Objective To design the family support scale for adolescent patients with nephritic syndrome. Methods 192 adolescent patients with nephritic syndrome were selected in the pilot investigation, and then formed the first questionnaire. The reliability and the validity of the questionnaire were evaluated by the experts. Results The questionnaire involved 15 items and its reliability and the validity were satisfied. There was a positive correlation between the family support and the self-nursing degree. Conclusion The reliability and the validity of this questionnaire are both up to the demands, it can used to study the condition of family support for adolescent patients with nephrotic syndrome.

Objective To report the clinical features and inwardly rectifying potassium channel 18 (KCNJ18) gene mutation in a group of patients with thyrotoxic periodic paralysis (TTP).Methods Fiftyseven TTP cases (55 male and 2 female) were collected in our clinic from July 2002 to October 2011.The KCNJ18 gene was directly sequenced in 57 TTP patients and 50 health Chinese controls through the nested PCR.According to the results of gene screening,the clinical features of KCNJ18 patients and non-KCNJ18 patients were retrospectively summarized and analyzed.Results In 4 male patients with TPP,we found 3 novel heterogeneous mutations (p.Q126X,p.K360T,p.E388K) and 1 reported mutation (p.A200P) in the KCNJ18 gene.The age of onset was 19-25 years old,and the duration ranged from 2 to 8 hours.The 4 patients all presented severe muscle weakness.The attacks of muscle weakness preceded overt symptoms of hyperthyroidism in the 4 patients. Three patients showed recurrent weakness during the 13-28 months follow-up,while the episodic weakness never appeared when patients got euthyroid. Conclusions The mutations in the KCNJ18 gene are responsible for a part of Chinese patients with TPP.The patients with KCNJ18 mutations have a shorter disease course,severer manifestation,and higher prevalence of recurrence as compared with those TPP patients without KCNJ18 mutations.

AIM:To investigate the effect of growth differentiation factor 11 ( GDF11 ) on the expansion of CD8 +memory stem T cells ( Tscm) and to further improve the effect of adoptive immunotherapy.METHODS:Healthy human peripheral blood mononuclear cells ( PBMCs) were isolated by density gradient centrifugation at first.Among the i-solated PBMCs, CD8 +T cells were further purified with MACS microbeads.The CD8 +T cells were then randomly divided into experimental groups and control group.The same volume of different concentrations of GDF11 were added into the ex-perimental groups, and the same volume of PBS solution was added into the control group.Finally, the expansion of Tscm in experimental groups and control group was measured by flow cytometry at several time points.RESULTS:GDF11 sig-nificantly increased the number of Tscm in CD8 +T cells in vitro expansion and also dramatically increased the ratio of Tscm in CD8 +T cells.Furthermore, 400 μg/L GDF11 treatment for 3 weeks was the optimal condition to induce CD8 +Tscm. CONCLUSION:GDF11 effectively increases the number and ratio of Tscm in the CD8 +T cells in cell culture growth, thereby creating a new strategy to further improve the efficiency of adoptive immunotherapy.

AIM:To investigate the effects of myeloid-related protein 8/14 ( MRP8/14 ) on the survival and apoptosis of human alveolar epithelial cell line A549, and to explore the role of nuclear factor-κB (NF-κB) in this process. METHODS:A549 cells were treated with different doses of MRP8/14 or stimulated with MRP8/14 for different time.The effect of MRP8/14 on the viability of A549 cells was determined by CCK-8 assay.The apoptotic rates were tested by flow cytometry.The nuclear translocation of NF-κB p65 was detected by Western blot and indirect immunofluorescence.Be-sides, the phosphorylation level of NF-κB p65 was determined by Western blot.NF-κB-specific inhibitor Bay 11-7082 was used to further analyze the role of NF-κB in the apoptosis induced by MRP8/14.RESULTS:The viability of the A549 cells was affected by MRP8/14 in a dose-and time-dependent manner.Flow cytometric analysis showed that the apoptotic rates were increased in the cells treated with MRP8/14 (P<0.01).In A549 cells administered with MRP8/14, NF-κB p65 was significantly phosphorylated and translocated into the nuclei, suggesting the activation of NF-κB signaling pathway. However, NF-κB-specific inhibitor Bay 11-7082 significantly attenuated the cell apoptosis induced by MRP8/14 ( P <0.01).CONCLUSION:NF-κB plays an important role in regulating the apoptosis of human alveolar epithelial cells in-duced by MRP8/14.

AIM:To investigate the inhibitory effect of PDE4 inhibitor rolipram on the releases of inflammatory cytokines in mouse macrophages (RAW264.7 cells) induced by myeloid-related protein 8/14 (MRP8/14), and to explore the role of nuclear factor-κB (NF-κB) in this process.METHODS:RAW264.7 cells were treated with MRP8/14.The inflammatory cytokines TNF-α and IL-6 were determined by LiquiChip and qPCR.In contrast, RAW264.7 cells were pretreated with rolipram prior to MRP8/14 exposure.After MRP8/14 challenge, the inflammatory cytokines TNF-α and IL-6 were determined by LiquiChip and qPCR.Moreover, the phosphorylation level of NF-κB P65 was determined by Western blot.The nuclear translocation of NF-κB P65 in RAW264.7 cells was detected by indirect immunofluorescence.RESULTS:The results of LiquiChip and qPCR showed that MRP8/14 enhanced the expression of TNF-α and IL-6 (P<0.01),while pretreatment with rolipram markedly down-regulated the level of inflammatory cytokines induced by MRP8/14 (P<0.05).Meanwhile, MRP8/14 significantly activated the phosphorylation of NF-κB P65, and the protein expression of p65 in the nucleus was increased,while pretreatment with rolipram suppressed the phosphorylation of NF-κB P65 induced by MRP8/14.CONCLUSION:Rolipram may significantly reduce the releases of the inflammatory cytokines induced by MRP8/14 through the NF-κB signaling.

AIM:To explore the effects of stanniocalcin 2 (STC2) on the proliferation, migration and the process of epithelial-mesenchymal transition (EMT) in human hepatocellular carcinoma HepG2 cells.METHODS:The expression levels of STC2 in the hepatocellular carcinoma cell lines and normal liver cells were assessed by Western blot.Colony formation assay was used to test the effect of STC2 on the proliferation of HepG2 cells.The effects of STC2 on the expression of proliferation-related molecules at mRNA and protein levels were determined by RT-qPCR and Western blot.The effect of STC2 on the migration ability was measured by Transwell assay.The mRNA and protein levels of vimentin and E-cadherin in STC2-overexpressing and-silencing cell lines were detected by RT-qPCR and Western blot.RESULTS:Compared with the normal liver cell line, the protein expression of STC2 was up-regulated in the hepatocellular carcinoma cell lines.The results of colony formation assay indicated that STC2 promoted the proliferation of HepG2 cells.STC2 significantly regulated the proliferation-related gene expression, such as cyclin D1.The results of Transwell assay showed that STC2 enhanced the migration ability of the HepG2 cells and influenced the EMT process.CONCLUSION:STC2 promotes the proliferation of HepG2 cells and affects the expression of proliferation-related genes.STC2 influences the process of EMT and promotes the migration of HepG2 cells.

AIM:To explore the mitochondrial pathway in the apoptosis of PC3 cells induced by PXD101 (also named as belinostat).METHODS:PC3 cells were treated with PXD101 at different doses or stimulated with PXD101 for different time.The effect of PXD101 on the viability of PC3 cells was measured by CCK-8 assay.The apoptotic rates and the mitochondrial membrane potential (MMP) were analyzed by flow cytometry.The protein levels of Bcl-2, Bax and cytochrome C (Cyt C) were determined by Western blot.The caspase-3 activity were tested by caspase-3 activity assay kit.RESULTS:The viability of the PC3 cells was inhibited by PXD101 in a dose-and time-dependent manner.Flow cytometric analysis showed that the apoptotic rates were increased in the cells treated with PXD101 (P<0.01).At the same time, PXD101 induced the decreases in MMP and Bcl-2, the release of Cyt C, and the increase in caspase-3 activity.CONCLUSION:PXD101 induces the apoptosis of human prostate cancer cell line PC3 by mitochondrial signal pathway.

0.05). The mean growth values in AdCMV-tk/GCV- and AdVEGF-tk/GCV-treated tumors were significantly lower than those in untreated tumors and AdVEGF-tk/saline-untreated tumors( P

AIM: To investigate the expression and function of apoptosis-related protein, Fas, FasL, and Bcl-2 in the pathogenesis of autoimmune thyroiditis. METHODS: Immunohistochemical staining was performed on 20 Hashimoto's thyroiditis (HT), 20 Graves' disease (GD), and 20 thyroid follicular adenoma (TFA, as control). RESULTS: All the cases expressed Fas, mainly on the cell surface and cytoplasm. FasL was found in all except 3 of the TFA. Bcl-2 in 15 of HT, 19 of GD, 17 of TFA. In TFA follicular cells expressed moderate Fas and minimal or absent FasL. In HT, follicles adjacent to infiltrating lymphocytes showed a increased levels of Fas and FasL, but infiltrating lymphocytes exhibited weaker staining of Fas and FasL than thyrocytes. In GD, thyrocytes and lymphocytes showed nearly similar Fas with HT, but rather weaker for FasL than HT. Bcl-2 was nearly similar in GD and TFA, but follicular cells in vicinity of lymphocytes and lymphocytes located in germinal centers of HT tissues exhibited significantly weaker. CONCLUSION: The expression of Fas, FasL and Bcl-2 in Hashimoto's thyroiditis and Graves' disease was nearly similar. Strong FasL expression and weak Bcl-2 expression on the follicles in HT may induce apoptosis. These results provide further proof that the functions of Fas and its ligand and Bcl-2 may play an important part in the pathogenesis of autoimmune thyroid diseases. The lymphocytes do not seem to be directly engaged in the process with their own FasL, but they may provide some cytokines that, in turn, up-regulates Fas and/or FasL leading to apoptosis.

Objective To explore the effects of ecoimmunonutrition support on the intestinal barrier function and pancreas in rats with severe acute pancreatitis (SAP). Methods Totally 64 SPF rats were randomly divided into sham operation group (control group) , SAP without enteral nutrition support group (SAP group), SAP with early enteral nutrition support group (EEN group), and SAP with early ecoimmunonutrition support group (EIN group). Bacteria translocation (BT), plasma endotoxin (ET) , gut permeability, pancreas pathology score,and distant ileum pathology were determined on the 4th and 7th post-modeling day. Results The BT rate was significantly higher in SAP group, EEN group, and EIN group than in control group (P ＜ 0.05), was significantly lower in EEN group and EIN group than in SAP group (P ＜ 0.05), and was significantly lower in EIN group than in EEN group (P ＜ 0.05). ET and FD-40 levels in blood were both significantly higher in SAP group, EEN group, and EIN group than in control group (P ＜0.01)and were significantly lower in EIN group and EEN group than in SAP group (P ＜0.01); ET was significantly lower in EIN group than in control group (P ＜0.05). Pathological scores were significantly higher in SAP group, EEN group, and EIN group than in control group (P ＜0.01)and were significantly lower in EEN group and EIN group than in SAP group (P ＜ 0.01). The individual pathological scores of EIN group were not significantly different from EEN group (P ＞ 0.05), while the total score was significantly lower in EIN group than in EEN group (P ＞ 0.05). Distant iliac mucosa was significantly thicker in EIN group than in other groups. Conclusions Early enteral nutrition support protects the intestinal barrier and pancreas in rats with SAP. Ecoimmunonutrition has better nutritional effectiveness than the normal enteral nutrition.