Objective:To explore the clinical application of mobile-intelligent medical management system for gout patients.Methods:This study was a randomized controlled trial. One hundred and two patients with gout who visited rheumatology department of the First Hospital of Jilin University from January 2022 to October 2023 were randomly divided into study group ( n=53) and the control group ( n=49). Patients in the study group were managed by the mobil-gout(M-G) health management system which consists of a distant management plateform and an App. The body weight and blood uric acid levels were regularly self-tested by patients, and the information was sent to the system, the doctor gave feed-back advice on medication adjustment and dietary management every 2 weeks. While patients in the control group were managed following the conventional outpatient consultation mode. The serum uric acid levels, liver and kidney function tests and physical examinations were conducted on the day of enrollment and 3 and 6 months after treatment. The number of affected joints and the frequency of attacks were evaluated, and pain was assessed using the visual analog scale (VAS). The efficacy of treatment were compared between two groups. Results:After 3 and 6 months of treatment, the serum uric acid levels in study group were significantly lower than those in control group (408.0 (345.0, 450.0)μmol/L vs. 458.0 (409.0, 482.0)μmol/L, 371.0 (338.5, 409.0) μmol/L vs. 412.0 (368.5, 445.0)μmol/L; Z=3.37, 4.61, P<0.01); and VAS scores were also significantly lower than those in control group (6.66±1.46 vs. 4.68±1.80, 7.45±1.06 vs. 5.88±1.52; t=14.12, 13.72, P<0.01). After 6 months of treatment, the frequency of gout attacks in the study group was significantly lower than that in the control group ( χ2=9.30, P<0.05). As the follow-up period was extended, the average number of joints affected by gout attacks and the frequency of gout attacks in the study group showed a reducing trend compared to the control group, but the differences were not statistically significant ( P>0.05). Conclusions:The M-G medical management system can more effectively control uric acid levels and alleviate symptome for gout patients.

ObjectiveTo explore the potential mechanism by which Huangqi Baijiang Yiren decoction （HBY） repairs the intestinal mucosal injury in the rat model of ulcerative colitis （UC） via the miR-21/suppressor of cytokine signaling 1 （SOCS1）/Janus kinase 1 （JAK1）/signal transducer and activator of transcription 6 （STAT6） signaling pathway. MethodsSixty SPF-grade male SD rats were randomly assigned into six groups： blank， model， low-dose （3.68 g·kg^-1） HBY， medium-dose （7.35 g·kg^-1） HBY， high-dose （14.5 g·kg^-1） HBY， and mesalazine （0.035 g·kg^-1）， with 10 rats in each group. The rat model of UC was established in other groups except the blank group by 3% dextran sulfate sodium solution. The rats were administrated with corresponding drugs once a day for 7 consecutive days since the 3th day after modeling. The histopathological changes of the colon were observed by hematoxylin-eosin staining， and the Robarts histopathology index （RHI） was scored. Enzyme-linked immunosorbent assay was employed to measure the levels of pro-inflammatory cytokines ［interleukin （IL）-6， IL-18， IL-1β， and tumor necrosis factor-α （TNF-α）］ in the serum. Real-time PCR was employed to determine the mRNA levels of miR-21， SOCS1， JAK1， and STAT6 in the colon tissue. Western blot was employed to determine the protein levels of SOCS1， JAK1， phosphorylated （p）-JAK1， STAT6， p-STAT6， Occludin， and Claudin-1 in the colon tissue. ResultsCompared with the blank group， the model group showed an increase in disease activity index （DAI） （P<0.01）， shortening of colon length （P<0.01）， severe histopathological damage in the colon tissue， and an increase in RHI， rises in serum levels of IL-6， IL-1β， IL-18， and TNF-α （P<0.01）， up-regulation in mRNA levels of miR-21， JAK1， and STAT6 and protein levels of p-JAK1 and p-STAT6 （P<0.01）， and down-regulation in mRNA and protein levels of SOCS1 and protein levels of Occludin and Claudin-1 （P<0.01）. The treatment with HBY reduced the DAI （P<0.01）， alleviated colon shortening and histopathological damage in the colon tissue， decreased the RHI （P<0.01）， lowered the serum levels of IL-6， IL-1β， IL-18， and TNF-α （P<0.01）， down-regulated the mRNA levels of miR-21， JAK1， and STAT6 （P<0.05， P<0.01）， up-regulated the mRNA level of SOCS1 （P<0.05）， up-regulated the protein levels of SOCS1， Occludin， and Claudin-1 （P<0.05， P<0.01）， and down-regulated the protein levels of p-JAK1 and p-STAT6 （P<0.05， P<0.01）. ConclusionHBY may modulate the miR-21/SOCS1/JAK1/STAT6 signaling pathway to suppress inflammatory responses and restore the intestinal mucosal barrier in UC rats.

Objective:To explore the clinical application of mobile-intelligent medical management system for gout patients.Methods:This study was a randomized controlled trial. One hundred and two patients with gout who visited rheumatology department of the First Hospital of Jilin University from January 2022 to October 2023 were randomly divided into study group ( n=53) and the control group ( n=49). Patients in the study group were managed by the mobil-gout(M-G) health management system which consists of a distant management plateform and an App. The body weight and blood uric acid levels were regularly self-tested by patients, and the information was sent to the system, the doctor gave feed-back advice on medication adjustment and dietary management every 2 weeks. While patients in the control group were managed following the conventional outpatient consultation mode. The serum uric acid levels, liver and kidney function tests and physical examinations were conducted on the day of enrollment and 3 and 6 months after treatment. The number of affected joints and the frequency of attacks were evaluated, and pain was assessed using the visual analog scale (VAS). The efficacy of treatment were compared between two groups. Results:After 3 and 6 months of treatment, the serum uric acid levels in study group were significantly lower than those in control group (408.0 (345.0, 450.0)μmol/L vs. 458.0 (409.0, 482.0)μmol/L, 371.0 (338.5, 409.0) μmol/L vs. 412.0 (368.5, 445.0)μmol/L; Z=3.37, 4.61, P<0.01); and VAS scores were also significantly lower than those in control group (6.66±1.46 vs. 4.68±1.80, 7.45±1.06 vs. 5.88±1.52; t=14.12, 13.72, P<0.01). After 6 months of treatment, the frequency of gout attacks in the study group was significantly lower than that in the control group ( χ2=9.30, P<0.05). As the follow-up period was extended, the average number of joints affected by gout attacks and the frequency of gout attacks in the study group showed a reducing trend compared to the control group, but the differences were not statistically significant ( P>0.05). Conclusions:The M-G medical management system can more effectively control uric acid levels and alleviate symptome for gout patients.

Objective The aim of this study was to establish a rat model of inflammation-cancer transformation of inflammatory bowel disease(IBD)and to explore the associated characteristics of the intestinal flora.Methods Adult male Wistar rats were divided randomly into control and model groups(M1,M2,M3)with different dextran sulfate sodium(DSS)intervention cycles.Colitis-cancer transformation was induced in all rats in the model group by a single intraperitoneal injection of azoxymethane(AOM)combined with free drinking of DSS in different cycles,and disease activity index(DAI)scores were recorded.Rats in the M1,M2 and M3 groups were killed at the end of the first,second,and third cycles of DSS,respectively,and spleen and colon tissues and colon contents were collected.Histological damage and colon carcinogenesis were evaluated in each group using hematoxylin and eosin staining and transmission electron microscopy.Characteristic changes in the intestinal flora were analyzed by 16S rRNA sequencing.Results AOM/DSS administration significantly increased the DAI score,shortened the colon,and increased the spleen index.The intestinal mucosal barrier was progressively destroyed from groups M1 to M3,and the pathological score was gradually increased.Abnormal crypt foci,polyps,low-and high-grade intraepithelial neoplasia,and mucosal carcinoma appeared in turn,while the pathological process showed similar characteristics to carcinogenesis in human inflammatory bowel disease.Screening using 16S rRNA sequencing with two differential abundance testing tools,Wilcoxon and ALDEx2,indicated that changes in flora abundance represented by Bacteroidetes and Monoglobus may be involved in the progression of colitis-cancer transformation.The functions of the differential flora were mainly enriched in metabolic pathways,such as lipid and carbohydrate metabolism.Conclusions The current rat model induced by AOM/DSS can dynamically simulate the pathological characteristics of colitis-cancer transformation,accompanied by changes in the abundance of specific intestinal flora,which may be closely related to the metabolic pathways mediated by the flora.

Objective This study aims to systematically evaluate the protective role of quercetin(QCT),a naturally occurring flavonoid,against oxidative damage in human endometrial stromal cells(HESCs)induced by hydrogen peroxide(H2O2).Oxidative stress,such as that induced by H2O2,is known to contribute significantly to cellular damage and has been implicated in various reproductive health issues.The study is focused on investigating how QCT interacts with specific molecular pathways to mitigate this damage.Special attention was given to the p38 MAPK/NOX4 signaling pathway,which is crucial to the regulation of oxidative stress responses in cellular systems.By elucidating these mechanisms,the study seeks to confirm the potential of QCT not only as a protective agent against oxidative stress but also as a therapeutic agent that could be integrated in treatments of conditions characterized by heightened oxidative stress in endometrial cells.Methods In vitro cultures of HESCs were treated with QCT at different concentrations(0,10,20,and 40 μmol/L)for 24 h to verify the non-toxic effects of QCT on normal endometrial cells.Subsequently,250 μmol/L H2O2 was used to incubate the cells for 12 h to establish an H2O2-induced HESCs injury model.HESCs were pretreated with QCT for 24 h,which was followed by stimulation with H2O2.Then,CCK-8 assay was performed to examine the cell viability and to screen for the effective intervention concentration.HESCs were divided into 3 groups,the control group,the H2O2 model group,and the H2O2+QCT group.Intracellular levels of reactive oxygen species(ROS)were precisely quantified using the DCFH-DA fluorescence assay,a method known for its accuracy in detecting and quantifying oxidative changes within the cell.The mitochondrial membrane potential was determined by JC-1 staining.Annexin Ⅴ/PI double staining and flow cytometry were performed to determine the effect of QCT on H2O2-induced apoptosis of HESCs.Furthermore,to delve deeper into the cellular mechanisms underlying the observed effects,Western blot analysis was conducted to measure the expression levels of the critical proteins involved in oxidative stress response,including NADPH oxidase 4(NOX4),p38 mitogen-activated protein kinase(p38 MAPK),and phosphorylated p38 MAPK(p-p38 MAPK).This analysis helps increase understanding of the specific intracellular signaling pathways affected by QCT treatment,giving special attention to its potential for modulation of the p38 MAPK/NOX4 pathway,which plays a significant role in cellular defense mechanisms against oxidative stress.Results In this study,we started off by assessing the toxicity of QCT on normal endometrial cells.Our findings revealed that QCT at various concentrations(0,10,20,and 40 μmol/L)did not exhibit any cytotoxic effects,which laid the foundation for further investigation into its protective roles.In the H2O2-induced HESCs injury model,a significant reduction in cell viability was observed,which was linked to the generation of ROS and the resultant oxidative damage.However,pretreatment with QCT(10 μmol/L and 20 μmol/L)significantly enhanced cell viability after 24 h(P<0.05),with the 20 μmol/L concentration showing the most substantial effect.This suggests that QCT can effectively reverse the cellular damage caused by H2O2.Furthermore,the apoptosis assays demonstrated a significant increase in the apoptosis rates in the H2O2 model group compared to those in the control group(P<0.01).However,co-treatment with QCT significantly reversed this trend(P<0.05),indicating QCT's potential protective role in mitigating cell apoptosis.ROS assays showed that,compared to that in the control group,the average fluorescence intensity of ROS in the H2O2 model group significantly increased(P<0.01).QCT treatment significantly reduced the ROS fluorescence intensity in the H2O2+QCT group compared to the that in the H2O2 model group,suggesting an effective alleviation of oxidative damage(P<0.05).JC-1 staining for mitochondrial membrane potential changes revealed that compared to that in the control,the proportion of cells with decreased mitochondrial membrane potential significantly increased in the H2O2 model group(P<0.01).However,this proportion was significantly reduced in the QCT-treated group compared to that of the H2O2 model group(P<0.05).Finally,Western blot analysis indicated that the expression levels of NOX4 and p-p38 MAPK proteins were elevated in the H2O2 model group compared to those of the control group(P<0.05).Following QCT treatment,these protein levels significantly decreased compared to those of the H2O2 model group(P<0.05).These results suggest that QCT may exert its protective effects against oxidative stress by modulating the p38 MAPK/NOX4 signaling pathway.Conclusion QCT has demonstrated significant protective effects against H2O2-induced oxidative damage in HESCs.This protection is primarily achieved through the effective reduction of ROS accumulation and the inhibition of critical signaling pathways involved in the oxidative stress response,notably the p38 MAPK/NOX4 pathway.The results of this study reveal that QCT's ability to modulate these pathways plays a key role in alleviating cellular damage associated with oxidative stress conditions.This indicates not only its potential as a protective agent against cellular oxidative stress,but also highlights its potential for therapeutic applications in treating conditions characterized by increased oxidative stress in the endometrium,thereby offering the prospect of enhancing reproductive health.Future studies should explore the long-term effects of QCT and its clinical efficacy in vivo,thereby providing a clear path toward its integration into therapeutic protocols.

Objective The aim of this study was to establish a rat model of inflammation-cancer transformation of inflammatory bowel disease(IBD)and to explore the associated characteristics of the intestinal flora.Methods Adult male Wistar rats were divided randomly into control and model groups(M1,M2,M3)with different dextran sulfate sodium(DSS)intervention cycles.Colitis-cancer transformation was induced in all rats in the model group by a single intraperitoneal injection of azoxymethane(AOM)combined with free drinking of DSS in different cycles,and disease activity index(DAI)scores were recorded.Rats in the M1,M2 and M3 groups were killed at the end of the first,second,and third cycles of DSS,respectively,and spleen and colon tissues and colon contents were collected.Histological damage and colon carcinogenesis were evaluated in each group using hematoxylin and eosin staining and transmission electron microscopy.Characteristic changes in the intestinal flora were analyzed by 16S rRNA sequencing.Results AOM/DSS administration significantly increased the DAI score,shortened the colon,and increased the spleen index.The intestinal mucosal barrier was progressively destroyed from groups M1 to M3,and the pathological score was gradually increased.Abnormal crypt foci,polyps,low-and high-grade intraepithelial neoplasia,and mucosal carcinoma appeared in turn,while the pathological process showed similar characteristics to carcinogenesis in human inflammatory bowel disease.Screening using 16S rRNA sequencing with two differential abundance testing tools,Wilcoxon and ALDEx2,indicated that changes in flora abundance represented by Bacteroidetes and Monoglobus may be involved in the progression of colitis-cancer transformation.The functions of the differential flora were mainly enriched in metabolic pathways,such as lipid and carbohydrate metabolism.Conclusions The current rat model induced by AOM/DSS can dynamically simulate the pathological characteristics of colitis-cancer transformation,accompanied by changes in the abundance of specific intestinal flora,which may be closely related to the metabolic pathways mediated by the flora.

Objective:To explore the efficacy of the oncoplastic round block technique in surgical management of idiopathic granulomatous mastitis (IGM).Methods:From January 2014 to December 2019, a total of 18 patients (24 to 38 years old, 32.2 years in average) with IGM underwent excision of the inflammatory breast mass with oncoplastic round block technique, the postoperative clinical efficacy was summarized and analyzed.Results:All 18 patients with IGM underwent excision of the inflammatory breast mass with oncoplastic round block technique, among them 2 patients underwent round-block reduction surgery of contralateral breast at the same time. The median follow-up duration was 16.1 months (from 6 to 36 months). Incision poor healing occurred in two cases which was cured after dressing change. Recurrence occurred in one case at 6 months after operation, and then cured with conservative measures. No other severe complications occurred. All patients were satisfacted with the results.Conclusions:Application of oncoplastic round block technique in surgical management of IGM may remove more tissue in order to reduce the recurrent rate, and get a better cosmetic results.

Objective:To investigate how urothelial carcinoma-associated 1 (UCA1) and miR-18a modulates acquired tamoxifen resistance and the relevant mechanisms in estrogen receptor (ER) positive cancer cells.Methods: qRT-PCR was performed to detect UCA1 and miR-18a expression in breast cancer cells.Dual luciferase assay was performed to detect the binding between miR-18a and UCA1 3′UTR.Tamoxifen sensitive MCF-7 cells were transfected with UCA1 expression vector or miR-18a inhi-bitors.Tamoxifen resistant LCC9 and BT474 cells were transfected with UCA1 siRNA or miR-18a mi-mics.CCK-8 assay was performed to detect cell viability.Soft agar assay was performed to assess cell colony formation.Flow cytometric analysis was performed to check cell cycle distribution.Results: UCA1 was significantly upregulated in tamoxifen resistant LCC2,LCC9,and BT474 cells than in tamoxifen sensitive MCF-7 cells.UCA1 expression was significantly upregulated in MCF-7 cells after treatment with 0.1 μmol/L tamoxifen.UCA1 overexpression enhanced cell viability of MCF-7 cells after tamoxifen treatment,while UCA1 siRNA significantly suppressed viability of LCC9 and BT474 cells after tamoxifen treatment.In MCF-7 cells,compared with vector control+tamoxifen group,the average cell colony number and colony size of the UCA1+tamoxifen group was 19.0％ more and 29.0％ larger respectively,while the proportions of the cells in G1 phase and in S phase were 7.3％ lower and 6.7％ higher respectively.In BT474 cells,compared with siRNA control+tamoxifen group,the average cell colony number and colony size of the si-UCA1+tamoxifen group were 54.0％ less and 42.0％ smaller respectively,while the proportions of the cells in G1 phase and in S phase were 9.0％ higher and 6.2％ lower respectively.UCA1 directly interacted with miR-18a and reduced its expression in ER positive breast cancer cells.Knockdown of miR-18a increased viability of MCF-7 cells after tamoxifen treatment,while miR-18a overexpression significantly reduced viability of BT474 cells after tamoxifen treatment.In MCF-7 cells,compared with miRNA inhibitor control+tamoxifen group,the average cell colony number and colony size of the miR-18a inhibitor+tamoxifen group were 15.0％ more and 33.0％ larger respectively,while the proportions of the cells in G1 phase and in S phase were 8.8％ lower and 5.3％ higher respectively.In BT474 cells,compared with miRNA control+tamoxifen group,the average cell colony number and colony size of the miR-18a mimics+tamoxifen group were 47.0％ less and 25.0％ smaller respectively,while the proportions of the cells in G1 phase and in S phase were 13.3％ higher and 7.9％ lower respectively.Conclusion: UCA1 can increase tamoxifen resistance of ER positive breast cancer cells via competitively inhibiting of miR-18a.

OBJECTIVE To investigate chemical properties of a fructooligosaccharide (ABP-50-FOS)separated from Achyranthes bidentata and immune response in mice immunized H1N1 influenza vaccine. METHODS The methods of GPC,CE,IR and NMR were used to study chemical properties of ABP-50-FOS. BALB/c mice were immunized intramuscularly twice with H1N1 influenza vaccine (3 μg)plus ABP-50-FOS(200 μg)each mouse. The serum total antibody titer and its isotypes titers were analyzed by ELISA. The populations of CD4+,CD8+,CD3+and CD19+lymphocytes were deter?mined by flow cytometry. The proliferation activities of spleen T and B lymphocytes were determined with MTT method. The levels of cytokines interferon-γ(IFN-γ),tumor necrosis factor-α(TNF-α),inter?leukin-4(IL-4),IL-12 and NO were measured by ELISA kits. RESULTS ABP-50-FOS was a fructooli?gosaccharide with moleculer mass 1885 u. Its bone linkages contained 1,2-and 1,6-fructose residues. ABP-50-FOS could induce high specific-IgG,IgG1,IgG2a,IgG2b and IgM titers after immunization with H1N1 influenza antigen twice(P<0.01). ABP-50-FOS significantly elevated the percentage of CD3+,CD4+ and CD8+ spleen lymphocytes and IFN-γ secretions(P<0.01)in vitro. It also stimulated peritoneal macrophage of mice and DC2.4 dendritic cells to produce TNF-αand IL-12p70 respectively (P<0.01). However,ABP-50-FOS inhibited secretions of NO in macrophage. CONCLUSION The fruc?tooligosaccharide ABP-50-FOS separated from A. bidentata can exhibit strong adjuvant activity for H1N1 influenza vaccine.

Objective To study the effect of black granule capsules(BGCs) on growth of transplanted mouse hepatocarcinoma cells, cell proliferation cycle and apoptosis.Methods KM mouse were subcutaneously inoculated with Hepatocarcinoma cells (H22) and randomly divided into the model control group, the positive control group, the low, medium and high does of BGC group after 24h. The positive control group received intraperitoneal injection with 30 mg/kg cyclophosphamide. Mice of BGC groups were intragastricaly with different dosage of BGC (400, 800, 1 600 mg/kg). The model control group received intragastricaly with normal saline. The drugs were administrated once a day for seven days. The tumor inhibition rate was calculated at 24 h after the last administration. Flow cytometry was used to detect changes of cell cycle and apoptosis in harvested H22 tumor cells.Results The group of high does showed significant inhibitory effect on the growth of transplanted H22 tumor cells withthe inhibitory rate 38.78% (male) and 43.57% (female). Compared with model control group, groups of different dosages decreased time of G0-G1 phase (58.06% ± 9.65%, 55.10% ± 5.89%, 61.36% ± 15.95%vs. 74.47% ± 2.63%), increased tiem of Sphase (33.96% ± 11.90%, 32.67% ± 4.04%, 33.89% ± 9.82%vs. 14.37% ± 4.92%), and increased the apoptosis rate (31.12% ± 1.85%, 31.89% ± 2.16%, 40.64% ± 0.55%vs.21.75% ± 2.64%).Conclusion BGC has antitumor effect on mouse hepatocarcinoma H22 tumor cells, and its mechanism was to regulate cell proliferation cycle and induce the apoptosis.