5 research outputs found

    MODELING OF CEREBROSPINAL FLUID FOR IMPACT BIOMECHANICS

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    Numerical Investigation of Spinal Cord Injury After Flexion-Distraction Injuries at the Cervical Spine

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    Abstract Flexion-distraction injuries frequently cause traumatic cervical spinal cord injury (SCI). Post-traumatic instability can cause aggravation of the secondary SCI during patient care. However, there is little information on how the pattern of disco-ligamentous injury affects the SCI severity and mechanism. This study objective was to analyze how posterior disco-ligamentous injuries affect spinal cord compression and stress and strain patterns in the spinal cord during post-traumatic flexion and extension. A cervical spine finite element model including the spinal cord was used and different combinations of partial or complete intervertebral disc (IVD) rupture and disruption of various posterior ligaments were modeled at C4–C5, C5–C6, or C6–C7. In flexion, complete IVD rupture combined with posterior ligamentous complex rupture was the most severe injury leading to the highest von Mises stress (47–66 kPa), principal strains p1 (0.32–0.41 in white matter) and p3 (−0.78 to −0.96 in white matter) in the spinal cord and the highest spinal cord compression (35–48%). The main post-trauma SCI mechanism was identified as the compression of the anterior white matter at the injured level combined with distraction of the posterior spinal cord during flexion. There was also a concentration of the maximum stresses in the gray matter during post-traumatic flexion. Finally, in extension, the injuries tested had little impact on the spinal cord. The capsular ligament was the most important structure to protect the spinal cord. Its status should be carefully examined during the patient's management

    Restored immune cell functions upon clearance of senescence in the irradiated splenic environment

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    Some studies show eliminating senescent cells rejuvenate aged mice and attenuate deleterious effects of chemotherapy. Nevertheless, it remains unclear whether senescence affects immune cell function. We provide evidence that exposure of mice to ionizing radiation (IR) promotes the senescent-associated secretory phenotype (SASP) and expression of p16(INK4a) in splenic cell populations. We observe splenic T cells exhibit a reduced proliferative response when cultured with allogenic cells in vitro and following viral infection in vivo. Using p16-3MR mice that allow elimination of p16(INK4a)-positive cells with exposure to ganciclovir, we show that impaired T-cell proliferation is partially reversed, mechanistically dependent on p16(INK4a) expression and the SASP. Moreover, we found macrophages isolated from irradiated spleens to have a reduced phagocytosis activity in vitro, a defect also restored by the elimination of p16(INK4a) expression. Our results provide molecular insight on how senescence-inducing IR promotes loss of immune cell fitness, which suggest senolytic drugs may improve immune cell function in aged and patients undergoing cancer treatment
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