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Sökning: db:Swepub > Persson Anders > Göteborgs universitet

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2.
  • Bull, Cecilia, 1977-, et al. (författare)
  • Exercise in Adulthood after Irradiation of the Juvenile Brain Ameliorates Long-Term Depletion of Oligodendroglial Cells.
  • 2017
  • Ingår i: Radiation research. - 1938-5404. ; 188:4, s. 443-454
  • Tidskriftsartikel (refereegranskat)abstract
    • Cranial radiation severely affects brain health and function, including glial cell production and myelination. Recent studies indicate that voluntary exercise has beneficial effects on oligodendrogenesis and myelination. Here, we hypothesized that voluntary running would increase oligodendrocyte numbers in the corpus callosum after irradiation of the juvenile mouse brain. The brains of C57Bl/6J male mice were 6 Gy irradiated on postnatal day 9 during the main gliogenic developmental phase, resulting in a loss of oligodendrocyte precursor cells. Upon adulthood, the mice were injected with bromodeoxyuridine and allowed to exercise on a running wheel for four weeks. Cell proliferation and survival, Ascl1(+) oligodendrocyte precursor and Olig2(+) oligodendrocyte cell numbers as well as CC1(+) mature oligodendrocytes were quantified using immunohistology. Radiation induced a reduction in the number of Olig2(+) oligodendrocytes by nearly 50% without affecting production or survival of new Olig2(+) cells. Ascl1(+) cells earlier in the oligodendroglial cell lineage were also profoundly affected, with numbers reduced by half. By three weeks of age, Olig2(+) cell numbers had not recovered, and this was paralleled by a volumetric loss in the corpus callosum. The deficiency of Olig2(+) oligodendrocytes persisted into adulthood. Additionally, the depletion of Ascl1(+) progenitor cells was irreversible, and was even more pronounced at 12 weeks postirradiation compared to day 2 postirradiation. Furthermore, the overall number of CC1(+) mature oligodendrocytes decreased by 28%. The depletion of Olig2(+) cells in irradiated animals was reversed by 4 weeks of voluntary exercise. Moreover, voluntary exercise also increased the number of Ascl1(+) progenitor cells in irradiated animals. Taken together, these results demonstrate that exercise in adulthood significantly ameliorates the profound and long-lasting effects of moderate exposure to immature oligodendrocytes during postnatal development.
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3.
  • Chantzichristos, Dimitrios, 1976-, et al. (författare)
  • Incidence, prevalence and seasonal onset variation of Addison's disease among persons with type 1 diabetes mellitus: nationwide, matched cohort studies.
  • 2018
  • Ingår i: European journal of endocrinology. - 1479-683X. ; 178:1, s. 115-122
  • Tidskriftsartikel (refereegranskat)abstract
    • We determined the incidence and prevalence of Addison's disease (AD) among persons with or without type 1 diabetes mellitus (T1DM) in nationwide, matched cohort studies.Persons with T1DM were identified from the Swedish National Diabetes Register and each was matched for age, sex, year and county to five controls randomly selected from the general population. Persons with AD were identified from the Swedish National Inpatient Register. Baseline demographics and seasonal onset variation of AD were presented by descriptive statistics. Prevalence and incidence were estimated by proportions and incidence rates, respectively. Times to AD were analyzed using the Cox proportional hazard model.Between 1998 and 2013, 66 persons with T1DM were diagnosed with AD at a mean age (s.d.) of 36.4 (13.0) years among 36 514 persons with T1DM, while 32 were diagnosed with AD at a mean age of 42.7 (15.2) years among 182 570 controls. The difference in mean age at diagnosis of AD between the groups was 6.3 years (P value = 0.036). The incidence of AD for a person with or without T1DM was therefore 193 and 18 per million person-years, respectively. The adjusted relative risk increase of developing AD in T1DM was 10.8 (95% CI: 7.1-16.5). The highest incidence of AD was observed during February-March and September-October. The prevalence of AD in persons with or without T1DM in December 2012 was 3410 and 208 per million, respectively. The odds ratio for AD in persons with T1DM vs controls was 16.5 (95% CI: 11.1-24.5).The risk to develop AD among persons with T1DM is more than 10 times higher than in persons without T1DM. Persons with T1DM develop AD at a younger age. The incidence of AD may have a seasonal pattern.
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4.
  • Chantzichristos, Dimitrios, 1976-, et al. (författare)
  • Mortality in patients with diabetes mellitus and Addison's disease: a nationwide, matched, observational cohort study.
  • 2017
  • Ingår i: European journal of endocrinology. - 1479-683X. ; 176:1, s. 31-39
  • Tidskriftsartikel (refereegranskat)abstract
    • Our hypothesis was that patients with diabetes mellitus obtain an additional risk of death if they develop Addison's disease (AD).Nationwide, matched, observational cohort study cross-referencing the Swedish National Diabetes Register with Inpatient, Cancer and Cause of Death Registers in patients with diabetes (type 1 and 2) and AD and matched controls with diabetes. Clinical characteristics at baseline, overall, and cause-specific mortality were assessed. The relative risk of death was assessed using a Cox proportional hazards regression model.Between January 1996 and December 2012, 226 patients with diabetes and AD were identified and matched with 1129 controls with diabetes. Median (interquartile range) follow-up was 5.9 (2.7-8.6) years. When patients with diabetes were diagnosed with AD, they had an increased frequency of diabetes complications, but both medical history of cancer and coronary heart disease did not differ compared with controls. Sixty-four of the 226 patients with diabetes and AD (28%) died, while 112 of the 1129 controls (10%) died. The estimated relative risk increase (hazard ratio) in overall mortality in the diabetes and AD group was 3.89 (95% confidence interval 2.84-5.32) compared with controls with diabetes. The most common cause of death was cardiovascular in both groups, but patients with diabetes and AD showed an increased death rate from diabetes complications, infectious diseases and unknown causes.Patients with the rare combination of diabetes and AD showed a markedly increased mortality and died more frequently from infections and unknown causes than patients with diabetes alone. Improved strategy for the management of this combination of metabolic disorders is needed.
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6.
  • Lidell, Martin E., et al. (författare)
  • Evidence for two types of brown adipose tissue in humans
  • 2013
  • Ingår i: Nature Medicine. - Nature Publishing Group. - 1078-8956. ; 19:5, s. 631-634
  • Tidskriftsartikel (refereegranskat)abstract
    • The previously observed supraclavicular depot of brown adipose tissue (BAT) in adult humans was commonly believed to be the equivalent of the interscapular thermogenic organ of small mammals. This view was recently disputed on the basis of the demonstration that this depot consists of beige (also called brite) brown adipocytes, a newly identified type of brown adipocyte that is distinct from the classical brown adipocytes that make up the interscapular thermogenic organs of other mammals. A combination of high-resolution imaging techniques and histological and biochemical analyses showed evidence for an anatomically distinguishable interscapular BAT (iBAT) depot in human infants that consists of classical brown adipocytes, a cell type that has so far not been shown to exist in humans. On the basis of these findings, we conclude that infants, similarly to rodents, have the bona fide iBAT thermogenic organ consisting of classical brown adipocytes that is essential for the survival of small mammals in a cold environment.
7.
  • Ljungberg, Peter, et al. (författare)
  • Effects of small-scale habitat fragmentation on predator-prey interactions in a temperate sea grass system
  • 2013
  • Ingår i: Marine Biology. - Springer. - 0025-3162. ; 160:3, s. 667-675
  • Tidskriftsartikel (refereegranskat)abstract
    • During the last decades, fragmentation has become an important issue in ecological research. Habitat fragmentation operates on spatial scales ranging over several magnitudes from patches to landscapes. We focus on small-scale fragmentation effects relevant to animal foraging decision making that could ultimately generate distribution patterns. In a controlled experimental environment, we tested small-scale fragmentation effects in artificial sea grass on the feeding behaviour of juvenile cod (Gadus morhua). Moreover, we examined the influence of fragmentation on the distribution of one of the juvenile cod's main prey resources, the grass shrimp (Palaemon elegans), in association with three levels of risk provided by cod (no cod, cod chemical cues and actively foraging cod). Time spent by cod within sea grass was lower in fragmented landscapes, but total shrimp consumption was not affected. Shrimp utilised vegetation to a greater extent in fragmented treatments in combination with active predation. We suggest that shrimp choose between sand and vegetation habitats to minimize risk of predation according to cod habitat-specific foraging capacities, while cod aim to maximize prey-dependent foraging rates, generating a habitat-choice game between predator and prey. Moreover, aggregating behaviour in grass shrimp was only found in treatments with active predation. Hence, we argue that both aggregation and vegetation use are anti-predator defence strategies applied by shrimp. We therefore stress the importance of considering small-scale behavioural mechanisms when evaluating consequences from habitat fragmentation on trophic processes in coastal environments.
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8.
  • Naylor, Andrew Stuart, 1977-, et al. (författare)
  • Extended voluntary running inhibits exercise-induced adult hippocampal progenitor proliferation in the spontaneously hypertensive rat.
  • 2005
  • Ingår i: Journal of neurophysiology. - 0022-3077. ; 93:5, s. 2406-14
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous work has shown that voluntary running increases cell proliferation and neurogenesis in the dentate gyrus of the adult hippocampus. Here we report that long-term running for 24 days results in a down-regulation of hippocampal progenitor proliferation to one-half the level of nonrunning controls compared with a fivefold increase in progenitor proliferation seen after 9 days of voluntary running (short-term running). The negative effects seen on proliferation after 24 days of running were prevented by restricting daily running distances (by 30-50%) during 24 days. Long-term running for 24 days increases the response of the hypothalamic-pituitary-adrenal axis, with an increase in adrenal gland weight and increased plasma corticosterone levels, as well as decreased thymus weight, indicating a stress response as a possible mediator of decreased progenitor proliferation. Furthermore, the negative effects seen on the observed stress response after 24 days of running were prevented by restricting daily running distance. Short-term running did not alter these stress parameters compared with nonrunning controls. However, it increased phosphorylated cyclic AMP response element binding protein (pCREB) in the dentate gyrus, an increase that was not seen in nonrunning controls or after 24 days of running. Taken together, these data suggest that voluntary running does not always enhance proliferation and that the decrease in progenitor proliferation seen in long-term running is possibly mediated by mechanisms involving a stress response in the animal. However, a moderate level of long-term running was able to prevent the negative stress-related changes seen in unrestricted long-term running.
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9.
  • Paulson, Linda, et al. (författare)
  • Comparative genome- and proteome analysis of cerebral cortex from MK-801-treated rats.
  • 2003
  • Ingår i: Journal of neuroscience research. - 0360-4012. ; 71:4, s. 526-33
  • Tidskriftsartikel (refereegranskat)abstract
    • cDNA microarrays and two-dimensional gel-electrophoresis in combination with mass spectrometry, were used to screen alterations in mRNA and protein levels, respectively, in cerebral cortex of MK-801-treated rats. The rats were divided in two groups; group 1 (short-term treated) and group 2 (long-term treated). In group 1, four genes were up-regulated and five down-regulated. In group 2, seven genes were up-regulated and six down-regulated. In group 1, the levels of one protein was increased and eight proteins reduced. In group 2, the levels of two proteins were increased and four proteins reduced. Several of the altered genes (casein kinase 2, glutamic acid decarboxylase, synaptotagmin, gamma aminobutyric acid [GABA] transporter, creatine kinase, and cytochrome c oxidase) and proteins (superoxide dismutase, hsp 60, hsp 72 and gamma-enolase) have previously been connected to schizophrenia. Alterations of the genes (microglobulin, c-jun proto-oncogene, 40S ribosomal protein S19, adenosine diphosphate (ADP)-ribosylation factors, platelet-derived growth factor, fructose-bisphophate aldolase A, and myelin proteolipid) and the proteins (stathmin, H+-transp. Adenosine triphosphate (ATP) synthase, pyruvate dehydrogenase, beta-actin and alpha-enolase), have not, to our knowledge, earlier been implicated in schizophrenia pathology. Overall, these results with a combined approach of genomics and proteomics add to the validity of subchronic N-methyl-D-aspartate (NMDA)-receptor antagonist treatment as an animal model of schizophrenia.
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