Early diagnosis is vital for the reduction of mortality caused by neonatal infections. Since TNF-α can be used as a marker for the early diagnosis, the detection of TNF-α with high sensitivity and specificity has great clinical significance. Herein, a highly sensitive and reusable electrochemical sensor was fabricated. Due to the high specificity of aptamers, TNF-α could be accurately detected from five similar cytokines, even from serum samples. In addition, Au nanoparticles (AuNPs) with a high surface area were able to combine a large number of doxorubicin hydrochloride (DOXh), which made the sensor have a high sensitivity. The sensor had a good linear relationship with TNF-α concentration in the range from 1 to 1 × 10⁴ pg/mL and the lowest detection limit is 0.7 pg/mL. More important was that the sensor could be reused 6 times by a crafty use of chain replacement reaction. Meanwhile, the detection time and cost were greatly reduced. Thus, we believe that these advantages of higher specificity and sensitivity, lower cost, and shorter detection time will provide a stronger potential for early diagnosis of neonatal infections in clinical applications.

Xenon (Xe) is an inert, colorless and odorless heavy gas and has many biological functions. However, little is known about whether and how Xe can modulate hypoxic-ischemic brain damage (HIBD) in neonatal rats. This study employed a neonatal rat model to explore the potential effect of Xe on neuron autophagy and the severity of HIBD. Neonatal Sprague–Dawley rats were subjected to HIBD, randomized and treated with Xe or mild hypothermia (at 32 °C) for 3 h. The degrees of HIBD, neuron autophagy and the neuronal functions in some neonates from each group were tested by histopathology, immunochemistry, transmission electron microscopy, western blot, open-field and Trapeze tests at 3 and 28 days post-induction of HIBD, respectively. Compared with the Sham group, hypoxic-ischemia caused larger volumes of cerebral infarction and severe brain damage, and increased autophagosome formation and Beclin-1 and microtubule-associated protein 1A/1B-light chain 3 class II (LC3-II) expression in the brain of rats, accompanied by the defect in neuronal functions. In contrast, treatment with Xe and/or hypothermia significantly reduced infarct volumes and ameliorated neurological defects in the HIBD rats, particularly for the combination of Xe and hypothermia. Xe significantly mitigated the relative levels of Beclin-1 and LC3-II expression and autophagosome formation induced by HIBD in rats. Xe acted as a neuroprotective factor against HIBD, possibly by inhibiting the hypoxia-induced neuron autophagy in rats.

The main causes of abnormal white matter development (periventricular leukomalacia) in premature infants are perinatal inflammation and the consequent oxidant/antioxidant imbalance in oligodendrocyte precursor cells (OPCs); however, the underlying mechanisms remain largely unclear. In this work, a rat model of prenatal inflammation was used to examine the mechanism by which artemisinin (ART) protects against white matter dysplasia. We established a primary OPC model and rat model of perinatal inflammation. ART was identified from the FDA-approved medicinal chemical library to be beneficial for treating OPC inflammation in model systems. Based on bioinformatics analysis of protein interactions and molecular docking analysis, we further identified the possible targets of ART and evaluated its specific effects and the underlying molecular mechanisms in vivo and in vitro. Following inflammatory stimulation, ART strongly promoted the maturation of OPCs and the development of white matter in the brain. A Cellular thermal shift assay (CETSA) demonstrated that interleukin-1 receptor-associated kinase-4 (IRAK-4) and interleukin-1 receptor-associated kinase-1 (IRAK-1) may be targets of ART, which was consistent with the findings from molecular modelling with Autodock software. Experiments conducted both in vivo and in vitro demonstrated the activation of the IRAK-4/IRAK-1/nuclear factor kappa-B (NF-κB) pathway and the production of inflammatory factors (IL-1β, IL-6, and TNF-α) in OPCs were greatly suppressed in the group treated with ART compared to the lipopolysaccharide (LPS)-treated group. Moreover, ART dramatically decreased reactive oxygen species (ROS) levels in OPCs while increasing nuclear factor e2-related factor 2 (Nrf2) levels. Our findings suggest that ART can significantly reduce OPC perinatal inflammation and consequent oxidative stress. The targeted inhibition of IRAK-4 and IRAK-1 by ART may be a potential therapeutic strategy for alleviating abnormalities in white matter development in premature newborns.

Neuronal development in newborns is often constrained by perinatal inflammation, with limited research available on the pathogenesis and treatment strategies for this condition. This study aimed to investigate the neuroprotective effects of Embelin in mitigating perinatal inflammation‐induced neuronal development limitations by targeting 5‐lipoxygenase (5‐LOX) and reducing oxidative stress and ferroptosis. This study utilized in vivo and in vitro inflammation models to assess the therapeutic potential of Embelin, a small molecule drug from the FDA compound library. Using Autodock software and surface plasmon resonance detection technology, 5‐LOX was identified as the molecular target of Embelin. Neuronal ferroptosis and oxidative stress were analyzed in rat models and PC12 cells treated with lipopolysaccharide (LPS) and Embelin. Biochemical assays, immunofluorescence staining, and western blotting were performed to quantify protein expression and oxidative stress markers. Embelin, along with the 5‐LOX inhibitor Zileuton and 5‐LOX mRNA silencing, significantly inhibited 5‐LOX expression in neurons. Conversely, overexpressed 5‐LOX promoted ferroptosis, and this effect could be inhibited by Embelin. These interventions reduced oxidative stress, suppressed ferroptosis, and promoted normal neuronal development in the cerebral cortex and hippocampus. The findings highlight Embelin's ability to specifically target and mitigate 5‐LOX‐induced ferroptosis, facilitating recovery from perinatal inflammation‐induced neurodevelopmental deficits. Embelin demonstrates significant neuroprotective potential by inhibiting 5‐LOX‐mediated ferroptosis and oxidative stress, offering a promising therapeutic strategy for perinatal brain injury and related neurodevelopmental disorders.

Congenital nephrotic syndrome (CNS), which is defined as heavy proteinuria, hypoalbuminemia, hyperlipidemia and edema, is most caused by monogenic defects in structural proteins of the glomerular filtration barrier in the kidneys. 22q11.2 duplication syndrome was a chromosomal disease with variable clinical featuresranging from normal to mental retardation and with congenital defects. Co-occurrence of two genetic disorders in a single patient is rare. The proband was born at 36 weeks of gestational age spontaneously and weighed 2350 g at birth. Six days after birth, the proband was admitted to our hospital due to fever of 38.5 °C lasting for 6 h. Physical examination at admission time showed dysmorphic features of hypertelorism, palpebral edema, broad nose bridge, upturned nose, dysmorphic auricle, long philtrum, and a thin upper lip. Additionally, we found left wrist drop and bilateral strephexopodia, bilateral knee joint flexion contracture in this patient. A series of indicators were detected and showed abnormalities. Albumin was used to remit the hypoproteinemia and edema. However, the parents refused to accept further therapy and the boy died at age 3 months due to cachexy. To confirm the pathogenesis, genetic analysis were performed and revealed two mutations of NPHS1 gene: Exon18: c.2386G > C; p. (Gly796Arg) inherited from mother, and intron24: c.3286 + 5G > A; p.? inherited from father. And he also had a 22q11.2 duplication which was inherited from his mild affected mother. The pathogenesis of the intronic mutation has been further identified that it can defect alternative splicing of NPHS1. We present a patient who was caught in congenital nephrotic syndrome and 22q11.2 duplication syndrome simultaneously, emphasizing the importance of new sequencing technology on diagnosis of different genetic disorders.

Objective: This study aimed to investigate the correlation between serum 25-hydroxyvitamin D (25(OH)D) levels and retinopathy of prematurity (ROP) in premature infants one month after birth.Methods: Preterm infants (gestational age <32 weeks) admitted to the Affiliated Hospital of Qingdao University from 2017 to 2022 were divided into ROP and non-ROP groups based on ROP occurrence any stage. Serum 25(OH)D levels and clinical data were compared between the two groups at 1 month after birth, and the relationship between vitamin D levels and ROP was analyzed.Results: Among the 217 premature infants included, 55 (25.35%) were in the ROP group, and 162 (74.65%) were in the non-ROP group. The ROP group had lower gestational age and birth weight, longer invasive ventilation (IV), non-invasive ventilation (NIV), and oxygen therapy times compared to the non-ROP group. Apgar scores, cesarean delivery, and antenatal steroids ratios were lower in the ROP group, while sepsis and pulmonary surfactant utilization ratios were higher (all p < 0.05). Significant differences in serum 25-(OH)D levels were observed among children in the non-ROP group (14.20 ± 5.07 ng/ml), ROP treated group (7.891 ± 1.878 ng/ml), and untreated group (12.168 ± 4.354 ng/ml) (p < 0.001). Multivariate regression analysis identified antenatal steroids as protective factors and lower birth weight, serum 25-(OH)D levels, long-term invasive mechanical ventilation, and sepsis as independent risk factors for ROP in premature infants.Conclusion: Vitamin D, lower birth weight, long-term invasive mechanical ventilation, and sepsis were associated with incidence of ROP in preterm infants. Vitamin D was associated with the severity of ROP, emphasizing the importance of prudent vitamin D supplementation and regular monitoring of serum 25-(OH)D levels.