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PURPOSE: To examine the clinical outcomes of intraocular lens (IOL) scleral fixation with the friction knot technique. METHODS: Retrospective case series of 152 eyes of 152 patients with inadequate capsular bag support operated with the friction knot IOL scleral fixation technique by a single surgeon. The fixated IOLs were one-piece or three-piece models all with open loop haptics. Main outcome measures were change in corrected distance visual acuity (CDVA) and postoperative complications. RESULTS: The mean follow-up time was 11.7 months (median 4.9, range 0.7-64.8). The mean logarithm of the minimum angle of resolution CDVA improved from preoperative 0.77 ± 0.73 (Snellen 20/118 ± 7.3 lines) to 0.44 ± 0.56 (Snellen 20/55 ± 5.6 lines) at the final visit (p < 0.001). The main postoperative complications were ocular hypertension (30.3%), uveitis-glaucoma-hyphaema syndrome (12.5%; UGHS), vitreous haemorrhage (11.2%) and retinal detachment (8.6%). Two (1.3%) cases of suture breakage were seen. In multivariate Cox regression analysis, age under 60 years [hazard ratio (HR) = 5.41; 95% confidence interval (CI) 1.95-15.01] and scleral fixated one-piece IOL (HR = 4.23; 95% CI 1.44-12.44) were found as significant independent risk factors for developing new UGHS. CONCLUSION: The friction knot technique provides a firm scleral fixation. Scleral fixation may successfully be utilized in dislocated three-piece IOLs with loop haptics. We recommend avoiding scleral fixation of one-piece IOLs in young patients due to a high risk of UGHS.

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OBJECTIVES: To evaluate the quality of cardiopulmonary resuscitation (CPR) in a physician staffed helicopter emergency medical service (HEMS) using a monitor-defibrillator with a quality analysis feature. As a post hoc analysis, the potential barriers to implementation were surveyed. METHODS: The quality of CPR performed by the HEMS from November 2008 to April 2010 was analysed. To evaluate the implementation rate of quality analysis, the HEMS database was screened for all cardiac arrest missions during the study period. As a consequence of the observed low implementation rate, a survey was sent to physicians working in the HEMS to evaluate the possible reasons for not utilizing the automated quality analysis feature. RESULTS: During the study period, the quality analysis was used for 52 out of 187 patients (28%). In these cases the mean compression depth was < 40 mm in 46% and < 50 mm in 96% of the 1-min analysis intervals, but otherwise CPR quality corresponded with the 2005 resuscitation guidelines. In particular, the no-flow fraction was remarkably low 0.10 (0.07, 0.16). The most common reasons for not using quality-controlled CPR were that the device itself was not taken to the scene, or not applied to the patient, because another EMS unit was already treating the patient with another defibrillator. CONCLUSIONS: When quality-controlled CPR technology was used, the indicators of good quality CPR as described in the 2005 resuscitation guidelines were mostly achieved albeit with sufficient compression depth. The use of the well-described technology in improving patient care was low. Wider implementation of the automated quality control and feedback feature in defibrillators could further improve the quality of CPR on the field. TRIAL REGISTRATION: ClinicalTrials.gov (NCT00951704).

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BACKGROUND: Patients with type 1 diabetes typically develop autoantibodies to antigens of the pancreatic islet cells including insulin, glutamic acid decarboxylase and the protein tyrosine phosphatase-related islet antigen 2 protein. Nephrin is a protein shared by the kidney glomeruli, pancreatic beta-cells and islet microendothelia. Since circulating antibodies to nephrin have been shown to cause proteinuria, we wanted to test whether such autoantibodies can be detected in diabetic patients. METHODS: We developed a radioimmunoprecipitation assay and analysed samples in a follow-up series of 66 patients with type 1 diabetes. RESULTS: A total of 24% of the patients tested positive for nephrin autoantibodies at diagnosis, whereas 23, 14 and 18% had these antibodies at 2, 5 and 10 years, respectively. During the follow-up at 16-19 years after diagnosis, 14 patients had signs of renal injury and 29% of them tested positive for nephrin autoantibodies in at least one sample. CONCLUSIONS: We conclude that a subset of patients with type 1 diabetes present with circulating autoantibodies to nephrin. However, the present data do not allow conclusions of a causative role for these antibodies in the pathogenesis of proteinuria in diabetes.

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BACKGROUND AND AIM: The development of autoantibodies against antigens of the pancreatic islet cells is a typical phenomenon in patients with type 1 diabetes. The expression of densin, recently shown to be present in kidney podocytes, was explored in the pancreas. Additionally, we studied whether densin and filtrin, another molecule shared between the kidney podocytes and pancreatic islet cells, can act as autoantigens and whether autoantibodies against these can be detected in patients with type 1 diabetes. METHODS: Expression of pancreatic densin was studied with reverse transcription polymerase chain reaction (RT-PCR) and immunofluorescence. Children and adolescents (n = 66) with type 1 diabetes and control subjects were analysed for densin autoantibodies (DAA) and filtrin autoantibodies (FAA) using radioimmunoprecipitation assay. The serum samples were obtained at the time of diagnosis and after a duration of 2, 5 and 10 years. RESULTS: Densin expression was observed in the pancreas, localising to the beta cells. DAA were detected in 33% of the patients and the positivity was typically seen already at diagnosis. FAA were observed in 11% of the patients. The proportion of islet cell antibody (ICA) positive, GADA positive and protein tyrosine phosphatase-related islet antigen 2 antibody (IA-2A)-positive patients decreased during the follow-up period, and a similar trend was seen for DAA but not for FAA. Among the 14 patients with signs of renal injury, four tested positive for DAA and two for FAA. CONCLUSIONS: Densin is a novel molecule shared by the kidney glomerular podocytes and pancreatic islet cells. Densin and filtrin can act as autoantigens, and autoantibodies against these can be detected in patients with type 1 diabetes.

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BACKGROUND: Mutations in the gene coding for the podocyte slit-pore membrane protein, nephrin, are responsible for the Finnish-type congenital nephrotic syndrome. The present study sought to examine whether nephrin expression may also be altered in experimental diabetes, and how such changes related to the development of proteinuria. In addition, the study also sought to examine nephrin expression in animals treated with different anti-proteinuric therapies. METHODS: Nephrin gene expression and localization were examined in rats with streptozotocin-induced diabetes at 6 months duration (proteinuric phase) and at 7 days (pre-proteinuric phase). In addition, the effects of anti-proteinuric drug therapies were also assessed in long-term diabetic rats, treated with either the angiotensin-converting enzyme inhibitor perindopril, or the blocker of advanced glycation end-product formation, aminoguanidine. Nephrin expression was determined using quantitative real-time PCR and in situ hybridization. RESULTS: When compared with control animals, nephrin expression was reduced in the late proteinuric phase (45% reduction vs controls, P<0.01) but not in the early, pre-proteinuric phase of experimental diabetic nephropathy. While ACE inhibition and aminoguanidine both reduced proteinuria, only the former attenuated the diabetes-associated reduction in nephrin expression. CONCLUSIONS: These findings suggests that reduction in nephrin may be a determinant of glomerular hyperpermeability in diabetic nephropathy. Attenuation of these changes with ACE inhibition suggest that this mechanism may contribute to the anti-proteinuric effects of this, but not all classes of drug which reduce urinary protein in diabetic nephropathy.

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