RESUMEN
Background. Patients with AAA face a complex decision, and knowledge of the risks and benefits of each treatment option is essential to informed decision-making. Here we assess the current information on the internet accessible to patients regarding the management of AAA. Study Design. We performed a search on Google using the keywords "abdominal aortic aneurysm" and reviewed the top 50 web sites. We focused on information related to treatment options and alternatives to treatment and the risks of each option. Results. Twenty-seven websites were included in the study. Nearly 30% of websites discussed the risk of mortality and myocardial infarction after open surgery, compared to only 7.4% for both risks after EVAR. Other complications were listed by fewer websites. Fifty-five percent of websites reported that patients had a faster recovery following EVAR, but only 18.5% mentioned the risk of reintervention after EVAR or the need for long-term surveillance with CT scans. Conclusions. While most websites included descriptive information on AAA and mentioned the potential treatment options available to patients, the discussion of the risks of open surgery and EVAR was inadequate. These results suggest that websites frequently accessed by patients lack important information regarding surgical risk.
RESUMEN
Gap junctions (GJs) are membrane-spanning channels that facilitate intercellular communication by allowing small signaling molecules (e.g. calcium ions, inositol phosphates, and cyclic nucleotides) to pass from cell to cell. Over the past two decades, many studies have described a role for GJ intercellular communication (GJIC) in the proliferation and differentiation of many cells, including bone cells. Recently, we reported that megakaryocytes (MKs) enhance osteoblast (OB) proliferation by a juxtacrine signaling mechanism. Here we determine whether this response is facilitated by GJIC. First we demonstrate that MKs express connexin 43 (Cx43), the predominant GJ protein expressed by bone cells, including OBs. Next, we provide data showing that MKs can communicate with OBs via GJIC, and that the addition of two distinct GJ uncouplers, 18alpha-glycyrrhetinic acid (alphaGA) or oleamide, inhibits this communication. We then demonstrate that inhibiting MK-mediated GJIC further enhances the ability of MKs to stimulate OB proliferation. Finally, we show that while culturing MKs with OBs reduces gene expression of several differentiation markers/matrix proteins (type I collagen, osteocalcin, and alkaline phosphatase), reduces alkaline phosphatase enzymatic activity, and decreases mineralization in OBs, blocking GJIC does not result in MK-induced reductions in OB gene expression, enzymatic levels, or mineralized nodule formation. Overall, these data provide evidence that GJIC between MKs and OBs is functional, and that inhibiting GJIC in MK-OB cultures enhances OB proliferation without apparently altering differentiation when compared to similarly treated OB cultures. Thus, these observations regarding MK-OB GJIC inhibition may provide insight regarding potential novel targets for anabolic bone formation.