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- Olsen, O E, et al.
(författare)
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Bone morphogenetic protein-9 suppresses growth of myeloma cells by signaling through ALK2 but is inhibited by endoglin.
- 2014
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Ingår i: Blood Cancer Journal. - : Springer Science and Business Media LLC. - 2044-5385. ; 4:Mar 21, s. 196-196
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Tidskriftsartikel (refereegranskat)abstract
- Multiple myeloma is a malignancy of plasma cells predominantly located in the bone marrow. A number of bone morphogenetic proteins (BMPs) induce apoptosis in myeloma cells in vitro, and with this study we add BMP-9 to the list. BMP-9 has been found in human serum at concentrations that inhibit cancer cell growth in vitro. We here show that the level of BMP-9 in serum was elevated in myeloma patients (median 176 pg/ml, range 8-809) compared with healthy controls (median 110 pg/ml, range 8-359). BMP-9 was also present in the bone marrow and was able to induce apoptosis in 4 out of 11 primary myeloma cell samples by signaling through ALK2. BMP-9-induced apoptosis in myeloma cells was associated with c-MYC downregulation. The effects of BMP-9 were counteracted by membrane-bound (CD105) or soluble endoglin present in the bone marrow microenvironment, suggesting a mechanism for how myeloma cells can evade the tumor suppressing activity of BMP-9 in multiple myeloma.
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| 2. |
- Stahl, M. G., et al.
(författare)
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Childhood growth prior to screen-detected celiac disease: prospective follow-up of an at-risk birth cohort
- 2020
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 55:11, s. 1284-1290
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: To determine the association between childhood growth prior to the development of celiac disease (CD) and CD autoimmunity (CDA) identified by periodic serological screening. Study design: The Diabetes Autoimmunity Study in the Young cohort includes 1979 genetically at-risk children from Denver, Colorado, with annual growth measurements from age nine months until ten years. Between 1993 and February 2019, 120 children developed CDA defined by persistent positive tissue transglutaminase autoantibodies (TGA); among these, 71 met our criteria for CD based on histopathological findings or high TGA levels. Age- and sex-specific z-scores of weight, body mass index (BMI), and height prior to seroconversion were derived using US reference charts as standards. Joint modeling of serial growth measurements was used to estimate adjusted hazard ratios (aHRs) accounting for celiac-associated human leukocyte antigens, early-life feeding practices, and socio-demographics. Results: In the first 10 years of life, there were no significant associations between the child’s current weight, BMI and height and the risk of screening-detected CDA or CD, neither was the weight nor BMI velocity associated with CDA or CD as identified by screening (all aHRs approximated 1). Increased height velocity was associated with later CD, but not CDA, development (aHR per 0.01-z score/year, 1.28; 95% confidence interval [CI] 1.18–1.38 and 1.03; 0.97–1.09, respectively). Conclusions: In the first 10 years of life, from prospectively collected serial growth measurements, we found no evidence of impaired childhood growth before CD and CDA development as identified through early and periodic screening. © 2020 Informa UK Limited, trading as Taylor & Francis Group.
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| 4. |
- Lund-Blix, N. A., et al.
(författare)
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Maternal and child gluten intake and association with type 1 diabetes: The Norwegian Mother and Child Cohort Study
- 2020
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Ingår i: PLoS medicine. - : Public Library of Science (PLoS). - 1549-1676. ; 17:3
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The relationship between maternal gluten intake in pregnancy, offspring intake in childhood, and offspring risk of type 1 diabetes has not been examined jointly in any studies. Our aim was to study the relationship between maternal and child intake of gluten and risk of type 1 diabetes in children. METHODS AND FINDINGS: We included 86,306 children in an observational nationwide cohort study, the Norwegian Mother and Child Cohort Study (MoBa), with recruitment from 1999 to 2008 and with follow-up time to April 15, 2018. We used registration of type 1 diabetes in the Norwegian childhood diabetes registry as the outcome. We used Cox proportional hazard regression to estimate hazard ratios (HRs) for the mother's intake of gluten up to week 22 of pregnancy and offspring gluten intake when the child was 18 months old. The average time followed was 12.3 years (0.70-16.0). A total of 346 children (0.4%) children were diagnosed with type 1 diabetes, resulting in an incidence rate of 32.6/100,000 person-years. Mean gluten intake per day was 13.6 g for mothers and 8.8 g for children. There was no association between the mother's intake of gluten in pregnancy and offspring type 1 diabetes, with an adjusted HR (aHR) of 1.02 (95% confidence interval [CI] 0.73-1.43, p = 0.91) for each 10-g-per-day increment. There was an association between offspring intake of gluten and a higher risk of type 1 diabetes, with an aHR of 1.46 (95% CI 1.06-2.01, p = 0.02) for each 10-g-per-day increment. Among the limitations are the likely imprecision in estimation of gluten intake and that we only had information regarding gluten intake at 2 time points in early life. CONCLUSIONS: Our results show that, while the mother's intake of gluten in pregnancy was not associated with type 1 diabetes, a higher intake of gluten by the child at an early age may give a higher risk of type 1 diabetes.
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| 5. |
- Mårild, Karl, 1982, et al.
(författare)
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Growth and Pubertal Timing in Boys With Adult-diagnosed Celiac Disease: A Population-based Longitudinal Cohort Study
- 2020
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Ingår i: Journal of pediatric gastroenterology and nutrition. - 1536-4801. ; 70:6, s. 853-857
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Tidskriftsartikel (refereegranskat)abstract
- There are few longitudinal data on whether childhood growth and pubertal timing may be impaired by adult-diagnosed celiac disease (CD). Through school health care records and national registers, we retrieved serial growth measurements on 37,672 Swedish boys born in 1945 to 1961, out of whom 72 (0.2%) were clinically diagnosed with CD as adults. Boys with, versus without, adult-diagnosed CD exhibited no appreciable mean differences in body mass index (BMI, kg/m) and height (cm) at ages 8 or 20 to 21 years (childhood BMI, 15.9 [CD] vs 15.7 [comparators]; childhood height, 129.1 [CD] vs 128.6 [comparators]; adult BMI, 21.3 [CD] vs 21.4 [comparators]; adult height, 180.7 [CD] vs 180.4 [comparators]). Neither did we observe any between-group differences in growth development during puberty nor in the timing of pubertal growth spurt (all P values ≥0.30). Conclusively, in this population-based longitudinal study, boys with adult-diagnosed CD had similar growth and pubertal timing as their peers.
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