Objective To explore the risk factors of thrombotic events in trauma patients by using random forest algorithm. Methods The data of 255 trauma patients admitted to the intensive care unit from July 2016 to December 2021 were retrospectively analyzed. These patients were divided into thrombosis group and non-thrombosis group by propensity score matching and according to the occurrence of thrombosis after trauma. The risk factors of 24 clinical variables including age, gender, injury severity score (ISS), acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ), white blood cell count, red blood cell count, platelet count, hemoglobin, alanine aminotransferase, aspartate aminotransferase, total bilirubin, creatinine, total protein, prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, fibrin degradation products, D-dimer, antithrombin 3, coagulation reaction time (CRT), clot formation rate, clot formation kinetics and maximum clot strength (maximal amplitude, MA) within 2 hours after admission were analyzed by random forest algorithm. The predictive values of the variables were evaluated by receiver operating characteristic (ROC) curve and verified by bootstrap method. Results One hundred and ten trauma patients were divided into thrombosis group (n=22) and non-thrombosis group (n=88) by propensity score matching. The results of random forest algorithms showed that high MA level was an important risk factor for thrombotic events after trauma(P<0.05). The area under ROC curve (AUC) of using MA value to predict thrombotic events in trauma patients was 0.70 (95%CI 0.56-0.81, P<0.01), and the bootstrap method confirmed that the AUC of using MA value to predict thrombotic events in trauma patients was 0.70 (95%CI 0.57-0.80, P<0.01). When the cut-off value of MA was 63.3 mm, the sensitivity and specificity of the trauma patients suffering thrombotic events were 63.6% and 78.4%, respectively. Conclusion The high MA level is an important risk factor for thrombotic events in trauma patients.

Objective To summarize the clinical features, diagnosing and treating passes of a case of primary ciliary dyskinesia (PCD) in newborns, and by literature review to increase awareness of PCD. Methods The clinical data of an infant patient, admitted in Children's Hospital Affiliated to Chongqing Medical University and diagnosed as PCD, was collected and retrospectively analyzed. CNKI, Wanfang, PubMed, Cochrane Library and Online Mendelian Inheritance in Man (OMIM) were searched, eligible literature was analyzed. Results A term female infant aged 1 month and 13 days was admitted to the hospital with 1-month history of cyanosis and 3-week of cough and wheeze, which aggravated 3 days prior to admission. She developed cyanosis on postnatal day 1, then cough and wheeze gradually. Her symptoms deteriorated due to pneumonia, non-invasive ventilation was performed, and continued CO₂ retention existed. Hypercapnia and oxygen dependence were found throughout the hospital stay even after clinical improvement. Whole exon sequencing test revealed DNAH1 compound heterozygous mutation in this patient, which leaded to the diagnosis of PCD. A total of 9 papers of neonatal respiratory distress caused by PCD were retrieved. All 12 patients in those papers were term infants, presented with varying degree of respiratory distress, which mainly manifested as tachypnea, retractions, elevated work of breath, cyanosis, hypoxemia, oxygen dependence. Of the 12 patients, 8 (66.7%) had situs inversus viscerum, 6 (50.0%) had atelectasis, 6 (50.0%) needed non-invasive or invasive ventilation. A total of 3 papers of PCD caused by DNAH1 mutation with 9 patients were retrieved. Of these patients, 7 were diagnosed in childhood and 2 in adulthood. The main clinical manifestations were Kartagener syndrome (55.5%), bronchiectasis (33.3%), atelectasis (22.2%), post-infectious bronchiolitis obliterans (33.3%), neonatal respiratory distress (11.1%), and female infertility (11.1%). Conclusions The clinical features of PCD in neonates are mainly unexplained respiratory distress, higher incidence of situs inversus viscerum and atelectasis, and the demand for respiratory support is high. Raising awareness of the clinical features of PCD in infants is helpful for early diagnosis and intervention.

Objective By literature review to retrospectively study the clinical characteristics, diagnosis and treatment process, and prognosis of anti-melanoma differentiation associated gene 5 (MDA5) autoantibody-positive dermatomyositis-associated with interstitial lung disease (ILD) treated with tofacitinib (TOF), so as to improve the understanding of the disease. Methods Retrospectively analyze the clinical and laboratory characteristics, imaging findings and adverse reactions before and after TOF treatment in seven patients who admitted to the First Medical Center of Chinese PLA General Hospital from January 2018 to October 2021. Thirty-six cases were found by searching databases to summarize the efficacy and safety of TOF in treating patients with anti-MDA5 autoantibody-positive dermatomyositis-associated ILD. Results Of the 7 patients, 5 were female and 2 were male with mean age of 50(30-64) years, the mean disease duration was 3(1-36) months, and the mean follow-up time was 12(1-35) months. Of them, 4 received previously the other immunosuppressive therapy, and 3 were newly treated. One patient died, and the remaining 6 patients were in relatively stable condition and maintenance treatment. One patient experienced fungal infection in the 18th month after TOF treatment. A total of 36 cases of anti-MDA5 autoantibody-positive dermatomyositis have been reported in databases. Clinical symptoms, laboratory tests and imaging findings were all improved after TOF therapy. Opportunistic infection occurred in 9(25%) cases after application of TOF. Conclusion Application of TOF is an effective and safe regimen in treatment of anti-MDA5 autoantibody-positive dermatomyositis-associated ILD, while attention should be paid for monitoring the opportunistic infection during treatment.

Intestinal tract is the largest immune organ of human body where hundreds of millions of microorganisms are colonized which are called intestinal flora. Each intestinal flora checks and balances each other, depends on and complements each other, and forms a mutually beneficial symbiotic relationship with the host. Changes in quantity and type of intestinal flora will cause the imbalance of intestinal microecology, affect the systemic immune function through immune regulation, and then affect the progress of the disease. At present, it has been found that intestinal microecology is closely related to rheumatic immune diseases such as systemic lupus erythematosus, ankylosing spondylitis, gouty arthritis and rheumatoid arthritis. Taking intestinal flora as the starting point to explore the pathogenesis of gout has become a new research hotspot. Based on the current research, the relevant literature was consulted in present paper, and the intestinal microecological composition and function, the structural characteristics of intestinal flora in patients with gout, the mechanism of intestinal flora in the pathogenesis of gout, and the treatment of probiotics, traditional Chinese medicine and fecal microbial transplantation were reviewed, in order to provide new ideas and directions for prevention and treatment of gout in the future.

Malocclusion seriously affect oral health and general health of patients, and keep a high prevalence remaining for many years. Orthodontics is an effective treatment. It is reported that osteogenesis by drag reduction distraction of the periodontal ligament can safely and efficiently accelerate the movement of orthodontic tooth, so might be used to solve some difficult problems caused by traditional correcting methods which took a long treatment duration, increased the risk of dental caries, periodontitis and root resorption. However, periodontal ligament distraction (PDLD) has not been widely used in clinical practice due to large force, inconvenient exertion, and poor comfort of patients. With the rapid development of high-throughput sequencing technology, more mechanical force-sensitive genes, non-coding RNA and lncRNAs/circRNA-miRNAs-mRNAs regulatory network maps involved in regulation have been found. At the same time, the research and development of accurate measurement and control and automatic distraction devices have also made great progress, which can gradually overcome the technical defects of PDLD in the past. A variety of new automatic distraction devices such as motor system, hydraulic system, shape memory alloy and piezoelectric motor have been developed, which have achieved encouraging results in animal experiments and clinical trials. Therefore, PDLD has made rapid progress in minimally invasive and automated aspects. The previous studies addressing the development history, important technical parameters, molecular biological mechanism, histological characteristics, technical advantages and innovation of PDLD have been reviewed in present article, in order to make a comprehensive summary of the latest progress in research and provide reference for accelerating the technical innovation and clinical application of orthodontic tooth movement.

Vesicovaginal fistula (VVF) is an abnormal anatomical structure formed between the bladder and vagina, which usually occurs after gyneco-obstetric or pelvic surgery. VVF is one of the most common female genitourinary fistulas, causing serious distress to patients' physical and mental health and the quality of life. At present, the majority of VVF patients have poor outcomes in conservative therapy such as continuous bladder drainage and electrocoagulation, surgical repair is the main treatment option. The traditional surgical methods include transvaginal repair and transabdominal open repair. In recent years, with the development of minimally invasive techniques such as laparoscopic/robot-assisted laparoscopic surgery, the selection of VVF repair procedures has become more diverse, and the safety and efficacy of the operation have been continuously improved. However, there is no uniform standard for the timing and optimal surgical method for VVF repair. This article reviews the current progress in the treatment of VVF, and provides a reference for surgeons to formulate the optimal options for individual differences.

Antithrombotic drugs are important means to prevent and treat thrombotic diseases. With the wider use of antithrombotic drugs, the incidence of antithrombotic drug-related bleeding has increased year by year. Anticoagulant drugs, antiplatelet drugs and thrombolytic drugs can all cause subcutaneous hemorrhage, gastrointestinal hemorrhage and even intracranial hemorrhage, resulting in death or disability. Therefore, the Chinese Society of Thrombosis, Hemostasis and Critical Care organized multidisciplinary experts to jointly write this specification to help clinicians regulate the treatment of antithrombotic drug-related bleeding. This specification includes four parts: antithrombotic drug monitoring, bleeding evaluation, reversal treatment and restart of antithrombotic treatment.

Objective To explore the phenotypes of erythroblastic island-like (EBI-like) macrophages during erythroid differentiation from human embryonic stem cells in vitro and the function of EBI-like macrophages in the differentiation of erythroid. Methods To study the function of EBI- like macrophages in the differentiation of erythroid, we used the Spin-EB method to induce human embryonic stem cells (hESCs) to differentiate into red blood cells. The expression of specific surface markers of erythrocytes and macrophages and the cell morphology were tested by flow cytometry and imaging flow cytometry. Multiple gene expressions were detected by qRT-PCR. An immunofluorescence assay was used to identify the phenotype of EBI-like macrophages. Results Erythroid cells were induced by embryonic stem cells in vitro. Giemsa staining revealed that EBI-like structures derived from the hESCs were similar to natural EBI. Immunofluorescence staining confirmed that the erythroid cells (CD235a) were surrounded by macrophages (CD68); CD45⁺CD235a⁺CD163⁺CD169⁺CD106⁺ EBI-like macrophage (0.092%±0.013%) resembles in vivo EBI macrophage. Imaging flow cytometry observed that CD45⁺CD235a⁺CD163⁺CD106⁺CD169⁺ EBI-like macrophages were surrounded by CD235a⁺ erythroid cells. The proportion of induced CD71⁺CD235a⁺ cells was 37.37%±1.68% after removing the EBI structure, which was significantly lower than the untreated group (46.97%±4.16%). We found that central macrophages of EBI-like may play a role in promoting erythroid differentiation through the interaction of CD169 and CD43. Conclusions EBI-like structure in the erythroid induction system of hESCs is similar to the natural EBI. The central EBI-like macrophages maybe promote the differentiation of erythrocytes in vitro through the interaction of CD169 and CD43. We provided a theoretical and practical reference for optimizing the erythroid induction system in vitro.

Objective To explore the molecular mechanism of a classic traditional Chinese medicine compatibility combination of Astragalus membranaceus (A.m) and Angelica sinensis (A.s) in treatment of diabetes mellitus with cardiovascular complications. Methods The BATMAN database was used to analyze A.m and A.s respectively. The chips data related to diabetes mellitus with cardiovascular complications were retrieved from GEO database. The differential genes were analyzed by GEO2R to construct the protein-protein interaction (PPI) network, and the key target genes of A.m-A.s were obtained by topology, and DAVID database was used for gene ontology (GO) and KEGG pathway enrichment analysis of key genes. A total of 20 SD rats were randomly divided into healthy control group, diabetes mellitus complicated with cardiovascular complications group, metformin group, and A.m-A.s group (5 each). All the rats except those in HC group were fed with high fat and high sugar feeds, and used to establish the model of diabetes mellitus with cardiovascular complications. The expressions of PI3K and Akt3 in cardiomyocytes of the rats in each group were observed. Results (1) A total of 1332 target genes related to A.m-A.s combination were analysis obtained from BATMAN database, and 3 chip data files related to diabetes with cardiovascular diseases (GSE26887, GSE43950 and GSE46262)were retrieved from GEO database including 2759 differential genes screened by GEO2R analysis and 247 key genes of A.m-A.s combination in treatment of diabetes mellitus with cardiovascular complications. (2) The protein-protein interaction (PPI) network diagram of key targets was constructed by STRING database, and the "A.m-A.s- active ingredients-targets" network was constructed by Cytoscape 3.7.2. The functional enrichment analysis with DAVID database showed that the biological process of A.m-A.s in treatment of diabetes mellitus and cardiovascular complications was mainly concentrated in positive and negative regulation of RNA polymerase II promoter transcription, redox process, signal transduction, apoptosis process, inflammatory reaction, and positive regulation of cell proliferation, etc. The signaling pathways mainly include metabolic pathway, cancer pathway, TNF signaling pathway, cAMP signaling pathway, cGMP-PKG signaling pathway, PI3K-Akt signaling pathway, non-alcoholic fatty liver disease pathway, and insulin resistance pathway and so on. (3) The animal model experiment with SD rats in vivo of A.m-A.s combination in treatment of diabetes mellitus with cardiovascular complications suggested that, compared with healthy control group, the expressions of PI3K and Akt3 decreased in cardiomyocytes of the untreated model group, and the difference was statistically significant (P<0.05, P<0.01); the expressions of PI3K in the treatment groups were higher than that in the model group, but lower than that in the healthy control group, and the difference was statistically significant (P<0.01). Conclusion The characteristics of A.m-A.s combination in treatment of diabetes mellitus with cardiovascular complications are "multi-components, multi-targets and multi-pathways", and multiple key genes and signal pathways can play important roles. Further research is expected to broaden the ideas of diagnosis and treatments of diabetes with traditional Chinese medicine.

Objective To explore the effect and mechanism of silybin on improving pulmonary fibrosis and oxidative stress in mice. Methods A total of 120 mice were randomly divided into sham operation group, lung injury model group, dexamethasone group, low-dose, medium-dose and high-dose silybin groups (20 mice each). The models of pulmonary injury mice were induced by bleomycin. Mice in dexamethasone group, low-, medium- and high-dose silybin groups were given intragastric administration of dexamethasone (3 mg/kg) and silybin (120, 240, 480 mg/kg), while sham operation group and lung injury model group were given the same volume of normal saline for 28 d. The bronchoalveolar lavage fluid (BALF) and pulmonary tissues of each group were collected. The count of inflammatory cells in BALF was examined by microscopy. The pathological damage of pulmonary tissues was observed by HE staining. The pulmonary wet/dry weight ratio (W/D) was detected by wet-dry weighting method. The content of hydroxyproline (HYP) in pulmonary tissues, and levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β in BALF were detected by ELISA. The expressions of bone morphogenetic protein 9 (BMP9)/bone morphogenetic protein receptor 2(BMPR2)/SMAD signaling pathways-related proteins were detected by Western blotting. Results Compared with sham operation group, count of BALF inflammatory cells, scores of pulmonary injury and fibrosis, W/D, HYP, and MDA, TNF-α, IL-1β and IL-6 levels in BALF increased significantly, while SOD, GSH-Px activity, T-AOC levels in BALF, as well as the relative expression levels of BMP9, BMPR2 and p-SMAD1/5/9 in lung tissues decreased significantly in lung injury model group (P<0.05). Compared with lung injury model group, count of BALF inflammatory cells, scores of pulmonary injury and fibrosis, W/D, HYP, and MDA, TNF-α,IL-1β and IL-6 levels in BALF decreased significantly, while SOD, GSH-Px activity, T-AOC level in BALF, and BMP9, BMPR2 and p-SMAD1/5/9 expression levels in lung tissues increased significantly in high-dose silybin group and dexamethasone group(P<0.05). Conclusion The silybin may improve bleomycin-induced pulmonary fibrosis and oxidative stress in lung injury mice by mediating BMP9/SMAD signaling pathways, and thereby repairing pulmonary injury.