ObjectiveTo explore the clinical efficacy and mechanism of Bupi Qingfei prescription （BPQF） in treating stable bronchiectasis in the patients with syndromes of lung-spleen Qi deficiency and phlegm-heat accumulation in the lungs. MethodsA randomized， double-blind， placebo-controlled trial was conducted. Patients were randomized into BPQF and placebo control （PC） groups. On the basis of conventional Western medicine treatment， the BPQF granules and placebo were respectively administered at 10 g each time， twice a day， for a course of 24 weeks. The TCM symptom scores， Quality of Life Questionnaire for Bronchiectasis （QOL-B） scores， lung function indicators， T lymphocyte subsets， level of inflammatory factors in the sputum， level of neutrophil elastase （NE） in the sputum， and occurrence of adverse reactions were observed before and after treatment in the two groups. ResultsA total of 64 patients completed the study， encompassing 32 in the BPQF group and 32 in the PC group. After treatment， the BPQF group showed decreased TCM symptom scores （P<0.01）， increased QOL-B scores （P<0.01）， and declined levels of tumor necrosis factor （TNF）-α and NE （P<0.05， P<0.01）. The PC group showed decreased TCM symptom （except spleen deficiency） scores （P<0.01）， increased the QOL-B health cognition and respiratory symptom domain scores （P<0.05， P<0.01）， and a declined TNF-α level （P<0.01）. Moreover， the BPQF group had lower TCM symptom （except chest tightness） scores （P<0.05， P<0.01）， higher QOL-B （except treatment burden） scores （P<0.05， P<0.01）， and lower levels of interleukin-6 and TNF-α （P<0.05） than the PC group. Neither group showed serious adverse reactions during the treatment process. ConclusionBPQF can ameliorate the clinical symptoms of stable bronchiectasis patients who have lung-spleen Qi deficiency or phlegm-heat accumulation in the lungs by regulating the immune balance and inhibiting airway inflammatory responses.

Objective To investigate the expression profile, prognostic value, gene co-expression network, and immunomodulatory role of BRF1 in a pan-cancer context, and to explore its biological functions and molecular regulatory mechanisms in esophageal squamous cell carcinoma (ESCC). Methods The pan-cancer dataset from The Cancer Genome Atlas (TCGA) was utilized to analyze the differential expression of BRF1 in tumor versus normal tissues, its association with patient survival, pathway enrichment for co-expressed genes, and immune features (including immune checkpoints, cytokines, and immune cell infiltration). The expression profile of BRF1 in ESCC was validated using the Gene Expression Omnibus (GEO) database. In vitro, BRF1 was knocked down in ESCC cells using siRNA. Cell proliferation and migration were assessed by MTT and Transwell assays, respectively. The expression levels of proliferation- and migration-related proteins were detected by Western blotting. The correlation between BRF1 and ferroptosis was analyzed using TCGA data. Results BRF1 was significantly upregulated in over 20 types of cancer, and its high expression was associated with poor prognosis in patients with adrenocortical carcinoma and prostate adenocarcinoma. BRF1 was found to positively regulate the T-cell-mediated cell death pathway in esophageal adenocarcinoma and was associated with the circadian rhythm regulation pathway in pancreatic adenocarcinoma. The correlation of BRF1 with immune checkpoints, cytokine networks, and immune cell infiltration was found to be cancer type-specific. In vitro experiments demonstrated that knocking down BRF1 significantly inhibited the proliferation of ESCC cells, accompanied by the downregulation of the proliferation marker PCNA. Cell migration was also significantly impaired, with decreased expression of Vimentin and MMPs and increased expression of E-cadherin. Furthermore, the expression of BRF1 was positively correlated with that of ferroptosis-antagonizing genes, such as GPX4, HSPA5, and SLC7A11. Conclusion BRF1 plays complex roles in pan-cancer, participating in the regulation of tumorigenesis, progression, and immune infiltration. BRF1 promotes the proliferation and migration of ESCC cells, a mechanism potentially associated with the regulation of ferroptosis resistance. These findings suggest that BRF1 could be a potential therapeutic target for ESCC.

Since the beginning of the 21st century, the severe respiratory infectious diseases worldwide [such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), influenza A H1N1 and novel coronavirus infection have attracted wide attention from all walks of life due to their superior pathogenicity and transmissibility. Aerosols-carrying pathogens are the main transmission route of many severe respiratory infectious diseases, which can lead to severe respiratory failure and even acute respiratory distress syndrome (ARDS) in infected individuals. Mechanical ventilation is the primary treatment for ARDS, and the small tidal volume, appropriate level of positive end-expiratory pressure based lung protective ventilation strategy can effectively reduce the incidence of ventilator-induced lung injury (VILI). However, in the process of clinical treatment, it is sometimes necessary to briefly disconnect the connection between the artificial airway and the ventilator circuit, which will not only cause the residual aerosol in the respiratory system to spill out and pollute the surrounding environment, increase the risk of nosocomial infection including medical staff, but also interfere with the implementation of lung protective ventilation strategy and aggravate ventilator-induced lung injury. In addition, studies have shown that a lot of medical staff have nosocomial infections, especially staff involved in tracheal intubation, extubation and other airway related operations. In addition to enhancing personal protective measures, it is crucial to safeguard healthcare workers from aerosol contamination and minimize associated risks during airway management. At present, there are few researches on the temporary sealing of airway lines and ventilator system, and there is a lack of clear guidance. This review summarizes the research status in related fields to provide a reference for corresponding solutions and programs.
Humans ; Respiratory Distress Syndrome/etiology* ; Respiration, Artificial ; Ventilator-Induced Lung Injury/prevention & control* ; Severe Acute Respiratory Syndrome ; COVID-19 ; Clinical Relevance

OBJECTIVE: To investigate the frequency and related factors of ineffective triggering (IT) and double triggering (DT) in patients with acute brain injury undergoing invasive mechanical ventilation. METHODS: A retrospective cohort study was conducted using data from a single-center observational trial. Patients with acute brain injury [traumatic brain injury, stroke, and post-craniotomy for brain tumors] undergoing mechanical ventilation in the intensive care unit (ICU) of Beijing Tiantan Hospital, Capital Medical University between June 2017 and July 2019 were retrospectively analyzed. Demographic and clinical data were collected. Respiratory parameters and waveforms during the first 3 days of mechanical ventilation were recorded, with 15-minute waveform segments collected 4 times daily. Airway occlusion pressure (P_0.1) was measured via end-expiratory hold at the end of each recording. IT and DT were identified based on airway pressure, flow, and esophageal pressure waveforms, and the ineffective triggering index (ITI) and DT incidence were calculated. Multivariate Logistic regression was used to identify factors associated with IT and DT. RESULTS: A total of 94 patients with acute brain injury were ultimately enrolled, including 19 cases of traumatic brain injury (20.2%), 39 cases of stroke (41.5%), and 36 cases of post-craniotomy for brain tumor (38.3%). Supratentorial injury was observed in 49 patients (52.1%), while infratentorial injury was identified in 45 patients (47.9%). A total of 94 patients with 1 018 datasets were analyzed; 684 (67.2%) datasets were on pressure support ventilation (PSV), and 334 (32.8%) were on mandatory ventilation. IT was detected in 810 (79.6%) datasets, with a median incidence of 2.1% (0.3%, 12.0%). Datasets demonstrating IT were characterized by lower P_0.1, higher tidal volume (VT), reduced respiratory rate (RR), and decreased minute ventilation (MV) compared to those without IT. The proportion of datasets exhibiting IT was higher during PSV than in mandatory ventilation [83.8% (573/684) vs. 71.0% (237/334), P < 0.05], while, the prevalence of ITI ≥ 10% was lower [23.8% (163/684) vs. 33.5% (112/334), P < 0.05]. DT was detected in 305 datasets (30%), with a median incidence of 0.6% (0.4%, 1.3%). Datasets exhibiting DT were characterized by higher VT, reduced RR, and lower pressure support levels. The incidence of DT was lower in PSV compared to mandatory ventilation modes [0% (0%, 0.3%) vs. 0% (0%, 0.5%), P < 0.05]. The post-craniotomy for brain tumors group exhibited higher ITI, lower RR, reduced MV, and a greater proportion of infratentorial lesions, compared to the TBI group. The infratentorial lesion group demonstrated higher ITI and incidence of DT compared to the supratentorial lesion group [ITI: 3.1% (0.7%, 17.8%) vs. 1.5% (0%, 8.3%), incidence of DT: 0% (0%, 0.5%) vs. 0% (0%, 0%), both P < 0.05]. After adjusting for confounding factors through multivariate logistic regression analysis, infratentorial lesion [odds ratio (OR) = 2.029, 95% confidence interval (95%CI) was 1.465-2.811, P < 0.001], lower P_0.1 (OR = 0.714, 95%CI was 0.616-0.827, P < 0.001), and mandatory ventilation (OR = 1.613, 95%CI was 1.164-2.236, P = 0.004) were independently associated with IT. Additionally, infratentorial lesion (OR = 1.618, 95%CI was 1.213-2.157, P = 0.001), large tidal volume (OR = 1.222, 95%CI was 1.137-1.314, P < 0.001), lower pressure support levels (OR = 0.876, 95%CI was 0.829-0.925, P < 0.001), and mandatory ventilation (OR = 2.750, 95%CI was 1.983-3.814, P < 0.001) were independently associated with DT. CONCLUSION IT and DT were common in patients with acute brain injury. Infratentorial lesions and mandatory ventilation were independently associated with both IT and DT.
Humans ; Respiration, Artificial/methods* ; Retrospective Studies ; Brain Injuries/therapy* ; Intensive Care Units ; Male ; Female ; Middle Aged ; Brain Injuries, Traumatic/therapy* ; Logistic Models ; Aged ; Adult

Objective To investigate the impact of the artificial intelligence iterative reconstruction (AIIR) algorithm on image quality in chest computed tomography (CT) at different radiation doses, and assess its value in reducing radiation dose during chest CT examinations. Methods A simulated chest phantom was scanned with 12 groups of tube voltages and milliampere-seconds, and the radiation dose was recorded for each group. The images of each group were reconstructed using seven methods: AIIR with noise levels 1-5, KARL iterative reconstruction, and filtered back projection (FBP). The CT values and standard deviations of soft tissue, thoracic vertebrae, pulmonary nodules, and the mediastinum were measured, with standard deviation representing image noise. Subjective evaluation of image quality was performed. The Friedman test was used to compare CT values among the seven reconstruction groups, a linear mixed model was employed for statistical analysis of image noise, and the Friedman test was also used for comparing subjective evaluation scores. Results The reconstruction algorithm, tube voltage, milliampere-seconds, and their interactions all showed statistically significant effects on image noise for the four tissues (F = 2.041-391.283, P < 0.05). Among the reconstruction algorithms, noise reduction capability decreased in the following order: AIIR levels 1-5, KARL, and FBP. The interaction between the reconstruction algorithm and tube voltage or milliampere-seconds indicated that AIIR exhibited improved noise reduction efficacy under low tube voltage and low milliampere-second conditions (|t| = 1.892-8.245, P < 0.05). In terms of subjective evaluation of image quality, there was no statistically significant difference among AIIR levels 3-5 (|Z| ≤ 0.567, P > 0.05), and the score of AIIR level 3 was significantly higher than those of AIIR level 1, AIIR level 2, FBP, and KARL level 2 (|Z| = 3.449-5.906, P < 0.05). Conclusion The AIIR reconstruction algorithm significantly reduced image noise in chest CT examinations. For improving image quality while maintaining image realism, AIIR level 3 is recommended, which can reduce the radiation dose by more than 75%. Furthermore, AIIR showed superior performance in noise reduction under low tube voltage and low milliampere-second conditions, demonstrating significant potential for reducing radiation dose.

The introduction of immunotherapy has significantly improved the pathological complete response (pCR) rate and tumor downstaging effect in patients receiving neoadjuvant therapy for gastric cancer, while simultaneously presenting new challenges and opportunities for surgical decision-making. The recommended number of cycles for neoadjuvant therapy is 2 to 4 cycles, and the recommended time interval for surgery is within 4 to 6 weeks after the last treatment. Laparoscopic and robotic-assisted minimally invasive surgeries have demonstrated relative advantages in postoperative recovery and safety. For cases achieving pCR or significant tumor regression after immunotherapy, active function-preserving surgeries or enrollment in clinical trial cohorts may be explored. Basic research indicates that preserving unaffected lymph nodes may maintain immune activity, challenging the traditional D2 lymphadenectomy scope, which requires further clinical evidence. Neoadjuvant immunotherapy has not significantly increased perioperative complications. This article aims to discuss the core issues in surgical decision-making for gastric cancer after neoadjuvant therapy, providing a detailed analysis from the perspectives of surgical timing, approach, scope, and complication management, with the hope of offering more references for surgical decision-making after neoadjuvant therapy.

Objective To investigate the effects of artesunate(Art)on the proliferation,apoptosis,and autophagy of nephroblastoma cell line(SK-NEP-1).Methods SK-NEP-1 cells were intervened with different concentrations of Art(0,10,20,40 and 80 μmol/L),and MTT method was applied to calculate the cell proliferation inhibition rate to screen the optimal intervention concentration;SK-NEP-1 cells were separated into control group,Art group,3-MA group(Art+autophagy inhibitor,3-methyladenine),and Rapa group(Art+autophagy activator rapamycin).EdU and flow cytometry were applied to detect cell proliferation and apoptosis,respectively;MDC staining was applied to detect autophagy in cells;the level of reactive oxygen species(ROS)in cells was detected by DCFH-DA fluorescent probe;the expression of proliferating cell nuclear antigen(PCNA),anti apoptotic factor B cell lym-phomatoma-2(Bcl-2),Bcl-2 associated X protein(Bax),microtubule junction protein 1 light chain 3 Ⅱ/3 Ⅰ(LC3 Ⅱ/LC3 Ⅰ),selective autophagy junction protein 1(p62),and benzyl chloride 1(Beclin-1)proteins in cells were detected by Western blot.Results Compared with 0 μmol/L Art,the proliferation inhibition rate of SK-NEP-1 cells was gradually increased after 10,20,40 and 80 μmol/L Art treatment(P＜0.05),and the IC50 value was 46.881 μmol/L,so 40 μmol/L Art was selected for follow-up experiments.Compared with the control group,the apoptosis rate,relative autophagy fluorescence intensity,ROS level,Bax,LC3 Ⅱ/LC3 Ⅰ,Beclin-1,PINK1,and Parkin protein expression levels of SK-NEP-1 cells in the Art group were obviously increased,the EdU positive cell rate,PCNA,Bcl-2,and P62 protein expression levels were obviously reduced(P＜0.05);The auto-phagy inhibitor 3-MA inhibited the promoting effect of Art on apoptosis and autophagy of nephroblastoma cells and inhibit proliferation(P＜0.05).Conclusions Art inhibits the proliferation of nephroblastoma cell line SK-NEP-1,and promotes autophagy and apoptosis.

Objective To review the damage outcomes of patients in medical damage events and to analyze the influencing factors of medical causality determination in medical damage events in Tianjin city,with a view to reducing the occurrence of medical damage events by avoiding risk factors and standardizing the diagnostic and therapeutic activities of medical personnel.Methods 316 cases of medical damage events handled by the Medical Damage Identification Office of Tianjin Medical Association from 2017 to 2023 were selected as the research object,and descriptive analysis was used to summarize the basic situation of medical damage events,and the medical fault factors affecting the magnitude of the cause force of the medical side of medical damage events were explored through single-factor analysis and the construction of multiomal logistic regression models.Results Medical malpractice(OR=3.140)and incomplete preoperative assessment(OR=6.008)are factors that influence the determination of the liability of the medical institution in medical malpractice events(P＜0.05),and all three regression coefficients were greater than 0,all three were positively correlated with the probability that the medical cause power was judged to be greater than or equal to the equivalent cause.Conclusion The number of medical damage incidents in Tianjin shows a fluctuating downward trend.In Tianjin,the number of medical injury incidents showed a fluctuating downward trend,and the number of medical injury incidents in tertiary public general hospitals was the largest.Therefore,medical institutions should establish and improve multidisciplinary diagnosis and treatment mode to improve the level of diagnosis and treatment.Strengthen preoperative evaluation to avoid surgical risk.

ObjectiveTo observe the effect of Weichang'an prescription-containing serum on ferroptosis of human gastric cancer cells and explore the possible mechanism. MethodsSD rats were administrated with 18， 36， 72 g·kg^-1·d^-1 Weichang'an prescription by gavage for preparation of serum samples containing different doses of Weichang'an prescription， which were then used to treat MKN-45 cells. The cell proliferation was examined by the cell counting kit-8 （CCK-8）. In addition， inhibitors of apoptosis， necroptosis， and ferroptosis were added， and the survival of the cells treated with the serum samples was observed. The fluorescent probe dichlorodihydrofluorescein diacetate （DCF-DA） and the lipid peroxidation sensor C11-BODIPY were employed to detect the intracellular levels of reactive oxygen species （ROS） and lipid peroxidation， respectively. The levels of ferrous ion （Fe²⁺）， glutathione （GSH）， and malondialdehyde （MDA） were detected by enzyme-linked immunosorbent assay （ELISA）. Real-time PCR and Western blotting were employed to determine the expression of nuclear factor erythroid 2-related factor 2 （Nrf2）， aldo-keto reductase family 1 member B1 （AKR1B1）， glutathione peroxidase 4 （GPX4）， acyl-CoA synthetase long-chain family member 4 （ACSL4）， signal transducer and activator of transcription 3 （STAT3）， and mitogen-activated protein kinase （MAPK）. ResultsCompared with the blank group， Weichang'an prescription-containing serum decreased the viability of MKN-45 cells （P<0.05， P<0.01） in a time- and dose-dependent manner. Compared with the Weichang'an prescription group， the apoptosis inhibitor+Weichang'an prescription group and the ferroptosis inhibitor+Weichang'an prescription group showed increased cell viability （P<0.05， P<0.01）. Compared with the blank group， Weichang'an prescription elevated the levels of ROS， lipid peroxidation， and intracellular Fe²⁺ and MDA （P<0.05， P<0.01） and lowered the level of GSH （P<0.05， P<0.01） in a dose-dependent manner. Compared with the blank group， Weichang'an prescription down-regulated the mRNA and protein levels of Nrf2， AKR1B1， and GPX4 （P<0.05， P<0.01） and up-regulated the mRNA and protein levels of ACSL4 （P<0.05， P<0.01） in a dose-dependent manner. Compared with the blank group， Weichang'an prescription down-regulated the protein levels of p-STAT3 and p-ERK （P<0.05， P<0.01） in a dose-dependent manner. ConclusionThe Weichang'an prescription-containing serum can promote the ferroptosis and inhibit the proliferation of MKN-45 cells by regulating the STAT3 and MAPK pathways.