Objective:To explore the impacts of Yiqi Wenfei Tongqiao Formula on inflammatory response and T helper cell(Th)1/Th2 immune balance in rats with lung Qi deficiency cold type allergic rhinitis.Methods:Sixty SD rats were randomly divided into model group,low dose Yiqi Wenfei Tongqiao Formula group,medium dose Yiqi Wenfei Tongqiao Formula group,high dose Yiqi Wenfei Tongqiao Formula group,and desloratadine group,with 12 rats in each group,using a combination of smoking,cold stimula-tion combined with ovalbumin(OVA)sensitization and stimulation construct lung Qi deficiency cold type allergic rhinitis model.An-other 12 normal SD rats were selected as control group.Each group of rats was treated with corresponding drugs once a day for 14 days.Model group and control group rats were given physiological saline.Scoring method was used to analyze the behavioral score and lung index of rats with allergic rhinitis.HE staining was applied to detect pathological changes in rat nasal mucosa tissue.ELISA was ap-plied to detect levels of IFN-γ,IL-4 and TNF-α in rats serum;flow cytometry was applied to detect Th1/Th2.Western blot was applied to detect expressions of T-bet and GATA-3 protein in nasal mucosa tissues of rats in each group.Results:Compared with control group,pathological damage to nasal mucosa tissue of model group rats was severe,allergic rhinitis behavior score(days 41,48,56),lung index,levels of IL-4 and TNF-α,Th2 and protein expression of GATA-3 were increased,while levels of IFN-γ,Th1,Th1/Th2,and protein expression of T-bet were decreased(P<0.05);compared with model group,pathological damage to nasal mucosa tissue of rats in low,medium,high doses Yiqi Wenfei Tongqiao Formula groups and desloratadine group were alleviated,the allergic rhinitis behavior score(days 48,56),lung index,levels of IL-4 and TNF-α,Th2 and protein expression of GATA-3 were decreased,while levels of IFN-γ,Th1,Th1/Th2,and protein expression of T-bet were increased(P<0.05).Conclusion:Yiqi Wenfei Tongqiao Formula can inhibit inflammatory response of lung Qi deficiency cold type allergic rhinitis rats By regulating Th1/Th2 immune balance.

Objective To investigate the effect of Yiqi Wenfei Tongqiao decoction on the inflammatory response in rats with allergic rhi-nitis(AR)of lung qi deficiency and cold type based on the Janus kinase 1(JAK1)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Methods A AR model of lung qi deficiency and cold type was established in rats using ovalbumin(OVA)combined with smoking and cold stimulation.After modeling,the rats were randomly divided into model,loratadine,low-dose Chinese medicine,high-dose Chinese medicine,and high-dose Chinese medicine+RO8191(JAK1/STAT3 signaling pathway activator)groups,with 12 rats per group.Twelve healthy rats were used as controls.After 14 days of drug intervention,the changes in the symptoms of lung qi deficiency and cold syndrome and AR were observed in the rats.Enzyme-linked immunosorbent assay was used to detect the serum levels of tumor necrosis factor α(TNF-α),interleukin(IL)-4,interferon-γ(IFN--γ),and ovalbumin-specific immunoglobulin E(OVA-sIgE).The number of inflammatory cells in the nasal lavage fluid was determined and the eosinophil(EOS)percentage was calculated.Pathological changes in the nasal mucosal tissue were observed after hematoxylin and eosin(HE)staining.Western blotting was used to detect the expression of JAK1/STAT3 signaling pathway-related proteins in nasal mucosal tissue.Results Compared with those in the model group,the AR symptom score,serum IL-4,TNF-α,and OVA-sIgE levels,EOS percentage in nasal lavage fluid,and levels of p-JAK1/JAK1 and p-STAT3/STAT3 in the nasal mucosal tissue of rats in the loratadine,low-dose Chinese medicine,and high-dose Chinese medicine groups were lower,whereas the serum IFN-γ level was higher(P＜0.05).RO8191 weakened the inhibitory effect of Yiqi Wenfei Tongqiao decoction on the inflammatory response in rats with AR of lung qi deficiency and cold type.Conclusion Overall,Yiqi Wenfei Tongqiao decoction can alleviate the inflammatory response in rats with AR of lung qi deficiency and cold type by inhibiting JAK1/STAT3 signaling pathway acti-vation and regulating the balance of Th1/Th2 cytokines.

Objective:To comprehensively retrieve and evaluate the best available evidence on perioperative fluid management in patients undergoing hepatectomy for liver cancer, and to provide references for clinical practice.Methods:A systematic search was conducted across multiple platforms, including UpToDate, BMJ Best Practice, Guidelines International Network, National Institute for Health and Care Excellence, PubMed, Web of Science, China National Knowledge Infrastructure, and Wanfang Data, for clinical decisions, guidelines, expert consensus, systematic reviews, evidence summaries, and randomized controlled trials related to perioperative fluid management in patients undergoing hepatectomy for liver cancer. The search period was from database inception to March 13, 2024. The 2014 version of the Joanna Briggs Institute evidence pre-grading and recommendation grading system was used to classify the evidence.Results:A total of 14 articles were included: 3 clinical decision articles, 3 guidelines, 1 evidence summary, 5 expert consensuses, 1 systematic review, and 1 randomized controlled trial. A total of 27 best evidence items were extracted, covering seven aspects: principles of fluid therapy, preoperative fluid management, intraoperative fluid management, postoperative fluid management, fluid type selection, assessment and monitoring, and training and education.Conclusions:This study summarizes the best evidence on perioperative fluid management for hepatectomy in liver cancer patients and provides an evidence-based reference for clinical nursing practice. Healthcare professionals should apply the evidence in a personalized manner based on the actual clinical context to promote scientific fluid management in the perioperative period.

Objective:To explore the impacts of Yiqi Wenfei Tongqiao Formula on inflammatory response and T helper cell(Th)1/Th2 immune balance in rats with lung Qi deficiency cold type allergic rhinitis.Methods:Sixty SD rats were randomly divided into model group,low dose Yiqi Wenfei Tongqiao Formula group,medium dose Yiqi Wenfei Tongqiao Formula group,high dose Yiqi Wenfei Tongqiao Formula group,and desloratadine group,with 12 rats in each group,using a combination of smoking,cold stimula-tion combined with ovalbumin(OVA)sensitization and stimulation construct lung Qi deficiency cold type allergic rhinitis model.An-other 12 normal SD rats were selected as control group.Each group of rats was treated with corresponding drugs once a day for 14 days.Model group and control group rats were given physiological saline.Scoring method was used to analyze the behavioral score and lung index of rats with allergic rhinitis.HE staining was applied to detect pathological changes in rat nasal mucosa tissue.ELISA was ap-plied to detect levels of IFN-γ,IL-4 and TNF-α in rats serum;flow cytometry was applied to detect Th1/Th2.Western blot was applied to detect expressions of T-bet and GATA-3 protein in nasal mucosa tissues of rats in each group.Results:Compared with control group,pathological damage to nasal mucosa tissue of model group rats was severe,allergic rhinitis behavior score(days 41,48,56),lung index,levels of IL-4 and TNF-α,Th2 and protein expression of GATA-3 were increased,while levels of IFN-γ,Th1,Th1/Th2,and protein expression of T-bet were decreased(P<0.05);compared with model group,pathological damage to nasal mucosa tissue of rats in low,medium,high doses Yiqi Wenfei Tongqiao Formula groups and desloratadine group were alleviated,the allergic rhinitis behavior score(days 48,56),lung index,levels of IL-4 and TNF-α,Th2 and protein expression of GATA-3 were decreased,while levels of IFN-γ,Th1,Th1/Th2,and protein expression of T-bet were increased(P<0.05).Conclusion:Yiqi Wenfei Tongqiao Formula can inhibit inflammatory response of lung Qi deficiency cold type allergic rhinitis rats By regulating Th1/Th2 immune balance.

Objective To investigate the effect of Yiqi Wenfei Tongqiao decoction on the inflammatory response in rats with allergic rhi-nitis(AR)of lung qi deficiency and cold type based on the Janus kinase 1(JAK1)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Methods A AR model of lung qi deficiency and cold type was established in rats using ovalbumin(OVA)combined with smoking and cold stimulation.After modeling,the rats were randomly divided into model,loratadine,low-dose Chinese medicine,high-dose Chinese medicine,and high-dose Chinese medicine+RO8191(JAK1/STAT3 signaling pathway activator)groups,with 12 rats per group.Twelve healthy rats were used as controls.After 14 days of drug intervention,the changes in the symptoms of lung qi deficiency and cold syndrome and AR were observed in the rats.Enzyme-linked immunosorbent assay was used to detect the serum levels of tumor necrosis factor α(TNF-α),interleukin(IL)-4,interferon-γ(IFN--γ),and ovalbumin-specific immunoglobulin E(OVA-sIgE).The number of inflammatory cells in the nasal lavage fluid was determined and the eosinophil(EOS)percentage was calculated.Pathological changes in the nasal mucosal tissue were observed after hematoxylin and eosin(HE)staining.Western blotting was used to detect the expression of JAK1/STAT3 signaling pathway-related proteins in nasal mucosal tissue.Results Compared with those in the model group,the AR symptom score,serum IL-4,TNF-α,and OVA-sIgE levels,EOS percentage in nasal lavage fluid,and levels of p-JAK1/JAK1 and p-STAT3/STAT3 in the nasal mucosal tissue of rats in the loratadine,low-dose Chinese medicine,and high-dose Chinese medicine groups were lower,whereas the serum IFN-γ level was higher(P＜0.05).RO8191 weakened the inhibitory effect of Yiqi Wenfei Tongqiao decoction on the inflammatory response in rats with AR of lung qi deficiency and cold type.Conclusion Overall,Yiqi Wenfei Tongqiao decoction can alleviate the inflammatory response in rats with AR of lung qi deficiency and cold type by inhibiting JAK1/STAT3 signaling pathway acti-vation and regulating the balance of Th1/Th2 cytokines.

Objective:To comprehensively retrieve and evaluate the best available evidence on perioperative fluid management in patients undergoing hepatectomy for liver cancer, and to provide references for clinical practice.Methods:A systematic search was conducted across multiple platforms, including UpToDate, BMJ Best Practice, Guidelines International Network, National Institute for Health and Care Excellence, PubMed, Web of Science, China National Knowledge Infrastructure, and Wanfang Data, for clinical decisions, guidelines, expert consensus, systematic reviews, evidence summaries, and randomized controlled trials related to perioperative fluid management in patients undergoing hepatectomy for liver cancer. The search period was from database inception to March 13, 2024. The 2014 version of the Joanna Briggs Institute evidence pre-grading and recommendation grading system was used to classify the evidence.Results:A total of 14 articles were included: 3 clinical decision articles, 3 guidelines, 1 evidence summary, 5 expert consensuses, 1 systematic review, and 1 randomized controlled trial. A total of 27 best evidence items were extracted, covering seven aspects: principles of fluid therapy, preoperative fluid management, intraoperative fluid management, postoperative fluid management, fluid type selection, assessment and monitoring, and training and education.Conclusions:This study summarizes the best evidence on perioperative fluid management for hepatectomy in liver cancer patients and provides an evidence-based reference for clinical nursing practice. Healthcare professionals should apply the evidence in a personalized manner based on the actual clinical context to promote scientific fluid management in the perioperative period.

Objective:To evaluate the relationship between microRNA-29a (miR-29a) and p53 up-regulated modulator of apoptosis (PUMA) in propofol-induced reduction of glucose deprivation (GD)-induced injury to human glioma cells.Methods:Human glioma U87 cells were cultured in vitro to the logarithmic growth phase. Cells were then divided into 6 groups ( n=24 each) by the random number table method: control group (group C), group GD, propofol + GD group (group P+ GD), miR-29a inhibitor group (group I), miR-29a inhibitor + GD group (group I+ GD) and miR-29a inhibitor+ propofol+ GD group (group I+ P+ GD). Cells were cultured in normal condition in group C. The culture medium was changed to glucose-free DMEM solution, and the cells were cultured for 12 h in group GD. In group P+ GD, cells were incubated with propofol 10 μmol/L for 12 h and then incubated in glucose-free DMEM solution for 12 h. In group I, group I+ GD and group I+ P+ GD, miR-29a inhibitor was transfected into cells using lipofectamine transfection kit, and then the cells were cultured for 48 h, and the other treatments were similar to those previously described in group P+ GD. The cell survival rate, mitochondrial membrane potential and level of reactive oxygen species (ROS) were determined. The expression of miR-29a was detected by quantitative real-time polymerase chain reaction, and the expression PUMA was detected by Western blot. Results:Compared with group C, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group GD and group I ( P<0.05). Compared with group GD, the cell survival rate and mitochondrial membrane potential were significantly increased, the level of ROS was decreased, the expression of miR-29a was up-regulated, and the expression of PUMA was down-regulated in group P+ GD, and the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ GD ( P<0.05). Compared with group P+ GD, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ P+ GD ( P<0.05). Conclusions:The mechanism by which propofol reduces glucose deprivation-induced injury to human glioma cells is related to up-regulation of miR-29a expression and down-regulation of PUMA expression.

Objective:To explore the mechanism of metformin on osteogenic differentiation of rat jaw bone marrow mesenchymal cells(BMSCs)under high sugar and high fat environment.Methods:BMSCs of male SD rats were isolated and cultured in vitro and divided into 4 groups:Control group(C group),high sugar and high fat group(H group),control cells and H group cells were respectively stimulated with metformin(CM group and HM group).EDU staining was used to detect the cell proliferation;after osteogenesis and adi-pogenesis induction of BMSCs,alkaline phosphatase staining,alizarin red(O)staining and oil red O staining were respectively used to detect the osteogenic and adipogenic differentiation of the cells.The protein expression of Runx2 and OCN was detected by Western blot and immunofluorescence staining respectively.Results:Compared with the H group,in the HM group the cell proliferation ability was enhanced,the expression levels of Runx2 and OCN were increased(P＜0.05),the osteogenic differentiation ability was significantly in-creased,and the adipogenic differentiation ability was significantly decreased.Conclusion:In vitro,metformin promotes the prolifera-tion and osteogenic differentiation of rat jaw BMSCs cultured with a high sugar and high fat environment by increase of the expression of Runx2 and OCN.

Objective To explore the changes in serum energy metabolites in patients with peripheral T-cell lymphoma,and investigate serum biomarkers for monitoring peripheral T-cell lymphoma from the perspective of energy metabolism.Methods Multiple/selected reaction monitoring(MRM/SRM)was used to detect the energy-related metabolites in the sera of 16 patients with newly diagnosed peripheral T-cell lymphoma admitted in the Hematology Medical Center of the Second Affiliated Hospital of Army Medical University from November 2020 to December 2021,as well as 10 recruited healthy volunteers.The corresponding clinical data including medical history,laboratory results and image data were collected and retrospectively analyzed.Results Significant differences were seen in the contents and expression profiles of serum energy metabolism-related products between the patients and the healthy volunteers.The patients had significantly reduced serum contents of cyclic AMP,succinate,citrate and cis-aconitate(P＜0.05),and elevated D-glucose 6-phosphate content(P＜0.05).The serum contents of citrate and succinate were negatively correlated with the risk stratification(low-,moderate-and high-risk)and clinical stage of the disease(P＜0.05).Meanwhile,there was a negative correlation between the contents of L-malic acid and citrate and the mid-term efficacy evaluation results,such as complete/partial response(CR/PR)or stable disease(SD)(P＜0.05).For patients with extranodal NK/T cell lymphoma(n=10),there were also significant reductions in the contents of cyclic AMP,succinate,citrate,isocitrate and cis-aconitate in the sera of patients compared with healthy volunteers(P＜0.05),and the contents of citrate and succinate were negatively correlated with the clinical stage(P＜0.05)and were rather correlated with mid-term efficacy evaluation results(CR/PR or SD)(P＜0.05).For patients with angioimmunoblastic T-cell lymphoma(n=6),the serum contents of cyclic AMP,citrate and succinate were significantly lower,while the content of D-glucose 6-phosphate was higher when compared with the healthy volunteers(P＜0.05),and the content of succinate was negatively correlated with both clinical stage and risk grade of the patients(P＜0.05).Conclusion There are 5 serum differential metabolites identified between patients with peripheral T-cell lymphoma and healthy controls,and succinate and citrate are expected to be serum biomarkers of peripheral T-cell lymphoma.

Objective:To evaluate the relationship between microRNA-29a (miR-29a) and p53 up-regulated modulator of apoptosis (PUMA) in propofol-induced reduction of glucose deprivation (GD)-induced injury to human glioma cells.Methods:Human glioma U87 cells were cultured in vitro to the logarithmic growth phase. Cells were then divided into 6 groups ( n=24 each) by the random number table method: control group (group C), group GD, propofol + GD group (group P+ GD), miR-29a inhibitor group (group I), miR-29a inhibitor + GD group (group I+ GD) and miR-29a inhibitor+ propofol+ GD group (group I+ P+ GD). Cells were cultured in normal condition in group C. The culture medium was changed to glucose-free DMEM solution, and the cells were cultured for 12 h in group GD. In group P+ GD, cells were incubated with propofol 10 μmol/L for 12 h and then incubated in glucose-free DMEM solution for 12 h. In group I, group I+ GD and group I+ P+ GD, miR-29a inhibitor was transfected into cells using lipofectamine transfection kit, and then the cells were cultured for 48 h, and the other treatments were similar to those previously described in group P+ GD. The cell survival rate, mitochondrial membrane potential and level of reactive oxygen species (ROS) were determined. The expression of miR-29a was detected by quantitative real-time polymerase chain reaction, and the expression PUMA was detected by Western blot. Results:Compared with group C, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group GD and group I ( P<0.05). Compared with group GD, the cell survival rate and mitochondrial membrane potential were significantly increased, the level of ROS was decreased, the expression of miR-29a was up-regulated, and the expression of PUMA was down-regulated in group P+ GD, and the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ GD ( P<0.05). Compared with group P+ GD, the cell survival rate and mitochondrial membrane potential were significantly decreased, the level of ROS was increased, the expression of miR-29a was down-regulated, and the expression of PUMA was up-regulated in group I+ P+ GD ( P<0.05). Conclusions:The mechanism by which propofol reduces glucose deprivation-induced injury to human glioma cells is related to up-regulation of miR-29a expression and down-regulation of PUMA expression.