Glial cells play a critical role in shaping neuronal development, structure, and function. In a screen for Caenorhabditis elegans mutants that display dopamine (DA)-dependent, Swimming-Induced Paralysis (Swip), we identified a novel gene, swip-10, the expression of which in glia is required to support normal swimming behavior. swip-10 mutants display reduced locomotion rates on plates, consistent with our findings of elevated rates of presynaptic DA vesicle fusion using fluorescence recovery after photobleaching. In addition, swip-10 mutants exhibit elevated DA neuron excitability upon contact with food, as detected by in vivo Ca²⁺ monitoring, that can be rescued by glial expression of swip-10. Mammalian glia exert powerful control of neuronal excitability via transporter-dependent buffering of extracellular glutamate (Glu). Consistent with this idea, swip-10 paralysis was blunted in mutants deficient in either vesicular Glu release or Glu receptor expression and could be phenocopied by mutations that disrupt the function of plasma membrane Glu transporters, most noticeably glt-1, the ortholog of mammalian astrocytic GLT1 (EAAT2). swip-10 encodes a protein containing a highly conserved metallo-β-lactamase domain, within which our swip-10 mutations are located and where engineered mutations disrupt Swip rescue. Sequence alignments identify the CNS-expressed gene MBLAC1 as a putative mammalian ortholog. Together, our studies provide evidence of a novel pathway in glial cells regulated by swip-10 that limits DA neuron excitability, DA secretion, and DA-dependent behaviors through modulation of Glu signaling.

Fetuin-A, also known as alpha-2-Heremans-Schmid-glycoprotein (Ahsg), is a multifunctional molecule with diverse roles in biological processes such as mineralization, tumor growth, and inflammation. This review explores the involvement of Ahsg in various cancers, including liver, breast, prostate, colorectal, brain, osteosarcoma, and lung cancers. In many cancer types, Ahsg promotes tumor growth, invasion, and metastasis through various mechanisms, including cellular adhesion, spreading, chemotaxis, and modulation of cell-growth signaling pathways. Additionally, Ahsg has been implicated in the regulation of inflammatory cytokine production, making it a potential marker of inflammation in cancer. The complex interplay between Ahsg and cancer progression highlights its potential as a diagnostic biomarker and therapeutic target in various cancers. However, further research is needed to fully elucidate the mechanisms of action of Ahsg in cancer and to explore its clinical implications in cancer diagnosis, prognosis, and treatment.

Claudin-4 is part of the Claudin family of transmembrane tight junction (TJ) proteins found in almost all tissues and, together with adherens junctions and desmosomes, forms epithelial and endothelial junctional complexes. Although the distribution of Claudin-4 occurs in many cell types, the level of expression is cell-specific. Claudin proteins regulate cell proliferation and differentiation by binding cell-signaling ligands, and its expression is upregulated in several cancers. As a result, alterations in Claudin expression patterns or distribution are vital in the pathology of cancer. Profiling the genetic expression of Claudin-4 showed that Claudin-4 is also a receptor for the clostridium perfringens enterotoxin (CPE) and that Claudin-4 has a high sequence similarity with CPE’s high-affinity receptor. CPE is cytolytic due to its ability to form pores in cellular membranes, and CPE treatment in breast cancer cells have shown promising results due to the high expression of Claudin-4. The C-terminal fragment of CPE (c-CPE) provides a less toxic alternative for drug delivery into breast cancer cells, particularly metastatic tumors in the brain, especially as Claudin-4 expression in the central nervous system (CNS) is low. Therefore, c-CPE provides a unique avenue for the treatment of breast–brain metastatic tumors.

Acute and chronic upper respiratory illnesses such as asthma, and allergic rhinitis (AR) have been linked to the presence of microorganisms in the nose. Microorganisms can exist in symbiotic or commensal relationships with the human body. However, in certain cases, opportunistic pathogens can take over, leading to altered states (dysbiosis) and causing disease. Thus, the microflora present in a host can be useful to reflect health status. The human body contains 10 trillion to 100 trillion microorganisms. Of these populations, certain pathogens have been identified to promote or undermine wellbeing. Therefore, knowledge of the microbiome is potentially helpful as a diagnostic tool for many diseases. Variations have been recognized in the types of microbes that inhabit various populations based on geography, diet, and lifestyle choices and various microbiota have been shown to modulate immune responses in allergic disease. Interestingly, the diseases affected by these changes are prevalent in certain racial or ethnic populations. These prevalent microbiome variations in these groups suggest that the presence of these microorganisms may be significantly associated with health disparities. We review current research in the search for correlations between ethnic diversity, microbiome communities in the nasal cavity and health outcomes in neurological and respiratory functions.

Study Design: Systematic Review with Proportional Meta-Analysis Objectives: Dexamethasone use in pediatric neurosurgical trauma remains controversial, with varying reports of its overall efficacy. Our study aims to assess the use of dexamethasone in pediatric neurosurgery regarding patient characteristics, risk factors, and dosing. Methods: A systematic review was conducted using PubMed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to identify literature presenting dexamethasone use in pediatric neurosurgical trauma. Results: A total of 597 publications were identified, of which 13 met inclusion criteria (2 case reports, 11 retrospective studies). Case reports (N=4 patients, mean age 13.5 years) demonstrated traumatic brain injury with cerebral edema, hematoma, or swelling. All patients received dexamethasone (5–7 days), experienced no treatment-related complications, and 75% showed neurological improvement. Across 11 retrospective studies (N=493 patients, mean age 7.3 years), most presented with severe TBI and cerebral edema. Management strategies included conservative therapy (83%) or surgical intervention (13%). Dexamethasone was used in 61% of patients (average 0.92 mg/kg/day for 4.7 days). Reported outcomes were mixed: some studies demonstrated reduced mortality, improved neurological recovery, and lower ICP with dexamethasone, while others reported increased infection risk, catabolic effects, and no significant benefit. Pooled subgroup analysis showed patients who improved neurologically were more likely to have received dexamethasone (80.6% vs. 58.7%, p = 0.0347), whereas those who declined were less likely to have received it (19.4% vs. 41.3%, p = 0.0347). Infection was more common in dexamethasone-treated patients (52.0% vs. 16.7%, p = 0.0049). Conclusion: Evidence regarding dexamethasone use in pediatric traumatic brain injury is conflicting. Although some older studies suggest benefits including reduced ICP and mortality, most studies report limited efficacy and increased complications such as hyperglycemia, hypertension, gastrointestinal bleeding, and infections. Given the small number of available studies, no definitive recommendation can be made at this time. Further high-quality research is needed to clarify its role and establish guidelines for use in pediatric neurosurgical trauma.