Knee osteoarthritis is a common cause of pain and disability in old subjects. Pain may predispose to the development of frailty. Studies on mechanisms underlying pain in osteoarthritis models during aging are lacking. In this work, we used the monosodium iodoacetate model of osteoarthritis in adult (11-week-old) and old (20-month-old) C57BL/6J mice to compare hypersensitivity, locomotion, neuroinflammation, and the effects of morphine treatment. After osteoarthritis induction in adult and old mice, weight-bearing asymmetry, mechanical allodynia, and thermal hyperalgesia similarly developed, while locomotion and frailty were more affected in old than in adult animals. When behavioral deficits were present, the animals were treated for 7 days with morphine. This opioid counteracts the behavioral alterations and the frailty index worsening both in adult and old mice. To address the mechanisms that underlie pain, we evaluated neuroinflammatory markers and proinflammatory cytokine expression in the sciatic nerve, DRGs, and spinal cord. Overexpression of cytokines and glia markers were present in osteoarthritis adult and old mice, but the activation was qualitatively and quantitatively more evident in aged mice. Morphine was able to counteract neuroinflammation in both age groups. We demonstrate that old mice are more vulnerable to pain’s detrimental effects, but prompt treatment is successful at mitigating these effects.

Background: Appropriate levels and patterns of sound and light in an intensive care room help to maintain the patient's normal physiological functions. High sound levels can disrupt the patient's normal sleep architecture, cause hearing deficits, and induce the onset of delirium. Intensive care unit patients frequently report poor sleep, partly due to the environment.Objectives: An observational pilot prospective study was designed to record sound pressure and light pollution levels in an Italian intensive care unit, without windows to provide natural light.Method: Sound levels were measured in decibel A (dBA) every 10 seconds. Sound data were analyzed for sound peak, defined as the number of times sound levels exceeded 45, 50, 60, 65, 70, 75, 80, and 85 dBA. Light measures were taken every 10 seconds on a continuous basis. Light data were analyzed for light "peaks," defined as the number of times light levels exceeded 100, 200, 300, 400, and 500 lux.Results: The overall median sound level during the study period was equal to 54.60 (interquartile range [IQR], 51.70-57.70) dBA. The daytime median sound level was 56.00 (IQR, 53.00-59.50) dBA, and the nighttime median was 53.00 (IQR,) dBA ( P < .001). The overall median light level was equal to 114 (IQR, 0-225) lux. The daytime median light level was 184 (IQR, 114-293) lux, and the nighttime median was 0 (IQR, 0-50) lux ( P < .001). With respect to room lighting, rooms were observed to have "no lights on" 12.6% of daytime and 41% of nighttime.Discussion: The sound levels recorded in our sample demonstrated that peaks >45 dBA during daytime and nighttime are, respectively, equal to 99.9% and 98.6% of all readings. The Environmental Protection Agency/World Health Organization recommended thresholds for both day (45 dBA) and night (35 dBA). Sound levels reached "toxic levels" when sound-generating activities were performed by nurses and physicians.

The scientific objectives of CAGE22-1 expedition were to 1) explore the seafloor at the historical disposal area in Repparfjord using a TowCam-multicorer system. The visual seafloor observations allow to characterize the composition and distribution of benthic communities and for targeted sediment samplings. 2) Collect sediment cores in and out of the disposal area and extract pore fluids for trace metals and gas analyses. The cruise may be known as: CAGE22_1

Knee osteoarthritis (OA) is a chronic degenerative inflammatory-based condition caused by a cascade of different intra-articular molecules including several cytokines. Among the cytokines, prokineticins (PKs) have recently been identified as important mediators of inflammation and pain. This observational study examined the potential involvement of PK2 in degenerative or traumatic knee disease. Fifteen patients presenting knee osteoarthritis (OA group) and 15 patients presenting a traumatic meniscal tear (TM group) were studied. Synovial fluid samples from affected knees were assessed for PK2, IL-10, and TNF-α using the ELISA method. At a long-term follow-up (minimum 5 years, mean = 6.1 years), patients in the TM group underwent clinical re-evaluation with PROMs (Tegner Activity Scale, IKDC, Lysholm, SKV); in addition, X-ray visualization was used to assess the presence of secondary OA. PK2 was detected in synovial fluids of both TM and OA patients and the levels were comparable between the two groups, while IL-10 levels were significantly greater in the OA group than those in TM patients. PK2 levels correlated with those of IL-10. PK2 levels were greater in blood effusions compared to clear samples, did not differ significantly between sexes, nor were they related to differences in weight, height, or injury (meniscal laterality, time since dosing). No correlation was found between PROMs and radiological classifications in patients in the TM group at final follow-up. These data are the first observations of PK2 in synovial fluid following traumatic meniscus injury. These findings suggest possible further prognostic indices and therapeutic targets to limit the development of secondary OA.