Reduced incidence of foot-related hospitalisation and amputation amongst persons with diabetes in Queensland, Australia

Objective To determine trends in the incidence of foot-related hospitalisation and amputation amongst persons with diabetes in Queensland (Australia) between 2005 and 2010 that coincided with changes in state-wide ambulatory diabetic foot-related complication management. Methods All data from cases admitted for the principal reason of diabetes foot-related hospitalisation or amputation in Queensland from 2005–2010 were obtained from the Queensland Hospital Admitted Patient Data Collection dataset. Incidence rates for foot-related hospitalisation (admissions, bed days used) and amputation (total, minor, major) cases amongst persons with diabetes were calculated per 1,000 person-years with diabetes (diabetes population) and per 100,000 person-years (general population). Age-sex standardised incidence and age-sex adjusted Poisson regression models were also calculated for the general population. Results There were 4,443 amputations, 24,917 hospital admissions and 260,085 bed days used for diabetes foot-related complications in Queensland. Incidence per 1,000 person-years with diabetes decreased from 2005 to 2010: 43.0% for hospital admissions (36.6 to 20.9), 40.1% bed days (391 to 234), 40.0% total amputations (6.47 to 3.88), 45.0% major amputations (2.18 to 1.20), 37.5% minor amputations (4.29 to 2.68) (p < 0.01 respectively). Age-sex standardised incidence per 100,000 person-years in the general population also decreased from 2005 to 2010: 23.3% hospital admissions (105.1 to 80.6), 19.5% bed days (1,122 to 903), 19.3% total amputations (18.57 to 14.99), 26.4% major amputations (6.26 to 4.61), 15.7% minor amputations (12.32 to 10.38) (p < 0.01 respectively). The age-sex adjusted incidence rates per calendar year decreased in the general population (rate ratio (95% CI)); hospital admissions 0.949 (0.942–0.956), bed days 0.964 (0.962–0.966), total amputations 0.962 (0.946–0.979), major amputations 0.945 (0.917–0.974), minor amputations 0.970 (0.950–0.991) (p < 0.05 respectively). Conclusions There were significant reductions in the incidence of foot-related hospitalisation and amputation amongst persons with diabetes in the population of Queensland over a recent six-year period.

Kinetics and mechanism of hot corrosion of γ-Y 2Si 2O 7 in thin-film Na 2SO 4 molten salt

γ-Y 2Si 2O 7 is a promising candidate material both for hightemperature structural applications and as an environmental/thermal barrier coating material due to its unique properties such as high melting point, machinability, thermal stability, low linear thermal expansion coefficient (3.9×10 -6/K, 200°-1300°C), and low thermal conductivity (<3.0 W/ṁK above 300°C). The hot corrosion behavior of γ-Y 2Si 2O 7 in thin-film molten Na 2SO 4 at 850°-1000°C for 20 h in flowing air was investigated using a thermogravimetric analyzer (TGA) and a mass spectrometer (MS). γ-Y 2Si 2O 7 exhibited good resistance against Na 2SO 4 molten salt. The kinetic curves were well fitted by a paralinear equation: the linear part was caused by the evaporation of Na2SO4 and the parabolic part came from gas products evolved from the hotcorrosion reaction. A thin silica film formed under the corrosion scale was the key factor for retarding the hot corrosion. The apparent activation energy for the corrosion of γ-Y 2Si 2O 7 in Na 2SO 4 molten salt with flowing air was evaluated to be 255 kJ/mol.

Kallikrein-related peptidase 4 induces tumour microenvironment alterations that support tumour growth

Kallikrein-related peptidase 4 (KLK4) is a protease with elevated production in prostate cancer versus benign tissue. KLK4 expression is associated with prostate cancer risk, and its activity favours tumour progression through increasing cell motility and growth. Importantly, over-production of KLK4 in prostate glandular cells precedes tumour formation, positioning the enzyme to play a role in early remodelling of the tumour microenvironment, a process essential for tumour growth. We sought to identify the proteins and downstream signalling pathways targeted by KLK4 activity, to define its role in tumour microenvironment remodelling and evaluate the efficacy of KLK4 inhibition as a cancer therapy.