Enhanced Oxygen Accumulation for a Hydrophobic Cathode in Lean-Oxygen Seawater Batteries.

The unsatisfactory oxygen reduction reaction (ORR) kinetics caused by the inherent lean-oxygen marine environment brings low power density for metal-dissolved oxygen seawater batteries (SWBs). In this study, we propose a seawater/electrode interfacial engineering strategy by constructing a hydrophobic coating to realize enhanced mass transfer of dissolved oxygen for the fully immersed cathode of SWBs. Accumulation of dissolved oxygen from seawater to the catalyst is particularly beneficial for improving the ORR performance under lean-oxygen conditions. As a result, SWB assembled with a hydrophobic cathode achieved a power density of up to 2.32 mW cm-2 and sustained discharge at 1.3 V for 250 h. Remarkably, even in environments with an oxygen concentration of 4 mg L-1, it can operate at a voltage approximately 100 mV higher than that of an unmodified SWB. The introduction of a hydrophobic interface enhances the discharge voltage and power of SWBs by improving interfacial oxygen mass transfer, providing new insights into improving the underwater ORR performance for practical SWBs.

Qualitative study on the perception of good death in patients with end-stage cancer in oncology nurses.

OBJECTIVE: To explore the perception of good death of patients with end-stage cancer by nurses in the oncology department. METHOD: In the study we used a phenomenological approach and semi-structured interviews. A total of 11 nurses from the oncology department of a Grade A hospital in Taizhou were interviewed on the cognition of good death from July 1 to September 30, 2022. Colaizzi's analysis method was used to analyse the interview data. This study followed the consolidated criteria for reporting qualitative research (COREQ). RESULT: Four themes were identified: a strong sense of responsibility and mission; To sustain hope and faith; The important role of family members; Improve patients' quality of life. CONCLUSION: The nurses in the department of oncology have a low level of knowledge about the "good death", and the correct understanding and view of the "good death" is the premise of the realization of " good death". The ability of nursing staff to improve the "good death", attention, and meet the needs and wishes of individuals and families, is the guarantee of the realization of "good death".

DNA-based ForceChrono probes for deciphering single-molecule force dynamics in living cells.

Understanding cellular force transmission dynamics is crucial in mechanobiology. We developed the DNA-based ForceChrono probe to measure force magnitude, duration, and loading rates at the single-molecule level within living cells. The ForceChrono probe circumvents the limitations of in vitro single-molecule force spectroscopy by enabling direct measurements within the dynamic cellular environment. Our findings reveal integrin force loading rates of 0.5-2 pN/s and durations ranging from tens of seconds in nascent adhesions to approximately 100 s in mature focal adhesions. The probe's robust and reversible design allows for continuous monitoring of these dynamic changes as cells undergo morphological transformations. Additionally, by analyzing how mutations, deletions, or pharmacological interventions affect these parameters, we can deduce the functional roles of specific proteins or domains in cellular mechanotransduction. The ForceChrono probe provides detailed insights into the dynamics of mechanical forces, advancing our understanding of cellular mechanics and the molecular mechanisms of mechanotransduction.

Engineering Short Antimicrobial Peptides to Specifically Target Fusobacterium nucleatum in the Mixed Microbial Population.

Antimicrobial peptides (AMPs) are becoming next-generation alternative antibacterial agents because of the rapid increase in resistance in bacteria against existing antibiotics, which can also be attributed to the formation of resilient biofilms. However, their widespread use is limited because of their poor absorption, higher dosage requirements, and delayed onset of the bioactivity to elicit a desired response. Here we developed a short AMP that specifically targeted Fusobacterium nucleatum. We conjugated 23R to a statherin-derived peptide (SDP) through rational design; this conjugate binds to FomA, a major porin protein of F. nucleatum. The SDP-tagged 23R exhibited rapid and highly specific bactericidal efficacy against F. nucleatum. Further, IC50 values were in the nanomolar range, and they were 100-fold lower than those obtained with unconjugated 23R. In a human gut microbiota model, 0.1 nM SDP-23R achieved 99% clearance of F. nucleatum ATCC 25586 without markedly altering resident microbiota. Here we demonstrated that binding-peptide-coupled AMPs show increased killing efficacy and specificity for the target pathogen without affecting the resident microbiota.

The influence of psychosocial work environment, personal perceived health and job crafting on nurses' well-being: a cross-sectional survey study.

BACKGROUND: The World Health Organization urged governments to prioritize the health and work well-being of nursing staff by promoting a positive working environment. A safe and healthy physical and psychosocial work environment is a basic human right for nurses. Job crafting is a necessary skill when facing challenging working conditions. OBJECTIVES: This cross-sectional correlational research based on the Job Demands-Resources Model aimed to explore the correlation between psychosocial work environment and work well-being among nurses working in the intensive care unit (ICU) and determine whether personal perceived health could mediate the relationship and whether job crafting can moderate the mediating effect. The study hypothesized that: 1. The psychosocial work environment would impact nurses' work well-being; 2. Personal perceived health would play a role as a mediator in the relationship between psychosocial work environment and work well-being; 3. Job crafting would moderate the relationship between personal perceived health and work well-being. METHODS: A total of 655 registered nurses (RNs) from 7 ICUs in a teaching hospital in Beijing participated in this study. The RNs completed a battery questionnaire measuring their health, psychosocial work environment, well-being, and job crafting. PROCESS macros analysis was used to test mediating and moderating effects. RESULTS: Personal perceived health mediated the relationship between psychosocial work environment and work well-being (b = 0.012, 95% CI [0.008, 0.016]). The moderated mediated analysis revealed that job crafting moderated perceived health's impact on work well-being (b = -0.007, 95% CI [- 0.010, - 0.003]). CONCLUSION: A better psychosocial work environment with well-designed work organization and job content through job crafting could positively impact nurses' health and work well-being.

TMC6 functions as a GPCR-like receptor to sense noxious heat via Gαq signaling.

Thermosensation is vital for the survival, propagation, and adaption of all organisms, but its mechanism is not fully understood yet. Here, we find that TMC6, a membrane protein of unknown function, is highly expressed in dorsal root ganglion (DRG) neurons and functions as a Gαq-coupled G protein-coupled receptor (GPCR)-like receptor to sense noxious heat. TMC6-deficient mice display a substantial impairment in noxious heat sensation while maintaining normal perception of cold, warmth, touch, and mechanical pain. Further studies show that TMC6 interacts with Gαq via its intracellular C-terminal region spanning Ser780 to Pro810. Specifically disrupting such interaction using polypeptide in DRG neurons, genetically ablating Gαq, or pharmacologically blocking Gαq-coupled GPCR signaling can replicate the phenotype of TMC6 deficient mice regarding noxious heat sensation. Noxious heat stimulation triggers intracellular calcium release from the endoplasmic reticulum (ER) of TMC6- but not control vector-transfected HEK293T cell, which can be significantly inhibited by blocking PLC or IP3R. Consistently, noxious heat-induced intracellular Ca2+ release from ER and action potentials of DRG neurons largely reduced when ablating TMC6 or blocking Gαq/PLC/IP3R signaling pathway as well. In summary, our findings indicate that TMC6 can directly function as a Gαq-coupled GPCR-like receptor sensing noxious heat.

Impact of summer hypoxia on macrobenthic communities in a semi-enclosed bay: A long-term observation in the North Yellow sea of China.

The O2 content of the global ocean has been declining progressively over the past decades, mainly because of human activities and global warming. Despite this situation, the responses of macrobenthos under hypoxic conditions remain poorly understood. In this study, we conducted a long-term observation (2015-2022) to investigate the intricate impact of summer hypoxia on macrobenthic communities in a semi-enclosed bay of the North Yellow Sea. Comparative analyses revealed higher macrobenthos abundance (1956.8 ± 1507.5 ind./m2 vs. 871.8 ± 636.9 ind./m2) and biomass (8.2 ± 4.1 g/m2 vs. 5.6 ± 3.2 g/m2) at hypoxic sites compared to normoxic sites during hypoxic years. Notably, polychaete species demonstrated remarkable adaptability, dominating hypoxic sites, and shaping community structure. The decline in biodiversity underscored the vulnerability and diminished resilience of macrobenthic communities to hypoxic stressors. Stable isotope analysis provided valuable insights into food web structures. The average trophic level of macrobenthos measured 2.84 ± 0.70 at hypoxic sites, contrasting with the higher value of 3.14 ± 0.74 observed at normoxic sites, indicating the absence of predators at high trophic levels under hypoxic conditions. Moreover, trophic interactions were significantly altered, resulting in a simplified and more vulnerable macrobenthic trophic structure. The findings underscored the importance of comprehensive research to understand the complex responses of macrobenthic communities to hypoxia, thereby informing future conservation efforts in impacted ecosystems.

A case of heat stroke with significantly elevated troponin and dynamic ECG changes: Myocardial infarction or Myocardial injury?

We described an 82-year-old man who was taken to our emergency department after being found unconscious. His electrocardiogram (ECG) showed ST-segment elevation in leads V4-V6 and cardiac troponin I (cTnI) was abnormally elevated. In addition to ECG and cTnI changes, this patient was combined with unconsciousness, high fever, abnormal liver function, acute renal failure, and rhabdomyolysis. The initial diagnosis was heat stroke, so cooling measures were initiated immediately, but a concurrent myocardial infarction was suspected. Meanwhile, emergency coronary angiography was performed, but no severe coronary stenosis or thrombosis was found. We first evaluated quantitative flow ratio (QFR) and coronary angiography-derived index of microvascular resistance (ca-IMR) in patients with heat stroke. Ca-IMR was 260 mmHg*s/m in the left circumflex artery, indicating the presence of coronary microvascular dysfunction (CMD). After several days of treatment, the patient recovered from multiple organ damage. Therefore, ECG and troponin results should be interpreted carefully in patients with high fever and coma during high temperature seasons.

Wnt5a-mediated autophagy contributes to the epithelial-mesenchymal transition of human bronchial epithelial cells during asthma.

BACKGROUND: The epithelial-mesenchymal transition (EMT) of human bronchial epithelial cells (HBECs) is essential for airway remodeling during asthma. Wnt5a has been implicated in various lung diseases, while its role in the EMT of HBECs during asthma is yet to be determined. This study sought to define whether Wnt5a initiated EMT, leading to airway remodeling through the induction of autophagy in HBECs. METHODS: Microarray analysis was used to investigate the expression change of WNT5A in asthma patients. In parallel, EMT models were induced using 16HBE cells by exposing them to house dust mites (HDM) or interleukin-4 (IL-4), and then the expression of Wnt5a was observed. Using in vitro gain- and loss-of-function approaches via Wnt5a mimic peptide FOXY5 and Wnt5a inhibitor BOX5, the alterations in the expression of the epithelial marker E-cadherin and the mesenchymal marker protein were observed. Mechanistically, the Ca2+/CaMKII signaling pathway and autophagy were evaluated. An autophagy inhibitor 3-MA was used to examine Wnt5a in the regulation of autophagy during EMT. Furthermore, we used a CaMKII inhibitor KN-93 to determine whether Wnt5a induced autophagy overactivation and EMT via the Ca2+/CaMKII signaling pathway. RESULTS: Asthma patients exhibited a significant increase in the gene expression of WNT5A compared to the healthy control. Upon HDM and IL-4 treatments, we observed that Wnt5a gene and protein expression levels were significantly increased in 16HBE cells. Interestingly, Wnt5a mimic peptide FOXY5 significantly inhibited E-cadherin and upregulated α-SMA, Collagen I, and autophagy marker proteins (Beclin1 and LC3-II). Rhodamine-phalloidin staining showed that FOXY5 resulted in a rearrangement of the cytoskeleton and an increase in the quantity of stress fibers in 16HBE cells. Importantly, blocking Wnt5a with BOX5 significantly inhibited autophagy and EMT induced by IL-4 in 16HBE cells. Mechanistically, autophagy inhibitor 3-MA and CaMKII inhibitor KN-93 reduced the EMT of 16HBE cells caused by FOXY5, as well as the increase in stress fibers, cell adhesion, and autophagy. CONCLUSION: This study illustrates a new link in the Wnt5a-Ca2+/CaMKII-autophagy axis to triggering airway remodeling. Our findings may provide novel strategies for the treatment of EMT-related diseases.

Aberrant patterns of spontaneous brain activity in schizophrenia: A resting-state fMRI study and classification analysis.

BACKGROUND: Schizophrenia is a prevalent mental disorder, leading to severe disability. Currently, the absence of objective biomarkers hinders effective diagnosis. This study was conducted to explore the aberrant spontaneous brain activity and investigate the potential of abnormal brain indices as diagnostic biomarkers employing machine learning methods. METHODS: A total of sixty-one schizophrenia patients and seventy demographically matched healthy controls were enrolled in this study. The static indices of resting-state functional magnetic resonance imaging (rs-fMRI) including amplitude of low frequency fluctuations (ALFF), fractional ALFF (fALFF), regional homogeneity (ReHo), and degree centrality (DC) were calculated to evaluate spontaneous brain activity. Subsequently, a sliding-window method was then used to conduct temporal dynamic analysis. The comparison of static and dynamic rs-fMRI indices between the patient and control groups was conducted using a two-sample t-test. Finally, the machine learning analysis was applied to estimate the diagnostic value of abnormal indices of brain activity. RESULTS: Schizophrenia patients exhibited a significant increase ALFF value in inferior frontal gyrus, alongside significant decreases in fALFF values observed in left postcentral gyrus and right cerebellum posterior lobe. Pervasive aberrations in ReHo indices were observed among schizophrenia patients, particularly in frontal lobe and cerebellum. A noteworthy reduction in voxel-wise concordance of dynamic indices was observed across gray matter regions encompassing the bilateral frontal, parietal, occipital, temporal, and insular cortices. The classification analysis achieved the highest values for area under curve at 0.87 and accuracy at 81.28% when applying linear support vector machine and leveraging a combination of abnormal static and dynamic indices in the specified brain regions as features. CONCLUSIONS: The static and dynamic indices of brain activity exhibited as potential neuroimaging biomarkers for the diagnosis of schizophrenia.

Mechanism of polygonum capitatum intervention in pulmonary nodule based on network pharmacology and molecular docking technology.

The present study utilizes network pharmacology and molecular docking methodologies to investigate the mechanism of action behind the intervention of Polygonum capitatum Buch.-Ham.ex D. Don (THL) in treating pulmonary nodules (PN). This research aims to provide a theoretical foundation for broadening the clinical application of THL. Active components of THL were identified and screened through an extensive literature review and the PharmMapper database, followed by an analysis of their target interactions. Relevant targets associated with PN were selected using databases such as OMIM and GeneCards, with an intersection of the two sets being determined. STRING11.5 facilitated the acquisition of protein-protein interaction data, which was then imported into Cytoscape 3.7.2 to establish a protein interaction network topology. This enabled the identification of pivotal targets affected by THL intervention in PN. The study further employed the Metascape database to conduct GO and KEGG bioinformatics enrichment analyses, which illuminated core pathways involved in THL's therapeutic effects on PN. A comprehensive component-target-pathway diagram was constructed utilizing Cytoscape 3.7.2 software, with molecular docking validations carried out via Maestro software. A total of 49 active THL ingredients were discerned, implicating 67 PN-relevant targets. Subsequent software analysis pinpointed 10 key targets, including ALB, EGFR, and SRC. Molecular docking studies indicated strong binding affinities for most protein-compound pairs, with 44 out of 60 docking results exhibiting binding energies below -5 kcal/mol. Enrichment analysis highlights that key targets are mainly involved in pathways such as cancer, lipid metabolism and atherosclerosis, estrogen signaling, IL-17 signaling, complement and coagulation cascades, and chemical carcinogenesis through receptor activation. Through comprehensive network pharmacological approaches, this research delineates the synergy of THL's multiple components, targets, and pathways in mitigating PN. It posits that primary active ingredients of THL - quercetin, salidroside, and oleanolic acid - may exert effects on targets like ALB, EGFR, SRC, potentially modulating pathways associated with cancer, lipid and atherosclerosis, and IL-17 signaling in the context of PN intervention.

Age-related changes in the mitochondrial, synthesis of steroids, and cellular homeostasis of the chicken ovary.

In poultry reproduction, the decline of ovarian function due to aging is related to dysfunction of mitochondria exacerbated by a reduction in antioxidant capacity, ultimately leading to follicle atresia and decreased egg production. However, the mechanisms of mitochondrial dysfunction in the chicken ovary in aging have remained to be understood. Hence, this study aims to investigate the effects of aging on mitochondrial function and cellular homeostasis. We collect ovarian tissue, small white follicles (SWF), large white follicles (LWF), and small yellow follicles (SYF) from three different laying periods of hens. The transmission electron microscopy (TEM) results showed that mitochondrial damage occurred in ovarian tissue during the late laying period (LP), characterized by structural swelling, scattered mitochondrial cristae, and an increase in the vacuoles. At the same time, with age, the synthesis of steroid hormones in the ovaries and follicular tissues is reduced. The levels of autophagy and cell apoptosis in ovarian tissues were both increased in the LP. In addition, aging adversely impacts mitochondrial function, leading to a decrease in mitochondrial unfolded protein response (UPRmt) functions. This study will expand the knowledge about regressing ovarian aging in hens and increasing egg production in older layers for poultry production.

Physalis Calyx seu Fructus inhibited pulmonary fibrosis through regulating Wnt/ß-catenin signaling pathway.

BACKGROUND: Pulmonary fibrosis is a chronic and advancing interstitial lung disease, and there is an urgent need for novel agents for its therapy. Physalis Calyx seu Fructus (PCF) has been utilized in traditional Chinese medicine to treat respiratory disorders with a long history, however, the therapeutic effect and mechanism of PCF against pulmonary fibrosis are still unclear. PURPOSE: To assess therapeutic efficacy and underlying mechanism of 75 % ethanol extract of PCF (PCF-EtOH) against pulmonary fibrosis, as well as to discover active constituents in PCF. METHODS: A bleomycin-stimulated mice model was established to assess potential therapy of PCF-EtOH against pulmonary fibrosis in vivo. A lipopolysaccharide-induced inflammatory model in RAW 264.7 cells and a transforming growth factor ß1-induced fibrosis model in MRC-5 cells were established to assess potential therapy and mechanisms of purified constituents in PCF-EtOH. UPLC-MS/MS analysis was adopted to ascertain the constituents of PCF-EtOH. Network pharmacology was employed to forecast targets of PCF against pulmonary fibrosis. RESULTS: PCF-EtOH ameliorated bleomycin-induced pulmonary fibrosis through repressing inflammatory response and extracellular matrix deposition. Meanwhile, PCF-EtOH inhibited Wnt/ß-catenin pathway through decreasing ß-catenin nuclear accumulation and promoting phosphorylation. Furthermore, withanolides and flavonoids were presumed to be main active compounds of PCF against pulmonary fibrosis based on the network pharmacology. Importantly, we found an extensive presence of withanolides in PCF-EtOH. Physapubescin, a typical withanolide in PCF-EtOH, inhibited the inflammatory response, extracellular matrix deposition, and Wnt/ß-catenin pathway. Notably, physapubescin demonstrated a more potent antifibrotic effect than pirfenidone, a clinically approved antifibrotic drug, in the tested model. CONCLUSION: Withanolides and flavonoids are responsible for the inhibitory effect of PCF-EtOH against pulmonary fibrosis. Withanolides may represent a class of promising therapeutic agents against pulmonary fibrosis, and an in-depth exploration is warranted to validate this proposition.

IL-38 Aggravates Atopic Dermatitis via Facilitating Migration of Langerhans cells.

Atopic dermatitis (AD) is a common inflammation skin disease that involves dysregulated interplay between immune cells and keratinocytes. Interleukin-38 (IL-38), a poorly characterized IL-1 family cytokine, its role and mechanism in the pathogenesis of AD is elusive. Here, we show that IL-38 is mainly secreted by epidermal keratinocytes and highly expressed in the skin and downregulated in AD lesions. We generated IL-38 keratinocyte-specific knockout mice (K14Cre/+-IL-38f/f ) and induced AD models by 2,4-dinitrofluorobenzene (DNFB). Unexpectedly, after treatment with DNFB, K14Cre/+-IL-38f/f mice were less susceptible to cutaneous inflammation of AD. Moreover, keratinocyte-specific deletion of IL-38 suppressed the migration of Langerhans cells (LCs) into lymph nodes which results in disturbed differentiation of CD4+T cells and decreased the infiltration of immune cells into AD lesions. LCs are a type of dendritic cell that reside specifically in the epidermis and regulate immune responses. We developed LC-like cells in vitro from mouse bone marrow (BM) and treated with recombined IL-38. The results show that IL-38 depended on IL-36R, activated the phosphorylated expression of IRAK4 and NF-κB P65 and upregulated the expression of CCR7 to promoting the migration of LCs, nevertheless, the upregulation disappeared with the addition of IL-36 receptor antagonist (IL-36RA), IRAK4 or NF-κB P65 inhibitor. Furthermore, after treatment with IRAK4 inhibitors, the experimental AD phenotypes were alleviated and so IRAK4 is considered a promising target for the treatment of inflammatory diseases. Overall, our findings indicated a potential pathway that IL-38 depends on IL-36R, leading to LCs migration to promote AD by upregulating CCR7 via IRAK4/NF-κB and implied the prevention and treatment of AD, supporting potential clinical utilization of IRAK4 inhibitors in AD treatment.

Non-Abelian Braiding of Topological Edge Bands.

Braiding is a geometric concept that manifests itself in a variety of scientific contexts from biology to physics, and has been employed to classify bulk band topology in topological materials. Topological edge states can also form braiding structures, as demonstrated recently in a type of topological insulators known as Möbius insulators, whose topological edge states form two braided bands exhibiting a Möbius twist. While the formation of Möbius twist is inspiring, it belongs to the simple Abelian braid group B_{2}. The most fascinating features about topological braids rely on the non-Abelianness in the higher-order braid group B_{N} (N≥3), which necessitates multiple edge bands, but so far it has not been discussed. Here, based on the gauge enriched symmetry, we develop a scheme to realize non-Abelian braiding of multiple topological edge bands. We propose tight-binding models of topological insulators that are able to generate topological edge states forming non-Abelian braiding structures. Experimental demonstrations are conducted in two acoustic crystals, which carry three and four braided acoustic edge bands, respectively. The observed braiding structure can correspond to the topological winding in the complex eigenvalue space of projective translation operator, akin to the previously established point-gap winding topology in the bulk of the Hatano-Nelson model. Our Letter also constitutes the realization of non-Abelian braiding topology on an actual crystal platform, but not based on the "virtual" synthetic dimensions.

Brassinosteroid-signaling kinase ZmBSK7 enhances salt stress tolerance in maize.

Salinity has become a crucial environmental factor that restricts plant growth, development, and productivity. Nevertheless, the mechanisms by which plants react to salt stress remain inadequately comprehended. In this study, we identified maize brassinosteroid-signaling kinase gene ZmBSK7 which is homologous to AtBSK1. Our results showed that ZmBSK7 is induced by salt stress and ZmBSK7 localizes in the plasma membrane. ZmBSK7 overexpression increases salt tolerance, while its knockdown decreases salt tolerance in maize. ZmBSK7 reduces the malondialdehyde (MDA) content and the percentage of electrolyte leakage, and also elevates the activities of antioxidant enzymes. Furthermore, ZmBSK7 promotes K+ content accumulation and reduces Na+/K+ ratio. Further found that ZmBSK7 physically interacts with K+ efflux antiporter 2 (ZmKEA2) in vivo and in vitro. Salt stress also increased the expression of ZmKEA2. Thus, ZmBSK7 improves salt tolerance in maize by affecting ZmKEA2 expression to promote K+ content accumulation and reduce Na+/K+ ratio. This study enhances the comprehension of BSK proteins and establishes a theoretical foundation for investigating salt stress tolerance in plants.

Protocol for preparation of electrifiable carbon membrane reactor for non-oxidative alkane dehydrogenation.

A membrane reactor (MR) offers a solution to overcome thermodynamic equilibrium limitations by enabling in situ product separation, enhancing product yields and energy efficiency. Here we present a protocol for synthesizing a carbon MR that couples a H2-permeable carbon molecular sieve hollow fiber membrane and a metal supported on zeolite catalyst for non-oxidative propane and ethane dehydrogenation. We describe steps for catalyst preparation, membrane fabrication, and MR construction. The as-developed MR has significant improvements in alkene yield and a record-high stability. For complete details on the use and execution of this protocol, please refer to Liu et al.1.

The high expression of ADRM1 in hepatocellular carcinoma is closely related to tumor immune infiltration and is regulated by miR-891a-5p.

Liver cancer is one of the most common malignant tumors worldwide. Although some progress has been made in the diagnosis and treatment of Hepatocellular carcinoma (HCC), the diagnosis and treatment of HCC is still facing great challenges because of the high mortality rate and poor prognosis of HCC. The purpose of this study was to explore the relationship between adhesion-regulating molecule1 (ADRM1), and liver cancer, and the relationship between prognoses. ADRM1 is highly expressed in tumors and is closely associated with the prognosis of patients with liver cancer. In our previous study, we found that ADRM1 was highly expressed in HCC and was closely related to tumor immune and immune checkpoint levels in HCC. We validated the immune expression of ADRM1 in liver cancer cells using flow cytometry. In hepatocellular carcinoma tissues, miR-891a-5p regulates ADRM1. Upregulation of miR-891a-5p upregulates ADRM1, and downregulation of miR-891a-5p downregulates ADRM1. It is suggested that ADRM1 plays a key role in the occurrence and development of hepatocellular carcinoma. This study is expected to provide new ideas for the research and development of anti-HCC drugs targeting miR-891a-5p/ADRM1. However, further trials are needed to confirm these results and explore the actual results in patients with HCC.