ライフサイエンスコーパス: SIDS

1 SIDS rates declined significantly from 1989-1991 to 1995

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

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

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

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

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

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

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

9 69 consecutive unexpected infant deaths (300 SIDS and 69 explained deaths) in Avon over 20 years (198

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

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

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

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

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

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

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

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

18 -1KO mice did not reveal differences between SIDS blockade and vehicle treatment in functional long-t

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

20 of polyradiculitis, which were diminished by SIDS blockade.

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

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

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

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

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

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

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

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

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

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

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

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

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

34 s the leading candidate ion channel gene for SIDS.

35 s that may have significant implications for SIDS.

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

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

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

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

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

41 on identifying infants at continued risk for SIDS.

42 ogenic substrate in some infants at risk for SIDS.

43 renatal nicotine, creating a higher risk for SIDS.

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

45 mutation as a novel pathogenic substrate for SIDS.

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

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

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

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

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

51 2008 and consisted of 41 infants dying from SIDS (cases), 7 infants with acute death from known caus

52 rol have been reported in infants dying from SIDS.

53 However, SIDS might represent an adaptive mechanism preventing au

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

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

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

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

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

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

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

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

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

63 life threatening and have been implicated in SIDS.

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

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

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

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

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

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

70 basis for further substantial reductions in SIDS incidence rates.

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

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

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

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

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

76 Most SIDS deaths now occur in deprived families.

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

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

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

80 to identify the pathophysiological basis of SIDS.

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

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

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

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

85 o be progress in understanding the causes of SIDS.

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

87 omeostasis and contribute to the etiology of SIDS.

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

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

90 This models features of SIDS.

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

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

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

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

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

96 which may contribute to the pathogenesis of SIDS.

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

98 ge could potentially reduce the high rate of SIDS.

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

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

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

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

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

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

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

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

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

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

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

110 -fetoprotein levels also predict the risk of SIDS.

111 alpha-fetoprotein and the subsequent risk of SIDS.

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

113 haring are associated with decreased risk of SIDS.

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

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

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

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

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

119 No significant impact on SIDS was observed.

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

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

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

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

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

125 partly explain why some women have recurrent SIDS.

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

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

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

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

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

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

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

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

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

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

136 10% to 15% of sudden infant death syndrome (SIDS) cases may stem from channelopathy-mediated lethal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 iomyopathy and sudden infant death syndrome (SIDS).

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

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

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

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

165 esponsible for sudden infant death syndrome (SIDS).

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

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

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

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

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

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

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

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

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

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

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

177 plain the increased vulnerability of boys to SIDS.

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

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

180 and prenatal factors that may contribute to SIDS.

181 cardia during hypoxia that may contribute to SIDS.

182 ate from multiple hypoxic events, leading to SIDS.

183 al chemoreception, which may be pertinent to SIDS.

184 are not likely to be immediate precursors to SIDS.

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

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

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

188 ght make affected infants more vulnerable to SIDS.

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

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