| 1. |
- Almemark, Mats, et al.
(author)
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Analysis and Development of the Interpretation process in LCA
- 2000
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Reports (other academic/artistic)abstract
- The objective of this work is to study interpretation as a procedure to use the quantitative results of a life-cycle inventory to compare process alternatives with the aim to conclude, whether or not significant differences exist with regard to the studied issues (individual emissions or impact categories). As a result of an introductory survey a procedure for quantitative interpretations is suggested, with data-quality scoring, statistical experimental planning, and multivariate data analysis as basic tools. The procedure has been tested on a case study of treatment of paper packaging waste, either by material recycling or by energy recovery (incineration). The inventory of an earlier study has been used. With the aid of what is called a conceptual model five variables, which could be presumed to have an influence on the environmental impact of paper packaging waste treatment, were identified. The choice of technology, material recycling or energy recovery, was one of these variables. Subsequently 36 scenario calculations, organised in an experimental matrix, were performed. The result was interpreted with the multivariate techniques principal component analysis (PCA), partial least-square modelling (PLS), and uncertainty analysis. The multivariate analysis made it possible to isolate the influence of the variable 'choice of technology' on the environmental impact of the system.
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| 2. |
- Björkenstam, Charlotte, et al.
(author)
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Sickness absence and disability pension before and after first childbirth and in nulliparous women : longitudinal analyses of three cohorts in Sweden
- 2019
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In: BMJ Open. - : BMJ. - 2044-6055. ; 9:9
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Journal article (peer-reviewed)abstract
- Objective Childbirth is suggested to be associated with elevated levels of sickness absence (SA) and disability pension (DP). However, detailed knowledge about SA/DP patterns around childbirth is lacking. We aimed to compare SA/DP across different time periods among women according to their childbirth status.Design Register-based longitudinal cohort study.Setting Sweden.Participants Three population-based cohorts of nulliparous women aged 18–39 years, living in Sweden 31 December 1994, 1999 or 2004 (nearly 500 000/cohort).Primary and secondary outcome measures Sum of SA >14 and DP net days/year.Methods We compared crude and standardised mean SA and DP days/year during the 3 years preceding and the 3 years after first childbirth date (Y−3 to Y+3), among women having (1) their first and only birth during the subsequent 3 years (B1), (2) their first birth and at least another delivery (B1+), and (3) no childbirths during follow-up (B0).Results Despite an increase in SA in the year preceding the first childbirth, women in the B1 group, and especially in B1+, tended to have fewer SA/DP days throughout the years than women in the B0 group. For cohort 2005, the mean SA/DP days/year (95% CIs) in the B0, B1 and B1+ groups were for Y−3: 25.3 (24.9–25.7), 14.5 (13.6–15.5) and 8.5 (7.9–9.2); Y−2: 27.5 (27.1–27.9), 16.6 (15.5–17.6) and 9.6 (8.9–10.4); Y−1: 29.2 (28.8–29.6), 31.4 (30.2–32.6) and 22.0 (21.2–22.9); Y+1: 30.2 (29.8–30.7), 11.2 (10.4–12.1) and 5.5 (5.0–6.1); Y+2: 31.7 (31.3–32.1), 15.3 (14.2–16.3) and 10.9 (10.3–11.6); Y+3: 32.3 (31.9–32.7), 18.1 (17.0–19.3) and 12.4 (11.7–13.0), respectively. These patterns were the same in all three cohorts.Conclusions Women with more than one childbirth had fewer SA/DP days/year compared with women with one childbirth or with no births. Women who did not give birth had markedly more DP days than those giving birth, suggesting a health selection into childbirth.
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| 3. |
- Björkenstam, Charlotte, et al.
(author)
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Sickness absence and disability pension in relation to first childbirth and in nulliparous women according to occupational groups : a cohort study of 492,504 women in Sweden
- 2020
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In: BMC Public Health. - : Springer Science and Business Media LLC. - 1471-2458. ; 20:1
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Journal article (peer-reviewed)abstract
- Background: Childbirth has been suggested to increase sickness absence (SA) and disability pension (DP). This may vary by occupation; however, knowledge in this field remains limited. We explored SA and DP in the years before and after childbirth among women in four occupational groups and those without occupation.Methods: We studied nulliparous women aged 18–39 years, living in Sweden on December 31, 2004 (n = 492,504). Women were categorized into five skill-level based occupational groups and three childbirth groups; no childbirths within 3 years (B0), first childbirth in 2005 with no childbirth within 3 years (B1), and first childbirth in 2005 with at least one more birth within 3 years (B1+). We compared crude and standardized annual mean SA (in spells> 14 days) and DP net days in the 3 years before and 3 years after first childbirth date.Results: Women in the highest skill level occupations and managers, had less mean SA/DP days during most study years than women in the lowest skill level occupations group. In B1 and B1+, absolute differences in mean SA/DP, particularly in SA, among occupational groups were highest during the year before childbirth. DP was most common in B0, regardless of group and year.Conclusions: We found that women’s mean SA/DP days before and after first childbirth was higher with decreasing skill-level of the occupational group and these differences were most pronounced in the year before childbirth. DP was most common among women not giving birth, regardless of occupational group.
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| 4. |
- László, Krisztina D., et al.
(author)
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Sickness absence and disability pension before and after first childbirth and in nulliparous women by numerical gender segregation of occupations : A Swedish population-based longitudinal cohort study
- 2019
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In: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 14:12
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Journal article (peer-reviewed)abstract
- Background: Pregnancy is associated with a temporarily increased sickness absence (SA) risk. This association may vary by the level of occupational gender segregation; however, knowledge in this area is limited. We studied whether trends in SA and disability pension (DP) in the years before and after first childbirth among women with one or more childbirths and with no childbirth during the study period varied by occupational gender segregation.Methods: We conducted a population-based register study involving nulliparous women aged 18–39 years, living in Sweden in 2002–2004 (n = 364,411). We classified participants in three childbirth groups as: (1) no childbirth in 2005 or in the next 3.75 years, (2) first childbirth in 2005 and no births in the subsequent 3.75 years, and (3) first childbirth in 2005 and at least one additional birth in the subsequent 3.75 years, and into five categories based on the rate of women in their occupations. We compared crude and standardized mean annual net SA and DP days during the three years before and the three years after 2005 across the childbirth and occupational gender segregation categories.Results: Women in extremely male-dominated occupations had or tended to have somewhat higher mean combined SA and DP days than women in gender-integrated occupations; women in female-dominated occupations had comparable or tended to have slightly higher mean SA and DP days than women in gender-integrated occupations. Except for the year before the first childbirth, women who gave birth, especially those who gave several births, had generally a lower mean combined standardized SA and DP days than nulliparous women. We found no substantial differences in trends in SA and DP around the time of first childbirth according to occupational gender segregation.Conclusions: Trends in SA and DP around the time of first childbirth did not vary by occupational gender segregation.
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| 5. |
- Lindfors, Charlotte
(author)
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Appetite control : genetic, immunological and neurobiological aspects
- 2017
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Doctoral thesis (other academic/artistic)abstract
- The overall goal of this thesis is to develop a better understanding of the brain’s regulation of appetite, i.e. the hypothalamic regulation of hunger and satiety signals. The correct regulation of appetite is crucial, potentially involved both in traditional eating disorders, such as anorexia nervosa and bulimia nervosa, as well as overweight, obesity and failure to thrive in infants and children. Anorexia/cachexia is also a severe and frequent complication to several common disorders such as cancer, HIV, renal failure and Alzheimer’s disease and is one of the most important factors determining both quality of life and mortality in these conditions. In this thesis, the anx/anx mouse is used as a tool to develop a better understanding of the hypothalamic regulation of food intake in an anorectic condition. Previous studies on the anx/anx mouse hypothalamus showed several abnormalities in the expression of neurotransmitters and neuropeptides in the orexigenic NPY/AgRP and the anorexigenic POMC/CART system. In order to elucidate when this abnormal phenotype first appears, we studied the development of the NPY/AgRP system in Paper I. The development of the NPY/AgRP system in the anx/anx mice is normal until P12. From this day, a gradual decrease in fiber density is seen with the weakest expression at P21, results that clearly show an impaired development of the NPY/AgRP system in the anx/anx mouse. A second aim for Paper I was to study the underlying mechanisms for this impaired development. We therefore analyzed the expression of markers of activated microglia and detected a gradual increase in these markers in the same areas and at the same time points as was seen for the gradual decrease in density of AgRP fibers. The impaired development of the AgRP system and the overlapping activation of microglia in the hypothalamus of the anx/anx mouse indicate an inflammatory/degenerative process. This was further investigated in Paper II, where we detected expression of MHC class I mRNA and protein in the arcuate nucleus, both in glial cells and in neurons. We also found that the neurons expressing the MHC class I subunit are ‘silenced’ or have a very low activity. Further evidence for neurodegeneration was seen in Paper II, as we detected a significantly increased number of apoptotic cells in several hypothalamic areas of the anx/anx mouse, as well as a double-labeling of NPY and active caspase 6, a marker for axonal degeneration, in neuronal fibers. Altogether, these results point to a neurodegenerative process in the hypothalamus of the anx/anx mouse. In Paper III, we continued the search for the anx gene/mutation to find the causes leading to the anorectic phenotype. Through a microarray study and the following pathway analysis the first indications were given that the anorectic phenotype in the anx/anx mouse is related to mitochondrial dysfunction and oxidative stress. We also detected that the anx mutation leads to decreased expression of the Ndufaf1 gene and protein. This gene, located within the anx interval, encodes an assembly factor for mitochondrial complex I. We show that the downregulation of Ndufaf1 is associated with the anx-allele and not due to a secondary effect of the starvation. We could also see that the downregulation of the Ndufaf1 gene leads to a less completely assembled mitochondrial complex I and the accumulation of sub-complexes, as well as increased levels of reactive oxygen species, in the anx/anx hypothalamus. Based on these results, we concluded that the anorexia and premature death of the anx/anx mouse is related to mitochondrial dysfunction and oxidative stress. In Paper V, we evaluated whether the activity in the hypothalamus is attenuated in the anx/anx mouse as a consequence of the defect mitochondrial complex I. We could see that hypothalamic glucose uptake in the fasted state was reduced in the anx/anx mouse. Further, the anx/anx hypothalamus had elevated levels of one of the glucose transporters, GLUT4 and a key metabolic molecule, AMPK. However, the hypothalamic activation state of AMPK was significantly decreased. Finally, during metabolic stress, levels of both AMP and IMP (both breakdown products of ATP) were decreased, while ATP levels were increased in the anx/anx hypothalamus. Together these results indicate that the anx/anx mouse has a reduced hypothalamic metabolism. This may contribute to the anorectic behavior of this mouse i.e. its inability to regulate food intake in response to the energy status. In Paper IV, we evaluated whether the inflammation and the mitochondrial dysfunction in the hypothalamus of the anx/anx mouse also could be detected in the endocrine pancreas, and if glucose homeostasis is disturbed. We found a strong downregulation of the Ndufaf1 gene, paralleled by a reduced mitochondrial complex I activity in isolated anx/anx islets. In addition, there was an increased macrophage infiltration in anx/anx islets, indicating inflammation. Moreover, elevated levels of free fatty acids were seen in anx/anx serum. In contrast, isolated islets from anx/anx mice cultured in the absence of free fatty acids did not show any inflammation. Also, an intraperitoneal injection of glucose to the anx/anx mouse revealed a marked glucose intolerance associated with reduced insulin release. However, the insulin release from isolated anx/anx islets was increased after stimulation either with glucose or KCl. The conclusion of Paper IV is that the anx/anx endocrine pancreas display marked reduction in insulin release that correlates with the increased serum levels of free fatty acids, and that the accompanying in vivo inflammation may lead to inhibition of insulin secretion.
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| 6. |
- Lindfors, Charlotte, et al.
(author)
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Hypothalamic mitochondrial dysfunction associated with anorexia in the anx/anx mouse
- 2011
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In: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 108:44, s. 18108-18113
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Journal article (peer-reviewed)abstract
- The anorectic anx/anx mouse exhibits disturbed feeding behavior and aberrances, including neurodegeneration, in peptidergic neurons in the appetite regulating hypothalamic arcuate nucleus. Poor feeding in infants, as well as neurodegeneration, are common phenotypes in human disorders caused by dysfunction of the mitochondrial oxidative phosphorylation system (OXPHOS). We therefore hypothesized that the anorexia and degenerative phenotypes in the anx/anx mouse could be related to defects in the OXPHOS. In this study, we found reduced efficiency of hypothalamic OXPHOS complex I assembly and activity in the anx/anx mouse. We also recorded signs of increased oxidative stress in anx/anx hypothalamus, possibly as an effect of the decreased hypothalamic levels of fully assembled complex I, that were demonstrated by native Western blots. Furthermore, the Ndufaf1 gene, encoding a complex I assembly factor, was genetically mapped to the anx interval and found to be down-regulated in anx/anx mice. These results suggest that the anorexia and hypothalamic neurodegeneration of the anx/anx mouse are associated with dysfunction of mitochondrial complex I.
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| 7. |
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