The chemoreflex is a vital protective reflex that is crucial in restoring normal blood gas and pH levels. The carotid bodies are peripheral chemoreceptors activated by hypoxia (primarily), hypercapnia, acidaemia, temperature, lactate and potassium fluctuations. They are crucial for maintaining physiological conditions based on underlying causes and blood gas abnormalities. Central chemoreceptors in the brain stem are responsive to hypercapnia and contribute to blood gas regulation. Chemoreceptors regained attention during the SARS‐CoV‐2 (COVID‐19) pandemic, potentially contributing to disease severity. In conditions like chronic intermittent hypoxia, chemoreflex sensitization may lead to respiratory disorders, impacting quality of life. There has been substantial research/evidence linking chemoreflex dysfunction to cardiovascular illnesses such as heart failure and hypertension. However, little emphasis has been placed on the role of the chemoreflex in mediating cardiopulmonary dysfunction during and after pulmonary disorders such as acute lung injury. The current review summarizes recent advances in the study of chemoreflex malfunction and the underlying mechanisms in acute and chronic lung diseases such as COVID‐19 infection, chronic obstructive pulmonary disease, asthma, obstructive sleep apnoea and acute lung injury. image

Etomidate is commonly used to induce anesthesia in cardiac surgery patients due to its favorable cardiovascular profile. Sedative-hypnotic effects are mediated by gammaaminobutyric acid (GABA) receptor complexes in the central nervous system. There are numerous studies in which etomidate and other drugs are compared in terms of their clinical outcomes. The relative efficacy and safety of etomidate, however, remains inconclusive. In this study, we performed a systematic analysis of randomized controlled trials to assess the impact of etomidate, on patients undergoing cardiac surgery, with respect to patient outcome and adverse events. A systematic review was conducted of all existing clinical trials exploring the safety and efficacy of etomidate in patients undergoing cardiac surgery. Randomized controlled trials (RCTs) that compared etomidate with other drugs during induction in adult cardiac surgery assessing hemodynamic parameters and clinical outcomes were included, while studies involving non-cardiac or pediatric surgery and those lacking relevant outcome data were excluded. Primary outcomes were all-cause 30-day mortality. Secondary outcomes included duration of tracheal intubation, duration of intensive care unit (ICU) stay, duration of hospital stay, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR) and other hemodynamic parameters, vasopressor requirements after induction and intubation, cortisol levels, and incidence of myoclonus. Sixteen randomized controlled trials involving 1162 patients were included. Etomidate did not affect the all-cause 30-day mortality of patients undergoing cardiac surgery compared to comparator drugs (RR, 0.96; 95 % CI, 0.26 to 3.49; P = 0.95). There were no significant differences in the duration of tracheal intubation (MD, -0.08 h; 95 % CI, -1.96 to 1.81; P = 0.94), the duration of ICU stay (MD, -2.07 h; 95 % CI, -8.09 to 3.96; P = 0.50) or the duration of hospital stay (MD, -0.62 d; 95 % CI, -2.25 to 1.00; P = 0.45) when etomidate was compared to comparator drugs. Patients receiving etomidate demonstrated a more stable hemodynamic profile after induction and intubation compared to those receiving comparator drugs. The requirement of a vasopressor after induction and intubation was significantly reduced with etomidate compared with those with comparator drugs (RR, 0.37; 95 % CI, 0.25 to 0.56; P < 0.00001). This systematic meta-analysis found a significant heterogeneity among included studies. In addition, most studies focused only on the hemodynamic profile of etomidate. Thus, efficacy and safety of etomidate could not be answered within this context. Nevertheless, for patients undergoing cardiac surgery, etomidate seems to offer a minimal beneficial cardiovascular profile in comparison with other agents during induction and intubation. However, improved hemodynamics did not improve clinical outcomes as Etomidate did not affect mortality, duration of tracheal intubation, the length of stay in ICU and hospital. Finally, infectious side effects as one important trigger for increased mortality in ICU patients due to the use of Etomidate could not be analyzed as data were mostly missing.

Background and Aims: Extracellular vesicles (EVs) are nanoscale carriers, including exosomes, microvesicles, and apoptotic bodies, that mediate intercellular communication by transporting proteins, nucleic acids, lipids, and metabolites. They regulate immunity, tissue repair, and cell differentiation. Increasing evidence highlights their dual roles in disease, where they may promote tumor growth and immune evasion but also serve as diagnostic and therapeutic tools. This review synthesizes advances in EV biology, their roles in health and disease, and their therapeutic potential. Methods: We conducted a narrative review of recent literature, focusing on EV isolation methods, biological functions, and clinical applications. Sources were selected to capture both mechanistic insights and translational perspectives. Results: Advances in isolation technologies, from ultracentrifugation to microfluidics, have improved the precision of EV characterization. EVs exhibit distinct molecular signatures, positioning them as promising biomarkers in cancer, cardiovascular, neurodegenerative, autoimmune, and infectious diseases. Mechanistic studies demonstrate their roles in immune modulation, tissue remodeling, and regeneration. As therapeutic agents, EVs show promise as drug delivery systems and as platforms for gene and immunotherapies, offering enhanced targeting and reduced toxicity compared to synthetic nanoparticles. Engineered EVs and hybrid EV–liposome systems further expand their applications, though challenges persist in scalability, standardization, and safety. Conclusion: EVs are central mediators of intercellular communication with transformative potential in diagnostics and therapeutics. Their biological properties position them as valuable biomarkers and delivery vehicles in precision medicine. Overcoming translational challenges, such as immunogenicity, oncogenic risks, and manufacturing limitations, will be essential for their successful clinical integration.

Background: Maternal oxycodone (oxy) exposure can disrupt placental function and fetal neurodevelopment, but the molecular mechanisms remain unclear. We investigated whether prenatal oxy exposure activates inflammation and stress response pathways in the placenta and fetal brain, and if maternal melatonin supplementation attenuates these effects. Methods: Female Sprague-Dawley rats received either saline or oxy via oral gavage for 15 days before mating (10-15mg/kg/day dose escalation) and throughout pregnancy (15mg/kg/day). From gestational day (GD) 12.5, half of the dams received melatonin (10mg/kg/day). On GD 19.5, placental and fetal brain tissues were collected. Changes in expression of markers of oxidative stress, antioxidant defense signaling, inflammation, ER stress, and apoptosis were assessed by western blotting. Data were analyzed by two-way ANOVA with Tukey’s post hoc test. Results: Neither oxy exposure nor melatonin treatment increased markers of oxidative stress or antioxidant defenses in the placenta and fetal brain. Oxy exposure increased placental IL-1β expression but did not alter expression of the other inflammatory markers examined. Oxy increased phosphorylation of eIF2α and increased the phospho-eIF2α:eIF2α ratio in the placentas of male fetuses, and fetal brains of both sexes. CHOP expression was increased in the placentas and brains of female, but not male fetuses after oxy exposure. Oxy exposure increased levels of cleaved caspase-3 and cleaved caspase-9 in the fetal brain, but not the placenta; melatonin treatment attenuated the oxy-induced increase in cleaved caspase-9, but not cleaved caspase-3. Conclusion: Prenatal oxy exposure induced a modest inflammatory response in the placenta and activated the integrated stress response and intrinsic apoptotic signaling in the fetal brain. Maternal melatonin supplementation partially mitigated the oxy-induced upregulation of caspase-9 but did not prevent stress signaling in either tissue. These findings demonstrate the presence of sex-specific placental and fetal brain responses to prenatal oxy exposure but suggest that melatonin may not provide complete protection against oxy-induced neurodevelopmental impairment.

Background: The gut–skin axis links intestinal microbial activity with inflammatory skin disease, yet findings across atopic dermatitis, acne vulgaris, and psoriasis remain inconsistent. This review examines how disease biology and host context shape microbiome‐related effects and responses to probiotics. Materials and Methods: Published clinical and experimental evidence on gut microbiota, immune and metabolic signaling, barrier dysfunction, inter‐organ communication, and probiotic interventions was narratively reviewed across atopic dermatitis, acne vulgaris, and psoriasis. Results: Microbiome‐related mechanisms differ by disease. In atopic dermatitis, they intersect with barrier dysfunction and altered immune regulation. In acne vulgaris, metabolic, hormonal, dietary, and neuroendocrine factors modify their effects. In psoriasis, gut dysbiosis occurs within a broader setting of systemic immune activation. Probiotic outcomes are similarly variable and depend on strain, host characteristics, disease context, and study design. Discussion: Gut–skin communication is better interpreted as part of an interconnected physiological network rather than a uniform linear pathway. Disease‐specific evaluation of microbiome changes and probiotic interventions may help explain conflicting findings and guide more targeted future studies.

Respiratory diseases remain major causes of morbidity and mortality; however, inadequate pulmonary drug exposure and systemic toxicity continue to limit treatment efficacy. Inhaled nanomedicines offer opportunities for localized, sustained, and targeted therapy. This review examines how disease biology informs pulmonary delivery design across pulmonary fibrosis, lung cancer, chronic obstructive pulmonary disease, pulmonary infections, and acute lung injury/acute respiratory distress syndrome. It outlines anatomical and biological barriers and compares liposomes, lipid nanoparticles, polymeric and hybrid systems, biomimetic carriers, and stimuli‐responsive formulations. Particular attention is given to matching therapeutic cargo and carrier properties to fibroblasts, macrophages, tumor cells, and alveolar type II cells. Emerging approaches include mRNA delivery, siRNA‐mediated gene silencing, antisense oligonucleotides, and CRISPR‐based editing, alongside alveolar regeneration and biomarker‐guided treatment. These strategies are evaluated in relation to their delivery requirements and stage of development. The review also addresses aerosol‐device compatibility, manufacturing, repeated‐dose safety, regulatory considerations, and clinical outcomes. By connecting delivery mechanisms with disease‐specific applications and clinical evidence, this review identifies both therapeutic opportunities and barriers to translation. This integrated perspective can guide the development of inhaled nanomedicines with more reproducible pulmonary delivery, improved treatment efficacy, and acceptable safety.