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Background Selective fetal restriction growth (sFGR) is one of the common diseases of monochorionic diamniotic (MCDA) twin pregnancies, resulting in many adverse outcomes. At present, second trimester ultrasonography is widely used in the prenatal diagnosis of sFGR, but the diagnostic effectiveness is still uncertain. The aim of this study is to assess the diagnostic accuracy of second trimester Doppler ultrasound measurements for sFGR. Methods A retrospective study included 280 pregnant women (118 with and 162 without sFGR) with MCDA pregnancies was conducted in the fetal medicine center from Leiden University Medical Center from January 2008 to December 2013. The women participating had already undergone an ultrasound examination in the second trimester. The postnatal criteria of sFGR was a single birth weight (BW) 95th percentile). According to the diagnosis of sFGR after birth, we evaluate diagnostic effectiveness of Doppler ultrasound in the second trimester for sFGR. Results Of these 280 participants, the mean age was 32.06 ± 4.76 years. About 43.9% of pregnant women were primiparas. The ability of second trimester Doppler ultrasound to accurately diagnosed sFGR is 75.4%, missed diagnosis rate and the misdiagnosis rate were 24.6% and 10.5% respectively. The ROC curve indicated that the combination of AC discordance, EFW discordance, and small fetal UA blood flow was the best diagnostic indicator of sFGR in MCDA pregnancy with the AUC was 0.882 (95%CI, 0.839–0.926). Conclusions Second trimester Doppler and ultrasound measurements is an effective method for early prenatal diagnosis of sFGR. The combined indicator of AC discordance, EFW discordance, and the small fetal UA blood flow reaches highest diagnostic value.

Background Osteoporotic vertebral compression fracture, always accompanied with pain and height loss of vertebral body, has a significant negative impact on life quality of patients. Vertebroplasty or kyphoplasty is minimal invasive techniques to reconstruct the vertebral height and prevent further collapse of the fractured vertebrae by injecting polymethylmethacrylate into vertebral body. However, recompression of polymethylmethacrylate augmented vertebrae with significant vertebral height loss and aggressive local kyphotic was observed frequently after VP or KP. The purpose of this study was to investigate the effect of polymethylmethacrylate distribution on recompression of the vertebral body after vertebroplasty or kyphoplasty surgery for osteoporotic vertebral compression fracture. Methods A total of 281 patients who were diagnosed with vertebral compression fracture (T5-L5) from June 2014 to June 2016 and underwent vertebroplasty or kyphoplasty by polymethylmethacrylate were retrospectively analyzed. The X-ray films at 1 day and 12 months after surgery were compared to evaluate the recompression of operated vertebral body. Patients were divided into those without recompression (non-recompression group) and those with recompression (recompression group). Polymethylmethacrylate distribution pattern, including location and relationship to endplates, was compared between the two groups by lateral X-ray film. Multivariate logistic regression analysis was performed to assess the potential risk factors associated with polymethylmethacrylate distribution for recompression. Results One hundred and six (37.7%) patients experienced recompression after surgery during the follow-up period. The polymethylmethacrylate distributed in the middle of vertebral body showed significant differences between two groups. In non-recompression group, the polymethylmethacrylate in the middle portion of vertebral body were closer to endplates than that in the recompression group (upper: t = 31.41, p

Background Cancer stem cells (CSCs) are proposed to be responsible for high recurrence rate in cervical carcinoma. Reagents that can suppress the proliferation and differentiation of CSCs would provide new opportunities to fight against tumor recurrence. Doxycycline has been reported as a potential anti-cancer compound. However, few studies investigated its inhibitory effect against cervical cancer stem cells. Methods HeLa cells were cultured in cancer stem cell conditional media in a poly-hema-treated dish. In this non-adhesive culture system, HeLa cells were treated with cisplatin until some cells survived and formed spheroids, which were then collected and injected into the immunodeficient mice. Cisplatin was administered every three days for five times. The tumor xenografts with CSC enrichment were cultured in cancer stem cell specific medium again to form tumorsphere, which we called HeLa-CSCs. Expression of cancer stem cell markers in HeLa-CSCs was measured by flow cytometry and qPCR. HeLa-CSCs were then treated with doxycycline. Proliferation and differentiation rates were determined by the size of spheres formed in vitro and tumor formed in vivo. Results We developed a new strategy to selectively enrich CSCs from human cervical carcinoma cell line HeLa, and these HeLa-CSCs are CD133+/CD49f+ cell populations with significantly enhanced expression of stem cell markers. When these HeLa-CSCs were treated with doxycycline, the colony formation, proliferation, migration and invasion, and differentiation were all suppressed. Meanwhile, stem cell markers SOX-2, OCT-4, NANOG, NOTCH and BMI-1 decreased in doxycycline treated cells, so as the surface markers CD133 and CD49f. Furthermore, proliferation markers Ki67 and PCNA were also decreased by doxycycline treatment in the in vivo xenograft mouse model. Conclusions Cancer stem cells are enriched from sphere-forming and chemoresistant HeLa-derived tumor xenografts in immunodeficient mice. Doxycycline inhibits proliferation, invasion, and differentiation, and also induces apoptosis of these HeLa-CSCs in vitro and in vivo.

STIM1 is a Ca2+ sensor within the ER membrane known to activate the plasma membrane store-operated Ca2+ channel upon depletion of its target ion in the ER lumen. This activation is a crucial step to initiate the Ca2+ signaling cascades within various cell types. Human STIM1 is a 77.4 kDa protein consisting of various domains that are involved in Ca2+ sensing, oligomerization, and channel activation and deactivation. In this study, we identify the domains and boundaries in which functional and stable recombinant human STIM1 can be produced in large quantities. To achieve this goal, we cloned nearly 200 constructs that vary in their initial and terminal residues, length and presence of the transmembrane domain, and we conducted expression and purification analyses using these constructs. The results revealed that nearly half of the constructs could be expressed and purified with high quality, out of which 25% contained the integral membrane domain. Further analyses using surface plasmon resonance, nuclear magnetic resonance and a thermostability assay verified the functionality and integrity of these constructs. Thus, we have been able to identify the most stable and well-behaved domains of the hSTIM1 protein, which can be used for future in vitro biochemical and biophysical studies. Published version

Inflammation plays an important role in the etiology and pathophysiology of spontaneous preterm birth (SPTB), and selenoprotein S (SEPS1) is involved in regulating the inflammatory response. Recently the G-105A promoter polymorphism in SEPS1 was shown to increase pro-inflammatory cytokine expression. We examined whether this functional polymorphism was related to the risk of SPTB in a Chinese population. We also examined the impact of premature rupture of membranes (PROM) on susceptibility to SPTB. The SEPS1 G-105A polymorphism was genotyped in 569 preterm singleton neonates and 673 term neonates by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. χ (2) tests and logistic regression analyses were used to calculate the odds ratios (ORs) and 95% confidence intervals (95% CIs). We observed that, compared with the GG genotype, -105A positive genotypes (GA + AA genotypes) were associated with significantly increased susceptibility to SPTB (adjusted OR, 1.87; 95% CI, 1.36-2.57; P

Coxsackieviruses A10 (CV-A10) and A6 (CV-A6) have been associated with increasingly occurred sporadic hand-foot-mouth disease (HFMD) cases and outbreak events globally. However, our understanding of epidemiological and genetic characteristics of these new agents remains far from complete. This study was to explore the circulation of CV-A10 and CV-A6 in HFMD and their genetic characteristics in China. A hospital based surveillance was performed in three heavily inflicted regions with HFMD from March 2009 to August 2011. Feces samples were collected from children with clinical diagnosis of HFMD. The detection and genotyping of enteroviruses was performed by real-time PCR and sequencing of 5′UTR/VP1 regions. Phylogenetic analysis and selection pressure were performed based on the VP1 sequences. Logistic regression model was used to identify the effect of predominant enterovirus serotypes in causing severe HFMD. The results showed 92.0% of 1748 feces samples were detected positive for enterovirus, with the most frequently presented serotypes as EV-71 (944, 54.0%) and CV-A16 (451, 25.8%). CV-A10 and CV-A6 were detected as a sole pathogen in 82 (4.7%) and 44 (2.5%) cases, respectively. Infection with CV-A10 and EV-71 were independently associated with high risk of severe HFMD (OR = 2.66, 95% CI: 1.40–5.06; OR = 4.81, 95% CI: 3.07–7.53), when adjusted for age and sex. Phylogenetic analysis revealed that distinct geographic and temporal origins correlated with the gene clusters based on VP1 sequences. An overall ω value of the VP1 was 0.046 for CV-A10 and 0.047 for CV-A6, and no positively selected site was detected in VP1 of both CV-A10 and CV-A6, indicating that purifying selection shaped the evolution of CV-A10 and CV-A6. Our study demonstrates variety of enterovirus genotypes as viral pathogens in causing HFMD in China. CV-A10 and CV-A6 were co-circulating together with EV-71 and CV-A16 in recent years. CV-A10 infection might also be independently associated with severe HFMD.