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- Song, Fei, et al.
(författare)
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The prevalence and determinants of hypothyroidism in hospitalized patients with type 2 diabetes mellitus
- 2017
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Ingår i: Endocrine. - : Springer Science and Business Media LLC. - 1355-008X .- 1559-0100. ; 55:1, s. 188-194
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of this study was to investigate the prevalence of hypothyroidism among hospitalized patients with type 2 diabetes mellitus and its related factors, and to assess the prevalence of macrovascular and microvascular diseases among type 2 diabetes mellitus inpatients with hypothyroidism and euthyroidism. A total of 1662 type 2 diabetes mellitus inpatients hospitalized at the Metabolic Diseases Hospital, Tianjin Medical University from 1 January 2008 to 1 March 2013 were included in this study. Information on demographic and anthropometric factors and additional variables related to hypothyroidism were collected from medical records. Prevalence rates were calculated and standardized using direct method based on the age-specific and sex-specific structure of all participants. Data were analyzed using binary logistic regression with adjustment for potential confounders. The prevalence of hypothyroidism among type 2 diabetes mellitus inpatients was 6.8 %, and 77.0% of the patients with hypothyroidism had subclinical hypothyroidism. The prevalence of hypothyroidism increased with age, and was higher in women (10.8 %) than in men (3.4 %). Older age (odds ratio, 1.74; 95% confidence interval, 1. 05 to 2.89), female gender (odds ratio, 2.02; 95% confidence interval, 1.05 to 3.87), and positive thyroid peroxidase antibody (odds ratio, 4.99; 95% confidence interval, 2.83 to 8.79) were associated with higher odds of hypothyroidism among type 2 diabetes mellitus inpatients. The type 2 diabetes mellitus inpatients with hypothyroidism had higher prevalence of cerebrovascular diseases than those with euthyroidism after adjustment for age and gender. The prevalence of hypothyroidism among type 2 diabetes mellitus inpatients was 6.8 %, and most patients had subclinical hypothyroidism. Older age, female gender, and positive thyroid peroxidase antibody could be indicators for detecting hypothyroidism in type 2 diabetes mellitus inpatients.
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| 2. |
- Edfeldt, Katarina, et al.
(författare)
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TCEB3C a putative tumor suppressor gene of small intestine neuroendocrine tumors
- 2014
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Ingår i: Endocrine-Related Cancer. - 1351-0088 .- 1479-6821. ; 21:2, s. 275-284
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Tidskriftsartikel (refereegranskat)abstract
- Small intestinal neuroendocrine tumors (SI-NETs), formerly midgut carcinoids, are rare and slow-growing neoplasms. Frequent loss of one copy of chromosome 18 in primary tumors and metastases has been observed. The aim of the study was to investigate a possible role of TCEB3C (Elongin A3), currently the only imprinted gene on chromosome 18, as a tumor suppressor gene in SI-NETs, and whether its expression is epigenetically regulated. Primary tumors, metastases, the human SI-NET cell line CNDT2.5, and two other cell lines were included. Immunohistochemistry, gene copy number determination by PCR, colony formation assay, Western blotting, real-time quantitative RT-PCR, RNA interference, and quantitative CpG methylation analysis by pyrosequencing were performed. The large majority of tumors (33/43) showed very low to undetectable Elongin A3 expression and as expected 89% (40/45) displayed one TCEB3C gene copy. The DNA hypomethylating agent 5-aza-2'-deoxycytidine induced TCEB3C expression in CNDT2.5 cells, in primary SI-NET cells prepared directly after surgery, but not in two other cell lines. Also siRNA to DNMT1 and treatment with the general histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in a cell type-specific way. CpG methylation at the TCEB3C promoter was observed in all analyzed tissues and thus not related to expression. Overexpression of TCEB3C resulted in a 50% decrease of clonogenic survival of CNDT2.5 cells, but not of control cells. The results support a putative role of TCEB3C as a tumor suppressor gene in SI-NETs. Epigenetic repression of TCEB3C seems to be tumor cell type-specific and involves both DNA and histone methylation.
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| 3. |
- Edfeldt, Katarina, 1979-, et al.
(författare)
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A Plausible Role for Actin Gamma Smooth Muscle 2 (ACTG2) in Small Intestinal Neuroendocrine Tumorgenesis
- 2016
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Ingår i: BMC Endocrine Disorders. - : BioMed Central (BMC). - 1472-6823. ; 16
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Small intestinal neuroendocrine tumors (SI-NETs) originate from the enterochromaffin cells in the ileum and jejunum. The knowledge about genetic and epigenetic abnormalities is limited. Low mRNA expression levels of actin gamma smooth muscle 2 (ACTG2) have been demonstrated in metastases relative to primary SI-NETs. ACTG2 and microRNA-145 (miR-145) are aberrantly expressed in other cancers and ACTG2 can be induced by miR-145. The aim of this study was to investigate the role of ACTG2 in small intestinal neuroendocrine tumorigenesis.METHODS: Protein expression was analyzed in SI-NETs (n = 24) and in enterochromaffin cells by immunohistochemistry. The cell line CNDT2.5 was treated with the histone methyltransferase inhibitor 3-deazaneplanocin A (DZNep), the selective EZH2 inhibitor EPZ-6438, or 5-aza-2'-deoxycytidine, a DNA hypomethylating agent. Cells were transfected with ACTG2 expression plasmid or miR-145. Western blotting analysis, quantitative RT-PCR, colony formation- and viability assays were performed. miR-145 expression levels were measured in tumors.RESULTS: Eight primary tumors and two lymph node metastases displayed variable levels of positive staining. Fourteen SI-NETs and normal enterochromaffin cells stained negatively. Overexpression of ACTG2 significantly inhibited CNDT2.5 cell growth. Treatment with DZNep or transfection with miR-145 induced ACTG2 expression (>10-fold), but no effects were detected after treatment with EPZ-6438 or 5-aza-2'-deoxycytidine. DZNep also induced miR-145 expression. SI-NETs expressed relatively low levels of miR-145, with reduced expression in metastases compared to primary tumors.CONCLUSIONS: ACTG2 is expressed in a fraction of SI-NETs, can inhibit cell growth in vitro, and is positively regulated by miR-145. Theoretical therapeutic strategies based on these results are discussed.
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