Memories of studying life in Emory University

<p>Gestational-age specific risks^{<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0155692#t004fn001" target="_blank">*</a>} of adverse perinatal outcomes comparing cesarean-section (130,808 infants) vs. vaginal (n = 232,812 infants) deliveries in twin pregnancies.</p

Maternal, pregnancy and newborn characteristics in gestational hypertensive versus non-hypertensive twin pregnancies in the study population, U.S. 1995–2000.

<p>Data presented are n (%). P values are from Chi-square tests for differences between diabetic and non-diabetic pregnancies. *SGA = Small-for-gestational-age <10^th percentile, LGA = large-for-gestational-age >90^th percentile, according to birth weight percentiles in non-malformation births to non-smoking mothers in the study cohort.</p>c<p> One or more of the following conditions: diabetes, heart disease, acute or chronic lung disease, renal disease, genital herpes and RH sensitization.</p>t<p> There were significant numbers of missing value (>10%) for smoking (n = 49494 mothers) (17.8%) and mode of delivery (101368 mothers) (36.4%). The numbers of missing for other variables were: race 0, marital status 705 (0.3%) mothers, age 0, education 3389 (1.2%) mothers, parity 12 (0.0%), other maternal illness 20721 (7.4%) mothers, preterm birth 0, low birth weight, SGA or LGA 8615 (1.5%) newborns. The rates for smoking and caesarean section, SGA, et al. are based on births with non-missing information.</p

Stillbirth in gestational hypertensive versus non-hypertensive twin pregnancies, U.S. matched multiple birth data 1995–2000.

<p>HR = Hazard ratio; CI =  confidence interval.</p><p>*Hazard ratios adjusted for maternal race, marital status, age, education, parity, smoking, other maternal major illnesses, fetal sex, mode of delivery and twin-cluster level dependence in Cox regression models.</p><p>**There were a significant number of stillbirths with missing birth weights.</p>t<p> Gestational age group-specific mortality rates and hazard ratios were calculated using the number of foetuses at risk and the number of stillbirths in the time interval specified.</p

Perinatal mortality in gestational hypertensive versus non-hypertensive twin pregnancies, U.S. matched multiple birth data 1995–2000.

<p>HR = Hazard ratio; CI =  confidence interval.</p><p>*Hazard ratios adjusted for maternal race, marital status, age, education, parity, smoking, other maternal major illnesses, fetal sex, mode of delivery and twin-cluster level dependence in Cox regression models.</p><p>**There were a significant number of perinatal deaths with missing birth weights.</p>t<p> Gestational age group-specific mortality rates and hazard ratios were calculated using the number of foetuses at risk and the number of perinatal deaths in the time interval specified.</p

Survival probabilities during the perinatal period (from 20 weeks gestation to 4 weeks postpartum) in gestational hypertensive vs. non-hypertensive twin pregnancies.

<p>Survival probabilities during the perinatal period (from 20 weeks gestation to 4 weeks postpartum) in gestational hypertensive vs. non-hypertensive twin pregnancies.</p

Maternal Smoking and Metabolic Health Biomarkers in Newborns

<div><p>Background</p><p>Maternal smoking has been associated with elevated risk of type 2 diabetes among the offspring in adulthood. The mechanisms underlying this fetal “programming” effect remain unclear. The present study sought to explore whether maternal smoking affects metabolic health biomarkers in fetuses/newborns.</p><p>Methods</p><p>In a prospective singleton pregnancy cohort (n = 248), we compared metabolic health biomarkers in the newborns of smoking and non-smoking mothers. Outcomes included cord plasma insulin, proinsulin, insulin-like growth factor I (IGF-I), IGF-II, leptin and adiponectin concentrations, glucose-to-insulin ratio (an indicator of insulin sensitivity) and proinsulin-to-insulin ratio (an indicator of β-cell function).</p><p>Results</p><p>Independent of maternal (glucose tolerance, age, ethnicity, parity, education, body mass index, alcohol use) and infant (sex, gestational age, birth weight z score, mode of delivery, cord blood glucose concentration) characteristics, the newborns of smoking mothers had lower IGF-I concentrations (mean: 6.7 vs. 8.4 nmol/L, adjusted p = 0.006), and marginally higher proinsulin-to-insulin ratios (0.94 vs. 0.72, adjusted p = 0.06) than the newborns of non-smoking mothers. Cord plasma insulin, proinsulin, IGF-II, leptin and adiponectin concentrations and glucose-to-insulin ratios were similar in the newborns of smoking and non-smoking mothers.</p><p>Conclusions</p><p>Maternal smoking was associated with decreased fetal IGF-I levels, and borderline lower fetal β-cell function. Larger cohort studies are required to confirm the latter finding. The preliminary findings prompt the hypothesis that these early life metabolic changes may be involved in the impact of maternal smoking on future risk of metabolic syndrome related disorders in the offspring.</p></div

Effects of exposure to the Chinese Great Famine <i>during fetal development only</i> by trimester of exposure on blood pressure, height and BMI.

<p>Data presented are adjusted least square mean±standard error, or adjusted mean difference (95% CI) for continuous outcomes (blood pressure, BMI, height), and n (%) or odds ratio (95% CI) for dichotomous outcomes (hypertension, obesity, short stature).</p>*<p>Adjusted for socio-demographic and lifestyle characteristics (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0049720#pone-0049720-t002" target="_blank">Table 2</a>); for blood pressure and hypertension, further adjusted for short stature and BMI; subjects with anti-hypertensive treatment were included in the models for hypertension, but excluded in the models for SBP and DBP.</p>†<p>p<0.05,</p>‡<p>p<0.01,</p>τ<p>p<0.001 for comparisons to the non-famine reference cohort.</p><p>SBP = systolic blood pressure; DBP = diastolic blood pressure; BMI = Body mass index; OR = odds ratio; CI = confidence interval.</p

Blood pressure, height and BMI by exposure to the 1959–1961 Chinese Great Famine during fetal development and infancy (<2 years postnatal).

<p>Data presented are adjusted least square mean±standard error, or adjusted mean difference (95% CI) for continuous outcomes (blood pressure, BMI, height), and n (%) or odds ratio (95% CI) for dichotomous outcomes (hypertension, obesity, short stature).</p>*<p>Adjusted for socio-demographic and lifestyle characteristics (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0049720#pone-0049720-t002" target="_blank">Table 2</a>); for blood pressure and hypertension, further adjusted for short stature and BMI; subjects with anti-hypertensive treatment were included in the models for hypertension, but excluded in the models for SBP and DBP.</p>†<p>p<0.05,</p>‡<p>p<0.01,</p>τ<p>p<0.001 for comparisons to the non-famine reference cohort. All p values were<0.05 in tests for the overall differences in mean blood pressure or the risk of hypertension across the four study groups.</p><p>SBP = systolic blood pressure; DBP = diastolic blood pressure; BMI = Body mass index; OR = odds ratio; CI = confidence interval.</p

Characteristics of study participants in the 1957–1964 birth cohort from Zhongshan and Nanhai municipalities, Guangdong province, China.

<p>Data presented are mean±SD for continuous variables, and n (%) for frequency variables.</p>*<p>P values in t tests for differences in means or Chi-square tests for differences in proportions between men and women.</p

Windows of exposure to the 1959–1961 Chinese Great Famine in the 1957–1964 birth cohort, Zhongshan and Nanhai municipalities, Guangdong province, China.

<p>Windows of exposure to the 1959–1961 Chinese Great Famine in the 1957–1964 birth cohort, Zhongshan and Nanhai municipalities, Guangdong province, China.</p