Treatment of Children With Autistic Spectrum Disorder With Autologous Umbilical Cord Blood, a Pilot Study

Author(s):  
2019 ◽  
Vol 09 (01) ◽  
pp. e60-e66
Author(s):  
Neeta Vora ◽  
Joel Parker ◽  
Piotr Mieckowski ◽  
Lisa Smeester ◽  
Rebecca Fry ◽  
...  

Objective To analyze the transcriptomic gene expression of umbilical cord blood leukocytes using RNA-sequencing from preterm birth (PTB) and term birth (TB). Study Design Eight women with spontaneous PTB (sPTB) and eight women with unlabored TB were enrolled prospectively. The sPTB and TB cohorts were matched for maternal age, race, mode of delivery, and fetal sex. Cord blood RNA was extracted and a globin depletion protocol was applied, then sequenced on the Illumina HiSeq 4000. Raw read counts were analyzed with DESeq2 to test for gene expression differences between sPTB and TB. Results 148 genes had significant differential expression (q < 0.01). Cell cycle/metabolism gene expression was significantly higher and immune/inflammatory signaling gene expression significantly lower in the sPTB cohort compared with term. In African American (AA) infants, 18 genes specific to cell signaling, neutrophil activity, and major histocompatibility complex type 1 had lower expression in preterm compared with term cohort; the opposite pattern was seen in non-Hispanic Whites (NHWs). Conclusion Compared with term, preterm fetuses have higher cell cycle/metabolism gene expression, suggesting metabolic focus on growth and development. Immune function gene expression in this pilot study is lower in the sPTB group compared with term and differs in AA compared with NHW infants.


Transfusion ◽  
2010 ◽  
Vol 50 (9) ◽  
pp. 1980-1987 ◽  
Author(s):  
Jessica Sun ◽  
June Allison ◽  
Colleen McLaughlin ◽  
Linda Sledge ◽  
Barbara Waters-Pick ◽  
...  

Pathology ◽  
2017 ◽  
Vol 49 ◽  
pp. S101-S102
Author(s):  
Fatima Vally ◽  
Thomas J. Cade ◽  
Edward Smith ◽  
Steve Holt

2014 ◽  
Vol 13 (3) ◽  
pp. 291-294 ◽  
Author(s):  
Michael Boettcher ◽  
Susanne Goettler ◽  
Georg Eschenburg ◽  
Thorben Kracht ◽  
Philip Kunkel ◽  
...  

Object Patients with spina bifida are particularly vulnerable to developing immunoglobulin E (IgE)–mediated latex sensitization. Even though many risk factors leading to latex allergy in these patients have been described, it is still unclear whether the increased prevalence of latex sensitization is disease associated or due to the procedures used to treat spina bifida. The aim of this study was to assess prenatal latex sensitization in patients with spina bifida by examining IgE levels in umbilical cord blood. Methods Patients with spina bifida and matched healthy infants were recruited from the University Medical Center Hamburg-Eppendorf and Children's Hospital Altona. Latex-specific and total IgE were assessed in umbilical cord blood using ImmunoCAP testing to evaluate the degree of prenatal latex sensitization. Results Twenty-two subjects, 10 with spina bifida and 12 healthy individuals, were included. Subjects were selected after matching for sex, gestational age, weight, parental allergy profile, number of prenatal examinations, and utilization of latex tools during pregnancy (propensity score estimates, p = 0.36). In patients with spina bifida, latex-specific and total IgE levels were significantly higher than those in healthy individuals (p = 0.001). After normalization to total IgE, latex-specific IgE levels were higher, yet not significantly increased (p = 0.085). Conclusions Perinatally, there is a significant augmentation of total and latex-specific IgE in patients with spina bifida. After correcting for total IgE, latex-specific IgE was increased, yet not significantly higher than in matched, healthy controls. This pilot study gives novel insights in the immunological reactions related to spina bifida. The increased latex-specific IgE levels could possibly be associated with the occurrence of a latex allergy in the future.


2018 ◽  
pp. 1-5
Author(s):  
Anthony Codd ◽  
Bryan Burford ◽  
Gabriella Petruso ◽  
Neil Davidson ◽  
Gillian Vance

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