Tumor immunotherapy has altered the therapeutic landscape of melanoma, lung cancer, renal cancer, hematologic malignancies, and several mismatch repair deficient tumors, yet durable responses remain uneven across tumor types and patient populations. Major restrictions arise from inefficient antigen presentation, inadequate trafficking and persistence of effector lymphocytes, stromal exclusion, suppressive myeloid compartments, hypoxia, aberrant vasculature, and systemic immune toxicity after nonselective immune activation. Nanomedicine delivery systems provide a materials-based route to adjust where, when, and in which cellular compartment immunomodulators are released. Lipid nanoparticles, polymeric particles, protein and lipoprotein mimetics, inorganic nanomaterials, biomimetic vesicles, and responsive hybrid platforms can co-deliver antigens, adjuvants, checkpoint inhibitors, cytokine modulators, nucleic acids, photosensitizers, or metabolic regulators to tumors and lymphoid tissues. This review summarizes the immunological rationale for nanomedicine design in cancer immunotherapy, with emphasis on active targeting, stimulus-responsive release, multifunctional immune remodeling, checkpoint blockade delivery, nanovaccines, suppressive microenvironment modulation, and combined therapeutic strategies. Current evidence indicates that nanomedicine can improve pharmacokinetics, concentrate immune signals in relevant tissues, reduce systemic exposure, and synchronize innate and adaptive immune activation. Clinical translation still depends on reproducible manufacturing, validated biomarkers of delivery, immune safety, and trial designs that distinguish material effects from payload effects.

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Intervertebral disc degeneration (IDD) is the underlying cause of many spinal diseases, such as disc herniation and chronic low back pain. The pathogenesis of IDD has been the focus of many studies, but its underling mechanisms are complex and not totally clear. Disrupted cells with deficient protein folding capacity or intracellular degradation equilibrium will elicit endoplasmic reticulum stress (ERS), and ERS has recently attracted considerable attention for its pervasive regulatory role in cell function. To respond to this stress, activation of the unfolded protein response (UPR) modifies the function of cell by tuning intracellular processes, including programmed cell death, autophagic flux, inflammatory signalling, metabolic modulation and so on. Increasing evidence has emerged indicating the role of endoplasmic reticulum stress (ERS) in promoting IDD mainly through modulating cellular integrity and extracellular matrix. Such information endows ERS as a potential target for future treatment of IDD. Collectively, we summarize current knowledge about ERS-related mechanisms in IDD and describe emerging intervention strategies, with the aim to contribute to the knowledge and to guide clinical management of IDD.

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As the urbanization process accelerates, the effect of air pollutants with respect to the health of the population has become more apparent, especially as far as its possible hazards to the quality of sleep are concerned, which has gradually gained traction. This paper concentrate on the fine particulate matter (PM 2.5) as the intended research object and adhere to PRISMA guidelines to perform systematic synthesis of the research on the topic published during the period of 2020-2025. The study examines the pathophysiology between PM2.5 exposure and sleep quality in adults. The findings showed that higher levels of PM2.5 are linked with greater Pittsburgh Sleep Quality Index (PSQI) scores, lowest Apnea-Hypopnea Index (AHI) scores, sleep efficiency. Precisely, an average decrease of 1.2 percent in sleep efficiency is caused by a 10 μg/m 3 increment in PM 2.5 concentration. It is also found that the sensitivity to pollution varies among the various age groups with the most pronounced effects being witnessed in the elderly population. Air pollution has become a major environmental risk factor in the context of which sleep health is endangered and the improved management of air quality and personal protection measures are required.

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Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma, and patients with relapsed or refractory (R/R) disease still have few treatment options and poor long-term results after the failure of standard therapy. Recently, some good clinical results have been achieved in the application of CD20×CD3 bispecific antibodies (BsAbs) to direct T cells to malignant B cells. The response of the treated people varies, and not everyone can maintain remission for a long time. More and more studies have shown that the tumour microenvironment can affect the response to therapy. Radiotherapy (RT) is used to treat cancer locally, and now it is also known for modulating the immune system. RT can cause immunogenic cell death, release tumor antigens, and increase the infiltration of immune cells in the tumour microenvironment; thus, it is one of the reasons for combination therapy with BsAbs. Review of Recent Research on RT in Combination with BsAbs for R/R DLBCL: Treatment Sequence, Radiation Dose and Fractionation, Differences among BsAb Platforms. At present, it is known that RT can enhance the antitumor effect of BsAb by promoting immune activation and T-cell migration; however, clinical results have been inconsistent in various studies. There is no standard RT protocol and reliable predictive biomarkers, so some patients have been harmed by the treatment so far.

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