Positron annihilation spectroscopy has been applied to measure the free-volume hole distributions in polystyrene (Tg = 95 °C, molar weight 105 000) as a function of temperature. The hole volume distributions are determined from orthopositronium distributions. The hole volumes are distributed between 35 and 200 Á3. The fractions of free volumes are distributed from 2.0% to 11% of total volume. The obtained free-volume distributions are compared and discussed with the experimental distributions obtained by photochromic and florescent probes and with the Turnbull-Cohen free-volume theory. The distributions of free-volume fractions fit well with the theoretical function according to the Simha-Somcynsky lattice model.

Free‐volume hole sizes, fractions, and distributions in a series of polycarbonate‐based polymers are measured by using positron annihilation lifetime (PAL) spectroscopy. Correlations between the obtained free‐volume hole properties and gas diffusion coefficients are observed. © 1995 John Wiley & Sons, Inc.

Positron annihilation spectroscopy has been applied to measure the free-volume hole distributions in an epoxy (DGEBA/DDH/DAB) polymer (Tg = 62 "C) as a function of quasi-isotropic pressure in the range of 0-14 kbar. The hole radius and volume distributions determined from orthopositronium lifetime distributions are found to be dramatically shifted to small values and to be narrower as a function of preasure. The hole radius distributions are found to be between 3.5 and 0.5 A and to have maxima at 2.45, 2.02, 1.40, and 0.78 A under the external pressure of 0.001, 1.8, 4.9, and 14.0 kbar, respectively.

Although TRPV1 channels represent a key player of noxious heat sensation, the precise mechanisms for thermal hyperalgesia remain unknown. We report here that conditional knockout of deSUMOylation enzyme, SENP1, in mouse dorsal root ganglion (DRG) neurons exacerbated thermal hyperalgesia in both carrageenan- and Complete Freund’s adjuvant-induced inflammation models. TRPV1 is SUMOylated at a C-terminal Lys residue (K822), which specifically enhances the channel sensitivity to stimulation by heat, but not capsaicin, protons or voltage. TRPV1 SUMOylation is decreased by SENP1 but upregulated upon peripheral inflammation. More importantly, the reduced ability of TRPV1 knockout mice to develop inflammatory thermal hyperalgesia was rescued by viral infection of lumbar 3/4 DRG neurons of wild-type TRPV1, but not its SUMOylation-deficient mutant, K822R. These data suggest that TRPV1 SUMOylation is essential for the development of inflammatory thermal hyperalgesia, through a mechanism that involves sensitization of the channel response specifically to thermal stimulation.

Indian Hedgehog (IHH) signaling, a key regulator of skeletal development, is highly activated in cartilage and bone tumors. Yet deletion of Ptch1, encoding an inhibitor of IHH receptor Smoothened (SMO), in chondrocyte or osteoblasts does not cause tumorigenesis. Here, we show that Ptch1 deletion in mice Prrx1+mesenchymal stem/stromal cells (MSCs) promotes MSC proliferation and osteogenic and chondrogenic differentiation but inhibits adipogenic differentiation. Moreover, Ptch1 deletion led to development of osteoarthritis-like phenotypes, exostoses, enchondroma, and osteosarcoma in Smo-Gli1/2-dependent manners. The cartilage and bone tumors are originated from Prrx1+ lineage cells and express low levels of osteoblast and chondrocyte markers, respectively. Mechanistically, Ptch1 deletion increases the expression of Wnt5a/6 and leads to enhanced β-Catenin activation. Inhibiting Wnt/β-Catenin pathway suppresses development of skeletal anomalies including enchondroma and osteosarcoma. These findings suggest that cartilage/bone tumors arise from their early progenitor cells and identify the Wnt/β-Catenin pathway as a pharmacological target for cartilage/bone neoplasms.