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Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Gastroenterologi) > (2010-2019) > Linnéuniversitetet

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1.
  • Lexne, Erik, et al. (författare)
  • Temperament and character in patients with acute abdominal pain
  • 2018
  • Ingår i: Comprehensive Psychiatry. - : Saunders Elsevier. - 0010-440X .- 1532-8384. ; 87, s. 128-133
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundSeveral conditions presenting with abdominal pain are associated with specific personality factors although it is unclear if this is true also in emergency clinic settings.ObjectiveTo study personality factors among patients with acute abdominal pain in an emergency ward.MethodsConsecutive patients (N = 165) with abdominal symptoms at an emergency clinic were administrated the Temperament and Character Inventory (TCI). Three main groups were identified; specific abdominal diagnoses, (N = 77), non-specific abdominal pain, (N = 67) and organic dyspepsia (N = 21). TCI results were compared between clinical groups and a control group (N = 122).ResultsAs compared to individuals with specific abdominal diagnoses and controls, those with organic dyspepsia were significantly more anxious (harm avoidance), (p = 0.003), and had lower ability to cooperate (cooperativeness) (p = 0.048 and p = 0.004 respectively). They were also significantly more unpretentious (self-transcendence) compared to individuals with specific abdominal diagnoses (p = 0.048), non-specific abdominal pain (p = 0.012) and controls (p = 0.004) and evidenced less mature character (sum of self-directedness and cooperativeness) compared to those with specific abdominal diagnoses and controls (p = 0.003).ConclusionIndividuals seeking care at an emergency clinic with organic dyspepsia showed a distinguishable pattern of personality features that distinguished them from the other comparison groups. Therefore an evaluation of personality factors may add a new dimension to the diagnostic investigation in the emergency care of abdominal pain and contribute to the optimization of the treatment of organic dyspepsia.
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2.
  • Röckert Tjernberg, Anna, 1975-, et al. (författare)
  • Coeliac disease and invasive pneumococcal disease : a population-based cohort study
  • 2017
  • Ingår i: Epidemiology and Infection. - : Cambridge University Press. - 0950-2688 .- 1469-4409. ; 145:6, s. 1203-1209
  • Tidskriftsartikel (refereegranskat)abstract
    • Severe infections are recognized complications of coeliac disease (CD). In the present study we aimed to examine whether individuals with CD are at increased risk of invasive pneumococcal disease (IPD). To do so, we performed a population-based cohort study including 29 012 individuals with biopsy-proven CD identified through biopsy reports from all pathology departments in Sweden. Each individual with CD was matched with up to five controls (n = 144 257). IPD events were identified through regional and national microbiological databases, including the National Surveillance System for Infectious Diseases. We used Cox regression analyses to estimate hazard ratios (HRs) for diagnosed IPD. A total of 207 individuals had a record of IPD whereas 45/29 012 had CD (0.15%) and 162/144 257 were controls (0.11%). This corresponded to a 46% increased risk for IPD [HR 1.46, 95% confidence interval (CI) 1.05-2.03]. The risk estimate was similar after adjustment for socioeconomic status, educational level and comorbidities, but then failed to attain statistical significance (adjusted HR 1.40, 95% CI 0.99-1.97). Nonetheless, our study shows a trend towards an increased risk for IPD in CD patients. The findings support results seen in earlier research and taking that into consideration individuals with CD may be considered for pneumococcal vaccination.
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3.
  • Pernow, Ylva, et al. (författare)
  • Aberrant tryptophan transport in cultured fibroblast from patients with Male Idiopathic Osteoporosis : an in vitro study
  • 2018
  • Ingår i: Bone Reports. - Amsterdam, Netherlands : Elsevier. - 2352-1872. ; 8, s. 25-28
  • Tidskriftsartikel (refereegranskat)abstract
    • It has been demonstrated, that long-term chronic tryptophan deficiency, results in decreased serotonin synthesis, which may lead to low bone mass and low bone formation. Findings from studies in male patients with idiopathic osteoporosis suggested a decreased transport of tryptophan in erythrocytes of osteoporotic patients, indicating that serotonin system defects may be involved in the etiology of low bone mass. Tryptophan is the precursor of serotonin, and a disturbed transport of tryptophan is implicated in altered serotonin synthesis. However, no study has investigated the tryptophan transport kinetics in MIO patients. The aim of this study is to investigate the kinetic parameters of tryptophan transport in fibroblasts derived from MIO patients compared to age and sex matched controls.Fibroblast cells were cultured from skin biopsies obtained from 14 patients diagnosed with Male Idiopathic Osteoporosis and from 13 healthy age-sex matched controls, without a diagnosis of osteoporosis. Transport of the amino acid tryptophan across the cell membrane was measured by the cluster tray method. The kinetic parameters, maximal transport capacity (Vmax) and affinity constant (Km) were determined by using the Lineweaver-Burke plot equation.The results of this study have shown a significantly lower mean value for Vmax (p = 0.0138) and lower Km mean value (p = 0.0009) of tryptophan transport in fibroblasts of MIO patients compared to the control group. A lower Vmax implied a decreased tryptophan transport availability in MIO patients.In conclusion, reduced cellular tryptophan availability in MIO patients might result in reduced brain serotonin synthesis and its endogenous levels in peripheral tissues, and this may contribute to low bone mass/formation. The findings of the present study could contribute to the etiology of idiopathic osteoporosis and for the development of novel approaches for diagnosis, treatment and management strategies of MIO.
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5.
  • Thorgersen, Ebbe Billmann, et al. (författare)
  • The Role of Complement in Liver Injury, Regeneration, and Transplantation
  • 2019
  • Ingår i: Hepatology. - : John Wiley & Sons. - 0270-9139 .- 1527-3350. ; 70:2, s. 725-736
  • Tidskriftsartikel (refereegranskat)abstract
    • The liver is both an immunologically complex and a privileged organ. The innate immune system is a central player, in which the complement system emerges as a pivotal part of liver homeostasis, immune responses, and crosstalk with other effector systems in both innate and adaptive immunity. The liver produces the majority of the complement proteins and is the home of important immune cells such as Kupffer cells. Liver immune responses are delicately tuned between tolerance to many antigens flowing in from the alimentary tract, a tolerance that likely makes the liver less prone to rejection than other solid organ transplants, and reaction to local injury, systemic inflammation, and regeneration. Notably, complement is a double-edged sword as activation is detrimental by inducing inflammatory tissue damage in, for example, ischemia-reperfusion injury and transplant rejection yet is beneficial for liver tissue regeneration. Therapeutic complement inhibition is rapidly developing for routine clinical treatment of several diseases. In the liver, targeted inhibition of damaged tissue may be a rational and promising approach to avoid further tissue destruction and simultaneously preserve beneficial effects of complement in areas of proliferation. Here, we argue that complement is a key system to manipulate in the liver in several clinical settings, including liver injury and regeneration after major surgery and preservation of the organ during transplantation.
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