Laboratory-acquired infections (LAIs) have been documented since the first report of typhoid fever in 1885 and continue to endanger laboratory professionals despite decades of biosafety advances. This review provides a comprehensive overview of LAIs, emphasizing their history, modes of transmission, and strategies for prevention.

A systematic review of historical records, case series, and biosafety guidance (1885–2025) identified documented LAIs, their transmission routes, and preventive measures. Data were extracted on pathogen spectrum, geographic distribution, incident outcomes, and the effectiveness of biosafety interventions.

Historical analysis identified 50 laboratory-acquired typhoid infections with six deaths from 1885 to 1915, largely due to mouth pipetting and aerosol exposure. A sharp decline in fatal bacterial infections was observed following the introduction of Class II biosafety cabinets in the 1960s. From 2000 to 2021, 309 LAIs were reported across 94 studies, most commonly Salmonella enterica (56.6%), vaccinia virus (4.2%), and Brucella species (3.9%), with Brucella responsible for over half of hospital-laboratory cases (60 per 100,000 personnel-years). In Canada during 2023, 63 exposure events occurred, including three confirmed infections despite adherence to biosafety level protocols. Environmental persistence studies underscored surface-borne risks. The most effective preventative measures included abolishing mouth pipetting, mandatory use of gloves and eye/face protection, routine Class II biosafety cabinet use for aerosol-generating procedures, surface disinfection with 0.5% sodium hypochlorite, and annual competency-based biosafety training with incident reporting.

LAIs remain geographically widespread and pathogen-diverse. Quantitative historical trends and contemporary surveillance highlight critical transmission routes, including ingestion, inoculation, mucosal splash, and inhalation, while reinforcing evidence-based prevention strategies. Sustained investment in biosafety infrastructure, real-time exposure reporting, and pathogen-specific training is essential to further reduce LAI incidence and severity in the face of emerging antimicrobial resistance and novel agents.

Breast cancer remains one of the most common cancers affecting women globally, with late detection frequently contributing to its high mortality rate. Multiple factors drive these delays, including a lack of awareness, financial constraints in low-income countries, and limited access to non-invasive and accurate biomarkers. This review aims to introduce biomarkers, particularly hematological and biochemical serum markers, as essential, non-invasive, and accurate tools for improving the diagnosis, prognosis, and therapeutic management of breast cancer. Hematological markers are measurable blood parameters that reflect physiological and pathological processes such as inflammation, infection, cardiovascular stress, autoimmune conditions, and cancer. Routinely measured hematological markers, such as the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and red blood cell indices, are typically obtained from standard tests like the complete blood count. Regular monitoring through complete blood count is essential during cancer treatment to evaluate changes in blood cell counts and detect potential adverse effects. Because of their affordability, minimal infrastructure requirements, and broad accessibility, hematological parameters have been increasingly studied for their association with high-risk factors in breast cancer, particularly in resource-limited settings. Their utility underscores their critical role in improving patient outcomes across diverse healthcare environments. This review summarizes the clinical value of various hematological and serum-based biochemical markers in the screening and diagnosis of breast cancer. Prediction methods that incorporate hematological and serum-based biochemical parameters can support screening, diagnosis, and staging. Overall, individual or combined blood indicators hold significant potential to enhance diagnostic accuracy and effectiveness.

Uterine fibroids (UFs) are common hormone-dependent tumors with a complex etiology involving both genetic and environmental factors. This study aimed to investigate, for the first time, the associations between loci from genome-wide association studies (GWAS) and environmental risk factors in UF development, with a particular focus on gene–environment interactions.

DNA samples from 737 women with UF and 451 healthy controls were genotyped for ten UF-associated GWAS single nucleotide polymorphisms (SNPs) using probe-based polymerase chain reaction in this case-control study.

SNP rs66998222 (LOC102723323, G/A) was associated with decreased UF risk in the total sample (odds ratio (OR) = 0.81, p = 0.038) and in patients with a history of induced abortion (OR = 0.70, p = 0.009). SNP rs11031731 (THEM7P, WT1, G/A) increased UF risk overall (OR = 1.39, p = 0.01), and in women with abortion history (OR = 1.60, p = 0.008) or without pelvic inflammatory disease (OR = 1.43, p = 0.02). SNPs rs641760 (PITPNM2, C/T) and rs2553772 (LOC105376626, G/T) showed protective effects depending on abortion history. SNP rs1986649 (FOXO1, C/T) was associated with later UF onset (p = 0.049) and slower growth (p = 0.017). GWAS loci influence UF-related genes involved in proliferation, inflammation, and hormone metabolism, underscoring their pathogenic role.

Induced abortions and inflammation modify the effects of GWAS-identified UF risk loci, with allele-specific impacts on hormonal, inflammatory, and repair pathways. Replication in diverse cohorts is needed to validate these population-specific effects.

Mitochondrial respiratory complexes (Complexes I–V) and their assembly into respiratory supercomplexes (SCs) are fundamental to liver bioenergetics, redox homeostasis, and metabolic adaptability. Disruption of these systems contributes to major liver diseases, including non-alcoholic fatty liver disease, alcoholic liver disease, drug-induced liver injury, viral hepatitis, and hepatocellular carcinoma, by impairing adenosine triphosphate synthesis, increasing oxidative stress, and altering metabolic pathways. Recent advances have clarified the structural-functional interdependence of individual complexes within SCs, revealing their dynamic remodeling in response to physiological stress and pathological injury. These insights open opportunities for clinical translation, such as targeting SC stability with pharmacological agents, nutritional strategies, or gene therapy, and employing mitochondrial transplantation in cases of severe mitochondrial failure. Precision medicine approaches, incorporating multi-omics profiling and patient-derived models, may enable individualized interventions and early detection using SC integrity as a biomarker. By linking molecular mechanisms to therapeutic strategies, this review underscores the potential of mitochondrial-targeted interventions to improve outcomes in patients with liver disease.

Ischemic stroke is a complex cerebrovascular disorder characterized by highly unpredictable outcomes influenced by patient-specific variables, including age, stroke severity, and preventable stroke-related complications such as infections. Analyses of clinical data have indicated a cumulative post-stroke infection rate of approximately 30%, with reported rates ranging from 5% to 65%. Post-stroke infections pose a significant challenge, as they not only increase the financial burden of stroke care but are also associated with adverse clinical outcomes, prolonged hospital stays, and a higher risk of stroke recurrence. The inflammatory response plays a pivotal role in the pathophysiology of ischemic stroke, encompassing the activation of inflammatory cells, the release of inflammatory mediators, and the engagement of inflammatory signaling pathways. Recent advances in molecular biology have facilitated the identification and investigation of numerous inflammation-related biomarkers. This article reviews the roles and mechanisms of key inflammatory biomarkers, including cytokines, chemokines, adhesion molecules, inflammation-related enzymes and mediators, receptors, signaling pathway molecules, and acute-phase proteins in the context of ischemic stroke, highlighting their significance in stroke pathophysiology and prognostic assessment. Additionally, in conjunction with the latest research advances, the article discusses novel biomarkers such as microRNAs and galectin-3, which are emerging as important tools in multiple domains, including diagnosis and treatment. Drawing on clinical diagnostic and therapeutic practices, this review analyzes the diagnostic and therapeutic roles of both novel and traditional biomarkers in the progression of ischemic stroke, following the temporal sequence from disease onset to prognosis. Finally, the article addresses the limitations of current research and offers perspectives on future directions, providing insights that may contribute to the advancement of precision medicine in the management of ischemic stroke.

It is established that administration of the COVID-19 vaccine may be associated with an exaggerated immune response leading to enlargement of several lymph nodes. Although most cases are benign and self-limiting, some have been reported in the literature as B-cell or T-cell lymphomas, with no reported cases of chronic lymphocytic leukaemia (CLL). We report two cases of follicular lymphoma and CLL that occurred a few weeks after COVID-19 vaccination. Case 1 is a 48-year-old woman who noticed two significantly palpable masses, one in each axilla, 48 h after receiving the first dose of the Pfizer-BioNTech BNT162b2 vaccine for COVID-19. Seven days later, she noticed another mass on the right side of her neck, which was biopsied within 48 hours. Case 2 is a 75-year-old man who presented with localized swellings in the axilla and on the neck, noted 24 h after the first dose of the Moderna messenger RNA-1273 COVID-19 vaccine. Neither patient reported any constitutional or associated symptoms. Surgical biopsy of the axillary lymph node in case 1 revealed a non-Hodgkin lymphoma, confirmed via immunohistochemistry as CD20-positive B-cell follicular lymphoma. The patient also had multiple pre- and para-aortic lymph nodes. In case 2, complete blood count showed lymphocytosis (total white blood cell – 148 × 109/L; lymphocyte differential – 92%), while peripheral blood film showed lymphocytosis with a predominance of small, mature-looking lymphocytes, both suggesting CLL. Although requested, immunophenotyping and molecular testing were not performed due to patient-related challenges. Although a chance occurrence is possible, lymphoid malignancies should be considered a strong differential. The vaccination history of patients presenting with clinical manifestations suggestive of a lymphoid malignancy should be thoroughly investigated, while ruling out other possible differentials such as a benign, self-limiting inflammatory process.

Chimeric antigen receptor (CAR)-T cell therapy faces significant challenges in treating solid tumors, including immune evasion, suppressive tumor microenvironments, and on-target/off-tumor toxicity, which limit its clinical efficacy. Although it has revolutionized treatment for hematological malignancies, these obstacles hinder its broader application in solid tumors. Nanotechnology offers innovative strategies to address these limitations through enhanced delivery, localization, and control. This review summarizes recent advances in nanotechnology-assisted CAR-T cell therapies for gynecologic cancers, with a particular focus on messenger RNA (mRNA)-based delivery systems, lipid nanoparticles, hydrogels, and external activation techniques such as photothermal and acoustogenetic modulation. The integration of nanotechnology, especially mRNA-based delivery systems, holds transformative potential for overcoming these barriers. mRNA enables transient, non-integrating expression of CARs, meaning the genetic modifications are temporary. This improves safety and allows flexible control over treatment intensity, while rational sequence optimization (e.g., codon usage, guanine-cytosine content, secondary structure) enhances mRNA stability and protein translation efficiency. Lipid nanoparticles, the leading delivery platform, can be engineered for cell-type specificity and tissue targeting through modulation of their components and surface functionalization. Recent innovations, including siloxane-modified lipid nanoparticles, injectable hydrogels, and photothermal or acoustogenetic activation strategies, enable precise spatiotemporal control of CAR-T cell function in vivo. In ovarian cancer, preclinical studies targeting nfP2X7 and employing multifunctional nanoparticles have demonstrated synergistic efficacy and tumor-specific delivery. This review highlights how nanotechnology platforms can be integrated with CAR-T cell therapies to enhance safety, precision, and therapeutic outcomes in ovarian cancer.

Medulloblastoma (MB) is a malignant neoplasm that is relatively common in children but rare in young adults, accounting for less than 1% of all intracranial tumors. This study reports a rare case of MB metastasis to the right temporoparietal region in a 42-year-old woman, presenting with focal neurological symptoms such as weakness in the left arm and leg, speech disturbances, and impaired coordination. The patient had a history of cerebellar MB and underwent surgical resection, radiation therapy, and chemotherapy. Despite treatment, metastasis occurred, highlighting the diagnostic and therapeutic challenges in adult MB cases. The article also reviews the literature on MB in young adults, emphasizing the importance of dynamic neuroclinical monitoring and timely instrumental diagnosis for early detection and management of MB metastases.

Craniopharyngioma (CP), although histologically benign, is a surgically challenging sellar-region tumor for which stereotactic irradiation is increasingly used as an alternative or adjuvant strategy. This review summarizes the role of stereotactic radiosurgery (SRS) in managing CP, with a focus on treatment outcomes, technical advances, and emerging strategies to support evidence-based clinical practice. Literature reports indicate that Gamma Knife radiosurgery achieves variable tumor control rates (36–100%), with optimal outcomes (79.6–91.4%) when marginal doses ≥12 Gy are delivered and patients receive adequate follow-up. Smaller tumors (<5 cm3) and those with higher solid components show particularly favorable outcomes. SRS demonstrates a favorable safety profile, with visual impairment occurring in approximately 4% of cases and endocrine dysfunction in 6%. Compared to conventional radiotherapy, SRS significantly reduces the risk of hypothalamic obesity in pediatric patients. The identification of BRAF mutations in papillary CPs has created novel opportunities for combining targeted therapies with SRS. Collectively, these advances underscore the role of SRS as an essential component of multidisciplinary CP management, particularly in the treatment of residual or recurrent lesions. It offers a more favorable toxicity profile and may improve quality of life outcomes compared to conventional radiotherapy. Further studies are needed to optimize patient selection, dosing strategies, and integration with novel systemic therapies.