Objective To investigate the effect and mechanism of verteporfin (Vp) in airway remodeling of experimental asthma. Methods (1) Animal experiment: Twelve female BALB/c mice were divided into 3 groups (4 each): control group experimental asthma group and Vp intervention asthma group. Mice in experimental asthma group were treated by intranasal delivery of house dust mite (HDM) extract, in Vp intervention group were treated with intraperitoneal injection of Vp before HDM stimulation, and in control group was treated with the same amount of normal saline. Lung tissues and bronchoalveolar lavage fluid (BALF) of mice were collected, HE staining, Masson staining and Periodic Acid-Schiff (PAS) staining were used to observe the pathological changes of lung tissue, Wright-Giemsa staining was used to count the inflammatory cells in BALF, and the expressions of Yes-associated protein (YAP) and phosphorylated Yes-associated protein (p-YAP) in lung tissues were detected with immunohistochemistry, RT-PCR and Western blotting were performed to detect the expressions of YAP, p-YAP, osteopontin (OPN)and smooth muscle myosin heavy chain (SMMHC). (2) Cell experiment: Human airway smooth muscle cells (HASMC) were divided into control group (treated with the same amount of normal saline), HDM group (treated with 50 μg/ml HDM for 24 hours)and HDM+Vp group (treated with 0.05 mg/L Vp for 2 hours, and then with 50 μg/ml HDM for 24 hours). The cell proliferation of HASMC was detected by CCK-8. The apoptosis rate of HASMC were detected by flow cytometry. The protein levels of YAP, OPN and SMMHC in cells were detected by Western blotting. Results (1) Animal experiment: Compared with control group, the lung inflammation was aggravated, the bronchial basement membrane, airway smooth muscle (ASM) and airway wall were thickened in experimental asthma group [(1.13±0.38) μm vs. (0.79±0.36) μm, (6.49±2.36) μm vs. (4.56±1.52) μm, (33.85±5.95) μm vs. (22.08±3.30) μm, P<0.05]. The deposition proportion of collagen fiber around airway and PAS staining area increased(5.85%±2.35% vs. 0.36%±0.12%, 28.81%±5.89% vs. 13.57%±2.08%, P<0.01). The mRNA and protein expression levels of YAP and OPN increased (P<0.05 or P<0.01), and the ratio of p-YAP/YAP and the mRNA and protein expression levels of SMMHC decreased (P<0.05 or P<0.01). Compared with experimental asthma group, the lung inflammation was reduced, and the thickness of bronchial basement membrane, ASM and airway wall were thinned in Vp intervention group [(0.93±0.27) μm, (4.99±1.75) μm,(26.59±2.76) μm, P<0.05]. The deposition proportion of collagen fiber around airway and PAS staining area decreased obviously(2.14%±0.89%, 17.92%±1.89%, P<0.05). The mRNA and protein expression levels of YAP and OPN decreased markedly (P<0.05 or P<0.01), and the ratio of p-YAP/YAP and the mRNA and protein expression levels of SMMHC increased (P<0.05). (2) Cell experiment: Compared with control group, the cell proliferation ability was higher (0.2874±0.0055 vs. 0.2626±0.0051, P<0.01)and apoptosis rate was lower in HDM group (5.14%±0.82% vs. 6.75%±0.21%, P<0.05). The protein expressions of YAP and OPN increased (3.14±0.48 vs. 1.51±0.61, 5.87±2.42 vs. 0.94±0.23, P<0.01), while of SMMHC decreased (0.80±0.19 vs. 2.96±0.96,P<0.01). Compared with HDM group, the cell proliferation ability reduced (0.2748±0.0043, P<0.05) and apoptosis rate increased(6.29%±0.49%, P<0.05), the protein expressions of YAP and OPN decreased (2.02±0.53, 2.93±1.09, P<0.05), while of SMMHC increased (2.11±0.85, P<0.05) in HDM+Vp group. Conclusions The abnormal expression of YAP may be involved in the airway remodeling in experimental asthma, and Vp may restrain the airway remodeling in experimental asthma by decreasing the YAP activity and nuclear shift, and reversing the HASMC phenotypic transformation.

Objective To prepare fibrin-targeted, integration of diagnosis and treatment and multi-functional gelatin nanoparticles, explore their potential of dual-mode imaging and the mechanism and effect of photothermal synergistic drug thrombolytic therapy in vitro, and observe the active-targeting ability of thrombus in vivo. Methods Loaded with alteplase (rt-PA)and Fe₃O₄ mediated by targeting fibrin polypeptide (Cys-Arg-Glu-Lys-Ala, CREKA), the magnetic gelatin nanoparticles (CREKA-Fe-rt-PA-Gel) were prepared by two-step desolvation and carbodiimide method. The morphology of CREKA-Fe-rt-PA-Gel was observed, and its physical and chemical properties and in vitro safety were detected. Its photoacoustic (PA) and magnetic resonance(MR) imaging features were also verified in vitro. The photothermal performance was monitored, the fibrin and hemoglobin indexes were used to evaluate the thrombolytic effect of photothermal therapy and the ability to damage fibrin network. Carotid artery thrombosis model was constructed with rats and HE staining section was performed to observe the targeting thrombus ability in vivo of the nanoparticles. Results CREKA-Fe-rt-PA-Gel were with uniform particle size, diameter of (254.79±6.83) nm, polydispersity coefficient of 0.09±0.05, surface potential of (5.48±4.60) mV. The CREKA peptide was successfully connected with the target connection rate of 98.66%, the encapsulation efficiency of rt-PA was 23.03%±0.05%, and of Fe₃O₄ was 92.78%±0.57%, the magnetization curve showed that it has good paramagnetism. The cytotoxicity and hemolysis test in vitro confirmed that CREKA-Fe-rt-PA-Gel had appropriate biological compatibility. At the same time, CREKA-Fe-rt-PA-Gel showed excellent imaging ability of PA and MR imaging in vitro. After laser irradiation, the nano solution heated up rapidly in a concentration-dependent manner,hemoglobin and fibrin in solution increased significantly after incubation with thrombus by near infrared irradiation (P<0.01), and nanoparticles released drugs combined with photothermal therapy could damage the fibrin network. HE staining of carotid artery thrombosis in rats showed good thrombus targeting ability of the nanoparticles in vivo. Conclusion The constructed CREKA-Fe-rt-PA-Gel have potential in dual-mode (PA/MR) imaging, good photothermal properties, outstanding targeting ability for thrombus(fibrin), and excellent thrombolytic ability when combined with photothermal, which is expected to be used in early diagnosis and multi-form treatment in clinical thrombotic diseases.

Objective To investigate the mechanism of artificial ulcer fibrosis of stenosis after full circumcision of esophageal mucosal dissection in porcine model based on TGF-β₁/Smads/ACTA2 signaling pathway. Methods A total of eight pigs were randomized into two groups (4 in each group): sham operation group and model group. Animals in the model group received full circumcision of ESD to establish the esophageal artificial ulcer fibrosis model. Three weeks after the surgery, we collected esophageal tissues from animals. We further analyzed the tissues with Hematoxylin-eosin (HE) staining to observe the pathological characteristics of esophageal tissues. The real-time quantitative polymerase chain reaction (qRT-PCR) was employed to detect the mRNA relative expression levels of TGF-β₁, Smad2, Smad3, and ACTA2. We then examined the positive expression of CTGF and ACTA2 using immunohistochemistry. Lastly, we detected the protein relative expression levels of TGF-β₁, Smad2/3,p-Smad2/3, Smad4, Smad7, CTGF, and ACTA2 using Western blotting. Results Compared with the sham operation group, the fibroblasts in the artificial ulcer site proliferated rapidly with a more transformed myofibroblast phenotype in the model group. In the model group, the qRT-PCR results showed up-regulated mRNA levels of TGF-β₁ (P<0.001), Smad3 (P=0.004), and ACTA2(P=0.001). The results of immunohistochemistry showed that the positive expression of CTGF (P<0.001) and ACTA2 (P<0.001)in the model group were higher than those in the sham operation group. We also observed up-regulated levels of TGF-β₁ (P=0.002),Smad2/3 (P=0.003), p-Smad2/3 (P=0.002), Smad4 (P<0.001), Smad7 (P=0.016), CTGF (P<0.001), and ACTA2 in the model group, compared with the sham operation group. Conclusion A porcine model of stenosis after full circumcision of esophageal mucosal dissection was successfully established, and the mechanism may be related to the artificial ulcer fibrosis by TGF-β₁/Smads/ACTA2 signaling pathway.

Objective To screen and validate the traditional Chinese medicine (TCM) monomer that may regulate adipocyte function and improve obesity. Methods Data sets GSE70353 and GSE72158 were downloaded from Gene Expression Omnibus(GEO) database. The former contains 770 men (45-73 years old) with different BMI corresponding gene expression in subcutaneous white adipose tissue (SAT), and the latter contains 42 women (before and 1 year after bariatric surgery) corresponding SAT. The differentially expressed genes (DEGs) of data sets GSE70353 and GSE72158 in GEO were analyzed with R language, and the co-expressed DEGs of the two data sets were screened. Functional annotation Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of co-expressed DEGs were conducted by R language,protein-protein interaction (PPI) network construction and the hub genes screening were completed by STRING database and Cytoscape software. Connectivity map (cMAP) was used to screen the TCMs that can regulate the hub gene. The bergenin (0, 0.4, 2,10 μmol/L) and ginkgolide A (0, 0.01, 0.1, 1 μmol/L) were selected to treat mature white adipocytes (WAT) induced by 3T3-L1 cells for 24 h. The mRNA levels of interleukin-6 (IL-6) and peroxisome proliferator-activated receptor γ (PPARγ) were detected by qRT-PCR. Results There were 64 co-expressed DEGs in the two data sets, GO and KEGG analysis showed that DEGs were enriched in immune cell chemotaxis, complement-related cascade activation, and various inflammatory signaling pathway, responding to nutrient and lipid protein. The 18 hub genes [APOB (up-regulated), ACP5, C1QB, C1QC, CCL2, CCND1, CD163, CD68, FCER1G, ITGB2,MMP9, MS4A6A, MS4A7, PLEK, SPP1, TNFRSF11B, TYROBP, VSIG4 (down-regulated)] were identified by Cytoscape. Twenty-eight TCMs that could regulate hub genes were screened by cMAP, and 22 of them showed the ability of improving obesity. Compared with the control group, the mRNA level of PPARγ decreased in 0.4 μmol/L bergenin group and 0.1 μmol/L ginkgolide A group(P<0.05), and IL-6 mRNA levels decreased in 0.4 μmol/L bergenin group, 10 μmol/L bergenin group and 0.1 μmol/L ginkgolide A group (P<0.05). Conclusion A total of 28 TCMs were screened, of which 22 TCMs have been proved to be able to improve obesity.It has been initially confirmed in present study that bergenin and ginkgolide A could regulate the function of adipocyte.

Objective To observe the effect of iron overload on the cardiac function of mice and cardiac myocytes ferroptosis of rats, and explore the mechanism of action of iron transporter receptor (TFRC) in cardiac myocytes ferroptosis of rats. Methods Fourteen C57BL/6J mice were randomly divided into normal-iron diet (NID) group and high-iron diet (HID)group (7 each), fed with normal diet or high-iron diet for 8 weeks, respectively. The mice cardiac function was then detected by echocardiography; The content of malondialdehyde (MDA) in the heart was detected with ELISA; Masson staining was performed to detect the cardiac fibrosis; Propidium iodide (PI) staining and lipophilic fluorescent dye (C11) were used to detect the cell mortality and the content of lipid peroxide. The effect was observed of ferric ammonium citrate (AIC) and ferroptosis inhibitor ferrostatin-1 (Fer-1) on the cardiac myocytes of H9C2 rat. H9C2 cells were treated with AIC and ferroptosis inducer Erastin,Western blotting was performed to detect the expression level of TFRC and glutathione peroxidase 4 (GPX4) protein, qRT-PCR was used to detect the mRNA level; at the same condition, small interfering RNA was applied to knock-down the expression of TFRC,detect the mortality of H9C2 cells and the content of lipid peroxide. Results Compared with mice in NID group, the mice in HID group showed obviously increased interventricular septal thickness (IVSd), left ventricular posterior wall thickness (LVPWd), MDA relative content and area of collagen deposition (0.96±0.12 vs. 0.73±0.09, 1.18±0.28 vs. 0.84±0.07, 2.08±0.8 vs. 1.00±0.50,4.04±0.60 vs. 1.00±0.21, P<0.05); But no significant difference between the two groups on left ventricular ejection fraction and shortening fraction. Treated with 500 μmol/L AIC, the death rate and lipid peroxide content of H9C2 increased obviously(33.73%±1.20% vs. 2.30%±1.73%, 5.36±0.06 vs. 1.00±0.19, P<0.05), while after treatment with Fer-1, the death rate and lipid peroxide content of H9C2 decreased markedly (19.63%±0.81% vs. 33.73%±1.20%, 2.03±0.12 vs. 5.36±0.06, P<0.05). Treated with 500 μmol/L AIC, the expression level increased obviously of TFRC in H9C2 cell (P<0.05), while knocked-down of TFRC, the cell death rate and the content of lipid peroxide induced by high-iron decreased markedly (P<0.05). Under inducement of Erastin,the expression levels of TFRC and GPX4 protein in H9C2 cells obviously up- and down-regulated, respectively; and after knocked-down of TFRC, the cell death rate induced by Erastin decreased markedly (P<0.05). Conclusions HID may induce the damage of myocardial ferroptosis, and TFRC participated in the pathologic process induced by iron overload, which may be as a new target point for the treatment of heart diseases.

Objective To study the effect of Fritillaria cirrhosae bulbus on ovalbumin (OVA)-sensitized asthmatic mice and its mechanism. Methods We set up the study including a blank control group, OVA model group (intraperitoneal injection of 0.2 mg OVA to induce sensitization), dexamethasone group (after successful modeling, intraperitoneal injection of 0.5 mg/kg dexamethasone), and Fritillaria cirrhosae bulbus low, medium and high dose groups (after successful modeling, gavage 7.0 mg/kg,14.0 mg/kg, 21.0 mg/kg Fritillaria cirrhosae bulbus), once a day for 4 weeks, with 10 mice in each group (total=60 BALB/c mice).After drug administration, we measured the amount of phenol red excretion in the airway and collected the bronchoalveolar lavage fluid (BALF) to determine the content of brain-derived neurotrophic factor (BDNF) and the number of inflammatory cells. We also took the blood samples through eyeballs followed by quantifying the concentration of serum immunoglobulin E (IgE), interleukin-4(IL-4), IL-13, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) using ELISA. We further collected the lung tissues and detected the mRNA and protein expressions of Janus kinase 3 (JAK3), signal transducer and activator of transcription 6 (STAT6),and IL-4 by RT-qPCR and Western blotting. Results Compared with the blank control group, the level of phenol red in the airway of the OVA model group reduced significantly, the content of BDNF as well as the number of inflammatory cells in BALF increased significantly, the contents of IgE, IL-4, IL-13, and TNF-α in serum were significantly elevated, the concentration of IFN-γ and IFN-γ/IL-4 ratio decreased significantly, the relative expression levels of JAK3, STAT6, IL-4 mRNA and p-JAK3/JAK3, p-STAT6/STAT6, and IL-4 protein in lung tissue increased significantly (P<0.05). Compared with the OVA model group, the above indexes were all significantly improved in each dose of the Fritillaria cirrhosae bulbus groups, and the high Fritillaria cirrhosae bulbus dose group had the best index (P<0.05). Conclusion The mechanism of Fritillaria cirrhosae bulbus regulating airway and lung inflammation in asthmatic mice may be related to inhibiting the activation of JAK3/STAT6 signal pathway.

Objective To investigate the influencing factors for prognosis in non-severe (mild to moderate) pulmonary acute respiratory distress syndrome (ARDS) patients, and evaluate the efficacy of the risk factors to predict the prognosis. Methods The data of 123 patients with non-severe pulmonary ARDS, hospitalized in the Department of Respiratory and Critical Care Medicine of Beijing Chaoyang Hospital (West Campus) from January 2017 to June 2021, were retrospectively enrolled, and divided into two groups according to 30-day survival condition, i.e., non-survivor group (n=45) and survivor group (n=78). Baseline characteristics, complications, arterial blood gas, blood routine, and levels of fibrinogen, C-reactive protein (CRP), procalcitonin,albumin and brain natriuretic peptide (BNP) were compared between the two groups. Kaplan-Meier and Cox survival analysis were adopted to analyze the risk factors which could affect the survival situation of patients with non-severe pulmonary ARDS.ROC curves were used to assess the efficacy of the risk factors to predict prognosis. Results Compared with survivor group, the proportion of patients with renal insufficiency, deep venous thrombosis and shock, APACHE Ⅱ score, body temperature, respiratory rate, neutrophil to lymphocyte ratio (NLR), fibrinogen and CRP levels in non-survivor group increased, and arterial partial pressure of carbon dioxide (PaCO₂), platelet count and albumin levels decreased (P<0.05). Kaplan-Meier survival analysis showed that kidney failure, deep venous thrombosis and shock were the risk factors of 30-day death in patients with non-severe pulmonary ARDS (P<0.05). Univariate Cox analysis demonstrated that heart rate, temperature, respiratory rate, PaCO₂, NLR, WBC, platelet count, fibrinogen, CRP, albumin and APACHE Ⅱ score were the risk factors of 30-day death in patients with non-severe pulmonary ARDS (P<0.05). Multivariate Cox analysis showed that higher APACHE Ⅱ score (HR=1.094, 95%CI 1.009-1.120, P=0.031), higher NLR (HR=1.087, 95%CI 1.012-1.167, P=0.021) and the presence of shock presented during course (HR=3.135, 95%CI 1.315-6.964, P=0.010) were independent risk factors for 30-day death of patients with non-severe pulmonary ARDS. The cut-off value of APACHE Ⅱ score and NLR in predicting mortality were 16.5 and 8.13, and the area under the curve (AUC) were 0.803 (95%CI 0.727-0.879) and 0.772 (95%CI 0.688-0.856), respectively. Conclusions APACHE Ⅱ score >16.5, NLR >8.13 and presence of shock were the independent risk factors of mortality for patients with non-severe pulmonary ARDS, and these factors could effectively predict prognosis.

Objective To screen the risk factors of preeclampsia and construct the predictive model of preeclampsia based on machine learning algorithm. Methods A retrospective study was conducted to collect the clinical data of 1609 hospitalized pregnant women from January 2016 to December 2018 on the big data platform of Academy of Medical Data Science of Chongqing Medical University. The 1609 cases were divided into preeclampsia group (n=291) and non-preeclampsia group (n=1318) according to the occurrence of preeclampsia during hospitalization. The clinical data of 70% patients were randomly selected as the training set (n=1126) to construct the prediction model, and the remaining 30% were used as the test set (n=483) for verification, and a consistency check between training set and test set was performed. The independent risk factors were screened by univariate analysis and logistic regression analysis, and the optimal parameters of LightGBM algorithm were searched by 5-fold cross-validation algorithm, and the prediction model was constructed based on LightGBM machine learning algorithm. Results A total of 58 indicators were collected, 13 indicators with missing rate ≥30% were excluded, and 45 indicators were finally included. Significant differences of 35 indicators existed between preeclampsia group and non-preeclampsia group (P<0.05) such as gamma-glutamyl transferase (GGT), alanine aminotrans ferase (ALT), thrombin time, aspartase transaminase (AST) and specific gravity of urine.Logistic regression analysis showed that specific gravity of urine, uric acid, hemoglobin concentration of erythrocyte, globulin, platelet distribution width, potassium ion, visiting age, family history of hypertension, systolic blood pressure, diastolic blood pressure,pulse and gestational age ≥34 weeks were independent risk factors for preeclampsia. The results of 5-fold cross-validation showed that, when num_leaves=5, max_depth=3, min_data_in_leaf=91, feature_fraction=0.8, bagging_fraction=0.6, and bagging_freq=5,the LightGBM model achieved the best effect the area under the curve (AUC), sensitivity and specificity of LightGBM model were 0.964, 84.9% and 92.7%. Conclusion The prediction model of preeclampsia based on LightGBM machine learning algorithm has a higher prediction effect, which can effectively predict the occurrence of preeclampsia in pregnant women in Chongqing, and provide decisions for clinicians.

Objective To explore the mutation status of KRAS, NRAS, PIK3CA, and BRAF, and the relations with clinicopathological features and hormone expression levels in ovarian low-grade serous tumors. Methods Tissue specimens (23 cases of common-type serous borderline tumor, 27 cases of micropapillary serous borderline tumor and 14 cases of low-grade serous carcinoma) were collected from the First People's Hospital of Yunnan Province during January 2017 to April 2021, and then retrospectively analyzed. The mutation status of human KRAS, NRAS, PIK3CA and BRAF genes were detected by expression status in tumor tissues was detected by immunohistochemistry, the relationship was analyzed between gene mutation status and clinicopathological features and hormone expression levels. Results A total of 36 mutations were detected in 64 tumor tissues,including 21 KRAS mutation, 12 BRAF mutation, 2 PIK3CA mutation and 1 NRAS mutation. KRAS and BRAF mutations were common in younger women ≤35 years old. In the KRAS mutant subtype, G12S and G12D mutations are common in micropapillary serous borderline tumor (P<0.05); G12C, G12R*, G12V, G12A, and G13C* mutations are common in common-type serous borderline tumor (P<0.05); G13D mutation was only detected in low-grade serous carcinoma. Patients with BRAF mutations were all seen in the early stages of the disease. Immunohistochemistry showed the positive expression rates of both estrogen receptor and progesterone receptor were 76.6% (49/64). The positive expression rate of common-type serous borderline tumor was similar to that of micropapillary serous borderline tumor, and both of them were significantly higher than that in lower-grade serous carcinoma(P<0.05). KRAS G13D mutation was significantly associated with low progesterone expression (P<0.05). Conclusion Gene mutations were mutual exclusion. KRAS mutation was an oncogenic driving factor in serous tumors, and different mutant subtypes were associated with histological type and progesterone receptor expression status. As the disease progresses, BRAF mutation rate gradually decreased and associated with a variety of clinicopathological features and good prognosis and might have a protective effect against disease progression. The mutation rates of NRAS and PIK3CA were lower.

Objective To report a case of gastric ulcer associated with cytomegalovirus (CMV) infection in immunocompetent for improving the clinical recognition of the disease. Methods A 69-year-old patient with gastric ulcer caused by CMV infection was admitted to the 900th Hospital of the Joint Logistics Team on August 10, 2020. Biopsies were performed at the gastric ulcer and biopsy gastric mucosa samples were measured by hematoxylin-eosin (HE) staining and immunohistochemistry.The microscopic characteristics of the mucosal tissues, diagnosis and treatment experience of this case were analyzed and summarized. A literature review about CMV infection in gastric in inmmunocompetent patients was performed using PubMed search from database inception to July 2021. Results A total of 20 literatures were retrieved, involving 57 patients. A total of 58 patients were included in this article, including 39 males (67.2%) and 19 females (32.8%), with a ratio of men to women of 2.05:1. The average onset age of male was (52.4±16.0) years old, while (72.3±17.7) years old in female. The overwhelming majority of those patients were complicated with hypertension or type 2 diabetes mellitus. The most common symptoms were upper abdominal pain and gastrointestinal bleeding. The antrum of stomach was the most frequently affected site in gastric CMV disease, isolated gastric ulcer and multiple mucosal erosion were the main endoscopic appearance. CMV inclusion bodies were found either at the ulcer base or at the ulcer edges. There were 51.1% (24/47) of the patients treated with ganciclovir. However, 48.9% (23/47) of the patients were cured by symptomatic treatment. Conclusions On no consideration can clinically ignore CMV gastritis in adults without apparent immunosuppression when the symptoms as hematemesis, melena, and abdominal pain occur and antral gastric ulcer or multiple mucosal inflammation is seen endoscopically. Biopsies for CMV related tests, especially for pathological examination or histopathologic diagnosis are recommended. Antiviral therapy in people with clinical risk factors is essential for management of gastric CMV disease.

Vascular complications of type 2 diabetes mellitus (T2DM) include macrovascular complications and microvascular complications, of which the increased incidence is often accompanied with a high incidence of obesity. Obesity is an independent risk factor for T2DM. In obese patients, body fat distribution rather than total body fat is associated with metabolic and cardiovascular risk. Body mass index (BMI) and waist circumference (WC) cannot accurately reflect body fat distribution in obese patients, so visceral fat has received more and more attention and may be as a related risk factor for vascular complications in T2DM.The research progress on the relationship between visceral fat and vascular complications of T2DM and its action mechanism have been reviewed in present paper, in order to provide a reference for in-depth research and clinical examination of visceral fat.

The incidence and mortality of malignant tumors are gradually increasing all the world, and the existing diagnosis and treatment methods still can not effectively block the occurrence and development of tumors. Some studies have found that cancer stem cells (CSCs) are the cells of tumor origin, and closely related to the occurrence, development and metastasis of tumors.Early detection and intervention with effective treatment of CSCs are expected to prevent the occurrence and development of tumors. Many studies have shown that the activation of Wnt/β-catenin signaling pathway is an important link in the initiation of CSCs and the formation of tumors. Therefore, by regulating the key upstream and downstream factors of the Wnt/β-catenin pathway in CSCs, thereby regulating the activity of the Wnt/β-catenin signaling pathway, controlling tumor growth and metastasis,can provide new targets and directions for the treatment and prevention of malignant tumors. The key role of Wnt/β-catenin signal pathway in CSCs, and the related mechanisms of the important factors of the pathway in regulating the tumor growth, development and metastasis of CSCs in different organs are reviewed in present paper.

Small cell lung cancer (SCLC) is an aggressive malignancy with a 5-year survival rate of 7.2%, which is characterized by exceptionally high proliferation rate, early metastasis, and poor prognosis. In the face of DNA damage and replicative stress, the DNA damage response (DDR) elicits activation of cell cycle checkpoints to promote repair by pausing the cell cycle or, in cases of unrepairable DNA damage, stimulate programmed cell death. SCLC carries a high mutation burden and genomic instability, and almost all SCLC tumors have functional inactivation of both TP53 and RB1, which leads to the form of a dysfunctional G₁/S checkpoint and results in an increased reliance on subsequent cell cycle checkpoints (S, G₂/M) to ensure genome stability and correct chromosomal segregation. Therefore, under the use of radio-chemotherapy for DNA damaging, promoting the cell cycle progress by inhibiting the cycle checkpoints and increasing DNA damage by inhibiting DNA damage repair can be new strategies for targeted therapies in SCLC. In the present article, we review the advances of targeting DDR and it's pathway inhibitors in SCLC, and provide some thoughts for the targeted treatment strategies of SCLC.

Artificial intelligence has made breakthroughs in medicine in the past decade. Compared with the traditional statistical model, the advantage of artificial intelligence is that it can establish algorithm and prediction model through machine learning to efficiently and effectively identify the patterns in large data sets, and combine a variety of factors to create more accurate prediction model. Therefore, artificial intelligence is particularly suitable for huge and complex or high-dimensional clinical data analysis and predictive modeling tasks. There are many kinds of data formats in the clinical practice of hepatology. Many studies have applied artificial intelligence in the diagnosis and classification of liver diseases, assisting treatment, predicting efficacy and prognosis, and evaluation of liver imaging and pathology. Based on the study outcomes in related fields at home and aboard, this paper summarizes the research progress and application of artificial intelligence in the field of diagnosis and treatment of chronic liver diseases.