A MEMS Design for an Intelligent Pacifier for Preventing Sudden Infant＇s Death Syndrome （SIDS Alarm）

Sudden Infant Death Syndrome （SIDS） is an unexpected death of infants under one year old. SIDS is the most common cause of death for infants after the first month of birth, commonly between two and four months. MEMS （Micro-Electro-Mechanical Systems） technology can be very useful to help us to avoid this horrible tragedy. In the present work, using a MEMS technology, an intelligent pacifier is designed to alarm any unusual changes in breathing during sleeping. A PZT （Piezoelectric） sensor is utilized to detect the force generated by breathing and convert it to a measurable voltage and alarm the risky breathing during infant＇s sleeping. This voltage can subsequently drive some simple alarm and make parents aware of hazard.

Prenatal and postnatal factors associated with sudden infant death syndrome:an umbrella review of meta-analyses

Background Comprehensive quantitative evidence on the risk and protective factors for sudden infant death syndrome(SIDS)effects is lacking.We investigated the risk and protective factors related to SIDS.Methods We conducted an umbrella review of meta-analyses of observational and interventional studies assessing SIDS-related factors.PubMed/MEDLINE,Embase,EBSCO,and Google Scholar were searched from inception until January 18,2023.Data extraction,quality assessment,and certainty of evidence were assessed by using A Measurement Tool Assessment Systematic Reviews 2 following PRISMA guidelines.According to observational evidence,credibility was graded and classified by class and quality of evidence(CE;convincing,highly suggestive,suggestive,weak,or not significant).Our study protocol was registered with PROSPERO(CRD42023458696).The risk and protective factors related to SIDS are presented as equivalent odds ratios(eORs).Results We identified eight original meta-analyses,including 152 original articles,covering 12 unique risk and protective factors for SIDS across 21 countries/regions and five continents.Several risk factors,including prenatal drug exposure[eOR=7.84(95%CI=4.81–12.79),CE=highly suggestive],prenatal opioid exposure[9.55(95%CI=4.87–18.72),CE=suggestive],prenatal methadone exposure[9.52(95%CI=3.34–27.10),CE=weak],prenatal cocaine exposure[4.38(95%CI=1.95–9.86),CE=weak],prenatal maternal smoking[2.25(95%CI=1.95–2.60),CE=highly suggestive],postnatal maternal smoking[1.97(95%CI=1.75–2.22),CE=weak],bed sharing[2.89(95%CI=1.81–4.60),CE=weak],and infants found with heads covered by bedclothes after last sleep[11.01(95%CI=5.40–22.45),CE=suggestive],were identified.On the other hand,three protective factors,namely,breastfeeding[0.57(95%CI=0.39–0.83),CE=non-significant],supine sleeping position[0.48(95%CI=0.37–0.63),CE=suggestive],and pacifier use[0.44(95%CI=0.30–0.65),CE=weak],were also identified.Conclusions Based on the evidence,we propose several risk and protective factors for SIDS.This study suggests the need for further studies on SIDS-related factors supported by weak credibility,no association,or a lack of adequate research.

Study on Pulmonary Surfactant of Sudden Death of Infant

Objective To find the pathogenesis of sudden infant death syndrome (SIDS) from changes of pulmonary surfactant. Methods By means of thin layer chromatography technique, surfactant in whole lung specimens of 10 infants with SIDS and 10 control infants without SIDS (dead of nonrespiratory diseases) were examined qualitatively and quantitatively. Results Eleven components in pulmonary surfactant were examined qualitatively, including lysophosphatidylcholine, sphingomyelin, phosphatidylcholine, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, phosphatidylglycerol, diphosphatidylglycerol, phosphatidic acid, cholesterol and neutral lipids. Quantitative examination showed that the amount of surfactant of whole lung specimens in sudden death group [(8.9±1.0) mg/g wet lung weight] was significantly less than that in control group [(12.6±1.4) mg/g wet lung weight, P<0.01]. Qualitative variance showed that the percentages of phosphatidylcholine (49.4%±2.0%) and phosphatidylglycerol (2.6%±0.7%) decreased markedly in sudden death group compared with those in control group (61.5%±3.0% and 4.3%±1.5%, P<0.01). Conclusion Before death there is serious defect on metabolism of pulmonary surfactant in sudden death infants, with the amount decreasing and the ratio of its components being disturbed, which is one of the important pathogenies of SIDS.

Incidence and determinants of sudden infant death syndrome:a population-based study on 37 million births

Background:The objective of our study is to measure the incidence of sudden infant death syndrome(SIDS),estimate the birth to death interval,and identify associated maternal and infant risk factors.Methods:We carried out a population-based cohort study on 37418280 births using data from the Centers for Disease Control and Prevention's"Linked Birth-Infant Death"and"Fetal Death"data files from 1995 to 2004.Descriptive statistics and cox-proportional hazard models were used to estimate the adjusted effect of maternal and newborn characteristics on the risk of SIDS.Results:There were 24101 cases of SIDS identified for an overall 10-year incidence of 6.4 cases per 10000 births.Over the study period,the incidence decreased from 8.1 to 5.6 per 10000 and appeared to be most common among infants aged 2-4 months.Risk factors inchuded maternal age<20 years,black,non-Hispanic race,smoking,increasing parity,inadequate prenatal care,prematurity and growth restriction.Conclusions:While the incidence of SIDS in the US has declined,it currently remains the leading cause of post-neonatal mortality,highlighting an important public health priority.Educational campaigns should be targeted towards mothers at increased risk in order to raise their awareness of modifiable risk factors for SIDS such as maternal smoking and inadequate prenatal care.

CHANGES OF MYOCARDIAL MYOGLOBIN, MYOSIN AND CREATINE KINASE IN CASES OF SUDDEN NOCTURNAL DEATH SYNDROME

Myoglobin, myosin creatine kinase MM (CK-MM),creatine kinase BB(CK-BB) in cardiac muscle and H chain ofmyosin in atrial and ventricular muscle were studied in speci-mens from 8 patients who died of sudden nocturnal deathsyndrome(SNDS) by avidin-biotin complex (ABC) method toinvestigate the possible early or very early myocardial ischemiain the syndrome. Hematoxylin-eosin staining was conductedfor comparison. The results showed evident loss of CK-MM,CK-BB, myoglobin and myosin from cardiac muscle cells, indi-caring that occurrence of SNDS is closely associated withacute myocardial ischemia.

Meta‑analysis of the Association between Serotonin Transporter Polymorphisms and Sudden Infant Death Syndrome

The serotonin transporter(5‑HTT)gene has been considered one of the risk factors for sudden infant death syndrome(SIDS),but the association remains unconfirmed.This meta‑analysis was performed to quantitatively summarize the evidence for such a relationship.PubMed,EMBASE,and China National Knowledge Infrastructure databases were searched for eligible studies within a range of published years from 1990 to December 2015.The odds ratios(ORs)with 95%confidence intervals(CIs)were used to assess the different associations.A total of 8 studies with 624 cases and 796 controls were included for 5‑HTT promoter polymorphism,5 studies with 418 cases and 542 controls for intron 2,and 3 studies with 253 cases and 334 controls for haplotype.The pooled examinations showed an overall increased SIDS risk for the 5‑HTT promoter polymorphism(OR=1.65,95%CI=1.03–2.63,P=0.035 for LL vs.LS and SS;OR=1.46,95%CI=1.04–2.04,P=0.028 for L vs.S),but no association(OR=1.00,95%CI=0.75–1.33,P=0.994 for 10+9 carriers vs.12/12;OR=0.97,95%CI=0.79–1.19,P=0.753 for 10+9 vs.12)for intron 2 polymorphism,and an unreliable association(OR=0.52,95%CI=0.31–0.87,P=0.013)for S‑9 and S‑10 haplotypes.This meta‑analysis suggests that the L allele or LL homozygote of 5‑HTT promoter polymorphism has an increased risk for SIDS,while intron 2 polymorphism has no association with SIDS.

Altered Expression of Nicotinic Receptors in Perinatal Life Related to Prenatal Exposure to Toxics—An Overview of the Research Carried Out on This Topic at the “Lino Rossi” Research Center of the Milan University

The article aims to underline the impact of nicotine and pesticides on neuronal α7-nicotinic acetylcholine receptors expression in brainstem regions receiving cholinergic projections, given their fundamental role during the neuronal development. The in-depth histopathological/immunohistochemical examination of the autonomic nervous system performed at the “Lino Rossi” Research Center of the Milan University on a wide group of sudden unexpected fetal and infant deaths, highlighted the frequent hypodevelopment of brainstem structures checking the vital functions associated to altered expression of α7-nicotinic acetylcholine receptors and smoke absorption in pregnancy. A dysregulation of the catecholamine system was also observed in the cerebellar cortex of the same cases. However, in a not negligible percentage of sudden deaths with altered expression of α7-nicotinic receptors, the mothers never smoked but lived in rural areas. Specific analytical procedures showed the presence of agricultural pesticides in cerebral cortex samples of these victims. Therefore, it is possible to believe that the exposition to pesticides during pregnancy can produce the same harmful effects as nicotine on the nicotinic acetylcholine receptors. Moreover, alterations of α7-nicotinic acetylcholine receptors receptor expression were also detected in the lungs of many sudden perinatal death victims, allowing to consider even these findings as possible consequence of maternal exposure to toxic factors.