ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

Electromagnetic fields can regulate the fundamental biological processes involved in bone remodeling. As a non-invasive physical therapy, electromagnetic fields with specific parameters have demonstrated therapeutic effects on bone remodeling diseases, such as fractures and osteoporosis. Electromagnetic fields can be generated by the movement of charged particles or induced by varying currents. Based on whether the strength and direction of the electric field change over time, electromagnetic fields can be classified into static and time-varying fields. The treatment of bone remodeling diseases with static magnetic fields primarily focuses on fractures, often using magnetic splints to immobilize the fracture site while studying the effects of static magnetic fields on bone healing. However, there has been relatively little research on the prevention and treatment of osteoporosis using static magnetic fields. Pulsed electromagnetic fields, a type of time-varying field, have been widely used in clinical studies for treating fractures, osteoporosis, and non-union. However, current clinical applications are limited to low-frequency, and research on the relationship between frequency and biological effects remains insufficient. We believe that different types of electromagnetic fields acting on bone can induce various “secondary physical quantities”, such as magnetism, force, electricity, acoustics, and thermal energy, which can stimulate bone cells either individually or simultaneously. Bone cells possess specific electromagnetic properties, and in a static magnetic field, the presence of a magnetic field gradient can exert a certain magnetism on the bone tissue, leading to observable effects. In a time-varying magnetic field, the charged particles within the bone experience varying Lorentz forces, causing vibrations and generating acoustic effects. Additionally, as the frequency of the time-varying field increases, induced currents or potentials can be generated within the bone, leading to electrical effects. When the frequency and power exceed a certain threshold, electromagnetic energy can be converted into thermal energy, producing thermal effects. In summary, external electromagnetic fields with different characteristics can generate multiple physical quantities within biological tissues, such as magnetic, electric, mechanical, acoustic, and thermal effects. These physical quantities may also interact and couple with each other, stimulating the biological tissues in a combined or composite manner, thereby producing biological effects. This understanding is key to elucidating the electromagnetic mechanisms of how electromagnetic fields influence biological tissues. In the study of electromagnetic fields for bone remodeling diseases, attention should be paid to the biological effects of bone remodeling under different electromagnetic wave characteristics. This includes exploring innovative electromagnetic source technologies applicable to bone remodeling, identifying safe and effective electromagnetic field parameters, and combining basic research with technological invention to develop scientifically grounded, advanced key technologies for innovative electromagnetic treatment devices targeting bone remodeling diseases. In conclusion, electromagnetic fields and multiple physical factors have the potential to prevent and treat bone remodeling diseases, and have significant application prospects.

BACKGROUND:In the initial stage of growth plate injury inflammation,platelet-derived growth factor BB promotes the repair of growth plate injury by promoting mesenchymal progenitor cell infiltration,chondrogenesis,osteogenic response,and regulating bone remodeling. OBJECTIVE:To elucidate the action mechanism of platelet-derived growth factor BB after growth plate injury. METHODS:PubMed,VIP,WanFang,and CNKI databases were used as the literature sources.The search terms were"growth plate injury,bone bridge,platelet-derived growth factor BB,repair"in English and Chinese.Finally,66 articles were screened for this review. RESULTS AND CONCLUSION:Growth plate injury experienced early inflammation,vascular reconstruction,fibroossification,structural remodeling and other pathological processes,accompanied by the crosstalk of chondrocytes,vascular endothelial cells,stem cells,osteoblasts,osteoclasts and other cells.Platelet-derived growth factor BB,as an important factor in the early inflammatory response of injury,regulates the injury repair process by mediating a variety of cellular inflammatory responses.Targeting the inflammatory stimulation mediated by platelet-derived growth factor BB may delay the bone bridge formation process by improving the functional activities of osteoclasts,osteoblasts,and chondrocytes,so as to achieve the injury repair of growth plate.Platelet-derived growth factor BB plays an important role in angiogenesis and bone repair tissue formation at the injured site of growth plate and intrachondral bone lengthening function of uninjured growth plate.Inhibition of the coupling effect between angiogenesis initiated by platelet-derived growth factor BB and intrachondral bone formation may achieve the repair of growth plate injury.

Purpose To investigate the immunohistochemical HER2 expression in a large group of patients with urothelial carcinoma and to compare the results with the pathologic features and survival rate.Methods A total of 519 urothelial carcinoma specimens were collected from two centers.HER2 expression was measured by EnVision immuno-histochemistry.HER2 expression was compared with clinicopathological parameters,and further analyzed in relation to patient prognosis.Results The median age of the 519 patients was 66 years with a male to female ratio of 1.93∶1.Among them,160 cases were radical specimens,and 359 were transurethral resection specimens.The overall HER2 positivity rate was 61.7％(320/519),of which 148 cases(28.5％)were HER2 1+,238(45.9％)were HER2 2+,and 82(15.8％)were HER2 3+.In addition,51 cases(9.8％)were HER2-negative.HER2-positive ex-pression was associated with age,tumor location,histological grade,histological type,surgical approach,lymphovas-cular invasion,and neural invasion(all P＜0.05),but there was no significant correlation with gender,pT stage,muscular invasion,or lymph node metastasis.Univariate and multivariate logistic regression analysis showed that age≥ 66 years,higher tumor grade,and lymphovascular invasion were risk factors for positive HER2 expression,and high histological grade and lymphovascular invasion were independent risk factors affecting HER2 expression after controlling for confounders.Survival analysis showed no significant difference in recurrence-free survival between patients with HER2-positive and HER2-negative non-muscle-invasive urothelial carcinoma(P=0.274).Conclusion High histologic grade,tumor lymphovascular invasion,and neural invasion were associated with positive HER2 expression in patients with urothelial carcinoma,and higher histologic grade and lymphovascular invasion are important factors affect-ing HER2 expression.However,HER2-positive expression may not affect the prognosis of patients with non-muscle-invasive bladder urothelial carcinoma.

Objective:To investigate the effect of oral administration of vitamin D3 on intestinal barrier function in patients after gastric cancer surgery,and to provide a reference for perioperative nutritional therapy in patients with gastric cancer.Methods:The conve-nience sampling method was used to select 80 patients with gastric cancer who were admitted to Department of Gastrointestinal Surgery in a grade A tertiary hospital in Xiamen,China,from June 2021 to May 2023,and the patients were divided into intervention group and control group using a random number table.The patients in the intervention group were given oral administration of vitamin D3 800 IU/d for 14 consecutive days before surgery.ELISA was used to measure the serum levels of 25-hydroxyvitamin D3[25(OH)D3],intestinal barrier indicators(D-lactate,Zonulin),and inflammatory indicators(C-reactive protein,interleukin-6)within 24 hours after admis-sion and on days 1,4,and 7 after surgery,and the changes in these indicators were compared between the two groups.Results:A total of 71 patients were enrolled finally,with 34 in the intervention group and 37 in the control group.On days 1,4,and 7 after surgery,the intervention group had a significantly lower level of D-lactate than the control group(F=3.978,P=0.026;F=9.649,P=0.005;F=4.389,P=0.021).On day 4 after surgery,the intervention group had a significantly lower level of Zonulin than the control group(F=3.198,P=0.035).Conclusion:Oral administration of vitamin D3 before surgery may accelerate the recovery of intestinal barrier function in pa-tients with gastric cancer.

Widespread utilization of glyphosate has led to environmental residues,posing potential threats to ecological systems and human health.Traditional methods for detection of glyphosate are limited by specialized equipment and operational techniques,resulting in inefficient responses.Therefore,it is urgent to develop a convenient,sensitive and accurate detection method for detection of glyphosate.Herein,a new naphthalenesulfonamide-based"Turn-on"fluorescent probe was synthesized using 2-chloroaniline and dansyl chloride as raw materials through a one-step process,which showed a good linear relationship between the glyphosate concentration in concentration range of 0.003-70 μmol/L and the fluorescence intensity(R2=0.995),with a detection limit of 2.73 nmol/L(S/N=3).Analytical techniques such as nuclear magnetic resonance(NMR)spectroscopy and high-resolution mass spectrometry(HRMS)were used to investigate the interaction mechanism between the fluorescent probe and glyphosate.The results indicated that a nucleophilic substitution reaction occurred between the probe and the secondary amine(—NH—)of glyphosate,inducing a photoinduced electron transfer(PET)effect which enhanced the fluorescence intensity by 11.2 times.The probe showed good anti-interference ability towards coexisting metal ions,anions and pesticides in water.When applied to determination of glyphosate in the samples such as tap water,river water(Xiangxi River Reservoir),soil,soybeans,and corn,the spiking recoveries ranged from 94.7％to 109.9％,demonstrating the high accuracy and broad applicability of this detection method.A portable test strip based on this fluorescent probe was developed for rapid semi-quantitative analysis of glyphosate.The developed method was rapid,sensitive,and portable,providing theoretical and technical support for on-site measurement of environmental contaminants.

Objective:To investigate the changes in and correlations between melanin-concentrating hormone (MCH) and androgen levels in the serum of patients with polycystic ovary syndrome (PCOS), aiming to provide a novel research perspective for its diagnosis.Methods:A cross-sectional study. A total of 307 subjects were enrolled from the physical examination center and endocrinology clinic of the Affiliated Hospital of Zunyi Medical University from June 2023 to June 2024. The cohort comprised 114 healthy controls and 193 patients with PCOS, diagnosed according to the Rotterdam criteria. The patients were grouped into four phenotypes: Phenotype A (hyperandrogenemia [HA]+ovulatory dysfunction [OA]+polycystic ovarian morphology [PCOM], n=44), Phenotype B (HA+OA, n=50), Phenotype C (HA+PCOM, n=46), and Phenotype D (OA+PCOM, n=53). Clinical data were collected for all subjects. Serum MCH levels were determined by enzyme-linked immunosorbent assay. The relationship between MCH and androgen-related risk factors for PCOS was analyzed using Spearman partial correlation analysis and stepwise multiple linear hierarchical regression. Binary logistic regression was used to analyze factors influencing PCOS onset. The diagnostic value of MCH for PCOS was evaluated using a receiver operating characteristic (ROC) curve. Results:There were no significant differences in age and height between the healthy control group and the PCOS phenotypic groups (both P>0.05). MCH levels [17.63 (12.69, 22.00), 17.31 (11.05, 20.09), 17.82 (11.47, 19.40), 16.50 (11.14, 19.41) μg/L vs. 12.14 (9.78, 15.05) μg/L], homeostatic model assessment of insulin resistance, fasting plasma glucose, fasting serum lisulin, body mass index, and weight were significantly higher across all four PCOS phenotypes (A, B, C, and D) than in healthy controls (all P<0.05), whereas sex hormone-binding globulin (SHBG) contents were significantly lower ( P<0.05). Free androgen index (FAI), total testosterone (TES) and dehydroepiandrosterone (DHEA) levels were significantly higher in PCOS phenotypes A, B, and C than in the control group and PCOS phenotype D (all P<0.05). Spearman partial correlation analysis revealed no significant correlation between MCH and TES, DHEA, or FAI in healthy controls and patients with non-HA PCOS (all P>0.05). However, in PCOS patients with HA, MCH showed a significant positive correlation with TES and DHEA ( r=0.227 and 0.196, respectively; both P<0.05), but not FAI ( P>0.05). Stepwise multiple linear hierarchical regression analysis showed that MCH was positively correlated with TES, DHEA and luteinizing hormone and negatively correlated with SHBG (all P<0.05). Binary logistic regression indicated that an increase in MCH may be a potential risk factor for PCOS occurrence ( OR=1.113, 95% CI 1.012-1.224, P=0.028). ROC analysis showed that MCH has diagnostic value for PCOS ( P<0.05), with an area under the curve of 0.713. Conclusion:Serum MCH is closely related to FAI, TES, and DHEA levels in PCOS patients and may play an important role in the etiology and progression of the syndrome.

Objective To explore the publication trends and future directions in the field of value of MRI for diagnosing uterine fibroids using bibliometrics.Methods Literature related to diagnostic value of MRI for uterine fibroids in CNKI,Wanfang Med Online,SinoMed and WOSCC databases from 2006 to 2024 were retrieved,and 460 Chinese and 166 English articles were included.A bibliometric analysis was conducted to examine annual publication volume,country/region collaborations,journal distribution,core authors,highly cited literatures and keywords related to MRI for diagnosing uterine fibroids.Results From 2006 to 2024,the number of publications showed a fluctuating upward trend,with Chinese literature dominating.Authors from United States led research in this field and had the closest collaboration with those from France.Chinese and English articles were published in 221 and 81 journals,respectively,with several journals demonstrating significant influence.Highly cited articles mainly focused on differential diagnosis in early publications.Keywords analysis indicated that Chinese studies emphasized diagnosis and pathological typing,while English studies were more concerned with technical comparisons and accuracy assessment.Since 2020,research focus shifted toward image analysis technology and MRI-guided therapy.Conclusion The research on value of MRI for diagnosing uterine fibroids has been continuously developing.In the future,application of new technologies could be further explored,and multi-center cooperation and clinical transformation should be strengthened to promote the development and innovation in this field.

AIM To investigate the impact of varying dosages of Supplemented Wendan Decoction on the PI3K/Akt/FOXO1 glycolipid metabolic pathway in 3T3-L1 adipocytes.METHODS The CCK-8 assay was used to determine the concentration of Supplemented Wendan Decoction-medicated serum.The mature adipocytes differentiated from 3T3-L1 preadipocytes after induction were further divided into the blank control group,the model group,the rosiglitazone group(10 mg/L),and the Supplemented Wendan Decoction groups(5％,10％,and 20％),followed by the sample collections after 48 hours of treatment.Oil red O staining quantified lipid accumulation in 3T3-L1 adipocytes;extracellular glucose levels were measured using glucose oxidase(GOD)assay;RT-qPCR analyzed mRNA expressions of IRS-1,PI3K,Akt,GLUT4,IL-6,TNF-α and IL-1β;Western blot assessed protein expressions of INSR,IRS-1,PI3K-p85,Akt,FOXO1 and GLUT4.RESULTS No significant changes in cell viability(P＞0.05)were observed in 3T3-L1 preadipocytes exposed to serum containing supplemented Wendan Decoction at different concentrations for 24,48,or 72 hours.The 3T3-L1 preadipocytes held the capacity to differentiate into mature adipocytes within a 14-day induction period.Compared to the model group,all supplemented Wendan Decoction groups exhibited reduced lipid accumulation in adipocytes and downregulated mRNA expression of IRS-1,IL-6,TNF-α and IL-1β(P＜0.01);the low-dose group demonstrated increased mRNA expressions of PI3K and GLUT4(P＜0.05,P＜0.01),alongside elevated protein expressions of INSR,IRS-1,PI3K-p85,Akt and GLUT4(P＜0.05,P＜0.01);the medium-dose group showed enhanced GLUT4 mRNA expression,and upregulated protein expressions of INSR and FOXO1(P＜0.01).After 24 hours intervention,the high-dose Supplemented Wendan Decoction group exhibited increased glucose consumption in adipocytes(P＜0.01),and elevated protein expression of INSR,Akt and FOXO1(P＜0.05,P＜0.01).CONCLUSION Supplemented Wendan Decoction reduces lipid accumulation in adipocytes,regulates glucose and lipid metabolism,and promotes metabolic homeostasis through PI3K/Akt/FOXO1 signaling pathway.