| 1. |
- Berntorp, Kerstin, et al.
(författare)
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Initiation of biphasic insulin aspart 30/70 in subjects with type 2 diabetes mellitus in a largely primary care-based setting in Sweden.
- 2011
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Ingår i: Primary Care Diabetes. - : Elsevier BV. - 1878-0210 .- 1751-9918. ; 5, s. 89-94
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: Despite a wealth of clinical trial data supporting use of the premixed insulin analogue, biphasic insulin aspart 30 (BIAsp 30) in the treatment of type 2 diabetes mellitus (T2DM), there is limited documentation of its use in primary care-based clinical practice. METHODS: An observational study investigating the safety and efficacy of BIAsp 30 in routine clinical practice was conducted. Patients were followed up 3 and 6 months after initiating insulin treatment. Safety and efficacy measures were documented. RESULTS: During the course of the study, 1154 patients were included (age range 20-95years), of whom 89% completed the 6-month follow-up period. Mean HbA(1c) at baseline was 8.8% (73mmol/mol), and had improved to 7.2% (55mmol/mol) after 6 months of treatment. The rate of total hypoglycaemia at completion of the study was 4.1 events per patient year. Major hypoglycaemic events were rare (two in total). CONCLUSIONS: BIAsp 30 was initiated safely and effectively in insulin-naïve patients with T2DM. The safety and efficacy profile observed in clinical trials was confirmed in this largely primary care-based setting in Sweden.
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| 2. |
- Ek Olofsson, Henric, et al.
(författare)
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Are cortical microvascular raspberries caused by cerebral hypoperfusion? An exploratory pathological study
- 2021
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Ingår i: Cerebral Circulation - Cognition and Behavior. - : Elsevier BV. - 2666-2450. ; 2
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: This retrospective study investigated a cortical microvascular formation, termed a ‘raspberry’ due to its appearance under a bright-field microscope. We examined whether there is support for the hypothesis that raspberry formation is an angiogenic process induced by cerebral hypoperfusion. Materials and Methods: Raspberries were manually quantified in haematoxylin and eosin-stained cortical sections from the anterior frontal lobe of deceased individuals who had undergone a diagnostic neuropathological examination at the Department of Pathology, Lund, Sweden, during April 2019–January 2021. Subjects represented consecutively received cases during this 22-month period. The raspberry density was compared between subjects according to variables collected from medical records and autopsy reports: age, sex, hypertension, diabetes mellitus, atrial fibrillation, orthostatic hypotension, chronic heart failure, acute circulatory failure, aortic atherosclerosis, atherosclerosis of the basal cerebral arteries (referred to as ‘cerebral atherosclerosis’), cerebral small vessel disease, cerebral amyloid angiopathy, cerebral infarction, and ischaemic white matter disease. Results: 62 subjects were included. The mean age was 71.9 years (range 46–97 years). 21 subjects (33.9%) were female. Independent-samples t-test showed a higher raspberry density in subjects with cerebral atherosclerosis (p = 0.029; 95% CI 0.7, 11.6 raspberries/cm²). The higher raspberry density in subjects with cerebral atherosclerosis remained in multiple linear regression (p = 0.003; 95% CI 2.3, 11.1 raspberries/cm²). Conclusion: This exploratory study indicates that cortical raspberries could be associated with cerebral atherosclerosis. The remaining results were inconclusive but motivate further examination of variables such as acute circulatory failure.
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| 3. |
- Ek Olofsson, Henric, et al.
(författare)
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On the regional distribution of cerebral microvascular ‘raspberries’ and their association with cerebral atherosclerosis and acute circulatory failure
- 2023
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Ingår i: Cerebral Circulation - Cognition and Behavior. - : Elsevier BV. - 2666-2450. ; 4, s. 1-5
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Tidskriftsartikel (refereegranskat)abstract
- IntroductionIn this follow-up study, cerebral microvascular formations termed ‘raspberries’ were quantified according to cerebral atherosclerosis (C-ASCL) and acute circulatory failure (ACF). We also examined the regional distribution of raspberries throughout the brain.Materials and methodsThe study population consisted of adult individuals who had undergone a diagnostic neuropathological autopsy. Groups were formed to examine the association between raspberries, C-ASCL and ACF (control group, C-ASCL group, C-ASCL+ACF group [n = 47 per group] and a combined C-ASCL-tot group [n = 94]). To examine the regional distribution, additional groups were formed based on previously known raspberry densities of the frontal cortex (high-, medium- and low-density group [n = 6 per group]). Raspberries were quantified on scanned haematoxylin-eosin-stained sections.ResultsCortical raspberry density did not differ at a statistically significant level between the control group, the C-ASCL group and the C-ASCL+ACF group (P = 0.10) but did so between the control group and the C-ASCL-tot group (P = 0.033). The total raspberry density of the high-, medium- and low-density groups differed at a statistically significant level (P = 0.005), which remained in group-to-group comparisons of the high- and medium-density groups (P = 0.015) and the high- and low-density groups (P = 0.002). Raspberries were rare in cerebral white matter and in the cerebellum.ConclusionAn association between raspberry density and C-ASCL is supported but is weaker than previously indicated. An association with ACF is not indicated. The raspberry density of the frontal cortex provides an approximation of the brain's total raspberry density.
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| 4. |
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| 5. |
- Haglund, Håkan, et al.
(författare)
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Snow Accumulation in Real-time
- 2002
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Ingår i: Proceedings from SIGRAD 2002. ; , s. 11-15
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Konferensbidrag (refereegranskat)abstract
- Whenever real-time snowfall is animated in computer games, no snow accumulation is simulated, as far as we know. Instead, so-called zero thickness is used, which means that the blanket of snow does not grow when the snowflakes reach the ground. In this paper we present a method for simulation of snow accumulation, which simulates the different stages, starting with a snow free environment and ending with a totally snow covered scene, all in real-time. The main focus is not on the physical properties of snow but on speed and visual result.
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| 6. |
- Haglund, Mattias, et al.
(författare)
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A methodological study of locus coeruleus degeneration in dementing disorders
- 2016
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Ingår i: Clinical Neuropathology. - 0722-5091. ; 35:5, s. 287-294
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Tidskriftsartikel (refereegranskat)abstract
- Background: Degeneration of the locus coeruleus (LC) of the brain stem is a recognized phenomenon in Alzheimer's disease (AD), in dementia with Lewy bodies (DLB), and in Parkinson's disease with dementia (PDD). Prior studies have suggested that LC degeneration can be used to differentiate various dementing disorders histologically, but the paucity of methodological data may hamper systematic research on this nucleus. Purpose: The purpose of this study was to evaluate various approaches to quantifying LC degeneration in dementing disorders, and to inform future decisions regarding the most appropriate method for diagnostics and research. Methods: 105 LCs from brains of demented individuals with AD, DLB/PDD, vascular dementia (VaD), mixed dementia (AD+VaD), or frontotemporal lobar degeneration (FTLD) were examined, and the extent of LC degeneration was assessed using macroscopic evaluation, cell counting, and two degeneration scales. Scores were compared across diagnostic categories; diagnostic utility and intra- and interobserver reliability were assessed. Results: AD and DLB/PDD were associated with greater LC damage using either assessment method, significantly different from VaD and FTLD. Macroscopic appearance was informative, but cell counting was more sensitive and specific. The degeneration scales did not add significant diagnostic value over cell counting and were associated with greater observer variability. Conclusions: The LC degenerates in certain dementia subtypes, especially in AD and DLB/PDD. Macroscopic assessment of the LC postmortem can be used to differentiate between disorders associated with degeneration (AD, DLB/PDD) or sparing (VaD) of the LC, but counting LC cells in a representative pontine section is the most appropriate method by which to assess LC degeneration.
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| 7. |
- Haglund, Mattias, et al.
(författare)
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Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia.
- 2006
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Ingår i: International Journal of Geriatric Psychiatry. - : Wiley. - 1099-1166 .- 0885-6230. ; 21:7, s. 681-687
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Tidskriftsartikel (refereegranskat)abstract
- Background and purpose Vascular dementia (VaD) has occasionally been associated with cerebral amyloid angiopathy (CAA), but the prevalence and significance of this counterintuitive relationship are poorly known. Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases. Methods We examined temporal and parietal regions of the cerebral cortex of 26 consecutive VaD cases from the Lund Longitudinal Dementia Study. We carried out immunohistochemistry and routine stainings, determined Apolipoprotein E (ApoE) genotypes, and obtained clinical characteristics on the studied group for retrospective analysis. Results CAA was marked in eight out of 26 cases, and correlated strongly with the presence of cortical microinfarcts, both in the temporal lobe and in the parietal lobe. Based on comparisons with eight age-matched VaD cases without CAA, the clinical records suggested that VaD cases with CAA as a group exhibited less pronounced neurological symptoms. A clear contribution of the ApoE genotype could not be identified. Conclusions Based on a combination of the clinical and pathological data, we suggest that microinfarcts in the cerebral cortex associated with severe CAA may be the primary pathological substrate in a significant proportion of VaD cases. Future studies should be undertaken to confirm or dismiss the hypothesis that these cases exhibit a different symptom profile than VaD cases without CAA. Copyright (c) 2006 John Wiley & Sons, Ltd.
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| 8. |
- Haglund, Mattias, et al.
(författare)
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Cerebral amyloid angiopathy, white matter lesions and Alzheimer encephalopathy - A histopathological assessment
- 2002
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Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 14:3, s. 161-166
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Tidskriftsartikel (refereegranskat)abstract
- To test the hypothesis that the cerebral amyloid angiopathy (CAA) of Alzheimer's disease (AD) is quantitatively associated with white matter lesions (WML), the brains of 63 demented patients exhibiting varying degrees of Alzheimer encephalopathy (AE) were examined, along with those of 10 nondemented control cases. The ratio of amyloid-positive to amyloid-negative vessels in the leptomeninges of the frontal pole from each patient was calculated subsequent to microscopical examination, and the severity of WML was graded according to previously published criteria. In AD cases without a significant component of vascular dementia, the level of CAA was found to correlate with the degree of WML diagnosed and graded by neuropathology. Neither age nor severity of AE correlated significantly with WML. There may be several reasons for the conflicting results of this study vis-a-vis earlier investigations; the roles played by different methods of staining, CAA quantitation and patient subgroup selection are also discussed. Copyright (C)2002 S. Karger AG, Basel.
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| 9. |
- Haglund, Mattias, et al.
(författare)
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Differential deposition of amyloid beta peptides in cerebral amyloid angiopathy associated with Alzheimer's disease and vascular dementia.
- 2006
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Ingår i: Acta Neuropathologica. - : Springer Science and Business Media LLC. - 1432-0533 .- 0001-6322. ; 111:5, s. 430-435
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Tidskriftsartikel (refereegranskat)abstract
- Cerebral amyloid angiopathy (CAA) caused by deposition of amyloid beta (A beta) peptides in the cerebrovasculature, involves degeneration of normal vascular components and increases the risk of infarction and cerebral hemorrhage. Accumulating evidence suggests that sporadic CAA is also a significant contributor to cognitive decline and dementia in the elderly. However, the mechanisms by which CAA arises are poorly understood. While neuronal sources of A beta peptides are sufficient to cause CAA in transgenic mice overexpressing the amyloid precursor protein, there is reason to believe that in aging man, vascular disease modulates the disease process. To better understand CAA mechanisms in dementia, we assessed the frontal cortex of 62 consecutive cases of Alzheimer's disease (AD), vascular dementia (VaD), and mixed dementia (MD) using immunohistochemistry with antibodies to A beta, smooth muscle actin and the carboxyl-terminal peptides to detect A beta(40) and A beta(42). While vascular A beta deposition was invariably associated with smooth muscle degeneration as indicated by absence of smooth muscle cell actin reactivity, VaD/MD cases exhibited markedly more vascular A beta(42) deposits and smooth muscle actin loss compared to AD cases with similar degrees of CAA and A beta(40) deposition. This suggests that distinct mechanisms are responsible for the differential deposition of A beta in CAA associated with AD and that associated with ischemic/cerebrovascular disease. It is plausible that experimental studies on the effects of cerebrovascular disease on A beta production and elimination will yield important clues on the pathogenesis of CAA.
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| 10. |
- Haglund, Mattias, et al.
(författare)
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Hippocampus and basal ganglia as potential sentinel sites for ischemic pathology after resuscitated cardiac arrest
- 2019
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Ingår i: Resuscitation. - : Elsevier BV. - 0300-9572. ; 139, s. 230-233
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Tidskriftsartikel (refereegranskat)abstract
- Aims of the study: Neurological impairment after resuscitated cardiac arrest (CA) remains a significant unmet medical need. Brain ischemia associated with CA and subsequent reperfusion is evident as two fundamentally different types of damage on neuropathological examination: frank necrosis (involving all cell types) and selective eosinophilic neuronal death (SEND). These types of damage are not only dissimilar in micromorphology, but also differently detectable with clinical brain imaging methods. In a previous study, SEND was reported in most patients surviving the initial CA. This study was undertaken to further characterize and map SEND in an expanded dataset. Methods: A cohort of 46 cases was included from an observational study on targeted temperature management (TTM) of resuscitated CA. Six brain and brain stem regions and 21 subregions were examined, and SEND severity was tested for correlation with time to ROSC. Representativity of all regions vis-à-vis global SEND was assessed, to investigate whether any particular region could be used as a “sentinel site” for overall damage. Results: The thalamus, the CA4 subregion of the hippocampus and the Purkinje cell layer of the cerebellum were the most severely affected subregions. Involvement of the hippocampus, cerebellum, cortex or basal ganglia indicated presence of SEND in other regions. There was a significant correlation between time to ROSC and SEND. Conclusion: There are regional differences in SEND distribution. Cases free of SEND in the hippocampus or basal ganglia are unlikely to have significant SEND in other regions, suggesting that these regions could be used as “sentinel sites” for global SEND in future studies.
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