Neonatal Stage Research Articles

Guide to the treatment of paediatric strokes. Iberoamerican Academy of Pediatric Neurology

A paediatric stroke is a rare entity that can occur at any age. It may be arterial or venous, ischemic or haemorrhagic, and may occur in the neonatal or paediatric stage of life, as well as in adolescence. Prompt diagnosis means that adequate treatment can be administered and prevents recurrence, minimising the percentage of sequelae. This guide aimed to analyse, prepare and classify the literature currently available in order to determine the best recommendations on the treatment of strokes in paediatric patients. In each section, we attempted to answer the following questions: when should we think in terms of a stroke and thrombosis of the cerebral venous sinuses in a newborn or paediatric patient? What are the recommended complementary studies? Is treatment indicated? What are the recommended treatments? This guide was prepared based on the opinion of experts in the field, in order to determine how the recommendations were assessed according to the 2011 Oxford Levels of Evidence. Finally, the guidelines were reviewed by the scientific committee of the Iberoamerican Academy of Pediatric Neurology for subsequent dissemination.

Biologically informed machine learning modeling of immune cells to reveal physiological and pathological aging process

The immune system undergoes progressive functional remodeling from neonatal stages to old age. Therefore, understanding how aging shapes immune cell function is vital for precise treatment of patients at different life stages. Here, we constructed the first transcriptomic atlas of immune cells encompassing human lifespan, ranging from newborns to supercentenarians, and comprehensively examined gene expression signatures involving cell signaling, metabolism, differentiation, and functions in all cell types to investigate immune aging changes. By comparing immune cell composition among different age groups, HLA highly expressing NK cells and CD83 positive B cells were identified with high percentages exclusively in the teenager (Tg) group, whereas unknown_T cells were exclusively enriched in the supercentenarian (Sc) group. Notably, we found that the biological age (BA) of pediatric COVID-19 patients with multisystem inflammatory syndrome accelerated aging according to their chronological age (CA). Besides, we proved that inflammatory shift- myeloid abundance and signature correlate with the progression of complications in Kawasaki disease (KD). The shift- myeloid signature was also found to be associated with KD treatment resistance, and effective therapies improve treatment outcomes by reducing this signaling. Finally, based on those age-related immune cell compositions, we developed a novel BA prediction model PHARE (https://xiazlab.org/phare/), which can apply to both scRNA-seq and bulk RNA-seq data. Using this model, we found patients with coronary artery disease (CAD) also exhibit accelerated aging compared to healthy individuals. Overall, our study revealed changes in immune cell proportions and function associated with aging, both in health and disease, and provided a novel tool for successfully capturing features that accelerate or delay aging.

Environmental exposure to tobacco smoke and the onset of respiratory infections in neonatal, infant, and childhood stages: A systematic review

Environmental exposure to tobacco smoke and the onset of respiratory infections in neonatal, infant, and childhood stages: A systematic review

Impact of Bifidobacterium longum Subspecies infantis on Pediatric Gut Health and Nutrition: Current Evidence and Future Directions.

Background: the intestinal microbiota, a complex community vital to human health, is shaped by microbial competition and host-driven selective pressures. Among these microbes, Bifidobacterium plays a crucial role in early gut colonization during neonatal stages, where Bifidobacterium longum subspecies infantis (B. infantis) predominates and is particularly prevalent in healthy breastfed infants. Objectives: as we embark on a new era in nutrition of the pediatric population, this study seeks to examine the existing understanding regarding B. infantis, encompassing both preclinical insights and clinical evidence. Methods: through a narrative disceptation of the current literature, we focus on its genetic capacity to break down various substances that support its survival and dominance in the intestine. Results: using "omics" technologies, researchers have identified beneficial mechanisms of B. infantis, including the production of short-chain fatty acids, serine protease inhibitors, and polysaccharides. While B. infantis declines with age and in various diseases, it remains a widely used probiotic with documented benefits for infant and child health in numerous studies. Conclusions: the current scientific evidence underscores the importance for ongoing research and clinical trials for a deeper understanding of B. infantis's role in promoting long-term health.

Gitelman Syndrome in a 37-Years Old Woman with Urinary Tract Syndrome and History of Caesarean Section: A Case Report

Gitelman Syndrome (GS) is a rare genetic disorder often underdiagnosed due to its non-specific symptoms that can appear from neonatal stages to adulthood. It is more frequently observed in Asians, with a prevalence of approximately 1 in 40,000 people. Accurate diagnosis requires a comprehensive clinical interview and laboratory examinations. This report presents the case of a 37-year-old woman with GS who also experienced a urinary tract infection and had a history of cesarean section. Upon admission, she reported feeling fatigued and weak in all extremities. She had undergone a cesarean section a month prior due to pre-eclampsia. Initial laboratory tests revealed hypokalaemia, hyponatremia, and hypochloraemia. Further evaluation during hospitalization detected a urinary tract infection, hypocalciuria, and hypomagnesemia. The patient also suffered from carpopedal spasms and muscle cramps. Treatment included magnesium sulfate, calcium gluconate, potassium chloride, and sodium chloride infusions to restore electrolyte balance. The patient was discharged after six days, with a diagnosis of Gitelman Syndrome, which was unusual given her late onset of symptoms, as most cases are identified in childhood. The clinical presentation was largely driven by the patient’s electrolyte imbalances, especially hypokalaemia and hypomagnesemia, with hypomagnesemia further contributing to hypocalcemia and vitamin D deficiency. The patient’s symptoms improved after appropriate electrolyte supplementation. This case emphasizes the importance of a detailed clinical history and laboratory assessments in diagnosing GS, along with timely correction of electrolyte disturbances to improve the patient’s condition and prevent complications.

Loss of NAT10 Reduces the Translation of Kmt5a mRNA Through ac4C Modification in Cardiomyocytes and Induces Heart Failure.

In the past decade, the biological functions of various RNA modifications in mammals have been uncovered. N4-acetylcytidine (ac4C), a highly conserved RNA modification, has been implicated in human diseases. Despite this, the involvement of RNA ac4C modification in cardiac physiology and pathology remains incompletely understood. NAT10 (N-acetyltransferase 10) stands as the sole acetyltransferase known to catalyze RNA ac4C modification. This study aims to explore the role of NAT10 and ac4C modification in cardiac physiology and pathology. Cardiac-specific knockout of NAT10, leading to reduced RNA ac4C modification, during both neonatal and adult stages resulted in severe heart failure. NAT10 deficiency induced cardiomyocyte apoptosis, a crucial step in heart failure pathogenesis, supported by invitro data. Activation of the p53 signaling pathway was closely associated with enhanced apoptosis in NAT10-deficient cardiomyocytes. As ac4C modification on mRNA influences translational efficiency, we employed ribosome footprints coupled with RNA sequencing to explore genome-wide translational efficiency changes caused by NAT10 deficiency. We identified and validated that the translational efficiency of Kmt5a was suppressed in NAT10 knockout hearts due to reduced ac4C modification on its mRNA. This finding was consistent with the observation that Kmt5a protein levels were reduced in heart failure despite unchanged mRNA expression. Knockdown of Kmt5a in cardiomyocytes recapitulated the phenotype of NAT10 deficiency, including increased cardiomyocyte apoptosis and activated p53 signaling. Finally, overexpression of Kmt5a rescued cardiomyocyte apoptosis and p53 activation induced by NAT10 inhibition. Our study highlights the significance of NAT10 in cardiomyocyte physiology, demonstrating that NAT10 loss is sufficient to induce cardiomyocyte apoptosis and heart failure. NAT10 regulates the translational efficiency of Kmt5a, a key mediator, through mRNA ac4C modification during heart failure.

Selective vulnerability of parvocellular oxytocin neurons in social dysfunction

Selective vulnerability offers a conceptual framework for understanding neurodegenerative disorders such as Parkinson’s disease, where specific neuronal types are selectively affected and adjacent ones are spared. However, the applicability of this framework to neurodevelopmental disorders, particularly those characterized by atypical social behaviors, such as autism spectrum disorder, remains uncertain. Here we show that an embryonic disturbance, known to induce social dysfunction in male mice, preferentially impaired the gene expression crucial for neural functions in parvocellular oxytocin (OT) neurons—a subtype linked to social rewards—while neighboring cell types experienced a lesser impact. Chemogenetic stimulation of OT neurons at the neonatal stage ameliorated social deficits in early adulthood, concurrent with cell-type-specific sustained recovery of pivotal gene expression within parvocellular OT neurons. Collectively, our data shed light on the transcriptomic selective vulnerability within the hypothalamic social behavioral center and provide a potential therapeutic target through specific neonatal neurostimulation.

12246 The Stage-Dependent Transcriptome And Methylome Reveal Significance Of The Neonatal Period In Postnatal Metabolic Maturation Of The Mouse Liver

Abstract Disclosure: S. Yano: None. N. Sato: None. H. Araki: None. F. Miura: None. T. Ito: None. Y. Ogawa: None. The mammalian liver serves as an extramedullary hematopoietic organ during the fetus and matures into a metabolic organ after birth, adapting to changes in the nutritional environment. DNA demethylation upregulates fatty acid β-oxidation (FAO) genes in the postnatal mouse liver to produce energy from breast milk lipids. However, the detailed interactions between DNA methylation (DNAme) and gene expression through the perinatal stages remain poorly understood. Here, we perform an integrative analysis of the transcriptome and methylome of the mouse liver at the fetal, neonatal, and postweaning stages. We found a drastic loss of DNAme at the neonatal stage in specific regions associated with metabolic pathways such as FAO and gluconeogenesis in concordance with the activation of metabolic processes. Moreover, in silico analysis predicted transcription factors including HNF4α, PPARα, and NR1H2 as key epigenetic regulators within the neonatal period. We also observed an inactivation of erythrocyte development with a concordant gain of DNAme. This analysis extends the epigenetic landscape of postnatal hepatic maturation, suggesting the importance of the nutritional environment during the neonatal period for epigenetic regulation. Presentation: 6/3/2024

Automated counting and classifying Daphnia magna using machine vision

Daphnia magna (D. magna) is a model organism widely used in aquatic ecotoxicology research due to its sensitivity to environmental changes. The survival and reproduction rates of D. magna are easily affected by toxic environments. However, their small size, fragility, and transparency, especially in neonate stages, make them challenging to count accurately. Traditionally, counting adult and neonate D. magna relies on manual separation and visual observation, which is not only tedious but also prone to inaccuracies. Previous attempts to aid counting with optical sensors have faced issues such as inducing stress damage due to vertical movement and an inability to distinguish between adults and neonates. With the advancement of deep learning technologies, our study employs a simple light source culture device and utilizes the Mask2Former model to analyze D. magna against the background. Additionally, the U-Net model is used for comparative analysis. We also applied OpenCV technology for automatic counting of adult and neonate D. magna. The model's results were compared against manual counting performed by experienced technicians. Our approach achieves an average relative accuracy of 99.72 % for adult D. magna and 98.30 % for neonate. This method not only enhances counting accuracy but also provides a fast and reliable technique for studying the survival and reproduction rates of D. magna as a model organism.

Heat wave impacts on crop‐pest dynamics are dependent upon insect ontogeny and plant resistance

AbstractHeat waves, brief periods of unusually high temperatures, are damaging to agroecosystems and are increasing in frequency and intensity due to climate change. Despite growing appreciation for the threat that heat waves pose to agricultural sustainability, we have a poor understanding of what determines their impact on agroecological interactions in the field. Here, we report the results of a field experiment that examined how heat waves and their timing interact with crop pest resistance to influence the interactions between potato (Solanum tuberosum) and its most damaging pest, the Colorado potato beetle (CPB; Leptinotarsa decemlineata). We used open‐top chambers and ceramic heaters to generate heat wave conditions in field plots with pest‐resistant and pest‐susceptible potato varieties at four CPB developmental stages. We then assessed CPB performance, leaf herbivory, and tuber yield. The neonate‐stage heat wave reduced larval survival by 10%, but the surviving larvae were 18% larger and developed 15% faster. However, these effects occurred only on the susceptible variety; both larval survival and growth were unaffected by the heat wave in the pest‐resistant variety. Moreover, the neonate‐stage heat wave reduced adult survival by 15%, suggesting negative carry‐over effects of early‐life heat exposure. Heat wave events after the neonate stage had no effects on CPB performance, crop damage, or tuber yield. Our results indicate that timing and pest resistance in crops are essential for understanding the impacts of extreme heat events on crop‐pest dynamics. Agroecological pest management in an increasingly variable and extreme climate will likely benefit from the development of strategies that account for the seasonal timing of potential heat events and from the continued use of crop varieties bred for pest resistance, which our results suggest may dampen the impacts of extreme temperatures on crop‐pest interactions.

The miR-203/ZBTB20/MAFA Axis Orchestrates Pancreatic β-Cell Maturation and Identity During Weaning and Diabetes.

Maturation of postnatal β cells is regulated in a cell-autonomous manner, and metabolically stressed β cells regress to an immature state, ensuring defective β-cell function and the onset of type 2 diabetes. The molecular mechanisms connecting the nutritional transition to β-cell maturation remain largely unknown. Here, we report a miR-203/ZBTB20/MAFA regulatory axis that mediates the β-cell maturation process. We show that miR-203 level in β cells changes during the nutritional transition and that miR-203 inhibits β-cell maturation at the neonatal stage and under high-fat diet (HFD) conditions. Using single-cell RNA sequencing, we demonstrated that miR-203 elevation promoted the transition of immature β cells into CgBHi endocrine cells, while suppressing gene expressions associated with β-cell maturation in a ZBTB20/MAFA-dependent manner. ZBTB20 is an authentic target of miR-203 and transcriptionally upregulates MAFA expression. Manipulating the miR-203/ZBTB20/MAFA axis may therefore offer a novel strategy for boosting functional β-cell numbers to alleviate diabetes.

Seasonal variation in newborn hip dysplasia: Unraveling the impact of weather on hip development

BackgroundBabies born in winter have greater incidence of developmental dysplasia of the hip (DDH) and related surgeries. How weather conditions impact hip development and how screening program reacts weather issue remain unknown. This study tests a hypothesis that winter born babies have more newborn acetabular dysplasia and laxity that is responsible of later DDH. MethodsRetrospective data from newborns who had hip ultrasonography in the first 3 days of life were analyzed. The Graf type IIc, III, IV (shallow acetabulum) and type D (laxity) were classified as abnormal. The association and risks of an abnormal hip were analyzed with gender, gestational age, fetal presentation, parity and external temperature of birth month and the last 3 months before birth using the Pearson chi-square test and logistic regression. ResultsA total of 10962 newborns participated in hip ultrasound exams voluntarily in nurseries from 2016 to 2022. Distribution of babies with Graf type I, IIa, IIc, D, III/IV hips were 88.8%, 10%, 0.5%, 0.6%, and 0.1%, respectively. Female was the most significant factor for congenital shallow acetabulum (3.8x) and hip laxity (4x) compared to male (p <0.001). Preterm babies had a borderline lower risk of abnormal hips (0.4x, p = 0.05). Winter season is not associated with newborn abnormal hips (p = 0.36, statistical power = 80%), but a positive correlation was noted between external temperature and incidence of abnormal hips (r = 0.62, p = 0.03). Cold weather does not have a direct internal effect in acetabular dysplasia or hip laxity at birth. ConclusionsBabies who were born in winter were not associated with acetabular dysplasia and hip laxity at birth but had greater risks of late-diagnosed DDH and surgeries. The postnatal effects from weather should be addressed by a public awareness campaign, and hip screening may not be limited on the neonatal stage. Level of evidencelevel III, diagnostic

A critical review of neonatal parent support programme in United Kingdom: the effect of kangaroo mother care in NHS.

It has become critically important to provide a thorough understanding of the effects of the Kangaroo mother care (KMC) phenomenon on infants in the neonatal stage within the United Kingdom (UK). The current body of knowledge suggests numerous research publications globally, but the UK has yet to scale up its KMC practice. This study provides a critical review of the subject for a more nuanced understanding of the subject effect and to identify the current stage of KMC research in the UK. The findings were consistent with the body of knowledge on KMC with slight variations. Specifically, the UK has limited primary study in KMC. Randomized clinical trials (RCT) in KMC are minimal hence the UK is dependent on MedTech like an infant incubator which is a potential threat to KMC scale-up. Breastfeeding figures in the UK suggest depleting practice of KMC. The National and local policies captured KMC components but have impacted morbidity and mortality indices. It also showed three areas of divergence in practice and standardization. To enhance UK national and local policies uniformized guidelines and standardization of postnatal follow-up and community-based supervision are necessary.

Group III metabotropic glutamate receptors: guardians against excitotoxicity in ischemic brain injury, with implications for neonatal contexts

AbstractThe group III metabotropic glutamate receptors (mGluRs), comprising mGluR4, mGluR6, mGluR7, and mGluR8, offer neuroprotective potential in mitigating excitotoxicity during ischemic brain injury, particularly in neonatal contexts. They are G-protein coupled receptors that inhibit adenylyl cyclase and reduce neurotransmitter release, mainly located presynaptically and acting as autoreceptors. This review aims to examine the differential expression and function of group III mGluRs across various brain regions such as the cortex, hippocampus, and cerebellum, with a special focus on the neonatal stage of development. Glutamate excitotoxicity plays a crucial role in the pathophysiology of brain ischemia in neonates. While ionotropic glutamate receptors are traditional targets for neuroprotection, their direct inhibition often leads to severe side effects due to their critical roles in normal neurotransmission and synaptic plasticity. Group III mGluRs provide a more nuanced and potentially safer approach by modulating rather than blocking glutamatergic transmission. Their downstream signaling cascade results in the regulation of intracellular calcium levels, neuronal hyperpolarization, and reduced neurotransmitter release, effectively decreasing excitotoxic signaling without completely suppressing essential glutamatergic functions. Importantly, the neuroprotective effects of group III mGluRs extend beyond direct modulation of glutamate release influencing glial cell function, neuroinflammation, and oxidative stress, all of which contribute to secondary injury cascades in brain ischemia. This comprehensive analysis of group III mGluRs multifaceted neuroprotective potential provides valuable insights for developing novel therapeutic strategies to combat excitotoxicity in neonatal ischemic brain injury.

Cardiac Fibroblasts regulate myocardium and coronary vasculature development via the collagen signaling pathway.

The fibroblast (FB), cardiomyocyte (CM), and vascular endothelial cell (Vas_EC) are the three major cell types in the heart, yet their relationships during development are largely unexplored. To address this gap, we employed RNA staining of the FB marker gene Col1a1 together with the CM marker gene Actn2 and the Vas_EC marker gene Cdh5 at different stages. This approach enabled us to discern the anatomical pattern of cardiac FBs and identify approximately one EC and four CMs directly interacting with each FB. Molecularly, through the analysis of single-cell mRNA sequencing (scRNA-seq) data, we unveiled collagen as the top signaling molecule derived from FBs influencing CM and Vas_EC development. Subsequently, we used a Pdgfra-CreER controlled diphtheria toxin A (DTA) system to ablate the FBs at different stages. We found that the ablation of FBs disrupted myocardium and vasculature development and led to embryonic heart defects. Using scRNA-seq, we further profiled the ablated hearts and identified molecular defects in their ventricular CMs and Vas_ECs compared to control hearts. Moreover, we identified a reduction of collagen in the ablated hearts and predicted collagen as the major signaling pathway regulating the differentially expressed genes in the ablated ventricular CMs. Finally, we performed both short-term and long-term fibroblast ablation at the neonatal stage. We found that short-term ablation caused a reduction in collagen and Vas_EC density, while long-term ablation may induce compensatory collagen expression without causing heart function reduction. In summary, our study has identified the function of fibroblasts in regulating myocardium and vasculature development and implicated an important role for the collagen pathway in this process.

Neonatal vitamin A but not retinoic acid administration increases intramuscular adipocyte number in sheep by promoting vascularization

This study investigated whether vitamin A (VA) administration during the neonatal stage could increase the number of intramuscular adipocytes in Hu sheep by promoting vascularity. A total of 56 newborn male Hu sheep were divided into four groups and received intramuscular injections of either 0, 7500 IU retinoic acid (RA), 7500 IU VA, or a combination of 7500 IU VA and 5 mg SU5416 (an angiogenic inhibitor), at 1, 7, 14, and 21 days of age. At 15 days of age, 6 sheep from each group were randomly selected and sacrificed for intramuscular adipogenic capacity analysis. The remaining 8 sheep in each group were raised until they were 8 months old. VA-treated sheep exhibited an increase in preadipocytes, elevated expression of adipogenic genes (CCAAT enhancer binding protein alpha [CEBPA] and CCAAT enhancer binding protein beta [CEBPB]) and angiogenic genes (vascular endothelial growth factor A [VEGFA]), and stromal vascular fraction cells in the longissimus dorsi (LD) muscle with enhanced adipogenic capacity (P ＜ 0.05). These effects were entirely negated by SU5416. Upon slaughter, VA increased final weight, carcass weight, and average daily gain (P ＜ 0.05) but did not affect feed intake at 21-32 weeks (P = 0.824). VA increased the number of intramuscular adipocytes in the LD and semitendinosus (ST) muscle (P ＜ 0.05) without changing the adipocyte number of the omentum, perirenal and subcutaneous fats (P ＞ 0.05). VA injections also increased intramuscular triglyceride (TG) content (P = 0.016) without changing the omentum fat weight or subcutaneous fat thickness (P ＞ 0.05), but it did increase the perirenal fat weight (P = 0.011). Consistently, SU5416 mitigated the effects of VA on intramuscular TG content and adipocyte count, correlating with a decrease in vascularity. In contrast, RA injections didn’t affect the intramuscular fat (P = 0.744) but reduced the TG content of the omentum and perirenal fat (P ＜ 0.05). In conclusion, intramuscular injections of VA but not RA at the neonatal stage improved the growth performance of Hu sheep, increasing the number of intramuscular adipocytes and marbling by promoting angiogenesis.

The effects of Atoh8 on postnatal murine neurogenesis.

Introduction Basic helix-loop-helix (bHLH) transcription factors are expressed in various organs and are involved in diverse developmental processes. The mouse atonal homolog 8 (Atoh8), a bHLH transcription factor plays a crucial role in various developmental processes, especially as a regulator of neurogenesis in the retina. Besides, Atoh8 expression has been observed in the central nervous system. The function of Atoh8 during the postnatal neurogenesis is still unclear. Methods This study focuses on elucidating the impact of Atoh8 on postnatal neurogenesis in the brain, particularly in selected regions; the subventricular zone (SVZ), rostral migration stream (RMS) and olfactory bulb (OB), across different life stages, using male homozygous Atoh8-knockout (M6KO) mice. Our morphometric analysis is based on immunohistochemically labeled markers for neuroblasts (Doublecortin) and proliferation (Phospho-Histone H3, PHH3) as well as pan neuronal markers. Results In Atoh8-/- mice alteration in the postnatal neurogenesis can be observed. Immunohistochemical analysis revealed a significant reduction in doublecortin-positive neuroblasts within the SVZ of neonatal M6KO mice compared to wildtype (WT) mice. Interestingly, no differences in cell number and distribution was observed in the subsequent migration of neuroblasts through the rostral migration stream (RMS) to the olfactory bulb (OB). Proliferating PHH3-positive neuronal progenitor cells were significantly diminished in proliferation rate in both the SVZ and RMS of neonatal and young M6KO mice. Furthermore, in the glomerular layer of the OB significantly fewer neurons were detected in the neonatal stage. Conclusion In conclusion, Atoh8 emerges as a positive regulator of postnatal neurogenesis in the brain. Its role encompasses the promotion of neuroblast formation, modulation of proliferation rates, differentiation, and maintenance of mature neurons. Understanding the intricacies of Atoh8 function provides valuable insights into the complex regulatory mechanisms governing neurogenesis.

Influence of an iron dextran injection in various diseases on hematological blood parameters, including serum ferritin, neonatal dairy calves

BackgroundFeeding milk substitutes with low iron content or whole milk without iron supplementation is considered a major factor in developing iron-deficiency anemia in neonatal dairy calves. Young calves are often supplemented with iron dextran injections on the first day of life to prevent anemia. However, the effects of preventive treatment and the presence of disease on serum iron (Fe) concentrations, serum ferritin levels, and hematological blood parameters during the early neonatal stages have not been examined in detail. Therefore, we examined and evaluated the effects of iron dextran injections and health status on the development of hematocrit (Ht), red blood cells (RBC), hemoglobin concentration (Hb), erythrocyte indices (mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration), Fe, and serum ferritin concentrations in dairy calves within the first 10 days of life. The suitability of serum ferritin as a reliable indicator of anemia in very young calves was evaluated by correlating ferritin concentrations with known laboratory diagnostic parameters of anemia.ResultsIron supplementation significantly increased Fe levels (P = 0.048) but did not affect serum ferritin levels in neonatal calves. Fe concentrations were significantly lower in diseased than healthy calves (P = 0.0417). Iron supplementation significantly affected the health status, as observed in Ht (Ptreat=0.0057; Phealth=0.0097), RBC (Ptreat=0.0342; Phealth=0.0243), and Hb (Ptreat=0.0170; Phealth=0.0168). Serum ferritin levels did not significantly correlate with Fe levels. Both groups showed marked differences in ferritin levels, with the highest levels measured on day 2. Fe concentrations showed weak negative correlations with Hb and Ht levels on day 3 (ρ=-0.45; P = 0.0034 and ρ=-0.045; P = 0.0032, respectively). RBC count showed strong positive correlations with Hb and Ht levels (ρ = 0.91 and ρ = 0.93; P < 0.001).ConclusionIron dextran injections increased Fe concentrations but reduced Ht level, RBC count, and Hb level. The presence of diseases led to a reduction in Fe and higher values of Ht, RBC, and Hb in moderate disease than in severe disease. Due to physiological fluctuations during the first 3 days of life, serum ferritin level seems unuseful for evaluating iron storage before day 4 of life.

The global burden of disease attributable to preterm birth and low birth weight in 204 countries and territories from 1990 to 2019: An analysis of the Global Burden of Disease Study.

Preterm birth and low birth weight (PBLBW), recognised globally as primary contributors to infant mortality in children under five, have not been sufficiently investigated in terms of their worldwide impact. In this study we aimed to thoroughly evaluate the contemporary trends in disease burden attributable to PBLBW. We analysed data from 204 countries and territories between 1990-2019, as sourced from the 2019 Global Burden of Disease Study. We analysed the global incidence of mortality and disability-adjusted life years (DALYs) associated with PBLBW, stratified by age, gender, year, and geographic location, alongside the socio-demographic index (SDI). We calculated the annual percentage changes to evaluate the dynamic trends over time. We employed a generalised linear model and scrutinised the relationship between the SDI and the disease burden attributed to PBLBW. In 2019, the global age-standardised rate of deaths and DALYs related to PBLBW showed significant declines. Over the period 1990-2019, both death and DALY rates displayed substantial downward trends, with similar change trends observed for both females and males. Age-specific ratios revealed a decrease in PBLBW-related deaths and DALYs with increasing age, primarily during the neonatal stages (zero to 27 days). The leading three causes of PBLBW-related DALYs in 2019 were neonatal disorders, lower respiratory infections, and sudden infant death syndrome. Furthermore, the association between SDI and PBLBW-related DALYs indicated that the age-standardised DALY rates in 204 countries and territories worldwide were negatively correlated with SDI in 2019. From 1990 to 2019, the age-standardised DALY rates decreased linearly in most regions, except sub-Saharan Africa. The persistent global burden of disease associated with PBLBW is particularly pronounced in neonates aged less than 28 days and in regions with low SDI. In this study, we highlighted the critical need for tailored interventions aimed at mitigating the detrimental effects of PBLBW to attain specific sustainable development goals, particularly those centred on enhancing child survival and overall well-being.

Neonatal Exposure to Polystyrene Nanoplastics Impairs Microglia-Mediated Synaptic Pruning and Causes Social Behavioral Defects in Adulthood.

The increasing prevalence and persistence of nanoplastics (NPs) have become critical environmental concerns. These particles have the potential to enter the food chain and accumulate in living organisms, which exerts their adverse effects on human health. The release of nanoparticles from feeding bottles raises concerns about potential health issues, especially for newborns exposed to NPs at the neonatal stage. In this study, we examined the impacts of neonatal exposure to polystyrene nanoplastics (PS-NPs) on neurodevelopment. Our study demonstrates that exposure to PS-NPs in newborn mice impairs microglial autophagic function and energy metabolism, leading to the disruption of microglia-mediated synaptic pruning during early neurodevelopment. These mice subsequently develop social behavioral defects in adulthood, suggesting the long-lasting effects of neonatal PS-NP exposure on brain development and behavior. Together, these data provide insights into the mechanism by which PS-NPs affect early neurodevelopment, thus emphasizing the crucial need to address plastic pollution globally.