ObjectiveTo explore the mechanism of ventricular remodeling mediated by the p38 mitogen-activated protein kinase （MAPK）/nuclear factor kappa B （NF-κB） signaling pathway in the rat model of chronic heart failure （CHF） with heart-blood stasis syndrome， as well as the intervention effect of Danhong injection. MethodsIn vivo experiment： SPF-grade male SD rats were assigned via the random number table method into 4 groups： Sham operation， model， captopril （8.8 mg·kg^-1）， and Danhong injection （6.0 mL·kg^-1）. The model of CHF with heart-blood stasis syndrome was established by abdominal aortic constriction， and the sham operation group only underwent laparotomy without constriction. All the groups were treated continuously for 15 days. The tongue color of rats was observed. Echocardiography， hemorheology， heart mass index （HMI）， and left ventricular mass index （LVMI） were measured. Hematoxylin-eosin （HE） staining and Masson staining were performed to observe the pathological and fibrotic changes of the myocardial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to quantify the levels of N-terminal pro-B-type natriuretic peptide （NT-proBNP）， interleukin-6 （IL-6）， angiotensin Ⅱ （AngⅡ）， tumor necrosis factor-α （TNF-α）， and Creactive protein （CRP） in the serum， as well as the levels of matrix metalloproteinase-2 （MMP-2） and matrix metalloproteinase-9 （MMP-9） in the myocardial tissue. Western blot was used to quantify the protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 in the myocardial tissue. In vitro experiment： H9C2 cardiomyocytes were treated with 1×10^-6 mol·L^-1 AngⅡ to establish a model of myocardial hypertrophy. H9C2 cardiomyocytes were allocated into normal， model， inhibitor + Danhong injection， Danhong injection （20 mL·L^-1）， and inhibitor （SB203580， 5 μmol·L^-1） groups. CCK-8 assay was used to detect the viability of H9C2 cardiomyocytes. Rhodamine-labeled phalloidin staining was used to reveal the area of cardiomyocytes. Real-time PCR was performed to determine the mRNA levels of atrial natriuretic peptide （ANP） and brain natriuretic peptide （BNP）. Western blot was used to assess the protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65. ResultsIn vivo experiment： Compared with the sham operation group， the model group showed purplish-dark tongue with decreased R， G， B values of the tongue surface （P<0.01）， increased whole blood viscosity （at low， medium， and high shear rates） （P<0.01）， decreased left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01）， increased left ventricular end-diastolic diameter （LVIDd）， left ventricular end-systolic diameter （LVIDs）， and left ventricular posterior wall thickness at end-diastole （LVPWd） （P<0.01）， raised LVMI and HMI （P<0.01）， and elevated levels of NT-proBNP， TNF-α， IL-6， and CRP in the serum and MMP-2 and MMP-9 in the myocardial tissue （P<0.01）. The HE and Masson staining of the myocardial tissue showed compensatory myocardial hypertrophy， fibrosis， and massive inflammatory cell infiltration in the model group. Additionally， the model group presented up-regulated protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 in the myocardial tissue （P<0.01）. Compared with the model group， each administration group showed increased R， G， B values of the tongue surface （P<0.05， P<0.01）， decreased whole blood viscosity （at low， medium， and high shear rates） （P<0.05， P<0.01）， increased LVEF and LVFS （P<0.01）， decreased LVIDd， LVIDs， and LVPWd （P<0.05， P<0.01）， declined LVMI and HMI （P<0.05， P<0.01）， and lowered levels of NT-proBNP， TNF-α， IL-6， and CRP in the serum and MMP-2 and MMP-9 in the myocardial tissue （P<0.01）. HE and Masson staining showed alleviated compensatory myocardial hypertrophy， reduced fibrosis， and decreased expression of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 in the myocardial tissue （P<0.01）. In vitro experiment： When the concentration of Danhong injection reached 20 mL·L^-1， the survival rate of H9C2 cardiomyocytes was the highest （P<0.01）. Compared with the normal group， the model group showed up-regulated mRNA levels of ANP and BNP （P<0.01）， increased relative cell surface area （P<0.01）， and raised protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 （P<0.01）. Compared with the model group， each administration group showed down-regulated mRNA levels of ANP and BNP （P<0.01）， reduced relative cell surface area （P<0.05， P<0.01）， and down-regulated protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 （P<0.05， P<0.01）. ConclusionDanhong injection can regulate ventricular remodeling through the p38 MAPK/NF-κB pathway， thereby exerting a protective effect on the rat model of CHF with heart-blood stasis syndrome.

Chronic heart failure （CHF） is a major global public health problem， and myocardial infarction is one of its main causes. The mouse model of heart failure induced by coronary artery ligation is widely used in the study of CHF， while the TCM syndrome attributes of this model have not yet been clarified. According to the theory of correspondence between prescriptions and syndromes， the method of syndrome identification by prescription efficacy is an important means of current syndrome research of animal models. This method deduces the syndrome characteristics of animal models through prescription efficacy. Taking the four basic syndrome elements of Qi， blood， Yin and Yang as the classification reference， this study used coronary artery ligation to construct a mouse model of CHF and treated the model with four representative TCM injections with the effects of replenishing Qi， warming Yang， nourishing Yin， and activating blood and enalapril. Echocardiography， tongue color parameters， histopathology， serum N-terminal pro-brain natriuretic peptide （NT-proBNP） and cardiac troponin Ⅰ （cTnⅠ） levels， and systematically explored the TCM syndrome attributes of this model. The results showed that the coronary ligation model presented an obvious cardiac function decline， myocardial fibrosis， infarct size expansion， and purple dark tongue， which were consistent with the basic syndrome characteristics of blood stasis in CHF. Danhong injection had significant effects of improving the cardiac function， alleviating myocardial fibrosis， and reducing serum NT-proBNP and cTnⅠ levels. Huangqi Injection and Shenfu injection can improve the cardiac function and tongue color parameters， with limited effects. The effect of Shenmai injection group was not obvious. This study verifies that the established model conforms to blood stasis syndrome through the method of syndrome identification by prescription efficacy， which provides an experimental basis for the study of TCM syndrome mechanism of CHF.

Objective To detect the isocenter of a medical linear accelerator using an optical surface monitoring system (OSMS) combined with a self-made 3D-printed phantom, and compare with the conventional front pointer measurement method. Methods A phantom that could be fixed to the front pointer of the accelerator was fabricated using 3D printing technology. The front pointer method and OSMS were used to detect the rotation isocenter deviations of the accelerator. During the experiments, the collimator, gantry, and couch linear displacement readings were recorded at different angles. We also recorded the measurement time of different surveyors. Results Compared to the front pointer measurement method, the OSMS method showed lower standard deviations. The reductions in standard deviations showed statistical significance in the Lat direction for the collimator rotation isocenter as well as in the Lat and Vrt directions for the gantry rotation isocenter. The mean deviation of Mag values for the collimator rotation isocenter using the OSMS method was 0.50 mm, which was larger than the 0.42 mm using the front pointer method. However, the standard deviation was 0.06 using the OSMS method, which was smaller than the 0.18 using the front pointer method. The mean deviation and standard deviation of Sag values for the gantry rotation isocenter using the OSMS method were 1.03 mm and 0.12, respectively, which were both larger than 0.47 mm and 0.06 using the front pointer method. For the couch rotation isocenter, the mean deviation and standard deviation using the OSMS method were 0.32 mm and 0.04, respectively, which were both smaller than the 0.55 mm and 0.20 using the front pointer method. All surveyors spent less time in isocenter measurements using the OSMS method compared to the front pointer method. Conclusion Compared with the front pointer method, the OSMS method significantly reduces the standard deviation among surveyors, effectively reduces the influence of the angle deviation of the accelerator on the measurement results, reduces detection time, improves detection efficiency, and provides a powerful practical basis for the application of OSMS in detecting the mechanical accuracy of the linear accelerator.

Objective To detect the isocenter of a medical linear accelerator using an optical surface monitoring system (OSMS) combined with a self-made 3D-printed phantom, and compare with the conventional front pointer measurement method. Methods A phantom that could be fixed to the front pointer of the accelerator was fabricated using 3D printing technology. The front pointer method and OSMS were used to detect the rotation isocenter deviations of the accelerator. During the experiments, the collimator, gantry, and couch linear displacement readings were recorded at different angles. We also recorded the measurement time of different surveyors. Results Compared to the front pointer measurement method, the OSMS method showed lower standard deviations. The reductions in standard deviations showed statistical significance in the Lat direction for the collimator rotation isocenter as well as in the Lat and Vrt directions for the gantry rotation isocenter. The mean deviation of Mag values for the collimator rotation isocenter using the OSMS method was 0.50 mm, which was larger than the 0.42 mm using the front pointer method. However, the standard deviation was 0.06 using the OSMS method, which was smaller than the 0.18 using the front pointer method. The mean deviation and standard deviation of Sag values for the gantry rotation isocenter using the OSMS method were 1.03 mm and 0.12, respectively, which were both larger than 0.47 mm and 0.06 using the front pointer method. For the couch rotation isocenter, the mean deviation and standard deviation using the OSMS method were 0.32 mm and 0.04, respectively, which were both smaller than the 0.55 mm and 0.20 using the front pointer method. All surveyors spent less time in isocenter measurements using the OSMS method compared to the front pointer method. Conclusion Compared with the front pointer method, the OSMS method significantly reduces the standard deviation among surveyors, effectively reduces the influence of the angle deviation of the accelerator on the measurement results, reduces detection time, improves detection efficiency, and provides a powerful practical basis for the application of OSMS in detecting the mechanical accuracy of the linear accelerator.

Objective To detect the isocenter of a medical linear accelerator using an optical surface monitoring system (OSMS) combined with a self-made 3D-printed phantom, and compare with the conventional front pointer measurement method. Methods A phantom that could be fixed to the front pointer of the accelerator was fabricated using 3D printing technology. The front pointer method and OSMS were used to detect the rotation isocenter deviations of the accelerator. During the experiments, the collimator, gantry, and couch linear displacement readings were recorded at different angles. We also recorded the measurement time of different surveyors. Results Compared to the front pointer measurement method, the OSMS method showed lower standard deviations. The reductions in standard deviations showed statistical significance in the Lat direction for the collimator rotation isocenter as well as in the Lat and Vrt directions for the gantry rotation isocenter. The mean deviation of Mag values for the collimator rotation isocenter using the OSMS method was 0.50 mm, which was larger than the 0.42 mm using the front pointer method. However, the standard deviation was 0.06 using the OSMS method, which was smaller than the 0.18 using the front pointer method. The mean deviation and standard deviation of Sag values for the gantry rotation isocenter using the OSMS method were 1.03 mm and 0.12, respectively, which were both larger than 0.47 mm and 0.06 using the front pointer method. For the couch rotation isocenter, the mean deviation and standard deviation using the OSMS method were 0.32 mm and 0.04, respectively, which were both smaller than the 0.55 mm and 0.20 using the front pointer method. All surveyors spent less time in isocenter measurements using the OSMS method compared to the front pointer method. Conclusion Compared with the front pointer method, the OSMS method significantly reduces the standard deviation among surveyors, effectively reduces the influence of the angle deviation of the accelerator on the measurement results, reduces detection time, improves detection efficiency, and provides a powerful practical basis for the application of OSMS in detecting the mechanical accuracy of the linear accelerator.

Chronic heart failure （CHF）， as the terminal stage of various cardiovascular diseases， is characterized by a prolonged course and a high mortality rate， posing a serious threat to human health and life. According to physician Sun Yikui's theory of "Mingmen Dongqi" （dynamic Qi of life gate） in the Ming Dynasty and the modern medicine concept of mitochondrial quality control （MQC）， this paper systematically explores the pathogenic mechanisms and evolutionary patterns of CHF， as well as its intrinsic connection with microstructural homeostasis， and further proposes potential traditional Chinese medicine （TCM） intervention strategies. CHF is often caused by damage to the heart Qi at the early stage. As the disease progresses， prolonged illness affects the kidneys， leading to the dynamic Qi decline of life gate. Further， it results in the failure of the functions of sustaining and consolidating， causing the disintegration of the physical form， which corresponds to mitochondrial kinetic disorders. The deficiency in primary driving force results in impaired Qi transformation， corresponding to mitochondrial autophagy dysfunction， forming a pathological transmission chain of "life gate-mitochondrion" that ultimately leads to myocardial structural disintegration and energy metabolism failure. Modern research indicates that patients with CHF exhibit significant MQC imbalance. Disrupted mitochondrial dynamics lead to network fragmentation， and impaired autophagy causes metabolic blockage， constituting the key microscopic mechanisms underlying ventricular remodeling and pump failure. Chinese herbal medicines， such as those with the effects of warming and tonifying kidney Yang or reinforcing healthy Qi， can intervene in multiple signaling pathways-including PTEN-inducible kinase 1 （PINK1）/Parkin and AMP-activated protein kinase/dynamin-related protein 1 （AMPK/Drp1）-to regulate mitochondrial dynamics and autophagy activity. This repairs damaged MQC networks and improves the microenvironment of myocardial energy metabolism. These intervention strategies align closely with the TCM therapeutic principles of warming and tonifying life gate， replenishing Qi， and activating blood， demonstrating the advantages of holistic regulation based on kidney-centered treatment and mitochondrial-targeted approaches. By integrating the "Mingmen Dongqi" theory with the MQC mechanism， this paper establishes a theoretical framework for the integrated prevention and treatment of CHF， offering new perspectives and insights for clinical practice and future research.

Chronic heart failure （CHF）， as the terminal stage of various cardiovascular diseases， is characterized by a prolonged course and a high mortality rate， posing a serious threat to human health and life. According to physician Sun Yikui's theory of "Mingmen Dongqi" （dynamic Qi of life gate） in the Ming Dynasty and the modern medicine concept of mitochondrial quality control （MQC）， this paper systematically explores the pathogenic mechanisms and evolutionary patterns of CHF， as well as its intrinsic connection with microstructural homeostasis， and further proposes potential traditional Chinese medicine （TCM） intervention strategies. CHF is often caused by damage to the heart Qi at the early stage. As the disease progresses， prolonged illness affects the kidneys， leading to the dynamic Qi decline of life gate. Further， it results in the failure of the functions of sustaining and consolidating， causing the disintegration of the physical form， which corresponds to mitochondrial kinetic disorders. The deficiency in primary driving force results in impaired Qi transformation， corresponding to mitochondrial autophagy dysfunction， forming a pathological transmission chain of "life gate-mitochondrion" that ultimately leads to myocardial structural disintegration and energy metabolism failure. Modern research indicates that patients with CHF exhibit significant MQC imbalance. Disrupted mitochondrial dynamics lead to network fragmentation， and impaired autophagy causes metabolic blockage， constituting the key microscopic mechanisms underlying ventricular remodeling and pump failure. Chinese herbal medicines， such as those with the effects of warming and tonifying kidney Yang or reinforcing healthy Qi， can intervene in multiple signaling pathways-including PTEN-inducible kinase 1 （PINK1）/Parkin and AMP-activated protein kinase/dynamin-related protein 1 （AMPK/Drp1）-to regulate mitochondrial dynamics and autophagy activity. This repairs damaged MQC networks and improves the microenvironment of myocardial energy metabolism. These intervention strategies align closely with the TCM therapeutic principles of warming and tonifying life gate， replenishing Qi， and activating blood， demonstrating the advantages of holistic regulation based on kidney-centered treatment and mitochondrial-targeted approaches. By integrating the "Mingmen Dongqi" theory with the MQC mechanism， this paper establishes a theoretical framework for the integrated prevention and treatment of CHF， offering new perspectives and insights for clinical practice and future research.

Objective This study aims to explore the efficacy of tetrahydrocurcumin(THC),the major active metabolite of curcumin,on high glucose(HG)-induced human platelet aggregation and activation as well as to clarify the underlying mechanisms in vitro.Methods Purified platelets prepared from healthy subjects were pre-incubated with various concentrations of THC(0.5 μmol/L,1 μmol/L or 10 μmol/L)or vehicle control(0.05％DMSO)for 40 min at 37℃,followed by the stimulation of normal glucose(NG,5 mmol/L)or HG(25 mmol/L)for additional 90 min.The maximal aggregation rate was determined by an aggregometer.Flow cytometry was used to measure platelet surface expression of CD62P(a typical marker of platelet activation)and generation of total intraplatelet reactive oxygen species(ROS).Meanwhile,the phosphorylation level of platelet p53 was detected by Western blot assay.Results Compared with NG group,HG intervention significantly increased platelet aggrega-tion(P<0.05)and CD62P expression(P<0.001),which were greatly inhibited by different concentrations of THC(P<0.05).Mechanistically,when compared with solvent control,THC significantly decreased the level of total ROS production(P<0.001)and p53 phosphorylation(P<0.05).In addition,HG-induced total intraplatelet ROS generation(P<0.001)and p53 phosphorylation(P<0.05)were greatly attenuated by adding a ROS scavenger N-acetyl-L-cysteine(NAC).The combination of NAC with THC(10 μmol/L)showed no additive inhibitory effects(P>0.05).Moreover,platelet aggregation and activation induced by HG were greatly decreased by NAC and a p53 specific inhibitor PFT-μ(P<0.05).The combination of THC(10 μmol/L)and NAC resulted no additive inhibitory effects on HG-increased platelet aggregation and activation(P>0.05).THC(10 μmol/L)exhibited additive inhibitory effects on platelet aggregation(P<0.05)but no additive inhibitory effects on platelet activation when combined with PFT-μ(P>0.05).Conclusions THC exerts a protective effect on HG-induced platelet aggregation and activation possibly through down-regulating ROS/p53 signaling pathway in human platelets in vitro.The current study may provide potential value for THC to improve thrombosis in diabetes mellitus and the related chronic metabolic diseases.

Objective This study aims to explore the efficacy of tetrahydrocurcumin(THC),the major active metabolite of curcumin,on high glucose(HG)-induced human platelet aggregation and activation as well as to clarify the underlying mechanisms in vitro.Methods Purified platelets prepared from healthy subjects were pre-incubated with various concentrations of THC(0.5 μmol/L,1 μmol/L or 10 μmol/L)or vehicle control(0.05％DMSO)for 40 min at 37℃,followed by the stimulation of normal glucose(NG,5 mmol/L)or HG(25 mmol/L)for additional 90 min.The maximal aggregation rate was determined by an aggregometer.Flow cytometry was used to measure platelet surface expression of CD62P(a typical marker of platelet activation)and generation of total intraplatelet reactive oxygen species(ROS).Meanwhile,the phosphorylation level of platelet p53 was detected by Western blot assay.Results Compared with NG group,HG intervention significantly increased platelet aggrega-tion(P<0.05)and CD62P expression(P<0.001),which were greatly inhibited by different concentrations of THC(P<0.05).Mechanistically,when compared with solvent control,THC significantly decreased the level of total ROS production(P<0.001)and p53 phosphorylation(P<0.05).In addition,HG-induced total intraplatelet ROS generation(P<0.001)and p53 phosphorylation(P<0.05)were greatly attenuated by adding a ROS scavenger N-acetyl-L-cysteine(NAC).The combination of NAC with THC(10 μmol/L)showed no additive inhibitory effects(P>0.05).Moreover,platelet aggregation and activation induced by HG were greatly decreased by NAC and a p53 specific inhibitor PFT-μ(P<0.05).The combination of THC(10 μmol/L)and NAC resulted no additive inhibitory effects on HG-increased platelet aggregation and activation(P>0.05).THC(10 μmol/L)exhibited additive inhibitory effects on platelet aggregation(P<0.05)but no additive inhibitory effects on platelet activation when combined with PFT-μ(P>0.05).Conclusions THC exerts a protective effect on HG-induced platelet aggregation and activation possibly through down-regulating ROS/p53 signaling pathway in human platelets in vitro.The current study may provide potential value for THC to improve thrombosis in diabetes mellitus and the related chronic metabolic diseases.

Objective:To investigate the predictive value of differential distribution of peripheral lymphocyte subsets before and after the first 131I treatment on the therapeutic response to 131I treatment in patients with papillary thyroid cancer (PTC). Methods:A retrospective study was conducted on 46 PTC patients (16 males, 30 females, age 20-77 years) who underwent total thyroidectomy and received 131I treatment between January 2021 and August 2021 in First Hospital of Shanxi Medical University. Peripheral blood lymphocyte subsets (T, B, CD4 + T, CD8 + T, natural killer (NK), helper T (Th)1, Th2, Th17, and regulatory T (Treg) cells) were measured 1-2 d before and 30 d after 131I treatment. Based on serological and imaging evidence, therapeutic response at 6-12 months post- 131I therapy was categorized as either excellent response (ER) or non-excellent response (NER). Differences of preablative stimulated thyroglobulin (psTg) and clinical baseline characteristics between two groups were assessed by using independent-sample t test, paired t test, or Mann-Whitney U test. Predictive value of lymphocyte subsets before and after 131I treatment for therapeutic response was assessed through logistic regression analysis, ROC curve analysis, and decision curve analysis (DCA). Results:In ER group ( n=33) and NER group ( n=13), most lymphocyte subsets showed different degrees of reduction 30 d after 131I treatment compared to before 131I treatment, such as T, B, CD4 + T and Th1 cells in ER group, as well as T, B, CD4 + T, Th1, Th2, Th17, and Treg cells in NER group ( t values: 2.41-9.57, all P<0.05). Before 131I treatment, NER group had significantly higher levels of psTg, Th2, Th17, and Treg cells compared to the ER group ( t values: from -3.32 to -2.48, U=29.00, all P<0.05). After 131I treatment, most of lymphocyte subsets in NER group (T, B, CD4 + T, CD8 + T, Th1 and Treg cells) showed higher trend than those in ER group but without statistical significances ( t values: from -1.12 to -0.06, all P>0.05). Th2 cells before 131I treatment (odds ratio ( OR)=25.00, 95% CI: 1.36-459.10, P=0.030) was identified as a risk factor for NER. ROC curve analysis indicated that AUCs of psTg and Th2 cells for predicting therapeutic response were 0.932 and 0.790, respectively, which was 0.958 for the combined psTg and Th2 cells. DCA showed that within the threshold probability range of 10%-60%, the curves for psTg, Th2 cells, and the combined psTg and Th2 cells were all higher than the extreme curve, suggesting good effect. Conclusions:Most lymphocyte subsets decrease to varying degrees, and NER group shows a significant decrease 30 d after 131I treatment. Th2 cells may be a risk factor for poor response to 131I treatment, providing a certain value in predicting the therapeutic response to 131I treatment.