Endochondral bone formation is complex and requires the coordination of signals from several factors and multiple cell types. Thus, chondrocyte differentiation is regulated by factors synthesized by both chondrocytes and cells in the perichondrium. Previously, we showed that expression of a dominant-negative form of the transforming growth factor beta (TGF-beta) type II receptor in perichondrium/periosteum resulted in increased hypertrophic differentiation in growth plate chondrocytes, suggesting a role for TGF-beta signaling to the perichondrium in limiting terminal differentiation in vivo. Using an organ culture model, we later demonstrated that TGF-beta1 inhibits chondrocyte proliferation and hypertrophic differentiation by two separate mechanisms. Inhibition of hypertrophic differentiation was shown to be dependent on Parathyroid hormone-related peptide (PTHrP) and expression of PTHrP mRNA was stimulated in the perichondrium after treatment with TGF-beta1. In this report, the hypothesis that the perichondrium is required for the effects of TGF-beta1 on growth and/or hypertrophic differentiation in mouse metatarsal organ cultures is tested. Treatment with TGF-beta1 inhibited expression of type X collagen mRNA in metatarsal cultures with the perichondrium intact. In contrast, hypertrophic differentiation as measured by expression of Type X collagen was not inhibited by TGF-beta1 in perichondrium-free cultures. TGF-beta1 added to intact cultures inhibited BrdU incorporation in chondrocytes and increased incorporation in the perichondrium; however, TGF-beta1 treatment stimulated chondrocyte proliferation in metatarsals from which the perichondrium had been enzymatically removed. These results suggest that the TGF-beta1-mediated regulation of both chondrocyte proliferation and hypertrophic differentiation is dependent upon the perichondrium. Thus, one or several factors from the perichondrium might mediate the way chondrocytes respond to TGF-beta1.

Purpose This paper reports the results of a survey of library staff members working with a library makerspace or with makerspace-related technologies. The purpose of this paper is to identify who is working with library makerspaces, what methods of training they have used, what training methods they prefer, and what topics they would like to see included in professional development and continuing education. Design/methodology/approach A 17-question survey was posted to two library makerspace-related listservs for two weeks. Findings The survey results found a varied array of job title of individuals working with library makerspaces. It also identified the preferred training methods, as well as the varied topics requested for professional development, showing a large need for a makerspace training in library staff. Originality/value This is the first study conducted about the preferred methods and topics of professional development and continuing education of library staff members working with makerspaces or makerspace-related technologies.

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Electrical stimulation and low intensity pulsed ultrasound technologies for bone healing may have some beneficial effects on radiographic assessment outcomes (e.g., spinal fusion rate, radiographic nonunion rates, number of days to radiographic healing) and clinical assessment outcomes (e.g., mouth opening, wrist and shoulder mobility, exteroceptive sensation, and wound healing), but may not improve outcomes that are important to patients (e.g., functional recovery). Pain may be reduced by electrical bone growth stimulation devices, but not by low intensity pulsed ultrasound. No adverse events (AEs) related to the low intensity pulsed ultrasound device were reported. It is unknown if there are AEs related to electrical stimulation devices (no evidence found). Low intensity pulsed ultrasound for treatment of fresh tibial fractures was not cost-effective compared with placebo from either a payer perspective or societal perspective within the Canadian context. It is unknown if electrical bone growth stimulator devices are cost-effective (no evidence found).