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.

Peri-implant keratinized mucosa (PIKM) augmentation refers to surgical procedures aimed at increasing the width of PIKM. Consensus reports emphasize the necessity of maintaining a minimum width of PIKM to ensure long-term peri-implant health. Currently, several surgical techniques have been validated for their effectiveness in increasing PIKM. However, the selection and application of PIKM augmentation methods may present challenges for dental practitioners due to heterogeneity in surgical techniques, variations in clinical scenarios, and anatomical differences. Therefore, clear guidelines and considerations for PIKM augmentation are needed. This expert consensus focuses on the commonly employed surgical techniques for PIKM augmentation and the factors influencing their selection at second-stage surgery. It aims to establish a standardized framework for assessing, planning, and executing PIKM augmentation procedures, with the goal of offering evidence-based guidance to enhance the predictability and success of PIKM augmentation.
Humans ; Consensus ; Dental Implants ; Mouth Mucosa/surgery* ; Keratins

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.

As a chronic liver inflammation disease caused by the lack of immune tolerance, autoimmune hepatitis is regulated by various signaling pathways, such as the NF-κB/NLRP3 pathway, the SIRT1/Nrf2/HO-1 pathway, the Hippo-YAP/TAZ pathway, the JAK/STAT pathway, the PI3K/Akt pathway, and the TRAF6/JNK pathway. These pathways can play a role against autoimmune hepatitis by participating in the processes including the proliferation and apoptosis of cytokines, immune response, and oxidative stress. In view of the problems of suboptimal response, obvious adverse reactions, and high recurrence rate in the clinical application of hormones and immune preparations for the treatment of autoimmune hepatitis, this article summarizes the research articles on autoimmune hepatitis-related signaling pathways and the mechanism of effective constituents (glycosides, terpenoids, flavonoids, quinones, and phenols) in traditional Chinese medicine intervening against the disease process of autoimmune hepatitis through the above signaling pathways, in order to provide a theoretical basis for scientific and effective utilization of effective constituents in traditional Chinese medicine to develop anti-autoimmune hepatitis drugs.

Objective To explore the predictive value of the expression of CD44v6 and EGFR on the efficacy of neoadjuvant chemotherapy (NACT) in stageⅡ-Ⅲ cervical cancer. Methods A total of 53 patients with stageⅡ-Ⅲ cervical cancer diagnosed by pathology were selected. All patients received two cycles of paclitaxel+platinum NACT. The pathological tissue samples of cervical tumors before NACT treatment were collected. The expression of CD44v6 and EGFR were detected by the immunohistochemical SP method, and we analyzed their predictive value of NACT in stageⅡ-Ⅲ cervical cancer. Results Among the 53 patients, 38 were in the NACT effective group (CR+PR), and 15 were in the NACT ineffective group (SD+PD). The expression of CD44v6 in the ineffective group was significantly higher than that in the effective group (P < 0.05). The expression of CD44v6 was significantly different in patients with CR, PR, and SD (P < 0.05). The AUC of CD44v6 to NACT effect on stage Ⅱ-Ⅲ cervical cancer was 0.74 (P < 0.05). The patients in the high expression group of CD44v6 had worse efficacy in NACT than those in the low expression group of CD44v6 (P < 0.05). Pearson test showed that CD44v6 and EGFR expression were correlated (R=0.34, P < 0.05). Conclusion High expression of CD44v6 may reduce the efficacy of NACT in stageⅡ-Ⅲ cervical cancer, suggesting that the expression of CD44v6 has a certain predictive value and clinical significance in the efficacy of paclitaxel+platinum NACT on cervical cancer. Moreover, CD44v6 is positively correlated with EGFR expression.

Hepatic fibrosis is a common pathological stage of many chronic liver diseases. Activation of hepatic stellate cells is considered as a key event in the progression of hepatic fibrosis. The pathogenesis of liver fibrosis is modulated by various cytokines involved in several signal pathways, including NF-κB, TGF-β/Smad, Wnt/β-catenin, Hedgehog etc. With the rapid development of modern pharmacology and biotechnology, the underlying molecular mechanism of anti-liver fibrosis of active components from traditional Chinese medicine has been further elucidated. This article summarizes scientific outcomes of signal pathways involved in liver fibrosis and how active components of Chinese herbal medicines exhibit anti-liver fibrosis effects, aiming to provide a potential drug candidate as a treatment for liver fibrosis and to open up a new research field of therapeutics for liver fibrosis.

Silicosis is one of the most common forms of pneumoconiosis globally. Workers who engage in mining, construction, ceramics, and many other industries have a high risk of developing silicosis. Chronic and repeated inhalation of free silica (SiO₂) dust (<5 μm) during working can lead to inflammatory reactions, resulting in interstitial lung disease characterized by extensive nodular fibrosis in both lungs. Once silicosis occurs, it will develop progressively even when the workers are removed from the silica dust environment. The pathogenesis of silicosis is complex, especially the role of nod-like receptor family protein 3 (NLRP3) inflammasome in the pathogenesis and progression of silicosis remains to be further studied. NLRP3 inflammasome, a multi-protein complex composed of NLRP3, apoptosis-associated speck-like protein, and cysteinyl aspartate specific proteinase 1 is involved in oxidative stress, inflammatory response, apoptosis, and pyroptosis, and has become one of the hot spots in silicosis research. This review summarized the structure, function, and activation mechanism of NLRP3 inflammasome. Furthermore, the cellular and molecular mechanisms of NLRP3 in mediating oxidative stress, inflammatory response, apoptosis, and pyroptosis in the progression of silicosis were reviewed. Finally, the potential therapeutic drugs for silicosis based on NLRP3-associated mechanisms were outlined. More attention should be paid to the role of NLRP3 inflammasome in the pathogenesis and progression of silicosis in the future, which will provide new ideas for the prevention and treatment of silicosis.

Lipids are important components of living organisms that participate in and regulate a variety of life activities. Lipids in plants also play important physiological functions in response to a variety of abiotic stresses (e.g. salt stress, drought stress, temperature stress). However, most research on lipids focused on animal cells and medical fields, while the functions of lipids in plants were overlooked. With the rapid development of "omics" technologies and biotechnology, the lipidomics has received much attention in recent years because it can reveal the composition and function of lipids in a deep and comprehensive way. This review summarizes the recent advances in the functions and classification of lipids, the development of lipidomics technology, and the responses of plant lipids against drought stress, salt stress and temperature stress. In addition, challenges and prospects were proposed for future lipidomics research and further exploration of the physiological functions of lipids in plant stress resistance.
Droughts ; Gene Expression Regulation, Plant ; Lipids ; Plants ; Stress, Physiological

Uridine-cytidine kinase, an important catalyst in the compensation pathway of nucleotide metabolism, can catalyze the phosphorylation reaction of cytidine to 5'-cytidine monophosphate (CMP), but the reaction needs NTP as the phosphate donor. To increase the production efficiency of CMP, uridine-cytidine kinase gene from Thermus thermophilus HB8 and polyphosphate kinase gene from Rhodobacter sphaeroides were cloned and expressed in Escherichia coli BL21(DE3). Uridine-cytidine kinase was used for the generation of CMP from cytidine and ATP, and polyphosphate kinase was used for the regeneration of ATP. Then, the D403 metal chelate resin was used to adsorb Ni²⁺ to form an immobilized carrier, and the immobilized carrier was specifically combined with the recombinant enzymes to form the immobilized enzymes. Finally, single-factor optimization experiment was carried out to determine the reaction conditions of the immobilized enzyme. At 30 °C and pH 8.0, 60 mmol/L cytidine and 0.5 mmol/L ATP were used as substrates to achieve 5 batches of high-efficiency continuous catalytic reaction, and the average molar yield of CMP reached 91.2%. The above method has the advantages of low reaction cost, high product yield and high enzyme utilization rate, and has good applied value for industrial production.
Cytidine Monophosphate ; metabolism ; Escherichia coli ; genetics ; Industrial Microbiology ; methods ; Phosphotransferases (Phosphate Group Acceptor) ; metabolism ; Uridine Kinase

ObjectiveTo systematically evaluate the association between smoking and the risk of primary biliary cirrhosis (PBC) from the perspective of evidence-based medicine. MethodsA literature search was performed in PubMed, EMBASE, CBM, CNKI, Wanfang Data, and VIP database to collect the case-control studies on the association between smoking and the risk of PBC published in the last two decades. Chinese search words were “吸烟”, “香烟”, “原发性胆汁性肝硬化”, “危险因素”, “队列研究”, and “病例对照研究”, and English search words were “smoking”, “cigarette”, “tobacco”, “risk factors”, “primary biliary cirrhosis”, “cohort studies”, and “case-control studies”. And then a meta-analysis was performed using Review Manager 5.2. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated, and the publication bias was analyzed by funnel plots. ResultsA total of 7 case-control studies involving 5459 subjects (2652 patients with PBC vs 2807 controls) were included in the meta-analysis. The analysis results showed that smokers had a significantly higher risk of PBC compared with non-smokers (OR=1.49, 95% CI: 1.11-2.00, P=0.009). The geographical subgroup analysis results showed that there was a significant difference in the risk of PBC between non-smokers and smokers in North America (OR=1.57, 95% CI: 1.20-2.04, P=0.0008). However, there was no significant difference in the risk of PBC between non-smokers and smokers in Europe (OR=1.41, 95% CI: 0.73-2.73, P=0.31). ConclusionSmoking can increase the risk of PBC. However, it needs to be confirmed in high-quality prospective studies with larger samples because of the heterogeneity of current included studies.