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Lung cancer is a highly prevalent and lethal type of cancer. Although targeted therapy and immunotherapy have received considerable attention in the treatment of lung cancer, particularly non-small cell lung cancer (NSCLC), there has been limited improvement in the overall recovery and survival rates of lung cancer patients. Thus, there is currently a substantial need for more effective therapies for NSCLC. This study aimed to define a new approach for treating NSCLC by employing a nanoparticle-based strategy for co- delivering PD-L1 inhibitor and a targeted candidate, sotorasib. Sotorasib is a small molecule that specifically and irreversibly inhibits KRASG12C, which is the most prevalent KRAS mutation observed in non-small cell lung cancer (NSCLC). This indicates that the combination of targeted therapy with immunotherapy, resulting in a synergistic impact, holds promise as a potential treatment for NSCLC.

The global healthcare system faces increasing threats from emerging and re-emerging pathogens. Current understanding of host-pathogen interactions and underlying immune mechanisms remains incomplete, which hinders the development of effective diagnostic tools and therapeutic strategies. The receptor for activated C kinase 1 (RACK1) is a multifunctional scaffolding protein that integrates diverse signaling pathways, modulates translation, and regulates key cellular processes. Despite accumulating evidence implicating RACK1 in host immune response to infections, its multifaceted roles and mechanisms remain poorly defined. Hence, this review systematically discusses the involvement of RACK1 in host defense against bacterial and viral pathogens, with a focus on its regulation of inflammatory signaling, inflammasome activation, hormone-mediated immune regulation, reactive oxygen species production, adaptive immunity, and different pathogen infections. Together, current evidence suggests that RACK1 links signaling and translation to shape immune responses in different infectious settings and may provide a basis for host-directed therapeutic strategies.

Long non-coding RNAs (lncRNAs) are emerging as master regulators of the lung cancer tumor microenvironment (TME), where they reprogram immune cell functions, cytokine networks, and checkpoint signaling to create an immunosuppressive and therapy-resistant landscape. This review offers a comprehensive analysis of how lncRNAs mediate the interplay between tumor cells and immune components, underscoring their context-dependent roles as both oncogenic drivers and microenvironmental suppressors. It also highlights their clinical utility as liquid-biopsy biomarkers and their central role in conferring resistance to chemo- and radio-therapy. This review synthesizes current knowledge on the interplay between lncRNAs and the TME, highlighting the targeting of specific lncRNAs as a novel therapeutic strategy for precision lung cancer therapy.

Despite significant advances in preventive and early-detection strategies, cervical cancer (CC) continues to pose a substantial clinical burden, especially when confronting the challenge of therapy-resistant or recurrent disease. Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in the development and progression of CC, particularly in mediating resistance to conventional and emerging therapies, including chemotherapy, radiotherapy, and immunotherapy. This review summarizes how specific lncRNAs drive therapeutic resistance through diverse mechanisms such as acting as competitive endogenous RNAs (ceRNAs) to sponge tumor-suppressive microRNAs, and by modulating key signaling pathways like PI3K/Akt and Wnt/β-catenin. Furthermore, we discuss the significant potential of lncRNAs as non-invasive diagnostic and prognostic biomarkers, detectable in liquid biopsies from patient serum or plasma, and as novel therapeutic targets. Advances in targeted strategies have primarily focused on the implementation of precise degradation or interference through antisense oligonucleotides (ASOs) and CRISPR-based systems, highlighting the translational potential of lncRNAs in overcoming refractory therapeutic resistance. Collectively, this review aims to provide a comprehensive overview of the multifaceted roles of lncRNAs in CC therapeutic resistance, offering critical insights that may accelerate the translation of lncRNA-based strategies into clinically actionable interventions to improve patient outcomes in therapy-resistant CC.

As a pivotal member of the p53 family, the p63 gene plays an indispensable role in skin homeostasis and development. The gene encodes multiple isoforms, primarily TAp63 and ΔNp63, which differentially regulate cell proliferation, differentiation, and stress responses through complementary mechanisms. This comprehensive review systematically examines the molecular mechanisms and cellular functions of p63 in cutaneous biology, with particular emphasis on its dual roles in maintaining skin integrity and contributing to disease pathogenesis. We detail the essential functions of p63 in skin development, encompassing epithelial fate determination, chromatin remodeling, cell adhesion, and barrier formation, while also exploring its involvement in skin regeneration and differentiation via metabolic reprogramming and stem cell modulation. Furthermore, we analyze how mutations in p63 underlie ectodermal dysplasia and various dermatological disorders, underscoring the gene’s fundamental importance in cutaneous health. By integrating current knowledge of the diverse biological roles of p63 and its associated therapeutic potential as a target, this review highlights its central significance in both skin physiology and pathology.

Background In critically ill sepsis patients the use of certain antibiotics can be associated with adverse effects. This study investigates the relationship between the use of different classes of antibiotic during the intensive care unit stay and the 30-day mortality risk in patients with sepsis-associated encephalopathy. Methods This retrospective observational study collected data from the Medical Information Mart for Intensive Care IV database between 2008 and 2019. The antibiotic classes assessed included cephalosporins, penicillins, carbapenems, quinolones, macrolides, and metronidazole. The Cox proportional hazards model was employed to assess the association between the use of different classes of antibiotic and mortality risk in patients with sepsis-associated encephalopathy. Results The 30-day mortality was 16.19% (643 out of 3974 patients). The use of penicillins (hazard ratio: 1.32, 95% confidence interval: 1.11–1.58, P  = 0.002), macrolides (hazard ratio: 1.50, 95% confidence interval: 1.13–2.00, P  = 0.005), and metronidazole (hazard ratio: 1.32, 95% confidence interval: 1.11–1.57, P  = 0.002) were associated with a higher risk of 30-day mortality. The use of one, two, or more than three antibiotic classes were associated with an increased risk of 30-day mortality (all P  < 0.05). In sepsis-associated encephalopathy patients aged ≥ 65 years, with Sequential Organ Failure Assessment scores ≥ 6, Charlson comorbidity index scores ≥ 2, Glasgow Coma Scale ≥ 8, experiencing acute kidney injury, and receiving opiates or propofol, the number of administered antibiotic classes was significantly associated with increased 30-day mortality risk. Conclusion We found an association between penicillins, macrolides, and metronidazole usage and 30-day mortality in sepsis-associated encephalopathy patients that needs future prospective randomized control trials to establish causal relationship.

Objective Long non‐coding RNA (lncRNA) has become an important regulator of many human malignancies. However, the biological role and clinical significance of most lncRNA in gastric cancer (GC) remain unclear. Methods We investigate the biological function, mechanism of action and clinical expression of lncRNA MYOSLID in GC. First, we analysed the differential expression of lncRNA MYOSLID in GC tissues and non‐cancerous tissues by analysing the sequencing data obtained from The Cancer Genome Atlas. Subsequently, we verified that lncRNA MYOSLID regulates the proliferation and apoptosis of GC cells by acting as a ceRNA against miR‐29c‐3p. The nude mouse xenograft was used to further confirm the functional significance of lncRNA MYOSLID in vivo. Results We found for the first time that the expression of lncRNA MYOSLID was significantly up‐regulated in GC tissues, and the up‐regulation of lncRNA MYOSLID in GC was correlated with tumour size, AJCC stage, depth of invasion and survival time. In addition, apoptosis and growth arrest can be induced in vitro after knockdown of lncRNA MYOSLID, which inhibits tumorigenesis in mouse xenografts in vivo. Further in‐depth studies revealed that lncRNA MYOSLID acts as a ceRNA of miR‐29c‐3p, resulting in de‐repression of its downstream target gene MCL‐1. Conclusion The lncRNA MYOSLID‐miR‐29c‐3p‐MCL‐1 axis plays a key role in the development of GC. Our findings may provide potential new targets for the diagnosis and treatment of human GC.

Background Assessing residual motor function in motor complete spinal cord injury (SCI) patients using surface electromyography (sEMG) is clinically important. Due to the prolonged loss of motor control and peripheral sensory input, patients may struggle to effectively activate residual motor function during sEMG assessments. The study proposes using virtual reality (VR) technology to enhance embodiment, motor imagery (MI), and memory, aiming to improve the activation of residual motor function and increase the sensitivity of sEMG assessments. Methods By Recruiting a sample of 12 patients with AIS A/B and capturing surface electromyographic signals before, druing and after VR training, Results Most patients showed significant electromyographic improvements in activation frequency and or 5-rank frequency during or after VR training. However, one patient with severe lower limb neuropathic pain did not exhibit volitional electromyographic activation, though their pain diminished during the VR training. Conclusions VR can enhance the activation of patients’ residual motor function by improving body awareness and MI, thereby increasing the sensitivity of sEMG assessments.

Low-cost electrocatalysts with high catalytic activity for hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) are essential for electrochemical water splitting to produce hydrogen. In this study, we report the combination of porosification and doping strategy to improve the catalytic activity of NiCo.sub.2O.sub.4-based electrocatalysts for HER and OER. A facile porosification method was proposed and demonstrated by annealing the NiCo.sub.2O.sub.4 nanosheets in a reductive atmosphere to synthesize porous NiCo.sub.2O.sub.4 nanosheets. In order to further improve the catalytic activity for HER and OER, the porous NiCo.sub.2O.sub.4 nanosheets were doped with P and Fe, respectively, which tailored the electronic structure of the electrocatalysts, improved the intrinsic catalytic activity, and increased the number of active sites. HER or OER experiments were performed on the porous P-NiCo.sub.2O.sub.4 nanosheets or the porous NiCo.sub.1.5Fe.sub.0.5O.sub.4 nanosheets, which required an overpotential of 160 mV or 222 mV to deliver a current density of 10 mA/cm.sup.2, respectively. Furthermore, overall water splitting was achieved using the porous P-NiCo.sub.2O.sub.4 nanosheet cathode and the porous NiCo.sub.2-xFe.sub.xO.sub.4 nanosheet anode with a Faraday Efficiency of 98.22%. The present paper proposes a strategy to fabricate doped porous electrocatalysts with a view to providing insights for the design and synthesis of efficient and inexpensive electrocatalysts for water splitting.

Low-cost electrocatalysts with high catalytic activity for hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) are essential for electrochemical water splitting to produce hydrogen. In this study, we report the combination of porosification and doping strategy to improve the catalytic activity of NiCo 2 O 4 -based electrocatalysts for HER and OER. A facile porosification method was proposed and demonstrated by annealing the NiCo 2 O 4 nanosheets in a reductive atmosphere to synthesize porous NiCo 2 O 4 nanosheets. In order to further improve the catalytic activity for HER and OER, the porous NiCo 2 O 4 nanosheets were doped with P and Fe, respectively, which tailored the electronic structure of the electrocatalysts, improved the intrinsic catalytic activity, and increased the number of active sites. HER or OER experiments were performed on the porous P-NiCo 2 O 4 nanosheets or the porous NiCo 1.5 Fe 0.5 O 4 nanosheets, which required an overpotential of 160 mV or 222 mV to deliver a current density of 10 mA/cm 2 , respectively. Furthermore, overall water splitting was achieved using the porous P-NiCo 2 O 4 nanosheet cathode and the porous NiCo 2-x Fe x O 4 nanosheet anode with a Faraday Efficiency of 98.22%. The present paper proposes a strategy to fabricate doped porous electrocatalysts with a view to providing insights for the design and synthesis of efficient and inexpensive electrocatalysts for water splitting. Graphical abstract