To evaluate the application efficacy of structured symptom intervention program in patients with chronic kidney disease (CKD) during the peri-dialysis period.

A non-simultaneous control study was conducted on 151 peri-dialysis outpatients having not yet initiated dialysis and being followed up who were subjected with convenience sampling from Department of Nephrology of Second Affiliated Hospital of Army Medical University from April to September 2024. According to the time period of their visits, the patients who visited from April to June 2024 were assigned into a control group (n=75), and those from July to September 2024 into an experimental group (n=76). The control group received conventional symptom intervention (telephone symptom reporting + health education), while the experimental group received the intervention as the control group and a structured symptom intervention program covering 4 evidence-based modules: symptom identification, assessment, intervention, and outcome. The efficacy of above treatments was evaluated before and at 3 months after intervention. Dialysis symptom index was used to assess the degree of symptom distress and the number of symptoms. MOS 36-Item Short Form Health Survey (SF-36) was employed to evaluate the quality of life. The differences in clinical indicators and endpoint events were compared between the 2 groups after intervention.

The experimental group obtained more significant reduction in the total score of symptom distress than the control group (P=0.021). After intervention, the number of symptoms was decreased in both groups (P<0.001), but no statistical difference was observed between the groups. The score of mental health dimension in SF-36 was obviously improved in the experimental group (P=0.004), which was notably better than that in the control group (P=0.033). The experimental group exhibited significantly higher prealbumin level than the control group (P=0.019), and stable albumin level, which was significantly decreased in the control group (P=0.035). The incidence of endpoint events was remarkably lower in the experimental group than the control group (P=0.028).

The structured symptom intervention program implements intervention through a closed-loop symptom module, which can effectively alleviate the symptom distress of patients during the peri-dialysis period, improve mental health and reduce the short-term risk for endpoint events.

To explore the networked association among the dimensions of self-efficacy in patients with rheumatoid arthritis (RA) and to identify core efficacy and bridge efficacy, and provide a basis for formulating precise nursing intervention strategies.

A total of 652 RA patients admitted in our hospital from September 2024 to January 2025 were enrolled with convenience sampling. The general information questionnaire and Rheumatoid Arthritis Self-Efficacy Scale (RASE) were used for assessment. Exploratory factor analysis was used to extract efficacy symptom clusters. With aid of R project, network analysis was employed to construct an association network among efficacy dimensions to calculate centrality indicators (strength, closeness, betweenness) to identify core efficacy and bridge efficacy.

Exploratory factor analysis extracted 7 efficacy symptom clusters, with a cumulative variance contribution rate of 64.539% (P<0.001). Network analysis showed that the network density was 0.143, suggesting that there were moderate correlations among the self-efficacy dimensions. “Relaxation efficacy 1 (r1)” and “pain efficacy 1 (a1)” had the strongest correlation (r=0.73). Interpersonal efficacy 2 (i2) had the highest intensity centrality (6.88), and relaxation efficacy 3 (r3) had the highest tightness (0.0125), and medication efficacy 1 (m1) had the highest mediation (116), which were the core efficacy and bridge efficacy in this network group.

There are complex network-like correlations among the various dimensions of self-efficacy in RA patients. Interpersonal efficacy is the core driving factor, while relaxation and medication efficacies play the bridging role, jointly influencing the overall level of patients’ self-management ability.

To analyze the electrophysiological and genetic examination results of children with congenital stationary night blindness (CSNB) without fundus abnormalities.

A retrospective study was conducted on 11 children diagnosed with CSNB in our department from August 2019 to March 2025. Their full-field electroretinogram (ffERG) and the results of genetic testing were analyzed.

Among the 11 patients, there were 10 males and 1 female, at a mean age of 7.5±2.1 years. In the optometry, 1 patient had hyperopia and the other had myopia, and all of them obtained a corrected visual acuity of 0.48±0.11 after wearing glasses. In fundus photography examination, except for the leopard pattern changes in high myopia, no obvious abnormalities were found in the remaining fundus. In ffERG examination for all patients, the amplitude of the a-wave of scotopic ERG 3.0/10.0 was normal or slightly to moderately decreased, the amplitude of the b-wave was decreased significantly, and the amplitude ratio of the b-wave to the a-wave was <1, showing a negative-phase wave, which belonged to the CSNB Schubert-Bornschein waveform. The results of genetic test revealed that all the 11 patients carried pathogenic mutations, including 6 cases with CACNA1F mutations, 2 cases with GPR179 mutations, 2 cases with NYX mutations, and 1 case with GRM6 mutation.

For children with normal fundus manifestations but corrected visual acuity lower than normal after wearing glasses, ffERG examination should be carried out as soon as possible to screen for CSNB, and a diagnosis should be made in combination with genetic testing. This is helpful for evaluating the heredity and prognosis of the disease, increasing the chance of early detection, and reducing excessive amblyopia training and treatment.

To analyze the burden of pressure ulcers and its changing trends among the general population (all age groups) and the elderly aged 65 years and above in China based on the global burden of disease (GBD) data from 1990 to 2021, predict the burden trends from 2022 to 2035, and address the public health issues of its unclear medium- and long-term trends and insufficient precise interventions in its prevention and control in order to provide support for formulating targeted prevention and control strategies.

The GBD database was used to extract the incidence, mortality and disability-adjusted life years (DALYs) of pressure ulcers in the general population and in the elderly aged 65 years and above in China from 1990 to 2021. Meanwhile, the age-standardized incidence rate (ASIR), mortality rate (ASMR), and disability-adjusted life rate (ASDR) of the general population were also extracted, and the age-standardized rate (ASRs) corresponding to the elderly population aged 65 years and above were estimated based on the GBD 2021 standard population. The average annual percentage changes (EAPCs) of ASRs were calculated to assess the trends. Bayesian age-period-cohort (BAPC) model was adopted to predict the ASRs and their changing trends of the general and elderly population from 2022 to 2035, respectively.

From 1990 to 2021, the number of pressure ulcer cases in the general population of China increased from 163 508.67 (95%CI: 142 891.48~184 055.10) cases to 397 312.27 (95%CI: 360 058.44~444 875.78) cases, the number of deaths soared from 242.51 (95%CI: 125.26~702.84) cases to 3 131.54 (95%CI: 1 562.60~4 126.85) cases, and DALYs increased from 11 965.10 (95%CI: 7 820.54~21 703.78) to 61 933.91 (95%CI: 36 313.26~77 402.42). During the same period, the EAPCs of ASIR, ASMR and ASDR were 1.06 (95%CI: 0.84~1.28), 3.63 (95%CI: 3.45~3.81), and 2.76 (95%CI: 2.60~2.92), respectively. In 2021, the number of male cases and DALYs were both higher than those of females, while the number of deaths was similar. The ASIR, ASMR and ASDR of the males were all higher than those of the females, and the growth rates of both genders were relatively fast. All indicators were increased significantly with age. It is predicted that by 2035, the ASIR, ASMR, and ASDR in the general Chinese population will continue to rise significantly. From 1990 to 2021, the number of pressure ulcer cases among the elderly (≥65 years old) in China increased from 42 334.95 (95%CI: 35 739.05~48 930.84) to 238 431.65 (95%CI: 212 539.53~264 323.77). The number of deaths rose from 204.97 (95%CI: 93.33~316.60) to 2 871.02 (95%CI: 2 334.39~3 407.66), and DALYs increased from 4 619.74 (95%CI: 2 990.73~6 248.76) to 43 968.28 (95%CI: 37 542.85~50 393.70). The EAPCs of ASIR, ASMR, and ASDR were 2.62 (95%CI: 2.44~2.80), 3.54 (95%CI: 3.38~3.70), and 3.28 (95%CI: 3.14~3.42), all of which increased significantly. In 2021, the number of cases, deaths and DALYs among elderly men and women were similar, but the ASIR, ASMR and ASDR of men were all higher than those of women, and their growth rates were faster. It is projected that by 2035, the ASIR of the elderly population will significantly decline to 146.24(95%CI: 140.35~152.14), with an EAPC of -0.57 (95%CI: -0.64~-0.50), while the ASMR and ASDR will continue to rise and remain higher in males than in females.

From 1990 to 2021, the number of pressure ulcer cases, deaths and DALYs among the general population and the elderly in China increased significantly, and the ASRs rose rapidly. The burden of pressure ulcers increases significantly with age and is higher in men than in women. Predictions show that ASIR in the general population will continue to rise, while that in the elderly will slightly decline. However, the ASMR and ASDR will continue to increase. Countermeasures　Continuously strengthen the prevention and control of pressure ulcers, implement precise intervention for the elderly, especially older men, promote standardized nursing guidelines, enhance training and resource input in primary medical care, and establish a national pressure ulcer monitoring system.

To investigate the ameliorative effect of deferoxamine (DFO) on cognitive impairment in a rat model of type 1 diabetes mellitus (T1DM) and to elucidate the molecular mechanisms underlying cerebral iron overload in T1DM rats.

Thirty-six healthy male SD rats (weighing 180~250 g) were randomly assigned into a blank control group (Ctrl), a T1DM model group and a DFO group, with 12 rats in each group. A single dose of 65 mg/kg streptozotocin (STZ) was intraperitoneally injected to the rats to establish a T1DM model, and those with fasting blood glucose ≥16.7 mmol/L at 3 d later were designated as the T1DM group. Intracerebroventricular administration of DFO (5 μg/kg·d) was given to the DFO group for 28 consecutive days since 21 d after STZ injection. Morris water maze test was carried out to assess the spatial learning and memory abilities. Nissl staining and immunofluorescence assay were applied to observe neuronal morphology and number in the hippocampus and cortex. The iron content in the hippocampus was measured with inductively coupled plasma mass spectrometry (ICP-MS). The expression levels of iron metabolism related proteins were detected with Western blotting.

In the T1DM group, significant declines in learning and memory abilities (P<0.01) and impaired neuronal morphology and reduced neuronal counts in the hippocampal CA1 region (P<0.01), CA3 region (P<0.01), and cortex (P<0.05) were observed when compared with those in the Ctrl group. ICP-MS analysis showed a marked increase in the hippocampal iron content in the T1DM group (P<0.01). Western blot results demonstrated that T1DM rats exhibited obviously up-regulated expression of iron storage proteins FTH and FTL in both the hippocampus (P<0.01, P<0.05) and the cortex (P<0.05, P<0.01), enhanced expression of iron import protein DMT1 in both the hippocampus and the cortex (P<0.05), while decreased expression of iron export protein FPN1 in the hippocampus (P<0.01) and the cortex (P<0.05). DFO treatment significantly ameliorated all above abnormalities.

The declines in learning and memory in T1DM rats are closely associated with neuronal damage induced by cerebral iron overload. Iron import protein DMT1 and export protein FPN1 jointly regulate cerebral iron content in T1DM rats. DFO reduces brain iron levels and mitigates iron overload-mediated neuronal injury by modulating the expression of DMT1 and FPN1.

To investigate the potential therapeutic targets and underlying molecular mechanisms of Z-ligustilide (Z-LIG) in treating retinitis pigmentosa (RP).

By integrating multiple databases, such as GeneCards and TargetNet, common targets for RP and Z-LIG were identified. Protein-protein interaction (PPI) network analysis of the targets was conducted using the STRING database and analyzed in Cytoscape to identify core targets. The DAVID database was employed for the functional enrichment analysis of Gene Ontology (GO) and the pathway enrichment analysis of Kyoto Encyclopedia of Genes and Genomes (KEGG) for the core targets. The PubChem database was accessed for molecular docking verification to validate the binding affinity between Z-LIG and the core targets. Finally, male rd10 mice were randomly divided into a control group (n=5) and a Z-LIG treatment group (n=5). The protective effect of Z-LIG on the visual function in rd10 mice was verified through visual electrophysiology and behavioral tests. Western blotting and RT-qPCR were utilized to investigate the molecular mechanism of action.

A total of 66 shared targets between RP and Z-LIG were identified through the screening process. PPI network analysis identified 55 key targets. GO enrichment analysis yielded 623 terms, which covering 3 dimensions, including cellular component (CC), molecular function (MF), and biological process (BP), such as inflammatory response. KEGG pathway enrichment analysis further concentrated 124 terms, which were enriched in the PI3K-Akt signaling pathway. Molecular docking suggested that Z-LIG could specifically bind with high affinity to RP-related core targets (such as EGFR and STAT3) via hydrogen bonds. In animal experiments, compared to the control group, the rd10 mice from the Z-LIG group showed a greater preference for the dark environment in the light/dark transition test (P<0.05), exhibited significantly higher amplitudes of A-wave and B-wave in electroretinogram (ERG) (P<0.05), greater number of outer nuclear layers, with fewer apoptotic cells and less microglial activation (P<0.05), demonstrated obviously reduced protein levels of p-PI3K/PI3K and p-AKT/AKT in the retina (P<0.05), and had notably down-regulated mRNA levels of pro-inflammatory cytokines IL-1β and IL-6 (P<0.05).

Z-LIG may exert a protective effect on the retina of rd10 mice by inhibiting the activation of the PI3K/AKT-inflammatory axis, thereby delaying retinal degeneration.

To investigate the effect and mechanisms of celecoxib on right heart function in mice with acute high-altitude hypoxia exposure.

Male C57BL/6J mice (7 weeks old) were housed in a hypobaric chamber simulating an altitude of 5 800 m for 2 d to establish an animal model of acute hypobaric hypoxia. ①Eighteen mice were randomly assigned to plain+saline (P+S), high-altitude hypoxia exposure+saline (H+S), and high-altitude hypoxia exposure+celecoxib (H+Cel). Body weight and routine blood indicators were measured, and cardiac ultrasound examination were performed for heart rate (HR), pulmonary artery acceleration time to ejection time ratio (AT/ET), tricuspid annular plane systolic excursion (TAPSE), tricuspid annular systolic velocity (S’), and left ventricular ejection fraction (LVEF) and fractional shortening (FS). Targeted metabolomic profiling was applied to detect the cardiac arachidonic acid (AA) metabolite levels. The contents of 12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) in the heart, liver, brown adipose tissue, and plasma were quantified by ELISA. ② Eighteen mice were randomly assigned into plain+saline (P+S), high-altitude hypoxia exposure+saline (H+S) and high-altitude hypoxia exposure+12,13-diHOME (H+di) groups. Body weight, routine blood tests, and echocardiography were performed as above. ③ Thirty-two mice were randomly divided into high-altitude hypoxia exposure+saline (H+S), high-altitude hypoxia exposure+celecoxib (H+Cel), high-altitude hypoxia exposure+soluble epoxide hydrolase inhibitor (sEHI) (H+sEHI), and high-altitude hypoxia exposure+sEHI+celecoxib (H+sEHI+Cel) groups. Body weight, routine blood tests, and echocardiography were performed as above. Cardiac and plasma contents of 12,13-diHOME and epoxyeicosatrienoic acids (EETs) were measured by ELISA.

① Compared to the P+S group, the H+S group exhibited significantly reduction of cardiac 12,13-diHOME level (P<0.001), increased counts of white blood cells (WBC) and neutrophils (P<0.01) and decreased TAPSE, S’ and AT/ET both at resting state and under stress (P<0.01, P<0.001). Compared to the H+S group, the H+Cel group exhibited significantly increase of cardiac 12,13-diHOME level (P<0.05), reduced WBC and lymphocyte counts (P<0.01, P<0.05) and improved TAPSE and S' levels at resting state and under stress (P<0.01, P<0.001). ② Compared to the H+S group, the H+di group demonstrated significantly improvement of TAPSE at basal and under stress (P<0.001) and a trend towards improved TAPSE at resting state (P=0.0532), but no obvious differences was observed in WBC and neutrophil counts between the H+di group and the H+S group. ③ Compared to the H+Cel group, both the H+sEHI and H+sEHI+Cel groups exhibited significantly reduction of cardiac 12,13-diHOME level (P<0.01, P<0.05) though no statistical changes in cardiac function indicators. Compared to the H+S group, WBC counts and lymphocyte were decreased, and serum EETs level was incrased in the H+Cel group, H+sEHI group and H+sEHI+Cel group (P<0.01, P<0.001).

Celecoxib can elevate cardiac level of 12,13-diHOME and improves right heart function in mice after acute high-altitude hypoxia exposure through the CYP450-sEH metabolic pathway.

To investigate the characteristics of immune exhaustion in sepsis and analyze its association with gut microbiota translocation.

A total of 130 mice were randomly divided into a cecal ligation and puncture (CLP) group (n=100) and a Sham group (n=30) Mouse model of sepsis was established with CLP procedure. Flow cytometry was used to analyze the proportions of peripheral blood CD4⁺ T and CD8⁺T cells and programmed cell death protein 1 (PD-1) positive T cell subsets in mice. Bacterial colonization in organs such as the heart, liver and kidneys was quantified by plating homogenates of the organs. Pathological changes in immune organs were observed with HE staining. The expression and localization of CD4⁺, CD8⁺, and PD-1⁺cells in immune organs were detected with immunohistochemical staining, and Image J software was employed for subsequent quantification of the number of the positive cells.

HE staining demonstrated that immune organs exhibited varying degrees of pathological damages with disease progression. Compared with the Sham mice, the CLP mice exhibited significantly increased bacterial colonization in parenchymal organs and peripheral blood (P<0.05), notably in the liver, which showed the most severe infection. In the CLP group, the proportion of CD4⁺ T lymphocytes in peripheral blood at days 1, 3, and 5 postoperatively was decreased by 56%, 70.57%, and 87.42%, respectively, when compared with the Sham group (P<0.001). The proportion of CD8⁺ T lymphocytes was decreased by 48.33% relative to the Sham group only at day 5 (P<0.001). In contrast, the proportion of CD4⁺ T cell subsets expressing PD-1 was increased to 673.08, 423.08, and 600 times that of the Sham group, respectively, at the same postoperative time points (P<0.001). Immunohistochemical results showed that, in the CLP group, the proportion of CD4⁺ T cells in the thymus, spleen, and mesenteric lymph nodes was increased to 7.65, 2.66, and 3.7 times that of the Sham group, respectively, at the early-stage peak (P<0.001), and then these proportions were decreased by 82.8% (P<0.001), 41.9% (P<0.01), and 60.15% (P<0.001), respectively, at the late-stage trough when compared with the early-stage peak in the corresponding organs. The proportion of CD8⁺ positive cells was increased in the early stage and then decreased insignificantly, while the proportion of PD-1⁺ positive cells was increased continuously, and reached 6.24, 13.9, and 20.96 times that of the Sham group at the peak in the thymus, spleen, and mesenteric lymph nodes respectively (P<0.001), with their expression regions showing a rough overlap with those of CD4⁺ cells.

During sepsis, the inflammatory response can cause severe damage to immune organs and persistent exhaustion of CD4⁺T lymphocytes, leading to declined defenses against infection, which may be the main causes for exacerbated gut microbiota translocation and then systemic infection.

To investigate the role of poly(rC)-binding protein 1 (PCBP1) in cadmium (Cd)-induced ferroptosis in mouse neuroblastoma Neuro-2a (N2A) cells.

N2A cells were exposed to a concentration gradient of CdCl₂ (0, 1, 2, 4 μmol/L) for 72 h. Cell viability was assessed by trypan blue staining. Western blotting was employed to detect the expression of ferroptosis-related proteins (GPX4, HMOX1, ACSL4) and PCBP1. Intracellular Fe²⁺ level and lipid peroxidation were detected using FerroOrange and BODIPY^581/591 C11 probes, respectively. Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, was applied to confirm the critical role of ferroptosis in Cd-induced cytotoxicity. Molecular docking was performed to elucidate the interaction between PCBP1 and ferritin, as well as the binding sites of Cd²⁺. PCBP1 overexpression plasmid was further constructed for functional validation.

Cd exposure suppressed cell viability in N2A cells in a dose-dependent manner (P<0.01), significantly down-regulated GPX4 expression (P<0.05), up-regulated HMOX1 expression (P<0.01), and induced Fe²⁺ overload and lipid peroxidation (P<0.01). Molecular docking revealed that Cd²⁺ directly bound to the KH2 domain of PCBP1 and then co-localized on the outer surface of ferritin heavy chain. Overexpression of PCBP1 markedly reversed Cd-induced Fe²⁺ accumulation, GPX4 down-regulation, lipid peroxidation, and cell death.

Cd exposure disrupts PCBP1-mediated iron homeostasis via transcriptional suppression and competitive displacement of metal ions, and then synergistically drives Fe²⁺ overload-triggered ferroptosis cascades, ultimately leading to neurotoxicity. Targeting PCBP1-mediated iron homeostasis can effectively mitigate Cd-induced neurotoxicity, and may serve as a novel therapeutic strategy.

To explore the differences in therapeutic efficacy and possible mechanism of different routes of administration of fullerene nanoparticles in the treatment of radiation retinopathy.

Eight-week-old adult male SD rats were randomly divided into blank group (Control), irradiation group (X-Ray), irradiation＋vitreous cavity administration group [X+F(IVT)], irradiation＋ocular surface administration group [X+F(OS)], and irradiation＋intravenous administration group [X+F (IV)], with 5 rats in each group. The blank group was not treated, the irradiation groups exposed to X-ray irradiation to establish the model, and fullerenol nanoparticles were given to the treatment groups through different routes after irradiation. At 7, 14, and 28 d after modeling, body weight and fundus changes were measured to evaluate drug safety, retinal optical coherence tomography (OCT) was used to observe the change in retinal tissue structure, and electroretinography (ERG) was applied for oscillatory potentials (OPs) to evaluate visual function. CD31 immunofluorescence staining was carried out to evaluate retinal endothelial vascular status, and in vivo imaging was utilized to evaluate the accumulation of fullerenol nanoparticles in the eyes.

The growth curves of body weight demonstrated that fullerenol nanoparticles did not affect the growth and development of rats, with no statistical difference between the treatment groups and the control group. Irradiation resulted in a significant reduction in visual function, decreased amplitudes of a-wave and b-wave, and declined OPs (P<0.01), and significantly increased thicknesses of the ganglion cell layer (GCL) and the inner nuclear layer (INL) in the retinas, as evidenced by OCT (P<0.01), along with a notably absent presence of CD31-positive cells (P<0.01). Notably, the X+F(IVT) group obtained significantly improved visual function after intravitreal administration, effectively maintained thickness of the GCL and INL, and prevention against the loss of CD31-positive cells (P<0.01). However, no such effective results were observed in the irradiated groups receiving intravenous either ocular surface administration. In vivo imaging revealed that intravitreal administration maintained high ocular accumulation of fullerene for 96 h, while ocular surface administration sustained these concentrations for only 12 h. Intravenous administration, in contrast, only led to a predominant drug distribution in vascular-rich areas, but reduced ocular accumulation.

Fullerene nanoparticles possess a therapeutic effect on radiation retinopathy, and the intravitreal administration route demonstrates better efficacy than ocular surface and intravenous administration.