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Biological age is a better measure of functional capacity than chronological age.1 One of the measures of biological age is telomere length. Telomeres are nucleoprotein complexes that protect chromosome ends from damage. The DNA component of telomeres progressively shortens as biological age increases and thus acts as a read out for ‘miles on the biological clock’. 2 Telomere length progressively shortens as biological age increases. Within health care, ageing is almost exclusively described in terms of chronological age. Recent studies explored using biological age to stratify patients and predict outcomes.3 This project acts as a pilot study to investigate whether biological age is related to intensive care unit (ICU) outcomes and whether ICU patients age biologically at an accelerated rate. This project used blood samples from a previous study where patients underwent cardiac surgery and were admitted to the ICU. Blood samples were obtained before surgery and on days 1, 2, and 3 after surgery. The database contained the following physiological parameters: haemoglobin, urea, creatinine, RIFLE score, length of ICU stay, and whether renal replacement therapy was required. Information on co-morbidities and medication was also provided. DNA was isolated using a Maxwell machine and telomere length determined via quantitative PCR. One hundred and fifty-five blood samples from 46 patients underwent analysis. Telomere length did not differ significantly over the 4 days (P=0.662). No relationship was found between telomere length and any physiological parameter, co-morbidity, or medication. There was a trend towards significance with RIFLE score at day 3 increasing as telomere length decreased, although this was not statistically significant (P=0.09). No relationship between telomere length and the available physiological parameters, comorbidities, or medication was found. Telomere length did not vary during ICU stay. This study was limited by its small sample size. Future studies would benefit from a larger sample size; in addition, blood samples could also be obtained at 6 months after discharge to allow gradual alterations in biological age to be determined. Recent studies give evidence that telomere length is a weak biomarker of ageing,3 and that more meaningful data might be obtained using superior markers, such as CDKN2A expression or expression levels of non-coding RNAs.3

Diabet. Med. 29, e191–e198 (2012) Abstract Aims This study characterized UK primary care patients with Type 2 diabetes who initiated insulin treatment, and described the initial insulin regimens used, overall metabolic changes and health-care resource usage. Methods A retrospective cohort study was performed using quality-checked patient data from The Health Improvement Network database. Eligible patients who initiated insulin for the first time between 2004 and 2006 were grouped into four cohorts according to the type of insulin regimen initiated. Data on patient characteristics, metabolic and clinical outcomes and health-care resource use were collected at baseline and during 6 months of follow-up. Results In total, 4045 eligible adults [2269 male, 1776 female; mean age 62.6 ± 13.3 years; mean baseline HbA1c 82 ± 22 mmol/mol (9.6% ± 2.0%)] initiated insulin. Approximately half (52.4%) initiated insulin as basal insulin only, 41.6% as premixed only, 4.0% as basal-bolus and 2.1% as prandial insulin only. Among patients with ≥ 180 days follow-up (n = 3815), the initial insulin regimen was not changed during follow-up in 75.1% of patients, while 13.7% discontinued, 7.0% switched and 4.7% intensified insulin therapy. The mean change in HbA1c was −14 mmol/mol (−1.3%, n = 2881), with 17.3% of patients achieving an HbA1c of

Diabet. Med. 29, e13–e20 (2012) Abstract Aims To describe patients with Type 2 diabetes mellitus treated with basal insulin, with or without oral antidiabetics in UK primary care, and evaluate insulin treatment patterns and factors explaining changes in therapy. Methods Retrospective analysis of patients with Type 2 diabetes within The Health Improvement Network UK primary care database. Patients receiving basal insulin between January and June 2006 were followed until July 2009. Results Analysis included 3185 patients, mean age 65.6 years [standard deviation (SD) 12.4], 50.9% men, median diabetes duration 9.6 years, median basal insulin use 1.3 years, 86.5% had received oral antidiabetics in the previous 12 months. Mean follow-up was 2.9 years (SD 1.0), 59.8% patients maintained basal insulin throughout follow-up with a mean HbA1C of 69 mmol/mol (SD 19; 8.4%, SD 1.7) at baseline and 65 mmol/mol (SD 17; 8.1%, SD 1.6) during follow-up. During follow-up, 6.9% of patients discontinued, 19.3% intensified with and 14.1% switched to prandial or premixed insulin. Patients who intensified (prandial) had a mean HbA1c of 77 mmol/mol (SD 18; 9.2%, SD 1.6) before change and a mean HbA1c of 71 mmol/mol (SD 21; 8.6%, SD 2.0) at the end of the study. Those switching to premixed insulin had a mean HbA1c of 80 mmol/mol (SD 18; 9.5%, SD 1.7) before change and a mean HbA1c of 69 mmol/mol (SD 17; 8.5%, SD 1.5) at the end of the study. Increasing HbA1c and longer diabetes duration explained intensification and switch. Conclusions The majority of patients had HbA1c above the 53 mmol/mol (

The effects of formaldehyde, acetaldehyde, and glutaraldehyde on human red blood cells were investigated. It was found that (a) The surface negative charge of the erythrocytes at pH 7 was increased 10% by glutaraldehyde, but not by the other two aldehydes. (b) The effect of incomplete fixation of the red blood cells was demonstrated by hemoglobin leakage studies The leakage of hemoglobin subsequent to formaldehyde treatment was especially pronounced Acetaldehyde-fixed cells showed some leakage of hemoglobin after an hour of exposure to the fixative, whereas glutaraldehyde-fixed cells showed no hemoglobin leakage. (c) All three aldehydes caused K+ leakage during fixation. The concentrations of K+ in the fixing solutions all reached the same level, but whereas the leakage with glutaraldehyde was immediate, that with formaldehyde was more gradual and that with acetaldehyde reached a steady state only after 24 hr. (d) The effects of the aldehydes on red cell deformability and swelling revealed that glutaraldehyde hardened the cells within 15 min, formaldehyde within 5 hr, while acetaldehyde required at least 24 hr to produce appreciable fixation. (e) The hematocrit changes accompanying the fixation process depended upon cell volume changes and loss of deformability.