Pulsed radiofrequency (PRF) fields applied by an electrode to neural structures, such as the peripheral sensory nociceptor axons and dorsal root ganglion, are clinically effective in reducing pain and other neuropathic syndromes. However, a full understanding of the underlying mechanisms by which this occurs has not yet been clarified. In this study, PRF is applied to the afferent axons of the sciatic nerves of rats. A standard radiofrequency (RF) electrode and RF generator is used to apply the RF signal output to the sciatic nerve using standard PRF parameters that have been successfully used in clinical practice. The ultrastructure of the treated axons is observed after 10 days by electron microscopy. A control, sham application is simultaneously applied to the contralateral sciatic nerve to provide a statistical differential comparison. It is found that the internal ultrastructural components of the axons show microscopic damage after PRF exposure, including: abnormal membranes and morphology of mitochondria, and disruption and disorganization of microfilaments and microtubules. The damage appears to be more pronounced for C-fibers than for A-delta and A-beta fibers. The results are discussed in terms of internal electric field strengths and thermodynamic parameters.

Lesioning using radiofrequency (RF) current has been increasingly used in clinical practice for the treatment of pain syndromes. Although formation of heat causing "thermocoagulation" of the nervous tissues is thought to be responsible of the clinical outcome, a more recent modality of RF application named pulsed radiofrequency (PRF) delivers the RF current without producing destructive levels of heat. In our study, we compared the effects of conventional RF (CRF) and PRF on rabbit dorsal root ganglion (DRG) morphology, including also control and sham operated groups. The setting of the experiment and the RF parameters used were similar to those used in current clinical practice. The specimens were analyzed both with light microscopy and electron microscopy, two weeks after the procedure. At the light microscopic level, all groups had preserved the normal DRG morphology and no differences were observed between them. In the electron microscopic analysis there were no pathological findings in the control and sham operated groups. But the ganglion cells in the RF groups had enlarged endoplasmic reticulum cisterns and increased number of cytoplasmic vacuoles which were more evident in the CRF group. Some of the ganglion cells in the CRF group had mitochondrial degeneration, nuclear membrane disorders or loss of nuclear membrane and neurolemma integrity. The myelinated and unmyelinated nerve fibers were of normal morphology in all groups. Our results suggest that PRF application is less destructive of cellular morphology than CRF at clinically used "doses". Before making certain judgements, more experimental and clinical studies should be planned.

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The use of wider-diameter cannulas can potentially improve fat graft survival and reduce fat graft resorption.

Melatonin may have a positive effect on both angiogenesis and wound healing.

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Abstract. The purpose of the study was to investigate whether carvedilol has an antiproliferative effect alone and whether carvedilol provides an additive, synergistic or antagonistic effect on imatinib mesylate-induced cytotoxicity in both C6 glioma monolayer and spheroid culture. The C6 rat glioma chemoresistant experimental brain tumour cell line, that is notoriously difficult to treat with combination chemotherapy, was used both in monolayer and spheroid cultures. We treated C6 glioma cells with carvedilol alone and a combination of carvedilol and imatinib mesylate at a concentration of 10 μM. Following treatment, we evaluated cell proliferation index, bromodeoxyuridine labelling index (BrDU-LI), cell cycle distributions, apoptotic cell percentages, cAMP levels and three dimensional cell morphology at monolayer cultures. In addition BrDU-LI, volume and morphology of spheroids were also assessed. Carvedilol and imatinib mesylate alone reduced cell number, BrDU-LI, cAMP levels and spheroid volume. Carvedilol and imatinib mesylate arrested cells at G0/ G1 phase in a time-dependent manner and time-independent manner, respectively. Carvedilol increased apoptosis rate only at the 24th h, but imatinib mesylate did for all time intervals. Interestingly carvedilol, drug with well-known protective effect on mitochondria, induced severe mitochondria damage, and imatinib mesylate induced autophagy confirmed only by transmission electron microscopy. These results suggest that carvedilol showed antitumour activity against rat C6 glioma cells and a combination of carvedilol with imatinib mesylate resulted in enhanced in vitro antitumour activity.

Our results suggest that OLE modulates the expression of some miRNAs related to anticancer activity in GBM and the response to TMZ. Further studies and validations are needed, but we suggest that OLE might be used for in vivo studies and future medical drug studies.