Acute kidney injury (AKI) following cardiac surgery significantly increases morbidity and mortality risks. Improving existing clinical methods of identifying patients at risk of perioperative AKI may advance management and treatment options. This study investigated whether a combination of biomarkers and clinical factors pre and post cardiac surgery could stratify patients at risk of developing AKI. Patients (n = 401) consecutively scheduled for elective cardiac surgery were prospectively studied. Clinical data was recorded and blood samples were tested for 31 biomarkers. Areas under receiver operating characteristic (AUROCs) were generated for biomarkers pre and postoperatively to stratify patients at risk of AKI. Preoperatively sTNFR1 had the highest predictive ability to identify risk of developing AKI postoperatively (AUROC 0.748). Postoperatively a combination of H-FABP, midkine and sTNFR2 had the highest predictive ability to identify AKI risk (AUROC 0.836). Preoperative clinical risk factors included patient age, body mass index and diabetes. Perioperative factors included cardio pulmonary bypass, cross-clamp and operation times, intra-aortic balloon pump, blood products and resternotomy. Combining biomarker risk score (BRS) with clinical risk score (CRS) enabled pre and postoperative assignment of patients to AKI risk categories. Combining BRS with CRS will allow better management of cardiac patients at risk of developing AKI.

Acute kidney injury (AKI) after major trauma is associated with increased mortality. The aim of this study was to assess if measurement of blood biomarkers in combination with clinical characteristics could be used to develop a tool to assist clinicians in identifying which orthopaedic trauma patients are at risk of AKI. This is a prospective study of 237 orthopaedic trauma patients who were consecutively scheduled for open reduction and internal fixation of their fracture between May 2012 and August 2013. Clinical characteristics were recorded, and 28 biomarkers were analysed in patient blood samples. Post operatively a combination of H-FABP, sTNFR1 and MK had the highest predictive ability to identify patients at risk of developing AKI (AUROC 0.885). Three clinical characteristics; age, dementia and hypertension were identified in the orthopaedic trauma patients as potential risks for the development of AKI. Combining biomarker data with clinical characteristics allowed us to develop a proactive AKI clinical tool, which grouped patients into four risk categories that were associated with a clinical management regime that impacted patient care, management, length of hospital stay, and efficient use of hospital resources.

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Background: Sleep disturbances (SD) are the most impactful and commonly reported symptoms in post-traumatic stress disorder (PTSD). Yet, they are often resistant to primary PTSD therapies. Research has identified two distinct SDs highly prevalent in PTSD; insomnia and nightmares. Those who report SDs prior to a traumatic event are at greater risk for developing PTSD; highlighting that sleep potentially plays a role in PTSD's pathology. To further understand the pathobiological mechanisms that lead to the development of PTSD, it is first imperative to understand the interplay which exists between sleep and PTSD on a biological level. The aim of this systematic review is to determine if biological or physiological markers are related to SD in PTSD. Methods: A systematic literature search was conducted on the electronic databases; Medline, Embase, AMED and PsycINFO, using Medical Subject Headings and associated keywords. Results: Sixteen studies were included in the final analyses. Physiological makers of autonomic function, and biochemical markers of HPA-axis activity; inflammatory processes; and trophic factor regulation were related to the severity of SDs in PTSD. Conclusion: These findings add to the growing literature base supporting a central focus on sleep in research aiming to define the pathophysiological processes which result in PTSD, as well as emphasising the importance of specifically targeting sleep as part of a successful PTSD intervention strategy. Resolving SDs will not only reduce PTSD symptom severity and improve quality of life but will also reduce all-cause mortality, hospital admissions and lifetime healthcare costs for those with PTSD. Limitations of the current literature are discussed, and key recommendations future research must adhere to are made within.

Background: Decreased expression of thrombomodulin (TM) in bladder cancer tissue has been shown to be associated with cell proliferation, increased malignancy and a poor prognosis. The aim of this study was to investigate the immunoexpression of TM in bladder tissue cores by immunohistochemistry (IHC) and the relationship between TM score and patient survival for the following pathologies: transitional cell papillary carcinoma (TCPC), transitional cell carcinoma (non-papillary) (TCC), squamous cell carcinoma (SCC), adenocarcinoma, and sarcoma. TM immunoexpression was also evaluated in normal adjacent bladder tissue cores. Methods: TM immunoexpression was assessed in n=185 formalin-fixed paraffin-embedded (FFPE) bladder tissue cores from n=98 patients by IHC. Tissue cores included TCPC (n=29), TCC (n=85), SCC (n=21), adenocarcinoma (n=12), sarcoma (n=4), and normal tissue cores (n=34). Results: TM immunoexpression scores are stronger in TCPC, TCC and SCC bladder cancer tissue cores with respect to adenocarcinoma and sarcoma (mean TM immunoexpression scores: 3.04, 2.57, 2.55, 1.55 and 1.19, respectively) (Kruskal-Wallis p<0.001). TM immunoexpression scores significantly decreased in bladder cancer tissue cores across both stage (p<0.001) and grade (p<0.001) (Kruskal-Wallis). Survival data were available for n=45 bladder cancer patients (mean follow-up of 34 months). Applying a TM immunoexpression cut-off score of 3.0 demonstrated that patients with bladder cancer who had a TM immunoexpression score <3.0 had lower survival rates (median survival 23.5 months). In contrast, patients with TM immunoexpression scores ≥3.0 had longer survival rates (median survival 40 months) (log-rank; p=0.045). Conclusion: TM immunoexpression in bladder cancer tissue may be a clinically relevant predictor of tumor progression and survival. Low expression of TM in bladder cancer biopsies or in recurrent bladder cancer may be indicative of a poor prognosis. TM immunoexpression could be used to guide clinical decision making.