BackgroundDiabetic foot ulcers (DFU) are a common problem in longstanding diabetes. However, mortality outcomes in Australian patients with DFU are still unclear.MethodsAll patients with DFU presenting for the first time to the Multi-Disciplinary Foot Clinic (MDFC) at Royal Darwin Hospital, Northern Territory Australia, between January 2003 and June 2015 were included in this study. These patients were followed until 2017, or death. Individual patient data was extracted from hospital and primary care information systems. Kaplan-Meier survival curves were developed. The association between various risk factors and mortality was analysed using Cox regression.ResultsIn total 666 subjects were screened, and 513 were included in the final analysis. Of these subjects, 247 were Indigenous and 266 were non-Indigenous. The median follow-up period was 5.8 years (IQR, 3.1–9.8). The mean age at inclusion was 59.9 ± 12.3 years and 62.8% were males. The majority (93.6%) had type 2 diabetes and the median diabetes duration was 7 years (IQR, 3–12). There were 199 deaths, with a 5-year-mortality rate of 24.6%, and a 10-year-mortality rate of 45.4%. The mean age at death was 64.6 ± 11.8 years. In a multivariate analysis, the following variables were associated with mortality (adjusted HR, 95% CI): age 1.04 (1.02–1.05, P < 0.001); chronic kidney disease 1.22 (1.11–1.33, P < 0.001), and plasma albumin 0.96 (0.94–0.99, P < 0.05). The most common causes of death were chronic kidney disease (24.6%), cardiovascular events (19.6%), sepsis (15.6%), respiratory failure (10.0%), malignancy (9.5%) and multi-organ failure (5.0%).ConclusionPatients with DFU have high mortality. Age, chronic kidney disease, and low albumin levels increase the risk of mortality. Strategies should focus on ulcer prevention and aggressive risk factor reduction.

Macrophages have been proposed as the major effector cell in T cell-mediated xenograft rejection. To determine their role in this response, NOD-SCID mice were transplanted with fetal pig pancreas (FPP) before reconstitution with CD4+ T cells from BALB/c mice. Twelve days after CD4+ T cell reconstitution, purified macrophages (depleted of T cells) were isolated from CD4+ T cell-reconstituted FPP recipient mice and adoptively transferred to their nonreconstituted counterparts. After adoptive macrophage transfer, FPP recipient mice transferred with macrophages from CD4+ T cell-reconstituted mice demonstrated xenograft destruction along with massive macrophage infiltration at day 4 and complete graft destruction at day 8 postmacrophage transfer. By contrast, FPP recipients that received macrophages from nonreconstituted mice showed intact FPP xenografts with few infiltrating macrophages at both days 4 and 8 after macrophage transfer. The graft-infiltrating macrophages showed increased expression of their activation markers. Depletion of endogenous macrophages or any remaining CD4+ T cells did not delay graft rejection in the macrophage-transferred FPP recipients, whereas depletion of transferred macrophages with clodronate liposomes prevented graft rejection. Our results show that macrophages primed by FPP and activated by CD4+ T cells were attracted from the peripheral circulation and were capable of specific targeting and destruction of FPP xenografts. This suggests that in xenograft rejection, there are macrophage-specific recognition and targeting signals that are independent of those received by T cells.

Primary nonfunction of transplanted islets results in part from their sensitivity to reactive oxygen species (ROS) generated during the isolation and transplantation process. Our aim was to examine whether coexpression of antioxidant enzymes to detoxify multiple ROS increased the resistance of mouse islets to oxidative stress and improved the initial function of islet grafts. Islets from transgenic mice expressing combinations of human copper/zinc superoxide dismutase (SOD), extracellular SOD, and cellular glutathione peroxidase (Gpx-1) were subjected to oxidative stress in vitro. Relative viability after hypoxanthine/xanthine oxidase treatment was as follows: extracellular SOD ؉ Gpx-1 ؉ Cu/Zn SOD > extracellular SOD ؉ Gpx-1 > extracellular SOD > wild type. Expression of all three enzymes was the only combination protective against hypoxia/ reoxygenation. Islets from transgenic or control wildtype mice were then transplanted into streptozotocininduced diabetic recipients in a syngeneic marginal islet mass model, and blood glucose levels were monitored for 7 days. In contrast to single-and double-transgenic grafts, triple-transgenic grafts significantly improved control of blood glucose compared with wild type. Our results indicate that coexpression of antioxidant enzymes has a complementary beneficial effect and may be a useful approach to reduce primary nonfunction of islet grafts. Diabetes 54:2109 -2116, 2005

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CSI-EMR with submucosal injection of succinylated gelatin is safe and superior to conventional EMR, consistently resulting in en bloc resections larger than 50 x 40 mm. With experience, total procedure duration is comparable.

Colour duplex US provides an accurate diagnostic assessment of a dysfunctional autogneous AVF, and is an important planning tool for subsequent open or endovascular intervention. It is particularly accurate in the peri-anastomotic area of the fistula which harbours the majority of fistula problems.

These results demonstrate that CCR5 is involved in both the activation and recruitment of macrophages to rejecting islet xenografts but other pathways are involved.

Background Lower extremity amputations (LEAs) in diabetic patients are common in the indigenous population. There is no published data from the Northern Territory. Methods All patients with diabetic foot ulcer, presenting for the first time to the multi‐disciplinary foot clinic at Royal Darwin Hospital, between January 2003 and June 2015, were included. These patients were followed until 2017, or death. LEA rates over the follow‐up period and the risk factors were studied. Results Of the 513 included patients, 62.8% were males and 48.2% were indigenous. The majority (93.6%) had type 2 diabetes with median diabetes duration of 7.0 years (interquartile range 3–12). During the follow‐up period of 5.8 years (interquartile range 3.1–9.8), a total of 435 LEAs (16.6% major; 34.7% minor) occurred in 263 patients (mean age 57.0 ± 11.8 years). In multivariate analysis, the following variables were associated with LEAs (adjusted odds ratio (95% confidence interval)): prior LEA (4.49 (1.69–11.9)); peripheral vascular disease (2.67 (1.27–5.59)); forefoot ulcer (7.72 (2.61–22.7)); Wagner grade 2 (3.71 (1.87–7.36)); and Wagner grade 3 (17.02 (3.77–76.72)). Indigenous patients were 1.8 times more likely to have LEAs than non‐indigenous patients. Indigenous amputees were approximately 9 years younger than their non‐indigenous counterparts. Conclusion Half of patients presenting with diabetic foot ulcer had LEA during follow‐up. Prior LEAs, peripheral vascular disease, forefoot ulcers and higher Wagner grades were independent risk factors for LEA. Indigenous patients were at higher risk for LEAs and were younger at the time of amputation.