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- Samsöe Andersen, Eva, et al.
(author)
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A novel diode laser system for photodynamic therapy
- 2001
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In: LASER-TISSUE INTERACTIONS, THERAPEUTIC APPLICATIONS, AND PHOTODYNAMIC THERAPY. - : SPIE. - 0277-786X .- 1996-756X. - 0819441473 ; 4433:33, s. 134-139
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Conference paper (peer-reviewed)abstract
- In this paper a novel diode laser system for photodynamic therapy is demonstrated. The system is based on linear spatial filtering and optical phase conjugate feedback from a photorefractive BaTiO3 crystal. The spatial coherence properties of the diode laser are significantly improved. The system provides an almost diffraction limited output which is efficiently coupled into a 50 mum core diameter fiber. The optical power transmitted through the fiber is increased by a factor of six when the feedback is applied to the diode laser. 85 percent of the power from the freely running laser diode is extracted in a high-quality beam and 80 percent of the output power is extracted through the fiber. The power transmitted through tile fiber scales linearly with the power of the laser diode. which means that a laser diode emitting 1.7 W multi-mode radiation would provide 1 W of optical power through a 50 mum core diameter fiber. The system is compact, portable, stable, and easy to operate.
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| 12. |
- Samsöe Andersen, Eva, et al.
(author)
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Improvement of brightness and output power of high-power laser diodes in the visible spectral region
- 2003
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In: Optics Communications. - 0030-4018. ; 219:1-6, s. 369-375
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Journal article (peer-reviewed)abstract
- This paper reports on a novel design for a high-brightness quantum-well AlGaInP laser-diode system operating at 635 nm. The spatial coherence of two broad area laser diodes is improved using spatial filtering and optical feedback from a narrow mirror stripe on each laser. To increase power, the outputs from the two systems are passively combined using a polarizing beam splitter. The result is a compact system providing a high-brightness beam. The beam-quality parameter is improved in one direction from M-2 = 12 and M-2 = 16 for the two lasers, to M-2 = 2.1 for the combined beam. The other direction of the beam is left unchanged due to its natural high quality with an M-2 value around 1.5. A procedure for efficient coupling of the two lasers into a small core-diameter optical fiber is given. This capability facilitates a wide range of applications including interstitial medical therapies, where delivery of the treatment light through thin optical fibers is essential. (C) 2003 Elsevier Science B.V. All rights reserved.
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| 13. |
- van Rheenen, W, et al.
(author)
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Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology
- 2021
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In: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 53:12, s. 1636-
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Journal article (peer-reviewed)abstract
- Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons.
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- Abe, O, et al.
(author)
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Effects of chemotherapy and hormonal therapy for early breast cancer on recurrence and 15-year survival: an overview of the randomised trials
- 2005
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In: The Lancet. - 1474-547X. ; 365:9472, s. 1687-1717
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Journal article (peer-reviewed)abstract
- Background Quinquennial overviews (1985-2000) of the randomised trials in early breast cancer have assessed the 5-year and 10-year effects of various systemic adjuvant therapies on breast cancer recurrence and survival. Here, we report the 10-year and 15-year effects. Methods Collaborative meta-analyses were undertaken of 194 unconfounded randomised trials of adjuvant chemotherapy or hormonal therapy that began by 1995. Many trials involved CMF (cyclophosphamide, methotrexate, fluorouracil), anthracycline-based combinations such as FAC (fluorouracil, doxombicin, cyclophosphamide) or FEC (fluorouracil, epirubicin, cyclophosphamide), tamoxifen, or ovarian suppression: none involved taxanes, trastuzumab, raloxifene, or modem aromatase inhibitors. Findings Allocation to about 6 months of anthracycline-based polychemotherapy (eg, with FAC or FEC) reduces the annual breast cancer death rate by about 38% (SE 5) for women younger than 50 years of age when diagnosed and by about 20% (SE 4) for those of age 50-69 years when diagnosed, largely irrespective of the use of tamoxifen and of oestrogen receptor (ER) status, nodal status, or other tumour characteristics. Such regimens are significantly (2p=0 . 0001 for recurrence, 2p<0 . 00001 for breast cancer mortality) more effective than CMF chemotherapy. Few women of age 70 years or older entered these chemotherapy trials. For ER-positive disease only, allocation to about 5 years of adjuvant tamoxifen reduces the annual breast cancer death rate by 31% (SE 3), largely irrespective of the use of chemotherapy and of age (<50, 50-69, &GE; 70 years), progesterone receptor status, or other tumour characteristics. 5 years is significantly (2p<0 . 00001 for recurrence, 2p=0 . 01 for breast cancer mortality) more effective than just 1-2 years of tamoxifen. For ER-positive tumours, the annual breast cancer mortality rates are similar during years 0-4 and 5-14, as are the proportional reductions in them by 5 years of tamoxifen, so the cumulative reduction in mortality is more than twice as big at 15 years as at 5 years after diagnosis. These results combine six meta-analyses: anthracycline-based versus no chemotherapy (8000 women); CMF-based versus no chemotherapy (14 000); anthracycline-based versus CMF-based chemotherapy (14 000); about 5 years of tamoxifen versus none (15 000); about 1-2 years of tamoxifen versus none (33 000); and about 5 years versus 1-2 years of tamoxifen (18 000). Finally, allocation to ovarian ablation or suppression (8000 women) also significantly reduces breast cancer mortality, but appears to do so only in the absence of other systemic treatments. For middle-aged women with ER-positive disease (the commonest type of breast cancer), the breast cancer mortality rate throughout the next 15 years would be approximately halved by 6 months of anthracycline-based chemotherapy (with a combination such as FAC or FEC) followed by 5 years of adjuvant tamoxifen. For, if mortality reductions of 38% (age <50 years) and 20% (age 50-69 years) from such chemotherapy were followed by a further reduction of 31% from tamoxifen in the risks that remain, the final mortality reductions would be 57% and 45%, respectively (and, the trial results could well have been somewhat stronger if there had been full compliance with the allocated treatments). Overall survival would be comparably improved, since these treatments have relatively small effects on mortality from the aggregate of all other causes. Interpretation Some of the widely practicable adjuvant drug treatments that were being tested in the 1980s, which substantially reduced 5-year recurrence rates (but had somewhat less effect on 5-year mortality rates), also substantially reduce 15-year mortality rates. Further improvements in long-term survival could well be available from newer drugs, or better use of older drugs.
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- Mishra, A, et al.
(author)
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Diminishing benefits of urban living for children and adolescents' growth and development
- 2023
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In: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 615:7954, s. 874-883
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Journal article (peer-reviewed)abstract
- Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being1–6. Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was <1.1 kg m–2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have amplified.
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| 28. |
- Raval, NR, et al.
(author)
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Synaptic Density and Neuronal Metabolic Function Measured by Positron Emission Tomography in the Unilateral 6-OHDA Rat Model of Parkinson's Disease
- 2021
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In: Frontiers in synaptic neuroscience. - : Frontiers Media SA. - 1663-3563. ; 13, s. 715811-
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Journal article (peer-reviewed)abstract
- Parkinson’s disease (PD) is caused by progressive neurodegeneration and characterised by motor dysfunction. Neurodegeneration of dopaminergic neurons also causes aberrations within the cortico-striato-thalamo-cortical (CSTC) circuit, which has been hypothesised to lead to non-motor symptoms such as depression. Individuals with PD have both lower synaptic density and changes in neuronal metabolic function in the basal ganglia, as measured using [11C]UCB-J and [18F]FDG positron emission tomography (PET), respectively. However, the two radioligands have not been directly compared in the same PD subject or in neurodegeneration animal models. Here, we investigate [11C]UCB-J binding and [18F]FDG uptake in the CSTC circuit following a unilateral dopaminergic lesion in rats and compare it to sham lesioned rats. Rats received either a unilateral injection of 6-hydroxydopamine (6-OHDA) or saline in the medial forebrain bundle and rostral substantia nigra (n = 4/group). After 3 weeks, all rats underwent two PET scans using [18F]FDG, followed by [11C]UCB-J on a separate day. [18F]FDG uptake and [11C]UCB-J binding were both lower in the ipsilateral striatal regions compared to the contralateral regions. Using [11C]UCB-J, we could detect an 8.7% decrease in the ipsilateral ventral midbrain, compared to a 2.9% decrease in ventral midbrain using [18F]FDG. Differential changes between hemispheres for [11C]UCB-J and [18F]FDG outcomes were also evident in the CSTC circuit’s cortical regions, especially in the orbitofrontal cortex and medial prefrontal cortex where higher synaptic density yet lower neuronal metabolic function was observed, following lesioning. In conclusion, [11C]UCB-J and [18F]FDG PET can detect divergent changes following a dopaminergic lesion in rats, especially in cortical regions that are not directly affected by the neurotoxin. These results suggest that combined [11C]UCB-J and [18F]FDG scans could yield a better picture of the heterogeneous cerebral changes in neurodegenerative disorders.
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| 30. |
- Samsoe, E, et al.
(author)
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Improvement of spatial and temporal coherence of a broad area laser diode using an external-cavity design with double grating feedback
- 2004
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In: Optics Express. - 1094-4087. ; 12:4, s. 609-616
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Journal article (peer-reviewed)abstract
- We demonstrate a novel technique for narrow bandwidth and highly improved lateral mode operation of a high-power broad area laser diode. The system uses simultaneous feedback from the first diffracted order and the zeroth reflected order of a diffraction grating. The two feedback paths lead to simultaneously improvement of the spectral and spatial properties of the laser diode. The laser system operates in the well-known asymmetric double-lobed far field pattern with the larger lobe being extracted as the output. The bandwidth of the output beam is measured to 0.07 nm, which corresponds to an improvement of a factor of 17 compared to the bandwidth of the freely running laser. The output from the system contains 54% of the energy reaching the grating, or 75% of the power reflected into the zeroth order. The improvements in both the spatial and temporal coherence opens the possibility of using this laser system in applications such as frequency doubling and pumping of optical parametric oscillators. (C) 2004 Optical Society of America.
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| 34. |
- Weber, M., et al.
(author)
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Preserved slow conducting corticomotoneuronal projections in ALS patients with autosomal recessive D90A CuZn-SOD mutation.
- 2000
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In: Brain. - : Oxford University Press (OUP). - 0006-8950 .- 1460-2156. ; 123:7, s. 1505-1515
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Journal article (peer-reviewed)abstract
- Recently, a subgroup of the amyotrophic lateral sclerosis (ALS) syndrome associated with mutations in the gene encoding the free radical scavenging enzyme CuZn-superoxide dismutase (CuZn-SOD, SOD1) has been identified. Some 67 different mutations have been reported worldwide to date, comprising about one-fifth of familial ALS cases in the populations studied. The autosomal recessively inherited D90A CuZn-SOD mutation has been associated with a very slowly progressive, clinically distinct phenotype, and is neurophysiologically characterized by very slow central motor conduction. It is not known which physiological and/or biochemical mechanisms are responsible for the different clinical course. To delineate ALS associated with this particular CuZn-SOD mutation from ALS without mutations, we performed a detailed neurophysiological study of the corticomotoneuronal function using peristimulus time histograms (PSTHs) in eight ALS patients homozygous for the D90A CuZn-SOD mutation. The results were compared with those obtained in 12 non-hereditary ALS patients and 11 healthy subjects. PSTHs were constructed from three to seven different, voluntarily recruited motor units of the extensor digitorum communis muscle (EDC) in each patient. The onset latency, number of excess bins, duration and synchrony of the primary peak were analysed. All measurements differed significantly between healthy controls and the D90A patients (P < 0.0007). The mean onset latency of the primary peak in D90A patients was 35.3 ms, compared with 24.2 ms for non-hereditary ALS patients and 19.3 ms for normal subjects (P < 0.0000). Delayed primary peaks in the D90A patients were desynchronized and characteristically preceded by a marked suppression phase. This suppression phase was not seen in non-hereditary ALS patients. We conclude that the mainly slow conducting and/or polysynaptic corticomotoneuronal connections are preserved in the D90A homozygous cases, and that the cortical and possibly spinal inhibitory circuitry is preserved. These events may partially protect the motor neurons, slowing down the degenerative process.
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| 35. |
- Weber, M., et al.
(author)
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The physiological basis of conduction slowing in ALS patients homozygous for the autosomal recessive D90A CuZn-SOD mutation
- 2001
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In: Muscle and Nerve. - 0148-639X .- 1097-4598. ; 24:1, s. 89-97
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Journal article (peer-reviewed)abstract
- Familial amyotrophic lateral sclerosis (ALS) with the autosomal-recessively inherited D90A CuZn-superoxide dismutase (CuZn-SOD) mutation is characterized by a stereotypic slowly progressive, distinctive phenotype and very slow central motor conduction. To determine the basis of this slowing, we assessed corticomotoneuronal function using peristimulus time histograms (PSTHs) in 8 ALS patients homozygous for the D90A CuZn-SOD mutation. The results were compared with findings in 10 patients with multiple sclerosis (MS), in which slowing of central motor conduction is common, and 11 healthy subjects. PSTHs were constructed from 3-7 different, voluntarily recruited motor units recorded in each patient from the extensor digitorum communis muscle (EDC). In D90A and MS patients, the stimulus threshold, onset latency, number of excess bins, duration, amplitude, and synchrony of the primary peak differed significantly from controls (P < 0.0004). The mean onset latency of the primary peak in D90A patients was 35.3 ms, compared to 23.6 ms for MS patients and 19.3 ms for normal subjects (P < 0.0001). In the D90A patients, the onset latencies of the primary peak had a bimodal distribution, whereas in MS the distribution showed a continuum. Loss of synchrony was similar in D90A and MS patients, but the threshold, number of excess bins, and duration differed significantly (P < 0.0057), which suggests that either axonal loss or demyelination can result in delayed and desynchronized primary peaks. We propose that conduction slowing in the D90A homozygotes results from selective loss of fast-conducting large pyramidal cells with preservation of slow-conducting mono- or polysynaptic corticomotoneuronal connections. Copyright 2001 John Wiley & Sons, Inc.
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