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1.
J Clin Endocrinol Metab ; 107(9): 2411-2423, 2022 08 18.
Artículo en Inglés | MEDLINE | ID: mdl-35763540

RESUMEN

BACKGROUND: Gestational diabetes mellitus (GDM) complicates up to 10% of pregnancies and is a well-known risk factor for type 2 diabetes mellitus (T2DM) and cardiovascular disease. Little is known about possible long-term risks of other diseases. BACKGROUND: The aim was to review the literature for evidence of associations with morbidity other than T2DM and cardiovascular disease and with long-term mortality. METHODS: A systematic review based on searches in Medline, Embase, and Cochrane Library until March 31, 2021, using a broad range of keywords. We extracted study characteristics and results on associations between GDM and disease occurrence at least 10 years postpartum, excluding studies on women with diabetes prior to pregnancy or only diabetes prior to outcome. The results are reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Newcastle-Ottawa Scale was used to assess risk of bias. RESULTS: We screened 3084 titles, 81 articles were assessed full-text, and 15 included in the review. The strongest evidence for an association was for kidney diseases, particularly in Black women. We found indication of an association with liver disease, possibly restricted to women with T2DM postpartum. The association between GDM and breast cancer had been studied extensively, but in most cases based on self-reported diagnosis and with conflicting results. Only sparse and inconsistent results were found for other cancers. No study on thyroid diseases was found, and no study reported on short-term or long-term mortality in women with a history of GDM. CONCLUSION: Given the frequency of GDM, there is a need for better evidence on possible long-term health consequences, in particular, studies based on comprehensive records of diagnosis of GDM and long-term health outcomes.


Asunto(s)
Enfermedades Cardiovasculares , Diabetes Mellitus Tipo 2 , Diabetes Gestacional , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/etiología , Diabetes Mellitus Tipo 2/epidemiología , Diabetes Gestacional/diagnóstico , Diabetes Gestacional/epidemiología , Femenino , Estudios de Seguimiento , Humanos , Morbilidad , Embarazo
2.
BMJ Open ; 9(12): e034502, 2019 12 15.
Artículo en Inglés | MEDLINE | ID: mdl-31843856

RESUMEN

OBJECTIVES: Characterisation of worker injuries on board merchant ships is modest. Using telemedical service contacts in Denmark, we describe the worker injuries patterns and factors related to injury incidence. METHODS: The data for this study were based on contacts (n=1401) from ships to Telemedical Assistance Service (TMAS) in Denmark in 2004-2014, which were supplemented with data on the annual estimation of all seafarers from the Danish Maritime Authority (n=73 336). The final data included information on broad age groups, occupation and nationality. The outcomes were injuries from any cause and six broad categories of injuries characterised by anatomic location or type of injury. RESULTS: During the observation period of 11 years, there were 1401 contacts to TMAS due to injuries, of which 36% were in upper limb, 18% in lower limb and 13% in the head. Age-adjusted incidence rates for all injuries varied between 13.6 and 26.8 incidences per 1000 person-years in 2004-2014. In most types of injuries, younger and older seafarers had higher risk for injuries than seafarers aged 30-49 years. Depending on the type of injury, non-officers had threefold to fivefold increased odds of injuries compared with officers, the risk being highest for head injuries with an OR of 5.00 (95% CI 3.19 to 7.83). Non-officers from the European Union (EU) had higher risk in most types of injuries than non-officers from outside the EU, whereas the pattern of this risk was inverse among officers. CONCLUSIONS: These findings suggest that non-officers and European seafarers have an increased risk for several types of injuries on board Danish-flagged merchant ships. Additionally, age affected risk with the younger (<30 years) and older (>50 years) seafarers having increased risk.


Asunto(s)
Personal Militar , Traumatismos Ocupacionales/epidemiología , Telemedicina/estadística & datos numéricos , Adulto , Factores de Edad , Estudios de Cohortes , Dinamarca/epidemiología , Europa (Continente)/epidemiología , Femenino , Humanos , Incidencia , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Factores de Riesgo , Navíos
3.
J Cell Physiol ; 232(11): 3112-3127, 2017 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-28019653

RESUMEN

Receptor tyrosine kinase (RTK) signaling controls key aspects of cellular differentiation, proliferation, survival, metabolism, and migration. Deregulated RTK signaling also underlies many cancers. Glycosphingolipids (GSL) are essential elements of the plasma membrane. By affecting clustering and activity of membrane receptors, GSL modulate signal transduction, including that mediated by the RTK. GSL are abundant in the nervous system, and glial development in Drosophila is emerging as a useful model for studying how GSL modulate RTK signaling. Drosophila has a simple GSL biosynthetic pathway, in which the mannosyltransferase Egghead controls conversion of glucosylceramide (GlcCer) to mactosylceramide (MacCer). Lack of elongated GSL in egghead (egh) mutants causes overgrowth of subperineurial glia (SPG), largely due to aberrant activation of phosphatidylinositol 3-kinase (PI3K). However, to what extent this effect involves changes in upstream signaling events is unresolved. We show here that glial overgrowth in egh is strongly linked to increased activation of Insulin and fibroblast growth factor receptors (FGFR). Glial hypertrophy is phenocopied when overexpressing gain-of-function mutants of the Drosophila insulin receptor (InR) and the FGFR homolog Heartless (Htl) in wild type SPG, and is suppressed by inhibiting Htl and InR activity in egh. Knockdown of GlcCer synthase in the SPG fails to suppress glial overgrowth in egh nerves, and slightly promotes overgrowth in wild type, suggesting that RTK hyperactivation is caused by absence of MacCer and not by GlcCer accumulation. We conclude that an early product in GSL biosynthesis, MacCer, prevents inappropriate activation of insulin and fibroblast growth factor receptors in Drosophila glia.


Asunto(s)
Aumento de la Célula , Ceramidas/metabolismo , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/metabolismo , Neuroglía/metabolismo , Proteínas Tirosina Quinasas/metabolismo , Proteínas Tirosina Quinasas Receptoras/metabolismo , Receptores de Factores de Crecimiento de Fibroblastos/metabolismo , Transducción de Señal , Animales , Animales Modificados Genéticamente , Proteínas de Drosophila/genética , Drosophila melanogaster/genética , Drosophila melanogaster/inmunología , Galactosiltransferasas/genética , Galactosiltransferasas/metabolismo , Genotipo , Hipertrofia , Ligandos , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , Mutación , Neuroglía/inmunología , Neuroglía/patología , Fenotipo , Proteínas Tirosina Quinasas/genética , Proteínas Tirosina Quinasas Receptoras/genética , Receptores de Factores de Crecimiento de Fibroblastos/genética
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