BACKGROUND:The relationship between rheumatoid arthritis and coronary atherosclerosis has received extensive attention.Inflammation is related to rheumatoid arthritis and coronary atherosclerosis,indicating that there may be a common pathophysiological pathway between the two diseases.However,observational studies have not yet clarified the causal relationship.OBJECTIVE:To explore whether there is a causal relationship between rheumatoid arthritis and coronary atherosclerosis,as well as the potential causal relationship with 1 400 serum metabolites and 91 inflammatory factors through a Mendelian randomization analysis.METHODS:Coronary atherosclerosis data are from Finngen database,rheumatoid arthritis data are from IEU OpenGWAS database,serum metabolites data are from Canadian Longitudinal Study on Aging,Augsburg Cooperative Health Research and British Twin Project Research,and data of 91 inflammatory proteins are from research published in Nature Immunology in 2023.Mendelian randomization analysis was performed using data from genome-wide association studies,and causal effects were evaluated using inverse variance weighting,MR-Egger regression,weighted median,weighted model,and simple model methods,with inverse variance weighting being the primary analysis method.To enhance robustness,Cochran's Q-test MR-Egger intercept was used for sensitivity analysis.RESULTS AND CONCLUSION:(1)Inverse variance weighting results showed that rheumatoid arthritis was positively correlated with the increased relative risk of coronary atherosclerosis(odds ratio=1.002,95％confidence interval=1.001-1.003,P=0.003).There was no reverse causal relationship between coronary atherosclerosis and rheumatoid arthritis.In addition,96 serum metabolites and 9 inflammatory factors were found to have causal relationships with coronary atherosclerosis.There was a causal relationship between 51 serum metabolites and 7 inflammatory factors and rheumatoid arthritis.(2)This study provided epidemiological evidence between rheumatoid arthritis and coronary atherosclerosis,and emphasized the potential role of serum metabolites and inflammatory factors in the pathogenesis of these diseases.These findings may contribute to the development of new treatment strategies.Due to the limited inclusion of data from Asian populations,most contemporary studies used international databases and European population analyses.By collecting and analyzing the health data of European populations,it is conducive to a better understanding of the effects and potential role of Chinese medicine in Europe,and to further promote the practice of modern integration of Western and Chinese medicine.Meanwhile,through the comparative study with the European databases,it is possible to reveal the genetic differences and susceptibility to diseases among different populations,providing more dimensions and perspectives for global health research.

BACKGROUND:Studies at home and abroad have shown that sarcopenia is closely related to metabolites.At present,the relationship between the latest 1400 blood metabolites and sarcopenia is still unknown.OBJECTIVE:To analyze the causal relationship between 1 400 metabolites and sarcopenia and its relevance with cardiovascular disease using Mendelian randomization.METHODS:Genome-wide association study(GWAS)data of sarcopenia-related characteristics(grip strength,limb muscle lean body mass,and walking speed)were obtained from the OPEN GWAS website as outcome data.A GWAS containing 1 400 metabolites was used as an exposure factor,and single nucleotide polymorphisms significantly associated with exposure factors were selected as instrumental variables.The causal association between 1 400 metabolites and sarcopenia was analyzed by"TwoSampleMR"and"gwasglue"packages of R software(V4.3.2).The research methods included inverse variance weighting,MR-Eggeer regression intercept,weighted median method,and simple mode.Heterogeneity,pleiotropic,sensitivity and other verification analysis were performed.Finally,reverse Mendelian randomization analysis was performed.RESULTS AND CONCLUSION:(1)The causal relationship between 1 400 serum metabolites and sarcopenia was analyzed by inverse variance weighting.The results showed that 1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate were protective factors,and the risk of disease decreased with the increase of metabolites(P＜0.01).(2)Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate were risk factors.With the increase of two unknown metabolites(X-12822 and X-15486),the degree of low grip strength of male hands increased.Similarly,with the increase of trans-3,4-methylene heptanoate,the risk of disease also increased(P＜0.01).(3)To conclude,1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate have inhibitory effects on sarcopenia.Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate can promote sarcopenia.This may be a new idea and new basis for sarcopenia research and treatment in the future.This study will also provide a reference for the study of the role of related metabolites in the Chinese population.

Objective To explore the impact of Qiangxin Tang on myocardial fibrosis in rats with chronic heart failure by mediating myocardial mitochondrial autophagy through the Bcl-2/adenovirus E1B 19kDa interacting protein 3/NIP3 like protein X and FUN14domain-containing protein 1.Methods Forty Sprague Dawley rats were divided into five groups randomly by the random number table:sham operation group,model group,Qiangxin Tang group,Captopril group,and Qiangxin Tang+Captopril group,with a total of eight rats in each group.Only the sham operation group threaded without ligating the left coronary artery of the heart.In all the other groups,CHF rat models were established after myocardial infarction by ligating the left coronary artery of the heart.From the day after successful modeling,each group was given corresponding drugs by gavage,and the left ventricular myocardial tissue of each group was de-tected.Western blot was used to detect the expression of NIX,BNIP3,and FUNDC1 proteins in each group.ELISA was used to detect brain natriuretic peptide and cardiac troponin T level.Mitochondrial morphology was observed under transmission electron microscopy.Masson staining was used to observe left ventricular myocardial fibrosis.Results Compared with the sham surgery group,the expression of NIX,BNIP3 and FUNDC1 proteins in the model group was significantly reduced,while the levels of BNP and cTnT were significantly increased(P＜0.05).The left ventricular myocardial tissue showed significant fibrosisand mitochondrial swelling.Compared with the model group,the expression of NIX,BNIP3,and FUNDC1 proteins was significantly increased in Qiangxin Tang group and Captopril group,while the levels of BNP and cTnT were significantly decreased(P＜0.05).The left ventricular myocardial tissue fibrosis was sig-nificantly reduced,and the mitochondrial morphology was mildly altered.Compared with Qiangxin Tang group and Captopril group,the Qiangxin Tang+Captopril group showed significant improvement in the above indicators,and there was no significant difference in the in-dicators between Qiangxin Tang group and Captopril group.Conclusion Qiangxin Tang may promote mitochondrial autophagy and ensure the morphology and function of mitochondrial by upregulating the expression of NIX,BNIP3 and FUNDC1,thereby reducing myocardial injury and fibrosis.In addition,the combination of Qiangxin Tang and Captopril has a better therapeutic effect on CHF.

BACKGROUND:Studies at home and abroad have shown that sarcopenia is closely related to metabolites.At present,the relationship between the latest 1400 blood metabolites and sarcopenia is still unknown.OBJECTIVE:To analyze the causal relationship between 1 400 metabolites and sarcopenia and its relevance with cardiovascular disease using Mendelian randomization.METHODS:Genome-wide association study(GWAS)data of sarcopenia-related characteristics(grip strength,limb muscle lean body mass,and walking speed)were obtained from the OPEN GWAS website as outcome data.A GWAS containing 1 400 metabolites was used as an exposure factor,and single nucleotide polymorphisms significantly associated with exposure factors were selected as instrumental variables.The causal association between 1 400 metabolites and sarcopenia was analyzed by"TwoSampleMR"and"gwasglue"packages of R software(V4.3.2).The research methods included inverse variance weighting,MR-Eggeer regression intercept,weighted median method,and simple mode.Heterogeneity,pleiotropic,sensitivity and other verification analysis were performed.Finally,reverse Mendelian randomization analysis was performed.RESULTS AND CONCLUSION:(1)The causal relationship between 1 400 serum metabolites and sarcopenia was analyzed by inverse variance weighting.The results showed that 1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate were protective factors,and the risk of disease decreased with the increase of metabolites(P＜0.01).(2)Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate were risk factors.With the increase of two unknown metabolites(X-12822 and X-15486),the degree of low grip strength of male hands increased.Similarly,with the increase of trans-3,4-methylene heptanoate,the risk of disease also increased(P＜0.01).(3)To conclude,1-linoleoyl-2-linoleoyl-GPC(18:2/18:3)and glycodeoxycholate 3-sulfate have inhibitory effects on sarcopenia.Two unknown metabolites(X-12822 and X-15486)and trans-3,4-methyleneheptanoate can promote sarcopenia.This may be a new idea and new basis for sarcopenia research and treatment in the future.This study will also provide a reference for the study of the role of related metabolites in the Chinese population.

Objective To explore the impact of Qiangxin Tang on myocardial fibrosis in rats with chronic heart failure by mediating myocardial mitochondrial autophagy through the Bcl-2/adenovirus E1B 19kDa interacting protein 3/NIP3 like protein X and FUN14domain-containing protein 1.Methods Forty Sprague Dawley rats were divided into five groups randomly by the random number table:sham operation group,model group,Qiangxin Tang group,Captopril group,and Qiangxin Tang+Captopril group,with a total of eight rats in each group.Only the sham operation group threaded without ligating the left coronary artery of the heart.In all the other groups,CHF rat models were established after myocardial infarction by ligating the left coronary artery of the heart.From the day after successful modeling,each group was given corresponding drugs by gavage,and the left ventricular myocardial tissue of each group was de-tected.Western blot was used to detect the expression of NIX,BNIP3,and FUNDC1 proteins in each group.ELISA was used to detect brain natriuretic peptide and cardiac troponin T level.Mitochondrial morphology was observed under transmission electron microscopy.Masson staining was used to observe left ventricular myocardial fibrosis.Results Compared with the sham surgery group,the expression of NIX,BNIP3 and FUNDC1 proteins in the model group was significantly reduced,while the levels of BNP and cTnT were significantly increased(P＜0.05).The left ventricular myocardial tissue showed significant fibrosisand mitochondrial swelling.Compared with the model group,the expression of NIX,BNIP3,and FUNDC1 proteins was significantly increased in Qiangxin Tang group and Captopril group,while the levels of BNP and cTnT were significantly decreased(P＜0.05).The left ventricular myocardial tissue fibrosis was sig-nificantly reduced,and the mitochondrial morphology was mildly altered.Compared with Qiangxin Tang group and Captopril group,the Qiangxin Tang+Captopril group showed significant improvement in the above indicators,and there was no significant difference in the in-dicators between Qiangxin Tang group and Captopril group.Conclusion Qiangxin Tang may promote mitochondrial autophagy and ensure the morphology and function of mitochondrial by upregulating the expression of NIX,BNIP3 and FUNDC1,thereby reducing myocardial injury and fibrosis.In addition,the combination of Qiangxin Tang and Captopril has a better therapeutic effect on CHF.

BACKGROUND:The relationship between rheumatoid arthritis and coronary atherosclerosis has received extensive attention.Inflammation is related to rheumatoid arthritis and coronary atherosclerosis,indicating that there may be a common pathophysiological pathway between the two diseases.However,observational studies have not yet clarified the causal relationship.OBJECTIVE:To explore whether there is a causal relationship between rheumatoid arthritis and coronary atherosclerosis,as well as the potential causal relationship with 1 400 serum metabolites and 91 inflammatory factors through a Mendelian randomization analysis.METHODS:Coronary atherosclerosis data are from Finngen database,rheumatoid arthritis data are from IEU OpenGWAS database,serum metabolites data are from Canadian Longitudinal Study on Aging,Augsburg Cooperative Health Research and British Twin Project Research,and data of 91 inflammatory proteins are from research published in Nature Immunology in 2023.Mendelian randomization analysis was performed using data from genome-wide association studies,and causal effects were evaluated using inverse variance weighting,MR-Egger regression,weighted median,weighted model,and simple model methods,with inverse variance weighting being the primary analysis method.To enhance robustness,Cochran's Q-test MR-Egger intercept was used for sensitivity analysis.RESULTS AND CONCLUSION:(1)Inverse variance weighting results showed that rheumatoid arthritis was positively correlated with the increased relative risk of coronary atherosclerosis(odds ratio=1.002,95％confidence interval=1.001-1.003,P=0.003).There was no reverse causal relationship between coronary atherosclerosis and rheumatoid arthritis.In addition,96 serum metabolites and 9 inflammatory factors were found to have causal relationships with coronary atherosclerosis.There was a causal relationship between 51 serum metabolites and 7 inflammatory factors and rheumatoid arthritis.(2)This study provided epidemiological evidence between rheumatoid arthritis and coronary atherosclerosis,and emphasized the potential role of serum metabolites and inflammatory factors in the pathogenesis of these diseases.These findings may contribute to the development of new treatment strategies.Due to the limited inclusion of data from Asian populations,most contemporary studies used international databases and European population analyses.By collecting and analyzing the health data of European populations,it is conducive to a better understanding of the effects and potential role of Chinese medicine in Europe,and to further promote the practice of modern integration of Western and Chinese medicine.Meanwhile,through the comparative study with the European databases,it is possible to reveal the genetic differences and susceptibility to diseases among different populations,providing more dimensions and perspectives for global health research.

OBJECTIVE To investigate the effects and potential mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure(CHF).METHODS The CHF model was established by ligating the left anterior descending branch of the coronary artery.Modeled rats were divided into model group,Qiangxin decoction low-dose and high-dose groups(12.25,24.50 g/kg,calculated by crude drug),and chemical medicine group(Sacubitril valsartan sodium tablets,10.42 mg/kg),with 10 rats in each group;control group was set up without treatment.Each group of rats was orally administered with the corresponding medication or normal saline twice a day for 28 consecutive days.After the last medication,the contents of N-terminal pro-brain natriuretic peptide(NT-proBNP)and adenosine triphosphate(ATP)in serum and phosphatidic acid(PA)and cardiolipin(CL)in myocardial tissue were all detected;the pathological damage and collagen fibrosis of rat myocardial tissue were observed;the apoptosis of myocardial cells was determined;the ultrastructure of myocardial tissue was observed;the protein expressions of mitofusin 1(Mfn1),Mfn2,optic atrophy protein 1(OPA1)and dynamin-related protein 1(Drp1)were all detected in myocardial tissue.RESULTS Compared with control group,the serum content of NT-proBNP,apoptotic rate of myocardial cells,and relative expressions of S-OPA1 and Drp1 proteins were all increased significantly;serum content of ATP,contents of PA and CL,and relative expressions of Mfn1,Mfn2 and L-OPA1 proteins were all significantly reduced(P＜0.05).There were abnormal membrane tissue structure in various layers of myocardial tissue,degeneration and necrosis of myocardial cells,and severe fibrosis;the mitochondria were swollen,with reduced or absent cristae,and uneven matrix density.After intervention with Qiangxin decoction,the levels of the aforementioned quantitative indicators in serum and myocardial tissue of rats(excluding CL content in the Qiangxin decoction low-dose group)were significantly reversed(P＜0.05);the pathological damage of myocardial tissue had significantly improved,fibrosis had significantly reduced,mitochondrial morphology tended to be normal,cristae had increased,and matrix density was uniform.CONCLUSIONS Qiangxin decoction can regulate myocardial mitochondrial function and structural integrity of CHF rats,thereby improving myocardial energy metabolism and antagonizing myocardial fibrosis,the mechanism of which may be associated with activating PA/Mfn/CL signaling pathway.

OBJECTIVE To investigate the effects of Qiangxin decoction on myocardial mitochondrial and energy metabolism in rats with chronic heart failure （CHF） based on mitophagy. METHODS Male SD rats were collected to establish CHF model by ligating the left anterior descending branch of coronary artery. The successful modeling rats were divided into model group， Qiangxin decoction group [12.25 g/（kg·d）， calculated by crude drug]， captopril group [10.38 mg/（kg·d）]， and Qiangxin decoction+captopril group （the same usage and dosage as single drug group） according to a random number table method， with 8 rats in each group. Another 8 normal rats were selected and received threading in the left anterior descending branch of the coronary artery without ligation as the sham operation group. Starting from the second day after successful modeling， the rats in administration groups were given relevant drug intragastrically， twice a day， for consecutive 28 days. After the last medication， the levels of adenosine triphosphate （ATP）， adenosine monophosphate （AMP） and free fatty acid （FFA） in infarcted myocardial tissues were detected， the pathological changes and mitochondrial morphology of the infarcted myocardial tissue were observed， as well as the protein expressions of B cell lymphoma-2 （Bcl-2）， Bcl-2 related X protein （Bax）， TANK-binding kinase 1 （TBK1）， p62 were detected in each group. RESULTS Compared with the sham operation group， the infarcted myocardial tissue fibrosis was changed evidently， with a large number of mitochondrial swelling and fusion， and internal cristae rupture； the levels of AMP and FFA， the protein expressions of Bax and p62 were all increased or up-regulated significantly in infarcted myocardial tissue， while the level of ATP， and the protein expressions of Bcl-2 and TBK1 were all decreased or down-regulated significantly （P＜0.05）. Compared with the model group， the pathological changes of infarcted myocardial tissue and mitochondrial swelling had been improved； the levels of AMP and FFA， and the protein expressions of Bax and p62 in infarcted myocardial tissue were significantly decreased or down-regulated in administration groups， while the level of ATP， and the protein expressions of Bcl-2 and TBK1 were increased or up-regulated significantly （P＜0.05）. And the effect of Qiangxin decoction+captopril group was better than that of single drug group. CONCLUSIONS Qiangxin decoction can alleviate myocardial fibrosis and mitochondrial swelling in CHF rats， and improve their myocardial energy metabolism， which may be related to regulating the expression of Bcl-2， Bax， TBK1 and p62 proteins and promoting myocardial mitophagy.

Objective To investigate the feasibility of the optimally designed"I"shaped structure mag-net based on the principle of magnetic compression technique for the preparation of rectovaginal fistula animal model.Methods Using 10 New Zealand female rabbits as the model animals,two self-designed magnets were inserted through the vagina and anus respectively after anesthesia,and the two magnets were adjusted to the appropriate position and made them attraction each other to form a magnet-rectovaginal partition-magnet structure.When the compression tissue between the magnets became ischemic necrosis and fell off,the two magnets formed the"1"shape structure and were located in the stoma of rectovaginal fistula to prevent the stoma from becoming smaller or even closing itself.The operation time and rectovaginal fistula formation time were recorded.The experimental rabbits were killed in postoperative 2 weeks,and the rectovaginal fistula specimens were obtained.The formation of fistula orifice was observed and the size of fistula orifice was meas-ured.Results The animal model of rectovaginal fistula was successfully prepared in all 10 experimental rab-bits.The procedure of intraoperative magnet placement was smooth and the operation time was(1.55±0.65)min.The experimental animals were generally in good condition after surgery,and the fistula orifice was formed on postoperative(4.80±0.75)d.After taking the gross specimen of rectovaginal septum in postopera-tive 2 weeks,the magnet was removed.The fistula orifice of rectovaginal fistula was visible with the diameter of(5.86±0.38)mm.Conclusion The"I"shaped structure magnet designed based on the principle of mag-netic compression technique could be used in the preparation of the rectovaginal fistula animal model.Its oper-ation is simple with high success rate of model preparation and good uniformity in fistula orifice.

Objective To explore the key nursing cooperation points in single-port laparoscopic cholecystectomy based on magnetic anchor technique. Methods The general information of 24 patients with transumbilical single-port laparoscopic cholecystectomy based on magnetic anchor technique was analyzed. Combined with the surgical procedure, the key nursing cooperation points of this innovative surgery were analyzed from the perspective of operating room nurses. Results By learning the principles of magnetic anchor technique before surgery, understanding the usage and precautions of the magnetic anchor device, accurately passing the magnetic anchor device during surgery, and avoiding mutual interference between the magnetic anchor device and conventional surgical instruments, the operating room nurses successfully assisted the surgeons in completing 24 cases of transumbilical single-port laparoscopic cholecystectomy based on magnetic anchor technique. Conclusion Real-time understanding of the surgeon's operation progress during surgery, accurate delivery of instruments, and avoidance of interference between the magnetic anchor device and conventional surgical instruments are important factors in the nursing cooperation of this surgical procedure.