Applications of Cryoneurolysis in Chronic Pain Management: a Review of the Current Literature.

PURPOSE OF REVIEW: The purpose of this review is to evaluate and summarize the literature investigating cryoneurolysis in the treatment of various chronic pain pathologies. RECENT FINDINGS: There is an increasing amount of interest in the use of cryoneurolysis in chronic pain, and various studies have investigated its use in lumbar facet joint pain, SI joint pain, post-thoracotomy syndrome, temporomandibular joint pain, chronic knee pain, phantom limb pain, neuropathic pain, and abdominal pain. Numerous retrospective studies and a more limited number of prospective, sham-controlled prospective studies suggest the efficacy of cryoneurolysis in managing these chronic pain pathologies with a low complication rate. However, more blinded, controlled, prospective studies comparing cryoneurolysis to other techniques are needed to clarify its relative risks and advantages.

Effects of neuropeptide Y on the microvasculature of human skeletal muscle.

BACKGROUND: Neuropeptide Y acts directly on the vasculature as a cotransmitter with norepinephrine for an augmented contraction. Little, however, is known about the effects of neuropeptide Y on the microvasculature of human skeletal muscle. Neuropeptide Y signaling has not been studied in the setting of cardiac surgery and cardiopulmonary bypass. We investigated the role of neuropeptide Y signaling on vasomotor tone in the microvessels of human skeletal muscle, as well as the effect of cardiopulmonary bypass on neuropeptide Y-induced responsiveness. METHODS: Specimens taken from intercostal muscles were collected from patients, pre- and post-cardiopulmonary bypass, undergoing coronary artery bypass grafting or cardiac valve surgery (n = 8/group). Microvessels (157 ± 47 microns) were isolated in vitro in a no-flow state. Arterial microvascular responses to a neuropeptide Y agonist, a Y1 receptor antagonist, phenylephrine, and the coadministration of neuropeptide Y and phenylephrine were examined. The abundance and localization of the Y1 receptor were measured using Western blot and immunofluorescence, respectively. RESULTS: Arterial microvessels showed responsiveness to the neuropeptide Y agonist (10-9 to 4 × 10-7 mol/L) both before and after cardiopulmonary bypass, reaching a 12.5% vasoconstriction from the baseline luminal diameter. With administration of the Y1 receptor antagonist after neuropeptide Y, the contractile response was eliminated (n = 3/group, P = .04). No difference in vasoconstriction was observed between pre- and post-cardiopulmonary bypass groups (P = .73). The coadministration of neuropeptide Y and phenylephrine (10-9 to 10-4 mol/L) elicited no difference in vasoconstriction (n = 7/group, P = .06 both pre- and post-cardiopulmonary bypass) when compared with phenylephrine alone (10-9 to 10-4 mol/L). No change in the protein expression or localization of the Y1 receptor was detected by Western blotting (n = 6/group, P = .44) or immunofluorescence (n = 6/group, P = .13). CONCLUSION: Neuropeptide Y induced vasoconstriction, suggesting that neuropeptide Y may play an important role in the regulation of the peripheral microvasculature. There was no change in microvascular responsiveness to neuropeptide Y after cardiopulmonary bypass nor were there any synergistic effects of neuropeptide Y on phenylephrine-induced vasoconstriction in the skeletal muscle microvasculature.

Advancement of multidisciplinary education and research in translational sciences: MERITS program development at Duke University.

INTRODUCTION: The Duke Multidisciplinary Education and Research in Translational Sciences Program provides educational resources for faculty and trainees in translational research. METHODS: To aid in program development, we assessed perceptions of translational science through focus groups targeting different career stages. RESULTS: In total, 3 essential themes emerged: collaboration, movement toward application, and public health impact. Facilitators and barriers varied among groups. CONCLUSION: Training programs must provide specific strategies for collaboration and selectively accelerating discoveries to therapies.