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1.
Neurosurgery ; 2024 Feb 21.
Article in English | MEDLINE | ID: mdl-38380924

ABSTRACT

BACKGROUND AND OBJECTIVES: Although risk factors for unplanned readmission after cervical spine surgery have been widely reported, less is known about how readmission itself affects patient-reported outcome measures (PROMs). Using the Quality Outcomes Database registry of patients undergoing elective cervical spine surgery, we sought to (1) determine the impact of unplanned readmission on PROMs and (2) compare the effect of specific readmission reasons on PROMs. METHODS: An observational study was performed using a multi-institution, retrospective registry for patients undergoing cervical spine surgery. The occurrence of 90-day unplanned readmission classified into medical, surgical, pain only, and no readmissions was the exposure variable. Outcome variables included 12-month PROMs of Neck Disability Index (NDI), Numeric Rating Scale (NRS)-neck/arm pain, EuroQol-5D (EQ-5D), and patient dissatisfaction. Multivariable models predicting each PROM were built using readmission reasons controlling for demographics, clinical characteristics, and preoperative PROMs. RESULTS: Data from 13 355 patients undergoing elective cervical spine surgery (82% anterior approach and 18% posterior approach) were analyzed. Unplanned readmission within 90 days of surgery occurred in 3.8% patients, including medical (1.6%), surgical (1.8%), and pain (0.3%). Besides medical reasons, wound infection/dehiscence was the most common reason for unplanned readmission for the total cohort (0.5%), dysphagia in the anterior approach (0.6%), and wound infection/dehiscence in the posterior approach (1.5%). Based on multivariable regression, surgical readmission was significantly associated with worse 12-month NDI, NRS-neck pain, NRS-arm pain, EQ-5D, and higher odds of dissatisfaction. Pain readmissions were associated with worse 12-month NDI and NRS-neck pain scores, and worse dissatisfaction. For specific readmission reasons, pain, surgical site infection/wound dehiscence, hematoma/seroma, revision surgery, deep vein thrombosis, and pulmonary embolism were significantly associated with worsened 12-month PROMs. CONCLUSION: In patients undergoing elective cervical spine surgery, 90-day unplanned surgical and pain readmissions were associated with worse 12-month PROMs compared with patients with medical readmissions and no readmissions.

2.
Genes Dev ; 19(12): 1432-7, 2005 Jun 15.
Article in English | MEDLINE | ID: mdl-15964994

ABSTRACT

Bmi-1 is required for the post-natal maintenance of stem cells in multiple tissues including the central nervous system (CNS) and peripheral nervous system (PNS). Deletion of Ink4a or Arf from Bmi-1(-/-) mice partially rescued stem cell self-renewal and stem cell frequency in the CNS and PNS, as well as forebrain proliferation and gut neurogenesis. Arf deficiency, but not Ink4a deficiency, partially rescued cerebellum development, demonstrating regional differences in the sensitivity of progenitors to p16Ink4a and p19Arf. Deletion of both Ink4a and Arf did not affect the growth or survival of Bmi-1(-/-) mice or completely rescue neural development. Bmi-1 thus prevents the premature senescence of neural stem cells by repressing Ink4a and Arf, but additional pathways must also function downstream of Bmi-1.


Subject(s)
Cyclin-Dependent Kinase Inhibitor p16/metabolism , Multipotent Stem Cells/cytology , Multipotent Stem Cells/metabolism , Neurons/cytology , Neurons/metabolism , Nuclear Proteins/metabolism , Proto-Oncogene Proteins/metabolism , Repressor Proteins/metabolism , Tumor Suppressor Protein p14ARF/metabolism , Animals , Cell Differentiation , Cell Proliferation , Cellular Senescence , Cerebellum/growth & development , Cyclin-Dependent Kinase Inhibitor p16/deficiency , Genes, p16 , Mice , Mice, Inbred C57BL , Mice, Knockout , Nuclear Proteins/deficiency , Nuclear Proteins/genetics , Polycomb Repressive Complex 1 , Proto-Oncogene Proteins/deficiency , Proto-Oncogene Proteins/genetics , Repressor Proteins/genetics , Tumor Suppressor Protein p14ARF/deficiency , Tumor Suppressor Protein p14ARF/genetics
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