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Birth is an inflammatory event for the newborn, characterized by elevations in interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α peripherally and/or centrally, as well as changes in brain microglia. However, the mechanism(s) underlying these responses is unknown. Toll-like receptors (TLRs) play crucial roles in innate immunity and initiate inflammatory cascades upon recognition of endogenous or exogenous antigens. Most TLR signaling depends on the adaptor molecule myeloid differentiation primary response 88 (MyD88). We independently varied MyD88 gene status in mouse dams and their offspring to determine whether the inflammatory response to birth depends on MyD88 signaling and, if so, whether that signaling occurs in the offspring, the mother, or both. We find that the perinatal surges in plasma IL-6 and brain expression of TNF-α depend solely on MyD88 gene status of the offspring, whereas postnatal increases in plasma IL-10 and TNF-α depend on MyD88 in both the pup and dam. Interestingly, MyD88 genotype of the dam primarily drives differences in offspring brain microglial density and has robust effects on developmental neuronal cell death. Milk cytokines were evaluated as a possible source of postnatal maternal influence; although we found high levels of CXCL1/GROα and several other cytokines in ingested post-partum milk, their presence did not require MyD88. Thus, the inflammatory response previously described in the late-term fetus and newborn depends on MyD88 (and, by extension, TLRs), with signaling in both the dam and offspring contributing. Unexpectedly, naturally-occuring neuronal cell death in the newborn is modulated primarily by maternal MyD88 gene status. 

Localized surface plasmon resonance (LSPR) of Cu 2− x S nanorods is quenched during the initial Cu 2− x S/Cu 2− x Te core/shell stage of anion exchange then returns as Cu 2− x Te progresses into the nanorod. Phase change within the core accounts for this behaviour illustrating the complexity emergent from anion exchange. 

Long-standing clinical findings report a dramatic surge of vasopressin in umbilical cord blood of the human neonate, but the neural underpinnings and function(s) of this phenomenon remain obscure. We studied neural activation in perinatal mice and rats, and found that birth triggers activation of the suprachiasmatic, supraoptic, and paraventricular nuclei of the hypothalamus. This was seen whether mice were born vaginally or via Cesarean section (C-section), and when birthtimingwas experimentally manipulated. Neuronal phenotyping showed that the activated neurons were predominantly vasopressinergic, and vasopressin mRNA increased fivefold in the hypothalamus during the 2–3 days before birth. Copeptin, a surrogate marker of vasopressin, was elevated 30-to 50-fold in plasma of perinatal mice, with higher levels after a vaginal than a C-section birth. We also found an acute decrease in plasma osmolality after a vaginal, but not C-section birth, suggesting that the difference in vasopressin release between birth modes is functionally meaningful. When vasopressin was administered centrally to newborns, we found an ~ 50% reduction in neuronal cell death in specific brain areas. Collectively, our results identify a conserved neuroendocrine response to birth that is sensitive to birth mode, and influences peripheral physiology and neurodevelopment.

 

Liquid interfaces facilitate the organization of nanometer‐scale biomaterials with plasmonic properties suitable for molecular diagnostics. Using hierarchical assemblage of 2D hafnium disulfide nanoplatelets and zero‐dimensional spherical gold nanoparticles, the design of a multifunctional material is reported. When the target analyte is present, the nanocomposites’ self‐assembling pattern changes, altering their plasmonic response. Using monkeypox virus (MPXV) as an example, the findings reveal that adding genomic DNA to the nanocomposite surface increases the agglomeration between gold nanoparticles and decreases the π‐stacking distance between hafnium disulfide nanoplatelets. Further, this self‐assembled nanomaterial is found to have minimal cross‐reactivity toward other pathogens and a limit of detection of 7.6 pg µL⁻¹(i.e., 3.57 × 10⁴copies µL⁻¹) toward MPXV. Overall, this study helped to gain a better understanding of the genomic organization of MPXV to chemically design and develop targeted nucleotides. The study has been validated by UV–vis spectroscopy, X‐ray diffraction, scanning transmission electron microscopy, surface‐enhanced Raman microscopy and electromagnetic simulation studies. To the best knowledge, this is the first study in literature reporting selective molecular detection of MPXV within a few minutes and without the use of any high‐end instrumental techniques like polymerase chain reactions.