Association of clinical signs of chorioamnionitis with histological chorioamnionitis and neonatal outcomes.

BACKGROUND: Chorioamnionitis is a risk factor for fetal and neonatal outcomes. Therefore, predicting histological chorioamnionitis (HCA) and neonatal outcomes using clinical parameters could be helpful in management and preventing morbidities. OBJECTIVE: To determine if parameters of clinical chorioamnionitis (CCA) would be associated with HCA and neonatal outcomes. STUDY DESIGN: In this cohort study using a retrospective design, we analyzed the performance of signs of CCA in predicting HCA, and neonatal outcomes. Data were extracted from the electronic health record for all neonates with documented CCA delivered at our institution from 2011 to 2016. We compared our findings based on the old ACOG definition of CCA and the new definition released in 2017 - maternal fever plus any of fetal tachycardia, maternal leukocytosis, and purulent vaginal discharge. Maternal tachycardia and uterine tenderness were removed from the new criteria. Neonatal laboratory samples on admission, 12 h and 24 h were used to define the three time points of neonatal suspected sepsis. RESULTS: There were 530 mothers-infant dyads with chorioamnionitis. Seventy-three were preterm, and 457 were term. Eighty-eight percent of the preterm mothers had CCA, and HCA was present in 62.5% of 72 preterm placentas. Preterm infants with placental HCA significantly had lower birth weight, gestational age, placental weight, and more infants with lower 5-minute Apgar scores, compared to those with no HCA. In preterm infants, maternal urinary tract infection was significantly associated with decreased odds for HCA (OR 0.22, CI 0.10 - 0.71). More preterm babies with suspected sepsis criteria at the 3 time points had HCA (all p ≤ .01). In the term cohort, 95.4% and 65.6% had CCA and HCA, respectively. In term infants (n = 457), maternal leukocytosis (p = .002) and prolonged rupture of membranes (PROM; p = 002) were associated with HCA. Suspected sepsis was associated with PROM (p = .04), HCA (p = .0001), and maternal leukocytosis (p ≤ .05) in at least 1 of the 3 time points. CONCLUSION: Though maternal leukocytosis was significantly associated with the presence of HCA in the term cohort, there were no CCA criteria that accurately predicted presence of HCA in either the preterm or the term infants.

Eliminating Contamination in Umbilical Cord Blood Culture Sampling for Early-Onset Neonatal Sepsis.

Introduction: Despite the advantages of umbilical cord blood culture (UCBC) use for diagnosis of early onset sepsis (EOS), contamination rates have deterred neonatologists from its widespread use. We aimed to implement UCBC collection in a level III neonatal intensive care unit (NICU) and apply quality improvement (QI) methods to reduce contamination in the diagnosis of early onset sepsis. Methods: Single-center implementation study utilizing quality improvement methodology to achieve 0% contamination rate in UCBC samples using the Plan-Do-Study-Act (PDSA) model for improvement. UCBC was obtained in conjunction with peripheral blood cultures (PBC) in neonates admitted to the NICU due to maternal chorioamnionitis. Maternal and neonatal characteristics between clinical sepsis and asymptomatic groups were compared. Process, outcome, and balancing measures were monitored. Results: Eighty-two UCBC samples were collected in addition to peripheral blood culture from neonates admitted due to maternal chorioamnionitis. Ten (12%) neonates had a diagnosis of clinical sepsis. All PBCs were negative and 5 UCBCs were positive in the study period. After 2 PDSA cycles, there was special cause variation with improvement in the percent of contaminated samples from 7.3 to 0%. There was no change in antibiotic duration among asymptomatic neonates. Conclusions: Implementation of UCBC for the diagnosis of EOS in term infants is feasible and contamination can be minimized with the implementation of a core team of trained providers and a proper sterile technique without increasing antibiotic duration.

Dietary Exposure to Excess Saturated Fat During Early Life Alters Hippocampal Gene Expression and Increases Risk for Behavioral Disorders in Adulthood.

PURPOSE: Maternal and postnatal diets result in long-term changes in offspring brain and behavior; however, the key mediators of these developmental changes are not well-defined. In this study, we investigated the impact of maternal and post-weaning high-fat diets on gene expression of key components mediating hippocampal synaptic efficacy. In addition, we evaluated the risk for impaired stress-coping and anxiety-like behaviors in adult offspring exposed to obesogenic diets during early life. METHODS: Dams were fed a control (C) or high-fat (HF) diet prior to mating, pregnancy, and lactation. Male offspring from control chow and high-fat fed dams were weaned to control chow or HF diets. The forced swim test (FST) and the elevated-plus maze (EPM) were used to detect stress-coping and anxiety-like behavior, respectively. Real-time RT-PCR and ELISA were used to analyze hippocampal expression of genes mediating synaptic function. RESULTS: Animals fed a HF diet post-weaning spent more time immobile in the FST. Swimming time was reduced in response to both maternal and post-weaning HF diets. Both maternal and post-weaning HF diets contributed to anxiety-like behavior in animals exposed to the EPM. Maternal and post-weaning HF diets were associated with a significant decrease in mRNA and protein expression for hippocampal GDNF, MAP2, SNAP25, and synaptophysin. Hippocampal mRNA expression of key serotonergic and glutamatergic receptors also exhibited differential responses to maternal and post-weaning HF diets. Hippocampal serotonergic receptor 5HT1A mRNA was reduced in response to both the maternal and post-weaning diet, whereas, 5HT2A receptor mRNA expression was increased in response to the maternal HF diet. The glutamate AMPA receptor subunit, GluA1, mRNA expression was significantly reduced in response to both diets, whereas no change was detected in GluA2 subunit mRNA expression. CONCLUSION: These data demonstrate that the expression of genes mediating synaptic function are differentially affected by maternal and post-weaning high-fat diets. The post-weaning high-fat diet clearly disturbs both behavior and gene expression. In addition, although the transition to control diet at weaning partially compensates for the adverse effects of the maternal HF diet, the negative consequence of the maternal HF diet is exacerbated by continuing the high-fat diet post-weaning. We present evidence to support the claim that these dietary influences increase the risk for anxiety and impaired stress-coping abilities in adulthood.

On the Use of Knitted Antennas and Inductively Coupled RFID Tags for Wearable Applications.

Recent advancements in conductive yarns and fabrication technologies offer exciting opportunities to design and knit seamless garments equipped with sensors for biomedical applications. In this paper, we discuss the design and application of a wearable strain sensor, which can be used for biomedical monitoring such as contraction, respiration, or limb movements. The system takes advantage of the intensity variations of the backscattered power (RSSI) from an inductively-coupled RFID tag under physical stretching. First, we describe the antenna design along with the modeling of the sheet impedance, which characterizes the conductive textile. Experimental results with custom fabricated prototypes showed good agreement with the numerical simulation of input impedance and radiation pattern. Finally, the wearable sensor has been applied for infant breathing monitoring using a medical programmable mannequin. A machine learning technique has been developed and applied to post-process the RSSI data, and the results show that breathing and non-breathing patterns can be successfully classified.

Maternal and postweaning high-fat diets disturb hippocampal gene expression, learning, and memory function.

We tested the hypothesis that excess saturated fat consumption during pregnancy, lactation, and/or postweaning alters the expression of genes mediating hippocampal synaptic efficacy and impairs spatial learning and memory in adulthood. Dams were fed control chow or a diet high in saturated fat before mating, during pregnancy, and into lactation. Offspring were weaned to either standard chow or a diet high in saturated fat. The Morris Water Maze was used to evaluate spatial learning and memory. Open field testing was used to evaluate motor activity. Hippocampal gene expression in adult males was measured using RT-PCR and ELISA. Offspring from high fat-fed dams took longer, swam farther, and faster to try and find the hidden platform during the 5-day learning period. Control offspring consuming standard chow spent the most time in memory quadrant during the probe test. Offspring from high fat-fed dams consuming excess saturated fat spent the least. The levels of mRNA and protein for brain-derived neurotrophic factor and activity-regulated cytoskeletal-associated protein were significantly decreased by maternal diet effects. Nerve growth factor mRNA and protein levels were significantly reduced in response to both maternal and postweaning high-fat diets. Expression levels for the N-methyl-d-aspartate receptor (NMDA) receptor subunit NR2B as well as synaptophysin were significantly decreased in response to both maternal and postweaning diets. Synaptotagmin was significantly increased in offspring from high fat-fed dams. These data support the hypothesis that exposure to excess saturated fat during hippocampal development is associated with complex patterns of gene expression and deficits in learning and memory.

Maternal and postweaning diet interaction alters hypothalamic gene expression and modulates response to a high-fat diet in male offspring.

Epidemiological data and results from animal studies indicate that imbalances in maternal nutrition impact the expression of metabolic disorders in the offspring. We tested the hypothesis that consumption of excess saturated fats during pregnancy and lactation contributes to adult metabolic dysfunction and that these disturbances can be further influenced by the postweaning diet. Adult male offspring from chow-fed dams were compared with males from dams fed a diet high in saturated fat (45 kcal/100 kcal) before mating, pregnancy, and lactation. Offspring were weaned to a standard chow diet or high fat diet. Animals were killed at 120 days after a 24-h fast. Body weight, energy intake, fat deposition, serum leptin, and insulin were significantly higher in offspring from control or high-fat dams if fed a high-fat diet from weaning to adulthood. Only fat-fed offspring from fat-fed dams were hyperglycemic. Leptin receptor, proopiomelanocortin, and neuropeptide Y (NPY) were also significantly increased in offspring exposed to excess saturated fat during gestation and into adulthood, whereas NPY(1) receptor was downregulated. Signal transducer and activator of transcription 3 mRNA level was significantly higher in offspring from high-fat-fed dams compared with controls; however, no change was detected in cocaine and amphetamine-regulated transcript or suppressor of cytokine signaling 3. An increase in agouti-related protein expression did not reach significance. A significant reduction in phosphatidylinositol 3-kinase regulatory subunit (p85alpha) coupled to an upregulation of protein kinase B was observed in offspring from high-fat-fed dams transitioned to chow food, whereas p85alpha expression was significantly increased in high-fat offspring weaned to the high-fat diet. These data support the hypothesis that early life exposure to excess fat is associated with changes in hypothalamic regulation of body weight and energy homeostasis and that postweaning diet influences development of metabolic dysfunction and obesity.

Urinary tract infection with Trichomonas vaginalis in a premature newborn infant and the development of chronic lung disease.

We report a case of a low-birth-weight infant with an infection of the urinary tract with Trichomonas vaginalis, who later developed cystic chronic lung disease suggestive of Wilson-Mikity syndrome. Although she had mild respiratory distress syndrome at birth, the extent of the chronic lung disease was out of proportion to the initial illness. We speculate that maternal infection with this organism may have resulted in an inflammatory response that led to its development.