Objective To investigate the relationship between regular exercise habit and coronary collaterals of patients with acute coronary syndrome (ACS).Methods TWo hundred and thirty-night patients diagnosed ACS and operated coronary angiography (CAG) showing severe coronary stenosis were enrolled hospitalized from May 2012 to October 2012.They were divided into regular exercise group (n =102) and irregular exercise group(n =137) according to the exercise frequency.The information of the general data,the information of CAG and other relevant index were collected.The coronary artery score was recorded according to the Censini and the coronary collateral class was made according to the Rentrop.Other characters in clinical and laboratory were recorded.Multi-factor regression analysis was used to analysis the influence factors of coronary collateral.Results The proportion of coronary collaterals (41.2％ (42/102)) in the regular exercise group was higher than that in the irregular exercise group (24.1％ (33/137)),and the difference was statistically significant(x2 =7.929,P =0.005).Lg(Gensini score) was (1.89 ± 0.18) the and (1.94 ± 0.19) in the regular exercise group,The left ventricular ejection fraction was 57.0％ (52.0％,60.0％) in the regular exercise group and 50.0％ (45.0％,57.0％) in the irregular exercise group,and the difference was statistically significant (Z =-5.152,P =0.000).Multi-factor regression analysis showed that regular exercise (OR =3.423,95％ CI:1.790-4.578),diabetes mellitus (OR =0.451,95％ CI:0.212-0.962),B-type natriuretic peptide (OR =2.412,95 ％ CI:1.271-4.578),non-ST-segment elevation ACS (OR =2.383,95％ CI:1.185-4.791),chest pain history (OR =2.207,95％ CI:1.175-4.145),Gensini score (OR =1.538,95％ CI:1.141-2.073) were independent influence factors of coronary collateral(P ＜ 0.05).After adjusting other factors,the patients with regular exercise had better coronary collaterals than that with irregular exercise (OR=3.423,95％CI:1.790-6.548,P ＜0.001).Conclusion The regular exercise can promote coronary collateral emergence for the patients with ACS.

Objective To explore the effect of resveratrol on the expression of matrix metalloproteinases-9 (MMP-9) in soluble CD40 ligand (sCD40L)-activated macrophages. Methods Human monocytic cell line THP-1 cells under an inducing of phorbol ester differentiated into macrophages. Then the macrophages were sitimulated by sCD40L independently and after a preincubation with resveratrol. The mRNA expression of MMP-9 and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in macrophages were investigated by semiquantitative RT-PCR. The secretions of MMP-9 and TIMP-1 protein were measured by Western blot. The MMP-9 activity was analyzed by gelatin zymography technique. Results The expressions of MMP-9 gene(1.53±0.04 vs. 0.75±0.01,P＜0.05) and protein(244 930.8±31 268.6 vs. 192 976.8±20 223.1,P＜0.05)were higher in macrophages when stimulated by sCD40L. Resveratrol (10 μmol/L and 50 μmol/L)can inhibit the CD40L-induced gene expression and the protein secretion of MMP-9 (P＜0.01). The activity of MMP-9 was degraded by resveratrol (P＜0.05). Meanwhile resveratrol could increase the gene expression and protein secretion of TIMP-1 (P＜0.05). Conclusions Resveratrol can inhibit the CD40L-activated macrophage expression of MMP-9. It may be one of its mechanisms on antiatherosclerosis and stabilization of atheromatous plaques.

Background Resveratrol has been unanimously recognized as an cardiovascular protective substance in red wine. It has been speculated that the anti-atherosclerosis effect of resveratrol is ascribed to its powerful anti-inflammatory effect. Objective To investigate the effects of resveratrol on injured human umbilical veno-endothelial cells (HUVEC) and the reactive oxygen species(ROS) production induced by TNF-? or soluble CD40L (sCD40L). Methods Cultured HUVEC were pre-incubated with resveratrol(1-50 ?mol/L) for 2 hours and then treated with TNF-?(10 ?g/L) or sCD40L?(10 ?g/L) for another 4 hours. MTT assay was used to detect proliterative activity of HUVEC. Immunofluorescence microscopy was used for determination of ROS expression. Results Both TNF-? and sCD40L impaired HUVEC proliferation (-32.7% and -26% vs control,P

ObjectiveTo investigate the effect of resveratrol on the expressions of E-selectin and monocyte chemoattractant protein-1 (MCP-1) in activated endothelial cells.Methods After being pretreated with resveratrol followed by tumor necrosis factor-α (TNF-α) stimulation, human umbilical vein endothelial cells (HUVEC) were randomly divided into three groups: TNF group,resveratrol+TNF-α group and control group. The expression of E-selectin molecule on the surface of HUVEC was detected by flow cytometric analysis and the mRNA expressions of E-selectin and MCP -1 were determined by semiquantitative RT-PCR. ResultsTNF-α induced the expression of E-selectin and MCP-I of HUVEC.Resveratrol (10 μmol/L) inhibited E-selectin expression.The positive cells of E-selectin in TNF group, resveratrol + TNF-α group and control group were(47.84±3.2)%, (15.3±1.7)% and (3.74±1.6)%, respectively, and the differences among the three groups were statistically significant (P<0.05). Conclusions Resveratrol may contribute to the anti-atherosclerotic effect by inhibiting the expression of E-seleetin and MCP-1 of HUVEC.

OBJECTIVE： To systematically review the efficacy and safety of colesevelam hydrochloride combined with other hypoglycemic drugs in the treatment of T2DM， and to provide evidence-based reference for clinical treatment of T2DM. METHODS： Retrieved from PubMed， Embase， Medline， Cochrane Library， CJFD， VIP and Wanfang database during database establishement-Jul. 2019， randomized controlled trials （RCT） about the efficacy and safety of colesevelam hydrochloride combined with other hypoglycemic drugs （trial group） vs. placebo or other hypoglycemic drugs （control group） in the treatment of T2DM were collected. After extracting data from clinical studies that met the inclusion criteria， the quality of the studies was evaluated by Cochrane System Evaluator Manual 5.1.0. Meta-analysis was conducted by using Rev Man 5.3 statistical software in respects of the levels HbA1c， FPG， LDL-C， the incidence of total ADR， incidence of hypoglycemia and incidence of gastrointestinal ADR. RESULTS： A total of 11 RCTs were included， involving 2 625 patients. Results of Meta-analysis showed that HbA1c levels [MD＝－0.37， 95％CI（－0.51， －0.22），P＜0.001]， FPG level [MD＝－0.47， 95％CI（－0.88， －0.07）， P＝0.02] and LDL-C level [MD＝－0.38， 95％CI（－0.49， －0.28）， P＜0.001] in trial group were significantly lower than control group， with statistical significance. In terms of safety， the incidence of total ADR [OR＝1.24， 95％CI（1.06， 1.45）， P＝0.007] and gastrointestinal ADR [OR＝1.78，95％CI（1.05， 3.02），P＝0.03] in trial group were significantly higher than control group， with statistical significance. There was no significant difference in the incidence of hypoglycemia [OR＝1.03， 95％CI（0.62，1.72），P＝0.90]. CONCLUSIONS： Colesevelam hydrochloride combined with other hypoglycemic drugs can effectively reduce the levels of HbA1c， FPG and LDL-C in T2DM patients， but attention should be paid to the occurrence of gastrointestinal ADR.

Objective:To explore the interventional effect of β-sitosterol on ovalbumin(OVA)-induced allergic asthma rats and its potential mechanism.Methods:SD male rats were randomly divided into normal group(CON),model group(M),positive drug dexamethasone group(DEX,0.075 mg/kg)and β-sitosterol group(Sit,50 mg/kg).A rat model of allergic asthma was estab-lished by intraperitoneal injection of OVA with aluminum hydrogen solution,and nebulized inhalation of OVA to stimulate.Rats were given intragastric administration 30 min before aerosol challenge,and after continuous administration for 7 days,the indicators of cough and asthma and tracheal phenol red excretion were detected.HE staining was used to observe pathological changes of lung tis-sue.Flow cytometry was used to detect reactive oxygen species(ROS)generation,apoptosis level and ratios of Th17 and Treg cells in peripheral blood.Biochemical method was used to detect contents of MDA,and activities of T-SOD and GSH-Px in rat lung tissues.ELISA was used to detect levels of Th17 and Treg-related cytokines(TNF-α,IL-4,IL-6,IL-17A,and IL-35).Results:Compared with model group,β-sitosterol significantly prolonged the incubation period of cough and gasp in rats with allergic asthma,reduced the frequency of cough and gasping,and promoted the excretion of phenol red in trachea;significantly reduced inflammatory infiltration in lung tissue of asthmatic rats;observably reduced MDA content in lung tissue,ROS of primary lung cell and apoptosis levels of asthmatic rats,increased the activities of T-SOD and GSH-Px;markedly reduced proportion of Th17 cells and levels of pro-inflammatory cyto-kines TNF-α,IL-4,IL-6 and IL-17A,increased proportion of Treg cells and levels of anti-inflammatory cytokine IL-35.Conclusion:β-sitosterol can ameliorate airway inflammation and oxidative damage in OVA-induced allergic asthmatic rats,and its mecha-nism may be related to the regulation of β-sitosterol on Th17/Treg immune imbalance and oxidative stress response.

Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

ObjectiveTo explore the mechanism of Xianglian Huazhuo prescription in the treatment of chronic atrophic gastritis （CAG） based on network pharmacology and animal experiments，so as to provide scientific basis for clinical application. MethodThe possible targets and pathways of Xianglian Huazhuo prescription in the treatment of CAG were obtained based on the prediction of network pharmacology. The CAG rat model was induced by sodium salicylate，N-methyl-N'-nitro-N-nitrosoguanidine （MNNG） and hunger and satiety disorder. Then the CAG rats were treated with Xianglian Huazhuo prescription and morodan for 60 days. After administration，the rats were sacrificed，and the content of interleukin-6 （IL-6），tumor necrosis factor-α （TNF-α），interleukin-1β （IL-1β） and vascular endothelial growth factor （VEGF） in serum was determined by enzyme linked immunosorbent assay（ELISA）. In addition， the protein expression of Bad and Bcl-2 in gastric mucosa was detected by immunohistochemistry （IHC）. ResultA total of 241 active components of Xianglian Huazhuo prescription and 53 core targets were obtained. Xianglian Huazhuo prescription affected multiple biological processes，such as cell proliferation and apoptosis，inflammatory reaction，regulation of DNA metabolism，and cell response to redox，as well as phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt），TNF，mitogen-activated protein kinase （MAPK），cancer and cancer-related signaling pathways. The animal model verification showed that Xianglian Huazhuo prescription lowered the levels of IL-6，TNF-α，IL-1β and VEGF in serum of CAG rats，and reduced the protein expression of Bad and Bcl-2 in gastric tissue. ConclusionXianglian Huazhuo prescription could regulate PI3K/Akt signal pathway and improve gastric mucosal injury in CAG by participating in biological processes such as cell proliferation，apoptosis and inflammation.

Objective:To analyze the clinical characteristics and prognosis of patients with infant acute lymphoblastic leukemia (IALL).Methods:A retrospective cohort study.Clinical data, treatment and prognosis of 28 cases of IALL who have been treated at Beijing Children′s Hospital, Capital Medical University and Baoding Children′s Hospital from October 2013 to May 2023 were analyzed retrospectively. Based on the results of fluorescence in situ hybridization (FISH), all patients were divided into KMT2A gene rearrangement (KMT2A-R) positive group and KMT2A-R negative group. The prognosis of two groups were compared. Kaplan-Meier method and Log-Rank test were used to analyze the survival of the patients.Results:Among 28 cases of IALL, there were 10 males and 18 females, with the onset age of 10.9 (9.4,11.8) months. In terms of immune classification, 25 cases were B-ALL (89%), while the remaining 3 cases were T-ALL (11%). Most infant B-ALL showed pro-B lymphocyte phenotype (16/25,64%). A total of 22 cases (79%) obtained chromosome karyotype results, of which 7 were normal karyotypes, no complex karyotypes and 15 were abnormal karyotypes were found. Among abnormal karyotypes, there were 4 cases of t (9; 11), 2 cases of t (4; 11), 2 cases of t (11; 19), 1 case of t (1; 11) and 6 cases of other abnormal karyotypes. A total of 19 cases (68%) were positive for KMT2A-R detected by FISH. The KMT2A fusion gene was detected by real-time PCR in 16 cases (57%). A total of 24 patients completed standardized induction chemotherapy and were able to undergo efficacy evaluation, 23 cases (96%) achieved complete remission through induction chemotherapy, 4 cases (17%) died of relapse. The 5-year event free survival rate (EFS) was (46±13)%, and the 5-year overall survival rate (OS) was (73±10)%.The survival time was 31.3 (3.3, 62.5) months. There was no significant statistical difference in 5-year EFS ((46±14)% vs. (61±18)%) and 5-year OS ((64±13)% vs. (86±13)%) between the KMT2A-R positive group (15 cases) and the KMT2A-R negative group (9 cases) ( χ2=1.88, 1.47, P=0.170, 0.224). Conclusions:Most IALL patients were accompanied by KMT2A-R. They had poor tolerance to traditional chemotherapy, the relapse rate during treatment was high and the prognosis was poor.