Objective To observe the clinical effect of Shiwei Wendan Decoction on coronary heart disease stable angina pectoris of qi deficiency and stasis-phlegm type. Methods Sixty patients of stable angina pectoris which belonged to the type of qi deficiency and stasis-phlegm were divided randomly into the treatment group and the control group,and each group has 30 cases. The treatment group was given Shiwei Wendan Decoction and the control group was given Tongxinluo Capsule for 4 week,one course. The changes of symptoms integral,ECG,clinical efficacy,blood-fat and CRP of the two groups were observed after the treatment. Results The total effective power of the treatment group was higher than that of the control group (P

Objective To quantify the expressions of collagen metabolic markers carboxy terminal propeptide of type I procollagen(PICP),nitrogen terminal propeptide of type I procollagen (PINP),nitrogen terminal propeptide of typeⅢprocollagen(PⅢNP),type I collagen carboxy terminal telopeptide (ICTP), matrix metalloproteinases(MMPs)and the tissue inhibitor of metalloproteinases(TIMPs)in the serum of atrial fibrillation patients by enzyme linked immunosorbent assay(ELISA),and to discuss the atrial structural remodeling during atrial fibrillation(AF).Methods 71 elderly patients were enrolled,24 patients had permanent AF,24 patients had paroxysmal AF,and 23 patients were in sinus rhythm.The serum levels of all markers were measured by ELISA. Results PICP was increased in permanent AF group versus the paroxysmal AF group and sinus rhythm group by 25.4%and 42.8%(all P<0.05),respectively.PⅢNP was increased in permanent AF group versus the paroxysmal AF group and sinus rhythm group by 17.9a% and 35.6%(all P<0.05),respectively,and was increased in the paroxysmal AF group versus the sinus rhythm group by 15.0%(P<0.05).PINP and ICTP did not differ significantly between the 3 groups(all P >0.05).MMP-1 was significantly increased by 25.6%(P<0.05)in the paroxysmal AF group versus the sinus rhythm group.MMP-2 was also significantly increased in permanent AF group versus the paroxysmal AF group and sinus rhythm group by 54.9%and 37.9%(all P<0.05),respectively.MMP-7,MMp-9 and TIMP-1 did not differ significantly between the 3 groups(P>0.05).TIMP-2was significantly decreased in the permanent AF group and paroxysmal AF group versus the sinus rhythm group by 21.8%and 11.8%(P<0.05),respectively. Conclusions Disturbance in the balance of MMP/TIMP system may perturb the balance of collagen synthesis and degradation during atrial fibrillation.This may be a contributing mechanism to atrial structural remodeling in atrial fibrillation,and may correlate with the initiation and maintenance of AF.

We have designed and carried out problem based learning (PBL) pedagogy since 2004. According to clinical eases, students learnt the pathophysiology of heart failure knowledge by themselves. Each group recommen-ded one student to make an oral presentation and wrote a review about heart failure. Preparing clinical cases and group discussions are very important. At the same time we should pay attention to the change in role of the teacher in PBL and cooperation with other disciplines.

Objective:To analyze the clinical characteristics and risk stratification of 182 patients with acute pulmonary embolism (APE), and to investigate the correlation of neutrophil (N)/lymphocyte (L) ratio (NLR) and risk stratification/prognosis.Methods:The clinical data of 182 APE patients admitted to Peking University People’s Hospital from January 2015 to March 2021 were retrospectively collected, including age, sex, symptoms and signs, blood pressure, blood gas analysis, blood routine parameters, cardiac biomarkers, coagulation parameters, and right ventricular imaging parameters. The patients were divided into groups according to the risk stratification at admission and prognosis in hospital. χ2 test, t test or nonparametric test were used to analyze the differences in clinical characteristics, blood routine parameters, blood gas analysis, coagulation parameters and other parameters between the groups. Multivariate logistic regression analysis was used to study the independent risk factors for the prognosis of APE. Results:Among the 182 patients, 79 were male and 103 were female, 23 were in the high-risk group, 51 were in the intermediate-high-risk group, 46 were in the intermediate-low risk group, and 62 were in the low-risk group. There were 27 deaths and 155 survivors. The respiratory rate of the high/intermediate-high-risk group was significantly higher than that of the low/intermediate-low-risk group. Compared with the other three groups, pH, oxygen partial pressure (PO 2) and blood oxygen saturation (SO 2) in the high-risk group were significantly lower ( both P<0.05). There were statistically significant differences in WBC, N, and NLR levels between the high/intermediate-high-risk group and low/intermediate-low-risk group ( both P<0.05). However there were no significant differences in PLT, PLT/MPV, PLT/PDW, and coagulation related parameters PT, FIB, APTT and D-D between groups (all P > 0.05). MPV and PDW were only significantly different between the low-risk group, intermediate-low-risk group and high-risk group ( both P<0.05). Multivariate logistic regression analysis showed that NLR ( OR=1.179,95% CI:1.029-1.410, P=0.039) and PH ( OR=1.156,95% CI:1.031-1.522, P=0.041) were independent predictors of in-hospital mortality. The ROC curve was used to analyze the predictive value of NLR for in-hospital mortality. When the cutoff value of NLR was 8.38, the AUC of NLR was 0.824 (95% CI: 0.829-0.913), the corresponding sensitivity was 0.831, and the specificity was 0.887. Conclusions:NLR is correlated with risk stratification and prognosis of APE, and is an independent risk factor for poor prognosis.

Background Silica nanoparticles (SiNPs) enter the human body through respiratory tract, digestive tract, and skin, causing body damage. Lung is one of the main damaged organs. Objective To observe the expressions of complement activated fragment C3a and its receptor C3aR in the lungs of mice exposed to SiNPs through respiratory tract, and to explore the involvement of C3a/C3aR in lung injury induced by SiNPs exposure. Methods The ultrastructure of SiNPs (particle size 5-20 nm) was determined under a transmission electron microscope, and the hydrodynamic diameter and surface Zeta potential of SiNPs were determined using a nanoparticle size analyzer. A total of 88 SPF C57BL/6J mice were randomly divided into five groups: a blank control group without any treatment (14 mice), a vehicle control group treated with 50 μL stroke-physiological saline solution by intratracheal instillation (14 mice), and three SiNPs exposure groups (low-dose group, medium-dose group, and high-dose group with 20 mice in each group, who were given 50 μL SiNPs suspension of 7, 21, and 35 mg·kg⁻¹ respectively and exposed once every 3 days for 5 times). The mice were anesthetized on day 1 (1-day model group) and day 15 (15-day model group) after exposure, then sacrificed after extraction of bronchoalveolar lavage fluid (BALF), and lung tissues were retained. The morphological changes of lung tissues were observed by HE staining, the expression level of C3a in BALF was detected by enzyme-linked immunosorbent assay, the deposition of C3a and C3aR in lung tissues were observed by immunohistochemistry, the protein expression level of C3aR was determined by Western blotting, and the localization and semi-quantitative detection of C3a and C3aR in lung tissues was observed by immunofluorescence. Results SiNPs agglomerated in stroke-physiological saline solution. The average hydrodynamic diameter was (185.60±7.39) nm and the absolute value of Zeta potential was (43.33±0.76) mV. The condition of mice in the 1-day model group and the 15-day model group was good, while 2 mice died in the medium-dose group of the 1-day model group due to misoperation. The autopsy results of the two mice showed congestion of the lung tissue, emphysema, and no imperfection of trachea integrity. No death was observed in other dose groups. The HE staining results showed pathological damage to the mouse lung, including alveolar wall thickening and inflammatory cell infiltration after SiNPs exposure. The pathological damage became more serious with the increase of dose. Regarding pathological changes, the 15-day model group was slightly relieved compared with the 1-day model group, but there were still pathological changes. The enzyme-linked immunosorbent assay results showed that there was no difference in the expression level of C3a between the blank control group and the vehicle control group (P＞0.05), the expression levels of C3a in the medium-dose group and the high-dose group were significantly higher than that in the vehicle control group (P<0.05). The immunohistochemistry results showed that C3a deposition was consistent with the enzyme-linked immunosorbent assay results. The Western blotting and the immunohistochemistry results showed that C3aR expression was low in the blank control group and the vehicle control group, while the expression in each dose group tended to increase with the increase of dose. The immunofluorescence results showed that the fluorescence signals of C3a and C3aR were weak in the blank control group and the vehicle control group in the 1-day model group and the 15-day model group, while the fluorescence signals in the lung tissues of mice in the SiNPs exposure groups tended to increase with the increase of dose. Conclusion The increased expressions of C3a and C3aR in complement activation may be related to lung injury induced by intratracheal instillation of SiNPs, suggesting that C3a/C3aR may be involved in lung injury induced by SiNPs exposure.