Nanoparticles are becoming an increasingly popular tool for biomedical imaging and drug delivery. While the prevalence of nanoparticle drug-delivery systems reported in the literature increases yearly, relatively little translation from the bench to the bedside has occurred. It is crucial for the scientific community to recognize this shortcoming and re-evaluate standard practices in the field, to increase clinical translatability. Currently, nanoparticle drug-delivery systems are designed to increase circulation, target disease states, enhance retention in diseased tissues, and provide targeted payload release. To manage these demands, the surface of the particle is often modified with a variety of chemical and biological moieties, including PEG, tumor targeting peptides, and environmentally responsive linkers. Regardless of the surface modifications, the nano–bio interface, which is mediated by opsonization and the protein corona, often remains problematic. While fabrication and assessment techniques for nanoparticles have seen continued advances, a thorough evaluation of the particle’s interaction with the immune system has lagged behind, seemingly taking a backseat to particle characterization. This review explores current limitations in the evaluation of surface-modified nanoparticle biocompatibility and in vivo model selection, suggesting a promising standardized pathway to clinical translation.

Nausea and vomiting during pregnancy (NVP), particularly its severe form, Hyperemesis gravidarum (HG), affects up to 70% of pregnancies and significantly impacts the quality of life for those with the condition as well as generates a great economic burden, with annual costs exceeding $1.7 billion in the United States. Despite the available treatments targeting neurotransmitters like serotonin and dopamine, many patients experience inadequate relief and suffer from severe side effects, including headaches and dizziness. Recent research has underscored the role of GDF15, a protein mainly produced by the placenta and linked to NVP symptoms. This protein, part of the TGF-β superfamily, has been implicated in appetite and weight regulation and is altered in those with HG due to specific genetic mutations. Addressing the challenges of delivering effective treatments, current innovations focus on targeting GDF15 to reduce symptoms while ensuring fetal safety. Promising therapeutic strategies include non-IgG immunotherapies, small peptide and molecule antagonists, and novel administration methods such as transdermal patches. These approaches aim to optimize dosage and reduce adverse effects. The effective development and testing of these treatments necessitate advanced animal models that closely resemble human pregnancy physiology, highlighting the need for further research and funding. This ongoing research holds significant potential to improve the clinical outcomes for HG patients and decrease the economic impact on healthcare systems, urging a dedicated response from the scientific and medical communities to advance these promising treatments.

The current lack of a comprehensive understanding of brain metastasis mechanisms presents a significant gap in cancer research. This review outlines the role that Schwann cells (SCs) have in this process. SCs are already known for their role in myelination and nerve repair within the peripheral nervous system (PNS), but there is less information on their function in facilitating the transport and activation of neoplastic cells to aid in the invasion of the blood–brain barrier and brain. Detailed insights into SCs’ interactions with various cancers, including lung, breast, melanoma, colon, kidney, and pancreatic cancers, reveal how these cells are coerced into repair-like phenotypes to accelerate cancer spread and modulate immune responses. By outlining SCs’ involvement in perineural invasion and BBB modification, this review highlights their functions in facilitating brain metastasis.

1. Extracellular vesicles (EVs) are lipid bilayer-bound nanoparticles (<200 nm), secreted by nearly all cells and can be detected in biological fluids, including bovine milk [1–3]. EVs are commonly...

Astrocytes regulate key aspects of the neural microenvironment that can be co-opted by cancer to support tumor growth and invasion. Secreted protein acidic and rich in cysteine-like 1 (SPARCL1) is a matricellular glycoprotein expressed by astrocytes and stromal cells, whose expression varies across cancer types. While SPARCL1 is downregulated in many peripheral cancers, reports of its expression in gliomas, specifically glioblastoma (GBM), are inconsistent. The biological context underlying these divergent findings, and the role of SPARCL1 in GBM malignancy, remains unclear. Publicly available transcriptomic datasets from the Ivy Glioblastoma Atlas Project (Ivy GAP), GlioVis, and TCGA were analyzed to evaluate SPARCL1 expression across GBM cohorts. Spatially resolved gene expression data from Ivy GAP were used to assess SPARCL1 expression from defined tumor regions. Microarray and RNA sequencing datasets from GlioVis and TCGA, respectively, were used to assess SPARCL1 expression across whole-tumor samples. Spatial transcriptomics from Ivy GAP show SPARCL1 expression was upregulated along the leading edge and in infiltrating tumor regions. Microarray datasets showed greater SPARCL1 expression in tumors of astrocyte lineage as opposed to oligodendrocyte lineage. Bulk RNA sequencing showed high SPARCL1 expression in low-grade gliomas, which is consistent with astrocytic lineage, IDH mutation, and spatial averaging effects that might obscure regional associations. These findings demonstrate that SPARCL1 expression in GBM is shaped by tumor architecture, molecular classification, and microenvironment interactions. Enrichment of SPARCl1 at invasive tumor margins is consistent with prior studies linking SPARCL1 to neuron–glioma synapse formation and angiogenesis.