Objective:To explore the impact of changes of myocardial infarct size on left ventricular adverse remodeling in patients with acute ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI).Methods:This was a prospective cohort study. The STEMI patients who underwent primary PCI in the First Medical Center of the Chinese People′s Liberation Army General Hospital, Beijing Anzhen Hospital, Hainan Hospital of the Chinese People′s Liberation Army General Hospital and Guangxi Yulin First People Hospital from January 1, 2017 to January 1, 2022 were enrolled. Cardiac magnetic resonance (CMR) was performed to dynamically assess the myocardial infarct size and calculate the rate of infarct size change between the acute phase (5 to 7 days post-primary PCI) and 6-month follow-up. The endpoint was left ventricular adverse remodeling which was defined as an increase of more than 20% in left ventricular end-diastolic volume (LVEDV) assessed by CMR at 6 months after primary PCI compared with LVEDV at 1 week after primary PCI. Based on serial CMR assessments, the patients were divided into left ventricular adverse remodeling group and non-remodeling group. The receiver operating characteristic (ROC) curve was used to evaluate the predictive performance of infarct size change for left ventricular adverse remodeling, and according to the optimal cutoff value, improved infarct size was defined as a decrease of >20% in the infarct size measured by CMR at 6 months after primary PCI compared with infarct size at 1 week after primary PCI. Multivariate logistic regression analysis was performed to identify the protective factors and risk factors for left ventricular adverse remodeling.Results:A total of 267 patients were enrolled, aged (58±11) years, with 234 males (87.6%). And 73 cases in the left ventricular remodeling group and 194 cases in the non-remodeling group. Infarct size assessed by CMR at 6 months after primary PCI decreased significantly compared with infarct size at 1 week after primary PCI in the left ventricular remodeling group ((23±13)% vs. (27±12)%, P=0.004), the same as in the non-remodeling group ((18±10)% vs. (23±10)%, P<0.001). The area under the ROC curve for the rate of infarct size change in predicting left ventricular remodeling was 0.735 (95% CI 0.670-0.799, P<0.001), a 20% reduction was the optimal cut-off value. Compared to the patients with non-improved infarct size, the incidence of left ventricular adverse remodeling was significantly lower in the patients with improved infarct size (18% (24/133) vs. 37% (49/134), P=0.001). Multivariate logistic regression analysis showed that improvement in IS was a protective factor for left ventricular adverse remodeling ( OR=0.376, 95% CI 0.236-0.721, P=0.002). Conclusion:Patients with STEMI who experience obvious reduction in infarct size after primary PCI have a significantly reduced risk of left ventricular adverse remodeling.

Endothelial dysfunction is a pivotal contributor to atherosclerosis(As)pathogenesis.A comprehensive understanding of the mechanisms of endothelial dysfunction would provide novel insights into effective treatment of As.Recent advances in genome and transcripome technology have enabled researchers to further explore the molecular mecha-nisms of endothelial dysfunction.It has been found that the regulatory network of competitive endogenous RNA(ceRNA)mediated by long non-coding RNA(lncRNA)plays a key role in endothelial dysfunction.lncRNA acts as a"molecular sponge"for microRNA(miRNA)to block the post-transcriptional repression of miRNA on downstream target gene messen-ger RNA(mRNA)by binding to miRNA,thereby regulating the function and phenotypic conversion of endothelial cell(EC)lncRNA-miRNA-mRNA interactions are widely involved in play an essential role EC inflammatory responses,apopto-sis,autophagy,angiogenesis,and endothelial-mesenchymal transition(EndMT).Which suggests that it may be a poten-tial therapeutic targets for As.

Endothelial dysfunction is a pivotal contributor to atherosclerosis(As)pathogenesis.A comprehensive understanding of the mechanisms of endothelial dysfunction would provide novel insights into effective treatment of As.Recent advances in genome and transcripome technology have enabled researchers to further explore the molecular mecha-nisms of endothelial dysfunction.It has been found that the regulatory network of competitive endogenous RNA(ceRNA)mediated by long non-coding RNA(lncRNA)plays a key role in endothelial dysfunction.lncRNA acts as a"molecular sponge"for microRNA(miRNA)to block the post-transcriptional repression of miRNA on downstream target gene messen-ger RNA(mRNA)by binding to miRNA,thereby regulating the function and phenotypic conversion of endothelial cell(EC)lncRNA-miRNA-mRNA interactions are widely involved in play an essential role EC inflammatory responses,apopto-sis,autophagy,angiogenesis,and endothelial-mesenchymal transition(EndMT).Which suggests that it may be a poten-tial therapeutic targets for As.

The theory of blood stasis originated from"The Yellow Emperor's Inner Canon(huang Di Nei Jing)",and the drugs used for promoting blood stasis originated from"Shennong's Classic of Materia Medica(Shen Nong Ben Cao Jing)".Finally,the medical sage Zhang Zhong-jing first put forward the name of"blood stasis"in"Synopsis of the Golden Chamber(Jin Gui Yao Lue)",and used the method of promoting blood stasis to treat various diseases,which provided ideas for the future study on the mechanism and treatment of blood stasis syndrome.Therefore,Zhang Zhong-jing was the founder of the theory of blood stasis.Moreover,the principles,methods,prescriptions and medicines which he put forward were still appropriate effectively in the clinic.On the basis of comprehensively combing the research achievements of Zhongjing's blood stasis theory,with combination with the current research hotspots,the review gives a novel understanding of the theory,method,prescription and medicine of Zhongjing's blood stasis theory from new aspects,including etiology,pathogenesis,treatment of blood stasis theory,and the active ingredients of anti-blood stasis Chinese medicines.We intend to promote the research progress of the scientific connotation of blood stasis theory,and improve the diagnosis and treatment level of clinicians in preventing and treating difficult diseases related to blood stasis syndrome through integrated summary and novel interpretation.

Objective:To explore the diagnostic value of the combined detection of v-Kirsten Ras viral oncogene homolog(KRAS),transmembrane protein 243(TMEM243),cell division cycle protein 42(CDC42)and RAS like family 11 member B(RASL11B)for different types of Hashimoto's thyroiditis(HT).Methods:From January 2023 to December 2024,a total of 185 HT patients who received detection in Hebei Yanda Hospital were selected by using a random number table method,and they were divided into three groups according to HT type,which included the euthyroid HT group(65 cases),the hypothyroid HT group(60 cases)and the hyperthyroidism HT group(60 cases).Another 65 healthy individuals who underwent physical examination during the same period were selected as the healthy control group.An analyzer of enzyme-linked immunosorbent assay(ELISA)was used to measure and analyze the levels of KRAS,TMEM243,CDC42 and RASL11B in the four groups.Differences in autoantibody levels among different HT patients were compared.Logistic regression analysis was conducted to assess influence factors for HT.A nomogram model was constructed to realize visual presentation on the basis of the influence factors.Receiver operating characteristic(ROC)curves were adopted to assess the diagnostic efficacy of antibodies for subjects in the four groups.Results:The KRAS,TMEM243,CDC42 and RASL11B levels in the three HT groups were significantly higher than those in the healthy control group(F=906.962,840.078,830.290,846.182,P<0.05),respectively.Multivariate logistic regression analysis showed that KRAS,TMEM243,CDC42 and RASL11B were risk factors for HT(OR=4.071,1.424,1.026,1.031,P<0.05).The area under curve(AUC)of the ROC curve of the combined detection of four indicators of autoantibodies was 0.975,which sensitivity and specificity were respectively 94.05%and 92.31%.Conclusion:There were overexpression of KRAS,TMEM243,CDC42 and RASL11B in HT patients,especially,the overexpression of hyperthyroidism HT patients is more significant.The combined detection of the four indicators of autoantibody has favorable performance and clinical reference value in diagnosing HT.

The theory of blood stasis originated from"The Yellow Emperor's Inner Canon(huang Di Nei Jing)",and the drugs used for promoting blood stasis originated from"Shennong's Classic of Materia Medica(Shen Nong Ben Cao Jing)".Finally,the medical sage Zhang Zhong-jing first put forward the name of"blood stasis"in"Synopsis of the Golden Chamber(Jin Gui Yao Lue)",and used the method of promoting blood stasis to treat various diseases,which provided ideas for the future study on the mechanism and treatment of blood stasis syndrome.Therefore,Zhang Zhong-jing was the founder of the theory of blood stasis.Moreover,the principles,methods,prescriptions and medicines which he put forward were still appropriate effectively in the clinic.On the basis of comprehensively combing the research achievements of Zhongjing's blood stasis theory,with combination with the current research hotspots,the review gives a novel understanding of the theory,method,prescription and medicine of Zhongjing's blood stasis theory from new aspects,including etiology,pathogenesis,treatment of blood stasis theory,and the active ingredients of anti-blood stasis Chinese medicines.We intend to promote the research progress of the scientific connotation of blood stasis theory,and improve the diagnosis and treatment level of clinicians in preventing and treating difficult diseases related to blood stasis syndrome through integrated summary and novel interpretation.

Objective:To explore the diagnostic value of the combined detection of v-Kirsten Ras viral oncogene homolog(KRAS),transmembrane protein 243(TMEM243),cell division cycle protein 42(CDC42)and RAS like family 11 member B(RASL11B)for different types of Hashimoto's thyroiditis(HT).Methods:From January 2023 to December 2024,a total of 185 HT patients who received detection in Hebei Yanda Hospital were selected by using a random number table method,and they were divided into three groups according to HT type,which included the euthyroid HT group(65 cases),the hypothyroid HT group(60 cases)and the hyperthyroidism HT group(60 cases).Another 65 healthy individuals who underwent physical examination during the same period were selected as the healthy control group.An analyzer of enzyme-linked immunosorbent assay(ELISA)was used to measure and analyze the levels of KRAS,TMEM243,CDC42 and RASL11B in the four groups.Differences in autoantibody levels among different HT patients were compared.Logistic regression analysis was conducted to assess influence factors for HT.A nomogram model was constructed to realize visual presentation on the basis of the influence factors.Receiver operating characteristic(ROC)curves were adopted to assess the diagnostic efficacy of antibodies for subjects in the four groups.Results:The KRAS,TMEM243,CDC42 and RASL11B levels in the three HT groups were significantly higher than those in the healthy control group(F=906.962,840.078,830.290,846.182,P<0.05),respectively.Multivariate logistic regression analysis showed that KRAS,TMEM243,CDC42 and RASL11B were risk factors for HT(OR=4.071,1.424,1.026,1.031,P<0.05).The area under curve(AUC)of the ROC curve of the combined detection of four indicators of autoantibodies was 0.975,which sensitivity and specificity were respectively 94.05%and 92.31%.Conclusion:There were overexpression of KRAS,TMEM243,CDC42 and RASL11B in HT patients,especially,the overexpression of hyperthyroidism HT patients is more significant.The combined detection of the four indicators of autoantibody has favorable performance and clinical reference value in diagnosing HT.

Objective:To explore the impact of changes of myocardial infarct size on left ventricular adverse remodeling in patients with acute ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI).Methods:This was a prospective cohort study. The STEMI patients who underwent primary PCI in the First Medical Center of the Chinese People′s Liberation Army General Hospital, Beijing Anzhen Hospital, Hainan Hospital of the Chinese People′s Liberation Army General Hospital and Guangxi Yulin First People Hospital from January 1, 2017 to January 1, 2022 were enrolled. Cardiac magnetic resonance (CMR) was performed to dynamically assess the myocardial infarct size and calculate the rate of infarct size change between the acute phase (5 to 7 days post-primary PCI) and 6-month follow-up. The endpoint was left ventricular adverse remodeling which was defined as an increase of more than 20% in left ventricular end-diastolic volume (LVEDV) assessed by CMR at 6 months after primary PCI compared with LVEDV at 1 week after primary PCI. Based on serial CMR assessments, the patients were divided into left ventricular adverse remodeling group and non-remodeling group. The receiver operating characteristic (ROC) curve was used to evaluate the predictive performance of infarct size change for left ventricular adverse remodeling, and according to the optimal cutoff value, improved infarct size was defined as a decrease of >20% in the infarct size measured by CMR at 6 months after primary PCI compared with infarct size at 1 week after primary PCI. Multivariate logistic regression analysis was performed to identify the protective factors and risk factors for left ventricular adverse remodeling.Results:A total of 267 patients were enrolled, aged (58±11) years, with 234 males (87.6%). And 73 cases in the left ventricular remodeling group and 194 cases in the non-remodeling group. Infarct size assessed by CMR at 6 months after primary PCI decreased significantly compared with infarct size at 1 week after primary PCI in the left ventricular remodeling group ((23±13)% vs. (27±12)%, P=0.004), the same as in the non-remodeling group ((18±10)% vs. (23±10)%, P<0.001). The area under the ROC curve for the rate of infarct size change in predicting left ventricular remodeling was 0.735 (95% CI 0.670-0.799, P<0.001), a 20% reduction was the optimal cut-off value. Compared to the patients with non-improved infarct size, the incidence of left ventricular adverse remodeling was significantly lower in the patients with improved infarct size (18% (24/133) vs. 37% (49/134), P=0.001). Multivariate logistic regression analysis showed that improvement in IS was a protective factor for left ventricular adverse remodeling ( OR=0.376, 95% CI 0.236-0.721, P=0.002). Conclusion:Patients with STEMI who experience obvious reduction in infarct size after primary PCI have a significantly reduced risk of left ventricular adverse remodeling.

Objective:To dynamically monitor the prevalence and trend of dental fluorosis in children in Shandong Province, and to evaluate the prevention and control measures for drinking water-borne endemic fluorosis (referred to as drinking water-borne fluorosis), and to provide scientific basis for the next step.Methods:Totally 40 counties (cities, districts) were selected as project counties (cities, districts) from drinking water-borne fluorosis areas in Shandong Province in 2018, and all counties (cities, districts) were selected in 2019 and 2020, to investigate the situation of water improvement, detect water fluoride content, and investigate the prevalence of dental fluorosis in children aged 8 - 12 years.Results:From 2018 to 2020, the detection rates of dental fluorosis in children aged 8 - 12 years were 10.30% (503/4 884), 8.94% (25 895/289 539) and 8.66% (24 061/277 689), respectively, with statistically significant differences (χ 2 = 27.10, P < 0.001), and the dental fluorosis indexes were 0.21, 0.18 and 0.17, respectively. The total detection rates of dental fluorosis in children of different age groups in the 3 years were 7.26% (6 590/90 775), 7.97% (9 303/116 680), 9.29% (12 167/130 915), 9.29% (12 238/131 670) and 9.95% (10 161/102 072), the differences were statistically significant (χ 2 = 615.71, P < 0.001). In the 3 years, the total detection rate of dental fluorosis was 8.93% (28 101/314 737) in boys and 8.69% (22 358/257 375) in girls, the difference was statistically significant (χ 2 = 10.27, P = 0.001). In 2018 and 2019, the detection rates of dental fluorosis of children aged 8 - 12 years in water fluoride qualified villages [5.74% (235/4 095) and 7.98% (20 200/253 082)] were significantly lower than those in villages with excessive water fluoride [33.97% (268/789) and 15.62% (5 695/36 457), χ 2 = 570.61, 2 283.76, P < 0.001]. Conclusions:The prevalence of dental fluorosis among children aged 8 - 12 years has been effectively controlled, and remarkable results have been achieved in prevention and treatment of drinking water-borne fluorosis in Shandong Province. However, the detection rate of dental fluorosis among children in a few endemic villages is high, so it is necessary to continue to strengthen the monitoring of fluoride content in drinking water and the condition of dental fluorosis among children.

With continually improving reperfusion strategies and patient care, the overall mortality of acute myocardial infarction (AMI) has been significantly reduced during the past two decades. However, this success is a double-edged sword, as many patients surviving an AMI will progress towards ischemic heart failure (HF) over time. The pathologic causes of ischemic HF are undoubtedly multifactorial. However, the inflammatory response is considered one of the most important causes of pathological remodeling because it spans the whole process of HF development. The macrophage-mediated inflammatory response was once considered a purely harmful factor leading to pathological remodeling and HF. However, growing evidence demonstrates that multiple subgroups of macrophage exist and contribute differently to ischemic HF development. Understanding macrophage populations and how they contribute to post-MI remodeling and consequent ischemic HF is, therefore, critical to understanding and treating the disease. This review focuses on different macrophage populations that regulate post-MI cardiac injury and how immunoregulation therapy may benefit patients with ischemic HF.