Objective To investigate the prevalence of soil-transmitted nematode human infections in Hubei Province from 2016 to 2023, so as to provide insights into formulation of soil-transmitted nematodiasis control strategies and evaluation of soil-transmitted nematodiasis control effectiveness. Methods There were 10 surveillance points established in Hubei Province for soil-transmitted nematodiasis each year from 2016 to 2023. The surveillance points were divided into eastern, western, southern, northern and central regions according to geographical locations, and one administrative village was sampled from a township in each region as a surveillance point. Then, at least 200 permanent residents at ages of over 3 years were randomly sampled at each point, with at least 1 000 individuals sampled. Soil-transmitted nematode infection was detected using a modified Kato-Katz thick smear method (two slides for one stool sample), and Enterobius vermicularis infection was additionally detected with a cellophane tape test among children at ages of 3 to 9 years. The prevalence of soil-transmitted nematode human infections was descriptively analyzed. Results A total of 80 547 individuals underwent surveillance for soil-transmitted nematodiasis in Hubei Province from 2016 to 2023, and a total of 262 individuals were detected with soil-transmitted nematode infections, including two cases with mixed infections, yielding an overall prevalence rate of 0.33% (262/80 547). The prevalence rates of hookworm, Ascaris lumbricoides, Trichuris trichiura, and E. vermicularis infections were 0.02% (20/80 547), 0.07% (55/80 547), 0.02% (15/80 547) and 0.22% (174/80 547), respectively, appearing a parasite species-specific prevalence rate (χ² = 250.235, P < 0.05), and the prevalence rates of soil-transmitted nematode infections were 0.50%(51/10271),0.37%(34/9120),0.39%(39/10099),0.40%(41/10168), 0.36% (37/10 234), 0.45% (46/10 211), 0.03% (3/10 238) and 0.11% (11/10 206) in Hubei Province from 2016 to 2023, respectively, showing a year-specific prevalence rate (χ² = 60.589, P < 0.05). Soil-transmitted nematode infections were detected across 36 surveillance points, and there was a significant difference in the prevalence of soil-transmitted nematode infections among surveillance points (0.02% to 3.30%, P < 0.001). In addition, the differences in prevalence rates of human soil-transmitted nematode infection among different age groups (χ² = 531.091, P < 0.05), occupations (P < 0.001), and education levels (P < 0.001) were all statistically significant. Among these, the children at ages of 3 to 9 years old (1.40%, 174/12 461), nursery-school children (1.69%, 90/5 312) and preschool-aged children (1.56%, 93/5 969) were relatively high. Conclusions The overall prevalence of soil-transmitted nematodiasis was low in Hubei Province from 2016 to 2023; however, the prevalence varied across regions and among populations, with E. vermicularis as the predominant species of soil-transmitted nematode. Soil-transmitted nematodiasis control should be given a high priority in key areas in Hubei Province, and preschool children, primary school students, and individuals with a low educational level are recommended as key target populations for health education and interventions.

Diabetic sarcopenia (DS) is a common but often ignored skeletal muscle complication in individuals with diabetes mellitus. It is characterized by progressive loss of skeletal muscle mass, reduced muscle strength, and impaired physical performance, which may further increase the risk of falls, disabilities, metabolic disorders, and adverse clinical outcomes. Traditionally, DS has been attributed mainly to hyperglycemia, insulin resistance, aging-related muscle decline, and chronic complications of diabetes. However, increasing evidence suggests that lipid metabolic disturbance and pathological lipid metabolic reprogramming are not merely secondary consequences of diabetes, but may actively participate in the initiation and progression of DS. Under diabetic conditions, impaired fatty acid uptake, transport, oxidation, and storage disrupt skeletal muscle metabolic homeostasis, leading to ectopic lipid deposition and accumulation of lipotoxic intermediates. These lipid-derived metabolites can aggravate insulin resistance, impair mitochondrial energy production, enhance oxidative stress, activate chronic low-grade inflammation, and disturb protein synthesis and degradation balance, thereby accelerating skeletal muscle atrophy and functional decline. Lipid metabolic dysregulation may also interact with multiple pathological processes involved in DS, including mitochondrial dysfunction, inflammatory signaling, oxidative damage, impaired autophagy, and gut microbiota imbalance. These mechanisms do not occur independently; instead, they form a complex bidirectional vicious cycle with diabetes-related metabolic disorders. Specifically, mitochondrial dysfunction reduces fatty acid oxidative capacity, which further promotes lipid accumulation and lipotoxicity. Inflammatory activation can impair insulin signaling and muscle protein metabolism, while lipid overload may in turn amplify inflammatory responses. Similarly, gut microbiota dysbiosis and altered microbial metabolites may influence systemic inflammation, lipid metabolism, and skeletal muscle homeostasis. Therefore, lipid metabolic reprogramming provides an important mechanistic perspective for understanding the progression of DS from metabolic disturbance to structural and functional muscle impairment. Exercise intervention is an effective and clinically feasible non-pharmacological strategy for the prevention and management of DS. Both aerobic exercise and resistance training have been shown to improve insulin sensitivity, enhance fatty acid oxidation, increase mitochondrial biogenesis, reduce ectopic lipid deposition, and attenuate lipotoxic metabolite accumulation. These adaptations not only improved glucose and lipid metabolism, but also increased the preservation of muscle mass, muscle strength, and physical function. Moreover, combined exercise strategies may provide complementary benefits by integrating the metabolic advantages of aerobic exercise with the anabolic and functional effects of resistance training. Based on analyses of publicly available datasets and literature evidences, this review systematically summarizes the role of lipid metabolic disorders in the pathogenesis of DS, with particular attention to the molecular mechanisms linking lipid dysregulation to insulin resistance, chronic inflammation, oxidative stress, mitochondrial dysfunction, and gut microbiota disturbance. Furthermore, this review discusses the potential mechanisms by which exercise intervention improves DS through the regulation of lipid metabolic reprogramming, and outlines exercise prescription strategies in terms of modality, intensity, frequency, and duration. Understanding the interaction between lipid metabolism and skeletal muscle dysfunction may provide new theoretical evidence for early identification, mechanistic research, and precision exercise therapy in DS. Overall, targeting pathological lipid metabolic reprogramming through exercise intervention represents a promising and clinically actionable approach for improving muscle health and prognosis in individuals with DS.

ObjectiveTo explore the anti-eczema efficacy and mechanism of Mongolian medicine Cymbaria dahurica n-butanol extract. MethodsThe compounds of C. dahurica n-butanol extract were obtained by ultra-performance liquid chromatography-quadrupole-electrostatic field orbital trap high resolution mass spectrometry （UPLC-Q-Exactive MS） analysis and literature mining. GEO chip analysis and network pharmacology were employed to predict potential targets and pathways for the anti-eczema effect. Seventy-five mice were randomized into a normal group （10 mice） and a modeling group （65 mice）. The model was induced by 1% dinitrochlorobenzene （DNCB） for 3 days. The modeled mice were grouped as follows： Positive drug （hydrocortisone butyrate cream， 250 mg·kg^-1·d^-1） and low-， medium-， and high-dose （95.94， 191.88， and 383.76 mg·kg^-1·d^-1， respectively） C. dahurica n-butanol extract， with 13 mice in each group. From day 5 of the experiment， 0.5% DNCB was applied， once every other day， until day 22. At the same time， drugs were applied daily from day 5. The appearance damage of back skin of mice in each group was analyzed. The pathological changes of the back skin of mice in each group were observed by hematoxylin-eosin （HE） staining and toluidine blue （TB） staining. The levels of inflammatory factors ［histamine （HIS）， interleukin-4 （IL-4）， interleukin-6 （IL-6）， interleukin-8 （IL-8）， and tumor necrosis factor-α （TFN-α）］， thymic stromal lymphopoietin （TSLP）， and immunoglobulin E （IgE） in the serum were determined by enzyme-linked immunosorbent assay （ELISA）. Metabolomics analysis was performed for the mouse skin. The HaCaT cell model of eczema was induced with TNF-α/interferon-γ （IFN-γ）. The secretion levels of IL-6， IL-8， thymus and activation-regulated chemokine （TARC/CCL17）， macrophage-derived chemokine （MDC）， and TSLP in the cell supernatant from each group were measured by ELISA， while the protein levels of phosphorylated （p）-Janus kinase 2 （JAK2）， JAK2， p-signal transducer and activator of transcription 3 （STAT3）， and STAT3 were assessed by Western blot. ResultsThrough UPLC-Q-Exactive MS and literature review， a total of 125 compounds of C. dahurica n-butanol extract were obtained. The Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis showed that the anti-eczema mechanism of C. dahurica n-butanol extract may be related to the Janus kinase/signal transducer and activator of transcription （JAK/STAT） pathway. The results of animal experiments showed that compared with the normal group， the modeling group exhibited redness， swelling， exudation， erosion， and scab formation on the back skin surface， and thickened dermis and epidermis with inflammatory cell infiltration. Compared with the modeling group， the positive drug and C. dahurica n-butanol alleviated the skin lesions （including redness， swelling， exudation， roughness， and keratosis and scab formation on the back）， reduced the thickness of dermis and epidermis， mitigated inflammatory cell infiltration， and restored the skin tissue structure. Compared with the normal group， the modeling group showed elevated levels of HIS， IL-4， IL-6， IL-8， TNF-α， TSLP， and IgE （P<0.05， P<0.01）， which were reversed in the positive drug group and C. dahurica n-butanol extract groups （P<0.05， P<0.01）. The results of metabolomics analysis showed that 12 differential metabolites might be the key substances for mitigating metabolic disorders of the skin and were closely related to the JAK/STAT signaling pathway. The cell experiement showed that compared with the normal group， the model group exhibited upregulated expression levels of IL-6， IL-8， MDC， TARC， TSLP， p-JAK2， p-STAT3， p-JAK2/JAK2， and p-STAT3/STAT3 in HaCaT cells （P<0.05， P<0.01）. Compared with the model group， C. dahurica n-butanol extract and dexamethasone downregulated the expression levles of these molecules （P<0.05， P<0.01）. ConclusionC. dahurica n-butanol extract may play an anti-eczema role by inhibiting the JAK2/STAT3 signaling pathway， reducing the inflammatory response， and correcting the metabolic disorder.

Intestinal aging is central to systemic aging, characterized by a progressive decline in intestinal structure and function. The core mechanisms involve dysregulation of epithelial cell renewal and gut microbiota dysbiosis. In addition to previous results in model organisms like Drosophila melanogaster, recent studies have shown that in mammalian models, aging causes increased intestinal permeability and intestinal-derived systemic inflammation, thereby affecting longevity. Therefore, anti-intestinal aging can be an important strategy for reducing frailty and promoting longevity. There are three key gaps remaining in the study of intestinal aging: (1) overemphasis on aging-related diseases rather than the primary aging mechanisms; (2) lack of specific drugs or treatments to prevent or treat intestinal aging; (3) limited aging-specific dysbiosis research. In this review, the basic structures and renewal mechanisms of intestinal epithelium, and mechanisms and potential therapies for intestinal aging are discussed to advance understanding of the causes, consequences, and treatments of age-related intestinal dysfunction.

Poly(ADP-ribosyl)ation (PARylation) is a specific form of post-translational modification (PTM) predominantly triggered by the activation of poly-ADP-ribose polymerase 1 (PARP1). However, the role and mechanism of PARylation in the advancement of acute kidney injury (AKI) remain undetermined. Here, we demonstrated the significant upregulation of PARP1 and its associated PARylation in murine models of AKI, consistent with renal biopsy findings in patients with AKI. This elevation in PARP1 expression might be attributed to trimethylation of histone H3 lysine 4 (H3K4me3). Furthermore, a reduction in PARylation levels mitigated renal dysfunction in the AKI mouse models. Mechanistically, liquid chromatography-mass spectrometry indicated that PARylation mainly occurred in receptor for activated C kinase 1 (RACK1), thereby facilitating its subsequent phosphorylation. Moreover, the phosphorylation of RACK1 enhanced its dimerization and accelerated the ubiquitination-mediated hypoxia inducible factor-1α (HIF-1α) degradation, thereby exacerbating kidney injury. Additionally, we identified a PARP1 proteolysis-targeting chimera (PROTAC), A19, as a PARP1 degrader that demonstrated superior protective effects against renal injury compared with PJ34, a previously identified PARP1 inhibitor. Collectively, both genetic and drug-based inhibition of PARylation mitigated kidney injury, indicating that the PARylated RACK1/HIF-1α axis could be a promising therapeutic target for AKI treatment.

Patients suffering from nerve injury often experience exacerbated pain responses and complain of memory deficits. The dorsal hippocampus (dHPC), a well-defined region responsible for learning and memory, displays maladaptive plasticity upon injury, which is assumed to underlie pain hypersensitivity and cognitive deficits. However, much attention has thus far been paid to intracellular mechanisms of plasticity rather than extracellular alterations that might trigger and facilitate intracellular changes. Emerging evidence has shown that nerve injury alters the microarchitecture of the extracellular matrix (ECM) and decreases ECM rigidity in the dHPC. Despite this, it remains elusive which element of the ECM in the dHPC is affected and how it contributes to neuropathic pain and comorbid cognitive deficits. Laminin, a key element of the ECM, consists of α-, β-, and γ-chains and has been implicated in several pathophysiological processes. Here, we showed that peripheral nerve injury downregulates laminin β1 (LAMB1) in the dHPC. Silencing of hippocampal LAMB1 exacerbates pain sensitivity and induces cognitive dysfunction. Further mechanistic analysis revealed that loss of hippocampal LAMB1 causes dysregulated Src/NR2A signaling cascades via interaction with integrin β1, leading to decreased Ca²⁺ levels in pyramidal neurons, which in turn orchestrates structural and functional plasticity and eventually results in exaggerated pain responses and cognitive deficits. In this study, we shed new light on the functional capability of hippocampal ECM LAMB1 in the modulation of neuropathic pain and comorbid cognitive deficits, and reveal a mechanism that conveys extracellular alterations to intracellular plasticity. Moreover, we identified hippocampal LAMB1/integrin β1 signaling as a potential therapeutic target for the treatment of neuropathic pain and related memory loss.
Animals ; Laminin/genetics* ; Hippocampus/metabolism* ; Neuralgia/metabolism* ; Cognitive Dysfunction/etiology* ; Male ; Peripheral Nerve Injuries/metabolism* ; Extracellular Matrix/metabolism* ; Integrin beta1/metabolism* ; Pyramidal Cells/metabolism* ; Signal Transduction

This study aimed to investigate the inhibitory effect of tubuloside B (Tub B) on amyloid β-protein (Aβ), and analyse the potential mechanism. A model of amyloid fibril was established by incubation of Aβ_1-42 in vitro. Thioflavin-T (ThT), Congo red (CR), 8-anilino-1-naphthene sulfonic acid (ANS) staining and transmission electron microscopy (TEM) were applied to detect the suppression of Tub B on the formation of Aβ_1-42 fibril. Circular dichroism (CD) was used to analyse the regulatory effect of Tub B on the secondary structure of Aβ_1-42. 3-(4,5-Dimethyl-2-thiazole) -2,5-diphenyltetrazolium bromide (MTT) and red blood cell hemolysis experiments were used to investigate the attenuation of Tub B on Aβ_1-42 induced cytotoxicity. 2',7'-Dichlorofluorescin diacetate (DCFH-DA) staining was used to assess the expression of intracellular reactive oxygen species (ROS) induced by Aβ_1-42. And molecular docking experiment was used to explore the interaction between Tub B and Aβ_1-42. The results indicated that Tub B could inhibit Aβ_1-42 fibrillization in a certain extent, which retarded the structural transition of α-helix to β-sheet of Aβ_1-42, hampered the exposure of hydrophobic regions, and attenuated amyloid-induced cytotoxicity and hemolysis. In summary, Tub B can prevent the formation of Aβ_1-42 amyloid fibril, which may be related to its antioxidant activity and hydrogen bonding and hydrophobic interactions with protein molecules. All animal experiments were approved by the Experimental Animal Research Center of Air Force Medical University (No. 20190051).

OBJECTIVE: To explore the improvement effect of rehabilitation nursing based on information-knowledge-belief-behavior (IKAP) theory on urinary incontinence patients after radical prostatectomy. METHODS Sixty-six patients with urinary incontinence who received robot-assisted laparoscopic radical prostatectomy in General Hospital of Eastern Theater Command from January 2021 to January 2023 were selected and divided into control group (n=33) and observation group (n=33) according to random number table method. The patients in the control group were treated with rehabilitation nursing. The patients in the observation group were treated with rehabilitation nursing guided by IKAP theory. The recovery of urinary incontinence, duration of urinary incontinence, subjective well-being, quality of life, psychological and emotional indexes of patients in the two groups were compared. Results： The total effective rate of urinary incontinence recovery in the observation group was significantly higher than that in the control group (90.91% vs 60.61%，P<0.05). The duration of urinary incontinence in the observation group was significantly shorter than that in the control group (［3.36±1.54］d vs ［4.15±1.36］d，P<0.05). And the subjective well-being score in observation group was significantly higher than that in the control group (［19.36±2.69］points vs ［11.65±2.65］points， P<0.05). There was no significant difference in preoperative physical function, social function，and mental health scores between the two groups (P>0.05). And all scores in the observation group were significantly higher than those in the control group after surgery (P<0.05). There was no significant difference in the preoperative SAS and SDS scores between the two groups of patients (P>0.05). And the scores of SAS and SDS in observation group were lower than those of the control group after the operation (P<0.05). Conclusion： Rehabilitation nursing based on IKAP theory can significantly improve urinary incontinence in patients with prostate cancer after surgery, which promotes the recovery of urinary incontinence, shortens the time of urinary incontinence, and improves the subjective well-being and quality of life, as well as reduces the negative impact of negative emotions. Therefore, it can be widely promoted and implemented in clinical practice.
Humans ; Prostatectomy/adverse effects* ; Urinary Incontinence/etiology* ; Male ; Quality of Life ; Rehabilitation Nursing ; Middle Aged ; Aged

Objective:To investigate the effect and mechanism of ginkgo acid(GA)on hepatic fibrosis in rats.Methods:CCl4 and TAA were used to construct rat liver fibrosis model,and GA or combined ferroptosis inhibitor(Fer-1)was given to intervene.The liver tissue and serum of rats were obtained and histopathologically evaluated by HE,Masson and Sirius red staining,respecively.The expression of HA,LN,Ⅳ-C and PC-Ⅲ in serum were detected by Elisa and the expression of GPX4 and FTH1 were detected by Western blot.Results:HE staining showed that,com-pared with TAA and CCl4 groups,the fibrosis level of GA group was significantly decreased.The results of Masoon and Sirius red staining showed that compared with TAA and CCl4 groups,the rate of collagen fibers in liver of GA group was significantly decreased(P＜0.05).Elisa results showed that compared with TAA and CCl4 groups,the levels of HA,LN,Ⅳ-C and PC-Ⅲ in serum of rats in GA group were significantly decreased(P＜0.05).After the intervention of GA com-bined with Fer-1,Western blot results showed that compared with TAA and CCl4 groups,the expression of GPX4 and FTH1 in liver of rats in GA group were significantly increased(P＜0.05).Compared with GA group,GPX4 and FTH1 levels in Fer group were significantly decreased(P＜0.05);The histopathological results showed that compared with GA group,the rate of liver collagen fibers in Fer group was significantly increased(P＜0.05).Conclusion:GA has anti-hepatic fi-brosis effect,which is associated with inducing ferroptosis.