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According to current estimates, atmospheric new particle formation (NPF) produces a large fraction of aerosol particles and cloud condensation nuclei in the Earth's atmosphere, which have implications for health and climate. Despite recent advances, atmospheric NPF is still insufficiently understood in the lower troposphere, especially above the mixed layer (ML). This paper presents new results from co-located airborne and ground-based measurements in a boreal forest environment, showing that many NPF events (∼42 %) appear to start in the topmost part of the residual layer (RL). The freshly formed particles may be entrained into the growing mixed layer (ML) where they continue to grow in size, similar to the aerosol particles formed within the ML. The results suggest that in the boreal forest environment, NPF in the upper RL has an important contribution to the aerosol load in the boundary layer (BL).

Heritability of Proliferative Diabetic Retinopathy Kustaa Hietala 1 2 , Carol Forsblom 1 3 , Paula Summanen 2 , Per-Henrik Groop 1 3 and on behalf of the FinnDiane Study Group 1 Folkhälsan Institute of Genetics, Folkhälsan Research Center, Biomedicum Helsinki, Helsinki, Finland 2 Department of Ophthalmology, Helsinki University Central Hospital, Helsinki, Finland 3 Division of Nephrology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland Corresponding author: Per-Henrik Groop, per-henrik.groop{at}helsinki.fi Abstract OBJECTIVE— Diabetic nephropathy clusters in families, suggesting that genetic factors play a role in its pathogenesis. We investigated whether similar clustering exists for proliferative retinopathy in families with two or more siblings with type 1 diabetes. RESEARCH DESIGN AND METHODS— The FinnDiane Study has characterized 20% (4,800 patients) of adults with type 1 diabetes in Finland. In 188 families, there were at least two siblings with type 1 diabetes. Ophthalmic records were obtained for 369 of 396 (93%) and fundus photographs for 251 of 369 (68%) patients. Retinopathy was graded based on photographs and/or repeated ophthalmic examinations using the Early Treatment of Diabetic Retinopathy grading scale. RESULTS— Mean age at onset of diabetes was 14.3 ± 10.2 years, and mean duration was 25.9 ± 11.8 years. Proliferative retinopathy was found in 115 of 369 patients (31%). The familial risk of proliferative retinopathy was estimated in 168 of 188 sibships, adjusted for A1C, duration, and mean blood pressure. Proliferative retinopathy in the probands (48 of 168) was associated with an increased risk (odds ratio 2.76 [95% CI 1.25- 6.11], P = 0.01) of proliferative retinopathy in the siblings of probands (61 of 182). The heritability of proliferative retinopathy was h 2 = 0.52 ± 0.31 ( P < 0.05). CONCLUSIONS— We found a familial clustering of proliferative retinopathy in patients with type 1 diabetes. The observation cannot be accounted for by conventional risk factors, suggesting a genetic component in the pathogenesis of proliferative retinopathy in type 1 diabetes. Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 28 April 2008. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted April 22, 2008. Received October 22, 2007. DIABETES

Diabetic retinopathy (DR) is a sight-threatening condition caused by diabetes. Screening programmes for DR include eye examinations, where the patient’s fundi are photographed, and the findings, including DR severity, are recorded in the medical report. However, statistical analyses based on DR severity require structured labels that calls for laborious manual annotation process if the report format is unstructured. In this work, we propose a large language model DR-GPT for classification of the DR severity from unstructured medical reports. On a clinical set of medical reports, DR-GPT reaches 0.975 quadratic weighted Cohen’s kappa using truncated Early Treatment Diabetic Retinopathy Study scale. When DR-GPT annotations for unlabeled data are paired with corresponding fundus images, the additional data improves image classifier performance with statistical significance. Our analysis shows that large language models can be applied for unstructured medical report databases to classify diabetic retinopathy with a variety of applications.

Background As the retina is suggested to mirror the brain, we hypothesized that diabetic retinopathy and macular edema are indicative of stroke risk in type 1 diabetes and sought to assess this association in individuals with type 1 diabetes. Methods We included 1,268 adult FinnDiane Study participants with type 1 diabetes (age 38.7 ± 11.8 years, 51.7% men vs. 48.3% women, and 31.5% had diabetic kidney disease), data on baseline diabetic retinopathy severity, and first stroke during our observational follow-up. Retinopathy was graded by the Early Treatment Diabetic Retinopathy Study (ETDRS) scale, and macular edema as clinically significant (CSME) or not. Strokes identified from registries were confirmed from medical files. Adjusted hazard ratios (HR) for stroke by retinopathy severity and CSME were calculated by Cox models adjusted for clinical confounders, including diabetic kidney disease. Results During median 18.0 (14.1–19.3) follow-up years, 130 strokes (96 ischemic, 34 hemorrhagic) occurred. With no–very mild (ETDRS 10–20) retinopathy as reference, the adjusted HR for stroke was 1.79 (95%CI 1.02–3.15) in non-proliferative (ETDRS 35–53), and 1.69 (1.02–2.82) in proliferative (ETDRS 61–85) retinopathy. Corresponding adjusted HR for ischemic stroke was 1.68 (0.91–3.10) in non-proliferative and 1.35 (0.77–2.36) in proliferative retinopathy. The adjusted HR for hemorrhagic stroke was 2.84 (0.66–12.28) in non-proliferative and 4.31 (1.16–16.10) in proliferative retinopathy. CSME did not increase HR for any stroke type after adjustment for clinical confounders (data not shown). Conclusions Stroke incidence increases with the severity of diabetic retinopathy independently of comorbid conditions, including diabetic kidney disease.

OBJECTIVE: Age at onset of type 1 diabetes influences the risk of microvascular complications. However, the long-term risk of proliferative retinopathy within the wide spectrum of age at onset of type 1 diabetes is less well known. RESEARCH DESIGN AND METHODS: A sample of 1,117 consecutively recruited patients was drawn from the FinnDiane Study population (4,800 patients). Type 1 diabetes was defined as age at onset [less-than or equal to]40 years, insulin treatment initiated within 1 year, and C-peptide [less-than or equal to]0.3 nmol/l. Retinopathy status was graded based on ophthalmic records and/or fundus photographs. The risk of proliferative retinopathy was studied in age-at-onset groups 0-4, 5-14, and 15-40 years. RESULTS: The mean durations to proliferative retinopathy were 24.3 (22.7-25.9) years in the 0-4 years group, 20.1 (19.2-21.1) years in the 5-14 years group, and 21.6 (19.8-23.3) years in the 15-40 years group (P < 0.001). In a Cox regression model, with A1C, blood pressure, sex, and BMI as covariates, the highest risk of proliferative retinopathy was observed in the 5-14 years group (hazard ratio 1.90 [95% CI 1.45-2.48], P < 0.001). Diabetes onset 0-4 vs. 5-14 years made no difference in the long-term risk of proliferative retinopathy (P = 0.2). When split into two groups, age at onset <15 years was associated with a higher long-term risk than age at onset ≥15 years (1.82 [1.40-2.36], P < 0.001). CONCLUSIONS: Age at onset significantly modifies the long-term risk of proliferative retinopathy. The highest risk is in age-at-onset group 5-14 years, whereas the lowest risk is in age-at-onset group 15-40 years.

To determine if the cumulative incidence of severe retinopathy in patients with type 1 diabetes has changed. The study looked at 3,781 patients diagnosed with type 1 diabetes (1939-2005), median age at onset 13 (interquartile range [IQR] 9-21) years, and duration of diabetes 19 (IQR 13-27) years. The severe retinopathy was based on a history of laser treatment. Patients were divided into <1975, 1975-1979, 1980-1984, and ≥1985 cohorts according to the diagnosis of diabetes. The cumulative incidence of severe retinopathy has declined (P < 0.0001). After 20 years of duration, the cumulative incidence was 23% (95% CI 21-25) and 33 (30-35) in the earliest cohorts, 18 (15-21) in the next cohort, and 6 (4-9) in the recent cohort. After 30 years, the cumulative incidence was 52 and 48% in the earliest cohorts, while it was 62% after 40 years in the earliest cohort. The cumulative incidence of severe retinopathy has declined in patients with type 1 diabetes.

The behavior of biodegradable polylactide as a stent material has not yet been fully established in small vessels such as arteries with a diameter <3 mm. The aim of this study was to investigate the long-term effect of a copolymeric polylactide (PLA96) stent. Appropriately sized spiral PLA96 stents were implanted into the infrarenal aortas of 20 rabbits. Intraoperative systemic heparinization (150 IU/kg), perioperative subcutaneous enoxaheparin sodium (10 mg), ticlopidine (250 mg/day) for 1 month, and acetosalicylic acid (12.5 mg/day) were continuously administered. Animals were euthanized according to a fixed timetable for up to 34 months for histologic and scanning-electron-microscopic assessment. Endothelialization was complete within 1 month. In 2 of the 3 aortas sampled 3 months after implantation, a mild inflammatory reaction was visible, with no sign of granulomatous or foreign-body reaction in the vessel wall. Instead, in 1 sample examined at the same time point, neointimal chondroid metaplasia was detected. After 6 months, inflammatory reaction declined in the vessel wall. Hydrolyzation of the stent was histologically evident at 12 months, with mild foreign-body reaction detectable in 2 of 5 aortas sampled at this time point. The stent disintegrated without fragmentation by 24 months, as it was gradually replaced by fibrosis. The vessel lumen remained patent at all time points. We conclude that the PLA96 stent degraded with minimal tissue response within 24 months. PLA96 may thus be a promising stent core material for small vessels in the future, although further investigation is needed to establish its final biocompatibility.

Intravascular metallic stents cause magnetic field distortions, disturbing luminal detection. Our aim was to evaluate the effect of polylactic acid (PLA) stents on magnetic resonance angiography (MRA). Biodegradable double spiral helical PLA stents ( n=12) or stainless steel (SS) ( n=6) stents were implanted into the infrarenal aortas of New Zealand White rabbits. All SS- and 6 PLA-stented animals as well as 6 non-operated control rabbits were imaged with gadolinium-enhanced MRA (1.5 T), and infrarenal aortic diameters (proximal, distal, and narrowest), together with the stent artifact, were measured. Six of the PLA-stented rabbits were followed up, and MRA was assessed at 2, 6, 9, and 12 months after the stent implantation. Image artifacts caused by the SS stents were visualized in all cases. The PLA stents caused no magnetic field distortion, allowing imaging of the underlying vessel including the vessel lumen. In the follow-up group of 6 rabbits with a PLA stent, 5 of 6 were patent at the end of the follow-up of 12 months. These stents allowed luminal detection at all time points, with no significant differences in aortic measurements emerging during the whole follow-up period. When immediately postoperatively scanned SS and PLA rabbits were compared with controls, no differences were observable in proximal diameters. Instead, the percentage of distal luminal loss was greater in the PLA-stented rabbits, as compared with SS stents ( p<0.01). The PLA stenting in small vessels allows evaluation of luminal patency with MRA both immediately after implantation and during follow-up.

The behavior of biodegradable polylactide as a stent material has not yet been fully established in small vessels such as arteries with a diameter <3 mm. The aim of this study was to investigate the long-term effect of a copolymeric polylactide (PLA96) stent. Appropriately sized spiral PLA96 stents were implanted into the infrarenal aortas of 20 rabbits. Intraoperative systemic heparinization (150 IU/kg), perioperative subcutaneous enoxaheparin sodium (10 mg), ticlopidine (250 mg/day) for 1 month, and acetosalicylic acid (12.5 mg/day) were continuously administered. Animals were euthanized according to a fixed timetable for up to 34 months for histologic and scanning-electron-microscopic assessment. Endothelialization was complete within 1 month. In 2 of the 3 aortas sampled 3 months after implantation, a mild inflammatory reaction was visible, with no sign of granulomatous or foreign-body reaction in the vessel wall. Instead, in 1 sample examined at the same time point, neointimal chondroid metaplasia was detected. After 6 months, inflammatory reaction declined in the vessel wall. Hydrolyzation of the stent was histologically evident at 12 months, with mild foreign-body reaction detectable in 2 of 5 aortas sampled at this time point. The stent disintegrated without fragmentation by 24 months, as it was gradually replaced by fibrosis. The vessel lumen remained patent at all time points. We conclude that the PLA96 stent degraded with minimal tissue response within 24 months. PLA96 may thus be a promising stent core material for small vessels in the future, although further investigation is needed to establish its final biocompatibility.