ライフサイエンスコーパス: SIDS

1 SIDS cases were matched to controls at a ratio of 1:4 by

2 SIDS rates declined significantly from 1989-1991 to 1995

3 SIDS rates increased with the amount smoked for all US r

4 They identified 2,107 SIDS cases, 96% of whom were diagnosed through autopsy.

5 Three of 133 SIDS cases were homozygous for the variant S1103Y.

6 ) compared with autopsied controls (n = 15) [SIDS, 177.2 +/- 15.1 (mean +/- SE) ng/mL versus controls

7 in-person interviews with the mothers of 185 SIDS cases and 312 randomly selected race/ethnicity- and

8 y, and direct DNA sequencing on DNA from 292 SIDS cases.

9 s, E42K and S272P, were detected in 2 of 292 SIDS cases, a 2-month-old white boy and a 3-month-old wh

10 69 consecutive unexpected infant deaths (300 SIDS and 69 explained deaths) in Avon over 20 years (198

11 Of 2 276 578 eligible infants, 354 SIDS (0.016%) cases (mean [SD] gestational age, 38.3 [2.

12 Tissues from 6 SIDS cases were further analyzed.

13 A total of 6 SIDS cases (9.3%) with high CSF neopterin were identifie

14 CSF neopterin was screened in 64 SIDS cases and 15 controls, with no exclusions.

15 A cohort of 71 SIDS cases (mean [SD] age, 55.2 [11.4] postconceptional

16 ere extracted from anonymised records of 745 SIDS cases and 2411 live controls.

17 een aberrant metabolic analytes at birth and SIDS.

18 markers combined with known risk factors and SIDS.

19 nal surveillance systems, except for NEC and SIDS, which were estimated from the literature.

20 ong association between maternal smoking and SIDS persisted after controlling for maternal age and li

21 to be the link between maternal smoking and SIDS, we examined the cardiorespiratory responses to hyp

22 lepsy, sudden death syndromes like SUDEP and SIDS, and cardiac arrhythmia.

23 outcomes were the monthly rates of SUID and SIDS during the COVID-19 pandemic compared with the prep

24 study found increased rates of both SUID and SIDS during the COVID-19 pandemic, with a significant sh

25 ation into the role of infection in SUID and SIDS is needed.

26 s regarding seasonal infections and SUID and SIDS.

27 th sudden unexpected infant death (SUID) and SIDS rates before and during the pandemic offers an oppo

28 ibutions suggest that cases once reported as SIDS are now being reported as ASSB and cause unknown/un

29 of SIDS should be considered when assessing SIDS risk in clinical settings.

30 40 infants died of SIDS (median [IQR] age at SIDS, 3 [2-4] months) during a 39-year study period.

31 on revealed significant associations between SIDS and 2 or more layers of clothing on the infant (adj

32 rkers of 5-HT function were compared between SIDS cases and controls, adjusted for postconceptional a

33 -1KO mice did not reveal differences between SIDS blockade and vehicle treatment in functional long-t

34 ribute to SIDS, yet the relationship between SIDS and biomarkers of metabolism remains unclear.

35 bral artery occlusion the effect of blocking SIDS by inhibiting body's main stress axes, the sympathe

36 of polyradiculitis, which were diminished by SIDS blockade.

37 Compared with controls, SIDS cases had a significantly higher 5-HT neuron count

38 Compared with controls, SIDS was associated with lower 5-HT and TPH2 levels, con

39 Current SIDS research has focused on the genetics of SIDS, brain

40 in rates of sudden unexplained infant death (SIDS) around 1990, four large case-control studies were

41 , the "Back to Sleep" campaign has decreased SIDS prevalence, consistent with a role for environmenta

42 and until age 1 year, emigration, developing SIDS, death, or study end.

43 first child had died in infancy from either SIDS (n = 84) or some other cause (n = 305) were identif

44 importance of aquatic foods in an emblematic SIDS, emphasizing their vulnerability to declining aquat

45 aquatic food consumption is high, to enable SIDS to meet key SDGs.

46 e for each analysis ranged from 16 to 31 for SIDS cases and 6 to 10 for controls.

47 ed Health Problems, Tenth Revision codes for SIDS (R95), unknown (R99), and accidental suffocation an

48 espiratory acidosis--a known risk factor for SIDS--produced abnormal gain-of-function late reopenings

49 s of clothing are important risk factors for SIDS among Northern Plains Indians.

50 xplained by common maternal risk factors for SIDS and obstetric complications and by the likelihood o

51 As risk factors for SIDS include apnea and respiratory acidosis, Y1103 and w

52 en markers and 6 recognized risk factors for SIDS was performed.

53 most important preventable risk factors for SIDS, and smoking prevention/intervention programs have

54 ured by NBS and established risk factors for SIDS.

55 s the leading candidate ion channel gene for SIDS.

56 s that may have significant implications for SIDS.

57 compared cause-specific mortality rates for SIDS, other sudden, unexpected infant deaths, and cause

58 s a referent, the unadjusted odds ratios for SIDS for the second through fifth quintiles were 1.7 (95

59 tment for these factors, the odds ratios for SIDS were 1.7 (95 percent confidence interval, 0.8 to 3.

60 le to identify infants at increased risk for SIDS soon after birth, which could inform further mechan

61 rm infants and 6 groups of those at risk for SIDS) who, during the first 6 months after birth, were o

62 hild care centers have an increased risk for SIDS, which is of particular concern as the number of in

63 on identifying infants at continued risk for SIDS.

64 ogenic substrate in some infants at risk for SIDS.

65 renatal nicotine, creating a higher risk for SIDS.

66 of S1103Y have a 24-fold increased risk for SIDS.

67 mutation as a novel pathogenic substrate for SIDS.

68 Women whose infants die from SIDS are more likely to have complications in their othe

69 Women who had an infant who died from SIDS were at increased risk in their next pregnancy of d

70 rs, the proportion of children who died from SIDS while co-sleeping with their parents, has risen fro

71 ostulated that women whose infants died from SIDS would be more likely to have had obstetric complica

72 NTS: Frozen medullae from infants dying from SIDS (cases) or from causes other than SIDS (controls) w

73 2008 and consisted of 41 infants dying from SIDS (cases), 7 infants with acute death from known caus

74 rol have been reported in infants dying from SIDS.

75 s case-control study, postmortem fluids from SIDS cases and controls collected between July 2011 and

76 CSF, liver, and brain tissue from SIDS cases with elevated CSF neopterin were subjected to

77 greater than 0.5, a total of 20 (62.5%) had SIDS.

78 times the odds (95% CI, 6.0-34.5) of having SIDS compared with those with a model-predicted probabil

79 However, SIDS might represent an adaptive mechanism preventing au

80 Stroke-induced immunodepression (SIDS) is an essential cause of poststroke infections.

81 , lobbying to enforce state law to implement SIDS education campaigns for child care centers and with

82 nal age, was significantly elevated (95%) in SIDS infants (n = 61) compared with autopsied controls (

83 ys similar to brain neurons, are abnormal in SIDS.

84 of the environment and genetic background in SIDS and also raise interesting questions about the link

85 Most of the decline in SIDS rates since 1999 is likely due to increased reporti

86 From 1999-2001, the decline in SIDS rates was offset by increasing rates of cause unkno

87 Serum and plasma 5-HT were also elevated in SIDS compared to controls.

88 the evidence for the brainstem hypothesis in SIDS with a focus upon abnormalities related to the neur

89 ycardia and apnea and has been implicated in SIDS pathogenesis, how PNE affects the SLCF-mediated car

90 ergic system has recently been implicated in SIDS, we conducted a large-scale investigation of the 5-

91 life threatening and have been implicated in SIDS.

92 tem to study 5-HT and 14-3-3 interactions in SIDS.

93 Recent literature in SIDS research has focused on identifying infants at cont

94 ued review of the most current literature in SIDS research to keep ourselves current and well informe

95 Serotonin levels were 26% lower in SIDS cases (n = 35) compared with age-adjusted controls

96 nt in the medulla was significantly lower in SIDS cases compared with controls (mean [SD], 0.70 [0.33

97 suggest an important underlying mechanism in SIDS that may help lead to identification of infants at

98 Medullary 5-HT pathology in SIDS is more extensive than previously delineated, poten

99 The presence in SIDS of both platelet and brainstem 5-HT and 14-3-3 abno

100 basis for further substantial reductions in SIDS incidence rates.

101 In conclusion, inhibiting SIDS by pharmacological blockade of body's stress axes i

102 ant data meta-analysis of five international SIDS/SUDI case-control studies.

103 ms have the potential to substantially lower SIDS rates in the United States and Sweden and presumabl

104 Male SIDS cases had significantly lower 5-HT(1A) binding dens

105 Although many SIDS infants come from large families, first-born infant

106 a portion of the raphe, as observed in many SIDS cases, can impair ability to autoresuscitate at cri

107 erating characteristic curve for a 14-marker SIDS model, which included 8 metabolites, was 0.75 (95%

108 matory functions compared with 3 age-matched SIDS cases with normal CSF neopterin levels.

109 For CSF neopterin measures, SIDS samples were from infants with mean (SD) age of 54.

110 Most SIDS deaths now occur in deprived families.

111 oradic SCN5A mutation in an infant with near SIDS, SCN5A has emerged as the leading candidate ion cha

112 ously, we reported that approximately 40% of SIDS deaths are associated with abnormalities in seroton

113 Thirty-one percent (19/61) of SIDS cases had 5-HT levels greater than 2 SDs above the

114 to identify the pathophysiological basis of SIDS.

115 espite these protective effects, blockade of SIDS increased CNS antigen-specific Type1 T helper cell

116 th singleton births, there were 114 cases of SIDS (incidence, 2.7 per 10,000 births among women with

117 Two of the 93 cases of SIDS possessed SCN5A mutations: a 6-week-old white male

118 Although the cause of SIDS is unknown, immature cardiorespiratory autonomic co

119 o be progress in understanding the causes of SIDS.

120 may contribute to the observed clustering of SIDS.

121 this prospective, population-based cohort of SIDS cases had an identifiable SCN5A channel defect, sug

122 re followed up from the index cases' date of SIDS, date of birth, or immigration, whichever came firs

123 ers may aid in the forensic determination of SIDS and have the potential to be predictive of SIDS ris

124 (1 395 199 [52%] male), 1540 infants died of SIDS (median [IQR] age at SIDS, 3 [2-4] months) during a

125 tionwide study, having a sibling who died of SIDS was associated with a 4-fold higher risk of SIDS co

126 , including siblings of children who died of SIDS.

127 d was autopsy material from infants dying of SIDS and age-matched controls dying of known causes.

128 In infants dying of SIDS compared to infants dying of known causes, we found

129 The etiology of SIDS is complex and remains largely unknown.

130 omeostasis and contribute to the etiology of SIDS.

131 The fatal events of SIDS are characterized by severe bradycardia and life-th

132 he definition, etiology, and risk factors of SIDS.

133 This models features of SIDS.

134 SIDS research has focused on the genetics of SIDS, brainstem abnormalities and arousal failures, the

135 The family history of SIDS should be considered when assessing SIDS risk in cl

136 ns should be to ensure that the incidence of SIDS continues to decline.

137 Pharmacological inhibition of SIDS appears promising in preventing life-threatening in

138 to 50% (p<0.0001), but the actual number of SIDS deaths in the parental bed has halved (p=0.01).

139 a continued downward trend in the number of SIDS deaths.

140 which may contribute to the pathogenesis of SIDS.

141 S and have the potential to be predictive of SIDS risk in living infants.

142 ta has also suggested that the prevention of SIDS should not be an indication for use of home cardior

143 A higher rate of SIDS was observed among siblings compared with the gener

144 ge could potentially reduce the high rate of SIDS.

145 Rates of SIDS were elevated throughout the intrapandemic period c

146 d position) had a significantly high risk of SIDS (AOR = 8.2 (95% CI: 2.6, 26.0) and AOR = 6.9 (95% C

147 ons are associated with an increased risk of SIDS and are likely to recur in subsequent pregnancies.

148 was associated with a 4-fold higher risk of SIDS compared with the general population.

149 abruption and placenta previa on the risk of SIDS did not differ significantly.

150 iated with a twofold increase in the risk of SIDS in offspring (odds ratio = 2.1, 95% confidence inte

151 side sleeping position had a higher risk of SIDS than infants who were always placed prone or on the

152 one or side position were at greater risk of SIDS than were infants who had last been put down on the

153 The risk of SIDS varied inversely with the birth-weight percentile a

154 The risk of SIDS was especially high for an unstable side position i

155 The risk of SIDS was higher for the children of women whose previous

156 Risk of SIDS was higher with a history of parental inpatient car

157 rum alpha-fetoprotein levels and the risk of SIDS, which may be mediated in part through impaired fet

158 -fetoprotein levels also predict the risk of SIDS.

159 alpha-fetoprotein and the subsequent risk of SIDS.

160 y may predispose an infant to a high risk of SIDS.

161 haring are associated with decreased risk of SIDS.

162 Standardized incidence ratios (SIRs) of SIDS were calculated with Poisson regression models rela

163 n of the controls, thus defining a subset of SIDS cases with elevated 5-HT.

164 sfunction may be responsible for a subset of SIDS cases.

165 A subset of SIDS infants has abnormalities in the neurotransmitter,

166 e replicated, prospective genetic testing of SIDS cases and screening with counseling for at-risk fam

167 The European Concerted Action on SIDS (ECAS) investigation was planned to bring together

168 th weight had a strong independent effect on SIDS, the addition of birth weight to the models lowered

169 No significant impact on SIDS was observed.

170 g for gap junction proteins was performed on SIDS-associated paraffin-embedded cardiac tissue.

171 ly, suggesting that the effect of smoking on SIDS is not mediated through birth weight.

172 excessive mortality to anoxia (a postulated SIDS stressor) at P5 and P8.

173 Although causality cannot be proved, SIDS rates declined approximately 38% during this period

174 muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5

175 partly explain why some women have recurrent SIDS.

176 gns for risk reduction have helped to reduce SIDS incidence by 50-90%.

177 ir side) or supine (on their back) to reduce SIDS risk, and in 1994, the national public education ca

178 Many Small Island Developing States (SIDS) are experiencing a nutrition transition, wherein h

179 mong the five US race/ethnic groups studied, SIDS rates ranged from a high of 3.0 infant deaths per 1

180 Despite this success, SIDS continues to be the most common cause of unexplaine

181 Circumstances surrounding SIDS and SUDEP deaths often facilitate CO(2) elevation,

182 d succumbed to sudden infant death syndrome (SIDS) (and no other cause of death) would be associated

183 iation between sudden infant death syndrome (SIDS) and maternal smoking was compared between the Unit

184 implicated in sudden infant death syndrome (SIDS) and obstructive sleep apnoea.

185 isk factor for sudden infant death syndrome (SIDS) and prenatal nicotine exposure is proposed to be t

186 tanding of how sudden infant death syndrome (SIDS) and the symptom complex seen in acute life-threate

187 driver in the sudden infant death syndrome (SIDS) cascade.

188 Many sudden infant death syndrome (SIDS) cases exhibit a partial ( approximately 26%) brain

189 10% to 15% of sudden infant death syndrome (SIDS) cases may stem from channelopathy-mediated lethal

190 Sudden infant death syndrome (SIDS) cases often have abnormalities of the brainstem ra

191 t two decades, sudden infant death syndrome (SIDS) continues to be the leading cause of death for inf

192 een conducted, sudden infant death syndrome (SIDS) has become increasingly concentrated among disadva

193 on the risk of sudden infant death syndrome (SIDS) has been reported previously, but with conflicting

194 pidemiology of sudden infant death syndrome (SIDS) has changed since the 1991 UK Back to Sleep campai

195 on and risk of sudden infant death syndrome (SIDS) in an ethnically diverse US population, the author

196 Sudden infant death syndrome (SIDS) is a leading cause of postneonatal mortality among

197 Sudden infant death syndrome (SIDS) is a major cause of infant death in the US.

198 recurrence of sudden infant death syndrome (SIDS) is an issue of biological, clinical, and legal int

199 Sudden infant death syndrome (SIDS) is postulated to result from abnormalities in brai

200 Sudden infant death syndrome (SIDS) is the leading cause of post-neonatal infant morta

201 The sudden infant death syndrome (SIDS) is the sudden death of an infant under one year of

202 US decline in sudden infant death syndrome (SIDS) rates may be explained by a shift in how these dea

203 Sudden infant death syndrome (SIDS) remains a leading cause of death during the first

204 proposal that sudden infant death syndrome (SIDS) results from a developmental abnormality of medull

205 lbirth and the sudden infant death syndrome (SIDS) share some features.

206 ch relevant to sudden infant death syndrome (SIDS) to determine whether there is a place for home mon

207 nts dying from sudden infant death syndrome (SIDS) were identified, suggesting that medullary 5-HT dy

208 re at risk for sudden infant death syndrome (SIDS), and patients with epilepsy are at risk for sudden

209 ndrome (CCHS), Sudden Infant Death Syndrome (SIDS), and Rett Syndrome.

210 reased risk of sudden infant death syndrome (SIDS), but few studies have assessed factors associated

211 eased risk for sudden infant death syndrome (SIDS), but the efficacy of such devices for this use is

212 tiology of the sudden infant death syndrome (SIDS), in which there is medullary 5-HT deficiency and i

213 plications for sudden infant death syndrome (SIDS), insofar as seemingly normal infants succumb to SI

214 who died from sudden infant death syndrome (SIDS), one with documented prolonged QTc and Torsade de

215 a high risk of sudden infant death syndrome (SIDS), the authors conducted a population-based case-con

216 Sudden infant death syndrome (SIDS), the leading cause of postneonatal infant mortalit

217 isk factor for sudden infant death syndrome (SIDS)-the leading postneonatal cause of infant mortality

218 esponsible for sudden infant death syndrome (SIDS).

219 nts who die of sudden infant death syndrome (SIDS).

220 sk factors for sudden infant death syndrome (SIDS).

221 iomyopathy and sudden infant death syndrome (SIDS).

222 some cases of sudden infant death syndrome (SIDS).

223 e stomach) and sudden infant death syndrome (SIDS).

224 tis (NEC), and sudden infant death syndrome (SIDS).

225 isk factor for sudden infant death syndrome (SIDS).

226 reased risk of sudden infant death syndrome (SIDS).

227 each year from sudden infant death syndrome (SIDS).

228 y cases of the sudden infant death syndrome (SIDS).Mice with a targeted disruption of the serotonin t

229 from SIDS (cases) or from causes other than SIDS (controls) were obtained from the San Diego Medical

230 orn child had died due to a cause other than SIDS.

231 This study demonstrates that SIDS is associated with peripheral abnormalities in the

232 Here we tested the hypothesis that SIDS is associated with an alteration in serum 5-HT leve

233 To evaluate our hypothesis that SIDS is, at least in part, a multi-organ dysregulation o

234 The SIDS rate for Sweden (using 1983-1992 data) was 0.9.

235 In addition, the SIDS rate among black infants continues to be more than

236 rmalities differed significantly between the SIDS and hospitalized groups (5-HT in the raphe obscurus

237 obscurus, TPH2 levels were 22% lower in the SIDS cases (n = 34) compared with controls (n = 5) (151.

238 with age in 5-HT(1A) receptor binding in the SIDS cases but no change in the controls (age x diagnosi

239 plain the increased vulnerability of boys to SIDS.

240 uggest that parents who have lost a child to SIDS may wish to delay a new pregnancy for at least 6 mo

241 Factors that contribute to SIDS have changed in their importance over the past 20 y

242 nborn errors of metabolism may contribute to SIDS, yet the relationship between SIDS and biomarkers o

243 and prenatal factors that may contribute to SIDS.

244 cardia during hypoxia that may contribute to SIDS.

245 ate from multiple hypoxic events, leading to SIDS.

246 al chemoreception, which may be pertinent to SIDS.

247 are not likely to be immediate precursors to SIDS.

248 e of pregnancy complications predisposing to SIDS could partly explain why some women have recurrent

249 sofar as seemingly normal infants succumb to SIDS when exposed to respiratory stressors (e.g., hypoxi

250 When the firstborn child had succumbed to SIDS, the mean birth weight of the next baby was 314 g (

251 ght make affected infants more vulnerable to SIDS.

252 Enquiries identified 18 families with two SIDS(sudden infant death syndrome) deaths and two famili

253 tabolites were significantly associated with SIDS in a univariate analysis: 17-hydroxyprogesterone, a

254 iplinary genetic evaluation of families with SIDS could provide additional evidence.

255 forensic biomarker in autopsied infants with SIDS with serotonergic defects.

256 s (cases) to index cases (first sibling with SIDS) were identified.