Birth asphyxia and its main sequel, hypoxic-ischemic encephalopathy, are one of the leading causes of children’s deaths worldwide and can potentially worsen the quality of life in subsequent years. Despite extensive research efforts, efficient therapy against the consequences of hypoxia-ischemia occurring in the perinatal period of life is still lacking. The use of hyperbaric oxygen, improving such vital consequences of birth asphyxia as lowered partial oxygen pressure in tissue, apoptosis of neuronal cells, and impaired angiogenesis, is a promising approach. This review focused on the selected aspects of mainly experimental hyperbaric oxygen therapy. The therapeutic window for the treatment of perinatal asphyxia is very narrow, but administering hyperbaric oxygen within those days improves outcomes. Several miRNAs (e.g., mir-107) mediate the therapeutic effect of hyperbaric oxygen by modulating the Wnt pathway, inhibiting apoptosis, increasing angiogenesis, or inducing neural stem cells. Combining hyperbaric oxygen therapy with drugs, such as memantine or ephedrine, produced promising results. A separate aspect is the use of preconditioning with hyperbaric oxygen. Overall, preliminary clinical trials with hyperbaric oxygen therapy used in perinatal asphyxia give auspicious results.

The 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.

Background: The aim of the study was to investigate if feto-maternal transfusion was related to the size of the fetal-maternal interface, and, therefore, was larger in twin pregnancy in comparison with singleton pregnancy. Methods: Blood samples from women with singleton (n = 11), and monochorionic (n = 11) and dichorionic (n = 13) twin gestations were tested. Flow cytometry tests with hemoglobin F, glycophorin A, and hemoglobin F and carbonic anhydrase simultaneous staining were used to detect fetal red blood cells and maternal F cells. Results: In all cases, the volume of feto-maternal transfusion was estimated to be low. The highest rate of fetal red blood cells in the maternal circulation was observed in the blood of women with dichorionic twin gestations both before and after delivery. An increase in fetal red blood cells was observed after cesarean section in singletons and twins. The median rate of maternal F cells was 2.23% in singleton, 2.1% in monochorionic and 3.95% in dichorionic pregnancy. Conclusions: Feto-maternal transfusion during pregnancy may be related to the multiplicity and chorionicity of pregnancy.

Neonatal hypoxic–ischemic encephalopathy (HIE) remains a major cause of neonatal mortality and long-term neurological disability. Although therapeutic hypothermia (TH) improves outcomes in eligible infants with moderate-to-severe HIE, its efficacy is incomplete, highlighting the need for additional neuroprotective strategies. Endogenous neuroprotective compounds are particularly attractive candidates because they participate in intrinsic cellular defense mechanisms and can modulate components of the hypoxic–ischemic injury cascade. This review focuses on five endogenous molecules—carnosine, citicoline, kynurenic acid (KYNA), lactoferrin, and N-acetylaspartylglutamate (NAAG)—whose neuroprotective effects have been demonstrated in experimental models of neonatal hypoxia-ischemia (HI). These molecules act through distinct but partly overlapping mechanisms involving modulation of glutamatergic neurotransmission, antioxidant defense, mitochondrial protection, anti-inflammatory signaling, and inhibition of regulated cell death. Their complementary actions suggest that they may represent components of a broader endogenous neuroprotective network rather than independent protective mechanisms. However, differences in blood–brain barrier accessibility, pharmacokinetics, therapeutic windows, and the predominantly preclinical nature of the available evidence remain important limitations to translation. Future studies should define optimal dosing, establish safety in the developing brain, and determine whether rational combinations of these compounds, particularly as adjuncts to TH, can provide more effective protection against neonatal hypoxic–ischemic brain injury.

Chalcones have garnered significant research interest due to their various medical bioactivities. Several chalcone compounds have been approved for marketing and clinical use in the treatment of various diseases. A critical aspect of the action of chalcones is their effect on microtubules. They are considered an excellent target for chemotherapeutic agents for the treatment of cancer. Consequently, scientists are constantly developing novel chalcone drug agents and also innovative drug delivery strategies. In this manuscript, we report the first synthesis of 12 new visible-light-activated, photoswitchable chalcone-based microtubule inhibitors (17a–17l). Among the obtained compounds, one photoswitch demonstrated light-dependent cytotoxicity in the PC-3 cancer cell line. The IC₅₀ value of the Z conformer was determined to be 4.75 ± 1.00 μM after 48 h of treatment. The E conformer exhibited slightly lower activity compared to the Z conformer, with an IC₅₀ value of 5.80 ± 0.80 µM following 48 h of incubation. In this study, NMR and UV spectroscopy, along with computational methods, were employed.

Neonatal hypoxic–ischemic encephalopathy (HIE) remains a major cause of neonatal mortality and long-term neurological disability. Although therapeutic hypothermia (TH) improves outcomes in eligible infants with moderate-to-severe HIE, its efficacy is incomplete, highlighting the need for additional neuroprotective strategies. Endogenous neuroprotec-tive compounds are particularly attractive candidates because they participate in intrinsic cellular defense mechanisms and can modulate components of the hypoxic–ischemic (HI) injury cascade. This review focuses on five endogenous molecules — carnosine, citicoline, kynurenic acid (KYNA), lactoferrin, and N-acetylaspartylglutamate (NAAG) — whose neuroprotective effects have been demonstrated in experimental models of neonatal HI. These molecules act through distinct but partly overlapping mechanisms involving mod-ulation of glutamatergic neurotransmission, antioxidant defense, mitochondrial protection, anti-inflammatory signaling, and inhibition of regulated cell death. Their complementary actions suggest that they may represent components of a broader endogenous neuropro-tective network rather than independent protective mechanisms. However, differences in blood–brain barrier accessibility, pharmacokinetics, therapeutic windows, and the pre-dominantly preclinical nature of the available evidence remain important limitations to translation. Future studies should define optimal dosing, establish safety in the developing brain, and determine whether rational combinations of these compounds, particularly as adjuncts to therapeutic hypothermia, can provide more effective protection against neonatal hypoxic–ischemic brain injury.