Ontology highlight
ABSTRACT:
PROVIDER: PRJNA733860 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14692600_1.fastq.gz | Fastqsanger.gz | |||
| SRR14692600_2.fastq.gz | Fastqsanger.gz | |||
| SRR14692601_1.fastq.gz | Fastqsanger.gz | |||
| SRR14692601_2.fastq.gz | Fastqsanger.gz | |||
| SRR14692602_1.fastq.gz | Fastqsanger.gz |
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Project description:Injury occurring during critical periods of development may have long-term effects on inflammatory responses. Periventricular leukomalacia (PVL) is the most common cause of cerebral palsy (CP) in preterm infant. Activated leukocytes are the main source of inflammatory cytokines that give rise to white matter damage and CP in preterm infant. Here, we tested the hypothesis that inflammation profiles as pathogenic mediators for the occurrence of PVL in the neonatal period may persist in preterm children with CP at school age.
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Project description:Microbial colonization of the human gastrointestinal tract plays an important role in establishing health and homeostasis. However, the time-dependent and related functional signatures of microbial and human proteins during early colonization of the gut have yet to be determined. Thus, we employed shotgun proteomics via nano-2D-LC-MS/MS to simultaneously monitor microbial and human proteins in fecal samples from a healthy preterm infant during early development. ). All MS/MS spectra were searched against a predicted protein database containing 25 microbial species along with the Human RefSeq2011 genome using the SEQUEST algorithm (Eng et al, 1994), and filtered with DTASelect version 1.9 (Tabb et al, 2002) at the peptide level with standard filters [SEQUEST Xcorrs of at least 1.8 (+1), 2.5 (+2) 3.5 (+3)] organizing identified peptides to their corresponding protein sequences. This study provides the first elucidation of coordinated human and microbial proteins in the infant gut during early development.
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Project description:91 preterm infant gut metaproteomes measured in technical duplicate using an eleven salt pulse 2D-LC-MS/MS method. Samples represent 17 preterm infants over the first several weeks of life, of which 6 preterm infants eventually developed necrotizing enterocolitis.
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Project description:Mammalian feces can be collected non-invasively during field research and provides valuable information on the ecology and evolution of the host individuals. Undigested food objects, genome/metagenome, steroid hormones, and stable isotopes obtained from fecal samples provide evidence on diet, host/symbiont genetics, and physiological status of the individuals. However, proteins in mammalian feces have hardly been studied, which hampers the molecular investigations into the behavior and physiology of the host individuals. Here, we apply mass spectrometry-based proteomics to fecal samples (n = 10) that were collected from infant, juvenile, and adult captive Japanese macaques (Macaca fuscata) to describe the proteomes of the host, food, and intestinal microbes. The results show that fecal proteomics is a useful method to investigate dietary changes along with breastfeeding and weaning, to reveal the organ/tissue and taxonomy of dietary items, and to estimate physiological status inside intestinal tracts. These types of insights are difficult or impossible to obtain through other molecular approaches. Most mammalian species are facing extinction risk and there is an urgent need to obtain knowledge on their ecology and evolution for better conservation strategy. The fecal proteomics framework we present here is easily applicable to wild settings and other mammalian species, and provides direct evidence of their behavior and physiology.
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Project description:Retinopathy of prematurity (ROP), a blinding condition affecting preterm infants, accounts for up to 40% of all childhood blindness worldwide. ROP is an interruption of retinal vascular maturation, which is physiologically complete at full term and thus ongoing at the time of preterm birth. Although ROP demonstrates delayed onset following preterm birth, representing a window for therapeutic intervention, we cannot cure or prevent this disease. The in-utero environment, including placental function, is increasingly recognized for contributions to preterm infant disease risk. Herein, we examine the clinical associations between presence and severity of acute placental inflammation to ROP risk. Using logistic regression, we find a protective relationship between presence and severity of acute placental inflammation and preterm infant development of ROP. This is most significant for infants born in the absence of maternal preeclampsia. Further, we examine the underlying molecular mediators that may inform this protective paradigm. Adopting a candidate approach analyzing proteins with described ROP risk associations, we find that placental HTRA1 and FABP4 protein expression is significantly decreased within placental tissues characterized by acute inflammation. Additionally, HTRA1 and VEGFA demonstrate inverse longitudinal trends within the peripheral circulation for infants born in the presence compared to absence of acute placental inflammation. An agnostic approach, including whole transcriptome and differential methylation placental analysis, identifies novel mediators and pathways that may underly protection. Taken together, these data build on emerging literature showing disparate associations between acute placental inflammation and ROP development within preeclamptic or non-preeclamptic preterm infant populations and identifies novel placental mechanisms that may inform postnatal risk associations in preterm infants.
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