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Objective:To investigate the mediating effect of rumination in primiparae on the expectation gap of social support and postpartum depression, so as to provide a reference basis for early detection and intervention in the regulation of meternal postpartum depression.Methods:In this cross-sectional study, questionnaires were administered from November 2021 to March 2022 using the general information questionnaire, the Ruminant Thinking Response Scale, the Postpartum Social Support Scale, and the Edinburgh Postpartum Depression Scale to 266 primiparae at three tertiary level A hospitals, the First Affiliated Hospital of Xi′an Jiaotong University, the Second Affiliated Hospital of Xi′an Jiaotong University, and the Northwest Women′s and Children′s Hospital, for postpartum review, and the relationship between ruminant thinking, social support expectation gap, and postpartum depression was analyzed using correlation analysis, structural equation modeling, and application of Bootsrap method.Results:The social support expectation gap, ruminative thinking, and postpartum depression average scores were (16.74 ± 12.77), (39.43 ± 4.14), (6.77 ± 2.77) points, respectively.There were positive correlations between social support expectation gap and ruminative thinking, postpartum depression, and ruminative thinking and postpartum depression ( r=0.62, 0.75, 0.70, all P<0.01). Primiparae ruminative thinking partially mediated the relationship between social support expectation gap and postpartum depression, with the mediating effect accounting for 22% of the total effect. Conclusions:Social support expectation gap can directly affect the occurrence of postpartum depression, but also indirectly through ruminative thinking, and postpartum depression can be prevented and intervened from the perspective of reducing ruminative thinking in clinical practice.
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Objective:To excavate the mechanism of the combination of Radix Ophiopogonis and Schisandra chinensis to treatatherosclerosisbased on network pharmacology to discuss its mechnism.Methods:This paper excavated the associated proteins with Radix Ophiopogonis and Schisandra chinensis from the TCMGeneDIT database, and constructed the multicomponent protein network of Radix Ophiopogonis, Schisandra chinensis and proteins ApoE-/- mice were randomly divided into control group, model group, low, medium, high dose group and atorvastatin calcium group. Except the control group, other groups were fed with H10540 high fat diet for 12 weeks. From the 4th week, the atrovastatin calcium group was given atrovastatin calcium liquid 6 mg/kg by gavage. The low, medium and high dose groups were administed 4.68, 2.34 and 1.17 g/kg, respectively, once a day by gavage for 8 weeks. The oil red staining was applied to observe the pathological changes of atherosclerotic aortic wall. Western blot was subjected to detect the expression change of mitogen activated protein kinases p38 (p38), ATP binding cassette subfamily G member 1 (ABCG1), Toll like receptor 4 (TLR4), heat shock protein 90 alpha family class a member 1 (HSP90AA1), MMP-9 and arachidonate 5-lipoxygenase (ALOX5) in liver tissue, as well as nuclear factor related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in brain tissue.Results:It was found that eleven components were interacted with 37 proteins, forming a protein interaction network with 48 nodes and 190 boundaries without isolated nodes. Compared to the model group, the level of p-p38/p38 (2.12 ± 0.12, 1.76 ± 0.11, 1.69 ± 0.10 vs. 2.45 ± 0.16), TLR4 (1.98 ± 0.10, 1.64 ± 0.11, 1.55 ± 0.12 vs. 2.68 ± 0.06), HSP90AA1 (1.79 ± 0.10, 1.66 ± 0.09, 1.59 ± 0.11 vs. 2.06 ± 0.07), MMP9 (1.84 ± 0.11, 1.75 ± 0.12, 1.66 ± 0.08 vs. 2.68 ± 0.10) in liver tissue of low, medium and high dose groups significantly decreased, the level of ABCG1 (0.53 ± 0.08, 0.78 ± 0.09, 0.81 ± 0.10 vs. 0.45 ± 0.04), ALOX5 (0.59 ± 0.04, 0.67 ± 0.09, 0.88 ± 0.07 vs. 0.47 ± 0.02) in liver tissue of low, medium and high dose groups significantly increased ( P<0.05). The expression of Nrf2 (1.62 ± 0.12, 1.32 ± 0.09, 1.14 ± 0.06 vs. 2.12 ± 0.08) in cytoplasm of brain tissue significantly decreased, and Nrf2 (1.12 ± 0.09, 1.61 ± 0.07, 1.68 ± 0.11 vs. 1.07 ± 0.08) in cell nucleus of brain tissue significantly increased. The expression of HO-1 (1.16 ± 0.09, 1.73 ± 0.11, 1.82 ± 0.08 vs. 1.05 ± 0.04) in brain tissue significantly increased. Conclusions:Network pharmacology and molecular biology were used to elucidate the molecular mechanism of the combination of Schisandra chinensis and Ophiopogon japonicus in the prevention and treatment of atherosclerosis, also to validate the related mechanism via Nrf2 pathway, which provided a reference for the further study of the combined prescription.
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Objective:To investigate the effect of IA10 regimen induction therapy on newly diagnosed adult acute myeloid leukemia (AML) patients without allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the influencing factors of prognosis.Methods:The clinical data of 99 adult patients with newly diagnosed AML treated with IA10 regimen and without allo-HSCT in the Third Hospital of Yuncheng City in Shanxi Province from January 2007 to April 2017 were retrospectively analyzed. The baseline disease characteristics, relapse and survival status and minimal residual disease (MRD) levels were obtained. The influencing factors of prognosis were evaluated by Cox regression model.Results:All the 99 patients did not undergo allo-HSCT after achieved morphologic leukemia-free state (MLFS), the blood cells of 84 cases (84.8%) recovered to complete remission (CR) when reaching MLFS, 8 cases (8.1%) had CR with incomplete recovery of platelet count (CRp), 7 cases (7.1%) had CR with incomplete recovery of blood cell count (CRi). The median relapse time, median disease-free survival time, and median overall survival time were 35 months (6-54 months), 22 months (4-49 months) and 39 months (9-73 months). Multivariate analysis showed that FLT3-ITD was an independent risk factor for relapse, disease-free survival and overall survival in all patients and patients with consolidation therapy ≥1 course (all patients: HR=3.46, 95% CI 2.03-5.97, HR=2.49, 95% CI 1.40-5.47, HR=2.70, 95% CI 1.86-5.90; patients with consolidation therapy ≥1 course: HR=2.14, 95 CI 1.67-5.64, HR=2.63, 95 CI 1.54-5.03, HR=2.06, 95 CI 1.12-4.34; all P < 0.05); the high risk group of South West Oncology Group (SWOG) was an independent risk factor for relapse and disease-free survival in all patients ( HR=2.54, 95% CI 1.16-5.30; HR=2.57, 95% CI 1.38-5.10; both P < 0.05); CRi when achieving MLFS was an independent risk factor for disease-free survival and overall survival in all patients and patients with consolidation therapy ≥ 1 course (all patients: HR=5.71, 95% CI 2.66-11.03, HR=4.46, 95% CI 2.51-9.14; patients with consolidation therapy ≥ 1 course: HR=3.87, 95% CI 1.56-9.83, HR=4.67, 95% CI 2.33-11.59; all P < 0.05), and it was an independent risk factor for relapse in all patients ( HR=3.37, 95 CI 1.26-8.91, P < 0.01); the proportion of peripheral blood primitive cells ≥ 0.50 and the positive MRD after 1 course of consolidation therapy were the independent risk factors for relapse and disease-free survival in patients with consolidation therapy ≥ 1 course (proportion of peripheral blood primitive cells ≥ 0.50: HR=1.96, 95% CI 1.25-3.41, HR=1.56, 95% CI 1.02-2.94; positive MRD after 1 course of consolidation therapy: HR=2.21, 95% CI 1.37-4.05, HR=2.46, 95% CI 1.51-4.23; all P < 0.05). There were significant differences in cumulative relapse, disease-free survival and overall survival of patients without and with 1, 2 and 3 prognostic risk factors (all P < 0.05). Conclusions:IA10 regimen is effective in the induction therapy of newly diagnosed adult AML patients without allo-HSCT. The poor molecular genetic characteristics and CRi when achieving MLFS at the first diagnosis are risk factors for the prognosis of patients, and the high proportion of peripheral blood primitive cells, the combination of monokaryotype and positive MRD after 1 course of consolidation therapy are also closely related to the poor prognosis of patients.
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Objective@#To excavate the mechanism of the combination of Radix Ophiopogonis and Schisandra chinensis to treatatherosclerosisbased on network pharmacology to discuss its mechnism.@*Methods@#This paper excavated the associated proteins with Radix Ophiopogonis and Schisandra chinensis from the TCMGeneDIT database, and constructed the multicomponent protein network of Radix Ophiopogonis, Schisandra chinensis and proteins ApoE-/- mice were randomly divided into control group, model group, low, medium, high dose group and atorvastatin calcium group. Except the control group, other groups were fed with H10540 high fat diet for 12 weeks. From the 4th week, the atrovastatin calcium group was given atrovastatin calcium liquid 6 mg/kg by gavage. The low, medium and high dose groups were administed 4.68, 2.34 and 1.17 g/kg, respectively, once a day by gavage for 8 weeks. The oil red staining was applied to observe the pathological changes of atherosclerotic aortic wall. Western blot was subjected to detect the expression change of mitogen activated protein kinases p38 (p38), ATP binding cassette subfamily G member 1 (ABCG1), Toll like receptor 4 (TLR4), heat shock protein 90 alpha family class a member 1 (HSP90AA1), MMP-9 and arachidonate 5-lipoxygenase (ALOX5) in liver tissue, as well as nuclear factor related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in brain tissue.@*Results@#It was found that eleven components were interacted with 37 proteins, forming a protein interaction network with 48 nodes and 190 boundaries without isolated nodes. Compared to the model group, the level of p-p38/p38 (2.12 ± 0.12, 1.76 ± 0.11, 1.69 ± 0.10 vs. 2.45 ± 0.16), TLR4 (1.98 ± 0.10, 1.64 ± 0.11, 1.55 ± 0.12 vs. 2.68 ± 0.06), HSP90AA1 (1.79 ± 0.10, 1.66 ± 0.09, 1.59 ± 0.11 vs. 2.06 ± 0.07), MMP9 (1.84 ± 0.11, 1.75 ± 0.12, 1.66 ± 0.08 vs. 2.68 ± 0.10) in liver tissue of low, medium and high dose groups significantly decreased, the level of ABCG1 (0.53 ± 0.08, 0.78 ± 0.09, 0.81 ± 0.10 vs. 0.45 ± 0.04), ALOX5 (0.59 ± 0.04, 0.67 ± 0.09, 0.88 ± 0.07 vs. 0.47 ± 0.02) in liver tissue of low, medium and high dose groups significantly increased (P<0.05). The expression of Nrf2 (1.62 ± 0.12, 1.32 ± 0.09, 1.14 ± 0.06 vs. 2.12 ± 0.08) in cytoplasm of brain tissue significantly decreased, and Nrf2 (1.12 ± 0.09, 1.61 ± 0.07, 1.68 ± 0.11 vs. 1.07 ± 0.08) in cell nucleus of brain tissue significantly increased. The expression of HO-1 (1.16 ± 0.09, 1.73 ± 0.11, 1.82 ± 0.08 vs. 1.05 ± 0.04) in brain tissue significantly increased.@*Conclusions@#Network pharmacology and molecular biology were used to elucidate the molecular mechanism of the combination of Schisandra chinensis and Ophiopogon japonicus in the prevention and treatment of atherosclerosis, also to validate the related mechanism via Nrf2 pathway, which provided a reference for the further study of the combined prescription.
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According to the quality requirements of clinical trials and the work characteristics and the development trend of clinical research coordinators ( CRCs),we proposed that converting non-hospital CRCs to hospital CRCs or ‘hospital Staffs’ and arranging them to assist quality management in clinical trials are very important and significant for improving the quality of clinical trials. In present study, we also analyzed the methods about how to convert non-hospital clinical research coordinators to hospital CRC and briefly described their role in quality management.
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Aim To investigate the change of miR-124 expression in methamphetamine-induced addiction in PC12 cells and the possible regulatory mechanism that it involves.Methods PC12 cells were randomly divided into 6 groups as follows: control group, methamphetamine group, agomir Negative Control group, miR-124 agomir group, agomir Negative Control+methamphetamine group and miR-124 agomir+methamphetamine group.After the treatment, the total RNA and protein were extracted in PC12 cells.The expression of miR-124 was measured by Real-time PCR and the expression of GluR2 was determined by Western blot in PC12 cells.Results Compared with those in the control group, the expression of miR-124 was remarkably decreased and the expression of GluR2 was significantly increased in the methamphetamine group in PC12 cells.Compared with those in the agomir Negative Control+methamphetamine group, the expression of miR-124 was remarkably increased and the expression of GluR2 was significantly decreased in the miR-124 agomir+methamphetamine group in PC12 cells.Conclusion MiR-124 might involve in methamphetamine-induced addiction in PC12 cells by inhibiting GluR2.
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The study was designed to explore the drug-drug interactions mechanisms mediated by OATP1B1 between traditional Chinese medicine Danshensu and rosuvastatin. First, the changes of rosuvastatin pharmacokinetics were investigated in presence of Danshensu in rats. Then, the primary rat hepatocytes model was established to explore the effects of Danshensu on the uptake of rosuvastatin by hepatocytes. Finally, HEK293T cells with overexpression of OATP1B1*a and OATP1B1*5 were established using a lentiviral delivery system to explore the effects of Danshensu on the uptake of rosuvastatin. Rosuvastatin pharmacokinetic parameters of C(max0, AUCO(0-t), AUC(0-∞) were increased about 123%, 194% and 195%, by Danshensu in rats, while the CL z/F value was decreased by 60%. Uptake of rosuvastatin in the primary rat hepatocytes was decreased by 3.13%, 41.15% and 74.62%, respectively in the presence of 20, 40 and 80 μmol x L(-1) Danshensu. The IC50 parameters was (53.04 ± 2.43) μmol x L(-1). The inhibitory effect of Danshensu on OATP1B1 mediated transport of rosuvastatin was related to the OATP1B1 gene type. In OATP1B1*5-HEK293T mutant cells, transport of rosuvastatin were reduced by (39.11 ± 4.94)% and (63.61 ± 3.94)%, respectively, by Danshensu at 1 and 10 μmol x L(-1). While transport of rosuvastatin was reduced by (8.22 ± 2.40)% and (11.56 ± 3.04)% and in OATP1B1*1a cells, respectively. Danshensu significantly altered the pharmacokinetics of rosuvastatin in rats, which was related to competitive inhibition of transport by OATPJBI. Danshensu exhibited a significant activity in the inhibition of rosuvastatin transport by OATP1B1*5-HEK293T, but not by OATP1B1*1a, suggesting a dependence on OATP1B1 sequence.
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Objective To study the effect of curcumin on the radiosensitivity of the human papillary thyroid cancer cell line TPC?1, to investigate the signaling pathway probably targeted by curcumin, and to provide new insights for the development of radiosensitizers for thyroid cancer. Methods The human papillary thyroid cancer cell line TPC?1 was treated with curcumin and radioactive iodine. CCK?8 assay, colony formation assay, and flow cytometry were used to evaluate cell proliferation, colony formation ability, and cell apoptosis, respectively. Western blot was used to measure the expression of p50, p65, and apoptosis?related proteins, Bcl?2 and Bax. Cell proliferation, colony formation ability, and cell apoptosis were determined again after the activity of the NF?κB signaling pathway was blocked by a NF?κB signaling pathway inhibitor PDTC. Results After treatment with curcumin and radioactive iodine, the human papillary thyroid cancer TPC?1 cells had reduced cell proliferation and colony formation, an elevated apoptosis rate, downregulated expression of anti?apoptotic Bcl?2, and upregulated expression of pro?apoptotic Bax in a dose?dependent manner. These results indicated that curcumin enhanced the radiosensitivity of TPC?1 cells. Curcumin inhibited the activation of the NF?κB signaling pathway in the TPC?1 cells treated with radioactive iodine. When the activity of the NF?κB pathway was blocked by PDTC, cell proliferation and colony formation were reduced and the apoptosis rate was increased, indicating an enhanced radiosensitivity of TPC?1 cells. Conclusions Curcumin is likely to target the NF?κB signaling pathway. It regulates the radiosensitivity of thyroid cancer cells by inhibiting the activity of the NF?κB signaling pathway.
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Aim To investigate the effect of indirubin derivative PHⅡ-7 and TRAIL on proliferation in breast cancer cell MCF-7 and its MDR counterpart MCF-7/ADR and the mechanism.Methods Growth inhibition rate was examined respectively by MTT assay under treatment with TRAIL or PHⅡ-7 or in combination. Cell apoptosis and ROS production were examined by flow cytometry.The change of TRAIL receptors(DR4/DR5 )in mRNA was analysed by realtime PCR.Re-sults IC50 of PHⅡ-7 on MCF-7 and MCF-7/ADR was (4.49 ±1.55 ),(3.44 ±0.90 )μmol · L-1 respec-tively;MDA-MB-231 was TRAIL sensitive cell line, and apparently TRAIL induced apoptosis in MDA-MB-23 1 .Low concentration of PHⅡ-7 in combination with TRAIL could augment TRAIL-induced cytotoxic effect including apoptosis while TRAIL or PHⅡ-7 treatment alone had limited cytotoxity to those cells.Besides, PHⅡ-7 at this concentration had little toxicity to hu-man peripheral blood mononuclear cells even if in com-bination with TRAIL.PHⅡ-7 generated ROS produc-tion inside MCF-7 and MCF-7/ADR cells and up-regu-lated DR4/DR5 expression concentration dependently. Once upon ROS scavenger NAC involved,the effect of TRAIL receptors up-regualtion by expression was abro-gated.Conclusions PHⅡ-7 at low concentration could improve the sensitivities of breast cancer cell MCF-7 and MCF-7/ADR to TRAIL,the mechanism of which may be the ability of ROS production by PHⅡ-7 help up-regulated TRAIL receptor DR4,DR5 .Our re-search set a solid foundation for PHⅡ-7 in combination with TRAIL in future clinical application.
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Background and purpose:Breast cancer is one of the most common carcinoma among female patients with high mortalities. Drug-resistance is the major reason that leads to chemotherapy failure in clinical practice. MCF-7/ADR is a multi-drug resistant cell line that was established on the basis of breast cancer cell line MCF-7. This research aimed to investigate the anti-apoptotic effect of c-fos in resistant breast cancer cell MCF-7/ADR, and to compare with its sensitive counterpart MCF-7.Methods:Doxorubicin with various concentrations was used to treat MCF-7 as well as its MDR- counterpart MCF-7/ADR. The growth inhibitory rate of MCF-7 and MCF-7/ADR wasdetermined by MTT assay. Additionally, RT-PCR was used to test the expression of P-gp and c-fos mRNA in MCF-7 and MCF-7/ADR; The expression of c-fos mRNA was detected by RT-PCR after 3 μmol doxorubicin treatment;We further established cell lines that stably interfered with c-fos, named MCF-7/ADR/si-fos-8B, MCF-7/ADR/si-fos-3D. Flow cytometry and MTT assay were used to investigate the apoptosis rate and inhibitory rate in these above cells under the treatment of 5-FU, CDDP or γ-radiation. At last, RT-PCR and Western blot analysis were used to detect the expression of bax, bcl-2, puma, p53.Results:The expression of c-fos and P-gp (MDR-1) was up-regulated in MCF-7/ADR, compared with its sensitive counterpart MCF-7. Additionally, the resistant fold of MCF-7/ADR to doxorubicin was nearly 40; The expression of c-fos was gradually up-regulated after 3 μmol doxorubicin treatment; The sensitivity to drugs (5-FU and CDDP) was increased after c-fos interference while the apoptosis rate was also increased after 5-FU, CDDP and γ-radiation treatment. RT-PCR and Western blot analysis indicated that up-regulation ofbax,puma,p53 after c-fos interference while the expression of bcl-2 was down-regulated.Conclusion:c-fos may act as an anti-apoptotic protein in resistant breast cancer cell line MCF-7/ADR by regulating the expression of apoptosis related proteins, and may play a vital role in the formation of multi-drug resistance phenotype.
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Objective To detect the proliferation and the expression levels of downstream target genes of Notch pathway of T-ALL CCRF-CEM(CEM)cell line treated with exogenous DLK1 protein,in order to investigatethe effects of DLK1 protein on the Notch pathway in CEM cells.Methods CCK-8 assay was performed to examine the proliferation of CCRF-CEM cells,which were treated with various concentration(0.5,1.0,1.5 μg/ml)DLK1 for various time(24,48,72 h).RFQ-PCR was applied to assess the mRNA expression level of Notch1 receptor and downstream target genes of Notch pathway in CEM cells,which were treated for various time(24,48,72 h).Results DLK1 protein stimulated the proliferation of CCRF-CEM cells,and the proliferation rates with different concentrations of DLK1 were 0.14±0.03,0.17±0.04,0.55±0.01 in 72 hours,respectively,there were statistic differences between that in the experimental group and that in the control group(P＜0.05).DLK1 protein up-regulated the Notch1 receptor and its downstream target genes HES1,c-myc and NF-κB.The relative transcript levels of target genes HES1 in 72 hours,c-myc in 48 hours and NF-κB in 72 hours were 3.2551±0.3100,1.6086±0.0941,2.0515±0.3453 respectively,and there were statistic differences between that in the experimental group and that in the control group(P＜0.05).Conclusion DLK1 protein stimulates the proliferation of T-ALL CCRF-CEM cells by up-regulating Notch1 receptor and downstream target genes HES1,c-myc and NF-κB of Notch pathway.
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Objective To dynamically monitor the base excess(BE) in traumatic brain injury(TBI) patients within 3 d after admission,and to assess the impact of the early BE on prognosis.Methods Blood BE was monitored for 3 d in 56 TBI patients.Patients were classified into mild group(15 patients),moderate group (22 patients) and severe group (19 patients) according to the scores of Glasgow coma scale(GCS).Patients were classified into survival group(42 patients) and dead group(14 patients) according to prognosis.Patients were classified into high BE group (35 patients,BE≥-8 mmol/L) and low BE group (21 patients,BE ＜-8 mmol/L).The relations among BE,degree of injury and prognosis were analyzed.Results The level of BE in mild group,moderate group and severe group was increased after treatment for 1,2,3 d than that before treatment.The level of BE was consistent with the degree of injury [mild group:(-3.02 ± 0.21)mmol/L; moderate group:(-8.49 ± 1.44) mmol/L;severe group:(-9.64 ± 1.19) mmol/L].The level of BE in mild group and severe group had significant difference than that in moderate group (P＜ 0.01).The level of BE in dead group before treatment and after treatment for 1,2,3 d was significantly lower than that in survival group [(-11.97 ±2.13) mmol/L vs.(-6.29 ± 1.16) mmol/L,(-9.84 ± 1.33) mmol/L vs.(-4.89 ± 1.78)mmol/L,(-8.78 ± 2.01) mmol/L vs.(-3.61 ± 1.43) mmol/L,(-7.84 ± 1.42) mmol/L vs.(-3.10 ±0.98)mmol/L] (P ＜0.01).The scores of APACHE Ⅱ before treatment and fatality rate in low BE group were significantly higher than those in high BE group [(24.84 ± 3.68) scores vs.(16.27 ± 2.21) scores,52.4％ (11/21) vs.8.6％(3/35)] (P ＜ 0.01).The scores of GCS before treatment in low BE group was significantly higher than that in high BE group [(7.56 ± 3.09) scores vs.(10.51 ± 2.43) scores](P ＜ 0.01).Conclusion The level of early BE is a good factor on evaluating the condition and prognosis in TBI patients.
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BACKGROUND: CpG oligonucleotide has been shown to strengthen the function of peripheral blood mononuclear cells (PBMCs), but its effects on type 1 diabetes mellitus has been rarely reported. OBJECTIVE: To investigate the effects of CpG oligonucleotide on the expression of interferon γ (IFN-γ), interleukin (IL) -12 and IL-10 in PBMCs in patients with type 1 diabetes mellitus versus healthy controls. METHODS: PBMCs were isolated from patients with type 1 diabetes mellitus and healthy controls and then cultured in RPMI-1640 with non-stimulator (control group) and CpG oligonucleotide (CpG oligonucleotide group), respectively. The mRNA expression of IFN-γ, IL-10, and IL-12 in PBMCs was detected by reverse transcription-polymerase chain reaction. RESULTS AND CONCLUSION: mRNA expression of IFN-γ and IL-10 was significantly lower in patients with type 1 diametes mellitus than in healthy controls (P < 0.01). In the CpG oligonucleotide group, the mRNA expression of IFN-γand IL-12 was significantly higher than in the healthy control group (P < 0.01), but the mRNA expression of IL-10 was similar to that in the healthy control group (P > 0.05). These findings demonstrated that CpG oligonucleotide can promote the production of IFN-γ and IL-12 in PBMCs of type 1 diametes mellitus.