Stroke is the main cause of death and disability among adults in China and is characterized by high incidence， disability， mortality， and recurrence rates. The combination of traditional Chinese and Western medicine has great potential in treating stroke and its sequelae. The classic traditional Chinese medicine prescription Da Chengqitang （DCQT） has a long history and proven efficacy in treating stroke. Clinically， DCQT is often used to treat stroke and its sequelae. However， the number and quality of clinical trials of DCQT in treating stroke need to be improved. Because of the insufficient basic research， the active ingredients and multi-target mechanism of action of DCQT remain unclear. Our research group has previously confirmed that DCQT can effectively reverse neurological damage， reduce iron deposition， and downregulate the levels of pro-inflammatory cytokines in the rat model of hemorrhagic stroke. The treatment mechanism is related to the nuclear factor erythroid 2-related factor 2 （Nrf2）-mediated signaling pathway and p38 mitogen-activated protein kinase （MAPK） signaling-mediated microglia activation. To clarify the pharmacodynamic basis and anti-stroke mechanism of DCQT， this article reviews the research progress in the treatment of stroke with DCQT in terms of clinical trials， pharmacodynamic material basis， safety evaluation， and mechanisms of absorbed components. This article summarizes 45 major phytochemical components of DCQT， 11 of which are currently confirmed absorbed components. Among them， emodin， rhein， chrysophanol， aloe-emodin， synephrine， hesperidin， naringin， magnolol， and honokiol can be used as quality markers （Q-markers） of DCQT. The mechanism of DCQT in treating stroke is complex， involving regulation of inflammatory responses， neuronal damage， oxidative stress， blood-brain barrier， brain-derived neurotrophic factor， and anti-platelet aggregation. This article helps to deeply understand the pharmacodynamic basis and mechanism of DCQT in treating stroke and provides a theoretical basis for the clinical application of DCQT in treating stroke and the development of stroke drugs.

Background: To enhance perioperative outcomes, a perioperative registry that integrates high-quality real-world data throughout the perioperative period is essential. Singapore General Hospital established the Perioperative and Anesthesia Subject Area Registry (PASAR) to unify data from the preoperative, intraoperative, and postoperative stages. This study presents the methodology employed to create this database. Methods: Since 2016, data from surgical patients have been collected from the hospital electronic medical record systems, de-identified, and stored securely in compliance with privacy and data protection laws. As a representative sample, data from initiation in 2016 to December 2022 were collected. Results: As of December 2022, PASAR data comprise 26 tables, encompassing 153,312 patient admissions and 168,977 operation sessions. For this period, the median age of the patients was 60.0 years, sex distribution was balanced, and the majority were Chinese. Hypertension and cardiovascular comorbidities were also prevalent. Information including operation type and time, intensive care unit (ICU) length of stay, and 30-day and 1-year mortality rates were collected. Emergency surgeries resulted in longer ICU stays, but shorter operation times than elective surgeries. Conclusions The PASAR provides a comprehensive and automated approach to gathering high-quality perioperative patient data.

In recent years， the field of network pharmacology （NP） has developed rapidly， but the flawed and routine workflow has seriously affected the scientificity and reliability of NP analysis results. For complex diseases caused by environmental and genetic factors， symptomatic treatment or drugs targeting a single pathophysiological process cannot prevent or delay the progression of the disease， so the drug development fails or withdraws from the market. Therefore， there is an urgent need to develop new ideas for NP analysis that combines multiple pathophysiological processes. The key pathophysiological process is an important and complete set of pathological changes in the process of the occurrence， development， and outcome of the disease， which represents the current comprehensive and profound understanding of the nature of the disease. In order to improve the quality of NP research and promote the healthy development of the NP field， this paper proposes a new idea of NP analysis based on key pathophysiological processes. Based on the long-term clinical practice of traditional Chinese medicine and the key pathophysiological process of the disease， the method comprehensively analyzes the pharmacological mechanism and active ingredients of traditional Chinese medicine compound from the perspective of key pathophysiological process， which increases the scientifically， reliability， and repeatability of the analysis results. This paper takes Alzheimer's disease （AD） as an example to illustrate the necessity， feasibility， main workflow， advantages， and disadvantages of this method， and it is expected to screen disease-modifying drugs that prevent or reverse the course of the disease and promote the clinical transformation of research results.

Nasopharyngeal carcinoma is one of the most common malignant head and neck tumors, and radiotherapy is the main treatment. However, radio-resistance is a key cause of local recurrence of nasopharyngeal carcinoma. Therefore, overcoming the radio-resistance of nasopharyngeal carcinoma and enhancing the radiosensitivity have become urgent problems in the treatment of nasopharyngeal carcinoma, which also play a key role in improving the overall survival rate of patients. In this article, recent studies on DNA, non-coding RNA (ncRNA), protein and cell behaviors related to radio-resistance of nasopharyngeal carcinoma were reviewed, aiming to provide valuable ideas for clinical treatment of nasopharyngeal carcinoma.

Objective To study the protective effect and mechanism of adenosine A2a receptor(A2aR)activation in the pathogenesis of systemic sclerosis associated interstitial lung disease(SSc-ILD).Methods A total of 24 healthy female Balb/c mice were randomly divided into three groups:wild normal control(WN)group,wild model(WM)group,WM with CGS21680(WMC)group.Two weeks after the end of injections,the lung samples and serum of mice were collected.A part of lung tissues were obtained for hematoxylin eosinstaining,Masson staining and determination of hydroxyprolineto observe the degree of inflammation and fibrosis.Enzyme linked immunosorbent assay(ELISA)was used to detect advanced oxidative protein products in mouse serum and lung tissue,reduced glutathione in lung tissue,and oxidative stress levels in serum and lung tissue.Results①Underhematoxylin eosinstaining and Masson staining,the lungs of mice in WM group showed inflammation infiltration and fibrosis,while mice in WMC group showed a reduction compared to mice in WM group;②The content of hydroxyproline in lung tissue,serum and late stage oxidative protein products in lung tissue of WM group mice increased compared to WN group mice(P<0.01),while the content of WMC group mice decreased compared to WM group mice(P<0.01);③The reduced glutathione content in lung tissue of WM group mice was lower than that of WN group mice(P<0.01),while WMC group mice were higher than WM group mice(P<0.05).Conclusion The activation of A2aR ameliorated the degree of inflammation and fibrosis in SSc-ILD,possibly through the antioxidant mechanism.

Objective:To establish a radioresistant nasopharyngeal carcinoma cell line in vitro and provide experimental basis for further research of the molecular mechanism of radioresistance. Methods:A radioresistant cell line 5-8F-IR was established by dose gradient irradiation. Cell morphological changes were observed by optical microscope. The formation of colony was detected by colony formation assay. Cell viability was detected by CCK-8 assay. Cell proliferation was assessed by 5-ethynyl-2'-deoxyuridine (EdU) assay. DNA damage repair ability was measured by immunofluorescence staining and comet assay. Cell apoptosis and cycle were detected by flow cytometry. The expression levels of DNA damage related protein γH2AX and apoptosis related protein Caspase-3 were measured by Western blot.Results:The 5-8F-IR cells became longer than that of parental generation 5-8F cells after dose gradient irradiation. The colony formation ability ( P<0.01), cell viability ( P<0.001), cell proliferation ability ( P<0.05) and DNA damage repair ability ( P<0.05) of 5-8F-IR cells were significantly stronger than those of parental generation 5-8F cells. The apoptosis rate of 5-8F-IR cells after irradiation was significantly lower than that of parental generation 5-8F cells ( P<0.01). The 5-8F-IR cells showed higher percentage of cells in S phase without irradiation, and obvious G 2/M phase arrest after irradiation ( P<0.01). Western blot showed that the expression levels of γH2AX ( P<0.001) and Caspase-3 ( P<0.05) in 5-8F-IR cells after irradiation were significantly lower compared with those of parental generation 5-8F cells. Conclusion:5-8F-IR cells induced by dose gradient irradiation of human nasopharyngeal carcinoma cell line 5-8F cells exhibit radioresistance and exhibit different biological characteristics compared to their parental 5-8F cells, providing a research tool for exploring radioresistance mechanism of nasopharyngeal carcinoma.

Objective To identify the influence factors and construct a predicted model for liver, lung, bone, or brain metastasis among patients with left or right colorectal cancer. Methods Patients with colorectal cancer with information on liver, lung, bone, and brain metastasis were retrospectively filtered and analyzed from 2010 to 2018 from the SEER database. These patients were divided into three groups based on their primary tumor location. Multivariate logistic regression analysis was conducted to identify the influence factors on metastasis. A nomogram that could predict metastasis was established and further validated by the AUC of ROC curves. Results A total of 49335 eligible patients were chosen from the SEER database. N stage and CEA were identified as risk factors for all metastases, which were unrelated to primary tumor location. By contrast, race had varying effects on liver metastasis between different groups (P < 0.05). The nomogram model predicting liver metastasis was successfully established, and the AUCs based on the three groups were 0.821 (95%CI: 0.813-0.830), 0.841 (95%CI: 0.833-0.848), and 0.796 (95%CI: 0.782-0.811), respectively. Conclusion The influence factors and predictive models on liver metastasis were different in patients with colorectal cancer and different primary tumor locations.

OBJECTIVE：To investigate the occurrence of medication errors （ME）in patients with hyperuricemia/gout and its related factors ，in order to avoid and reduce the occurrence of related ADE and ensure the safety of drug use in patients. METHODS：The ME reports related to hyperuricemia/gout were collected from National Monitoring Network for Clinical Safe Drug Use during Sept. 22nd，2012 to Jul. 9th，2020，and then analyzed in terms of reporting provinces ，classification and drugs involved，error content ，initiator and error factors. RESULTS ：A total of 179 ME reports ，which met inclusion criteria ，were included from 47 hospitals in 11 provinces. The drugs involved mainly included benbromarone （36 cases，20.11％），allopurinol （31 cases，17.32％），calcium carbonate D 3（30 cases，16.76％），inverting sugar electrolyte （24 cases，13.41％）and sodium bicarbonate（22 cases，12.29％）. Grade B ME were the most frequently reported （124 cases，69.27％）；severe ME occurred in 3 cases（1.68％）. The main errors were contraindications ，accounting for 70 cases（37.43％，mainly involving calcium carbonate D 3 and inverting sugar electrolyte ）. The people who caused ME were mainly doctors ，involving 126 cases（70.39％，the main content of errors was contraindications ）. The main error factors for ME were personnel factors ，involving 120 cases（67.04％，mainly lacking of knowledge ），followed by environmental factors （33 cases，mainly equipment failure ）. CONCLUSIONS ：ME in patients with hyperuricemia/gout are mainly caused by uric acid-lowering drugs and non-uric acid-lowering drugs that cause changes in uric acid. The main error contents include contraindications ，which were mostly caused by non-uric acid-lowering drugs and doctors. The main error factors are lack of knowledge and equipment failure. It is suggested to strengthen personnel training or introduce clinical medication support decision-making system ，while pay attention to the correct use and maintenance of related equipment in the process of drug use.

Background: Gastric cancer, especially intestinal-type gastric cancer, is considered as the result of the process of non-atrophic gastritis-atrophic gastritis-dysplasia-carcinogenesis. Aims: To explore the phenotypic characteristics and differentially expressed genes (DEGs) enrichment pathway of inflammatory cells between gastritis that prone to canceration (atrophic gastritis) and gastritis that not prone to canceration (non-atrophic gastritis). Methods: The datasets of GSE2669, GSE83389, GSE106656 and GSE27411 were downloaded from GEO database. DEGs were screened by R language and verified by GSE116312 dataset. DEGs screened from 3 datasets of 'non-atrophic gastritis-atrophic gastritis' were overlapped with inflammatory cell phenotypic characteristic genes. REACTOME and KEGG analyses of DEGs were performed. Results: A variety of DEGs in the 'normal gastric mucosa-non-atrophic gastritis-atrophic gastritis' dynamic process were screened, and 5 common genes were verified by GSE116312 dataset. A total of 85 inflammatory cell phenotypic characteristic genes were screened from 3 datasets. The percentage of neutrophil was high during 'normal gastric mucosa-non-atrophic gastritis' process while the percentages of fibroblast and macrophage were high during 'non-atrophic gastritis-atrophic gastritis' process. REACTOME and KEGG analyses showed that DEGs of inflammatory cell phenotype during 'non-atrophic gastritis-atrophic gastritis' process were mainly enriched in IL-10, IL-4 and IL-13 signaling pathways and antigen presentation pathway. Conclusions: Macrophage, neutrophil and fibroblast are the inflammatory cell phenotypic characteristics of gastritis with cancerous potential, which enriched in IL and antigen presentation pathways.

Objective: To analyze the relationship between serum lactic acid value and risk of death in patients with extensive burn during shock stage and the related influencing factors. Methods: Clinical data of 127 patients (111 males and 16 females) with extensive burn admitted to Institute of Burn Research of the First Affiliated Hospital of Army Medical University from January 2009 to December 2013 and Department of Plastic Surgery and Burns of the Affiliated Hospital of Southwest Medical University from January 2016 to December 2018, who met the admission criteria, were retrospectively analyzed. The patients aged 21 to 62 years, with total burn area more than 50% total body surface area. All patients were treated with antishock therapy after admission. (1) According to the treatment outcome, the patients were divided into survival group (n=98) and death group (n=29). The gender, age, total burn area, partial-thickness burn area, full-thickness burn area, abbreviated burn severity index (ABSI), admission time after injury, number of patients with inhalation injury, number of patients with acute renal failure, and serum lactic acid values on admission and at post admission hour (PAH) 12, 24, 36, and 48 were recorded. (2) According to the optimal positive cut-off value of serum lactic acid 48 hours after admission, the patients were divided into high lactic acid group and normal lactic acid group. Age, gender, total burn area, indexes at PAH 48 including urea nitrogen, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total serum bilirubin, alkaline phosphatase (ALP), albumin, white blood cell count, platelet count, lymphocyte count, prothrombin time (PT), hematocrit value, oxygenation index, respiratory index (RI), the alveolar-arterial oxygen partial pressure difference, mean arterial pressure (MAP) at PAH 48, the average urine volume within 48 hours after admission, the total volume of intravenous fluid infusion within 48 hours after admission, the volume of fluid infusion per kilogram of body mass within the first 24 hours after admission, the volume of fluid infusion per one percent of body surface area per kilogram of body mass within the first 24 hours after admission, the volume of urine per kilogram of body mass per hour within the first 24 hours after admission, and the percentage of hospital death were recorded. Data were processed with t test, chi-square test, and Fisher′s exact probability test. Cox regression analysis was used to screen independent risk factors affecting the prognosis of patients. Receiver operating characteristic curve (ROC) of serum lactic acid value at PAH 48 of 127 patients was drawn to predict patients′ death and determine the optimal positive cut-off value. Multivariate logistic regression analysis was used to screen independent risk factors causing increase of serum lactic acid. Results: (1) There were significantly statistical differences in total burn area, full-thickness burn area, and ABSI of patients between survival group and death group (t=6.257, 4.476, 5.727, P<0.01), while other indexes between the two groups were close. (2) The serum values of lactic acid of patients in death group on admission and at PAH 12, 24, 36, and 48 were (4.00±0.28), (4.50±0.26), (4.02±0.31), (3.48±0.22), (3.40±0.19) mmol/L, respectively, which were significantly higher than those in survival group [(3.30±0.21), (3.20±0.19), (2.33±0.17), (1.85±0.18), (1.50±0.09) mmol/L, t=14.552, 29.603, 38.133, 40.648, 74.973, P<0.05 or P<0.01]. (3) Cox regression analysis showed that the serum value of lactic acid at PAH 48 was the independent risk factor affecting the prognosis of patients, with risk ratio of 1.853 and 95% confidence interval of 1.342-2.559, P<0.01. (4) The total area under ROC of serum value of lactic acid at PAH 48 to predict death of 127 patients was 0.811, with 95% confidence interval of 0.699-0.924, P<0.01. The optimal positive cut-off value of serum value of lactic acid was 1.75 mmol/L, with sensitivity of 75.0% and specificity of 79.5% for predicting death. (5) There were significantly statistical differences in total burn area, ALT, AST, ALP, PT, total serum bilirubin, total volume of intravenous fluid infusion within 48 hours after admission, volume of fluid infusion per kilogram of body mass within the first 24 hours after admission, and percentage of hospital deaths of patients between high lactic acid group (n=34) and normal lactic acid group (n=93), t=3.592, 6.797, 10.367, 2.089, 2.880, 4.517, 2.984, 4.044, χ²=58.498, P<0.05 or P<0.01, while other indexes were close between the two groups. (6) Multivariate logistic regression analysis showed that AST and total serum bilirubin were independent risk factors for increase of serum lactic acid, with odds ratios of 1.021 and 1.064 and 95% confidence intervals of 1.001-1.040 and 1.001-1.132, P<0.05. Conclusions Serum value of lactic acid at PAH 48 can independently predict the death of patients with extensive burns. Liver injury is an important risk factor causing hyperlacticemia during burn shock stage. Widespread increase of vascular permeability and large amount of fluid resuscitation are the core factors leading to aggravation of abdominal organ injury.