Caesarean scar-unusual site of ectopic pregnancy: a rare case report

Scar ectopic pregnancy is the rarest type of ectopic pregnancy; however, it is becoming more common around the world. It is a life-threatening condition caused by abnormal embryo implantation in the myometrium and fibrous tissue of the prior scar after a caesarean section, hysterotomy, myomectomy, or metroplasty. With a better understanding of the disease and an increased rate of caesarean section, there is a significant increase in this condition. Early and correct diagnosis, combined with prompt treatment, can help to avoid pregnancy problems including haemorrhage and uterine rupture, as well as preserve fertility

Semaphorin 3B Is a 1,25-Dihydroxyvitamin D 3 -Induced Gene in Osteoblasts that Promotes Osteoclastogenesis and Induces Osteopenia in Mice

The vitamin D endocrine system is important for skeletal homeostasis. ] is the bioactive metabolite of vitamin D. This hormone functions through the vitamin D receptor (VDR), a member of the nuclear hormone receptor superfamily, to regulate the transcription of target genes in a number of tissues including the intestine, bone, parathyroid gland, skin, and a variety of other systems (1, 2). The 1,25-(OH) 2 D 3 /VDR endocrine system functions in diverse biological processes, such as hair follicle cycling, mammary gland development, and immune cell function (2). One of the most profound actions of 1,25-(OH) 2 D 3 is to protect skeletal integrity because deficiencies in either the hormone or the receptor result in undermineralized bones Acting in concert with PTH, 1,25-(OH) 2 D 3 preserves bone mineralization primarily by maintaining calcium and phosphate homeostasis. 1,25-(OH) 2 D 3 controls serum levels of these minerals by stimulating calcium and phosphate absorption by the intestine, by increasing reabsorption of calcium and phosphate in the kidney, and by liberating calcium and phosphate from skeletal stores (3). When dietary sources of calcium are inadequate, 1,25-(OH) 2 D 3 promotes osteoclastogenesis and bone resorption, in part, by stimulating osteoblasts to express receptor activator of nuclear factor-B ligand (RANKL) (5), a molecule essential for osteoclast formation and function (6, 7). Under conditions of normocalcemia, the 1,25-(OH) 2 D 3 /VDR endocrine system also modulates osteoblast differentiation and mineralization (8-11). Thus, 1,25-(OH) 2 D 3 functions both systemically to regulate serum concentrations of calcium and phosphate and locally to fine-tune the balance between bone formation and bone resorption. However, with the exception of RANKL and a few bone matrix protein

The peroxisome proliferator-activated receptor (PPAR) alpha agonist fenofibrate maintains bone mass, while the PPAR gamma agonist pioglitazone exaggerates bone loss, in ovariectomized rats

<p>Abstract</p> <p>Background</p> <p>Activation of peroxisome proliferator-activated receptor (PPAR)gamma is associated with bone loss and increased fracture risk, while PPARalpha activation seems to have positive skeletal effects. To further explore these effects we have examined the effect of the PPARalpha agonists fenofibrate and Wyeth 14643, and the PPARgamma agonist pioglitazone, on bone mineral density (BMD), bone architecture and biomechanical strength in ovariectomized rats.</p> <p>Methods</p> <p>Fifty-five female Sprague-Dawley rats were assigned to five groups. One group was sham-operated and given vehicle (methylcellulose), the other groups were ovariectomized and given vehicle, fenofibrate, Wyeth 14643 and pioglitazone, respectively, daily for four months. Whole body and femoral BMD were measured by dual X-ray absorptiometry (DXA), and biomechanical testing of femurs, and micro-computed tomography (microCT) of the femoral shaft and head, were performed.</p> <p>Results</p> <p>Whole body and femoral BMD were significantly higher in sham controls and ovariectomized animals given fenofibrate, compared to ovariectomized controls. Ovariectomized rats given Wyeth 14643, maintained whole body BMD at sham levels, while rats on pioglitazone had lower whole body and femoral BMD, impaired bone quality and less mechanical strength compared to sham and ovariectomized controls. In contrast, cortical volume, trabecular bone volume and thickness, and endocortical volume were maintained at sham levels in rats given fenofibrate.</p> <p>Conclusions</p> <p>The PPARalpha agonist fenofibrate, and to a lesser extent the PPARaplha agonist Wyeth 14643, maintained BMD and bone architecture at sham levels, while the PPARgamma agonist pioglitazone exaggerated bone loss and negatively affected bone architecture, in ovariectomized rats.</p

Estrogen/Estrogen Receptor Alpha Signaling in Mouse Posterofrontal Cranial Suture Fusion

BACKGROUND: While premature suture fusion, or craniosynostosis, is a relatively common condition, the cause is often unknown. Estrogens are associated with growth plate fusion of endochondral bones. In the following study, we explore the previously unknown significance of estrogen/estrogen receptor signaling in cranial suture biology. METHODOLOGY/PRINCIPAL FINDINGS: Firstly, estrogen receptor (ER) expression was examined in physiologically fusing (posterofrontal) and patent (sagittal) mouse cranial sutures by quantitative RT-PCR. Next, the cranial suture phenotype of ER alpha and ER beta knockout (alphaERKO, betaERKO) mice was studied. Subsequently, mouse suture-derived mesenchymal cells (SMCs) were isolated; the effects of 17-beta estradiol or the estrogen antagonist Fulvestrant on gene expression, osteogenic and chondrogenic differentiation were examined in vitro. Finally, in vivo experiments were performed in which Fulvestrant was administered subcutaneously to the mouse calvaria. Results showed that increased ERalpha but not ERbeta transcript abundance temporally coincided with posterofrontal suture fusion. The alphaERKO but not betaERKO mouse exhibited delayed posterofrontal suture fusion. In vitro, addition of 17-beta estradiol enhanced both osteogenic and chondrogenic differentiation in suture-derived mesenchymal cells, effects reversible by Fulvestrant. Finally, in vivo application of Fulvestrant significantly diminished calvarial osteogenesis, inhibiting suture fusion. CONCLUSIONS/SIGNIFICANCE: Estrogen signaling through ERalpha but not ERbeta is associated with and necessary for normal mouse posterofrontal suture fusion. In vitro studies suggest that estrogens may play a role in osteoblast and/or chondrocyte differentiation within the cranial suture complex

An evaluation of morphine dependence in the rat

A semiquantitatiye method for assessing the degree of physical dependence upon morphine in rats has been examined. A time-course measure of dependence due to repetitive and increasing daily doses of morphine was obtained between one and eleven days of treatment utilizing a narcotic antagonist to precipitate withdrawal and scoring six specific withdrawal symptoms. High starting doses of morphine produced a miximal withdrawal score after two days which remained constant until the eleventh day. However, low starting doses of morphine produced a more typical dose-effect relationship from day one through day seven. The scoring system utilized in this study was analyzed and found to be acceptable, but by no means optimal to assess the degree of morphine physical dependence. The effects upon the narcotic antagonist precipitated withdrawal score, and therefore, the degree of physical dependence upon morphine, of concomitantly administered drugs was investigated. Dextroamphetamine, apomorphine and atropine were shown to decrease the total withdrawal score whereas levoamphetamine, haloperidol and atropine methyl nitrate failed to reduce significantly the total withdrawal score. Based upon these data a hypothetical model for the development of morphine physical dependence was, proposed. Although this model appeared to hold for total withdrawal scores certain discrepancies became apparent when drug-induced effects upon individual withdrawal symptoms were analyzed. Irrespective of mechanism, the research shows a clear differential effect between the two isomers of amphetamine, which could be due to differences on central dopaminergic mechanisms.Pharmacy, College o

The Wnt antagonist secreted frizzled-related protein-1 is a negative regulator of trabecular bone formation in adult mice

Previous studies have associated activation of canonical Wnt signaling in osteoblasts with elevated bone formation. Here we report that deletion of the murine Wnt antagonist, secreted frizzled-related protein (sFRP)-1, prolongs and enhances trabecular bone accrual in adult animals. sFRP-1 mRNA was expressed in bones and other tissues of +/+ mice but was not observed in -/- animals. Despite its broad tissue distribution, ablation of sFRP-1 did not affect blood and urine chemistries, most nonskeletal organs, or cortical bone. However, sFRP-1-/- mice exhibited increased trabecular bone mineral density, volume, and mineral apposition rate when compared with +/+ controls. The heightened trabecular bone mass of sFRP-1-/- mice was observed in adult animals between the ages of 13-52 wk, occurred in multiple skeletal sites, and was seen in both sexes. Mechanistically, loss of sFRP-1 reduced osteoblast and osteocyte apoptosis in vivo. In addition, deletion of sFRP-1 inhibited osteoblast lineage cell apoptosis while enhancing the proliferation and differentiation of these cells in vitro. Ablation of sFRP-1 also increased osteoclastogenesis in vitro, although changes in bone resorption were not observed in intact animals in vivo. Our findings demonstrate that deletion of sFRP-1 preferentially activates Wnt signaling in osteoblasts, leading to enhanced trabecular bone formation in adults