Nursing Team Training and Standardized Management in Hybrid OR.

Objective: Analyzing the impact of nursing workforce development, training and standardization on hybrid operating theatres. Methods: Thirty nurses in the mixed operating room of the First Affiliated Hospital of Nanchang University from January 2021 to December 2021 were selected as the control group to receive routine nursing management and training methods and another thirty nurses were selected as the experimental group to receive nursing team construction, training and standardized management based on conventional methods. Nurses' theoretical and operational scores, nurses' satisfaction, surgeon satisfaction with nurses, and nursing service quality scores were compared between two groups at baseline and after intervention. Results: After the intervention, nurses in both groups had a significant improvement in theoretical and operational scores than those at baseline, and nurses in the experimental group had better scores than those in the control group, The difference was statistically significant (P = .002, P = .004). Nursing quality of surgical preparation, environmental management, surgical safety, and instrument management in the intervention group were significantly better than those at baseline and better than those in the control group. The difference was statistically significant (P = .001, P = .001, P = .001, P = .001). Satisfaction of nurses and doctors in the intervention group was significantly better than those at baseline and better than those in the control group. The difference was statistically significant (P = .002, P = .001). Conclusion: The effect of nursing team construction and training and standardized management of hybrid operating Room was ideal, which can improve nurses' theoretical knowledge and practical skills, and enhance the satisfaction of nurses and surgeons, providing patients with higher quality nursing services, which is worth adopting.

Research on driving factors and mechanism of Minority Village tourism development in Guizhou Province, China1.

The fundamental purpose of tourism destination development is to improve the quality of life of local residents. For the minority areas in Guizhou Province in China, tourism development can achieve good ecological, economic and social benefits. This research is aimed at to exploring the key driving factors which can improve the quality of local destinations. On the basis of literature analysis and to visit many villages, 8 variables are found, which are tourism resources, tourism location, tourism development environment, tourists' preference, tourism stakeholders, tourism products, tourism innovation and the development tourism destination. 19 hypotheses are proposed and a theoretical models is established. Through the sequential mixed method of qualitative phase and quantitative phase and model test with SEM, it is found: 1) all factors have significant positive effects on the development of rural tourism destinations. 2) The primary factors driving the development of rural tourism destinations are CTR, TL and tourism innovation. 3) Most factors interact with each other to drive the development of minority tourism destinations. Finally, according to the research results, combined with the current situation of the development of rural tourism destinations, the study puts forward suggestions and prospects to promote the development of rural minority tourism destinations.

Discovery of an effective anti-inflammatory agent for inhibiting the activation of NF-κB.

In this study, based on the effect of compounds on the activation of NF-κB and NO release, compound 51 was discovered as the best one with NO release inhibition IC50 value was 3.1 ± 1.1 µM and NF-κB activity inhibition IC50 value was 172.2 ± 11.4 nM. Compound 51 could inhibit the activation of NF-κB through suppressing phosphorylation and nuclear translocation of NF-κB, and suppress LPS-induced inflammatory response in RAW264.7 cells, such as the over-expression of TNF-α and IL-6, which were target genes of NF-κB. This compound also showed preferable anti-inflammatory activity in vivo, including alleviating significantly gastric distention and splenomegaly caused by LPS stimulation, reducing the level of oxidative stress induced by LPS, and inhibiting the expression of IL-6 and TNF-α in serum. Thus, it's reasonable to consider that this compound is a promising small molecule with anti-inflammatory effect for inhibiting the NF-κB signalling pathway.

A novel CDK8 inhibitor with poly-substituted pyridine core: Discovery and anti-inflammatory activity evaluation in vivo.

As an ideal anti-inflammatory target, cyclin-dependent kinase 8 (CDK8) has gradually attracted the attention of researchers. CDK8 inhibition up-regulates Interleukin-10 (IL-10) expression by enhancing the transcriptional activity of activator protein-1 (AP-1), and augmenting IL-10 abundance is a viable strategy for the treatment of inflammatory bowel disease (IBD). In this research, through structure-based drug design and dominant fragment hybridization, a series of poly-substituted pyridine derivatives were designed and synthesized as CDK8 inhibitors. Ultimately, compound CR16 was identified as the best one, which exhibited good inhibitory activity against CDK8 (IC50 = 74.4 nM). In vitro and in vivo studies indicated that CR16 could enhance the transcriptional activity of AP-1, augment the abundance of IL-10, and affect CDK8-related signaling pathways including TLR7/NF-κB/MAPK and IL-10-JAK1-STAT3 pathways. In addition, CR16 showed potent therapeutic effect in an animal model of IBD.

An insight into algicidal characteristics of Bacillus altitudinis G3 from dysfunctional photosystem and overproduction of reactive oxygen species.

Cyanobacterial blooms negatively affect aquatic ecosystems and human health. Algicidal bacteria can efficiently kill bloom-causing cyanobacteria. Bacillus altitudinis G3 isolated from Dianchi Lake shows high algicidal activity against Microcystis aeruginosa. In this study, we investigated its algicidal characteristics including attack mode, photosynthesis responses, and source and the contribution of reactive oxygen species (ROS). The results showed that G3 efficiently and specifically killed M. aeruginosa mainly by releasing both thermolabile and thermostable algicidal substances, which exhibited the highest algicidal activity (99.8%, 72 h) in bacterial mid-logarithmic growth phase. The algicidal ratio under full-light conditions (99.5%, 60 h) was significantly higher than under dark conditions (<20%, P < 0.001). G3 filtrate caused photosystem dysfunction by decreasing photosynthetic efficiency, as indicated by significantly decreased Fv/Fm and PIABS (P < 0.001) values. It also inhibited photosynthetic electron transfer as indicated by significantly decreased rETR (P < 0.001), especially QA- downstream, as revealed by significantly decreased φEo and ψo, and increased Mo (P < 0.001). These results indicated that the algicidal activity of G3 filtrate is light-dependent, and the cyanobacterial photosystem is an important target. Cyanobacterial ROS and malondialdehyde contents greatly increased by 37.1% and 208% at 36 h, respectively. ROS levels decreased by 49.2% (9 h) when diuron (3-(3-4-dichlorophenyl)-1,1-dimethylurea) partially blocked photosynthetic electron transport from QA to QB. Therefore, excessive ROS were produced from disrupted photosynthesis, especially the inhibited electron transport area in QA- downstream, and caused severe lipid peroxidation with significantly increased MDA content and oxidative stress in cyanobacteria. The ROS scavenger N-acetyl-l-cysteine significantly decreased both cyanobacterial ROS levels (34%) and algicidal ratio (52%, P < 0.05) at 39 h. Thus, excessive ROS production due to G3 filtrate administration significantly contributed to its algicidal effect. G3 could be an excellent algicide to control M. aeruginosa blooms in waters under suitable light conditions.

Novel 2-phenyl-4H-chromen derivatives: synthesis and anti-inflammatory activity evaluation in vitro and in vivo.

It is significant to design, synthesise and optimise flavonoid derivatives with better anti-inflammatory activity. This study aims to design and synthesise a series of novel 2-phenyl-4H-chromen-4-one compounds with anti-inflammatory; among them, compound 8 was discovered as the best one. And then, the effects of compound 8 on the TLR4/MAPK signalling pathway was carried out in vivo, the results indicated that compound 8 could downregulate NO, IL-6, and TNF-α expression, and suppress LPS-induced inflammation by inhibiting the TLR4/MAPK pathways. Furthermore, compound 8 reduced inflammation by a mouse model of LPS-induced inflammatory disease in vivo. The results suggest that compound 8 has the potential against inflammation through regulating TLR4/MAPK pathway and can be assessed further for drug development.

Discovery and Anti-Inflammatory Activity Evaluation of a Novel CDK8 Inhibitor through Upregulation of IL-10 for the Treatment of Inflammatory Bowel Disease In Vivo.

Increasing the anti-inflammatory cytokine interleukin-10 (IL-10) level is a promising strategy to suppress the progression of pathogenic inflammation including inflammatory bowel disease (IBD). Since cyclin-dependent kinase 8 (CDK8) inhibition can upregulate IL-10 abundance in activated myeloid-derived dendritic cells, it is considered to be an effective target for IBD treatment. Here, the complete discovery process of a novel CDK8 inhibitor as an anti-inflammatory agent was described. Starting with wogonin, structure-based optimization and structure-activity relationship (SAR) study were comprehensively carried out, and then lead compound 85 (N-(2-ethylphenyl)-5-(4-(piperazine-1-carbonyl)phenyl)nicotinamide) was developed as a potent druglike CDK8 inhibitor upregulating IL-10 both in vivo and in vitro. Also, compound 85 (with CDK8 IC50 = 56 nM, IL-10 enhancement rate 88%) exhibited effective anti-inflammatory activity in an animal model of IBD. These results confirmed that certain CDK8 inhibitor could be used as an effective anti-IBD drug.

Non-peptidyl non-covalent cathepsin C inhibitoEEr bearing a unique thiophene-substituted pyridine: Design, structure-activity relationship and anti-inflammatory activity in vivo.

Cathepsin C (Cat C) is involved in inflammation regulation by activating neutrophil serine proteases (NSPs). Therefore, Cat C is an attractive target for treatment of inflammatory diseases mediated by NSPs overactivation. In previous study, compounds 54 and 77 were reported to be the first non-peptidyl non-covalent Cat C inhibitors, with good enzyme inhibitory activity and NSPs activation inhibition, but their pharmacokinetic (PK) properties were unsatisfactory. In this study, starting from 77, after several rounds of structure-based design and modification, compound SF38, a novel Cat C inhibitor bearing a unique thiophene structure was identified, which exhibited strong inhibitory activity against Cat C (IC50 = 59.9 nM). Further mechanism study and in vivo evaluation showed that SF38 inhibited the Cat C activity in bone marrow and blood, decreased the activation of NSPs, and exhibited anti-inflammatory activity in an animal model of acute lung injury, with acceptable PK properties (F = 42.07%). These results enriched the structure-activity relationship (SAR) of Cat C inhibitor with thiophene structure characteristic, and proved the broad prospect of non-peptidyl non-covalent Cat C inhibitor.

Design and synthesis of the 4H-chromenone derivatives against psoriasis.

On basis of Quercetin moiety, two series of 20 new compounds were designed and synthesized accordingly in this study, and their anti-inflammatory activities in vitro and in vivo were evaluated. At last, compound 8A2: 3- (1- (2- (4- (5-bromo-2-chlorobenzoyl) piperazin-1-yl) ethyl)-1H-1,2,3-triazol-4-yl) methoxy)-5,7-dimethoxy-2-(3,4,5-trimethoxyphenyl)-4H-chromen-4-one with low toxicity was found the best one for inhibiting of NO. Meanwhile, this compound could significantly inhibit the expression of IL-6 (Interleukin-6), TNF-α (Tumor necrosis factor-α) and IL-17 (Interleukin-17), and also significantly down-regulate IL-17 mRNA psoriasis model in vitro. Further studies were performed to establish mouse psoriasis model induced by Imiquimod (IMQ), and the preliminary mechanism indicated that compound 8A2 may alleviate mouse psoriasis through obstructed the JAK1/2-STAT1/3 pathway. This study should be provide a basis for further study of effective treatment of psoriasis.

Discovery and In Vivo Anti-inflammatory Activity Evaluation of a Novel Non-peptidyl Non-covalent Cathepsin C Inhibitor.

Cathepsin C (Cat C) participates in inflammation and immune regulation by affecting the activation of neutrophil serine proteases (NSPs). Therefore, cathepsin C is an attractive target for treatment of NSP-related inflammatory diseases. Here, the complete discovery process of the first potent "non-peptidyl non-covalent cathepsin C inhibitor" was described with hit finding, structure optimization, and lead discovery. Starting with hit 14, structure-based optimization and structure-activity relationship study were comprehensively carried out, and lead compound 54 was discovered as a potent drug-like cathepsin C inhibitor both in vivo and in vitro. Also, compound 54 (with cathepsin C Enz IC50 = 57.4 nM) exhibited effective anti-inflammatory activity in an animal model of chronic obstructive pulmonary disease. These results confirmed that the non-peptidyl and non-covalent derivative could be used as an effective cathepsin C inhibitor and encouraged us to continue further drug discovery on the basis of this finding.

Angel or Devil ? - CDK8 as the new drug target.

Cyclin-dependent kinase 8 (CDK8) plays an momentous role in transcription regulation by forming kinase module or transcription factor phosphorylation. A large number of evidences have identified CDK8 as an important factor in cancer occurrence and development. In addition, CDK8 also participates in the regulation of cancer cell stress response to radiotherapy and chemotherapy, assists tumor cell invasion, metastasis, and drug resistance. Therefore, CDK8 is regarded as a promising target for cancer therapy. Most studies in recent years supported the role of CDK8 as a carcinogen, however, under certain conditions, CDK8 exists as a tumor suppressor. The functional diversity of CDK8 and its exceptional role in different types of cancer have aroused great interest from scientists but even more controversy during the discovery of CDK8 inhibitors. In addition, CDK8 appears to be an effective target for inflammation diseases and immune system disorders. Therefore, we summarized the research results of CDK8, involving physiological/pathogenic mechanisms and the development status of compounds targeting CDK8, provide a reference for the feasibility evaluation of CDK8 as a therapeutic target, and guidance for researchers who are involved in this field for the first time.

The expression and significance of serum caveolin-1 in patients with Kawasaki disease.

We investigated the expression of caveolin-1 (Cav-1) in Kawasaki disease (KD) and analyzed its relationship with coronary artery lesions (CALs). Cav-1 participated in the progression of CAL in KD. A total of 68 children with KD (23 with CALs), age matched with a fever control group (F, n = 28) and a normal control group (N, n = 24) were enrolled in this study. Cav-1 expression was detected using an enzyme-linked immunosorbent assay. The results are the following: (1) Compared with the F and N, Cav-1 expression was significantly increased in the children with KD (P < 0.05); there was no significant difference in Cav-1 between the F and N. (2) The serum level of Cav-1 was significantly higher in children with KD and CALs during the acute phase than in children with KD without CALs (P < 0.05). (3) Serum Cav-1 may be a biomarker that reflects CALs in children with KD based on a receiver operating characteristic (ROC) curve analysis. (4) Those children with KD who were given intravenous immunoglobulin (2 g/kg, 10-12 h) during the acute phase showed decreased expression of Cav-1 compared to the N. Conclusions are as follows: (1) The serum level of Cav-1 during the acute phase of KD increased significantly, while in KD patients with CALs the increase was even greater. (2) Based on our ROC curve analysis, Cav-1 may be a predictor of CALs in children with KD.

Discovery and SARs of 5-Chloro-N4-phenyl-N2-(pyridin-2-yl)pyrimidine-2,4-diamine Derivatives as Oral Available and Dual CDK 6 and 9 Inhibitors with Potent Antitumor Activity.

Cyclin-dependent kinases (CDKs) are promising therapeutic targets for cancer therapy. Herein, we describe our efforts toward the discovery of a series of 5-chloro-N4-phenyl-N2-(pyridin-2-yl)pyrimidine-2,4-diamine derivatives as dual CDK6 and 9 inhibitors. Intensive structural modifications lead to the identification of compound 66 as the most active dual CDK6/9 inhibitor with balancing potency against these two targets and good selectivity over CDK2. Further biological studies revealed that compound 66 was directly bound to CDK6/9, resulting in suppression of their downstream signaling pathway and inhibition of cell proliferation by blocking cell cycle progression and inducing cellular apoptosis. More importantly, compound 66 significantly inhibited tumor growth in a xenograft mouse model with no obvious toxicity, indicating the promising therapeutic potential of CDK6/9 dual inhibitors for cancer treatment. Therefore, the above results are of great importance in the development of dual CDK6/9 inhibitors for cancer therapy.

Short- and medium-term follow-up of transcatheter closure of perimembranous ventricular septal defects.

BACKGROUND: Transcatheter closure of perimembranous ventricular septal defects is one of the greatest challenges in interventional cardiology. Short- and midium-term follow-up data for large samples are limited. This report presents our experience with transcatheter closure of perimembranous ventricular septal defects using an occluder. METHODS: Two hundred fifty-three patients included in the database of the Second Affiliated Hospital and Yuying Children's Hospital from January 2011- December 2015 with transcatheter closure of perimembranous ventricular septal defects and discharged from follow-up. All patients were invited for clinical and transthoracic echocardiography, electrocardiogram, and thoracic radiography check-up. RESULTS: Device implantation was successful in 252 of 253 patients (99.6%). The median age was 42 months (range 27-216 months). The median follow-up duration was 36 months (range 6-60 months). The mean defect diameter was 3.5 ± 1.4 mm and the mean size of the ventricular septal defect rim below the aortic valve was 3.7 ± 1.8 mm. The mean diameter of the devices used was 4 mm. Thirty-seven patients developed arrhythmia after the procedure and recovered within 24 months; four patients had hemolysis and four had moderate tricuspid valve regurgitation. No other serious adverse event occurred during the follow-up period. CONCLUSION: Transcatheter closure of perimembranous ventricular septal defects using an occluder is safe and effective in most patients.

Piceatannol alleviates inflammation and oxidative stress via modulation of the Nrf2/HO-1 and NF-κB pathways in diabetic cardiomyopathy.

Diabetic cardiomyopathy (DCM) is one of the leading causes of morbidity and mortality in diabetic patients. Piceatannol (PIC) has protective effects against cardiovascular disease; however, it remains unknown whether it also protects against DCM. A Cell Counting Kit-8 (CCK-8) assay was used to evaluate the effects of PIC on the viability of high glucose (HG)-induced H9C2 cells. Protein expression and mRNA levels were detected by western blotting and real-time polymerase chain reaction (RT-PCR), respectively. In vivo, physical and biochemical analyses, together with transthoracic echocardiography and hemodynamic measurements, were used to detect the effects of PIC treatment on cardiac function in DCM rats. Reactive oxygen species production was determined using an ELISA kit, and inflammatory cytokines were detected by RT-PCR. Pathological changes were assessed by hematoxylin-eosin staining, immunohistochemical staining, and TUNEL staining. According to the results, PIC treatment improved cell viability and inhibited cell apoptosis in HG-induced H9C2 cardiac myoblasts. In addition, PIC not only attenuated the over-production of interleukin-6 (IL-6) (P < 0.05) and tumor necrosis factor alpha (TNF-α) (P < 0.05), but also improved the expression of nuclear factor E2-related factor 2 (Nrf2) (P < 0.05) and heme oxygenase-1 (HO-1) (P < 0.01). Importantly, knockdown of Nrf2 suppressed PIC-mediated activation of the Nrf2/HO-1 pathway and abolished its anti-inflammatory effects. In vivo, oral administration of PIC suppressed STZ-induced inflammation, oxidative stress hypertrophy, fibrosis(myocardial collagen volume fraction in 5 mg/kg and 10 mg/kg PIC group was decreased 25.83% and 55.61% compared with the DM group), and apoptosis(Caspase-3 level in 5 mg/kg and 10 mg/kg PIC group was decreased 13.21% and 33.91% compared with the DM group), thereby relieving cardiac dysfunction and improving both fibrosis and pathological changes in cardiac tissues of diabetic rats. These findings define for the first time that the effects of PIC against DCM can be attributed to its role in inflammation and oxidative stress inhibition.

Nicotinic Agonist Inhibits Cardiomyocyte Apoptosis in CVB3-Induced Myocarditis via α3ß4-nAChR/PI3K/Akt-Dependent Survivin Upregulation.

BACKGROUND: Cardiomyocyte apoptosis is critical for the development of coxsackievirus B3- (CVB3-) induced myocarditis, which is a common cardiac disease that may result in heart failure or even sudden death. Previous studies have associated CVB3-induced apoptosis with the downregulation of antiapoptotic proteins. Here, attempts were made to examine whether nicotinic acetylcholine receptors (nAChRs), especially α3ß4-nAChRs, were a novel therapeutic antiapoptotic target via the activation of survivin, a strong antiapoptotic protein, in viral myocarditis (VMC). METHODS AND RESULTS: In the present study, we demonstrated that nAChRs, α3ß4-nAChR subunits in particular, were present and upregulated in CVB3-infected neonatal rat cardiomyocytes (NRC) and H9c2 cells by RT-qPCR. The function of α3ß4-nAChRs was next examined using its specific blocker α-CTX AuIB in vitro. The results of the TUNEL assay and western blot experiments showed that the block of α3ß4-nAChRs abrogated nicotine-mediated protection of NRC from CVB3-induced apoptosis, and this effect displayed a substantial correlation with the protein expressions of pAkt, survivin, and Cleaved Caspase-3. Hence, the involvement of the PI3K/Akt pathway was further verified by LY294002, a selective inhibitor of PI3K. As a result, nicotine-mediated induction of pAkt and survivin was abolished by LY294002; meanwhile, apoptotic NRC were increased accompanied by an increase of Cleaved Caspase-3 expression. Regarding CVB3-infected BALB/c mice, the α-CTX AuIB- and LY294002-treated groups had a lower survival rate, deteriorative ventricular systolic function, and more severe inflammation than the nicotine-treated group and the modulation of pAkt, survivin, and Cleaved Caspase-3 protein expressions was similar to that in CVB3-infected NRC. In addition, we found that a nicotinic agonist reduced CVB3 replication in a dose-dependent manner in vitro, which indicates that nAChR activation may serve as a possible protection mechanism of CVB3-induced myocarditis. CONCLUSIONS: Our study demonstrated that α3ß4-nAChR subunits are essential in the nicotine-mediated antiapoptotic effect of protecting cardiomyocytes from CVB3-induced apoptosis in vivo and in vitro. This protection correlated with the PI3K/Akt pathway and the inducement of the antiapoptotic protein survivin. A combination of these mechanisms serves as a novel protective response to treat viral myocarditis.

The Neural Mechanism Underlying Cognitive and Emotional Processes in Creativity.

Creativity is related to both cognition and emotion, which are the two major mental processes, interacting with each other to form psychological processes. Emotion is the major driving force of almost all creativities, sometimes in an unconscious way. Even though there are many studies concerning the relationship between creativity and cognition, there are few studies about the neural mechanisms of the emotional effects on creativity. Here, we introduce a novel model to explain the relationship between emotions and creativities: Three Primary Color model, which proposes that there are four major basic emotions; these basic emotions are subsided by three monoamines, just like the three primary colors: dopamine-joy, norepinephrine-stress (fear and anger), and serotonin-punishment. Interestingly, these three neuromodulators play similar roles in creativity, whose core features are value and novelty (surprise), like the characteristics of the core features of basic emotions (hedonic value and arousal value). Dysfunctions of these neuromodulators may be the reasons for both psychopathology and creativity, in that they can change the thinking styles such as novelty seeking behavior, hyper-connectivity of brain areas, and/or cognitive disinhibition to induce both creativity and psychopathology. This new model will not only help researchers understand the dynamics of basic emotion elements, it can also bring an entirely new perspective into the relationship between psychopathology and creativity.

The Optimal Intervention Time of Bone Marrow Mesenchymal Stem Cells in Ameliorating Cardiac Fibrosis Induced by Viral Myocarditis: A Randomized Controlled Trial in Mice.

Bone marrow-derived mesenchymal stem cells (BMSCs) have recently been introduced to treat cardiovascular diseases, such as myocardial infarction and dilated cardiomyopathy. Nevertheless, there are few researches focused on the application of BMSCs in treating viral myocarditis, not to mention its optimal intervention timer potential mechanisms. In our study, we concentrated on finding an optimal time window to perform BMSCs treatment in a murine model of myocarditis induced by coxsackievirus B3 (CVB3). On the 1st day, 3rd day, 7th day, and 14th day after BALB/c mice were infected by CVB3, we intravenously injected equivalent BMSCs into the treatment groups. With a 28-day follow-up after inoculation, we found that the ventricular function was significantly improved in the BMSCs treatment group and cardiac fibrosis markedly ameliorated, especially when BMSCs were injected between 1 and 2 weeks after CVB3 inoculation. Furthermore, we demonstrated that after BMSCs treatment, the expressions of TGF-ß, col1α1, and col3α1 were significantly decreased. Therefore, we conclude that BMSCs may have a potential to improve CVB3-induced myocarditis by ameliorating cardiac fibrosis through the inhibition of TGF-ß expression.

Study on the diversity of Bacteroides and Clostridium in patients with primary gout.

To analyze the diversity of both Bacteroides and Clostridium in patients with primary gout and the difference from that of normal individuals. And to investigate the relationship between the primary gout and the intestinal flora. Fecal samples of 90 cases with the primary gout and 94 cases normal comparison group were selected, together with the cases that match the filter criteria. The DNA is extracted from the feces. 16S rRNA specific primers of both Bacteroides and Clostridium were adopted for the PCR amplification. The molecular fingerprints of Bacteroides and Clostridium in both the primary gout group and the normal control group were obtained through DGGE and subjected for further analysis on both the diversity and the similarity. Compared with normal individuals, the number of bands and Shannon-Weaver (H') of Bacteroides in patients with primary gout was not reduced, but significantly decreased in Clostridium. Furthermore, the intra-group and inter-group similarity of both Bacteroides and Clostridium were lower. The primary gout has caused the structural change of both Bacteroides and Clostridium, inducing the low similarity, especially for Clostridium. It has statistic significance. The gut predominant flora may play an important role in the development of primary gout.