Development and validation of a nomogram for predicting late-onset sepsis in preterm infants on the basis of thyroid function and other risk factors: Mixed retrospective and prospective cohort study.

Preterm birth and infection are common causes of neonatal death. In this study, we aimed to develop a nomogram for assessing the individual prior probability of late-onset sepsis on the basis of risk factors in preterm infants. This study is a mixed retrospective and prospective cohort study conducted in three centers. Data from January 2014 to December 2017 was used for the development cohort, and data from January 2018 to December 2018 was used for the validation cohort. In the development cohort, we identified the predicting variables of late-onset sepsis in preterm infants, from which a nomogram was obtained. Then we built nomograms, for with and without thyroid function, to predict late-onset sepsis. The nomogram was validated in the validation cohort concerning discrimination and calibration. A total of 1256 and 452 preterm infants were included in the development and validation cohort, respectively. We found thyroid hypofunction in preterm infants could increase the incidence of late-onset infection. The prediction model incorporated thyroid function, birth weight, use of endotracheal intubation, and duration of umbilical venous catheters was validated and developed as a nomogram for predicting late-onset sepsis in preterm infants. Nomogram in this study may contribute to clinical assessment and treatment decisions.

PKA-mediated phosphorylation of CREB and NMDA receptor 2B in the hippocampus of offspring rats is involved in transmission of mental disorders across a generation.

This study is aimed at the mechanism of transmission of mental disorders across a generation. We used 10 different stressors to establish an animal model of chronic unpredictable stress (CUS) before pregnancy. Forced swimming test (FST) and open field test (OFT) were used to analyze the behavior of 30-day-old adolescent offspring rats born to stress mothers. Magnetic resonance spectroscopy was used to measure glutamate, gamma-aminobutyric acid (GABA), and glutamine. Phosphate-activated glutaminase (PAG), glutamate decarboxylase (GAD), GABA-transaminase (GABA-T), protein kinase A (PKA), cAMP response element-binding protein (CREB), and N-methyl-D-aspartate (NMDA) receptor 2B (NR2B) were detected by western blot. Adolescent offspring rats in the CUS group exhibited depressive-like behavior in the FST and anxious behavior in the OFT. GAD was increased and GABA-T was decreased, which resulted in an increase in GABA levels and decrease of the glutamate/GABA ratio in the hippocampus of CUS offspring rats. Disruption of the glutamate/GABA-glutamine cycle was related to decrease PKA-mediated phosphorylation of CREB and NR2B in the hippocampus. These findings highlight the importance of mental health of females before pregnancy and suggest that CUS before pregnancy reduces p-CREB and p-NR2B in the offspring hippocampus, which could be responsible for behavioral disorders in the adolescent offspring.

Exposure of mother rats to chronic unpredictable stress before pregnancy alters the metabolism of gamma-aminobutyric acid and glutamate in the right hippocampus of offspring in early adolescence in a sexually dimorphic manner.

There is increasing evidence that mothers' exposure to stress before or during pregnancy is linked to an incidence of psychiatric disorders in offspring. However, a few studies have estimated the role of sex in the detrimental effects of pre-gestational stress on the offspring rats at early adolescence. Sex differences regarding the metabolism of gamma-aminobutyric acid and glutamate in the right hippocampus were investigated by MRS when the offspring rats reached 30 days. Additionally, the impact of pre-gestational stress exposed on an additional short-term acute stressor, such as forced swim, was examined in the male and female offspring rats. Our findings showed female offspring rats were more vulnerable to stressful conditions for either pre-gestational stress or acute stress in early adolescence, and had decreased GABA/Cr+PCr and Glu/Cr+PCr in the right hippocampus. Interestingly, in response to forced swim, male offspring rats whose mothers were exposed to pre-gestational stress were more affected by the short-term acute stressor and this was manifested by change of Glu/GABA and Glu/Gln in the right hippocampus. These data indicated that although female offspring rats were more vulnerable to pre-gestational stress from their mothers than males, in response to an additional acute stressor they showed better response. Therefore, both sexually dimorphic manner and combination of stressful procedures should be carefully considered in the study of stress-related psychiatric disorders in early adolescence.