While the association between serum albumin and eosinophils has been investigated in adult asthma, its role in any pediatric atopic triad - asthma, allergic rhinitis, or atopic dermatitis - remains unclear. We assessed the association between serum albumin and blood eosinophil counts in adolescents presenting with any atopic triad, using data from a 2-year National Health and Nutrition Examination Survey (NHANES) cycle. We analyzed data from 658 participants aged 12-18 years with any atopic triad condition from the 2005-2006 NHANES cycle. Multivariate linear regression models were employed to assess the potential association between serum albumin levels and blood eosinophil counts (BEOC). Trend tests, smooth curve fitting, and threshold effect models were applied to confirm this relationship, and stratified analyses were conducted to assess its consistency across subgroups. A significant negative association was observed between serum albumin and BEOC in the fully adjusted model (β = -0.08 × 103 cells/µL, 95% CI: -0.15, -0.01, P = .018). Moreover, curve fitting and threshold effect analyses confirmed a nonlinear relationship between serum albumin and BEOC, with an inflection point for threshold and saturation effects of 4.4 g/dL, beyond which the association attenuated. Stratified analyses confirmed robustness across key subpopulations. Our study identified a nonlinear association between serum albumin levels and BEOC in adolescents with any atopic triad, exhibiting an L-shaped relationship. These findings highlight albumin as a potential biomarker for nutritional-immunological interplay in allergic inflammation and support targeted nutritional strategies in at-risk pediatric populations.

Obstructive sleep apnea (OSA), obesity, and cancer constitute an interconnected pathophysiological triad withi mportant implications for morbidity and mortality. Obesity is a major upstream driver of both OSA and tumorigenesis, while OSA contributes independently through intermittent hypoxia, sleep fragmentation, systemici nflammation, oxidative stress, immune dysregulation, and sympathetic activation. Emerging evidence links OSA-associated hypoxemia to cancer initiation, progression, and treatment response, with hypoxic burden and nocturnal oxygen desaturation metrics outperforming the apnea-hypopnea index in predicting cancer-related outcomes. Mechanistic advances implicate immune checkpoint signaling, extracellular matrix remodeling, and metabolic-hepatic pathways as key mediators of OSA-related oncogenesis. Epidemiological studies support associations between OSA and several malignancies independent of obesity, although residual confounding remains a challenge. Therapeutically, continuous positive airway pressure may mitigate hypoxemia-related pathways, whereas bariatric surgery and GLP-1/GIP receptor agonists off er the potential to simultaneously reduce obesity, OSA severity, and cancer risk. Precision medicine approaches integrating hypoxemia phenotyping, immune profi ling, and targeted interventions are needed to optimize prevention and treatment strategies.

In the aftermath of the COVID-19 pandemic, telemedicine has evolved from a contingency-based alternative into a structural pillar of healthcare delivery, increasingly being integrated with artificial intelligence. Algorithms for triage, clinical decision support, remote monitoring, and generative language models now actively participate in medical care. This integration is more than just functional; it reorganizes the foundational aspects of medicine-ontological, ethical, and epistemological-by redefining what qualifies as valid knowledge, who has legitimate authority, and how care is organized when an algorithmic agent facilitates the clinical interaction. This article critically examines the emergence of the patient-clinician-algorithm triad in telemedicine, and analyzes its implications for autonomy, informed consent, epistemic trust, privacy, justice, responsibility, and the phenomenology of care. It argues that the future of medicine will not be human or algorithmic but human-algorithmic, provided clinical judgment, explainability, and moral responsibility remain central.

The lung is among the most radiosensitive organs and a principal dose-limiting organ in thoracic radiotherapy, yet the acute metabolic consequences of irradiation at the lipidomic level remain poorly characterized. We constructed a time-resolved lipidomic atlas of the murine lung response to high-dose irradiation. Male C57BL/6 J mice received a single 10 Gy whole-body X-ray dose, and lungs were collected at 5 minutes, 1 hour, 4 hours, and 24 hours post-exposure (n = 5 per group) and analyzed by untargeted liquid chromatography-tandem mass spectrometry. Radiation triggered rapid and coordinated lipid remodeling. Principal component analysis revealed a structured temporal trajectory, and oxidized lipid species increased significantly by 24 hours. Pulmonary surfactant lipids, including dipalmitoylphosphatidylcholine and phosphatidylglycerol, underwent early and progressive oxidation. Membrane signaling lipids shifted in a manner consistent with a transient pro-survival bias, with ceramide depletion, sphingomyelin accumulation, and phosphatidylserine oxidation. Mitochondrial lipids displayed a coordinated triad of early cardiolipin oxidation, progressive coenzyme Q depletion, and sustained phosphatidylethanolamine accumulation. Lysobisphosphatidic acid accumulated steadily, consistent with endolysosomal activation, while storage triglycerides and diglycerides were rapidly mobilized and free fatty acids accumulated at later time points. Class-level changes were temporally ordered and compartmentally organized, indicating that the acute lipid response is not confined to oxidative damage. The lipid classes involved overlap with those implicated in ferroptosis, mitophagy, lipophagy, and surfactant biology, although these processes were not assessed directly here. This atlas is offered as a descriptive resource for mechanistic study of radiation-induced lung injury.

Despite rapid advances in clear aligner therapy, the low predictability of aligner tooth movements remains a clinical challenge. This article (part 2) translates the conceptual biomechanical triad of anchorage, stress continuity, and aligner-tooth contact, along with the related determinant factors, described in part 1 into practical strategies to enhance the predictability of tooth movements with clear aligners. This paper features 3 interrelated strategic domains: patient-centered, aligner-mediated, and practitioner-directed strategies. Patient-centered strategies emphasize appropriate aligner case selection, aligner-favored treatment planning, and difficulty-based patient management. Aligner-mediated strategies focus on choosing optimal aligner materials, reducing aligner stress concentration, and optimizing aligner designs. Furthermore, practitioner-directed strategies highlight the practitioner's active role in managing the fundamental prerequisites of tooth movements (ie, force, space, and time). This is achieved through deliberate overtreatment with aligners, biomechanical augmentation with attachments and auxiliaries, judicious staging sequences that prioritize predictable movements, and dynamic monitoring and troubleshooting protocols. Collectively, in clinical practice, the 3 strategic domains should not be isolated but rather be integrated to achieve predictable tooth movements with clear aligners.

Zinner syndrome is a rare congenital malformation of the urogenital system characterized by the triad of unilateral renal agenesis, ipsilateral seminal vesicle cyst, and ipsilateral ejaculatory duct obstruction. A variant of Zinner syndrome is present when, instead of a seminal vesicle cyst, there is agenesis of the ipsilateral seminal vesicle. Although Zinner syndrome has been associated with urogenital neoplasms in some cases, to our knowledge, no case of a patient with Zinner syndrome and a contralateral neuroendocrine tumor (NET) has been previously described. The patient is a 26-year-old man who developed urinary retention due to a tumor of the right seminal vesicle infiltrating the prostate and obstructing the prostatic urethra. Abdominal and bladder MRI showed dysgenesis of the left kidney, seminal vesicle, and ejaculatory duct, as well as a mildly contrast-enhancing mass of the right seminal vesicle infiltrating the adjacent prostate. Gallium-68 PET-CT showed increased somatostatin receptor (SSTR) expression in the right seminal vesicle. Histologically, it was a well-differentiated NET with infiltrates of epithelial tumor cells that were positive for chromogranin, synaptophysin, and CD56. Chromogranin was also increased in the serum. The patient underwent radical prostatectomy, and it was decided not to proceed with chemotherapy or radiotherapy. Zinner syndrome may be associated with a contralateral NET of the genitourinary tract. Therefore, patients with Zinner syndrome should be regularly followed up to avoid overlooking a co-occurring malignancy.

BACKGROUND Zinner syndrome is a rare congenital anomaly of the male genitourinary system, characterized by the classic triad of features: a seminal vesicle cyst, unilateral renal agenesis, and vas deferens obstruction. This article presents a clinical case of a 36-year-old patient with this rare condition and describes the results of his successful laparoscopic surgical treatment. CASE REPORT A 36-year-old man with a 2-year history of infertility and chronic pelvic pain received a diagnosis of Zinner syndrome, characterized by the triad of left renal agenesis, ipsilateral ureteral atresia, and a large seminal vesicle cyst. He underwent successful laparoscopic excision of the cyst. The cyst contents (approximately 120 mL of light-brown fluid) were aspirated, followed by meticulous enucleation. The cyst, remnant seminal vesicle tissue, and distal atretic ureter (3 cm) were completely resected. Histopathological examination confirmed a benign, multilocular cyst lined by columnar epithelium with glandular metaplasia and chronic inflammation, with no evidence of malignancy. The postoperative course was uneventful. At 3-month follow-up, the patient reported complete resolution of pain and normalized urination. Semen analysis showed significant improvement: ejaculate volume increased to 1.6 mL, sperm concentration to 1.4×10[7]/mL, and progressive motility to 35%, indicating partial recovery of ejaculatory function. The case demonstrates that laparoscopic surgery is an effective treatment for Zinner syndrome, alleviating symptoms and potentially improving fertility parameters. CONCLUSIONS This case highlights the importance of timely recognition of Zinner syndrome, especially in patients with unilateral renal agenesis and pelvic pain, and demonstrates the effectiveness of the laparoscopic approach as a method of choice in the symptomatic course of this pathology.

Melanocyte homeostasis is highly dependent on mitochondrial function and redox balance, while oxidative stress and mitochondrial dysfunction are considered key pathogenic factors in vitiligo. However, the upstream regulatory mechanisms remain incompletely understood. In this study, we investigated the roles of histidine triad nucleotide-binding protein 1 (HINT1) and armadillo repeat-containing protein 10 (ARMC10) in melanogenesis and their potential mechanisms in vitiligo. Clinical sample analysis revealed that the expression levels of HINT1 and ARMC10 were significantly altered in lesional skin of vitiligo patients compared with normal controls. In vitro, knockdown of HINT1 or ARMC10 in B16 cells markedly affected melanin production, as evidenced by changes in melanin content, tyrosinase activity, and the expression of melanogenesis-related genes including MITF, TYR, TRP-1, and TRP-2. HINT1 or ARMC10 deficiency was associated with increased mitochondrial reactive oxygen species (ROS) accumulation and impaired mitochondrial membrane potential, indicating mitochondrial dysfunction. Furthermore, transmission electron microscopy and protein analysis suggested the involvement of mitochondrial quality control processes. Transcriptomic analysis further supported the enrichment of oxidative stress- and mitochondrial-related pathways. In vivo, knockdown of HINT1 or ARMC10 affected depigmentation and melanogenesis-related markers in a vitiligo mouse model. In conclusion, our findings suggest that HINT1 and ARMC10 are involved in the regulation of melanogenesis and are associated with oxidative stress and mitochondrial dysfunction in melanocytes.

The gut-brain axis represents an emerging therapeutic target. This study seeks to investigate the regulatory effects of LXTL on the brain-gut axis and to elucidate its mechanism of action during the ischemic stroke recovery period. This study investigated the effects of LXTL on a middle cerebral artery occlusion and reperfusion model. The assessment of recovery effects was conducted through the evaluation of brain injury scores, Y-maze performance, open field tests. Furthermore, comprehensive analyses were conducted on the gut microbiota, damaged brain tissue, cecal contents, and brain samples using metagenomic sequencing, transcriptomic sequencing, and non-targeted metabolomics. And the selected targets were verified. Integrated analyses were conducted by constructing correlation networks and performing joint pathway enrichment to elucidate the connections between microbial alterations, metabolite changes, and gene expression modifications. LXTL improved cognitive and exploratory behaviors, reduced brain damage and neuron loss, and enhanced gut health by increasing beneficial bacteria like Eubacterium and Kurthia. It boosted SCFAs, neuroactive metabolites, and altered nucleotide metabolism. LXTL is linked to genes involved in neurorepair and immune homeostasis, correlates with microglial polarization, and is associated with genes such as Ngfr, Card9, Chat, Nkg7, and Gch1 within the pertinent pathways. The integrated network linked LXTL-enhanced microbiota, gut and brain metabolites, and repair genes, facilitating recovery through a neurorepair-immune-metabolic triad. LXTL aids ischemic stroke recovery by altering gut microbiota and gut-brain metabolite profiles, while regulating brain gene networks related to neuroplasticity, inflammation, and metabolism. This demonstrates LXTL's multi-target effects through the gut-brain axis, underscoring the potential of herbal medicine in stroke rehabilitation.