产前38周检查与新生儿窒息的关系分析

目的探讨妊娠38周产前检查结果与新生儿窒息的关系。方法回顾性分析我院在妊娠38周进行产前检查的3 846例孕产妇中138例发生新生儿窒息的临床资料,统计其危险分数及发生窒息的几率。结果危险分数越高,发生窒息几率越高,组间比较有显著性差异（P〈0.05）;新生儿窒息与孕妇、胎盘、脐带等多种因素有关。结论 38周产前检查结果及危险分数对评价新生儿窒息发生几率有重要的价值。     

Mercury as a possible link between maternal obesity and autism spectrum disorder

The incidence of both obesity and autism spectrum disorders (ASD) has dramatically increased during the last decades. Moreover, the most recent studies have revealed increased risk of ASD in offspring of overweight and obese women. However, the mechanisms of association between ASD and maternal obesity are unknown. Taking into account the existing data indicating the association between mercury (Hg) exposure and development of obesity and ASD, we hypothesize that Hg may serve as an additional link between maternal obesity and ASD. In particular, it is supposed that obesity is associated with excessive accumulation of Hg in the maternal organism. After conception, the fetus is developing in the conditions of Hg overload within the body of obese women thus predisposing to the development of ASD. The proposed hypothesis may be confirmed by the existing data. In particular, previous studies demonstrated that overweight and obese persons are characterized by a significantly higher level of Hg in hair, blood and urine than the lean ones. Therefore, an obese organism is characterized by elevated Hg burden that may be transferred to the fetus during pregnancy. Moreover, multiple studies have demonstrated a tight association between maternal and children Hg status being indicative of placental transfer of metal from maternal organism to offspring. Finally, a growing body of data indicates the influence of Hg exposure and Hg status on the risk of ASD in children. However, additional experimental and clinical studies are required to prove the hypothesis and provide novel data on the role of Hg in maternal obesity-associated ASD development. In particular, the contribution of Hg to ASD development in children from obese mothers should be determined. If a significant role of Hg in maternal obesity ASD risk will be confirmed, this will open additional perspectives of risk modification. Taking into account the universal mechanisms of Hg toxicity, transport, and accumulation, further preventive actions may be undertaken to reduce the risk of Hg toxicity and Hg-associated ASD development. In particular, it is supposed that the use of Hg chelators (like N,N′bis-(2-mercaptoethyl)isophthalamide, NMBI), antioxidants, and anti-inflammatory compounds prior or during pregnancy may have a beneficial effect. However, the safety of such actions should repeatedly be tested to avoid adverse health effects in a developing fetus.     

Prenatal alcohol exposure and traumatic childhood experiences: A systematic review

Prenatal alcohol exposure (PAE) and traumatic childhood experiences (trauma) such as abuse or neglect can each cause central nervous system neurobiological changes or structural damage which can manifest as cognitive and behavioural dysfunction. In cases where both exposures have occurred, the risk of neurodevelopmental impairment may be greater, but this interaction has not been well studied. Here we present a systematic review that identified five primary research studies which investigated either the impact of trauma in children with PAE, or of PAE in children with trauma. Due to the heterogeneity of studies, narrative analysis was applied. Children in these cohorts with both exposures were more likely to show deficits in language, attention, memory and intelligence, and exhibit more severe behavioural problems than children with one exposure in absence of the other. However, the current literature is scarce and methodologically flawed. Further studies are required that: assess dual exposure in other neurodevelopmental domains; feature developmentally impaired yet non-exposed controls; and account for the wide spectrum of effects and different diagnostic criteria associated with PAE.     

Behavioral economic analysis of cue‐elicited craving for alcohol

Aims Craving as a motivational determinant of drug use remains controversial because of ambiguous empirical findings. A behavioral economic approach may clarify the nature of craving, theorizing that subjective craving functionally reflects an acute increase in a drug's value. The current study tested this hypothesis via a multidimensional assessment of alcohol demand over the course of an alcohol cue reactivity procedure. Design One‐way within‐subjects design. Setting Human laboratory environment. Participants Heavy drinkers (n = 92) underwent exposures to neutral (water) cues followed by personalized alcohol cues. Assessments Participants were assessed for craving, alcohol demand, affect, and salivation following each exposure. Findings Alcohol versus neutral cues significantly increased craving and multiple behavioral economic measures of the relative value of alcohol, including alcohol consumption under conditions of zero cost (intensity), maximum expenditure on alcohol (O_max), persistence in drinking to higher prices (breakpoint) and proportionate price insensitivity (normalized P_max). Craving was significantly correlated with demand measures at levels ranging from 0.21–0.43. Conclusions These findings support the potential utility of a behavioral economic approach to understanding the role of environmental stimuli in alcohol‐related decision making. Specifically, they suggest that the behavioral economic indices of demand may provide complementary motivational information that is related to though not entirely redundant with measures of subjective craving.     

Animal house: University risk environments and the regulation of students’ alcohol use

BackgroundThis article extends the risk environment framework to understand the factors that universities identify as influencing university students’ risky drinking behaviours and universities attempts at managing risky alcohol use on their campuses.MethodsThis article examines data collected as part of qualitative fieldwork on university corporate security services, and others involved in university alcohol policy implementation (e.g., residence services), conducted at five Canadian universities. Interviews (n = 56), fieldnotes from 246 h of observations of university corporate security personnel, and university policy documents (i.e., codes of student behaviour, residence policies) were analysed to understand the influence of risk environments on high-risk alcohol use.ResultsWe identify three risk environments on university campuses in relation to the use and regulation of alcohol: the physical, social, and policy environments. Residence buildings and abutting spaces (physical risk environment) and the university “party” culture (social risk environment) are principal contributors to risk within their risk environments. University policies and practices (policy risk environment) attempt to modify these environments in order to manage risky alcohol use.ConclusionWe suggest current approaches to regulating student alcohol use may not be the best approach to preventing harms (e.g., health problems, legal troubles) to students. Given university policies and practices have the potential to shape and influence risky alcohol use and associated harms we argue it is necessary for university administrators to adopt the best practices of “harm reduction” and seek new ways to address on-campus alcohol use.