Risk Factors For Sudden Infant Death Syndrome Research Articles

The α7 and β2 nicotinic acetylcholine receptor subunits regulate apoptosis in the infant hippocampus, and in sudden infant death syndrome (SIDS).

Apoptosis is increased in the hippocampus of infants who died of sudden infant death syndrome (SIDS), yet it is not known via which mechanism this has occurred. Following existing support for a role of the α7 and β2 nicotinic acetylcholine receptor (nAChR) subunits in apoptotic regulation, we aimed to determine whether these subunits are altered in the SIDS hippocampus and if they are correlated with cell death markers of active caspase-3 (Casp-3)and TUNEL. Further analyses were run according to the presence of major SIDS risk factors related to hypoxia (bed-sharing and prone sleeping), infection (presence of an upper respiratory tract infection (URTI)), cigarette smoke exposure and gender. Immunohistochemical expression of the markers was studied in 4 regions of the hippocampus (Cornu Ammonis (CA)1, CA2, CA3, CA4) and subiculum amongst 52 infants (aged 1-7months) who died suddenly and unexpectedly (SUDI) and for whom the cause of death was explained (eSUDI; n = 9), or not and characterised as SIDS I (n = 8) and SIDS II (n = 35) according to the San Diego diagnostic criteria. Results showed that SIDS II infants had widespread increases in TUNEL compared with eSUDI and SIDS I infants, as well as increased α7 and Casp-3 in CA2 compared to eSUDI infants, although these changes were predominant amongst infants who did not bed-share. Cigarette smoke exposure had minimal effects on the markers, while an URTI was associated with changes in all markers (after accounting for bed-sharing). Our findings support the role of nAChRs in regulating apoptosis in the SIDS hippocampus, and highlight the need for separate analysis according to risk factors.

Cotinine enhances the nicotine‐mediated decrease in respiratory burst amplitude recorded from the hypoglossal nerve in the brainstem spinal cord preparation from nicotine‐exposed neonatal rats

Cotinine, the primary metabolite of nicotine, can be detected in the blood of infants born to mothers who used nicotine products during pregnancy and breast feeding, and is used as a marker of nicotine exposure. Previous research shows that prenatal nicotine exposure alters the regions of the brain that control breathing and results in impaired protective breathing reflexes in exposed human and animal neonates. These abnormalities are proposed as a mechanism to explain Sudden Infant Death Syndrome (SIDS), and maternal smoking is the number one risk factor for SIDS. While it has long been known that nicotine has direct effects on brain function and development, it has only recently been established that cotinine may act on the brain as well. Both nicotine and cotinine bind to nicotinic acetylcholine receptors (nAChRs) which are expressed on neurons throughout the nervous system. Preliminary data using the in vitro brainstem spinal‐cord preparation from nicotine‐exposed neonatal rats shows that activation of nAChRs produces a decrease in the amplitude of respiratory bursts recorded from hypoglossal nerve roots (−30.74±18.2 % baseline, n=4), and that this effect is enhanced by cotinine (−60.34±16.1 % baseline, n=4). This supports the hypothesis that cotinine modulates the function of nAChRs in regions of the brain that control breathing (P<0.0001).Support or Funding Information5R01HD071302‐07

Sudden infant death syndrome: Do the parents follow the recommendations?

IntroductionProne sleeping position is the main known modifiable risk factor for sudden infant death syndrome (SIDS). At the end of the twentieth century, preventive campaigns were initiated, which recommended parents to have their children sleep in the supine position, with a significant reduction of SIDS rates worldwide being observing after this. There are other SIDS recommendations apart from the sleeping position, although with less impact. The objective of this study is to describe the prevalence of prone position during sleep in a sample of Spanish babies and infants, as well as other risk factors associated with SIDS. MethodsCross-sectional study carried out on 640 families with children from 0 months to 11 months. In addition to the sleep position, the adherence to four other recommendations regarding SIDS was analysed: place where infant sleeps, breastfeeding, use of non-nutritive suction, and maternal smoking. ResultsA total of 41.3% of infants under 6 months and 59.7% of infants aged 6–11 months slept in a non-recommended position. Only 6.4% of families analysed followed all five recommendations. DiscussionThere is a high, and therefore concerning, prevalence of modifiable risk factors for SIDS among the population studied. Personalised education should be promoted, along with other campaigns to raise awareness and prevent SIDS.

Determinants of infant mortality in Pakistan: evidence from Pakistan Demographic and Health Survey 2017–18

The infant mortality rate was very high in Pakistan until the early 1990s, at 86 deaths/1000 live births. It has decreased 24 points and declined to 62 deaths/1000 in the last 3 decades, but Pakistan is still in the group of countries with highest infant mortality rate. The present study aimed to assess the magnitude of infant mortality in Pakistan and its causes and associated risk factors. For this study, data from the 2018 Pakistan Demographic and Health Survey were used. Risk factors for infant mortality were first examined in bivariate analyses. Chi-square test was employed to understand the significance level of the categorical difference of independent variables. The Cox proportional hazard model was used to account for potential confounders that function as risk factors for infant deaths. Large differentials in infant survival by socioeconomic and demographic factors indicate poor coverage of social and health schemes for the public. Mothers who did not use the ANC services experienced about 1.5 times higher infant mortality than those who did (52 vs. 36/1000 LB; p = 0.007). The hazard model shows that rich households experienced about 30% (HR = 0.735; 95% CI = 0.614–0.878) less infant mortality than poor ones. The rural-urban differential in public health services and gender inequities are the underlying causes of the stagnation of infant mortality in Pakistan. The low status of women’s education, poor economic conditions and low level of using public health care services are closely tied to higher infant death rates in Pakistan. Health interventions in Pakistan should be designed to reach the most under-served—women and children—especially in rural areas.

Knowledge assessment of sudden infant death syndrome risk factors in expectant mothers: A prospective monocentric descriptive study

In France, approximately 500 deaths per year are related to sudden infant death syndrome (SIDS). After a 75% reduction of SIDS-related deaths in the 1990s, thanks to large prevention campaigns directing parents to put their infants to sleep on their back, the number of SIDS-related deaths remains stable. However, we estimate that 100–200 infant deaths per year in France could be prevented with better education on the risk factors for SIDS. In this prospective, descriptive monocentric study, we aimed to evaluate the level of expectant women's knowledge about SIDS. Questionnaires were distributed during a midwife consultation. A score on sleeping conditions, environmental and protective factors was determined with coefficients attributed according to their relevance to SIDS. Of 296 questionnaires distributed, 202 were completed and included in the analysis from March 1 to September 21, 2018. Scores were distributed from 2 to 46/50. The average score was 28.6/50. Information was principally obtained from media and not health professionals. When the information was delivered by a caregiver, in particular by a paediatrician, we observed better knowledge among these women. This study shows that it is important for health professionals to take the time to inform future mothers about the risk factors for SIDS, especially the least informed population groups such as young mothers and those from lower socioeconomic status, in order to reduce the number of avoidable infant deaths.

P4387Environmental tobacco smoke exposure affects the QT interval during early infancy

Abstract Background The association between long QT interval and sudden infant death syndrome (SIDS) has been clearly established. Environmental tobacco smoke (ETS) exposure is associated with increased risk for SIDS. However, there has been little focus on the relationship between the QT interval and ETS exposure during early infancy. To clarify this, we examined the QT interval with ETS exposure during early infancy. Methods Electrocardiographic study was performed in 624 infants (age: 1–5 months) who have been exposed to tobacco smoking since intrauterine life and 1119 age-matched children without ETS exposure. QT data were extracted from the electrocardiogram monitor built-in echocardiogram. Recordings from lead II on the monitor ECG were used to measure the QT interval. The QT intervals of 5 consecutive beats were measured manually. The QT interval was measured on the first, second, third, fourth, and fifth month. The corrected QT interval (QTc) was calculated by dividing the QT interval by the square root of the RR interval (Bazett's formula). The data of the number of cigarettes per day were collected by a questionnaire. Results In the total study population, the mean QTc showed the highest peak at the second month. The mean QTc at the first and second month (399±21 and 402±18 msec) was significantly longer (p<0.05) than that at the third, fourth, and fifth month (394±19, 393±21, and 392±22 msec) as shown in Figure 1A. The mean QTc in ETS infants at the first, second and third month was significantly greater than that in infants without ETS (404±20 vs. 397±21 msec, 407±19 vs. 399±17 msec and 404±17 vs. 390±18 msec, p<0.01, respectively), but the mean QTc at the fourth and fifth was similar in the 2 groups as shown in Figure 1B. The QTc increased significantly as the category of number of cigarettes per day increased, with a significant prolongation as of the category 6–10 cigarettes per day as shown in Figure 1C. Figure 1 Conclusions The present study indicates that the QT interval during early infancy lengthens by ETS exposure. Further study is needed as to whether QT prolongation associated with ETS exposure is a risk factor for SIDS.

Sudden infant death syndrome: Do the parents follow the recommendations?

Prone sleeping position is the main known modifiable risk factor for sudden infant death syndrome (SIDS). There are other SIDS recommendations although with less impact. The objective of this study is to describe the prevalence of prone position during sleep as well as other risk factors associated with SIDS in a sample of Spanish babies and infants. Cross-sectional study carried out on 640 families with children from 0 months to 11 months. In addition to the sleep position, the adherence to four other recommendations regarding SIDS was analysed: place where infant sleeps, breastfeeding, use of non-nutritive suction, and maternal smoking. A total of 41.3% of infants under 6 months and 59.7% of infants aged 6 to 11 months slept in a non-recommended position. Only 6.4% of families analysed followed all five recommendations. There is a high prevalence of modifiable risk factors for SIDS among the studied population. Personalized education should be promoted, along with other campaigns to raise awareness and prevent SIDS.

Prevalence and Predictors of Infant Mortality of Respiratory Distress Syndrome in Beijing and Jiangxi Provinces of PR China: A Retrospective Cohort Analysis

Background: Like any other countries, respiratory distress syndrome is a major cause of infantile mortality in China, especially in low birth weight infants. Objectives: The study aimed to determine the incidence of respiratory distress syndrome and identify some predictors of mortality in Chinese infants with confirmed respiratory distress syndrome (Level of Evidence: III). Methods: We retrospectively analyzed the demographic characteristics, perinatal risk factors, and clinical manifestations of 600 infants with Downes’ score of ≥ 4 admitted to the Affiliated BaYi Children’s Hospital, China, and the Second Affiliated Hospital of Nanchang University, China, from 1 January 2013 to 1 December 2018. Infants were divided into two cohorts, non-survivors (who died, n = 109) and survivors (who survived, n = 491). Factors predicting infant mortality were determined using univariate and multivariate logistic regression analysis at a 95% confidence level. Results: Infants of the non-survivor cohort were more likely to have severer respiratory distress (P = 0.003), to be of low birth weight ( 6, extreme low birth weight (< 1,000 g, P = 0.001), preterm delivery (gestational age < 37 weeks, P = 0.003), and cesarean delivery (P = 0.002) were found to be the independent risk factors of infant death. Conclusions: Preterm delivery, extremely low birth weight, and cesarean section were the risk factors of infant death from respiratory distress syndrome.

Aerodynamic factors affecting rebreathing in infants.

The rebreathing of expire air, with high carbon dioxide and low oxygen concentrations, has long been implicated in unexplained Sudden Infant Death Syndrome (SIDS) when infants are placed to sleep in a prone (facedown) position. This study elucidates the effect of the aerodynamic parameters Reynolds number, Strouhal number, and Froude number on the percentage of expired air that is reinspired (rebreathed). A nasal module was designed that served as a simplified geometric representation of infant nostrils and placed above a hard, flat surface. Quantitative and flow visualization experiments were performed to measure rebreathing, using water as the working medium, under conditions of dynamic similarity. Different anatomic (e.g., tidal volume, nostril diameter), physiological (e.g., breathing frequency), and environmental (e.g., temperature, distance from the surface) factors were considered. Increases in Strouhal number (simultaneously faster and shallower breathing) always produced higher rebreathed percentages, because rolled-up vortices in the vicinity of the nostrils had less time to move away by self-induction. Positively and negatively buoyant flows resulted in significant rebreathing. In the latter case, consistent with a warm environment and a high percentage of rebreathed CO2, denser gas pooled in the vicinity of the nostrils. Reynolds numbers below 200 also dramatically increased rebreathing because the expired gas pooled much closer to the nostrils. These results clearly elucidated how the prone position dramatically increases rebreathing by a number of different mechanisms. Furthermore, the results offer plausible explanations of why a high-temperature environment and low birthweight are SIDS risk factors. NEW & NOTEWORTHY A fundamentally new aerodynamics-based approach to the study of rebreathing of expired air in infants is presented. Rebreathing is implicated in unexplained Sudden Infant Death Syndrome (SIDS) when infants sleep in a prone position. This is the first time that aerodynamic parameters are systematically varied and their effects on rebreathing quantified. The study provides us with a deeper understanding of the effects of breathing frequency, tidal volume (birthweight) and environmental conditions.

Cell death in the human infant central nervous system and in sudden infant death syndrome (SIDS).

The brainstem has been a focus of sudden infant death syndrome (SIDS) research with amassing evidence of increased neuronal apoptosis. The present study extends the scope of brain regions examined and determines associations with known SIDS risk factors. Immunohistochemical expression of cell death markers, active caspase-3 and TUNEL, was studied in 37 defined brain regions in infants (aged 1-12 months) who died suddenly and unexpectedly (SUDI). A semi-quantitative mean score of marker expression was derived for each region and scores compared between three SUDI subgroups: explained SUDI (eSUDI; n = 7), SIDS I (n = 8) and SIDS II (n = 13). In eSUDI, active caspase-3 scores were highest in several nuclei of the rostral medulla, and lowest in the hypothalamus and cerebellar grey matter (GM). TUNEL was highest in regions of the hippocampus and basal ganglia, and lowest in the thalamus and cerebellar GM. TUNEL scores were higher in SIDS II compared to eSUDI in the amygdala (p = 0.03) and 5/9 nuclei in the rostral medulla (p = 0.04 - 0.01), and higher in SIDS II compared to SIDS I in the amygdala (p < 0.01), putamen (p = 0.01), lentiform nucleus (p = 0.03) and parietal (p = 0.03) and posterior frontal (p = 0.02) cortex. Active caspase-3 was greater in the hypoglossal nucleus (p = 0.03) of SIDS I compared to eSUDI infants. Co-sleeping, cigarette smoke exposure and the presence of an upper respiratory tract infection in SIDS infants was associated with differences in marker expression. This study affirms the sensitivity of the brainstem medulla to cell death in SIDS, and highlights the amygdala as a new region of interest.

Creating a Safe Sleep Environment for the Infant: What the Pediatric Nurse Needs to Know

Despite the release of guidelines by the American Academy of Pediatrics (AAP) on safe infant sleep and public service campaigns aimed at reducing risk factors over the past 25 years, deaths due to Sudden Infant Death Syndrome (SIDS) and Sudden Unexplained Infant Death (SUID) are still the 4th leading causes of infant death in the United States. Findings from several studies demonstrate that nurses do not consistently model safe sleep practices with infants due to a lack of education on evidence-based practice and misconceptions regarding safe infant sleep. The aim of this paper is to demonstrate the need for expanded education to both nurses and parents on the principles of safe infant sleep and the impact it can have on decreasing risk factors for SIDS and SUID. Strategies are outlined for additional education for nurses and parents to enhance adherence to safe sleep guidelines and quality improvement projects aimed at the implementation of culture change are discussed. Going forward it is critical that nurses take an active role in seeking additional education on modifiable risk factors linked to SIDS and SUID and use that education to model and teach safe infant sleep practices with every infant at every encounter.

Karakteristik Ibu dan Faktor Risiko Kejadian Kematian Bayi di Kabupaten Banjarnegara

Latar Belakang: Kabupaten Banjarnegara pada tahun 2012 menjadi Kabupaten dengan angka kematian bayi (AKB) tertinggi di Provinsi Jawa tengah. Dalam lima tahun terakhir angka kematian bayi sudah mengalami penurunan namun belum signifikan. Tujuan penelitian ini adalah untuk menganalisis karakteristik ibu dan beberapa faktor risiko yang berhubungan dengan kejadian kematian bayi di kabupaten Banjarnegara. Metode: Penelitian ini merupakan penelitian survei dengan pendekatan kasus kontrol dengan jumlah kelompok kasus 47 ibu dan kelompok kontrol 47 ibu. Sampel diambil secara purposive dengan kriteria inklusi kelompok kasus yaitu ibu yang mempunyai bayi meninggal sebelum berusia 24 hari di tahun 2017 dan tercatat di puskesmas Punggelan dan pejawaran. Data primer diambil dengan menggunakan kuesioner dengan teknik wawancara tatap muka. Data sekunder diambil dari buku catatan KIA ibu. Data dianalisis dengan menggunakan uji Chi-Square.Hasil: Dari hasil penelitian didapatkan bahwa faktor risiko yang berhubungan dengan kejadian kematian bayi di Kabupaten Banjarnegara adalah komplikasi persalinan, riwayat anemia, berat bayi lahir rendah, asfiksia, kelainan kongenital, dan bayi lahir prematur. Sedangkan umur ibu pengetahuan ibu, Pendidikan ibu, Paritas, Jarak kehamilan, berat badan ibu, lingkar lengan atas ibu, riwayat penyakit kronik ibu, perdarahan, hipertensi, penolong persalinan, tidak berhubungan secara signifikan dengan kejadian kematian bayi. Diharapkan dari hasil penelitian ini petugas kesehatan dapat mencegah faktor risiko yang berhubungan dengan kematian bayi dengan cara menganjurkan dan mengunjungi ibu hamil untuk melakukan ANC tepat waktu dan lengkap termasuk pemberian tablet Fe kepada ibu dan memonitornya melalui petugas surveilance KIA.Kata Kunci: kematian bayi, faktor risiko, karakteristik ibu hamil

Sudden Infant Death Syndrome and Safe Sleep on Twitter: Analysis of Influences and Themes to Guide Health Promotion Efforts.

BackgroundIn the United States, sudden infant death syndrome (SIDS) is the leading cause of death in infants aged 1 month to 1 year. Approximately 3500 infants die from SIDS and sleep-related reasons on a yearly basis. Unintentional sleep-related deaths and bed sharing, a known risk factor for SIDS, are on the rise. Furthermore, ethnic disparities exist among those most affected by SIDS. Despite public health campaigns, infant mortality persists. Given the popularity of social media, understanding social media conversations around SIDS and safe sleep may assist the medical and public health communities with information needed to spread, reinforce, or counteract false information regarding SIDS and safe sleep.ObjectiveThe objective of our study was to investigate the social media conversation around SIDS and safe sleep to understand the possible influences and guide health promotion efforts and public health research as well as enable health professionals to engage in directed communication regarding this topic.MethodsWe used textual analytics to identify topics and extract meanings contained in unstructured textual data. Twitter messages were captured during September, October, and November in 2017. Tweets and retweets were collected using NUVI software in conjunction with Twitter’s search API using the keywords: “sids,” “infant death syndrome,” “sudden infant death syndrome,” and “safe sleep.” This returned a total of 41,358 messages, which were analyzed using text mining and social media monitoring software.ResultsMultiple themes were identified, including recommendations for safe sleep to prevent SIDS, safe sleep devices, the potential causes of SIDS, and how breastfeeding reduces SIDS. Compared with September and November, more personal and specific stories of infant loss were demonstrated in October (Pregnancy and Infant Loss Awareness Month). The top influencers were news organizations, universities, and health-related organizations.ConclusionsWe identified valuable topics discussed and shared on Twitter regarding SIDS and safe sleep. The study results highlight the contradicting information a subset of the population is exposed to regarding SIDS and the continued controversy over vaccines. In addition, this analysis emphasizes the lack of public health organizations’ presence on Twitter compared with the influence of universities and news media organizations. The results also demonstrate the prevalence of safe sleep products that are embedded in safe sleep messaging. These findings can assist providers in speaking about relevant topics when engaging in conversations about the prevention of SIDS and the promotion of safe sleep. Furthermore, public health agencies and advocates should utilize social media and Twitter to better communicate accurate health information as well as continue to combat the spread of false information.

Central and peripheral chemoreceptors in sudden infant death syndrome.

The pathogenesis of sudden infant death syndrome (SIDS) has been ascribed to an underlying biological vulnerability to stressors during a critical period of development. This paper reviews the main data in the literature supporting the role of central (e.g. retrotrapezoid nucleus, serotoninergic raphe nuclei, locus coeruleus, orexinergic neurons, ventral medullary surface, solitary tract nucleus) and peripheral (e.g. carotid body) chemoreceptors in the pathogenesis of SIDS. Clinical and experimental studies indicate that central and peripheral chemoreceptors undergo critical development during the initial postnatal period, consistent with the age range of SIDS (<1year). Most of the risk factors for SIDS (gender, genetic factors, prematurity, hypoxic/hyperoxic stimuli, inflammation, perinatal exposure to cigarette smoke and/or substance abuse) may structurally and functionally affect the developmental plasticity of central and peripheral chemoreceptors, strongly suggesting the involvement of these structures in the pathogenesis of SIDS. Morphometric and neurochemical changes have been found in the carotid body and brainstem respiratory chemoreceptors of SIDS victims, together with functional signs of chemoreception impairment in some clinical studies. However, the methodological problems of SIDS research will have to be addressed in the future, requiring large and highly standardized case series. Up-to-date autopsy protocols should be produced, involving substantial, and exhaustive sampling of all potentially involved structures (including peripheral arterial chemoreceptors). Morphometric approaches should include unbiased stereological methods with three-dimensional probes. Prospective clinical studies addressing functional tests and risk factors (including genetic traits) would probably be the gold standard, allowing markers of intrinsic or acquired vulnerability to be properly identified.

Effects of neonatal hyperoxia on the critical period of postnatal development of neurochemical expressions in brain stem respiratory-related nuclei in the rat.

We have identified a critical period of respiratory development in rats at postnatal days P12‐13, when inhibitory influence dominates and when the response to hypoxia is at its weakest. This critical period has significant implications for Sudden Infant Death Syndrome (SIDS), the cause of which remains elusive. One of the known risk factors for SIDS is prematurity. A common intervention used in premature infants is hyperoxic therapy, which, if prolonged, can alter the ventilatory response to hypoxia and induce sustained inhibition of lung alveolar growth and pulmonary remodeling. The goal of this study was to test our hypothesis that neonatal hyperoxia from postnatal day (P) 0 to P10 in rat pups perturbs the critical period by altering the normal progression of neurochemical development in brain stem respiratory‐related nuclei. An in‐depth, semiquantitative immunohistochemical study was undertaken at P10 (immediately after hyperoxia and before the critical period), P12 (during the critical period), P14 (immediately after the critical period), and P17 (a week after the cessation of hyperoxia). In agreement with our previous findings, levels of cytochrome oxidase, brain‐derived neurotrophic factor (BDNF), TrkB (BDNF receptor), and several serotonergic proteins (5‐HT1A and 2A receptors, 5‐HT synthesizing enzyme tryptophan hydroxylase [TPH], and serotonin transporter [SERT]) all fell in several brain stem respiratory‐related nuclei during the critical period (P12) in control animals. However, in hyperoxic animals, these neurochemicals exhibited a significant fall at P14 instead. Thus, neonatal hyperoxia delayed but did not eliminate the critical period of postnatal development in multiple brain stem respiratory‐related nuclei, with little effect on the nonrespiratory cuneate nucleus.

Sudden Infant Death Syndrome: A Review.

Sudden infant death syndrome (SIDS) is the sudden unexpected death of an apparently healthy infant younger than age 12 months whose cause of death remains unknown despite a thorough death scene investigation, a review of the clinical history, and an autopsy. Despite the huge achievement of the Back to Sleep program, SIDS remains one of the leading causes of infant death in the United States. In recent years, the SIDS rate has remained stationary despite major public health efforts aimed at high-risk groups to improve sleep environment and strategies. This review focuses on SIDS epidemiology, pathogenesis and risk factors, the American Academy of Pediatrics recommendations on safe infant sleeping environment, and the US Centers for Disease Control and Prevention's multistate registry to improve knowledge on SIDS, evaluate trends, and analyze circumstances and events surrounding SIDS cases. [Pediatr Ann. 2018;47(3):e118-e123.].

Detoxification genes polymorphisms in SIDS exposed to tobacco smoke

The best hypothesis to explain Sudden Infant Death Syndrome (SIDS) pathogenesis is offered by the “triple risk model”, which suggests that an interaction of different variables related to exogenous stressors and infant vulnerability may lead to the syndrome. Environmental factors are triggers that act during a particular sensible period, modulated by intrinsic genetic characteristics. Although literature data show that one of the major SIDS risk factors is smoking exposure, a specific involvement of molecular components has never been highlighted. Starting from these observations and considering the role of GSTT1 and GSTM1 genes functional polymorphisms in the detoxification process, we analyzed GSTM1 and GSTT1 null genotype frequencies in 47 SIDS exposed to tobacco smoke and 75 healthy individuals.A significant association (p < .0001) between the GSTM1 null genotype and SIDS exposed to smoke was found. On the contrary, no association between GSTT1 polymorphism and SIDS was determined. Results indicated the contribution of the GSTM1 −/− genotype resulting in null detoxification activity in SIDS cases, and led to a better comprehension of the triple risk model, highlighting smoking exposure as a real SIDS risk factor on a biochemical basis.

Cardiovascular autonomic dysfunction in sudden infant death syndrome.

A failure of cardiorespiratory control mechanisms, together with an impaired arousal response from sleep, are believed to play an important role in the final event of sudden infant death syndrome (SIDS). The 'triple risk model' describes SIDS as an event that results from the intersection of three overlapping factors: (1) a vulnerable infant, (2) a critical developmental period in homeostatic control and (3) an exogenous stressor. In an attempt to understand how the triple risk hypothesis is related to infant cardiorespiratory physiology, many researchers have examined how the known risk and protective factors for SIDS alter infant cardiovascular control during sleep. This review discusses the association between the three components of the triple risk hypothesis and major risk factors for SIDS, such as prone sleeping, maternal smoking, together with three "protective" factors, and cardiovascular control during sleep in infants, and discusses their potential involvement in SIDS.

Ambient Temperature and Sudden Infant Death Syndrome in the United States.

Sudden infant death syndrome (SIDS) is a leading cause of infant mortality in the United States. While thermal stress is implicated in many risk factors for SIDS, the association between ambient temperature and SIDS remains unclear. We obtained daily individual-level infant mortality data and outdoor temperature data from 1972 to 2006 for 210 US cities. We applied a time-stratified case-crossover analysis to determine the effect of ambient temperature on the risk of SIDS by season. We stratified the analysis by race, infant age, and climate. There were a total of 60,364 SIDS cases during our study period. A 5.6°C (10°F) higher daily temperature on the same day was associated with an increased SIDS risk of 8.6% (95% confidence interval [CI] = 3.6%, 13.8%) in the summer, compared with a 3.1% decrease (95% CI = -5.0%, -1.3%) in the winter. Summer risks were greater among black infants (18.5%; 95% CI = 9.3%, 28.5%) than white infants (3.6%; 95% CI = -2.3%, 9.9%), and among infants 3-11 months old (16.9%; 95% CI = 8.9%, 25.5%) than infants 0-2 months old (2.7%; 95% CI = -3.5%, 9.2%). The temperature-SIDS association was stronger in climate clusters in the Midwest and surrounding northern regions. Temperature increases were associated with an elevated risk of SIDS in the summer, particularly among infants who were black, 3 months old and older, and living in the Midwest and surrounding northern regions.

Hypoxia and nicotine effects on Pituitary adenylate cyclase activating polypeptide (PACAP) and its receptor 1 (PAC1) in the developing piglet brainstem

Pituitary adenylate cyclase activating polypeptide (PACAP) and its cognate receptor 1 (PAC1), have been implicated in the pathophysiology of the Sudden Infant Death Syndrome (SIDS). Two main risk factors for SIDS are prone sleeping and cigarette smoke exposure. Using piglet models of these risk factors, intermittent hypercapnic hypoxia (IHH-mimicking rebreathing in prone position) and nicotine (main reinforcing element of cigarettes), this study aimed to determine their effects on PACAP and PAC1 protein expression in the medulla. IHH was delivered for 1 (n=7), 2 (n=6), 3 (n=6) and 4 (n=7) days prior to euthanasia at 13–14days of age, while nicotine (n=7) was continuous for the first 14days of life. An additional group of combined nicotine and 1day IHH (1DIHH) was studied to determine the combined effects of the risk factors. Changes in expression were seen after the acute 1DIHH exposure (none after repeated daily exposures) and included a decrease in PACAP in the dorsal motor nucleus of vagus (DMNV; p=0.024), nucleus of the solitary tract (NTS; p=0.024) and the gracile nucleus (GRAC; p=0.001), and a decrease in PAC1 in the NTS (p=0.01). No PACAP change was noted in the nicotine-exposed piglets, however, a decrease in PAC1 was found in the DMNV (p=0.02). IHH exposure in piglets with pre-exposure to nicotine led to a significant decrease in PACAP in the Grac (p=0.04) but had no effect on PAC1. These findings show for the first time, the vulnerability of PACAP in the brainstem during early development to an acute hypercapnic hypoxic exposure and that those effects are greater than from nicotine exposure.