Our findings provide further understanding of the association between maternal hepatitis B or C carrier status and perinatal outcomes. Infants born to women with hepatitis C infection appear to be at risk for poor birth outcomes, including preterm birth, LBW and congenital anomaly.
Research investigating the role of paternal age in adverse birth outcomes is limited. This population-based retrospective cohort study used the Missouri maternally linked data set from 1989 to 2005 to assess whether paternal age affects fetal birth outcomes: low birth weight (LBW), preterm birth (PTB), stillbirth, and small size for gestational age (SGA). We examined these outcomes among infants across seven paternal age-groups (<20, 20-24, 25-29, 30-34, 35-39, 40-45, and >45 years) using the generalized estimating equation framework. Compared with infants born to younger fathers (25-29 years), infants born to fathers aged 40 to 45 years had a 24% increased risk of stillbirth but a reduced risk of SGA. A 48% increased risk of late stillbirth was observed in infants born to advanced paternal age (>45 years). Moreover, advanced paternal age (>45 years) was observed to result in a 19%, 13%, and 29% greater risk for LBW, PTB, and VPTB (very preterm birth) infants, respectively. Infants born to fathers aged 30 to 39 years had a lower risk of LBW, PTB, and SGA, whereas those born to fathers aged 24 years or younger had an elevated likelihood of experiencing these same adverse outcomes. These findings demonstrate that paternal age influences birth outcomes and warrants further investigation.
Among women that experience hypertension in pregnancy, the recurrence rate in a next pregnancy is relatively low, and the course of disease is milder for most women with recurrent disease. These reassuring data should be used for shared decision-making in women who consider a new pregnancy after a pregnancy that was complicated by hypertension.
Few studies have examined paternal involvement in relation to feto-infant health; therefore we aim to assess the impact of absence of the father on birth outcomes among racial-ethnic subgroups. Florida vital statistics records for singleton births occurring between 1998 and 2005 were used for this study. Births to women less than 20 years of age and births outside the gestational age range of 20-44 weeks were excluded. Adjusted and unadjusted odds ratios and 95% confidence intervals were generated to examine the impact of paternal involvement, as defined by presence of paternal information on the birth certificate, on feto-infant morbidity across racial-ethnic sub-populations. There were higher rates of low birth weight, very low birth weight, preterm birth, very preterm birth, and small for gestational age (SGA) among father-absent births. Within each racial-ethnic subgroup, women with absent fathers had higher risks of poor birth outcomes than their counterparts with involved fathers. Black women with absent fathers had the highest risk of low birth weight, very low birth weight, preterm birth, very preterm birth, and SGA. Promoting paternal involvement during the perinatal period may provide a means to decrease the proportion of infants born of very low birth weight or very preterm, thus potentially reducing the black-white disparity in infant mortality.
We sought to assess the contribution of paternal involvement to racial disparities in infant mortality. Using vital records data from singleton births in Florida between 1998 and 2005, we generated odds ratios (OR), 95% confidence intervals (CI), and preventative fractions to assess the association between paternal involvement and infant mortality. Paternal involvement status was based on presence/absence of paternal first and/or last name on the birth certificate. Disparities in infant mortality were observed between and within racial/ethnic subpopulations. When compared to Hispanic (NH)-white women with involved fathers, NH-black women with involved fathers had a two-fold increased risk of infant mortality whereas infants born to black women with absent fathers had a seven-fold increased risk of infant mortality. Elevated risks of infant mortality were also observed for Hispanic infants with absent fathers (OR = 3.33. 95%CI = 2.66-4.17). About 65-75% of excess mortality could be prevented with increased paternal involvement. Paternal absence widens the black-white gap in infant mortality almost four-fold. Intervention programs to improve perinatal paternal involvement may decrease the burden of absent father-associated infant mortality.
Study Objectives To determine the effect of self-reported clinical diagnosis of obstructive sleep apnea (OSA) on longitudinal changes in brain amyloid PET and CSF biomarkers (Aβ42, T-tau, and P-tau) in cognitively normal (NL), mild cognitive impairment (MCI), and Alzheimer’s disease (AD) elderly. Methods Longitudinal study with mean follow-up time of 2.52 ± 0.51 years. Data were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. Participants included 516 NL, 798 MCI, and 325 AD elderly. Main outcomes were annual rate of change in brain amyloid burden (i.e. longitudinal increases in florbetapir PET uptake or decreases in CSF Aβ42 levels); and tau protein aggregation (i.e. longitudinal increases in CSF total tau [T-tau] and phosphorylated tau [P-tau]). Adjusted multilevel mixed effects linear regression models with randomly varying intercepts and slopes was used to test whether the rate of biomarker change differed between participants with and without OSA. Results In NL and MCI groups, OSA+ subjects experienced faster annual increase in florbetapir uptake (B = .06, 95% CI = .02, .11 and B = .08, 95% CI = .05, .12, respectively) and decrease in CSF Aβ42 levels (B = −2.71, 95% CI = −3.11, −2.35 and B = −2.62, 95% CI = −3.23, −2.03, respectively); as well as increases in CSF T-tau (B = 3.68, 95% CI = 3.31, 4.07 and B = 2.21, 95% CI = 1.58, 2.86, respectively) and P-tau (B = 1.221, 95% CI = 1.02, 1.42 and B = 1.74, 95% CI = 1.22, 2.27, respectively); compared with OSA− participants. No significant variations in the biomarker changes over time were seen in the AD group. Conclusions In both NL and MCI, elderly, clinical interventions aimed to treat OSA are needed to test if OSA treatment may affect the progression of cognitive impairment due to AD.
African couples with high rates of ATV concor- dance experience higher risks for IPV, with some variation in magnitude of risk across countries. In African settings, ATV positive concordance could serve as a supplemental screening tool to detect spousal violence. Understanding ATV could potentially enhance our ability to formulate public health intervention to detect and prevent spousal abuse.
Study Objectives: To determine the effect of self-reported clinical diagnosis of Obstructive Sleep Apnea (OSA) on longitudinal changes in brain amyloid-PET and CSF-biomarkers (Aβ42, T-tau and P-tau) in cognitively normal (NL), mild cognitive impairment (MCI) and Alzheimer's Disease (AD) elderly. Methods: Longitudinal study with mean follow-up time of 2.52±0.51 years. Data was obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Participants included 516 NL, 798 MCI and 325 AD elderly. Main Outcomes were annual rate-of-change in brain amyloid-burden (i.e. longitudinal increases in florbetapir-PET uptake or decreases in CSF-Aβ42 levels); and tau-protein aggregation (i.e. longitudinal increases in CSF total-tau (T-tau) and phosphorylated-tau (P-tau)). Adjusted multi-level mixed effects linear regression models with randomly varying intercepts and slopes was used to test whether the rate-of-biomarker-change differed between participants with and without OSA. Results: In NL and MCI groups, OSA+ subjects experienced faster annual increase in
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.