BackgroundVirtual reality (VR) therapy has been successfully used as an adjunct therapy for the management of acute pain in adults and children, and evidence of potential efficacy in other health applications is growing. However, minimal research exists on the value of VR as an intervention for chronic pain.ObjectiveThis case series examined the value of VR to be used as an adjunctive therapy for chronic pain patients in their own homes.MethodsAn exploratory approach using a case series and personal interviews was used. Ten chronic pain patients received VR therapy for 30 min on alternate days for 1 month. Pre- and postexposure (immediately afterwards, 3 h, and at 24 h) pain assessment was recorded using the Numerical Rating Scale (NRS), and weekly using the Brief Pain Inventory (BPI) and Self-completed Leeds Assessment of Neuropathic Symptoms and Signs pain scale (S-LANSS). Terminal semistructured personal interviews with the patients were also undertaken.ResultsOf the 8 patients who completed the study, 5 of them reported that pain was reduced during the VR experience but no overall treatment difference in pain scores postexposure was observed. VR was not associated with any serious adverse events, although 60% of patients reported some cybersickness during some of the experiences.ConclusionsOf note is that the majority of these study participants reported a reduction in pain while using the VR but with highly individualized responses. One patient also reported some short-term improved mobility following VR use. Some evidence was found for the short-term efficacy of VR in chronic pain but no evidence for persistent benefits.
Human GWAS and Mendelian genetic studies have linked polymorphic variants and mutations in the human uromodulin gene (UMOD) with chronic kidney disease. The primary function of this kidney‐specific and secreted protein remains elusive. This study investigated whether UMOD deficiency modified responses to unilateral ureteral obstruction (UUO)‐induced kidney injury. Kidneys harvested from groups of wild‐type (UMOD+/+) and knockout (UMOD−/−) male mice (n = 7–10 each) were studied on days 7, 14, and 21. Compared to sham kidneys, UMOD protein levels increased 9–13x after UUO and were associated with increased urinary UMOD levels. Kidney KIM‐1 protein levels were higher in the UMOD−/− groups at all time‐points (4–14x). The UMOD−/− groups also had higher KIM‐1 kidney‐to‐urine relative ratios (5–35x). In vitro studies using KIM‐1 expressing 769‐P cells showed lower KIM‐1 levels in the presence of UMOD protein. Levels of proapoptotic genes and the epithelial cell apoptotic protein marker M30 were significantly lower in the UMOD−/− groups. Both M30 and KIM‐1 colocalized with intraluminal UMOD protein deposits. Interstitial inflammation was less intense in the UMOD−/− groups. Renal fibrosis severity (kidney collagen mRNA and protein) was similar in both genotypic groups on days 7, 14, and 21. Our findings suggest a role for UMOD‐dependent inhibition of KIM‐1 expression and its apoptotic cell scavenging responses during chronic obstruction‐associated tubular injury.
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