Emerging evidence highlights the critical role of circular RNAs (circRNAs) in regulating pathological processes in various diseases, including organ fibrosis. Endometrial fibrosis, commonly referred to as intrauterine adhesions (IUA), is a major cause of uterine infertility. However, the involvement of circRNAs in the pathogenesis of IUA remains largely unexplored, necessitating further research. This study aimed to identify a specific circRNA that may serve as a diagnostic biomarker and therapeutic target for IUA. CircRNA microarray analysis was performed to compare circRNA expression profiles between paired fibrotic and normal endometrial samples from patients with IUA. The expression of hsa_circ_0079474 was significantly upregulated in fibrotic tissues compared with normal tissues. Functional analyses demonstrated that hsa_circ_0079474 enhanced cell proliferation, promoted cell cycle progression, and facilitated epithelial-mesenchymal transition (EMT) in vitro, as assessed by qRT-PCR, CCK-8 assays, EdU assays, flow cytometry, and Masson staining. Mechanistically, dual-luciferase reporter assays and RNA immunoprecipitation confirmed that hsa_circ_0079474 acted as a molecular sponge for miR-630, leading to the upregulation of YAP1. In an IUA rat model, hsa_circ_0079474 was found to drive EMT, whereas miR-630 administration reversed this process and ameliorated endometrial fibrosis. Consequently, these findings indicate that hsa_circ_0079474 contributes to the progression of IUA by modulating the miR-630/YAP1 axis, providing new insights into circRNA-mediated mechanisms in IUA and highlighting hsa_circ_0079474 as a potential therapeutic target.

Metabolic reprogramming constitutes a hallmark of malignant neoplasms. Purine metabolism emerges as a pivotal regulator in cellular metabolic networks through multiple mechanisms, including dysregulation of de novo biosynthesis/salvage pathway coordination, adenosine-mediated immunosuppressive microenvironment formation, and collective contributions to tumorigenesis and malignant progression. During metastatic progression, purine metabolism reinforces tumor cell plasticity through mitochondrial energy regulation and modulation of cell cycle checkpoints (eg, G1/S transition). These mechanistic revelations have positioned purine metabolism-targeting strategies as promising oncotherapeutic candidates. This review methodically analyzes (1) purine metabolic pathways and their regulatory dynamics, (2) adenosine-mediated pathophysiological interactions, and (3) the synergistic impacts of these pathways in malignant transformation. We propose a unified mechanistic framework that clarifies oncogenic purine metabolic rewiring while evaluating translational potential through three clinical dimensions: pathogenesis elucidation, diagnostic biomarker discovery, and targeted therapeutic development. This comprehensive synthesis aims to advance precision oncology through mechanistic insights and therapeutic innovation.

Abstract Insufficient understanding exists of the molecular mechanisms underlying circRNA involvement in IUA and requires further investigation. This research aims to examine the role of hsa_circ_0079474 (circDGKB-009) and its potential mechanisms in intrauterine adhesion (IUA). A circRNA microarray was utilized to identify differences in circRNA expression between fibrotic endometrial samples and normal endometrial samples. Subsequent studies confirmed the expression and biological functions of hsa_circ_0079474 both in vivo and in vitro using various experimental techniques such as CCK-8, EdU, flow cytometry, FISH, RT-PCR, Western blot and IHC/ICC. The interactions between hsa_circ_0079474 and miR-630, as well as miR-630 and YAP1 were determined using dual-luciferase reporter assay and RNA immunoprecipitation. Hsa_circ_0079474 was dramatically elevated in IUA tissues compared to normal tissues. Hsa_circ_0079474 was found to enhance cell proliferation, expedite cell cycle progression, and facilitate epithelial-mesenchymal transition (EMT). Mechanistically, hsa_circ_0079474 acted as a sponge for miR-630, resulting in upregulation of YAP1 expression. This, in turn, promoted the progression of IUA. Hsa_circ_0079474 improves IUA by regulating the miR-630/YAP1 axis, providing a novel understanding of the molecular mechanisms underlying circRNA in IUA.

In critical care medicine, sepsis is a dangerous systemic condition that is highly prevalent and is associated with high morbidity and mortality rates[1]. The high mortality rate associated with sepsis is closely related to multi-organ dysfunction, with heart injury being particularly critical and considered the starting point of multi-organ injury[2].

Avamectin (AVM), a macrolide antibiotic, is widely used in fisheries, agriculture, and animal husbandry, however, its irrational use poses a great danger to aquatic organisms. Ferulic acid (FA) is a natural chemical found in the cell walls of plants. It absorbs free radicals from the surrounding environment and acts as an antioxidant. However, the protective effect of FA against kidney injury caused by AVM has not been demonstrated. In this study, 60 carp were divided into the control group, AVM group (2.404 μg/L), FA+AVM group and FA group (400 mg/kg). Pathological examination, quantitative real-time PCR (qPCR), reactive oxygen species (ROS) and western blot were used to evaluate the preventive effect of FA on renal tissue injury after AVM exposure. Histological findings indicated that FA significantly reduced the swelling and infiltration of inflammatory cells in the kidney tissues of carp triggered by AVM. Dihydroethidium (DHE) fluorescent probe assay showed that FA inhibited the accumulation of kidney ROS. Biochemical results showed that FA significantly increased glutathione (GSH) content, total antioxidant capacity (T-AOC) and catalase (CAT) activity, and decreased intracellular malondialdehyde (MDA) content. In addition, western blot results revealed that the protein expression levels of Nrf2 and p-NF-κBp65 in the carp kidney were inhibited by AVM, but reversed by the FA. The qPCR results exhibited that FA significantly increased the mRNA levels of tgf-β1 and il-10, while significantly down-regulated the gene expression levels of tnf-α, il-6 and il-1β. These data suggest that FA can reduce oxidative stress and renal tissue inflammation induced by AVM. At the same time, FA inhibited the apoptosis of renal cells induced by AVM by decreasing the transcription level and protein expression level of Bax, and increasing the transcription level and protein expression level of Bcl2, PI3K and AKT. This study provides preliminary evidence for the theory that FA reduces the level of oxidative stress, inflammation response and kidney tissue damage caused by apoptosis in carp, providing a theoretical basis for the prevention and treatment of the AVM.

As a broad-spectrum and efficient triazole fungicide, difenoconazole is widely used, which not only pollutes the environment but also exerts toxic effects on non-target organisms. The spleen plays an important role in immune protection as an important secondary lymphoid organ in carp. In this study, we assessed the protective impact of silybin as a dietary additive on spleen tissues of carp during exposure to difenoconazole. Sixty carp were separated into four groups for this investigation including control group, difenoconazole group, silybin group, and silybin and difenoconazole group. By hematoxylin-eosin staining, dihydroethidium staining, immunohistochemical staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, quantitative real-time PCR assay, Western blot analysis, biochemical assays, and immune function indicator assays, we found that silybin could prevent difenoconazole-induced spleen tissue damage, oxidative stress, and immune dysfunction, and inhibited apoptosis of carp spleen tissue cells by suppressing the formation of p53-driven caspase-9-apoptotic protease activating factor-1-cytochrome C complex. The results suggested that silybin as a dietary additive could improve spleen tissue damage and immune dysfunction induced by difenoconazole in aquaculture carp.

Avermectins, as a new type of environmental pollutant, have received significant attention in recent years. Previous research has shown that acute exposure to avermectins can induce oxidative stress and inflammation in non-target fish species, such as carp. Flavonoid lignans, particularly Silybin, have demonstrated promising biological activities, including regulation of non-alcoholic fatty liver and cerebral ischemia-reperfusion injury. This study aims to investigate the impact of dietary supplementation with Silybin on the intestinal damage in carp caused by chronic exposure to avermectins and to improve the health status and production of carp in aquaculture. Silybin was used as a dietary supplement by adding it to the experimental feed, and an animal experimental model was utilized to assess its effects on oxidative stress, inflammation, and cell apoptosis in carp intestine. Additionally, intestinal barrier integrity, digestive capacity, and fish growth were evaluated. The results indicated that dietary supplementation with Silybin effectively alleviated the oxidative stress induced by chronic exposure to avermectins in carp intestine. Furthermore, Silybin improved intestinal barrier integrity and digestive capacity by modulating the Nrf2/Keap1 pathway. This study demonstrates that dietary supplementation with Silybin can effectively mitigate the intestinal damage caused by chronic exposure to avermectins in carp, providing a sustainable solution for the aquaculture industry to enhance the overall health and production of cultured fish. The research expands our understanding of avermectin environmental pollution and offers a potential remediation approach.

Difenoconazole (DFZ) is a widely used triazole fungicide in agricultural production. However, the presence of DFZ residue in the environment poses a significant risk to non-target organisms. Ferulic acid (FA) is a phenolic compound known for its antioxidant and anti-inflammatory properties. This study aims to investigate the hepatic damage caused by DFZ in carp and explore the mechanism through which FA alleviates this damage. The findings revealed that FA enhanced the antioxidant capability of the carp's liver and reduced the accumulation of reactive oxygen species (ROS) in the liver tissue. Moreover, FA regulated the transcriptional levels of inflammation-related factors, effectively preventing the inflammatory response triggered by the NF-κB signaling pathway. Additionally, TUNEL results demonstrated that DFZ initiated apoptosis, while dietary supplementation with FA decreased the protein expression levels of Bax and Cytochrome C (Cyt c) and the transcriptional levels of bax, caspase3, caspase9, p53 genes. Furthermore, FA increased the protein expression and transcriptional levels of Bcl-2. In conclusion, FA protects against liver injury induced by DFZ exposure in carp by modulating oxidative damage, inflammation, and apoptosis.

Tumour-induced immunosuppressive microenvironments facilitate oncogenesis, with regulatory T cells (Tregs) serving as a crucial component. The significance of Treg-associated genes within the context of ovarian cancer (OC) remains elucidated insufficiently. Utilizing single-cell RNA sequencing (scRNA-Seq) for the identification of Treg-specific biomarkers, this investigation employed single-sample gene set enrichment analysis (ssGSEA) for the derivation of a Treg signature score. Weighted gene co-expression network analysis (WGCNA) facilitated the identification of Treg-correlated genes. Machine learning algorithms were employed to determine an optimal prognostic model, subsequently exploring disparities across risk strata in terms of survival outcomes, immunological infiltration, pathway activation and responsiveness to immunotherapy. Through WGCNA, a cohort of 365 Treg-associated genes was discerned, with 70 implicated in the prognostication of OC. A Tregs-associated signature (TAS), synthesized from random survival forest (RSF) and Least Absolute Shrinkage and Selection Operator (LASSO) algorithms, exhibited robust predictive validity across both internal and external cohorts. Low TAS OC patients demonstrated superior survival outcomes, augmented by increased immunological cell infiltration, upregulated immune checkpoint expression, distinct pathway enrichment and differential response to immunotherapeutic interventions. The devised TAS proficiently prognosticates patient outcomes and delineates the immunological milieu within OC, offering a strategic instrument for the clinical stratification and selection of patients.

Background Important roles of INHBB in various malignancies are increasingly identified. The underlying mechanisms in gastric cancer (GC) microenvironment are still greatly unexplored. Methods The clinical significance of INHBB and the correlation between INHBB and p-p65 in GC were assessed through analyzing publicly available databases and human paraffin embedded GC tissues. The biological crosstalk of INHBB between GC cells and fibroblasts was explored both in vitro and in vivo. RNA-seq analyses were performed to determine the mechanisms which regulating fibroblasts reprogramming. Luciferase reporter assay and chromatin immunoprecipitation (CHIP) assay were used to verify the binding relationship of p65 and INHBB in GC cells. Results Our study showed that INHBB level was significantly higher in GC, and that increased INHBB was associated with poor survival. INHBB positively regulates the proliferation, migration, and invasion of GC cells in vitro. Also, activin B promotes the occurrence of GC by reprogramming fibroblasts into cancer-associated fibroblasts (CAFs). The high expression of INHBB in GC cells activates the NF-κB pathway of normal gastric fibroblasts by secreting activin B, and promotes fibroblasts proliferation, migration, and invasion. In addition, activin B activates NF-κB pathway by controlling TRAF6 autoubiquitination to induce TAK1 phosphorylation in fibroblasts. Fibroblasts activated by activin B can induce the activation of p65 phosphorylation of GC cells by releasing pro-inflammatory factors IL-1β. p65 can directly bind to the INHBB promoter and increase the INHBB transcription of GC cells, thus establishing a positive regulatory feedback loop to promote the progression of GC. Conclusions GC cells p65/INHBB/activin B and fibroblasts p65/IL-1β signal loop led to the formation of a whole tumor-promoting inflammatory microenvironment, which might be a promising therapeutic target for GC.

Abstract Background Immunosuppression is a key feature of cancer, promoting tumor growth and progression. Regulatory T cells (Tregs) are a specialized subset of T lymphocytes that mediate immunosuppression in cancer. However, the role of Treg-related genes in ovarian cancer (OC) remains largely unexplored.Methods To identify marker genes related to Tregs in OC, we utilized scRNA-seq analysis. Treg scores were then constructed using single-sample gene set enrichment analysis (ssGSEA) based on these markers. To identify gene modules with the strongest correlation with Treg scores in bulk RNA-seq data, we employed the Weighted Gene Co-expression Network Analysis (WGCNA) algorithm. Multiple machine learning algorithms were then used to construct risk models with superior predictive performance, which were validated using external independent datasets. A risk score was developed for each OC sample based on the optimal model to evaluate differences in prognosis, immune infiltration, pathway activity, and immunotherapy between high and low-risk groups.Results We identified 365 genes regulating Treg activity using the WGCNA algorithm, and found that 70 of these genes were associated with the prognosis of OC based on univariate cox analysis. Using a combination of the Random Survival Forest (RSF) and Lasso algorithms, we constructed a risk model with the highest c-index based on the assigned risk scores. The model's performance was validated using four external datasets. Our analysis revealed that the low-risk group had a better prognosis, more immune cell infiltration, higher immune checkpoint expression, and significant differences in pathway enrichment and immunotherapy efficacy between the different risk groups.Conclusion Our findings provide new insights into the role of Treg cells in the development and progression of OC and highlight the potential for developing novel Treg-targeted therapies for the treatment of this disease.

In order to fill the gap between training needs and short training time in the offline teaching of periodontology, the teaching and research group of periodontology at Nanjing Medical University has developed an onlineself-directed learning platform. It has been one year since the implementation of this online platform, in order to evaluate its effect, 97 undergraduates majoring in stomatology from grade 2017 in Nanjing Medical University were enrolled for the research survey. This paper expounds the design and implementation of the periodontology online self-directed learning platform, and the application effect was evaluated by final examination scores, questionnaire surveys and interviews. The results showed that average final examination score of students from periodontology rotation was (78.64±10.14) points, the excellent rate was 50% (48/96), and the pass rate was 92.71%(89/96). The overall satisfaction of the students with online self-directed learning platform was 90.7% (88/97). Therefore, the online self-learning platform helps students to master theoretical knowledge systematically and is widely acknowledged by students. In addition, students think that the platform is efficient and practical, real-time interactive, and full of challenges.

目的 探讨支气管肺发育不良(BPD)早产儿不同阶段(出生后7 d、28 d、1年、2年)肺功能情况.方法 选取2018年3月至2019年11月南京医科大学附属淮安第一医院收治的BPD早产儿91例为研究组,另选取同期南京医科大学附属淮安第一医院收治的非BPD早产儿87例为对照组.对所有患儿进行随访,记录其出生后7 d、28 d、1年、2年肺功能指标,包括呼吸频率(RR)、潮气量(TV)、潮气呼气峰流量(PTEF)、吸气时间/总呼吸时间(Ti/Tt)、达峰时间比(TPTEF/TE)、25％潮气量呼气流量(TEF25)、50％潮气量呼气流量(TEF50)、75％潮气量呼气流量(TEF75).结果 出生后1年,对照组有4例失访,研究组有3例失访;出生后2年,对照组有8例失访,研究组有7例失访;最终对照组有79例、研究组有84例完成随访.方法 与时间在RR、TV、PTEF、Ti/Tt、TPTEF/TE、TEF25、TEF50、TEF75上存在交互作用(P<0.05);方法 、时间在RR、TV、PTEF、Ti/Tt、TPTEF/TE、TEF25、TEF50、TEF75上主效应显著(P<0.05).研究组出生后7 d、28 d、1年RR快于对照组,TPTEF/TE低于对照组(P<0.05);研究组出生后2年RR慢于对照组(P<0.05);研究组出生后7 d、28 d TV、PTEF、TEF25、TEF50、TEF75低于对照组,Ti/Tt高于对照组(P<0.05).两组出生后28 d、1年、2年RR分别慢于本组出生后7 d,TV、PTEF、TEF25、TEF50、TEF75分别高于本组出生后7 d,Ti/Tt分别低于本组出生后7 d(P<0.05);两组出生后1年、2年RR分别慢于本组出生后28 d,TV、PTEF、TEF25、TEF50、TEF75分别高于本组出生后28 d,Ti/Tt分别低于本组出生后28 d(P<0.05);两组出生后2年RR分别慢于本组出生后1年,TV、PTEF、TEF25、TEF50分别高于本组出生后1年(P<0.05);两组出生后1年、2年TPTEF/TE分别高于本组出生后7 d、28 d(P<0.05).结论 BPD早产儿新生儿期肺功能异常,婴儿期、幼儿期肺功能有所改善,但呼吸效率仍较低,动态监测BPD早产儿不同阶段肺功能指标可评估其肺发育情况,进而有利于对其进行对症治疗.

Objective:To observe the short-term clinical effect of Edaravone Dexborneol injection for acute anterior circulatory ischemic stroke.Methods:A retrospective study of 80 patients with acute anterior circulatory ischemic stroke admitted to the Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University from August to December 2020 without intravenous thrombolysis or endovascular treatment was conducted. The observation group (32 cases) was treated with conventional treatment combining Edaravone Dexborneol injection, while the control group (48 cases) was treated with only conventional treatment. Both groups were treated for 14 days. Independent sample t-test was used to compare the National Institute of Health stroke scale (NIHSS) scores at admission, 7 14 days after treatment. The total efficacy of the two groups on 7 and 14 days after treatment was compared by chi-square test.Results:No statistically significant difference was observed in NIHSS scores of the two groups at baseline before treatment (P＞0.05). NIHSS score of the observation group on 7 and 14 days after treatment were lower than those of the control group [(6.31±4.81) vs (8.48±4.77); (4.40±2.95) vs (6.56±4.27)], and the differences were statistically significant (t=-2.167, P=0.033; t=-2.485, P=0.015). The total efficacy of the observation group on 7 and 14 days after treatment were higher than those of the control group (90.63% vs 70.83%; 96.88% vs 77.08%), and the differences were statistically significant (χ2=4.494, P=0.034; χ2=5.899, P=0.015).Conclusion:Edaravone Dexborneol injection was effective in short time for acute anterior circulatory ischemic brain injury.

Endotoxin tolerance refers to a state refractory to subsequent lipopolysaccharide (LPS) stimulations following a primary LPS exposure. To study the relationship between endotoxin tolerance and macrophage polarization, endotoxin tolerance was induced by 1 μg/mL LPS from the periodontal pathogen, Porphyromonas gingivalis (P. gingivalis), in peritoneal macrophages (PMs) and bone marrow-derived macrophages (BMDMs). Repeated P. gingivalis LPS challenges increased the quantities of CD206+ PMs, while the number of CD86+CD206+ PMs was reduced compared with the non-tolerant group (p < 0.05). However, there were no changes in BMDMs (p > 0.05). Down regulations of TNF-α, IL-12, nitric oxide and MMP-2 production, and upregulated IL-10, MMP-9 levels and arginase-1 activities occurred in tolerant PMs and BMDMs (p < 0.05). P. gingivalis LPS-tolerant PMs and BMDMs also enhanced scrape-wound healing abilities of 15p-1 cells (p < 0.05). Expressions of phospho-signal transducer and activator of transcription 6 (p-STAT6) and protein tyrosine phosphatase 1B (PTP1B) were increased, while p-MEK1/2 levels were downregulated in tolerant PMs and BMDMs (p < 0.05). IL-10 production in tolerant Stat6 knockdown RAW264.7 cells was lower than tolerant control cells (p < 0.05). P. gingivalis LPS-tolerant macrophages represented an intermediate state between M1/M2 polarization, which functioned as M2-like cells, and led to limited inflammatory responses and enhanced wound healing activities. The PTP1B-MEK1/2-STAT6 signaling pathway might be involved in the polarization of tolerant macrophages.

Urticaria is an immune-mediated allergic disease. This study explored the effect of Jingfang Mixture on spleen T lymphocyte subsets of urticaria mice. A total of 50 Kunming mice were randomized into normal group(C), model group(V), and low-(JF-L, 0.5 g·kg~(-1)), medium-(JF-M, 1 g·kg~(-1)) and high-dose(JF-H, 2 g·kg~(-1)) Jingfang Mixture groups, with 10 mice in each group. The mixture of ovalbumin and aluminum hydroxide(0.1 mg + 0.1 mL) was used(intraperitoneal injection) to induce urticaria in mice. The administration began 6 days after the first immunization, and the second immunization was carried out 10 days after the first immunization. The pruritus index was detected within 30 min after the second immunization. The administration lasted 21 days. After 21 days, the serum was taken to detect the total IgE level. Based on hematoxylin and eosin(HE) staining, the pathological changes of skin tissue were observed, and Western blot was used to detect the levels of p-Janus kinase 2(JAK2)/JAK2 and p-signal transducer and activator of transcription 3(STAT3)/STAT3 in skin tissue. The spleen was taken to detect the spleen index, and flow cytometry was employed to determine the expression of lymphocyte subsets. The results showed that group V had obvious pathological changes in skin tissue compared with group C. Moreover, group V showed more scratches, higher spleen index, and higher level of total serum IgE than group C. In addition, higher levels of p-JAK2 and p-STAT3, lower proportions of CD4~+T, Th1, and Treg, higher proportions of CD8~+T, Th2, and Th17, and lower ratios of CD4~+/CD8~+, Th1/Th2, and Terg/Th17 were observed in group V than in group C. Compared with group V, each administration group showed alleviation of the pathological morphology of skin tissue, obvious epidermal thickening, relatively intact collagen fiber structure of dermal reticular layer, alleviated edema, and relief of vasodilation and peripheral inflammatory cell infiltration. Moreover, less scratching, lower spleen index, lower p-JAK2/JAK2 and p-STAT3/STAT3 were observed in the administration groups than in group V. JF-M group and JF-H group demonstrated lower levels of total IgE, larger proportions of CD4~+T, Th1, and Treg, smaller proportions of CD8~+ T, Th2, and Th17, and higher ratios of CD4~+/CD8~+, Th1/Th2, and Terg/Th17. In conclusion, Jingfang Mixture may improve the symptoms of urticaria mice by regulating the balance of spleen T lymphocyte subsets through JAK2-STAT3 signaling pathway.

Tolerance is defined to be a hyporesponsive state following repeated stimulations with bacteria or their virulence factors and has potential impacts on the development of periodontitis. Recently, macrophages have been reported to release chromatin and antimicrobial peptides to form extracellular traps upon bacterial or chemical stimulations. Thus, we explored the roles and mechanisms of tolerance induced by Porphyromonas gingivalis (P. gingivalis) in macrophage extracellular traps (METs). Tolerance in peritoneal macrophages from mice was triggered by repeated P. gingivalis stimulation. METs were observed using fluorescence microscopy, and the levels of extracellular DNA were determined by microplate reader assays. The expression of p-RAF, p-MEK, and p-ERK was examined by Western blot, and reactive oxygen species (ROS) production was explored using flow cytometry. Moreover, the levels of intracellular Ca2+ were also determined by confocal microscopy to identify the possible mechanisms related to the changes in METs in P. gingivalis–pretreated macrophages. Repeated P. gingivalis stimulation contributed to the formation of METs and increased levels of extracellular DNA (p < 0.05). ROS generation and RAF/MEK/ERK phosphorylation were decreased in P. gingivalis–pretreated macrophages compared with non-pretreated cells (p < 0.05), which was inconsistent with the changes in METs. However, in P. gingivalis–pretreated macrophages, the levels of intracellular Ca2+ were significantly increased compared with the single stimulation group. Additionally, inhibition of intracellular Ca2+ resulted in a decrease in the levels of extracellular DNA in P. gingivalis–pretreated cells (p < 0.05). Taken together, P. gingivalis–pretreated macrophages released more METs, possibly related to the increased levels of intracellular Ca2+.

目的:探讨牙周基础治疗对一氧化氮(NO)代谢和血压的影响.方法:纳入45名血压正常的中、重度牙周炎患者,记录牙周基础治疗前及治疗后1月患者的菌斑指数、牙龈指数、探诊深度、临床附着丧失(CAL)及血压,采用Griess法测量治疗前后唾液及血浆NO氧化产物亚硝酸钠(NaNO2)水平,实时定量PCR技术检测治疗前后龈下菌斑中牙龈卟啉单胞菌(P.gin-givalis)、中间普氏菌(P.intermedia)及总菌水平,ELISA法检测治疗前后龈沟液(GCF)和血清中的白介素(IL)-6水平,以及血清C-反应蛋白(CRP)水平,并对治疗前血压、牙周临床指标、细菌数量、NaNO2、CRP、IL-6水平间的关系进行相关性分析.结果:牙周基础治疗后1月,患者各牙周临床指标、血压、唾液及血浆NaNO2水平、龈下菌斑中的P.gingivalis、P.intermedia及总菌水平、血清及GCF中的IL-6及CRP水平均显著下降(P<0.05).治疗前收缩压与GCF中IL-6水平、唾液NaNO2水平、CAL均存在中度相关性;舒张压与总菌水平、P.intermedia存在中度相关性(P<0.05).结论:牙周基础治疗能降低唾液及血浆NO水平,同时改善全身炎症状态,为伴高血压的牙周炎患者的治疗提供参考.

Objective: The present study aimed to screen hub genes for pathology of uterine leiomyoma.Methods: The microarray data of GSE31699, containing 16 uterine leiomyoma tissue samples and 16 matched normal myometrium samples, were downloaded from the Gene Expression Omnibus database (GEO).The "limma" R language package was used to identify di ferently-expressed genes (DEGs) between uterine leiomyoma and myometrium.Gene Ontology (GO) and pathway enrichment analyses were performed by using clusterprofiler, the DEGs were mostly enriched in post-synapse assembly, response to glucocorticoid, extracellular matrix receptor interaction and coagulation cascades.Subsequently, a protein-protein interaction (PPI) network of DEGs was constructed by Search Tool for the Retrieval of Interacting Genes Database (STRING) and visualized by utilizing Cytoscape so tware.We screened hub clusters of PPI network by the plug-in Molecular Complex Detection (MCODE) in Cytoscape, then clusterprofiler was also utilized to analyze functions and pathways enrichment of the genes in the hub clusters.Furthermore, we employed the "WGCNA" package in R to conduct co-expression network for all genes in GSE31699.Ultimately, we selected the overlapped genes in hub clusters of DEGs' PPI network and WGCNA.Results: Five genes (COL5A2, ALDH1A1, GNG11, EFEMP1, ANXA1) were finally validated in other GEO datasets (GSE64763, GSE764, GSE593) and Oncomine database.Gene set enrichment analysis (GSEA) was also performed for the hub genes.The expression of COL5A2 was significantly higher in uterine leiomyoma compared with that in myometrium, while the expression of the other hub genes was significantly lower in uterine leiomyoma.Conclusion: The results indicated that COL5A2, ALDH1A1, GNG11, EFEMP1 and ANXA1 may be the key pathological genes in uterine leiomyoma.

目的:从龈下菌斑总菌数、牙龈卟啉单胞菌(P.gingivalis)、伴放线聚集杆菌(A.actinomycetemcomitans)及白细胞毒素(LTX)在江苏汉族牙周炎人群中分布的角度,比较牙周病2018年新分类与1999年分类.方法:纳入73名牙周炎患者和26名牙周健康者,分别按照牙周病2018年新分类与1999年分类对牙周炎人群分组.初诊时记录全口探诊深度(PD)、临床附着丧失(CAL)、牙龈指数(GI)和菌斑指数(PLI),并收集龈下菌斑.采用实时定量PCR检测龈下菌斑中总菌、P.gingivalis和A.actinomycetemcomitans数量,采用PCR检测A.actinomycetemcomitans毒力因子LTX的携带率,比较上述指标在不同的牙周炎分类法间的分布差异.结果:慢性牙周炎和侵袭性牙周炎患者之间,总菌和P.gingivalis数量无显著差异(P>0.05),A.actinomy-cetemcomitans数量和LTX阳性率存在差异(P<0.05),所有检出的LTX均为低毒型.不同牙周炎分期分级组间,菌量和LTX阳性率存在差异(P<0.05).PD、CAL、GI与总菌、P.gingivalis、A.actinomycetemcomitans数量间存在相关性(P<0.05).结论:2018年牙周病新分类能较好地反映江苏汉族牙周炎患者的微生物学特征.