Ferroptosis is an oxidative damage-related, iron-dependent regulated cell death with intracellular lipid peroxide accumulation, which is associated with many physiological and pathological processes. It exhibits unique features that are morphologically, biochemically, and immunologically distinct from other regulated cell death forms. Ferroptosis is regulated by iron metabolism, lipid metabolism, anti-oxidant defense systems, as well as various signal pathways. Hypoxia, which is found in a group of physiological and pathological conditions, can affect multiple cellular functions by activation of the hypoxia-inducible factor (HIF) signaling and other mechanisms. Emerging evidence demonstrated that hypoxia regulates ferroptosis in certain cell types and conditions. In this review, we summarize the basic mechanisms and regulations of ferroptosis and hypoxia, as well as the regulation of ferroptosis by hypoxia in physiological and pathological conditions, which may contribute to the numerous diseases therapies.

/pdf/ferroptosis-regulated-by-hypoxia-in-cells-g9jx9ks7.pdf

Ferroptosis Regulated by Hypoxia in Cells

Manganese dioxide (MnO2)-based nanostructures have emerged as promising tumour microenvironment (TME) responsive platforms. Herein, we used a one-pot reaction to prepare MnO2 nanostructures with Pt(iv) prodrugs as redox- (and thus TME-) responsive theranostics for cancer therapy, in which the Pt(iv) complexes act as prodrugs of cisplatin (Pt(ii)), a clinical chemotherapeutic drug. The cytotoxicity of these MnO2–Pt(iv) probes was evaluated in two and three dimensional (2D and 3D) A549 cell models and found to be as effective as active drug cisplatin in 3D models. Moreover, MnO2–Pt(iv) nanoparticles exhibited strong off/ON magnetic resonance (MR) contrast in response to reducing agents, with the longitudinal relaxivity (r1) increasing 136-fold upon treatment with ascorbic acid. This off/ON MR switch was also observed in (2D and 3D) cells in vitro. In vivo MRI experiments revealed that the nanostructures induce a strong and long-lasting T1 signal enhancement upon intratumoral injection in A549 tumour-bearing mice. These results show the potential of MnO2–Pt(iv) NPs as redox responsive MR theranostics for cancer therapy.

/pdf/redox-double-switch-cancer-theranostics-through-pt-iv-1b0msl01.pdf

Redox double-switch cancer theranostics through Pt(iv) functionalised manganese dioxide nanostructures

Key Points Question Can the artificial neural network (ANN) predict risk for neonatal metabolic bone disease (MBD) in the prenatal and postnatal periods? Findings In this diagnostic study of 10 801 participants, among 5 ANN models with different exposures, the models including significant prenatal and postnatal factors and postnatal factors alone had the best ability to predict infants at risk for MBD. Meaning These findings suggest that the ANN, using prenatal and postnatal factors, could be an efficient tool for identifying neonates at risk for BMD.

https://jamanetwork.com/journals/jamanetworkopen/articlepdf/2800708/jiang_2023_oi_221476_1673621643.32259.pdf

Artificial Neural Network Modeling to Predict Neonatal Metabolic Bone Disease in the Prenatal and Postnatal Periods

Bone health starts with maternal health and nutrition, which influences bone mass and density already in utero. The mechanisms underlying the effect of the intrauterine environment on bone health are partly unknown but certainly include the ‘foetal programming’ of oxidative stress and endocrine systems, which influence later skeletal growth and development. With this narrative review, we describe the current evidence for identifying patients with risk factors for developing osteopenia, today’s management of these populations, and screening and prevention programs based on gestational age, weight, and morbidity. Challenges for bone health prevention include the need for new technologies that are specific and applicable to pregnant women, the foetus, and, later, the newborn. Radiofrequency ultrasound spectrometry (REMS) has proven to be a useful tool in the assessment of bone mineral density (BMD) in pregnant women. Few studies have reported that transmission ultrasound can also be used to assess BMD in newborns. The advantages of this technology in the foetus and newborn are the absence of ionising radiation, ease of use, and, above all, the possibility of performing longitudinal studies from intrauterine to extrauterine life. The use of these technologies already in the intrauterine period could help prevent associated diseases, such as osteoporosis and osteopenia, which are characterised by a reduction in bone mass and degeneration of bone structure and lead to an increased risk of fractures in adulthood with considerable social repercussions for the related direct and indirect costs. 

Prenatal and Neonatal Bone Health: Updated Review on Early Identification of Newborns at High Risk for Osteopenia

Abstract Objective Vitamin D deficiency in pregnant women is of special concern as mother is the only source of vitamin D for the developing fetus, and maternal hypovitaminosis D has been implicated in a number of maternal and neonatal adverse outcomes. The objective of this study was to assess the association of maternal circulating 25-hydroxy vitamin D3 [25(OH)D] concentration with cord blood 25(OH)D and adverse birth and neonatal outcomes. Methods This prospective cohort study was conducted in Mahatma Gandhi Medical College and Research Institute (MGMCRI) from January 2020 to December 2020. 121 babies born to mothers with singleton pregnancy tested for serum 25(OH)D level on admission for safe confinement were included in the study and cord blood of the babies were sampled for 25(OH)D. Based on the maternal 25(OH)D level, babies were categorized as those born to mothers with sufficient vitamin D level and those born to mothers with hypovitaminosis D (deficient/insufficient) and primary and secondary outcome was compared between two groups. Results Maternal and cord blood hypovitaminosis D was observed in 65% of mothers and 68.6% of babies, respectively. Maternal vitamin D level was the single most significant predictor of cord blood vitamin D level with five-fold increased risk of cord blood hypovitaminosis D in babies born to mothers with hypovitaminosis D. Birthweight (t = −2.219, p = .028) and preterm birth (aOR = 4.417, 95% CI: 1.03–18.9) was significantly associated with maternal hypovitaminosis D and a trend toward increased risk of LBW (aOR − 2.1, 95%CI: 0.6–7.3), SGA babies (aOR − 1.5, 95% CI: 0.5–4.7), perinatal depression (aOR − 1.5, 95% CI: 0.4–5.8) and neonatal hyperbilirubinemia (aOR = 2.68, 95%CI: 0.942–7.6) was observed. Conclusions Hypovitaminosis D in pregnant women is a significant health issue affecting both the mother and her baby. Safest dose for supplementation during pregnancy to prevent adverse perinatal outcome needs to be evaluated.

Impact of maternal hypovitaminosis D on birth and neonatal outcome – a prospective cohort study

The relationship between High-mobility group box 1 (HMGB1) and febrile seizures (FS) in children remains unclear. This study aimed to apply meta-analysis to reveal the correlation between HMGB1 levels and FS in children. Databases including PubMed, EMBASE, Web of science, Cochrane library, CNKI, SinoMed and WanFangData were searched for relevant studies. Pooled standard mean deviation and 95% confidence interval were calculated as effect size since the random-effects model was used when I2 > 50%. Meanwhile, between-study heterogeneity was determined by performing subgroup and sensitivity analyses. A total of 9 studies were finally included. Meta-analysis showed that the children with FS had significantly higher HMGB1 levels compared with healthy children and children with fever but no seizures (P<0.05). Additionally, subgroup analysis showed that the HMGB1 level in children with complex FS was higher than those with simple FS (P<0.05), and children with duration >15 min were higher than those with duration ≤15min (P<0.05). There were no statistical differences between children with or without a family history of FS (P>0.05). Finally, children with FS who converted to epilepsy exhibited higher HMGB1 levels than those who did not convert to epilepsy (P<0.05). The level of HMGB1 may be implicated in the prolongation, recurrence and development of FS in children. Thus, it was necessary to evaluate the precise concentrations of HMGB1 in FS patients and to further determine the various activities of HMGB1 during FS by well-designed, large-scale, and case-controlled trials. 

/pdf/association-between-high-mobility-group-box-1-levels-and-k8ifveuc.pdf

Association between high-mobility group box 1 levels and febrile seizures in children: a systematic review and meta-analysis

Background: The mechanisms underlying ferroptosis in neonatal hypoxic-ischemic brain damage (HIBD) remain unclear. Method: Four microarray datasets were collected from the GEO database (three mRNA datasets GSE23317, GSE144456, and GSE112137, and one miRNA microarray dataset GSE184939). Weighted gene co-expression network analysis (WGCNA) was used to identify modules of HIBD-related genes. The ferroptosis-related genes were extracted from FerrDb, of which closely correlated to HIBD were obtained after the intersection with existing HIBD’s DEGs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, as well as protein–protein interaction (PPI) network analysis were subsequently conducted. Cytoscape was used to identify central genes. Immune cell infiltration analysis was performed by the CIBERSORT algorithm. Result: Fifty-six ferroptosis-related differentially expressed genes (FRDEGs) were screened, mainly related to ferroptosis, autophagy, hypoxia response, metabolic pathways, and immune inflammation. The seven optimal hub FRDEGs were obtained by intersecting with key modules of WGCNA. Then, the expression levels of the seven optimal hub FRDEGs were validated in the GSE144456 and GSE112137 datasets, and the ferroptosis-related mRNA-miRNA network was established. In addition, this study revealed immune cell infiltration in the HIBD cerebral cortex and the interaction between immune cells. Moreover, notably, specific FRDEGs were strongly positively correlated with immune function. Conclusions: The mechanism of ferroptosis is intricate and closely related to neonatal HIBD. Therefore, targeting ferroptosis-related gene therapy and immunotherapy may have therapeutic prospects for neonatal HIBD.

/pdf/new-insights-into-mechanisms-of-ferroptosis-associated-with-2g0wkvw6.pdf

New Insights into Mechanisms of Ferroptosis Associated with Immune Infiltration in Neonatal Hypoxic-Ischemic Brain Damage

/pdf/publisher-correction-association-between-high-mobility-group-256kvppx.pdf

Publisher Correction: Association between high-mobility group box 1 levels and febrile seizures in children: a systematic review and meta-analysis

/pdf/micrornas-in-blood-as-diagnostic-biomarkers-for-neonatal-2n5c6g1j.pdf

MicroRNAs in Blood as Diagnostic Biomarkers for Neonatal Hypoxic–Ischemic Encephalopathy

Background In recent years, studies have examined the relationship between febrile seizures in children and S100B protein with contradictory results. We systematically evaluated the relationship between children's febrile seizures and S100B protein levels. Methods We used Stata 11.0 software to conduct a meta-analysis of the included studies published in The China National Knowledge Infrastructure, VIP, Wanfang, Chinese Biology Medicine Disc, PubMed, Web of Science, Cochrane Library, and EMBASE databases as well as clinical trial registries in China, Europe, and the United States. Results Six case-control studies were finally included in the meta-analysis. The results of the meta-analysis showed that the serum S100B protein level of children with febrile seizures was 0.72 higher than the serum S100B protein level of healthy children (Z=6.85, 95% CI 0.52∼0.93, P 0.05). Conclusion The level of serum S100B protein in children with febrile seizures was higher than that of healthy children and was statistically significant, whereas the increase in children with higher fever without seizures was not statistically significant. Because there was only a difference in serum S100B protein levels between children with febrile seizures and healthy children but not in febrile children without seizures as the strongest confounding factors for the results, febrile seizures do not elevate the level of S100B protein levels any more than fever.

No association between children's febrile seizures and S100B protein levels: A meta-analysis.

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