Objective:To develop and validate a risk prediction model for in-stent restenosis (ISR) after percutaneous coronary intervention (PCI).Methods:This prospective study included 126 patients with acute myocardial infarction (AMI) who underwent PCI at Lishui Central Hospital from May 2021 to April 2023. The patients were divided into two groups based on whether they experienced ISR after PCI: ISR group ( n = 33) and non-ISR group ( n = 93). Clinical data were compared between the two groups. Binary logistic regression was used to identify independent risk factors for ISR in patients with AMI after PCI. A risk prediction model was then developed, and the predictive value of the model was assessed using receiver operating characteristic curve analysis. Results:After surgery, significant differences were observed between the ISR and non-ISR groups regarding postoperative smoking [21(63.64%) vs. 27(29.03%)], elevated uric acid level [19 (57.58%) vs. 28(30.11%)], serum amyloid A (SAA) ≥ 10 mg/L [20(60.61%) vs. 26(27.96%)], and lipoprotein(a) [Lp(a)] ≥ 300 mg/L [21(63.64%) vs. 32(34.41%)] [ χ2 = 12.36, 7.85, 11.20, 8.53, all P < 0.05]. Postoperative smoking, elevated uric acid levels, SAA ≥ 10 mg/L, and Lp(a) ≥ 300 mg/L were identified as independent risk factors for ISR in patients with AMI after PCI ( OR = 0.234, 0.317, 0.252, 0.300, all P < 0.05). A risk prediction model for ISR after PCI was developed based on postoperative smoking, elevated uric acid levels, SAA levels, and Lp(a) levels ≥ 300 mg/L. Receiver operating characteristic curve analysis revealed the areas under the curve were 0.673 [95% CI(0.564, 0.782)], 0.637 [95% CI(0.525, 0.750)], 0.663 [95% CI(0.552, 0.774)], 0.646 [95% CI(0.536, 0.757)], and 0.889 [95% CI(0.821, 0.958)] for ostoperative smoking, elevated uric acid levels, SAA levels, Lp(a) levels ≥ 300 mg/L, and the risk prediction model, respectively. At the critical threshold values, the sensitivities for these variables were 0.636, 0.576, 0.606, 0.636, and 0.909, respectively, while the specificities were 0.710, 0.699, 0.720, 0.656, and 0.763, respectively. The bootstrap method (B = 1000) was used for the internal validation of the risk prediction model. After bias correction, the predicted curve approached the ideal curve, yielding a consistency index of 0.778, which indicates a high predictive value for the model. Moreover, the risk prediction model demonstrated a net benefit greater than 0 within a threshold probability range of 0.02 to 0.93, exceeding two ineffective thresholds. Conclusions:Postoperative smoking, elevated uric acid levels, SAA, and Lp(a) are independent risk factors for ISR in patients with AMI after PCI. The risk prediction model developed based on these four factors demonstrates a high predictive value, which can aid in assessing the risk of ISR in AMI patients with AMI after PCI and in formulating appropriate intervention measures.

Objective:To develop and validate a risk prediction model for in-stent restenosis (ISR) after percutaneous coronary intervention (PCI).Methods:This prospective study included 126 patients with acute myocardial infarction (AMI) who underwent PCI at Lishui Central Hospital from May 2021 to April 2023. The patients were divided into two groups based on whether they experienced ISR after PCI: ISR group ( n = 33) and non-ISR group ( n = 93). Clinical data were compared between the two groups. Binary logistic regression was used to identify independent risk factors for ISR in patients with AMI after PCI. A risk prediction model was then developed, and the predictive value of the model was assessed using receiver operating characteristic curve analysis. Results:After surgery, significant differences were observed between the ISR and non-ISR groups regarding postoperative smoking [21(63.64%) vs. 27(29.03%)], elevated uric acid level [19 (57.58%) vs. 28(30.11%)], serum amyloid A (SAA) ≥ 10 mg/L [20(60.61%) vs. 26(27.96%)], and lipoprotein(a) [Lp(a)] ≥ 300 mg/L [21(63.64%) vs. 32(34.41%)] [ χ2 = 12.36, 7.85, 11.20, 8.53, all P < 0.05]. Postoperative smoking, elevated uric acid levels, SAA ≥ 10 mg/L, and Lp(a) ≥ 300 mg/L were identified as independent risk factors for ISR in patients with AMI after PCI ( OR = 0.234, 0.317, 0.252, 0.300, all P < 0.05). A risk prediction model for ISR after PCI was developed based on postoperative smoking, elevated uric acid levels, SAA levels, and Lp(a) levels ≥ 300 mg/L. Receiver operating characteristic curve analysis revealed the areas under the curve were 0.673 [95% CI(0.564, 0.782)], 0.637 [95% CI(0.525, 0.750)], 0.663 [95% CI(0.552, 0.774)], 0.646 [95% CI(0.536, 0.757)], and 0.889 [95% CI(0.821, 0.958)] for ostoperative smoking, elevated uric acid levels, SAA levels, Lp(a) levels ≥ 300 mg/L, and the risk prediction model, respectively. At the critical threshold values, the sensitivities for these variables were 0.636, 0.576, 0.606, 0.636, and 0.909, respectively, while the specificities were 0.710, 0.699, 0.720, 0.656, and 0.763, respectively. The bootstrap method (B = 1000) was used for the internal validation of the risk prediction model. After bias correction, the predicted curve approached the ideal curve, yielding a consistency index of 0.778, which indicates a high predictive value for the model. Moreover, the risk prediction model demonstrated a net benefit greater than 0 within a threshold probability range of 0.02 to 0.93, exceeding two ineffective thresholds. Conclusions:Postoperative smoking, elevated uric acid levels, SAA, and Lp(a) are independent risk factors for ISR in patients with AMI after PCI. The risk prediction model developed based on these four factors demonstrates a high predictive value, which can aid in assessing the risk of ISR in AMI patients with AMI after PCI and in formulating appropriate intervention measures.

Currently, there is still no effective curative treatment for the development of late-stage liver fibrosis. Here, we have illustrated that TB001, a dual glucagon-like peptide-1 receptor/glucagon receptor (GLP-1R/GCGR) agonist with higher affinity towards GCGR, could retard the progression of liver fibrosis in various rodent models, with remarkable potency, selectivity, extended half-life and low toxicity. Four types of liver fibrosis animal models which were induced by CCl₄, α-naphthyl-isothiocyanate (ANIT), bile duct ligation (BDL) and Schistosoma japonicum were used in our study. We found that TB001 treatment dose-dependently significantly attenuated liver injury and collagen accumulation in these animal models. In addition to decreased levels of extracellular matrix (ECM) accumulation during hepatic injury, activation of hepatic stellate cells was also inhibited via suppression of TGF-β expression as well as downstream Smad signaling pathways particularly in CCl₄-and S. japonicum-induced liver fibrosis. Moreover, TB001 attenuated liver fibrosis through blocking downstream activation of pro-inflammatory nuclear factor kappa B/NF-kappa-B inhibitor alpha (NFκB/IKBα) pathways as well as c-Jun N-terminal kinase (JNK)-dependent induction of hepatocyte apoptosis. Furthermore, GLP-1R and/or GCGR knock-down results represented GCGR played an important role in ameliorating CCl₄-induced hepatic fibrosis. Therefore, TB001 can be used as a promising therapeutic candidate for the treatment of multiple causes of hepatic fibrosis demonstrated by our extensive pre-clinical evaluation of TB001.

The antimicrobial peptide APKGVQGPNG (named YD), a natural peptide originating from Bacillus amyloliquefaciens CBSYD1, exhibited excellent antibacterial and antioxidant properties in vitro. These characteristics are closely related to inflammatory responses which is the central trigger for liver fibrosis. However, the therapeutic effects of YD against hepatic fibrosis and the underlying mechanisms are rarely studied. In this study, we show that YD improved liver function and inhibited the progression of liver fibrosis by measuring the serum transaminase activity and the expression of α-smooth muscle actin and collagen I in carbon tetrachloride-induced mice. Then we found that YD inhibited the level of miR-155, which plays an important role in inflammation and liver fibrosis. Bioinformatics analysis and luciferase reporter assay indicate that Casp12 is a new target of miR-155. We demonstrate that YD significantly decreases the contents of inflammatory cytokines and suppresses the NF-κB signaling pathway. Further studies show that transfection of the miR-155 mimic in RAW264.7 cells partially reversed the YD-mediated CASP12 upregulation, the downregulated levels of inflammatory cytokines, and the inactivation of the NF-κB pathways. Collectively, our study indicates that YD reduces inflammation through the miR-155–Casp12–NF-κB axis during liver fibrosis and provides a promising therapeutic candidate for hepatic fibrosis.

Objective To discuss the application and practice of TBL teaching mode in the clinical teaching of oncology . Methods Physicians on rotational medical tour in Huadong hospital from April 2017 to August 2017 were selected as research sub-jects, and were randomly divided into 2 groups:the experimental group and the control group .Theory test and manipulation test scores were compared and analyzed between the physicians of the 2 groups.Questionnaire feedback was used to evaluate the effect of TBL teaching mode.Results Total average scores of the experimental group were 84.15 ±4.50, while those of the control group were 78.80 ±2.38, and statistically significance could be noted , when comparisons were made between the 2 groups.Results of the questionnaire survey indicated that most of the students thought that TBL teaching mode was more beneficial to comprehensive grasp of oncology knowl -edge , and TBL teaching mode was more interesting , as compared with the conventional teaching mode .More importantly , TBL teaching mode could not only improve their learning initiative , but enhance the spirit of teamwork and cooperation .Conclusion The application of TBL teaching mode in oncology clinical teaching could fully improve learning initiative of the students , strengthen the spirit of team-work, and enhance the quality of teaching .

Cinobufacino injection is a significant anti-tumor medicine for the treatment of various tumors in clinic, which was made from water extraction of the skin of Bufo bufo gargarizans. In present paper, HPLC-DAD-FT-ICR-MS method was used to identify the major bufadienolides in cinobufacino for the first time. Solid-phase extraction with dichloromethane and silica was used to enrich the total bufadienolides in cinobufacino. Based on the UV and high resolution MS/MS data, 33 bufadienolides were analyzed and characterized. Among them, eight compounds were identified by comparing with standard references unambiguously. This study elucidated the major bufadienolides in cinobufacino, which provided material foundation of cinobufacino and will be benefit for the further pharmacological research.

Cinobufacino injection is purified from water extraction of the skin of Bufo bufo gargarizans, which has been widely used for various cancers in clinic with significant anti-tumor effects. Bufadienolides were regarded as the main active constituents of cinobufacino injection in previous reports. In present study, 6 bufadienolides were isolated and purified from Cinobufacino injection. Their structures were identified as 3-epi-ψ-bufarenogin (1), ψ-bufarenogin (2), 3-epi-arenobufagin (3), arenobufagin (4), 3-epi-gamabufotalin (5), and 3-oxo-arenobufagin (6), separately. Among them, 1 and 3 were new compounds, 5 and 6 were new natural products. Compounds 1, 2 and compounds 3, 4 were two pairs configuration isomers at C-3, separately.