Fetal magnetic resonance imaging is well accepted as secondary image tool for the evaluation of pathologies affecting the fetal brain as detected on prenatal ultrasonography. Significantly, fewer articles have focused on the fetal spinal canal and its contents. Many malformations and pathologies involving the spinal canal and cord may however have a significant impact on the quality of life. In addition, anomalies of the spinal cord may affect the development of the fetal brain or may be part of a more extensive malformation that may also affect the major thoracic and abdominal organs. A thorough knowledge of the nor- mal and abnormal development of the spinal column and its contents is necessary to diagnose and understand the encountered findings. In the current review the value of fetal magnetic resonance imaging of the spinal column and cord is discussed. The most frequently encountered malformations will be presented and discussed in the context of the most relevant embryological processes.
To estimate the diagnostic accuracy of electronic fetal heart rate abnormalities in the identification of neonates with encephalopathy treated with whole-body hypothermia.
A transcranial photoacoustic (PA) imaging can non-invasively quantify graded oxyhemoglobin (HbO 2 ) saturation changes at the superior sagittal sinus (SSS) and brain tissue through intact skull and scalp of large animal models and humans, which strongly implies its potential to address urgent clinical problems to identify brain distress in patients. However, effective signal processing to compensate for substantial transcranial signal attenuation is still desired to secure high imaging contrast. In this study, we present a spectral system denoising scheme for the spectroscopic PA neuroimaging using in vivo neonatal piglets, which well resembles the skull thickness and neurophysiology of term human neonates.
Abstract Introduction The purpose of this study was to evaluate whether there are additional benefits of 17‐hydroxyprogesterone caproate (17‐ OHPC ) supplementation in preventing recurrent spontaneous preterm birth in women with a prophylactic cerclage. Material and methods Electronic databases (MEDLINE, Scopus, ClinicalTrials.gov, PROSPERO, EMBASE, Scielo and the Cochrane Central Register of Controlled Trials) were searched for studies published before June 2018. Keywords included “preterm birth”, “prophylactic cerclage”, “history‐indicated cerclage”, “pregnancy” and “17‐hydroxyprogesterone caproate”. Studies comparing history‐indicated cerclage alone with cerclage+17‐ OHPC were included. The primary outcome measure was preterm birth at <24 weeks of gestation. Secondary outcome measures include preterm birth at <28 weeks, <32 weeks and <37 weeks of gestation, respiratory distress syndrome, necrotizing enterocolitis, fetal birthweight, neonatal intensive care unit stay, mean gestational age at delivery, fetal/neonatal death, neurological morbidity (intraventricular hemorrhage plus periventricular leukomalacia), neonatal sepsis and a composite of severe neonatal morbidity. Severe neonatal morbidity was defined as a composite measure of periventricular leukomalacia, intraventricular hemorrhage (grades III and IV), necrotizing enterocolitis or respiratory distress syndrome. Meta‐analysis was performed using the random‐effects model of DerSimonian and Laird. Risk of bias and quality assessment were performed using the ROBINS‐I and GRADE tools, respectively. PROSPERO Registration Number: CRD42018094559. Results Five studies met the inclusion criteria and were included in the final analysis. Of the 546 women, 357 (75%) received history‐indicated cerclage alone and 189 (35%) received adjuvant 17‐OHPC. The composite endpoint, severe neonatal morbidity, was present in 84 of 1515 neonates. Though there was a trend toward a reduced risk of preterm birth, the summary estimate of effect was not statistically significant when comparing cerclage alone with cerclage+17‐OHPC at <24 weeks (relative risk [RR] .86, 95% confidence interval [CI] .45‐1.65). Similarly, we found no differences in preterm birth at <37 weeks (RR .90, 95% CI .70‐1.17) and <28 weeks (RR .85, 95% CI .54‐1.32) when comparing cerclage alone with cerclage+17‐OHPC. There were no differences in fetal birthweight, respiratory distress syndrome or necrotizing enterocolitis comparing cerclage alone with cerclage+17‐OHPC. Conclusions Intramuscular 17‐OHPC in combination with prophylactic cerclage in women with prior preterm birth had no synergistic effect in reducing spontaneous recurrent preterm birth or improving perinatal outcomes.
Necrostatin-1 inhibits receptor-interacting protein (RIP)-1 kinase and programmed necrosis and is neuroprotective in adult rodent models. Owing to the prominence of necrosis and continuum cell death in neonatal hypoxia-ischemia (HI), we tested whether necrostatin was neuroprotective in the developing brain. Postnatal day (P)7 mice were exposed to HI and injected intracerebroventricularly with 0.1 μL of 80 μmol necrostatin, Nec-1, 5-(1H-Indol-3-ylmethyl)-(2-thio-3-methyl) hydantoin, or vehicle. Necrostatin significantly decreased injury in the forebrain and thalamus at P11 and P28. There was specific neuroprotection in necrostatin-treated males. Necrostatin treatment decreased necrotic cell death and increased apoptotic cell death. Hypoxia-ischemia enforced RIP1-RIP3 complex formation and inhibited RIP3-FADD (Fas-associated protein with death domain) interaction, and these effects were blocked by necrostatin. Necrostatin also decreased HI-induced oxidative damage to proteins and attenuated markers of inflammation coincidental with decreased nuclear factor-κB and caspase 1 activation, and FLIP ((Fas-associated death-domain-like IL-1β-converting enzyme)-inhibitory protein) gene and protein expression. In this model of severe neonatal brain injury, we find that cellular necrosis can be managed therapeutically by a single dose of necrostatin, administered after HI, possibly by interrupting RIP1-RIP3-driven oxidative injury and inflammation. The effects of necrostatin treatment after HI reflect the importance of necrosis in the delayed phases of neonatal brain injury and represent a new direction for therapy of neonatal HI.
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