RESUMEN
ObjectivesãAlthough more than half of women who smoke attempt to stop smoking after conception, many relapse after delivery. We conducted a population-based longitudinal study to identify the predictors of postpartum smoking relapse.MethodsãParticipants were expectant mothers living in Nagoya city, Japan, who notified Health Centers of their pregnancy from April 2014 to March 2015. A self-administered questionnaire was given to the expectant mothers that includes individual factors in the pregnancy: expectant mother's smoking status, age, marital status, experience of parturition, (mother's and father's) occupations, infertility treatment reception, feelings when pregnancy was confirmed, plans to return to parents' house for delivery, accessibility to help with childcare, household member(s) smoking in the same room, alcohol consumption, and depressive symptoms continuing more than 2 weeks.ãWe followed their smoking status at their children's "3-month-old health check-up" (3 months) and "1-year-and-6-months-old health check-up" (18 months) held in Health Centers until March 2017.ãThe data were analyzed using a combination of Chi-square or Fisher's exact test and logistic regression modeling. The analyses were conducted separately in primiparas and multiparas in addition to all expectant mothers.ResultsãParticipants were 24,413 mothers; 18,041 were followed up at 3 months and 14,163 at 18 months.ãOf the 18,041 mothers at 3 months, 1,031 primiparas and 695 multiparas stopped smoking when they confirmed pregnancy; 89 (8.6%) primiparas and 107 (15.4%) multiparas relapsed at 3 months. Of the 14,163 mothers at 18 months, 789 primiparas and 568 multiparas stopped smoking when they confirmed pregnancy; 155 (19.6%) primiparas and 174 (30.6%) multiparas relapsed smoking at 18 months.ãAs a result of logistic regression modeling, "multiparas," "younger (<25 years old)," "not married (only in multiparas)," "no plan to return to mother's parent's house for delivery," "household member(s) smoking in the same room (only in primiparas)," and "depressive symptoms (only in all mothers and primiparas)" were the predictors of postpartum smoking relapse at 3 months. "Multiparas," "not married (only in all mothers)," "no help with childcare (only in all mothers)," and "household member(s) smoking in the same room" were the predictors of postpartum smoking relapse at 18 months.ConclusionãMore mothers relapsed with smoking after 3 months than before 3 months. The predictors of postpartum smoking relapse differed between 3 and 18 months. Support to continue smoking cessation was needed for each mother at an appropriate time not only in pregnancy but also after delivery.
Asunto(s)
Periodo Posparto/psicología , Embarazo/psicología , Fumar/epidemiología , Adulto , Factores de Edad , Consumo de Bebidas Alcohólicas , Femenino , Humanos , Lactante , Modelos Logísticos , Estudios Longitudinales , Estado Civil , Ocupaciones , Parto , Recurrencia , Factores de Riesgo , Prevención Secundaria , Prevención del Hábito de Fumar , Apoyo Social , Encuestas y Cuestionarios , Factores de Tiempo , Adulto JovenRESUMEN
AIM: Apoptosis and necrosis occur in nonalcoholic steatohepatitis (NASH) and are thought to be related to fibrosis. A stroke-prone spontaneously hypertensive (SHRSP5/Dmcr) rat fed a high-fat-cholesterol (HFC) diet exhibited similar pathological features to human NASH with severe liver fibrosis. We aimed to reveal the molecular pathway and to confirm the relationship between cell death, fibrosis and K18Asp396 levels, a neoepitope generated during cleavage of keratin 18 by caspases, as a candidate for biomarker of hepatic damage in this animal model. MAIN METHODS: Male rats were fed with control and HFC diets for 2, 8 and 14 weeks. Liver apoptosis cells, necrosis score, and the molecular mechanism and K18Asp396 levels were investigated. KEY FINDINGS: HFC diet increased TUNEL-positive cells only at 2 weeks and necrosis scores strongly in the livers of rats during the entire period. This diet increased hepatic Bax/Bak but decreased Bcl-2/Bcl-xl expression during the entire period; however, it upregulated caspase 8, 9, and 3/7 activities only at 2 weeks, but downregulated them at 14 weeks. Additionally, this diet did not increase hepatic cytochrome c expression. Serum K18Asp396 levels have a positive correlation with necrosis score. SIGNIFICANCE: In SHRSP5/Dmcr rats, HFC diet caused hepatocyte necrosis rather than apoptosis by the downregulation of all caspase activity. Serum K18Asp396 levels may be a good biomarker of hepatocyte necrosis.