ライフサイエンスコーパス: BPD

1 BPD is associated with significant short-term morbidity,

2 BPD is the most common serious complication experienced

3 BPD was associated with decreased fractional anisotropy

4 dary measures (positive affect scale p = .02 BPD, p = .002 combined group).

5 nalysis and comprised a pooled sample of 154 BPD patients and 150 healthy control subjects.

6 We performed exome sequencing on 50 BPD-affected and unaffected twin pairs using DNA isolate

7 group (F=0.63; p=0.64); however, at week 8, BPD patients on pramipexole demonstrated a significantly

8 al BPD factor that strongly influenced all 9 BPD criteria (standardized path coefficients, 0.53-0.79)

9 sibly disrupts lung development leading to a BPD-like condition with hypoalveolarization, decreased a

10 sitivity and a lower detection limit using a BPD.

11 (benzoporphyrin derivative monoacid ring A; BPD) is increased by the in vivo administration of erlot

12 tes to the decreased serum cholesterol after BPD.

13 sensitivity and cholesterol metabolism after BPD.

14 n obese subjects and reduced to normal after BPD.

15 Seven weeks after BPD, insulin sensitivity had doubled and serum cholester

16 ge (risk ratio, 1.21; 95% CI, 1.10-1.32) and BPD (risk ratio, 1.33; 95% CI, 1.19-1.50).

17 .06), medical NEC (1.57), sepsis (1.43), and BPD (1.30) (P < 0.001).

18 ociation signals for both SCZ (P<10(-7)) and BPD (P=0.029).

19 ne receptor-dependent exacerbation of AA and BPD in mice.

20 ontributing to increased incidence of AA and BPD in the progenies.

21 y SS-exposed mice exhibit exacerbated AA and BPD that is not dependent on the decrease in peroxisome

22 er the observed comorbidity between ADHD and BPD could be due to shared genetic risks.

23 m-based genetic correlation between ADHD and BPD in the full and age-restricted samples (rGfull = .64

24 m-based genetic correlation between ADHD and BPD is substantial, significant, and consistent with the

25 xistence of genetic overlap between ADHD and BPD, with potential differential genetic mechanisms invo

26 sess associations between levels of care and BPD rates.

27 preterm infants completed echocardiogram and BPD assessments at 36 weeks PMA.

28 ciations between SigmaPBDEs and AC, EFW, and BPD at weeks 20-34 and HC at birth.

29 e associations being found with AC, EFW, and BPD at weeks 20-34, and with BW and HC at delivery.

30 cused on the prevention of preterm labor and BPD, novel research aimed at promoting postnatal alveola

31 of NSAID treatment for PDA on mortality and BPD.

32 miR-34a improves the pulmonary phenotype and BPD-associated pulmonary arterial hypertension (PAH) in

33 he genes differentially expressed in SCZ and BPD are concordant in their expression level (q0.01, 53

34 53 genes differentially expressed in SCZ and BPD, respectively.

35 expression and association for both SCZ and BPD.

36 se processes have been implicated in SCZ and BPD.

37 nates with respiratory distress syndrome and BPD.

38 xchange surface area of the lung and causing BPD.

39 Combined BPD or death rates across 116 NICUs varied from 17.7% to

40 Core BPD symptoms, history of childhood traumatization, and p

41 val (95% CI) 0.25-1.55] (P = 0.31) for death/BPD for conventional mechanical ventilation vs high-freq

42 able chromophore (benzoporphyrin derivative, BPD) in the lipid bilayer, and a nanoparticle containing

43 preterm infants who now survive and develop BPD, we hypothesized that risk loci underlying this dise

44 cells of premature infants who later develop BPD or die have impaired mitochondrial bioenergetic capa

45 , HUVECs obtained from infants who developed BPD or died had a lower maximal oxygen consumption rate

46 ypertension increase the odds for developing BPD after preterm birth, and that maternal smoking is st

47 with level IV NICUs, the risk for developing BPD was higher for level II NICUs (odds ratio, 1.23; 95%

48 Using a bioplasmonic paper device (BPD), we demonstrate the selective and sensitive detecti

49 Infants with diagnosed BPD had significantly greater volume of high-signal lung

50 zed clinical trials of adults with diagnosed BPD randomized to psychotherapy exclusively or to a cont

51 PD, six premature patients without diagnosed BPD, and six full-term NICU patients (gestational ages,

52 femur length (FL), and biparietal diameter (BPD) during gestation were measured by ultrasounds.

53 e variant in subjects with bipolar disorder (BPD) and autism spectrum disorder (ASD).

54 tivity disorder (ADHD) and bipolar disorder (BPD) are frequently co-occurring and highly heritable me

55 ), schizophrenia (SCZ) and bipolar disorder (BPD) are of great societal and medical importance, but t

56 Schizophrenia (SCZ) and bipolar disorder (BPD) are severe mental disorders with high heritability.

57 Depression in bipolar disorder (BPD) is challenging to treat.

58 Lastly, deep sequencing of bipolar disorder (BPD) patients and controls identified several rare novel

59 of schizophrenia (SZ) and bipolar disorder (BPD), and use functional magnetic resonance imaging (fMR

60 our groups: schizophrenia, bipolar disorder (BPD), major depression (MD) and unaffected controls.

61 in depressed patients with bipolar disorder (BPD).

62 rol kinase eta (DGKeta) to bipolar disorder (BPD).

63 )) is widely used to treat bipolar disorder (BPD).

64 in euthymic patients with bipolar disorder (BPD); however, the emergence of impulse-control disorder

65 the core of borderline personality disorder (BPD) involve a dysfunction of frontolimbic systems subse

66 Borderline personality disorder (BPD) is a debilitating condition, but several psychother

67 ogenesis of borderline personality disorder (BPD) is complex and not fully understood.

68 gression in borderline personality disorder (BPD) is thought to be mediated through emotion dysregula

69 gulation in borderline personality disorder (BPD), as increased levels of depersonalization, body ima

70 ose without borderline personality disorder (BPD), both health- and work-related life events were key

71 s common in borderline personality disorder (BPD), especially when severe, and the molecular underpin

72 tients with borderline personality disorder (BPD), with impulsivity and emotional dysregulation as co

73 Although borderline personality disorder (BPD)-one of the most common, burdensome, and costly psyc

74 symptoms of borderline personality disorder (BPD).

75 the BRIDGE Bleeding and Platelet Disorders (BPD) collection who carry a TPM4 variant that causes tru

76 Biliopancreatic diversion (BPD) improves insulin sensitivity and decreases serum ch

77 ocedures, such as biliopancreatic diversion (BPD), and a combination of both methods, such as Roux-en

78 l bypass surgery (biliopancreatic diversion [BPD]).

79 d bacterial phosphoinositide-binding domain (BPD) that is found in functionally diverse Type III effe

80 ve cells pre-loaded with the photoactive dye BPD.

81 mary outcome was bronchopulmonary dysplasia (BPD) among survivors.

82 igh incidence of bronchopulmonary dysplasia (BPD) and chronic respiratory morbidity.

83 creased risk for bronchopulmonary dysplasia (BPD) and respiratory disease during early childhood afte

84 of infants with bronchopulmonary dysplasia (BPD) demonstrate impaired alveolar development with larg

85 of Ureaplasma in bronchopulmonary dysplasia (BPD) development, the use of azithromycin for BPD preven

86 the pathology of bronchopulmonary dysplasia (BPD) from one of acute lung injury to a disease of disru

87 e risk of AA and bronchopulmonary dysplasia (BPD) in children and animal models.

88 pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which no specific preventive or th

89 Bronchopulmonary dysplasia (BPD) is a chronic respiratory disease associated with pr

90 Bronchopulmonary dysplasia (BPD) is a common lung disease of premature infants, with

91 Bronchopulmonary dysplasia (BPD) is a prevalent yet poorly characterized pulmonary c

92 Bronchopulmonary dysplasia (BPD) is characterized by lifelong obstructive lung disea

93 Bronchopulmonary dysplasia (BPD) occurs in approximately 40% of infants born at youn

94 Bronchopulmonary dysplasia (BPD) remains a serious morbidity in very low-birth-weigh

95 pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity that often l

96 pathogenesis of bronchopulmonary dysplasia (BPD), a devastating lung disease in preterm infants, inc

97 rders, including bronchopulmonary dysplasia (BPD), a respiratory condition that affects preterm infan

98 erm infants with bronchopulmonary dysplasia (BPD), but whether early signs of pulmonary vascular dise

99 comes, including bronchopulmonary dysplasia (BPD), in preterm infants.

100 Bronchopulmonary dysplasia (BPD), the main consequence of prematurity, has a signifi

101 ease the risk of bronchopulmonary dysplasia (BPD)-a developmental lung condition primarily seen in ne

102 e of infancy, or bronchopulmonary dysplasia (BPD).

103 y increased with bronchopulmonary dysplasia (BPD; 1.77), whereas total cost increased with surgical N

104 ly medicated, depressed patients with either BPD (n = 41) or major depressive disorder (n = 22).

105 therapies that prevent or treat established BPD.

106 op effective strategies to treat established BPD.

107 reward-dependent decision making in euthymic BPD patients pre- and post 8 weeks of treatment with pra

108 ated decision-making performance in euthymic BPD.

109 ges were used for the first time to evaluate BPD-related brain abnormalities from resting functional

110 bipolar I disorder with psychotic features [BPD+; N = 269].

111 PD) development, the use of azithromycin for BPD prevention, and the factors influencing azithromycin

112 ent currently fulfilling DSM-IV criteria for BPD (cBPD) (n = 23), a patient in remission for 2 years

113 ogical nature of the individual criteria for BPD as defined by the DSM-IV has not been explored.

114 The 9 criteria for BPD assessed by the Structured Interview for DSM-IV Pers

115 analyzed to identify early risk factors for BPD and late PH.

116 ts, the two major perceived risk factors for BPD were prematurity of <28 weeks and high oxygen requir

117 s used to assess individual risk factors for BPD.

118 th a twofold (P = 0.04) increase in odds for BPD.

119 Only 38% of NICUs had a protocol for BPD prevention and 47% routinely tested for Ureaplasma.

120 o assess the efficacy of psychotherapies for BPD populations.

121 ilation course, the adjusted odds ratios for BPD ranged from 1.88 (95% CI, 1.54-2.31) among infants w

122 ul tool to identify infants at high risk for BPD and PH.

123 reterm infants were associated with risk for BPD or death before 36 weeks postmenstrual age.

124 ction was associated with increased risk for BPD.

125 nd represents a novel therapeutic target for BPD.

126 f 210]) and postnatal corticosteroid use for BPD (41.0% [91 of 222] vs 41.5% [95 of 229]) and the mea

127 Thirty-four BPD patients completed both assessments (18 placebo and

128 dules were also built from RNA-seq data from BPD cases or from MD cases but were not preserved when u

129 use it effectively shields newborn mice from BPD, IL-1Ra emerges as a promising treatment for a curre

130 The meta-analysis between the full BPD sample identified two genome-wide significant (prs70

131 ominated by 1 highly heritable (55%) general BPD factor that strongly influenced all 9 BPD criteria (

132 teria derive from 1 highly heritable general BPD factor, whereas the environmental influences were mo

133 onventional mechanical ventilation died/ had BPD compared with 43 patients (53.8%) in the high-freque

134 apeutic option to prevent or ameliorate HALI/BPD in neonates.

135 ivors, 1695 (59.1%) were diagnosed as having BPD, 856 (29.9%) received supplemental oxygen at dischar

136 Compared with HC, BPD patients showed relatively increased activation of t

137 In BPD, PFC and ACC MAO-A VT were positively correlated wit

138 but its potential to induce abnormalities in BPD patients is unknown.

139 hat structural and functional abnormality in BPD involves both temporolimbic and frontomedial structu

140 shold showed a convergence of alterations in BPD patients in genual and perigenual structures, with f

141 physical pain suggest poor body awareness in BPD.

142 d that impairment of alveolar development in BPD results in a decrease in both D(M) and Vc components

143 etwork of emotion processing is disrupted in BPD.

144 upport the hypothesis that CC dysfunction in BPD and SZ reflects a continuum of deficits that cuts ac

145 Processing of negative emotions in BPD might be subserved by an abnormal reciprocal relatio

146 Cross-brain information flow in BPD was examined from May 25, 2012, to December 4, 2015,

147 tic strategies for pulmonary hypertension in BPD are based on small observational studies with poorly

148 and G proteins, have long been implicated in BPD etiology; however, recent genetic studies link BPD t

149 ify with high confidence genes implicated in BPD, thereby providing important insights into its biolo

150 ted pulmonary arterial hypertension (PAH) in BPD mouse models, which, conversely, is worsened by miR-

151 ctrum of pulmonary vascular disease (PVD) in BPD rather than a simple question of whether or not pulm

152 As such, in BPD, a potential role for variants near CRP gene is prop

153 eroid pregnenolone on depressive symptoms in BPD was examined.

154 The wide variability in BPD occurrence across hospitals could offer insights int

155 study supports the role of rare variants in BPD, in contrast with the role of common variants target

156 Secondary outcomes included BPD severity, postnatal corticosteroid use, respiratory

157 ltiple indicators of BPD severity, including BPD symptomatology, mood symptoms, suicidality, and neur

158 Early PH was a risk factor for increased BPD severity (relative risk, 1.12; 95% confidence interv

159 ost of the genetic effects on the individual BPD criteria derive from 1 highly heritable general BPD

160 and survival of extremely premature infants, BPD remains a major clinical problem.

161 netic mechanisms involved in early and later BPD onset.

162 iology; however, recent genetic studies link BPD to other proteins, particularly ion channels.

163 tofrontal cortex coupling were shown in male BPD patients, while in female patients trait anger posit

164 x group interaction was found in which male BPD patients revealed higher activity in the left amygda

165 y, in severe BPD subjects (n = 14), moderate BPD subjects (n = 14), subjects with a major depressive

166 PFC and ACC MAO-A VT compared with moderate BPD, MDE, and healthy control subjects (multivariate ana

167 a pivotal role for IL-1alpha/beta in murine BPD and an involvement for MIP (macrophage inflammatory

168 receptor antagonist (IL-1Ra) prevents murine BPD.

169 After irradiation at 690 nm, BPD disrupted the endosomal membranes and delivered the

170 are consistent with the conceptualization of BPD as an emotion dysregulation disorder.

171 n our understanding of PVD in the context of BPD, including universally accepted definitions, approac

172 n addition, at least some neural deficits of BPD may be more reversible than is currently assumed for

173 isease is associated with the development of BPD and with late PH in preterm infants.

174 ssociated with the subsequent development of BPD or PH at 36 weeks post-menstrual age (PMA) is unknow

175 ome is a key mechanism in the development of BPD, and represents a novel therapeutic target for BPD.

176 ls with unknown impact on the development of BPD.

177 masome is associated with the development of BPD.

178 failure is predictive of the development of BPD.

179 during gestation blocked the development of BPD.

180 Of the 14396 individuals with a diagnosis of BPD, 6671 were included in the cohort, with 2148 prescri

181 e investigated the early and late effects of BPD on plasma BA levels, composition, and markers of BA

182 solidate current knowledge of the effects of BPD that are recognized at specific stages of life, incl

183 f erlotinib; nevertheless, this elevation of BPD levels only partially accounts for the benefit of er

184 s11265269 was identified as a risk factor of BPD (OR 1.8, p = 5.3 x 10(-5)), independently of the rob

185 mbic brain regions are a hallmark feature of BPD and therefore are consistent with the conceptualizat

186 or a core diagnostic and clinical feature of BPD.

187 ppear to be associated with core features of BPD.

188 VT is associated with multiple indicators of BPD severity, including BPD symptomatology, mood symptom

189 reness in psychotherapeutic interventions of BPD.

190 nosis phenotype, a clinical manifestation of BPD.

191 Using a neonatal mouse model of BPD, we show that hyperoxia increases activity and expre

192 stantially up-regulated in a murine model of BPD.

193 ation of mechanical ventilation, the odds of BPD were only increased among infants exposed to 4 or mo

194 nfants, or 44.8%, met the primary outcome of BPD or death prior to 36 weeks.

195 A combined outcome of BPD or mortality prior to 36 weeks was used.

196 The pathogenesis of BPD is multifactorial, but all triggers cause pulmonary

197 tions play a key role in the pathogenesis of BPD.

198 led to new insights into the pathogenesis of BPD; however, many unique issues persist regarding our u

199 es in Ureaplasma treatment and prevention of BPD highlight the need for further azithromycin evaluati

200 applied to determine risk-adjusted rates of BPD across hospitals and assess associations between lev

201 Rates of BPD have not improved over the past two decades; nor hav

202 ipitant for suicidal behavior, regardless of BPD comorbidity.

203 d plasma levels of CRP predicted the risk of BPD (OR 3.4, p = 2.9 x 10(-4)) and the SNP rs3093059 ass

204 d with a progressive increase in the risk of BPD and use of supplemental oxygen at discharge.

205 from the first week of life and the risk of BPD were assessed.

206 unanticipated results regarding the role of BPD and study limitations, these findings require replic

207 clinical data demonstrate that survivors of BPD have long-standing deficits in lung function and may

208 ty, and both cellular and genetic targets of BPD: GPCRs, G proteins, and ion channels.

209 To further elucidate neural underpinnings of BPD, the present meta-analysis summarizes functional neu

210 uals with BPD (5167 thereof with early-onset BPD), and 21,363 typically developing controls.

211 ratio, 0.73; 95% CI, 0.43-1.13; P = .18), or BPD (odds ratio, 1.01; 95% CI, 0.73-1.45; P = .94) in su

212 sociated with an increased risk for death or BPD at 36 weeks' postmenstrual age (risk ratio, 1.21; 95

213 tnatal CMV on the combined risk for death or BPD at 36 weeks' postmenstrual age.

214 The primary outcome was death or BPD at 36 weeks' postmenstrual age.

215 NSAID treatment and the odds of mortality or BPD (odds ratio, 0.94; 95% CI, 0.70-1.25; P = .69), mort

216 ence in the combined outcome of mortality or BPD between the 2 ventilation groups in prenatally diagn

217 revealed that after 8 weeks on pramipexole, BPD patients attended more readily to feedback related t

218 We precipitated BPD by perinatal inflammation (lipopolysaccharide inject

219 losure in improving mortality and preventing BPD is unclear.

220 ing mechanisms and the relevance to putative BPD targets are unknown.

221 ased regionalization of NICU care may reduce BPD among VLBW infants.

222 azithromycin safety and efficacy in reducing BPD rates.

223 m brain tissues (cingulate cortex) from SCZ, BPD and control subjects, and identified differentially

224 Overall, our study is the first to sequence BPD exomes from newborn blood spot samples and identify

225 Severe BPD was associated with greater PFC and ACC MAO-A VT com

226 Rates for severe BPD (26.6% [55 of 207] vs 20.5% [43 of 210]) and postnat

227 ls in PFC and ACC would be highest in severe BPD and would correlate with symptom magnitude.

228 -A VT), an index of MAO-A density, in severe BPD subjects (n = 14), moderate BPD subjects (n = 14), s

229 in the odds of mortality or moderate/severe BPD among similar preterm infants born at 28 weeks or yo

230 DA in reducing mortality and moderate/severe BPD at 36 weeks postmenstrual age.

231 lification, only appeared in the most severe BPD cases, although cystic appearance did increase with

232 e, and the molecular underpinnings of severe BPD are largely unknown.

233 osite outcome was death, moderate, or severe BPD at 36 weeks postmenstrual age.

234 Contrary to early studies, BPD patients showed less activation than control subject

235 Compared with healthy control subjects, BPD patients demonstrated greater activation within the

236 We hypothesized that BPD cases with an early age of onset (</=21 years old) w

237 targets of miR34a, is able to ameliorate the BPD pulmonary and PAH phenotypes.

238 e D(M)/Vc ratio would not differ between the BPD and FT groups.

239 Moreover, NMR studies reveal that the BPD of the newly identified Vibrio parahaemolyticus Type

240 ese findings suggest that in addition to the BPD diagnosis at 36 weeks, other factors modulate late r

241 Restricting the analyses to BPD cases with an early onset yielded one genome-wide si

242 o identify gene loci predisposing infants to BPD.

243 exhibiting levels of decline intermediate to BPD+ and SAD.

244 er revealed a continuum of deficits in which BPD showed intermediate levels of CC relative to control

245 Adults (n=80) with BPD, depressed mood state, were randomized to pregnenolo

246 obiology (e.g., analysis of adolescents with BPD; inclusion of clinical control groups) is missing.

247 leotide polymorphisms (SNPs) associated with BPD were genotyped in both Finnish (n = 555) and non-Fin

248 d birth weight z-scores were associated with BPD.

249 ically significant inverse associations with BPD, HC, and BW when using maternal serum, and for AC an

250 ing rs3093059, had nominal associations with BPD.

251 Twenty-two percent of infants diagnosed with BPD and 34% of preterm infants without BPD had no clinic

252 Length of stay increased with BPD (2.92) and NEC (surgical, 2.04; medical, 1.28) (P <

253 individuals with ADHD, 9650 individuals with BPD (5167 thereof with early-onset BPD), and 21,363 typi

254 he84Ser was only present in individuals with BPD and leads to marked increase monoamine transport in

255 increased the odds of having an infant with BPD by twofold (P = 0.02).

256 y length and did not differ for infants with BPD and FT subjects.

257 ncreasing body length; however, infants with BPD had significantly lower D(M) and Vc than FT subjects

258 ur findings are consistent with infants with BPD having impaired alveolar development with fewer but

259 -term respiratory morbidity for infants with BPD is a priority.

260 whether the decreased DL(CO) in infants with BPD results from a reduction in both components of DL(CO

261 tor to poor outcomes in preterm infants with BPD.

262 In the aggression phase, men with BPD exhibited higher activity in the lateral orbitofront

263 Twenty adolescent patients with BPD (aged 14-18 years), 20 healthy, and 20 clinical cont

264 ay matter abnormalities in 263 patients with BPD and 278 HC were analyzed.

265 tral stimuli in a total of 281 patients with BPD and 293 healthy control subjects (HC) were included.

266 hirty-three female and 23 male patients with BPD and 30 healthy women and 26 healthy men participated

267 improve depressive symptoms in patients with BPD and can be safely administered.

268 imaging data were acquired in patients with BPD and in an equal number of matched control subjects (

269 adjustment of behavior in male patients with BPD despite their efforts at control.

270 the respiratory problems that patients with BPD experience.

271 Patients with BPD had significantly reduced mean HEP amplitudes compar

272 aggression in female and male patients with BPD have been widely missing on the behavioral and parti

273 The analysis of patients with BPD in remission suggests an improvement in cortical rep

274 nteers, and 17 medication-free patients with BPD in remission.

275 ntrols, 24 recent (<1 y) onset patients with BPD Type I with psychotic features, and 70 recent onset

276 stigated in 34 medication-free patients with BPD, 31 healthy volunteers, and 17 medication-free patie

277 ignificant differences between patients with BPD, premature patients without BPD, and full-term contr

278 during quiet breathing in six patients with BPD, six premature patients without diagnosed BPD, and s

279 rocessing of bodily signals in patients with BPD, which appear to be associated with core features of

280 ioral and clinical symptoms in patients with BPD.

281 are nonsynonymous mutations in patients with BPD.

282 on is increased in tissue from patients with BPD.

283 connectivity was found in male patients with BPD.

284 normalities may occur in adult patients with BPD.

285 e interaction difficulties among people with BPD.

286 D PARTICIPANTS: Multivariate twin study with BPD criteria assessed by personal interview within a gen

287 increasing numbers of preterm survivors with BPD, improving the current state of knowledge of long-te

288 events to suicidal behavior among those with BPD was more complex.

289 noxide (DL(CO)) in infants and toddlers with BPD compared with healthy controls born at full term (FT

290 2%; P = 0.020) and premature infants without BPD (8.2 +/- 6.4%; P = 0.026).

291 with BPD and 34% of preterm infants without BPD had no clinical signs of late respiratory disease du

292 atients with BPD, premature patients without BPD, and full-term control subjects.

293 Survival without BPD at 36 weeks' gestational age.

294 be safe but did not improve survival without BPD at 36 weeks' PMA or respiratory and neurodevelopment

295 Survival without BPD at 36 weeks' PMA was similar between the placebo and

296 ary outcome was the rate of survival without BPD at 36 weeks' postmenstrual age (PMA).

297 LISA did not increase survival without BPD but was associated with increased survival without m

298 to 14 improves the rate of survival without BPD.

299 o received LISA, 72 (67.3%) survived without BPD compared with 61 (58.7%) of those in the control gro

300 ith HUVECs from infants who survived without BPD, HUVECs obtained from infants who developed BPD or d