Early pregnancy loss is the most common complication of human reproduction. Given the complexities of early development, it is likely that many mechanisms are involved. Knowledge of differences in protein expression in parallel profiling is essential to understand the comprehensive pathophysiological mechanism underlying early pregnancy loss. To identify proteins with different expression profiles related to early pregnancy loss, we applied a proteomic approach and performed two-dimensional gel electrophoresis (2-DE) on six placental villous tissues from patients with early pregnancy loss and six from normal pregnant women, followed by comparison of the silver-stained 2-DE profiles. It was found that 13 proteins were downregulated and 5 proteins were upregulated significantly (P < 0.05) in early pregnancy loss as determined by spot volume. Among them, 10 downregulated and 2 upregulated spots were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Anomalies of these proteins, including three principal antioxidant enzymes (copper/zinc-superoxide dismutase, peroxiredoxin 3, and thioredoxin-like 1 protein), S100 calcium binding protein, galectin-1, chorionic somatomammotropin hormone 1, transthyretin, fas inhibitory molecule, eukaryotic translation elongation factor, RNA-binding protein, ubiquitin-conjugating enzyme E2N, and proteasome beta-subunit, indicate widespread failure in cell regulations and processes such as antioxidative defense, differentiation, cell proliferation, metabolism, apoptosis, transcription, and proteolysis in early pregnancy loss. This study has identified several proteins that are associated with placentation and early development, shedding a new insight into the proteins that may be potentially involved in the pathophysiological mechanisms underlying early pregnancy loss.
Polycystic ovary syndrome (PCOS) is one of the most common female endocrine disorders and a leading cause of female subfertility. The mechanism underlying the pathophysiology of PCOS remains to be illustrated. Here, we identify two alternative splice variants (ASVs) of the androgen receptor (AR), insertion and deletion isoforms, in granulosa cells (GCs) in ∼62% of patients with PCOS. AR ASVs are strongly associated with remarkable hyperandrogenism and abnormalities in folliculogenesis, and are absent from all control subjects without PCOS. Alternative splicing dramatically alters genome-wide AR recruitment and androgeninduced expression of genes related to androgen metabolism and folliculogenesis in human GCs. These findings establish alternative splicing of AR in GCs as the major pathogenic mechanism for hyperandrogenism and abnormal folliculogenesis in PCOS.n ovarian follicles, oocytes are surrounded by granulosa cells (GCs), which have crucial endocrine functions. Polycystic ovary syndrome (PCOS) is a heterogeneous hormonal disorder affecting one in 15 women, and is one of the most common causes of female infertility (1). Hyperandrogenism and abnormal follicle development, associated with excessively small follicles and ovulatory dysfunction largely due to GCs dysfunction, characterize the pathogenesis of PCOS. Although the underlying etiology remains unclear, androgens and the androgen receptor (AR) are considered important on account of their critical roles in the prevalence of hyperandrogenism and ovarian folliculogenesis in this disorder (1-3).Androgens elicit their effects upon binding to AR, and AR functions primarily via genomic activities as a nuclear receptor. In the ovary, AR is predominantly expressed by GCs throughout most stages of follicular development. Nearly all reproductive phenotypes observed in global AR knockout mice have been attributed to a lack of AR expression in GCs (3). Haploinsufficiency for exon 3-deleted mutant AR is associated with a premature reduction in female fecundity (4), verifying the crucial role of classical genomic AR activity in normal ovarian function. Clinical studies have suggested that PCOS might be associated with AR (CAG)n repeats (5) and rs6152A (6) gene polymorphisms. These studies promoted interest in investigating the effects of AR in GC dysfunction in PCOS women. We therefore hypothesized that abnormally expressed and/or dysfunctional AR plays an important role in the pathogenesis of PCOS. ResultsAlternative Splice Variants of AR in GCs of PCOS Women. Nested RT-PCR (Fig. S1A) was used to amplify AR cDNAs from GCs of Southeastern Han Chinese women undergoing in vitro fertilization and embryo transfer. We identified two alternative splice variants (ASVs) expressed exclusively in PCOS women. One ASV inserted 69 bp into intron 2 (ivs2) between exons 2 and 3 (insertion isoform, ins) whereas the other skipped exon 3 (deletion isoform, del), as demonstrated by agarose gel electrophoresis (Fig. 1A) and PCR product sequencing (Fig. 1B). AR ASVs were not detected in ...
An effective iodized salt program has brought iodine sufficiency to most of China, but pregnant women in some areas may still risk deficiency and need further supplements. We suggest other countries and international agencies pay more attention to pregnancy, where iodine deficiency has its worst consequences.
Children born to ovarian-hyperstimulated women displayed cardiovascular dysfunctions. The underlying mechanisms may involve the effects of supraphysiological estradiol and progesterone levels.
High levels of serum CA-125 were found not only in the EOC, but also in some NMGDs, especially in the reproductive patients with complaints of acute abdomen symptoms or abnormal vaginal bleeding.
Ectopic pregnancy is identified with the widely-applied assisted reproductive technology (ART). Bilateral ectopic pregnancy is a rare form of ectopic pregnancy which is difficult to be diagnosed at the pre-operation stage. In this paper, we presented an unusual case of heterochronic bilateral ectopic pregnancy after stimulated intrauterine insemination (IUI), where there has been a delay of 22 d between the diagnoses of the two ectopic pregnancies. Literature was reviewed on the occurrence of bilateral ectopic pregnancy during the past four years in the MEDLINE database. We found 16 cases of bilateral ectopic pregnancy reported since 2008, and analyzed the characteristics of those cases of bilateral ectopic pregnancy. We emphasize that ovulation induction and other ARTs may increase the risk of bilateral ectopic pregnancy. Because of the difficulty in identification of bilateral ectopic pregnancy by ultrasonography, the clinician should be aware that the treatment of one ectopic pregnancy does not preclude the occurrence of a second ectopic pregnancy in the same patient and should pay attention to the intra-operation inspection of both side fallopian tubes in any ectopic pregnancy case.
The manual contour mode for 3D-PDA vascular measurements has better interobserver and intraobserver reproducibility than the automatic sphere contour mode. It is especially useful for measuring tumor tissues with irregular shapes and vascularity.
Congenital aortic arch anomaly is usually found in association with other cardiovascular malformations or chromosomal anomalies. Double aortic arch (DAA) is an uncommon but significant type of aortic arch anomaly, and it may lead to compression of the trachea and esophagus by forming a complete vascular ring. Aortic arch anomalies occur in about 15% of patients with D-transposition of the great arteries (D-TGA) (Cui et al., 2007). Here we report an unusual case of combined D-TGA and DAA diagnosed by ultrasound fetal echocardiogram. To the best of our knowledge, this is the first reported case in the literature.A 27-year-old Chinese woman presented at our hospital for a routine prenatal ultrasound examination at 24 weeks of gestation, with an unremarkable pregnancy history. She had an insignificant past pregnancy history and denied any family history of congenital malformations or genetic disorders. The routine ultrasound examination revealed an otherwise healthy female fetus with an abnormal outflow tract in the heart. To further evaluate the abnormality, we performed a complete ultrasound cardiovascular examination, using a GE Voluson 730 Expert Ultrasound Machine and a 3.5 MHz linear transducer. The fetal heart was found to be normally sized and normally situated in the chest cavity, with an atrial situs solitus, atrioventricular concordance, and ventriculo-arterial discordance. The foramen ovale flap was seen in the left atrium. A small ventricular septal defect was identified in the four-chamber view, showing a left-to-right shunt in the systolic phase and a rightto-left shunt in the diastolic phase through the defect. The great arteries arose from the heart in an abnormally parallel arrangement, with the aorta arising anteriorly from the right ventricle and the pulmonary trunk arising posteriorly from the left ventricle. The aorta and the pulmonary trunk were normal in size, measuring 5 and 6 mm in diameter, respectively. In transverse sonogram, the ascending aorta was found to give rise to two symmetrical aortic arches with one on the left and the other on the right (Figure 1). Each aortic arch gave rise to a brachiocephalic artery divided into the common carotid artery and then the subclavian artery. Distal to the brachiocephalic branches, two aortic arches joined posteriorly to form a left-sided descending aorta. The remaining anatomy of the heart and the great vessels was normal. Flow patterns were normal in the mitral valve, tricuspid valve, inferior vena cava, ductus venosus, and umbilical vein, upon pulsed Doppler interrogation. The maximum velocity across the pulmonary and the aortic valve was 73 and 90 cm/s, respectively.To further evaluate the fetal anomaly, we did an amniocentesis followed by karyotyping. The fetus was found to have a normal karyotype (46,XX). After receiving the reports and information of a poor postnatal prognosis, the parents decided to terminate the pregnancy. A female fetus was delivered stillborn. A full body autopsy was done, which confirmed the prenatal diagnosis of DAA an...
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