[ Objective ] To investigate the therapeutic effect of Chinese herbal medicines, which have the actions of dispersing stagnated liver-Qi and promoting bile secretion, clearing heat and removing damp, activating blood and removing blood-stasis, in the treatment of the third-level or above intrahepatic biliary duct stone. [Methods] After the routine surgical treatment including cholecystectomy, choledochotomy with T-tube drainage and choledochoscope lithotomy, 42 cases of third-level or above intrahepatic biliary duct stone received Dandao Paishi Mixture (DPM, mainly composed of Herba Lysimachiae, Radix Clematidis, Herba Artemisiae Scopariae, Radix Aucklandiae, Rhizoma Curcumae Longae, Radix Curcumae, etc.) for oral use. The effects of DPM on the intrahepatic biliary duct stone were evaluated after treatment. [Results] Before the treatment of DPM, the stones in third-level or above intrahepatic biliary ducts cannot be taken out; after the treatment of DPM, T-tube reverse biliary contrast examination showed that stones were removed in 39 (92.9%) cases, stones still existed in the common bile duct in 3 cases and then were removed by lithotomy through T-tube sinus of the common bile duct with Olympus fiber choledochoscope 8 weeks later. [Conclusion] DPM has good lytholytic and lithagogue effects for the treatment of third-level or above intrahepatic biliary duct stone and for intrahepatic biliary duct incarcerated stone. It can also reduce the postoperative residue of stone and recurrence rate.

Objective To investigate the effects of narrow-band ultraviolet B (NB-UVB) therapy on the levels of plasmin and CC chemokine ligand 20 (CCL20) in peripheral blood of patients with psoriasis vulgaris.Methods A total of 60 patients with psoriasis vulgaris in progressive stage were treated with NB-UVB radiation thrice a week for 8 weeks.Enzyme-linked immunosorbent assay (ELISA) was performed to detect the levels of plasmin and CCL20 in the peripheral blood of the patients before and after the treatment,as well as in the peripheral blood of 50 healthy controls.Results After the treatment,psoriasis area and severity index (PASI) scores in patients were significantly decreased compared with those before the treatment (2.54 ± 1.64 vs.10.26 ± 3.14,t =17.40,P ＜ 0.05),and the response rate was up to 87％ (52/60).Before the treatment,levels of plasmin and CCL20 were both significantly higher in the patient group than in the control group (plasmin:180.07 ± 40.62 μg/L vs.76.30 ± 26.92 μg/L,t =15.45,P ＜ 0.05;CCL20:422.41 ± 129.87 pg/L vs.205.33 ± 49.89 pg/L,t =11.15,P ＜ 0.05).After the treatment,levels of plasmin (148.22 ± 40.05 μg/L) and CCL20 (329.67 ± 100.73 pg/L) in patients were significantly decreased compared with those before the treatment (t =4.97,6.44,P ＜ 0.05),but still significantly higher than those in controls (t =10.82,7.95,P ＜ 0.05).Before the treatment,the level of plasmin was positively correlated with the level of CCL20 in peripheral blood of the patients (r =0.57,P ＜ 0.05),and the levels of plasmin and CCL20 were both positively correlated with the PASI score (r =0.49,0.62,respectively,both P ＜ 0.05).Conclusion NB-UVB radiation may exert a therapeutic effect on psoriasis vulgaris by reducing levels of plasmin and CCL20 in peripheral blood of patients.

Objective: To explore the relationship between platelet counts at admission and in-hospital mortality in patients with type A acute aortic dissection (AAD). Methods: We investigated 183 consecutive patients with CT conifrmed diagnosis of type A AAD treated in our hospital from 2012-02 to 2013-05. There were 126 (68.9%) male and the patients were divided into 3 sets of groups.①In-hospital surviving group,n=157 and In-hospital death group,n=26.②According to platelet counts, the patients were divided into 5 groups: Q1 group, platelet counts ≤ 119×109/L,n=36, Q2 group, platelet (120-149) ×109/L,n=37, Q3 group, platelet (150-173)×109/L, n=36, Q4 group, platelet (174-228)×109/L,n=37, Q5 group, platelet >228×109/L,n=37.③At admission, platelet ≤ 119×109/L,n=36 and platelet >119×109/L,n=147. In addition, the patients were further divided into another 4 groups based on operative condition: platelet ≤ 119×109/L with operation,n=18, without operation,n=18; platelet > 119×109/L with operation,n=96, without operation,n=51. The basic information at admission including platelet counts, WBC and D-dimer were studied in all groups, the primary endpoint was in-hospital mortality. Results: The overall in-hospital mortality was 14.3%. Compared with In-hospital surviving group, the In-hospital mortality group had decreased platelet counts, lower blood pressure and higher level of D-dimer. The mortality in Q1 group (38.9%) was higher than those in Q2, Q3, Q4 and Q5 groups (10.8%, 11.1%, 8.1% and 2.7%), allP<0.001. The risk of death in Q5 group was higher than Q1 group (HR=11.2, 95% CI 2.13-123.3,P=0.007). With adjusted age, gender and other relevant factors, when platelet counts ≤ 119×109/L, the risk of in-hospital mortality with Cox multivariate model I analysis was (HR3.90, 95% CI 1.67-9.09,P=0.002), with Cox model II was (HR=2.67, 95% CI 1.15 -6.19,P=0.023). Conclusion: AAD patients with admission platelet counts ≤ 119×109/L had the high risk of in-hospital death, even with operation, lower platelet counts was still related to in-hospital death.

Objective To investigate the effects and mechanism of IL-6 on invasion and metastasis of human pancreatic cancer cells. Methods IL-6 was added into the culture media of human pancreatic cancer cells Capan-2 and SW1990. Cell growth was measured by MTT assay. Western blot and immunocytochemistry were performed to detect Phosphorylated STAT3 (P-STAT3) protein. VEGF and MMP-2 mRNA and protein expression were examined using fluorescence quantitative polymerase chain reaction (RT-PCR) and Western blot, respectively. The invasion ability of SW1990 and Capan2 cells was determined by cell invasion assay in vitro. Results 100 ng/mL IL-6 significantly promoted growth and invasion ability of Capan-2 and SW1990 cells (P＜0.05). The use of IL-6 not only markedly increased the protein expression of P-STAT3, VEGF and MMP-2, but also greatly increased the mRNA expression of MMP-2 and VEGF. Conclusions STAT3 signal transducer pathway activation with IL-6 can promote the invasion ability of pancreatic cancer cells in vitro through up-regulation of MMP-2 and VEGF expression. STAT3 signal transducer may provide a novel therapeutic target for the treatment of pancreatic cancer.

Objective To explore the influence of coal-arsenic exposure on human T cells proliferation and its mechanism.Methods Blood samples colleoted from individuals which lived in arsenism area of coal-burning type and non-arsenism area in Guizhou Province were divided into exposed group(17),mild(35),moderate(38) and severe arsenism group(19)and control group(35)according to Diagnosis Smndard for Endemic Arsenism (WS/T 211-2001).T cell stimulation index wag determined by methyl thiazolyl tetrazolium(MTT)colorimetric method.The intracellular Ca2+ exponential(IECa2+)in peripheral blood mononuclear cell(PBMC)was analyzed by Fho-3/AM dye and flow cytometry.DNA binding activity of actively T cells nuclear factor(NF-AT)in PBMC was evaluated by electrophoretie mobility shift assay(EMSA).Results Concanavalin A(ConA)stimulation decreased the T cells stimulation indexes in exposed group,mild,moderate and severe arsenism groups(1.315±0.962, 1.611±1.224,1.114±0.545,1.289±0.875)compared with control group(2.322±1.241),all the differences being statistically significant(P＜0.01).After stimulated by anti-CD3 monoclonal antibody(McAb),the T cells stimulation index in exposed group,mild,moderate and severe arsenism group(0.997±0.177,1.103±0.291,1.007±0.221, 0.957±0.205) were lower than that of control group(1.842±0.429,P ＜ 0.01 ). IECa2+ of PBMC after treated by anti-CD3 McAb in mild,moderate and severe arsenism group( 110.130±49.637,92.429±31.191,77.640± 35.372) were lower compared with control group(145.986±59.450,P ＜0.01 ). Moreover,IECa2+ in moderat and severe arsenism group were lower than exposed group(121.337±46.410,P ＜ 0.05). DNA binding activity of PBMC NF-AT in mild,moderate and severe arsenism group(1.354±0.446,1.290±0.291,1.159±0.411 ) were lowered than that of control group(1.722±0.291,P ＜ 0.01) and exposed group(1.611±0.294,P ＜ 0.05). Conclusions The coal-arsenic exposure can reduce the human T cells stimulation indexes,IECa2+ in PBMC and the DNA binding activity of NF-AT. It suggest that arsenic may suppress the proliferation ability of human T cells,which may be partly related to the influence of arsenic on T cell receptor(TCR)/CD3 signal transduetion pathway.

Objective To investigate the activation of T lymphocytes in human peripheral blood and the signaling molecules in protein kinase C/nuclear factor KB(PKC/NF-κB) pathway expressivity or activity changes in human peripheral blood mononuclear cells(PBMCs) exposed to coal-arsenic,to explore the role of PKC/NF-κB signal pathway in activation of T cells in human exposed to coal-arsenic. Methods Blood samples were collected from individuals who lived in arsenism area of coal-burning in Guizhou province, and were divided into asymptomatically exposed group (12),mild arsenism group (33),moderate arsenism group (34) and severe arscnism group (15) according to Diagnosis Standard for Endemic Arsenism (WS/T 211-2001). The individuals who lived in non-arsenism area were control group(27). The ratio of activated T ceils was analyzed by flow cytometry. DNA binding activity of NF-κB in PBMCs was evaluated by electrophoretic mobility shift assay(EMSA). The expression of PKCθ and phospho-PKCθ(pPKCθ) in PBMCs were detected with western blotting analysis. Results The ratio of activating T cells in asymptomatically exposed group[(21.76±15.31)%],mild arsenism group[(18.41±11.36)%],moderate arsenism group[(17.78±11.93)%]and severe arsenism group[(18.79±13.38)%]were all higher than that of control group[(3.19±2.12)%],the difference among all groups being statistically significant(F = 7.893,P < 0.05). DNA binding activity of PBMCs NF-κB in asymptomatically exposed group,mild arsenism group,moderate arsenism group and severe arsenism group(1.49±0.24,1.58±0.30,1.57±0.34,1.51±0.16) were higher than that of the control group(1.30±0.17),the difference being statistically sign/ficant(P < 0.05 or < 0.01). The expression of PBMCs pPKCθ in mild arsenism group,moderate arsenism group and severe arsenism group(0.64± 0.14,0.64±0.27,0.62±0.12) were all lower than that of the control group(0.93±0.20),the difference being statistically significant(P < 0.05). There were significant negative correlations between the expression of pPKCθ and the activity of NF-κB(r =-0.565,P < 0.01). There were significant positive correlations between the activity of NF-κB and the ratio of activating T cells(r = 0.546,P < 0.01). Conclusion Coal-arsenic enhances the DNA binding activity of NF-κB,reduces the expression of PBMCs pPKCθ in human PBMCs and up-regulates the activity of T cells. It suggests that the PKC/NF-κB signal might be one of transduction pathway via activating of T cells by coal-arsenic.

Objective To investigate the clinical features of a patient diagnosed with Jacobsen syndrome (JBS) and Paris-Trousseau syndrome (PTS) using chromosomal microarray analysis. Method A retrospective analysis including the patients' clinical manifestations, laboratory examination and genetic analysis was carried out and related literature were reviewed. Results A 14 month-old girl with global development retardation was reported. The patient can sit but cannot walk independently. The patient also presented hypsicephaly, ocular hypertelorism, palpebral ptosis, flat nasal bridge, sparse eyebrows, and speech delay. Gesell development scale showed that the patient was global development retarded with a development level of 40 weeks. No o bvious abnormality was found in EEG but the MRI showed cerebral white matter abnormality. This patient was also diagnosed with neonatal thrombocytopenia in other hospital. Genomic CNVs were detected in this girl, and a 15.7Mb loss was found in the 11q23.3q25 region that covers JBS and PTS region. Conclusions Patient diagnosed with JBS and PTS often present with craniofacial abnormalities, cerebral white matter abnormality and neonatal thrombocytopenia. Chromosomal microarray analysis can help diagnosis.

OBJECTIVETo explore the therapeutic effect of Hejie Decoction (HJD) in treating chronic hepatitis B and its relationship with T-cell receptor V beta 7 (TCRV beta 7) gene expression.

METHODSForty-five patients of chronic hepatitis B were randomly divided into two groups. The 30 patients in the treated group were treated by HJD, and the 15 patients in the control group were treated by conventional western medicine. The therapeutic effect and changes of TCRV beta 7 gene expression after treatment were observed.

RESULTSAfter 6 months treatment, the ALT level in the two groups were obviously decreased (P < 0.01). No significant difference was shown in comparison of the total effective rate between the two groups but it did show in comparison of markedly effective rate between them. TCRV beta 7 expression was detected in 5 patients of the treated group, and HBV-DNA and HBeAg in the 5 patients were all negatively converted. While in the control group, no one had TCRV beta 7 expression detected, either no one with negative conversion of HBV-DNA and HBeAg. TCRV beta 7 could not be detected in all the patients whose HBV-DNA and HBeAg hasn't negatively converted, though their liver function could be normalized.

CONCLUSIONHJD might have the effect of regulation on TCRV beta 7 expression, it possibly is the important way for HBV replication inhibition and virucidal action of HJD.

Adolescent ; Adult ; Aged ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Genes, T-Cell Receptor beta ; genetics ; Hepatitis B e Antigens ; blood ; Hepatitis B, Chronic ; drug therapy ; genetics ; immunology ; Humans ; Male ; Middle Aged ; Phytotherapy ; Receptors, Antigen, T-Cell, alpha-beta ; biosynthesis ; genetics

Objective To analyze variations of hepatic vein in healthy people with 64-slice spiral CT.Methods Seventy-five healthy subjects underwent multi-slice spiral computed(MSCT)hepatic venography.The anatomy of the junction of the hepatic veins with the inferior vena cava and the intrahepatic drainage territory of the hepatic veins and tributaries were evaluated.The hepatic veins were classified according to three anatomic classification(Nakamura's,Marcos's and Kawasaki's classification)methods respectively.Results There was a common trunk of the middle and left hepatic veins before joining the IVC in 86.7%(65/75)of the cases.In 13.3%(10/75)of the cases,the three main hepatic veins joined the IVC separately.The ratios of Nakamura's classification type A,B,C of hepatic veins were 49.4% (37/75),37.3%(28/75),and 13.3%(10/75)respectively.The ratios of Marcos's classification type A,B,C of hepatic veins were 56.0%(42/75),24.0%(18/75),and 20.0%(15/75)respectively. The ratios of Kawasaki's classification type Ⅰ,Ⅱ of hepatic vein were 40.0%(30/75)and 60.0% (45/75).Conclusion Multi-slice spiral CT hepatic venography can provide visualization of peripheral hepatic venous branches in details.

Objective To construct an adenoviral vector carrying the gene encoding ciliary neurotrophic factor (CNTF). Methods The gene fragment encoding CNTF was amplified from pMEG-CNTF plasmid by PCR and the Psp-CNTF-IRES-GFP and PDC316-CNTF-IRES-GFP plasmids were constructed. Using PDC316-CNTF-IRES-GFP and PBHG plasmids, the Ad-CNTF-IRES-GFP vector was constructed, and the constructed vector was amplified, purified and identified in 293-LP cells. Ectopic overexpression of CNTF was induced using the constructed vector in human bone marrow-derived mesenchymal stem cells (MSCs) to investigate the role of CNTF in promoting remyelination. Results The Ad-CNTF-IRES-GFP vector was successfully constructed with a pfu of 2.3x1011. CNTF concentration in the MSCs transfeeted with Ad-CNTF-IRES-GFP vector was 20-fold higher than that in either non-transfected or Ad-EGFP-transfected MSCs. Conclusion The constructed Ad-CNTF-IRES-GFP vector allows CNTF overexpression in human MSCs by 20 folds, which provides a strategy for gene therapy targeting CNTF.