| 1. |
|
|
| 2. |
- Kehoe, Laura, et al.
(författare)
-
Make EU trade with Brazil sustainable
- 2019
-
Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 364:6438, s. 341-
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
|
|
| 3. |
|
|
| 4. |
- Abdelmagid, N., et al.
(författare)
-
Von Willebrand Factor Gene Variants Associate with Herpes simplex Encephalitis
- 2016
-
Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 11:5
-
Tidskriftsartikel (refereegranskat)abstract
- Herpes simplex encephalitis (HSE) is a rare complication of Herpes simplex virus type-1 infection. It results in severe parenchymal damage in the brain. Although viral latency in neurons is very common in the population, it remains unclear why certain individuals develop HSE. Here we explore potential host genetic variants predisposing to HSE. In order to investigate this we used a rat HSE model comparing the HSE susceptible SHR (Spontaneously Hypertensive Rats) with the asymptomatic infection of BN (Brown Norway). Notably, both strains have HSV-1 spread to the CNS at four days after infection. A genome wide linkage analysis of 29 infected HXB/BXH RILs (recombinant inbred lines-generated from the prior two strains), displayed variable susceptibility to HSE enabling the definition of a significant QTL (quantitative trait locus) named Hse6 towards the end of chromosome 4 (160.89-174Mb) containing the Vwf (von Willebrand factor) gene. This was the only gene in the QTL with both cis-regulation in the brain and included several non-synonymous SNPs (single nucleotide polymorphism). Intriguingly, in human chromosome 12 several SNPs within the intronic region between exon 43 and 44 of the VWF gene were associated with human HSE pathogenesis. In particular, rs917859 is nominally associated with an odds ratio of 1.5 (95% CI 1.11-2.02; p-value = 0.008) after genotyping in 115 HSE cases and 428 controls. Although there are possibly several genetic and environmental factors involved in development of HSE, our study identifies variants of the VWF gene as candidates for susceptibility in experimental and human HSE.
|
|
| 5. |
- Adeboye, Peter, 1982, et al.
(författare)
-
In situ conversion of phenolic compounds as a tool to phenolic tolerance development by S. cerevisiae
- 2015
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Phenolic compounds in hydrolysates are degradation products from the lignin component of wood. They are diverse in nature and they account for some of the inhibitory activities observed during lignocellulosic fermentation. S. cerevisiae possesses the ability to convert some phenolic compounds. We are currently studying the interaction between S. cerevisiae and selected phenolic compounds namely; coniferyl aldehyde, ferulic acid and p-coumaric acid to understand the ability of S. cerevisiae to convert the selected compounds. Preliminary results show that the three phenolic compounds are being converted into several other less inhibitory phenolic compounds common to the three compounds. We hypothesised a conversion route and engineered S. cerevisiae strains to test the hypothesis, the preliminary result shows faster conversion in an engineered strain.
|
|
| 6. |
- Aeinehband, Shahin, et al.
(författare)
-
Cerebrospinal fluid kynurenines in multiple sclerosis : relation to disease course and neurocognitive symptoms
- 2016
-
Ingår i: Brain, behavior, and immunity. - : Elsevier. - 0889-1591 .- 1090-2139. ; 51, s. 47-55
-
Tidskriftsartikel (refereegranskat)abstract
- Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease of the central nervous system, with a high rate of neurocognitive symptoms for which the molecular background is still uncertain. There is accumulating evidence for dysregulation of the kynurenine pathway (KP) in different psychiatric and neurodegenerative conditions. We here report the first comprehensive analysis of cerebrospinal fluid (CSF) kynurenine metabolites in MS patients of different disease stages and in relation to neurocognitive symptoms. Levels of tryptophan (TRP), kynurenine (KYN), kynurenic acid (KYNA) and quinolinic acid (QUIN) were determined with liquid chromatography mass spectrometry in cell-free CSF. At the group level MS patients (cohort 1; n = 71) did not differ in absolute levels of TRP, KYN, KYNA or QUIN as compared to non-inflammatory neurological disease controls (n = 20). Stratification of patients into different disease courses revealed that both absolute QUIN levels and the QUIN/KYN ratio were increased in relapsing-remitting MS (RRMS) patients in relapse. Interestingly, secondary progressive MS (SPMS) displayed a trend for lower TRP and KYNA, while primary progressive (PPMS) patients displayed increased levels of all metabolites, similar to a group of inflammatory neurological disease controls (n = 13). In the second cohort (n = 48), MS patients with active disease and short disease duration were prospectively evaluated for neuropsychiatric symptoms. In a supervised multivariate analysis using orthogonal projection to latent structures (OPLS-DA) depressed patients displayed higher KYNA/TRP and KYN/TRP ratios, mainly due to low TRP levels. Still, this model had low predictive value and could not completely separate the clinically depressed patients from the non-depressed MS patients. No correlation was evident for other neurocognitive measures. Taken together these results demonstrate that clinical disease activity and differences in disease courses are reflected by changes in KP metabolites. Increased QUIN levels of RRMS patients in relapse and generally decreased levels of TRP in SPMS may relate to neurotoxicity and failure of remyelination, respectively. In contrast, PPMS patients displayed a more divergent pattern more resembling inflammatory conditions such as systemic lupus erythematosus. The pattern of KP metabolites in RRMS patients could not predict neurocognitive symptoms.
|
|
| 7. |
- Aeinehband, Shahin, et al.
(författare)
-
Complement Component C3 and Butyrylcholinesterase Activity Are Associated with Neurodegeneration and Clinical Disability in Multiple Sclerosis
- 2015
-
Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 10:4
-
Tidskriftsartikel (refereegranskat)abstract
- Dysregulation of the complement system is evident in many CNS diseases but mechanisms regulating complement activation in the CNS remain unclear. In a recent large rat genomewide expression profiling and linkage analysis we found co-regulation of complement C3 immediately downstream of butyrylcholinesterase (BuChE), an enzyme hydrolyzing acetylcholine (ACh), a classical neurotransmitter with immunoregulatory effects. We here determined levels of neurofilament-light (NFL), a marker for ongoing nerve injury, C3 and activity of the two main ACh hydrolyzing enzymes, acetylcholinesterase (AChE) and BuChE, in cerebrospinal fluid (CSF) from patients with MS (n = 48) and non-inflammatory controls (n = 18). C3 levels were elevated in MS patients compared to controls and correlated both to disability and NFL. C3 levels were not induced by relapses, but were increased in patients with >= 9 cerebral lesions on magnetic resonance imaging and in patients with progressive disease. BuChE activity did not differ at the group level, but was correlated to both C3 and NFL levels in individual samples. In conclusion, we show that CSF C3 correlates both to a marker for ongoing nerve injury and degree of disease disability. Moreover, our results also suggest a potential link between intrathecal cholinergic activity and complement activation. These results motivate further efforts directed at elucidating the regulation and effector functions of the complement system in MS, and its relation to cholinergic tone.
|
|
| 8. |
- Ahlsson, Anders, et al.
(författare)
-
Is There a Weekend Effect in Surgery for Type A Dissection? : Results From the Nordic Consortium for Acute Type A Aortic Dissection Database
- 2019
-
Ingår i: Annals of Thoracic Surgery. - : Elsevier. - 0003-4975 .- 1552-6259. ; 108:3, s. 770-776
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Aortic dissection type A requires immediate surgery. In general surgery populations, patients operated on during weekends have higher mortality rates compared with patients whose operations occur on weekdays. The weekend effect in aortic dissection type A has not been studied in detail.Methods: The Nordic Consortium for Acute Type A Aortic Dissection (NORCAAD) registry includes data for 1,159 patients who underwent type A dissection surgery at 8 Nordic centers during 2005 to 2014. This study is based on data relating to surgery conducted during weekdays versus weekends and starting between 8:00 AM and 8:00 Pm ("daytime") versus from 8:00 Pm to 8:00 AM ("nighttime"), as well as time from symptoms, admittance, and diagnosis to surgery. The influence of timing of surgery on the 30-day mortality rate was assessed using logistic regression analysis.Results: The 30-day mortality was 18% (204 of 1,159), with no difference in mortality between surgery performed on weekdays (17% [150 of 889]) and on weekends (20% [54 of 270], p = 0.45), or during nighttime (19% [87 of 467]) versus daytime (17% [117 of 680], p = 0.54). Time from symptoms to surgery (median 7.0 hours vs 6.5 hours, p = 0.31) did not differ between patients who survived and those who died at 30 days. Multivariable regression analysis of risk factors for 30-day mortality showed no weekend effect (odds ratio, 1.04; 95% confidence interval, 60.67 to 1.60; p = 0.875), but nighttime surgery was a risk factor (odds ratio, 2.43; 95% confidence interval, 1.29 to 4.56; p = 0.006).Conclusions: The 30-day mortality in surgical repair of aortic dissection type A was not significantly affected by timing of surgery during weekends versus weekdays. Nighttime surgery seems to predict increased 30-day mortality, after correction for other risk factors.
|
|
| 9. |
- Ahlsson, Anders, et al.
(författare)
-
Is there a weekend effect in surgery for type A dissection? - Results from the NORCAAD database
- 2019
-
Ingår i: Annals of Thoracic Surgery. - : Elsevier BV. - 1552-6259 .- 0003-4975. ; 108:3, s. 770-776
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Aortic dissection type A requires immediate surgery. In general surgery populations, patients operated during weekends have higher mortality rates compared to patients operated on weekdays. The weekend effect in aortic dissection type A has not been studied in detail.METHODS: The Nordic Consortium for Acute Type A Aortic Dissection (NORCAAD) registry includes patients (N=1,159) who underwent type A dissection surgery at eight Nordic centers during 2005-2014. This study is based on data relating to surgery conducted during weekdays vs. weekends, and starting between 8 am and 8 pm ("daytime") vs. from 8 pm to 8 am ("nighttime"), as well as time from symptoms/admittance/diagnosis to surgery. The influence of timing of surgery on 30-day mortality was assessed using logistic regression analysis.RESULTS: The 30-day mortality was 18% (204/1,159), with no difference in mortality between surgery performed on weekdays (17%, 150/889) and on weekends (20%, 54/270, p=0.45), or during nighttime (19%, 87/467) vs. daytime (17%, 117/680, p=0.54). Time from symptoms to surgery (median 7.0 hours vs. 6.5 hours, p=0.31) did not differ between patients who survived and those dead at 30 days. Multivariable regression analysis of risk factors for 30-day mortality showed no weekend effect (OR 1.04 [0.67-1.60], p=0.875), but nighttime surgery was a risk factor (OR 2.43 [1.29-4.56], p=0.006).CONCLUSIONS: Thirty-day mortality in surgical repair of aortic dissection type A was not significantly affected by timing of surgery during weekends vs. weekdays. Nighttime surgery seems to predict increased 30-day mortality, after correction for other risk factors.
|
|
| 10. |
- Al Nimer, Faiez, et al.
(författare)
-
Lipocalin-2 is increased in progressive multiple sclerosis and inhibits remyelination
- 2016
-
Ingår i: Neurology. - 2332-7812. ; 3:1
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: We aimed to examine the regulation of lipocalin-2 (LCN2) in multiple sclerosis (MS) and its potential functional relevance with regard to myelination and neurodegeneration. Methods: We determined LCN2 levels in 3 different studies: (1) in CSF and plasma from a case-control study comparing patients with MS (n = 147) with controls (n = 50) and patients with relapsing-remitting MS (n = 75) with patients with progressive MS (n = 72); (2) in CSF and brain tissue microdialysates from a case series of 7 patients with progressive MS; and (3) in CSF at baseline and 60 weeks after natalizumab treatment in a cohort study of 17 patients with progressive MS. Correlation to neurofilament light, a marker of neuroaxonal injury, was tested. The effect of LCN2 on myelination and neurodegeneration was studied in a rat in vitro neuroglial cell coculture model. Results: Intrathecal production of LCN2 was increased predominantly in patients with progressive MS (p < 0.005 vs relapsing-remitting MS) and displayed a positive correlation to neurofilament light (p = 0.005). Levels of LCN2 in brain microdialysates were severalfold higher than in the CSF, suggesting local production in progressive MS. Treatment with natalizumab in progressive MS reduced LCN2 levels an average of 13% (p < 0.0001). LCN2 was found to inhibit remyelination in a dose-dependent manner in vitro. Conclusions: LCN2 production is predominantly increased in progressive MS. Although this moderate increase does not support the use of LCN2 as a biomarker, the correlation to neurofilament light and the inhibitory effect on remyelination suggest that LCN2 might contribute to neurodegeneration through myelination-dependent pathways.
|
|
