This study reports the clinical course of two patients with osteogenesis imperfecta who received prenatal human fetal mesenchymal stem cell (MSC) transplantation and postnatal boosting with same‐donor MSCs. Findings suggest that prenatal transplantation of allogeneic human fetal MSCs in osteogenesis imperfecta appears safe and is of likely clinical benefit and that retransplantation with same‐donor cells is feasible. Further studies are required.

Although there is as yet no evidence for a causal link between irisin and/or GIP and PCOS, it is conceivable that irisin and GIP might contribute to the development of PCOS and may also represent novel PCOS biomarkers.

Our results revealed PUR was a common phenomenon in patients who had a cesarean delivery, and morphine-related postoperative analgesia was the main contributing factor.

No abstract

Women with intrauterine fluid accumulation during pregnancy may be at risk for coexistent ectopic pregnancy. High resolution transvaginal color Doppler sonography may be useful to identify a heterotopic pregnancy preoperatively.

This paper investigates the stability of thin viscoelastic liquid film flowing down on a vertical wall using a long-wave perturbation method to find the solution for generalized nonlinear kinematic equations with a free film interface. To begin with, a normal mode approach is employed to obtain the linear stability solution for the film flow. The linear growth rate of the amplitudes, the wave speeds and the threshold conditions are obtained subsequently as the by-products of linear solutions. The results of linear analysis indicate that the viscoelastic parameter k = k 0 /(ρh * 2 0 ) destabilizes the film flow as its magnitude increases. To further investigate practical flow stability conditions, the weak nonlinear dynamics of a film flow are presented by using the method of multiple scales. It is shown that the necessary condition for the existence of such a solution is governed by the Ginzburg-Landau equation.Modelling results indicate that both the subcritical instability and the supercritical stability conditions are possible in a viscoelastic film flow system. The results of nonlinear modelling further indicate that the threshold amplitude εa 0 in the subcritical instability region becomes smaller as the viscoelastic parameter k increases. If the initial finite amplitude of disturbance is greater than the value of threshold amplitude, the system becomes explosively unstable. It is also interesting to note that both the the threshold amplitude and the nonlinear wave speed in the supercritical stability region increase as the value of k increases. Therefore, the flow becomes unstable when the value of k increases. The viscoelastic parameter k indeed plays a significant role in destabilizing the film flow travelling down along a vertical plate.

In mammals, carcinoembryonic antigen cell adhesion molecules (CEACAMs) and pregnancy-specific glycoproteins (PSGs) play important roles in the regulation of pathogen transmission, tumorigenesis, insulin signaling turnover, and fetal–maternal interactions. However, how these genes evolved and to what extent they diverged in humans remain to be investigated specifically. Based on syntenic mapping of chordate genomes, we reveal that diverging homologs with a prototypic CEACAM architecture–including an extracellular domain with immunoglobulin variable and constant domain-like regions, and an intracellular domain containing ITAM motif–are present from cartilaginous fish to humans, but are absent in sea lamprey, cephalochordate or urochordate. Interestingly, the CEACAM/PSG gene inventory underwent radical divergence in various vertebrate lineages: from zero in avian species to dozens in therian mammals. In addition, analyses of genetic variations in human populations showed the presence of various types of copy number variations (CNVs) at the CEACAM/PSG locus. These copy number polymorphisms have 3–80% frequency in select populations, and encompass single to more than six PSG genes. Furthermore, we found that CEACAM/PSG genes contain a significantly higher density of nonsynonymous single nucleotide polymorphism (SNP) compared to the chromosome average, and many CEACAM/PSG SNPs exhibit high population differentiation. Taken together, our study suggested that CEACAM/PSG genes have had a more dynamic evolutionary history in vertebrates than previously thought. Given that CEACAM/PSGs play important roles in maternal–fetal interaction and pathogen recognition, these data have laid the groundwork for future analysis of adaptive CEACAM/PSG genotype-phenotypic relationships in normal and complicated pregnancies as well as other etiologies.

PurposeLovastatin is an effective inhibitor of cholesterol synthesis. A previous study demonstrated that lovastatin can also suppress airway hyperresponsiveness (AHR) in murine model of asthma. We aimed to investigate the effect of lovastatin on mucus secretion and inflammation-associated gene expression in the lungs of murine model of asthma.MethodsFemale BALB/c mice were sensitized and challenged with ovalbumin (OVA) by intraperitoneal injection, and orally administered lovastatin from days 14 to 27 post-injection. Gene expression in lung tissues was analyzed using real-time polymerase chain reaction. AHR and goblet cell hyperplasia were also examined. BEAS-2B human bronchial epithelial cells were used to evaluate the effect of lovastatin on the expression of cell adhesion molecules, chemokines, and proinflammatory cytokines in vitro.ResultsWe showed that lovastatin inhibits the expression of Th2-associated genes, including eotaxins and adhesion molecules, in the lungs of murine model of asthma. Mucin 5AC expression, eosinophil infiltration and goblet cell hyperplasia were significantly decreased in the lung tissue of murine model of asthma treated with lovastatin. Furthermore, lovastatin inhibited AHR and expression of Th2-associated cytokines in bronchoalveolar lavage fluid. However, a high dose (40 mg/kg) of lovastatin was required to decrease specific IgE to OVA levels in serum, and suppress the expression of Th2-associated cytokines in splenocytes. Activated BEAS-2B cells treated with lovastatin exhibited reduced IL-6, eotaxins (CCL11 and CCL24), and intercellular adhesion molecule-1 protein expression. Consistent with this, lovastatin also suppressed the ability of HL-60 cells to adhere to inflammatory BEAS-2B cells.ConclusionsThese data suggest that lovastatin suppresses mucus secretion and airway inflammation by inhibiting the production of eotaxins and Th2 cytokines in murine model of asthma.