Zhang X, Ding L, Diao Z, Yan G, Sun H, Hu Y. CYR61 modulates the vascular endothelial growth factor C expression of decidual NK cells via PI3K/AKT pathway. Am J Reprod Immunol 2012; 67: 216-223 Problem Either vascular endothelial growth factor C (VEGFC) or CYR61 plays an important role in placental development and may be involved in pre-eclampsia. Decidual natural killer (dNK) cells are the main source of VEGFC in the maternal-fetal interface. However, it is unclear about CYR61 on the regulation of VEGFC secretion in dNK cells. Method of study Decidual natural killer cells were isolated from decidual tissues of first trimester of pregnancy with anti-human CD56-conjugated microbeads. Integrin αvβ3 was detected using immunofluorescent staining. dNK cells were cultured in the presence of CYR61, anti-human αvβ3 integrin antibody (LM609), PI3K inhibitor (LY294002), or MEK inhibitor (U0126). VEGFC mRNA and protein were evaluated by real-time PCR and ELISA, respectively. Results Exogenous CYR61 induced the expression of VEGFC in dNK cells in both mRNA and protein levels. Integrin αvβ3 was strongly expressed on dNK cell surface. Anti-αvβ3 integrin antibody inhibited the effect of CYR61 on VEGFC expression. LY294002, but not U0126, significantly reduced this promotion effect of CYR61 on dNK cells. Conclusions The upregulation of VEGFC secretion mainly depends on CYR61 binding with integrin αvβ3 on the surface of dNK cells. PI3K/AKT, rather than the ERK/MAPK signal, is involved in the regulation. [ABSTRACT FROM AUTHOR]

Background: The rates of preterm birth in Chinese women and the potential effects of differing environments are poorly understood. Aim: To determine the rate of preterm birth in Chinese women in China, Hong Kong and Western Australia. Methods: The rates of preterm birth were obtained from records of 26 611 pregnancies in Jiangsu Province in mainland China, 48 976 pregnancies in Hong Kong and 185 798 pregnancies in Western Australia. Results: Preterm birth rates increased from 2.6 and 2.9% in urban and rural Jiangsu Province, respectively, and 2.5% in China-born women in Western Australia who required an interpreter; to 4.9% in China-born women in Western Australia who did not require an interpreter; to 5.6% in non-resident Chinese women in Hong Kong; and 7.6% for women resident in Hong Kong. Within Western Australia, the rate of preterm birth was significantly less in women who were born in China and declared themselves to be Chinese (4.4%) than Caucasians (7.8%), other women who declared themselves to be 'Asian' (8.7%) and women of Aboriginal heritage (14.5%). Conclusions: The rate of preterm birth in China is relatively low but appears to differ in Chinese women in other environments. Differences between traditional Chinese and contemporary Western lifestyles, possibly including smoking and sexual practices, may contribute to the different rates of preterm birth. Further research in this area may provide avenues for the prevention of preterm birth and also help to prevent a possible rise in this complication of pregnancy as Chinese society continues on the path of economic and social reform. [ABSTRACT FROM AUTHOR]

Objective: To estimate the prevalence of hepatitis B surface antigen (HBsAg) among pregnant women in Jiangsu Province, eastern China, 17years after vaccination against hepatitis B virus (HBV) was introduced.Methods: From August 2002 to July 2004, serum samples from 6398 women between 15 and 20weeks of pregnancy and from 6 urban and 8 rural areas across Jiangsu Province were tested for markers of HBV. The results were then compared with the rates before 1980.Results: The overall rates of 6.71% for HBsAg and 36.84% for anti-HBs were significantly lower and higher, respectively, than the prevaccination rates. The rate for HBsAg was lower in urban areas than in rural areas (5.75% vs 7.14%, P=0.04). Although the rate used to be much higher in the northern part of Jiangsu Province, which is less prosperous than the southern part, the rates are now similar in both parts (6.60% vs 6.97%).Conclusion: These findings demonstrate a drop in the prevalence of HBsAg among pregnant women in Jiangsu Province since the introduction of vaccination programs in 1980, and indicate that HBV infection can also be controlled in less prosperous areas. [ABSTRACT FROM AUTHOR]

Problem Extensive studies have demonstrated that Th1 type immunity is predominant in pre-eclampsia, but there is little concern with regard to the intracellular mechanisms behind this initial T-cell polarization. In this study, we investigated whether the imbalance of the T-cell transcription factors contributes to it. Method of study A total of 15 pre-eclamptic patients and 15 healthy pregnant women were enrolled in this study. The expression levels of transcription factors for Th1 (T-bet), Th2 (GATA3), Th17 (RORc) and Treg (FOXP3) cells, together with the Th1/Th2 status, were simultaneously investigated in both peripheral blood mononuclear cells (PBMCs) and decidua. Results The expression levels of FOXP3 mRNA were decreased in both PBMCs and decidua from pre-eclamptic patients compared with healthy pregnant women ( P < 0.05), and T-bet mRNA and RORc mRNA were significantly increased ( P < 0.05), while Th1/Th2 balance shifted toward the Th1 immunity. Furthermore, there was a negative correlation between FOXP3 mRNA and Th1 cells ( P < 0.05), and the expression level of T-bet mRNA correlated strongly with Th1 cells ( P < 0.05). Conclusion Decreased expression of FOXP3 mRNA and increased expression of T-bet mRNA may contribute to Th1 type immunity predominant in pre-eclampsia. [ABSTRACT FROM AUTHOR]

Abstract: The great shortage of human hepatic cells makes it desirable to generate extrahepatic stem or precursor cells. In recent years, it has been reported that human multipotential mesenchymal stem cells (hMSCs) differentiate into hepatocyte-like cells. The fetal lung is one of the largest organs containing many MSCs that can be easily obtained. Whether MSCs from fetal lung can differentiate into hepatocytes or bile duct cells is an important issue in basic medicine and clinical application. We isolated fetal lung cells, and expanded and analyzed them. At passage 4, their morphologic, immunophenotyping and cytokine secretions were similar to adult bone marrow-derived MSCs. We conclude that these cells from fetal lung are MSCs, indicating that human fetal lung is an ideal source of hMSCs. hMSCs from fetal lung induced in special differentiation medium showed homogeneous and small polygonal endothelial-like morphology, expressing weak mRNA, as well as Alb and AFP. This implies that hMSCs from fetal lung can differentiate into hepatocyte-like cells. [Copyright &y& Elsevier]

Objectives: To evaluate the feasibility and superiority of comparative genomic hybridization (CGH) in the genetic analysis of spontaneously aborted tissues.Methods: 38 conceptuses from early failed pregnancies were studied, of which, 27 samples were fresh and 11 were old. Each sample was divided into two parts, one part for conventional cytogenetic analysis and the other for CGH analysis.Results: All 38 spontaneously aborted tissues were analyzed successfully by the CGH approach, but only 31 samples received results from the cytogenetic karyotype analysis, while 7 other tissues failed to get data due to failure in tissue culturing. Among the specimen successfully analyzed by both approaches, 90% (28 out of 31) obtained identical results, and 14 aneuploidies were found. The only structural chromosome aberration in this series, 46, XY, del(3) (q22-24), was found using the CGH approach, which appeared as a normal male karyotype on the chromosomal metaphase spread. Also, two cases indicated triploidies under cytogenetic analysis but appeared to be normal on the CGH profile. In addition, among the seven samples of tissue culture failure, CGH identified three to be aneuploidies.Conclusion: The CGH analysis accurately identifies chromosomal unbalanced abnormalities related to spontaneous abortions with low failure rate. [ABSTRACT FROM AUTHOR]

Objectives To develop a reliable and specific technique for rapid prenatal diagnosis of Down syndrome. Methods High throughput real-time PCR technique was used to measure the DSCR3 gene dosage of genomic DNAs from uncultured amniocytes of fetuses, lymphocytes of trisomy 21 syndrome patients, and normal people, compared to conventional cytogenetic karyotype analysis. Results The DSCR3/GAPDH ratio of uncultured amniocytes in trisomy 21 syndrome fetuses to normal fetuses was 1.69 ± 0.17 to 1.06 ± 0.14, respectively ( p < 0.001); and the DSCR3/GAPDH ratio of lymphocytes in trisomy 21 syndrome children to normal people was 1.67 ± 0.13 to 0.99 ± 0.10, respectively ( p < 0.001). Real-time PCR technique effectively differentiates the normal fetuses from the trisomy 21 syndrome fetuses; therefore, compared to the results of the conventional cytogenetic karyotype analysis, the DSCR3/ GAPDH ratios of trisomy 21 syndrome fetuses are significantly higher than those of normal fetuses. Conclusion Because the DSCR3/GAPDH ratio of trisomy 21 syndrome fetuses is significantly higher than that of normal fetuses, the genomic DNA real-time PCR technique may be a reliable and specific method for the rapid prenatal diagnosis of Down syndrome. Copyright © 2004 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Problem: Asherman's syndrome (AS) is characterized by endometrial fibrosis leading to intrauterine adhesions and symptoms like hypomenorrhea, infertility, and recurrent pregnancy loss. Macrophages are key regulators of inflammation, tissue repair, regeneration, and fibrosis. However, the role of macrophages in AS remains unclear. Method of study: Endometrial biopsies of AS patients and controls were collected during the late proliferating phase of menstrual cycle. Fibrosis and proliferation markers were detected by Masson's trichrome staining and immunohistochemistry. Macrophages were examined by immunostaining and flow cytometry. The expression levels of CCL2, CSF1, CSF1R, and GM‐CSF were detected by quantitative real‐time polymerase chain reaction (q‐PCR) and immunohistochemistry. A well‐differentiated endometrial cell line Ishikawa (IK) was used for in vitro studies. Macrophages differentiating from THP‐1 monocytic cells were polarized by IL‐4/IL‐13. Their culture supernatants (M(IL‐4/13)‐S) were applied to H2O2 or bleomycin‐damaged IK cells. Results: In AS patients, endometrial stroma was replaced by fibrous tissue and cell proliferation was reduced. Macrophages in endometrial tissue were mainly alternative activated macrophages and their number was significantly decreased in AS patients. The CSF1 expression level was reduced in AS patients. M(IL‐4/13)‐S promoted the growth and migration of IK cells and inhibited H2O2‐induced apoptosis. M(IL‐4/13)‐S protected IK cells from bleomycin‐induced fibrosis. Conclusion: Macrophages are critical cells involved in the process of endometrial repair and fibrosis. The decreased amount of endometrial macrophages may be attributed to the reduced expression level of CSF1. Manipulation of macrophage activation/function may provide a novel therapeutic target for AS. [ABSTRACT FROM AUTHOR]

Macrophages are a key and heterogeneous cell population involved in endometrial repair and regeneration during the menstrual cycle, but their role in the development of intrauterine adhesion (IUA) and sequential endometrial fibrosis remains unclear. Here, we reported that CD301 + macrophages were significantly increased and showed their most active interaction with profibrotic cells in the endometria of IUA patients compared with the normal endometria by single-cell RNA sequencing, bulk RNA sequencing, and experimental verification. Increasing CD301 + macrophages promoted the differentiation of endometrial stromal cells into myofibroblasts and resulted in extracellular matrix accumulation, which destroyed the physiological architecture of endometrial tissue, drove endometrial fibrosis, and ultimately led to female infertility or adverse pregnancy outcomes. Mechanistically, CD301 + macrophages secreted GAS6 to activate the AXL/NF-κB pathway, upregulating the profibrotic protein synthesis. Targeted deletion of CD301 + macrophages or inhibition of AXL by Bemcentinib blunted the pathology and improved the outcomes of pregnancy in mice, supporting the therapeutic potential of targeting CD301 + macrophages for treating endometrial fibrosis., (© 2023 The Authors. Published under the terms of the CC BY 4.0 license.)