Objective: To investigate factors influencing perioperative blood transfusion in patients with scarred uterus during pregnancy undergoing cesarean section, construct and validate a transfusion risk prediction model, and provide evidence for preoperative assessment and blood management. Methods: Clinical data of 405 patients undergoing cesarean section for scarred uterus during pregnancy at the First Affiliated Hospital of Xi'an Jiaotong University from January 2020 to December 2024 were retrospectively collected. The dataset was randomly divided into a training set (n=284) and a validation set (n=121) at a 7∶3 ratio. Within the training set, Firth-penalized logistic regression was employed for multivariate analysis to identify independent factors influencing perioperative blood transfusion and construct a predictive model. Model performance was evaluated in the validation set. Results: Multivariate Firth regression analysis showed that severe placenta previa (OR=75.566, 95%CI: 8.603-9979.174) and placenta accreta (OR=4.591, 95%CI: 1.120-19.416) were independent risk factors for perioperative blood transfusion, while preoperative red blood cell count (OR=0.189, 95%CI: 0.083-0.405) and fibrinogen levels (OR=0.588, 95%CI: 0.395-0.855) were protective factors. The predictive model constructed based on these four variables demonstrated good discriminatory performance, with areas under the receiver operating characteristic curves of 0.803 (95%CI: 0.740-0.867) and 0.753 (95%CI: 0.644-0.862) in the training and validation sets, respectively. Conclusion: For patients with scarred uterus during pregnancy undergoing cesarean section, severe placenta previa and placenta accreta significantly increase the risk of transfusion, while higher preoperative red blood cell count and fibrinogen levels exert a protective effect. The predictive model established in this study facilitates the identification of patients requiring transfusion, thereby enabling preoperative blood preparation and optimized blood management.

Spine fracture and dislocation are common traumatic spinal conditions that often require surgical intervention due to compromised spinal stability. Surgical approaches include anterior, posterior, and combined anterior-posterior spinal procedures. According to the specific surgical requirements, patients may be placed in the prone position or repositioned between prone and supine positions during surgery. Intraoperative repositioning has become an essential step in patient positioning. However, during repositioning, patients with spinal fracture and dislocation are at increased risk for complications such as hemodynamic instability, nerve injury, and pressure injuries to the skin and soft tissue. Notably, due to the instability of the spinal cord, even minor manipulations can further exacerbate the damage, potentially leading to severe outcomes like paraplegia. Although the current clinical guidelines provide instructive recommendations for standard position, there remains no specific protocols for intraoperative repositioning in patients with spine fracture and dislocation. With a concern for the lack of clinical studies on positioning techniques, risk prevention, and operational norms for special patients, no applicable guidelines or standards are available. A consensus was required to provide clinical reference, meet the requirements of surgical treatment, and minimize the safety risks of patients caused by improper placement of positions. Professional Committee of Operating Room Nursing of Shaanxi Nursing Association organized experts in nursing management and operating room nursing from major hospitals across China to formulate Expert consensus on intraoperative repositioning for patients with spinal fracture and dislocation ( version 2025). The consensus provides 11 recommendations covering pre-repositioning preparation, intraoperative maneuvers, and post-repositioning observation, aiming to provide references for clinical standardization of the intraoperative repositioning process and protection of patients′ safety.

Objective To analyze the predictive value of apolipoprotein B(apoB)and apoB to apolipoprotein A1(apoA1)ratio(apoB/A1)in acute myocardial infarction(AMI)of phlegm blended with blood stasis syndrome.Methods A total of 200 patients with AMI confirmed by coronary angiography in Foshan Hospital of Traditional Chinese Medicine during the trial period were collected.Data collection covered the basic information of gender,age,medical history of hypertension,coronary heart disease and diabetes mellitus,and smoking history,the information of four diagnostic methods of traditional Chinese medicine(TCM),and relevant indicators of blood lipids,the number of lesioned branches of coronary arteries and the Gensini scores.The predictive value of apoB and apoB/A1 for AMI of phlegm blended with blood stasis syndrome was explored by univariate Logistic regression analysis and multivariate Logistic regression analysis as well as by plotting the Receiver Operating Characteristic(ROC)curves.Results(1)Among the 200 AMI patients,41 cases were differentiated as qi deficiency and blood stasis syndrome,36 cases as qi stagnation and blood stasis syndrome,74 cases as phlegm blended with blood stasis syndrome,and 49 cases as other syndromes(including 16 cases of cold accumulation in heart vessels syndrome,22 cases of qi and yin deficiency syndrome,and 11 cases of healthy-qi deficiency and yang collapse syndrome).(2)The difference of Gensini scores among the patients with various TCM syndrome types were statistically significant(H=43.735,P=0.000<0.001).And the Gensini scores in the patients with syndromes of qi deficiency and blood stasis,qi stagnation and blood stasis,and phlegm blended with blood stasis were relatively high,being 60.0(43.0,87.0),70.0(48.5,84.0)and 65.0(40.0,95.0)points,respectively,which were higher than that of the other TCM syndrome types[44.0(32.0,64.0)points].The pairwise comparison between various TCM syndrome types showed that the differences were statistically significant(P<0.05).However,there was no statistically significant difference in the number of lesioned branches of coronary arteries among the patients with various TCM syndrome types(H=1.180,P=0.758>0.05).(3)The results of correlation analysis showed that the number of lesioned branches of coronary arteries,Gensini score and apoB/A1 were significantly and positively correlated(r=0.140,P=0.049<0.05;r=0.205,P=0.004<0.01).(4)The results of univariate Logistic regression analysis and multivariate Logistic regression analysis showed that apoB and apoB/A1 were the independent risk factors for phlegm blended with blood stasis syndrome(P<0.01).ROC curve analysis showed that apoB/A-1 exerted a high predictive value for AMI of phlegm blended with blood stasis syndrome,with high sensitivity and specificity.Conclusion It is indicated that ApoB/A1 can be used as an objective indicator for predicting AMI of phlegm blended with blood stasis syndrome in clinical practice.

Objective To explore the scheme for the deployment and withdrawal of the surgical module of the new-type tent hospital system.Methods A set of standardized scheme for deploying and withdrawing the surgical module of the new-type tent hosital system was proposed and implemented in terms of labor division,operation precedure,operation technique and precaution.The operating time,number of operational errors and number of equipment damages were recorded for each of the five deployment and withdrawal operations before and after the program was executed,and the team members'immediate heart rate,percentage of maximum heart rate(MHR)and rating of perceived exercise(RPE)at the end of the operation were recorded after the program was implemented.SPSS 26.0 software was used for statistical analysis.Results The standardized scheme had the deployment time shortened from(85.15±11.430)min to(58.23±8.513)min,withdrawal time decreased from(65.36±9.369)min to(48.92±7.129)min,with the differences being statistically significant(P＜0.05);the numbers of operatio-nal errors and equipment damages were both reduced when compared with those before the implementation of the schemce;the immediate heart rate of the team members at the end of the operation ranged from 43 to 157 beats/min,with an average value of 151.1 beats/min,the individual MHR percentages were from 75％to 87％,with an average value of 81.1％,and the RPE scores were from 14 to 17,with an average value of 15.3,which all could be categorized as moderate-operation intensity.Condusion The standardized deployment and withdrawal scheme for the surgical module meets the needs of actual combat and training assessment,and thus is worthy promoting in medical institutions equipped with the surgical module of the new-type tent hosital system.[Chinese Medical Equipment Journal,2025,46(2):74-79]

Objective To investigate the effect of cordyceps sinensis(CS)on the activation of fibroblasts through IL-6 trans-signaling pathway and its specific mechanism in the treatment of renal fibrosis.Methods Renal fibrosis mouse model was established by unilateral ischemia/reperfusion(UIR),and the mice were administered intragastrically CS,soluble glycoprotein 130 Fc(sgp130Fc)or Hyper-IL-6.Masson's trichrome staining was utilized to identify tubulointerstitial fibrosis.PAS staining was utilized to assess the extent of renal injury.Western blot was employed to analyze the expression levels of fibrosis markers[alpha-smooth muscle actin(α-SMA),fibronectin(FN)]and proteins associated with IL-6 trans-signaling pathway[phosphorylated signal transducer and activator of transcription 3(p-STAT3),soluble interleukin-6 receptor(sIL-6R)].The expression and localization of proteins were additionally detected by immunohistochemistry,immunofluorescence and qPCR.The effect of cordyceps sinensis extract cordycepin on IL-6 trans-signaling in fibroblasts was further investigated in vitro.Results The results from in vivo experiments showed that administration of CS during the chronic phase demonstrated a beneficial protective impact on inflammation and fibrosis in the affected kidney,and serum creatinine levels and collagen deposition were decreased.Western blot analysis revealed a decrease in the expression levels of α-SMA,FN,as well as IL-6 trans-signaling pathway protein p-STAT3,sIL-6R in the treatment group.Additionally,the mRNA expression levels of chemokines monocyte chemoattractant protein-1(MCP-1)and C-X-C motif chemokine ligand 12(CXCL12)were also decreased in the CS treatment group.Additionally,Hyper-IL-6 can partially counteract the therapeutic effects of CS.In vitro experiments further demonstrated that cordycepin inhibited the secretion of IL-6 from NRK-52E.Combined treatment of recombinant IL-6 and sIL-6R protein activated NRK-49F,leading to a significant increase in α-SMA,FN,and p-STAT3 expression levels.Cordycepin or sgp130Fc treatment significantly inhibited the proliferation of fibroblasts induced by IL-6 trans-signaling pathway.Conclusion CS can significantly reduce IL-6 secretion by renal tubular epithelial cells and inhibit the activation of IL-6 trans-signaling pathway in fibroblasts,thereby ameliorating renal interstitial fibrosis.

Objective:To elucidate the inhibitory effect of interferon-γ(IFN-γ)on the proliferation of neuroblastoma cells and the protentral gene signature of IFN-γ and the relationship between the expression of gene signature of IFN-γ in the neuroblastoma cells and its adverse prognosis,and to clarify the effect of IFN-γ and its gene signture in the neuroblastoma.Methods:The SK-N-BE(2)(proto-oncogene N-MYC amplification type)and SH-SY5Y(proto-oncogene N-MYC non-amplification type)neuroblastoma cells were selected and treated with different concentrations(0,500,750,1 000 and 1 500 μg·L-1)of IFN-γ for 24 h,followed by cell proliferation assays using cell counting kit-8(CCK-8).Transcriptome sequencing was then performed to identify the gene signature of IFN-γ.Additionally,the tissue microarrays from 23 cases of neuroblastoma and 6 cases of normal adrenal gland samples were collected,immunohistochemistry(IHC)analysis was used to to detect the expression of gene signature of IFN-γ.Based on the expression levels of gene signature of IFN-γ,the samples were divided into SULT2B1 low and high expression groups.The correlation between the expression of gene signature of IFN-γ and poor prognosis of the patients was analyzed.Results:The CCK-8 assay results showed that as IFN-γconcentration increased,the proliferation of SK-N-BE(2)cells was significantly inhibited(P＜0.01),with inhibitory rates of SK-N-BE(2)cells in four groups were 6.73％,6.77％,7.67％,and 9.19％,respectively.In contrast,the proliferation rate of SH-SY5Y cells were significantly increased with the increase of IFN-γ concentrations(P＜0.01),and the proliferation rates of SH-SY5Y cells in four groups were 46.80％,79.19％,70.30％,and 72.33％,respectively.Transcrip tome sequencing identified hydroxysteroid sulfotransferase 2B1(SULT2B1)as a potential gene signature of IFN-γ.The IHC analysis results showed the expression amount of SULT2B1 protein in neuroblastoma tissues was increased.The clinical data analysis results revealed significant differences in age(Z=-2.618,P=0.018),lymphnode metastasis(x2=4.439,P=0.035),and distant metastasis(x2=5.856,P=0.016)between low and high SULT2B1 expression groups.Conclusion:IFN-γ can inhibit the proliferation of SK-N-BE(2)cells while promoting the proliferation of SH-SY5Y cells.SULT2B1 is a potential gene signature of IFN-γ,and its expression is upregulated in neuroblastoma tissue.SULT2B1 high expression is significantly associated with poor prognosis in the neuroblastoma patients.

The innate immune system detects cellular stressors and microbial infections, activating programmed cell death (PCD) pathways to eliminate intracellular pathogens and maintain homeostasis. Among these pathways, pyroptosis, apoptosis, and necroptosis represent the most characteristic forms of PCD. Although initially regarded as mechanistically distinct, emerging research has revealed significant crosstalk among their signaling cascades. Consequently, the concept of PANoptosis has been proposed—an inflammatory cell death pathway driven by caspases and receptor-interacting protein kinases (RIPKs), and regulated by the PANoptosome, which integrates key features of pyroptosis, apoptosis, and necroptosis. The core mechanism of PANoptosis involves the assembly and activation of the PANoptosome, a macromolecular complex composed of three structural components: sensor proteins, adaptor proteins, and effector proteins. Sensors detect upstream stimuli and transmit signals downstream, recruiting critical molecules via adaptors to form a molecular scaffold. This scaffold activates effectors, triggering intracellular signaling cascades that culminate in PANoptosis. The PANoptosome is regulated by upstream molecules such as interferon regulatory factor 1 (IRF1), transforming growth factor beta-activated kinase 1 (TAK1), and adenosine deaminase acting on RNA 1 (ADAR1), which function as molecular switches to control PANoptosis. Targeting these switches represents a promising therapeutic strategy. Furthermore, PANoptosis is influenced by organelle functions, including those of the mitochondria, endoplasmic reticulum, and lysosomes, highlighting organelle-targeted interventions as effective regulatory approaches. Cardiovascular diseases (CVDs), the leading global cause of morbidity and mortality, are profoundly impacted by PCD. Extensive crosstalk among multiple cell death pathways in CVDs suggests a complex regulatory network. As a novel cell death modality bridging pyroptosis, apoptosis, and necroptosis, PANoptosis offers fresh insights into the complexity of cell death and provides innovative strategies for CVD treatment. This review summarizes current evidence linking PANoptosis to various CVDs, including myocardial ischemia/reperfusion injury, myocardial infarction, heart failure, arrhythmogenic cardiomyopathy, sepsis-induced cardiomyopathy, cardiotoxic injury, atherosclerosis, abdominal aortic aneurysm, thoracic aortic aneurysm and dissection, and vascular toxic injury, thereby providing critical clinical insights into CVD pathophysiology. However, the current understanding of PANoptosis in CVDs remains incomplete. First, while PANoptosis in cardiomyocytes and vascular smooth muscle cells has been implicated in CVD pathogenesis, its role in other cell types—such as vascular endothelial cells and immune cells (e.g., macrophages)—warrants further investigation. Second, although pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) are known to activate the PANoptosome in infectious diseases, the stimuli driving PANoptosis in CVDs remain poorly defined. Additionally, methodological challenges persist in identifying PANoptosome assembly in CVDs and in establishing reliable PANoptosis models. Beyond the diseases discussed, PANoptosis may also play a role in viral myocarditis and diabetic cardiomyopathy, necessitating further exploration. In conclusion, elucidating the role of PANoptosis in CVDs opens new avenues for drug development. Targeting this pathway could yield transformative therapies, addressing unmet clinical needs in cardiovascular medicine.

OBJECTIVE: Aloin, the main active component in Aloe vera (L.) Burm. f., has shown promising anti-tumor effects. This study investigated the impact of aloin in lung squamous cell carcinoma (LUSC) and explored its functional mechanism. METHODS: We analyzed the viability, migration, invasion, proliferation, and apoptosis of two LUSC cell lines after treatment with aloin. Target molecules of aloin and downstream target transcripts of nuclear receptor subfamily 3 group C member 2 (NR3C2) were predicted by bioinformatics. The biological functions of NR3C2 and metallothionein 1 M (MT1M) in the malignant properties of LUSC cells were determined. A co-culture system of LUSC cells with monocyte-derived macrophages was constructed. Mouse xenograft tumor models were generated to analyze the functions of aloin and NR3C2 in the tumorigenic activity of LUSC cells and macrophage polarization in vivo. RESULTS: Aloin suppressed malignant properties of LUSC cells in vitro. However, these effects were negated by the silencing of NR3C2. NR3C2 was found to activate MT1M transcription by binding to its promoter. Additional upregulation of MT1M suppressed the malignant behavior of LUSC cells augmented by NR3C2 silencing. Analysis of the M1 and M2 markers/cytokines in the macrophages or the culture supernatant revealed that aloin treatment or MT1M overexpression in LUSC cells enhanced M1 polarization while suppressing M2 polarization of macrophages, whereas NR3C2 silencing led to reverse trends. Consistent findings were reproduced in vivo. CONCLUSION This study demonstrated that aloin activates the NR3C2/MT1M axis to suppress the malignant behavior of LUSC cells and M2 macrophage polarization. Please cite this article as: Chen YN, Lu JY, Gao CF, Fang ZR, Zhou Y. Aloin blocks the malignant behavior of lung squamous cell carcinoma cells and M2 macrophage polarization by modulating the NR3C2/MT1M axis. J Integr Med. 2025; 23(2): 195-208.
Lung Neoplasms/metabolism* ; Humans ; Animals ; Cell Line, Tumor ; Carcinoma, Squamous Cell/metabolism* ; Mice ; Macrophages/drug effects* ; Emodin/analogs & derivatives* ; Metallothionein/genetics* ; Cell Proliferation/drug effects* ; Cell Movement/drug effects* ; Apoptosis/drug effects* ; Receptors, Glucocorticoid/genetics*

Objective:To explore the feasibility of shortening the time of long exercise test (LET) from 120 to 60 minutes by analyzing the positive rate within 60 minutes among periodic paralysis (PP) patients who were positive in 120-minute test.Methods:The data of patients undergoing 120-minute LET from January 2015 to October 2021 in Beijing Tiantan Hospital, Capital Medical University were retrospectively analyzed, with 30%, 33%, and 40% as diagnostic cut-off values, respectively. PP patients with positive results within 120 minutes after exercise were enrolled in the study. The positive rate within 30 minutes and 60 minutes after exercise was calculated. The change rates of compound muscle action potential (CMAP) amplitude and the sensitivity and specificity of LET at 30 minutes, 60 minutes, and 120 minutes after exercise were analyzed. The change rate of CMAP amplitude in PP patients who did not show positive results within 60 minutes was further calculated.Results:A total of 254 patients were examined, including 114 PP patients. With 30%, 33%, and 40% as diagnostic cut-off values, the results showed that there were 88, 88, and 82 positive PP patients, respectively. Under each diagnostic cut-off values, the age of positive PP patients was (32±10) years, with a male proportion of 98% (86/88), 98% (86/88), and 99% (81/82), respectively; the positive rate of PP patients within 30 minutes after exercise was 60% (53/88), 58% (51/88), and 41% (34/82), respectively; the positive rate of PP patients within 60 minutes after exercise was 91% (80/88), 86% (76/88), and 83% (68/82), respectively. At the cut-off values of 30%, 33% and 40%, the change rate of CMAP amplitude at 30 minutes [-36% (-49%, -23%), -36% (-49%, -23%), -37% (-51%, -24%)], 60 minutes [-51% (-66%, -40%), -51% (-66%, -40%), -53% (-66%, -42%)] and 120 minutes [-57% (-67%, -45%), -57% (-67%, -45%), -58% (-67%, -46%)] after exercise showed statistically significant difference among 3 time points ( H=57.764, 57.764, 59.616, respectively, all P<0.001); the further comparison between time points showed that there was statistically significant difference in the change rate of CMAP amplitude between 60 minutes ( Z=5.419, 5.419, 5.531, respectively, all P<0.001), 120 minutes ( Z=7.325, 7.325, 7.431, respectively, all P<0.001) and 30 minutes after exercise, but there was no statistically significant difference in the change rate of CMAP amplitude between 120 minutes and 60 minutes after exercise ( Z=1.906, 1.906, 1.899, respectively, all P>0.05); the sensitivity of LET for the diagnosis of PP at 60 minutes after exercise was 70.2% (80/114), 66.7% (76/114) and 59.6% (68/114), and the specificity of LET for the diagnosis of PP was 77.9% (109/140), 84.3% (118/140) and 91.4%(128/140), respectively. When 30%, 33% and 40% were used as the diagnostic cut-off values, and the change rate of CMAP amplitude at 60 minutes after exercise fell below these cut-off values but showed a decline of ≥20%, ≥22% and ≥24%, respectively, the detection time should be extended to 120 minutes. Conclusions:Whether using 30%, 33%, or 40% as diagnostic cut-off values, it is feasible to shorten the LET time from 120 minutes to 60 minutes. The 60-minute LET has good sensitivity and specificity for the diagnosis of PP. It is recommended to extend the detection time to 120 minutes for patients with a ≥20%, ≥22%, or ≥24% decline in CMAP amplitude at 60 minutes after exercise while falling short of corresponding diagnostic cut-off values when 30%, 33%, and 40% are used as diagnostic cut-off values. This method can not only improve the examination efficiency of LET, but also minimize the missed diagnosis as much as possible.