Challenge-Hindrance Stressors and Academic Engagement Among Medical Postgraduates in China: A Moderated Mediation Model.

Background: Improving academic engagement of medical postgraduates is crucial for enhancing the quality of learning and the development of medical education. Due to medical postgraduates face high levels of stress and rigorous demands, yet the mechanisms linking challenge-hindrance stressors to academic engagement in this context remain largely unexplored. This study aims to explore the comprehensive relationship between challenge-hindrance stressors and academic engagement among medical postgraduates in China. Methods: Data were collected from 437 medical postgraduates in China, to investigate their challenge-hindrance stressors, emotional exhaustion, learning, relaxation and academic engagement. Among these postgraduates, 40.3% were male and 59.7% were female, with the mean age of the participants being 25.71 years. Statistical procedures were conducted using Mplus 8.3, ensuring a robust analysis of the data collected. Results: Our study showed that both challenge and hindrance stressors are significantly positively correlated with emotional exhaustion among Chinese medical postgraduates, and emotional exhaustion is negatively associated with academic engagement. Emotional exhaustion mediates the relationship between challenge-hindrance stressors and academic engagement. Learning plays a protective role, moderating the challenge stressors and emotional exhaustion relationship and its indirect effect on academic engagement. However, relaxation was not identified as a significant moderating factor in this context. Conclusion: Our findings not only revealed emotional exhaustion as a potential mechanism underlying the relationship between challenge-hindrance stressors and academic engagement but also validated the moderating role of learning in mitigating the adverse effects of challenge stressors on emotional exhaustion and academic engagement among Chinese medical postgraduates. This comprehensive insight into the complex dynamics between different stressors and academic engagement provides both theoretical and empirical evidence for medical universities. It underscores the importance of interventions to enhance academic engagement in stressful environments and serves as a valuable reference for the development of reasonable assessment systems. These contributions are crucial for fostering a supportive educational atmosphere and promoting the well-being of medical postgraduates.

Anxiety prevalence and associated factors among frontline nurses following the COVID-19 pandemic: a large-scale cross-sectional study.

Introduction: Nurses are more likely to experience anxiety following the coronavirus 2019 epidemic. Anxiety could compromise nurses' work efficiency and diminish their professional commitment. This study aims to investigate nurses' anxiety prevalence and related factors following the pandemic in multiple hospitals across China. Methods: An online survey was conducted from April 16 to July 3, 2023, targeting frontline nurses who had actively participated in China. Anxiety and depression symptoms were assessed using the Self-rating Anxiety Scale and the Self-rating Depression Scale (SDS), respectively. Multivariable logistic regression analysis was employed to identify factors linked with anxiety. Results: A total of 2,210 frontline nurses participated in the study. Overall, 65.07% of participants displayed clinically significant anxiety symptoms. Multivariable logistic regression revealed that nurses living with their families [2.52(95% CI: 1.68-3.77)] and those with higher SDS scores [1.26(95% CI: 1.24-1.29)] faced an elevated risk of anxiety. Conversely, female nurses [0.02(95% CI: 0.00-0.90)] and those who had recovered from infection [0.05(95%CI: 0.07-0.18)] demonstrated lower rates of anxiety. Discussion: This study highlights the association between SDS score, gender, virus infection, living arrangements and anxiety. Frontline nurses need to be provided with emotional support to prevent anxiety. These insights can guide interventions to protect the mental well-being of frontline nurses in the post-pandemic period.

Effect of Sevoflurane Anesthesia on Intraoperative Spikes, High-Frequency Oscillations, and Phase-Amplitude Coupling in MRI-Normal Hippocampus.

INTRODUCTION: The purpose of this study was to determine the effect of sevoflurane anesthesia on spikes, high-frequency oscillations (HFOs), and phase-amplitude coupling using a modulation index in MRI-normal hippocampus, with the aim of evaluating the utility of intraoperative electrocorticography in identifying the epileptogenic hippocampus during sevoflurane administration. METHODS: Eleven patients with intractable temporal lobe epilepsy with a normal hippocampus on MRI underwent extra-operative electrocorticography evaluation. Patients were assigned to the Ictal (+) or Ictal (-) group depending on whether the parahippocampal gyrus was included in the seizure onset zone. Intraoperative electrocorticography was performed under 0.5 and 1.5 minimum alveolar concentration of sevoflurane. The rates of spikes, ripples, fast ripples (FRs), ripples on spikes, FRs on spikes, and MI HFO(3-4 Hz) were evaluated. RESULTS: During the intraoperative electrocorticography procedure, sevoflurane administration was found to significantly increase the rate of spikes, ripples on spikes, fast ripples on spikes, and MI HFO(3-4 Hz) in the Ictal (+) group (P < 0.01). By contrast, the Ictal (-) group exhibited a paradoxical increase in the rate of ripples and fast ripple (P < 0.05). CONCLUSIONS: Our findings indicate that the administration of sevoflurane during intraoperative electrocorticography in patients with MRI-normal hippocampus can lead to a dose-dependent enhancement of epileptic biomarkers (spikes, ripples on spikes, fast ripples on spikes, and MI (HFO 3-4)) in the epileptogenic hippocampus, while paradoxically increasing the rate of ripples and fast ripple in the nonepileptogenic hippocampus. These results have significant implications for the identification of the MRI-normal hippocampus that requires surgical intervention and preservation of the nonepileptogenic hippocampus.

Establishment and validation of a torsade de pointes prediction model based on human iPSC­derived cardiomyocytes.

Drug-induced cardiotoxicity is one of the main causes of drug failure, which leads to subsequent withdrawal from pharmaceutical development. Therefore, identifying the potential toxic candidate in the early stages of drug development is important. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are a useful tool for assessing candidate compounds for arrhythmias. However, a suitable model using hiPSC-CMs to predict the risk of torsade de pointes (TdP) has not been fully established. The present study aimed to establish a predictive TdP model based on hiPSC-CMs. In the current study, 28 compounds recommended by the Comprehensive in vitro Proarrhythmia Assay (CiPA) were used as training set and models were established in different risk groups, high- and intermediate-risk versus low-risk groups. Subsequently, six endpoints of electrophysiological responses were used as potential model predictors. Accuracy, sensitivity and area under the curve (AUC) were used as evaluation indices of the models and seven compounds with known TdP risk were used to verify model differentiation and calibration. The results showed that among the seven models, the AUC of logistic regression and AdaBoost model was higher and had little difference in both training and test sets, which indicated that the discriminative ability and model stability was good and excellent, respectively. Therefore, these two models were taken as submodels, similar weight was configured and a new TdP risk prediction model was constructed using a soft voting strategy. The classification accuracy, sensitivity and AUC of the new model were 0.93, 0.95 and 0.92 on the training set, respectively and all 1.00 on the test set, which indicated good discrimination ability on both training and test sets. The risk threshold was defined as 0.50 and the consistency between the predicted and observed results were 92.8 and 100% on the training and test sets, respectively. Overall, the present study established a risk prediction model for TdP based on hiPSC-CMs which could be an effective predictive tool for compound-induced arrhythmias.

Comprehensive transcriptomic analysis of immune-related eRNAs associated with prognosis and immune microenvironment in melanoma.

Background: Recent evidence suggests that enhancer RNAs (eRNAs) play key roles in cancers. Identification of immune-related eRNAs (ireRNAs) in melanoma can provide novel insights into the mechanisms underlying its genesis and progression, along with potential therapeutic targets. Aim: To establish an ireRNA-related prognostic signature for melanoma and identify potential drug candidates. Methods: The ireRNAs associated with the overall survival (OS-ireRNAs) of melanoma patients were screened using data from The Cancer Genome Atlas (TCGA) via WGCNA and univariate Cox analysis. A prognostic signature based on these OS-ireRNAs was then constructed by performing the least absolute shrinkage and selection operator (LASSO) Cox regression analysis. The immune landscape associated with the prognostic model was evaluated by the ESTIMATE algorithm and CIBERSORT method. Finally, the potential drug candidates for melanoma were screened through the cMap database. Results: A total of 24 OS-ireRNAs were obtained, of which 7 ireRNAs were used to construct a prognostic signature. The ireRNAs-related signature performed well in predicting the overall survival (OS) of melanoma patients. The risk score of the established signature was further verified as an independent risk factor, and was associated with the unique tumor microenvironment in melanoma. We also identified several potential anti-cancer drugs for melanoma, of which corticosterone ranked first. Conclusions: The ireRNA-related signature is an effective prognostic predictor and provides reliable information to better understand the mechanism of ireRNAs in the progression of melanoma.

Evaluation of biomarkers for doxorubicin­induced cardiac injury in rats.

Drug-induced cardiotoxicity is a leading cause of failure in drug development and predicting its occurrence in non-clinical studies is the primary preventive measure. The present study aimed to evaluate the changes in biomarkers during acute and chronic myocardial injury induced by doxorubicin (DOX) in rats. A rat model of acute myocardial injury was established through a single-dose, intraperitoneal injection of DOX (40 mg/kg), the changes in biomarkers were measured at 2, 4, 8 and 24 h after administration, following DOX administration, creatine kinase (CK) and fatty acid-binding protein 3 (FABP3) levels increased between 8 and 24 h, whereas cardiac troponin I (cTnI) peaked at 8 h. To establish a chronic myocardial injury model, rats received 1, 2 or 3 mg/kg DOX weekly by caudal vein injection for 2, 4, 6 or 7 weeks, the changes in biomarkers were detected at 2, 4, 6 and 8 weeks, the results showed that cTnI increased significantly after 2 and 8 weeks of administration. A significant increase in FABP3 and microRNA (miR)-146b levels was observed after 8 weeks of administration. Receiver operating characteristic curve and correlation analysis showed that cTnI and miR-146b had relatively high predictive values for chronic myocardial injury (area under the curve, 0.83 and 0.71, respectively) and were closely correlated with myocardial damage. These data suggested that CK, cTnI and FABP3 were relatively sensitive to DOX-induced acute myocardial injury, whereas cTnI and miR-146b were relatively sensitive to DOX-induced chronic myocardial injury.

Clinical safety study of photobiomodulation in acute spinal cord injury by scattering fiber.

The study aimed to design a reliable and straightforward PBM method by implanting a medical scattering fiber above surgically exposed spinal cord in SCI patients. Moreover, the safety of this method was examined. Twelve patients with acute SCI (ASIA B) requiring posterior decompression were recruited. The medical scattering fiber was implanted above the spinal cord, and was continuously irradiated at 810 nm, 300 mW, 30 min/day, once per day for 7 days. The vital signs (temperature, blood pressure, respiratory rate, heart rate, and oxygen saturation), infection indicators (WBC, NEUT, hs-CRP, and PCT), photo-allergic reaction indicators (Eosinophil and Basophil), coagulation function indicators (PT, APTT, TT) and neurological stability indicators (ASIA sensory and motor scores) were recorded to evaluate the safety of PBM. Three months after surgery, 12 patients completed follow-up. In our study, direct PBM on SCI site did not cause clinically pathologic changes in vital signs of the patients. All patients had higher WBC, NEUT, and hs-CRP at day 3 during irradiation than those before surgery, and returned to normal at day 7. The changes in Eosinophil and Basophil that were closely associated with allergic reactions were within normal limits throughout the course of irradiation. The coagulation function (PT, APTT, and TT) of patients were also in the normal range. The ASIA sensory and motor scores of all patients had no changes throughout the irradiation process. However, in the follow-up, both ASIA sensory and motor scores of all patients had minor improvement than those in pre-irradiation, and 7 patients had adverse events, but they were not considered to be related to PBM. Our study might firstly employ direct PBM in the SCI by using scattered optical fibers. In a limited sample size, our study concluded that direct PBM at the site of SCI would not produce adverse effects within the appropriate irradiation parameters. The method is safe, feasible, and does not add additional trauma to the patient. Our preliminary study might provide a new methodology for the clinical PBM treatment of acute SCI.

RIP2 knockdown inhibits cartilage degradation and oxidative stress in IL-1ß-treated chondrocytes via regulating TRAF3 and inhibiting p38 MAPK pathway.

Receptor-interacting protein 2 (RIP2) is a key mediator implicated in multiple cellular processes, and its dysregulation has been recently reported in colitis, asthma and other inflammatory diseases. However, the effects of RIP2 on osteoarthritis (OA) and the underlying mechanisms remain unclear. In this study, we found that RIP2 expression was upregulated in human articular cartilage tissues with OA and interleukin-1ß (IL-1ß)-treated chondrocytes. Knockdown of RIP2 inhibited IL-1ß-induced extracellular matrix (ECM) and oxidative stress. Moreover, knockdown of TRAF3 reversed the effects of RIP2 silencing on cartilage degradation and oxidative stress in IL-1ß-induced chondrocytes. In addition, p38 mitogen-activated protein kinase (MAPK) activator dehydrocorydalmine chloride (Dc) also reversed the effects of RIP2 silencing on IL-1ß-induced chondrocytes. Taken together, our data reveal that RIP2 knockdown inhibits cartilage degradation and oxidative stress in IL-1ß-treated chondrocytes by regulating TRAF3 expression and p38 MAPK pathway activation.

Rational Construction of a N, F Co-doped Mesoporous Cobalt Phosphate with Rich-Oxygen Vacancies for Oxygen Evolution Reaction and Supercapacitors.

Transition-metal phosphates have been widely applied as promising candidates for electrochemical energy storage and conversion. In this study, we report a simple method to prepare a N, F co-doped mesoporous cobalt phosphate with rich-oxygen vacancies by in-situ pyrolysis of a Co-phosphate precursor with NH4 + cations and F- anions. Due to this heteroatom doping, it could achieve a current density of 10 mA/cm2 at lower overpotential of 276 mV and smaller Tafel slope of 57.11 mV dec-1 on glassy carbon. Moreover, it could keep 92 % of initial current density for 35 h, indicating it has an excellent stability and durability. Furthermore, the optimal material applied in supercapacitor displays specific capacitance of 206.3 F g-1 at 1 A ⋅ g-1 and maintains cycling stability with 80 % after 3000 cycles. The excellent electrochemical properties should be attributed to N, F co-doping into this Co-based phosphate, which effectively modulates its electronic structure. In addition, its amorphous structure provides more active sites; moreover, its mesoporous structure should be beneficial to mass transfer and electrolyte diffusion.

Rational Design of a N,S Co-Doped Supermicroporous CoFe-Organic Framework Platform for Water Oxidation.

It remains a challenge to rational design of a new metal-organic framework (MOF) as highly efficient direct electrocatalysts for the oxygen evolution reaction (OER). Herein, we developed a simple and effective method to explore a new pillared-layered MOF with syringic acid as a promising OER electrocatalyst. The isostructural mono-, heterobimetallic MOF and N,S co-doped MOF by mixing thiourea were quickly synthesized in a high yield under solvothermal condition. Moreover, the optimized N,S co-doped MOF exhibits the lowest overpotential of 254 mV at 10 mA cm-2 on a glass carbon electrode and a small Tafel slope of 50 mV dec-1 , especially, this catalyst also possesses long-term electrochemical durability for at least 16 h. According to the characterization, the incorporation of N and S atoms into this heterobimetallic CoFe-based MOF could modify its pore structure, tune the electronic structure, accordingly, improve the mass and electron transportation, and facilitate the formation of active species, as a consequence, the improved activity of this new N,S co-doped MOF for OER should be mainly be ascribed to higher electrochemical activation toward the active species via in situ surface modification during the OER process.

Anti-biofouling therapeutic nanoparticles with removable shell and highly efficient internalization by cancer cells.

Cationic gelatin nanoparticles ((+)nGNPs) were prepared by in situ polymerization upon the surfaces of monodispersed gelatin nanoparticles (GNPs) using N-(3-Aminopropyl)methacrylamide (APm) as monomer, which were then decorated with doxorubicin terminated poly(2-methylacryloyloxyethyl phosphorylcholine) (DOX-pMPC) via EDC/NHS conjugation to obtain core-shell nanoparticles ((+)nGNPs@DOX-pMPC) for cancer therapy. The non-fouling pMPC shell could effectively shield the positively charged surface of inner nanoparticle and prevent non-specific protein adsorption, thus endowing the materials with potential for long-acting cancer treatment. Furthermore, the acyl hydrazone bond connecting DOX and pMPC chain could be easily hydrolyzed in the weakly acidic tumor microenvironment. After decladding of the pMPC shell, electropositive (+)nGNPs carrying the drugs can be effectively internalized by cancer cells to induce apoptosis, avoiding undesirable hindrance caused by the superhydrophilic outer layer. On combining the above properties, this drug delivery system can be a promising candidate for long-acting, low-toxicity and high-efficiency cancer therapy.

Endothelin B receptor promotes the proliferation and immune escape of malignant gliomas.

PURPOSE: As a kind of difficult to cure tumour, malignant gliomas have attracted widespread attention. The proliferation and immune escape of tumour cells were closely related to the development of malignant gliomas. The aim of this study was to investigate the role of endothelin B receptor (NTBR) in gliomas. METHODS: RT-PCR was used to detect the expression of NTBR mRNA in glioma tissue and glioma cell lines. The expression of NTBR in glioma tissues was detected by immunohistochemistry. MTT assay was used to detect the viability of U87 cells after adding NTBR. Cell cloning assay was used to detect the cell proliferation ability. Western blot was used to detect the expression of TGF-ß and the expression of Treg after adding NTBR to U87. RESULT: The expression of NTBR in glioma tissues and cells was significantly higher than that in the control group by RT-PCR. After adding NTBR, cell proliferation of U87 was significantly enhanced and TGF-ß and Treg were significantly expressed. It was suggested that NTBR could contribute to tumour immune escape in glioma, and it was found that there was a positive correlation between NTBR expression and different stages in malignant gliomas. CONCLUSION: Endothelin B receptor can increase the proliferation of glioma cells and tumour immune escape. The expression of endothelin B is closely related to the clinical stage of glioma.

Recombinant adenoviral vector expressing human wild-type p53, GM-CSF, and B7-1 genes suppresses the growth of glioma in vivo.

Malignant gliomas are the most common of primary brain tumors and have been proven incurable with conventional treatments. Evidence have shown that a recombinant adenoviral vector expressing human wild-type p53, granulocyte-macrophage colony-stimulating factor (GM-CSF), and B7-1 genes (BB-102) may have antitumor effects in vitro. In this study, we investigated the effects of BB-102-based vaccine on glioma in vivo. An animal model using nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice with human immune system was established. The mice were vaccinated with inactivated U251 glioma cells transduced with BB-102 or adenoviral vector expressing green fluorescence protein (Ad-GFP) as a control and followed by the challenge of live U251 glioma cells. Tumor growth and antitumor responses were measured. Data showed that mice vaccinated with BB-102 had significantly reduced local tumor growth compared to mice with Ad-GFP vaccination or the control group. Histopathological analysis displayed low tumor cell density and significant infiltration of human peripheral blood lymphocytes (HuPBLs) in the tumor tissues of mice transduced with BB-102. Immunohistochemical analysis showed that mutant p53 was not expressed in tumor tissues of mice with BB-102 vaccination, and the expression level of Ki67 was significantly lower in the tumor tissues of the BB-102 group than those in the Ad-GFP group or the control group. Further study demonstrated that mice with BB-102 vaccination had significantly increased total T cell numbers, total T cell proportion, CD4+ T cell proportion, and CD8+ T cell proportion in spleens, as well as higher value of IgG, IgA, and IgE in sera. These data suggest that the recombinant adenoviral vector expressing human wild-type p53, GM-CSF, and B7-1 genes could suppress glioma in NOD/SCID mice model and might be considered as a novel strategy for glioma therapy.

Alkaloids from Lycoris caldwellii and their particular cytotoxicities against the astrocytoma and glioma cell lines.

Phytochemical investigation of the ethanol extract of the bulbs of Lycoris caldwellii afforded four new alkaloids, (+)-N-methoxylcarbonyl-nandigerine (1), (+)-N-methoxycarbonyl-lindcarpine (2), (+)-10-O-methylhernovine N-oxide (3), and (+)-3-hydroxy-anhydrolycorine N-oxide (4). Structural elucidation of all the compounds were performed by spectral methods such as 1D and 2D (¹H-¹H COSY, HMQC, and HMBC) NMR spectroscopy, in addition to high resolution mass spectrometry. All the alkaloids were in vitro evaluated for their cytotoxic activities against eight tumor cell lines (BEN-MEN-1, CCF-STTG1, CHG-5, SHG-44, U251, BGC-823, HepG2, and SK-OV-3). Alkaloids 1 and 2 exhibited particular cytotoxic activities against astrocytoma and glioma cell lines with IC50 of 9.2-11.3 µM and 10.4-12.2 µM respectively.

The risk of second cancers after diagnosis of primary thyroid cancer is elevated in thyroid microcarcinomas.

BACKGROUND: Thyroid cancers have increased dramatically over the past few decades. Comorbidities may be important, and previous studies have indicated elevated second cancer risk after initial primary thyroid cancers. This study examined the risk of second cancers after development of a thyroid cancer, primary utilizing the Surveillance, Epidemiology, and End Results (SEER) program database. METHODS: The cohort consisted of men and women diagnosed with first primary thyroid cancer who were reported to a SEER database in 1973-2008 (n=52,103). Standardized incidence ratios (SIR) were calculated for all secondary cancers. Confidence intervals and p-values are at 0.05 significance alpha level and are two-sided based on Poisson exact methods. RESULTS: In this cohort, 4457 individuals developed second cancers. The risk of developing second cancers after a primary thyroid cancer varied from 10% to 150% depending on different cancer types. Cancers in all sites, breast, skin, prostate, kidney, brain, salivary gland, second thyroid, lymphoma, myeloma, and leukemia were elevated. The magnitude of the risk varied by histology, tumor size, calendar year of first primary thyroid cancer diagnosis, and the treatment of the primary thyroid cancer. The risk of a second cancer was elevated in patients whose first primary thyroid carcinomas were small, or were diagnosed after 1994, or in whom some form of radiation treatment was administered. CONCLUSIONS: This large population-based analysis of second cancers among thyroid cancer patients suggests that there was an increase of second cancers in all sites, and the most commonly elevated second cancers were the salivary gland and kidney. Additionally, the increase in second cancers in patients with recently diagnosed thyroid microcarcinomas (<10 mm) suggests that aggressive radiation treatment of the first primary thyroid cancer, the environment, and genetic susceptibility, may increase the risk of a second cancer.

Polymorphisms in Th1/Th2 cytokine genes, hormone replacement therapy, and risk of non-Hodgkin lymphoma.

We conducted a population-based case-control study in Connecticut women to test the hypothesis that genetic variations in Th1 and Th2 cytokine genes modify the relationship between hormone replacement therapy (HRT) and risk of non-Hodgkin lymphoma (NHL). Compared to women without a history of HRT use, women with a history of HRT use had a significantly decreased risk of NHL if they carried IFNGR2 (rs1059293) CT/TT genotypes (OR = 0.5, 95%CI: 0.3-0.9), IL13 (rs20541) GG genotype (OR = 0.6, 95%CI: 0.4-0.9), and IL13 (rs1295686) CC genotype (OR = 0.6, 95%CI: 0.4-0.8), but not among women who carried IFNGR2 CC, IL13 AG/AA, and IL13CT/TT genotypes. A similar pattern was also observed for B-cell lymphoma but not for T-cell lymphoma. A statistically significant interaction was observed for IFNGR2 (rs1059293 P(for interaction) = 0.024), IL13(rs20541 P(for interaction) = 0.005), IL13 (rs1295686 P(for interaction) = 0.008), and IL15RA (rs2296135 P(for interaction) = 0.049) for NHL overall; IL13 (rs20541 P(for interaction) = 0.0009), IL13(rs1295686 P(for interaction) = 0.0002), and IL15RA (rs2296135 P(for interaction) = 0.041) for B-cell lymphoma. The results suggest that common genetic variation in Th1/Th2 pathway genes may modify the association between HRT and NHL risk.

Adenovirus mediated transfer of p53, GM-CSF and B7-1 suppresses growth and enhances immunogenicity of glioma cells.

OBJECTIVES: Malignant gliomas are good targets for gene therapy because they have been proven incurable with conventional treatments. However, malignant gliomas are genetically and physiologically highly heterogeneous, and current gene therapy interventions have been designed to target only a few variations of this kind of disease. Hence, we developed a combined gene therapy approach using a recombinant adenovirus carrying human wild-type p53 (WT-p53), granulocyte-macrophage colony-stimulating factor (GM-CSF) and B7-1 genes (designated BB-102) to combat the disease. METHODS: Human malignant glioma cells U251 and U87 were transduced with BB-102. Expression of WT-p53, GM-CSF and B7-1 genes were determined by Western blot, enzyme linked immunosorbent assay and flow cytometric analysis, respectively. Growth rates were determined by serial cell counts. Apoptosis was detected by flow cytometric analysis. Proliferation of autologous peripheral blood lymphocytes (PBLs) and cytotoxicity against primary glioma cells were assessed by cell proliferation and cytotoxicity assay kits, respectively. RESULTS: By the transduction of BB-102, high expression levels of the three exogenesis genes were detected in glioma cells. Cell growth was inhibited and apoptosis was induced. Significant proliferation of autologous PBLs and specific cytotoxicity against primary glioma cells were also induced by the infection of BB-102 in vitro, with the effect being more evident than that of Ad-p53. CONCLUSION: These results suggest that glioma cell vaccination co-transferred with p53, GM-CSF and B7-1 genes may be a feasible and effective immunotherapeutic approach in glioma treatments.