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  • 1.
    Beeckmans, Dorien
    et al.
    Katholieke Univ Leuven, Belgium.
    Farre, Ricard
    Katholieke Univ Leuven, Belgium.
    Riethorst, Danny
    Katholieke Univ Leuven, Belgium.
    Keita, Åsa
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för kirurgi, ortopedi och onkologi. Linköpings universitet, Medicinska fakulteten.
    Augustijns, Patrick
    Katholieke Univ Leuven, Belgium.
    Söderholm, Johan D
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för kirurgi, ortopedi och onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    Vanuytsel, Tim
    Katholieke Univ Leuven, Belgium.
    Vanheel, Hanne
    Katholieke Univ Leuven, Belgium.
    Tack, Jan
    Katholieke Univ Leuven, Belgium.
    Relationship between bile salts, bacterial translocation, and duodenal mucosal integrity in functional dyspepsia2020Inngår i: Neurogastroenterology and Motility, ISSN 1350-1925, E-ISSN 1365-2982, artikkel-id e13788Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background Functional dyspepsia (FD) is a complex disorder, in which multiple mechanisms underlie symptom generation, including impaired duodenal barrier function. Moreover, an altered duodenal bile salt pool was recently discovered in patients with FD. We aimed to evaluate the relationship between bile salts, bacterial translocation, and duodenal mucosal permeability in FD. Methods Duodenal biopsies from patients with FD and healthy volunteers (HV) were mounted in Ussing chambers to measure mucosal resistance and bacterial passage in the absence and presence of fluorescein-conjugated Escherichia coli and glyco-ursodeoxycholic acid (GUDCA) exposure. In parallel, duodenal fluid aspirates were collected from patients and bile salts were analyzed. Key results The transepithelial electrical resistance of duodenal biopsies from patients was lower compared with HV (21.4 +/- 1.3 omega.cm(2) vs. 24.4 +/- 1.2 omega.cm(2); P = .02; N = 21). The ratio of glyco-cholic and glyco-chenodeoxycholic acid (GCDCA) to tauro- and GUDCA correlated positively with transepithelial electrical resistance in patients. Glyco-ursodeoxycholic acid slightly altered the mucosal resistance, resulting in similar values between patient and healthy biopsies (22.1 +/- 1.0 omega.cm(2) vs. 23.0 +/- 1.0 omega.cm(2); P = .5). Bacterial passage after 120 minutes was lower for patient than for healthy biopsies (0.0 [0.0-681.8] vs. 1684.0 [0.0-4773.0] E coli units; P = .02). Glyco-ursodeoxycholic acid increased bacterial passage in patient biopsies (102.1 [0.0-733.0] vs. 638.9 [280.6-2124.0] E coli units; P = .009). No correlation was found between mucosal resistance and bacterial passage. Conclusions amp; inferences Patients with FD displayed decreased duodenal mucosal resistance associated with bile salts, however, not associated with bacterial passage in vitro. In addition, the hydrophilic bile salt glyco-ursodeoxycholic acid abolished differences in mucosal resistance and bacterial passage between patient and control group.

  • 2.
    Derolf, Asa
    et al.
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Juliusson, Gunnar
    Skane Univ Hosp, Sweden.
    Benson, Lina
    Epidemiol and Reg Oncol Ctr Stockholm, Sweden.
    Floisand, Yngvar
    Oslo Univ Hosp, Norway.
    Lazarevic, Vladimir
    Skane Univ Hosp, Sweden.
    Antunovic, Petar
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för kirurgi, ortopedi och onkologi. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Hematologiska kliniken US.
    Mollgard, Lars
    Sahlgrens Univ Hosp, Sweden.
    Lehmann, Soren
    Uppsala Univ, Sweden.
    Uggla, Bertil
    Orebro Univ Hosp, Sweden.
    Wahlin, Anders
    Umea Univ, Sweden.
    Hoglund, Martin
    Uppsala Univ, Sweden.
    Deneberg, Stefan
    Karolinska Univ Hosp, Sweden; Karolinska Inst, Sweden.
    Letter: Decreasing early mortality in acute myeloid leukaemia in Sweden 1997-2014: improving performance status is a major contributing factor in BRITISH JOURNAL OF HAEMATOLOGY, vol 188, issue 1, pp 187-1912020Inngår i: British Journal of Haematology, ISSN 0007-1048, E-ISSN 1365-2141, Vol. 188, nr 1, s. 187-191Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    n/a

  • 3.
    Eriksson, Per
    et al.
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Segelmark, Mårten
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US.
    Systemisk vaskulit2018Inngår i: Internmedicin / [ed] Ulf Dahlström, Stergios Kechagias, Leif Stenke, Stockholm: Liber, 2018, 6, Vol. Sidorna 939-949, s. 939-949Kapittel i bok, del av antologi (Annet vitenskapelig)
  • 4.
    Eskilsson, Anna
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Inflammatory Signaling Across the Blood-Brain Barrier and the Generation of Fever2020Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Fever is a cardinal sign of inflammation and is evolutionary conserved. Fever is known to be beneficial during acute inflammation, but over time and if very high it can be detrimental. The signaling pathways by which fever is initiated by the brain and the peripheral mechanisms through which the temperature increase is generated were studied from several point of views. Fever is known to be dependent on prostaglandin E2 (PGE2) binding to its receptors in the median preoptic nucleus of the hypothalamus, which signals to the brainstem and through sympathetic nerves to heat conserving and heat producing effector organs. This thesis focuses on identifying the cells that produce the PGE2 critical for the fever response; showing where in the brain the critical PGE2 production takes place; demonstrating how peripheral inflammation activates these cells to produce PGE2; and finally, identifying the effector mechanisms behind the temperature elevation in fever. By using a newly developed specific antibody we showed that the enzyme responsible for the terminal step in the production of PGE2, microsomal prostaglandin E-synthase 1 (mPGES-1), is expressed in endothelial cells of brain blood vessels in mice where it is co-expressed with the enzyme cyclooxygenase-2 (Cox-2), which is known to be induced in these cells and to be rate limiting for the PGE2 production. The mPGES-1 enzyme was also expressed in several other cell types and structures which however did not express Cox-2, such as capillary-associated pericytes, astroglial cells, leptomeninges, and the choroid plexus. The role of the mPGES-1 in these other cells/structures remains unknown. Next, by using mice with selective deletion of Cox-2 in brain endothelial cells, we showed that local PGE2 production in deep brain areas, such as the hypothalamus, is critical for the febrile response to peripheral inflammation. In contrast, PGE2 production in other brain areas and the overall PGE2 level in the brain were not critical for the febrile response. Partly restoring the PGE2 synthesizing capacity in the anterior hypothalamus of mice lacking such capacity with a lentiviral vector resulted in a temperature elevation in response to an intraperitoneal injection of bacterial wall lipopolysaccharide (LPS). The data show that the febrile response is dependent on the local release of PGE2 onto its target neurons, possibly by a paracrine mechanism. Deletion of the receptor for the pyrogenic cytokine IL-6 on brain endothelial cells, but not on neurons or peripheral nerves, strongly attenuated the febrile response to LPS and reduced the induction of the Cox-2 expression in the hypothalamus. Furthermore, mice deficient of the IL- 6Rα gene in the brain endothelial cells showed a reduced SOCS3 mRNA induction, whereas IκB mRNA-levels were unaffected, suggesting that the IL-6 signaling occurs via STAT3 activation and not signaling through the transcription factor NF-κB. This idea was confirmed by the observation of attenuated fever in mice deficient of STAT3 in brain endothelial cells. These data show that IL-6, when endogenously released during systemic inflammation, is pyrogenic by binding to IL-6R on brain endothelial cells to induce prostaglandin synthesis in these cells. Finally, we demonstrate that mice with genetic deletion of uncoupling protein-1 (UCP-1), hence lacking functional brown adipose tissue, had a normal fever response to LPS, and that LPS caused no activation of brown adipose tissue in wild type mice. However, blocking peripheral cutaneous vasoconstriction resulted in a blunted fever response to LPS, suggesting that heat conservation, possibly together with shivering or non-shivering thermogenesis in the musculature, is responsible for the generation of immune-induced fever, whereas brown adipose tissue thermogenesis is not involved.  

    Delarbeid
    1. Distribution of microsomal prostaglandin E synthase-1 in the mouse brain
    Åpne denne publikasjonen i ny fane eller vindu >>Distribution of microsomal prostaglandin E synthase-1 in the mouse brain
    2014 (engelsk)Inngår i: Journal of Comparative Neurology, ISSN 0021-9967, E-ISSN 1096-9861, Vol. 522, nr 14, s. 3229-3244Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Previous studies in rats have demonstrated that microsomal prostaglandin E synthase-1 (mPGES-1) is induced in brain vascular cells that also express inducible cyclooxygenase-2, suggesting that such cells are the source of the increased PGE2 levels that are seen in the brain following peripheral immune stimulation, and that are associated with sickness responses such as fever, anorexia, and stress hormone release. However, while most of what is known about the functional role of mPGES-1 for these centrally evoked symptoms is based on studies on genetically modified mice, the cellular localization of mPGES-1 in the mouse brain has not been thoroughly determined. Here, using a newly developed antibody that specifically recognizes mouse mPGES-1 and dual-labeling for cell-specific markers, we report that mPGES-1 is constitutively expressed in the mouse brain, being present not only in brain endothelial cells, but also in several other cell types and structures, such as capillary-associated pericytes, astroglial cells, leptomeninges, and the choroid plexus. Regional differences were seen with particularly prominent labeling in autonomic relay structures such as the area postrema, the subfornical organ, the paraventricular hypothalamic nucleus, the arcuate nucleus, and the preoptic area. Following immune stimulation, mPGES-1 in brain endothelial cells, but not in other mPGES-1-positive cells, was coexpressed with cyclooxygenase-2, whereas there was no coexpression between mPGES-1 and cyclooxygenase-1. These data imply a widespread synthesis of PGE2 or other mPGES-1-dependent products in the mouse brain that may be related to inflammation-induced sickness symptom as well as other functions, such as blood flow regulation.

    sted, utgiver, år, opplag, sider
    John Wiley & Sons, 2014
    Emneord
    Astroglial cells; Cyclooxygenase; Endothelial cells; Immune challenge; Pericytes; Prostaglandin synthesis
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-109962 (URN)10.1002/cne.23593 (DOI)000339967300006 ()24668417 (PubMedID)2-s2.0-84904553311 (Scopus ID)
    Tilgjengelig fra: 2014-09-12 Laget: 2014-08-29 Sist oppdatert: 2020-01-08
    2. Immune-Induced Fever Is Dependent on Local But Not Generalized Prostaglandin E-2 Synthesis in the Brain
    Åpne denne publikasjonen i ny fane eller vindu >>Immune-Induced Fever Is Dependent on Local But Not Generalized Prostaglandin E-2 Synthesis in the Brain
    Vise andre…
    2017 (engelsk)Inngår i: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 37, nr 19, s. 5035-5044Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Fever occurs upon binding of prostaglandin E-2 (PGE(2)) to EP3 receptors in the median preoptic nucleus of the hypothalamus, but the origin of the pyrogenic PGE(2) has not been clearly determined. Here, using mice of both sexes, we examined the role of local versus generalized PGE(2) production in the brain for the febrile response. In wild-type mice and in mice with genetic deletion of the prostaglandin synthesizing enzyme cyclooxygenase-2 in the brain endothelium, generated with an inducible CreER(T2) under the Slco1c1 promoter, PGE(2) levels in the CSF were only weakly related to the magnitude of the febrile response, whereas the PGE(2) synthesizing capacity in the hypothalamus, as reflected in the levels of cyclooxygenase-2 mRNA, showed strong correlation with the immune-induced fever. Histological analysis showed that the deletion of cyclooxygenase-2 in brain endothelial cells occurred preferentially in small-and medium-sized vessels deep in the brain parenchyma, such as in the hypothalamus, whereas larger vessels, and particularly those close to the neocortical surface and in the meninges, were left unaffected, hence leaving PGE(2) synthesis largely intact in major parts of the brain while significantly reducing it in the region critical for the febrile response. Furthermore, injection of a virus vector expressing microsomal prostaglandin E synthase-1 (mPGES-1) into the median preoptic nucleus of fever-refractive mPGES-1 knock-out mice, resulted in a temperature elevation in response to LPS. We conclude that the febrile response is dependent on local release of PGE(2) onto its target neurons and not on the overall PGE(2) production in the brain.

    sted, utgiver, år, opplag, sider
    SOC NEUROSCIENCE, 2017
    Emneord
    cyclooxygenase-2; endothelial cells; fever; median preoptic nucleus; microsomal prostaglandin E synthase-1; prostaglandin E2
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-138257 (URN)10.1523/JNEUROSCI.3846-16.2017 (DOI)000401118600015 ()28438967 (PubMedID)
    Merknad

    Funding Agencies|Swedish Medical Research Council; Swedish Cancer Foundation; European Research Council; Knut and Alice Wallenberg Foundation; Swedish Brain foundation; County Council of Ostergotland

    Tilgjengelig fra: 2017-06-13 Laget: 2017-06-13 Sist oppdatert: 2020-01-08
    3. Immune-Induced Fever Is Mediated by IL-6 Receptors on Brain Endothelial Cells Coupled to STAT3-Dependent Induction of Brain Endothelial Prostaglandin Synthesis
    Åpne denne publikasjonen i ny fane eller vindu >>Immune-Induced Fever Is Mediated by IL-6 Receptors on Brain Endothelial Cells Coupled to STAT3-Dependent Induction of Brain Endothelial Prostaglandin Synthesis
    Vise andre…
    2014 (engelsk)Inngår i: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 34, nr 48, s. 15957-15961Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    The cytokine IL-6, which is released upon peripheral immune challenge, is critical for the febrile response, but the mechanism by which IL-6 is pyrogenic has remained obscure. Herewegenerated mice with deletion of themembranebound IL-6 receptor alpha (IL-6R alpha) onneural cells, on peripheral nerves, on fine sensory afferent fibers, and on brain endothelial cells, respectively, and examined its role for the febrile response to peripherally injected lipopolysaccharide. We show that IL-6R alpha on neural cells, peripheral nerves, and fine sensory afferents are dispensable for the lipopolysaccharide-induced fever, whereas IL-6R alpha in the brain endothelium plays an important role. Hence deletion of IL-6R alpha on brain endothelial cells strongly attenuated the febrile response, and also led to reduced induction of the prostaglandin synthesizing enzyme Cox-2 in the hypothalamus, the temperature-regulating center in the brain, as well as reduced expression of SOCS3, suggesting involvement of the STAT signaling pathway. Furthermore, deletion of STAT3 in the brain endothelium also resulted in attenuated fever. These data show that IL-6, when endogenously released during systemic inflammation, is pyrogenic by binding to IL-6R alpha on brain endothelial cells to induce prostaglandin synthesis in these cells, probably in concerted action with other peripherally released cytokines.

    sted, utgiver, år, opplag, sider
    Society for Neuroscience, 2014
    Emneord
    blood-brain barrier; cell-specific gene deletions; fever; interleukin-6; prostaglandins; STAT3
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-113199 (URN)10.1523/JNEUROSCI.3520-14.2014 (DOI)000345923600013 ()25429137 (PubMedID)
    Merknad

    Funding Agencies|Swedish Medical Research Council; Swedish Cancer Foundation; European Research Council; Knut and Alice Wallenberg Foundation; Swedish Brain foundation; County CouncilO Ostergotland

    Tilgjengelig fra: 2015-01-13 Laget: 2015-01-12 Sist oppdatert: 2020-01-08
  • 5.
    Gutefeldt, Kerstin
    et al.
    Linköpings universitet, Institutionen för hälsa, medicin och vård, Avdelningen för diagnostik och specialistmedicin. Region Östergötland, Hjärt- och Medicincentrum, Endokrinmedicinska kliniken.
    Hedman, Christina
    Linköpings universitet, Institutionen för hälsa, medicin och vård, Avdelningen för diagnostik och specialistmedicin. Region Östergötland, Hjärt- och Medicincentrum, Endokrinmedicinska kliniken.
    Thyberg, Ingrid
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Bachrack Lindström, Margareta
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för omvårdnad. Linköpings universitet, Medicinska fakulteten.
    Arnqvist, Hans
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Endokrinmedicinska kliniken.
    Spångeus, Anna
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Endokrinmedicinska kliniken.
    Low health-related quality of life is strongly linked to upper extremity impairments in type 1 diabetes with a long duration2020Inngår i: Disability and Rehabilitation, ISSN 0963-8288, E-ISSN 1464-5165Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Purpose: To compare health-related quality of life (HRQOL) in type 1 diabetes and non-diabetic controls and possible links to upper extremity impairments (UEIs). Prevalence of sick-leave and causes were investigated. Materials and methods: This Swedish population-based case-control study included type 1 diabetes patients amp;lt;67 years old and with a diabetes duration amp;gt;= 20 years. Participants completed a postal questionnaire including Short Form 36, and questions regarding UEIs, and sick-leave. Results: In total, 773 patients, aged 50 +/- 10 years (diabetes duration 35 +/- 10 years), and 708 non-diabetic controls, aged 54 +/- 9 years, completed the study. Patients reported significantly lower HRQOL compared with controls. The difference was greatest for general health, vitality, and bodily pain. Patients with shoulder or hand but not finger impairments scored significantly lower than asymptomatic patients. The prevalence of sick leave was higher in patients vs. controls (23% vs. 9%, p amp;lt; 0.001), and nearly half cited impairments from back, muscles, or joints as the main reason. Conclusions: Health-related quality of life is lower in type 1 diabetes than controls and in patients with shoulder and hand impairments than in asymptomatic. Musculoskeletal impairments (back/muscle/joints) have impact on work ability. Identification of UEIs is important for initiating preventative-, therapeutic-, and rehabilitative interventions.

  • 6.
    Håkansson, Irene
    et al.
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Neurologiska kliniken i Linköping.
    Ernerudh, Jan
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk immunologi och transfusionsmedicin.
    Vrethem, Magnus
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Neurologiska kliniken i Linköping.
    Dahle, Charlotte
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk immunologi och transfusionsmedicin.
    Ekdahl, Kristina N.
    Centre of Biomaterials Chemistry, Linnaeus University, Kalmar, Sweden ; Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Complement activation in cerebrospinal fluid in clinically isolated syndrome and early stages of relapsing remitting multiple sclerosis2020Inngår i: Journal of Neuroimmunology, ISSN 0165-5728, E-ISSN 1872-8421, Vol. 340, artikkel-id 577147Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    To assess if markers of complement activation are associated with disease activity, C1q, C3, C3a and sC5b-9 levels in plasma and cerebrospinal fluid (CSF) were determined in 41 patients with clinically isolated syndrome (CIS) or remitting multiple sclerosis (RRMS), in a prospective longitudinal four-year cohort study. C1q in CSF (CSF-C1q) was significantly higher in patients than in controls. Baseline CSF-C1q and CSF-C3a correlated with several neuroinflammatory markers and neurofilament light chain levels. Baseline CSF-C3a correlated with the number of T2 lesions at baseline and new T2 lesions during follow-up. Baseline CSF-C3a was also significantly higher in patients with (n = 21) than in patients without (n = 20) signs of disease activity according to the NEDA-3 concept during one year of follow-up (p ≀ .01) Study results support that complement activation is involved in MS pathophysiology and that CSF-C3a carries prognostic information.

  • 7.
    Kallner, Anders
    et al.
    Karolinska Univ Hosp, Sweden.
    Theodorsson, Elvar
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för klinisk kemi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk kemi.
    Repeatability imprecision from analysis of duplicates of patient samples and control materials2020Inngår i: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Measurement imprecision is usually calculated from measurement results of the same stabilized control material(s) obtained over time, and is therefore, principally, only valid at the concentration(s) of the selected control material(s). The resulting uncertainty has been obtained under reproducibility conditions and corresponds to the conventional analytical goals. Furthermore, the commutability of the control materials used determines whether the imprecision calculated from the control materials reflects the imprecision of measuring patient samples. Imprecision estimated by measurements of patient samples uses fully commutable samples, freely available in the laboratories. It is commonly performed by calculating the results of routine patient samples measured twice each. Since the duplicates are usually analysed throughout the entire concentration interval of the patient samples processed in the laboratory, the result will be a weighted average of the repeatability imprecision measured in the chosen measurement intervals or throughout the entire interval of concentrations encountered in patient care. In contrast, the uncertainty derived from many measurements of control materials over periods of weeks is usually made under reproducibility conditions. Consequently, the repeatability and reproducibility imprecision play different roles in the inference of results in clinical medicine. The purpose of the present review is to detail the properties of the imprecision calculated by duplicates of natural samples, to explain how it differs from imprecision calculated from single concentrations of control materials, and to elucidate what precautions need to be taken in case of bias, e.g. due to carry-over effects.

  • 8.
    Lin, Chung-Ying
    et al.
    Hong Kong Polytech Univ, Peoples R China.
    Cheng, Andy S. K.
    Hong Kong Polytech Univ, Peoples R China.
    Nejati, Babak
    Tabriz Univ Med Sci, Iran.
    Imani, Vida
    Tabriz Univ Med Sci, Iran.
    Ulander, Martin
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Neurofysiologiska kliniken US.
    Browall, Maria
    Jonkoping Univ, Sweden.
    Griffiths, Mark D.
    Nottingham Trent Univ, England.
    Broström, Anders
    Region Östergötland, Sinnescentrum, Neurofysiologiska kliniken US. Jonkoping Univ, Sweden.
    Pakpour, Amir H.
    Jonkoping Univ, Sweden; Qazvin Univ Med Sci, Iran.
    A thorough psychometric comparison between Athens Insomnia Scale and Insomnia Severity Index among patients with advanced cancer2020Inngår i: Journal of Sleep Research, ISSN 0962-1105, E-ISSN 1365-2869, Vol. 29, nr 1, artikkel-id e12891Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    For patients with cancer, sleep disturbance is commonplace. Using classical test theory and Rasch analyses, the present study compared two commonly used psychometric instruments for insomnia - Athens Insomnia Scale and Insomnia Severity Index - among patients with advanced cancer. Through convenience sampling, patients with cancer at stage III or IV (n = 573; 326 males; mean age = 61.3 years; SD = 10.7) from eight oncology units of university hospitals in Iran participated in the study. All the participants completed the Athens Insomnia Scale, Insomnia Severity Index, Edmonton Symptom Assessment Scale, Hospital Anxiety and Depression Scale, General Health Questionnaire-12, Epworth Sleepiness Scale and Pittsburgh Sleep Quality Index. Additionally, 433 participants wore an Actigraph device for two continuous weekdays. Classical test theory and Rasch analysis both supported the construct validity for Athens Insomnia Scale (factor loadings from confirmatory factor analysis = 0.61-0.87; test-retest reliability = 0.72-0.82; infit mean square = 0.81-1.17; outfit MnSq = 0.79-1.14) and for Insomnia Severity Index (factor loadings from confirmatory factor analysis = 0.61-0.81; test-retest reliability = 0.72-0.82; infit mean square = 0.72-1.14; outfit mean square = 0.76-1.11). Both Athens Insomnia Scale and Insomnia Severity Index had significant associations with Edmonton Symptom Assessment Scale, Hospital Anxiety and Depression Scale, General Health Questionnaire-12, Epworth Sleepiness Scale and Pittsburgh Sleep Quality Index, as well as having good sensitivity and specificity. Significant differences in the actigraphy measure were found between insomniacs and non-insomniacs based on Athens Insomnia Scale or Insomnia Severity Index score. With promising results, healthcare providers can use either Athens Insomnia Scale or Insomnia Severity Index to understand the insomnia of patients with advanced cancer.

  • 9.
    Magnusson, Per
    et al.
    Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för klinisk kemi. Region Östergötland, Diagnostikcentrum, Klinisk kemi.
    Nilsen, Per
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten.
    Schedvin, Göran
    Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för klinisk kemi. Region Östergötland, Diagnostikcentrum, Klinisk kemi.
    Appropriate Use of Vitamin D Assessments in Primary Health Care: Impact of New Strategies for the Introduction and Follow-Up of Analyses in Östergötland2019Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 116, nr 14, artikkel-id FFPXArtikkel i tidsskrift (Fagfellevurdert)
  • 10.
    Nätt, Daniel
    et al.
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Örtegren Kugelberg, Unn
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Casas, Eduard
    Josep Carreras Leukaemia Res Inst IJC, Spain.
    Nedstrand, Elizabeth
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
    Zalavary, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Medicinska fakulteten.
    Henriksson, Pontus
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden.
    Nijm, Carola
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten.
    Jaderquist, Julia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten.
    Sandborg, Johanna
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden.
    Flinke Carlsson, Eva
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten.
    Ramesh, Rashmi
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Örkenby, Lovisa
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Appelkvist, Filip
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Lingg, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Guzzi, Nicola
    Lund Univ, Sweden.
    Bellodi, Cristian
    Lund Univ, Sweden.
    Löf, Marie
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden.
    Vavouri, Tanya
    Josep Carreras Leukaemia Res Inst IJC, Spain.
    Öst, Anita
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Human sperm displays rapid responses to diet2019Inngår i: PLoS biology, ISSN 1544-9173, E-ISSN 1545-7885, Vol. 17, nr 12, artikkel-id e3000559Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The global rise in obesity and steady decline in sperm quality are two alarming trends that have emerged during recent decades. In parallel, evidence from model organisms shows that paternal diet can affect offspring metabolic health in a process involving sperm tRNA-derived small RNA (tsRNA). Here, we report that human sperm are acutely sensitive to nutrient flux, both in terms of sperm motility and changes in sperm tsRNA. Over the course of a 2-week diet intervention, in which we first introduced a healthy diet followed by a diet rich in sugar, sperm motility increased and stabilized at high levels. Small RNA-seq on repeatedly sampled sperm from the same individuals revealed that tsRNAs were up-regulated by eating a high-sugar diet for just 1 week. Unsupervised clustering identified two independent pathways for the biogenesis of these tsRNAs: one involving a novel class of fragments with specific cleavage in the T-loop of mature nuclear tRNAs and the other exclusively involving mitochondrial tsRNAs. Mitochondrial involvement was further supported by a similar up-regulation of mitochondrial rRNA-derived small RNA (rsRNA). Notably, the changes in sugar-sensitive tsRNA were positively associated with simultaneous changes in sperm motility and negatively associated with obesity in an independent clinical cohort. This rapid response to a dietary intervention on tsRNA in human sperm is attuned with the paternal intergenerational metabolic responses found in model organisms. More importantly, our findings suggest shared diet-sensitive mechanisms between sperm motility and the biogenesis of tsRNA, which provide novel insights about the interplay between nutrition and male reproductive health.

  • 11.
    Silverå Ejneby, Malin
    et al.
    Linköpings universitet, Institutionen för teknik och naturvetenskap, Laboratoriet för organisk elektronik. Linköpings universitet, Tekniska fakulteten.
    Migliaccio, Ludovico
    Linköpings universitet, Institutionen för teknik och naturvetenskap, Laboratoriet för organisk elektronik. Linköpings universitet, Tekniska fakulteten.
    Gicevicius, Mindaugas
    Linköpings universitet, Institutionen för teknik och naturvetenskap, Fysik och elektroteknik. Linköpings universitet, Tekniska fakulteten. Vilnius Univ, Lithuania.
    Derek, Vedran
    Linköpings universitet, Institutionen för teknik och naturvetenskap, Fysik och elektroteknik. Linköpings universitet, Tekniska fakulteten.
    Jakesova, Marie
    Linköpings universitet, Institutionen för teknik och naturvetenskap, Laboratoriet för organisk elektronik. Linköpings universitet, Tekniska fakulteten.
    Elinder, Fredrik
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Glowacki, Eric
    Linköpings universitet, Institutionen för teknik och naturvetenskap, Laboratoriet för organisk elektronik. Linköpings universitet, Tekniska fakulteten. Warsaw Univ Technol, Poland.
    Extracellular Photovoltage Clamp Using Conducting Polymer-Modified Organic Photocapacitors2020Inngår i: ADVANCED MATERIALS TECHNOLOGIES, ISSN 2365-709X, artikkel-id 1900860Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Optoelectronic control of physiological processes accounts for new possibilities ranging from fundamental research to treatment of disease. Among nongenetic light-driven approaches, organic semiconductor-based device platforms such as the organic electrolytic photocapacitor (OEPC) offer the possibility of localized and wireless stimulation with a minimal mechanical footprint. Optimization of efficiency hinges on increasing effective capacitive charge delivery. Herein, a simple strategy to significantly enhance the photostimulation performance of OEPC devices by employing coatings of the conducting polymer formulation poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate), or PEDOT:PSS is reported. This modification increases the charge density of the stimulating photoelectrodes by a factor of 2-3 and simultaneously decreases the interfacial impedance. The electrophysiological effects of PEDOT:PSS-derivatized OEPCs on Xenopus laevis oocyte cells on membrane potential are measured and voltage-clamp techniques are used, finding an at-least twofold increase in capacitive coupling. The large electrolytic capacitance of PEDOT:PSS allows the OEPC to locally alter the extracellular voltage and keep it constant for long periods of time, effectively enabling a unique type of light-controlled membrane depolarization for measurements of ion channel opening. The finding that PEDOT:PSS-coated OEPCs can remain stable after a 50-day accelerated ageing test demonstrates that PEDOT:PSS modification can be applied for fabricating reliable and efficient optoelectronic stimulation devices.

  • 12.
    Sjöwall, Christopher
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Reumatiska systemsjukdomar2018Inngår i: Internmedicin / [ed] Ulf Dahlström, Stergios Kechagias, Leif Stenke, Stockholm: Liber, 2018, 6, Vol. Sidorna 920-939, s. 920-939Kapittel i bok, del av antologi (Annet vitenskapelig)
  • 13.
    Sorbo, Ann
    et al.
    Sodra Alvsborg Hosp, Sweden; Uddevalla Cent Hosp, Sweden; Univ Gothenburg, Sweden.
    Eiving, Ingrid
    Sahlgrens Univ Hosp, Sweden.
    Theodorsson, Elvar
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för klinisk kemi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk kemi.
    Rydenhag, Bertil
    Univ Gothenburg, Sweden; Sahlgrens Univ Hosp, Sweden.
    Jonsdottir, Ingibjorg H.
    Inst Stress Med, Sweden.
    Pre-traumatic conditions can influence cortisol levels before and after a brain injury2020Inngår i: Acta Neurologica Scandinavica, ISSN 0001-6314, E-ISSN 1600-0404Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective Satisfactory anabolic reactions, including the activation of the hypothalamic-pituitary-adrenal (HPA) axis, are essential following severe traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH). Many factors may influence this activation. This study aimed to investigate whether individuals who reported chronic diseases, psychosocial afflictions, or stressful events before a severe brain injury display a different pattern regarding cortisol levels retrospectively and up to three months compared with those who did not report stressful experiences. Materials and Methods Fifty-five patients aged 16-68 years who were admitted to the neurointensive care unit (NICU) were included. Hair cortisol measurements offer a unique opportunity to monitor cortisol levels retrospectively and after the trauma. Hair strands were collected as soon as possible after admission to the NICU and every month until three months after the injury/insult. The participants/relatives were asked about stressful events, psychosocial afflictions and recent and chronic diseases. Results The group who reported chronic diseases and/or stressful events before the brain injury had more than twice as high median hair cortisol levels before the brain injury compared with those who did not report stress, but the difference was not statistically significant (P = .12). Those who reported stress before the brain injury had statistically significantly lower hair cortisol values after the brain injury and they remained until three months after the injury. Conclusions Stressful events and/or chronic disease before brain injury might affect mobilization of adequate stress reactions following the trauma. However, the large variability in cortisol levels in these patients does not allow firm conclusions and more studies are needed.

  • 14.
    Svedberg, Anna
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten.
    Toxicity and pharmacokinetic biomarkers for personalized non-small cell lung cancer treatment2020Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Lung cancer is the leading cause of cancer-related deaths worldwide. Unfortunately, lung cancer is usually discovered at a late stage when the curative treatment options are limited. The treatment can include surgery, radiation, chemotherapy, targeted therapy and now also immunotherapy.

    The challenge in cancer treatment is to eradicate cancer by the use of harsh treatments, while still, keeping the patient alive. For this purpose, treatments with severe toxicities are usually accepted but regularly lead to dose reductions or postponed treatment. Large variations in response are generally observed between patients treated with the same drug at the same dose. The dose may be adequate in one patient while ineffective or cause severe adverse drug reactions in other patients. The occurrence of drug-induced toxicities can, however, also be a positive indicator of treatment response. In personalized treatment it is of importance to select the most suitable treatment option and give it at the most favorable dose, to enable the patients to stay on treatment during the time the treatment is able to affect cancer since the tumor commonly develops resistance towards the treatment eventually.

    In this thesis, inter-individual variability in pharmacokinetics and toxicity for the targeted therapy erlotinib, associated with the adverse events skin rash and diarrhea was studied. Inter-individual variability in toxicity was also studied for the chemotherapy treatment gemcitabine/carboplatin linked to the hematological toxicities neutropenia and leukopenia.

    Erlotinib was studied in papers I-IV. Erlotinib and its metabolite concentrations were determined using a validated LC-MS/MS method. Diarrhea was associated with erlotinib and the metabolite M13, while skin rash was associated with the activity of the erlotinib metabolizing enzyme CYP3A and the ABCG2 single nucleotide polymorphism rs10856870. CYP3A was also shown to be induced during treatment. Additionally, in vitro studies showed that genetic variability in ABCG2 contributes to differences in intracellular concentrations. Genes and gene variants were found to be associated with gemcitabine/carboplatininduced toxicity in paper V. The variants were partially validated, and two models were developed to estimate the risk of leukopenia or neutropenia based on a set of genetic variants.

    Delarbeid
    1. A validated liquid chromatography tandem mass spectrometry method for quantification of erlotinib, OSI-420 and didesmethyl erlotinib and semi-quantification of erlotinib metabolites in human plasma
    Åpne denne publikasjonen i ny fane eller vindu >>A validated liquid chromatography tandem mass spectrometry method for quantification of erlotinib, OSI-420 and didesmethyl erlotinib and semi-quantification of erlotinib metabolites in human plasma
    Vise andre…
    2015 (engelsk)Inngår i: Journal of Pharmaceutical and Biomedical Analysis, ISSN 0731-7085, E-ISSN 1873-264X, Vol. 107, s. 186-195Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    A liquid chromatography tandem mass spectrometry method was developed and validated for quantification of erlotinib and its metabolites in human plasma. The method is suitable for therapeutic drug monitoring and pharmacokinetic studies. The substances were extracted using protein precipitation, separated on a BEH XBridge C18 column (100 x 2.1 mm, 1.7 mu m) by gradient elution at 0.7 mL/min of acetonitrile and 5 mM ammonium acetate. The concentration was determined using a Waters Xevo triple quadrupole mass spectrometer in a multi reaction monitoring mode. The total run time was 7 min. Deuterated erlotinib and OSI-597 were used as internal standard for erlotinib and its metabolites, respectively. Erlotinib, OSI-420 and didesmethyl erlotinib were quantified in the concentration range 25-5000 ng/mL, 0.5-500 ng/mL and 0.15-10 ng/mL, respectively. Precision and accuracy was less than14% except for OSI-420 at LLOQ (17%). Extraction recovery was above 89%, 99% and 89% for erlotinib, OSI-420 and didesmethyl erlotinib, respectively. The human liver microsomes generated 14 metabolites, three of them not previously reported. Twelve metabolites were measured semi-quantitatively and validated with respect to selectivity, precision and stability. (C) 2014 Elsevier B.V. All rights reserved.

    sted, utgiver, år, opplag, sider
    Elsevier, 2015
    Emneord
    LC-MS/MS; Human liver microsomes; Non-small cell lung cancer; EGFR; Tyrosine kinase inhibitor
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-117227 (URN)10.1016/j.jpba.2014.12.022 (DOI)000351116900024 ()25594896 (PubMedID)
    Merknad

    Funding Agencies|Swedish Research Council [C0592901, A0671101]; Swedish Cancer Society [130335]; Medical Research Council of Southeast Sweden [388611]

    Tilgjengelig fra: 2015-04-23 Laget: 2015-04-21 Sist oppdatert: 2020-01-14
    2. Erlotinib treatment induces cytochrome P450 3A activity in non-small cell lung cancer patients
    Åpne denne publikasjonen i ny fane eller vindu >>Erlotinib treatment induces cytochrome P450 3A activity in non-small cell lung cancer patients
    Vise andre…
    2019 (engelsk)Inngår i: British Journal of Clinical Pharmacology, ISSN 0306-5251, E-ISSN 1365-2125, Vol. 85, nr 8, s. 1704-1709Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Aims Erlotinib is a tyrosine kinase inhibitor used in the treatment of non-small cell lung cancer highly metabolized by the cytochrome P450 (CYP) 3A. Hence, CYP3A4 activity might be a useful predictor of erlotinib pharmacokinetics in personalized medicine. The effect of erlotinib on CYP3A activity was therefore studied in non-small cell lung cancer patients. Methods The study included 32 patients scheduled for erlotinib monotherapy. CYP3A activity was assessed using quinine as a probe before and during erlotinib treatment. Plasma from blood samples drawn 16 hours post quinine administration were analysed using HPLC with fluorescence detection to determine the quinine/3-OH-quinine ratio. Results Matched samples, available from 13 patients, showed an induction of CYP3A activity (P = 0.003, Wilcoxons signed rank test) after 2 months of treatment. The quinine/3-OH-quinine ratio decreased from 20.2 (+/- 13.4) at baseline to 11.0 (+/- 4.34). Single-point samples, available from 19 patients, supported the decrease in ratio (P = 0.007, Mann-Whitney U-test). Generally, females had a higher CYP3A activity both at baseline and after two months of treatment. Statistical analysis by gender also showed significant increase in CYP3A activity (males, n = 10, P = 0.001, and females, n = 22, P = 0.001). Conclusions An induction of CYP3A activity was observed after 2 months of erlotinib treatment which was also seen when subdividing based on gender. It could be important to take this into consideration for patients co-administering other CYP3A-metabolizing drugs during erlotinib treatment and also makes it difficult to use baseline CYP3A activity to predict erlotinib pharmacokinetics.

    sted, utgiver, år, opplag, sider
    WILEY, 2019
    Emneord
    CYP3A activity; erlotinib; non-small cell lung cancer; quinine; Tarceva
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-159123 (URN)10.1111/bcp.13953 (DOI)000475399400007 ()30945322 (PubMedID)
    Merknad

    Funding Agencies|Cancerfonden [CAN 2016/602]; Forskningsradet i Sydostra Sverige [760411]; Swedish Research Council; Linkoping University

    Tilgjengelig fra: 2019-07-30 Laget: 2019-07-30 Sist oppdatert: 2020-01-14
  • 15.
    Svärd, Anna
    et al.
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Uppsala Univ, Sweden.
    Roos, Karin
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Uppsala Univ, Sweden.
    Brink, M.
    Umea Univ, Sweden.
    Martinsson, Klara
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten.
    Sjöwall, Christopher
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Dahlqvist, S. Rantapaa
    Umea Univ, Sweden.
    Kastbom, Alf
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för inflammation och infektion. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Secretory antibodies to citrullinated peptides in plasma and saliva from rheumatoid arthritis patients and their unaffected first-degree relatives2020Inngår i: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 199, nr 2, s. 143-149Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to evaluate secretory antibodies to citrullinated proteins (ACPA) in plasma and immunoglobulin (Ig)A ACPA in saliva from patients with rheumatoid arthritis (RA) and their unaffected first-degree relatives (FDRs). Patients with RA (n = 194) and first-degree relatives unaffected by RA (n = 191) were recruited for analysis of secretory antibodies to second-generation cyclic citrullinated peptides (anti-CCP) in plasma. From a subpopulation (25 RA patients, 21 first-degree relatives and 11 controls), saliva samples were obtained for IgA anti-CCP analysis. The presence of secretory ACPA was compared between subject categories, and related to genetic and environmental risk factors. Secretory ACPA occurred in 37 (19%) plasma samples from patients with RA, but only in two (1%) of FDRs. IgA ACPA in saliva was found in three of 25 (12%) patients with RA, but not in any of the 21 FDRs (amp;lt; 5%). No significant associations were seen between the presence of secretory ACPA and SE or smoking, either among RA patients or among FDRs. Despite occurring in 19% of RA plasma, secretory ACPA was rare in both saliva and plasma among FDRs, even among those positive for conventional ACPA of non-mucosal origin. Longitudinal studies are warranted to determine whether circulating secretory ACPA occurs before or in parallel with the development of clinical arthritis.

  • 16.
    Wu, Wendy Yi-Ying
    et al.
    Umea Univ, Sweden.
    Johansson, Gunnar
    Umea Univ, Sweden.
    Wibom, Carl
    Umea Univ, Sweden.
    Brannstrom, Thomas
    Umea Univ, Sweden.
    Malmström, Annika
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, LAH Linköping.
    Henriksson, Roger
    Umea Univ, Sweden.
    Golovleva, Irina
    Umea Univ, Sweden.
    Bondy, Melissa L.
    Stanford Univ, CA 94305 USA; Baylor Coll Med, TX 77030 USA.
    Andersson, Ulrika
    Umea Univ, Sweden.
    Dahlin, Anna M.
    Umea Univ, Sweden.
    Melin, Beatrice
    Umea Univ, Sweden.
    The Genetic Architecture of Gliomagenesis-Genetic Risk Variants Linked to Specific Molecular Subtypes2019Inngår i: CANCERS, Vol. 11, nr 12, artikkel-id 2001Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Genome-wide association studies have identified 25 germline genetic loci that increase the risk of glioma. The somatic tumor molecular alterations, including IDH-mutation status and 1p/19q co-deletion, have been included into the WHO 2016 classification system for glioma. To investigate how the germline genetic risk variants correlate with the somatic molecular subtypes put forward by WHO, we performed a meta-analysis that combined findings from 330 Swedish cases and 876 controls with two other recent studies. In total, 5,103 cases and 10,915 controls were included. Three categories of associations were found. First, variants in TERT and TP53 were associated with increased risk of all glioma subtypes. Second, variants in CDKN2B-AS1, EGFR, and RTEL1 were associated with IDH-wildtype glioma. Third, variants in CCDC26 (the 8q24 locus), C2orf80 (close to IDH), LRIG1, PHLDB1, ETFA, MAML2 and ZBTB16 were associated with IDH-mutant glioma. We therefore propose three etiopathological pathways in gliomagenesis based on germline variants for future guidance of diagnosis and potential functional targets for therapies. Future prospective clinical trials of patients with suspicion of glioma diagnoses, using the genetic variants as biomarkers, are necessary to disentangle how strongly they can predict glioma diagnosis.

  • 17.
    Xiao, Jiaxin
    et al.
    Univ Oslo, Norway; Oslo Univ Hosp, Norway.
    Adil, Mohammed Yasin
    Univ Oslo, Norway; Oslo Univ Hosp, Norway.
    Chen, Xiangjun
    Norwegian Dry Eye Clin, Norway; Sorlandet Hosp, Norway; Oslo Univ Hosp, Norway; Univ Oslo, Norway; Univ Coll Southeast Norway, Norway.
    Utheim, Oygunn A.
    Norwegian Dry Eye Clin, Norway.
    Raeder, Sten
    Norwegian Dry Eye Clin, Norway.
    Tonseth, Kim Alexander
    Oslo Univ Hosp, Norway; Oslo Univ Hosp, Norway.
    Lagali, Neil
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för logopedi, otorhinolaryngologi och audiologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Sinnescentrum, Ögonkliniken US/LiM. Sorlandet Hosp, Norway.
    Dartt, Darlene A.
    Harvard Med Sch, MA 02115 USA.
    Utheim, Tor P.
    Oslo Univ Hosp, Norway; Sorlandet Hosp, Norway; Oslo Univ Hosp, Norway; Univ Oslo, Norway; Univ Coll Southeast Norway, Norway; Oslo Univ Hosp, Norway; Stavanger Univ Hosp, Norway.
    Functional and Morphological Evaluation of Meibomian Glands in the Assessment of Meibomian Gland Dysfunction Subtype and Severity2020Inngår i: American Journal of Ophthalmology, ISSN 0002-9394, E-ISSN 1879-1891, Vol. 209, s. 160-167Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    PURPOSE: To classify subtypes of meibomian gland dysfunction (MGD) and evaluate the dependency of dry eye signs, symptoms, and parameters on MGD subtype. DESIGN: Cross-sectional study. Study Population: the right eyes of 447 patients with MGD of various subtypes and 20 healthy volunteers. METHODS: Patients were divided into 4 subtypes of MGD based on meibum expression, meibum quality, and MG loss on meibography images (meibograde of 0-6). Subtypes were patients with high meibum delivery (hypersecretory and nonobvious MGD) and those with low meibum delivery (hyposecretory and obstructive MGD). Additional clinical tests included tear film break-up time (TFBUT), ocular staining, osmolarity, Schirmer I, blink interval timing and the Ocular Surface Disease Index (OSDI) questionnaire. RESULTS: A total of 78 eyes had hypersecretory MGD; 49 eyes had nonobvious MGD; 66 eyes had hyposecretory MGD; and 254 eyes had obstructive MGD. Increased tear film osmolarity and lower TFBUT were found in the low-delivery groups; hyposecretory (P = 0.006, P = 0.016) and obstructive MGD (P = 0.008, P = 0.006) relative to high-delivery MGD (hypersecretory and nonobvious groups, respectively). Worse ocular symptoms and ocular staining were also found in low-delivery MGD groups than the high delivery MGD groups (P amp;lt; 0.01 and P amp;lt; 0.006, respectively). " CONCLUSIONS: Patients with low-delivery MGD had worse dry eye parameters and ocular symptoms than those with high meibum delivery, indicating the pivotal role of meibum secretion in ocular surface health that should be targeted in MGD therapy. Furthermore, nonobvious MGD cannot be diagnosed using conventional dry eye tests and requires morphologic assessment of meibography images to confirm MG loss. ((C) 2019 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).)

  • 18.
    Yngman Uhlin, Pia
    et al.
    Linköpings universitet, Institutionen för hälsa, medicin och vård, Avdelningen för omvårdnad och reproduktiv hälsa. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Ledningsstab Region Östergötland, Enheten för forskningsstöd.
    Kjellsdotter, Anna
    Univ Skovde, Sweden.
    Uhlin, Fredrik
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Njurmedicinska kliniken US. Tallinn Univ Technol, Estonia.
    Edéll-Gustafsson, Ulla
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för omvårdnad. Linköpings universitet, Medicinska fakulteten.
    Sleep Quality, Fatigue, and Health-Related Quality of Life in Patients on Initial Peritoneal Dialysis and Multiple Modalities after Two Years: A Prospective Study2019Inngår i: Nephrology Nursing Journal : Journal of The American Nephrology Nurses Association, ISSN 1526-744X, E-ISSN 2163-5390, Vol. 46, nr 6, s. 615-+Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The purpose of this study was to investigate changes in sleep quality, fatigue, mental health, and health-related quality of life (HRQoL) over a two-year period among patients undergoing peritoneal dialysis treatment at home. We further explored the extent to which sleep quality, fatigue, and mental health predicted health-related quality of life outcomes. This prospective study included 55 patients. Sleep parameters changed over two years, independently of treatment. Sleep variables at baseline, to some extent, predicted sleep quality after two years. Daytime sleepiness can be a long-term problem. Findings indicate improvements in nocturnal sleep over a two-year time period, independently of dialysis treatment. In contrast, fatigue remained unchanged over the same time period Dansplantation seems to generally benefit the outcome of HRQoL. Strategies to improve sleep and HRQoL may include systematic risk factor modification and efforts to optimise symptomatic treatment.

  • 19.
    Zetterqvist, Maria
    et al.
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Barn- och ungdomspsykiatriska kliniken.
    Hanell, H. Erneroth
    Stockholm City Council, Sweden.
    Wadsby, Marie
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Cocozza, Madeleine
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Gustafsson, Per
    Linköpings universitet, Institutionen för biomedicinska och kliniska vetenskaper, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Närsjukvården i centrala Östergötland, Barn- och ungdomspsykiatriska kliniken.
    Validation of the Systemic Clinical Outcome and Routine Evaluation (SCORE-15) self-report questionnaire: index of family functioning and change in Swedish families2020Inngår i: Journal of Family Therapy, ISSN 0163-4445, E-ISSN 1467-6427, Vol. 42, nr 1, s. 129-148Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Instruments for evaluating the progress and outcome of systemic therapeutic treatments in clinical practice need to be easily administered and have sound psychometric properties. The Systemic Clinical Outcome and Routine Evaluation, 15-item version (SCORE-15), is a self-report instrument that measures aspects of family functioning. This study investigates the psychometric qualities of a Swedish version of SCORE-15. Seventy Swedish families with healthy children and 159 families with children with psychiatric or behavioural problems were included in the study, resulting in a total of 397 individuals. Results showed that SCORE-15 differentiated clinical from non-clinical families with acceptable psychometric properties for test-retest, internal consistency, convergent and construct validity, as well as sensitivity to change for the clinical sample. The three-factor solution of strengths, difficulties and communication was tested. Results imply preliminary psychometric support for the use of the Swedish version of SCORE-15 to evaluate progress and outcome in clinical practice. Practitioner points SCORE-15 is an easily administered questionnaire suitable for use in clinical practice to evaluate systemic therapeutic progress and outcome The Swedish version of SCORE-15 has acceptable psychometric properties

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