A retrospective cohort study comparing outcomes following hip fractures in Australian indigenous patients with non-Australian indigenous patients.

BACKGROUND: Australian Indigenous (AI) populations face significant socioeconomic disadvantage and have poorer health outcomes when compared to their non-AI counterparts. There is a paucity of published literature on outcomes following hip fracture in the AI population. METHODS: We performed a retrospective cohort study comparing outcomes following hip fracture in AI and non- AI patients presenting to a single regional trauma centre. The primary outcome of interest was all-cause mortality. Secondary outcomes of interest were the odds of postoperative delirium and length of stay in hospital. All outcomes were adjusted against collected baseline covariates. RESULTS: One hundred and twenty-seven hip fractures were identified across 125 patients. There were 62 hip fractures in the AI group and 65 in the non-AI group. The adjusted hazard ratio (HR) for all-cause mortality was not statistically significant when comparing Indigenous versus non-Indigenous patients (HR = 2.37, P = 0.055). Adjusted odds of postoperative delirium was lower in Indigenous patients (OR = 0.12; P = 0.018). The AI cohort had a 4 day longer median length of stay, which was not statistically significant when adjusted for covariates. CONCLUSION: AI patients with hip fractures were younger, had a higher Charlson Comorbidity Index Score and American Society of Anaesthesiologists grade, as well as a higher incidence of diabetes and associated end-organ sequalae. There was no difference in all-cause mortality. Odds of postoperative delirium was lower in the AI group. We did not find any difference in the length of hospital stay.

CDCP1 enhances Wnt signaling in colorectal cancer promoting nuclear localization of ß-catenin and E-cadherin.

Elevated CUB-domain containing protein 1 (CDCP1) is predictive of colorectal cancer (CRC) recurrence and poor patient survival. While CDCP1 expression identifies stem cell populations that mediate lung metastasis, mechanisms underlying the role of this cell surface receptor in CRC have not been defined. We sought to identify CDCP1 regulated processes in CRC using stem cell populations, enriched from primary cells and cell lines, in extensive in vitro and in vivo assays. These experiments, demonstrating that CDCP1 is functionally important in CRC tumor initiation, growth and metastasis, identified CDCP1 as a positive regulator of Wnt signaling. Detailed cell fractionation, immunoprecipitation, microscopy, and immunohistochemical analyses demonstrated that CDCP1 promotes translocation of the key regulators of Wnt signaling, ß-catenin, and E-cadherin, to the nucleus. Of functional importance, disruption of CDCP1 reduces nuclear localized, chromatin-associated ß-catenin and nuclear localized E-cadherin, increases sequestration of these proteins in cell membranes, disrupts regulation of CRC promoting genes, and reduces CRC tumor burden. Thus, disruption of CDCP1 perturbs pro-cancerous Wnt signaling including nuclear localization of ß-catenin and E-cadherin.