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Sökning: L773:0172 780X > (2015-2019)

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1.
  • Fotouhi, Omid, et al. (författare)
  • Regional differences in somatostatin receptor 2 (SSTR2) immunoreactivity is coupled to level of bowel invasion in small intestinal neuroendocrine tumors
  • 2018
  • Ingår i: Neuro - endocrinology letters. - Stockholm, Sweden : Maghira & Maas Publications. - 0172-780X. ; 39:4, s. 305-309
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Somatostatin receptor (SSTR) expression constitutes a pivotal cornerstone for accurate radiological detection and medical treatment of small intestinal neuroendocrine tumors (SI-NETs), and the development of somatostatin analogues for these purposes have revolutionized the clinical work-up. Previous assessments of SSTR isoform expression in SI-NETs have found correlations to overall prognosis and treatment response, however these analyses usually report overall tumoral immunoreactivity, and little is reported regarding histo-regional differences in expressional patterns.METHODS: Thirty-seven primary SI-NETs (WHO grade I, n=32 and WHO grade II, n=5) were collected and assessed for SSTR2 immunohistochemistry. Samples were stratified with regards to histological level of bowel infiltration and spread (mucosal region, muscularis propria region, subserosal region) and each of these tumoral regions was separately scored by SSTR2 staining localization (membrane, cytoplasmic), overall staining intensity and local staining differences within each region.RESULTS: SSTR2 immunoreactivity was progressively weaker as the tumor cells advanced through the small intestinal layers. This was exemplified by a reduction in the amount of tumor samples with strong SSTR2 expression in the deeper histological levels of the section; 56% of tumors displayed strong SSTR2 expression in the mucosal region, as compared to 29% and 30% of tumors within muscularis propria and subserosal layers, respectively.CONCLUSIONS: This observation indicates a down-regulation of SSTR2 expression as the tumors progress through the intestinal wall, which might signify underlying biological processes of importance for SI-NET invasion behavior.
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  • Melkersson, Kristina, et al. (författare)
  • Early-onset inguinal hernia as risk factor for schizophrenia or related psychosis : a nationwide register-based cohort study
  • 2017
  • Ingår i: Neuro - endocrinology letters. - : MAGHIRA & MAAS PUBLICATIONS. - 0172-780X. ; 27, s. S900-S901
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: In an earlier interview study, we found that more men with familial schizophrenia had undergone inguinal hernia operation, than men with sporadic schizophrenia. However, there are no other studies published specifically on inguinal hernia and schizophrenia. Therefore, the aim of this study was to carry out a Swedish register-based cohort study on the association between inguinal hernia and schizophrenia or related psychosis. METHODS: Data from the Total Population-and Medical Birth-Registers were used to create a cohort of all individuals born in Sweden 1987-1999 (n=1 406 168). The cohort individuals were linked with the In-and Out-patient Registers and followed from birth to 2015 to identify onset of schizophrenia, schizoaffective disorder and inguinal hernia. Cox proportional hazards regression models were used to assess the association between inguinal hernia before age 13 and risk of developing schizophrenia or schizoaffective disorder during a follow-up from age 13. RESULTS: Inguinal hernia before age 13 was identified in 21 095 individuals, and during the follow-up in total 1314 individuals developed schizophrenia or schizoaffective disorder. The risk of schizophrenia or schizoaffective disorder was higher among individuals with inguinal hernia before age 13, than among individuals without such a diagnosis, especially among the men [adjusted hazard ratio (95% confidence interval); all: 1.44 (1.01-2.06), p=0.0452, men: 1.46 (1.01-2.12), p=0.0460, women: 0.56 (0.14-2.27), p=0.4173]. CONCLUSIONS: This study shows that early-onset inguinal hernia is associated with increased risk of developing schizophrenia or schizoaffective disorder, especially in men. Such an association may point to a common biological basis for the development of inguinal hernia and schizophrenia or related psychosis.
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  • Melkersson, Kristina, et al. (författare)
  • Type 1 diabetes mellitus and the risk for schizophrenia or schizoaffective disorder : a Swedish nationwide register-based cohort study
  • 2019
  • Ingår i: Neuro - endocrinology letters. - : MAGHIRA & MAAS PUBLICATIONS. - 0172-780X .- 2354-4716. ; 29, s. S75-S75
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: Type 1 diabetes mellitus (T1DM), resulting from an immune-associated destruction of insulin-secreting pancreatic beta-cells, has been reported in a few earlier studies to be inversely associated with schizophrenia, but not with schizophrenia-like psychoses. The aim of this study was to verify this finding by carrying out a Swedish register study.METHODS: Data from the Total Population- and Medical Birth-Registers were used to create a cohort of all individuals born in Sweden 1987-2004. The cohort individuals were linked with the Inpatient- and Outpatient-Registers and followed from birth to 2017 to identify onset of T1DM, schizophrenia and schizoaffective disorder. Cox proportional hazard regression models were used to assess the association between T1DM and risk of developing schizophrenia or schizoaffective disorder during a follow-up from age 13.RESULTS: The study population included 1 745 977 individuals and the length of follow-up was maximally 18.0 (median 9.7) years. During the follow-up, 1 280 individuals developed schizophrenia and 649 individuals schizoaffective disorder. The risk of developing schizophrenia was significantly lower among individuals with, than among individuals without, a diagnosis of T1DM, whereas the risk of developing schizoaffective disorder did not differ among individuals with or without a T1DM diagnosis [adjusted hazard ratio (95% confidence interval); schizophrenia: 0.29 (0.09-0.91), p=0.0338, schizoaffective disorder: 1.50 (0.71-3.16), p=0.29091].CONCLUSIONS: This study, in line with previous studies, shows that a diagnosis of T1DM is associated with a decreased risk of schizophrenia. This finding of an inverse association between T1DM and schizophrenia may bring an interesting piece, related to autoimmunity, into the schizophrenia-aetiology puzzle.
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  • Walser, Marion, 1961, et al. (författare)
  • Effects of peripheral administration of GH and IGF-I on gene expression in the hippocampus of hypophysectomised rats
  • 2018
  • Ingår i: Neuroendocrinology Letters. - 0172-780X. ; 39:7, s. 525-531
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Growth hormone (GH) increases insulin-like growth factor I (IGF-I) production and both hormones affect hippocampal plasticity. We have previously shown that Hbb and Alas2 in the rat hippocampus were robustly regulated by GH-infusions for six days, whereas other transcripts were weakly affected. Here, weexplored the effects of prolonged GH administration on transcripts linked to neuroprotection and investigated whether serum IGF-I administration may exert similar effects. DESIGN: Hypophysectomised female rats were infused with GH or IGF-I for 19 days. Hbb, Alas2 and seven additional GH- and IGF-I-related transcripts were quantified by Q-RT-PCR in rat hippocampus. RESULTS: Three transcripts, Hbb, Alas2, and Aloxl5 were increased by both GH and IGF-I administration. The other transcripts were marginally affected. CONCLUSION: The 19-day GH-infusion induced similar effects as those reported after 6-day GH treatment, with the addition of the regulation of transcript Aloxl5. IGF-I induced altered gene expression in relation to its effect on weight gain. This study underlines that there is an entity of transcripts involved in neuroprotection and vascular tone that is regulated by both systemic GH and IGF-I. For other transcripts, the longer duration of this study did not significantly enhance the marginal effects of GH administration seen previously. © 2018 Neuroendocrinology Letters
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