Objective To investigate the possible mechanism of Xuebijing injection in regulating abnormal degradation of pulmonary vascular endothelial calyx to improve acute lung injury induced by severe heatstroke. Methods Forty-eight Wistar rats were randomly divided into control group, heatstroke group and Xuebijing group. Before heatstroke induction, rats in Xuebijing group were administrated with Xuebijing injection (2 ml/kg, 2 times/d) for 3 days. All rats were exposed to an environment with temperature of (40±2) ℃ and humidity of 65%±5% for 60 minutes to induce heatstroke. Two hours later, the lung wet/dry weight ratio was recorded; the concentration of proteins in BALF was measured; the pulmonary vascular permeability was measured by Evans blue (EB); HE staining was used to observe the pathological changes of lung tissue; the changes of hyaluronic acid (HA) on the surface of pulmonary vessels were observed by immunofluorescence; Western blotting was used to detect the expression of Syndecan-1, Glypican-1, VE-Cadherin, Occludin, VCAM-1 and E-selectin in lung tissues; Enzyme-linked immunosorbent assay (ELISA) was utilized to quantify the concentration of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) in serum and heparanase (HPA) in lung tissue. Results Xuebijing could decrease the lung wet/dry weight ratio, reduce protein exudation and improve pulmonary vascular permeability (P<0.01); reduce the histological injury (P<0.01); reduce the degradation of HA, Syndecan-1 and Glypican-1 on the surface of pulmonary vessels (P<0.01); increase the expression of VE-Cadherin and Occludin (P<0.01); regulate the overexpression of VCAM-1 and E-selectin (P<0.01); down-regulate the expression of TNF-α, IL-6 and HPA (P<0.01). Conclusion Xuebijing injection decrease the expression of HPA, improve the disintegration of pulmonary vascular endothelial calyx, repair the integrity of pulmonary vessels, reduce the damage of cell connections, down-regulate the expression of adhesion molecules, inhibit the inflammatory reaction, relieving acute lung injury caused by severe heat stroke.

Dexmedetomidine is a highly selective α₂ adrenergic receptor agonist, exerting anti-sympathetic, sedative, analgesic and anti-anxiety effects, with minimal impact on respiration. In recent years, dexmedetomidine has been widely used in clinical anesthesia, perioperative treatment, and intensive care. Organ-protection is an important focus of anesthesia and perioperative medicine, with clinical significance in reducing complications and improving short- and long-term outcomes. Increasing clinical evidence and basic research have shown that the application of dexmedetomidine could protect the heart, brain, lung, kidney, liver, gastrointestinal tract and other important organs. The mechanism may be related to dexmedetomidine's effects of anti-inflammation, anti-oxidation, anti-apoptosis, and autophagy regulation. From our perspectives, clinical use should follow the principle of individualization, and the dose should be adjusted in time according to patients' responses, so as to avoid adverse reactions such as hypotension and bradycardia while protecting the organs. Moreover, more strictly designed clinical studies and in-depth mechanistic investigations are needed for the optimal dexmedetomidine therapy and better organ protection during the perioperative course. In order to facilitate better understanding of clinicians, this paper reviews the organ-protective effects and underlying mechanisms of dexmedetomidine.

For axial spondyloarthritis/ankylosing spondylitis, rehabilitation is very important for controlling disease activity, preventing disease progression and improving quality of life. Initiated by China Spine Alliance and jointly formulated by Air Force Specialty Medical Center and Chinese PLA General Hospital, the current guidelines were developed according to World Health Organization Guidelines Development Manual and the Basic Methods and Procedures for the Development/Revision of the Clinical Diagnosis and Treatment Guidelines, Appraisal of Guidelines for Research and Evaluation Ⅱ (AGREEⅡ), Grading of Recommendations Assessment, Development and Evaluation (GRADE). Two basic princlples and 12 suggestions were made for important issues such as diagnosis, rehabilitation assessment, rehabilitation intervention and management for axial spondyloarthritis/ankylosing spondylitis.

Neurological impairment in the form of stroke, cognitive dysfunction and delirium is a common complication after cardiac surgery and a major cause of postoperative death and long-term disability in patients undergoing cardiac surgery. There have been many studies attempting to identify intervention and treatment strategies, but no standardized protocols for neurological protection have been developed. The purpose of this article is to discuss the risk factors, mechanisms and neuroprotective measures to improve patient prognosis of neurological injury after cardiac surgery, and to review the recent research progress from three aspects: preoperative assessment and intervention, intraoperative management and monitoring, and postoperative diagnosis and treatment, emphasizing that the focus of perioperative prevention and treatment should be on the prevention of ischemic-hypoxic injury. Future research directions should focus on translational research of preclinical experiments and the development of novel imaging techniques to reduce the incidence of neurological complications and improve clinical outcome.

With aging of population and improvement of medical technology, the number of elderly patients receiving surgical treatment is increasing. Cardiovascular events after noncardiac surgery are one of the leading causes of death. Perioperative cardiovascular events have a high risk and incidence rate, thus severely affecting the prognosis of patients. In recent years, a growing number of studies have focused on the prevention and treatment of perioperative cardiovascular events in elderly patients. Assessing the risk of perioperative cardiovascular events and using effective interventions can effectively reduce the incidence of cardiovascular events and improve the prognosis of elderly patients. This article discusses cardiovascular risk assessment and management in elderly patients during noncardiac surgeries from the perspective of preoperative, intraoperative, postoperative periods, and perioperative medication used to provide assistance to clinical practice.

Chronic obstructive pulmonary disease (COPD) is a frequent and common disease of the respiratory system. The problem of low early diagnosis rate, low treatment compliance, and low treatment standardization has persisted in the diagnosis and treatment of COPD. Heterogeneity found in clinical practice is one of the reasons why COPD is difficult to treat. In recent years, it has been gradually recognized that the occurrence and development of COPD are closely related to the immune state of the body. At present, it become one of the hot spots in clinical and basic research that searching for specific and sensitive cell and molecular biomarkers to early diagnose acute exacerbation and subtype differentiation of COPD, which ultimately provide individual diagnosis and treatment strategies for COPD patients. This review focuses on the research progress of immunocytes and immunologic factors as biomarkers to different phenotypes and progression of COPD in recent years, providing a reference for the research on diagnosis and treatment of COPD.

With the continuous development and progress of medicine, the total number of general anesthetic surgery is increasing, and postoperative complications are also on the rise, especially postoperative pulmonary complications (PPCs) caused by perioperative lung injury. PPCs are the main cause of prolonged hospitalization, increased morbidity and mortality, poor prognosis, and increased medical burden in patients undergoing general anesthesia. With the enhancement of awareness of mechanical ventilation and the implementation of the enhanced recovery after surgery (ERAS) concept, lung-protective ventilation strategies (LPVS) are receiving more and more attention. However, the debate continues on how to apply the LPVS effectively. The recent introduction of diaphragm-protective ventilation as a novel concept has led to the realization that the application of protective ventilation strategies should limit the adverse effects of mechanical ventilation on diaphragm function within the context of lung protective ventilation. How to apply protective ventilation strategies effectively to prevent the development of ventilator-induced lung injury (VILI) and ventilator-induced diaphragm dysfunction (VIDD), reduce the incidence of PPCs, improve patient prognosis, and reduce the medical burden is an important challenge in the management of mechanically ventilated patients. In this paper, we will focus on ventilation strategies of lung and diaphragm combined with the latest progress of LPVS, to elaborate the research on the application of individualized ventilation strategies and the mechanisms of VILI and VIDD occurrence. Finally, prospecting the future research direction of protective ventilation strategies.

Objective To investigate the effects and mechanisms of TAR DNA-binding protein 43 (TDP-43) on oxygen-glucose deprivation (OGD)-induced apoptosis in mouse atrial myocytes (HL-1 cells). Methods The in vitro cultured mouse atrial myocytes (HL-1 cells) were divided into: (1) control group and groups with different OGD treatment times (2, 4, 8, 16 h), and cell viability was detected by CCK-8 assay, and TDP-43 protein expression level was detected by Western blotting, which was used to determine the time point of OGD induction for the subsequent study; (2) control and OGD groups, flow cytometry was used to detect apoptosis, JC-1 staining to detect mitochondrial membrane potential, chemiluminescence to detect adenosine triphosphate (ATP) relative content, microplate method to detect malondialdehyde (MDA) content, and WST-1 method to detect superoxide dismutase (SOD) content. Mouse atrial myocytes (HL-1 cells) transfected with lentivirus were divided into: (1) negative control lentiviral intervention group (NC-shRNA), TDP-43 knockdown lentiviral intervention group (TDP-43-shRNA1, TDP-43-shRNA2, TDP-43-shRNA3), and Western blotting was used to detect the TDP-43 protein expression level, and the group with the highest lentiviral knockdown efficiency was selected as the TDP-43-shRNA for subsequent experiments; (2) NC-shRNA group, TDP-43-shRNA group, OGD+NC-shRNA group, OGD+TDP-43-shRNA group, under normoxic and OGD conditions, flow cytometry was used to detect the apoptosis rate, MitoTracker staining to detect mitochondrial morphology, JC-1 staining to detect mitochondrial membrane potential, chemiluminescence to detect the relative content of ATP, flow cytometry to detect the fluorescence intensity of reactive oxygen species (ROS), microplate to detect the content of MDA, and WST-1 to detect the content of SOD. Results CCK-8 method showed that, with the prolongation of OGD time, the viability of mouse atrial myocytes (HL-1 cells) gradually decreased; Western blotting assay showed that the expression level of TDP-43 protein gradually increased, and both of them showed a strong time-dependence. Compared with control group, mouse atrial myocytes (HL-1 cells) viability was the lowest (P<0.05) and TDP-43 protein expression was the highest (P<0.05) at 16 h of OGD, accordingly, OGD 16 h was chosen as the induction time point for subsequent experiments. Compared with control group, the apoptosis rate, the fluorescence intensity ratio of mitochondrial membrane potential and the content of MDA increased, the relative content of ATP and SOD decreased in OGD group, and the differences were all statistically significant (P<0.05). Western blotting detection showed that compared with NC-shRNA group, the TDP-43-shRNA2 group had the most obvious reduction in TDP-43 protein expression level (P<0.05) and the highest knockdown efficiency, so the TDP-43-shRNA2 group was selected for subsequent experiments. The results of flow cytometry showed that under normoxic conditions, there was no significant change in the apoptosis rate in TDP-43-shRNA group compared with NC-shRNA group (P>0.05); and under OGD conditions, the apoptosis rate in OGD+TDP-43-shRNA group reduced when compared with OGD+NC-shRNA group (P<0.05). MitoTracker staining results showed that the mitochondrial morphology of TDP-43-shRNA group was intact without significant changes compared with NC-shRNA group; the mitochondria of OGD+NC-shRNA group increased in number, most of which were fragmented and scattered in distribution; compared with OGD+NC-shRNA group, the mitochondrial morphology of OGD+TDP-43-shRNA group was restored. Under normoxic conditions, there were no significant changes in mitochondrial membrane potential, relative ATP content, ROS fluorescence intensity, MDA content, and SOD content in TDP-43-shRNA group compared with NC-shRNA group (P>0.05); however, under OGD conditions, the ratio of fluorescence intensity of mitochondrial membrane potential of cells the fluorescence intensity of ROS, and the content of MDA decreased, and the relative content of ATP and the content of SOD increased in OGD+TDP-43-shRNA group compared with that of OGD+NC-shRNA group, and all of these differences was statistically significant (P<0.05). Conclusion TDP-43 exacerbates OGD-induced mitochondrial dysfunction by regulating cardiomyocyte apoptosis; therefore, knockdown of TDP-43 expression is expected to be a potential therapeutic strategy for ischemic cardiomyopathy.

Objective To evaluate the efficacy and safety of modified decompressive craniectomy in treatment of traumatic brain injury and its impact on the serum levels of inflammatory mediators and prognosis. Methods According to different surgical methods, 82 patients with traumatic brain injury admitted to the department of neurosurgery of Nanyang Central Hospital from June 2020 to January 2022 were divided into standard group (n=41) and modified group (n=41). The standard group was given standard decompressive craniectomy, and the modified group was given modified decompressive craniectomy. The intraoperative blood loss, operation time and hospital stay, the levels of neuron-specific enolase (NSE), S-100 calcium binding protein B (S-100β), C-reaction protein (CRP), procalcitonin (PCT), and interleukin-6 (IL-6) before operation, 6 hours after operation, and 3 days after operation, Glasgow Outcome Scale (GOS), incidence of complications, and incision healing grade 1 month after operation were compared between two groups. Results Compared with standard group, the hospital stay was significant shorter in modified group (P<0.05), and intraoperative blood loss and operation time were no significant difference in modified group (P>0.05). At 6 hours and 3 days after operation, the levels of NSE, S-100β, CRP, PCT and IL-6 in modified group were lower than those in standard group (P<0.05). Compared with standard group, the good prognosis rate based of GOS was higher in modified group [82.9% (34/41) vs. 63.4% (26/41), P<0.05]; the total incidence of complications was lower in modified group [2.4%(1/41) vs. 19.5%(26/41), P<0.05]; and the grade of incision healing was better in modified group (P<0.05). Conclusions Modified decompressive craniectomy in the treatment of traumatic brain injury could reduce stress of brain injury and surgical trauma, and the incidence of complications, help to speed up the postoperative recovery process, improve the rate of good prognosis and the grade of incision healing. Its efficacy and safety is better than standard decompressive craniectomy.

Objective To explore the risk factors for renal injury in tumors patients treated with programmed death receptor-1 (PD-1) inhibitor, and further construct a column chart model to predict the likelihood of renal injury in patients. Methods The present study is a single center retrospective analysis. 447 patients with tumors treated with PD-1 inhibitors in the Third Affiliated Hospital of Soochow University between January 2018 and January 2021 were included and followed up until January 2022. Kidney injury was defined as acute kidney disease (AKD). All patients were divided into AKD group (n=71) and non-AKD group (n=376 according to whether PD-1 inhibitor associated with AKD development at the end of follow-up. Basic information, disease and medication situation, laboratory indicators, and the incidence of extrarenal immune related adverse events (irAEs) during follow-up period were compared between the two groups. Univariate and multivariate logistic regression models were used to identify independent risk factors for PD-1 inhibitor associated AKD. The present study randomly divided all samples (n=447) into training set (n=313) and validation set (n=134) in a 7:3 ratio, built nomogram prediction models in the training set according to the screened independent risk factors, drawn the receiver operating characteristic (ROC) curves to evaluate the discrimination of the models, drawn calibration curves to evaluate the calibration of the models, and drawn clinical decision curve analysis (DCA) to explore the clinical validity and benefit rate of the models. Results The combination of antibiotics, diabetes, hypertension, extrarenal irAEs and cystatin C (Cys C) in AKD group were significantly higher than those in non-AKD group (P<0.05), but hemoglobin (Hb) was significantly lower than that in non-AKD group (P<0.05). Single factor logistic regression analysis showed that combination of antibiotics, diabetes, hypertension, extrarenal irAEs, lower Hb, estimated glomerular filtration rate (eGFR), higher blood urea nitrogen (BUN), serum creatinine (SCr), Cys C, fasting blood glucose (FBG), and alanine transaminase (ALT) were risk factors for PD-1 inhibitor related AKD (P<0.05). Multivariate logistic regression analysis showed that concomitant extrarenal irAEs, lower Hb, higher SCr, and direct bilirubin (DBIL) were independent risk factors for PD-1 inhibitor associated AKD (P<0.05). Based on the independent risk factors mentioned above, a column chart prediction model was further established and validated. The results showed that the area under the ROC curve (AUC) of the training and validation sets of the model were 0.703 (95%CI 0.628-0.777) and 0.791 (95%CI 0.671-0.911), respectively, indicating good discrimination. The calibration curves of both the training and validation sets hover around the ideal line of 45°, indicating that the model has good calibration. DCA shows that the constructed model curve is far away from the two polar lines (the curve with a net benefit of 0 and the curve with all samples being positive), indicating that the model has good clinical benefits. Conclusion The combination of extrarenal irAEs, lower Hb, higher SCr, and higher DBIL are independent risk factors for the occurrence of PD-1 inhibitor related AKD; The established column chart model has good discrimination and calibration, which can provide guidance for clinical practice.