The industry standard Barium Sulfate Anti-Radiation Mortar (JC/T 2676—2022) was officially released on September 30, 2022, and came into effect on April 1, 2023. The promulgation and implementation of this standard play a significant role in improving the product quality of barium sulfate anti-radiation mortar, promoting industry development, and safeguarding the occupational health of workers. To facilitate accurate understanding of the standard clauses and ensure proper implementation of its requirements, this article elaborated on the background, objectives, and significance of the standard development, along with an interpretation of its key clauses.

Objective: To investigate the ability of different concentrations of piceatannol (PIC) solution to biomodify decalcified dentin matrices in primary teeth, thereby providing a theoretical basis for improving the durability of resin-dentin bonding. Methods: This study was approved by the Medical Ethics Committee of the institution. Molecular docking was performed to predict the interaction effects of PIC with type I collagen and matrix metalloproteinases (MMPs) in dentin. A total of 124 clinically extracted intact primary molars were selected due to retention; of these, 76 were prepared into 60 completely decalcified dentin beams and 24 dentin slices. The 60 beams were equally allocated for dry mass loss and swelling ratio testing (30 beams each). For both experiments, the beams were randomly divided into five groups (n = 6): a control group, 5% glutaraldehyde group, and 2.5, 5, and 10 mg/mL PIC solution groups. This was to evaluate the anti-enzymatic hydrolytic properties and mechanical performance of type I collagen. Of the 24 slices, 15 were assigned to the aforementioned five groups (n = 3) for Fourier-transform infrared spectroscopy (FTIR) to explore the cross-linking mechanism. The remaining nine slices were randomly divided into three groups (n = 3): distilled water group A (SEM examination prior to enzymatic hydrolysis), distilled water group B (SEM examination after enzymatic hydrolysis), and a 10 mg/mL PIC solution group (SEM examination after treatment with 10 mg/mL PIC and subsequent enzymatic hydrolysis). This was to evaluate the cross-linking effect on demineralized dentin collagen. The remaining 48 molars were fabricated into bonding specimens and randomly divided into four groups (n = 12): a control group (distilled water group) and 2.5, 5, and 10 mg/mL PIC groups. Immediate and aged shear bond strength (SBS) were measured, and failure modes were observed under a stereomicroscope to investigate the impact of different PIC concentrations on the bonding durability of primary tooth dentin. Results: Molecular docking revealed strong binding activity between PIC and type I collagen/MMPs via hydrogen bonds, electrostatic potential, and hydrophobic forces; the FTIR results confirmed hydrogen bond formation. In the dry mass loss test, mass loss rates in the 2.5, 5, and 10 mg/mL PIC groups were significantly lower than that in the control group (P < 0.05), with the 10 mg/mL PIC group showing the most optimized cross-linking effect. Swelling tests indicated that all three PIC concentrations reduced the swelling ratio of the demineralized matrix, effectively improving its mechanical properties. SEM showed that collagen from the 10 mg/mL PIC group retained its natural three-dimensional network post-enzymolysis, contrasting sharply with the disintegrated collagen in the enzymolyzed distilled water group B but resembling the morphology of the non-enzymolyzed distilled water group A. SBS results demonstrated that the 10 mg/mL PIC group exhibited significantly higher bond strengths than the control group in both the immediate and aged tests (P < 0.05); immediate SBS in the 10 mg/mL PIC group was also significantly greater than that in the 2.5 mg/mL PIC group (P < 0.05), while no other intergroup differences were found (P > 0.05). Failure mode analysis indicated predominantly mixed fractures, with the proportion of interfacial fractures decreasing as PIC concentration increased compared with the control group. Conclusion A 10 mg/mL PIC solution can effectively cross-link decalcified dentin matrices in primary teeth, enhancing the anti-enzymatic hydrolytic capacity and mechanical properties during clinical operation, thereby promoting bond strength and interface stability, which promises to improve the long-term durability of resin-dentin bonding.

BACKGROUND: Based on the China-VHD database, this study sought to develop and validate a Valvular Heart Disease- specific Age-adjusted Comorbidity Index (VHD-ACI) for predicting mortality risk in patients with VHD. METHODS & RESULTS: The China-VHD study was a nationwide, multi-centre multi-centre cohort study enrolling 13,917 patients with moderate or severe VHD across 46 medical centres in China between April-June 2018. After excluding cases with missing key variables, 11,459 patients were retained for final analysis. The primary endpoint was 2-year all-cause mortality, with 941 deaths (10.0%) observed during follow-up. The VHD-ACI was derived after identifying 13 independent mortality predictors: cardiomyopathy, myocardial infarction, chronic obstructive pulmonary disease, pulmonary artery hypertension, low body weight, anaemia, hypoalbuminaemia, renal insufficiency, moderate/severe hepatic dysfunction, heart failure, cancer, NYHA functional class and age. The index exhibited good discrimination (AUC, 0.79) and calibration (Brier score, 0.062) in the total cohort, outperforming both EuroSCORE II and ACCI (P < 0.001 for comparison). Internal validation through 100 bootstrap iterations yielded a C statistic of 0.694 (95% CI: 0.665-0.723) for 2-year mortality prediction. VHD-ACI scores, as a continuous variable (VHD-ACI score: adjusted HR (95% CI): 1.263 (1.245-1.282), P < 0.001) or categorized using thresholds determined by the Yoden index (VHD-ACI ≥ 9 vs. < 9, adjusted HR (95% CI): 6.216 (5.378-7.184), P < 0.001), were independently associated with mortality. The prognostic performance remained consistent across all VHD subtypes (aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation, tricuspid valve disease, mixed aortic/mitral valve disease and multiple VHD), and clinical subgroups stratified by therapeutic strategy, LVEF status (preserved vs. reduced), disease severity and etiology. CONCLUSION The VHD-ACI is a simple 13-comorbidity algorithm for the prediction of mortality in VHD patients and providing a simple and rapid tool for risk stratification.

Objective:This study aims to investigate the role of fatty acid-binding protein 4 (FABP4) in endothelial-to-mesenchymal transition (EndMT) during the formation of idiopathic pulmonary fibrosis (IPF) and its possible mechanism, and to evaluate the therapeutic potential ofFABP4 inhibitor BMS309403.Methods:A bleomycin (BLM)-induced mouse model of pulmonary fibrosis was established for in vivo experiments.hematoxylin-eosin(HE)and Masson staining were used to assess the histopathological changes and collagen deposition in lung tissue, while western blotting (WB) was used to assess EndMT-related protein expression in lung tissue.In vitro, human umbilical vein endothelial cells (HUVEC) were treated with transforming growth factor-β (TGF-β) to induce the EndMT model.After intervention with FABP4 protein or BMS309403, the expression levels of EndMT related genes and peroxisome proliferator-activated receptor γ (PPAR γ) were detected.Results:BLM-induced mice showed significant pulmonary fibrosis, inflammatory infiltration, and EndMT (upregulated expression of Fibronectin and α-SMA proteins expression, downregulated expression of VE cadherin and CD31 proteins), and BMS309403 treatment significantly alleviated these pathological changes.In vitro experiments confirmed that TGF-β could successfully induce EndMT in HUVECs, FABP4 enhanced the induction effect of TGF-β on EndMT, and BMS309403 could effectively reverse this effect.The co-treatment with TGF-β and FABP4 significantly inhibited the expression of PPARγ, BMS309403 significantly alleviated these changes.Conclusions:FABP4 may promote pulmonary fibrosis progression by facilitating EndMT through the PPARγ signaling pathway.FABP4 may serve as a promising therapeutic target for IPF.

Objective:This study aims to investigate the role of fatty acid-binding protein 4 (FABP4) in endothelial-to-mesenchymal transition (EndMT) during the formation of idiopathic pulmonary fibrosis (IPF) and its possible mechanism, and to evaluate the therapeutic potential ofFABP4 inhibitor BMS309403.Methods:A bleomycin (BLM)-induced mouse model of pulmonary fibrosis was established for in vivo experiments.hematoxylin-eosin(HE)and Masson staining were used to assess the histopathological changes and collagen deposition in lung tissue, while western blotting (WB) was used to assess EndMT-related protein expression in lung tissue.In vitro, human umbilical vein endothelial cells (HUVEC) were treated with transforming growth factor-β (TGF-β) to induce the EndMT model.After intervention with FABP4 protein or BMS309403, the expression levels of EndMT related genes and peroxisome proliferator-activated receptor γ (PPAR γ) were detected.Results:BLM-induced mice showed significant pulmonary fibrosis, inflammatory infiltration, and EndMT (upregulated expression of Fibronectin and α-SMA proteins expression, downregulated expression of VE cadherin and CD31 proteins), and BMS309403 treatment significantly alleviated these pathological changes.In vitro experiments confirmed that TGF-β could successfully induce EndMT in HUVECs, FABP4 enhanced the induction effect of TGF-β on EndMT, and BMS309403 could effectively reverse this effect.The co-treatment with TGF-β and FABP4 significantly inhibited the expression of PPARγ, BMS309403 significantly alleviated these changes.Conclusions:FABP4 may promote pulmonary fibrosis progression by facilitating EndMT through the PPARγ signaling pathway.FABP4 may serve as a promising therapeutic target for IPF.

Rare diseases still lack effective treatments, and the development of drugs for rare diseases (known as orphan drugs) is an urgent medical problem. As natural active ingredients in living organisms, some biomacromolecule drugs have good biocompatibility, low immunogenicity, and high targeting. They have become one of the most promising fields in drug research and development in the 21st century. However, there are still many obstacles in terms of in vivo delivery. In view of the unique advantages of nanocarriers prepared from polymers, lipids, organic biomimetic and inorganic materials in drug delivery, researchers are committed to building an efficient delivery system with versatility and synergy to solve the bottleneck issues in treating rare diseases with biomacromolecule drugs. Therefore, this article reviews the research progress of nanocarrier delivering proteins, peptides and nucleic acids in the field of rare disease treatment in the past ten years, which provides ideas for researches on biomacromolecule drug nanosystems in the field of treatment of rare diseases.

Objective To establish a Nomogram model for assessing the risk of intestinal colonization by Carbapenem-Resistant Klebsiella pneumoniae(CRKP)to determine the specific probability of colonization and adopt individualized prevention strategies for the purpose of reducing the occurrence of colonization and secondary infection of neonatal CRKP.Methods A total of 187 neonates hospitalized between January 2021 and October 2022 and diagnosed with CRKP colonization by rectal swab/fecal culture as well drug sensitivity identification 48 h after admission were assigned to the CRKP group.Another 187 neonates without non-CRKP colonization during the same period were set as the non-CRKP group.All the data of the two groups were used for a retrospective analysis.The caret package in R 4.2.1 was used to randomly divide the 374 cases into the model group and validation group at a ratio of 3∶1.Then the glmnet package in R 4.2.1 was used to conduct a LASSO regression analysis over the data from the model group to determine the predictive factors for modeling and the rms software package was used to build a Nomogram model.The pROC and rms packages in R 4.2.1 were used to examine the data,analyzing the consistency indexes(Cindex),receiver operating characteristic curves(ROC),and area under the curves(AUC)and performing the internal and external validation of the efficacy of the Nomogram model via the calibration curves.Results LASSO regression analysis determined eight predictors from the 35 factors probably affecting neonatal CRKP colonization:gender,cesarean section,breastfeeding,nasogastric tube,enema,carbapenems,probiotics,and hospital stay.The Nomogram model constructed using these eight predictors as variables could predict CRKP colonization to a moderate extent,with the area under the ROC curve of 0.835 and 0.800 in the model and validation group,respectively.The Hos-mer-Lemeshow test showed that the predicted probability was highly consistent with the actual probability(the modeling group:P = 0.678>0.05;the validation group:P = 0.208>0.05),presenting a higher degree of fitting.Conclusion The Nomogram model containing such variables as gender,cesarean section,breastfeeding,nasogastric tube,enema,carbapenems,probiotics,and hospital stay is more effective in predicting the risk of neonatal CRKP colonization.Therefore,preventive measures should be individualized based on the colonization probability predicted by the Nomogram model in order to keep neonates from CRKP colonization and reduce the incidence of secondary CRKP infections among them.

Platelets are reprogrammed by cancer via a process called education, which favors cancer development. The transcriptional profile of tumor-educated platelets (TEPs) is skewed and therefore practicable for cancer detection. This intercontinental, hospital-based, diagnostic study included 761 treatment-naïve inpatients with histologically confirmed adnexal masses and 167 healthy controls from nine medical centers (China, n = 3; Netherlands, n = 5; Poland, n = 1) between September 2016 and May 2019. The main outcomes were the performance of TEPs and their combination with CA125 in two Chinese (VC1 and VC2) and the European (VC3) validation cohorts collectively and independently. Exploratory outcome was the value of TEPs in public pan-cancer platelet transcriptome datasets. The AUCs for TEPs in the combined validation cohort, VC1, VC2, and VC3 were 0.918 (95% CI 0.889-0.948), 0.923 (0.855-0.990), 0.918 (0.872-0.963), and 0.887 (0.813-0.960), respectively. Combination of TEPs and CA125 demonstrated an AUC of 0.922 (0.889-0.955) in the combined validation cohort; 0.955 (0.912-0.997) in VC1; 0.939 (0.901-0.977) in VC2; 0.917 (0.824-1.000) in VC3. For subgroup analysis, TEPs exhibited an AUC of 0.858, 0.859, and 0.920 to detect early-stage, borderline, non-epithelial diseases and 0.899 to discriminate ovarian cancer from endometriosis. TEPs had robustness, compatibility, and universality for preoperative diagnosis of ovarian cancer since it withstood validations in populations of different ethnicities, heterogeneous histological subtypes, and early-stage ovarian cancer. However, these observations warrant prospective validations in a larger population before clinical utilities.
Humans ; Female ; Blood Platelets/pathology* ; Biomarkers, Tumor/genetics* ; Ovarian Neoplasms/pathology* ; China

Coronary heart disease (CHD) and stroke are the most well-known cardiovascular diseases, which share many common pathological basis. Yindan Xinnaotong soft capsule (YDXNT) is a commonly used Chinese patent medicine in the treatment of stroke and CHD. However, its action of mechanism of co-treatment for stroke and CHD is still unclear. The aim of this study was to explore the common mechanism of YDXNT in co-treatment of CHD and stroke using network pharmacology, experimental verification and molecular docking. An integrated literature mining and databases of IPA, ETCM, HERB, Swiss Target Prediction, OMIM and GeneCards were used to screen and predict active ingredients and potential targets of YDXNT in co-treatment of CHD and stroke. The protein-protein interaction network, GO analysis and pathway analysis were analyzed by IPA software. The effect of YDXNT on core targets was verified by immunofluorescence. UPLC-QTOF/MS and molecular docking were used to screen and predict the main active constituents of YDXNT and their interactions with core targets. A total of 151 potential targets are predicted for YDXNT in co-treatment of CHD and stroke. Hypoxia-inducible factor-1α (HIF1α)-matrix metalloproteinase-9 (MMP9)-mediated HIF1α signaling pathway serves as one of the common mechanisms. YDXNT could reduce the increase of mitochondrial fluorescence intensity and the protein expression of HIF1α and MMP9 in HL-1 and HA induced by oxygen and glucose deprivation/reperfusion (OGD/R) in a dose-dependent manner. Baicalin may be the material basis for treating stroke and CHD with YDXNT. In conclusion, the HIF1α signaling pathway is one of the common key mechanisms of YDXNT in the co-treatment of stroke and CHD. The study provides support and basis for the in-depth scientific connotation of the traditional Chinese medicine theory of "same treatment to different diseases".

OBJECTIVE: To develop and validate a user-friendly risk score for older mitral regurgitation (MR) patients, referred to as the Elder-MR score. METHODS: The China Senile Valvular Heart Disease (China-DVD) Cohort Study functioned as the development cohort, while the China Valvular Heart Disease (China-VHD) Study was employed for external validation. We included patients aged 60 years and above receiving medical treatment for moderate or severe MR (2274 patients in the development cohort and 1929 patients in the validation cohort). Candidate predictors were chosen using Cox's proportional hazards model and stepwise selection with Akaike's information criterion. RESULTS: Eight predictors were identified: age ≥ 75 years, body mass index < 20 kg/m², NYHA class III/IV, secondary MR, anemia, estimated glomerular filtration rate < 60 mL/min per 1.73 m², albumin < 35 g/L, and left ventricular ejection fraction < 60%. The model displayed satisfactory performance in predicting one-year mortality in both the development cohort (C-statistic = 0.73, 95% CI: 0.69-0.77, Brier score = 0.06) and the validation cohort (C-statistic = 0.73, 95% CI: 0.68-0.78, Brier score = 0.06). The Elder-MR score ranges from 0 to 15 points. At a one-year follow-up, each point increase in the Elder-MR score represents a 1.27-fold risk of death (HR = 1.27, 95% CI: 1.21-1.34, P < 0.001) in the development cohort and a 1.24-fold risk of death (HR = 1.24, 95% CI: 1.17-1.30, P < 0.001) in the validation cohort. Compared to EuroSCORE II, the Elder-MR score demonstrated superior predictive accuracy for one-year mortality in the validation cohort (C-statistic = 0.71 vs. 0.70, net reclassification improvement = 0.320, P < 0.01; integrated discrimination improvement = 0.029, P < 0.01). CONCLUSIONS The Elder-MR score may serve as an effective risk stratification tool to assist clinical decision-making in older MR patients.