Stretched exponential relaxation, exp[−(t/τ ) β ], fits many relaxation processes in disordered and quenched electronic and molecular systems, but it is widely believed that this function has no microscopic basis, especially in the case of molecular relaxation. For electronic relaxation the appearance of the stretched exponential is often described in the context of dispersive transport, where β is treated as an adjustable parameter, but in almost all cases it is generally assumed that no microscopic meaning can be assigned to 0 < β(T ) < 1 even at T = T g , a glass transition temperature. We show that for molecular relaxation β(T g ) can be understood, providing that one separates extrinsic and intrinsic effects, and that the intrinsic effects are dominated by two magic numbers, β SR = 3 5 for short-range forces, and β K = 3 7 for long-range Coulomb forces, as originally observed by Kohlrausch for the decay of residual charge on a Leyden jar. Our mathematical model treats relaxation kinetics using the Lifshitz-Kac-Luttinger diffusion to traps depletion model in a configuration space of effective dimensionality, the latter being determined using axiomatic set theory and Phillips-Thorpe constraint theory. The experiments discussed include ns neutron scattering experiments, particularly those based on neutron spin echoes which measure S(Q, t) directly, and the traditional linear response measurements which span the range from µs to s, as collected and analysed phenomenologically by Angell, Ngai, Böhmer and others. The electronic materials discussed include a-Si:H, granular C 60 , semiconductor nanocrystallites, charge density waves in TaS 3 , spin glasses, and vortex glasses in high-temperature semiconductors. The molecular materials discussed include polymers, network glasses, electrolytes and alcohols, Van der Waals supercooled liquids and glasses, orientational glasses, water, fused salts, and heme proteins. In the intrinsic cases the theory of β(T g ) is often accurate to 2%, which is often better than the quoted experimental accuracies ∼5%. The extrinsic cases are identified by explicit structural signatures which are discussed at length. The discussion also includes recent molecular dynamical simulations for metallic glasses, spin glasses, quasicrystals and polymers which have achieved the intermediate relaxed Kohlrausch state and which have obtained values of β in excellent agreement with the prediction of the microscopic theory.

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Introduction: Preclinical and clinical studies suggest that cannabidiol (CBD) found in Cannabis spp. has broad therapeutic value. CBD products can currently be purchased online, over the counter and at Cannabis-specific dispensaries throughout most of the country, despite the fact that CBD is generally deemed a Schedule I controlled substance by the U.S. Drug Enforcement Administration and renounced as a dietary supplement ingredient by the U.S. Food and Drug Administration. Consumer demand for CBD is high and growing, but few studies have examined the reasons for increasing CBD use.Materials and Methods: A self-selected convenience sample (n = 2409) was recruited via an online survey designed to characterize whom, how, and why individuals are currently using CBD. The anonymous questionnaire was accessed from October 25, 2017 to January 25, 2018. Participants were recruited through social media.Results: Almost 62% of CBD users reported using CBD to treat a medical condition. The top three medical conditions were pain, anxiety, and depression. Almost 36% of respondents reported that CBD treats their medical condition(s) “very well by itself,” while only 4.3% reported “not very well.” One out of every three users reported a nonserious adverse effect. The odds of using CBD to treat a medical condition were 1.44 (95% confidence interval, 1.16–1.79) times greater among nonregular users of Cannabis than among regular users.Conclusion: Consumers are using CBD as a specific therapy for multiple diverse medical conditions—particularly pain, anxiety, depression, and sleep disorders. These data provide a compelling rationale for further research to better understand the therapeutic potential of CBD.

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Osteoprotegerin (OPG) binds the ligand for receptor activator of nuclear factor B (RANKL) to prevent association with its receptor RANK and inhibit osteoclast-mediated bone resorption. OPG has been reported, recently, to inhibit tumor necrosis factor-related apoptosis-induced ligand (TRAIL)-induced tumor cell apoptosis. This raises the possibility that OPG may play a unique role in regulating these two signaling pathways. However, there are little data on the interactions between OPG, RANKL, and TRAIL, and the relative affinity of OPG for these two ligands is unknown. In the present study we examined the ability of OPG to bind native human TRAIL and RANKL under physiological conditions. Native TRAIL was expressed in Escherichia coli, purified to homogeneity, and shown to induce human myeloma cell apoptosis. OPG inhibited native TRAIL from binding the TRAILR1 at 37°C in vitro. Similarly, OPG prevented RANKL from binding to RANK. TRAIL also prevented OPG-mediated inhibition of RANKL from binding RANK. The affinity of OPG for native TRAIL and RANKL at 37°C was determined by plasmon surface resonance analysis. OPG had a binding affinity for TRAIL of 45 nM, whereas the affinity of OPG for RANKL was 23 nM. These data suggest that OPG can bind both RANKL and TRAIL and that the affinity of OPG for these two ligands is of a similar order of magnitude. Furthermore, OPG prevented TRAIL-mediated reductions in cell viability, whereas TRAIL inhibited OPG-mediated inhibition of osteoclastogenesis in vitro. This highlights the pivotal role of OPG in regulating the biology of both RANKL and TRAIL.Bone is a complex tissue that is constantly being replaced through the process of bone remodeling. This process is mediated by the removal of bone by osteoclasts and its subsequent replacement by osteoblasts. Disruptions to the normal, coupled, activity of these cell types leads to skeletal disorders. The activity of osteoclasts and osteoblasts is regulated by the concerted actions of specific messengers, including hormones, adhesion molecules, local growth factors, and cytokines. One family of cytokines that plays a central role in regulating osteoclast cell function is the tumor necrosis factor (TNF) 2 superfamily (1). Although a number of TNF family members has been shown to regulate osteoclast formation and function, one system has been shown to play a central role. This is the osteoprotegerin (OPG)/ligand for receptor activator of NFB (RANKL)/receptor activator of NFB (RANK) pathway (2).Osteoprotegerin was first identified through screening a fetal rat intestinal cDNA library, searching an expressed sequence tag data base, and by direct purification from the supernatant derived from human fibroblasts (3-5). Analysis of the protein sequence identified structural motifs that were similar to those seen in members of the TNF receptor family, and thus OPG was identified as a new member of the TNF receptor family (3, 6). However, OPG lacks a transmembrane domain and, unlike the majority of members of this family, is secreted into the ext...