The increasing radiofrequency (RF) electromagnetic radiation pollution resulting from the development and use of technologies utilizing RF has sparked debate about the possible biological effects of said radiation. Of particular concern is the potential impact on the brain, due to the close proximity of communication devices to the head. The main aim of this study was to examine the effects of long-term exposure to RF on the brains of mice in a real-life scenario simulation compared to a laboratory setting. The animals were exposed continuously for 16 weeks to RF using a household Wi-Fi router and a laboratory device with a frequency of 2.45 GHz, and were compared to a sham-exposed group. Before and after exposure, the mice underwent behavioral tests (open-field test and Y-maze); at the end of the exposure period, the brain was harvested for histopathological analysis and assessment of DNA methylation levels. Long-term exposure of mice to 2.45 GHz RF radiation increased their locomotor activity, yet did not cause significant structural or morphological changes in their brains. Global DNA methylation was lower in exposed mice compared to sham mice. Further research is needed to understand the mechanisms behind these effects and to understand the potential effects of RF radiation on brain function.

This review explores the maternal gut microbiome’s role in shaping neonatal neurodevelopmental outcomes following perinatal asphyxia (PA), a leading cause of infant mortality and disability with limited therapeutic options beyond hypothermia. We synthesized current evidence on microbiome-mediated neuroprotective mechanisms against hypoxic-ischemic brain injury. The maternal microbiome influences fetal development through bioactive metabolites (short-chain fatty acids, indole derivatives) that cross the placental barrier, bacterial antigen regulation, and infant microbiome colonization. These pathways activate multiple protective mechanisms: anti-inflammatory signaling via NF-κB suppression and regulatory T cell expansion; antioxidant defenses through Nrf2 activation; neural repair via BDNF upregulation and neurogenesis; and oxytocin system modulation. Animal models demonstrate that maternal dysbiosis from high-fat diet or antibiotics exacerbates PA-induced brain damage, increasing inflammatory markers and hippocampal injury. Conversely, probiotic supplementation, dietary fiber, and specific interventions (omega-3, resveratrol) reduce neuroinflammation and oxidative injury. Human studies link maternal dysbiosis-associated conditions (obesity, gestational diabetes) with adverse pregnancy outcomes, though direct clinical evidence for PA severity remains limited. Understanding the maternal microbiome-fetal brain axis opens therapeutic avenues, including prenatal probiotics, dietary modifications, and targeted metabolite supplementation to prevent or mitigate PA-related neurological sequelae, potentially complementing existing neuroprotective strategies.

Reconstructing the orbit following complex craniofacial fractures presents significant challenges. Throughout the years, several materials have been used for orbital reconstruction, taking into account factors such as their durability, compatibility with living tissue, cost efficiency, safety, and capacity to be adjusted during surgery. Nevertheless, a consensus has not yet been reached on the optimal material for orbital restoration. This study investigates the potential of a hybrid hydroxyapatite–collagen (HAp-COL) material 3D-printed on Ti mesh to be used as an implant for orbital wall reconstruction. HAp-COL powder was synthesized using a high-pressure hydrothermal technique. The powder was further used to 3D-print HAp-COL structures on titanium mesh, with the latter having potential uses in orbital wall reconstruction. Biocompatibility was assessed by evaluating the effects of the HAp-COL material on the adhesion and proliferation of fibroblasts (3T3) and mesenchymal stem cells (MSCs) in culture. In vitro and in vivo results showed that HAp-COL is highly biocompatible and has a good integration of the implant in the bone. The findings reported in this study offer convincing evidence to support the use of our designed HAp-COL for the restoration of orbital wall fractures, with a high level of safety.

Maternal gut microbiome impairment has garnered attention for its potential role in influencing neurodevelopmental outcomes in offspring, especially in situations that increase brain vulnerability such as perinatal asphyxia (PA). Maternal microbiome and fetal brain interplay emerge as a critical link between maternal health and offspring neurodevelopment. This study aims to generate a model to assess the impact of maternal dysbiosis triggered by gestational antibiotic administration and PA on offspring neurodevelopment. Wistar rats were subjected to antibiotics in drinking water from the 11th gestational day until birth. On the 6th postnatal day, pups were subjected to PA/normoxia, resulting in four experimental groups: control-normoxia, antibiotics-normoxia, control-asphyxia, and antibiotics-asphyxia. Early-life behavioral tests were conducted between postnatal days 7 and 9. The initial antimicrobial cocktail (ampicillin, vancomycin, neomycin, clindamycin, amphotericin-B) led to an increased number of miscarriages, poor weight gain during pregnancy, reduced offspring weight, and changes in the maternal gut microbiome compared to control. Offspring presented impaired neurodevelopmental reflexes in both PA and antibiotic groups and increased hippocampal neuroinflammation. Due to these detrimental effects, a more pregnancy-safe antibiotic cocktail was used for a second experiment (ampicillin, vancomycin, neomycin, meropenem). This resulted in no miscarriages or pregnancy-weight loss but was still linked to gut microbiome disruption. PA impaired neurodevelopmental reflexes and increased neuroinflammation, effects amplified by antibiotic administration. These preliminary findings reveal the cumulative potential of maternal dysbiosis and PA on neurodevelopment impairment, emphasizing caution in gestational antimicrobial use. Further investigations should include offspring long-term follow-up and maternal behavior and integrate probiotics to counteract antibiotic effects. Graphical Lay summary: This study investigates the impact of maternal gut microbiome disruptions caused by gestational antibiotic treatment and low oxygen exposure shortly after birth on the development of the rats’ babies. We found that both antibiotic exposure and reduced oxygen levels led to changes in early behavior and increased inflammation of the nervous tissue in the baby rats. Although using a different, potentially safer antibiotic combination reduced pregnancy complications, it still changed the bacteria in the mother’s gut and worsened early behavior. These findings show that antibiotics during pregnancy can affect the developing brain of baby rats and careful consideration should be used before prescribing them. Future research will explore longer-term effects and potential medicines.

Background/Objectives: Birth asphyxia is a frequent neonatal complication in humans. Its outcome is variable, and the factors underlying this variability remain incompletely understood. Maternal gut microbiome impairment has been proposed as one factor that may influence offspring neurodevelopment, especially when the immature brain is exposed to additional vulnerability such as perinatal asphyxia (PA). Building on our previous maternal microbiome disruption model and on our prior observation that electroencephalography (EEG) reactivity to photic stimulation under deep anesthesia detects functional impairment two months after PA, we assessed whether this reactivity was further impaired after prolonged gestational antibiotic administration and whether probiotics modulated this effect. Methods: Wistar dams received antibiotics, probiotics, antibiotics with probiotics, or control treatment, and offspring underwent PA. Adult EEG reactivity to photic stimulation was assessed during chloral hydrate-induced burst suppression. Burst count reactivity (BCR) was used as the primary event-based readout of stimulus-evoked burst recruitment and was compared with the suppression-ratio-based burst-suppression reactivity index (BSRi). Results: Burst suppression remained reactive to photic stimulation in all groups. BCR was lower after gestational antibiotic treatment than in controls. The magnitude of the effect was attenuated by probiotics coadministration. BSRi showed the same overall pattern. Conclusions: Prolonged gestational antibiotic exposure increased the severity of perinatal asphyxia as measured by EEG reactivity in the adult offspring. The converging BCR and BSRi results support burst-suppression reactivity as a functional neurophysiological readout in this PA model and support further methodological development of EEG reactivity measures for translational studies of hypoxic–ischemic brain injury.

Prolonged gestational antibiotic exposure was previously reported to impair EEG reactivity in adult offspring after perinatal asphyxia. It remained unclear to what extent the effect depended on perinatal insult. We assessed adult EEG reactivity after uncomplicated birth using the same gestational treatment paradigm. Pregnant Wistar rats received antibiotics (AB), probiotics (P), combined treatment (AB&P), or control (C). Adult offspring (AB: 5; P: 8; AB&P: 7; C: 9; 14 males) underwent intermittent photic stimulation during chloral-hydrate-induced EEG burst suppression. Reactivity to 60 s stimulation was quantified in 180 s trials using burst count reactivity (BCR) and the burst-suppression reactivity index (BSRi). After baseline burst count filtering, 200 trials were retained across groups. BCR did not differ significantly between groups. No multiplicity-corrected pairwise comparison identified a specific treatment-associated difference in BCR or BSRi. Mixed-effects models accounting for repeated trials likewise showed no significant overall group effect. Our small cohort did not provide evidence for a long-term effect of gestational antibiotic or probiotic exposure following uncomplicated birth. Together with the previous report, we suggest that gestational antibiotic administration could impair resilience to perinatal asphyxia at an exposure level without a readily detectable effect after uncomplicated birth.