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  • 1.
    Barathan, Muttiah
    et al.
    University of Malaya, Malaysia.
    Mohamed, Rosmawati
    University of Malaya, Malaysia.
    Saeidi, Alireza
    University of Malaya, Malaysia.
    Vadivelu, Jamuna
    University of Malaya, Malaysia.
    Chang, Li Y.
    University of Malaya, Malaysia.
    Gopal, Kaliappan
    University of Malaya, Malaysia.
    Ram, Mani R.
    University of Malaya, Malaysia.
    Ansari, Abdul W.
    University of Malaya, Malaysia.
    Kamarulzaman, Adeeba
    University of Malaya, Malaysia.
    Velu, Vijayakumar
    Emory Vaccine Centre, GA USA.
    Larsson, Marie
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Shankar, Esaki M.
    University of Malaya, Malaysia; University of Malaya, Malaysia.
    Increased frequency of late-senescent T cells lacking CD127 in chronic hepatitis C disease2015Ingår i: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 45, nr 5, s. 466-474Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BackgroundHepatitis C virus (HCV) causes persistent disease in similar to 85% of infected individuals, where the viral replication appears to be tightly controlled by HCV-specific CD8+ T cells. Accumulation of senescent T cells during infection results in considerable loss of functional HCV-specific immune responses. Materials and methodsWe characterized the distinct T-cell phenotypes based on the expression of costimulatory molecules CD28 and CD27, senescence markers PD-1 and CD57, chronic immune activation markers CD38 and HLA-DR, and survival marker CD127 (IL-7R) by flow cytometry following activation of T cells using HCV peptides and phytohemagglutinin. ResultsHCV-specific CD4+ and CD8+ T cells from chronic HCV (CHC) patients showed increased expression of PD-1. Furthermore, virus-specific CD4+ T cells of CHC-infected subjects displayed relatively increased expression of HLA-DR and CD38 relative to HCV-specific CD8+ T cells. The CD4+ and CD8+ T cells from HCV-infected individuals showed significant increase of late-differentiated T cells suggestive of immunosenescence. In addition, we found that the plasma viral loads positively correlated with the levels of CD57 and PD-1 expressed on T cells. ConclusionsChronic HCV infection results in increased turnover of late-senescent T cells that lack survival potentials, possibly contributing to viral persistence. Our findings challenge the prominence of senescent T-cell phenotypes in clinical hepatitis C infection.

  • 2.
    Barathan, Muttiah
    et al.
    University of Malaya, Malaysia.
    Mohamed, Rosmawati
    University of Malaya, Malaysia.
    Vadivelu, Jamuna
    University of Malaya, Malaysia.
    Chang, Li Y.
    University of Malaya, Malaysia.
    Saeidi, Alireza
    University of Malaya, Malaysia.
    Yong, Yean K.
    University of Malaya, Malaysia.
    Ravishankar Ram, M.
    University of Malaya, Malaysia.
    Gopal, Kaliappan
    University of Malaya, Malaysia.
    Velu, Vijayakumar
    Emory Vaccine Centre, GA 30329 USA.
    Larsson, Marie
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Shankar, Esaki M.
    University of Malaya, Malaysia.
    Peripheral loss of CD8(+)CD161(++)TCRV7 center dot 2(+) mucosal-associated invariant T cells in chronic hepatitis C virus-infected patients2016Ingår i: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 46, nr 2, s. 170-180Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BackgroundMucosal-associated invariant T (MAIT) cells play an important role in innate host defence. MAIT cells appear to undergo exhaustion and are functionally weakened in chronic viral infections. However, their role in chronic hepatitis C virus (HCV) infection remains unclear. Materials and methodsWe investigated the frequency of CD8(+)CD161(++)TCR V7.2(+) MAIT cells in a cross-sectional cohort of chronic HCV-infected patients (n = 25) and healthy controls (n = 25). Peripheral blood mononuclear cells were investigated for circulating MAIT cell frequency, liver-homing (CCR5 and CD103), biomarkers of immune exhaustion (PD-1, TIM-3 and CTLA-4), chronic immune activation (CD38 and HLA-DR), and immunosenescence (CD57) by flow cytometry. ResultsThe frequency of MAIT cells was significantly decreased, and increased signs of immune exhaustion and chronic immune activation were clearly evident on MAIT cells of HCV-infected patients. Decrease of CCR5 on circulating MAIT cells is suggestive of their peripheral loss in chronic HCV-infected patients. MAIT cells also showed significantly increased levels of HLA-DR, CD38, PD-1, TIM-3 and CTLA-4, besides CD57 in chronic HCV disease. ConclusionsImmune exhaustion and senescence of CD8(+)CD161(++)TCR V7.2(+) MAIT cells could contribute to diminished innate defence attributes likely facilitating viral persistence and HCV disease progression.

  • 3.
    Järemo, Peter
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Kardiologi. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Lindahl, Tomas
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Klinisk kemi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk kemi.
    Lennmarken, Claes
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Anestesiologi.
    Forsgren, H
    The use of platelet density and volume measurements to estimate the severity of pre-eclampsia.2001Ingår i: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 30, s. 1113-1118Artikel i tidskrift (Refereegranskat)
  • 4.
    Järemo, Petter
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i östra Östergötland, Medicinkliniken ViN.
    Milovanovic, Micha
    Linköpings universitet, Institutionen för samhälls- och välfärdsstudier, Hälsa, Aktivitet, Vård (HAV). Linköpings universitet, Hälsouniversitetet.
    Buller, Caroline
    Östergötlands Läns Landsting, Närsjukvården i östra Östergötland, Medicinkliniken ViN.
    Nilsson, Staffan
    Linköpings universitet, Institutionen för medicin och hälsa, Allmänmedicin. Linköpings universitet, Hälsouniversitetet.
    Winblad, Bengt
    Karolinska Institute, Huddinge, Sweden.
    Alzheimer's disease and granulocyte density diversity2013Ingår i: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 43, nr 6, s. 545-548Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND:

    The current study investigates circulating eosinophils and neutrophils in Alzheimer's (AD) type dementia with respect to density (kg/L). The existence of β-amyloid plaques in the brain is a feature of AD. Sporadic scientific reports indicate that the disease affects circulating neutrophils. In contrast, numerous publications investigate inflammatory reactions in AD brains. Locally, the plaques evoke a substantial inflammatory response involving activated microglia and astrocytes.

    METHODS:

    Subjects with probable AD (n = 39) were included and compared with elderly individuals (n = 22) lacking apparent memory problems. We sampled 10 mL venous blood in citrate. Granulocytes were separated according to density in linear Percoll™ gradients. Subsequently, the gradients were divided into density subfractions (n = 16). In every fraction, determination of eosinophil and neutrophil counts was carried out.

    RESULTS:

    AD sufferers displayed less granulocytes in fractions nos. 13-15 containing light cells. For these fractions, the P-values proved to be (P < 0·001; not significant; P = 0·03) and (P = 0·01; P = 0·01; not significant), for eosinophils and neutrophils, respectively.

    CONCLUSIONS:

    The present work describes that less circulating light granulocytes are a feature of AD demented individuals. It is to hypothesize that it is a sign of impaired granulocyte turnover and cell damage. It is concluded that AD affects inflammatory cells in the periphery and that the behaviour of granulocytes in dementia is worthwhile further studies.

  • 5.
    Lundberg, J. O. N.
    et al.
    Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Herulf, M.
    Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Olesen, Martin
    Department of Medicine, Division of Gastroenterology, Örebro Medical Center Hospital, Örebro, Sweden.
    Bohr, J.
    Department of Medicine, Division of Gastroenterology, Örebro Medical Center Hospital, Örebro, Sweden.
    Tysk, Curt
    Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.
    Morcos, E.
    Department of Urology, Karolinska Hospital, Stockholm, Sweden.
    Hellström, P. M.
    Department of Medicine, Division of Gastroenterology, Karolinska Hospital, Stockholm.
    Weitzberg, E.
    Department of Anaesthesiology and Intensive Care, Karolinska Hospital, Stockholm, Sweden.
    Järnerot, G.
    Department of Medicine, Division of Gastroenterology, Örebro Medical Center Hospital, Örebro, Sweden.
    Increased nitric oxide production in collagenous and lymphocytic colitis1997Ingår i: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 27, nr 10, s. 869-871Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The production of nitric oxide (NO) is increased in active ulcerative colitis and in Crohn's disease. We have studied NO production in collagenous colitis (CC) and lymphocytic colitis (LC), both of which are inflammatory bowel disorders of unknown aetiology. NO levels were measured directly in gas sampled from the colon during colonoscopy. Plasma levels of NO metabolites (nitrate/nitrite) were also measured. Luminal NO levels were more than 100 times higher in patients with CC compared with controls. In addition, plasma levels of nitrate/nitrite were increased in the patients as compared with controls. Measurements of NO directly in the colon or its oxidation products in plasma may be a helpful tool in further understanding the role of NO in the pathophysiology of CC and LC. Moreover, it is tempting to speculate that these measurements could be clinically useful in the diagnosis and therapy monitoring of these two inflammatory bowel diseases.

  • 6. Monstein, Hans-Jürg
    et al.
    Fransén, Karin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi.
    Dimberg, Jan
    Söderkvist, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi.
    K-ras and B-raf gene mutations are not associated with gastrin- and CCK2-receptor mRNA expression in human colorectal tumour tissues2004Ingår i: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 34, nr 2, s. 100-106Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Colorectal cancer is a multistep process caused by genetic alterations in cell growth regulatory genes such as K-ras and B-raf. It has been assumed that mutations in the K-ras gene induce gastrin gene expression and that gastrin stimulates the growth of colorectal cancer in an autocrine fashion by coexpressing gastrin and cholecystokinin (CCK)2 receptors. The aim of this study was to examine a possible association of K-ras and B-raf gene mutations with gastrin and CCK2 receptor mRNA expression in human colon and rectum tumour biopsy specimens. Methods: K-ras and B-raf gene mutations as well as gastrin and CCK2 receptor mRNA expression in 50 colon and 46 rectum biopsies, respectively, were determined using molecular biology methods. Results: K-ras mutations occurred in 44% colon and 30% rectum and B-raf mutations in 16% colon and 4% rectum tumours, respectively. Gastrin mRNA was expressed in 64% colon and 61% rectum tumours, whereas CCK2 receptor mRNAs was expressed in 32% colon and 13% rectum tumours. K-ras or B-raf gene mutations and simultaneous gastrin mRNA expression was observed in 40% colon and 17% rectum tumours, respectively. Coexpression of gastrin and CCK2 receptor mRNA occurred in 20% colon and 9% rectal tumours. Conclusions: The results do not support the hypothesis that K-ras and B-raf gene mutations have an impact on gastrin- and CCK-receptor mRNA expression in colorectal tumour tissues.

  • 7. Schmidt, PT
    et al.
    Degerblad, M
    Lindström, E
    Sundqvist, M
    Näslund, E
    Gillberg, PG
    Husebye, E
    Theodorsson, Elvar
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för klinisk kemi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk kemi.
    Hellström, PM
    Circulating ghrelin levels after food intake during different phases of the migrating motor complex in man2006Ingår i: European Journal of Clinical Investigation, ISSN 0014-2972, E-ISSN 1365-2362, Vol. 36, nr 7, s. 503-508Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The timing of the migrating motor complexes (MMC) at food intake may influence gastric emptying and release of regulatory hormones. This report studies the relationships between phases I (motor quiescence) and II (intermediate frequency contractions) of MMC and prandial gut hormone response. Materials and methods: Seven fasting volunteers ingested a meal during phase I or II of MMC verified by manometry, using paracetamol as a marker for gastric emptying. Blood was sampled before, during and 210 min after food intake for analysis of ghrelin, motilin, insulin and paracetamol. Results: The basal level of ghrelin during phase I was 127.5 ± 25.4 pmol L-1 and during phase II was 132.4 ± 24.8 pmol L-1. After food intake during phase I, ghrelin fell to 77.2 ± 10 pmol L-1, in phase II it fell to 82.7 ± 17.8 pmol L-1 within 60 min and returned to baseline levels after 120 min. Baseline levels of motilin were 16 ± 2 pmol L-1 and 18 ± 3 pmol L-1 during phases I and II, respectively. After food, motilin decreased to 8.5 ± 0.7 pmol L-1 and 8.7 ± 1.0 pmol L-1 within 60 min and returned to baseline after 90 min. Insulin levels in phases I and II were 8.1 ± 1.2 mU L-1 and 8.6 ± 0.7 mU L-1, respectively, reaching 138.9 ± 35.6 mU L-1 and 167.4 ± 30.0 mU L-1 at 45 min postprandially. Conclusions: The nutritional status of the gastrointestinal tract at food intake had only a limited impact on plasma ghrelin. After food intake, plasma ghrelin drops, similar to motilin, and resumes preprandial levels within 120 min. © 2006 Blackwell Publishing Ltd.

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