Introduction: The aim of this study was to assess core stabilization exercise effects in reducing functional disability in patients with chronic low back pain (CLBP).Methods: This study included total of 90 patients aged 40 to 60 years. After a ten-day rehabilitation program the patients from an examination group (n = 30) performed home exercise program five times a week, patients from a first control group (n = 30) three times a week, while patients from a second control group (n = 30) did not perform the exercises at all. The patients performed core stabilization exercises of moderate intensity once a day in 30 minutes sessions. The patient's functional disability was estimated using the Oswestry Disability Index (ODI).Results: After two months of rehabilitation there was a statistically significant increase in functional ability in patients who performed the core stabilization exercises five times a week(p = 0.0001) and in patients who performed the core stabilization exercises three times per week (p = 0.0001). A statistically significant difference in functional ability was not recorded in patients who did not perform the exercises. The analysis of the average values of the ODI differences at the beginning and after two months of rehabilitation showed a statistically significant difference between the group who did not perform the exercises and the group who performed the core stabilization exercises three times a week (p = 0.0001), and between the group who did not perform the exercises and the group who performed the core stabilization exercises five times a week (p = 0.0001).Conclusions: The implementation of the core stabilization exercises leads to a reduction of functional disability in patients with CLBP.

In addition to their role as effector cells in virus control, natural killer (NK) cells have an immunoregulatory function in shaping the antiviral T-cell response. This function is further pronounced in perforin-deficient mice that show the enhanced NK-cell proliferation and cytokine secretion upon mouse cytomegalovirus (MCMV) infection. Here, we confirmed that stronger activation and maturation of NK cells in perforin-deficient mice correlates with higher MCMV load. To further characterize the immunoregulatory potential of perforin, we compared the response of NK cells that express or do not express perforin using bone-marrow chimeras. Our results demonstrated that the enhanced proliferation and maturation of NK cells in MCMV-infected bone-marrow chimeras is an intrinsic property of perforin-deficient NK cells. Thus, in addition to confirming that NK-cell proliferation is virus load dependent, our data extend this notion demonstrating that perforin plays an intrinsic role as a feedback mechanism in the regulation of NK-cell proliferation during viral infections.